tbuckley/cabot-search huggingface dataset:
Peer Mentoring and Financial Incentives to Improve Glucose Control in African American Veterans
Authors: Judith A. Long, Erica C. Jahnle, Diane M. Richardson, George Loewenstein, Kevin G. Volpp
Journal: Annals of Internal Medicine (2012)

Background: Compared with white persons, African Americans have a greater incidence of diabetes, decreased control, and higher rates of microvascular complications. A peer mentorship model could be a scalable approach to improving control in this population and reducing disparities in diabetic outcomes. Objective: To determine whether peer mentors or financial incentives are superior to usual care in helping African American veterans decrease their hemoglobin A1c (HbA1c) levels. Design: A 6-month randomized, controlled trial. (ClinicalTrials.gov registration number: NCT01125956) Setting: Philadelphia Veterans Affairs Medical Center. Patients: African American veterans aged 50 to 70 years with persistently poor diabetes control. Intervention: 118 patients were randomly assigned to 1 of 3 groups: usual care, a peer mentoring group, and a financial incentives group. Usual care patients were notified of their starting HbA1c level and recommended goals for HbA1c. Those in the peer mentoring group were assigned a mentor who formerly had poor glycemic control but now had good control (HbA1c level ≤7.5%). The mentor was asked to talk with the patient at least once per week. Peer mentors were matched by race, sex, and age. Patients in the financial incentive group could earn $100 by decreasing their HbA1c level by 1% and $200 by decreasing it by 2% or to an HbA1c level of 6.5%. Measurements: Change in HbA1c level at 6 months. Results: Mentors and mentees talked the most in the first month (mean calls, 4; range, 0 to 30), but calls decreased to a mean of 2 calls (range, 0 to 10) by the sixth month. Levels of HbA1c decreased from 9.9% to 9.8% in the control group, from 9.8% to 8.7% in the peer mentor group, and from 9.5% to 9.1% in the financial incentive group. Mean change in HbA1c level from baseline to 6 months relative to control was −1.07% (95% CI, −1.84% to −0.31%) in the peer mentor group and −0.45% (CI, −1.23% to 0.32%) in the financial incentive group. Limitation: The study included only veterans and lasted only 6 months. Conclusion: Peer mentorship improved glucose control in a cohort of African American veterans with diabetes. Primary Funding Source: National Institute on Aging Roybal Center.
Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection
Authors: A. Haas, K. Zimmermann, F. Graw, E. Slack, P. Rusert, B. Ledergerber, W. Bossart, R. Weber, M. C. Thurnheer, M. Battegay, B. Hirschel, P. Vernazza, N. Patuto, A. J. Macpherson, H. F. Gunthard, A. Oxenius
Journal: Gut (2011)

<h3>Background</h3> Human systemic antibody responses to commensal microbiota are not well characterised during health and disease. Of particular interest is the analysis of their potential modulation caused by chronic HIV-1 infection which is associated with sustained enteropathy and systemic B cell disturbances reflected by impaired B cell responses and chronic B cell hyperactivity. The mechanisms underlying B cell hyperactivation and the specificities of the resulting hypergammaglobulinaemia are only poorly understood. <h3>Methods</h3> By a technique referred to as live bacterial FACS (fluorescence-activated cell sorting), the present study investigated systemic antibody responses to several gut and skin commensal bacteria as well as <i>Candida albicans</i> in longitudinal plasma and serum samples from healthy donors, chronic HIV-1-infected individuals with or without diarrhoea and patients with inflammatory bowel disease (IBD). <h3>Results</h3> The data show that systemic antibody responses to the commensal microbiota were abundantly present in humans and remained remarkably stable over years. Overall systemic antibody responses to gut commensal bacteria were not affected during chronic HIV-1 infection, with titres decreasing when normalised to elevated plasma immunoglobulin G (IgG) levels found in patients with HIV. In contrast, increases in the titres of high affinity antimicrobiota antibodies were detected in patients with IBD, demonstrating that conditions with known increased intestinal permeability and aberrant mutualism can induce changes in antibody titres observed in these assays. <h3>Conclusion</h3> Neither HIV-associated enteropathy nor B cell dysfunction impact on the high-affinity systemic antibody responses to gut commensal bacteria. HIV-associated hypergammaglobulinaemia is therefore unlikely to be driven by induction of antimicrobiota antibodies.
Sandblasting jeans kills young people
Authors: A. Çimrin, T. Sigsgaard, B. Nemery
Journal: European Respiratory Journal (2006)

To the Editors: 

At this year’s annual congress of the Turkish Thoracic Society (TTS), a mini-symposium was devoted to the occurrence of silicosis in the textile sector in Turkey. Clinicians from four cities reported on a total of 35 subjects with silicosis: 20, 10, four and one cases from Erzurum, Izmir, Tokat and Diyarbakir, respectively 1–4. Nearly all patients were young males in their early twenties or even younger. They had been employed, often as undeclared workers, for only …
The Treatment of Lupus
Authors: J. H. Stowers
Journal: BMJ (1885)

1Uof the placenta was the pulseless and flabby state of the cord.When this "was obtained, then each case could be treated on its own merits; if there were hTmorrhage, more or less active interference was required.If there were no haimorrhage there really was no heedfor activre interference, and simple means, such as gentle friction or expression, w-ould often caus the placenta to conme away.Mr. WADDELL (Newry), related a case which had occurred in his practice, in 1866.He was called to a woman in the sixth month of pregnancy, and found her in labour.She was delivered of a dead foetus, the placenta of which, after it had become detached, he removed.At the same time he felt the movements of another child.This was retained, and the woman was delivered of a healthy boy at full term, three months afterwards.He believed that if he had been in too great a hurry to remove the first placenta and had employed the usual means for doing so, the second child would have been lost.The PRESIDENT (Dr.Godson), considered that very different ideas were entertained as to tlle meaningo of the terms " Expression of the placenta," and " Expectant methoS." He could not over-estimate the
Does valganciclovir have a role in glioblastoma therapy?
Authors: C. S. Cobbs
Journal: Neuro-Oncology (2014)

In 2002, we published the first evidence that cytomegalovirus (CMV) infection is associated with a high percentage of malignant gliomas and glioblastomas (GBM).1 These findings have been confirmed independently by several groups, yet other groups have found no evidence of CMV in GBM.2,3 Ongoing investigations related to low-level viral copy number and possible abortive infection of CMV suggest that the CMV infection detected in GBM by many groups is quantitatively different from the typical fulminant infections seen in fetuses and immunocompromised patients.
Reversal of Warfarin-Induced Excessive Anticoagulation with Recombinant Human Factor VIIa Concentrate
Authors: Ruby Anne E. Deveras
Journal: Annals of Internal Medicine (2002)

Bleeding associated with warfarin anticoagulation correlates directly to duration and degree of international normalized ratio (INR) elevation above the therapeutic range. Safe and rapid reversal of excessive anticoagulation is occasionally needed to treat or avoid hemorrhagic complications.To evaluate the efficacy and safety of human recombinant factor VIIa (rFVIIa) concentrate in persons requiring rapid reversal of the effects of warfarin.Uncontrolled case series.Academic medical center.13 patients with critically increased INRs requiring immediate reversal of warfarin-induced anticoagulation.Prothrombin time and INR were measured before and after administration of varying doses of rFVIIa.Critically prolonged INR and bleeding complications were treated successively and rapidly in all patients, regardless of rFVIIa dose (range, 15 to 90 microg/kg of body weight). Indications for use of rFVIIa included an INR greater than 10 in high-risk persons (n = 5), clinical hemorrhage (n = 4), and diagnostic or therapeutic procedures (n = 4).Safe, rapid, and effective administration of rFVIIa corrects critically prolonged INRs and can avert or reverse bleeding associated with warfarin anticoagulation.
Protein Structural Influences in Rhodopsin Evolution
Authors: L. Marsh
Journal: Molecular Biology and Evolution (2005)

Incorporating specific structural information can be important for developing a realistic model of evolution for phylogenetic reconstruction of protein-coding genes. We analyzed 62 sequences of vertebrate rhodopsin. The bovine rhodopsin structure was used to label residue sites by surface accessibility, secondary structure, and transmembrane (TM) location. Residue sites with amino acid differences were identified; using maximum parsimony (MP), homoplasious residues were identified. Residues were analyzed for patterns that would indicate correlation of rate with secondary structure, surface accessibility, or position relative to the lipid bilayer. Surface residues, especially those residing in one of the seven TM helices, were significantly correlated with high rates of amino acid substitution. This category of residues, defined solely by protein structural characteristics, potentially defined a class enriched in homoplasious residues. MP analysis using all sites led to a tree with anomalies in the relationships of amphibian, mammalian, bird, and alligator species. Analysis excluding the structurally defined residue class recovered a more accurate phylogeny. A model is presented for including structural influences on rate in phylogenetic inference.
Resistance of Cancers to Immunologic Cytotoxicity and Adoptive Immunotherapy via X-Linked Inhibitor of Apoptosis Protein Expression and Coexisting Defects in Mitochondrial Death Signaling
Authors: Rajani Ravi, Ephraim J. Fuchs, Ajay Jain, Vui Pham, Kiyoshi Yoshimura, Traci Prouser, Sanju Jalla, Xianzheng Zhou, Elizabeth Garrett-Mayer, Scott H. Kaufmann, Richard D. Schulick, Drew M. Pardoll, Atul Bedi
Journal: Cancer Research (2006)

Abstract The ability of cancers to evade immune surveillance and resist immunotherapy raises a fundamental question of how tumor cells survive in the presence of a competent immune system. Studies to address this question have primarily focused on mechanisms by which tumor cells avoid recognition by or induce tolerance in the immune system. However, little is known about whether cancer cells also acquire an intrinsic ability to resist killing by immune effectors. We find that cancer cells enhance their ability to withstand an attack by cytotoxic immune effector cells via acquisition of specific genetic alterations that interfere with the shared mitochondrial death signaling pathway entrained by granzyme B, IFN-γ, and Apo2 ligand/tumor necrosis factor–related apoptosis inducing ligand (Apo2L/TRAIL), three key mediators of immunologic cell–mediated cytotoxicity. We show that the coexistence of specific mitochondrial signaling defects (either deletion of Bax, overexpression of Bcl-xL, or deletion of Smac) with expression of X-linked inhibitor of apoptosis protein decreases the sensitivity of cancer cells to IFN-γ/Apo2L/TRAIL– or granzyme B–induced apoptosis, lymphocyte-mediated cytotoxicity in vitro, and adoptive cellular immunotherapy in vivo. Conversely, negating X-linked inhibitor of apoptosis protein expression or function in tumor cells with defective mitochondrial signaling enables direct activation of caspase-3/-7 by granzyme B or Apo2L/TRAIL, and restores their susceptibility to immunologic cytotoxicity. These findings identify an important mechanism by which cancers evade elimination by immune effector cells and suggest that cancer immunotherapy might be improved by concurrent strategies to alleviate or circumvent the intrinsic mitochondrial death signaling defects that help cancer cells resist immunologic cytotoxicity. (Cancer Res 2006; 66(3): 1730-9)
Living donor for liver transplantation
Authors: C BROELSCH
Journal: Hepatology (1994)

Since living related liver transplantation was first performed in 1989, more than 150 cases have been performed worldwide, mostly in the United States and Japan. This paper reports the first series of living related liver transplantation in Europe. Twenty living related liver transplantation surgeries were performed over a 13-mo period, with an overall patient survival of 85%. For patients who underwent elective transplantation (n = 13), the survival rate was 100%. Technical complications included one arterial thrombosis necessitating retransplantation and five bile leaks requiring surgical revision. The technical improvements that permit avoidance of these complications are discussed. A detailed description of the living related liver procurement is given. All procurements yielded grafts of excellent quality. No intraoperative complications occurred, and no reoperations were necessary. No heterologous blood transfusion was needed. In two patients, incisional hernias developed after wound infection. Living related liver transplantation does not absolve the transplant community of efforts to promote cadaveric organ procurement. Nevertheless, living related liver transplantation does have the advantage of a readily available graft of excellent quality, permitting transplantation with optimal timing under elective conditions. Several centers are now preparing living related segmental liver transplants, following the model of our protocol, for three reasons: (a) to obtain superior results compared with cadaveric liver transplantation; (b) to overcome cadaveric organ shortage and further reduce pretransplantation mortality and (c) to provide viable organs in countries where cadaveric organ procurement is not established. When performed by a team experienced in pediatric liver transplantation and in adult liver resection, living related liver transplantation is an excellent modality for the treatment of end-stage liver disease in children.
Efficacy and treatment tolerance in older patients with NSCLC: a meta-analysis of five phase III randomized trials conducted by the Hellenic Oncology Research Group
Authors: A.G. Pallis, A. Karampeazis, L. Vamvakas, N. Vardakis, A. Kotsakis, V. Bozionelou, A. Kalykaki, D. Hatzidaki, D. Mavroudis, V. Georgoulias
Journal: Annals of Oncology (2011)
Genetic mapping of xenotropic murine leukemia virus-inducing loci in five mouse strains.
Authors: C A Kozak, W P Rowe
Journal: The Journal of Experimental Medicine (1980)

A single mendelian gene was identified for induction of the endogenous xenotropic murine leukemia virus in five mouse strains (C57BL/10, C57L, C57BR, AKR, and BALB/c). This locus, designated Bxv-1, mapped to the same site on chromosome 1 in all strains: Id-1-Pep-3-[Bxv-1-Lp]. Thus, inducibility loci for xenotropic virus are more limited in number and chromosomal distribution than ecotropic inducibility loci. Virus expression in mice with Bxv-1 was induced by treatment of fibroblasts with 5-iododeoxyuridine or by exposure of spleen cells to a B cell mitogen, bacterial lipopolysaccharide. An analysis of the hamster X mouse somatic cell hybrids indicated that chromosome 1, alone, was sufficient for virus induction.
Rheumatology in Dar-es-Salaam, Tanzania.
Authors: P E McGill
Journal: Annals of the Rheumatic Diseases (1991)

<h3>Abstract</h3> Recently, a 15-valent (PCV15) and a 20-valent pneumococcal conjugate vaccine (PCV20) have been licensed by the US Food and Drug Administration and are under evaluation by the European Medicines Agency. PCV15 contains all serotypes of the 13-valent conjugate vaccine (PCV13) plus serotype 22F and 33F and PCV20 includes PCV13 serotypes plus serotypes 8, 10A, 11A, 12F, 15B, 22F, 33F. We investigated pneumococcal serotype distribution, secular trends and proportion of pneumonia caused by serotypes included in PCV13, PCV15, PCV20, and the 23-valent pneumococcal polysaccharide vaccine (PPV23) among adult patients with all-cause community-acquired pneumonia (CAP) between 2013 and 2019. We applied logistic mixed regression modelling to assess annual trends. Urine samples from adult patients with CAP treated in the community or hospital in Germany and included in the CAPNETZ study, a prospective multi-centre cohort study, were analysed by two serotype-specific multiplex urinary antigen detection assays (UAD1/UAD2) at Pfizer’s Vaccines Research and Development Laboratory. UAD1 detects serotypes in PCV13, UAD2 detects additional serotypes in PCV20 plus serotypes 2, 9N, 17F and 20. Out of 1,831 patients screened, urine samples with a valid UAD test result were available for 1,343 patients (73.3%). Among those patients, 829 patients (61.7%) were male, 792 patients (59.0%) were aged ≥60 years, 1038 patients (77.3%) had at least one comorbidity and 1,204 patients (89.7%) were treated in the hospital. The overall proportion of vaccine-type pneumonia among all-cause CAP for PCV13, PCV15, PCV20 and PPV23 was 7.7% (n=103), 9.1% (n=122), 12.3% (n=165) and 13.3% (n=178). Over the entire observation period, we did not observe evidence for significant annual trends in pneumococcal vaccine serotype coverage against pneumonia in adults (PCV13: OR 0.94, 95% CI 0.83-1.05; PCV15: OR 0.93, 95% CI 0.84-1.03; PCV20: OR 0.95, 95% CI 0.86-1.04; PPV23: OR 0.99, 95% CI 0.90-1.08). In conclusion, our data show i) no decline of PCV13 serotypes in all-cause CAP between 2013-2019 mainly due to a persistently high proportion of serotype 3 suggesting no meaningful effect of childhood PCV13 vaccination on PCV13 coverage in pneumonia in adults during this time period and ii) that the gap in the coverage between PCV20 and PPV23 was small and did not increase over the entire observation time.
Role of cytoskeleton and acidification of endocytic compartment in asialoglycoprotein metabolism in isolated rat hepatocyte couplets
Authors: Masaru Harada, Shotaro Sakisaka, Masao Yoshitake, Masahito Ohishi, Satoshi Itano, Satoshi Shakado, Yoshihiro Mimura, Kazunori Noguchi, Michio Sata, Hiroshi Yoshida, Kyuichi Tanikawa
Journal: Hepatology (1995)

The process of receptor-mediated endocytosis is common to a variety of species and cell types. One of the best characterized receptor-ligand systems is the hepatocyte receptor for asialoglycoproteins. We investigated the morphological features of the uptake and intracellular transport of gold-conjugated asialofetuin in isolated rat hepatocyte couplets. We assessed the effects of colchicine, lumicolchicine, cytochalasin B, and chloroquine on the uptake and intracellular transport of asialoglycoproteins. Isolated rat hepatocyte couplets were incubated with gold-conjugated asialofetuin, and transmission electron micrographs of these cells were analyzed to determine the density and distribution of gold particles in the peripheral and pericanalicular areas. Results were analyzed morphometrically. Colchicine significantly inhibited the uptake and intracellular transport of asialoglycoproteins, but did not affect membrane fusion of endocytic compartments in the peripheral area. Lumicolchicine and cytochalasin B had minimal effects on these processes. Chloroquine inhibited the uptake of asialoglycoproteins, but did not affect the intracellular transport of asialoglycoproteins. Results suggest that the microtubule is essential for intracellular movement of endocytosed asialoglycoproteins and receptor recycling, and that endocytic structures in the peripheral regions can fuse in the absence of intact microtubules. We also found that uptake and intracellular transport of asialoglycoproteins were independent of the microfilaments, and the pH gradient in endocytic compartments was important in receptor-mediated endocytosis of asialoglycoproteins.
Biomarkers in early rheumatoid arthritis: longitudinal associations with inflammation and joint destruction measured by magnetic resonance imaging and conventional radiographs
Authors: S. W. Syversen, E. A. Haavardsholm, P. Boyesen, G. L. Goll, C. Okkenhaug, P. I. Gaarder, D. van der Heijde, T. K. Kvien
Journal: Annals of the Rheumatic Diseases (2010)

To examine associations between a panel of soluble biomarkers and progressive joint destruction assessed by magnetic resonance imaging (MRI) and conventional radiographs as well as longitudinal associations with disease activity assessed clinically and by MRI in early rheumatoid arthritis (RA) patients.84 early RA patients were evaluated at baseline, 3, 6 and 12 months with clinical examination, serum and urine sampling, MRI scans of the dominant wrist and conventional radiographs of the hands. A panel of biomarkers (sCTX-I, uCTX-II, sOPG, sYKL-40, sCOMP and sMMP-3) was assessed by ELISA. MRI images and conventional radiographs were scored according to the RA MRI score (RAMRIS) and the van der Heijde modified Sharp score (SHS), respectively. Longitudinal associations between biomarkers and MRI inflammation and disease activity score (DAS28) and association with the progression of damage were examined with adjustments for known predictors.The baseline sCTX-I level predicted progression in joint destruction assessed by MRI and conventional radiographs, whereas the uCTX-II level was a predictor of progression in SHS but not RAMRIS. Consistent associations, both with MRI inflammation (synovitis and bone marrow oedema) and DAS28 were found for sYKL-40 and sMMP-3 in addition to C-reactive protein at baseline and in longitudinal analyses. Associations remained significant in multivariate analyses.Levels of sCTX-I and uCTX-II were significant predictors of progressive joint destruction, whereas sMMP-3 and sYKL-40 were merely markers of joint inflammation. The clinical value of these markers for use in individual patients is limited due to a considerable overlap in levels of patients with progression and no progression.
Inherited variant on chromosome 11q23 increases susceptibility to IDH-mutated but not IDH-normal gliomas regardless of grade or histology
Authors: T. Rice, S. Zheng, P. A. Decker, K. M. Walsh, P. Bracci, Y. Xiao, L. S. McCoy, I. Smirnov, J. S. Patoka, H. M. Hansen, G. Hsuang, J. L. Wiemels, T. Tihan, A. R. Pico, M. D. Prados, S. M. Chang, M. S. Berger, A. Caron, S. Fink, T. Kollmeyer, A. Rynearson, J. Voss, M. L. Kosel, B. L. Fridley, D. H. Lachance, J. E. Eckel-Passow, H. Sicotte, B. P. O'Neill, C. Giannini, J. K. Wiencke, R. B. Jenkins, M. R. Wrensch
Journal: Neuro-Oncology (2013)

Recent discoveries of inherited glioma risk loci and acquired IDH mutations are providing new insights into glioma etiology. IDH mutations are common in lower grade gliomas and secondary glioblastomas and uncommon in primary glioblastomas. Because the inherited variant in 11q23 has been associated with risk of lower grade glioma and not with glioblastomas, we hypothesized that this variant increases susceptibility to IDH-mutated gliomas, but not to IDH-wild-type gliomas. We tested this hypothesis in patients with glioma and controls from the San Francisco Adult Glioma Study, the Mayo Clinic, and Illumina controls (1102 total patients, 5299 total controls). Case-control additive associations of 11q23 risk alleles (rs498872, T allele) were calculated using logistic regression, stratified by tumor IDH status (mutated or wild-type) and by histology and grade. We also adjusted for the recently discovered 8q24 glioma risk locus rs55705857 G allele. The 11q23 glioma risk locus was associated with increased risk of IDH-mutated gliomas of all histologies and grades (odds ratio [OR] = 1.50; 95% confidence interval [CI] = 1.29–1.74; P = 1.3X10−7) but not with IDH-wild-type gliomas of any histology or grade (OR = 0.91; 95% CI = 0.81–1.03; P = 0.14). The associations were independent of the rs55705857 G allele. A variant at the 11q23 locus increases risk for IDH-mutated but not IDH-wild-type gliomas, regardless of grade or histology.