tbuckley/cabot-search huggingface dataset:
Monocytes and Macrophages
Authors: R B Johnston
Journal: New England Journal of Medicine (1988)

MACROPHAGES play a central and essential part in the immune response by presenting antigen to lymphocytes during the development of specific immunity and by serving as supportive, "accessory" cells to lymphocytes, at least partly by releasing soluble factors. Macrophages also carry out the fundamental protective functions of ingesting and killing invading organisms, and as has recently been discovered, they release an enormous number of factors involved in host defense and inflammation. Adding to the excitement of those who study macrophages is the increasing understanding of how these cells can be "activated" pharmacologically to carry out their protective role more effectively. . . .
CD38 expression labels an activated subset within chronic lymphocytic leukemia clones enriched in proliferating B cells
Authors: Rajendra N. Damle, Sonal Temburni, Carlo Calissano, Sophia Yancopoulos, Taraneh Banapour, Cristina Sison, Steven L. Allen, Kanti R. Rai, Nicholas Chiorazzi
Journal: Blood (2007)
Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels.
Authors: M F Maturi, S E Martin, D Markle, M Maxwell, C R Burruss, E Speir, R Greene, Y M Ro, D Vitale, M V Green
Journal: Circulation (1991)

BACKGROUND We studied the effect of intracoronary administration of arginine-8-vasopressin on blood flow in nondiseased coronary arteries and determined whether this vasoconstriction was severe enough to produce ischemia in 30 dogs. METHODS AND RESULTS In group 1 (n = 6), after vasopressin administration coronary blood flow was decreased by 41% (p less than 0.002) without changes in heart rate or aortic pressure, and left ventricular ejection fraction measured by radionuclide angiocardiography was decreased by 18% (p less than 0.0005). In group 2 (n = 6), ischemia was confirmed by measurement of transmural pH changes. Administration of vasopressin decreased subendocardial pH of the infused zone from 7.40 +/- 0.03 to 7.31 +/- 0.07 (p less than 0.01). The subendocardial pH of the zone not infused with vasopressin did not change. To overcome the intrinsic regulation of blood flow, operating primarily in small coronary arteries, we hypothesized that vasopressin must increase resistance primarily in large rather than small coronary arteries. After intracoronary infusion in group 3 (n = 6), however, most (94%) of the increase in resistance during vasopressin administration was explained by an increase of resistance in small coronary arteries. In group 4 (n = 9), vasopressin decreased coronary blood flow by 50% and decreased local shortening by 90% at a time when systemic hemodynamics were unchanged. Coronary constriction induced by vasopressin, or the recovery from it, also was not altered by cyclooxygenase blockade. CONCLUSIONS Thus, vasopressin produces myocardial ischemia by constricting small, nondiseased coronary arteries severely enough to overcome the competition from normal coronary regulation, and this ischemic event is not mediated by prostaglandin products.
Association of Fibrinogen, C-reactive Protein, Albumin, or Leukocyte Count With Coronary Heart Disease
Authors: John Danesh, Rory Collins, Paul Appleby, Richard Peto
Journal: JAMA (1998)

Context.—A large number of epidemiologic studies have reported on associations between various "inflammatory" factors and coronary heart disease (CHD).Objective.—To assess the associations of blood levels of fibrinogen, C-reactive protein (CRP), and albumin and leukocyte count with the subsequent risk of CHD.Data Sources.—Meta-analyses of any long-term prospective studies of CHD published before 1998 on any of these 4 factors. Studies were identified by MEDLINE searches, scanning of relevant reference lists, hand searching of cardiology, epidemiology, and other relevant journals, and discussions with authors of relevant reports.Study Selection.—All relevant studies identified were included.Data Extraction.—The following information was abstracted from published reports (supplemented, in several cases, by the authors): size and type of cohort, mean age, mean duration of follow-up, assay methods, degree of adjustment for confounders, and relationship of CHD risk to the baseline assay results.Data Synthesis.—For fibrinogen, with 4018 CHD cases in 18 studies, comparison of individuals in the top third with those in the bottom third of the baseline measurements yielded a combined risk ratio of 1.8 (95% confidence interval [CI], 1.6-2.0) associated with a difference in long-term usual mean fibrinogen levels of 2.9 µmol/L (0.1 g/dL) between the top and bottom thirds (10.3 vs 7.4 µmol/L [0.35 vs 0.25 g/dL]). For CRP, with 1053 CHD cases in 7 studies, the combined risk ratio of 1.7 (95% CI, 1.4-2.1) was associated with a difference of 1.4 mg/L (2.4 vs 1.0 mg/L). For albumin, with 3770 CHD cases in 8 studies, the combined risk ratio of 1.5 (95% CI, 1.3-1.7) was associated with a difference of 4 g/L (38 vs 42 g/L, ie, an inverse association). For leukocyte count, with 5337 CHD cases in the 7 largest studies, the combined risk ratio of 1.4 (95% CI, 1.3-1.5) was associated with a difference of 2.8×109/L (8.4 vs 5.6×109/L). Each of these overall results was highly significant (P&lt;.0001).Conclusions.—The published results from these prospective studies are remarkably consistent for each factor, indicating moderate but highly statistically significant associations with CHD. Hence, even though mechanisms that might account for these associations are not clear, further study of the relevance of these factors to the causation of CHD is warranted.
The Intra-Uterine Feto-Fetal Transfusion
Authors: Eberhard H. Heinrichs
Journal: JAMA (1964)

THE INTRA-UTERINE feto-fetal transfusion, sometimes called the "human intra-uterine parabiotic syndrome" because of its similarity to the experimental vascular connection in animals, is a rarely recognized phenomenon. The diagnosis is made at the birth of monozygotic twins by observing unequal blood distribution; one twin is anemic, the other plethoric. To date, 35 cases have been reported.<sup>1-9</sup> This report describes a case with unusual findings and presents a pathophysiology of this syndrome. <h3>Report of a Case</h3> A 17-year-old white mother, after 24 weeks' gestation, delivered male twins precipitously. At birth one twin was cyanotic, the other pale in comparison. The hemoglobin values at birth were 20.6 gm/100 cc and 13.3 gm/100 cc, respectively. The first twin died after 4 hours, the second after 28 hours of life, showing symptoms of a respiratory distress syndrome. An autopsy was refused. The placenta was complete and of the monochorionic-diamnionic type. One umbilical cord
Abstract 136: PTEN phosphatase inhibits metastasis through negatively affecting Entpd5/IGF1R pathway
Authors: Yanlin Yu
Journal: Cancer Research (2014)

Abstract Migration of cancer cell is the key event in metastasis. Recent data suggest that PTEN phosphatase activity may be required for inhibiting cell migration; however, little in vivo experimental evidence exists directly demonstrating the efficacy of PTEN phosphatase in tumor metastasis. We showed here that PTEN loss was correlated with progression to metastatic state using tissue array analysis and UV-irradiated HGF/SF transgenic-PTEN deficient mouse melanoma model. Analysis of various human melanoma cell lines demonstrated that PTEN expression was related to metastatic behavior. To further dissect the role of PTEN activity in metastasis, we have established a model system containing mutant PTEN with various phosphatase activities. We found that wild type PTEN could inhibit cell motility and invasiveness. Moreover, wild type PTEN was able to reduce metastatic potential of melanoma cells in a dose-dependent manner; in contrast, PTEN phosphatase dead mutant promoted metastatic behavior of melanoma cell. To gain more insight into the regulation of tumor cell migration, invasion and metastasis by PTEN, we performed a microarray analysis of cells with various PTEN phosphatase mutants. We found that a protein N-glycosylation and folding promoter, Entpd5 was negatively regulated by PTEN phosphatase. Down regulation of Entpd5 by shRNA in cells with PTEN phosphatase dead mutant blocked PTEN phosphatase dead mutant mediated tumor metastasis in vivo, promoted cell ER stress and growth inhibition as well as reduction of IGF1R. In contrast, overexpression of Entpd5 in cell with PTEN wild-type form enhanced PTEN wild-type-inhibited tumor metastasis in vivo, inhibited cell ER stress, promoted cell growth and abundance of IGF1R. We provide mechanistic insight toward regulation of metastasis by PTEN phosphatase and demonstrate a link between PTEN and Entpd5/IGF1R activation in metastatic process. Citation Format: Yanlin Yu. PTEN phosphatase inhibits metastasis through negatively affecting Entpd5/IGF1R pathway. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 136. doi:10.1158/1538-7445.AM2014-136
A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism
Authors: Christopher R. Longo, Virendra I. Patel, Gautam V. Shrikhande, Salvatore T. Scali, Eva Csizmadia, Soizic Daniel, David W. Sun, Shane T. Grey, Maria B. Arvelo, Christiane Ferran
Journal: Hepatology (2005)

Abstract The liver has a remarkable regenerative capacity, allowing recovery following injury. Regeneration after injury is contingent on maintenance of healthy residual liver mass, otherwise fulminant hepatic failure (FHF) may arise. Understanding the protective mechanisms safeguarding hepatocytes and promoting their proliferation is critical for devising therapeutic strategies for FHF. We demonstrate that A20 is part of the physiological response of hepatocytes to injury. In particular, A20 is significantly upregulated in the liver following partial hepatectomy. A20 protects hepatocytes from apoptosis and ongoing inflammation by inhibiting NF-κB. Hepatic expression of A20 in BALB/c mice dramatically improves survival following extended and radical lethal hepatectomy. A20 expression in the liver limits hepatocellular damage hence maintains bilirubin clearance and the liver synthetic function. In addition, A20 confers a proliferative advantage to hepatocytes via decreased expression of the cyclin-dependent kinase inhibitor p21waf1. In conclusion , A20 provides a proliferative advantage to hepatocytes. By combining anti-inflammatory, antiapoptotic and pro-proliferative functions, A20-based therapies could be beneficial in prevention and treatment of FHF. (Hepatology 2005;42:156–164.)
Increased influx of myeloid dendritic cells during acute rejection is associated with interstitial fibrosis and tubular atrophy and predicts poor outcome
Authors: Kim Zuidwijk, Johan W. de Fijter, Marko J.K. Mallat, Michael Eikmans, Marian C. van Groningen, Natascha N. Goemaere, Ingeborg M. Bajema, Cees van Kooten
Journal: Kidney International (2011)
Left Ventricular Hypertrophy Decreases Slowly but Not Rapidly Activating Delayed Rectifier Potassium Currents of Epicardial and Endocardial Myocytes in Rabbits
Authors: Xiaoping Xu, Seth J. Rials, Ying Wu, Joseph J. Salata, Tengxian Liu, David B. Bharucha, Roger A. Marinchak, Peter R. Kowey
Journal: Circulation (2001)

Delayed rectifier K(+) currents are critical to action potential (AP) repolarization. The present study examines the effects of left ventricular hypertrophy (LVH) on delayed rectifier K(+) currents and their contribution to AP repolarization in both epicardial (Epi) and endocardial (Endo) myocytes.VH was induced in rabbits by a 1-kidney removal, 1-kidney vascular clamping method. Slowly (I(Ks)) and rapidly (I(Kr)) activating delayed rectifier K(+) currents were recorded by the whole-cell patch-clamp technique, and APs were recorded by the microelectrode technique. In normal rabbit left ventricular myocytes, I(Ks) densities were larger in Epi than in Endo (1.1+/-0.1 versus 0.43+/-0.07 pA/pF), whereas I(Kr) density was similar between Epi and Endo (0.31+/-0.05 versus 0.36+/-0.07 pA/pF) at 20 mV. LVH reduced I(Ks) density to a similar extent (approximately 40%) in both Epi and Endo but had no significant effect on I(Kr) in either Epi or Endo. Consequently, I(Kr) was expected to contribute more to AP repolarization in LVH than in control. This was confirmed by specific I(Kr) block with dofetilide, which prolonged AP significantly more in LVH than in control (31+/-3% versus 18+/-2% in Epi; 53+/-6% versus 32+/-4% in Endo at 2 Hz). In contrast, L-768,673 (a specific I(Ks) blocker) prolonged AP less in LVH than in control. The very small I(Ks) density in Endo with LVH is consistent with the greater incidence of early afterdepolarizations induced in this region by dofetilide.LVH induces a decrease in I(Ks) density and increases the propensity to develop early afterdepolarizations, especially in Endo.
Deletion of cognate CD8 T cells by immature dendritic cells: a novel role for perforin, granzyme A, TREM-1, and TLR7
Authors: Lior Zangi, Yael Zlotnikov Klionsky, Liran Yarimi, Esther Bachar-Lustig, Yaki Eidelstein, Elias Shezen, David Hagin, Yumi Ito, Toshiyuki Takai, Shlomit Reich-Zeliger, Assaf Lask, Oren Milstein, Steffen Jung, Vera Shinder, Yair Reisner
Journal: Blood (2012)
Classification of anti-FcϵRI and anti-IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity
Authors: Ruth A. Sabroe, Edda Fiebiger, David M. Francis, Dieter Maurer, Paul T. Seed, Clive E.H. Grattan, Anne Kobza Black, Georg Stingl, Malcolm W. Greaves, Robert M. Barr
Journal: Journal of Allergy and Clinical Immunology (2002)
F-18 Flurodeoxyglucose Negative, F-18 Fluoride Accumulating in a Brain Metastasis in a Treated Case of Carcinoma of the Breast
Authors: Madhavi Tripathi, Abhinav Jaimini, Namita Singh, Nikunj Jain, Maria D'Souza, Prabhjot Kaur, Dinesh Singh, Rajnish Sharma, Anupam Mondal
Journal: Clinical Nuclear Medicine (2009)

A 52-year-old woman undergoing treatment for carcinoma of the left breast with brain and bone metastases was referred for F-18 fluoride positron emission tomography-computed tomography (PET/CT) bone scan (FBS) to evaluate the status of a bone metastasis. Review of the plain fluoride-PET images section-wise revealed an intracranial focus of abnormal fluoride accumulation, which was localized to the right medial temporal lobe on the fused fluoride-PET/CT image, with no evidence of calcification corresponding to this lesion on CT. The pretreatment F-18 flurodeoxyglucose (FDG)-PET/CT study showed this lesion to correspond to the site of FDG accumulating in a brain metastasis. The patient had undergone radiation therapy (RT) for her brain metastasis. Brain FDG-PET/CT was then done, which failed to reveal FDG accumulation in the lesion. Magnetic resonance imaging and magnetic resonance spectroscopy of this lesion revealed features suggestive of radiation damage. The probable mechanism of fluoride accumulation in the metastatic brain lesion was related to cell membrane damage and protein denaturation post-RT. Thus, while reporting FBS the possibility of extraosseous accumulation in an intracranial metastasis must be kept in mind.
Carcinogen-Induced Gene Promoter Hypermethylation Is Mediated by DNMT1 and Causal for Transformation of Immortalized Bronchial Epithelial Cells
Authors: Leah A. Damiani, Christin M. Yingling, Shuguang Leng, Paul E. Romo, Jun Nakamura, Steven A. Belinsky
Journal: Cancer Research (2008)

Abstract A better understanding of key molecular changes during transformation of lung epithelial cells could affect strategies to reduce mortality from lung cancer. This study uses an in vitro model to identify key molecular changes that drive cell transformation and the likely clonal outgrowth of preneoplastic lung epithelial cells that occurs in the chronic smoker. Here, we show differences in transformation efficiency associated with DNA repair capacity for two hTERT/cyclin-dependent kinase 4, immortalized bronchial epithelial cell lines after low-dose treatment with the carcinogens methylnitrosourea, benzo(a)pyrene-diolepoxide 1, or both for 12 weeks. Levels of cytosine-DNA methyltransferase 1 (DNMT1) protein increased significantly during carcinogen exposure and were associated with the detection of promoter hypermethylation of 5 to 10 genes in each transformed cell line. Multiple members of the cadherin gene family were commonly methylated during transformation. Stable knockdown of DNMT1 reversed transformation and gene silencing. Moreover, stable knockdown of DNMT1 protein before carcinogen treatment prevented transformation and methylation of cadherin genes. These studies provide a mechanistic link between increased DNMT1 protein, de novo methylation of tumor suppressor genes, and reduced DNA repair capacity that together seem causal for transformation of lung epithelial cells. This finding supports the development of demethylation strategies for primary prevention of lung cancer in smokers. [Cancer Res 2008;68(21):9005–14]
Science, medicine, and the future: Bioinformatics
Authors: A. Bayat
Journal: BMJ (2002)

An unprecedented wealth of biological data has been generated by the human genome project and sequencing projects in other organisms.The huge demand for analysis and interpretation of these data is being managed by the evolving science of bioinformatics.Bioinformatics is defined as the application of tools of computation and analysis to the capture and interpretation of biological data.It is an interdisciplinary field, which harnesses computer science, mathematics, physics, and biology (fig 1).Bioinformatics is essential for management of data in modern biology and medicine.This paper describes the main tools of the bioinformatician and discusses how they are being used to interpret biological data and to further understanding of disease.The potential clinical applications of these data in drug discovery and development are also discussed.
Absence of anti-cyclic citrullinated peptide antibodies in erosive osteoarthritis: further serological evidence of the disease as a subset of osteoarthritis
Authors: G Morozzi
Journal: Annals of the Rheumatic Diseases (2005)

Erosive osteoarthritis (EOA) is considered to be a rare subset of osteoarthritis (OA) characterised by destructive changes involving the proximal interphalangeal and distal interphalangeal joints.1–3 Laboratory findings are usually negative even though a slight increase of erythrocyte sedimentation rate may occur.2,3 Radiologically, central erosions and the “gull wing” deformity characterise the disorder.4 Synovial pathology shows changes consistent with both rheumatoid arthritis (RA) and OA.1,2 Histological examination of synovium from patients with EOA joints shows lining cell hyperplasia, lymphocytic infiltration, and pannus formation, features indistinguishable from those of RA.1

The relationship between EOA and classical OA is controversial, as some authors consider it to be a separate disease entity, some regard it as one end of the …
Papillary Necrosis in Experimental Analgesic Nephropathy
Authors: B. M. Saker, P. Kincaid-Smith
Journal: BMJ (1969)

A proprietary aspirin, phenacetin, and caffeine preparation given to rats in a dose equivalent to that taken by patients with analgesic nephropathy produced papillary necrosis in 55%. There was a higher incidence in rats deprived of fluids overnight.Papillary necrosis was not noted in rats receiving twice as much phenacetin.These findings support the argument that phenacetin should not be singled out as the substance responsible for analgesic nephropathy in man.
281 THE NEURONAL GUIDANCE CUE AND SURVIVAL FACTOR, NETRIN-1, IN LIVER FIBROGENESIS
Authors: D. Lopez, M. Scheffler, F. Schulze, K. Wendland, S. Mesghenna, U. Töx, U. Drebber, D. Nierhoff, H.P. Dienes, M. Odenthal
Journal: Journal of Hepatology (2009)
Altered Breast Development in Young Girls from an Agricultural Environment
Authors: Elizabeth A. Guillette, Craig Conard, Fernando Lares, Maria Guadalupe Aguilar, John McLachlan, Louis J. Guillette
Journal: Environmental Health Perspectives (2005)

In several human populations, the age at which female breast development begins is reported to have declined over the last five decades. Much debate has occurred over whether this reported decline has actually occurred and what factors contribute to it. However, geographical patterns reflecting earlier developmental onset in some human populations suggest environmental factors influence this phenomenon. These factors include interactions between genetic makeup, nutrition, and possible cumulative exposure to estrogens, both endogenous as well as environmental beginning during in utero development. We examined the onset of breast development in a group of peripubertal girls from the Yaqui Valley of Sonora, Mexico. We observed that girls from valley towns, areas using modern agricultural practices, exhibited larger breast fields than those of girls living in the foothills who exhibited similar stature [e.g., weight, height, body mass index (BMI)], and genetic background. Further, girls from valley towns displayed a poorly defined relationship between breast size and mammary gland development, whereas girls from the Yaqui foothills, where traditional ranching occurs, show a robust positive relationship between breast size and mammary size. The differences noted were obtained by a medically based exam involving morphometric analysis and palpation of tissues, in contrast to visual staging alone. In fact, use of the Tanner scale, involving visual staging of breast development for puberty, detected no differences between the study populations. Mammary tissue, determined by palpation, was absent in 18.5% of the girls living in agricultural areas, although palpable breast adipose tissue was present. No relationship was seen between mammary diameter and weight or BMI in either population. These data suggest that future in-depth studies examining mammary tissue growth and fat deposition in breast tissue are required if we are to understand environmental influences on these phenomena.
Recent Suicides Highlight Need to Address Depression in Medical Students and Residents
Authors: Rita Rubin
Journal: JAMA (2014)

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