tbuckley/cabot-search huggingface dataset:
Do we know how to use steroids in acute severe colitis?
Authors: M. S. Islam, S. Grainger
Journal: Gut (2011)

<h3>Introduction</h3> Options in the treatment of acute severe ulcerative colitis have broadened with the recognition of the value of ciclosporin and infliximab, but corticosteroids remain the first-line treatment for active ulcerative colitis (UC) more than 50 years after the publication of the trial showing their benefit. But a standard regimen for drug, dose and duration has not been established. Patient intolerance, the side effects of corticosteroids – especially infection, and the availability of alternative drugs emphasises the importance of using corticosteroids in the most effective way. <h3>Methods</h3> To assess variation in UK practice in preparation for a study to determine the optimal regimen for the use of corticosteroids in acute severe colitis. In January 2010, the authors surveyed all members of the inflammatory bowel disease section of the British Society of Gastroenterology on their use of corticosteroids in a typical patient with acute severe colitis, as defined by Truelove and Witts. <h3>Results</h3> Responses were obtained from 94 hospitals out of the 174 Trusts/Health Boards treating acute severe UC in the UK. <h3>Initial corticosteroid</h3> 76% of units use intravenous hydrocortisone 100 mg, 6 h as the initial regimen. 15% of units use a different regimen for intravenous hydrocortisone. Intravenous methyl-prednisolone or dexamethasone is preferred by 9%. <h3>Transfer to oral corticosteroid</h3> 88% of units start prednisolone 40 mg daily when changing from intravenous administration. Possibly suboptimal dosing with prednisolone 30 mg daily is used by 4% units and 6% units use more than 40 mg when changing to oral steroid. Weight adjusted dosing (1 mg/kg) is used in only 2% of units. <h3>Tapering of oral prednisolone</h3> 47% of units prescribe oral steroids for 8 weeks, but more than 40% taper over a longer period, up to 12 weeks. The remainder withdraws steroids in less than 8 weeks. The commonest interval for dose reduction was 5 mg per week but 60% of units used different doses or intervals. <h3>Total exposure to oral steroids</h3> The total dose of prednisolone differed between units by more than threefold. <h3>Conclusion</h3> The authors did not ask units to report their success rates. If efficacy is similar, then some units are exposing their patients to three times more corticosteroid than necessary, with the potential for more side effects and risks. Alternatively, if greater doses are more effective some units are denying their patients optimal treatment. In the era of evidence-based medicine the time is right for a formal investigation of dose and duration of corticosteroid in the treatment of acute severe colitis.
Controversy Concerning the Cutoff Value for Depth of Submucosal Invasion after Endoscopic Mucosal Resection of Early Gastric Cancer
Authors: J. Cho, Y. Kim, I. Jung, C. Ryu, M. Lee, C. Shim, S. Jin
Journal: Endoscopy (2006)

We read with interest the recent article by the Endoscopic Classification Review Group [1]. Endoscopic mucosal resection (EMR) has become widely accepted as a curative treatment for mucosal cancer of the stomach [2], and recent advances in EMR techniques are extremely remarkable. A new endoscopic procedure, using multiple accessories, provides an en bloc specimen and therefore allows precise histologic staging.
Influence of setting on unattended respiratory monitoring in the sleep apnoea/hypopnoea syndrome
Authors: P. Lloberes, G. Sampol, G. Levy, D. Aristizabal, T. Sagales, M. De la Calzada, A. Roca, I. Cañas, F. Morell
Journal: European Respiratory Journal (2001)

The high demand for full polysomnography and the better quality of sleep at home are the main reasons for performing home sleep studies. Home respiratory monitoring has been evaluated in several studies, but the influence of setting on the results of unattended respiratory monitoring has not been assessed to date. Unattended monitoring of respiratory variables at home and in the sleep laboratory was conducted in 35 consecutive patients with suspected sleep apnoea/hypopnoea syndrome. Respiratory variables during sleep, rate of successful studies and patient preference were compared. The data acquisition failure rate was 2.8% in the sleep laboratory and 5.7% at home. The mean difference between apnoea/hypopnoea indices (AHI) obtained from home and laboratory studies was −0.21±8 (95% confidence interval 3.27–2.84). Using the method comparison approach of Bland and Altman, the limits of agreement of the mean difference between AHI home and AHI laboratory were −16.7 and 17.1. No difference was observed between the studies in time spent in different body positions. When patients were asked where they would prefer to repeat the sleep study, 53% replied at home, 28% in hospital and 19% showed no preference. It was concluded that the setting of unattended respiratory monitoring (home or sleep laboratory) influences neither the number of valid studies nor the results of the respiratory parameters measured; most patients, however, preferred home studies.
HIV Prevention for a Threatened Continent
Authors: Rebecca Bunnell, Jonathan Mermin, Kevin M. De Cock
Journal: JAMA (2006)

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
Long-Term Follow-up Study of Penicillin-Treated Subacute Bacterial Endocarditis
Authors: Richard Gorlin, Cutting B. Favour, F. Jean Emery
Journal: New England Journal of Medicine (1950)

SINCE 1944, when penicillin became available in quantity, subacute bacterial endocarditis has moved from the category of an almost uniformly fatal disorder to the ranks of curable disease. Among the many well documented papers1 2 3 4 5 6 7 8 9 10 11 12 13 14 supporting the efficacy of treatment is an earlier report from this clinic.15 During the past five years, the original group of patients described has been considerably augmented. It is the purpose of this paper to report on the altered clinical pattern seen in these patients since the advent of penicillin therapy, and the effect of this therapy on long-term results.Clinical MaterialFrom 1944 through 1947, . . .
Genetic hemochromatosis and Wilson'S disease: Role for oxidant stress?
Authors: Robert S. Britton, Kyle E. Brown
Journal: Hepatology (1995)

Hereditary haemochromatosis is characterised by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl radical formation that can cause increased lipid peroxidation and depletion of chain-breaking antioxidants. We have therefore assessed lipid peroxidation and antioxidant status in 15 subjects with hereditary haemochromatosis and age/sex matched controls. Subjects with haemochromatosis had increased serum iron (24.8 (19.1-30.5) vs. 17.8 (16.1-19.5) μmol/L, P = 0.021) and % saturation (51.8 (42.0-61.6) vs. 38.1 (32.8-44.0), P = 0.025). Thiobarbituric acid reactive substances (TBARS), a marker of lipid peroxidation, were increased in haemochromatosis (0.59 (0.48-0.70) vs. 0.46 (0.21-0.71) μmol/l, P = 0.045), and there were decreased levels of the chain-breaking antioxidants alpha-tocopherol (5.91 (5.17-6.60) vs. 7.24 (6.49-7.80) μmol/mmol cholesterol, P = 0.001), ascorbate (51.3 (33.7-69.0) vs. 89.1 (65.3-112.9), P = 0.013), and retinol (1.78 (1.46-2.10) vs. 2.46 (2.22-2.70) μmol/l, P - 0.001). Patients with hereditary haemochromatosis have reduced levels of antioxidant vitamins, and nutritional antioxidant supplementation may represent a novel approach to preventing tissue damage. However, the use of vitamin C may be deleterious in this setting as ascorbate can have prooxidant effects in the presence of iron overload. The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases ( n = 17; group A), hemochromatosis ( n 17;group B) and Wilson's disease ( n 12;group C). Lipidstandardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (&gt;180 μg/dl), a low free iron binding capacity (&lt;8 μmol/l) and high ferritin-levels (&gt;450 μg/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (&gt;10 μg/dl). The data support a role for free radicals in the pathogenesis of active liver diseases. © Journal of Hepatology.
Overexpression of Human Copper/Zinc Superoxide Dismutase (SOD1) Suppresses Ischemia–Reperfusion Injury and Subsequent Development of Graft Coronary Artery Disease in Murine Cardiac Grafts
Authors: Masashi Tanaka, Golnaz K. Mokhtari, Raya D. Terry, Leora B. Balsam, Keun-Ho Lee, Theo Kofidis, Philip S. Tsao, Robert C. Robbins
Journal: Circulation (2004)

Background— Ischemia–reperfusion injury is an important risk factor for graft coronary artery disease (GCAD). We hypothesized that overexpression of SOD1 in donor hearts would suppress ischemia—reperfusion injury and thereby reduce GCAD. Methods and Results— In one series, donor hearts of C57BL/6 (H-2 b ) transgenic mice overexpressing human SOD1 or C57BL/6 wild-type mice were heterotopically transplanted into C57BL/6 recipients and procured after 4 hours of reperfusion (n=6 each). Superoxide, TNF-α, and MCP-1/CCL2 production were significantly reduced in the SOD1 transgenic donor heart recipients, and graft injury determined by serum CPK-MB levels was significantly decreased. Cardiomyocyte apoptosis and caspase-3 and caspase-9 activities were significantly decreased in these recipients; caspase-8 activity was unchanged. Fas ligand but not Fas expression was also reduced. In a second series, transgenic and wild-type hearts were transplanted into C-H-2 bm12 KhEg (H-2 bm12 ) recipients, and then procured on day 56 (n=7 each). Cardiac graft beating was significantly better in the SOD1 transgenic donor heart recipients on days 28, 42, and 56 (but not day 14). Significant reduction in luminal narrowing, the intima/media ratio, and the percentage of diseased vessels was seen in the SOD1 transgenic donor heart recipients, and MCP-1/CCL2, ICAM-1, and VCAM-1 production were significantly reduced. Conclusions— Overexpression of SOD1 attenuates both apoptosis and the inflammatory response during ischemia—reperfusion injury and therefore mitigates against the subsequent development of GCAD.
The effects of levosimendan and glibenclamide on circulatory and metabolic variables in a canine model of acute hypoxia
Authors: Lothar A. Schwarte, Ingo Schwartges, Kai Thomas, Patrick Schober, Olaf Picker
Journal: Intensive Care Medicine (2011)

To study the effects of pretreatment with levosimendan (LEVO, a Ca2+-sensitizer and K ATP + channel opener) and/or the K ATP + channel antagonist glibenclamide (GLIB) on systemic hemodynamics, metabolism, and regional gastromucosal oxygenation during hypoxic hypoxemia. Chronically instrumented, healthy dogs (24–32 kg, n = 6 per group, randomized cross-over design) were repeatedly sedated, mechanically ventilated (FiO2 ~0.3) and subjected to the following interventions: no pretreatment, LEVO pretreatment, GLIB pretreatment, or combined LEVO + GLIB pretreatment, each followed by hypoxic hypoxemia (FiO2 ~0.1). We measured cardiac output (CO, ultrasonic flow probes), oxygen consumption (VO2, indirect calorimetry), and gastromucosal microvascular hemoglobin oxygenation (μHbO2, spectrophotometry). Statistics: data are presented as mean ± SEM and compared by one-way ANOVA (direct drug effects within group) and two-way ANOVA (between all hypoxic conditions) both with Bonferroni corrections; p < 0.05. In LEVO-pretreated hypoxemia, CO was significantly higher compared to unpretreated hypoxemia. The increased CO was neither associated with an increased VO2 nor with markers of aggravated anaerobiosis (pH, BE, lactate). In addition, LEVO pretreatment did not further compromise gastromucosal μHbO2 in hypoxemia. After combined LEVO + GLIB pretreatment, systemic effects of GLIB were apparent, however, CO was significantly higher than during unpretreated and GLIB-pretreated hypoxemia, but equal to LEVO-pretreated hypoxemia, indicating that GLIB did not prevent the increased CO in LEVO-pretreated hypoxia. LEVO pretreatment resulted in improved systemic circulation (CO) during hypoxemia without fueling systemic VO2, without aggravating systemic anaerobiosis markers, and without further compromising microvascular gastromucosal oxygenation. Thus, LEVO pretreatment may be an option to support the systemic circulation during hypoxia.
Abstract 477: Bcl-2 suppresses cell spreading, adhesion and migration in non-small cell lung cancer cells
Authors: Hasseri Halim, Pithi Chanvorachote
Journal: Cancer Research (2012)

Abstract Bcl-2 is mainly thought to regulate cell apoptosis. However, little is known about its regulation associated with cell metastasis. Here, we demonstrate that Bcl-2 plays an important role in the cell spreading, adhesion and migration of non-small cell lung cancer cells. To study the role of Bcl-2, mutant cell lines exhibiting stably up-regulated and down-regulated Bcl-2 were generated using Bcl-2 plasmid and RNA interference. As compared to control H460 cells, Bcl-2 overexpressed cells exhibited significantly decreased cell spreading, adhesion and migration. Consistent with these results, the loss of Bcl-2 in Bcl-2 knockdown cells increased cell spreading, adhesion and migration. The morphology characteristics study has shown that Bcl-2 increased mesenchymal-epithelial transition phenotype whereas the loss of Bcl-2 increased epithelial-mesenchymal transition phenotype. The increase of fluorescent intensity of phalloidin staining in Bcl-2 overexpressed cells suggesting actin polymerization might be responsible in the supression of cell spreading, adhesion and migration. This result may explain why Bcl-2 has been suggested as a prognostic factor for survival in lung cancer patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 477. doi:1538-7445.AM2012-477
Hypoxia-Inducible Factor-1-Independent Regulation of Vascular Endothelial Growth Factor by Hypoxia in Colon Cancer
Authors: Yusuke Mizukami, Jingnan Li, Xiaobo Zhang, Michael A. Zimmer, Othon Iliopoulos, Daniel C. Chung
Journal: Cancer Research (2004)

Abstract The induction of vascular endothelial growth factor (VEGF) is an essential feature of tumor angiogenesis, and the hypoxia-inducible factor-1 (HIF-1) transcription factor is known to be a key mediator of this process. In colon cancer, the frequently mutated K-ras oncogene also can regulate VEGF expression, but the role that K-ras may play in hypoxia is unknown. Hypoxia induced VEGF promoter activity, mRNA, and protein levels in colon cancer cells. Although HIF-1α was induced by hypoxia, VEGF reporter constructs with selectively mutated hypoxia-response elements remained responsive to hypoxia. In addition, “knockdown” of HIF-1α by RNA interference only minimally inhibited the hypoxic induction of VEGF. A region of the VEGF promoter between −420 and −90 bp mediated this HIF-independent induction by hypoxia. The introduction of K-rasVal12 augmented the hypoxic induction of VEGF, and this was observed in wild-type and HIF-1α knockdown colon cancer cells. Thus, VEGF may be induced by hypoxia through HIF-dependent and HIF-independent pathways, and K-ras also can induce VEGF in hypoxia independent of HIF-1. These findings suggest the existence of multiple mechanisms regulating the hypoxic induction of VEGF in colon cancer.
Prevalence and Characteristics of Chronic Pain Among Chemically Dependent Patients in Methadone Maintenance and Residential Treatment Facilities
Authors: Andrew Rosenblum
Journal: JAMA (2003)

ContextLittle is known about the prevalence and characteristics of chronic pain among patients with different types of chemical dependency.ObjectivesTo estimate the prevalence and to examine the characteristics of chronic severe pain in chemically dependent populations receiving methadone maintenance or inpatient residential treatment.Design, Setting, and ParticipantsRepresentative samples of 390 patients from 2 methadone maintenance treatment programs (MMTPs) and 531 patients from 13 short-term residential substance abuse treatment (inpatient) programs, all in New York State, were surveyed in late 2000 and early 2001.Main Outcome MeasurePrevalence of chronic severe pain, defined as pain that persisted for more than 6 months and was of moderate to severe intensity or that significantly interfered with daily activities.ResultsChronic severe pain was experienced by 37% of MMTP patients (95% confidence interval [CI], 32%-41%) and 24% of inpatients (95% CI, 20%-28%; P = .03). Pain of any type or duration during the past week was reported by 80% of MMTP patients and 78% of inpatients. Among those with chronic severe pain, 65% of MMTP patients and 48% of inpatients reported high levels of pain-related interference in physical and psychosocial functioning. Among MMTP patients, correlates of chronic pain in a multivariate model were age (odds ratio [OR], 2.08; 95% CI, 1.17-3.70), chronic illness (OR, 1.88; 95% CI, 1.07-3.29), lifetime psychiatric illness (OR, 1.77; 95% CI, 1.06-2.97), psychiatric distress (OR, 1.63; 95% CI, 1.22-2.18), and time in treatment (OR, 2.23; 95% CI, 1.06-4.68). Among inpatients, the correlates of chronic pain were race (blacks vs whites: OR, 0.52; 95% CI, 0.31-0.90; Hispanics vs whites: OR, 0.48; 95% CI, 0.24-0.95), drug craving (OR, 2.78; 95% CI, 1.54-5.02), chronic illness (OR, 2.17; 95% CI, 1.37-3.43), and psychiatric distress (OR, 1.36; 95% CI, 1.03-1.81). Among those with chronic severe pain, inpatients were significantly more likely than MMTP patients to have used illicit drugs, as well as alcohol, to treat their pain complaint (51% vs 34%, P = .005) but were less likely to have been prescribed pain medications (52% vs 67%, P = .01).ConclusionsChronic severe pain is prevalent among patients in substance abuse treatment, especially MMTP patients. Pain is associated with functional impairment and correlates of pain vary with the population. Self-medication for pain with psychoactive drugs appears especially problematic among substance users who enroll in drug-free treatment programs. Substance abuse treatment programs need to develop comprehensive and structured pain management programs.
Vaccination with genetically modified birch pollen allergens: Immune and clinical effects on oral allergy syndrome
Authors: Verena Niederberger, Jürgen Reisinger, Peter Valent, Maria-Theresa Krauth, Gabrielle Pauli, Marianne van Hage, Oliver Cromwell, Friedrich Horak, Rudolf Valenta
Journal: Journal of Allergy and Clinical Immunology (2007)
Subacute Thyroiditis: A Review of 105 Cases
Authors: MICHAEL I. KITCHNER, IAN M. CHAPMAN
Journal: Clinical Nuclear Medicine (1989)

A retrospective review of 4023 thyroid scans performed at the Royal Adelaide Hospital in the five years to February 1987 identified 105 cases of subacute thyroiditis. Subacute thyroiditis accounted for 9.9% of subjects scanned for hyperthyroidism. Eighty-four percent had painful thyroiditis, 6% postpartum thyroiditis, and 10% painless thyroiditis. Follow-up was obtained in 68% of cases, and 11% were taking thyroxine, probably indicating long-term hypothyroidism. Apart from the presence of antibodies in post-partum thyroiditis, no other factor was identified which predicted the development of long-term hypothyroidism. As subacute thyroiditis is a common cause of hyperthyroidism in our community, the authors believe all people with hyperthyroidism should have a thyroid scan unless they have distinctive features of Graves' disease.
Hepatitis Associated With Ranitidine-Reply
Authors: Jack D. Proctor
Journal: JAMA (1984)

In Reply.—  Several possible explanations were offered for the clinical hepatitis that I reported in a patient taking ranitidine. An attempt to include all relevant details was made so that the reader could reach some conclusion other than the one that came so readily to me—that ranitidine was the most likely cause. Since there have been hardly any reports of hepatotoxicity for a drug so frequently used as ranitidine, it seemed that speculation on a drug interaction or some other unusual coincidence was appropriate. Drs Jack and Smith satisfactorily refute the suggestion that ranitidine shares the defined hepatotoxic mechanism of other known hepatotoxic furans, and, thus, a toxic interaction with acetaminophen by that mechanism is unlikely.  I agree with Dr Souza Lima that my report is not a proved instance of ranitidine-induced hepatitis. Relapse on rechallenge is the best evidence that a drug reaction has occurred and is essential for
Which Comes First in Non—Insulin-Dependent Diabetes Mellitus: Insulin Resistance or Beta-Cell Failure? Both Come First
Authors: Gordon C. Weir
Journal: JAMA (1995)

The curious physician trying to understand the pathogenesis of non—insulin-dependent diabetes mellitus (NIDDM) has every reason to be mystified by the barrage of conflicting claims about the primacy of beta-cell failure and insulin resistance. How can the argument go on for so long without a clear answer? Probably because we keep trying to view NIDDM as being simpler than it really is, and because we expect that the first identifiable lesion will lead us to the primary cause. Since there is general agreement that a combination of both environmental and genetic forces leads to NIDDM, it is probably counterproductive to think in terms of a primary cause or something that comes first. The major environmental problem seems to be our modern obesity-promoting lifestyle of limited physical activity and abundant food. Not only is obesity associated with insulin resistance, but sedentary behavior by itself leads to reduced insulin action on muscle.