tbuckley/cabot-search huggingface dataset:
Axl and Growth Arrest–Specific Gene 6 Are Frequently Overexpressed in Human Gliomas and Predict Poor Prognosis in Patients with Glioblastoma Multiforme
Authors: Markus Hutterer, Pjotr Knyazev, Ariane Abate, Markus Reschke, Hans Maier, Nadia Stefanova, Tatjana Knyazeva, Verena Barbieri, Markus Reindl, Armin Muigg, Herwig Kostron, Guenther Stockhammer, Axel Ullrich
Journal: Clinical Cancer Research (2008)

Abstract Purpose: The receptor tyrosine kinase Axl has recently been identified as a critical element in the invasive properties of glioma cell lines. However, the effect of Axl and its ligand growth arrest–specific gene 6 (Gas6) in human gliomas is still unknown. Experimental Design: Axl and Gas6 expression was studied in 42 fresh-frozen and 79 paraffin-embedded glioma specimens by means of reverse transcription-PCR and immunohistochemistry. The prognostic value of Axl and Gas6 expression was evaluated using a population-based tissue microarray derived from a cohort of 55 glioblastoma multiforme (GBM) patients. Results: Axl and Gas6 were detectable in gliomas of malignancy grades WHO 2 to 4. Moderate to high Axl mRNA expression was found in 61%, Axl protein in 55%, Gas6 mRNA in 81%, and Gas6 protein in 74% of GBM samples, respectively. GBM patients with high Axl expression and Axl/Gas6 coexpression showed a significantly shorter time to tumor progression and an association with poorer overall survival. Comparative immunohistochemical studies showed that Axl staining was most pronounced in glioma cells of pseudopalisades and reactive astrocytes. Additionally, Axl/Gas6 coexpression was observed in glioma cells and tumor vessels. In contrast, Axl staining was not detectable in nonneoplastic brain tissue and Gas6 was strongly expressed in neurons. Conclusions: In human gliomas, Axl and Gas6 are frequently overexpressed in both glioma and vascular cells and predict poor prognosis in GBM patients. Our results indicate that specific targeting of the Axl/Gas6 signaling pathway may represent a potential new approach for glioma treatment.
Polymorphonuclear neutrophils express the common acute lymphoblastic leukemia antigen.
Authors: J Cossman, L M Neckers, W J Leonard, W C Greene
Journal: The Journal of Experimental Medicine (1983)

Monoclonal antibodies J5, VIL-A1, and BA-3, known to react with the common acute lymphoblastic leukemia antigen (CALLA) were found to specifically stain normal human polymorphonuclear neutrophils (PMN). The antigen detected on PMN had a molecular weight (95,000-110,000 mol wt) close to that of CALLA (95,000-100,000 mol wt) and thus these surface membrane antigens are likely related, if not identical. The fluorescent staining intensity of PMN is comparable to that of CALLA-positive leukemic cells and the presence of PMN in patient samples could potentially produce false-positive results in diagnosis.
Fibroblast-like synoviocytes support B-cell pseudoemperipolesis via a stromal cell–derived factor-1– and CD106 (VCAM-1)–dependent mechanism
Authors: Jan A. Burger, Nathan J. Zvaifler, Nobuhiro Tsukada, Gary S. Firestein, Thomas J. Kipps
Journal: Journal of Clinical Investigation (2001)

B-cell accumulation and formation of ectopic germinal centers are characteristic changes in the diseased joints of patients with rheumatoid arthritis (RA). Earlier studies suggested that interactions between B lymphocytes and specialized synovial "nurse-like" cells peculiar to the RA synovium may be responsible for the homing and sustained survival of B cells in the synovium. However, in this study, we found that B cells spontaneously migrate beneath ordinary fibroblast-like synoviocytes (FLSs) and then experience prolonged survival. FLSs isolated from joints of patients with osteoarthritis also supported this activity, termed B-cell pseudoemperipolesis. We found that FLSs constitutively expressed the chemokine stromal cell–derived factor-1 (SDF-1), and that pertussis toxin or antibodies to the SDF-1 receptor (CXCR4) could inhibit B-cell pseudoemperipolesis. However, expression of SDF-1 is not sufficient, as dermal fibroblasts also expressed this chemokine but were unable to support B-cell pseudoemperipolesis unless previously stimulated with IL-4 to express CD106 (VCAM-1), a ligand for the α4β1 integrin, very-late-antigen-4 (VLA-4 or CD49d). Furthermore, mAb's specific for CD49d and CD106, or the synthetic CS1 fibronectin peptide, could inhibit B-cell pseudoemperipolesis. We conclude that ordinary FLSs can support B-cell pseudoemperipolesis via a mechanism dependent upon fibroblast expression of SDF-1 and CD106.
PROXIMAL SARTORIUS TENDON RUPTURE AS A CAUSE OF TRAUMATIC ANTERIOR HIP PAIN-A CASE REPORT OF A PROFESSIONAL FOOTBALLER
Authors: Bhavesh Kumar, Dinesh Sirisena, Mike Rayner
Journal: British Journal of Sports Medicine (2013)

Background Sartorius injuries are seldom mentioned in medical literature. Thus developing an evidence-based management plan for sartorius muscle and tendon injuries can be challenging. In this case a grade 3 tear of the proximal sartorius tendon was identified in a player following a high-velocity contact injury to the pelvis during a professional match. Methods The athlete was able to continue playing for a further 30 minutes following the injury, but ultimately increasing pain and restriction in hip movements forced him to limp off. Examination revealed localised swelling, bruising and tenderness at the site of contact to the left anterior-superior iliac spine (ASIS), and painful muscle contraction. This was managed to good effect as a presumed muscle contusion, but with recurrence of symptoms, further swelling, bruising and limping by half time in the subsequent match one week later. The presumed contusion was thought to have deteriorated forming a suspected 10cm muscle haematoma. The merits of blind and sonography-guided aspiration were considered, and the latter option was chosen. Results Ultrasonography revealed soft tissue oedema and injury to the proximal sartorius tendon, and aspiration was therefore not attempted. A subsequent MRI scan demonstrated a grade 3 sartorius tendon tear at its insertion to the ASIS with 3cm separation. With no specific guidance available in the medical literature, consensus of opinion was to continue with conservative management. Rehabilitation methods were modified according to the new findings. Given importance of this player in the team and the next match being a cup final a week later, a pragmatic approach was taken to allowing him to play; he played effectively for one hour before he showed signs of limping. He went on to have three, weekly Prolotherapy injections into the site of the tear in order to facilitate healing in the off-season. Progressive rehabilitation of his thigh resulted in return to uninhibited play within six weeks. Discussion/ Conclusions ▸ The history and physical examination findings, as well as initial good response to conservative treatment of a presumed simple contusion provided our medical team false assurance and a small delay in the diagnosis of this rare injury. ▸ Attaining the exact diagnosis allowed a more hands-on and bespoke rehabilitation program, as well as informed decision-making as to suitability to play in a crucial match. ▸ The rarity of this injury and negligible functional deficit that results from a ruptured proximal sartorius tendon following good rehabilitation perhaps accounts for the paucity of medical literature available. ▸ We ask the audience to consider a sartorius tendon rupture in the differential diagnosis of acute anterior hip pain.
DNR and Autopsy: A Linked Bayesian System
Authors: Hampton R. Bates
Journal: JAMA (1990)

<h3>To the Editor.—</h3> The development of modern diagnostic techniques is perhaps the most important of several factors that have changed medical practice so that realistic and compassionate donot-resuscitate (DNR) orders are now commonplace. The careful evaluation that must precede a DNR decision anticipates the function of the autopsy and is, in fact, a form of autopsy (seeing for oneself). Thus, the autopsy approach to DNR patients begins with the use of diagnostic probes to secure aliquots and images of organs and tissues that provide more timely information than postmortem specimens. Information leading to a DNR decision coupled with postmortem data forms a linked Bayesian system in which the final posterior probability (P≈100%) of the primary disease is established before death. Because the postmortem part of the linked diagnostic system is limited to refining the principal diagnosis and turning up secondary diagnoses—pulmonary embolism, pneumonia, gallstones, and the like— that were not
Genetic instability in colorectal cancer
Authors: H J W THOMAS
Journal: Gut (1998)

See article on page553 

The development of neoplasia has been thought to be associated with genetic alterations for many years. In colorectal cancer two specific types of genetic instability have been defined. One is associated with chromosomal instability and the other with DNA microsatellite instability, also known as replication errors.1 The mechanism underlying tumorigenesis leads to profound differences in the pathological features, prognosis and response to chemotherapy of these two types of colorectal cancer.

The great majority of colorectal cancers are aneuploid with a variable chromosome complement. However, between 10 and 15% of colorectal cancers are near diploid and exhibit DNA microsatellite instability in which replication errors may be demonstrated within repetitive sequences of tumour DNA which are not present in the normal DNA of the individual. Tumours with microsatellite instability occur more frequently in younger patients, are more frequently proximal to the splenic flexure and exhibit exophytic growth, poor differentiation, extracellular mucin production, and a Crohn’s-like …
Reversible superior vena caval syndrome due to tuberculosis.
Authors: R G Harbecke, D P Schlueter, D Y Rosenzweig
Journal: Thorax (1979)

Obstruction of the superior vena cava is usually caused by neoplasia; however, benign diseases cause between 3 and 26% of the reported cases (Lokich and Good- man, 1975; Urschel and Paulson, 1966).We describe a superior vena caval syndrome that resolved with chemotherapy for tuberculosis. Case reportA 36-year-old man was admitted on 21 January 1976 after he lacerated the flexor tendon of his right index finger.He had a prominent superficial venous pattern on his chest and digital clubbing.A chest radiograph showed a large hilar mass (see figure).He had noticed distended veins on his neck and chest for the past year, but denied any history of tuberculosis or respiratory symptoms.He had smoked one packet of cigarettes a day, stopping five years before admission.Sputa for cytology and smear for acid-fast bacilli (AFB) were negative on several occasions.The 5 TU tuberculin skin test was positive.His superior venacavogram showed complete occlusion of the superior Routine admission chest radiograph showing right hilar mass.
HIV-induced apoptosis requires the CD4 receptor cytoplasmic tail and is accelerated by interaction of CD4 with p56lck.
Authors: J Corbeil, M Tremblay, D D Richman
Journal: The Journal of Experimental Medicine (1996)

The roles of the CD4 receptor and the src kinase p56lck were examined in the process of HIV-induced apoptosis of CD4+ T lymphocytes. The presence of the CD4 cytoplasmic tail was found to be essential in delivering an apoptotic signal, and interaction of CD4 with p56lck potentiated HIV-induced apoptosis. Apoptosis, but not HIV replication, was abrogated by deleting the NH2-terminal intracytoplasmic tail of CD4, or by mutating the two critical cysteines in this tail that are responsible for CD4-p56lck interaction. Introduction of p56lck in C8166-45 or MT-2 cells, CD4+ T cell lines deficient for this protein, greatly increased HIV-induced apoptosis and syncytium formation. The ability of p56lck to deliver an apoptotic signal did not depend on its kinase function, since a kinase-deficient mutant was as effective as its normal counterpart in inducing apoptosis, suggesting that p56lck may act as an adapter to anchor other proteins to transduce the death signal.
Recurrence of Membranoproliferative Glomerulonephritis Type II in Renal Allografts
Authors: Michael C. Braun, Don M. Stablein, Lorraine A. Hamiwka, Lorraine Bell, Sharon M. Bartosh, C. Frederic Strife
Journal: Journal of the American Society of Nephrology (2005)

Membranoproliferative glomerulonephritis type II (MPGN II) is an uncommon form of complement-dependent acquired renal disease. Although it has been recognized since the 1970s that MPGN II recurs almost universally in renal transplants, data regarding the long-term consequences of disease recurrence are limited. Therefore, a retrospective comparative analysis of 75 patients with MPGN II contained in the North American Pediatric Renal Transplant Cooperative Study transplantation database was performed. Five-year graft survival for patients with MPGN II was significantly worse (50.0 +/- 7.5%) compared with the database as a whole (74.3 +/- 0.6%; P < 0.001). Living related donor organs had a significantly better 5-yr survival (65.9 +/- 10.7%) compared with cadaveric donor organs (34.1 +/- 9.8%; P = 0.004). The primary cause of graft failure in 11 (14.7%) patients was recurrent disease. Supplemental surveys were obtained on 29 (38%) of 75 patients. Analysis of these data indicated that recurrent disease occurred in 12 (67%) of the 18 patients with posttransplantation biopsies. Although there was no correlation between pretransplantation presentation, pre- or posttransplantation C3 levels, and either disease recurrence or graft failure, there was a strong association between heavy proteinuria and disease recurrence. The presence of glomerular crescents in allograft biopsies had a significant negative correlation with graft survival. At last follow-up, patients with recurrent disease had significantly higher serum creatinine and qualitatively more proteinuria than patients without biopsy-proven disease. These data indicate that recurrent MPGN II has a significant negative impact on renal allograft function and survival.
Associations between active commuting, body fat, and body mass index: population based, cross sectional study in the United Kingdom
Authors: E. Flint, S. Cummins, A. Sacker
Journal: BMJ (2014)

<b>Objective</b> To determine if promotion of active modes of travel is an effective strategy for obesity prevention by assessing whether active commuting (walking or cycling for all or part of the journey to work) is independently associated with objectively assessed biological markers of obesity. <b>Design</b> Cross sectional study of data from the wave 2 Health Assessment subsample of Understanding Society, the UK Household Longitudinal Study (UKHLS). The exposure of interest, commuting mode, was self reported and categorised as three categories: private transport, public transport, and active transport. <b>Participants</b> The analytic samples (7534 for body mass index (BMI) analysis, 7424 for percentage body fat analysis) were drawn from the representative subsample of wave 2 respondents of UKHLS who provided health assessment data (n=15 777). <b>Main outcome measures</b> Body mass index (weight (kg)/height (m)<sup>2</sup>); percentage body fat (measured by electrical impedance). <b>Results</b> Results from multivariate linear regression analyses suggest that, compared with using private transport, commuting by public or active transport modes was significantly and independently predictive of lower BMI for both men and women. In fully adjusted models, men who commuted via public or active modes had BMI scores 1.10 (95% CI 0.53 to 1.67) and 0.97 (0.40 to 1.55) points lower, respectively, than those who used private transport. Women who commuted via public or active modes had BMI scores 0.72 (0.06 to 1.37) and 0.87 (0.36 to 0.87) points lower, respectively, than those using private transport. Results for percentage body fat were similar in terms of magnitude, significance, and direction of effects. <b>Conclusions</b> Men and women who commuted to work by active and public modes of transport had significantly lower BMI and percentage body fat than their counterparts who used private transport. These associations were not attenuated by adjustment for a range of hypothesised confounding factors.
Eukaryotic Initiation Factor 4E Binding Protein Family of Proteins: Sentinels at a Translational Control Checkpoint in Lung Tumor Defense
Authors: Yong Y. Kim, Linda Von Weymarn, Ola Larsson, Danhua Fan, Jon M. Underwood, Mark S. Peterson, Stephen S. Hecht, Vitaly A. Polunovsky, Peter B. Bitterman
Journal: Cancer Research (2009)

The usurping of translational control by sustained activation of translation initiation factors is oncogenic. Here, we show that the primary negative regulators of these oncogenic initiation factors--the 4E-BP protein family--operate as guardians of a translational control checkpoint in lung tumor defense. When challenged with the tobacco carcinogen 4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone (NNK), 4ebp1(-/-)/4ebp2(-/-) mice showed increased sensitivity to tumorigenesis compared with their wild-type counterparts. The 4E-BP-deficient state per se creates pro-oncogenic, genome-wide skewing of the molecular landscape, with translational activation of genes governing angiogenesis, growth, and proliferation, and translational activation of the precise cytochrome p450 enzyme isoform (CYP2A5) that bioactivates NNK into mutagenic metabolites. Our study provides in vivo proof for a translational control checkpoint in lung tumor defense.
Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL)
Authors: Carlo Briguori, Flavio Airoldi, Davide D’Andrea, Erminio Bonizzoni, Nuccia Morici, Amelia Focaccio, Iassen Michev, Matteo Montorfano, Mauro Carlino, John Cosgrave, Bruno Ricciardelli, Antonio Colombo
Journal: Circulation (2007)

Volume supplementation by saline infusion combined with N-acetylcysteine (NAC) represents an effective strategy to prevent contrast agent-induced nephrotoxicity (CIN). Preliminary data support the concept that sodium bicarbonate and ascorbic acid also may be effective in preventing CIN.Three hundred twenty-six consecutive patients with chronic kidney disease, referred to our institutions for coronary and/or peripheral procedures, were randomly assigned to prophylactic administration of 0.9% saline infusion plus NAC (n=111), sodium bicarbonate infusion plus NAC (n=108), and 0.9% saline plus ascorbic acid plus NAC (n=107). All enrolled patients had serum creatinine > or = 2.0 mg/dL and/or estimated glomerular filtration rate < 40 mL x min(-1) x 1.73 m(-2). Contrast nephropathy risk score was calculated in each patient. In all cases, iodixanol (an iso-osmolar, nonionic contrast agent) was administered. The primary end point was an increase of > or = 25% in the creatinine concentration 48 hours after the procedure (CIN). The amount of contrast media administered (179+/-102, 169+/-92, and 169+/-94 mL, respectively; P=0.69) and risk scores (9.1+/-3.4, 9.5+/-3.6, and 9.3+/-3.6; P=0.21) were similar in the 3 groups. CIN occurred in 11 of 111 patients (9.9%) in the saline plus NAC group, in 2 of 108 (1.9%) in the bicarbonate plus NAC group (P=0.019 by Fisher exact test versus saline plus NAC group), and in 11 of 107 (10.3%) in the saline plus ascorbic acid plus NAC group (P=1.00 versus saline plus NAC group).The strategy of volume supplementation by sodium bicarbonate plus NAC seems to be superior to the combination of normal saline with NAC alone or with the addition of ascorbic acid in preventing CIN in patients at medium to high risk.
Divergent evolution and evolution by the birth-and-death process in the immunoglobulin VH gene family.
Authors: T Ota, M Nei
Journal: Molecular Biology and Evolution (1994)

Immunoglobulin diversity is generated primarily by the heavy- and light-chain variable-region gene families. To understand the pattern of long-term evolution of the heavy-chain variable-region (VH) gene family, which is composed of a large number of member genes, the evolutionary relationships of representative VH genes from diverse organisms of vertebrates were studied by constructing a phylogenetic tree. This tree indicates that the vertebrate VH genes can be classified into group A, B, C, D, and E genes. All VH genes from cartilaginous fishes such as sharks and skates from a monophyletic group and belong to group E, whereas group D consists of bony-fish VH genes. By contrast, group C includes not only some fish genes but also amphibian, reptile, bird, and mammalian genes. Group A and B genes were composed of the genes from mammals and amphibians. The phylogenetic analysis also suggests that mammalian VH genes are classified into three clusters--i.e., mammalian clans I, II, and III-and that these clans have coexisted in the genome for >400 Myr. To study the short-term evolution of VH genes, the phylogenetic analysis of human group A (clan I) and C (clan III) genes was also conducted. The results obtained show that VH pseudogenes have evolved much faster than functional genes and that they have branched off from various functional VH genes. There is little indication that the VH gene family has been subject to concerted evolution that homogenizes member genes. These observations indicate that the VH genes are subject to divergent evolution due to diversifying selection and evolution by the birth-and-death process caused by gene duplication and dysfunctioning mutation. Thus, the evolutionary pattern of this monofunctional multigene family is quite different from that of such gene families as the ribosomal RNA and histone gene families.
Effects of adenine nucleotides on calcium binding by rat heart sarcoplasmic reticulum
Authors: S. PENPARGKUL
Journal: Cardiovascular Research (1979)

Journal Article Effects of adenine nucleotides on calcium binding by rat heart sarcoplasmic reticulum Get access SOMSONG PENPARGKUL SOMSONG PENPARGKUL 1 From the Division of Cardiology, Department of Medicine, Montefiore Hospital and Medical Center of the Albert Einstein College of Medicine Bronx, New York 1Address for reprints: Dr. Somsong Penpargkul, Division of Cardiology, Department of Medicine, Montefiore Hospital and Medical Center of the Albert Einstein College of Medicine. 111 E. 210th Street, Bronx, New York 10467, USA. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 13, Issue 5, May 1979, Pages 243–253, https://doi.org/10.1093/cvr/13.5.243 Published: 01 May 1979