tbuckley/cabot-search huggingface dataset:
Ergonovine-induced myocardial ischemia: no role for serotonergic receptors?
Authors: S B Freedman, S Chierchia, L Rodriguez-Plaza, R Bugiardini, G Smith, A Maseri
Journal: Circulation (1984)

Because ergonovine appears to produce coronary contractions by a serotonergic (5-HT) mechanism, we attempted to prevent ergonovine-induced ischemia in patients with vasospastic angina by pretreatment with ketanserin, a new selective 5-HT blocker. We studied seven patients with consistently positive results of ergonovine testing (ST segment elevation in three and ST segment depression in four). Ergonovine testing was performed before and after a bolus of 10 mg of ketanserin (all patients) and infusion of 2 to 4 mg/hr for 8 hr (six patients). To assess 5-HT blockade during ketanserin infusion, the constrictor response of hand veins to 5-HT was tested before and after ketanserin. Despite evidence of 5-HT blockade in hand veins, ergonovine-induced ischemia was not prevented by ketanserin in any patient, and there was no significant change in the dose of ergonovine required to provoke ischemia. In one patient, four spontaneous episodes of ST segment elevation occurred during infusion of ketanserin. The plasma concentrations of ketanserin at the time of ergonovine testing ranged from 61 to 127 ng/ml (mean 102) and were well above those that completely inhibit canine coronary 5-HT contractions in vitro. Although human coronary arteries may differ in their responsiveness to 5-HT or ketanserin, these data suggest that ischemia from ergonovine-induced coronary vasospasm is not mediated by 5-HT receptors.
An Immunoassay to Measure Free IgE in Individuals Receiving Anti-IgE Therapy
Authors: S. Roberts, M. Collwell, H. Wells, J. Myers, S. Oltremari, P. Walters, C. Brockus, M. Ling, J.F. Halsey, M. Altrich
Journal: Journal of Allergy and Clinical Immunology (2011)
Hyperglycemia Induced by Megestrol Acetate
Authors: Anand P. Panwalker
Journal: Annals of Internal Medicine (1992)

Letters15 May 1992Hyperglycemia Induced by Megestrol AcetateAnand P. Panwalker, MDAnand P. Panwalker, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-116-10-878_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors:Henry and coworkers' report (1) of diabetes mellitus induced by megestrol acetate prompts me to report a similar case. A 25-year-old man was diagnosed with the acquired immunodeficiency syndrome (AIDS) in December 1989 after he developed persistent genital ulcers caused by herpes simplex virus type 2. His CD4 count was 27/mm3. He received zidovudine, clotrimazole lozenges, prophylactic acyclovir, and monthly pentamidine isethionate by aerosol, and he remained well. Several blood glucose levels obtained between March 1989 and March 1991 were normal. Megestrol acetate (80 mg orally, twice a day) was prescribed in March 1991 because of a...Reference1. HenryRathgaberSullivanMcCabe KSCK. Diabetes mellitus induced by megestrol acetate in a patient with AIDS and cachexia. Ann Intern Med. 1992;116:53-4. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrug-Induced Acute Myocardial Infarction: Identifying ‘Prime Suspects’ from Electronic Healthcare Records-Based Surveillance SystemDescompensación hiperglucémica hiperosmolar en paciente trasplantado hepático en tratamiento con acetato de megestrolA comparison of megestrol acetate, nandrolone decanoate and dietary counselling for HIV associated weight lossSevere Hyperglycemia in an HIV Clinic: Preexisting Versus Drug-Associated Diabetes MellitusDiabète sucré médicamenteux au cours de l'infection par le VIH. A propos de cinq casHyperglycemia Induced by Megestrol Acetate in a Patient with AIDSInsulin resistance and development of diabetes mellitus associated with megestrol acetate therapy.Steroids and ProgestinsMegestrol 15 May 1992Volume 116, Issue 10Page: 878-878KeywordsAIDSBloodDiabetes mellitusGenital anatomyGlucoseHerpes simplexHyperglycemiaUlcers Issue Published: 15 May 1992 PDF downloadLoading ...
MEDICAL AND SURGICAL EXPERT TESTIMONY.
Authors: JOHN E. OWENS
Journal: JAMA (1897)

Medical and surgical expert testimony is frequently so unsatisfactory and useless to the attorney, who seeks for truth; to the judge, whose desire is the administration of justice; so subversive of the dignity and good name of the medical profession, and yet so helpful to the unscrupulous lawyer, who duly thrives and fattens at the expense of his client, that the subject must surely be worthy of your earnest consideration. As the matter now stands, it is too often a farce, and some of our ablest and most conscientious attorneys, being strongly impressed with its inutility in many cases, and disgusted with the senseless wrangle which instructs neither judge, the bar or the jury, are much inclined to get along without it. Does it not bring discredit to the medical profession that experts and medical attendants, on the side of the plaintiff, testify along certain lines, and that those on
Early Growth Response Factor-1 Is Associated With Intraluminal Thrombus Formation in Human Abdominal Aortic Aneurysm
Authors: In-Soon Shin, Jeong-Min Kim, Koung Li Kim, Shin Yi Jang, Eun-Seok Jeon, Seung Hyuk Choi, Duk-Kyung Kim, Wonhee Suh, Young-Wook Kim
Journal: Journal of the American College of Cardiology (2009)
Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial KATP channels in mouse cardiomyocytes
Authors: Dennis Rottlaender, Kerstin Boengler, Martin Wolny, Guido Michels, Jeannette Endres-Becker, Lukas J. Motloch, Astrid Schwaiger, Astrid Buechert, Rainer Schulz, Gerd Heusch, Uta C. Hoppe
Journal: Journal of Clinical Investigation (2012)

Potassium (K+) channels in the inner mitochondrial membrane influence cell function and survival. Increasing evidence indicates that multiple signaling pathways and pharmacological actions converge on mitochondrial ATP-sensitive K+ (mitoKATP) channels and PKC to confer cytoprotection against necrotic and apoptotic cell injury. However, the molecular structure of mitoKATP channels remains unresolved, and the mitochondrial phosphoprotein(s) that mediate cytoprotection by PKC remain to be determined. As mice deficient in the main sarcolemmal gap junction protein connexin 43 (Cx43) lack this cytoprotection, we set out to investigate a possible link among mitochondrial Cx43, mitoKATP channel function, and PKC activation. By patch-clamping the inner membrane of subsarcolemmal murine cardiac mitochondria, we found that genetic Cx43 deficiency, pharmacological connexin inhibition by carbenoxolone, and Cx43 blockade by the mimetic peptide 43GAP27 each substantially reduced diazoxide-mediated stimulation of mitoKATP channels. Suppression of mitochondrial Cx43 inhibited mitoKATP channel activation by PKC. MitoKATP channels of interfibrillar mitochondria, which do not contain any detectable Cx43, were insensitive to both PKC activation and diazoxide, further demonstrating the role of Cx43 in mitoKATP channel stimulation and the compartmentation of mitochondria in cell signaling. Our results define a role for mitochondrial Cx43 in protecting cardiac cells from death and provide a link between cytoprotective stimuli and mitoKATP channel opening, making Cx43 an attractive therapeutic target for protection against cell injury.
The characteristics and in vivo suppression of neointimal formation with sirolimus-eluting polymeric stents
Authors: Mei-Chin Chen, Yen Chang, Chin-Tang Liu, Wei-Yun Lai, Shu-Fen Peng, Yi-Wen Hung, Hung-Wen Tsai, Hsing-Wen Sung
Journal: Biomaterials (2008)
An important role of tachykinins in ozone-induced airway hyperresponsiveness.
Authors: H Koto, H Aizawa, S Takata, H Inoue, N Hara
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

We investigated the role of tachykinins in ozone-induced airway hyperresponsiveness (AHR) in guinea pigs. Airway responsiveness was assessed by determining the provocative concentration (PC200) of a histamine aerosol. Ozone exposure (3.0 ppm for 2 h) caused significant AHR. For vehicle-pretreated animals, the geometric mean pre- and post-ozone PC200 values were 0.87 mg/ml (GSEM 1.33) and 0.11 mg/ml (GSEM 1.17), respectively. Tachykinin depletion by capsaicin (50 mg/kg) prevented this AHR, whereas it did not alter pre-ozone airway responsiveness. The PC200 was 0.36 mg/kg (GSEM 1.64) before ozone and 0.24 mg/kg (GSEM 1.72) after ozone for this group. Ozone also caused a significant increase in neutrophils in bronchoalveolar lavage fluid (BALF) compared with BALF from a normal control group (1.71 +/- 0.69 versus 0.07 +/- 0.02 x 10(5)/ml, respectively). Capsaicin pretreatment attenuated this neutrophil influx (0.23 +/- 0.16 x 10(5)/ml). Morphometric assessment revealed edema of the bronchiolar wall after ozone exposure, which was not observed in the capsaicin group. BAL and morphometry revealed that the degree of ozone-induced epithelial desquamation was similar in both groups. These results suggest that tachykinins may be responsible for ozone-induced AHR, possibly via neurogenic inflammation.
Solitary Defect on Liver Sulfur Colloid Imaging Secondary to Focal Fatty Infiltration
Authors: RICHARD R. BLACK, DAVID F. WINFIELD, MARIANO FERNANDEZ-ULLOA
Journal: Clinical Nuclear Medicine (1989)

Radionuclide liver-spleen imaging using Tc-99m SC may identify focal defects on routine examinations. Fatty infiltration has generally been described as a diffuse process in the liver that may be manifested on Tc-99m SC liver imaging as a nonhomogeneous pattern of radiopharmaceutical distribution or multiple small defects. This case demonstrates a focal defect on radionuclide imaging, simulating a space-occupying lesion that ultimately proved to be focal fatty infiltration. Although not an uncommon finding on CT, to the authors' knowledge this has not been reported in the nuclear medicine literature to date.
Cardiac Asthma — A Fresh Look at an Old Wheeze
Authors: Alfred P. Fishman
Journal: New England Journal of Medicine (1989)

Soon after Laennec's description in 1819 of the invention of the stethoscope and its use in auscultation, the term "cardiac asthma" began to appear in cardiologic treatises. In 1835, Hope1 wrote that "an immense proportion of asthmas — and of the most dangerous and distressing cases, result from disease of the heart. . . . If the cause be overlooked, the asthmatic is harassed with a farrago of inappropriate and unavailing, not to say pernicious remedies. . . ." Clinicians who performed autopsies on their own patients realized that attacks of wheezing occurred in patients with severe heart disease and . . .
Test case may threaten abortion rights
Authors: C. Dyer
Journal: BMJ (2003)

A case heard by the European court of human rights in Strasbourg this week could force the 45 member states of the Council of Europe, including the United Kingdom, to rewrite their abortion laws.

A grand chamber of 17 judges—reserved for cases that raise serious questions of interpretation of the European convention on human rights or for those where there is a risk of departing from existing case law—heard the case of Thi-Nho Vo, who argues that under the convention an unborn child has the right to life.

The court is expected to deliver its judgment in nine to 12 months' time.

Mrs Vo's …
Prompt access to expert care is among advice to reduce perinatal deaths in Netherlands
Authors: T. Sheldon
Journal: BMJ (2010)

<h3>Background</h3> Thrombectomy for patients with emergent large vessel occlusion (ELVO) is currently recognized as the standard of care for appropriately selected patients. As proven in several randomized clinical trials and meta-analyses, treatment with thrombectomy lowers rates of poor functional outcomes after ELVO, compared with standard medical management. However, combined mortality rates of the most recent, high-quality clinical trials have not been collectively assessed. <h3>Objective</h3> The goal of this study was to assess the combined mortality rates of patients with ELVO following thrombectomy using data from the most recent, high-quality clinical trials. <h3>Methods</h3> Meta-analysis was performed in clinical trials comparing thrombectomy and medical management for patients with anterior circulation ELVO. Cumulative rates of mortality (mRS 6) as well as mortality or severe disability (mRS 5-6) were calculated. <h3>Results</h3> Ten clinical trials fit the inclusion criteria, including PISTE, REVASCAT, DAWN, THRACE, SWIFT PRIME, ESCAPE, DEFUSE 3, THERAPY, EXTEND-IA, and MR CLEAN, with 2233 patients assessed for mortality alone and 2229 for mortality or severe disability. There was a significantly reduced risk of death with thrombectomy compared with standard medical care (14.9% vs 18.3%, P=0.03; RR 0.81, 95% CI 0.67 to 0.98), as well as a reduced risk of mortality or severe disability (mRS 5–6) in ELVO patients treated with thrombectomy (21.1% vs 30.5%, P&lt;0.0001; RR 0.69, 95% CI 0.60 to 0.80). <h3>Conclusions</h3> Overall, these results suggest a lower risk of death, as well as death or severe disability, in patients with ELVO treated with thrombectomy compared with medical management alone.
Lineage fate of ductular reactions in liver injury and carcinogenesis
Authors: Simone Jörs, Petia Jeliazkova, Marc Ringelhan, Julian Thalhammer, Stephanie Dürl, Jorge Ferrer, Maike Sander, Mathias Heikenwalder, Roland M. Schmid, Jens T. Siveke, Fabian Geisler
Journal: Journal of Clinical Investigation (2015)

Ductular reactions (DRs) are observed in virtually all forms of human liver disease; however, the histogenesis and function of DRs in liver injury are not entirely understood. It is widely believed that DRs contain bipotential liver progenitor cells (LPCs) that serve as an emergency cell pool to regenerate both cholangiocytes and hepatocytes and may eventually give rise to hepatocellular carcinoma (HCC). Here, we used a murine model that allows highly efficient and specific lineage labeling of the biliary compartment to analyze the histogenesis of DRs and their potential contribution to liver regeneration and carcinogenesis. In multiple experimental and genetic liver injury models, biliary cells were the predominant precursors of DRs but lacked substantial capacity to produce new hepatocytes, even when liver injuries were prolonged up to 12 months. Genetic modulation of NOTCH and/or WNT/β-catenin signaling within lineage-tagged DRs impaired DR expansion but failed to redirect DRs from biliary differentiation toward the hepatocyte lineage. Further, lineage-labeled DRs did not produce tumors in genetic and chemical HCC mouse models. In summary, we found no evidence in our system to support mouse biliary-derived DRs as an LPC pool to replenish hepatocytes in a quantitatively relevant way in injury or evidence that DRs give rise to HCCs.
Distribution and Supervision of Oral Contraceptives
Authors: E. C. Bramwell
Journal: BMJ (1974)

Dr. Godfrey described the increased in- hibition of bronchoconstriction after 60 mg indoramin compared with 50 mg taken by the same patient on a different occasion as a "quite extraordinary dose-related phen- omenon."Admittedly the dose-response curve in this one patient appears to be steep, nevertheless the result is consistent with what one would expect of a drug with antagonist activity.Many more experiments with patients receiving several doses of indoramin seem necessary to determine that this dose relationship is unusual.Professor Bianco and his colleagues claimed that indoramin prevented specific airway conductance falling below the pretreatment con- trol level in all cases.This is inconsistent, however, with the results published for cases 2, 3, 9, and 10 in their table III.Fortunately, these inconsistencies do not detract from the authors' overall condlusions.From our analysis of their work we would conclude that under the limitations imposed by their methodology the evidence is consistent with indoramin preventing exercise-induced bronchoconstriction in five patients, decreas- ing it in five, and not leading to any im- provement in one.It would be of interest to learn from the investigators how the patients' symptomatology was affected by alpha-blockade.For it could be argued that if indoramin abolished the asthmatic symp- toms it prevented exercise-induced "asthma" while only partially antagonizing exercise- induced "bronchoconstriction."-We are, etc.,
Mutation of <i>Lkb1</i> and <i>p53</i> Genes Exert a Cooperative Effect on Tumorigenesis
Authors: Chongjuan Wei, Christopher I. Amos, L. Clifton Stephens, Imelda Campos, Jian Min Deng, Richard R. Behringer, Asif Rashid, Marsha L. Frazier
Journal: Cancer Research (2005)

Abstract Peutz-Jeghers syndrome (PJS) is a dominantly inherited disorder characterized by gastrointestinal hamartomatous polyps and mucocutaneous melanin pigmentation. Germ line mutations in LKB1 cause PJS. We have generated mice carrying an Lkb1 exon 2 to 8 deletion by gene targeting in embryonic stem cells. Heterozygotes develop gastric hamartomas that are histologically similar to those found in humans with PJS. LKB1 is also reportedly a mediator of p53-dependent apoptosis. To explore the potential combined effects of p53 and Lkb1 alterations on tumorigenesis, we carried out a series of matings with Lkb1+/− and p53 null mice to generate Lkb1+/−/p53+/− and Lkb1+/−/p53−/− mice. Similar to the Lkb1+/− mice, gastrointestinal hamartomas have also been detected in the mice with these two genotypes. The Lkb1+/−/p53+/− mice displayed a dramatically reduced life span and increased tumor incidence compared to the mice with either Lkb1 or p53 single gene knockout. The time to onset of polyposis in Lkb1+/−/p53−/− mice is ∼2 months earlier than Lkb1+/−/p53+/− and Lkb1+/− mice, whereas the latter two show a similar time to onset which is at ∼6 months of age. These results strongly suggested that mutations of p53 and Lkb1 gene cooperate in the acceleration of tumorigenesis. (Cancer Res 2005; 65(24): 11297-303)
Acetylator Phenotype, Aminobiphenyl-Hemoglobin Adduct Levels, and Bladder Cancer Risk in White, Black, and Asian Men in Los Angeles, California
Authors: M. C. Yu, P. L. Skipper, K. Taghizadeh, S. R. Tannenbaum, K. K. Chan, B. E. Henderson, R. K. Ross
Journal: JNCI Journal of the National Cancer Institute (1994)

There is a large body of epidemiologic and experimental data that have identified a number of arylamines as human bladder carcinogens. Metabolic activation is required to biotransform these arylamines into their carcinogenic forms, and N-hydroxylation, which is catalyzed by the hepatic cytochrome P4501A2 isoenzyme, is generally viewed as the first critical step. On the other hand, the N-acetylation reaction, catalyzed by the hepatic N -acetyltransferase enzyme, represents a detoxification pathway for such compounds. The N -acetyltransferase enzyme is coded by a single gene displaying two phenotypes, slow and rapid acetylators. In the United States, cigarette smoking is a major cause of bladder cancer in men, and carcinogenic arylamines present in cigarette smoke are believed to be responsible for inducing bladder cancer in smokers. Purpose : Our purpose was to test the differences in three ethnic/racial groups for the prevalence of acetylator phenotypes and to ascertain whether slow acetylators actually have higher levels of activated arylamines in comparison with rapid acetylators. Methods : One hundred thirty-three male residents of Los Angeles County who were either white, black, or Asian (Chinese or Japanese) and over the age of 35 years were assessed for their acetylator phenotype and levels of 3- and 4-aminobiphenyl (ABP) hemoglobin adducts. Subjects were either lifetime nonsmokers (n = 72) or current cigarette smokers of varying intensity (n = 61). Results : The proportion of slow acetylators was highest among whites (54%), intermediate among blacks (34%), and lowest among Asians (14%). Similarly, geometric mean levels of both 3- and 4-ABP-hemoglobin adducts were highest in whites (1.80 and 49.2 pg/g hemoglobin [Hb], respectively), intermediate in blacks (1.54 and 38.5 pg/g Hb), and lowest in Asians (0.73 and 36.0 pg/g Hb). As expected, cigarette smokers had significantly higher mean levels of both 3- and 4-ABP-hemoglobin adducts relative to nonsmokers, and the levels increased with the number of cigarettes smoked per day (P<.0005 for both adducts). Slow acetylators consistently exhibited higher mean levels of ABP-hemoglobin adducts relative to rapid acetylators, independent of race and level of smoking. Conclusion : The present cross-sectional survey supports acetylation phenotype as an important determinant of bladder cancer risk and a possible major factor in the varying bladder cancer risk among whites, blacks, and Asians. [J Natl Cancer Inst 86: 712–716, 1994]
A novel antagonist of CRTH2 blocks eosinophil release from bone marrow, chemotaxis and respiratory burst
Authors: J. F. Royer, P. Schratl, S. Lorenz, E. Kostenis, T. Ulven, R. Schuligoi, B. A. Peskar, A. Heinemann
Journal: Allergy (2007)

Background: Chemoattractant receptor‐homologous molecule expressed on Th2 cells (CRTH2) has been revealed to be a novel receptor for prostaglandin (PG) D 2 , which is a major mast cell product released during the allergic response. The aim of this study was to analyze the effects of a newly developed small molecule antagonist of CRTH2, Cay10471, on eosinophil function with respect to recruitment, respiratory burst and degranulation. Methods: Chemotaxis of guinea pig bone marrow eosinophils and human peripheral blood eosinophils were determined using microBoyden chambers. Eosinophil release from bone marrow was investigated in the in situ perfused guinea pig hind limb preparation. Respiratory burst and degranulation were measured by flow cytometry. Results: Cay10471 bound with high affinity to recombinant human and guinea pig CRTH2, but not DP, receptors. The antagonist prevented the PGD 2 ‐induced release of eosinophils from guinea pig bone marrow, and inhibited the chemotaxis of guinea pig bone marrow eosinophils and human peripheral blood eosinophils. Pretreatment with PGD 2 primed eosinophils for chemotaxis towards eotaxin, and this effect was prevented by Cay10471. In contrast, PGD 2 inhibited the C5a‐induced up‐regulation of CD63, a cellular marker of degranulation, in a Cay10471‐sensitive manner. Finally, Cay10471 abolished the respiratory burst of eosinophils upon stimulation by PGD 2 . Conclusion: These data further emphasize the importance of CRTH2 in eosinophil function and show that Cay10471 is a highly potent and selective antagonist of PGD 2 ‐induced eosinophil responses. Cay10471 might hence be a useful compound for the treatment of allergic diseases.
Induction of acute GVHD by sex-mismatched H-Y antigens in the absence of functional radiosensitive host hematopoietic–derived antigen-presenting cells
Authors: Tomomi Toubai, Isao Tawara, Yaping Sun, Chen Liu, Evelyn Nieves, Rebecca Evers, Thea Friedman, Robert Korngold, Pavan Reddy
Journal: Blood (2011)
Inhibition of vascular permeability changes in rats by captopril.
Authors: J C Fantone, D Schrier, B Weingarten
Journal: Journal of Clinical Investigation (1982)

Systemic treatment of rats with captopril (50 mg/kg body wt per os), a specific competitive inhibitor of angiotensin l-converting enzyme, significantly inhibits vascular permeability changes induced by the intradermal injection of the vasoactive mediators histamine, bradykinin, serotonin, and compound 48/80. This effect of captopril is both dose- and time-dependent with approximately 60% inhibition of edema formation observed 7 h after captopril treatment (100 mg/kg body wt per os). The inhibitory effect of captopril on edema formation is temporally unrelated to the inhibition of serum angiotensin l-converting enzyme activity or serum prostaglandin E2 levels and is not inhibited by systemic treatment of rats with indomethacin. The data suggest that captopril may have potent antiinflammatory activity through as yet undefined mechanisms.