tbuckley/cabot-search huggingface dataset:
Nitric oxide suppression reversibly attenuates mitochondrial dysfunction and cholestasis in endotoxemic rat liver†
Authors: Masaya Shiomi, Yoshiyuki Wakabayashi, Tsuyoshi Sano, Yuichi Shinoda, Yuji Nimura, Yuzuru Ishimura, Makoto Suematsu
Journal: Hepatology (1998)

This study aimed to examine whether nitric oxide (NO) plays a causal role in endotoxin-induced dysfunction of biliary transport. Rats were treated with intraperitoneal injection of endotoxin (O111B4, 4 mg/kg). At 2 hours, the liver was excised and perfused ex vivo with taurocholate (TC)-containing Krebs-Ringer solution under monitoring bile output and NO 2 in the perfusate and tissue cyclic guanosine monophosphate (cGMP) levels as indices of NO production. The endotoxin treatment evoked a marked decrease in the bile acid-dependent bile formation concurrent with the increasing NO 2 output, cGMP elevation, and a reduction of hepatic adenosine triphosphate (ATP) contents and oxygen consumption. Perfusion with 1 mmol/L aminoguanidine (AG), an inhibitor of inducible NO synthase, but not with l -nitroarginine methyl ester, an inhibitor of the constitutive form of the enzyme, significantly reversed the endotoxin-induced increment of the bile formation in concert with the recovery of oxygen consumption and ATP levels. Laser confocal microfluorography of the liver lobules using rhodamine 123 (Rh), a fluoroprobe sensitive to mitochondrial membrane potential, revealed that endotoxin elicited a significant mitochondrial dysfunction panlobularly. The AG administration reversed the endotoxin-induced decrease in mitochondrial membrane potential. Collectively, up-regulation of NO by inducible NO synthase accounts for a mechanism through which endotoxin impairs the bile formation, and its suppression serves as a therapeutic strategy for improvement of hepatobiliary function.
Hydration of sickle cells using the sodium ionophore Monensin. A model for therapy.
Authors: M R Clark, N Mohandas, S B Shohet
Journal: Journal of Clinical Investigation (1982)

Mean cell hemoglobin concentration (MCHC) is thought to have an important influence in sickle cell disease, both through the strong dependence of sickling rates on hemoglobin S concentration, and through the profoundly limiting effect of high MCHC on the rheologic competence of oxygenated, irreversibly sickled cells (ISC). Recent studies have tested the ability of antidiuretic hormone to reduce sickle cell MCHC by reducing plasma sodium (Na) and osmolality. An alternative means of reducing MCHC is to elevate intracellular cation content, rather than to depress extracellular cation concentration. In an effort to do this, we have treated sickle cells with Monensin, an antibiotic that selectively enhances membrane Na permeability. At submicromolar concentrations, Monensin substantially reduced the MCHC of whole sickle blood and isolated ISC, causing an improvement in cell deformability. Monensin's effectiveness in producing a controlled increase in erythrocyte water content suggests that agents that selectively increase membrane Na permeability could be therapeutically useful.
Successful topical treatment of focal epithelial hyperplasia (Heck's disease) with interferon-beta
Authors: M. Steinhoff, D. Metze, E. Stockfleth, T.A. Luger
Journal: British Journal of Dermatology (2001)

We report the successful topical treatment of focal epithelial hyperplasia (Heck’s disease) with interferon‐β (Fiblaferon gel®). Topical treatment with interferon‐β appears to be an effective, simple, non‐invasive, cheap and low‐risk alternative to other invasive or surgical therapeutic modalities.
Progression to Hepatitis and Fibrosis Secondary to Lomitapide Use
Authors: Marta A. Miyares
Journal: JAMA Internal Medicine (2014)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Antiepiligrin (laminin 5) cicatricial pemphigoid associated with an underlying gastric carcinoma producing laminin 5
Authors: None TANIUCHI, None TAKATA, None MATSUI, None FUSHIDA, None UCHIYAMA, None MORI, None KAWARA, None YANCEY, None TAKEHARA
Journal: British Journal of Dermatology (1999)

Although bullous pemphigoid and cicatricial pemphigoid are sometimes associated with malignancy, it remains uncertain whether such an association is pathogenetically related or just a coincidence attributable to the advanced age of the patients. We report a 61-year-old patient with antiepiligrin (laminin 5) cicatricial pemphigoid (AeCP) associated with an advanced gastric carcinoma. The gastric carcinoma cells in this patient were shown to produce laminin 5 by immunofluorescence microscopy, and the patient's serum contained autoantibodies directed against laminin 5 on immunoprecipitation. Furthermore, the blistering symptoms and the titre of antibasement membrane zone antibodies coordinately changed with the resection and subsequent relapse of the gastric cancer. These observations suggest that the gastric carcinoma producing laminin 5 may have induced the production of autoantibodies to this laminin, which were pathogenic to the skin and mucous membranes in this patient. This report demonstrates a link between this autoimmune subepithelial blistering disease and malignancy. It is of interest and potential great importance to examine other cases of AeCP for such a potential association.
"RENAL FAILURE CASTS"
Authors: William G. Exton
Journal: JAMA (1925)

To the Editor:  —Dr. Addis does a service by taking advantage of his extremely interesting observations on casts to point out the apparent lack of interest in morphology, as contrasted with function (The Journal, April 4). As a matter of fact, however, these broad types of casts have been discussed on rare occasions, although never in such a vivid concrete way as has Dr. Addis.  Professor von Jaksch first called my attention to them many years ago, and no student of his was ever allowed to miss seeing them. I am also under a distinct impression that they have been referred to in works by Quensel, Oertel and Senator.  In a paper which Dr. Addis could not reasonably be expected to have come across in his survey of the literature, mention of the existence of such casts was made with the mere statement that their presence suggested some distention of
THE ACTIVE AGENT IN JEQUIRITY INFLAMMATION.
Authors: R. Tilley
Journal: JAMA (1884)

Erroneous impressions about the influence of microbes is greatly to be deprecated, and by no one is this more keenly felt than by those who sincerely wish to give the microbe its due influence either for the weal or woe of the human race. It is consequently with regret that we find in the address of the Chairman of the Section of Practical Medicine of the American Medical Association, that the influence of the jequirity is said to be of special importance because "in it we have pressed into our service the ubiquitious microbe, which is receiving at present so much attention." See address Vol. I, No. 19, p. 517. This position taken by Sattler, and supported by Cornil and Berlioz, has been so completely overthrown by Neisser, of Berlin, and Salomonsen and Dirckinck—Holmfeld, of Copenhagen, and the question itself is of such intrinsic interest, that whilst the matter is
Plasma Brain Natriuretic Peptide as an Indicator of Left Ventricular Systolic Function and Long-term Survival After Acute Myocardial Infarction
Authors: Torbjørn Omland, Asbjørn Aakvaag, Vernon V. S. Bonarjee, Kenneth Caidahl, Rolv Terje Lie, Dennis W. T. Nilsen, Johan A. Sundsfjord, Kenneth Dickstein
Journal: Circulation (1996)

Elevated plasma levels of atrial natriuretic peptide (ANP) and the N-terminal fragment of the ANP prohormone (N-ANP) are associated with decreased left ventricular function and decreased long-term survival after acute myocardial infarction (AMI). Previous data suggest that plasma brain natriuretic peptide (BNP) may increase proportionally more than plasma ANP after AMI and in chronic heart failure. The diagnostic and prognostic value of plasma BNP as an indicator of left ventricular dysfunction and long-term survival after AMI, relative to that of ANP and N-ANP, remain to be established.Venous blood samples for analysis of ANP, N-ANP, and BNP were obtained on day 3 after symptom onset from 131 patients with documented AMI. Left ventricular ejection fraction was determined by echocardiography in a subsample of 79 patients. Twenty-eight cardiovascular and 3 noncardiovascular deaths occurred during the follow-up period (median, 1293 days). All three peptides proved to be powerful predictors of cardiovascular mortality by univariate Cox proportional hazards regression analyses (ANP: P < .0001; N-ANP: P = .0002; BNP: P < .0001). In a multivariate model, plasma BNP (P = .021) but not ANP (P = .638) or N-ANP (P = .782) provided additional prognostic information beyond left ventricular ejection fraction. Logistic regression analysis showed that ANP (P = .003) and N-ANP (P = .027) but not BNP (P = .14) were significantly associated with a left ventricular ejection fraction < or = 45%.These results suggest that plasma BNP determination provides important, independent prognostic information after AMI. Although plasma ANP appears to be a better predictor of left ventricular dysfunction, plasma BNP may have greater potential to complement standard prognostic indicators used in risk stratification after AMI because of its strong, independent association with long-term survival, enhanced in vitro stability, and simplicity of analysis.
Henry Vincent Corbett
Authors: R. Corbett
Journal: BMJ (2009)

After qualifying, Henry Vincent Corbett was a house surgeon at the Royal Southern Hospital in Liverpool. He obtained a physiology research lectureship at Liverpool University and submitted a thesis on colour blindness for his MD, discovering in the process that he was partially colour blind himself. By 1936 he had decided to train in obstetrics and gynaecology and was a house …
Cilastatin protects against cisplatin-induced nephrotoxicity without compromising its anticancer efficiency in rats
Authors: Blanca Humanes, Alberto Lazaro, Sonia Camano, Estefanía Moreno-Gordaliza, Jose A. Lazaro, Montserrat Blanco-Codesido, Jose M. Lara, Alberto Ortiz, Maria M. Gomez-Gomez, Pablo Martín-Vasallo, Alberto Tejedor
Journal: Kidney International (2012)
Sodium and Fluid Restriction
Authors: James Song-Jeng Yeh, Priyank Jain
Journal: JAMA Internal Medicine (2014)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Internal Medicine journal
Altered aldose reductase gene regulation in cultured human retinal pigment epithelial cells.
Authors: D N Henry, M Del Monte, D A Greene, P D Killen
Journal: Journal of Clinical Investigation (1993)

Aldose reductase (AR2), a putative "hypertonicity stress protein" whose gene is induced by hyperosmolarity, protects renal medullary cells against the interstitial hyperosmolarity of antidiuresis by catalyzing the synthesis of millimolar concentrations of intracellular sorbitol from glucose. Although AR2 gene induction has been noted in a variety of renal and nonrenal cells subjected to hypertonic stress in vitro, the functional significance of AR2 gene expression in cells not normally exposed to a hyperosmolar milieu is not fully understood. The physiological impact of basal AR2 expression in such cells may be limited to hyperglycemic states in which AR2 promotes pathological polyol accumulation, a mechanism invoked in the pathogenesis of diabetic complications. Since AR2 overexpression in the retinal pigment epithelium has been associated with diabetic retinopathy, the regulation of AR2 gene expression and associated changes in sorbitol and myo-inositol were studied in human retinal pigment epithelial cells in culture. The relative abundance of aldehyde reductase (AR1) and AR2 mRNA was quantitated by filter hybridization of RNA from several human retinal pigment epithelial cell lines exposed to hyperglycemic and hyperosmolar conditions in vitro. AR2 but not AR1 mRNA was significantly increased some 11- to 18-fold by hyperosmolarity in several retinal pigment epithelial cell lines. A single cell line with a 15-fold higher basal level of AR2 mRNA than other cell lines tested demonstrated no significant increase in AR2 mRNA in response to hypertonic stress. This cell line demonstrated accelerated and exaggerated production of sorbitol and depletion of myo-inositol upon exposure to 20 mM glucose. Therefore, abnormal AR2 expression may enhance the sensitivity of cells to the biochemical consequences of hyperglycemia potentiating the development of diabetic complications.
Long-term treatment of chronic obstructive pulmonary disease with salmeterol and the additive effect of ipratropium
Authors: J.A. van Noord, D.R.A.J. de Munck, Th.A. Bantje, W.C.J. Hop, M.L.m Akveld, A.m Bommer
Journal: European Respiratory Journal (2000)

The efficacy and safety of salmeterol alone was compared with the combination of salmeterol plus ipratropium and with placebo during long-term treatment in patients with stable chronic obstructive pulmonary disease. In addition, the single-dose effect in response to the first dose of treatment was studied over 12 h. The patients (n=144; age 64+/-7 yrs, forced expiratory volume in one second (FEV1) 44+/-11% pred) participated in a three-centre double-blind double-placebo parallel group study and were randomized after a run-in period of 2 weeks to receive either salmeterol 50 microg b.i.d., salmeterol 5 microg b.i.d. plus ipratropium 40 microg q.i.d. or placebo for a period of 12 weeks. The single-dose study demonstrated that salmeterol produced a significant increase in FEV1 (peak of 7% pred) and specific airway conductance (sGaw) (maximum of 60% baseline) for > or =12 h. The combination of salmeterol plus ipratropium elicited a greater bronchodilator response (11% and 94% increases respectively) than salmeterol alone during the first 6 h after inhalation. During treatment there were significant improvements in daytime symptom scores and morning peak expiratory flow in both the salmeterol and the salmeterol plus ipratropium groups (p<0.001), with an associated decrease in the use of rescue salbutamol. Improvements in FEV1 and sGaw were greater in the salmeterol plus ipratropium group than in the patients receiving only salmeterol. Thirty-five patients had an exacerbation; 11 (23%) in the salmeterol group (versus placebo NS), six (13%) in the salmeterol plus ipratropium group (versus placebo p<0.01) and 18 (36%) in the placebo group. In conclusion, in patients with severe stable chronic obstructive pulmonary disease, long-term treatment with either salmeterol alone or salmeterol plus ipratropium is safe and effective. There was added benefit from the combination therapy in terms of improvement in airways obstruction, but not for improvement in symptom control or need for rescue salbutamol.
Neurology and the Affordable Care Act
Authors: Daniel Gold, David E. Newman-Toker, Joshua M. Sharfstein
Journal: JAMA Neurology (2015)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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) 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 Neurology journal
Prostacyclin production by the deendothelialized rabbit aorta.
Authors: J M Boeynaems, N Galand, P Ketelbant
Journal: Journal of Clinical Investigation (1985)

The acute effect of in vitro deendothelialization on the production of prostacyclin (PGI2) by the rabbit aorta has been investigated. The effectiveness of removing endothelium by rubbing it against filter paper or scraping it with a scalpel was demonstrated by scanning electron microscopy and en face examination after silver staining. Endothelium removal produced an immediate stimulation of PGI2 release, resulting in 408% of the control after rubbing and 367% of the control after scraping, during the first 30-min period of incubation. This increased production of PGI2 gradually declined over time to reach values similar to the control after 2h. At that time, the deendothelialized aorta was totally unresponsive to the stimuli that increase PGI2 release in the intact aorta (acetylcholine, ADP, ionophore A23187, and arachidonic acid). The enhanced production of PGI2 in the deendothelialized aorta was associated with an increased release of free arachidonic acid (353% of the control): in contrast with PGI2, this stimulation was maintained for at least 150 min. A transient exposure of the deendothelialized aorta to ibuprofen (250 microM) was followed by a rebound of PGI2 production, which was also prolonged by BW-755C (3-10 microM). In conclusion, removal of the endothelium triggered an immediate and sustained mobilization of free arachidonic acid in the rabbit aorta: the resulting increase of PGI2 production was short-lived, probably as a consequence of cyclooxygenase self-inactivation. Our results indicate that the subendothelium has a significant capacity to produce PGI2, but that this capacity is expressed only briefly.
Angiotensin II receptor blockade attenuates the deleterious effects of exercise training on post-MI ventricular remodelling in rats
Authors: M Jain
Journal: Cardiovascular Research (2000)

Objectives: The effects of exercise training on LV remodelling following large anterior myocardial infarction (MI) remains controversial. Blockade of the renin–angiotensin system has been shown to prevent ventricular dilation and deleterious remodeling. We therefore tested, in a rat model of chronic MI, whether any potentially deleterious effects of exercise on post-MI remodelling could be ameliorated by angiotensin II receptor blockade. Methods: Male Wistar rats underwent coronary ligation or sham operation. Treatment with losartan (10 mg/kg/day) began 1 week post-MI and moderate treadmill exercise (25 m/min, 60 min/day, 5 days/week) was initiated 2 weeks post-MI. Systolic and diastolic pressure–volume relationships were measured in isolated, red-cell perfused, isovolumically beating hearts 8 weeks post-MI. Morphometric measurements were performed in trichrome stained cross sections of the heart. Five groups of animals were compared: sham (n=13), control MI (MI; n=11), MI plus losartan (MI–Los; n=13), MI plus exercise (MI–Ex; n=10) and MI plus exercise and losartan (MI–Ex–Los; n=12). Results: Infarct size (% of left ventricle, LV) was similar among the infarcted groups [MI=43±4%, MI–Los=49±2%, MI–Ex=45±1%, MI–Ex–Los=48±2% (NS)]. Exercise, losartan and exercise+losartan treatments all attenuated LV dilation post-MI to a similar degree. Exercise training increased LV developed pressure in both untreated and losartan treated hearts (P<0.05 vs. other MI groups). In addition, exercise resulted in additional scar thinning in untreated hearts, while no additional scar thinning was seen in post-infarct hearts receiving both losartan and exercise. Conclusions: Following large anterior MI, losartan attenuated LV dilation and scar thinning. In untreated animals, exercise decreased dilation, but also contributed to scar thinning. Therefore, exercise concurrent with blockade of the renin–angiotensin system may provide optimal therapeutic benefit following large anterior MI.
Tezosentan (an intravenous endothelin receptor A/B antagonist) reduces peripheral resistance and increases cardiac power therefore preventing a steep decrease in blood pressure in patients with congestive heart failure
Authors: Cotter Gad, Kiowski Wolfgang, Kaluski Edo, Kobrin Isaac, Milovanov Olga, Marmor Alon, Jafari Jamal, Reisin Leonardo, Krakover Ricardo, Vered Zvi, Caspi Avi
Journal: European Journal of Heart Failure (2001)
Rheumatic Heart Disease in the Framingham Study
Authors: Joseph Stokes, Thomas R. Dawber
Journal: New England Journal of Medicine (1956)

THE pattern of distribution of rheumatic heart disease in the general population is of particular interest not only to those studying the natural history of rheumatic fever but also to those concerned with the pre-eminence of heart disease as a cause of disability and death. Studies of the epidemiology of rheumatic fever have helped to establish the association between that disease and streptococcal infections as well as to describe the familial aggregation of cases of rheumatic fever1 , 2 and its predilection for northern latitudes.3 However, data on the epidemiology of the late cardiac sequelae of rheumatic fever have been largely restricted . . .
Radiogallium Scan in P. Carinii Pneumonia
Authors: K L PARTHASARATHY, SURAJ P. BAKSHI, MERRILL A. BENDER
Journal: Clinical Nuclear Medicine (1982)

A gallium scan performed on a patient with fever of unknown origin (FUO) revealed an abnormal uptake of radiotracer in the lungs despite negative chest roentgenographic examination and other routine diagnostic studies. Subsequent lung biopsy results confirmed the presence of Pneumocystis (P.) carinii infection. A repeat gallium scan obtained following appropriate antibiotic therapy was essentially normal. The importance of radiogallium scanning in an immunosuppressed patient with FUO is emphasized.