tbuckley/cabot-search huggingface dataset:
TREATMENT OF GAS POISONING IN TRANSVAAL MINES
Authors: A. H. Watt, L. G. Irvine
Journal: BMJ (1915)

Literature.I have not been able to finid in the literature any refer- enices to the immediate plhysiological action of clhlorine.''hlie ilost exact worlk on the effects of respiring mixtures of clhlorine and air is that of Lelhmann,2 Wllo plaCed afll-lais d(IuViug onie to six lhours in afftiosplheres contain- iiro fiuii I-part p-e 1,00,000 to 1 part erl1,000.He fouind thlat prolonged exp6ostie fo 1 pai't in 100,000 is suffidient to produce putliiuonary hlaemorlrhage and oedema wllilh lie regards as inflamunatory-whilst exposure to 1 part in 10,000 catnses in 'additioh a lbbrinous (" croupouis") exudat.oun in all ttie aiL passages, eVeh tlle flnest, and appea'rs ultiiimately to piodu'ce asp)lyxiatio,n.Numerous expert- mlental pathioiogfsts, 'inchling; W5eleh,83S."Miaybi,4 Salhli,5 indULt_Wit6 hlave 'n46ckavobir"ed to elti6idate tlh6 conditio'ns of 'pr6ductio'l of pulmonirly o6dema'.'T'h6se conditiidns liave also lately been studkid in' tlle I'siirviving " lung in Ma<,iius's laobdratory at"Utredlht by Mo'drakowski.7 IA these las`t-mleiftiioned paper's'tlhe literature of tLe subject is given, btht most oft thle Vb-rk refeired to hlas but little bearing lipon the oedemna puodu6cd by clhlorine.-Binz 8 fotuid in, tlhe frog that exposture to-clboiine gas hlas ,no influence on the lheart (as agaiuitt Falk', noi; on muscle and nerve, nlOLOr l ile e spinal cord, buit believes that it is-carried to tle brain, in' wllich, h&6 states, it can be detected by thle siunlle I liamie not noticed any snell of chlorine 2?ost inortehi7 in the animals I lhave dealt witlh.
Activation of Rabbit Hageman Factor by Homogenates of Cultured Rabbit Endothelial Cells
Authors: Roger C. Wiggins, David J. Loskutoff, Charles G. Cochrane, John H. Griffin, Thomas S. Edgington
Journal: Journal of Clinical Investigation (1980)

Rabbit Hageman factor was proteolytically cleaved and activated by a homogenate prepared from cultured rabbit endothelial cells. Cleavage of radiolabeled Hageman factor was monitored by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. Endothelial cell-mediated cleavage of Hageman factor was demonstrated both in a purified system and in plasma, was time and concentration dependent, and was associated with formation of the characteristic 28,000 Mr form of active Hageman factor. The rate of cleavage of Hageman factor was not affected by Triton X-100 (Rohm and Haas, Co., Philadelphia, Pa.), hexadimethrine bromide (Polybrene, Aldrich Chemical Co., Inc., Milwaukee, Wis.), hirudin, soybean trypsin inhibitor, or antisera to plasminogen or prekallikrein. However, cleavage was enhanced by kaolin, and was inhibited by diisopropyl-fluorophosphate. The enzyme responsible for cleavage of Hageman factor was localized to the 100,000-g-sedimentable, subcellular fraction of the endothelial cell homogenate and was relatively specific, because neither radiolabeled rabbit Factor XI nor rabbit prekallikrein were themselves proteolytically cleaved by the endothelial cell homogenate. However, when these molecules were incubated with the homogenate in the presence of Hageman factor, both Factor XI and prekallikrein were cleaved, demonstrating that Hageman factor had been activated by the endothelial cell homogenate. Furthermore, the kallikrein generated by endothelial cell homogenate-activated Hageman factor was capable of liberating kinin from high molecular weight kininogen as measured by bioassay. Cultured rabbit endothelial cells, therefore, possess the capacity to activate Hageman factor by proteolysis. This may be one mechanism for Hageman factor activation in vivo.
Prenatal Bisphenol A Exposure Induces Preneoplastic Lesions in the Mammary Gland in Wistar Rats
Authors: Milena Durando, Laura Kass, Julio Piva, Carlos Sonnenschein, Ana M. Soto, Enrique H. Luque, Mónica Muñoz-de-Toro
Journal: Environmental Health Perspectives (2006)

Humans are routinely exposed to bisphenol A (BPA), an estrogenic compound that leaches from dental materials, food and beverage containers, and other consumer products. Prenatal exposure to BPA has produced long-lasting and profound effects on rodent hormone-dependent tissues that are manifested 1-6 months after the end of exposure.The aim of the present work was to examine whether in utero exposure to BPA alters mammary gland development and increases its susceptibility to the carcinogen N-nitroso-N-methylurea (NMU).Pregnant Wistar rats were exposed to BPA (25 pg/kg body weight per day) or to vehicle. Female offspring were sacrificed on postnatal day (PND) 30, 50, 110, or 180. On PND50 a group of rats received a single subcarcinogenic dose of NMU (25 mg/kg) and they were sacrificed on either PND110 or PND180.At puberty, animals exposed prenatally to BPA showed an increased proliferation/apoptosis ratio in both the epithelial and stromal compartments. During adulthood (PND110 and PND180), BPA-exposed animals showed an increased number of hyperplastic ducts and augmented stromal nuclear density. Moreover, the stroma associated with hyperplastic ducts showed signs of desmoplasia and contained an increased number of mast cells, suggesting a heightened risk of neoplastic transformation. Administration of a subcarcinogenic dose of NMU to animals exposed prenatally to BPA increased the percentage of hyperplastic ducts and induced the development of neoplastic lesions.Our results demonstrate that the prenatal exposure to low doses of BPA perturbs mammary gland histoarchitecture and increases the carcinogenic susceptibility to a chemical challenge administered 50 days after the end of BPA exposure.
The use of the Psorilux 3050A machine in the management of psoriasis of the hands and feet
Authors: HELEN M. NELSON, RONA M. MacKIE
Journal: British Journal of Dermatology (1980)

Eleven patients with severe psoriasis involving the palms and soles have been treated using a high-energy source of UV-A and UV-B with no additional topical or systemic photosensitizing drug. The results showed marginal benefit of UV-A alone over conventional topical tar therapy. The high energy output of the machine makes it essential that personnel supervising therapy are adequately protected.
ABC of diabetes. clinical presentation: why is diabetes so often missed?
Authors: P J Watkins
Journal: BMJ (1982)

A 62-yr-old woman with a history of mental retardation, paranoid psychosis and agitated depression presented with deterioration in her baseline mental status and fever. No obvious source of fever was found on clinical exam or on initial laboratory studies. An <sup>111</sup>In-white blood cell (<sup>111</sup>In-WBC) study was performed 1 wk after hospital admission, which revealed increased uptake in the anterior neck and oral cavity. Subsequent laryngoscopy revealed a red, swollen epiglottis compatible with epiglottitis. While not advocating <sup>111</sup>In-WBC scintigraphy as part of the workup of epiglottitis, this case is presented to emphasize the possible milder presentation of epiglottitis in adults compared to children.
Secondary Left Ventricular Endocardial Fibroelastosis Following Mitral Valve Replacement
Authors: WILLIAM C. ROBERTS, ANDREW G. MORROW
Journal: Circulation (1968)

Secondary endocardial fibrosis of variable severity was observed in the left ventricle in 13 of 16 patients after mitral valve replacement. Similar lesions were not observed in any of 20 patients who died in the late postoperative period after isolated aortic valve replacement. The left ventricular endocardial thickening is believed to be the result of turbulent flow, produced in the left ventricle by the caged ball within it. Severe impairment of cardiac function appeared to result from the process in two of the 13 patients: each developed intractable and ultimately fatal cardiac failure several months after double valve replacement, and the extensive endocardial thickening was the only anatomical cause for failure in both patients. Thus, secondary left ventricular endocardial fibrosis appears to be another, although uncommon, cause of cardiac failure in the late postoperative period after replacement of the mitral valve with a cagedball prosthesis.
Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.
Authors: S Takata, M Matsubara, P G Allen, P A Janmey, C N Serhan, H R Brady
Journal: Journal of Clinical Investigation (1994)

5-Lipoxygenase products, such as leukotrienes, are important stimuli for leukocyte-mediated tissue injury in acute inflammation. 15-Hydroxyeicosatetraenoic acid (15-HETE) is an eicosanoid generated by a variety of cell types via the actions of 15-lipoxygenases and, in addition, cyclooxygenases and epoxygenases. 15-HETE levels are frequently elevated at sites of inflammation, and extracellular 15(S)-HETE is esterified rapidly into neutrophil (PMN) phospholipids in vitro to levels that are comparable with arachidonic acid. We present evidence that remodeling of PMN phospholipids with 15(S)-HETE stereoselectively inhibits PMN migration across endothelium in response to leukotriene B4 (LTB4) and other chemoattractants. Esterified 15(S)-HETE causes a striking reduction in the affinity of LTB4 cell-surface receptors for their ligand and inhibition of LTB4-triggered stimulus-response coupling. As a result of these actions, esterified 15(S)-HETE attenuates the cytoskeletal rearrangements and CD11/CD18-mediated adhesive events that subserve directed locomotion of PMN across endothelium. These observations indicate that products of the 5-lipoxygenase and 15-lipoxygenase pathways can exert counterbalancing influences on PMN trafficking across endothelium. They suggest that 15(S)-HETE may be a potent endogenous inhibitor of PMN-endothelial interactions in vivo and serve to limit or reverse acute inflammation.
P374 LONG-TERM TREATMENT OF PRIMARY BILIARY CIRRHOSIS WITH THE FXR AGONIST OBETICHOLIC ACID SHOWS DURABLE EFFICACY
Authors: K. Kowdley, G. Hirschfield, R. Chapman, C. Vincent, D. Jones, A. Pares, V. Luketic, S. Gordon, R. Pencek, T. Marmon, R. Hooshmand-Rad
Journal: Journal of Hepatology (2014)
Mechanism of chronic obstructive uropathy: Increased expression of apoptosis-promoting molecules
Authors: Yeong-Jin Choi, Elzbieta Baranowska-Daca, Vinh Nguyen, Takehiko Koji, Christie M. Ballantyne, David Sheikh-Hamad, Wadi N. Suki, Luan D. Truong
Journal: Kidney International (2000)
Multimerin is found in the alpha-granules of resting platelets and is synthesized by a megakaryocytic cell line.
Authors: C P Hayward, D F Bainton, J W Smith, P Horsewood, R H Stead, T J Podor, T E Warkentin, J G Kelton
Journal: Journal of Clinical Investigation (1993)

In this report, we describe the intracellular localization of multimerin in platelets and its biosynthesis by Dami cells, a megakaryocytic cell line. Immunoelectron microscopy was used to examine frozen thin sections of resting and activated platelets. Multimerin was localized within the platelet alpha-granule in an eccentric position. Within activated platelets, multimerin was found in the surface-connected open cannalicular system and on the external plasma membrane. Light microscopic immunocytochemistry demonstrated multimerin in normal megakaryocytes and in Dami cells after stimulation with PMA. Confirmation of multimerin biosynthesis by Dami cells was obtained by metabolic labeling studies. Both platelet and Dami cell multimerin demonstrated several subunit sizes on reduced SDS-PAGE. However, peptide mapping confirmed structural homology between the different multimerin subunits. Glycosidase digestion demonstrated that multimerin is heavily glycosylated with mainly complex, N-linked carbohydrate. In contrast to the multimerin isolated from platelets, cultured Dami cells secreted mainly smaller multimers of the protein. Biosynthesis of multimerin by a megakaryocytic cell line supports endogenous biosynthesis by megakaryocytes as the origin of this platelet alpha-granule protein.
Health bill arose from attempt to accommodate Lib Dem as well as Tory ideas, says commentator
Authors: N. Hawkes
Journal: BMJ (2012)

The widely held view that the health secretary for England, Andrew Lansley, was the sole begetter of his own political misfortunes over the Health and Social Care Act is mistaken, concludes a new account of the controversial legislation.1

Nick Timmins, former public policy editor of the Financial Times , finds the fingerprints of the Liberal Democrats all over the bill and identifies the confusion that arose in the weeks after the coalition was formed as the key to understanding why an evolutionary change became revolutionary turmoil.

In Never Again , published by the King’s Fund and the Institute for Government, Timmins traces the history of the legislation from published sources and through interviews with those involved. 

He told a meeting at the institute on 12 July that among the relatively few who declined his requests for interviews were Oliver Letwin and Danny Alexander, Conservative and Liberal Democrat respectively, who in the weeks after the coalition was formed had the job of turning the sketchy coalition agreement into a programme for government. This was done in haste and …
Abstract 2912: Inhibition of redox/Fyn/c-Cbl pathway function by Cdc42 controls tumor initiation capacity and tamoxifen sensitivity in basal-like breast cancer cells.
Authors: Hsing-Yu Chen, Yin Yang, Brett Stevens, Mark Noble
Journal: Cancer Research (2013)

Abstract Two of the substantial challenges in cancer research are to identify means overcoming resistance of malignant cells to existing therapies and to eliminate the unique small population within bulk tumors, named tumor initiating cells or cancer stem cells which have been proposed to regenerate resistant relapsed tumors. In this study, we offer a novel therapeutic target relevant to both of these goals on basal-like (triple-negative) breast cancer (BLBC) cells, one of the most challenging cancers to treat with current regimens. Our findings emerged from examining the puzzling differences in regulation of activation of the E3 ubiqutin ligase c-Cbl in normal cells and in cancer cells by low microM concentrations of tamoxifen (TMX). In normal progenitor cells, TMX causes oxidation and sequential activation of Fyn kinase and the c-Cbl ubiquitin ligase. Activation of c-Cbl via this redox/Fyn/c-Cbl (RFC) pathway leads to accelerated degradation of receptor tyrosine kinases that are critical in cell survival and division (such as the epidermal growth factor (EGFR)). In BLBC cells, in contrast, TMX does not activate c-Cbl despite making the cells more oxidized and causing activation of Fyn. Moreover, BLBC cells exposed to TMX show no reduction in levels of EGFR. We found that TMX-induced activation of c-Cbl in BLBC cells was inhibited due to expression of Cdc42. Cdc42 sequestered c-Cbl, prevented its activation and prevented EGFR from being degraded. Restoration of c-Cbl function, by inhibiting activation of Cdc42, reduced EGFR levels in these cells. More critically, restoring c-Cbl function sensitized these cells to TMX both in vitro and in vivo through estrogen receptor-independent mechanisms. Analysis of tumor growth and formation in vivo showed that reducing the levels of Cdc42 reduced the size of tumors, increased sensitivity to TMX and decreased tumor forming capacity of these cells. The results provide a novel defense mechanism that BLBC cells utilize to prevent EGFR degradation, which may have high relevance to treatment of these tumors. Of particular importance is the ability of cdc42 to confer TMX sensitivity on these otherwise resistant tumor cells. Moreover, as use of low microM levels of TMX has been attempted for over a dozen different kinds of cancers, at least some of which express increased levels of Cdc42, this strategy may be relevant to the treatment of multiple different cancers. Citation Format: Hsing-Yu Chen, Yin Yang, Brett Stevens, Mark Noble. Inhibition of redox/Fyn/c-Cbl pathway function by Cdc42 controls tumor initiation capacity and tamoxifen sensitivity in basal-like breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2912. doi:10.1158/1538-7445.AM2013-2912
THE RELATIVE REACTION WITHIN LIVING MAMMALIAN TISSUES
Authors: Peyton Rous
Journal: The Journal of Experimental Medicine (1925)

The present paper is the first of a series of reports on the relative reaction of living tissues as determined by vital staining with indicators. It is possible to bring about a localized and a general coloration of living rats and mice with litmus. The animals remain in good health and the coloration of some of the tissues persists for months. Much of the dye is stored in cell granules, especially in those of the reticulo-endothelial elements, but a diffuse staining of certain tissues occurs, notably of bone, epidermis, cartilage, and connective tissue everywhere. In the intensity and localization of the bony coloration litmus has resemblances to madder. Diffuse staining with it renders blue most, if not all, of the tissues affected, while a granular staining causes others to become notably pink, owing to the fact that the indicator, though introduced into the organism in the blue form and circulating as such in the body fluids, is ordinarily red when stored in cells. The polymorphonuclear elements and macrophages of a peritoneal exudate, may become so laden with material colored red by litmus that the blue color of the fluid constituent is masked and the exudate appears a deep, turbid red. The phenomenon is but one manifestation of a notable acidity within cell granules throughout the organism. Like many another in the stained animals it would appear to be of physiological import. Some of the questions suggested by the work will be dealt with in the paper immediately following.
KINETICS OF THE REACTION OF RENIN WITH NINE SYNTHETIC PEPTIDE SUBSTRATES
Authors: Leonard T. Skeggs, Kenneth E. Lentz, Joseph R. Kahn, Harry Hochstrasser
Journal: The Journal of Experimental Medicine (1968)

A number of peptides have been synthesized which represent portions of the tetradecapeptide renin substrate molecule, and which contain the hydrolyzable leu-leu bond. An automatic chemical method for determination of the velocity of the reaction of renin with these compounds was developed. Application of the method at several levels of substrate concentration permitted construction of Lineweaver-Burk plots, and calculation of Michaelis constants (Km) and maximal velocities (Vmax). The results show that the maximum affinity of the enzyme (lowest Km) for substrate is achieved only with the full tetradecapeptide molecule (asp1-arg2-val3-tyr4-ileu5-his6-pro7-phe8-his9-leu10-leu11-val12-tyr13-ser14). Removal of asp1 and arg2 from the N-terminal increases the Km eight-fold. Further, moderate increase in Km occurs when the next amino acids, val3, tyr4 and ileu5, are removed. The further removal of his6 results in a marked reduction in the Vmax. Removal of ser14 from the C-terminal of the nonapeptide his6-pro7-phe8-his9-leu10-leu11-val12-tyr13-ser14 does not greatly affect the Km nor the Vmax. Further removal of tyr13 from this compound results in complete loss of substrate activity. It is suggested that the compounds his6-pro7-phe8-his9-leu10-leu11-val12-tyr13-ser14 or his6-pro7-phe8-his9-leu10-leu11-val12-tyr13 might be used as substrates for the chemical assay and standardization of renin.
Observations on the Role of Serotonin in Shock due to Bacterial Endotoxin.
Authors: R. B. Davis
Journal: Annals of Internal Medicine (1961)

s1 May 1961Observations on the Role of Serotonin in Shock due to Bacterial Endotoxin.R. B. Davis, M.D., W. R. Meeker, M.D.R. B. Davis, M.D.Search for more papers by this author, W. R. Meeker, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-5-1054_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe possible role of serotonin in the trigger mechanism producing shock due to bacterial endotoxin has been investigated. Prior studies in our laboratory showed that profound alterations occurred in serotonin concentrations within 15 sec. after the injection of Escherichia coli endotoxin, coincident with significant hemodynamic changes and marked intravascular agglutination of platelets in the dog. Actual release of serotonin, however, was not conclusively demonstrated.After lethal amounts of endotoxin were injected in rabbits, the in vivo liberation of serotonin clearly was demonstrated in carotid artery blood. A statistically significant elevation of plasma serotonin was demonstrated after endotoxin, with serum and... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Minneapolis, Minn. (CI) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1961Volume 54, Issue 5Page: 1054-1055KeywordsBlood plasmaCarotid arteriesEndotoxinsEscherichia coliHemodynamicsPlateletsRabbitsResearch laboratoriesSerotoninShock ePublished: 1 December 2008 Issue Published: 1 May 1961 PDF downloadLoading ...
Epigastric Pain With Falling Hematocrit
Authors: Donald L. Roback
Journal: JAMA (1979)

<h3>History</h3> A 56-year-old woman was admitted with severe epigastric pain after having eaten a large meal. The patient was diaphoretic and had tachycardia. The pain radiated across the abdomen and was suggestive of biliary colic. The blood pressure was 110/70 mm Hg, with a regular pulse rate of 144 beats per minute. The hematocrit value was 34.3%, and the hemoglobin concentration was 12 g/dL. The initial diagnosis was cholecystitis, cholelithiasis, and gallbladder colic. An intravenous cholangiogram was normal. The hematocrit value fell to 25.7%, and the hemoglobin concentration fell to 8.8 g/dL in 24 hours, with a blood pressure of 70/40 mm Hg. There was no evidence of bleeding from the gastrointestinal tract. An emergency angiogram was performed (Fig 1 and 2). <h3>Diagnosis</h3> Aneurysm of the inferior pancreaticoduodenal artery with retroperitoneal bleeding. Subtraction film of the early arterial phase of the superior mesenteric angiogram (Fig 1) shows a 2-cm aneurysm