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Journal articles on the topic "863/.64 b"

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Yacoubi, Loubna, Soumia Farih, Noussaiba Benhamza, Abderazzak Seddari, and Adil maleb. "Health vigilance concerning Acinetobacter baumannii bacteremia at the mohammed VI university hospital of oujda (morocco): epidemiological profile and antibiotic resistance." E3S Web of Conferences 319 (2021): 01003. http://dx.doi.org/10.1051/e3sconf/202131901003.

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The objective of this work is to determine the epidemiological profile of Acinetobacter b aumannii (A.baumannii ) bacteremia in the microbiology laboratory of CHU Mohammed VI of Oujda and its antibiotic resistance rates. This is a retrospective and descriptive study of 27 months from June 24, 2016to September 19, 2018 including all positive blood cultures processed in the microbiology laboratory in accordance with REMIC (reference in medical microbiology)and EUCAST(European Committee on Antimicrobial Susceptibility Testing). Contaminated blood cultures were excluded. As results we collected 863 positive blood cultures, A. baumannii accounted for 7.41% (n = 64). 67% (n =43) of the strains were isolated from patients hospitalized in intensive care (adults, children and newborns). The two main risk factors described in patients with our series were wearing of intravascular device in 55% (n=35) Immunosuppression in 22% n=14). A. baumannii bacteremia was associated with care in 37.5% (n=24). 75% (n=48) of A. baumannii isolates were resistant to carbapenems. No strain of A. baumannii was resistant to colistin. In light of these results strengthening the control and prevention measures for healthcare associated infections would be the most reliable way to limit the spread of A. baumannii in our establishment.
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Duvic, M., A. Forero-Torres, F. Foss, E. Olsen, L. Pinter-Brown, and Y. Kim. "Long-term treatment of CTCL with the oral PNP inhibitor, forodesine." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 8552. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.8552.

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8552 Background: Forodesine is a potent inhibitor of purine nucleoside phosphorylase (PNP) that leads to T-cell selective intracellular accumulation of dGTP, resulting in apoptosis. Methods: An open-label dose escalation study of oral forodesine (40–320 mg/m2 daily) for 4 wks with extended therapy was performed to determine the maximum tolerated and/or optimal biologic dose (OBD). Additional subjects were accrued at an OBD (80 mg/m2) to further assess safety and clinical efficacy. Subjects with refractory CTCL, stages IB-IV were eligible. The primary efficacy endpoint (objective response rate [ORR]) was defined as ≥ 50% improvement by a severity-weighted assessment tool (mSWAT). Results: The overall intent to treat response rate was 17 of 64 (27%) subjects or 14 of 36 (39%) at the OBD. As of October 2008, nine of 64 subjects (14%) have received forodesine treatment for >12 months. This cohort of 9 subjects is further examined. Six discontinued treatment (median time on treatment 440 days): 4 for progressive disease, 1 withdrew consent, and 1 due to an adverse event (Diffuse Large B-cell Lymphoma). Three are continuing on therapy for 416, 710, and 863 days. Median age was 68 years (range 42, 81), and all but one was ≥ stage III. They had received a median of 3 prior systemic therapies including 8 of 9 with prior bexarotene. Five of 9 subjects had a response (2 with complete response, 3 with partial response, and 4 with stable disease). Related AEs were experienced by 7 of 9 subjects. The most frequent were nausea (44%), fatigue, peripheral edema, dyspnea, and urinary casts (all 22%). Grade 3 or higher related AEs were experienced by 2 of 9 subjects (Diffuse Large B-Cell Lymphoma as previously mentioned and peripheral edema). There were no hematologic or infection AEs related to forodesine. Grade 3 lymphopenia and CD4 count < 200 were noted in 8 of 9 and 4 of 9 subjects respectively. The risk of any infection AE regardless of cause in these 9 subjects was 15 per 100 person-months of forodesine exposure compared to 59 in all other subjects (n=55). Conclusions: Forodesine has an acceptable safety profile and efficacy in these CTCL subjects treated for 12 months or longer. [Table: see text]
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Matsuda, Shinichiro, Ritsuro Suzuki, Masaya Inoue, Ritsuko Seki, Koji Nagafuji, Hiroaki Miyoshi, Koichi Ohshima, and Junji Suzumiya. "Clinical and Prognostic Significance of Epstein-Barr Virus in Diffuse Large B-Cell Lymphoma." Blood 128, no. 22 (December 2, 2016): 108. http://dx.doi.org/10.1182/blood.v128.22.108.108.

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Abstract Introduction: Diffuse large B-cell lymphoma (DLBCL) is the largest subtype of lymphoma, but consists of heterogeneous groups with different prognosis. Many studies conducted to determine prognosis factors of DLBCL. Recently, several studies have been reported that the elderly Epstein-Barr virus (EBV)-positive DLBCL patients showed worse prognosis than the elderly EBV-negative DLBCL. (Oyama T et al. Clin Cancer Res 2007;13:5024-5032). On the other hand, other studies reported that EBV-positivity is not a prognosis factor in young-adult DLBCL patients (Hong JY et al. Annals of Oncology 2015;26:548-555, Nicolae A et al. BLOOD 2015;126:863-872). In the present study, retrospective analyses were carried out for patients with DLBCL diagnosed between 1990 and 2007 to analyze the clinical and prognostic significance of EBV. Patients: Those who met the following criteria were included in the study: (i) pathology confirmed de novo DLBCL, according to the WHO classification; (ii) adequate amount and quality of paraffin-embedded biopsy specimens or unstained slides for EBV-encoded RNA in situ hybridization. Statistical methods: Intergroup comparisons were carried out with Fisher's exact test for categorical variables and the Mann-Whitney test for age. For survival analysis, we carried out Kaplan-Meier and multivariate proportional hazard (Cox) analyses. Statistical analyses were carried out using the software Stata SE version 14.0. Results: A total of 456 patients were included. The median follow up duration of survivor was 100 months (range, 1.9-363). There were 236 male (51.75%) and 220 female patients (48.25%) with a median age of 67 (range, 22-94) years. 246 patients (54.0%) were in advanced (III/IV) stage, 134 (29.4%) presented with poor Eastern Cooperative Oncology Group Performance Status (ECOG-PS), 275 (60.3%) with elevated lactate dehydrogenase (LDH) level, 263 (57.7%) with extranodal involvement of 1 or more sites, and 64 (14.0%) with bulky mass. As a consequence, 211 patients (46.3%) were in high/high-intermediate International Prognostic Index (IPI) categories. 5 years overall survival (OS) was 66.2%, in total. EBV was detected in samples from 47 patients (10.3 %). The positivity was 10.6% (15 / 142) in patients of 60 years or younger, and 10.2 % (32 / 314) in those older than 60 years (p = 0.51). No differences in back ground date were found between EBV - positive and negative DLBCLs regarding age (median 66.5 vs. 64.8, P = 0.17), male sex (88.1% vs. 11.9%, P = 0.16), advanced stage (88.2% vs. 11.8%, P = 0.17), poor ECOG-PS (90.3% vs. 9.7%, P = 0.47), elevated LDH (89.5% vs. 10.6%, P = 0.48), extranodal sites of one or more (90.5% vs. 9.5%, P = 0.31), bulky mass (92.2% vs. 7.8%, P = 0.33), and higher IPI categories (88.6% vs. 11.4%, P = 0.29). The prognosis was also not different between EBV-positive and negative DLBCLs. The 5 years OS was 42.6% for EBV-positive DLBCLs, and 56.4% for EBV-negative DLBCLs (P = 0.11). The same results were found for the younger (53.3% vs. 66.9%, P = 0.30) and the elderly patients (42.9% vs. 51.8%, P = 0.18). Conclusion: In this practice based, uncontrolled study, EBV-positively wad not different in younger and elderly DLBCLs. Although EBV-positive DLBCL showed worse trend of prognosis, the difference was not statistically significant. The significance of EBV in DLBCL should be reconsidered in unbiased, large-scale patient date. Figure Figure. Disclosures Suzuki: Chugai: Honoraria; Bristol-Myers Squibb: Honoraria; Kyowa Hakko kirin: Honoraria. Suzumiya:Chugai: Research Funding, Speakers Bureau; Astellas: Research Funding; Toyama Chemical: Research Funding; Eizai: Research Funding; Takeda: Speakers Bureau; Kyowa Hakko Kirin: Research Funding.
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LU, X., X. ZHAO, C. BAI, C. ZHAO, G. LU, and G. XU. "Corrigendum to “LC–MS-based metabonomics analysis” [J. Chromatogr. B 866 (2008) 64]." Journal of Chromatography B 874, no. 1-2 (October 15, 2008): 125. http://dx.doi.org/10.1016/j.jchromb.2008.09.001.

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Howarth, David E., Jayne L. Kennedy, Andrew M. Will, Trevor F. Carr, and Wynn Robert. "Does the Use of Different Factor VIII Products Influence Inhibitor Formation in Patients with Haemaphilia A." Blood 106, no. 11 (November 16, 2005): 4029. http://dx.doi.org/10.1182/blood.v106.11.4029.4029.

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Abstract This retrospective study looked at all patients with Haemophilia A who attended Manchester Pendlebury Childrens Hospital for their first and subsequent Factor replacement therapy between January 1980 and May 2005. The aim was to determine :- Does an increased number of different products used influence inhibitor formation. Does using a B domain deleted factor (Refacto) concentrate influence inhibitor formation. Does changing from plasma derived to recombinant factor influence inhibitor formation. A total of 107 patients who received a cumulative total of 65,102 trearment days were identified and the following information was recorded for each patient :-severity of haemophilia (mild, moderate or severe) and baseline factor VIII level, date and age of first product, all types of products used, number of treatment days used of each product, detection of inhibitor and if present date of ocurrence and age of patient. The policy of the unit was to test for inhibitors every six months, pre operatively or when clinically indicated. Thirteen different products were in use during the period of the study :- AHFC(anti haemophilic factor concentrate), Cryoprecipitate, 8Y, 8SM, Alphanate, Replenate, Monoclate P, Helixate, Refacto, Recombinate, Hemophil M, Advate and Haemate P. Only 4 patients out of 107 developed inhibitors and all were exposed to less than 4 products. Inhibitor patient demographics Haemophilia type and baseline factor VIII Number of treatment days before inhibitor Products used with respective treatment days Severe (<1%) 249 Cryoprecipitate (128) 8Y(121) Severe (1%) 75 Alphanate(34) 8SM(34) Replinate(7) Moderate (2%) 39 Alphanate(30) Helixate(9) Moderate (2%) 18 Refacto(2) Helixate(16) A total of 37 patients received 6 or greater factor products. The mean number of treatment days was 1224 (median 1285, SDV 863) and the mean number of factor products used was 6.8 (median 7, SDV 0.81). In severe patients (baseline factor VIII of 2% or less) a total of 31 patients received 4 or greater factor products. The mean number of treatment days was 1512 (median 1501, SDV 776) and the mean number of factor products used was 6.45 (median 6, SDV 1.31). A total of 23 patients received 6 or greater factor products. The mean number of treatment days was 1664 (median 1525, SDV 776) and the mean number of products used was 7.04 (median 7, SDV 0.93). There were 10443 exposure days of Refacto in those patients that did not develop an inhibitor. 69 out of 103 patients were exposed to the product with a mean number of treatment days of 151 (median 43, SDV 237). In the same population 29 out of 43 severe patients (baseline factor VIII of 2% or less) were exposed to the product with a total number of exposure days of 6464 with a mean number of treatment days of 222 (median 241, SDV 241). There were only 2 exposure days of ReFacto in just one of the inhibitor patients. 64 patient changed from using plasma to recombinant products. Only one of these patients developed an inhibitor. In this study the number of different factors used, use of a B deleted domain factor and change from plasma derived to recombinant factors did not appear to be factors in the formation of inhibitors.
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Novak, Anne J., Takashi Akasaka, Michelle Manske, Tammy Price-Troska, Mamta Gupta, Thomas E. Witzig, Martin JS Dyer, Ahmet Dogan, and Stephen M. Ansell. "Elevated Expression of GPR34 in Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma and Its Association with Increased Cell Growth, Erk Activation, and AP-1 and CRE-Mediated Transcription." Blood 114, no. 22 (November 20, 2009): 3927. http://dx.doi.org/10.1182/blood.v114.22.3927.3927.

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Abstract Abstract 3927 Poster Board III-863 In previous studies we characterized the t(X;14)(p11.4;q32) translocation in a patient with MALT lymphoma and found that GPR34, an orphan G-protein coupled receptor (GPCR), was highly expressed due to its juxtaposition to the IGHSA2 switch region. As part of a larger MALT gene expression-profiling project, we have now acquired gene expression analysis on the patient carrying the t(X;14)(p11;q32) translocation and have confirmed overexpression of GPR34. We then measured GPR34 mRNA expression in a panel of MALT lymphomas (n=17) and found that GPR34 was expressed at levels higher than that seen in normal B cells (mean, 11.3 fold; median, 5.5; range, 1.4-64 fold). When analyzed separately, 70% (12/17) had an expression level greater than 3-fold over normal B cells. Of note, in a gastric MALT lymphoma specimen, we found a 64 fold increase in GPR34 mRNA expression. FISH studies performed on this specimen showed an extra intact GPR34 signal but no translocation involving IGH or GPR34, suggesting that other mechanisms, including gene dosage effect, can upregulate GPR34. Elevated expression of GPR34 mRNA was also detected in other histologic types of NHL, but not to the extent seen in MALT lymphoma. Taken together, these data suggest that GPR34 is commonly overexpressed in MALT lymphoma and that deregulation of GPR34 expression can occur independent of a t(X;14)(p11.4;q32) translocation. The receptor encoded by GPR34 is most similar to the PY2 receptor subfamily of GPCR and GPR34 mRNA transcripts are abundant in mast cells while lower levels were detected in other immune cells including B cells. Signals from GPR34 have been briefly described and the results to date suggest that overexpression of GPR34 results in an accumulation of inositol phosphates. To further characterize the impact of GPR34 overexpression on cell signaling, HeLa cells were transduced with a retroviral expression plasmid (pBMN-GFP) that expresses GPR34 and GFP. GFP expressing cells were isolated and overexpression of GPR34 mRNA was confirmed by PCR and GPR34 protein expression was detected by flow cytometry. When normalized to the isotype control, pBMN-GPR34 cells expressed 17-fold more GPR34 on their cell surface compared to the pBMN-vector control cells. To determine which signaling pathways were affected by GPR34 overexpression, pBMN-GPR34 or pBMN-vector control cells were transfected with an AP-1, CRE, NF-κB, E2F, SRE, NFAT, or ISRE- luciferase reporter plasmid. Upon normalization with renilla, pBMN-GPR34 expressing cells had increased luciferase activity (n=3) driven by AP-1 (5.35-fold), CRE (4.7), NF-κB (2.8-fold), and E2F (2.13) when compared to pBMN-vector control cells. ISRE, NFAT, and SRE mediated luciferase expression was similar in the GPR34 and control cells. AP-1 and CRE have been implicated in a large variety of cellular processes, including transformation, and both AP-1 and CRE activity is induced upon activation of MAP kinases. To determine if MAPK activity was also upregulated in GPR34 expressing cells, we analyzed the phosphorylation status of Erk1/2 in pBMN-GPR34 cells by western blot and found that Erk1/2 was constitutively phosphorylated in GRP34 expressing cells (1.8 fold increase) compared to vector control cells. Increased phosphorylation of PKC-α/β was also detected in pBMN-GPR34 cells (3.5 fold increase compared to control cells). To determine the biologic impact of GRP34 overexpression on cell growth, the proliferation rates of pBMN-control and pBMN-GPR34 cells were compared and it was found that proliferation of GPR34 expressing cells was 2.2 times higher than that seen in control cells. Because the MAPK kinase pathway was found to be active in the pBMN-GPR34 cells, we tested the effect of the MEK inhibitor PD98059 on proliferation and saw a dose dependent decrease in proliferation of GPR34 expressing cells. These results suggest that GPR34-mediated proliferation is Erk-dependent. In summary, these data suggest that deregulation of GPR34 is commonly found in MALT lymphoma and that overexpression of GPR34 results in activation of Erk1/2, phosphorylation of PKC, and results is AP-1 and CRE mediated transcription. Additionally, our data suggest that overexpression of GPR34 results in increased cell growth that is MAPK-dependent. Taken together, this studies indicate that overexpression of a GPCR, GPR34, may be a novel mechanism by which MALT, lymphoma, and potentially other subtypes of NHL, develop. Disclosures: No relevant conflicts of interest to declare.
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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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Bradwell, Arthur R., Neil D. Evans, Mike J. Chappell, Paul Cockwell, Steven D. Reid, John Harrison, Colin Hutchison, and Graham P. Mead. "Rapid Removal of Free Light Chains from Serum by Hemodialysis for Patients with Myeloma Kidney." Blood 106, no. 11 (November 16, 2005): 3482. http://dx.doi.org/10.1182/blood.v106.11.3482.3482.

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Abstract Introduction. Acute renal failure (ARF) develops in 10–15% of patients with multiple myeloma (MM). Typically, complexes of serum free light chains (sFLC) and Tamm-Horsfall protein form casts in the distal tubules that block urine flow. Many patients, subsequently, require long-term hemodialysis (HD) and may have reduced survival. In an attempt to minimise renal damage, plasma exchange (PE) has been used to reduce the pre-renal load of sFLC. Zucchelli et al., (Kidney Int1988; 33:1175–1180) showed that PE reduced HD requirements but subsequent controlled trials showed no benefit (Johnson WJ et al., Arch Intern Med1990; 150:863–869: Clarke WF et al., Haematologica2005; 90(s1) p117). The availability of sFLC immunoassays now allows an informed evaluation of the role of PE and/or HD in treating these patients. Methods. sFLC were measured in 1: 100 patients with chronic renal failure (CRF), GFR&lt; 15ml/min and not on dialysis; 2: 38 at the beginning and end of HD (dialyzer A) and 3: 25 on chronic ambulatory peritoneal dialysis (CAPD). sFLC hemofiltration efficiency was assessed, in-vitro, for three different dialyzers, using standard pump pressures and flow rates. Sera containing approximately 1,000 mg/L of monoclonal kappa (κ ) (NR &lt; 20mg/L) and lambda (λ ) FLC (NR &lt; 27mg/L) were recycled for ~45 minutes through the dialyzers and clearance rates assessed. A two-compartment, mathematical model was constructed to assess sFLC removal by HD and PE from hypothetical patients. The following parameters were considered:- sFLC concentrations in MM at clinical presentation; monomeric κ or dimeric λ clearance differences; partition of sFLC between vascular and extravascular compartments; flow of FLC between compartments; half-life of sFLC in ARF; sFLC production and tumour killing rates with chemotherapy. The model was interrogated for various dialysis times, different dialyzers and a PE protocol of 3L, x6 over 2 weeks. Results. Mean sFLC concentrations in severe CRF were: κ 93 mg/L (range 43–207); λ 64 mg/L (range 43–134). Mean sFLC before and after HD: κ 130 mg/L (range 40–567) to 49 (range 20–234); λ 100 mg/L (range 31–225) to 61 (range 24–159). Mean sFLC in CAPD patients: κ 118 mg/L (range 31–266); λ 114 mg/L (range 36–263). Clearances of sFLC by the 3 dialyzers were: A: BBraun high flux polyethersulfone 1.8sqm (HI PeS) (the dialyzer in routine use); κ 46%: λ 39%, B: Idmesa high flux polyethersulphone 2.0sqm (200MHP); κ 67%: λ 59%, C: Asahi high flux polysulphone 2.1sqm (APS 1050); κ 71%: λ 65%. Model calculations showed that sFLC reduced from a starting value of 14g/L (typical of light chain MM) to less than 0.5g/L in 14 days using PE. Membrane A, used for four hours, x3/week, was approximately 20% more efficient than PE and reduced κ sFLC approximately 50% faster than the natural clearance rate of patients in ARF. Dialyzers B and C were approximately twice as efficient. Performing initial, 16-hour dialyses daily for 3 days, with dialyzer C reduced sFLC to less than 0.5g/L in 2–3 days with ~95% of the sFLC being removed. Dimeric λ sFLC were removed ~50% more slowly. Conclusion. PE was less efficient at removing sFLC than routine HD. Prolonged HD with high-flux dialyzers removed monoclonal sFLC quickly and should be assessed in a clinical trial for patients with acute myeloma kidney. CAPD was inefficient at removing sFLC.
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Mirza, A., Z. Win Naing, P. Khonsari, H. Khan, P. Rezai, A. K. Abbas, and M. Nisar. "POS1421 AROMATASE INHIBITORS AND SKELETAL HEALTH – NATURAL HISTORY AND INTERVENTIONAL EPIDEMIOLOGY." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1054.1–1054. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2165.

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BackgroundBreast cancer remains the most common cancer diagnosed in women worldwide. Aromatase inhibitors (AI) are employed for hormone sensitive disease in mainly postmenopausal women. AI related bone loss (AIBL) is a known complication; although data regarding the natural history in the real-world, long-term outcomes and the role of bone active therapy in fracture prevention is sparse.ObjectivesOur aim was to determine the real-world impact of AIBL and whether bone sparing therapy utilising standard risk stratification model is sufficient for fracture prevention.MethodsWe undertook a longitudinal study of patients prescribed AI for breast cancer over a seven-year period at our university teaching hospital. All the data was recorded electronically with full access to demographics, disease parameters, investigations and drug management. DEXA scans performed prior to initiation of AI were compared with subsequent imaging over a mean follow up of 3 years. Outcome data for cancer and all fractures was collected. Statistical analysis was done to investigate significant relationships amongst the variables of interest.Results1001 women were identified during the study period. The mean age of the cohort was 64 years (range 29-93). 929 (93%) were Caucasian, 57 (6%) were Asian and 15 (1%) were Afro-Caribbean. 723 women (72%) were diagnosed with invasive ductal carcinoma and 863 women (86%) were postmenopausal. At diagnosis, 428 women (43%) had node positive disease and 35 women (4%) had metastases. 91 women (9%) had sustained fractures prior to their breast cancer diagnosis.All women had a baseline DEXA: 496 (49.6%) had osteopenia, 151 (15%) had osteoporosis and 354 (35.4%) had a normal result. 478 (48%) of women had a repeat scan available. Overall, there was a decline (from a mean of 0.888 g/cm2 to 0.858 g/cm2, p<0.0001) in left neck of femur (LNOF) bone mineral density (BMD) over time (mean of 3 years, with a range of 1-6).334 (33%) were prescribed bone active therapy with 276 women (83%) given oral bisphosphonates. This group had an improvement in BMD by 0.4% (LNOF mean BMD of 0.785 g/cm2 at baseline compared to LNOF mean BMD of 0.788 at repeat DEXA, p=0.82).Women who were not offered any treatment (n=667, 66%), showed a significant decline in bone density with the decline being -5%. (LNOF mean BMD of 0.939 g/cm2 at baseline compared to LNOF mean BMD of 0.888 g/cm2 at repeat DEXA, p< 0.0001).The rate of fractures remained the same between the treatment (19 fractures, 5.67%) and non-treatment group (38 fractures, 5.70%)ConclusionOur study provides long term data for AIBL and confirms a significant decline in BMD over seven years. It confirms that bone sparing therapy is effective in reducing the pace of decline in BMD. However standard risk stratification model such as FRAX based intervention thresholds in mainly those with WHO defined osteoporosis (T ≤-2.5) is ineffective in fracture prevention in keeping with prior literature. Since our study period overlaps with publication of newer guidelines recommending different T score-based risk model, further studies are required to confirm their utility.References[1]https://www.wcrf.org/dietandcancer/worldwide-cancer-data/. Date accessed: 26.01.2022[2]R. Coleman, J.J. Body, M. Aapro, et al., Bone health in cancer patients: ESMO clinical practice guidelines, Ann. Oncol. 25 (Suppl 3) (2014) iii124–iii137.[3]E. Amir, B. Seruga, S. Niraula, et al., Toxicity of adjuvant endocrine therapy in postmenopausal breast cancer patients: a systematic review and meta-analysis, J. Natl. Cancer Inst. 103 (2011) 1299–1309.Disclosure of InterestsNone declared
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Pho, Nguyen Van, Pham Tich Xuan, and Pham Thanh Dang. "Occurrence of supergene nickel ores in the Ha Tri Massive, Hoa An District, Cao Bang Province." VIETNAM JOURNAL OF EARTH SCIENCES 40, no. 2 (January 19, 2018): 154–65. http://dx.doi.org/10.15625/0866-7187/40/2/11676.

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Nickel (Ni) laterites are regolith materials derived from ultramafic rocks and play an important role in the world's Ni production. Ni-laterite deposits are the supergene enrichment of Ni formed from the intense chemical and mechanical weathering of ultramafic parental rocks. In Vietnam, the weathering profile containing Ni laterite was first discovered in the Ha Tri massive (Cao Bang). This profile develops on the Ha Tri serpentinized peridotite rocks classified to the Cao Bang mafic-ultramafic complex (North Vietnam) and exhibits thick weathered zone (10 - 15m). This work carried out a detailed study of the weathering profile at the center of Ha Tri massive. Samples from different horizons of the profile were collected and analyzed in detail by XRF, XRD and SEM-EDX methods to establish the relationship between the Ni-rich supergene products and the parental peridotites (lherzolite) rocks in Ha Tri massive. The results show that the saprolite horizon is most Ni-rich in the weathering profile in Ha Tri. In this horizon, Ni-silicate minerals of garnierite group such as pimelite, nepouite and other Mg-Ni silicates have been found. The appearance of minerals of garnierite group is due to the exchange of Mg by Ni during weathering of peridotite minerals, especially olivine, which leads to the enrichment of the supergene Ni. The occurrence of Ni silicates suggests the existence of the supergene Ni ore in the weathering profile of the Ha Tri massive.References Bosio N.J., Hurst J.V., Smith R.L., 1975. Nickelliferousnontronite, a 15 Å garnierite, at Niquelandia, Goias Brazil. Clays Clay Miner., 23, 400-403. Brand N.W., Butt C.R.M., Elias M., 1998. Nickel Laterites: Classification and features. AGSO Journal of Australian Geology & Geophysics, 17(4), 81-88. Bricker O.P., Nesbitt H.W. and Gunter W.D., 1973. The stability of talc. American Mineralogist, 58, 64-72. Brindley G.W. and Hang P.T., 1973. The nature of garnierites. Structures, chemical composition and color characteristics. Clay and Clay Minerals, 21, 27-40. Brindley G.W. and Maksimovic Z., 1974. The nature and nomenclature of hydrous nickel-containing silicates. Clay Minerals, 10, 271-277. Brindley G.W. and Wan H.M., 1975. Composition structures and thermal behavior of nickel containing minerals in thelizardite-ne´pouite series. American Mineralogist, 60, 863-871. Brindley G.W., Bish D.L. and Wan H.M., 1979. Compositions, structures and properties of nickel containing minerals in the kerolite-pimelite series. American Mineralogist, 64, 615-625. Cluzel D. and Vigier B., 2008. Syntectonic mobility of supergene nickel ores from New Caledonia (Southwest Pacific). Evidence from faulted regolith and garnierite veins. Resource Geology, 58, 161-170. Colin F., Nahon D., Trescases J.J., Melfi A.J., 1990. Lateritic weathering of pyroxenites at Niquelandia, Goais, Brazil: The supergene behavior ofnickel: Economic Geology, 85, 1010-1023. Das S.K., Sahoo R.K., Muralidhar J., Nayak B.K., 1999. Mineralogy and geochemistry of profilesthrough lateritic nickel deposits at Kansa,Sukinda, Orissa. Joural of Geoogical. SocietyIndia, 53, 649-668. Decarreau A., Colin F., Herbillon A., Manceau A., Nahon D., Paquet H., Trauth-Badaud D.,Trescases J.J., 1987. Domain segregation in NiFe-Mg-Smectites. Clay Minerals, 35, 1-10. Freyssinet P., Butt C.R.M. and Morris R.C., 2005. Oreforming processes related to lateritic weathering. Economic Geology, 100th aniversary volume, 681-722.Garnier J., Quantin C., Martins E.S., Becquer T., 2006. Solid speciation and availability of chromium in ultramafic soils from Niquelandia, Brazil. Journal of Geochemical Exploration, 88, 206-209. Garnier J., Quantin C., Guimarães E., Becquer T., 2008. Can chromite weathering be a source of Cr in soils? Mineralogy Magazine, 72, 49-53. Gleeson S.A., Butt C.R. and Elias M., 2003. Nickel laterites: A review. SEG Newsletter, 54, 11-18. Gleeson S.A., Butt C.R., Wlias M., 2003. Nickellaterites: a review. SEG Newsletter, Society of Economic Geology, 54. Available from www.segweb.org. Golightly J.P., 1981. Nickeliferous laterite deposits. Economic Geology, 75th Anniversary volume, 710-735. Golightly J.P., 2010. Progress in understanding the evolution of nickel laterite. Society of Economic Geology, In Special Publication, 15, 451-485. Manceau A. and Calas G., 1985. Heterogeneous distribution of nickel in hydrous silicates from New Caledonia ore deposits. American Mineralogist, 70, 549-558. Nguyen Van Pho, 2013. Tropic weathering in Vietnam (in Vietnamese). Pubisher Science and Technology, 365p.Ngo Xuan Thanh, Tran Thanh Hai, Nguyen Hoang, Vu Quang Lan, S. Kwon, Tetsumaru Itaya, M. Santosh, 2014. Backarc mafic-ultramafic magmatism in Northeastern Vietnam and its regional tectonic significance. Journal of Asian Earth Sciences, 90, 45-60.Pelletier B., 1983. Localisation du nickel dans les minerais ‘‘garnieritiques’’ de Nouvelle-Caledonie. Sciences Ge´ologique: Me´moires, 73, 173-183.Pelletier B., 1996. Serpentines in nickel silicate ores from New Caledonia. In Grimsey E.J., and Neuss I. (eds): Nickel ’96, Australasian Institute of Miningand Metallurgy, Melbourne, Publication Series 6(9), 197-205. Proenza J.A., Lewis J.F., Galı´ S., Tauler E., Labrador M., Melgarejo J.C., Longo F. and Bloise G., 2008. Garnierite mineralization from Falcondo Ni-laterite deposit (Dominican Republic). Macla, 9, 197-198. Soler J.M., Cama J., Galı´ S., Mele´ndez W., Ramı´rez, A., andEstanga, J., 2008. Composition and dissolution kinetics ofgarnierite from the Loma de Hierro Ni-laterite deposit,Venezuela. Chemical Geology, 249, 191-202. Springer G., 1974. Compositional and structural variations ingarnierites. The Canadian Mineralogist, 12, 381-388. Springer G., 1976. Falcondoite, nickel analogue of sepiolite. The Canadian Mineralogist, 14, 407-409.Svetlitskaya T.V., Tolstykh N.D., Izokh A.E., Phuong Ngo Thi, 2015. PGE geochemical constraints on the origin of the Ni-Cu-PGE sulfide mineralization in the Suoi Cun intrusion, Cao Bang province, Northeastern Vietnam. Miner Petrol, 109, 161-180.Tran Trong Hoa, Izokh A.E., Polyakov G.V., Borisenko A.S., Tran Tuan Anh, Balykin P.A., Ngo Thi Phuong, Rudnev S.N., Vu Van Van, Bui An Nien, 2008. Permo-Triassic magmatism and metallogeny of Northern Vietnam in relation to the Emeishan plume. Russ. Geol. Geophys., 49, 480-491.Trescases J.J., 1975. L'évolution supergene des roches ultrabasiques en zone tropicale: Formation de gisements nikelifères de Nouvelle Caledonie. Editions ORSTOM, Paris, 259p.Tri T.V., Khuc V. (eds), 2011. Geology and Earth Resources of Vietnam. Publishing House for Science and Technology, 645p (in English). Villanova-de-Benavent C., Proenza J.A., GalíS., Tauler E., Lewis J.F. and Longo F., 2011. Talc- and serpentine-like ‘‘garnierites’’ in the Falcondo Ni-laterite deposit, Dominican Republic. ‘Let’s talk ore deposits’, 11th Biennial Meeting SGA 2011, Antofagasta, Chile, 3p.Wells M.A., 2003. Goronickel laterite deposit. New Caledonia. CRC LEME, p.3.
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Books on the topic "863/.64 b"

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Marquez, Gabriel Garcia. Vivir para contarla. Barcelona: Mondadori, 2002.

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Marquez, Gabriel Garcia. Vivir para contarla. Nueva York: Alfred A. Knopf, 2002.

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Marquez, Gabriel Garcia. Vivir para contarla. Barcelona: Norma, 2002.

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Marquez, Gabriel Garcia. Living to tell the tale. London: Jonathan Cape, 2003.

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Marquez, Gabriel Garcia. Vivir para contarla. New York: Vintage Books, 2003.

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Marquez, Gabriel Garcia. Living to tell the tale. New York: Alfred A. Knopf, 2003.

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Marquez, Gabriel Garcia. Vivir para contarla. Barcelona: Debolsillo, 2004.

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Marquez, Gabriel Garcia. Vivir para contarla. Bogotá: Grupo Editorial Norma, 2002.

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Marquez, Gabriel Garcia. Living to tell the tale. New York: Vintage Books, 2004.

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Marquez, Gabriel Garcia. Vivre pour la raconter. Paris: Librairie Générale Française, 2006.

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Book chapters on the topic "863/.64 b"

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Feather, Leonard, and Ira Gitler. "l." In The Biographical Encyclopedia of Jazz, 395–424. Oxford University PressNew York, NY, 1999. http://dx.doi.org/10.1093/oso/9780195074185.003.0012.

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Abstract La porta, john d., cl., saxes, comp, arr; b. Philadelphia, PA, 4/1/20; d. Sarasota, FL, 5/12/04. Began on cl. at age 9. Stud. cl. w. Wm. Dietrich, Joseph Gigliotti, Leon Russianoff 1932–57. Pl. in Youth Symph. cond. by Leopold Stokowski ’37–8. Stud. comp. w. Ernst Toch, Alexis Haieff ’45–6; improv. w. Lennie Tristano ’47–8; received B. Mus. ’56, M. Mus. Ed. ’57 fr. Manh. Sch. of Mus. Pl. w. Bob Chester, Richard Himber, Ray McKinley early ’40s; Woody Herman ’44–6; Tristano late ’40s; Charles Mingus ’50–67; Metronome All-Stars ’51–2; own gps ’51–62. Founding member and mus. dir. of Jazz Composers Wkshp. ’52–4. App. w. Gunther Schuller at Brandeis Mus. Fest. ’57; Leonard Bernstein and N.Y. Philharm. perf. Teo Macero’s Fusion ’58–9. Taught at Parkway Mus. Inst., Bklyn. ’48–51. Reed coach for Marshall Brown’s Newport Youth Band ’53–8. Active as clinician ’59–81. Taught at Manh. Sch. of Mus. ’60–2; Berklee Sch. of Mus. fr. ’62. Dir. Greater Bost. HS Stage Band ’64–5. Pl. w. Bost. Sax Qt. w. Charlie Mariano ’60s; Berklee Sax Qt. fr. ’62; Herb Pomeroy Orch fr. ’76; John La Porta–Bob Winter Duo fr. ’81. La Porta was a founding member of the Nat’l Assoc. of Jazz Educs. and the author of eight instructional texts, incl. Tonal Organization of Improv. Techniques (Kendor); Guide to Improv. (Berklee); Guide to Jazz Phrasing and Interpretation (Berklee). His numerous arrs. for hs band are publ. by Berklee, Kendor, and Marshall Brown Music. La Porta taught and lectured at Berklee and in Fla. Polls: Play. ’61; NAJE Award ’86; Berklee Award ’87. Fests: all major ’50s–’60s. Film: Trocadero w. Bob Chester Orch. perf. La Porta comp. ’42. CDs: w. C. Parker (Verve); T. Macero (Stash); C. Mingus (Deb; Sav.; Atl.); W. Herman (Col.); H. Mobley (Sav.); H. Merrill (Em.; Verve).
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Feather, Leonard, and Ira Gitler. "i." In The Biographical Encyclopedia of Jazz, 339–43. Oxford University PressNew York, NY, 1999. http://dx.doi.org/10.1093/oso/9780195074185.003.0009.

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Abstract Ibrahim, abdullah (Adolphe Johannes Brand aka Dollar Brand), pno, comp, sop sax, fl, cello; b. Capetown, South Africa, 10/9/34. Studied priv. fr. age 7, pl. in church; then self-taught. Listened to Louis Jordan in his teens. First prof. job w. vocal gp. Streamline Bros.; also subbed w. Tuxedo Slickers. As Dollar Brand, pl. w. Willy Max in Capetown 1959; led own gp., Jazz Epistles, w. Hugh Masekela, Makaya Ntshoko, Kippie Moeketsi ’60–1. Moved w. wife, singer Sathima Bea Benjamin, to Zurich ’62. Led trio in Eur. ’62–5. Duke Ellington, who heard him at a club in Zurich, rec. him for Reprise ’63. Pl. at festivals in Juan-les-Pins, Palermo ’63; Montmartre club, Copenhagen ’64–5. Came to the US and app. at NJF ’65. Pl. w. Elvin Jones, also subbed for Ellington on tour ’66, then tour. Eur. w. Don Cherry, Gato Barbieri, M. Ntshoko, Johnny Gertze ’66–8. Stud. w. Hall Overton. Converted to Islam ’68; known by Muslim name fr. mid ’70s. Ret. to Africa ’68, living in Swaziland, Capetown, and Johannesburg ’68–76. Tour. Eur. frequently in mid ’70s, mainly as solo pno.; also w. 10–pc. band ’74. Moved to NYC ’76. Pl. in duo w. Carlos Ward fr. ’76; led own spt. Ekaya fr. ’83. Led perf. of mixedmedia opera, Kalahari Liberation, in Eur. ’82. Much of Ibrahim’s work reflects the influences of South African popular and folk musics, Ellington, and Thelonious Monk. Some of his orchestral work has an impressive African rhythmic sensitivity. Polls: DB critics TDWR ’75. Fests: prod. fests in Swaziland; all major in Eur. fr. ’60s. TV: Eur. TV, incl. apps. w. Danish Radio bb in ’60s and ’70s. Film: mus. for Chocolat ’87; No Fear No Die. CDs: Enja; BL; Japo; Tiptoe; Kaz; Rep. (as Dollar Brand); w. Barbieri (Aff.).
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Conference papers on the topic "863/.64 b"

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GOMPERTS, E. D., and K. WEINBERG. "LOSS OF IMMUNE TO RECALL ANTIGENS IN THERE HIV+ HEMOPHILIC CHILDREN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644140.

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Three children with severe inherited bleeding disorders have been followed for a number of years at this center. One child (DOB 3/71) initially presented with mild hemophilia A, (Factor VIII 6%). He subsequently developed an inhibitor to Factor VIII (maximum 45 B. U.) and seroconverted to HIV+ Status 12/83. In 12/86 he had virtually lost his antibody response to infused Factor VIII (previously withheld), with a maximum increase in inhibitor titre to1 B. U. on challenge. In addition, his antitetanus antibody titre was very low at 0.01 u/ml earlier in theyear. His absolute T4 cell number at this time was very low at 64 and did not respond to skin antigen testing to PPD, tetanus and Candida.The second patient (severe hemophilia A DOB 7/76) had seroconvertedto HIV+ Status in 9/78. This child has lost his a-HBs seropositive status with an absolute T4 count of 239. His current anti-tetanus titre is 0.01 u/ml.The third patient (von Willebrand disease, Type III, DOB 7/74) seroconverted to HIV+E status by 5/83. His T4 absolute numbers have fallen to 53. His anti-tetanus antibody titre has fallen to extremely low levels (0.01 u/ml), and this failed to respond to re-immunization with tetanus toxoid. These three patients indicate that previously immunized children may lose their immune status and their ability to respond to recall antigens. It is pertinent to note that lymphocytes from all 3 patients failed to respond mitogenically in vitro to tetanus antigen pari passu with the observed very low anti-tetanus antibody titres. These phenomena would indicate that these patients are probably susceptible to previously preventable infectious agents including poliovirus, measles, mumps, rubella, diphtheria, tetanus and hepatitis B virus.
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Félix, Jaqueline, João Refundini, Maria Carthery Goulart, Katerina Lukasova, and Raquel Fornari. "DEVELOPMENT OF A TOOL TO EVALUATE FACE-NAME LEARNING IN PORTUGUESE SPEAKERS." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda096.

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Background: Learning and retrieving proper names is one of the most common complaints among older adults. However, this aspect is not commonly assessed in this population. Objective: To develop an anterograde episodic memory assessment tool that measures the ability to learn, retain and retrieve face-name associations and test its application. Methods: The face-name association (FNAT) has 2 versions (A and B) and involves learning, free recall and recognition of 12 pairs. FNAT was applied to 86 community dwelling older adults, aged 69(±6), schooling 13(±3). (64 did version A, 57 B and 35 AB). Second test (AB) occurred 2-3 months after the first. Results: In both versions, recognition scores were higher than learning and free recall respectively (version A 47±24%, 34±25%, 76±20%; version B 51±26%, 41±26%, 74±24%). In the subgroup that performed both versions, no significant differences were found between the three subtests. Conclusion: FNAT was applied successfully in our sample. Test and retest effects were not observed and the two versions demonstrated an equivalent level of difficulty. Further studies are needed to explore cutoff scores according to aging and education.
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Silva, Maria Gabriela Ferreira, Isabella Cristina Santos Soares, Flávia Pinto Cardozo, Flávia Maria Souza Clímaco, and Aguinaldo Ferreira Leite Filho. "COMPLETE PATHOLOGICAL RESPONSE AFTER NEOADJUVANT CHEMOTHERAPY IN BREAST CANCER PATIENTS: ANALYSIS OF 83 PATIENTS TREATED AT A FEDERAL PUBLIC SERVICE." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1057.

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Introduction: Neoadjuvant chemotherapy is performed before surgical treatment and aims to make a locally advanced tumor operable, provide conservative treatment, demonstrate tumor sensitivity in vivo and evaluate the pathological response (PR) to treatment. PR is an important prognostic factor, and several studies have demonstrated a correlation between the biological factors of the tumor and its response rate. Patients with a pathologic complete response (PCR) present a longer survival rate compared to those with residual disease. Objectives: The main objective was to assess PCR in patients with breast cancer undergoing neoadjuvant chemotherapy. As secondary objectives, we identified clinical-pathological variables related to PCR and correlated the pathologic response in the breast with the axillary response after chemotherapy. Methods: Four hundred and forty-four medical records of patients seen in the Mastology sector were reviewed between January 2016 and July 2019. Eighty-three patients were selected, with 361 cases that did not meet the inclusion criteria being excluded. The exclusion criteria were benign disease, neoadjuvant hormone therapy, neoadjuvant radiation therapy, trastuzumab associated with chemotherapy, upfront surgery and patients who did not receive surgical treatment after chemotherapy. The variables analyzed were age, tumor size, axillary involvement, histological type and grade, molecular subtype and PCR. Results: Most patients were over 50 years of age (62%) and had tumors larger than 5 cm (75%). Fifty of them (60%) had initial axillary involvement. Among the 83 patients, 64 (77%) did not obtain a pathologic response in the breast and armpit. Two (3%) showed a response only in the breast. PCR was observed in 17 patients (20%) and almost half of them were under 50 years of age (47%). Moderately differentiated (grade 2) and undifferentiated (grade 3) tumors, accounted for 96% of cases and had a higher rate ofPCR than grade 1 tumors. In HER2 positive subtypes, PCR occurred in 36% and in negative triples in 22%, being higher than in luminous A and B subtypes (15% and 17%, respectively). Conclusions: The histological grade and molecular subtypes correlate with the pathologic response to neoadjuvant chemotherapy. More undifferentiated tumors and the triple negative and HER 2 positive molecular subtypes have a higher PCR rate. Despite the small sample, the results of this study were similar to those in the medical literature. A higher number of cases is necessary to corroborate the data obtained, as well as a longer follow-up time to demonstrate the relationship between PCR and survival.
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da Silva, Maria Gabriela Ferreira, Flávia Maria de Souza Climaco, Flávia Pinto Cardozo, Isabella Cristina Santos Soares, Cristina Milene Barbosa Maynart Aragão, and Aguinaldo Ferreira Leite Filho. "Resposta patológica completa após quimioterapia neoadjuvante em pacientes com câncer de mama: análise de 83 casos tratados no serviço público federal." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130217.

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Introdução: A quimioterapia neoadjuvante é aquela realizada antes do tratamento cirúrgico e tem como finalidade tornar operável um tumor localmente avançado, proporcionar tratamento conservador a pacientes inicialmente candidatas à mastectomia, demonstrar a sensibilidade in vivo e avaliar a resposta patológica ao tratamento instituído. A resposta patológica é considerada fator prognóstico e diversos estudos demonstram correlação entre os fatores biológicos do tumor e a taxa de resposta. Pacientes que apresentam resposta patológica completa (RPC) têm maior sobrevida em comparação àquelas com doença residual na mama ou na axila. Objetivo: O objetivo principal foi avaliar a RPC em pacientes com câncer de mama submetidas à quimioterapia neoadjuvante. Como objetivos secundários, identificamos as variáveis clínico-patológicas relacionadas à RPC e correlacionamos a resposta patológica na mama com a resposta axilar pós-quimioterapia. Material e Métodos: Neste estudo, foram revisados 444 prontuários de pacientes atendidas no setor de Mastologia, entre janeiro de 2016 e julho de 2019. Oitenta e três pacientes com diagnóstico de carcinoma invasivo foram selecionadas, sendo excluídos 361 casos, conforme os critérios de exclusão (doença benigna, hormonioterapia e radioterapia neoadjuvantes, trastuzumabe associado à quimioterapia, cirurgia upfront e pacientes que não receberam tratamento cirúrgico após a quimioterapia). As variáveis analisadas foram: idade, tamanho do tumor, acometimento axilar, tipo e grau histológico, subtipo molecular e RPC. Resultados e Conclusão: A maioria das pacientes tinha mais de 50 anos (62%) e tumores maiores que 5 cm (75%). Cinquenta pacientes (60%) apresentavam acometimento axilar inicial. Das 83 pacientes, 64 (77%) não obtiveram resposta patológica na mama e na axila. Duas mulheres (3%) apresentaram resposta somente na mama. A RPC foi observada em 17 pacientes (20%), e quase metade destas tinha menos de 50 anos (47%). Os tumores moderadamente diferenciados (grau 2) e indiferenciados (grau 3) somavam 96% dos casos e tiveram maior taxa de RPC que os tumores grau 1 (não obtida em nenhuma paciente). Nos subtipos HER2 positivos, a RPC ocorreu em 36% dos casos e nos triplos negativos em 22%, sendo maior que nos subtipos luminais A e B (15 e 17%, respectivamente). O grau histológico e os subtipos moleculares apresentaram correlação com RPC à quimioterapia neoadjuvante. Tumores mais indiferenciados e os subtipos moleculares triplo negativo e HER 2 positivo apresentaram maior taxa de RPC. Apesar da pequena casuística, os resultados deste estudo foram semelhantes aos da literatura médica sobre RPC pós-quimioterapia neoadjuvante. Um maior número de casos se faz necessário para corroborar os dados obtidos, assim como um tempo de seguimento maior para demonstrar a relação entre RPC e sobrevida.
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Reports on the topic "863/.64 b"

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Hajarizadeh, Behzad, Jennifer MacLachlan, Benjamin Cowie, and Gregory J. Dore. Population-level interventions to improve the health outcomes of people living with hepatitis B: an Evidence Check brokered by the Sax Institute for the NSW Ministry of Health, 2022. The Sax Institute, August 2022. http://dx.doi.org/10.57022/pxwj3682.

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Abstract:
Background An estimated 292 million people are living with chronic hepatitis B virus (HBV) infection globally, including 223,000 people in Australia. HBV diagnosis and linkage of people living with HBV to clinical care is suboptimal in Australia, with 27% of people living with HBV undiagnosed and 77% not receiving regular HBV clinical care. This systematic review aimed to characterize population-level interventions implemented to enhance all components of HBV care cascade and analyse the effectiveness of interventions. Review questions Question 1: What population-level interventions, programs or policy approaches have been shown to be effective in reducing the incidence of hepatitis B; and that may not yet be fully rolled out or evaluated in Australia demonstrate early effectiveness, or promise, in reducing the incidence of hepatitis B? Question 2: What population-level interventions and/or programs are effective at reducing disease burden for people in the community with hepatitis B? Methods Four bibliographic databases and 21 grey literature sources were searched. Studies were eligible for inclusion if the study population included people with or at risk of chronic HBV, and the study conducted a population-level interventions to decrease HBV incidence or disease burden or to enhance any components of HBV care cascade (i.e., diagnosis, linkage to care, treatment initiation, adherence to clinical care), or HBV vaccination coverage. Studies published in the past 10 years (since January 2012), with or without comparison groups were eligible for inclusion. Studies conducting an HBV screening intervention were eligible if they reported proportion of people participating in screening, proportion of newly diagnosed HBV (participant was unaware of their HBV status), proportion of people received HBV vaccination following screening, or proportion of participants diagnosed with chronic HBV infection who were linked to HBV clinical care. Studies were excluded if study population was less than 20 participants, intervention included a pharmaceutical intervention or a hospital-based intervention, or study was implemented in limited clinical services. The records were initially screened by title and abstract. The full texts of potentially eligible records were reviewed, and eligible studies were selected for inclusion. For each study included in analysis, the study outcome and corresponding 95% confidence intervals (95%CIs) were calculated. For studies including a comparison group, odds ratio (OR) and corresponding 95%CIs were calculated. Random effect meta-analysis models were used to calculate the pooled study outcome estimates. Stratified analyses were conducted by study setting, study population, and intervention-specific characteristics. Key findings A total of 61 studies were included in the analysis. A large majority of studies (study n=48, 79%) included single-arm studies with no concurrent control, with seven (12%) randomised controlled trials, and six (10%) non-randomised controlled studies. A total of 109 interventions were evaluated in 61 included studies. On-site or outreach HBV screening and linkage to HBV clinical care coordination were the most frequent interventions, conducted in 27 and 26 studies, respectively. Question 1 We found no studies reporting HBV incidence as the study outcome. One study conducted in remote area demonstrated that an intervention including education of pregnant women and training village health volunteers enhanced coverage of HBV birth dose vaccination (93% post-intervention, vs. 81% pre-intervention), but no data of HBV incidence among infants were reported. Question 2 Study outcomes most relevant to the HBV burden for people in the community with HBV included, HBV diagnosis, linkage to HBV care, and HBV vaccination coverage. Among randomised controlled trials aimed at enhancing HBV screening, a meta-analysis was conducted including three studies which implemented an intervention including community face-to-face education focused on HBV and/or liver cancer among migrants from high HBV prevalence areas. This analysis demonstrated a significantly higher HBV testing uptake in intervention groups with the likelihood of HBV testing 3.6 times higher among those participating in education programs compared to the control groups (OR: 3.62, 95% CI 2.72, 4.88). In another analysis, including 25 studies evaluating an intervention to enhance HBV screening, a pooled estimate of 66% of participants received HBV testing following the study intervention (95%CI: 58-75%), with high heterogeneity across studies (range: 17-98%; I-square: 99.9%). A stratified analysis by HBV screening strategy demonstrated that in the studies providing participants with on-site HBV testing, the proportion receiving HBV testing (80%, 95%CI: 72-87%) was significantly higher compared to the studies referring participants to an external site for HBV testing (54%, 95%CI: 37-71%). In the studies implementing an intervention to enhance linkage of people diagnosed with HBV infection to clinical care, the interventions included different components and varied across studies. The most common component was post-test counselling followed by assistance with scheduling clinical appointments, conducted in 52% and 38% of the studies, respectively. In meta-analysis, a pooled estimate of 73% of people with HBV infection were linked to HBV clinical care (95%CI: 64-81%), with high heterogeneity across studies (range: 28-100%; I-square: 99.2%). A stratified analysis by study population demonstrated that in the studies among general population in high prevalence countries, 94% of people (95%CI: 88-100%) who received the study intervention were linked to care, significantly higher than 72% (95%CI: 61-83%) in studies among migrants from high prevalence area living in a country with low prevalence. In 19 studies, HBV vaccination uptake was assessed after an intervention, among which one study assessed birth dose vaccination among infants, one study assessed vaccination in elementary school children and 17 studies assessed vaccination in adults. Among studies assessing adult vaccination, a pooled estimate of 38% (95%CI: 21-56%) of people initiated vaccination, with high heterogeneity across studies (range: 0.5-93%; I square: 99.9%). A stratified analysis by HBV vaccination strategy demonstrated that in the studies providing on-site vaccination, the uptake was 78% (95%CI: 62-94%), significantly higher compared to 27% (95%CI: 13-42%) in studies referring participants to an external site for vaccination. Conclusion This systematic review identified a wide variety of interventions, mostly multi-component interventions, to enhance HBV screening, linkage to HBV clinical care, and HBV vaccination coverage. High heterogeneity was observed in effectiveness of interventions in all three domains of screening, linkage to care, and vaccination. Strategies identified to boost the effectiveness of interventions included providing on-site HBV testing and vaccination (versus referral for testing and vaccination) and including community education focussed on HBV or liver cancer in an HBV screening program. Further studies are needed to evaluate the effectiveness of more novel interventions (e.g., point of care testing) and interventions specifically including Indigenous populations, people who inject drugs, men who have sex with men, and people incarcerated.
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