Статті в журналах: "697,1, 697.27"

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Agliano, Alice, Ines Martin-Padura, Paola Merighetti, Patrizia Mancuso, Cristina Rabascio, Leonard D. Shultz, and Francesco Bertolini. "Comparison of Three Different NOD/SCID-Related Strains in Preclinical Models of Acute Leukemia." Blood 108, no. 11 (November 1, 2006): 2361. http://dx.doi.org/10.1182/blood.v108.11.2361.2361.

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Abstract Transplantation of human acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) primary cells and cell lines in a variety of different strains of immunodeficient mice has led to preclinical models extensively used to investigate AML and ALL stem cells, biology, and drug sensitivity. We investigated the engraftment kinetics of two AML cell lines (HL-60 and KG-1), two ALL cell lines (MOLT-16 and 697) and AML primary cells from an AML M4 patient (QD1-EIO, described in Fusetti et al, Cancer Res 2000) in 3 different strains of NOD/LtSz-Prkdcscid (NOD/SCID, NS)-related immunodeficient mice. NS, NS/beta2 null (NSB) and NOD/SCID/IL-2Rgamma null (NSG) mice were injected ip with 10x106 AML or ALL cells. Mice were observed daily and sacrificed when leukemia-related symptoms were evident. Overall, leukemia-related symptoms were observed in 71, 84 and 86% of NS, NSB and NSG mice, respectively (n=42, p<0.01), after a median of 53, 49 and 35 days (p<0.001). Leukemia engraftment was investigated in the marrow, the blood and the spleen by means of morphology, flow cytometry and quantitative PCR for human genes. AML HL-60 and KG-1 cells accounted for 10-6, 5-1 and 7-3 % of peripheral blood cells in NS, NSB and NSG mice, respectively. ALL MOLT-16 and 697 cells accounted for 2-12, 22-27 and 1-27 % of blood cells in NS, NSB and NSG mice, respectively. AML primary cells QD1-EIO accounted for <1, <1 and 3% of blood cells in NS, NSB and NSG mice, respectively. Similar engraftment results were observed in the marrow and in the spleen. Leukemia cell-injected NSG mice, compared to NS and NSB, showed a significantly higher increase of circulating endothelial mature cells (CEC, enumerated by flow cytometry as CD45−, CD13+ VEGFR2+ cells) and progenitors (CEP, enumerated by flow cytometry as CD45−, CD13+ VEGFR2+ CD117+ cells, see Shaked et al, Cancer Cell 2005). This CEC and CEP increase paralleled leukemia engraftment. Taken together, our data indicate that the 3 different strains have significantly different leukemia engraftment behavior and kinetics. Engraftment in NSG mice is significantly faster compared to the other two strains, leukemia-related microenvironment is differently modulated, and less leukemic burden might be needed to observe leukemia-related symptoms. These data might have major implications to design future studies on leukemia-initiating stem cells, leukemia biology and preclinical leukemia treatment studies.

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Bugdayli, K., P. Ungprasert, K. J. Warrington, and M. Koster. "POS0800 VISUAL ISCHEMIA DURING RELAPSE AND FOLLOW-UP OF GIANT CELL ARTERITIS: A SYSTEMATIC REVIEW." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 652.2–652. http://dx.doi.org/10.1136/annrheumdis-2021-eular.697.

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Background:Visual ischemia (VI) is one of the most feared complications in giant cell arteritis (GCA). While the frequencies of VI development at or near diagnosis are better studied, limited information is available regarding the frequency of VI during relapse.Objectives:The purpose of this study was to characterize the frequency of visual ischemia (VI) as a manifestation of relapse or during follow-up in patients with GCA through performance of a systematic literature review.Methods:Potentially eligible studies were identified from Medline and EMBASE databases from inception to November 31, 2019 using a search strategy that comprised of terms for “giant cell arteritis,” “temporal arteritis,” or “Horton’s disease,” with “relapse,” “recurrence,” “flare,” “outcome,” “follow-up,” or “prognosis.” VI was defined as transient or permanent, full or partial, monocular or binocular visual field loss. VI occurring within 4 wks of GCA diagnosis was considered due to active disease and not included as a relapse event. Inclusion criteria used: (1) original research reported in English, (2) GCA definition provided, (3) VI outcome described as one of the following: (a) relapse rate/frequency denoting the presence or absence of VI, or (b) absolute number of VI events (> 4 weeks after GCA diagnosis) even if total cohort relapse rate/frequency was not provided. In order to reduce bias from under-reporting of negative results, studies that reported relapse rates/frequencies with accompanying relapse characteristics but did not provide initial detail regarding the presence/absence of VI were also identified. In such circumstances, the primary authors were directly contacted for patient-level data regarding VI and these studies were included in the final analysis if such data were available and provided.Results:A total of 913 unique articles were identified and underwent screening. Among these, 148 articles underwent independent full-text review by two physicians (K.B. and M.J.K). 33 articles met full inclusion criteria and an additional 21 articles included data on relapse but did not report VI patient data in the publication. Responses were received from authors of 11 of these 21 studies allowing for inclusion. 44 studies accounting for 3,649 patients with GCA were identified. Average percentage of baseline VI was 19% (range 0-66%). The average length of follow-up was 3.4 years (range 0.4 to 8.7). VI developing > 4 weeks after GCA diagnosis was recorded in a total of 53 patients (1.5%).Study-defined relapses were reported in 36 studies. A total of 1,215 patients with at least one or more relapses were recorded among 2,592 patients under observation (47%). Among these 36 studies, VI occurred in 37 patients (3.0%) with at least one study defined relapse event.Comparing trial design, retrospective studies (n=25) reported 27 of 2,718 (1%) patients developed VI during follow-up whereas 19 of 541 (3.5%) patients in randomized controlled trials (n=8) developed VI during the trial or post-trial follow-up.Conclusion:This report outlines the first systematic review evaluating VI as a manifestation of relapse and during follow-up in GCA. Overall, VI > 4 weeks after GCA diagnosis is uncommon (1.5%) but is noted in up to 3% of patients with at least one relapse event. Frequencies of reported VI were 3.5 times higher in randomized controlled trials compared to retrospective studies.Disclosure of Interests:Kubra Bugdayli: None declared, Patompong Ungprasert: None declared, Kenneth J Warrington Grant/research support from: Financial support for research from Kiniksa, Eli Lilly, Matthew Koster: None declared

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Gu, Yan, Chunhua Song, Sinisa Dovat, Qinglong Guo, Qinyu Ge, and Zheng Ge. "Oncogenesis of CRLF2 Overexpression and Effect of JAK2 Inhibitor in CRLF2 Overexpressed B-Cell Acute Lymphoblastic Leukemia." Blood 134, Supplement_1 (November 13, 2019): 2757. http://dx.doi.org/10.1182/blood-2019-125259.

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Backgroud: Cytokine receptor-like factor 2 (CRLF2) plays an important role in the development of normal B lymphocytes, which can mediate the proliferation of early B cells. However, the diect oncogenic effect of CRLF2 overexpression in acute lymhpoblastic leukemia (ALL) is far yet to be clarified. Here, we explored the effect of CRLF2 overexpression on cell proliferation and the effect of the novel JAK2 inhibitor on B-ALL cells with CRLF2 overexpression. Methods: The 83 patients with newly-diagnosed ALL (56 B-cell and 27 T-cell ALL; range from 14 to 77 years old) between June 2008 and June 2016 were studied at Zhongda Hospital Southeast University. The 21 normal bone marrow subjects were enrolled as controls. The qPCR method is developed for detection CRLF2 expression and the CRLF2 overexpression was determined with a cutoff value more than the highest sample of normal bone marrow control. Median differences between the cohorts were evaluated using a Mann-Whitney U-test. Frequency differences were analyzed using uni- and multivariate Cox model. Event-free survival (EFS) and overall survival (OS) were estimated by the Kaplan-Meier method and compared by log-rank test. CRLF2 F232C gain-of-function mutant which we previously reported or CRLF2 were expressed in Nalm6 and 697 B-ALL cells with lentiviral transduction. WST-1 cell proliferation assay and in vitro clonogenic assay were performed upon JAK2 inhibitor (BBT594) treatment. Nalm6-CRLF2-luc, Nalm6-F232C-luc, and Nalm6-vector-luc cells were injected via tail vein into the NSG mice. The leukemia engraftment was monitored once a week by living imaging. Results: The expression of CRLF2 in patietns with ALL was significantly higher than the normal control (P<0.0001). Patients with CRLF2 overexpression had a significantly higher WBC count (53*10^9/L vs. 29.5*10^9/L, P=0.041). Survival analysis showed that the patients with CRLF2 overexpression had a worse EFS and OS, the differences were statistically significant (11 months vs. 26 months, P=0.043 and 15 months vs. 32 months, P=0.015). Also, the CRLF2 expression is determined with flow cytometry after staining with FITC-CRLF2 antibody in 28 samples. The correlation analysis was performed on the CRLF2 expression detected by qPCR and flow cytometry, respectively. A significant positive correlation of the two methods was observed(r=0.957, P<0.0001). These data not only indicate that CRLF2 overexpression is a marker of poor outcome, but also reveal the qPCR might be a simple and quick method for screening CRLF2 overexpression in the clinic compared to flow cytometry which is commonly used. We further found that expression of CRLF2 or CRLF2 F232C mutant into Nalm6 and 697 B-ALL cells dramatically increase the CRLF2 mRNA level, which is 69 times than vector-only control. Moreover, CRLF2 or CRLF2 F232C significantly promotes the cell proliferation of Nalm6 and 697 cells compared to vector only (P<0.001). In addition, JAK2 inhibitor (BBT594) treatment showed the significant dose-dependent cell proliferation arrest and clonogenic inhibition in CRLF2 or CRLF2 F232C overexpressed Nalm6 and 697 cells compared to vector-only control. Furthermore, in vivo we observed the 5-fold higher signal intensity of leukemia engraftment in the mice injected with Nalm6-CRLF2-luc or Nalm6-F232C-luc compared to that of Nalm6-vector-luc control 1-3 weeks after the injection(P<0.001). The Nalm6-CRLF2-luc and Nalm6-F232C-luc infiltrations were observed in bone marrow, central nervous system, liver and spleen of the mice. Conclusion: We showed that CRLF2 overexpression could enhance the proliferation and infiltration of human B-ALL cells, and for the first time indicated that JAK2 inhibitor could suppress the cell proliferation and clonogenesis of the CRLF2 overexpressed B-ALL cells. Our data provide direct evidence of the oncogenic role of CRLF2 overexpression and the new therapeutic potential for targeting CRLF2 overexpressed B-ALL with JAK2 inhibitor. Disclosures No relevant conflicts of interest to declare.

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Biggs, JC, J. Szer, P. Crilley, K. Atkinson, K. Downs, A. Dodds, AJ Concannon, B. Avalos, P. Tutschka, and N. Kapoor. "Treatment of chronic myeloid leukemia with allogeneic bone marrow transplantation after preparation with BuCy2." Blood 80, no. 5 (September 1, 1992): 1352–57. http://dx.doi.org/10.1182/blood.v80.5.1352.1352.

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Abstract One hundred fifteen patients with chronic myelocytic leukemia (CML) were administered busulphan 4 mg/kg for 4 days and cyclophosphamide 60 mg/kg on each of 2 days (BuCy2) followed by allogeneic bone marrow transplantation from histocompatible sibling donors. For 62 patients in chronic phase, 26 in accelerated phase, and 27 in blast transformation, the actuarial survival at 3 years was 58%, 41%, and 25%, respectively. Actuarial probability of relapse was 3%, 12%, and 27%, respectively. Only two patients in chronic phase showed a transient cytogenetic relapse and one of these died from subsequent transplant-related complications, whereas the other remains cytogenetically normal 697 days posttransplant. Patients who were transplanted within 1 year of diagnosis in chronic phase had a survival of 70% compared with 40% when transplanted beyond 1 year from diagnosis. This significant difference in survival was due to transplant-related complications and was correlated with previous exposure to high doses of busulphan. This study indicates that BuCy2 is a useful conditioning regimen for marrow transplantation in patients with CML and results in similar survival statistics and transplant-related mortality as would be expected with conditioning regimens containing total body irradiation. It is possible that relapse after BuCy2 may be lower than expected with regimens containing total body irradiation, but larger analyses are required.

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Biggs, JC, J. Szer, P. Crilley, K. Atkinson, K. Downs, A. Dodds, AJ Concannon, B. Avalos, P. Tutschka, and N. Kapoor. "Treatment of chronic myeloid leukemia with allogeneic bone marrow transplantation after preparation with BuCy2." Blood 80, no. 5 (September 1, 1992): 1352–57. http://dx.doi.org/10.1182/blood.v80.5.1352.bloodjournal8051352.

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One hundred fifteen patients with chronic myelocytic leukemia (CML) were administered busulphan 4 mg/kg for 4 days and cyclophosphamide 60 mg/kg on each of 2 days (BuCy2) followed by allogeneic bone marrow transplantation from histocompatible sibling donors. For 62 patients in chronic phase, 26 in accelerated phase, and 27 in blast transformation, the actuarial survival at 3 years was 58%, 41%, and 25%, respectively. Actuarial probability of relapse was 3%, 12%, and 27%, respectively. Only two patients in chronic phase showed a transient cytogenetic relapse and one of these died from subsequent transplant-related complications, whereas the other remains cytogenetically normal 697 days posttransplant. Patients who were transplanted within 1 year of diagnosis in chronic phase had a survival of 70% compared with 40% when transplanted beyond 1 year from diagnosis. This significant difference in survival was due to transplant-related complications and was correlated with previous exposure to high doses of busulphan. This study indicates that BuCy2 is a useful conditioning regimen for marrow transplantation in patients with CML and results in similar survival statistics and transplant-related mortality as would be expected with conditioning regimens containing total body irradiation. It is possible that relapse after BuCy2 may be lower than expected with regimens containing total body irradiation, but larger analyses are required.

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LOOH, George Ashwehmbom, Fondzenyuy Cedric MANGEH (III), Xunwei WANG, and Xiushan WANG. "Performance Assessment of a Self-propelled Paddy Grain Thresher under Different Threshing Functional Parameters." Applied Engineering in Agriculture 36, no. 2 (2020): 141–49. http://dx.doi.org/10.13031/aea.13585.

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HighlightsThis research was aimed at assessing the performance of a self-propelled paddy grain thresher.Increasing cylinder speed increased the threshing percentage and percentage of broken grains of the machine.More broken grains were obtained at a lower concave clearance.The feed rate did not have much significance on the performance parameters that were evaluated. Abstract.This research was conducted to assess the performance of a self-propelled mini combine harvester, model number 4LZ-0.8 under different threshing functional parameters such as cylinder speed, concave clearance, and feed rate. An indoor experiment was conducted using the mini combine with an axial flow threshing cylinder and tangential feeding of material. These functional parameters were set at 5 levels each. The responses were obtained in terms of threshing percentage, percentage of unthreshed grains and percentage of broken grains. Response values were analyzed using the response surface tool (rstool) in MATLAB. Analysis of variance was done to determine the significant effects of the factor variations on the response values. MATLAB was used to present response surface graphs that were used to describe the variations of the responses as the factors changed from one level to the other. Results showed that with an increase in cylinder speed from 697 to 1202 rpm, the percentage of broken grains increased significantly from 0.0384% to 3.4052%, respectively. At cylinder speeds of 697 and 1202 rpm, the percentage of unthreshed grains increased from 0.1515% to 0.2162%, respectively. Furthermore, an increase in feed rate decreased the threshing percentage. The highest threshing percentage was obtained at an average concave clearance of 27 mm. Furthermore, it was realized that increasing the concave clearance from 18 to 35 mm, equally increased the percentage of unthreshed grains from 0.1478% to 0.3177%. The percentage of grain damage decreased from 3.2758% to 0.0268% with an increase in concave clearance from 18 to 35 mm, respectively. From the results obtained, it was tested and suggested that operating the threshing cylinder at a cylinder speed of 1100 rpm, concave clearance of 27 mm and feed rate of 0.9 kg s-1 offered the best machine performance. At these suggested values of the operating parameters, the threshing percentage was 99.9801%, the percentage of broken grains was 0.0134%, and the percentage of unthreshed grains was 0.0199%. Keywords: Assessment, Axial threshing unit, Cylinder speed, Concave clearance, Feed rate, Functional parameters, Threshing percentage.

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Pacora Portella, Percy. "Macrosomía fetal: Definición, Predicción, Riesgos y Prevención." Revista Peruana de Ginecología y Obstetricia 39, no. 17 (July 28, 2015): 42–50. http://dx.doi.org/10.31403/rpgo.v39i1633.

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Tradicionalmente la macrosomía fetal ha sido definida en base a un peso arbitrario. Sin embargo, la macrosomía fetal actualmente debe ser definida como el feto grande para la edad de gestación ( > percentil 90) en base al incrementado riesgo perinatal que presenta. En un estudio prospectivo que incluyó 1 697 gestaciones simples, 278 tuvieron fetos macrosómicos (GEG) y 1 336 fueron fetos de tamaño adecuado (AEG). Los factores predictivos de GEG en orden de especificidad fueron: ganancia ponderal excesiva (70%), feto de sexo varón (77%), grosor placentario > 4 cm (74%), edad mayor de 30 años (41,7%), obesidad (33,5%), antecedente de feto grande (27%), glicemia en ayunas > 79 mg/dl (21,6%), glucosa posprandial a las 2 horas > 110 mg/dl (20,7%), talla > 160 cm (20%), diabetes familiar (113,7%) y anemia (10,1 %). Las complicaciones maternas que debieran hacernos pensar en macrosomía fetal son ganancia ponderal excesiva, anemia, amenaza de aborto, placenta previa, polihidramnios, circular de cordón, hipertensión arterial asociada con ruptura prematura de membranas, labor disfuncional con enfoque de riesgo y el empleo de medidas de restricción calórica, insulina profiláctica y la inducción del parto antes de la semana 42, a fin de prevenir la macrosomía fetal.

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Asfandiyarova, Nailya S. "Risk factors of death in diabetes mellitus." Clinical Medicine (Russian Journal) 94, no. 9 (November 2, 2016): 697–700. http://dx.doi.org/10.18821/0023-2149-2016-94-9-697-700.

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Objective. To study risk factors of death in diabetes mellitus (DM). Materials and methods. This prospective cohort study included 337 patients with compromised carbohydrate metabolism (36 with impaired fasting glycemia or impaired glucose tolerance, 80 with type 1 diabetes, 194 with type 2 diabetes, 27 with diabetes due to chronic pancreatitis). Mean follow-up was 11.2±4.8 years (from 1 January 1995 through 31 December 2014). We investigated causes and risk factors of death in patients with impaired carbohydrate metabolism. Results. 115 patients died during the study period. The most common causes of death of patients with type 1 and 2 diabetes are cardiovascular diseases and cancer. Risk factors of death in type 1 DM include cardiovascular disease, diabetic nephropathy and retinopathy. Patients die at a younger age due to early onset of the disease. In type 2 diabetes risk factors of death are cardiovascular and oncologic diseases, nephropathy, the use of insulin. Patients die in elderly and senile age due to the late onset of diabetes. Gender differences in mortality associated with type 1 and 2 diabetes mellitus were not observed. Conclusion. Main causes of death in patients with type 1 and 2 DM are cardiovascular diseases and cancer. Risk factors of death include macro - and microvascular complications.

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Bentley, Robert F., Jeremy J. Walsh, Patrick J. Drouin, Aleksandra Velickovic, Sarah J. Kitner, Alyssa M. Fenuta, and Michael E. Tschakovsky. "Dietary nitrate restores compensatory vasodilation and exercise capacity in response to a compromise in oxygen delivery in the noncompensator phenotype." Journal of Applied Physiology 123, no. 3 (September 1, 2017): 594–605. http://dx.doi.org/10.1152/japplphysiol.00953.2016.

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Recently, dietary nitrate supplementation has been shown to improve exercise capacity in healthy individuals through a potential nitrate-nitrite-nitric oxide pathway. Nitric oxide has been shown to play an important role in compensatory vasodilation during exercise under hypoperfusion. Previously, we established that certain individuals lack a vasodilation response when perfusion pressure reductions compromise exercising muscle blood flow. Whether this lack of compensatory vasodilation in healthy, young individuals can be restored with dietary nitrate supplementation is unknown. Six healthy (21 ± 2 yr), recreationally active men completed a rhythmic forearm exercise. During steady-state exercise, the exercising arm was rapidly transitioned from an uncompromised (below heart) to a compromised (above heart) position, resulting in a reduction in local pressure of −31 ± 1 mmHg. Exercise was completed following 5 days of nitrate-rich (70 ml, 0.4 g nitrate) and nitrate-depleted (70 ml, ~0 g nitrate) beetroot juice consumption. Forearm blood flow (in milliliters per minute; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (in millimeters of mercury; finger photoplethysmography), exercising forearm venous effluent (ante-cubital vein catheter), and plasma nitrite concentrations (chemiluminescence) revealed two distinct vasodilatory responses: nitrate supplementation increased (plasma nitrite) compared with placebo (245 ± 60 vs. 39 ± 9 nmol/l; P < 0.001), and compensatory vasodilation was present following nitrate supplementation (568 ± 117 vs. 714 ± 139 ml ⋅ min−1 ⋅ 100 mmHg−1; P = 0.005) but not in placebo (687 ± 166 vs. 697 ± 171 min−1 ⋅ 100 mmHg−1; P = 0.42). As such, peak exercise capacity was reduced to a lesser degree (−4 ± 39 vs. −39 ± 27 N; P = 0.01). In conclusion, dietary nitrate supplementation during a perfusion pressure challenge is an effective means of restoring exercise capacity and enabling compensatory vasodilation. NEW & NOTEWORTHY Previously, we identified young, healthy persons who suffer compromised exercise tolerance when exercising muscle perfusion pressure is reduced as a result of a lack of compensatory vasodilation. The ability of nitrate supplementation to restore compensatory vasodilation in such noncompensators is unknown. We demonstrated that beetroot juice supplementation led to compensatory vasodilation and restored perfusion and exercise capacity. Elevated plasma nitrite is an effective intervention for correcting the absence of compensatory vasodilation in the noncompensator phenotype.

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Sri, Trisha, Eleanor Southgate, Sarah R. Kerry, Claire Nightingale, and Pippa Oakeshott. "Health-related quality of life and Chlamydia trachomatis infection in sexually experienced female inner-city students: a community-based cross-sectional study." International Journal of STD & AIDS 28, no. 4 (July 10, 2016): 367–71. http://dx.doi.org/10.1177/0956462416650095.

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This cross-sectional study was undertaken to compare health-related quality of life (EQ-5D) in women with and without undiagnosed Chlamydia trachomatis infection. We analysed data from 2401 multi-ethnic sexually active female students aged 16–27 years who were recruited to a randomised controlled trial of chlamydia screening – the prevention of pelvic infection trial in 2004–2006. At recruitment, all participants were asked to provide self-taken vaginal swabs for chlamydia testing and to complete a sexual health questionnaire including quality of life (EQ-5D). Most women (69%) had an EQ-5D of one representing ‘perfect health’ in the five dimensions: mobility, self-care, usual activities, pain/discomfort and anxiety/depression. We therefore compared the proportion of women with an EQ-5D score < 1 implying ‘less than perfect health’ in women with and without chlamydia infection, and women with symptomatic chlamydia versus the remainder. The proportion of women with EQ-5D score < 1 was similar in women with and without undiagnosed chlamydia: 34% (47/138) versus 31% (697/2263; RR 1.11, 95% CI 0.87 to 1.41). However, more women with symptomatic chlamydia had EQ-5D score < 1 than the remainder: 45% (25/55) versus 31% (714/2319; RR 1.47, CI 1.10 to 1.98). In this community-based study, EQ-5D scores were similar in women with and without undiagnosed chlamydia. However, a higher proportion of women with symptomatic chlamydia infection had ‘less than perfect health’. Undiagnosed chlamydia infection may not have a major short-term effect on health-related quality of life, but EQ-5D may not be the best tool to measure it in this group.

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Herbst, R. S., Y. Sun, S. Korfee, P. Germonpré, N. Saijo, C. Zhou, J. Wang, P. Langmuir, S. J. Kennedy, and B. E. Johnson. "Vandetanib plus docetaxel versus docetaxel as second-line treatment for patients with advanced non-small cell lung cancer (NSCLC): A randomized, double-blind phase III trial (ZODIAC)." Journal of Clinical Oncology 27, no. 18_suppl (June 20, 2009): CRA8003. http://dx.doi.org/10.1200/jco.2009.27.18_suppl.cra8003.

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CRA8003 Background: Vandetanib is a once-daily oral inhibitor of VEGFR, EGFR and RET signaling. Addition of vandetanib to docetaxel (doc) prolonged progression-free survival (PFS) in a randomized phase II study in patients (pts) with previously treated NSCLC (Heymach et al, JCO, 2007). Methods: The primary objective was to determine whether vandetanib 100 mg/day + doc 75 mg/m2 every 21 days (max 6 cycles) prolonged PFS vs placebo + doc. Secondary endpoints included overall survival, objective response rate (ORR), time to deterioration of symptoms (TDS) and safety. Efficacy and safety in females were assessed as a co-primary analysis population. Eligibility criteria included stage IIIB/IV NSCLC, PS 0–1, and previous first-line chemotherapy. Results: Between May 2006 and April 2008, 1,391 pts (mean age, 58 years; 30% female; 25% squamous; 10% brain mets) were randomized to vandetanib + doc (n=694) or placebo + doc (n=697). Baseline characteristics were similar in both arms. Median duration of follow-up was 12.8 months, with 87% patients progressed and 59% dead. Addition of vandetanib to doc showed a statistically significant improvement in PFS vs doc (hazard ratio [HR] 0.79, 97.58% CI 0.70–0.90; P<0.001), and a similar advantage in females (HR 0.79; P=0.024). Significant advantages for vandetanib + doc were also seen for ORR (17% vs 10%, P<0.001) and TDS (HR 0.78, P=0.002; FACT-L Lung Cancer Subscale). Overall survival showed a positive trend for vandetanib + doc that was not statistically significant (HR 0.91, 97.52% CI 0.78–1.07; P=0.196). The adverse event (AE) profile was consistent with that previously observed for vandetanib in NSCLC. Common AEs occurring more frequently in the vandetanib arm included diarrhea (42% vs 33%), rash (42% vs 24%) and neutropenia (32% vs 27%). Nausea (23% vs 32%), vomiting (16% vs 21%) and anemia (10% vs 15%) were less frequent in the vandetanib arm. The incidence of protocol-defined QTc prolongation was <2% in pts receiving vandetanib. Conclusions: The study met its primary objective of PFS prolongation with vandetanib + doc vs doc. Vandetanib is the first oral targeted therapy in phase III trials to show significant evidence of clinical benefit when added to standard chemotherapy in NSCLC. [Table: see text]

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Assaf-Balut, Carla, Nuria García de la Torre, Alejandra Duran, Manuel Fuentes, Elena Bordiú, Laura del Valle, Cristina Familiar, et al. "A Mediterranean Diet with an Enhanced Consumption of Extra Virgin Olive Oil and Pistachios Improves Pregnancy Outcomes in Women Without Gestational Diabetes Mellitus: A Sub-Analysis of the St. Carlos Gestational Diabetes Mellitus Prevention Study." Annals of Nutrition and Metabolism 74, no. 1 (December 14, 2018): 69–79. http://dx.doi.org/10.1159/000495793.

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Aims: The aim of the study was to evaluate the effect of a Mediterranean diet (MedDiet), enhanced with extra virgin olive oil (EVOO) and nuts, on a composite of adverse maternofoetal outcomes of women with normoglycemia during pregnancy. Methods: This was a sub-analysis of the St Carlos gestational diabetes mellitus Prevention Study. Only normoglycemic women were analysed (697). They were randomized (at 8–12th gestational weeks) to: standard-care control group (337), where fat consumption was limited to 30% of total caloric intake; or intervention group (360), where a MedDiet, enhanced with EVOO and pistachios (40–42% fats of total caloric intake) was recommended. The primary outcome was a composite of maternofoetal outcomes (CMFOs): at least having 1 event of emergency C-section, perineal trauma, pregnancy-induced hypertension and preeclampsia, prematurity, large-for-gestational-age and small-for gestational-age. Results: Crude relative risk showed that the intervention was associated with a significant reduction in the risk of CMFOs (0.48 [0.37–0.63]; p = 0.0001), with a number-needed-to-treat = 5. Risk of urinary tract infections, emergency C-sections, perineal trauma, large-for-gestational-age and small-for gestational age new-borns were also significantly reduced. Conclusion: A MedDiet, enhanced with EVOO and nuts, was associated with a risk reduction of CMFOs in over 50% in normoglycemic pregnant women. Therefore, it might be a potentially adequate diet for pregnant women. Trial registration: Identifier ISRCTN84389045. The study was registered on September 27, 2013. Last edited on September 26, 2018

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Elsayem, Ahmed F., Kelly W. Merriman, Carmen E. Gonzalez, Sai-Ching J. Yeung, Patrick S. Chaftari, Cielito Reyes-Gibby, and Knox H. Todd. "Presenting Symptoms in the Emergency Department as Predictors of Intensive Care Unit Admissions and Hospital Mortality in a Comprehensive Cancer Center." Journal of Oncology Practice 12, no. 5 (May 2016): e554-e563. http://dx.doi.org/10.1200/jop.2015.009019.

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Purpose: The identification of patients at high risk for poor outcomes may allow for earlier palliative care and prevent futile interventions. We examined the association of presenting symptoms on risk of intensive care unit (ICU) admission and hospital death among patients with cancer admitted through an emergency department (ED). Methods: We queried MD Anderson Cancer Center databases for all patients who visited the ED in 2010. Presenting symptoms, ICU admissions, and hospital deaths were reviewed; patient data analyzed; and risk factors for ICU admission and hospital mortality identified. Results: The main presenting symptoms were pain, fever, and respiratory distress. Of the patients with cancer who visited the ED, 5,362 (58%) were admitted to the hospital at least once (range, 1 to 13 admissions), 697 (13%) were admitted to the ICU at least once, and 587 (11%) died during hospitalization (31% of 233 patients with hematologic malignancies and 27% of 354 patients with solid tumors died in the ICU; P < .001). In multivariable logistic regression, presenting symptoms of respiratory distress or altered mental status; lung cancer, leukemia, or lymphoma; and nonwhite race were independent predictors of hospital death. Patients who died had a longer median length of hospital stay than patients discharged alive (14 v 6 days for hematologic malignancies and 7 v 5 days for solid tumors; P < .001). Conclusion: Patients with cancer admitted through an ED experience high ICU admission and hospital mortality rates. Patients with advanced cancer and respiratory distress or altered mental status may benefit from palliative care that avoids unnecessary interventions.

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14

Oran, B., A. Aleman, E. J. Shpall, C. Hosing, M. Korbling, P. Anderlini, R. Champlin, and M. Donato. "Higher Rate of Thrombotic Thrombocytopenic Pupura (TTP) Associated with Graft Versus Host Disease (GVHD) and Unrelated Donor Bone Marrow Transplantation (BMT)." Blood 106, no. 11 (November 16, 2005): 1111. http://dx.doi.org/10.1182/blood.v106.11.1111.1111.

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Abstract TTP is one of the complications of allogeneic hematopoietic stem cell transplantation (HSCT). In contrast to idiopathic cases, post-transplantation TTP may not be associated with severe von Willebrand factor-cleaving protease deficiency but rather a diffuse endothelial injury. Our aim was to define incidence, risk factors and mortality of TTP following allogeneic HSCT. 1312 patients with lymphoid malignancies (n=605), myeloid malignancies (n=688) or aplastic anemia (AA, n=18) who were treated with ablative preparative regimens (n=614) or reduced intensity regimens (n=697) followed by HSCT from an HLA matched related (MRD, n=694) or unrelated donor (MUD; n=461) and 1–3 antigen mismatched related (MMR, n=99) or unrelated donor (MMUD, n=57) between December 1997 and December 2004 were studied. Patients with prior allogeneic HSCT or graft failure were excluded. GVHD prophylaxis was tacrolimus-based in 1276 (97.3%) and cyclosporine based in 15 (1.1%) patients. Twenty patients did not receive GVHD prophylaxis per protocol. Anti-thymocyte-globulin (ATG) was added in 350 patients. Stem cell sources were bone marrow (n=626), peripheral blood (n=635) or cord blood (n=50). The following variables were evaluated: age, gender, primary diagnosis, disease status before HSCT, intensity of preparative regimen, stem cell source and acute GVHD(aGVHD) grade ≥2 (time dependent variable). Of the 1312 patients with a median follow-up from transplantation of 11.4 months (range, 5 days-7.2 years), 77 developed TTP (6%). The actuarial risk of developing TTP was 6.5% at 1 year. The median time of the onset of TTP was 67 days post HSCT (range, 11–1812) with 27 cases (35%) presenting after day 100. Female gender, lymphoid malignancies, unrelated or antigen mismatched related donor and aGVHD grade ≥2 were found to be independent risk factors. (Table1). Among the patients who had aGVHD grade≥2, the median time of interval between the onsets of two events was 25 days (range, 2–335 days). All patients were treated with therapeutic plasma exchange (PE). Of the 77 patients only 1 died of TTP (intracranial hemorrhage). The overall one-year survival after TTP was 29% and the most common cause of death were acute or chronic GVHD (n=35, 55%) and primary disease progression (n=10, 16%). Stem cell donors other than MRD, lymphoid malignancies and aGVHD≥2 have been established as risk factors associated with development of TTP and therapeutic PE has been shown to decrease TTP related mortality. Risk factors for TTP after allogeneic HSCT Variables sample size events HR 95% CI p Male 793 33 1.0 Female 518 44 2.2 1.3–3.6 0.002 Myleoid malignancy 688 33 1.0 Lymphoid malignancy 605 42 1.9 1.1–3.3 0.03 AA 18 2 1.3 0.2–8.0 0.75 MRD 694 28 1.0 MUD 461 40 2.9 1.6–5.1 <0.001 MMR 99 7 2.4 0.9–6.0 0.06 MMUD 57 2 1.7 0.4–7.6 0.5 aGVHD ≥2 370 39 3.3 2.0–5.5 <0.001

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15

Chance, Jenna A., Mike D. Tokach, Hilda I. Calderon, Jason C. Woodworth, Joel M. DeRouchey, and Robert D. Goodband. "245 Evaluation of Cellulose in Diets with and Without Added Zno on Nursery Pig Performance." Journal of Animal Science 99, Supplement_1 (May 1, 2021): 92–93. http://dx.doi.org/10.1093/jas/skab054.148.

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Abstract A total of 1,296 pigs (PIC L337×1050; initially 4.8 kg) were used in a 42-d study to evaluate cellulose in diets with and without pharmacological levels of Zn on nursery pig performance. Our hypothesis was that added fiber (cellulose) may provide more benefit in diets without ZnO. Pens were assigned to 1 of 4 dietary treatments in a RCBD by BW with 27 pigs/pen and 12 pens/treatment. Dietary treatments were arranged in a 2×2 factorial with main effects of cellulose (0 vs 1%; J. Rettenmaier USA, Schoolcraft, MI) and Zn (200 vs. 3,000 mg/kg in phase 1 and 110 vs. 2,000 mg/kg in phase 2). Treatment diets were formulated in two phases fed from d 0 to 7 and 7 to 21 with a common diet fed from d 21 to 42 post-weaning. Pig weights and feed disappearance were collected weekly to determine ADG, ADFI, and G:F. On d 16 or 17, fecal samples were collected from 3 pigs/pen to determine fecal DM, and all pens were visually evaluated for fecal consistency. There were no Zn×cellulose interactions. For the experimental and overall period, pigs fed diets containing added Zn had increased (P < 0.001) ADG, ADFI, G:F and BW while those that were fed cellulose had decreased (P < 0.05) ADG. For fecal dry matter, there was no evidence for difference (P >0.10) between any of the treatments but those fed added ZnO had visually firmer feces as evidenced by lower (P < 0.001) fecal scores. When fed a common diet from d 21 to 42, pigs previously fed added ZnO had increased (P < 0.001) ADG (502 vs. 523 g/d) and ADFI (697 vs. 734 g/d). In conclusion, there were no interactive effects between added cellulose and Zn; however, cellulose reduced ADG while the inclusion of pharmacological levels of Zn improved all growth criteria.

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16

Seward, F. D., R. M. Williams, Y. H. Chu, R. A. Gruendl, and J. R. Dickel. "ACHANDRAOBSERVATION OF SNR 0540 – 697." Astronomical Journal 140, no. 1 (June 8, 2010): 177–83. http://dx.doi.org/10.1088/0004-6256/140/1/177.

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17

Lucas, David M., Ellen J. Sass, Ryan B. Edwards, Li Pan, Gerard Lozanski, Nyla A. Heerema, John C. Byrd, A. Douglas Kinghorn, and Michael R. Grever. "Resistance to the Novel Translation Inhibitor Silvestrol Is Mediated by Elevated Mcl-1 Expression." Blood 114, no. 22 (November 20, 2009): 1737. http://dx.doi.org/10.1182/blood.v114.22.1737.1737.

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Abstract Abstract 1737 Poster Board I-763 We previously reported the efficacy and B-cell selectivity of the natural product silvestrol in acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL), using both primary cells and B-cell lines. We also showed that silvestrol inhibits translation, resulting in rapid depletion of the short half-life protein Mcl-1 followed by mitochondrial damage and apoptosis. Cencic et al. reported that silvestrol directly blocks translation initiation by aberrantly promoting interaction of eIF4A with capped mRNA (PLoS One 2009; 4(4):e5223). However, the loss of Mcl-1 in breast and prostate cancer cell lines is delayed relative to what we observe in B-leukemias (48 hr vs. 4-6 hr in CLL and ALL cells). Additionally, silvestrol does not reduce Mcl-1 expression in normal T-cells to the same extent that it does in B-cells, potentially explaining in part the relative resistance of T-cells to this agent. We therefore investigated cell-type differences, as well as the importance of Mcl-1, in silvestrol-mediated cytotoxicity. We incubated the ALL cell line 697 with gradually increasing concentrations of silvestrol to generate a cell line (697-R) with resistance to 30 nM silvestrol (IC50 of parental 697 < 5 nM). No differences between 697-R and the parental line were detected upon detailed immunophenotyping. However, cytogenetic analysis revealed a balanced 7q;9p translocation in 697-R not present in the parental 697 cell line that may be related to the emergence of a resistant clone. We also detected no difference in expression of multi-drug resistance proteins MDR-1 and MRP, which can contribute to resistance to complex amphipathic molecules such as silvestrol. In contrast, we found that baseline Mcl-1 protein expression is strikingly increased in 697-R cells relative to the parental line, although these cells still show similar percent-wise reduction in Mcl-1 upon re-exposure to 80 nM silvestrol. To investigate whether this resistance to silvestrol is reversible, 697-R cells were maintained without silvestrol for 6 weeks (∼18 passages). During this time, viability remained near 99%. Cells were then treated with 30 nM silvestrol. Viability was 94% at 48 hr post-treatment and returned to 99% within a week, while parental 697 cells with the same treatment were completely dead. Baseline Mcl-1 levels remained elevated in 697-R even with prolonged silvestrol-free incubation. These results indicate that the resistance phenotype is not rapidly reversible, as is seen with transient upregulation of multi-drug resistance or stress-response proteins. Additionally, silvestrol moderately induces the transcription of several pro-apoptotic Bcl-2 family members and results in elevated levels of these proteins despite its translation inhibitory activity. Interestingly, no such activity is detected in silvestrol-treated normal T-cells. Together, these results support the hypothesis that in B-cells, silvestrol induces cell death by altering the balance of pro- and anti-apoptotic factors, and that increased Mcl-1 protein can force the balance back toward survival. This work further underscores the importance of Mcl-1 in silvestrol-mediated cytotoxicity. We are now investigating the mechanism of Mcl-1 upregulation in 697-R cells to identify a factor or pathway that can be targeted therapeutically to circumvent resistance. Silvestrol is currently undergoing preclinical pharmacology and toxicology investigation by the U.S. National Cancer Institute Drug Development Group at the Stage IIA level to facilitate its progression to Phase I clinical testing. Disclosures No relevant conflicts of interest to declare.

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18

Li, P., X. X. Wu, Z. Y. Wang, H. H. Ho, Y. X. Wu, Z. C. Mao, and Y. Q. He. "First Report of Ralstonia solanacearum Causing Bacterial Wilt of Yacon in China." Plant Disease 96, no. 6 (June 2012): 904. http://dx.doi.org/10.1094/pdis-11-11-0940-pdn.

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Yacon (Smallanthus sonchifolius) is an important cash crop in Yunnan Province, China. In 2003, yacon was introduced to Yunnan province as a novelty root crop and as an experimental source of natural sugars; now more than 15 provinces cultivate the crop. Yunnan is one of the major yacon producing areas of China, with up to 10,000 ha yielding up to 50,000 t of yacon, which is nearly half of the production in China. In April and May 2010, bacterial wilt of yacon was observed in the fields of Lion Mountain of Wuding County, Yunnan Province, China. In 2011, the disease occurred in approximately 1 ha of yacon, resulting in 10% crop loss in that area. The initial symptoms observed were irregular, black, necrotic lesions on leaf margins. After 4 to 7 days, leaves became totally necrotic, plants wilted, and black stripes were observed on plant stems. Within 2 to 3 weeks, more than 70% of leaves within the crop were wilted. Subsequently, the plants died and stems became brittle. When dead plants were pulled from the soil, tubers were found to have turned black. When diseased stems and/or petioles were cut with a sterile sharp knife or razor blade, bacterial ooze appeared on the cut ends. High populations of morphologically uniform bacteria were isolated from the diseased plants by conventional methods. When cultured on TZC (2,3,5-Triphenylte tetrazolium chloride) agar medium (3), colonies were large, elevated, fluidal, and entirely white with a pale red center. The isolated bacterium was gram-negative, grew aerobically, and did not form endospores. The cells were 0.5 to 0.7 × 1.5 to 2.0 μm and nonencapsulated. Ralstonia solanacearum was identified and confirmed as the pathogen on the basis of morphological and physiological characteristics, pathogenicity test, and 16S rDNA sequence analysis (1,4). The nucleotide sequence is available in GenBank (Accession No. HQ176322.1). The pathogenic strain belonged to race 1 and biovar 3 according to the pathogenicity and carbohydrate utilization tests (2). Koch's postulates were tested in the greenhouse, with 10 plants inoculated per species. Plants were inoculated with 15 μl of cell suspension containing 106 to 107 CFU ml–1 deposited into the third axilla with a capillary tube. The bacteria could infect tomato, pepper, tobacco, potato, common sage (Salvia dugesii Fernald), and patchouli, and caused typical symptoms of wilt and black lesions, but could not infect leaves of swamp mahogany (Eucalyptus robusta Smith), stramonium (Dature stramonium Datura L.), ginger, or maize. To our knowledge, this is the first report of yacon as a host of R. solanacearum. Since the pathogen has a wide host range, monitoring of the vegetation in and around yacon fields should be implemented as a mandatory management measure to prevent disease spread. References: (1) C. A. Boucher et al. J. Bacteriol. 169:5626, 1987. (2) A. C. Hayward. J. Appl. Bacteriol. 27:265, 1964. (3) A. Kelman. Phytopathology 44:693, 1954. (4) W. G. Weisburg et al. J. Bacteriol. 173:697, 1991.

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19

Miyashita, T., and JC Reed. "Bcl-2 oncoprotein blocks chemotherapy-induced apoptosis in a human leukemia cell line." Blood 81, no. 1 (January 1, 1993): 151–57. http://dx.doi.org/10.1182/blood.v81.1.151.151.

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Abstract Previous studies have shown that the bcl-2 gene encodes a mitochondrial protein that contributes to neoplastic cell expansion primarily by promoting cell survival through interference with “programmed cell death” (PCD), also termed “apoptosis.” Because many chemotherapeutic drugs are capable of initiating pathways leading to apoptosis, we determined whether deregulated bcl-2 expression could render cells resistant to several drugs commonly used in the treatment of non- Hodgkin's lymphomas, including dexamethasone (DEX), methotrexate (MTX), 1-beta-D-arabinofuranosyl-cytosine (Ara-C), etoposide (VP-16), vincristine (VC), cisplatin (CP), and hydroperoxycyclophosphamide (4- HC). For these experiments, we achieved high levels of p26-Bcl-2 protein production in a human pre-B-cell leukemia line 697 by stable infection with a recombinant bcl-2-containing retrovirus and then compared these cells with control virus-infected 697 cells. Control 697 cells were induced to undergo apoptosis by all drugs tested as defined by DNA degradation into oligonucleosomal-length fragments, cell shrinkage, and subsequent cell death. In contrast, 697 cells with elevated Bcl-2 protein levels exhibited strikingly prolonged cell survival and markedly reduced DNA fragmentation when cultured in the presence of these antineoplastic agents. Although high levels of Bcl-2 protein protected 697 cells from the acute cytotoxic effects of DEX and the other drugs tested, Bcl-2 did not prevent these drugs from suppressing the proliferation of 697 cells. However, when 697 cells were treated with DEX or MTX for 3 days, then washed and cultured in semisolid media without drugs, bcl-2-virus-infected cells gave rise to colonies at much higher frequencies than 697 cells stably infected with control virus. These results indicate that by protecting 697 leukemic cells from the acute cytotoxicity of DEX and some other chemotherapeutic drugs, high levels of p26-Bcl-2 can create the opportunity for re-initiation of cell growth when drugs are withdrawn. The findings may be relevant to clinical correlative studies of non- Hodgkin's lymphoma patients that have found an association between worse prognosis and bcl-2 gene rearrangements or t[14;18] translocations.

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20

Miyashita, T., and JC Reed. "Bcl-2 oncoprotein blocks chemotherapy-induced apoptosis in a human leukemia cell line." Blood 81, no. 1 (January 1, 1993): 151–57. http://dx.doi.org/10.1182/blood.v81.1.151.bloodjournal811151.

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Previous studies have shown that the bcl-2 gene encodes a mitochondrial protein that contributes to neoplastic cell expansion primarily by promoting cell survival through interference with “programmed cell death” (PCD), also termed “apoptosis.” Because many chemotherapeutic drugs are capable of initiating pathways leading to apoptosis, we determined whether deregulated bcl-2 expression could render cells resistant to several drugs commonly used in the treatment of non- Hodgkin's lymphomas, including dexamethasone (DEX), methotrexate (MTX), 1-beta-D-arabinofuranosyl-cytosine (Ara-C), etoposide (VP-16), vincristine (VC), cisplatin (CP), and hydroperoxycyclophosphamide (4- HC). For these experiments, we achieved high levels of p26-Bcl-2 protein production in a human pre-B-cell leukemia line 697 by stable infection with a recombinant bcl-2-containing retrovirus and then compared these cells with control virus-infected 697 cells. Control 697 cells were induced to undergo apoptosis by all drugs tested as defined by DNA degradation into oligonucleosomal-length fragments, cell shrinkage, and subsequent cell death. In contrast, 697 cells with elevated Bcl-2 protein levels exhibited strikingly prolonged cell survival and markedly reduced DNA fragmentation when cultured in the presence of these antineoplastic agents. Although high levels of Bcl-2 protein protected 697 cells from the acute cytotoxic effects of DEX and the other drugs tested, Bcl-2 did not prevent these drugs from suppressing the proliferation of 697 cells. However, when 697 cells were treated with DEX or MTX for 3 days, then washed and cultured in semisolid media without drugs, bcl-2-virus-infected cells gave rise to colonies at much higher frequencies than 697 cells stably infected with control virus. These results indicate that by protecting 697 leukemic cells from the acute cytotoxicity of DEX and some other chemotherapeutic drugs, high levels of p26-Bcl-2 can create the opportunity for re-initiation of cell growth when drugs are withdrawn. The findings may be relevant to clinical correlative studies of non- Hodgkin's lymphoma patients that have found an association between worse prognosis and bcl-2 gene rearrangements or t[14;18] translocations.

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21

Wrobleski, Shirley, Chris Longo, Patricia Bedard, Neelu Kaila, George Shaw, Frank Londy, Suzan Rohrer, et al. "Resolution of venous thrombosis using a novel oral small-molecule inhibitor of P-selectin (PSI-697) without anticoagulation." Thrombosis and Haemostasis 97, no. 03 (2007): 400–407. http://dx.doi.org/10.1160/th06-11-0658.

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SummaryP-selectin inhibition has been shown to decrease thrombogenesis in multiple animal species. In this study, we show that a novel oral small-molecule inhibitor of P-selectin, PSI-697, promotes thrombus resolution and decreases inflammation in a baboon model of venous thrombosis. Experimental groups consisted of the following: 1) primates receiving a single oral dose of PSI-697 (30 mg/kg) daily starting three days pre-iliac vein balloon occlusion, and continued for six days; 2) primates receiving a single treatment dose of a low-molecular-weight-heparin (LMVVH) (1.5 mg/kg) daily starting one day pre-iliac balloon occlusion, and continued for six days; and 3) primates receiving a single oral dose of a vehicle control daily starting three days pre-iliac vein balloon occlusion, and continued for six days. Animals receiving PSI-697, although thrombosed after balloon deflation, demonstrated greater than 80% vein lumen opening over time, with no opening (0%) for vehicle control (p<0.01). LMVVH opening evident after balloon deflation slightly deteriorated overtime compared to PSI-697. PSI-697 therapy also significantly decreased vein wall inflammation determined by magnetic resonance venography (MRV). Importantly, this beneficial opening occurred without measured anticoagulation. Animals receiving PSI-697 demonstrated significantly increased plasma D-dimer levels versus LMVVH and control animals six hours post thrombus induction (p<0.01). This study is the first to demonstrate the effectiveness of oral P-selectin inhibition to modify venous thrombogenesis, increase vein lumen opening, and decrease inflammation in a large animal model.

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Biswas, Sabyasachi, Andrew P. Mone, Chandan K. Sen, Natarajan Muthusamy, and John C. Byrd. "Arsenic Trioxide and Ascorbic Acid Enhances the Cytotoxicity of Hu1D10 towards CLL Cells." Blood 104, no. 11 (November 16, 2004): 3479. http://dx.doi.org/10.1182/blood.v104.11.3479.3479.

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Abstract Hu1D10 (apolizumab), a humanized HLA-DR beta-chain-specific antibody directed to the 1D10 antigen, has been shown to be cytotoxic towards primary B-cell chronic lymphocytic leukemia (CLL) cells and is currently in clinical trials for this disease. Other second generation HLA-DR antibodies are also in late pre-clinical development at this time. We previously reported that in vitro Hu1D10 treatment of CLL cells resulted in generation of reactive oxygen species (ROS); however, antioxidant treatment did not modulate the cytotoxicity observed. It is known that CLL cells have a compromised antioxidant defense system, as evident from the low activities of the major antioxidant enzymes superoxide dismutase and catalase, and the accumulation of degradation products like malonaldialdehyde and 8-oxo-deoxyguanosine. Therefore, we hypothesized that CLL cells would be susceptible to damage by ROS generating agents, and that ROS generating agents would enhance the cytotoxicity of Hu1D10. Furthermore, CLL cells are reported to have high concentrations of the antioxidant glutathione (GSH), thus we expect GSH depletion by buthionine sulfoximine (BSO) treatment to enhance the cytotoxicity of Hu1D10. Arsenic trioxide (ATO), an agent that is approved for treatment of relapsed acute promyelocytic leukemia, is believed to exert its cytotoxicity through the generation of ROS and thiol depletion. The efficacy of ATO is enhanced by ascorbic acid. At high concentrations, ascorbic acid is also capable of generating ROS . We found that ATO was cytotoxic to both CLL cells and the 697 B-cell line in a dose dependant manner. Ascorbic acid alone was cytotoxic to CLL cells and 697 cells at very high doses, but not at 1mM. As a sole agent, ATO at clinically relevant concentrations (0.5 – 2 μM) was not cytotoxic towards 697 or CLL cells at 24 hrs; however, ATO (1 μM) in combination with 1mM ascorbic acid was toxic toward 697 cells as measured by annexin V-FITC/propidium iodide staining with FACS analysis (viability in Control = 94.5% ± 1.1, ATO + ascorbate = 31.7% ± 0.8). We found a similar cytotoxic response in two primary CLL cell samples treated with ATO (1 μM) + ascorbic acid (1 mM) [CLL-1 viability in Control = 64.4% ± 0.3, ATO + ascorbate = 12.3% ± 0.2; CLL-2 viability in Control = 83.3 ± 0.2, ATO + ascorbate = 30.9% ± 0.3]. Depletion of glutathione by BSO enhanced ATO/ascorbate cytotoxicity in 697 cells by 40%. However, this treatment was less effective in enhancing the cytotoxicity of Hu1D10 in 697 cells (8.7% increase). We next investigated whether ATO/ascorbate co-administration would be able to enhance the cytotoxicity of Hu1D10 as hypothesized. The addition of ATO (1 μM) and ascorbic acid (1 mM) enhanced the cytotoxicity of Hu1D10 towards 697 cells and CLL cells (viability in 3 CLL patients are: Control = 73.2% ± 10.5, Hu1D10 = 43.8% ± 16, Hu1D10 + ATO/ascorbate = 20.2% ±11). Combination treatment of CLL cells or 697 cells with ATO and ascorbic acid is cytotoxic at clinically relevant concentrations. Furthermore, the toxicity of Hu1D10 toward CLL and 697 cells is increased by the addition of ATO and ascorbic acid. These results suggest that ATO and ascorbic acid alone, or in combination with the antibody Hu1D10 could emerge as effective therapies for the treatment of CLL.

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23

Rycerz, L., and M. Gaune-Escard. "Phase Diagram of the TbBr3-KBr Binary System." Zeitschrift für Naturforschung A 59, no. 1-2 (February 1, 2004): 84–90. http://dx.doi.org/10.1515/zna-2004-1-212.

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The phase equilibrium of the TbBr3-KBr has been established by Differential Scanning Calorimetry. This system has the three compounds K3TbBr6, K2TbBr5, and KTb2Br7 and two eutectics located at (χTb = 0.163 (885 K) and (χTb = 0.433 (697 K). K3TbBr6 undergoes a solid-solid phase transition at 691 K and melts congruently at 983 K with the corresponding enthalpies 8.0 and 48.0 kJ mol−1. K2TbBr5 melts incongruently at 725 K, and KTb2Br7 at 741 K. The latter forms at 694 K, a temperature very close to that (697 K) of one of the two eutectics also existing in the binary system.

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24

Liang, Der-Cherng, Lee-Yung Shih, Chao-Ping Yang, Iou-Jih Hung, Hsi-Che Liu, Tang-Her Jaing, Ting-Chi Yeh, et al. "The Frequencies of ETV6-RUNX1 Fusion and Hyperdiploidy (>50 chromosomes) in Children with Acute Lymphoblastic Leukemia Are Lower in Far East Than the West.." Blood 114, no. 22 (November 20, 2009): 3064. http://dx.doi.org/10.1182/blood.v114.22.3064.3064.

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Abstract Abstract 3064 Poster Board III-1 Both ETV6-RUNX1 (TEL-AML1)fusion and hyperdiploidy (>50 chromosomes) of lymphoblasts are favorable outcome predictors in childhood acute lymphoblastic leukemia (ALL). In 433 children with ALL diagnosed at our hospitals between 1997 and 2007 in Taiwan, the frequency of ETV6-RUNX1 fusion was 15.8%, and the frequency of hyperdiploidy (>50 chromosomes) was 14.1%, both were lower than those of the West. While ETV6-RUNX1 fusion had borderline favorable impact on outcome (p=0.053-0.061), hyperdiploidy showed significant favorable impact on event-free survival (91.1% vs 76.6 %, p= 0.016) in our patients. A meta-analysis from literature enrolled reports in which the case numbers and frequency of ETV6-RUNX1 fusion or hyperdiploidy in childhood ALL were described. It revealed that the frequency of ETV6-RUNX1 fusion in childhood ALL in Far East (Japan, Korea, Hong Kong, Chinese in Singapore, and Taiwan) was 14.2% (127/893, range 10-17%), significantly lower than 21.8% (152/697, range 19-27%) in the West (USA, Germany, Italy, France and Chile) (p < 0.0001). The frequency of hyperdiploidy in Japan and Taiwan was 15.2% (140/921, range 13-20%), significantly lower than 31.6% in the West (977/3,158, range 19-34%) (USA, UK and Germany) (p < 0.0001). So far as we know, there were several articles, including ours, addressing that the frequency of ETV6-RUNX1 fusion in childhood ALL was lower in a Far East country. This is the first meta-analysis to demonstrate that the frequency of ETV6-RUNX1 fusion in childhood ALL in Far East was lower than that in the West. There was no report on that the frequency of hyperdiploidy in Far East was lower than that in the West. This is also the first meta-analysis to demonstrate that the frequency of hyperdiploidy in childhood ALL in Far East is significantly lower than that in the West. The nature of these differences, probably due to racial, needs further study. In Far East, with both a lower frequency of ETV6-RUNX1 fusion, and a lower frequency of hyperdiploidy, it warrants renewed effort to cure a higher proportion of children with ALL. Disclosures No relevant conflicts of interest to declare.

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25

Lambert, D. H., L. Levy, V. A. Mavrodieva, S. B. Johnson, M. J. Babcock, and M. E. Vayda. "First Report of Potato mop-top virus on Potato from the United States." Plant Disease 87, no. 7 (July 2003): 872. http://dx.doi.org/10.1094/pdis.2003.87.7.872a.

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Potato mop-top virus (PMTV) is a tripartite pomovirus vectored by the powdery scab plasmodiophoromycete Spongospora subterranea pv. subterranea (1). PMTV occurs on potato (Solanum tuberosum) in Europe, the Andes, Asia, and Canada. Internal necrotic arc and fleck tuber symptoms (“spraing”) may reduce commercial acceptance of some cultivars (3). PMTV symptoms were discovered in ‘Shepody’ tubers at the Aroostook Research Farm, Presque Isle, ME in May 2002 and subsequently in ‘Russet Burbank’ tubers in commercial storage from the 2001 Maine crop. Symptomatic tubers exhibited single or multiple concentric necrotic arcs that were partial or complete, but exhibited no distinct external symptoms. The presence of PMTV in eight ‘Shepody’ tubers was indicated by positive enzyme-linked immunosorbent assay (ELISA; Adgen, Ltd., Auchincruive, Ayr, Scotland) and confirmed by reverse transcription polymerase chain reaction (RT-PCR). ‘Russet Burbank’ potatoes were visually diagnosed, and the corresponding halves of 128 symptomatic tubers were forwarded to the University of Maine and APHIS (Beltsville, MD). Of these, ELISA readings in Maine were strongly positive (>3 × background) for 88, ambiguous (1.5-3 × background) for 13, and negative for 27. Subsamples from these three categories were positive by PCR in 17 of 17, 9 of 9, and 12 of 14 cases, respectively. A similar rating, positive or ambiguous, in ELISA testing was identical for all but one case at Beltsville. Confirmation of PMTV required PCR testing, resulting in a characteristic PCR product of 401 bp that was generated from the coat protein coding region on RNA 2 (2) using the primer pair PMTV 1 5′-GCAGCCGTCGAGAATAGATA-3′ (RNA nucleotides 316–335) and PMTV 4 5′-GCGAGTTGATGTGCC ACATT-3′ (complementary to RNA 2 nucleotides 716–697). An immunocapture RT-PCR using this primer set and the coating antibody from the Adgen ELISA kit was also successful in detecting PMTV. In separate reactions, a second product of 646 bp was generated from the triple gene block on RNA 3 (4) using the primer pair PMTV 5 5′-GGTGAACACGAGGACAAGGT-3′ (RNA 3 nucleotides 1417–1436) and PMTV 7 5′-AACAGTCCGGTCTTGTGAAC-3′ (complementary to RNA 3 nucleotides 2063–2044). The sequence of these products was 98 to 100% identical to PMTV published sequences. The discovery of this virus will result in adjustments to U.S. and Canadian seed potato certification standards and symptom characterization for common North American cultivars. References: (1) R. A. C. Jones and B. D. Harrison. Ann. Appl. Biol 63:1, 1969. (2) S. Kashiwazak et al. Virology 206:701, 1995. (3) M. Sandgren et al. Am. J. Potato Res. 79:205, 2002. (4) K. P. Scott et al. J. Gen. Virol.75:3561, 1994.

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Jasuja, Reema, Sunita Patel Hett, Neelu Kaila, and Debra Pittman. "Effect of PSI697, a Small Molecule Inhibitor of P-Selectin, in the Townes Model of Sickle Cell Disease." Blood 126, no. 23 (December 3, 2015): 3391. http://dx.doi.org/10.1182/blood.v126.23.3391.3391.

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Abstract Chronic vaso-occlusion is a major cause of morbidity and mortality in patients with sickle cell disease (SCD). Persistent vaso-occlusion can damage lungs, liver, kidneys or brain and ultimately lead to end-organ dysfunction. Vaso-occlusive pain crisis is a complex multistep process, initiated by adhesion of fragile sickle erythrocytes and rigid neutrophils to hypoxic and inflamed endothelium. Large multicellular aggregates of blood cells, including platelets and sickled erythrocytes, form on these adherent activated neutrophils in the microcirculation, ultimately causing vascular occlusion and tissue ischemia. Inflammatory mediators, such as P-selectin, play a key role in mediating these heterocellular interactions and attract additional leucocytes to the site of occlusion. P- and E-selectin mediate rolling and tethering of blood cells on the endothelium. Here, we explore cellular and animal models of sickle cell disease to assess PSI-697, an orally active small molecule antagonist of P-selectin. PSI-697 inhibits P-selectin binding to P-selectin glycoprotein ligand-1 (PSGL-1) with an IC50 of 50-125 µM (Bedard et al, JPET, 2008). Townes SCD mice were used to assess the efficacy for PSI-697 in preventing vaso-occlusion in SCD. Mice were randomized to treatment with vehicle or PSI-697. Animals were treated in a prophylactic setting prior to the surgical preparation. Surgical preparation induces a well described acute inflammatory response in the microcirculation associated with neutrophil adhesion to the endothelium and formation of multicellular aggregates. Alexa-488 labeled Ly-6G neutrophil antibody and Dylight-649 labeled CD42c platelet antibody were injected to quantify adherent neutrophils and neutrophil-platelet aggregates. Cremaster microvasculature was observed by intravital microscopy. Mice treated with 100 mg/kg of P-selectin inhibitor PSI-697 showed a 55% reduction in adherent neutrophils and a 78% decrease in the number of neutrophil-platelet aggregates compared to vehicle treated animals. Neutrophils showed ~7 fold increase in rolling velocity in mice treated with P-selectin inhibitor. Our results demonstrate that prophylactic administration of PSI-697, a small molecule P-selectin antagonist, improved parameters associated with vaso-occlusion in Townes SCD mice. Disclosures No relevant conflicts of interest to declare.

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Hackett, Benjamin, Varun Badami, Sunil Sharma, and Robert Stansbury. "697 Sleep Quality After COVID-19 Infection." Sleep 44, Supplement_2 (May 1, 2021): A272—A273. http://dx.doi.org/10.1093/sleep/zsab072.695.

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Abstract Introduction COVID-19 has proven to be a novel virus with significant complications to an expanding number of body systems. Hallmark characteristics of COVID-19 include substantial inflammatory response which has been linked to sleep dysregulation in previous studies. We examined the change in sleep quality after acute COVID-19 infections requiring hospitalization. Methods We performed a retrospective, single-center observational study of 20 patients with acute COVID-19 infection requiring hospitalization. Eligible patients were contacted and completed telephone surveys of the Pittsburgh Sleep Quality Index (PSQI) prior to and 1 month after hospital discharge. A score of ≥5 was indicative of poor sleep quality. Secondary data were collected from EMR. Results The mean PSQI prior to COVID-19 infection was 6.1, worsening to 10.3 one month after acute infection, denoting a delta-PSQI of 4.2 (p = 0.0004). There were noted statistically significant differences in certain components of the PSQI including: subjective sleep quality 0.8 to 1.7 (delta 0.9, p = 0.0003), sleep latency 1.25 to 1.85 (delta 0.6, p = 0.03), sleep disturbance 1.05 to 1.5 (delta 0.45, p = 0.0009), and daytime dysfunction 0.3 to 1.45 (delta 1.15, p = 0.0005). Sleep latency and daytime dysfunction accounted for the most change. Two groups declared themselves with 6 of the 20 patients having improvement/no change in PSQI, and 14 having worsening. Between these groups certain differences were seen including: Pre-infection PSQI 9.67 vs 4.57 (p = 0.009), delta global PSQI -0.83 vs 6.36 (p < 0.001), delta subjective sleep quality 0.17 vs 1.2 (p = 0.002), delta sleep latency -0.3 vs 1 (p = 0.01), delta sleep duration -0.3 vs 0.93 (p = 0.02), delta sleep efficiency -0.3 vs 0.71 (p = 0.02), and delta daytime dysfunction 0.17 vs 1.57 (p = 0.006). Conclusion In our study of patients hospitalized for COVID-19 infection specific components of sleep were different following infection. Sleep latency and daytime dysfunction contributed the most to PSQI change. Two groups declared themselves based on PSQI improvement vs worsening. Those with poor sleep prior to infection continued to have poor sleep, while those without prior sleep troubles developed worsened sleep quality. Support (if any):

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Michael C. J. Putnam. "Regina Aurea (Aen. 1. 697–98)." Illinois Classical Studies 43, no. 1 (2018): 176. http://dx.doi.org/10.5406/illiclasstud.43.1.0176.

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Myung, I. S., J. K. Choi, J. Y. Lee, M. J. Yoon, E. Y. Hwang, and H. S. Shim. "First Report of Bacterial Leaf Spot of Witloof, Caused by Pseudomonas cichorii in Korea." Plant Disease 97, no. 10 (October 2013): 1376. http://dx.doi.org/10.1094/pdis-04-13-0436-pdn.

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In August 2011, bacterial leaf spot was observed on witloof (Cichorium intybus L. var. foliosum) grown in a commercial field with 15% incidence in Injae, Korea. Symptoms on leaves included irregular brown to reddish brown spots in the center. Bacterial streaming from the lesions was observed microscopically. Bacterial isolates (BC3286, BC3287, and BC3308-BC3310) were recovered on Trypticase soy agar from lesions surface-sterilized in 70% ethyl alcohol for 30 s. The isolates were gram negative, urease negative, fluorescent on King's B agar, and had aerobic rods with 2 to 6 polar flagella. Pathogenicity tests were separately performed in different greenhouses located in Suwon (National Academy of Agricultural Science) and Chuncheon (Gangwondo Agricultural Research and Extension Services) in Korea. Pathogenicity was confirmed by spray inoculation of healthy, 10-day-old leaves of witloof plants (two plants/isolate) with a suspension of original field isolate (106 CFU/ml). Sterile distilled water was used as negative control. The inoculated plants were incubated in a growth chamber (25°C and 95% relative humidity [RH]) overnight, then transferred to a greenhouse at 23 to 27°C and 60 to 70% RH. Characteristic leaf spot symptoms were observed on inoculated witloof plants 8 days after inoculation. No symptoms were observed on control plants. The bacterium reisolated from the inoculated leaves was confirmed by analyzing sequence of the gyrB gene with direct sequencing method of PCR products using primers gyr-F and gyr-R (2). The sequence of reisolated bacteria shared 100% similarity with inoculated ones. In LOPAT (1) tests, all isolates and the reference strain of Pseudomonas cichorii CFBP2101T (=BC2595) were levan negative, oxidase positive, potato rot negative, arginine dihydrolase negative, and tobacco hypersensitivity positive, indicative of group III (–, +, –, –, +) of fluorescent pseudomonads. The 16S rRNA (1,408 bp), and gyrB (676 bp) regions were sequenced to aid in identification of the original field isolates as well as P. cichorii CFBP 2101T (=BC2595) using reported sets of PCR primers, fD1/rP2 and gyr-F/gyr-R, respectively (2,4). Phylogenetic analyses based on partial sequences of the gyrB and the 16S rRNA of Psudomonas spp. available in GenBank, the reference strain of P. cichorii CFBP2101T (=BC2595), and the witloof field isolates were conducted using the neighbor-joining method with Juke-Cantor model of distance calculation in MEGA version 5.1 (3). The isolates and the reference strain of P. cichorii CFBP2101T (=BC2595) was clustered in one group with P. cichorii strains in both phylogenetic trees based on the two sequences. Sequences of the 16S rRNA region had a distance index value ranging from 0.000 to 0.001 between the reference strain of P. cichori CFBP2101T (GenBank JX913784) and the field isolates (JX913785 to JX913789), and ranged from 0.000 to 0.001 within the field isolates. Sequences of the gyrB region had a distance index value ranging 0.029 to 0.033 between the reference strain (JX913790) and the field isolates (JX913791 to JX913795), and ranged from 0.000 to 0.041 within the field isolates. To our knowledge, this is the first report of bacterial leaf spot of witloof caused by P. cihorii in Korea. P. cichorii has a wide host range, and an important economic impact on vegetables. The disease is expected to result in a significant economic impact on root production of witloof in Korea. References: (1) R. A. Lelliott et al. J. Appl. Bacteriol. 29:470, 1966. (2) H. Sawada et al. J. Mol. Evol. 49:627, 1999. (3) K. Tamura et al. Mol. Biol. Evol. 28:2731, 2011. (4) W. G. Weinsburg et al. J. Bacteriol. 173, 697, 1991.

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Li, Ding-You, Pierre Hardy, Daniel Abran, Ana-Katherine Martinez-Bermudez, Anne-Marie Guerguerian, Mousumi Bhattacharya, Guillermina Almazan та ін. "Key role for cyclooxygenase-2 in PGE2 and PGF2α receptor regulation and cerebral blood f low of the newborn". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, № 4 (1 жовтня 1997): R1283—R1290. http://dx.doi.org/10.1152/ajpregu.1997.273.4.r1283.

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Ibuprofen, a cyclooxygenase (COX) inhibitor nonselective for either COX-1 or COX-2 isoform, upregulates cerebrovascular prostaglandin E2(PGE2) and PGF2α receptors in newborn pigs. COX-2 was shown to be the predominant form of COX and the main catalyst of prostaglandin synthesis in the newborn brain. We proceeded to establish direct evidence that COX-2-generated prostaglandins govern PGE2 and PGF2α receptor density and function in the cerebral vasculature of the newborn. Hence, we determined PGE2 and PGF2α receptor density and functions in brain vasculature by using newborn pigs treated with saline, ibuprofen, COX-1 inhibitor (valerylsalicylate), or COX-2 inhibitors (DUP-697 and NS-398). Newborn brain PGE2 and PGF2α concentrations were significantly reduced by ibuprofen, DUP-697, and NS-398 but not by valerylsalicylate. In newborn pigs treated with DUP-697, NS-398, and ibuprofen, PGE2 and PGF2α receptor densities in brain microvessels were increased to adult levels; there was also a significant increase in inositol 1,4,5-trisphosphate (IP3) production and cerebral vasoconstrictor effects of 17-phenyl trinor PGE2(EP1 receptor agonist), M&B-28767 (EP3 receptor agonist), PGF2α, and fenprostalene (PGF2αanalog). Treatment with ibuprofen or DUP-697 also increased the upper blood pressure limit of cerebral cortex and periventricular blood flow autoregulation from 85 to ≥125 mmHg (uppermost blood pressure studied). However, valerylsalicylate treatment did not affect cerebrovascular PGE2 and PGF2α receptors, IP3 production, or vasoconstrictor effects in newborn animals. These in vivo and in vitro observations indicate that COX-2 is mainly responsible for the regulation of PGE2 and PGF2α receptors and their functions in the newborn cerebral vasculature.

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Noyer, Jacques. "Michel Watin (Dir.) : Communication et espace public – Univers créoles 1." Études de communication, no. 25 (December 1, 2002): 169–72. http://dx.doi.org/10.4000/edc.697.

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Linger, Rachel M. A., Deborah DeRyckere, Luis Brandão, Kelly K. Sawczyn, Amy K. Keating, and Douglas K. Graham. "Synergistic Killing of E2A-PBX1+ B-ALL Cells by Chemotherapeutic Agents and MerTK Inhibition." Blood 112, no. 11 (November 16, 2008): 2843. http://dx.doi.org/10.1182/blood.v112.11.2843.2843.

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Abstract Acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy. Although cure rates have increased in recent years, significant risk of both short- and long-term toxicities persists including a 25% incidence of a severe late effect in pediatric cancer survivors. Thus, novel and less toxic therapies are needed. Most pediatric leukemias are of the B-cell lineage and a subset of these express the fusion protein E2A-PBX1 as a result of the chromosomal rearrangement t(1;19). A previous DNA microarray study suggested that the receptor tyrosine kinase Mer (MerTK) is aberrantly expressed in E2A-PBX1+ B-ALL (Yeoh et al., 2002, Cancer Cell 1:133–143). Within the hematopoietic lineages, MerTK is expressed in dendritic cells, monocytes/macrophages, NK cells, NKT cells, megakaryocytes, and platelets. However, MerTK is not expressed in normal lymphocytes. In studies of T-cell ALL, we have previously shown that ectopic expression of MerTK contributes to leukemogenesis. MerTK is known to activate anti-apoptotic signaling proteins such as Akt and Erk 1/2. These data led us to hypothesize that abnormal expression and activation of MerTK may provide a survival advantage for leukemia cells. Furthermore, inhibition of MerTK may enhance the sensitivity of leukemia cells to cytotoxic agents. In this study, we extended the findings of Yeoh et al. (2002) by confirming the ectopic expression of MerTK mRNA and protein in patient samples and human cell lines of E2A-PBX1+ B-ALL. In subsequent studies, we used lentiviral short hairpin RNA (shRNA) contructs to knockdown MerTK in the human E2A-PBX1+ B-ALL cell line, 697. In vitro assays of cell proliferation and survival demonstrated that inhibition of MerTK significantly increased the sensitivity of 697 cells to numerous chemotherapeutic agents. For example, when wildtype or non-silencing shRNA control (shControl) 697 cells were treated with 6-mercaptopurine (6-MP), an IC50 could not be determined because the cells were robustly resistant to killing with this agent. However, the MerTK knockdown lines demonstrated remarkable sensitivity (IC50 values ~ 4 μM) to 6-MP. In other cases, the wildtype/shControl 697 lines were sensitive to treatment with chemotherapeutic agents but a dramatic increase in sensitivity was observed with MerTK inhibition. These results were acquired via an assay of metabolically active cells which precludes determination of the contribution of changes in cell proliferation and cell death. To more specifically evaluate the role of cell death, we performed flow cytometric analysis of cells stained with propidium iodide and YO-PRO®-1. These experiments revealed that inhibition of MerTK results in increased induction of cell death in response to treatment with chemotherapeutic agents. Western blotting was used to compare the signaling pathways activated in shControl versus MerTK knockdown 697 cells following treatment with chemotherapeutic agents. Inhibition of MerTK leads to loss of ERK 1/2 and mTOR signaling in 697 cells. Further investigation demonstrated that inhibition of MerTK also correlates with robust activation of apoptotic proteins in response to treatment with chemotherapeutic agents. Specifically, cleavage of both Caspase 8 and Caspase 9 was observed suggesting that inhibition of MerTK permits activation of both intrinsic and extrinsic apoptosis pathways in response to treatment with chemotherapeutic agents. Taken together, these in vitro results suggest that inhibition of MerTK may increase the efficacy of standard chemotherapy and thereby allow for dose reduction and decreased toxicity. To demonstrate proof of concept in an in vivo setting, we evaluated the oncogenicity of wildtype, shControl and MerTK knockdown 697 cells in a mouse xenograft model of leukemia. We found that MerTK inhibition significantly delayed the onset of disease. Animals which received wildtype or shControl 697 cells exhibited median survival of 22 and 26 days, respectively. Median survival was significantly increased to 63 days for each of two clonal MerTK knockdown lines (P<0.0001). Our results demonstrate that MerTK is a novel biological target for treatment of leukemia and possibly a spectrum of other cancers known to aberrantly express MerTK.

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Gylling, Helena, David E. Laaksonen, Mustafa Atalay, Maarit Hallikainen, Leo Niskanen, and Tatu A. Miettinen. "Markers of absorption and synthesis of cholesterol in men with type 1 diabetes." Diabetes/Metabolism Research and Reviews 23, no. 5 (2007): 372–77. http://dx.doi.org/10.1002/dmrr.697.

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Zhang, Suping, Lin Song, Na Yuan, Weiwei Lin, Yan Cao, Fei Xu, Yixuan Fang, et al. "Autophagy Collaborates with Ubiquitination to Down-Regulate Oncoprotein E2A/Pbx1 in B Cell Acute Lymphoblastic Leukemia." Blood 124, no. 21 (December 6, 2014): 5276. http://dx.doi.org/10.1182/blood.v124.21.5276.5276.

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Abstract Background: B cell acute lymphoblastic leukemia (B-ALL) accounts for the most cancer incidences in children. The t(1;19) translocation leukemia accounts for a quarter of pre-B ALL and up to 5% of all ALL patients, in which the transcriptional activator E2A and homeobox pre-B-cell leukemia transcription factor 1 (PBX1) fuses, resulting in expression of the chimeric transcription factor E2A/PBX1. E2A/PBX1 has been proved to be an oncogene and could induce malignant transformation. Methods: (1) Childhood B-ALL patients were collected and the stem/progenitor cells (CD34+CD38-) and leukemia cells (CD19+) were sorted with BD FACS Aria III. The autophagy level in these cells was measured by real-time Q-PCR, including gene expression of Beclin1, Atg7, Atg5, LC3 and p62. Normal bone marrow cells from healthy donors were used as control. (2) E2A/PBX1 fusion gene positive pre-B ALL 697 cells were used to establish leukemia mouse model and the autophagy activity in the mice was enhanced by administration of rapamycin. Mice were sacrificed three weeks post treatment, leukemia phenotype was then identified and E2A/PBX1 oncoprotein of liver was detected by western blotting. (3) Autophagy and ubiquitination were manipulated with inhibitors or starvation in 697 cells and the degradation mechanism of E2A/PBX1 was explored. Co-localization of E2A/PBX1-LC3 and E2A/PBX1-Ub was observed by confocal microscopy and quantified by Amnis image flow cytometry. Results: (1) B-ALL primary cells from childhood patients show down-regulated level of autophagy. (2) The NOD-SCID mouse model study shows that activating autophagy of mice by rapamycin improved the survival of leukemia animals, prevented leukemiagenesis by inhibition on the transplanted leukemia cells (examined by blood cell counting, liver HE staining and expression of CD 45, 10, 19 from transplanted human 697 cells by flow cytometry), promoted the degradation of oncoprotein E2A/PBX1 (by Western blotting)), and more importantly, restored hematopoietic stem cells (LSKCD34- cell number detected by flow cytometry). (3) The ALL 697 cell line study shows that activation of autophagy by rapamycin and starvation could down-regulate E2A/PBX1 expression detected by flow cytometry and western blotting. The confocal microscopic results show co-localization of E2A/PBX1 with autophagy marker GFP-LC3 in both rapamycin and starvation treatment groups. To confirm the degradation mechanism, autophagy inhibitor (3-MA or Baf-A1) and ubiquitin-proteasome inhibitor (MG132) were used to treat 697 cells. The results show that inhibition of autophagy in the early stage by 3-MA fails to degrade E2A/PBX1 in 697 cells, but ubiquitination also contributes to the degradation of E2A/PBX1. Quantitative analysis shows increased co-localization percentage of E2A/PBX1-LC3 in rapamycin and starvation treatment groups and increased co-localization of E2A/PBX1 with Ubiquitin in starvation group; but MG132 treatment inhibited the co-localization of E2A/PBX1-Ub induced by starvation, indicating a collaborative role between autophagy and ubiquitination in the degradation of E2A/PBX1. Conclusions: B-ALL primary cells from patients show low autophagy activity; Autophagy activation fights against B-ALL by inhibition on transplanted leukemia cells, degradation of oncoprotein E2A/Pbx1 and restoration of hematopoietic stem cells in the NOD-SCID B-ALL mouse model; autophagy collaborates with ubiquitination in the degradation of E2A/PBX1 in the 697 cells, thereby proposing a novel strategy for targeted therapy on childhood B-ALL. Disclosures No relevant conflicts of interest to declare.

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Sonnenday, Christopher J., Daniel S. Warren, Sara K. Cooke, Harry C. Dietz, and Robert A. Montgomery. "A novel chimeric ribozyme vector produces potent inhibition of ICAM-1 expression on ischemic vascular endothelium." Journal of Gene Medicine 6, no. 12 (2004): 1394–402. http://dx.doi.org/10.1002/jgm.697.

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Donmez, D., B. Keleşoğlu, Z. C. Karahan, S. Sezer, M. E. Yayla, M. Torgutalp, E. G. Aydemir Gülöksüz, G. Kinikli, T. M. Turgay, and A. Ates. "AB0495 SERUM HIGH MOBILITY GROUP BOX-1 LEVEL IN PATIENTS WITH BEHCET’S SYNDROME AND ITS RELATIONSHIP WITH DISEASE ACTIVITY AND CLINICAL FEATURES." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1545–46. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4232.

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Background:Behcet’s Syndrome (BS) is a chronic, multisystemic inflammatory disease. High Mobility Group Box-1 (HMGB-1) is a nuclear protein and acts as a proinflammatory molecule. The serum HMGB-1 levels were found high in various chronic inflammatory diseases.Objectives:In this cross-sectional study, serum HMGB-1 levels in patients with BS and healthy controls were studied. Also, its association with disease activity scores and clinical findings in BS were evaluated.Methods:Between March 2018 and March 2019, 90 BS patients and 50 age-sex matched healthy controls were included. Disease activity scores were assessed by using Behcet Disease Current Activity Form (BDCAF) and Behcet Syndrome Activity Score (BSAS). A p-value of <0.05 was considered to be statistically significant.Results:The demographic and clinical features were summarized in Table 1. Serum HMGB-1 levels were significantly higher in BS than those in control group.(Table 1) The statistically significant corelation of serum HMGB-1 level with current clinical findings was found only in patients having eryhtema nodosum and genital ulcers in the last 1 month. The eye, central nervous system (CNS), gastrointestinal system (GIS), arterial and venous involvements were classified together as major organ involvement (MOI) (n=47). The serum HMGB-1 level was higher in patients with MOI compared to patients without MOI; however,it was not statistically significant.(40.5pg/mL and 37.2 pg/mL, p=0.560) BDCAF and BSAS scores were positively corelated with serum HMGB-1 level (p=0.022, p=0.026 respectively). (Table 2)Table 1.Demographic features and HMGB-1 levels of study groups with current clinical findings of BS patientsBehcet SyndromeControl GroupP valueAge (years) (±SD)42.1±9.639.5±10.60.128Sex (Women) n(%)51 (56.7)32 (64)0.401Disease Duration (years)10 (1-37)Serum HMGB-1 level (pg/mL)43.26 (0-221.3)16.730-41.9)<0.001Oral Ulcers n(%)100 (100.0)Genital Ulcers n(%)68 (75.6)Erythema Nodosum n(%)52 (57.8)Papulopustuler Eruption n(%)59 (65.6)Patergy pozitivity n(%)37 (41.1)Uveitis n(%)27 (30.0)Retinal vasculitis2 (2.2)CNS involvement n(%)7 (7.8)GIS involvement n(%)2 (2.2)Athralgia n(%)75(83.3)Arthritis n(%)15 (16.7)Arterial disease n(%)3 (3.3)Venous disease n(%)25 (27.8)Table 2.Corelation between Serum HMGB-1 level and inflammatory markers in BDHMGB-1rpESR (mm/h)-0,040.68CRP (mg/L)0,120.23Neutrophil/Lymphocyte0,140.20Platelet/Lymphocyte0,020.89BSAS0,240.02BDCAF0,240.03Conclusion:The two studies evaluating the relationship between serum HMGB-1 level and disease activity in BS found higher levels of serum HMGB-1 level in BS than in healthy controls as in our study1,2. This result supports the importance of HMGB-1 in the development of BS through its role in inflammation. De Souza et al. found no association between BDCAF and serum HMGB-1 level; whereas, we found a positive correlation with both BDCAF and BSAS2. This suggests that HMGB-1 can be used as a new disease activity parameter in BS. In conclusion, this study is unique as it involves the largest number of BS patients and uses BDCAF and BSAS together to assess disease activityReferences:[1]Ahn, J.K., et al., Extracellular high-mobility group box 1 is increased in patients with Behcet’s disease with intestinal involvement. Journal of Korean medical science, 2011. 26(5): p. 697-700.[2]de Souza, A.W., et al., High mobility group box 1 serum levels are increased in Behcet’s disease, but not associated with disease activity or disease manifestations. Rheumatology, 2015. 54(12): p. 2151-2155.Disclosure of Interests:None declared

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des Rivières-Pigeon, Catherine, Marie-Josèphe Saurel-Cubizolles, and Patrizia Romito. "Division of domestic work and psychological distress 1 year after childbirth: a comparison between France, Quebec and Italy." Journal of Community & Applied Social Psychology 12, no. 6 (November 2002): 397–409. http://dx.doi.org/10.1002/casp.697.

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Amenedo, E., C. Perchet, F. Perrin, and L. Garcia-Larrea. "697 Neurophysiological and behavioural interference caused by mobile phone conversations." International Journal of Psychophysiology 30, no. 1-2 (September 1998): 263–64. http://dx.doi.org/10.1016/s0167-8760(98)90696-1.

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39

Desbois, C., and P. Jalinot. "Int-6, nouveau constituant des corps nucléaires contenant PML, est délocalisée par la protéine Tax du virus HTLV-1." médecine/sciences 12, no. 12 (1996): 1450. http://dx.doi.org/10.4267/10608/697.

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Hogenschurz, Johannes. "Fristverlängerung zur Anspruchsbegründung nach Widerspruch gegen den Mahnbescheid?" Monatsschrift für Deutsches Recht 68, no. 18 (September 20, 2014): 1055–56. http://dx.doi.org/10.9785/mdtr-2014-1807.

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AbstractDie Angst des Anwalts vor der Fristversäumung führt reflexartig zum Fristverlängerungsantrag. Der folgende Beitrag zeigt, warum dieser Aufwand bei der Frist für die Anspruchsbegründung gem. § 697 Abs. 1 S. 1 ZPO nach vorangegangenem Mahnbescheid und Widerspruch schlecht investiert ist und zur folgenlosen Ablehnung führen muss.

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Lewis, Simon G. "The Holocene evolution of the London Thames. Archaeological excavations (1991-1998) for the London Underground Limited Jubilee Line Extension Project, J. Sidell, K. Wilkinson, R. Scaife and N. Cameron, Museum of London Archaeology Service Monograph no. 5, 2000 (144 pp) ISBN 1-901992-10-1." Journal of Quaternary Science 17, no. 8 (2002): 799–800. http://dx.doi.org/10.1002/jqs.697.

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Burns, Peter C. "X-ray powder diffraction data for the identification of boracite-group minerals." Powder Diffraction 10, no. 4 (December 1995): 250–60. http://dx.doi.org/10.1017/s0885715600014925.

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An X-ray powder-diffraction pattern for boracite, Mg3B7O13Cl, is reported. Boracite is orthorhombic, space group Pca21, and the refined unit-cell parameters are a=8.557(6), b=8.553(8), c= 12.09(1) Å. X-ray powder-diffraction patterns have been calculated for the boracite-group minerals boracite, ericaite, trembathite and congolite. The calculated pattern for boracite is in good agreement with the observed pattern reported here, but the PDF entry (5-710) for boracite is missing several intense peaks. The calculated pattern for ericaite is in poor agreement with the PDF entry (29-697) for ericaite, and PDF 29-697 is for congolite, not ericaite. The calculated powder patterns presented here for these four minerals will facilitate their identification via X-ray powder diffraction. © 1995 International Centre for Diffraction Data.

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Nunes, Suzana Gilioli. "Capacidade de Absorção do Conhecimento e a Comunicação com o Ambiente Externo: Uma Análise em Empresas de Palmas/TO." Revista Observatório 1, no. 1 (September 30, 2015): 123. http://dx.doi.org/10.20873/uft.2447-4266.2015v1n1p123.

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O objetivo principal desta pesquisa foi avaliar a capacidade de absorção do conhecimento organizacional, tendo como uma das suas dimensões a comunicação com o ambiente externo. Foi desenvolvida uma pesquisa de caráter quantitativo com cem empresas pertencentes aos setores de comércio e de serviços, localizadas na cidade de Palmas, TO. O questionário aplicado envolveu a utilização de uma escala da capacidade de absorção do conhecimento, desenvolvida por Matusik e Heeley (2005). Os autores avaliam que a capacidade de absorção é composta de múltiplas dimensões: 1) relação da empresa com seu ambiente externo, 2) a estrutura, as rotinas de conhecimentos, e o grupo principal de criação de valor e, 3) absorção de habilidades individuais. Os resultados demonstraram que as empresas pesquisadas possuíam alto grau de predominância de relacionamento com o ambiente.Palavras-chave: Capacidade de Absorção do Conhecimento; Conhecimento; Comunicação com o ambiente externo. ABSTRACTThe main objective of this research was to evaluate the absorption capacity of organizational knowledge, having as one of its dimensions communication with the external environment. One quantitative study with a hundred companies belonging to the trade and service sectors has been developed, located in the city of Palmas, TO. The questionnaire involved the use of a range of absorption capacity of the knowledge developed by Matusik and Heeley (2005). The authors estimate that the absorption capacity is made up of multiple dimensions: 1) the company's relationship with its external environment, 2) the structure, routines of knowledge, and the main group of value creation and, 3) absorption of individual skills . The results showed that the surveyed enterprises had a high degree of dominance relationship with the environment.Keywords: Absorption Capacity of Knowledge; Knowledge; Communication with the external environment. RESUMENEl principal objetivo de esta investigación fue evaluar la capacidad de absorción de conocimiento organizacional, teniendo como una de sus dimensiones de comunicación con el ambiente externo. Un estudio cuantitativo con un centenar de empresas pertenecientes a los sectores de comercio y servicios se ha desarrollado, que se encuentra en la ciudad de Palmas, TO. El cuestionario implicó el uso de una gama de capacidad de absorción del conocimiento desarrollado por Matusik y Heeley (2005). Los autores estiman que la capacidad de absorción se compone de múltiples dimensiones: 1) la relación de la empresa con su entorno externo, 2) la estructura, las rutinas de conocimiento, y el grupo principal de la creación de valor y, 3) la absorción de las capacidades individuales . Los resultados mostraron que las empresas encuestadas tenían un alto grado de relación de dominación con el medio ambiente.Palabras clave: Capacidad de absorción de conocimiento; el conocimiento; la comunicación con el ambiente externo. REFERÊNCIASCOHEN,W. M., LEVINTHAL, D. A. Absorptive capacity: A new perspective on learning and innovation. Administrative Science Quarterly, v. 35: 128-152, 1990.CRADWELL, D. The Norton history of technology. London: Norton.1995.FELDMAN, M. S.; PENTLAND, B., T. Reconceptualizing organizational routines as a source of flexibility and change. Administrative Science quarterly, v. 48, n. 1, 94-118, 2003.FLATTEN, T.; BRETTEL, M.; ENGELEN, A.; GREVE G. A measure of absorptive capacity: Development and validation. Academy of Management Proceedings Volume: 2009, Publisher: Academy of Management, Pages: 1-7, 2009.GOES, J. B.; PARK, S. H. Interorganizational links and innovation: The case of hospital services. Academy of Management Journal, v. 40: 673-697, 1997.GREVE, H.R. Exploration and exploitation in product innovation. Industrial and Corporate Change, 1-31, may, 2007.HUBER, G. P. Organizational learning: The contributing processes and the literatures. Organization Science, v. 2:88-115, 1991.JANSEN, J.J.P., VAN DEN BOSCH, F.A.J.; VOLBERDA, H.W. Exploratory innovation, exploitative innovation, and performance: Effects of organizational antecedents and environmental moderators. Management Science, v. 52, 1661-74, 2006.KIM, L. Crisis construction and organizational leanirg: capability bulding in catchinp-up at HyaundayMotor. Organization Science, 9: 506-521, 1998.KOGUT, B.; ZANDER, U. Knowledge of the firm, combinative capacidades and the replication of technology. Organization Studies, v. 3, p. 383-397, 1992.KHOJA, F. AND MARANVILLE, S. How do firms nurture absorptive capacity? Journal of Managerial Issues, Vol. 12, No. 2, pp. 262-278, 2010..LANE, P. J. LUBATKIN, M. Relative absorptive capacity and interorganizational learning. Strategic Management Journal, v.19, n. 5, 461-477. 1998.LEONARD-BARTON, D. Wellsprings of knowledge: Building and sustaining the source of innovation. Boston: Harvard Business School Press, 1995.MATUSIK, S.F.; HEELEY, M.B. Absorptive capacity in the software industry: Identifying factors that affect knowledge and knowledge creation activities. Journal of Management, v. 31, n.4, p. 549-572, 2005.MATUSIK, S. F.; HILL, C.W. L. The utilization of contingent work, knowledge creation, and competitive advantage., Academy of Management Review, v. 23: 680-697, 1998.NONAKA, I. A dynamic theory of organizational knowledge creation. Organization Science, v. 5: 14-37, 1994.NONAKA, I. TAKEUCHI, H. The knowledge-creating company: How japanese companies create the dynamics. Oxford: Oxford University Press. 1995.ROSA, A. C. ; RUFFONI, Janaina . Mensuração da Capacidade Absortiva de Empresas que possuem Interação com Universidades. Economia e Desenvolvimento (Santa Maria), v. 26, p. 80-104, 2014.ROXAS, B. Clarifying the link between social capital and MSME innovation performance: the role of absorptive capacity, Asia-Pacific social science review, vol. 7, no. 1, pp. 31-51, 2007.WAHYUNI, S.; SUDHARTIO, L. How to increase local partners' bargaining power and absorptive capacity in joint ventures? Global Management Journal. Vol. 2, n. 1, 86-93, 2010.ZAHRA, S. A., GEORGE, G. Absorptive capacity: A review, reconceptualization, and extension. Academy of Management Review, v. 27, n. 2, 185-203, 2002.ZANDER, U.; KOGUT, B. Knowledge and the speed of the transfer and imitation of organizational capabilities: An empirical test. Organization Science, v. 6, n. 1: 76-92, 1995. Disponível em:Url: http://opendepot.org/2720/ Abrir em (para melhor visualização em dispositivos móveis - Formato Flipbooks):Issuu / Calameo

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Buchanan, Alec. "Mental Health: The New Law. By Phil Fennell. Jordan Publishing Limited, 21 St Thomas Street, Bristol BS1 6JS, 2007, 646 pp. Paperback, ISBN 978‐1‐84661‐074‐5." Criminal Behaviour and Mental Health 18, no. 3 (July 2008): 203–5. http://dx.doi.org/10.1002/cbm.697.

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Sanchez-Bilbao, L., M. J. García-García, D. Martínez-López, M. Rivero-Tirado, B. Castro, I. González-Mazón, J. Crespo, M. A. González-Gay, and R. Blanco. "POS1376 UVEITIS IN 1449 PATIENTS WITH INFLAMMATORY BOWEL DISEASE. STUDY FROM A SINGLE UNIVERSITY CENTER." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 970.1–970. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3610.

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Background:Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD), and Ulcerative colitis (UC) are related to Spondyloarthritis (SpA). Ocular manifestations (OM) are well-stablished in axial SpA but not in IBD. It has been classically reported that whereas uveitis with axial SpA is predominantly anterior, unilateral, acute, and non-recurrent; in IBD it is bilateral, posterior, insidious, and chronic (1).Objectives:In a large unselected series of IBD, our aim was to assess a) epidemiology and clinical features of uveitis associated to IBD, b) to compare patients who developed uveitis and those who did not, and c) its relationship with biological treatment used in IBD.Methods:Study of all consecutive patients from a single University Hospital during the last 40 years with: a) IBD (CD and UC), and b) uveitis according to Standarization Uveitis Nomenclature (SUN) Working Group. Demographic features, clinical findings, occurrence of other extraintestinal manifestations and treatment were recorded.Results:We studied 1449 (714 women/735 men) patients with IBD, mean age of 55.2±15.9 years.Uveitis was present in 23 (1.6 %) (38 eyes) of 1448 IBD patients. The most common pattern of uveitis was typically anterior (n=18; 78.3%), unilateral (n=19; 82.6%), acute (n=19; 82.6%), and non-recurrent (n=12; 52.2%).The comparative study between patients with and without uveitis showed a significant predominance of women (Table 1) in patients with uveitis, as well as erythema nodosum, hidradenitis suppurativa and joint involvement.Regarding IBD severity, in terms of surgical interventions, and conventional and biological immunosuppressive treatments, there were no significant differences.Conclusion:Although uveitis is more infrequent in IBD than in axial SpA, it is also anterior, unilateral, acute, and non-recurrent in contrast with published data from selected series. Patients with uveitis do not seem to represent more severe phenotype of IBD.References:[1]Lyons & Rosenbaum JT. Arch Ophthalmol 1997; 115:61-4.Table 1.General features of 1448 patients with IBD with and without uveitis.Overall(n=1449)Uveitis(n=23)Non uveitis(n=1426)pMain general featuresAge, years, mean±SD55.2±15.949.1±14.655.2±15.90.8Sex, women/men, n, (% of women)714 / 735 (49.3)17 / 6 (73.9)697 / 729 (48.9)0.02*IBD duration, years, mean±SD13.2 ± 9.717.4 ± 10.213.1 ± 8.90.08IBD SeveritySurgical Interventions, n (%)289 (19.9)2 (8.7)284 (19.9)0.7Conventional Immunosuppressive drugs, n (%)878 (60.6)14 (60.9)863 (60.5)0.5Biological Therapy, n (%)384 (26.5)7 (30.4)378 (26.5))0.9TNFi monoclonal antibodies384 (26.5)7 (30.4)378 (26.5)0.9Ustekinumab27 (1.9)1 (4.3)27 (1.9)0.5Other23 (1.6)1 (4.3)22 (1.6)0.3Extraintestinal manifestationsCutaneous manifestations, n (%) (TOTAL)125 (8.6)9 (39.1)121 (8.7)0.1Erythema nodosum, n (%)26 (1.8)6 (26.1)24 (1.7)0.009*Pyoderma gangrenosum, n (%)13 (0.9)1 (4.3)13 (0.9)0.7Hidradenitis suppurativa, n (%)2 (0.1)1 (4.3)1 (0.1)0.0001*Joint involvement, n (%) (TOTAL)131 (9)10 (43.5)121 (8.5)0.0001*Axial pattern, n (%)65 (4.5)4 (17.4)58 (4.1)0.0001*Peripheral pattern, n (%)64 (4.4)4 (17.4)63 (4.4)0.9Disclosure of Interests:Lara Sanchez-Bilbao: None declared, María José García-García: None declared, David Martínez-López: None declared, Montserrat Rivero-Tirado: None declared, Beatriz Castro: None declared, Iñigo González-Mazón: None declared, Javier Crespo: None declared, Miguel A González-Gay Speakers bureau: AbbVie, Pfizer, Roche, Sanofi, Celgene and MSD., Grant/research support from: AbbVie, MSD, Jansen and Roche,, Ricardo Blanco Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD., Grant/research support from: AbbVie, MSD and Roche

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Franić Tomić, Viktoria. "Nepoznati dokumenti o Grgi Novaku i Miroslavu Krleži, koji osvjetljavaju kulturnu atmosferu sredine stoljeća u Hrvatskoj." Croatica et Slavica Iadertina, no. 6 (January 18, 2017): 313. http://dx.doi.org/10.15291/csi.697.

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U arhivu Mediteranskog instituta Grga Novak na Hvaru čuva se nekoliko neuočenih dokumenata koji osvjetljavaju život Grge Novaka, jednog od najznamenitijih Dalmatinaca XX. stoljeća, arheologa i historičara, pisca dvosveščane Prošlosti Dalmacije i trosveščane Povijesti Splita.1 U drugom, kraćem dijelu studijeautorica analizira i pismo Miroslava Krleže predsjedniku JAZU koje osvjetljava Krležin položaj u Titovoj Jugoslaviji. Analiziraju se neki aspekti Krležinog epistolarnog stila.

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Тихонов, Дмитрий. "COVID-19 некоторые особенности в Сибири". Siberian Research 5, № 1 (31 травня 2021): 6–9. http://dx.doi.org/10.33384/26587270.2021.05.01.01r.

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Географически определяемая территория Сибири составляет около 13 100 000 кв. км. больше по площади чем территории США, Китая, Канады, Бразилии, Австралии и Индии, но в нем всего проживает по состоянию на 1 января 2021 г. 31 140 697 человек [1]. Благодаря своему суровому климату развитие многих заболеваний, в том числе и инфекционных, на этой территории имеют свои особенности.

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Shestakova, E. A. "HOX GENE EXPRESSION IN HUMAN B-CELL PROGENITOR LEUKEMIA CELL LINES EXPRESSING E2A-PBX1 ONCOGENE." Russian Journal of Biotherapy 19, no. 1 (March 22, 2020): 89–95. http://dx.doi.org/10.17650/1726-9784-2019-19-1-89-95.

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Introduction. Acute lymphoblastic leukemia (ALL) is diagnosed mainly in children (2/3 of diseases) making this type of leukemia one of the most common oncological diseases among children. Oncogenes are involved in the development of ALL, in particular the product of chromosomes 1 and 19 translocation, the oncogene E2A-PBX1 that codes for E2A-PBX1 chimeric oncoprotein with strong transcription activation properties as well as oncogenes of HOX family, mainly HOXA and HOXB cluster genes. E2A-PBX1 chimeric oncoprotein and НОХА proteins are associated in vivo with factors participating in epigenetic regulation of gene expression such as chromatin modifying and remodeling enzymes that partially determines their oncogenic properties. In previous studies we obtained data indicating genetic interactions of E2A-PBX1 and НОХ genes participating in leukemia development.The aim of this research was to confirm the role of Е2А – РВХ1 oncogene in the activation of the expression of НОХА cluster genes coding for the proteins with high oncogenic potential.Materials and methods. The objects of the study were four B cell progenitor (pre-B) leukemia cell lines: RCH-ACV, KASUMI-2, 697 and NALM-6. Standard polymerase chain reaction (PCR) was used for the identification of chromosome 1 and 19 translocation product, E2A-PBX1 oncogene and its expression. Method of reverse transcription coupled with quantitative polymerase chain reaction (Q-RT-PCR) was used for the analysis of 11 HOXA cluster genes expression.Results. It is demonstrated that E2A-PBX1 oncogene is present and expressed in three studied human pre-B leukemia cell lines, RCH-ACV, KASUMI-2 and 697, while its expression is absent in NALM-6 cell line. High expression of 7 from 11 HOXА cluster genes is revealed in RCH-ACV, KASUMI-2 and 697 cell lines expressing E2A-PBX1 oncogene, whereas NALM-6 cell line, that does not express E2A-PBX1 oncogene, also does not express HOXA genes except low expression of two genes from this cluster.Conclusions. The data obtained in this study demonstrate that RCH-ACV, KASUMI-2 and 697 human leukemia pre-B cell lines, containing and expressing Е2А-РВХ1 oncogene, also express most of HOXA genes (7 genes of 11 genes) at high level in contrast to control NALM-6 cell line that does not comprise Е2А-РВХ1 oncogene and almost does not express НОХА genes. Therefore, the results of this study suggest the participation of strong transcriptional activator, chimeric oncoprotein Е2А-РВХ1, associated with chromatin modifying and remodeling enzymes, in the expression activation of HOXA cluster genes that also possess high oncogenic potential.

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Ruszczyk, Grażyna. "„Budowle służące zabawom przyjemnym a tem samem przy wodnej kuracji bardzo pożytecznym”. O drewnianych domach zdrojowych, teatrach i estradach w polskich uzdrowiskach w XIX i na początku XX wieku." Biuletyn Historii Sztuki 82, no. 4 (January 21, 2021): 601–40. http://dx.doi.org/10.36744/bhs.697.

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Właściciele i administratorzy uzdrowisk, aby sprostać wymaganiom stawianym przez zamożnych gości, którzy oczekiwali nie tylko skutecznej kuracji, ale również bogatej oferty kulturalnej i towarzyskiej, musieli zapewnić rozmaite rozrywki i atrakcje. W związku z tym organizowali występy zespołów teatralnych, koncerty, bale, spotkania, odczyty itp. Dlatego w uzdrowiskach powstawały domy zdrojowe mieszczące sale balowe, czytelnie, restauracje, kawiarnie, pokoje do gier. Budowano też teatry, a w parkach estrady muzyczne. Artykuł poświęcony jest właśnie tym budynkom, pochodzącym z kilku wybranych uzdrowisk uważanych za polskie, powstałych na terenie I Rzeczpospolitej. Są to uzdrowiska najstarsze (z 1. połowy XIX w.), największe i działające do dzisiaj: Busko, Ciechocinek, Druskienniki, Iwonicz, Krynica, Solec, Szczawnica i Truskawiec oraz młodsze (z 2. połowy XIX w.), ale znane i nadal funkcjonujące – Zakopane i Połąga. Tematem są budynki drewniane, ponieważ to one do początków XX w. decydowały o krajobrazie architektonicznym polskich uzdrowisk. Większość z nich uległa zniszczeniu, znane są jedynie z materiałów ikonograficznych i opisów.

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Vekeman, Francis, Medha Sasane, Wendy Y. Cheng, Agnihotram V. Ramanakumar, Jonathan Fortier, Mei S. Duh, Carole Paley, and Patricia Adams-Graves. "Adherence to Iron Chelation Therapy and Associated Healthcare Resource Utilization and Costs in Medicaid Patients with Sickle Cell Disease." Blood 124, no. 21 (December 6, 2014): 2177. http://dx.doi.org/10.1182/blood.v124.21.2177.2177.

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Abstract Introduction: While adherence to iron chelation therapy (ICT) is critical for successful iron overload (IO) treatment among patients with sickle cell disease (SCD), published data indicate it is often suboptimal. Deferoxamine (DFO) and Deferasirox (DFX) are ICTs indicated for the treatment of chronic IO in patients with SCD. Lack of patient adherence may impact patient outcomes and increase cost of care. This study evaluated the economic burden of ICT non-adherence in patients with SCD from the state Medicaid program’s perspective. Methods: Patients with SCD were identified from Florida, Iowa, Kansas, Mississippi, Missouri, and New Jersey (1997-2013) state Medicaid programs. Patients were required to have ≥1 ICD-9 diagnosis code for SCD (282.6), ≥1 prescription for DFO or DFX, and ≥6 months of continuous enrollment prior to the 1st DFO/DFX prescription (index date), which was defined as the baseline period. Adherence was estimated using the medication possession ratio (MPR), defined as the sum of the days of medication supply divided by the number of days between 1st and last prescription fill plus the days of supply of the last fill; a threshold of ≥0.80 was used to define optimal adherence. All-cause and SCD-specific resource utilization per-patient-per-month (PPPM) was assessed using cumulative rates, accounting for all visits observed, and compared between adherent and non-adherent patients using cumulative rate ratios (CRR). All-cause and SCD-specific healthcare costs were computed using mean cost PPPM. Regression models adjusting for baseline characteristics were used to assess resource utilization and cost differences between adherent and non-adherent patients. Results: A total of 846 eligible patients with SCD were included with 77 in DFO-only, 686 in DFX-only), and 83 in DFO/DFX switch cohort. Mean (SD) MPR was 0.68 (0.27) for DFO-only patients and 0.75 (0.26) for DFX-only patients (p<0.05). Among all users of ICT, 409 (48.3%) were considered adherent. Adherent patients were slightly younger (19 vs. 21 years, p=0.003) than non-adherent patients. Rates of transfusions were comparable between the two groups (mean [SD] transfusions PPPM, adherent: 0.41 [0.47]; non-adherent: 0.40 [0.54], p=0.456) at baseline. The adjusted rate of all-cause IP visits PPPM was lower in adherent versus non-adherent patients (CRR=0.87 [95% CI: 0.83, 0.91]; p<0.001). The adjusted rates of all-cause outpatient (OP) visits (1.10 [1.08, 1.13], p<0.001) and ER visits (1.06 [1.01, 1.10], p=0.010) PPPM of adherent patients were higher in adherent patients than those in non-adherent patients. A similar trend was observed in SCD-specific resource utilization except for rates of ER visits, which were similar between cohorts. From cost perspective, total all-cause and SCD-specific costs were lower in adherent versus non-adherent patients primarily due to lower IP costs (Table 1). SCD-specific ER and OP costs were similar in both cohorts. All-cause pharmacy costs were higher in adherent versus non-adherent patients. Conclusion: Published studies have reported low adherence to ICT, and a similar trend was found in this study. Adherent patients were observed to have less frequent hospitalizations and lower overall and SCD-specific IP costs compared to non-adherent patients. It should be noted that the rate of OP visits was higher in the adherent patients compared to non-adherent patients suggesting that adherent patients may be more closely monitored potentially resulting in better overall patient management and fewer hospitalizations. Additional analyses are needed to explore differences between adherent and non-adherent patients. Table 1 Costs PPPM Adherent patients (N=409) [A] Non-adherent patients (N=437) [B] Adjusted cost difference[A] – [B] P -value All-cause, mean [SD] $4,766 [$4,388] $5,304 [$4,725] -$724 0.072 Inpatient $1,911 [$3,647] $2,996 [$4,439] -$947 0.016 Emergency room $27 [$87] $40 [$88] -$203 0.104 Outpatient $580 [$697] $485 [$617] $49 0.500 Pharmacy $2,248 [$1,949] $1,783 [$1,449] $432 0.004 Pharmacy without ICT $215 [$482] $274 [$544] -$50 0.192 SCD-specific, mean [SD] $2,237 [$3,679] $3,116 [$4,301] -$952 0.0160 Inpatient $1,776 [$3,546] $2,782 [$4,268] -$855 0.0160 Emergency room $18 [$63] $28 [$69] -$199 0.1200 Outpatient $443 [$658] $306 [$548] $105 0.1120 Disclosures Vekeman: Novartis Pharmaceuticals: Research Funding. Sasane:Novartis Pharmaceuticals: Employment. Cheng:Novartis Pharmaceuticals: Research Funding. Ramanakumar:Novartis Pharmaceuticals: Research Funding. Fortier:Novartis Pharmaceuticals: Research Funding. Duh:Novartis Pharmaceuticals: Research Funding. Paley:Novartis Pharma: Employment. Adams-Graves:Novartis Pharmaceuticals: Consultancy, Honoraria, Speakers Bureau.

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