tbuckley/cabot-search huggingface dataset:
Chylothorax complicating pneumonectomy.
Authors: A Van Mulders, L M Lacquet, W Van Mieghem, G Deneffe
Journal: Thorax (1984)

Chylothorax is an uncommon clinical entity caused by obs- truction or rupture of the thoracic duct.Malignant disease, mostly lymphoma or metastatic carcinoma, accounts for half and surgical trauma for a quarter of all cases.'Occasionally, chylothorax is caused by thrombosis of the great veins, benign cysts, or lymphangiomas of the thoracic duct, tuberculosis, mediastinitis, paravertebral abscess, filariasis, or amyloidosis.We present an unusual case of postpneumonectomy chylothorax with serious haemodynamic effects necessitat- ing reoperation. Case reportIn February 1984 a 60 year old man was admitted to our hospital because of thoracic pain, weight loss, and progres- sive atelectasis of the left lung.On physical examination the breath sounds were absent over the left lung; there was no lymphadenopathy or hepatomegaly.The serum levels
Effects of the antibiotic ionophore X-537A on contractility and ionic exchange in rabbit ventricular myocardium.
Authors: I R Wendt, G A Langer
Journal: Circulation Research (1977)

The effects of the ionophore X-537A on mechanical function and on ionic exchange were studied in the isolated, arterially perfused rabbit interventricular septum. X-537A produced an initial positive inotropic response which was, however, transient in this preparation and appeared to be dependent on an effect of the ionophore on catecholamines. The positive inotropy gave way to a progressive decline in force development which was unrelated to the action of catecholamines and was not accompanied by the development of contracture. Isotope uptake experiments revealed that coincident with this decline in force development there was a continuous net loss of tissue K+ and a net gain of Na+. X-537A (5 micronM) perfused for 20 minutes resulted in a net K+ loss of 50.2 +/- 4.6 mmol/kg dry weight and a net Na+ gain of 74.0 +/- 4.5 mmol/kg dry weight. Isotope washout experiments confirmed that the entire net loss of K+ could be accounted for by increased K+ efflux. X-537A did not alter Na+ efflux nor did it have any detectable effect on 45Ca exchange of the perfused septum in which the ability to detect net movements is at a level of approximately +/- 550 micron mol/kg dry weight. On removal of the ionophore the decline in force development ceased and reversed to near control levels and the progressive ionic changes ceased. However, despite the near total recovery of contractile function the Na+ and K+ levels remained at values little different from those reached at the termination of X-537A perfusion. In addition, after removal of the ionophore, we found that K+ exchange rate remained significantly less than control and, furthermore, a kinetic inhomogeneity of tissue K+ was observed. The results emphasize a dissociation between cellular Na+ and K+ content and function following the ionic perturbations induced by the ionophore.
Treating non-ulcer dyspepsia and H pylori
Authors: S. J O V. van Zanten
Journal: BMJ (2000)

Papers p 659

H elicobacter pylori is the main cause of duodenal and gastric ulcers. The organism has also been linked to gastric cancer.1 Most researchers believe that there is a relation, although an imperfect one, between non-ulcer dyspepsia and infection with H pylori . The pathophysiological mechanisms by which the infection may cause dyspepsia are unclear, but may include changes in acid secretion, abnormal motility, or altered visceral perception.2 The prevalence of H pylori is higher in patients with non-ulcer dyspepsia than in healthy controls.3 A pivotal question is whether curing the infection leads to a sustained improvement in symptoms in patients with non-ulcer dyspepsia. The controversy surrounding this issue is addressed by the meta-analysis by Moayyedi et al in this issue of the journal (p 659).4

Dyspepsia is defined as pain or discomfort in the central upper abdomen which originates in the upper gastrointestinal tract.5 To make the diagnosis of non-ulcer (functional) dyspepsia patients need to have had symptoms for at least 12 weeks and the presence of an organic disease, such as a peptic ulcer or oesophagitis, must be ruled out. …
Testosterone, cortisol, dominance, and submission: Biologically prepared motivation, no psychological mechanisms involved
Authors: Jack van Honk, Dennis J. L. G. Schutter, Erno J. Hermans, Peter Putman
Journal: Behavioral and Brain Sciences (2004)

Mazur & Booth's (1998) target article concerns basal and reciprocal relations between testosterone and dominance, and has its roots in Mazur's (1985; 1994) model of primate dominance-submissiveness interactions. Threats are exchanged in these interactions and a psychological stress-manipulation mechanism is suggested to operate, making sure that face-to-face dominance contests are usually resolved without aggression. In this commentary, a recent line of evidence from human research on the relation between testosterone, cortisol, and vigilant (dominant) and avoidant (submissive) responses to threatening "angry" faces is discussed. Findings, to a certain extent, converge with Mazur & Booth's theorizing. However, the strongest relations have been found in subliminal exposure conditions, suggesting that biological instead of psychological mechanisms are involved.
Interleukin 13 blocks the release of collagen from bovine nasal cartilage treated with proinflammatory cytokines
Authors: C S Cleaver
Journal: Annals of the Rheumatic Diseases (2001)

To investigate whether interleukin 13 (IL13) could act in a chondroprotective manner and protect cartilage stimulated to resorb with a combination of IL1alpha and oncostatin M (OSM), in a similar way to the anti-inflammatory cytokine, IL4.IL13 was added to explant cultures of bovine nasal cartilage stimulated to resorb with IL1alpha and OSM, and the release of collagen and proteoglycan determined. Collagenolytic and tissue inhibitors of metalloproteinase (TIMP) activities were determined by bioassay. Northern blot analyses were performed to determine the effects of IL13 on the induction of matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, and TIMP-1 gene expression.IL13 can prevent the release of collagen from bovine nasal cartilage in a dose dependent manner. This was accompanied by a concomitant decrease in measurable collagenolytic activity in the culture supernates and an increase in TIMP activity. Northern blot analysis showed that IL13 down regulated MMP-3 and MMP-13 levels but up regulated MMP-1 and TIMP-1 gene expression in bovine nasal chondrocytes at 24 hours.This study showed for the first time that IL13 can block collagen release from resorbing cartilage in a similar manner to IL4. This is accompanied by a reduction in detectable collagenolytic activity, a decrease in MMP-3 and MMP-13 mRNA levels, and an up regulation of TIMP-1 expression.
Metabolic syndrome: relevant for all types of chronic liver diseases?
Authors: G. Marchesini, G. Bianchi
Journal: Gut (2010)

Hepatologists have some primary tasks to accomplish with their patients: (1) to eradicate or halt viral infections; (2) to stop alcohol abuse; (3) to prevent and, later, treat common life-threatening complications (ascites, variceal bleeding, encephalopathy); (4) to support liver function and keep patients under surveillance for the risk of liver cancer; and (5) to decide on the timing for possible liver transplantation. All these tasks point to reduced liver-related mortality as the ultimate target.

The nutritional status has long attracted attention as a factor generally associated with outcome; the majority of studies indicate a poor nutritional status (protein–calorie malnutrition) as potentially associated with mortality risk.1 This was mainly the case of skid-row patients with alcoholic liver disease (ALD), whereas a large observational Italian study in subjects with cirrhosis indicated that 29% of females and 18% of males were over-nourished.2 The precise aetiology of liver disease was not clearly defined at that time, but in the same years it became clear that obesity and other metabolic alterations were per se potential causes of liver disease, following the seminal observation linking fatty liver to ‘cryptogenic cirrhosis’, via non-alcoholic steatohepatitis. We now know that non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome,3 a …
Allergic contact dermatitis to tefillin
Authors: Bonnie Ross, Ronald R Brancaccio
Journal: Journal of the American Academy of Dermatology (1996)

Zidovudine and psoriasisTo the Editor: The article by Townsend, Cohen, and Duvie describes the use of zidovudine (formerly azidothymidine [AZT]) for the treatment of psoriasis in HlV
Cystic Disease of the Lungs
Authors: E. A. Perrott
Journal: BMJ (1956)

When fully established the disease is grossly dis- abling.Earlier recognition should lead to the more frequLent use of surgery in appropriate cases.ADDENDUM.-Sincewriting this account another patient has had-operative treatment-a successful pneumonectomy.He was one of the three extensive left-sided cases.My thanks ar-c duc to the Cumberland County Council for permission to undertake this work.I am indebtetd to Dr. R.Hambridge, chest physician to West Cumberland, for driawing my attention to these cases, advising me on this paper
Drinking from the fountain of promise: biomarkers in the surveillance of Barrett's oesophagus--the glass is half full!
Authors: S L Preston
Journal: Gut (2006)

Biomarkers for prognostication need large randomised controlled trials such as AspECT and BOSS. These trials will deliver surrogates which fulfil the validation criteria necessary for their introduction into the clinic

Barrett’s oesophagus (BO) is an acquired premaligant condition that is the only known precursor to oesophageal adenocarcinoma (OA); a malignancy whose incidence has risen steadily in the Western world in the last 20–30 years.1 The lifetime risk of developing an adenocarcinoma in the context of BO is 2–5%,2 and despite recent advances in its treatment the associated morbidity and mortality remain high.3 BO advances through a series of morphological stages: from metaplasia through dysplasia of different grades and finally to adenocarcinoma—the metaplasia-dysplasia-adenocarcinoma sequence (MCS).4,5 Although this genetic process is not as well outlined as in the colon,4 it is thought to be a similar multistep process consisting of genetic and epigenetic mutations, involving the same or a similar group of genes, which over many years leads to increasing genomic instability and ultimately to the formation of an autonomous clone of cells with invasive and metastatic properties.5

Knowledge of the natural history of the adenoma:carcinoma sequence in the colon has translated to clinical medicine, prompting the removal of adenomatous polyps at the premalignant stage, with an associated reduction in the incidence of colorectal cancer.6,7 Regrettably, thus far, such gains have not been made in dysplasia in the context of BO, with the effectiveness of current surveillance strategies yet to be conclusively proven; a matter soon to be addressed by the BOSS (Barrett’s Oesophagus Surveillance Study), a study integrated with the AspECT (Aspirin and Esomprazole Chemoprevention Trial of Cancer in Barrett’s Oesophagus) (7500 patients in total).8 At present, a patient with BO can only be risk stratified on the basis of either …
Randomized Study Comparing Combined Pulmonary Vein–Left Atrial Junction Disconnection and Cavotricuspid Isthmus Ablation Versus Pulmonary Vein–Left Atrial Junction Disconnection Alone in Patients Presenting With Typical Atrial Flutter and Atrial Fibrillation
Authors: Oussama Wazni, Nassir F. Marrouche, David O. Martin, A. Marc Gillinov, Walid Saliba, Eduardo Saad, Allan Klein, Mandeep Bhargava, Dianna Bash, Robert Schweikert, Demet Erciyes, Ahmad Abdul-Karim, Johannes Brachman, Jens Gunther, Ennio Pisano, Domenico Potenza, Raffaele Fanelli, Andrea Natale
Journal: Circulation (2003)

Background— Atrial flutter (AFL) and atrial fibrillation (AF) frequently coexist in the same patient. Recently it has been demonstrated that the triggers for both AF and AFL may originate in the pulmonary veins (PVs). We hypothesized that in patients with both AF and typical AFL, pulmonary vein–left atrial junction (PV-LAJ) disconnection may eliminate both arrhythmias. Methods and Results— Consecutive patients with documented symptomatic AF and typical AFL were randomly assigned to have PV-LAJ disconnection combined with cavotricuspid isthmus (CTI) ablation (group 1, n=49) or PV-LAJ disconnection alone (group 2, n=59). Within the first 8 weeks after ablation, 32 of the group 2 patients had typical AFL documented, whereas none was seen in group 1. Twenty of these 32 converted to sinus rhythm after initiating antiarrhythmic drugs (AADs). Twelve were cardioverted, and AADs were started. After 8 weeks, all AADS were stopped, and only 3 patients continued to have recurrent sustained typical AFL that was eliminated by CTI ablation. Beyond 8 weeks of follow-up, 7 patients in group 1 and 6 patients in group 2 (14% and 11%, respectively) continued to have AF. Ten of these 13 patients underwent a repeat PV-LAJ disconnection procedure and were cured. The remaining 3 remained in normal sinus rhythm while taking AADs. Conclusions— In patients with both AFL and AF, PV-LAJ disconnection alone may be sufficient to control both arrhythmias. CTI block reduced early postablation recurrence of arrhythmias, which in the majority of patients reflects a short-term clinical problem.
The measurement of the exchangeable pools of cholesterol in the baboon
Authors: Jean D. Wilson
Journal: Journal of Clinical Investigation (1970)

Five male baboons were fed cholesterol-1alpha-(3)H until an isotopic steady state was approached in which the ratio of serum to dietary cholesterol specific activity was constant. The animals were then given single intravenous injections of cholesterol-4-(14)C, and the disappearance curves of the (14)C from the circulation were followed for 70-85 days. The total exchangeable cholesterol pools under these conditions were determined by carcass analysis at the end of the experiment and were shown to agree closely with the sums of the two exchangeable cholesterol pools as predicted from analysis of the die-away curve in terms of a two exchangeable pool model, assuming that entry into and exit from the system occur predominantly through the more rapidly exchanging of the two pools. These results have been interpreted as support for the validity of a model consisting of two exchangeable pools and one nonexchangeable or very slowly exchangeable pool as an approximation of over-all cholesterol metabolism in this species. In addition, an anatomical and chemical dissection of these pools was performed. While the three pool model is not applicable to every tissue, it has been possible to show that its general applicability in the intact animal stems from the fact that the major portions of the three cholesterol pools of the body lie within a limited number of tissues.
Defining Severe Asthma In Childhood: A Descriptive Multicenter Study In Turkey
Authors: Bulent Enis Sekerel, Ozge Soyer, Fatih Celmeli, Yakup Canitez, Ozlem Keskin, Demet Can, Ferhat Catal, Mehtap Kilic, Burcin Nalbantoglu, Nail Yologlu, Suleyman T. Yavuz, Belgin Guc, Fadil Ozturk, Gulbin Karakoc, Suna Asilsoy, Mehmet Kilic, Cem Razi, Dost Zeyrek, Semanur Kuyucu, Hasan Yuksel, Omer Cevit, Aysen Bingol, Mehtap G. Yazicioglu, Ayse Yenigun
Journal: Journal of Allergy and Clinical Immunology (2014)
Depression and Risk of Incident Asthma in Adults. The CARDIA Study
Authors: Wendy M. Brunner, Pamela J. Schreiner, Akshay Sood, David R. Jacobs
Journal: American Journal of Respiratory and Critical Care Medicine (2014)

Rationale: Asthma is associated with depression, but the temporality of the association has not been established.Objectives: To examine the association between prevalent elevated depressive symptoms and incident asthma, and between prevalent asthma and incident elevated depressive symptoms in a cohort of young and middle-aged adults.Methods: We examined the longitudinal association between asthma and depressive symptoms bidirectionally in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. First, 3,614 participants, free of asthma, were classified by elevated depressive symptoms at the CARDIA Year-5 exam (n = 856 elevated vs. 2,758 not elevated; ages 23–35 yr) and followed for 20 years to incident asthma. Then, 3,016 participants, free of elevated depressive symptoms, were classified by self-reported current asthma status (n = 188 prevalent vs. 2,828 not prevalent) at the CARDIA Year-5 exam and followed for 20 years until onset of elevated depressive symptoms.Measurements and Main Results: The relative hazard of incident asthma among those with elevated depressive symptoms was 1.26 (95% confidence interval [CI] = 1.02–1.56) after adjustment for covariates. When depressive status was modeled as the total number of reports of elevated depressive symptoms before the onset of asthma, the adjusted hazard ratio was 1.15 (95% CI = 1.02–1.29). The hazard of incident elevated depressive symptoms for those with asthma was no different than the hazard in those without asthma (adjusted hazard ratio = 0.92; 95% CI = 0.70–1.20).Conclusions: This longitudinal observational study points to depression as a marker of risk for incident adult-onset asthma. On the other hand, prevalent asthma is not associated with incident adult-onset depression.
Genetic Modification of Mesenchymal Stem Cells Overexpressing CCR1 Increases Cell Viability, Migration, Engraftment, and Capillary Density in the Injured Myocardium
Authors: Jing Huang, Zhiping Zhang, Jian Guo, Aiguo Ni, Arjun Deb, Lunan Zhang, Maria Mirotsou, Richard E. Pratt, Victor J. Dzau
Journal: Circulation Research (2010)

Although mesenchymal stem cell (MSC) transplantation has been shown to promote cardiac repair in acute myocardial injury in vivo, its overall restorative capacity appears to be restricted mainly because of poor cell viability and low engraftment in the ischemic myocardium. Specific chemokines are upregulated in the infarcted myocardium. However the expression levels of the corresponding chemokine receptors (eg, CCR1, CXCR2) in MSCs are very low. We hypothesized that this discordance may account for the poor MSC engraftment and survival.To determine whether overexpression of CCR1 or CXCR2 chemokine receptors in MSCs augments their cell survival, migration and engraftment after injection in the infarcted myocardium.Overexpression of CCR1, but not CXCR2, dramatically increased chemokine-induced murine MSC migration and protected MSC from apoptosis in vitro. Moreover, when MSCs were injected intramyocardially one hour after coronary artery ligation, CCR1-MSCs accumulated in the infarcted myocardium at significantly higher levels than control-MSCs or CXCR2-MSCs 3 days postmyocardial infarction (MI). CCR1-MSC-injected hearts exhibited a significant reduction in infarct size, reduced cardiomyocytes apoptosis and increased capillary density in injured myocardium 3 days after MI. Furthermore, intramyocardial injection of CCR1-MSCs prevented cardiac remodeling and restored cardiac function 4 weeks after MI.Our results demonstrate the in vitro and in vivo salutary effects of genetic modification of stem cells. Specifically, overexpression of chemokine receptor enhances the migration, survival and engraftment of MSCs, and may provide a new therapeutic strategy for the injured myocardium.
Aspirin-triggered 15-Epi-Lipoxin A4 (LXA4) and LXA4 Stable Analogues Are Potent Inhibitors of Acute Inflammation: Evidence for Anti-inflammatory Receptors
Authors: Tomoko Takano, Stefano Fiore, Jane F. Maddox, Hugh R. Brady, Nicos A. Petasis, Charles N. Serhan
Journal: The Journal of Experimental Medicine (1997)

Lipoxins are bioactive eicosanoids that are immunomodulators. In human myeloid cells, lipoxin (LX) A4 actions are mediated by interaction with a G protein–coupled receptor. To explore functions of LXA4 and aspirin-triggered 5(S),6(R),15(R)-trihydroxy-7,9,13-trans-11-cis–eicosatetraenoic acid (15-epi-LXA4) in vivo, we cloned and characterized a mouse LXA4 receptor (LXA4R). When expressed in Chinese hamster ovary cells, the mouse LXA4R showed specific binding to [3H]LXA4 (Kd ≈ 1.5 nM), and with LXA4 activated GTP hydrolysis. Mouse LXA4R mRNA was most abundant in neutrophils. In addition to LXA4 and 15-epi-LXA4, bioactive LX stable analogues competed with both [3H]LXA4 and [3H]leukotriene D4 (LTD4)– specific binding in vitro to neutrophils and endothelial cells, respectively. Topical application of LXA4 analogues and novel aspirin-triggered 15-epi-LXA4 stable analogues to mouse ears markedly inhibited neutrophil infiltration in vivo as assessed by both light microscopy and reduced myeloperoxidase activity in skin biopsies. The 15(R)-16-phenoxy-17,18, 19,20-tetranorLXA4 methyl ester (15-epi-16-phenoxy-LXA4), an analogue of aspirin triggered 15-epi-LXA4, and 15(S)-16-phenoxy-17,18,19,20-tetranor-LXA4 methyl ester (16-phenoxy-LXA4) were each as potent as equimolar applications of the anti-inflammatory, dexamethasone. Thus, we identified murine LXA4R, which is highly expressed on murine neutrophils, and showed that both LXA4 and 15-epi-LXA4 stable analogues inhibit neutrophil infiltration in the mouse ear model of inflammation. These findings provide direct in vivo evidence for an anti-inflammatory action for both aspirin-triggered LXA4 and LXA4 stable analogues and their site of action in vivo.
NAFLD: A multisystem disease
Authors: Christopher D. Byrne, Giovanni Targher
Journal: Journal of Hepatology (2015)

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in Western countries that is predicted to become also the most frequent indication for liver transplantation by 2030. Over the last decade, it has been shown that the clinical burden of NAFLD is not only confined to liver-related morbidity and mortality, but there is now growing evidence that NAFLD is a multisystem disease, affecting extra-hepatic organs and regulatory pathways. For example, NAFLD increases risk of type 2 diabetes mellitus (T2DM), cardiovascular (CVD) and cardiac diseases, and chronic kidney disease (CKD). Although the primary liver pathology in NAFLD affects hepatic structure and function to cause morbidity and mortality from cirrhosis, liver failure and hepatocellular carcinoma, the majority of deaths among NAFLD patients are attributable to CVD. This narrative review focuses on the rapidly expanding body of clinical evidence that supports the concept of NAFLD as a multisystem disease. The review discusses the factors involved in the progression of liver disease in NAFLD and the factors linking NAFLD with other extra-hepatic chronic diseases, such as T2DM, CVD, cardiac diseases and CKD. The review will not discuss NAFLD treatments as these are discussed elsewhere in this issue of the Journal. For this review, PubMed was searched for articles using the keywords "non-alcoholic fatty liver disease" or "fatty liver" combined with "diabetes", "cardiovascular (or cardiac) disease", "cardiovascular mortality" or "chronic kidney disease" between 1990 and 2014. Articles published in languages other than English were excluded.
A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
Authors: Gerhard C. Hildebrandt, Ulrich A. Duffner, Krystyna M. Olkiewicz, Leigh A. Corrion, Nicole E. Willmarth, Debra L. Williams, Shawn G. Clouthier, Cory M. Hogaboam, Pavan R. Reddy, Bethany B. Moore, William A. Kuziel, Chen Liu, Gregory Yanik, Kenneth R. Cooke
Journal: Blood (2003)