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Academic literature on the topic 'Wm 172'

Author: Grafiati
Published: 26 July 2024
Last updated: 30 July 2024

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Journal articles on the topic "Wm 172"

1

Alotaibi, Abdulmajeed, Anna Podlasek, Amjad AlTokhis, Ali Aldhebaib, Rob A. Dineen, and Cris S. Constantinescu. "Investigating Microstructural Changes in White Matter in Multiple Sclerosis: A Systematic Review and Meta-Analysis of Neurite Orientation Dispersion and Density Imaging." Brain Sciences 11, no. 9 (August 29, 2021): 1151. http://dx.doi.org/10.3390/brainsci11091151.

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Multiple sclerosis (MS) is characterised by widespread damage of the central nervous system that includes alterations in normal-appearing white matter (NAWM) and demyelinating white matter (WM) lesions. Neurite orientation dispersion and density imaging (NODDI) has been proposed to provide a precise characterisation of WM microstructures. NODDI maps can be calculated for the Neurite Density Index (NDI) and Orientation Dispersion Index (ODI), which estimate orientation dispersion and neurite density. Although NODDI has not been widely applied in MS, this technique is promising in investigating the complexity of MS pathology, as it is more specific than diffusion tensor imaging (DTI) in capturing microstructural alterations. We conducted a meta-analysis of studies using NODDI metrics to assess brain microstructural changes and neuroaxonal pathology in WM lesions and NAWM in patients with MS. Three reviewers conducted a literature search of four electronic databases. We performed a random-effect meta-analysis and the extent of between-study heterogeneity was assessed with the I2 statistic. Funnel plots and Egger’s tests were used to assess publication bias. We identified seven studies analysing 374 participants (202 MS and 172 controls). The NDI in WM lesions and NAWM were significantly reduced compared to healthy WM and the standardised mean difference of each was −3.08 (95%CI −4.22 to (−1.95), p ≤ 0.00001, I2 = 88%) and −0.70 (95%CI −0.99 to (−0.40), p ≤ 0.00001, I2 = 35%), respectively. There was no statistically significant difference of the ODI in MS WM lesions and NAWM compared to healthy controls. This systematic review and meta-analysis confirmed that the NDI is significantly reduced in MS lesions and NAWM than in WM from healthy participants, corresponding to reduced intracellular signal fraction, which may reflect underlying damage or loss of neurites.
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Abeykoon, Jithma P., Saurabh Zanwar, Stephen M. Ansell, Shaji Kumar, Carrie A. Thompson, Thomas Matthew Habermann, Thomas E. Witzig, et al. "Outcomes with rituximab plus bendamustine (R-Benda), dexamethasone, rituximab, cyclophosphamide (DRC), and bortezomib, dexamethasone, rituximab (BDR) as primary therapy in patients with Waldenstrom macroglobulinemia (WM)." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 7509. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.7509.

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7509 Background: Waldenstrom macroglobulinemia (WM) is a rare lymphoma for which scant comparative data exist to guide frontline therapy. Herein, we compare 3 commonly used regimens in WM: R-Benda, DRC, and BDR in frontline setting. Methods: Patients (Pts) with active WM seen at Mayo Clinic between 2000 & 2018 who received R-Benda, DRC or BDR as primary therapy were included in this retrospective study. Response rates were assessed by Consensus Criteria. All time to event analyses were performed from the frontline therapy, using Kaplan-Meier method. Results: The study included 172 pts with active WM (R-Benda, n=67, DRC, n=75, BDR, n=30).The median follow-up for the entire cohort was 3.7 years (y) (95% CI 3.7-3.0). Baseline characteristics, including IPSS, and time to frontline therapy from WM diagnosis were similar across the 3 cohorts. Clinically relevant endpoints are shown in the Table. Hematologic and non-hematologic toxicities were similar across the 3 groups. Grade 3 neuropathy requiring treatment discontinuation was encountered in 13% pts treated with BDR. 56 pts received subsequent salvage therapy [(10% in R-Benda arm, 44% in DRC arm, & 53% in BDR arm]; 29% pts in the R-Benda arm and 30% pts in DRC arm received a PI-based regimen while 69% pts in the BDR arm received alkylator-rituximab based therapy. Conclusions: Outcomes (MRR, TTNT and EFS) with frontline R-Benda are superior in comparison to frontline DRC or BDR in patients with WM. Clinically relevant endpoints are not significantly different with DRC vs. BDR. The toxicity profile across the 3 groups was comparable. [Table: see text]
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Sabah, Katrina, Nachshon Meiran, and Gesine Dreisbach. "Examining the Trainability and Transferability of Working-Memory Gating Policies." Journal of Cognitive Enhancement 5, no. 3 (January 27, 2021): 330–42. http://dx.doi.org/10.1007/s41465-021-00205-8.

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AbstractInternal working memory (WM) gating control policies have been suggested to constitute a critical component of task-sets that can be learned and transferred to very similar task contexts (Bhandari and Badre (Cognition, 172, 33–43, 2018). Here, we attempt to expand these findings, examining whether such control policies can be also trained and transferred to other untrained cognitive control tasks, namely to task switching and AX-CPT. To this end, a context-processing WM task was used for training, allowing to manipulate either input (i.e., top-down selective entry of information into WM) or output (i.e., bottom-up selective retrieval of WM) gating control policies by employing either a context-first (CF) or context-last (CL) task structure, respectively. In this task, two contextual cues were each associated with two different stimuli. In CF condition, each trial began with a contextual cue, determining which of the two subsequent stimuli is target relevant. In contrast, in the CL condition the contextual cue appeared last, preceded by a target and non-target stimulus successively. Participants completed a task switching baseline assessment, followed by one practice and six training blocks with the WM context-processing training task. After completing training, task-switching and AX-CPT transfer blocks were administrated, respectively. As hypothesized, compared to CL training condition, CF training led to improved task-switching performance. However, contrary to our predictions, training type did not influence AX-CPT performance. Taken together, the current results provide further evidence that internal control policies are (1) inherent element of task-sets, also in task switching and (2) independent of S-R mappings. However, these results need to be cautiously interpreted due to baseline differences in task-switching performance between the conditions (overall slower RTs in the CF condition). Importantly though, our results open a new venue for the realm of cognitive enhancement, pointing here for the first time to the potential of control policies training in promoting wider transfer effects.
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4

Adamia, Sophia, Jennifer Hodges, Patrick M. Pilarski, Steven Treon, Michael J. Mant, Tony Reiman, Andrew R. Belch, and Linda M. Pilarski. "Accumulation of Inherited and Acquired Mutations in Hyaluronan Synthase1 Gene May Contribute Oncogenesis in Multiple Myeloma and Waldenstrom’s Macroglobulinemia." Blood 108, no. 11 (November 16, 2006): 3432. http://dx.doi.org/10.1182/blood.v108.11.3432.3432.

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Abstract In multiple myeloma (MM) and Waldenstrom’s macroglobulinemia (WM), we identified three alternatively and/or aberrantly spliced HAS1 transcripts—HAS1Va, HAS1Vb and HAS1Vc. Statistical analysis of samples taken from 172 untreated MM patients showed that expression of HAS1Vb, an intronic splice variant, strongly correlates with poor survival (P=0.005). We investigated the molecular basis of intron retention during HAS1 splicing in MM and WM patients. We speculated that aberrant HAS1 splicing and the associated reduced survival of MM patients, resulted from an accumulation of mutations in aberrantly spliced regions of HAS1. Exons and introns 3 and 4 of the HAS1 gene were sequenced, because they are hotspots for splicing aberrations. Sequencing of HAS1 was performed for a total 11 patients with WM and MM and 2 healthy donors. HAS1 gene templates for sequencing were isolated from a multiple sorted cell subpopulations, including malignant B and plasma cells (PC), non-malignant T cells and buccal epithelial cells (BECs), as well as hematopoietic progenitor cells (HPCs) from mobilized blood of MM patients. We detected sets of inherited and acquired genetic variations in HAS1 that were recurrent within 5–11 of the MM and WM patients analyzed, but absent from healthy donors. We also identified genetic variations that were unique to individual patients. Those HAS1 mutations found in all cell types tested, including BECs and from the hematopoietic cells (B, PC, T and HPCS) were classified as germline mutations. Those mutations found in hematopoietic cells but absent from BECs were classified as hematopoietic origin which acquired during the lifetime of the individual. Mutations identified only in malignant MM and WM B cells and PCs (absent from T cells, HPCs and BECs) were classified as acquired tumor specific mutations. Recurrent HAS1 mutations were found among both inherited and acquired sets of mutations. Some recurrent HAS1 mutations were common to both MM and WM. The high frequency of inherited HAS1 mutations suggests that they confer predisposition for developing MM or WM. Our sequencing analysis suggests that in MM and WM, sequential accumulation of genetic variations occurs as hematopoietic cells differentiate. Our data also suggest that hematopoietic origin mutations are necessary but by no means sufficient to drive HAS1 gene splicing. Effects of hematopoietic origin mutations on HAS1 splicing are manifested in malignant MM cells in context of additional tumor specific mutations, which are acquired by circulating B cells and passed to their plasma cell progeny. This suggests that mutations which lead to aberrant splicing of HAS1 pre-mRNA undergo mutational selection events, and leave a mutational “trace” throughout the hematopoietic cell lineage, including tumor cells. Existence of same mutational events detected in HAS1 gene from MM and WM supports the speculation that the precursors of both diseases may undergo a series of shared genetic events, diverging only when tumor specific mutations accumulate in distinct subsets of B lineage cells. In silico comparison of splicesomal assembly between wild type and mutated HAS1 gene gave a pattern that precisely predicts partial retention of intron and aberrant splicing of the HAS1 gene.
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5

Famdan, Famdan, and Arif Hartono. "The Influence of Leadership Style & Environment on Employee Performance With Work Motivation as a Mediation Variable PT. Unilab Perdana." Journal Research of Social Science, Economics, and Management 2, no. 03 (October 25, 2022): 301–10. http://dx.doi.org/10.59141/jrssem.v2i03.270.

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The title of this research is the analysis of the influence of leadership style (LS) and work environment (WE) on employee performance (EP) with work motivation (WM) as a mediating variable at PT. Prime Unilab. This study aims to determine the mediating effect of work motivation in the relationship between leadership style and work environment on employee performance. This research was conducted quantitatively and used a questionnaire as a data collection method. The population is 300 employees. The research sample used was 172 employees. Therefore, sampling is simple and multiple linear regression analysis and path analysis. The results of this study indicate that leadership style and work environment have a positive and significant influence on employee performance, leadership style and work environment have a positive and significant influence on work motivation. Work motivation can mediate the relationship between leadership style and work environment on employee performance.
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6

Dimopoulos, Meletios A., Marie-Christine Kyrtsonis, Evdoxia Hadjiharissi, Argiris Symeonidis, Eurydiki Michalis, Panayiotis Repoussis, Costas Tsatalas, et al. "Validation of the International Prognostic Scoring System (IPSS) for Waldenstrom's Macroglobulinemia (WM) and the Importance of Serum Lactate Dehydrogenase (LDH)." Blood 114, no. 22 (November 20, 2009): 2845. http://dx.doi.org/10.1182/blood.v114.22.2845.2845.

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Abstract Abstract 2845 Poster Board II-821 Recently, the IPSS has been proposed as a staging system for patients with WM who require treatment. This system is based on five adverse covariates: age >65 years, hemoglobin '11.5 g/dL, platelet count '100×109/L, beta2-microglobulin >3 mg/L and serum monoclonal protein concentration >7 g/dL. Low risk is defined by the presence of ' 1 adverse characteristic and age '65 years, intermediate risk by the presence of 2 adverse characteristics or only age >65 years and high risk by the presence of >2 adverse characteristics. The aim of our analysis was to independently validate the significance of IPSS not only for overall survival (OS) but also for cause-specific survival (CSS) (i.e deaths unrelated to WM or to complications of treatment are censored). Furthermore, we wanted to assess whether elevated serum LDH may add to the strength of IPSS. From the data base of the Greek Myeloma Study Group, we identified 335 patients with clearly defined criteria for diagnosis and for initiation of treatment who were treated over the last 20 years. Main primary therapies included alkylating agents (43%), CHOP (3%), nucleoside analogues (3%) and rituximab either alone (3%) or in combination with conventional chemotherapy (44%). Before the initiation of treatment the median age of patients was 68 years (range 28 to 89 years). Fifty-nine percent of patients were >65 years, while 75% of patients had hemoglobin levels of <11.5 g/dL, 57% had beta2-microglobulin of >3 mg/L, 33% had lymphadenopathy, 32% splenomegaly, 23% presence of B-symptoms, 12% platelet count of <100×109/L and 6% had serum monoclonal protein concentration of >7 g/dL. Among 152 patients who had died by the time of this analysis, 33 patients (22%) had died due to causes not related to WM, to disease transformation, to myelodysplasia or to complications of treatment. Most frequent causes were second primary solid tumors, celebrovascular accidents, coronary artery disease and congestive heart failure. For the whole group of patients median OS was 105 months and median CSS was 116 months. Patients were divided into low risk (23%), intermediate risk (38%) and high risk (39%), according to IPSS. Median OS was 161 months, 105 months and 64 months respectively (p<0.01) and median CSS was 172 months, 116 months and 94 months, respectively (p<0.01). Elevated serum LDH >250 IU/L (normal upper limit 225 IU/L) was found in 18% of patients. Serum LDH was elevated in 16%, 12% and 24% of patients with low, intermediate and high risk, respectively. Median OS according to low or elevated LDH was 109 versus 63 months (p<0.01) and median CSS was 116 versus 64 months, respectively (p<0.01). Serum LDH was able to divide high risk patients into two subgroups with different outcome. The median OS was 94 and 35 months, for normal and high LDH group, respectively (p<0.01) and the median CSS was 104 and 36 months, for normal and high LDH group, respectively (p<0.01). We conclude that the recently proposed IPSS for WM is a robust staging system and it is also applicable to patients who received primary treatment with rituximab-based regimens. Elevated serum LDH is an adverse prognostic factor in WM. The combination of high risk according to IPSS and elevated serum LDH identified a subset of patients with very poor outcome. Such patients should be included in trials that evaluate novel agents and new treatment strategies including upfront high dose therapy. Disclosures: No relevant conflicts of interest to declare.
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7

Chaul Barbosa, Caroline, Lisa Marie DeAngelis, and Christian Grommes. "Ibrutinib associated infections: A retrospective study." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e19020-e19020. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e19020.

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e19020 Background: Ibrutinib (IBRU) is a Bruton tyrosine kinase (BTK) inhibitor that has been FDA approved for chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL) and Waldenstrom's Macroglobulinemia (WM). BTK inhibition may contribute to immunosuppression through B- and T-cell inhibition, resulting in an increase in infections. We therefore characterized IBRU-related infections retrospectively. Methods: The study was an IRB approved retrospective review. Patients (pts) treated with IBRU between 4/2014-11/2016 who developed any infection were identified using ICD10 codes in a clinical database. Study population was defined using descriptive statistics. Results: 200 pts were identified: 78 pts had CLL (39%), 30 diffuse large B-cell lymphoma (15%), 28 MCL (14%), 19 WM (9.5%), 15 (7.5%) marginal zone lymphoma, 14 (7%) follicular lymphoma, 7 (3.5%) multiple myeloma, 7 (3.5%) T-cell lymphoma and 2 (1%) primary central nervous system lymphoma (PCNSL). Median age was 68 (range 28-96), 34% were men and median ECOG was 1. The majority of pts received IBRU as second line treatment (172, 86%) with a median of 2 prior lines of treatment; 23 pts (11.5%) were post transplant. Median IBRU dose was 420mg daily (range 140-840mg), administered a median of 316 days (range 3-1780). Single agent IBRU was used in 162 pts (81%). 105 pts (52%) developed an infection, with pneumonia (30%), upper airway infection (26%); skin infection (18%); and sinusitis (13%) being the most common. 10 (9.5%) had neutropenic fever and 1 (1%) cryptococcal pneumonia. Seven (7%) developed fungal infections, with invasive aspergillosis in 5 (5%). 34 (32%) developed ≥3 infections. 46 pts (44%) were hospitalized, 10 (9.5%) interrupted IBRU and 3 pts (2.9%) died due to infections (2 pneumonia; 1 neutropenic fever). The median time to infection after starting IBRU was 70 days (range 2-1261). The highest infection rate was seen in pts with PCNSL (100%, 2/2), MZL (67%, 10/14), followed by CLL (64%, 50/78). Conclusions: We identified infections in half of the pts treated with IBRU. Pts treated with IBRU should be monitored closely for the development of infections, particularly airway infections.
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Dale, David C., Steven P. Treon, David F. McDermott, Diego Cadavid, Xia Luo, Varun Garg, Weihua Tang, et al. "Oral Administration of Mavorixafor, a CXCR4 Antagonist, Increases Peripheral White Blood Cell Counts across Different Disease States." Blood 138, Supplement 1 (November 5, 2021): 2186. http://dx.doi.org/10.1182/blood-2021-152990.

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Abstract Introduction: Peripheral leukocyte deficiency is a common feature of multiple diseases and may render affected individuals susceptible to infections, both common and opportunistic. The CXCR4 chemokine receptor regulates the trafficking of leukocytes among the bone marrow, blood, and lymphatic system (Al Ustwani O, et al. Br J Haematol. 2014;164:15-23). Mavorixafor is an orally available investigational, small-molecule, selective antagonist of the CXCR4 receptor with potential to restore physiological trafficking and maturation of white blood cells (WBCs). Mavorixafor was previously shown to increase totals and subsets of WBCs in healthy volunteers and in a phase 2 clinical trial in adults with WHIM (Warts, Hypogammaglobulinemia, Infections, Myelokathexis) syndrome (Stone N, et al. Antimicrob Agents Chemother. 2007;51(7):2351-2358; Dale D, et al. Blood. 2020;136(26):2994-3003). Here, we report the effect of daily oral administration of mavorixafor on peripheral WBC counts and subsets in patients with clear cell renal cell carcinoma (ccRCC), WHIM syndrome, and Waldenström's macroglobulinemia (WM). Methods: Percentage changes in total peripheral WBC count, absolute neutrophil count (ANC), absolute lymphocyte count (ALC), and absolute monocyte count (AMC) from pretreatment levels were evaluated in the following settings: a phase 1/2 trial evaluating mavorixafor (200 mg twice daily or 400 mg once daily [QD]) in combination with axitinib (5 mg twice daily) in patients with advanced ccRCC who received ≥1 prior therapy; a phase 1b trial evaluating mavorixafor (400 mg QD) in combination with nivolumab (240 mg QD) in patients with metastatic ccRCC unresponsive to prior nivolumab monotherapy; a long-term extension of the aforementioned phase 2 trial evaluating mavorixafor 300 or 400 mg QD in patients with WHIM syndrome with pathogenic CXCR4 gain-of-function mutation and ANC ≤400/μL and/or ALC ≤650/μL; and an ongoing phase 1b trial evaluating mavorixafor (200 mg QD for 4 weeks, increased to 400 mg and 600 mg QD thereafter) in combination with ibrutinib (420 mg QD) in patients with WM with MYD88 and CXCR4 mutations. Results: In the study evaluating combination mavorixafor (400 mg QD) and axitinib in ccRCC, total WBC count, ANC, ALC, and AMC increased to 153%, 158%, 143%, and 182% of baseline after 4 weeks (n=49), and with increases sustained at 159%, 171%, 139% and 166% of baseline after 6 months' treatment (n=20). In the study evaluating mavorixafor in combination with nivolumab in ccRCC, total WBC count, ANC, ALC, and AMC increased to 146%, 143%, 141%, and 179% of baseline after 4 weeks (n=9), and with increases sustained at 147%, 136%, 152%, and 191% of baseline after 6 months (n=2). In an interim analysis of the phase 1b trial in WM, compared to screening values, total WBC count, ANC, ALC, and AMC increased to 192%, 170%, 219%, and 186% of baseline after 4 weeks (n=8), and with increases sustained at 163%, 192%, 106%, 172% of baseline after 6 months' (n=5) treatment. In the WHIM syndrome phase 2 extension, total WBC count, ANC, ALC, and AMC increased to 339%, 652%, 239%, and 486% of baseline after 6 months' (n=5) treatment, with annualized infection rate decreasing from 5.6 (SD ± 3.13) events at baseline to 2.2 (SD ± 0.93) events after 40 months. Mavorixafor was generally well tolerated, with manageable safety profile across all indications either alone or in combination with other drugs. Conclusions: Mavorixafor alone or in combination with other therapies is the first oral treatment to either acutely or chronically increase total peripheral WBCs 1.5- to 3-fold and WBC subsets across all disease populations examined, in both the presence (WHIM syndrome and WM) and absence (ccRCC and healthy volunteers) of CXCR4 gain-of-function mutation. Increases in WBC subsets occurred rapidly and were sustained during chronic treatment, with a larger treatment effect in patients with pre-existing cytopenia (WHIM syndrome) compared to patients without cytopenia at baseline (ccRCC and WM). Co-occurring reduction in infection burden was observed in the phase 2 trial in WHIM syndrome. Assessment of the beneficial effects of mavorixafor on total and WBC subsets is ongoing in a phase 3 trial of WHIM syndrome and a phase 1 trial of severe chronic neutropenia (SCN) that will assess the potential to correct cytopenias by elevating total WBC counts. Disclosures Dale: X4 Pharmaceuticals: Consultancy, Honoraria, Research Funding. Treon: AbbVie: Consultancy, Research Funding; Dana Farber Cancer Institute: Current Employment; Self: Patents & Royalties: Holder of multiple patents related to testing and treatment of MYD88 and CXCR4 mutated B-cell malignancies; BMS: Consultancy, Research Funding; BeiGene: Consultancy, Research Funding; Janssen: Consultancy, Research Funding; Pharmacyclics: Consultancy, Research Funding; X4: Research Funding. McDermott: Johnson and Johnson: Consultancy, Honoraria; Genentech: Research Funding; Eisia Inc.: Consultancy, Honoraria; Werewolf Therapeutics: Consultancy, Honoraria; Calithera Biosciences: Consultancy, Honoraria; X4 Pharmaceuticals: Research Funding; Iovance: Consultancy, Honoraria; EMD Serono: Consultancy, Honoraria; BMS: Consultancy, Honoraria, Research Funding; Merck: Consultancy, Honoraria, Research Funding; Pfizer: Consultancy, Honoraria, Research Funding; Exelixis: Research Funding; Alkermes, Inc.: Consultancy, Honoraria, Research Funding; Eli Lilly and Company: Consultancy, Honoraria. Cadavid: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Luo: X4 Pharmaceuticals: Consultancy. Garg: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Tang: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Jiang: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Chen: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Taveras: X4 Pharmaceuticals: Current Employment, Current equity holder in publicly-traded company. Bhandari: X4 Pharmaceuticals: Current Employment.
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9

Lu, Jiadong, Songli Zhang, Leizhi Zhang, Chenxi Wang, and Chunying Min. "Preparation and Properties of Hollow Glass Microspheres/Dicyclopentadiene Phenol Epoxy Resin Composite Materials." Materials 16, no. 10 (May 16, 2023): 3768. http://dx.doi.org/10.3390/ma16103768.

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With the development of the integrated circuit and chip industry, electronic products and their components are becoming increasingly miniaturized, high-frequency, and low-loss. These demand higher requirements for the dielectric properties and other aspects of epoxy resins to develop a novel epoxy resin system that meets the needs of current development. This paper employs ethyl phenylacetate cured dicyclopentadiene phenol (DCPD) epoxy resin as the matrix and incorporates KH550 coupling-agent-treated SiO2 hollow glass microspheres to produce composite materials with low dielectric, high heat resistance, and high modulus. These materials are applied as insulation films for high density interconnect (HDI) and substrate-like printed circuit board (SLP) boards. The Fourier transform infrared spectroscopy (FTIR) technique was used to characterize the reaction between the coupling agent and HGM, as well as the curing reaction between the epoxy resin and ethyl phenylacetate. The curing process of the DCPD epoxy resin system was determined using differential scanning calorimetry (DSC). The various properties of the composite material with different HGM contents were tested, and the mechanism of the impact of HGM on the properties of the composite material was discussed. The results indicate that the prepared epoxy resin composite material exhibits good comprehensive performance when the HGM content is 10 wt.%. The dielectric constant at 10 MHz is 2.39, with a dielectric loss of 0.018. The thermal conductivity is 0.1872 Wm−1 k−1, the coefficient of thermal expansion is 64.31 ppm/K, the glass transition temperature is 172 °C, and the elastic modulus is 1221.13 MPa.
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Kriangkum, Jitra, Andrew R. Belch, and Linda M. Pilarski. "Clinically Significant Aberrant HAS1Vb Splicing of the Hyaluronan Synthase 1 Gene (HAS1) Requires a Combination of Mutations and Deletions in Introns 3 and 4 of HAS1 Minigene,." Blood 118, no. 21 (November 18, 2011): 3931. http://dx.doi.org/10.1182/blood.v118.21.3931.3931.

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Abstract Abstract 3931 Clinically important aberrant splicing of the hyaluronan synthase 1 gene (HAS1) occurs in malignant B cells from multiple myeloma (MM) and Waldenstrom macroglobulimenia (WM) patients but is undetectable in B cells from healthy donors (HD)1. HAS1 splice variants are generated by aberrant alternative splicing (AS) within exons 3, 4 and 5, involving exon 4 skipping (Va), partial intron 4 retention (Vc, Vd) or a combination of both (Vb). Aberrant splicing of HAS1Vb has previously shown to correlate with reduced survival in a cohort of MM patients1. In patients, frequent mutations have been identified in introns 3 and 4, suggesting their roles in AS1. To identify genetic regions involved in splice site selection leading to HAS1Vb expression, we performed in vitro sequence manipulation of introns 3 and 4. We established a mammalian expression system to analyse HAS1 splicing by fusing a minigene extending from exon 3 to exon 5 with the upstream cDNA sequence. In an unaltered sequence of the HAS1 minigene, splicing of HAS1 full length predominated, with trace amount of variants, including the novel HAS1Vd, identified for the first time in transfectants. HAS1Vd shared an alternative acceptor site with HAS1Vb (retained 59 bp of downstream intron 4) but unlike HAS1Vb, retained exon 4. Analysis of peripheral blood mononuclear cells (PBMC) revealed that 9% of healthy donors (n=102) and MM patients (n=93) expressed HAS1Vd. About 2% coexpressed HAS1Vb and Vd. In this cohort of patients, HAS1Vb was found in 20% of unfractionated MM PBMC compared to 5% in HD PBMC, supporting our previous finding that HAS1Vb was restricted to sorted MM B cells1and suggesting that in HD PBMC, non-B cells are responsible for this splicing. While MM PBMCs expressed HAS1Vb>Vd, HD PBMCs and transfectants expressed HAS1Vd>Vb, indicating that splicing directed by the minigene construct was substantively different from that occurring in MM patients. In transfectants, partial deletion of HAS1 intron 4 increased HAS1Vd expression but did not affect HAS1Vb despite the fact that both variants use the same 3' splice site in intron 4. Proper joining of exons 3, 4 and 5 required a minimum of 172 bp of downstream intron 4 and acceptor site selection may be regulated by sequence between 172 and 84 bp upstream of exon 5. Thus, changes in intron 4 alone were insufficient to promote the splicing pattern observed in patients (i.e., elevated HAS1Vb). We then employed site directed mutagenesis to alter multiple G-rich regions in downstream intron 3, a strategy which enhanced exon 4 skipping as shown by increased HAS1Va expression, but did not lead to HAS1Vb splicing. Minimal manipulation to promote exon 4 skipping included base changes within the 2 tandem G-repeats (8 bp) located 73 bp upstream of exon 4, where splicing enhancer/silencer sequences were also identified. Thus, changes in intron 3 also affected the HAS1 splicing profile but like deletions in intron 4, were insufficient on their own to promote HAS1Vb expression. We next developed expression constructs that combined deletion in intron 4 with mutations in intron 3. We are able to demonstrate that when both introns were co-modified, the splicing pattern shifted towards increased HAS1Vb expression, similar to that observed in malignant cells from MM patients. Our previous work showed that deletions or mutations in the 3' end of intron 4 are frequent in MM; in silico analysis predicts splicing to form HAS1Vb2. To determine whether intron 3 genetic changes occur in patients, we sequenced intron 3 from genomic DNA of 50 MM PBMC. In 22/50 patients, 18 recurrent mutations unique to MM were identified in intron 3; many were also recurrent in our previous study2. Individual mutations recurred in 2–7 patients. Among these, 17/18 recurrent mutations increased the G-C content of intron 3 and 6/18 created or disrupted G runs in intron 3. This supports the idea that in MM patients, cumulative variations in introns 3 and 4 alter splice site selection, operationally resulting in loss of HAS1Vd and enhanced expression of the clinically relevant HAS1Vb variant. We speculate that individuals who accumulate genetic variations in introns 3 and 4 of HAS1 are predisposed to aberrant splicing of HAS1 which may contribute to development of malignancy in MM and WM. Disclosures: Belch: Celgene: Research Funding; Onyx: Research Funding.
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Books on the topic "Wm 172"

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L, Cooper Cary, and Payne Roy, eds. Personality and stress: Individual differences in the stress process. Chichester: Wiley, 1991.

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Van der Kolk, Bessel A., 1943-, ed. Psychological trauma. Washington, DC: American Psychiatric Press, 1987.

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Kabat-Zinn, Jon. Full catastrophe living: Using the wisdom of your body and mind to face stress, pain, and illness. New York, N.Y: Pub. by Dell Publishing, a division of Bantam Doubleday Dell Pub. Group, 1991.

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Caroline, Garland, ed. Understanding trauma: A psychoanalytical approach. London: Duckworth, 1998.

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R, Bancroft Pauline, and Ardley Leli B, eds. Major depression in women. New York: Nova Biomedical Books, 2008.

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Krin, Gabbard, ed. Psychiatry and the cinema. 2nd ed. Washington, DC: American Psychiatric Press, 1999.

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M, Drummond Lynne, ed. The practice of behavioural and cognitive psychotherapy. Cambridge: Cambridge University Press, 1991.

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1959-, Pathé Michele, and Purcell Rosemary 1969-, eds. Stalkers and their victims. 2nd ed. Cambridge: Cambridge University Press, 2009.

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Williams, Ruth, MA (Oxon), Dip. Psych. and Yule William, eds. Understanding post-traumatic stress: A psychosocial perspective on PTSD and treatment. Chichester: J. Wiley, 1997.

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J, Barnard Philip, ed. Affect, cognition, and change: Re-modelling depressive thought. Hove, UK: L. Erlbaum Associates, 1993.

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Book chapters on the topic "Wm 172"

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"M 18 a3c ( L 3) e : a2n07L -D 21 , 7 M , e1a9k7i5n . s TL, Taguchi K, Duignan TP, Dhillon KS, Gordon J. Ann Surg 4. Nielsen HJ, Hammer JH, Moesgaard F, Kehlet H. Surgery 105(6):711-719, 1989. 5. B 67 ro 6 w , n19R8 , 2 . Bancewicz J, Hamid J, Tillotson G, Ward C, Irving M. Ann Surg 196(6):672-6. Fernandez LA, MacSween JM, You CK, Gorelick M. Am J Surg 1613:263-270, 1992. 7. H 57 a , m 1 id 98J4 , . Bancewicz J, Brown R, Ward C, Irving MH, Ford WL. Clin Exp Immunol 56:49-8. Tartter PI, Steinberg B, Barron DM, Martinelli G. Arch Surg 122:1264-1268. 1987. 9. J M en o s ll eenr -N LS ie , ls A en ndCe , rsH en anAbJe , rg C -S hr oirse ti nasnesnenF , PHMo , klH an odk la M n . dBP, r J Ju Shul rg CO7 , 9 M :51 ad 3 s -5 en 16G , , 19M 92 o . rtensen J, 10. Fisher E, Lennard V, Siefert P Kluge A, Johannsen R. Human Immunol 3:187-194, 1980. 11. L 10 e1n5n , ar1d9V 83 , . Maassen G, Grosse-Wilde H, Wernet P, Opelz G. Transplant Proc 15(1): 1011-12. F1o9r8d7 . CD, Warnick CT, Sheets S, Quist R, Stevens LE. Transplant Proc 19( 1): 1:456-457, 13. Cox DR. Analysis of binary data, Methuen: London, 1970. 14. Murphy PJ, Connery C, Hicks GL Jr, Blumberg N. J Thoracic Cardiovasc Surgery (in press). 15. A Pa rc tc hheSnu rg Deerlyl in 1g2e3r ( E 1 , 1 ) M : 1i3 ll 2e0r -1 S3D2 , 7 , W1e9r8 tz 8 . MJ, Grypma M, Droppert B and Anderson PA. 16. D 12 e 3 ll : i1n3g2e0r -1 E3P2 , 5 M , 1 il 9 le 8r8 , SD, Wertz MJ, Grypha M, Droppert B, Anderson PA. Arch Surg 17. Dawes LG, Aprahamian C, Condon RE and Malongi MA. Surgery 100:796-803, 1986. 18. Tartter PI. Br J Surg 75:789-792,1988. 19. A Lo gsarAwnagleN le , s , MAuprrpihly1J9G 92 , . Cayten CG, Stahl WM. Presented to the Surgical Infection Society, 20. Truilzi DJ, Vanek K, Ryan DH and Blumberg N. Transfusion (accepted for publication). 21. Murphy P, Heal JM and Blumberg N. Transfusion 31:212-217,1991. 22. Mezrow CK, Berstein I and Tartter PI. Transfusion 32:27-30, 1992. 23. BMuesdch3R2C8 , : 1 H 37 o2p , W 19 C9J3 , . Hoynck van Zpapendrecht MAW, Marquet RL, Jeekel J. N Engl J 24. W 19 a8y7m . ackJP, Warden GD, Miskell P, Gonce S, Alexander JW. World J Surg 11:387-391, 25. WaymackJP, Robb E, Alexander JW. Arch Surg 122:935-939, 1987." In Transfusion Immunology and Medicine, 301. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-30.

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Conference papers on the topic "Wm 172"

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Horowitz, Moshe, and Baruch Fischer. "On the Buildup and Decay of Photorefractive Wave Mixing Processes." In Photorefractive Materials, Effects, and Devices II. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/pmed.1991.mb2.

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Photorefractive media have been used for many novel applications in image processing. One interesting use is the novelty filter which is an all optical processor based on the response of two wave mixing (2-WM) or four wave mixing (4-WM) [1,2]. It is obvious that the temporal dymnamics of the wave mixing process is essential to understand such processes. However, since the overall photorefractive dynamics, including the wave mixing part, is described by complicated nonlinear partial differential equations, it is hard to obtain a general solution. The study has been largely limited to steady state behavior and the response of the photorefractive material only, without taking into account the dynamics of the wave coupling effects.
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Pashayi, Kamyar, Hafez Raeisi Fard, Fengyuan Lai, Joel Plawsky, and Theodorian Borca-Tasciuc. "Annealing Temperature Effect on the Structure of High Thermal Conductivity Silver/Epoxy Nanocomposites." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-65578.

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The thermal conductivity κ of polymer nanoparticle composites is typically <10 Wm−1K−1, even when high κ nanofillers are employed, due to the thermal interface resistance between nanoparticles and the polymer matrix1 or the absence of high thermal conductivity pathways. We recently demonstrated high κ in bulk nanocomposites of silver nanoparticles dispersed in epoxy and cured at low temperature (150 °C). A nanocomposite with 30 vol. % 20nm particles exhibited κ ∼30 Wm−1K−1.2 The mechanism responsible for enhancing κ was found to be the self-construction, through in-situ sintering, of high aspect ratio metallic networks inside the nanocomposite.2 In order to control and optimize the network structure and subsequently increase κ even further, this work focuses on studying the effects of curing temperature and nanoparticle surface coating on the structure of the nanocomposite.
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Reifenberg, J., R. England Voss, P. Rao, W. Schmitt, Y. Yang, S. Shojaei-Zadeh, W. Liu, S. M. Sadeghipour, and M. Asheghi. "Thermal Conductivity Measurements of Thin Aluminum Layers Using Steady State Joule Heating and Electrical Resistance Thermometry in Suspended Bridges." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-42055.

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Thin metallic film layers are extensively used as the constituents of the micro-devices. The reliability of these devices, therefore, strongly depends on the thermal behavior of such film layers. Aluminum thin film layers are of particular interest in this respect. The lateral thermal conductivity of the aluminum film layers is measured, using the steady state electrical Joule heating and electrical resistance thermometry technique. Aluminum suspended microbridges of identical thicknesses (500 nm) and variable widths (16 to 18 μm) and/or lengths (200 to 500 μm) are fabricated, using conventional microfabrication processes. The lateral thermal conductivity of the 500 nm thick Aluminum film layer was found to be k = 174 ± 13 Wm−1 K−1, at room temperature (300 K).
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Son, Hye jin, Minki Lee, Seongrak Kim, Jai-Hee Moon, Hana Kim, Wonhwa Shin, Joseph Kim, et al. "Abstract 1216: New therapeutic antibody ("WM-A1") for treatment of low or no PD-L1 NSCLC patients." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1216.

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Hong, Chungpyo, and Yutaka Asako. "Heat Transfer Characteristics of Gaseous Flows in Micro-Channels With Negative Heat Flux." In ASME 4th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2006. http://dx.doi.org/10.1115/icnmm2006-96163.

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Two-dimensional compressible momentum and energy equations are solved to obtain the heat transfer characteristics of gaseous flows in micro-channels with CHF (constant heat flux) whose value is negative. The combined effect of viscous dissipation and compressibility is also investigated. The numerical methodology is based on the Arbitrary-Lagrangian-Eulerian (ALE) method. The computations are performed for channels with constant heat flux with range from −104 to −102 Wm−2. The channel height ranges from 10 to 100 μm and the aspect ratio of the channel height and length is 200. The stagnation pressure varies from 120 to 500 kPa. The outlet pressure is fixed at the atmosphere. The wall and bulk temperatures in micro-channels are compared with those of the case of positive heat flux and also compared with those of the incompressible flow in a conventional sized channel. In the case of negative heat flux, temperature profiles normalized by heat flux have different trends in the case of positive heat flux, when flow is fast. A gas temperature falls down due to the energy conversion. A correlation for the prediction of the wall temperature of the gaseous flow in the micro-channel is proposed.
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Ailawadhi, Sikander, Jarrod Longcor, Kate Oliver, and Igor D. Grachev. "Abstract PO-25: CLR 131 demonstrates 100% overall response rate in relapsed or refractory lymphoplasmacytic lymphoma (LPL)/Waldenstrom's macroglobulinemia (WM): initial results from ongoing phase 2 trial, CLOVER-1 study." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-po-25.

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Berndt, M. C., X. Du, L. Beutler, W. J. Booth, and P. A. Castaldi. "LOCALIZATION OF FUNCTIONAL DOMAINS ON HUMAN PLATELET GP Ib-IX COMPLEX BY EPITOPE ANALYSIS WITH MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642923.

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There is now considerable evidence that glycoprotein (GP) Ib plays an important functional role in the von Willebrand factor (vWF)-dependent adhesion of platelets to exposed vascular subendothelium and in the a-thrombin activation of platelets, and that GP IX is important for quinine/quinidine drug-dependent antibody platelet recognition. GP Ib (Mr = 170 KD) consists of two disulfide-linked subunits, Iba (Mr = 135 KD) and Ibβ (Mr = 25 KD), and exists as a heterodimer complex with GP IX (Mr = 22 KD). In this study we have used a panel of 10 antiGP Ib-IX complex monoclonal antibodies to define the functional domains on this complex. Immunoprecipitation of trypsin-treated GP Ib-IX complex revealed that the monoclonal antibodies mapped into three distinct groups: FMC 25, AK 1 and SZ 1, epitopes on the membrane-associated fragment (GP IX and an ≃25 KD remnant of the α-chain disulfide linked to the β-chain); AK 3 and WM 23, epitopes on the central macroglycopeptide core (90 KD); AN 51, SZ 2, AK 2, AP 1 and HIP 1, epitopes on peptide tail (45 KD). Crossblocking studies indicated that with the exception of AK 1 and SZ 1, the monoclonal antibodies were directed against distinct epitopes. All five monoclonal antibodies directed against the peptide tail region blocked ristocetin-dependent vWF-platelet interaction whereas the other five monoclonal antibodies were without effect, indicating that the 45 KD peptide tail region at the plasma end of the α-chain of GP Ib contained the vWF binding domain. Similarly, only the three monoclonal antibodies directed against the membrane-associated region interfered with drug-dependent antibody-platelet interaction.By western blot analysis, α-thrombin bound to the 45 KD peptide tail region. However, only AP 1 interfered significantly with the α-thrombin-dependent aggregation of platelets. This panel of epitope-defined monoclonal antibodies should be of value in further defining the structure-function relationships of this important membrane complex.
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