tbuckley/cabot-search huggingface dataset:
ADAPTATION OF GROUP B COXSACKIE VIRUS TO ADULT MOUSE PANCREAS
Authors: Gilbert Dalldorf, Rebecca Gifford
Journal: The Journal of Experimental Medicine (1952)

An alteration of tissue tropism of a Coxsackie virus has been observed following different methods of propagation of the virus in animals. Tropism for the adult mouse pancreas, as described by Pappenheimer, appeared to be irrevocably lost following prolonged brain-to-brain transfer. It was present in the same strain on reisolation from human feces, was intensified following pancreas transfers, and suppressed by brain transfers. Pancreatotropism may be correlated with the titer of virus in the pancreas.
Adenosine deaminase deficiency increases thymic apoptosis and causes defective T cell receptor signaling
Authors: Sergey G. Apasov, Michael R. Blackburn, Rodney E. Kellems, Patrick T. Smith, Michail V. Sitkovsky
Journal: Journal of Clinical Investigation (2001)

Adenosine deaminase (ADA) deficiency in humans results in a severe combined immunodeficiency (SCID). This immunodeficiency is associated with severe disturbances in purine metabolism that are thought to mediate lymphotoxicity. The recent generation of ADA-deficient (ADA–/–) mice has enabled the in vivo examination of mechanisms that may underlie the SCID resulting from ADA deficiency. We demonstrate severe depletion of T and B lymphocytes and defects in T and B cell development in ADA–/– mice. T cell apoptosis was abundant in thymi of ADA–/– mice, but no increase in apoptosis was detected in the spleen and lymph nodes of these animals, suggesting that the defect is specific to developing thymocytes. Studies of mature T cells recovered from spleens of ADA–/– mice revealed that ADA deficiency is accompanied by TCR activation defects of T cells in vivo. Furthermore, ex vivo experiments on ADA–/– T cells demonstrated that elevated adenosine is responsible for this abnormal TCR signaling. These findings suggest that the metabolic disturbances seen in ADA–/– mice affect various signaling pathways that regulate thymocyte survival and function. Experiments with thymocytes ex vivo confirmed that ADA deficiency reduces tyrosine phosphorylation of TCR-associated signaling molecules and blocks TCR-triggered calcium increases.
The Knee Joint: Recent Advances in Basic Research and Clinical Aspects
Authors: Kingsbury G. Heiple
Journal: JAMA (1975)

A book of 63 headings in only 329 pages can hardly be said to have chapters. Indeed the text comprises the papers from an International Congress on the Knee Joint held in Rotterdam in September 1973. The material covered is divided into six sections: I. Biomechanics of the Knee Joint, II. Degenerative Joint Disease, III. Trauma of the Knee Joint, IV. Congenital and Postural Deformities, V. Transplantation of Cartilage and Bone, and VI. Arthroplasty of the Knee Joint. Each section contains both short research reports and clinical material. In general, the research material is interesting and may be worth inspection by those actively engaged in the particular areas involved. This is particularly true of the biomechanics and transplantation sections, where some new and interesting material appears. Even here, however, much of the material appears to be either so preliminary as to be unsupported by data, or a rehash of the
Muscarinic receptor stimulation by carbachol improves functional recovery in isolated, blood perfused rabbit heart
Authors: M Hendrikx, Y Toshima, K Mubagwa, W Flameng
Journal: Cardiovascular Research (1993)

The aim was to test whether, besides adenosine A1 receptors, other receptors coupled to the "inhibitory" GTP binding protein Gi confer protection against ischaemic and reperfusion injury.Isolated hearts were Langendorff perfused at 37 degrees C with blood and were divided into five groups, all subjected to 45 min zero flow normothermic ischaemia, followed by 1 h reperfusion. Group 1 consisted of control untreated hearts (n = 5). Group 2 consisted of hearts treated with the muscarinic agonist carbachol (CCh, 10 microM; n = 5). In group 3 (CCh+atropine, n = 5) 5 microM atropine was given as well as CCh. Groups 1, 2, and 3 were paced at 3 Hz except during ischaemia. Groups 4 (n = 5) and 5 (n = 6) were similar to groups 1 and 2, except that pacing was continued throughout ischaemia.In group 1, left ventricular end diastolic pressure increased during ischaemia, from 7.2(SEM 1.2) mm Hg to 57(5.6) mm Hg, and remained increased during reperfusion, whereas in group 2, it increased moderately during ischaemia, from 9.2(0.9) mm Hg to 21.6(4.9) mm Hg and returned to preischaemic levels during reperfusion. In hearts paced during ischaemia, contracture developed faster than in unpaced hearts, but CCh still delayed contracture. Postischaemic recovery of isovolumetric left ventricular pressure or its first derivative (dP/dt) and reactive hyperaemia were significantly greater in CCh treated hearts [left ventricular pressure = 69.8(4.9)% of preischaemic value after 60 min reperfusion] than in control hearts [29.3(6.8)%]. Recovery of left ventricular pressure and dP/dt was worsened by pacing, but CCh still improved this recovery [left ventricular pressure = 13.1(8.4)% in control, 46.7(5.3)% in CCh treated hearts]. The CCh effect could be prevented by atropine. ATP breakdown and lactate accumulation during the first minute of ischaemia were lower in non-paced CCh treated hearts than in controls. ATP recovered better at the end of reperfusion in both non-paced [7.1(0.72) mumol.g-1] and paced [4.4(0.77) mumol.g-1] CCh treated hearts, as compared with non-paced [1.8(0.58) mumol.g-1] and paced [1.2(0.39) mumol.g-1] control hearts. In paced hearts, less creatine kinase and lactate dehydrogenase were released in the CCh treated group throughout the reperfusion phase.Carbachol improves functional recovery and confers cellular protection, and this protection depends mainly but not entirely on its bradycardic effect.
Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.
Authors: A Saito, J A Williams, T Kanno
Journal: Journal of Clinical Investigation (1980)

Using an isolated perfused rat pancreas preparation, the interrelationship between the endocrine and exocrine portions of the pancreas were studied. Addition of exogenous rat insulin (1-20 mU/ml) to the perfusing solution potentiated the action of cholecystokinin (CCK) (1 mU/ml) to increase both pancreatic juice flow and the release of the enzyme, amylase. Raising the glucose concentration in the perfusing solution from 2.5 to 17.5 mM both increased endogenous insulin release and potentiated the CCK-induced exocrine secretory response. Two lines of evidence indicated that this effect of glucose on the exocrine pancreas was mediated by endogenous insulin release. First, the addition of comparable amounts of xylose or galactose to the perfusion medium neither released insulin nor potentiated the CCK-induced response. Second, epinephrine blocked the effect of high glucose on both insulin release and potentiation of CCK action. Epinephrine alone did not affect the action of CCK. The magnitude of the exocrine response induced by high glucose was comparable to that of 2.5 mU/ml exogenous insulin. It seems possible that pancreatic acinar cells can be exposed to insulin levels of this magnitude in situ.
Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters
Authors: Abderrahim Nemmar, Peter H.M. Hoet, Jos Vermylen, Benoit Nemery, Marc F. Hoylaerts
Journal: Circulation (2004)

Background— Particulate air pollution is associated with cardiovascular diseases and myocardial infarction (MI). Methods and Results— We investigated the relationship between airway inflammation and thrombosis 24 hours after intratracheal (IT) instillation of diesel exhaust particles (DEP; 50 μg/hamster). Mild thrombosis was induced in the femoral vein by endothelial injury, and the consequences of airway inflammation on thrombogenicity were studied via online video microscopy. Lung inflammation and histamine analysis in bronchoalveolar lavage (BAL) and plasma were performed after pretreatment with dexamethasone (DEX) or sodium cromoglycate (SC). DEP induced airway inflammation and histamine release in BAL and in plasma, and increased thrombosis, without elevating plasma von Willebrand factor (vWF) levels. The IT instillation of 400-nm positively charged polystyrene particles (500 μg/hamster), serving as particles that do not penetrate into the circulation, equally produced airway inflammation, histamine release, and enhanced thrombosis. Histamine in plasma resulted from basophil activation. Intraperitoneal (IP) pretreatment with DEX (5 mg/kg) abolished the DEP-induced histamine increase in BAL and plasma and abrogated airway inflammation and thrombogenicity. The IT pretreatment with DEX (0.5 mg/kg) showed a partial but parallel inhibition of all of these parameters. Pretreatment with SC (40 mg/kg, IP) strongly inhibited airway inflammation, thrombogenicity, and histamine release. Conclusions— Our results are compatible with the triggering of mast cell degranulation and histamine release by DEP. Histamine plays an initial central role in airway inflammation, further release of histamine by circulating basophils, and peripheral thrombotic events. Antiinflammatory pretreatment can abrogate the peripheral thrombogenicity by preventing histamine release from mast cells.
Radial nerve palsy in an elite bodybuilder
Authors: A B Y Ng, J Borhan, H R Ashton, A N Misra, D R M Redfern
Journal: British Journal of Sports Medicine (2003)

A case is reported of high radial nerve palsy in an elite bodybuilder caused by an extrinsic mass effect of muscular hypertrophy. Surgical decompression resulted in complete clinical resolution.
Pigeon allergens in indoor environments: a preliminary study
Authors: L. Curtis, B.‐S. Lee, D. Cai, I. Morozova, J.‐L. Fan, P. Scheff, V. Persky, C. Einoder, S. Diblee
Journal: Allergy (2002)

Few studies have measured pigeon allergens in non pigeon coop environments. This study was conducted to determine approximate pigeon dropping allergen concentrations in indoor environments.Polyclonal antibody serum was prepared by injecting a rabbit three times with crude wild pigeon dropping extract in 50 mM Tris buffer with Freund's adjuvant. One hundred and fifteen dust samples were collected in a pigeon-infested school, pigeon coops, homes and hospitals and analyzed by a direct competitive pigeon enzyme-linked immunosorbent assay (ELISA).The highest level of pigeon allergen inhibitory activity were recorded in four samples from pigeon coop bedding samples with a median activity of 11.2% relative to pigeon droppings. The second highest level of pigeon allergens was in a pigeon-infested high school with a median or 7.4% activity relative to pigeon droppings. At an entrance underneath pigeon roosts, one sample had a relative inhibitory activity of 62.3%. Pigeon allergen inhibitory levels were generally low in the home and hospital samples, but nevertheless 46 out of 89 of these samples were still above detection limit.This study suggests that large concentrations of pigeon allergens can be found in buildings without domestic pigeons such as the pigeon-infested high school.
Scotland sets up its first forensic art unit
Authors: Bryan Christie
Journal: BMJ (2005)

A marriage of art and science is taking place at the University of Dundee that is desgned to advance techniques of facial reconstruction for both forensic and archaeological purposes. Scotland's first Forensic Art Unit has been established in a collaboration between the university and the local Duncan of Jordanstone College of Art. It is headed by Caroline Wilkinson who has been recruited from the University of Manchester.

Facial reconstruction techniques have traditionally involved the use of clay models to rebuild a face, based on skull structure. …
Enhanced Inhibition of Neointimal Hyperplasia by Genetically Engineered Endothelial Progenitor Cells
Authors: Deling Kong, Luis G. Melo, Abeel A. Mangi, Lunan Zhang, Marco Lopez-Ilasaca, Mark A. Perrella, Chong C. Liew, Richard E. Pratt, Victor J. Dzau
Journal: Circulation (2004)

Circulating endothelial progenitor cells (EPCs) have been reported previously. In this study, we examined the hypothesis that overexpression of vasculoprotective gene endothelial nitric oxide synthase (eNOS) and heme oxygenase-1 (HO-1) in EPCs enhances their ability to inhibit neointimal hyperplasia.EPCs were isolated from rabbit peripheral blood, expanded in culture, and transduced with pseudotyped retroviral vectors expressing human eNOS (eNOS-EPCs), HO-1 (HO-1-EPCs), or green fluorescent protein (GFP-EPCs). Transduction efficiency of EPCs ex vivo was >90%. Four groups of rabbits (n=5 to 6 per group) were subjected to balloon angioplasty of the common carotid artery. Immediately after injury, approximately 5x10(6) autologous eNOS-EPCs or HO-1-EPCs were transplanted into the injured vessel. Control animals received an equivalent number of GFP-EPCs or Ringer's saline. Two weeks after transplantation, eNOS and HO-1 transgene transcripts and proteins were detected in the transduced rabbit vessels. Endothelialization was enhanced in the EPC-transplanted vessels independently of gene transfer. Neointimal thickening was significantly reduced in the GFP-EPC-treated vessels relative to the saline control. Neointima size was further reduced in vessels treated with eNOS-EPCs. Surprisingly, no additional reduction was seen in vessels treated with HO-1-EPCs relative to GFP-EPCs. Thrombosis occurred in approximately 50% of the saline-treated vessels but was virtually absent in all EPC-transplanted vessels.We conclude that transplantation of autologous EPCs overexpressing eNOS in injured vessels enhances the vasculoprotective properties of the reconstituted endothelium, leading to inhibition of neointimal hyperplasia. This cell-based gene therapy strategy may be useful in treatment of vascular disease.
Abstract 1715: Induction of CYP1B1 expression in non-small cell lung carcinoma cells treated with B(a)P inhibits cisplatin-induced apoptosis
Authors: Juwon Park, Kyungseon Kim, Yang Seok Chae, Kwang-Sung Ahn, Nam Hee Won
Journal: Cancer Research (2011)

Abstract Cytochrome P450 1B1 (CYP1B1) is a key enzyme involved in metabolizing environment pollutants and whose expression is often significantly increased in human malignancies. In the past years, several studies focused on the possible role of CYP1B1 in tumor progression, invasion and drug resistance. CYP1B1 gene polymorphisms have been associated with the risk of lung and other cancer. However, there is no a evidence that induction of CYP1B1 by B(a)P has relevance to anticancer drug resistance. In this study, we found that CYP1B1 expression was increased by exposure of B(a)P in A549 cells and H1299 cells, respectively. Both A549 cells and H1299 cells prolonged exposed to B(a)P [A549-B(a)P and H1299-B(a)P] were resistant to cisplatin treatments. MTT assay showed that IC50 of A549-B(a)P and H1299-B(a)P was 2.3 folds and 3.2 folds higher than IC50 of parental cells. Results of immuocytostain revealed that induction of CYP1B1 and AhR was detected in A549-B(a)P and H1299-B(a)P. Reduction of CYP1B1 by shRNA of CYP1B1 in A549-B(a)P and H1299-B(a)P became to be sensitized to cisplatin treatments. The similar result was found in A549 cells and H1299 cells transfected with shRNA of AhR. Our data suggested that AhR-mediated CYP1B1 expression affected the response of cisplatin treatments on non-small cell lung cancer cells (NSCLCs). It suggested that, in exposure of B(a)P on lung cancer cells, AhR can modulate CYP 1B1 expression resulting in producing BPDE to form a bulk of DNA adducts. Exposure of B(a)P is committed to controlling proliferative/apoptotic balance, which has obvious and important implications in tumor progression and drug resistance. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1715. doi:10.1158/1538-7445.AM2011-1715
Gastric Ga-67 Uptake in Patients With Lymphoma
Authors: NAYER NIKPOOR, DAVID E. DRUM, PIRAN ALIABADI
Journal: Clinical Nuclear Medicine (1995)

Gastric accumulation of Ga-67 greater than that seen in the liver was observed in 16 of 162 (9.8%) patients with lymphoma. Endoscopic biopsies in six patients showed one instance each of histiocytic lymphoma, mixed cellularity Hodgkin's disease, adenocarcinoma, and hiatal hernia with mucosal deformity, as well as two instances of benign gastric ulcer. All six patients had chronic gastric symptoms, as well as persistent radiogallium accumulation on sequential examinations of 2 years duration. The remaining 10 patients exhibited transient radiotracer gastric uptake and only two has gastric symptoms. Persistent gastric Ga-67 accumulation is not common in lymphoma and warrants endoscopy when accompanied by prolonged symptoms.
THE TREATMENT OF ALL FRACTURES OF THE FOREARM, EXCEPT OF THE OLECRANON PROCESS, BY EXTENSION, COUNTER-EXTENSION AND FORCED SUPINATION.Read at the Annual Meeting of the Mississippi Valley Medical Association, at Louisville, Ky., October, 1890.
Authors: X. C. SCOTT
Journal: JAMA (1890)

In calling your attention to this mode of treatment I hope to convince you that it is superior to any other method, that you will not condemn it untried as an old doctor friend of mine did, and who said to me, "Doctor, it may be all right, but I do not think it will do because I have not tried it myself." Give it a fair trial and you will be convinced that it can be carried out in a simple manner and that it is better and far superior to any other method, by being adapted to every form of fracture of the forearm, except that of the olecranon process of the ulna. The splint is made of two pieces of board fas tened together securely at right angles. The shorter piece extending up the back of the arm about two-thirds the distance from the elbow to the
Platelet 12-LOX is essential for FcγRIIa-mediated platelet activation
Authors: Jennifer Yeung, Benjamin E. Tourdot, Pilar Fernandez-Perez, Joanne Vesci, Jin Ren, Christopher J. Smyrniotis, Diane K. Luci, Ajit Jadhav, Anton Simeonov, David J. Maloney, Theodore R. Holman, Steven E. McKenzie, Michael Holinstat
Journal: Blood (2014)
Growth factor-induced therapeutic angiogenesis in the heart: protein therapy
Authors: B ANNEX, M SIMONS
Journal: Cardiovascular Research (2004)

Therapeutic angiogenesis, stimulated growth of new vasculature to compensate for tissue ischemia, remains an unfulfilled promise. After nearly a decade of trials, the development of drugs capable of stimulating revascularization of underperfused tissues remains an exciting but unrealized goal in cardiovascular therapeutics. This review will summarize experiences in therapeutic angiogenesis studies employing protein therapies and will draw conclusions based on our current understanding of biological processes of new vessel growth.
Inflammation in Gut: Esophagitis, Duodenitis, Segmental Colitis
Authors: C. Wilmer Wirts
Journal: JAMA (1971)

This small volume is composed of 15 selected papers dealing with esophagitis, duodenitis, and segmental colitis prepared for presentation at the Eighth International Congress of Gastroenterology held in Prague, July 1968. In regard to esophagitis, the anatomy, histology, and pathology are discussed in detail; the interrelationship of pathophysiology and symptomatology are based on roentgen, endoscopic, and especially direct vision and blind biopsy findings. This sheds considerable light on a subject that continues to be a source of controversy. The topic of duodenitis is excessively belabored. Diagnosis based on biopsy fails to establish chronic nonspecific duodenitis as an entity, but, as expected, the duodenum may be affected by diffuse diseases of the small bowel and intestinal parasites such as giardiasis, ancylstomiasis, and strongyloidiasis. Finally, for segmental colitis a review of the incidence, symptomatology, diagnosis, pathology, and treatment is given.
Consequentialism and Harsh Interrogations
Authors: Matthew K. Wynia
Journal: The American Journal of Bioethics (2005)

With this issue, we begin a regular feature on bioethics and public health. We welcome Matthew K. Wynia, M.D., M.P.H., Director of the Institute for Ethics of the American Medical Association as our new Contributing Editor. If you have comments or suggestions regarding this feature, please email us at manuscript@ bioethics.net.
Comparative Imaging: Spinal Vascular Malformation
Authors: ROBERT G. WELLS, JOHN R. STY, DAVID C. GREGG, JOHN E. FELDMEIER
Journal: Clinical Nuclear Medicine (1988)

A case of an extradural spinal vascular malformation in a 14-year-old girl is presented. The imaging characteristics with radiographs, computed tomography, and Tc-99m labeled red blood cell imaging are correlated.
Meningococcemia Diagnosed by Peripheral Blood Smear
Authors: Edward J. Young
Journal: JAMA (1988)

A college student in previous good health presented with recent onset of fever, rigors, headache, and nuchal rigidity. A routine peripheral blood smear showed many intraleukocytic and extracellular cocci and diplococci (Figure). The organisms appeared purple in the Wright-stained preparation, but the presence of a high-grade bacteremia was unmistakable. The diagnosis of meningococcemia was confirmed by a lumbar puncture, which revealed gram-negative diplococci, and later<i>Neisseria meningitidis</i>group B was grown from both cerebrospinal fluid and blood. Microorganisms are infrequently visualized in peripheral blood films,<sup>1</sup>although it has been reported that examination of the buffy-coat layer is sometimes helpful in making an early diagnosis of septicemia.<sup>2</sup>In most instances only rare organisms are seen within phagocytic cells of the buffy coat, but their presence is strong evidence of bacteremia (or fungemia). When large numbers of organisms are present, it is important to rule out pseudobacteremia caused by contaminated
Endothelial Dysfunction and Cytomegalovirus Replication in Pediatric Heart Transplantation
Authors: Jacob Simmonds, Matthew Fenton, Catherine Dewar, Elizabeth Ellins, Clare Storry, David Cubitt, John Deanfield, Nigel Klein, Julian Halcox, Michael Burch
Journal: Circulation (2008)

Cardiac allograft vasculopathy is the major limiting factor to the long-term success of pediatric heart transplantation. Cytomegalovirus (CMV) has been shown to be a significant risk factor for the development of cardiac allograft vasculopathy. Recent work has demonstrated CMV DNA in leukocytes in the absence of direct allograft infection, suggesting that vascular changes may not be limited to the allograft.Systemic arterial endothelial function was assessed with high-resolution ultrasound to determine brachial artery flow-mediated dilation in 50 pediatric heart transplant recipients (8 to 17 years of age; 27 male). Patients were separated into 2 groups according to CMV status: those without evidence of CMV replication after transplantation (n=38; 19 male) and patients with evidence of viremia after transplantation (n=12; 8 male). No patient had detectable viremia at the time of study. Flow-mediated dilation was significantly impaired in patients with evidence of CMV replication after transplantation (6.64+/-1.12%, mean+/-SE) compared with those without (9.48+/-0.56%; P=0.02). This difference remained after adjustment for age, time since transplantation, and medication. Pretransplantation recipient and donor CMV status and traditional CMV risk were not associated with flow-mediated dilation.CMV replication after cardiac transplantation is associated with chronic endothelial dysfunction in the systemic circulation in children. The implication for both systemic and coronary vascular health requires prospective evaluation.