tbuckley/cabot-search huggingface dataset:
Barking mad? Another lunatic hypothesis bites the dust
Authors: S. Chapman, S. Morrell
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objective:</b> To assess whether dog bites requiring hospital admission occur more at the full moon. <b>Design:</b> Review of dates of admission for dog bites to accident and emergency departments, June 1997 to June 1998, compared with dates of the full moon. <b>Setting:</b> All public hospitals in Australia. <b>Main outcome measures:</b> Admissions for dog bites. <b>Results:</b> 12 peak clusters of admissions were unrelated to the time of the full moon. <b>Conclusion:</b> Dog bites are no more frequent on full moons than at any other time of the month. Sceptics rejoice.
Gestational changes in pulmonary vascular responses in fetal lambs in utero.
Authors: A B Lewis, M A Heymann, A M Rudolph
Journal: Circulation Research (1976)

Pulmonary arterial (PA) blood flow patterns, changes in pulmonary blood flow, and pulmonary vascular responses to graded hypoxemia and intravenous acetylcholine (ACh) were studied in 15 fetal lambs in utero 3-12 days after surgical implantation of an electromagnetic flow transducer and PA catheter. Phasic PA flow in the fetus was forward only during the first third of systole, almost zero during midsystole, and backward during late systole and early diastole. In contrast, neonatal lambs showed forward PA flow throughout systole. The constriction of the fetal pulmonary vasculature in response to progressive hypoxemia varied with gestational age. At 103 days there was no significant drop in PA flow and only a small increase in pulmonary vascular resistance (Rp) with hypoxemia. The greatest increase in Rp was seen in fetuses after 121 days of gestation. This response was unaffected by alpha- and beta-sympathetic and parasympathetic blockade. Similarly, the pulmonary vascular response to ACh injected into the fetal jugular vein depended on gestational age. Little or no increase in pulmonary flow was noted in the youngest fetus, whereas ACh produced a marked increase in pulmonary flow in festuses over 120 days of gestation. These data suggest that the mechanisms by which hypoxemia constricts and ACh relaxes the pulmonary vascular smooth muscle are not fully developed in fetal lambs at 100 days of gestation and furthermore, that these mechanisms progressively develop during the last third of gestation.
DIAPHRAGMATIC HERNIA AS A LATE SEQUEL OF WAR WOUND OF THE CHEST
Authors: Harold E. Waxman
Journal: JAMA (1922)

An interesting phase of the case here reported is the fact that diaphragmatic hernia may be confused with appendicitis. From a theoretical standpoint it scarcely seems probable that a condition pathologically and anatomically so different from diaphragmatic hernia as acute appendicitis could be confused with the former. Yet this did happen, and Borden<sup>1</sup>recently reported a similar mistake, although in a widely different and more chronic form of diaphragmatic hernia. <h3>REPORT OF CASE</h3><h3>History.</h3> —J. B., a white man, aged 28, a city fireman, was admitted to the hospital, Dec. 30, 1920, complaining of pain in the abdomen. December 23, while at a fire, the patient was overcome by smoke. He did not remember much of what had happened to him, but was told by companions that his asphyxia was rather profound, and the pulmotor was used. Before the accident, to the best of his knowledge, he was in
Sex is a potent modifier of the cardiovascular system
Authors: Leslie A. Leinwand
Journal: Journal of Clinical Investigation (2003)

Despite the growing number of reports in the literature identifying sex-related differences in cardiac function in both rodents and humans, the underlying mechanisms have yet to be determined. Here, variables of experimental studies such as diet, animal model utilized, and age, in addition to sex hormones and other factors that may play a role in sex-related variations in cardiac responses to various pathophysiological conditions are discussed, suggesting that current approaches used in the study of cardiac disease require reevaluation.

There are numerous health problems that are affected by gender. Women are more susceptible than men to depression, osteoporosis, asthma, lung cancer due to smoking, and autoimmune disease (1). Gender effects in disease are complex, however, as exemplified by the observation that while the incidence of melanoma is slightly higher among women than men, mortality from melanoma is higher in men. Not all medical problems show gender dimorphism. For example, males do not differ from females in terms of their responses to infection (1). When it comes to heart disease, generally, of those individuals diagnosed with heart disease, women fare much better than men. Little is known about the basis for this difference in cardiovascular disease. Much focus has been placed on the potential cardioprotective role of estrogen. However, the recent finding that estrogen replacement in postmenopausal women actually increased heart disease has challenged this view (2).

Deriving a coherent view of potential players in sex-dependent differences in the heart requires analysis of both the clinical literature and the literature on sex-dependent differences in the cardiovascular system of laboratory animals. There is a major limiting factor in comparing rodent laboratory studies: the vast majority have been carried out on males only. However, this limitation appears to be changing. In the past year, a number of studies have appeared in which both males and females have been analyzed. An article in a recent issue of the JCI by O’Connell et al. (3) provided a glimpse into what promises to be a new way of thinking about genetic sex. In this report, the authors found that the α1-adrenergic receptors are critical in determining heart size and the ability of the heart to respond to both pathologic and physiologic stimuli, but only in male animals. Intriguingly, this sex-related difference did not disappear following ovariectomy of females. This article will discuss the fact that sex is an extremely potent modifier of the myocardium and will identify which pathways have been implicated in some of these differences. I hope it will become clear that future research should focus on the mechanisms by which both sex and diet can modify cardiovascular phenotypes.
Relations between cardiac and vascular structure in patients with primary and secondary hypertension
Authors: Damiano Rizzoni, Maria Lorenza Muiesan, Enzo Porteri, Massimo Salvetti, Maurizio Castellano, Giorgio Bettoni, Guido Tiberio, Stefano Maria Giulini, Cristina Monteduro, Guido Garavelli, Enrico Agabiti-Rosei
Journal: Journal of the American College of Cardiology (1998)
An Address ENTITLED AFTER TWENTY YEARS: Delivered before the Walthamstow Division of the Metropolitan Counties Branch of the British Medical Association
Authors: P. Warner
Journal: BMJ (1905)

MARCH II, 19g5. metastatic disease, the older views in regard to the infective powers of the micro-organism must be set aside.The gono- *coccus must be regarded as a micro-organism capable under certain conditions of setting up widespread disease in the human body.It may be regarded as an occasional exciting agent of septicaemia, but, just as in the case of other microorganisms, the gonococcus in the production of disease shows preference for certain parts of the body-for example, the synovial membranes of joints, tendon sheaths, and the val ar apparatus of the heart.The affection of the heart by the gonococcus has been the subject of much discussion, more particularly in regard to the frequency of its occurrence.Clinically the condition is regarded as rare, and even post mortem the exciting agent may be lost sight of.It is true that the demonstration of the gonococcus is difficult in many cases, but with the routine examination of the blood in all cases of endocarditis ante mortem, as well as the bacterio- -logical examination of the valvular lesion post mortem, cases due to the micrococcus gonorrhoeae ought to be brought to light in greater abundance in the future.
Genetic variation in the PNPLA3 gene is associated with alcoholic liver injury in caucasians
Authors: Felix Stickel, Stephan Buch, Katharina Lau, Henriette Meyer zu Schwabedissen, Thomas Berg, Monika Ridinger, Marcella Rietschel, Clemens Schafmayer, Felix Braun, Holger Hinrichsen, Rainer Günther, Alexander Arlt, Marcus Seeger, Sebastian Müller, Helmut Karl Seitz, Michael Soyka, Markus Lerch, Frank Lammert, Christoph Sarrazin, Ralf Kubitz, Dieter Häussinger, Claus Hellerbrand, Dieter Bröring, Stefan Schreiber, Falk Kiefer, Rainer Spanagel, Karl Mann, Christian Datz, Michael Krawczak, Norbert Wodarz, Henry Völzke, Jochen Hampe
Journal: Hepatology (2010)

A recent genome-wide study revealed an association between variation in the PNPLA3 gene and liver fat content. In addition, the PNPLA3 single-nucleotide polymorphism rs738409 (M148I) was reported to be associated with advanced alcoholic liver disease in alcohol-dependent individuals of Mestizo descent. We therefore evaluated the impact of rs738409 on the manifestation of alcoholic liver disease in two independent German cohorts. Genotype and allele frequencies of rs738409 (M148I) were determined in 1,043 alcoholic patients with or without alcoholic liver injury and in 376 at-risk drinkers from a population-based cohort. Relative to alcoholic patients without liver damage (n = 439), rs738409 genotype GG was strongly overrepresented in patients with alcoholic liver cirrhosis (n = 210; OR 2.79; P(genotype) = 1.2 × 10(-5) ; P(allelic) = 1.6 × 10(-6) ) and in alcoholic patients without cirrhosis but with elevated alanine aminotransferase levels (n = 219; OR 2.33; P(genotype) = 0.0085; P(allelic) = 0.0042). The latter, biochemically defined association was confirmed in an independent population-based cohort of at-risk drinkers with a median alcohol intake of 300 g/week (OR 4.75; P(genotype) = 0.040; P(allelic) = 0.022), and for aspartate aminotransferase (AST) levels. Frequencies of allele PNPLA3 rs738409(G) in individuals with steatosis and normal alanine aminotransferase (ALT) and AST levels were lower than in alcoholics without steatosis and normal ALT/AST (P(combined) = 0.03). The population attributable risk of cirrhosis in alcoholic carriers of allele PNPLA3 rs738409(G) was estimated at 26.6%. Genotype PNPLA3 rs738409(GG) is associated with alcoholic liver cirrhosis and elevated aminotransferase levels in alcoholic Caucasians.
THE STAINING OF THICK SECTIONS OF SKIN
Authors: E. H. LEACH
Journal: British Journal of Dermatology (1952)

Journal Article THE STAINING OF THICK SECTIONS OF SKIN Get access E. H. LEACH, M.A., B.Sc. E. H. LEACH, M.A., B.Sc. University Laboratory of Physiology, Oxford Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 64, Issue 5, 1 May 1952, Pages 183–189, https://doi.org/10.1111/j.1365-2133.1952.tb15893.x Published: 01 May 1952
Raman profiles of the stratum corneum define 3 filaggrin genotype–determined atopic dermatitis endophenotypes
Authors: Gráinne M. O'Regan, Patrick M.J.H. Kemperman, Aileen Sandilands, Huijia Chen, Linda E. Campbell, Karin Kroboth, Rosemarie Watson, Marion Rowland, Gerwin J. Puppels, W.H. Irwin McLean, Peter J. Caspers, Alan D. Irvine
Journal: Journal of Allergy and Clinical Immunology (2010)

Filaggrin (FLG) has a central role in the pathogenesis of atopic dermatitis (AD). FLG is a complex repetitive gene; highly population-specific mutations and multiple rare mutations make routine genotyping complex. Furthermore, the mechanistic pathways through which mutations in FLG predispose to AD are unclear.We sought to determine whether specific Raman microspectroscopic natural moisturizing factor (NMF) signatures of the stratum corneum could be used as markers of FLG genotype in patients with moderate-to-severe AD.The composition and function of the stratum corneum in 132 well-characterized patients with moderate-to-severe AD were assessed by means of confocal Raman microspectroscopy and measurement of transepidermal water loss (TEWL). These parameters were compared with FLG genotype and clinical assessment.Three subpopulations closely corresponding with FLG genotype were identified by using Raman spectroscopy. The Raman signature of NMF discriminated between FLG-associated AD and non-FLG-associated AD (area under the curve, 0.94; 95% CI, 0.91-0.99). In addition, within the subset of FLG-associated AD, NMF distinguished between patients with 1 versus 2 mutations. Five novel FLG mutations were found on rescreening outlying patients with Raman signatures suggestive of undetected mutations (R3418X, G1138X, S1040X, 10085delC, and L2933X). TEWL did not associate with FLG genotype subgroups.Raman spectroscopy permits rapid and highly accurate stratification of FLG-associated AD. FLG mutations do not influence TEWL within established moderate-to-severe AD.
Association of in Vitro<i>Escherichia coli</i>Adherence to Vaginal and Buccal Epithelial Cells with Susceptibility of Women to Recurrent Urinary-Tract Infections
Authors: Anthony J. Schaeffer, Joanne M. Jones, Judith K. Dunn
Journal: New England Journal of Medicine (1981)

To identify changes in epithelial cells that were associated with susceptibility to recurrent urinary-tract infections, we investigated the adherence of Escherichia coli to vaginal and buccal cells obtained from 11 healthy controls and 24 patients who had had at least three such infections in the preceding year. Adherence to vaginal cells was greater in patients than in controls (10.1 +/- 0.92 vs. 3.8 +/- 0.47 bacteria per cell [mean +/- S.E.], P less than 0.001), as was adherence to buccal cells (11.7 +/- 1.29 vs. 7.1 +/- 0.49, P = 0.002). This increased adherence in patients persisted despite temporary remission of the infection. Vaginal cells from patients not receiving antimicrobial prophylaxis had greater adherence than cells from patients given prophylactic therapy (11.7 +/- 1.34 vs. 8.3 +/- 1.0; P = 0.027). The range and rapidity of change in adherence as well as in vivo colonization of the vaginal mucosa were greater in patients than controls. Our data suggest that susceptibility to urinary-tract infections in women is associated with changes in the adhesive characteristics of epithelial cells.
Clinical and Diagnostic Virology
Authors: Trudy A. Larson
Journal: JAMA (1994)

<i>Clinical and Diagnostic Virology</i>is a new journal in the field of virology. It is an international journal publishing papers on any aspect of human virology that directly pertains to virus-induced clinical conditions and falls under one of the journal's major section headings: epidemiology, pathogenesis, diagnosis, detection, prevention, and treatment. Articles from any field of virological study are accepted if relevant to the understanding or manipulation of a disease state. Clinicians will find<i>Clinical and Diagnostic Virology</i>to be fairly dry and its applicability limited by the small number of articles in each issue. Issues average 65 pages, with only seven to nine articles. Submissions of original research are well chosen and relevant. References are up-to-date and extensive. However, overall the articles are uneven with some very well written and others suffering from poor grammar. The journal is designed to meet the needs both of virologists working with viruses that
Activation of CREB by tauroursodeoxycholic acid protects cholangiocytes from apoptosis induced by mTOR inhibition
Authors: LiFu Wang, Anne‐Christine Piguet, Karin Schmidt, Thierry Tordjmann, Jean‐François Dufour
Journal: Hepatology (2005)

Tauroursodeoxycholic acid (TUDCA) is a cytoprotective bile acid frequently prescribed to patients with cholestatic diseases. Several mechanisms of action have been investigated, but the possibility that cyclic adenosine monophosphate responsive element binding protein (CREB), a transcription factor promoting cell survival, mediates TUDCA's protective effects has not been considered. We examined whether TUDCA activates CREB and whether this activation can protect biliary epithelial cells. Cholangiocytes were stressed by exposure to CCI-779, which inhibits signaling though the kinase mTOR (mammalian target of rapamycin), resulting in cell cycle arrest and apoptosis. Incubation of normal rat cholangiocytes (NRC) cells, with TUDCA resulted in phosphorylation of CREB (Western blotting analysis) and activation of CREB transcription activity (luciferase reporter assay). Inhibition of calcium signals and inhibition of protein kinase C prevented the TUDCA-induced activation of CREB. CCI-779 decreased the viability of rat cholangiocytes in a dose-dependent manner (MTT [3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay). TUDCA protected against CCI-779 cytotoxicity. A dominant negative form of CREB was stably transduced in NRC cells (NRC-M1). TUDCA protection was decreased in NRC-M1. While CCI-779 induced apoptosis in NRC cells as determined by caspase 3 activity, TUDCA attenuated CCI-779–induced apoptosis, an effect absent in NRC-M1. Finally, CCI-779 blocked proliferation of both NRC and NRC-M1 (thymidine incorporation) and this was unaffected by TUDCA. In conclusion, TUDCA activates CREB in cholangiocytes, reducing the apoptotic effect of CCI-779. These findings suggest a novel cytoprotective mechanism for this bile acid. (HEPATOLOGY 2005.)
Abstract 2467: Podoplanin expressing cancer stem cells show increased resistance to DNA damage induced by ionizing radiation
Authors: Ravesanker Ezhilarasan, Patrice N. Love, Lindsey D. Goodman, Kenneth D. Aldape, Erik P. Sulman
Journal: Cancer Research (2011)

Abstract The majority of patients with malignant gliomas, the most common and most lethal brain tumor, develop disease recurrence despite aggressive, multi-modality therapies. This treatment resistance has been attributed to a small population of tumor-initiating glioma cancer stem cells (GSCs). We recently described a new marker of GSCs, the transmembrane glycoprotein podoplanin (pdpn), based on analysis of gene expression profiling data and have found it to be more accurately identify the stem cell population than other described markers. Pdpn expression correlates with poor patient survival and decreased response to radiotherapy. Pdpn expressing cells form neurospheres at high rates in vitro, are more resistant to ionizing radiation, and initiate tumors in vivo. Silencing of pdpn leads to increased radiosensitivity. To identify the mechanism of radiation resistance in pdpn-expressing GSCs, we screened for putative binding partners and identified target of myb-like-1 (tom1l1), a known regulator of Src-pathway activation. We hypothesized that modulation of pdpn and/or tom1l1 expression would lead to alternations in the response of GSCs to radiation via src signaling. Mechanisms of radiation resistance in GSCs are poorly understood to date and the role of src family kinases in modulating radiosensitivity has not previously been reported in gliomas. Pdpn binding of tom1l1 was confirmed by co-immunoprecipation and src activation monitored by immunoblot. Pdpn and tom1l1 expression was downregulated by RNA interference and dsDNA damage and repair assayed by neutral comet assay and by scoring of γH2AX foci. Silencing of pdpn in primary culture, neurophere forming GSC-like cells resulted in increased DNA damage following 2 and 6 Gy ionizing radiation. We similarly examined effects of decreased tom1l1 to determine if the effects on DNA repair mediating by pdpn were acting via the src pathway. In summary, our data suggest that pdpn expression correlates with increased dsDNA repair following ionizing radiation and presents a possible mechanism by which GSCs resist treatment and regrow the tumor. 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 2467. doi:10.1158/1538-7445.AM2011-2467
Autoantibodies associated with RNA are more enriched than anti-dsDNA antibodies in circulating immune complexes in SLE
Authors: E. Ahlin, L. Mathsson, M.-L. Eloranta, T. Jonsdottir, I. Gunnarsson, L. Ronnblom, J. Ronnelid
Journal: Annals of the Rheumatic Diseases (2011)

<h3>Background and objective</h3> We have earlier shown that polyethylene glycol (PEG)-precipitated circulating immune complexes (CIC) from systemic lupus erythematosus (SLE) patients induce cytokines in vitro, and that levels of both CIC and CIC-induced cytokines are dependent on (1) SLE disease activity and (2) the occurrence of anti-SSA but not anti-dsDNA autoantibodies. These findings implicated anti-SSA in immune complex formation, but the formal proof that anti-SSA participates in the formation of SLE CIC to a greater degree than did other antinuclear antibody-associated autoantibodies was lacking. The aim of this study was to investigate to what extent different autoantibodies accumulate in SLE immune complexes, and whether such accumulation is dependent on SLE disease activity. <h3>Methods</h3> Circulating immune complexes were isolated from SLE sera by both PEG precipitation (n=19) and C1q binding (n=8). Autoantibody specificities were determined with a semiquantitative lineblot assay quantified by densitometry. To compare the relative levels of autoantibodies they were normalised against total IgG measured by ELISA in sera and CIC in parallel. Samples were investigated both in a cross-sectional design (n=19), as well as in a paired design with samples obtained during active and inactive SLE (n=10). <h3>Results</h3> All autoantibodies were enriched in CIC compared to in serum. The group of antibodies against RNA-associated antigens showed higher median enrichment than anti-dsDNA (anti-RNP/Sm p=0.0228, anti-Sm p=0.0392, anti-SSA/Ro60 p=0.0539, anti-SSA/Ro52 p=0.0122, anti-SSB/La p=0.0342). Similarly, the other DNA-associated antigens (antihistones and antinucleosomes) were also less enriched as compared with the RNA-associated specificities. These findings were corroborated by analysis of autoantibody content in C1q-bound CIC. There was no difference in degree of accumulation of the investigated autoantibodies in CIC during active and inactive SLE. <h3>Conclusion</h3> Our findings demonstrate a difference in enrichment between autoantibodies against RNA- and DNA-associated autoantigens in isolated SLE CIC, suggesting that the RNA-associated autoantibodies are more prone to form complexes in the circulation in SLE, in contrast to antibodies against DNA-associated autoantigens including dsDNA. These finding have implications on by what mechanisms different autoantibodies accumulate in target organs in SLE.