tbuckley/cabot-search huggingface dataset:
Islet Cell Antibodies at Diagnosis, But Not Leanness, Relate to a Better Cardiovascular Risk Factor Profile 5 Years After Diagnosis of NIDDM
Authors: Anders Gottsäter, Mubarik Ahmed, Bo Lilja, Per Fernlund, Göran Sundkvist
Journal: Diabetes Care (1996)

OBJECTIVE To evaluate the relationship between islet cell antibodies (ICAs) and the cardiovascular risk profile 5 years after clinical diagnosis of NIDDM. RESEARCH DESIGN AND METHODS Five years after clinical diagnosis, we evaluated blood pressure (BP) and lipids in 17 NIDDM patients with ICA at diagnosis (age 60 ± 4 years) and 133 NIDDM patients without ICA at diagnosis (age 61 ± 1 year). Urinary albumin excretion was evaluated in a subset of 12 NIDDM patients with ICA at diagnosis (age 60 ± 4 years) and 82 NIDDM patients without ICA at diagnosis (age 61 ± 1 year). RESULTS NIDDM patients without ICA showed higher BP (140/86 ± 2/1 mmHg vs. 128/79 ± 3/2 mmHg; P &amp;lt; 0.05), total cholesterol (6.10 ± 0.11 vs. 5.09 ± 0.29 mmol/l; P &amp;lt; 0.01), LDL-to-HDL ratio (3.85 ± 0.14 vs. 2.49 ± 0.18; P &amp;lt; 0.001), and triglycerides (2.58 ± 0.24 vs. 0.90 ± 0.06 mmol/l; P &amp;lt; 0.001), lower HDL cholesterol (1.08 ± 0.03 vs. 1.40 ± 0.08 mmol/l; P &amp;lt; 0.001), and higher urinary albumin excretion (0.16 ± 0.06 vs. 0.01 ± 0.01 g/24 h; P &amp;lt; 0.05) than NIDDM patients with ICA. Among NIDDM patients without ICA, no differences concerning BP or lipids were found between obese and nonobese patients. CONCLUSIONS ICA at diagnosis of NIDDM is a marker of more favorable cardiovascular risk profile 5 years after clinical diagnosis.
Insertion/Deletion Polymorphism in the Angiotensin-Converting Enzyme Gene Affects Heart Weight
Authors: Ken-ichi Nakahara, Satoru Matsushita, Hiroko Matsuoka, Takashi Inamatsu, Masanori Nishinaga, Masahiko Yonawa, Tadashi Aono, Tomio Arai, Yukiyoshi Ezaki, Hajime Orimo
Journal: Circulation (2000)

Angiotensin (Ang) II, a major regulatory factor for left ventricular mass, is generated from Ang I by ACE. ACE levels are associated with an insertion/deletion (I/D) polymorphism in the ACE gene. The ACE polymorphism should result in varied Ang II concentrations and hence affect left ventricular mass. We therefore investigated whether ACE genotype is a predictor of heart weight.From 693 consecutive patients autopsied between 1994 and 1998 in our hospital, patients with valvular disease, myocardial infarction, or cardiomyopathy were excluded. The remaining 443 autopsy patients were the subjects of our study. The heart weight at autopsy was corrected for body surface area. Genomic DNA was purified from the kidney, and ACE genotype was determined by polymerase chain reaction. Heart weight in the DD genotype (249. 9+/-49.9 g/m(2)) was significantly higher than that in the ID (230. 0+/-51.2 g/m(2); P<0.05) and II (226.8+/-49.8 g/m(2); P<0.01) genotypes. Heart weight was also positively related to age (r=0.145, P<0.0001) and coronary stenosis index (r=0.147, P=0.0019). Multiple regression analysis showed that a history of hypertension (P<0.0001), age (P=0.0001), and DD genotype (P=0.0154) were independent predictors of heart weight.ACE genotype predicts cardiac mass; however, it was less effective than epigenetic factors such as hypertension or age.
Three quarters of doctors are confident in GMC regulation, researchers say
Authors: A. Rimmer
Journal: BMJ (2015)

Three quarters of doctors say that they are confident or very confident in the way they are regulated by the UK General Medical Council, a survey has found.

The survey, carried out last year by IFF Research on behalf of the GMC and published by the GMC this week, asked doctors, medical students, patients and the general public, and others about their views of the regulator.1 The survey received 2722 responses from doctors, 267 …
Congenital Familial Cardiac Conduction Defects
Authors: PETER C. GAZES, RODNEY M. CULLER, ELSIE TABER, THADDEUS E. KELLY
Journal: Circulation (1965)

A family in which several members of three separate generations have evidence of congenital familial conduction disturbance has been described. The occurrence of Adams-Stokes seizures with congenital AV block was also noted. From the available information it is clear that the conduction disturbance was congenital in two generations, and the family history suggests that three or four generations were probably involved. The data suggest that in this family the congenital cardiac conduction defects were transmitted as an autosomal dominant trait with incomplete penetrance.
Europe's public health advocates need to have bigger impact, conference hears
Authors: T. Richards
Journal: BMJ (2011)

Europe’s public health professionals are failing to convince their governments that health is a societal “good” and that even in the financial crisis it makes economic sense to increase investment in health promotion and disease prevention, participants at last week’s annual European Health Forum in Bad Gastein, Austria agreed.

Concerns from public health experts about rising rates of obesity, non-communicable disease, and ageing populations are not being translated into effective advocacy, suggested Monica Kosinska, secretary general of the European Public Health Alliance. For example, …
Effect of a new aldose reductase inhibitor, 8′-chloro-2′,3′-dihydrospiro [pyrrolidine-3,6′(5′H)-pyrrolo[1,2,3,-de] [1,4]bezoxazine]-2,5,5′-trione (ADN-138), on delayed motor nerve conduction velocity in streptozotocin-diabetic rats
Authors: Yoshihiro Hirata, Shizuyoshi Fujimori, Kodo Okada
Journal: Metabolism (1988)
Abstract 2540: Evaluation of novel <i>bis</i>-amidine osmium complex as anti-proliferative agents
Authors: Matta Ajay, Leroi V. DeSouza, T. C. Lau, K.W. Michael Siu
Journal: Cancer Research (2011)

Abstract Introduction. Despite improvement in current treatment strategies, including surgery, chemotherapy (CT) and radiotherapy (RT), survival of cancer patients in advanced stages has not improved significantly over the last decade. Organometallic complexes of platinum (cisplatin, carboplatin and oxaliplatin) are in use as chemotherapeutic agents worldwide. However, acquired drug resistance to these platinum complexes has necessitated the search for novel strategies to overcome this limitation, which includes combination therapies and the development of novel platinum or non-platinum complexes as drugs. Methods. Anti-proliferative effects of a bis-amidine complex (Os-Sh1) was determined by measuring the inhibition of cell proliferation using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry-based cell-cycle analysis, annexin V dye binding assay and TUNEL assay in endometrial cancer (Hec1A and KLE) and cervical cancer (HeLa) cells. Results: Cell viability (MTT) assays revealed inhibition of cell proliferation on treatment with the bis-amidine osmium complex (Os-Sh1) in HEC1A, KLE and HeLa cell lines in a dose- (1μM – 50μM) and time-dependent manner (24h – 96h). Cell-cycle analysis showed increased cell death, i.e. the sub-G0 fraction, with G0/G1-arrest and reduction in the G2/M phase of cell cycle on treatment with the Os-Sh1 in these cell lines. Results of annexin V assay suggested apoptosis as the mechanisms of Os-complex induced cell death. Apoptosis was further confirmed by TUNEL assay using flow cytometry analysis. Western blot analysis showed cleavage of caspase 9, caspase 3 and poly-ADP ribose polymerase (PARP), suggesting activation of the intrinsic mitochondrial pathway of apoptosis. Interestingly, Os-Sh1 was more effective in inhibiting cell proliferation at a lower dose and shorter period of time (LD50=20 μM, 48h) in comparison to cisplatin, carboplatin and oxaliplatin in HEC1A, KLE and HeLa cell lines. Conclusions: Our in vitro data clearly demonstrated anti-proliferative effects of a novel bis-amidine osmium complex in endometrial and cervical cancer cells at a lower dose and in shorter period of time in comparison to platinum drugs. Based on these results, we hypothesize that such osmium complex has the potential as effective cytotoxic agents wherein cancer cells acquire resistance to commonly used platinum drugs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2540. doi:10.1158/1538-7445.AM2011-2540
The Interaction of Serum and Arterial Lipoproteins with Elastin of the Arterial Intima and Its Role in the Lipid Accumulation in Atherosclerotic Plaques
Authors: Dieter M. Kramsch, William Hollander
Journal: Journal of Clinical Investigation (1973)

Arterial elastin appears to be a proteinlipid complex with the lipid component being bound to elastin peptide groups. In atherosclerotic lesions the lipid content of elastin increases progressively with increasing severity of atherosclerosis. The increases in the lipid content of plaque elastin are mainly due to large increases in cholesterol with about 80% of the cholesterol being cholesterol ester. This deposition of cholesterol in elastin accounts for a substantial part of the total cholesterol accumulation in atherosclerotic lesions of all stages. The present in vitro study suggests that the mechanism involved in the deposition of lipids in arterial elastin may be an interaction of the elastin protein with serum or arterial low density or very low density lipoproteins (LDL and VLDL) resulting in a transfer of lipids, but not of lipoprotein protein to the elastin. No significant lipid transfer occurred from the high density lipoproteins or chylomicrons. The amount of lipid taken up by plaque elastin was strikingly higher than by normal elastin and consisted mainly of cholesterol with over 80% of the cholesterol being cholesterol ester. The precondition for the lipid accumulation in plaque elastin appeared to be an altered amino acid composition of the elastin protein consisting of an increase in polar amino acids and a reduction in cross-linking amino acids. Subsequent treatment of lipoprotein-incubated arterial elastin with hot alkali and apolipoproteins did not reverse the binding of lipoprotein lipid to diseased elastin.
Control of mouse hepatocyte proliferation and ploidy by p53 and p53ser246 mutationin vivo
Authors: Li Yin, Nader Ghebranious, Subhendu Chakraborty, Christine E. Sheehan, Zoran Ilic, Stewart Sell
Journal: Hepatology (1998)

The effect of expression of the p53 gene, in the presence or absence of the p53ser246 mutation (p53*), on ploidization (image cytometry), proliferation (expression of proliferating cell nuclear antigen and radioactive thymidine histoautoradiography), and apoptosis (in situ detection of DNA fragments) is determined in hepatocytes of p53-null and p53-transgenic mice. The mouse p53ser246 mutation is equivalent to the p53ser249 mutation found in human hepatomas associated with hepatitis B virus infection and aflatoxin exposure. The hepatocytes of heterozygous or homozygous p53-knockout mice (p53+/−; p53−/−), as well as knockout mice expressing one allele of p53ser246 (p53+/−, p53*; p53−/−, p53*), do not undergo normal polyploidization with aging and show an increase in the number of cycling (G1-, S-, and M-phase) cells. In addition, p53ser246-transgenic mice (p53+/+, p53*; p53+/−, p53*; and p53−/−, p53*) have a greatly increased number of hepatocytes in the G1 phase. No differences in rates of apoptotic hepatocytes are found among any of the mouse groups studied, so the increased proliferation results in a hyperplasia manifested by a increased number of small periportal cells. We conclude that loss of p53 removes blocks in the cell cycle, leading to increased proliferation, whereas expression of the p53ser246 mutation stimulates G0to G1and/or M to G1transition of hepatocytes. Increased proliferation of hepatocytes, combined with no concomitant increase in apoptosis, may in part explain the enhanced development of hepatocellular carcinomas in p53-knockout and p53-transgenic mice exposed to aflatoxin.
Some experience with deglycyrrhizinated liquorice in the treatment of gastric and duodenal ulcers with special reference to its spasmolytic effect.
Authors: S N Tewari, F C Trembalowicz
Journal: Gut (1968)

Some experience with deglycyrrhizinated liquorice in the treatment of gastric and duodenal ulcers with special reference to its spasmolytic effect
Poly(amido amine)-based multilayered thin films on 2D and 3D supports for surface-mediated cell transfection
Authors: Sry D Hujaya, Giulia Marchioli, Karin Roelofs, Aart A van Apeldoorn, Lorenzo Moroni, Marcel Karperien, Jos M J Paulusse, Johan F J Engbersen
Journal: Journal of Controlled Release (2015)
The Medical Traveler
Authors: John Lister
Journal: New England Journal of Medicine (1957)

THE medical traveler is no new phenomenon. Long ago Paracelsus, who was born near Zurich, said that a doctor must be a traveler because he must inquire of the world. He himself set out on his travels in 1513. His tour lasted twelve years and first took him to Bologna and Padua in Italy. Thence he went to France, Spain, the Netherlands and Sweden and later journeyed east to Turkey and Russia. Thomas Linacre, who became the first president of the Royal College of Physicians in 1551, graduated at Oxford and then went to Italy to travel. John Caius of . . .
What's the evidence that NICE guidance has been implemented?: More recent data on NICE implementation show different picture
Authors: Michael Rawlins, Andrew Dillon
Journal: BMJ (2005)

This week in the BMJ for the paper by Walsh et al are offered the conclusion that investment in intermediate care in community hospitals may be more cost effective than financing nurse led care for post-acute patients in acute hospitals. 1 2But the study itself, which confirms existing evidence on the costs of nurse led intermediate care in acute settings, 3 4 tackles neither the effect nor the cost of intermediate care in community hospitals.How then can such a conclusion be drawn?Walsh et al do not make this assertion.The author of the comment offers no support.Our own review of the evidence on nurse led intermediate care found no quality evidence for either the effect or cost of intermediate care in community settings. 5 The BMJ has been at the forefront of setting standards for the reporting of primary research.However, the editors must be aware that many readers simply pick up a take home message from comment, like this, 1 in the journal.
Theme Issue on Medical Education
Authors: Robert M. Golub
Journal: JAMA (2005)

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
Potassium Channel KIR4.1 as an Immune Target in Multiple Sclerosis
Authors: Rajneesh Srivastava, Muhammad Aslam, Sudhakar Reddy Kalluri, Lucas Schirmer, Dorothea Buck, Björn Tackenberg, Veit Rothhammer, Andrew Chan, Ralf Gold, Achim Berthele, Jeffrey L. Bennett, Thomas Korn, Bernhard Hemmer
Journal: New England Journal of Medicine (2012)

Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system. Many findings suggest that the disease has an autoimmune pathogenesis; the target of the immune response is not yet known.We screened serum IgG from persons with multiple sclerosis to identify antibodies that are capable of binding to brain tissue and observed specific binding of IgG to glial cells in a subgroup of patients. Using a proteomic approach focusing on membrane proteins, we identified the ATP-sensitive inward rectifying potassium channel KIR4.1 as the target of the IgG antibodies. We used a multifaceted validation strategy to confirm KIR4.1 as a target of the autoantibody response in multiple sclerosis and to show its potential pathogenicity in vivo.Serum levels of antibodies to KIR4.1 were higher in persons with multiple sclerosis than in persons with other neurologic diseases and healthy donors (P<0.001 for both comparisons). We replicated this finding in two independent groups of persons with multiple sclerosis or other neurologic diseases (P<0.001 for both comparisons). Analysis of the combined data sets indicated the presence of serum antibodies to KIR4.1 in 186 of 397 persons with multiple sclerosis (46.9%), in 3 of 329 persons with other neurologic diseases (0.9%), and in none of the 59 healthy donors. These antibodies bound to the first extracellular loop of KIR4.1. Injection of KIR4.1 serum IgG into the cisternae magnae of mice led to a profound loss of KIR4.1 expression, altered expression of glial fibrillary acidic protein in astrocytes, and activation of the complement cascade at sites of KIR4.1 expression in the cerebellum.KIR4.1 is a target of the autoantibody response in a subgroup of persons with multiple sclerosis. (Funded by the German Ministry for Education and Research and Deutsche Forschungsgemeinschaft.).
Treatment of Traumatized Victims of War and Torture: A Randomized Controlled Comparison of Narrative Exposure Therapy and Stress Inoculation Training
Authors: D. Hensel-Dittmann, M. Schauer, M. Ruf, C. Catani, M. Odenwald, T. Elbert, F. Neuner
Journal: Psychotherapy and Psychosomatics (2011)

&lt;i&gt;Background:&lt;/i&gt; The aim of the present randomized controlled trial was to compare the outcome of 2 active treatments for posttraumatic stress disorder (PTSD) as a consequence of war and torture: narrative exposure therapy (NET) and stress inoculation training (SIT). &lt;i&gt;Methods:&lt;/i&gt; Twenty-eight PTSD patients who had experienced war and torture, most of them asylum seekers, received 10 treatment sessions of either NET or SIT at the Outpatient Clinic for Refugees, University of Konstanz, Germany. Posttests were carried out 4 weeks after treatment, and follow-up tests were performed 6 months and 1 year after treatment. The main outcome measure was the PTSD severity score according to the Clinician-Administered PTSD Scale (CAPS) at each time point. &lt;i&gt;Results:&lt;/i&gt; A significant reduction in PTSD severity was found for NET, but not for SIT. A symptom reduction in the NET group occurred between pretest and the 6-month follow-up examination, the effect size being &lt;i&gt;d&lt;/i&gt; = 1.42 (for SIT: &lt;i&gt;d&lt;/i&gt; = 0.12), and between pretest and the 1-year follow-up, the effect size being &lt;i&gt;d&lt;/i&gt; = 1.59 (for SIT: &lt;i&gt;d&lt;/i&gt; = 0.19). The rates and scores of major depression and other comorbid disorders did not decrease significantly over time in either of the 2 treatment groups. &lt;i&gt;Conclusions:&lt;/i&gt; The results indicate that exposure treatments like NET lead to a significant PTSD symptom reduction even in severely traumatized refugees and asylum seekers.
Obstetrics in General Practice
Authors: P. D. Arnold, N. Gillman, J. Nickson, J. A. Richards
Journal: BMJ (1963)

<h3>Introduction</h3> Approximately 5% of patients with stable angina have disease of the left main stem (LMS). Three-year survival in patients with &gt;50% LMS stenosis may be as low as 50%. Single photon emission tomography (SPECT) fails to detect ischaemia in up to 15% of LMS stenoses, and identification of the “classical” pattern of both left anterior descending (LAD) and circumflex (LCx) coronary territory ischaemia is lower still. To date, the utility of cardiovascular magnetic resonance (CMR) perfusion in LMS disease is poorly established. The CE-MARC study was a prospective study of 752 patients with suspected coronary artery disease, enrolled to undergo CMR, SPECT and x-ray coronary angiography; we assessed the diagnostic performance of SPECT and CMR to detect LMS disease. <h3>Methods</h3> All patients with LMS disease ≥50% on quantitative angiography were identified from the CE-MARC study. All patients had undergone adenosine stress perfusion by CMR and SPECT and also invasive x-ray angiography.1 We compared detection rates for visual perfusion analysis from both the CMR and SPECT perfusion studies in patients with ≥50% and ≥70% LMS stenosis on angiography. <h3>Results</h3> Of 23 patients in the CE-MARC cohort with LMS stenosis ≥50%, one patient could not be analysed. CMR identified evidence of inducible perfusion defects in 18/22 (82%) of the LMS group; SPECT identified 13/22 (59%). For CMR and SPECT respectively, inducible perfusion defects were found in both LAD and LCx territories for 6/18 (33%) and 2/13 (15%). Only one patient had normal perfusion analyses (false negative) for both CMR and SPECT. Of 11 patients with ≥70% LMS stenosis, 10 (91%) had inducible perfusion defects with CMR vs 5 (45%) with SPECT. Six (55%) vs 2 (18%) had a LAD and LCx disease pattern. Perfusion abnormalities were detected with similar frequency in ≥50% and ≥70% groups by both CMR (p=0.64) and SPECT (p=0.49). Abstract 088 figures 1 and 2 summarise the detection rate of CMR and SPECT in LMS disease in the ≥50% and ≥70% LMS groups respectively. <h3>Conclusions</h3> CMR stress perfusion imaging identifies ischaemia in a higher proportion of patients with significant LMS disease than SPECT, and identifies a “classical” LMS pattern with higher frequency. Perfusion abnormalities are detected with similar frequency in patients with ≥50% and ≥70% LMS stenosis.