tbuckley/cabot-search huggingface dataset:
Does occult HBV infection have an impact on the evolution of chronic hepatitis C?
Authors: Fabien Zoulim
Journal: Journal of Hepatology (2013)

Viral co-infections with HBV or HIV are well known to aggravate the evolution of chronic hepatitis C (CHC). With respect to HBV, although the impact of overt infection has been well characterized, the role of occult HBV infection (OBI) on the outcome of CHC remains elusive [1,2]. OBI are mainly defined by the persistence of HBV genome in the liver of individuals testing negative for HBsAg [1]. The mechanisms by which the persistence of the viral genome is not associated with a full expression of viral antigens and viral replication are still partially known [3]. The pathobiological and clinical consequences of HBV genome persistence as an OBI, whether as a mono-infection or as a co-infection with HCV, include an increased severity of liver disease and an increased risk of HCC [4]. However, most of the published studies were cross-sectional and were therefore subjected to potential bias in patient selection. OBI is highly prevalent in patients with CHC, at least in areas of high HBV prevalence. Whether OBI might negatively influence CHC clinical outcome, favoring its progression toward cirrhosis, has been largely debated for many years. Controversies remains on the possible prooncogenic role exerted by OBI, particularly in CHC patients [5]. A recent meta-analysis suggested that OBI increases the risk of hepatocellular carcinoma (HCC) development in both HCV and non-HCV infected patients [6], but other studies performed in North America did not find such an association [7]. One main reason for the discussion of the possible contribution of OBI to a more severe evolution of CHC is the lack of longitudinal studies evaluating the clinical outcome of HCV patients according to the status of OBI during a sufficient period of observation to allow clinical events to occur. In this paper, Squadrito et al. [8] have performed a long awaited observational cohort study evaluating the clinical evolution of CHC patients according to their OBI status. From 1991 to 2000, 326 HBsAg negative CHC patients were tested for OBI by the analysis of HBV genome by PCR in liver biopsy samples. A total of 128/326 cases (39.2%) tested OBI positive and 198/326 (60.8%) OBI negative. Ninety-four of 326 patients (37 OBI positive, 57 OBI negative) were followed-up for a median time of
Kelch-Like Protein 2 Mediates Angiotensin II–With No Lysine 3 Signaling in the Regulation of Vascular Tonus
Authors: Moko Zeniya, Nobuhisa Morimoto, Daiei Takahashi, Yutaro Mori, Takayasu Mori, Fumiaki Ando, Yuya Araki, Yuki Yoshizaki, Yuichi Inoue, Kiyoshi Isobe, Naohiro Nomura, Katsuyuki Oi, Hidenori Nishida, Sei Sasaki, Eisei Sohara, Tatemitsu Rai, Shinichi Uchida
Journal: Journal of the American Society of Nephrology (2015)

Recently, the kelch-like protein 3 (KLHL3)-Cullin3 complex was identified as an E3 ubiquitin ligase for with no lysine (WNK) kinases, and the impaired ubiquitination of WNK4 causes pseudohypoaldosteronism type II (PHAII), a hereditary hypertensive disease. However, the involvement of WNK kinase regulation by ubiquitination in situations other than PHAII has not been identified. Previously, we identified the WNK3-STE20/SPS1-related proline/alanine-rich kinase-Na/K/Cl cotransporter isoform 1 phosphorylation cascade in vascular smooth muscle cells and found that it constitutes an important mechanism of vascular constriction by angiotensin II (AngII). In this study, we investigated the involvement of KLHL proteins in AngII-induced WNK3 activation of vascular smooth muscle cells. In the mouse aorta and mouse vascular smooth muscle (MOVAS) cells, KLHL3 was not expressed, but KLHL2, the closest homolog of KLHL3, was expressed. Salt depletion and acute infusion of AngII decreased KLHL2 and increased WNK3 levels in the mouse aorta. Notably, the AngII-induced changes in KLHL2 and WNK3 expression occurred within minutes in MOVAS cells. Results of KLHL2 overexpression and knockdown experiments in MOVAS cells confirmed that KLHL2 is the major regulator of WNK3 protein abundance. The AngII-induced decrease in KLHL2 was not caused by decreased transcription but increased autophagy-mediated degradation. Furthermore, knockdown of sequestosome 1/p62 prevented the decrease in KLHL2, suggesting that the mechanism of KLHL2 autophagy could be selective autophagy mediated by sequestosome 1/p62. Thus, we identified a novel component of signal transduction in AngII-induced vascular contraction that could be a promising drug target.
Pharmacological Evidence for the Persistent Activation of ATP-Sensitive K <sup>+</sup> Channels in Early Phase of Reperfusion and Its Protective Role Against Myocardial Stunning
Authors: Sakuji Shigematsu, Toshiaki Sato, Takako Abe, Tetsunori Saikawa, Toshiie Sakata, Makoto Arita
Journal: Circulation (1995)

The activation of cardiac ATP-sensitive potassium channels is reported to protect myocardium during ischemia. However, the behavior and role of this channel during reperfusion remain uncertain.Guinea pig right ventricular walls were studied by use of microelectrodes and a force transducer. Each preparation was perfused via the coronary artery at a constant flow rate and was stimulated at 3 Hz. In the first protocol, the preparation was subjected to 10 minutes of no-flow ischemia, which was followed by 60 minutes of reperfusion. Introduction of ischemia shortened the action potential duration (APD) to 58.7 +/- 3.1% of the preischemic values, in association with a decrease in the resting membrane potential (by 12 +/- 0.8 mV) and action potential amplitude (by 34.6 +/- 1.8 mV). On reperfusion, although the APD was restored, it remained shortened for up to approximately 30 minutes of reperfusion. In the presence of glibenclamide (10 mumol/L), the shortening of the APD during ischemia was significantly attenuated and the restoration of APD after reperfusion was significantly facilitated. When glibenclamide was applied from the onset of reperfusion, the persistent APD shortening was significantly suppressed. The developed tension decreased during ischemia and recovered after 60 minutes of reperfusion (up to 92.0 +/- 6.4% of preischemic values) in the untreated preparations. The application of glibenclamide that was started before ischemia or from the onset of reperfusion significantly suppressed the recovery of contractility (P < .05 versus untreated preparations). In the second series of experiments, 20 minutes of no-flow ischemia and 60 minutes of reperfusion were applied. This protocol produced a sustained contractile dysfunction after reperfusion (to 34.0 +/- 3.2% of preischemic values). In the presence of cromakalim (2 mumol/L), the APD shortening was enhanced during both ischemia and the early reperfusion period. Cromakalim significantly improved the contractile recovery (to 79.3 +/- 4.1% of preischemic values, P < .05 versus untreated preparations). The application of cromakalim that was started from the onset of reperfusion also improved the contractile recovery during this phase and this effect was associated with enhanced APD shortening. However, the cromakalim-treated preparations demonstrated a higher incidence of ventricular fibrillation during reperfusion.Cardiac ATP-sensitive potassium channels are activated by ischemia, and a fraction of these channels remains activated during the early reperfusion phase. The resulting shortening of the APD prevents the heart from developing myocardial stunning.
Cord Blood Transplants
Authors: Joan Stephenson
Journal: JAMA (2009)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
What is a sports injury?
Authors: T Timpka, J Jacobsson, J Ekberg, L Nordenfeldt
Journal: British Journal of Sports Medicine (2011)

Background While athletes and coaches, government policy-makers, and sports managers need evidence for decision-making, unambiguous terms and definitions for reporting and analyzing sports injuries across settings are lacking. Objective To define unambiguous concepts for reporting sports injuries across settings. Design Meta-analysis of sports injury-related concepts followed by development of an integrated conceptual framework and appraisal of current sports injury definition practices. Setting Definitions used in the scientific literature on sports injury, injury concepts related to the ICD and ICF, and action-theoretical notions used describe disability. Main outcome measures Definition of reportable episodes employed in consensus statements about injury reporting in specific sports and in epidemiological studies of athletics injuries published in PubMed before October 2009. Results A three-context framework for cross-referencing of sports injury-related concepts was developed using the WHO notion of impairment as foundation, that is, loss or abnormality of psychological, physiological, or anatomical structure or function. In each context, the concepts are differentiated with regard to the duration of the process leading to the loss or abnormality, reflecting the possibilities for prevention and clinical interventions. This three-context framework covered all definitions of sports injury in the evaluated studies (18/18). In comparison, no single study used a definition of sports injury that covered all contexts included in the three-context framework. The sports institution context (‘time loss from sports’) dominated the definitions of reportable events (13/18 studies). Data from the athlete self-evaluation context was only included in three of the 18 studies. None of the studies used clinical screening as the primary context for defining injury. Conclusion Present practices for definition of sports injury have important limitations. A three-context framework representing the major stakeholder perspectives (the athlete, clinical medicine, and sports institutions) have been defined and situated with regard to international definitions of injury, disease, and function.
Malabsorption induced by para-aminosalicylate.
Authors: D. J. Coltart
Journal: BMJ (1969)

MemorandaMEDICsJO 825 creatinine clearance 2-1 ml./min.).The plasma electrolytes were: sodium 120, potassium 5-6, chloride 70, and bicarbonate 8 mEq/1.Her urine contained protein (0'5 g./l.) with a normal sediment, and was sterile on culture.A skeletal survey showed renal osteodystrophy with changes of hyperparathyroidism and rickets.She was treated with intravenous saline and sodium bicarbonate with rapid improvement, and her blood urea fell to a minimum of 150 mg./100 ml.Subsequently she needed a high fluid intake, a diet restricted in protein, and an oral supplement of sodium bicarbonate.The first radiological investigation of her urinary tract was a micturating cystogram.This showed a large (700 ml.) bladder which emptied normally.There was no ureteric reflex.Urography was then carried out with 60 ml. of sodium iothalamate (Conray 420) and immediate tomography.This showed normal-size kidneys with smooth outlines.The pelvicaliceal systems were faintly opacified but appeared normal.The most striking finding was the presence of numerous translucent cysts in the cortico- medullary region (Figs. 1 and2).The appearances were thought to be characteristic of medullary cystic disease.COMMENT Clinically this patient showed features typical of medullary cystic disease.The age of presentation, failure to conserve sodium and water, lack of hypertension, and the presence of severe renal failure with renal osteodystrophy are all charac- teristic, but not diagnostic.Among several conditions which may present in this way is familial juvenile nephronophthisis (Royer et al., 1963), which is felt by some (Strauss and Sommers, 1967) to be pathologically indistinguishable, though a positive family history is found less often in medullary cystic disease (Strauss and Sommers, 1967).The condition is distinct from medullary sponge kidney (Strauss and Welt, 1963;Heptinstall, 1966), though several authors have confused the two conditions (Mulvaney and Collins, 1956; Lowen and
Spleen (No. 78)
Authors: Paula Tatarunis
Journal: JAMA (1998)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Diabetic Gustatory Sweating
Authors: DAVID D. STUART
Journal: Annals of Internal Medicine (1978)

Brief Reports1 August 1978Diabetic Gustatory SweatingDAVID D. STUART, M.D.DAVID D. STUART, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-89-2-223 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe term "gustatory sweating" refers to sweating induced by the ingestion of food. Facial sweating is a physiologic response to eating highly spiced food (1). In some persons facial sweating occurs as an idiosyncratic response to specific types of food; cheese is frequently a stimulant to sweating in susceptible persons (2). In contrast to physiologic gustatory sweating, which is diffuse and symmetrical (1), circumscribed gustatory sweating may develop after abscess, trauma, or surgery of the parotid gland, in which case it is known as Frey's syndrome (3). In 1973 Watkins (4) described the cases of six patients in whom diffuse...References1. LEE T: Physiological gustatory sweating in a warm climate. J Physiol (Lond) 124:528-542, 1954 CrossrefGoogle Scholar2. VAISRUB S: By the sweat of thy brow (editorial). JAMA 232:1360, 1975 CrossrefMedlineGoogle Scholar3. BEDNAREKREIDMATSUMOTO JWT: Frey's syndrome. Am J Surg 131:592-594, 1976 CrossrefMedlineGoogle Scholar4. WATKINS P: Facial sweating after food: new sign of diabetic autonomic neuropathy. Br Med J 1:583-587, 1973 CrossrefMedlineGoogle Scholar5. FRIEDMANPOMARICO WJ: The intratympanic correction of Frey's syndrome. Arch Surg 108:366-368, 1974 CrossrefMedlineGoogle Scholar6. FREEDBERGSHAWMCMANUS ARM: The auriculotemporal syndrome. A clinical and pharmacologic study. J Clin Invest 27:669-676, 1948 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Hennepin County Medical Center Minneapolis, Minnesota PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byGustatory sweating in people with type 1 and type 2 diabetes mellitus: Prevalence and risk factorsFrey's SyndromeDevelopment of a small wireless device for perspiration monitoringHyperhidrosisDiabetic Autonomic NeuropathyGustatory facial sweating subsequent to upper thoracic sympathectomyBilateral gustatory sweating as a sign of diabetic neuropathyFREY'S SYNDROME FOLLOWING PAROTID SURGERYAntisympathetic ganglia antibodies in a patient with gustatory sweatingBiology of sweat glands and their disorders. II. Disorders of sweat gland functionFrey's SyndromeEpisodic hyperhidrosis on the dorsum of handsClonidine hydrochloride: Review of pharmacologic and clinical aspectsClonidine Effect on Diabetic Gustatory SweatingH. U. JANKA, M.D., E. STANDL, M.D., H. MEHNERT, M.D.Treatment of Frey’s Syndrome 1 August 1978Volume 89, Issue 2Page: 223-224KeywordsAbscessesCheesesEatingFoodIngestionParotid glandsTrauma surgery Issue Published: 1 August 1978 PDF downloadLoading ...
Abstract 12069: Deceleration Capacity is a Powerful Predictor of Overall Mortality in Patients with Non-Ischemic Dilated Cardiomyopathy
Authors: Thomas Demming, Daniel Rzepka, Mark Ludde, Wanda Mauser, Norbert Frey, Hendrik Bonnemeier
Journal: Circulation (2011)

Introduction: Deceleration Capacity (DC), a surrogate parameter of tonic vagal modulation of the heart rate, is a prognostic parameter in patients surviving acute myocardial infarction as shown in ...
Hairy Cell Leukemia With Chylous Ascites
Authors: Gregg E. Davies
Journal: JAMA (1977)

HAIRY cell leukemia, or leukemic reticuloendotheliosis, is a rare chronic leukemia in which the bone marrow, liver, spleen, and abdominal lymph nodes are infiltrated by unique mononuclear cells with long cytoplasmic projections. Although retroperitoneal lymphadenopathy in the absence of noticeable peripheral lymphadenopathy is common in this disorder, to our knowledge, chylous ascites has not been previously reported. We describe a patient with hairy cell leukemia in whom chylous ascites were successfully treated with radiation therapy after several chemotherapy regimens failed. <h3>Report of a Case</h3> A 41-year-old man was referred because of ascites. Sixteen months earlier he was examined elsewhere for weight loss, night sweats, and splenomegaly. Hairy cell leukemia was diagnosed from blood smears and a bone marrow aspirate, and after a splenectomy, the patient became symptom-free. Three months prior to referral abdominal swelling developed. The patient then required paracentesis of several liters of milky, sometimes slightly pink fluid every
Cough threshold after upper abdominal surgery.
Authors: J P Dilworth, J C Pounsford, R J White
Journal: Thorax (1990)

The effect of upper abdominal surgery under general anaesthesia on the cough threshold was studied in 26 patients, on the basis of the concentrations of capsaicin and citric acid causing cough. Cough threshold was determined after administering doubling doses of nebulised aerosols of capsaicin and citric acid before operation and on the first and fourth postoperative days. There was an increase in cough threshold (decrease in cough sensitivity) in response to both inhaled irritants on the first postoperative day from the preoperative day and a return towards preoperative values by the fourth day after surgery. The increase in cough threshold on the first postoperative day correlated with the time since opiate administration (r = 0.7 for capsaicin, 0.52 for citric acid). These results show that the threshold concentration of chemical irritants causing cough is increased on the first postoperative day after upper abdominal surgery.
High percentage of CD34-positive cells in autologous AML peripheral blood stem cell products reflects inadequate in vivo purging and low chemotherapeutic toxicity in a subgroup of patients with poor clinical outcome
Authors: N Feller, G J Schuurhuis, M A van der Pol, G Westra, G W D Weijers, A van Stijn, P C Huijgens, G J Ossenkoppele
Journal: Leukemia (2003)
Essential Role of P-Selectin in the Initiation of the Inflammatory Response Induced by Hemorrhage and Reinfusion
Authors: Rosario Scalia, Valerie E. Armstead, Alexander G. Minchenko, Allan M. Lefer
Journal: The Journal of Experimental Medicine (1999)

Resuscitation from hemorrhage induces profound pathophysiologic alterations and activates inflammatory cascades able to initiate neutrophil accumulation in a variety of tissues. This process is accompanied by acute organ damage (e.g., lungs and liver). We have previously demonstrated that significant leukocyte–endothelium interactions occur very early in other forms of ischemia/reperfusion (i.e., splanchnic ischemia/reperfusion and traumatic shock) which are largely mediated by increased expression of the adhesion molecule, P-selectin, on the vascular endothelium. Here we postulated that increased endothelial expression of P-selectin in the microvasculature would play an essential role in initiating the inflammatory signaling of hemorrhagic shock. Using intravital microscopy, we found that hemorrhagic shock significantly increased the number of rolling and adherent leukocytes in the mouse splanchnic microcirculation. In contrast, mice genetically deficient in P-selectin, or wild-type mice given either an anti–P-selectin monoclonal antibody or a recombinant soluble P-selectin glycoprotein ligand (PSGL)-1 immunoglobulin, exhibited markedly attenuated leukocyte–endothelium interaction after hemorrhagic shock. Thus, activation of P-selectin protein on the microvascular endothelium is essential for the initial upregulation of the inflammatory response occurring in hemorrhagic shock. Moreover, endogenous levels of PSGL-1 mRNA were significantly increased in the lung, liver, and small intestine of wild-type mice subjected to hemorrhagic shock. Since PSGL-1 promotes adhesive interactions largely through P-selectin expressed on the vascular endothelium, this result further supports the crucial role played by P-selectin in the recruitment of leukocytes during hemorrhagic shock.