tbuckley/cabot-search huggingface dataset:
Opiate receptor antagonism in right-sided congestive heart failure. Naloxone exerts salutary hemodynamic effects through its action on the central nervous system.
Authors: S Sakamoto, C K Stone, P D Woolf, C S Liang
Journal: Circulation Research (1989)

Opiate receptor inhibition causes adrenergic receptor-mediated increases in aortic pressure, cardiac output, and left ventricular contractile function in right heart failure. To study whether the effects of opiate receptor inhibition are mediated by means of an action on the central opiate system, we administered equimolar doses of naloxone hydrochloride and naloxone methobromide (MeBr) and normal saline to heart failure dogs. Chronic stable right heart failure was produced by progressive pulmonary artery constriction and tricuspid valve avulsion. Naloxone hydrochloride caused an increase in mean aortic pressure, cardiac output, left ventricular dP/dt and dP/dt/P, plasma catecholamines, and regional blood flows to the myocardium, quadriceps muscle, kidneys, and splanchnic beds. Plasma beta-endorphin and adrenocorticotropin also increased. In contrast, neither normal saline nor naloxone MeBr (which does not cross the blood-brain barrier) affected the systemic or regional hemodynamics or neurohormones. Naloxone hydrochloride was also administered to anesthetized heart failure dogs. Pentobarbital anesthesia removed cortical perception of nociceptive stimulation, reduced the increase in plasma epinephrine, and abolished vasodilation in skeletal muscle that occurred in conscious dogs after naloxone hydrochloride administration but had no major effects on responses of plasma norepinephrine, systemic hemodynamics, or other regional blood flows to opiate receptor inhibition. Naloxone hydrochloride had no effect in sham-operated dogs. The results indicate that the hemodynamic effects of naloxone are mediated by an action within the central nervous system. Furthermore, since pentobarbital anesthesia did not markedly alter the hemodynamic responses to naloxone hydrochloride, the acute salutary effects of opiate receptor inhibition probably are not caused by removal of the antinociceptive effect of endogenous opioids in heart failure.
Splanchnic and Hepatic Metabolism of Somatostatin: A Study in Cirrhotic Patients with a Portacaval Shunt
Authors: Susan Webb, David Kravetz, Jaume Bosch, John A.H. Wass, Joan Evans, Ramon Gomis, Lesley H. Rees, Joan Rodes
Journal: Hepatology (1983)

Experimental data suggest that somatostatin is metabolized by both liver and kidneys. Results in humans are conflicting. By studying a group of cirrhotic patients with surgically induced end-to-side portacaval shunts, basally and during a somatostatin infusion, we have been able to analyze separately the hepatic and splanchnic metabolism of this peptide. After catheterization, samples were obtained from the pulmonary artery, portal and hepatic veins. Basal pulmonary artery immunoreactive somatostatin (IRS) was significantly higher (p less than 0.001) in the cirrhotic patients (96 +/- 11 pg per ml) than in a sex- and age-matched control group (31.4 +/- 5.8 pg per ml). During the infusion of exogenous somatostatin, IRS values were higher in arterial (12,269 +/- 1,198 pg per ml) than in hepatic venous blood (7,648 +/- 1,234 pg per ml), indicating hepatic extraction of the peptide; but there was also a substantial splanchnic extraction demonstrated by higher arterial (12,269 +/- 1,532 pg per ml) than portal values (6,754 +/- 1,040 pg per ml) of IRS. During the somatostatin infusion, at very high circulation IRS levels, the liver was able to extract 38% of the peptide. This suggests that the high basal IRS levels found in liver cirrhosis are not likely to be due to hepatic failure. Possible mechanisms may involve increased somatostatin secretion, predominance of high molecular weight moieties of IRS which may not be as effectively removed by the liver, and/or portal-systemic shunting.
Is Cardiac Migraine a Clinical Entity?
Authors: JEAN LETTE, LISE-ANDRÉE MERCIER, JACQUES LESPÉRANCE, ANDRÉ ARSENAULT, MICHEL CERINO, STANLEY NATTEL
Journal: Clinical Nuclear Medicine (1995)

Chest pain because of a disorder of the coronary circulation is assumed to be ischemic in nature. Irrespective of the underlying pathophysiological mechanism, it is accepted that all routes lead to myocardial ischemia in the pathway to anginal pain. The authors describe a patient with a history of vasoactive disorders including migraine, asthma, documented variant angina with prolonged episodes of chest pain, and scintigraphic evidence of inferior and posterior wall ischemia during exercise and ergonovine testing in the absence of significant underlying stenoses. Remarkably, severe retrosternal chest pain, ST segment depression in multiple leads, and relative increased uptake in the inferior and posterior walls on Tc-99m sestamibi tomographic images developed during pharmacologic coronary vasodilatation with dipyridamole, leading the authors to speculate as to the possible existence of a nonischemic chest pain syndrome caused by coronary vasodilatation either in association with variant angina or as a separate entity.
Some Addenda on the Role of Today's Autopsy
Authors: John Prutting
Journal: JAMA (1965)

<h3>To the Editor:—</h3> It is heartwarming to one who believes wholly in the importance of the autopsy to learn that the eminent symposiasts of the Sept 6Journalbelieve it is still important and indeed may be increasing in value. However, it seems to me that the occasional emphasis on the "lessening importance" of the procedure may well tend to increase the reluctance of many physicians to obtain them. The symposium says that some postmortems are of little value. In a recent survey in New York City, physicians, especially surgeons, maintained that postmortems are often unnecessary—for example, when the patient has widespread metastases. To cite an example of this fallacy, it has been shown that metastatic lung cancers are often diagnosed ante mortem as primary— only to find by autopsy that the disease was secondary from the pancreas, well-known for its silent morbid manifestations, or some other organ. Only through
Newborns in England are screened for four extra genetic conditions
Authors: N. Hawkes
Journal: BMJ (2015)

During chronic human immunodeficiency virus (HIV) infection, inhibitory molecules are upregulated and contribute to effector cell dysfunction and exhaustion. People living with (PLWH) HIV are at a greater risk for age-related morbidities, an issue magnified by human cytomegalovirus (HCMV) co-infection. As HCMV modifies NK cell phenotype and function, we considered the role of upregulated inhibitory molecules in this context and their potential to affect NK cell-based strategies to eliminate HIV-infection. To evaluate impacts of HCMV-driven NK cell adaptation in HIV infection, PLWH were distinguished by HCMV status or by high (&gt;20%) versus low (&lt;6%) percentages of adapted NK cells. Adapted NK cells did not display a classical exhausted phenotype as there was low LAG-3, PD-1 (&lt;1%), and TIM-3 (&lt;10%) expression. In contrast, TIGIT was present on a large fraction of NK and CD8<sup>pos</sup> T cells and levels were associated with HCMV status. Since CD4<sup>pos</sup> T cells latently infected with HIV upregulate CD155, a ligand for TIGIT, we investigated TIGIT modulation of NK cell functions. Blocking TIGIT/CD155 interactions increased NK cell cytotoxicity and correlated with the extent of NK cell adaptation to HCMV. Engaging TIGIT reduced levels of antibody-dependent cell-mediated cytotoxicity (ADCC) against pseudo HIV-infected (vPE16) P815 cells with the extent of reduction again reflecting NK cell adaptation to HCMV. Measuring HIV-specific ADCC against HIV-infected CEM.NK<sup>R</sup> CCR5<sup>pos</sup> cells transduced with CD155 will allow assessment of the role of TIGIT inhibition in a genuine HIV infection model. Blocking TIGIT may be an appropriate strategy to invigorate antibody-dependent NK cell activity against HIV reservoirs in cure or treatment strategies.
Parallel Retention of Pdx2 Genes in Cartilaginous Fish and Coelacanths
Authors: J. F. Mulley, P. W. H. Holland
Journal: Molecular Biology and Evolution (2010)

The Pdx1 or Ipf1 gene encodes an important homeodomain-containing protein with key roles in pancreas development and function. Mutations in human PDX1 are implicated in developmental defects and disease of the pancreas. Extensive research, including genome sequencing, has indicated that Pdx1 is the only member of its gene family in mammals, birds, amphibians, and ray-finned fish, and with the exception of teleost fish, this gene forms part of the ParaHox gene cluster along with Gsx1 and Cdx2. The ParaHox cluster, however, is a remnant of a 4-fold genome duplication; the three other ParaHox paralogues lack a Pdx-like gene in all vertebrate genomes examined to date. We have used bacterial artificial chromosome cloning and synteny analysis to show that the ancestor of living jawed vertebrates in fact had more ParaHox genes, including two Pdx genes (Pdx1 and Pdx2). Surprisingly, the two Pdx genes have been retained in parallel in two quite distantly related lineages, the cartilaginous fish (sharks, skates, and chimeras) and the Indonesian coelacanth, Latimeria menadoensis. The Pdx2 gene has been lost independently in ray-finned fish and in tetrapods.
Kan-1 (Bile acid CoA:Amino acid N-acyltransferase) messenger RNA as a novel predictive indicator for prognosis of hepatocellular carcinoma patients after partial hepatectomy
Authors: M Furutani
Journal: Hepatology (1996)

We identified kan-1 complementary DNA (cDNA), the sequence of which is identical to bile acid CoA:amino acid N-acyltransferase (BAT), a liver enzyme that catalyzes the conjugation of bile acids with glycine or taurine. Kan-1(BAT) messenger RNA (mRNA) levels of the resected specimens obtained from 37 hepatocellular carcinoma (HCC) patients were studied in an attempt to evaluate prognostic significance in HCC patients after partial hepatectomy. Using Northern blot hybridization, kan-1(BAT) mRNA levels were quantified in tumorous and nontumorous tissues, and the ratio of the former to the latter was defined as the kan-1(BAT) ratio. Twelve patients had a kan-1(BAT) ratio < 0.5 (low kan-1[BAT] ratio), and 25 patients had a ratio >0.5 (high kan-1[BAT] ratio). The patients with a low kan-1(BAT) ratio demonstrated poorer survival than the patients with a high kan-1(BAT) ratio (P = .0013). The overall estimated hazard ratio for death in patients with a low kan-1(BAT) ratio was 68.05 according to a multivariate model (P = .0005). Thus, the kan-1(BAT) ratio may serve as a new molecular prognostic marker in HCC patients, following hepatic resection.
NOTES OF THREE CASES
Authors: HOWARD MORROW
Journal: British Journal of Dermatology (1901)

Journal Article NOTES OF THREE CASES Get access HOWARD MORROW HOWARD MORROW SAN FRANCISCO Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 13, Issue 11, 1 November 1901, Pages 433–435, https://doi.org/10.1111/j.1365-2133.1901.tb16350.x Published: 01 November 1901
Elevated serum levels of <i>Wisteria floribunda</i> agglutinin‐positive human Mac‐2 binding protein predict the development of hepatocellular carcinoma in hepatitis C patients
Authors: Kazumi Yamasaki, Masakuni Tateyama, Seigo Abiru, Atsumasa Komori, Shinya Nagaoka, Akira Saeki, Satoru Hashimoto, Ryu Sasaki, Shigemune Bekki, Yuki Kugiyama, Yuri Miyazoe, Atsushi Kuno, Masaaki Korenaga, Akira Togayachi, Makoto Ocho, Masashi Mizokami, Hisashi Narimatsu, Hiroshi Yatsuhashi
Journal: Hepatology (2014)

The Wisteria floribunda agglutinin-positive human Mac-2-binding protein (WFA+-M2BP) was recently shown to be a liver fibrosis glycobiomarker with a unique fibrosis-related glycoalteration. We evaluated the ability of WFA+-M2BP to predict the development of hepatocellular carcinoma (HCC) in patients who were infected with the hepatitis C virus (HCV). A total of 707 patients who had been admitted to our hospital with chronic HCV infection without other potential risk factors were evaluated to determine the ability of WFA+-M2BP to predict the development of HCC; factors evaluated included age, sex, viral load, genotypes, fibrosis stage, aspartate and alanine aminotransferase levels, bilirubin, albumin, platelet count, alpha-fetoprotein (AFP), WFA+-M2BP, and the response to interferon (IFN) therapy. Serum WFA+-M2BP levels were significantly increased according to the progression of liver fibrosis stage ( P &lt; 0.001). In each distinctive stage of fibrosis (F0-F1, F2, F3, and F4), the risk of development of HCC was increased according to the elevation of WFA+-M2BP. Multivariate analysis identified age &gt; 57 years, F4, AFP &gt; 20 ng/mL, WFA+-M2BP ≥4, and WFA+-M2BP 1-4 as well as the response to IFN (no therapy vs. sustained virological response) as independent risk factors for the development of HCC. The time-dependent areas under the receiver operating characteristic curve demonstrated that the WFA+-M2BP assay predicted the development of HCC with higher diagnostic accuracy than AFP. Conclusion : WFA+-M2BP can be applied as a useful surrogate marker for the risk of HCC development, in addition to liver biopsy. (Hepatology 2014;60:1563–1570)
Review: Neurologic Manifestations of HIV Infection
Authors: David M. Simpson
Journal: Annals of Internal Medicine (1995)

Corrections15 February 1995Correction: Neurologic Manifestations of HIV InfectionFREEDavid M. Simpson and Michele TagliatiDavid M. SimpsonSearch for more papers by this author and Michele TagliatiSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-122-4-199502150-00023 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail In a review article [1], a study by Luft and colleagues [2] about clindamycin therapy for cerebral toxoplasmosis was incorrectly quoted. The dosage for clindamycin should have been 600 mg, four times a day.References1. Simpson DM, Tagliati M. Neurologic manifestations of HIV infection. Ann Intern Med. 1994; 121:769-85. Google Scholar2. Luft BJ, Hafner R, Korzun AH, Leport C, Antoniskis D, Bosler EM, et al. Toxoplasmic encephalitis in patients with the acquired immunodeficiency syndrome. Members of the ACTG 077p/ANRS 009 Study Team. N Engl J Med. 1993; 329:995-1000. Google Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 February 1995Volume 122, Issue 4Page: 317KeywordsClindamycinHIV infectionsToxoplasmosis Issue Published: 15 February 1995 CopyrightCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Common occurrence of anaemia at the end of pregnancy following exposure to zidovudine-free regimens
Authors: Carmela Pinnetti, Silvia Baroncelli, Atim Molinari, Giulia Nardini, Orazio Genovese, Bianca Maria Ricerca, Anna Franca Cavaliere, Giovanni Guaraldi, Anna Degli Antoni, Enrica Tamburrini, Marco Floridia
Journal: Journal of Infection (2011)
ETIOLOGY OF CHRONIC MYOCARDITIS
Authors: JAMES P. O'HARE
Journal: JAMA (1928)

The etiology of the cardiac condition familiarly known as chronic myocarditis has always remained vague and many theories have been evolved in the endeavor to explain the development of this common condition. It is well known that chronic valvular disease is a common cause of myocardial insufficiency; that hyperthyroidism is an occasional adequate cause, and that a similar condition is associated with hypertension—whether vascular or related to renal disease. There is a fourth group of nonvalvular cases in which the blood pressure is normal or low. This is the type of chronic myocarditis the etiology of which is so uncertain. Osler,<sup>1</sup>Assman<sup>2</sup>and other German writers, and most of the authors of the current textbooks on the subject, believe that the acute infections, especially diphtheria and rheumatic fever, are common causes of the myocarditic heart. They also assert that overexertion and certain toxic substances such as alcohol, lead
Abstract P127: Resuscitation with Liposome-Encapsulated Hemoglobin (Artificial Oxygen Carrier) from Lethal Hemorrhagic Shook and Its Effect on Nitoric Oxide and Tissue Expression of Hypoxia-Inducible Factor-1 alpha
Authors: Bonpei Takase, Yashiro Nogami, Manabu Kinoshita, Yoshitaka Ogata, Hidemi Hattori, Masayuki Ishihara
Journal: Circulation (2008)

Previously reported acellular hemoglobin-based oxygen carriers have a high affinity for nitric oxide (NO) and subsequently cause vasoconstriction leading to decrease peripheral perfusion due to NO ...
Endothelial nitric oxide synthase enhancer reduces oxidative stress and restores endothelial function in db/db mice
Authors: Wai San Cheang, Wing Tak Wong, Xiao Yu Tian, Qin Yang, Hung Kay Lee, Guo-Wei He, Xiaoqiang Yao, Yu Huang
Journal: Cardiovascular Research (2011)

AimsEndothelial dysfunction is caused by reduced nitric oxide (NO) bioavailability and/or over-produced reactive oxygen species (ROS). The present study investigated a vascular benefit of AVE3085, an endothelial nitric oxide synthase (eNOS) enhancer, in preserving endothelial function in diabetic mice and the mechanisms involved.
Law has a protective function for both patients and doctors
Authors: I. Finlay, P. Routledge, A. Freedma, K. Woodhouse, D P Davies, A B Hawthorne, M. Pritchard, M. Hall, P. Beck, C. Wilkinson
Journal: BMJ (1996)

EDITOR,—“Show me a hero and I will write you a tragedy”; so wrote F Scott Fitzgerald. Jack Kevorkian is a fanatic, not a hero.1

There are some practical reasons why the killing of a patient, even when problems seem insurmountable, must remain prohibited in law. The law has a protective function. It protects the vulnerable from misinformation due to mistakes by or the ignorance of the informer, from pressure by those with malintent, from economically driven judgments on their future, and from much more. It also protects us, as doctors, from ourselves: our ignorance or arrogance, any temptation to cover up medical mistakes, our difficulty in asking for help from a colleague, overinvolvement with a patient that colours our judgment, our fatigue, or personal prejudice or bias about clinical or social conditions. It protects us from undue pressure by relatives weary of caring or who stand to gain financially. Managers cannot put pressure on us to clear those who are dying from our beds rapidly, and purchasers cannot question why we strive to provide quality care to patients with a poor prognosis.

As a pathologist Kevorkian may be desensitised to corpses. We provide long term care and bereavement support and are increasingly aware of the absolute import of death. Currently, prognosis cannot be predicted accurately, there are errors of diagnosis, depression is difficult to diagnose in medically ill people, patients' priorities alter often during the course of a life threatening illness, hope can re-emerge from hopelessness, we find some patients' problems overwhelming at times, and sometimes our judgment is clouded by ignorance or fatigue. Why no cries to enshrine in law the right of all patients to a second opinion if their suffering remains intractable for a week? Why call for legalising carelessness?
CARDIAC I-123 METAIODOBENZYLGUANIDINE IMAGING COULD IDENTIFY PATIENTS WITH CHRONIC HEART FAILURE AND LVEF&lt;35% AT LOW RISK FOR SUDDEN CARDIAC DEATH FOR FIVE YEARS
Authors: Tsutomu Kawai, Takahisa Yamada, Takashi Morita, Yoshio Furukawa, Yusuke Iwasaki, Masato Kawasaki, Atsushi Kikuchi, Tadao Fujimoto, Takashi Naito, Kentaro Ozu, Hironori Yamamoto, Kaoruko Sengoku, Takumi Kondo, Satoshi Takahashi, Masatake Fukunami
Journal: Journal of the American College of Cardiology (2013)
Effect of knowledge of serum enzyme concentrations on doctors' interpretation of electrocardiographic manifestations in suspected myocardial infarction.
Authors: T Gjorup, H Kelbaek, L Stenbygard, F Sorensen, J Godtfredsen, A M Jensen
Journal: BMJ (1986)

Agreement between positive and negative interpretations of enzyme concentrations and electrocardiograms (ECG) in patients with suspected acute myocardial infarction. (Figures are numbers (%) ofpatients)
Pre-B cell receptor–mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC
Authors: Rahul Nahar, Parham Ramezani-Rad, Maximilian Mossner, Cihangir Duy, Leandro Cerchietti, Huimin Geng, Sinisa Dovat, Hassan Jumaa, B. Hilda Ye, Ari Melnick, Markus Müschen
Journal: Blood (2011)
Effects of Hypoxia and Metabolic Inhibitors on the Intrinsic Heart Rate and Myocardial Contractility in Dogs
Authors: ANTHONY D. JOSE, FRANK STITT
Journal: Circulation Research (1969)

Previous studies have shown that after autonomic blockade by propranolol and atropine, the intrinsic rate and contractile function of the heart were related in patients with myocardial failure. In this study the intrinsic rate and ventricular contractile force were measured in dogs during acute heart failure produced by agents which impair myocardial energy syntinesis, to see whether these conditions reproduced the relationship found in naturally occurring myocardial disease in man. Anesthetized dogs, after propranolol and atropine, were either ventilated with 6% oxygen or given sodium cyanide, parachloromercuribenzoate, or dinitrophenol by intravenous infusion. Hypoxia and cyanide initially increased and then depressed both rate and contraction. Parachloromercuribenzoate depressed both. Dinitrophenol depressed only contraction. During hypoxia, cyanide, and parachloromercuribenzoate the percent changes in contractile force and intrinsic rate were linearly related (r=0.87) with slopes of 3.2, 2.7, and 3.3, respectively. These results together with previous data during pentobarbital and aminophylline were consistent with a single linear relationship between rate and contractility (r=0.89, slope 3.2). This resembled closely the relationship found previously in man. It is suggested that in both situations, this relationship may be determined by a dependence of rate and contractility on similar limited sources of energy.
Folate-Induced Remission in Aplastic Anemia with Familial Defect of Cellular Folate Uptake
Authors: Richard F. Branda, Charles F. Moldow, James R. MacArthur, Maxwell M. Wintrobe, Bruce K. Anthony, Harry S. Jacob
Journal: New England Journal of Medicine (1978)

Severe aplastic anemia developed in a young man with an extensive family history of leukemia, pancytopenia, and neutropenia. Megaloblastic changes became evident, and treatment with high doses of folic acid resulted in striking clinical improvement. However, red-cell folate levels remained persistently low despite high serum folate levels. A defect in cellular folate uptake was suspected, and, indeed, uptake of 5–14CH3-H4-folate by stimulated lymphocytes and by bone-marrow cells from the patient was significantly reduced (P<0.05) as compared to normal cells. Further characterization of folate metabolism showed that intestinal absorption of the vitamin, membrane transport of 5–14CH3-H4-folate by mature red cells, folate utilization in the conversion of deoxyuridylate to thymidylate and polyglutamate formation were all normal. At least five other family members manifest decreased uptake of 5–14CH3–H4-folate by stimulated lymphocytes. These studies suggest that a genetically induced abnormality of folate uptake contributed to this patient's severe, but reversible, aplasia. (N Engl J Med 298:469–475, 1978)