tbuckley/cabot-search huggingface dataset:
Effects of long-term administration of octreotide in portal vein-stenosed rats
Authors: H Lin, M C Yang, M Hou, S Li, Y Huang, P Yu, Y Tsai, S Lee
Journal: Hepatology (1996)

The hemodynamic effects of long-term administration of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shunts has not yet been evaluated. Hence, the current study was undertaken to evaluate the effects of long-term administration of octreotide in rats with portal vein stenosis. Immediately after portal vein stenosis or sham operation, rats were given either a long-term octreotide administration of 100 μg/kg or a placebo every 12 hours by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree of mesenteric-systemic shunts, and plasma glucagon concentrations were measured after the final dose of octreotide or placebo. A fifth group of portal vein-stenosed rats received hemodynamic and plasma glucagon measurements after 1-day octreotide treatment given at 14 days after surgery. Long-term octreotide treatment modified the hyperdynamic circulation without affecting the degree of mesenteric-systemic shunts, and 1-day octreotide treatment decreased portal tributary blood flow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. Plasma glucagon levels were decreased in portal vein-stenosed rats receiving either long-term or 1-day octreodtide compared with rats receiving placebo. In contrast, chronic octreotide treatment did not affect any of the hemodynamic values or plasma glucagon levels in sham-operated rats. In conclusion, long-term administration of octreotide modified in part the development of portal hypertension and hyperdynamic circulation in portal vein-stenosed rats without affecting the degree of mesenteric-systemic shunts.
PSYCHO-ANATOMY OF A DISASTER: A LONG TERM STUDY OF POST-TRAUMATIC NEUROSES IN SURVIVORS OF A MARINE EXPLOSION
Authors: ROBERT L. LEOPOLD, HAROLD DILLON
Journal: American Journal of Psychiatry (1963)

This study reports the immediate psychological effects of a maritime explosion on 36 survivors, and the long term effects on 34 who were seen 3½ to 4½ years later. All were experienced seamen. The circumstamces of the accident were virtually identical for all. None received any systematic interim psychotherapy. All were guaranteed realistic compensation. Immediate effects in the majority of cases were appropriate to the circumstances, but long term investigation indicated appreciable deterioration in 71%, most frequent and most marked in the age group 36 and over. The long term psychological pictures were strikingly similar for all subjects. It was formulated from the data that repeated exposure to a potential danger apparently deprives the organism of its capacity to defend itself; when the danger has been converted to an actuality, it subsequently is perceived as a constant peril which is not amenable to repression, and the resultant reverberating anxiety accounts for the severity of the long term reactions. The data also supported the authors' previously stated hypotheses that the nature of the accident itself is a more significant determinant of post-traumatic psychological illness than the pre-accident personality; that such illness, if untreated, tends to worsen with time; and that litigation worries are a minor factor in producing the illness. It is suggested that the post-traumatic psychological states be considered diagnostic categories in themselves. This approach, because it shifts emphasis from the pre-accident personality to the accident itself, and recognizes that post-traumatic psychological damage is a discrete illness representing the failure of the individual's defense mechanisms, will best serve understanding and treatment of that illness.
Appeal of the week?
Authors: Trisha Greenhalgh
Journal: BMJ (2004)

Ever submitted a paper to the BMJ ? Ever had a reply saying your paper lacked originality, methodological rigour, or credibility on the Clapham omnibus? Believe it or not, the BMJ 's rejection letters are more comprehensive, fair, and sensitive than the ones from JAMA or the Lancet , and its reasons for trashing your work are more likely to be evidence based—at least if a content analysis of my own collection is anything to go by. I'm told …
Incremental prognostic value of kidney function decline over coronary artery disease for cardiovascular event prediction after coronary computed tomography
Authors: Marcio S. Bittencourt, Edward A. Hulten, Brian Ghoshhajra, Suhny Abbara, Venkatesh L. Murthy, Sanjay Divakaran, Khurram Nasir, Luis Henrique W. Gowdak, Leonardo V. Riella, Marco Chiumiento, Udo Hoffmann, Marcelo F. Di Carli, Ron Blankstein
Journal: Kidney International (2015)
Prevalence of non-organ-specific autoantibodies and chronic liver disease in the general population: a nested case-control study of the Dionysos cohort
Authors: M Lenzi, S Bellentani, G Saccoccio, P Muratori, F Masutti, L Muratori, F Cassani, F B Bianchi, C Tiribelli
Journal: Gut (1999)

Several retrospective and prospective studies report an increased prevalence of non-organ-specific autoantibodies (NOSAs) in patients with hepatitis C virus (HCV) related chronic liver disease (CLD). Some of the data so far available are controversial and the true prevalence of NOSAs in the general population is still not known.To explore the prevalence of NOSAs, their relation to different HCV genotypes, and the presence and severity of CLD in the general population of Northern Italy.All 226 anti-HCV positive and 87 hepatitis B surface antigen (HBsAg) positive patients of the Dionysos cohort study were analysed and compared with sex and age matched cases (226) negative for both anti-HCV antibody and HBsAg selected from the same cohort.Sera tested for the presence of NOSAs (anti-nuclear antibody (ANA), anti-smooth muscle antibody (SMA), and anti-liver/kidney microsomes type 1 antibody (LKM1)) were screened by indirect immunofluorescence at a 1:40 serum dilution. HCV RNA and HCV genotypes were also determined by nested polymerase chain reaction (PCR) of the 5' non-coding region and by PCR amplification of the core region with type specific primers.The overall prevalence of NOSA reactivity was significantly higher in anti-HCV positive subjects than in both normal and pathological controls (25% v 6% and 7% respectively, p<0.05). ANA, SMA, and LKM1 occurred in 16, 10, and 1. 3% of cases respectively. No specific association between NOSAs and a specific HCV genotype was found. NOSAs were found more often associated with more than one genotype (35.7%) and with untypable genotypes (34.6%), although the association was not statistically significant. NOSAs were associated with HCV RNA and CLD but not with the presence of cirrhosis and/or hepatocellular carcinoma. On univariate analysis, NOSA reactivity was independently associated with abnormal alanine aminotransferase (p<0.01) and gamma-glutamyltranspeptidase levels (p<0.05). The risk for the presence of NOSAs was 5.1 times higher in anti-HCV subjects than in controls.In the general population the prevalence of NOSAs is higher in anti-HCV positive subjects than in normal or disease controls. Moreover NOSAs are associated with CLD and with a more active disease in terms of alanine aminotransferase activity.
Faculty Opinion on Changes in Medical Education
Authors: Maurice B. Visscher
Journal: JAMA (1974)

<h3>To the Editor.—</h3> A one-page questionnaire was sent to 248 heads of departments of medicine, pediatrics, and surgery in 73 medical schools in operation for ten years or longer; 220 or 89% responded. The first question was whether the department chairman and his colleagues were well satisfied, reasonably well satisfied, or definitely dissatisfied with the basic science preparation of their students. The second was whether there had been improvement, deterioration, or no change in student preparation for clinical studies over the past ten years. The final question asked whether the change was due to more effective or less effective preclinical science instruction, or to changed student attitude, deterioration or improvement (Table). Relatively small numbers, 13% and 14%, respectively, of respondees said they were either well satisfied or definitely dissatisfied. Among those who indicated a change in satisfaction and were reasonably well satisfied, a majority indicated that it was in the
RU486-inducible retrovirus-mediated caspase-3 overexpression is cytotoxic to bcl-xl-expressing myeloma cells in vitro and in vivo
Authors: Jonathan B Pollett, Yuan-Xiao Zhu, Sonal Gandhi, Meena Bali, Esther Masih-Khan, Zhihua Li, Xiao-Yan Wen, A.Keith Stewart
Journal: Molecular Therapy (2003)

The antiapoptotic protein bcl-x(L) is upregulated in a variety of solid tumors and in primary hematologic malignancies such as multiple myeloma. Activated caspase-3 cleaves proteins essential for cell survival, including bcl-x(L). To explore the potential of caspase-3 as a cytotoxic and immunostimulatory molecule in the treatment of malignancy, an RU486-inducible caspase-3 retrovirus was constructed, validated, and used to transduce first 3T3 and subsequently murine myeloma B9BM1 cells (creating the cell line B9BM-C3). After induction, apoptotic cell death of 3T3 and B9BM-C3 cells began by 4 h and was complete by 48 h postinduction, while nontransduced cells remained viable. Annexin V staining demonstrated 43, 76, and 98% apoptotic cell death at 12, 18, and 24 h postinduction. Activation of caspase-3 was evident in induced cells and cell death could be inhibited by the addition of a caspase-3-specific inhibitor. Overexpression of the myeloma-associated oncogene FGFR3, which upregulates bcl-x(L), delayed but did not prevent caspase-3-mediated killing. B9BM-C3 cells formed tumors after subcutaneous injection in mice. Early treatment with RU486 eradicated tumors; however, rechallenge of treated mice failed to demonstrate evidence of immunoprotection. These results indicate that therapeutic attempts to induce caspase-3 in malignant cells may prove useful in the treatment of bcl-x(L)-expressing tumors.
Effects of morphine on glucose homeostasis in the conscious dog.
Authors: P M Radosevich, P E Williams, D B Lacy, J R McRae, K E Steiner, A D Cherrington, W W Lacy, N N Abumrad
Journal: Journal of Clinical Investigation (1984)

This study was designed to assess the effects of morphine sulfate on glucose kinetics and on glucoregulatory hormones in conscious overnight fasted dogs. One group of experiments established a dose-response range. We studied the mechanisms of morphine-induced hyperglycemia in a second group. We also examined the effect of low dose morphine on glucose kinetics independent of changes in the endocrine pancreas by the use of somatostatin plus intraportal replacement of basal insulin and glucagon. In the dose-response group, morphine at 2 mg/h did not change plasma glucose, while morphine at 8 and 16 mg/h caused a hyperglycemic response. In the second group of experiments, morphine (16 mg/h) caused an increase in plasma glucose from a basal 99 +/- 3 to 154 +/- 13 mg/dl (P less than 0.05). Glucose production peaked at 3.9 +/- 0.7 vs. 2.5 +/- 0.2 mg/kg per min basally, while glucose clearance declined to 1.7 +/- 0.2 from 2.5 +/- 0.1 ml/kg per min (both P less than 0.05). Morphine increased epinephrine (1400 +/- 300 vs. 62 +/- 8 pg/ml), norepinephrine (335 +/- 66 vs. 113 +/- 10 pg/ml), glucagon (242 +/- 53 vs. 74 +/- 14 pg/ml), insulin (30 +/- 9 vs. 10 +/- 2 microU/ml), cortisol (11.1 +/- 3.3 vs. 0.9 +/- 0.2 micrograms/dl), and plasma beta-endorphin (88 +/- 27 vs. 23 +/- 6 pg/ml); all values P less than 0.05 compared with basal. These results show that morphine-induced hyperglycemia results from both stimulation of glucose production as well as inhibition of glucose clearance. These changes can be explained by rises in epinephrine, glucagon, and cortisol. These in turn are part of a widespread catabolic response initiated by high dose morphine that involves activation of the sympathetic nervous system, the endocrine pancreas, and the pituitary-adrenal axis. Also, we report the effect of a 2 mg/h infusion of morphine on glucose kinetics when the endocrine pancreas is clamped at basal levels. Under these conditions, morphine exerts a hypoglycemic effect (25% fall in plasma glucose, P less than 0.05) that is due to inhibition of glucose production (by 25-43%, P less than 0.05). The hypoglycemia was independent of detectable changes in insulin, glucagon, epinephrine and cortisol, and was not reversed by concurrent infusion of a slight molar excess of naloxone. Therefore, we postulate that the hypoglycemic effect of morphine results from the interaction of the opiate with non-mu receptors either in the liver or the central nervous system.
Risk Factors for Recent HIV Infection in Uganda
Authors: Jonathan Mermin
Journal: JAMA (2008)

Studies of factors associated with acquiring human immunodeficiency virus (HIV) are often based on prevalence data that might not reflect recent infections.To determine demographic, biological, and behavioral factors for recent HIV infection in Uganda.Nationally representative household survey of cross-sectional design conducted in Uganda from August 2004 through January 2005; data were analyzed until November 2007.There were 11,454 women and 9905 men aged 15 to 59 years who were eligible. Questionnaires were completed for 10,826 women (95%) and 8830 men (89%); of those interviewed, blood specimens were collected for 10,227 women (94%) and 8298 men (94%).Specimens seropositive for HIV were tested with the BED IgG capture-based enzyme immunosorbent assay to identify recent seroconversions (median, 155 days) using normalized optical density of 0.8 and adjustments.Of the 1023 HIV infections with BED results, 172 (17%) tested as recent. In multivariate analysis, risk factors associated with recent HIV infection included female sex (adjusted odds ratio [aOR], 2.4; 95% confidence interval [CI], 1.1-5.2); current marital status (widowed vs never married, aOR, 6.1; 95% CI, 2.8-13.3; divorced vs never married, aOR, 3.0; 95% CI, 1.5-6.1); geographic region (north central Uganda vs central Uganda/Kampala, aOR, 2.6; 95% CI, 1.7-4.1); number of sex partners in past year (> or = 2 compared with none; aOR, 2.9; 95% CI, 1.6-5.5); herpes simplex virus type 2 infection (aOR, 3.9; 95% CI, 2.6-5.8); report of a sexually transmitted disease in the past year (aOR, 1.7; 95% CI, 1.2-2.4); and being an uncircumcised man (aOR, 2.5; 95% CI, 1.1-5.3). Among married participants, recent HIV infection was associated with never using condoms with partners outside of marriage (aOR, 3.2; 95% CI, 1.7-6.1) compared with individuals having no outside partners. The risk of incident HIV infection for married individuals who used condoms with at least 1 outside partner was similar to that of those who did not have any partners outside of marriage (aOR, 1.0; 95% CI, 0.3-2.7).A survey of individuals in Uganda who were tested with an HIV assay used to establish recent infection identified risk factors, which offers opportunities for prevention initiatives.
Discontinuation of evening surgery.
Authors: T Ternent
Journal: BMJ (1972)

My AS double-pocket wallet opens like a book with two inside gussetted pockets, which are able to take the usual hospital letter unfolded.The only item requiring folding is the large A4 hospital report.There are a number of minor advantages with this system.The Department of Health and Social Security and the General Medical Services Crommittee have already given their opinions on the new A4 record size folder for general practice.About 90%0/, of medical records in general practice do not require the large
Drug Evaluation After Marketing
Authors: DENNIS SLONE
Journal: Annals of Internal Medicine (1979)

After marketing, drugs should be evaluated for safety and for efficacy. Present national systems are inadequate for both tasks. Safety can be evaluated by means of nonexperimental research, whereas evaluation of efficacy in a variety of settings representing normal medical practice generally requires experiments, randomized and blinded. Research into safety requires the maintenance of routine, yet flexible, multipurpose data systems, different for established and newly marketed drugs. Ad hoc studies on safety and on efficacy can be mounted more swiftly and economically through the maintenance of "standby" capabilities, in addition to maximal use of resources outside the actual national system.
The effects of topically applied constituents of green tea (caffeine or (−)-epigallocatechin; EGCG) on UV-induced increase in p53 and apoptotic markers in the skin of human volunteers, a pilot study
Authors: Komal M Pandya, Melissa Magliocco, Rama Malaviya, Melissa Yao
Journal: Journal of the American Academy of Dermatology (2004)
Phagocyte-derived lactate stimulates oxygen consumption by Neisseria gonorrhoeae. An unrecognized aspect of the oxygen metabolism of phagocytosis.
Authors: B E Britigan, D Klapper, T Svendsen, M S Cohen
Journal: Journal of Clinical Investigation (1988)

O2 consumption resulting from interaction of Neisseria gonorrhoeae and human neutrophils represents a composite of O2 consumed by the two cell systems. Experiments studying the relative contribution of each system suggested the possibility that gonococci increased their metabolic activity in response to interaction with neutrophils. This hypothesis was confirmed by demonstrating that undifferentiated HL-60 cells, which are unable to undergo a respiratory burst, induce a two- to three-fold increase in gonococcal O2 consumption. Gonococcal capacity to adhere to HL-60 cells did not correlate with extent of metabolic stimulation. Stimulatory activity was demonstrable in cell-free supernatant from neutrophils or HL-60 cells, and increased with duration of incubation. Supernatant applied to a G-15 Sephadex column yielded fractions that stimulated gonococcal O2 consumption. Elution profiles were similar for HL-60 cells, neutrophils, and a stimulatory factor previously isolated from pooled human serum. This stimulatory factor(s) failed to adhere to DEAE or C-18 HPLC columns. Stimulatory activity release from myeloid cells was inhibited by incubation at 4 degrees C or in the presence of NaF, indicating a critical role for glucose metabolism. Lactate, the principal product of resting neutrophil glucose catabolism, was demonstrable in cell-free supernatants after incubation at 37 degrees C. Lactate accumulation was inhibited by NaF and decreased temperature of incubation. Lactate at levels present in cell-free supernatant increased gonococcal O2 consumption twofold and restored stimulatory activity to dialyzed serum. Live, but not heat-killed gonococci eliminated lactate released from neutrophils during phagocytosis. Gonococci are able to utilize host-derived lactate to enhance their rate of O2 metabolism.
Megakaryocyte-matrix interaction within bone marrow: new roles for fibronectin and factor XIII-A
Authors: Alessandro Malara, Cristian Gruppi, Paola Rebuzzini, Livia Visai, Cesare Perotti, Remigio Moratti, Cesare Balduini, Maria Enrica Tira, Alessandra Balduini
Journal: Blood (2010)
Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure
Authors: Ichiro Shiojima, Kaori Sato, Yasuhiro Izumiya, Stephan Schiekofer, Masahiro Ito, Ronglih Liao, Wilson S. Colucci, Kenneth Walsh
Journal: Journal of Clinical Investigation (2005)

Although increased external load initially induces cardiac hypertrophy with preserved contractility, sustained overload eventually leads to heart failure through poorly understood mechanisms. Here we describe a conditional transgenic system in mice characterized by the sequential development of adaptive cardiac hypertrophy with preserved contractility in the acute phase and dilated cardiomyopathy in the chronic phase following the induction of an activated Akt1 gene in the heart. Coronary angiogenesis was enhanced during the acute phase of adaptive cardiac growth but reduced as hearts underwent pathological remodeling. Enhanced angiogenesis in the acute phase was associated with mammalian target of rapamycin–dependent induction of myocardial VEGF and angiopoietin-2 expression. Inhibition of angiogenesis by a decoy VEGF receptor in the acute phase led to decreased capillary density, contractile dysfunction, and impaired cardiac growth. Thus, both heart size and cardiac function are angiogenesis dependent, and disruption of coordinated tissue growth and angiogenesis in the heart contributes to the progression from adaptive cardiac hypertrophy to heart failure.
HIV/hepatitis C co-infection and hepatic fibrosis: looking beyond HIV-associated immune suppression; the contribution of hepatic steatosis and insulin resistance
Authors: S. Bhagani
Journal: Gut (2009)

It is estimated that up to a third of the world’s HIV-infected population is co-infected with hepatitis C (HCV).1 Liver disease contributes significantly to overall morbidity and mortality in HIV-infected individuals.2 The interaction between these two viruses appears to be unidirectional. There is now ample data describing increased risk of hepatic fibrosis progression and faster progression to end-stage liver disease in HIV/HCV co-infected patients compared to HCV mono-infected patients.3 On the other hand there seems to be little effect of HCV on HIV-related progression of immune suppression or response to combination antiretroviral therapies (cART).4 Although, pegylated-interferon alpha and ribavirin combination therapy are standard of care for HCV treatment in this group of patients, sustained viral clearance rates are much lower than those seen in mono-infected patients.5 There is therefore an urgent need to understand and perhaps modify factors that may contribute to fibrosis progression whilst we await the arrival of more effective specifically-targeted antiviral therapies.

HIV-related immune suppression has a profound and complex effect on HCV-associated hepatic inflammation and fibrosis.6 This causes immune dysregulation in response to HCV that in turn promotes inflammation and fibrosis and is also associated with very high HCV viral loads. Furthermore, HIV may have direct or indirect effects on hepatic stallete cells leading to activation and promotion of fibrogenesis.7 Intuitively, cART-related suppression of HIV replication and reversal of immune suppression would thus be expected to slow down fibrosis progression and ultimately the risk of progression to end-stage liver disease. Although studies in the early cART era suggested a beneficial effect …
Duchenne Muscular Dystrophy
Authors: Sheldon Berrol
Journal: JAMA (1976)

<h3>To the Editor.—</h3> Dr Sadjadpour's observation (234:382, 1975) about the causes of toe walking in Duchenne muscular dystrophy certainly requires repeated emphasis and consideration in corrective surgical procedures. Toe walking does, indeed, precede contracture of the heel cords, and the unfortunate use of heel-cord lengthening commonly eliminates kinesiologic postural adjustment of the child, forcing him into braces. If we are to keep the child walking, we cannot eliminate the only compensatory mechanism that he has left. There is certainly good reason to consider iliotibial tract releases and posterial tibial tendon transfers, but there is rarely an indication for heel-cord lengthening procedures in Duchenne muscular dystrophy while the child still ambulates.