tbuckley/cabot-search huggingface dataset:
Insulin Resistance Associated With Compensatory Hyperinsulinemia as an Independent Risk Factor for Vasospastic Angina
Authors: Kazuya Shinozaki, Masaaki Suzuki, Motoyoshi Ikebuchi, Hiroshi Takaki, Yasushi Hara, Motoo Tsushima, Yutaka Harano
Journal: Circulation (1995)

It is generally believed that coronary artery spasm plays an important role in the progression of obstructive coronary artery disease. Since insulin resistance together with hyperinsulinemia plays an important role in the pathogenesis of coronary atherosclerosis, we investigated the association of hyperinsulinemia and insulin resistance with vasospastic angina (VAP).The study population consisted of 60 patients with VAP and 42 control subjects (62 subjects with normal glucose tolerance and 40 with impaired glucose tolerance). Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method for nondiabetic, normotensive, nonobese subjects (16 control subjects, 16 obstructive coronary artery disease patients, and 16 VAP patients). Compared with the control group, the 2-hour insulin area (area under the plasma insulin concentration-time curve) during a 75-g oral glucose tolerance test was significantly higher in both VAP groups with normal and impaired glucose tolerance. A high frequency of vasospastic angina was observed in subjects with clustered risk factors for insulin resistance syndrome, suggesting a close association of VAP with this syndrome. In stepwise discriminant analysis, the 2-hour insulin area was significantly associated with VAP independent of other risk factors. SSPG level in VAP was about twofold over control, indicating the presence of insulin resistance in patients with VAP. However, no differences were found between patients with VAP and obstructive coronary artery disease with respect to mean SSPG level.SSPG level was significantly elevated in patients with VAP and obstructive coronary artery disease compared with control subjects. This indicates that hyperinsulinemia is secondary to insulin resistance, both of which are thought to play important roles as risk factors for VAP in the early atheromatous lesion and in the future development of occlusive lesions when chronically present.
Small-for-Gestational-Age Infants and Risk of Fetal Death in Subsequent Pregnancies
Authors: Jun Zhang, Mark A. Klebanoff
Journal: New England Journal of Medicine (2004)

One of the triumphs of modern obstetrics has been the dramatic reduction in late fetal mortality (defined as the rate of antepartum or intrapartum fetal death at 20 weeks of gestation or later) in the developed world during the second half of the 20th century. The reduction can be attributed to better access to vastly improved antepartum and intrapartum care; improved antepartum fetal surveillance; the virtual elimination of Rh isoimmunization; and the revolution in neonatal care that enabled obstetricians to deliver a fetus, particularly one remote from term, when its health was in jeopardy. The fetal mortality rate in the . . .
Expression pattern of the bullous pemphigoid-180 antigen in normal and neoplastic epithelia
Authors: J.A. FAIRLKY, P.W. HEINTZ, M. NEUBURG, L.A. DIAZ, G.J. GIUDICE
Journal: British Journal of Dermatology (1995)

Journal Article Expression pattern of the bullous pemphigoid‐180 antigen in normal and neoplastic epithelia Get access J.A. FAIRLKY, J.A. FAIRLKY Departments of Dermatology and Biochmistry, MEDICAL College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar P.W. HEINTZ, P.W. HEINTZ Departments of Dermatology and Biochmistry, MEDICAL College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar M. NEUBURG, M. NEUBURG Departments of Dermatology and Biochmistry, MEDICAL College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar L.A. DIAZ, L.A. DIAZ Departments of Dermatology and Biochmistry, MEDICAL College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar G.J. GIUDICE G.J. GIUDICE Departments of Dermatology and Biochmistry, MEDICAL College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 133, Issue 3, 1 September 1995, Pages 385–391, https://doi.org/10.1111/j.1365-2133.1995.tb02665.x Published: 01 September 1995 Article history Accepted: 01 November 1994 Published: 01 September 1995
How Does Glucose Insulin Potassium Improve Hemodynamic Performance?
Authors: Aaron M. Ranasinghe, Christopher J. McCabe, David W. Quinn, Sally R. James, Domenico Pagano, Jayne A. Franklyn, Robert S. Bonser
Journal: Circulation (2006)

Glucose insulin potassium (GIK) improves hemodynamic performance after coronary artery surgery (CABG). We investigated whether this is associated with changes in gene expression of beta1-adrenergic receptor (ADRB1) or other calcium handling proteins.During a randomized double-blind placebo-controlled trial, 48 patients undergoing on-pump CABG, allocated to receive pre-ischemic placebo (5% dextrose) or GIK (40% dextrose, K+ 100 mmol.L(-1), insulin 70 u.L(-1); 0.75 mL.kg(-1).h(-1)) continued for 6 hours after the removal of the aortic cross-clamp (AXC), underwent left ventricular biopsy for analysis of specific mRNAs immediately before AXC, before release of AXC, and 10 minutes after reperfusion (placebo n=24, GIK n=24). GIK or placebo was infused for a mean of 79+/-21 minutes or 79+/-18 minutes pre-ischemia respectively. Serial hemodynamic measurements were performed. Biopsy samples were snap-frozen and stored at -80 degrees C, mRNA was extracted and TaqMan real-time polymerase chain reaction was performed to investigate expression of ADRB1, sarcoplasmic reticulum Ca-ATPase (SERCA2a), and phospholamban (PLB). GIK significantly increased cardiac index versus placebo (P=0.037). TaqMan reverse-transcriptase polymerase chain reaction showed significantly greater ADRB1 mRNA expression at all time points (4.9-fold, 7.4-fold, and 15.6-fold increase, respectively; P<0.001), significantly greater SERCA2a mRNA expression after reperfusion (13.2-fold; P<0.001), and increased PLB mRNA expression at pre-ischemia and reperfusion (P<0.001 for both time-points) in GIK groups versus placebo.The beneficial hemodynamic effects of GIK therapy are associated with increased ADRB1 and SERCA2a mRNA expression. Further work is therefore warranted to investigate these mRNA effects at the protein level.
Does Positive Hepatobiliary Scan in Cholecystitis Stay Positive, and for How Long?
Authors: JASON LIU, ISMAEL MENA, STEVE McCARTNEY
Journal: Clinical Nuclear Medicine (1986)

A prospective study of 11 patients who had undergone two sequential hepatobiliary scans prior to surgery demonstrated that initially positive scans could be due to acute cholecystitis, or chronic cholecystitis with exacerbation. A second hepatobiliary scan performed four to five days later differentiated acute from chronic cholecystitis. All five patients with surgery-proven acute cholecystitis remained hepatobiliary-positive, while patients with surgery-proven chronic cholecystitis reverted back to negative hepatobiliary scans if the second hepatobiliary scan was done properly.
Narrative vs Evidence-Based Medicine—And, Not Or
Authors: Zachary F. Meisel, Jason Karlawish
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Terminology for early pregnancy loss must be changed
Authors: D. J R Hutchon, S. Cooper
Journal: BMJ (1998)

Editorial p 1028

EDITOR —Miscarriage is distressing, giving rise to a range of emotional experiences for both the woman and her partner. The aim of medical and nursing staff must be to reduce distress, but the distress may be increased by staff taking the wrong approach or using inappropriate terminology. The lay public tend to interpret an “abortion” as a termination of pregnancy.1 We advise that when women are counselled about miscarriage the word abortion should be avoided.

The Royal College of Obstetricians and Gynaecologists has …
Modification by Suppressor Cells and Serum Factors of the Cell-Mediated Immune Response in Experimental Pyelonephritis
Authors: Thomas Miller, Lesley Scott, Elaine Stewart, Derek North
Journal: Journal of Clinical Investigation (1978)

A marked suppression of the thymusderived (T)-lymphocyte response to concanavalin A has been demonstrated in vitro during renal infection. Suppression of the T-lymphocyte response in vitro was seen as early as 2 h after the induction of renal infection, but maximum suppression was found 24-72 h later. A population of suppressor cells in the splenic lymphocyte population, generated during the host's response to infection, contributed to the depressed lymphocyte response. Removal of suppressor cells restored the mitogenic responsiveness of the remaining splenic lymphocytes. Conversely, in co-culture experiments, a suppressor cell present in the splenic lymphocyte population of pyelonephritic animals was shown to be capable of suppressing the mitogenic responsiveness of normal splenic lymphocytes. Significantly reduced host vs. graft responses by the pyelonephritic animals confirmed, in vivo, the depression of cell-mediated immune mechanisms. An additional suppressive factor was found in the serum of pyelonephritic animals which depressed in vitro the mitogenic responsiveness of splenic lymphocytes from normal animals. Support for the suppressive role of this serum factor was found when splenic lymphocytes from pyelonephritic animals were tested in vivo in the absence of homolgous serum (graft vs. host). Under these conditions, the lymphocytes showed an enhanced reaction compared with lymphocytes from normal animals. The presence of a suppressor cell population and a serum factor, both capable of depressing cell-mediated mechanisms, may be major factors contributing to the establishment of infection in the kidney.
Induction of Cellular Immunity to Coccidioides immitis After Sensitization with Dinitrochlorobenzene
Authors: WARNER M. BURCH
Journal: Annals of Internal Medicine (1982)

A patient had progressive disseminated coccidioidomycosis and depressed cellular immunity to Coccidiodes immitis. He developed a large nasal coccidioidal lesion that was unresponsive to conventional therapy. Application of dinitrochlorobenzene (DNCB) to the nasal lesion was temporally associated with resolution of the lesion and stabilization of the systemic disease. In addition, DNCB application was followed by signs of cellular immunity to C. immitis. These included development of delayed cutaneous hypersensitivity to coccidioidin, as well as lymphokine production and lymphoproliferative responses to coccidioidin. Similar forms of DNCB immunotherapy may prove useful in other patients with fungal disease and depressed cellular immunity.
Increased prebeta-high density lipoprotein, apolipoprotein AI, and phospholipid in mice expressing the human phospholipid transfer protein and human apolipoprotein AI transgenes.
Authors: X Jiang, O L Francone, C Bruce, R Milne, J Mar, A Walsh, J L Breslow, A R Tall
Journal: Journal of Clinical Investigation (1996)

Human plasma phospholipid transfer protein (PLTP) circulates bound to high density lipoprotein (HDL) and mediates both net transfer and exchange of phospholipids between different lipoproteins. However, its overall function in lipoprotein metabolism is unknown. To assess the effects of increased plasma levels of PLTP, human PLTP transgenic mice were established using the human PLTP gene driven by its natural promoter. One line of PLTP transgenic mice with moderate expression of PLTP mRNA and protein was obtained. The order of human PLTP mRNA expression in tissues was: liver, kidney, brain, small intestine > lung > spleen > heart, adipose tissue. Western blotting using a human PLTP monoclonal antibody revealed authentic human PLTP (Mr 80 kD) in plasma. Plasma PLTP activity was increased by 29% in PLTP transgenic mice. However, plasma lipoprotein analysis, comparing PLTP transgenic mice to control littermates, revealed no significant changes in the plasma lipoprotein lipids or apolipoproteins. Since previous studies have shown that human cholesteryl ester transfer protein and lecithin:cholesterol acyltransferase only function optimally in human apoAI transgenic mice, the human PLTP transgenic mice were cross-bred with human apoAI transgenic mice. In the human apoAI transgenic background, PLTP expression resulted in increased PLTP activity (47%), HDL phospholipid (26%), cholesteryl ester (24%), free cholesterol (37%), and apoAI (22%). There was a major increase of apoAI in prebeta-HDL (56%) and a small increase in alpha-HDL (14%). The size distribution of HDL particles within alpha- and prebeta-migrating species was not changed. The results suggest that PLTP increases the influx of phospholipid and secondarily cholesterol into HDL, leading to an increase in potentially antiatherogenic prebeta-HDL particles.
Malignant Diseases of Infancy, Childhood and Adolescence
Authors: Ruth Andrea Seeler
Journal: JAMA (1984)

This entirely rewritten second edition provides the reader with an up-to-date, authoritative, readable text for the field of oncology as seen in pediatrics. The second edition has eight contributors, which provides indepth coverage for all important clinical aspects of pediatric oncology. The first eight chapters are devoted to the important broad-based concepts of malignancy, chemotherapy, radiation therapy, psychological impact, and epidemiology. These chapters are important but are frequently skipped by readers who simply look up a particular malignant neoplasm in the index and focus all of their attention there. The chapter dealing with oncological emergencies is a complete litany of what can and does happen even during successful therapy. This should be read by all who have a child with a malignant neoplasm in their practice. The brief and well-written chapter dealing with dental problems should not be overlooked. The inclusion of a chapter on the late effects of cancer
Three Bs, please: More academic excellence, please
Authors: David McKean
Journal: BMJ (2006)

Evidence based diagnosis We may need to be open to new ideasEditor-If evidence based diagnosis is still in the dark ages, as Delamothe writes, 1 then so is evidence based treatment.The doctor's job is to choose the right treatment.If the diagnosis is wrong then the treatment will be wrong.Inaccurate diagnoses will also affect clinical trials.A treatment may be "evidence based" because it has worked in a published study, but some patients who would have responded might have been left out because of diagnostic inaccuracy while some patients with no prospect of responding might have been included incorrectly. 2vidence based diagnosis is about convincing others using shared rules of evidence that a diagnosis (and its implications in terms of treatment) should be accepted by others.Evidence is gathered from the individual and from groups of patients. 3Evidence based diagnosis means specifying the individual's facts in addition to pointing to facts relating to that diagnosis in the literature. 4ayes's theorem uses unconditional initial prior probabilities.Diagnostic leads are based on conditional probabilities and are used to initiate diagnostic thought processes. 4owever, closely related theorems can be used to interpret diagnostic leads, which allow doctors to reason with diagnostic evidence in a more familiar way, 3 thus reducing misunderstandings. 5So to improve evidence based diagnosis we also need to collect better data on diagnostic leads.The published evidence given for a diagnosis and any related actions cannot realistically be assembled when actually seeing a patient.A draft evidence based rationale might be prepared in advance.It would have to be capable of being accessed in seconds to provide evidence in support of a suspected diagnosis and decision arrived at by using kindness, imagination, and common sense.It could be put into context by inserting the patient's details into the draft evidence summoned up from a computer.If we are to make progress and allow evidence based diagnosis to emerge from the dark ages then in addition to doing more of the same, we may also have to be receptive to new ideas.
Insulin resistance of glucose uptake in skeletal muscle cannot be ameliorated by enhancing endothelium-dependent blood flow in obesity.
Authors: H Laine, H Yki-Jarvinen, O Kirvela, T Tolvanen, M Raitakari, O Solin, M Haaparanta, J Knuuti, P Nuutila
Journal: Journal of Clinical Investigation (1998)

We tested the hypothesis that endothelium-dependent vasodilatation is a determinant of insulin resistance of skeletal muscle glucose uptake in human obesity. Eight obese (age 26+/-1 yr, body mass index 37+/-1 kg/m2) and seven nonobese males (25+/-2 yr, 23+/-1 kg/m2) received an infusion of bradykinin into the femoral artery of one leg under intravenously maintained normoglycemic hyperinsulinemic conditions. Blood flow was measured simultaneously in the bradykinin and insulin- and the insulin-infused leg before and during hyperinsulinemia using [15O]-labeled water ([15O]H2O) and positron emission tomography (PET). Glucose uptake was quantitated immediately thereafter in both legs using [18F]- fluoro-deoxy-glucose ([18F]FDG) and PET. Whole body insulin-stimulated glucose uptake was lower in the obese (507+/-47 mumol/m2 . min) than the nonobese (1205+/-97 micromol/m2 . min, P < 0.001) subjects. Muscle glucose uptake in the insulin-infused leg was 66% lower in the obese (19+/-4 micromol/kg muscle . min) than in the nonobese (56+/-9 micromol/kg muscle . min, P < 0.005) subjects. Bradykinin increased blood flow during hyperinsulinemia in the obese subjects by 75% from 16+/-1 to 28+/-4 ml/kg muscle . min (P < 0.05), and in the normal subjects by 65% from 23+/-3 to 38+/-9 ml/kg muscle . min (P < 0.05). However, this flow increase required twice as much bradykinin in the obese (51+/-3 microg over 100 min) than in the normal (25+/-1 mug, P < 0.001) subjects. In the obese subjects, blood flow in the bradykinin and insulin-infused leg (28+/-4 ml/kg muscle . min) was comparable to that in the insulin-infused leg in the normal subjects during hyperinsulinemia (24+/-5 ml/kg muscle . min). Despite this, insulin-stimulated glucose uptake remained unchanged in the bradykinin and insulin-infused leg (18+/-4 mumol/kg . min) compared with the insulin-infused leg (19+/-4 micromol/kg muscle . min) in the obese subjects. Insulin-stimulated glucose uptake also was unaffected by bradykinin in the normal subjects (58+/-10 vs. 56+/-9 micromol/kg . min, bradykinin and insulin versus insulin leg). These data demonstrate that obesity is characterized by two distinct defects in skeletal muscle: insulin resistance of cellular glucose extraction and impaired endothelium-dependent vasodilatation. Since a 75% increase in blood flow does not alter glucose uptake, insulin resistance in obesity cannot be overcome by normalizing muscle blood flow.
Application of liposomes for cancer metastasis
Authors: Naoto Oku, Chieko Koike, Yoshihiro Tokudome, Shoji Okada, Naoyuki Nishikawa, Hideo Tsukada, Makoto Kiso, Akira Hasegawa, Hideki Fujii, Jun Murata, Ikuo Saiki
Journal: Advanced Drug Delivery Reviews (1997)
180 RECIPIENT'S VITAMIN D RECEPTOR GENETIC POLYMORPHISMS IDENTIFY HCV POSITIVE LIVER TRANSPLANTED PATIENTS AT LOWER RISK OF GRAFT FIBROSIS PROGRESSION DUE TO RECURRENT HEPATITIS C
Authors: D. Bitetto, E. Falleti, S. Cmet, A. Cussigh, E. Fornasiere, C. Avellini, C. Fabris, M. Pirisi, P. Toniutto
Journal: Journal of Hepatology (2012)
The Hot Clot Sign: A New Finding in Deep Venous Thrombosis on Bone Scintigraphy
Authors: Anita Moallem
Journal: Clinical Nuclear Medicine (1991)

Focal Tc-99m MDP uptake on bone scanning in regions of deep venous thrombosis (DVT) is reported in two patients with documented DVT. It is speculated that this uptake may be related to localized calcification or ossification, which is occasionally observed on radiographs of patients with chronic DVT.
Inhibition of pentagastrin-stimulated acid secretion after subcutaneous administration of a new somatostatin analogue.
Authors: I Whitehouse, C Beglinger, G Ruttimann, K Gyr
Journal: Gut (1986)

Somatostatin, a peptide present in hypothalamus, gastric mucosa, and pancreas suppresses several gastrointestinal functions. Its short half life has prevented clinical use. We have therefore evaluated the effect of subcutaneous administration of a new synthetic somatostatin analogue, in comparison with a placebo, on pentagastrin stimulated acid secretion in six healthy volunteers. On different days, acid secretion was measured continuously, after a basal 30 minutes, for six hours during 3 micrograms/kg/h of intravenous pentagastrin. Acid secretion was measured with a marker technique (0.1% phenol red) to correct for duodenal volume loss. Blood was drawn in regular intervals to measure plasma somatostatin concentrations by radio immunoassay. One hour after starting the pentagastrin infusion, a single subcutaneous injection of either 100 micrograms somatostatin analogue, or placebo (isotonic saline) was given. In a follow up study, somatostatin was given subcutaneously in a dose of 200 micrograms. No difference in efficacy was observed between the two doses. A single subcutaneous injection of the somatostatin analogue significantly suppressed acid secretion for five hours (p less than 0.01). Maximal inhibition was approximately 75%. Mean elimination half life of the analogue was approximately 80 minutes. We suggest that the new somatostatin analogue might be useful for clinical use.