tbuckley/cabot-search huggingface dataset:
A psychiatric study of patients with diseases of the small intestine
Authors: D. Goldberg
Journal: Gut (1970)

<h3>Abstract</h3> Conventional microbial cell cultivation techniques are typically labor intensive, low throughput, and poor parallelization, rendering them inefficient. The development of automated, modular microbial cell micro–cultivation systems, particularly those employing droplet microfluidics, has gained attention for their high–throughput, parallel and highly efficient cultivation capabilities. Here, we report the development of a microbial microdroplet culture system (MMC), which is an integrated platform for automated, high–throughput cultivation and adaptive evolution of microorganisms. We demonstrated that the MMC yielded both accurate and reproducible results for the manipulation and detection of droplets. The superior performance of MMC for microbial cell cultivation was validated by comparing the growth curves of six microbial strains grown in MMC, conventional shake flasks or well plates. The highest incipient growth rate for all six microbial cell lines was achieved using MMC. We also conducted an 18–day process of adaptive evolution of a methanol–essential <i>Escherichia coli</i> strain in MMC and obtained two strains exhibiting higher growth rates compared with the parent strain. Our study demonstrates the power of MMC to provide an efficient and reliable approach for automated, high–throughput microbial cultivation and adaptive evolution.
Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities
Authors: W. T. McNicholas, M. R. Bonsignore
Journal: European Respiratory Journal (2006)

Considerable evidence is available in support of an independent association between obstructive sleep apnoea syndrome (OSAS) and cardiovascular disease, which is particularly strong for systemic arterial hypertension and growing for ischaemic heart disease, stroke, heart failure, atrial fibrillation and cardiac sudden death. The pathogenesis of cardiovascular disease in OSAS is not completely understood but likely to be multifactorial, involving a diverse range of mechanisms including sympathetic nervous system overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormal coagulation and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism. The present report, which arose out of a European Union Cooperation in the field of Scientific and Technical Research (COST) action on OSAS (COST B26), reviews the current evidence for an independent association and proposes research priorities to identify the underlying mechanisms involved, with a view to identifying novel therapeutic strategies. Large-scale collaborative studies of carefully defined patient populations with obstructive sleep apnoea syndrome, adequately controlled for potential confounders, are needed. Such studies carry the prospect of evaluating potential interactions between different basic mechanisms operating in obstructive sleep apnoea syndrome and cardiovascular disease, and interactions with other related disorders, such as obesity, diabetes and dyslipidaemia. Furthermore, translational studies involving cell culture and animal models linked to studies of obstructive sleep apnoea syndrome patients are necessary to integrate basic mechanisms with the clinical disorder.
Repression of Cap-Dependent Translation Attenuates the Transformed Phenotype in Non–Small Cell Lung Cancer Both <i>In vitro</i> and <i>In vivo</i>
Authors: Blake A. Jacobson, Michael D. Alter, Marian G. Kratzke, Sandra P. Frizelle, Ying Zhang, Mark S. Peterson, Svetlana Avdulov, Riikka P. Mohorn, Bryan A. Whitson, Peter B. Bitterman, Vitaly A. Polunovsky, Robert A. Kratzke
Journal: Cancer Research (2006)

Aberrant hyperactivation of the cap-dependent protein synthesis apparatus has been documented in a wide range of solid tumors, including epithelial carcinomas, but causal linkage has only been established in breast carcinoma. In this report, we sought to determine if targeted disruption of deregulated cap-dependent translation abrogates tumorigenicity and enhances cell death in non-small cell lung cancer (NSCLC). NSCLC cell lines were stably transfected with either wild-type 4E-BP1 (HA-4E-BP1) or the dominant-active mutant 4E-BP1(A37/A46) (HA-TTAA). Transfected NSCLC cells with enhanced translational repression showed pronounced cell death following treatment with gemcitabine. In addition, transfected HA-TTAA and HA-4E-BP1wt proteins suppressed growth in a cloning efficiency assay. NSCLC cells transduced with HA-TTAA also show decreased tumorigenicity in xenograft models. Xenograft tumors expressing HA-TTAA were significantly smaller than control tumors. This work shows that hyperactivation of the translational machinery is necessary for maintenance of the malignant phenotype in NSCLC, identifies the molecular strategy used to activate translation, and supports the development of lung cancer therapies that directly target the cap-dependent translation initiation complex.
Factors affecting hydrogen production and consumption by human fecal flora. The critical roles of hydrogen tension and methanogenesis.
Authors: A Strocchi, M D Levitt
Journal: Journal of Clinical Investigation (1992)

We studied the influence of hydrogen tension (PH2) and methanogenesis on H2 production and consumption by human fecal bacteria. Hydrogen consumption varied directly with PH2, and methanogenic feces consumed H2 far more rapidly than did nonmethanogenic feces. At low PH2, H2 production greatly exceeded consumption and there was negligible accumulation of the products of H2 catabolism, methane and sulfide. Thus, incubation at low PH2 allowed the first reported measurements of absolute as opposed to net H2 production. Feces incubated at high and intermediate PH2 had a net H2 production of only 1/900 and 1/64 of absolute production. Glucose fermentation by fecal bacteria yielded an absolute H2 production of 80 ml/g, a value far in excess of that excreted by volunteers ingesting lactulose. We conclude that most H2 produced by colonic bacteria is consumed and methanogenesis and fecal stirring (via its influence on fecal PH2) are critical determinants of H2 consumption and, hence, net H2 production. Study of fecal samples from four subjects with low breath H2 excretion after lactulose showed that absolute H2 production was normal, and the low H2 excretion apparently reflected increased consumption due to rapid methanogenesis (two subjects) and decreased luminal stirring (two subjects).
Dissolving foreign bodies in the trachea and bronchus.
Authors: A J Mearns, R M England, A J Mearns, R M England
Journal: Thorax (1975)

Two young children inhaled sweets which dissolved in the tracheobronchial secretions and caused severe respiratory obstruction. The viscid fluid produced as the sweet dissolved was not expectorated and bronchoscopy was necessary. The oedema of the mucosa caused by the presence of a hyperosmolar sugar solution took up to 48 hours to resolve; antibiotics and steroid cover were considered necessary. The similarity of presentation with acute tracheobronchitis and the lack of reports in the literature suggest that such cases may be misdiagnosed.
Ventilatory post-stimulus potentiation in patients with brain damage.
Authors: D Georgopoulos, I Mitrouska, K Koletsos, K Markopoulou, D Riggos, D Patakas, N R Anthonisen
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

In normal humans when a brief hypoxic ventilatory stimulus is terminated abruptly by breathing 100% O2, ventilation during hyperoxia gradually declines to baseline prehypoxic levels without an undershoot. This has been interpreted as evidence of decay of short-term potentiation (STP), a mechanism located in the brainstem and not dependent upon higher center inputs. STP decay may be important in preventing periodic breathing by damping ventilatory responses to cyclic stimuli. Patients with brain damage commonly have periodic breathing that may be caused partly by impairment of STP activation. To test this 12 tracheostomized patients with severe brain damage (Glasgow score 9.9 +/- 0.6) were studied. Breathing stability was estimated by at least 6 h of capnography and from these records apnea index (AI, episodes/hour) and cyclic changes of end-tidal CO2 (c-PETCO2, cycles/hour) were derived. STP activation was examined by brief exposure to hypoxia (45 s, end-tidal O2 = 50 mm Hg) followed by hyperoxia. Forty-four hypoxic-hyperoxic runs were analyzed and compared with 19 normoxic-hyperoxic trials. At the end of the hypoxia ventilation (VI) increased 39.5 +/- 5.8% and PETCO2 decreased 2.7 +/- 0.6 mm Hg to 91.5 +/- 2.2% of baseline value. When hypoxia was terminated abruptly by hyperoxia VI dropped immediately to 63.2 +/- 7.2% of baseline, remaining for 35 s significantly lower than the corresponding values acquired during hyperoxia after normoxia. After hypoxia, apneas occurred in 19 of 44 hyperoxic runs. There was a negative relationship between nadir hyperoxic ventilation after hypoxia and both AI and c-PETCO2.(ABSTRACT TRUNCATED AT 250 WORDS)
Pitfalls of Measuring Total Blood Calcium in Patients with CKD
Authors: Ce[Combining Acute Accent]dric Gauci, Olivier Moranne, Bruno Fouqueray, Renaud de la Faille, Ge[Combining Acute Accent]rard Maruani, Jean-Philippe Haymann, Christian Jacquot, Jean-Jacques Boffa, Martin Flamant, Je[Combining Acute Accent]ro[Combining Circumflex Accent]me Rossert, Pablo Urena, Be[Combining Acute Accent]ne[Combining Acute Accent]dicte Stengel, Jean-Claude Souberbielle, Marc Froissart, Pascal Houillier
Journal: Journal of the American Society of Nephrology (2008)

Disorders of mineral and bone metabolism are prevalent in patients with chronic kidney disease (CKD). The recent National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend that blood calcium (Ca) be regularly measured in patients with stages 3 to 5 CKD. The Kidney Disease: Improving Global Outcomes (KDIGO) position states that the measurement of ionized Ca (iCa) is preferred and that if total Ca (tCa) concentration is used instead, then it should be adjusted in the setting of hypoalbuminemia. In 691 consecutive patients with stages 3 to 5 CKD, we compared the ability of noncorrected and albumin-corrected tCa concentration to identify low, normal, or high iCa concentration. The agreement between noncorrected or albumin-corrected tCa and iCa was only fair. The risk for underestimating ionized calcium was independently increased by a low total CO<sub>2</sub> concentration when either noncorrected or albumin-corrected Ca was used and by a low albumin concentration only when noncorrected tCa was used. The risk for overestimating iCa was increased by a low albumin concentration only when albumin-corrected Ca was used. In conclusion, albumin-corrected tCa does not predict iCa better than noncorrected tCa. Moreover, both noncorrected and albumin-corrected tCa concentrations poorly predict hypo- or hypercalcemia in patients with CKD.
Re-examining examination: misconceptions in clinical medicine
Authors: Joshua M Brostoff
Journal: Journal of the Royal Society of Medicine (2009)

The United Kingdom has a proud tradition of clinical teaching at undergraduate level. Furthermore, entry into higher training in most specialties is preceded by obligatory written and clinical examinations. This is at odds with, for example, the United States of America, where there is less emphasis on clinical examination, with most American Board exams purely a written test.

Nonetheless as with any branch of knowledge, some of what is taught is handed down as an almost unbroken lineage from teacher to pupil without critical appraisal of its value. Bad habits are often picked up in medical school or early in clinical training, and are then never eradicated. Clinical examination is still a cornerstone of our diagnostic armamentarium and improvement of our skills should be a lifelong pursuit.

This brief essay will concentrate on three traditional teachings that deserve re-examination.
A randomised, double blind, multicentre trial of octreotide in moderate to severe acute pancreatitis
Authors: W Uhl, M W Buchler, P Malfertheiner, H G Beger, G Adler, W Gaus, None the German Pancreatitis Study Group
Journal: Gut (1999)

The pharmacological inhibition of exocrine pancreatic secretion with the somatostatin analogue octreotide has been advocated as a specific treatment of acute pancreatitis.To investigate the efficacy of octreotide in acute pancreatitis in a randomised, placebo controlled trial.302 patients from 32 hospitals, fulfilling the criteria for moderate to severe acute pancreatitis within 96 hours of the onset of symptoms, were randomly assigned to one of three treatment groups: group P (n=103) received placebo, while groups O1 (n=98) and O2 (n=101) received 100 and 200 microg of octreotide, respectively, by subcutaneous injection three times daily for seven days. The primary outcome variable was a score composed of mortality and 15 typical complications of acute pancreatitis.The three groups were well matched with respect to pretreatment characteristics. An intent to treat analysis of all 302 patients revealed no significant differences among treatment groups with respect to mortality (P: 16%; O1: 15%; O2: 12%), the rate of newly developed complications, the duration of pain, surgical interventions, or the length of the hospital stay. A valid for efficacy analysis (251 patients) also revealed no significant differences.This trial shows no benefit of octreotide in the treatment of acute pancreatitis.
Effect of inhaled prostaglandin D2 in normal and atopic subjects, and of pretreatment with leukotriene D4
Authors: S. E. Sampson, A. P. Sampson, J. F. Costello
Journal: Thorax (1997)

BACKGROUND: Prostaglandin (PG) D2 is a potent bronchoconstrictor mediator and is found, together with leukotriene (LT) D4, in bronchoalveolar lavage fluid during the early response to allergen challenge in asthmatic subjects. The potency of PGD2 has not been established in normal and atopic non-asthmatic subjects, nor has the contribution of cholinergic mechanisms to PGD2 induced bronchoconstriction in normal subjects. Mediators released simultaneously may interact, so the effect of pre-inhalation of LTD4 on PGD2 responsiveness was investigated. METHODS: Six normal and six atopic non-asthmatic subjects performed histamine and PGD2 challenges on separate occasions. Eight normal subjects performed PGD2 challenges immediately before and 45 minutes after inhalation of 200 micrograms oxitropium bromide or placebo. Bronchial responsiveness to PGD2 was established in six normal subjects immediately after pretreatment with saline or non-bronchoconstricting doses of methacholine or LTD4 (challenge 1), and again at six hours (challenge 2). All studies were performed in a double blind, randomised, crossover fashion. RESULTS: PGD2 was 25-fold and 18-fold more potent as a bronchoconstrictor than histamine in atopic non-asthmatic and normal subjects, respectively. Responsiveness (PC35sGaw) to histamine and PGD2 correlated significantly (r = 0.917, n = 12, p &lt; 0.001). Oxitropium bromide in a dose of 200 micrograms inhibited PGD2 induced bronchoconstriction by 37.5%, although in two of these subjects no inhibition was seen. Pre-inhalation of LTD4 and methacholine shifted the dose-response curve of PGD2 to the left by 4.6-fold and 2.4-fold, respectively. CONCLUSIONS: PGD2 is a potent bronchoconstrictor in normal subjects, which is partly mediated by cholinergic mechanisms in some subjects. No significant interaction was found between LTD4 and PGD2 in six normal subjects.
Society of Surgical Oncology–American Society for Radiation Oncology Consensus Guideline on Margins for Breast-Conserving Surgery With Whole-Breast Irradiation in Stages I and II Invasive Breast Cancer
Authors: Meena S. Moran, Stuart J. Schnitt, Armando E. Giuliano, Jay R. Harris, Seema A. Khan, Janet Horton, Suzanne Klimberg, Mariana Chavez-MacGregor, Gary Freedman, Nehmat Houssami, Peggy L. Johnson, Monica Morrow
Journal: Journal of Clinical Oncology (2014)

Controversy exists regarding the optimal margin width in breast-conserving surgery for invasive breast cancer.A multidisciplinary consensus panel used a meta-analysis of margin width and ipsilateral breast tumor recurrence (IBTR) from a systematic review of 33 studies including 28,162 patients as the primary evidence base for consensus.Positive margins (ink on invasive carcinoma or ductal carcinoma in situ) are associated with a two-fold increase in the risk of IBTR compared with negative margins. This increased risk is not mitigated by favorable biology, endocrine therapy, or a radiation boost. More widely clear margins do not significantly decrease the rate of IBTR compared with no ink on tumor. There is no evidence that more widely clear margins reduce IBTR for young patients or for those with unfavorable biology, lobular cancers, or cancers with an extensive intraductal component.The use of no ink on tumor as the standard for an adequate margin in invasive cancer in the era of multidisciplinary therapy is associated with low rates of IBTR and has the potential to decrease re-excision rates, improve cosmetic outcomes, and decrease health care costs. J Clin Oncol 32. 2014 American Society of Clinical Oncology®, American Society for Radiation Oncology®, and Society of Surgical Oncology®. All rights reserved. No part of this document may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without written permission by the American Society of Clinical Oncology, American Society for Radiation Oncology, and Society of Surgical Oncology.
HLA antigens in Italian patients with primary Sjogren's syndrome.
Authors: C Vitali, A Tavoni, G Rizzo, R Neri, A D'Ascanio, R Cristofani, S Bombardieri
Journal: Annals of the Rheumatic Diseases (1986)

Twenty eight Italian patients with primary Sjögren9s syndrome were typed for class I and class II alloantigens of the major histocompatibility complex. Patients with Sjögren9s syndrome had higher prevalence of DR3 (46.4% v 14% in the control population, p corrected less than 0.02), while similar prevalence was found for DR2 and DRw52 alloantigens. DR3 correlated with DRw52 (p less than 0.0001), anti-Ro(SSA) (p less than 0.0002) and anti-La(SSB) (p less than 0.02) antibodies, and extraglandular manifestations (p less than 0.02). In addition, extraglandular involvement was associated with anti-Ro antibodies (p less than 0.05) and raised gammaglobulins (p less than 0.02). In Italian patients with primary Sjögren9s syndrome DR3 is the genetic marker related to this clinical entity and seems to identify a disease subset characterised by autoantibody production and extraglandular manifestations.
RELEASE OF KALLIKREIN FROM GUINEA PIG LUNG DURING ANAPHYLAXIS
Authors: O. Jonasson, E. L. Becker
Journal: The Journal of Experimental Medicine (1966)

An antigen-antibody reaction occurring in the perfused sensitized guinea pig lung, has been demonstrated to release kallikrein, a proteolytic enzyme related to the formation of kinins. This lung kallikrein is similar to plasma kallikrein in all properties studied, including susceptibility to the same inhibitors, electrophoretic mobility, and heterogeneity in molecular size. The release of kallikrein during anaphylaxis in the guinea pig lung occurs in the presence of ethylenediaminetetraacetate. Perfusion of ellagic acid into nonsensitized lungs will also release kallikrein, presumably through activation of Hageman factor. On the basis of these findings the hypothesis is suggested that the kallikrein in perfused lung activated by the antigen-antibody reaction is, in fact, plasma kallikrein. It is further suggested that activation of such kallikrein by the antigen-antibody reaction proceeds through Hageman factor.
Fire smoke inhalation and bronchial hyperresponsiveness
Authors: Cheol-Hong Kim, In-Gyu Hyun
Journal: European Respiratory Journal (2013)

Background: Fire smoke affects direct or indirect injury on airway because it has many harmful dusts to humans. Clinically, it is very similar to bronchial asthma. It is well known that airway reactivity increased in the early phase of smoke inhalation, however, it remains relationship between smoke inhalation and bronchial hyperresponsiveness.  Methods; Smoke inhalation injury was diagnosed by initial arterial carboxyhemoglobin (COHb) more than 5% or by bronchoscopy. The grade of inhalation injury was classified as follows; normal, mild, moderate and severe. Its lung parenchymal involvement was assessed by high resolution computer tomography (HRCT). We performed mannitol challenge test (AridolTM) to identify bronchial hyperresponsiveness and considered positive as FEV1 decreased more than 15% of basal FEV1 or more than 10% than previous FEV1, during the test.  Results: 15 patients (male 5, female 10) were enrolled consecutively. Initial COHb concentrations and PaO2/FiO2 ratio were 14.8±18.49% and 425.7±123.68, respectively. Bronchoscopic grades for inhalation injury as follows: normal, 3; mild, 9; moderate, 3; severe, none. Of 7 who performed HRCT, 4 showed abnormal radiographic opacities. Post-bronchodilator FVC, FEV1, FEV1/FVC, FEF25-75% and Dlco were 76.00±24.27%, 79.80±27.42%, 80.05±10.01%, 76.40±36.70% and 92.44±22.64%, of predicted values, respectively. Aridol test was performed on 4th day (median; 2-20 days) since the onset of fire and showed all negative results.  Conclusions; Fire smoke seems not to cause bronchial hyperresponsiveness in the early phase of smoke inhalation, however, it is required large scaled study to verify its relationship.