tbuckley/cabot-search huggingface dataset:
ACUTE APPENDICITIS IN A CASE OF STRANGULATED HERNIA
Authors: Vincent Anthony Lapenta
Journal: JAMA (1923)

Dr. A. W. Miller, Aug. 1, 1923, referred for examination to me a boy, aged 2 years, who had a large swelling in the scrotum and right inguinal region. The child appeared to be very sick and was vomiting frequently. The pulse was rapid and of good volume, the temperature was normal, and the abdomen was slightly distended. An attempt to reduce the hernia was unsuccessful. The mother reported that incarcerations had occurred at other times, which had been reduced by manipulation; this, however, was the first time that the child had shown such a sick appearance. On account of the irreducible strangulation, an immediate operation was advised. The patient was admitted to St. Francis Hospital, and under ether anesthesia, a classical incision was made, exposing the constriction near the internal inguinal ring. The contents of the sac, however, could not be reduced. The sac was dissected free from the
The Effect of Statin Therapy on Endothelial Function in Type 2 Diabetes Without Manifest Cardiovascular Disease
Authors: Edith D. Beishuizen, Jouke T. Tamsma, J. Wouter Jukema, Marcel A. van de Ree, J. Carel M. van der Vijver, A. Edo Meinders, Menno V. Huisman
Journal: Diabetes Care (2005)

OBJECTIVE—Cardiovascular disease (CVD) is the most important cause of mortality in patients with type 2 diabetes and is preceded by endothelial dysfunction. Flow-mediated dilation (FMD) is a noninvasive technique for measuring endothelial dysfunction. We aimed to determine the effect of long-term statin therapy versus placebo on FMD in patients with type 2 diabetes without manifest CVD. RESEARCH DESIGN AND METHODS—A randomized, placebo-controlled, double-blind trial was performed with 250 type 2 diabetic patients. Patients were given 0.4 mg cerivastatin or placebo daily. In August 2001, when cerivastatin was withdrawn from the market, the 0.4 mg cerivastatin was replaced by 20 mg simvastatin, without deblinding the study. The primary end point was the change in FMD, measured by B-mode ultrasound, after 2 years. RESULTS—Determinants of baseline FMD were diabetes duration, common carotid intima-media thickness, and brachial artery diameter. FMD at baseline was 1.51% in the placebo group and 1.66% in the statin group and did not change significantly after 2 years. CONCLUSIONS—The 2-year statin therapy had no effect on FMD in type 2 diabetes. Statin-induced improvement of cardiovascular risk in patients with type 2 diabetes may be mediated through mechanisms other than increased nitric oxide availability.
Molecular analysis of the influences of positive selection, tolerance induction, and antigen presentation on the T cell receptor repertoire.
Authors: P J Fink, M J Blair, L A Matis, S M Hedrick
Journal: The Journal of Experimental Medicine (1990)

Immunization of both B10.A and B10.S(9R) mice with pigeon cytochrome c (pcc) elicits T cells capable of proliferating to pcc presented on I-E major histocompatibility complex (MHC) molecules. The T cell receptor (TCR) repertoire used by pcc-specific T cells from these two strains is markedly different, even for T cells recognizing very similar antigen/MHC complexes. Our current studies have been directed toward explaining this differential expression between MHC congenic strains of TCR gene elements capable of recognizing similar ligands. Analysis of the TCR repertoire of pcc-specific T cells from F1[B10.A x B10.S (9R)]----parent radiation chimeras has demonstrated that much of this difference is a result of the positive selection of T cells for MHC restriction specificity. Further analysis of T cell lines from F1 mice and from radiation chimeras stimulated in vitro with pcc on both B10.A and B10.S(9R) antigen-presenting cells has provided clear-cut examples of the influence of positive selection, tolerance induction and of both in vivo and in vitro antigen presentation on the shaping of the TCR repertoire for a protein antigen. This is the first molecular analysis of how positive selection, tolerance induction, and antigen presentation can combine to mold the TCR repertoire.
Sphingosine-1-Phosphate–Dependent Activation of p38 MAPK Maintains Elevated Peripheral Resistance in Heart Failure Through Increased Myogenic Vasoconstriction
Authors: Judith Hoefer, M. Ali Azam, Jeffrey T.E. Kroetsch, Howard Leong-Poi, M. Abdul Momen, Julia Voigtlaender-Bolz, Elias Q. Scherer, Anja Meissner, Steffen-Sebastian Bolz, Mansoor Husain
Journal: Circulation Research (2010)

Mechanisms underlying vasomotor abnormalities and increased peripheral resistance exacerbating heart failure (HF) are poorly understood.To explore the role and molecular basis of myogenic responses in HF.10 weeks old C57Bl6 mice underwent experimental myocardial infarction (MI) or sham surgery. At 1 to 12 weeks postoperative, mice underwent hemodynamic studies, mesenteric, cerebral, and cremaster artery perfusion myography and Western blot. Organ weights and hemodynamics confirmed HF and increased peripheral resistance after MI. Myogenic responses, ie, pressure-induced vasoconstriction, were increased as early as 1 week after MI and remained elevated. Vasoconstrictor responses to phenylephrine were decreased 1 week after MI, but not at 2 to 6 weeks after MI, whereas those to endothelin (ET)-1 and sphingosine-1-phosphate (S1P) were increased at all time points after MI. An antagonist (JTE-013) for the most abundant S1P receptor detected in mesenteric arteries (S1P(2)R) abolished the enhanced myogenic responses of HF, with significantly less effect on controls. Mice with genetic absence of sphingosine-kinases or S1P(2)R (Sphk1(-/-); Sphk1(-/-)/Sphk2(+/-); S1P(2)R(-/-)) did not manifest enhanced myogenic responses after MI. Mesenteric arteries from HF mice exhibited increased phosphorylation of myosin light chain, with deactivation of its phosphatase (MLCP). Among known S1P-responsive regulators of MLCP, GTP-Rho levels were unexpectedly reduced in HF, whereas levels of activated p38 MAPK and ERK1/2 (extracellular signal-regulated kinase 1/2) were increased. Inhibiting p38 MAPK abolished the myogenic responses of animals with HF, with little effect on controls.Rho-independent p38 MAPK-mediated deactivation of MLCP underlies S1P/S1P(2)R-regulated increases in myogenic vasoconstriction observed in HF. Therapeutic targeting of these findings in HF models deserves study.
Muscle Injury During Critical Illness
Authors: Jane Batt, Claudia C. Dos Santos, Margaret S. Herridge
Journal: JAMA (2013)

understanding of its molecular mechanism were not appreciated or research priorities until recently. The mass, strength, and metabolic function of muscle affect its role as a major reservoir of amino acids, driver of metabolic homeostasis, and consumer of energy substrates. In the context of critical illness, muscle atrophy captured by direct or indirect measurements such as frailty 6 and reduced body mass index 7 have all been linked to poor outcome. Simultaneously, a decrease in muscle strength can occur independently as a result of multifactorial dysregulation in different processes such as myofiber calcium sequestration and homeostasis, and uncoupling of mitochondrial-dependent pathways. Even though there may be significant overlap in molecular biologic networks that regulate both mass and contractility, processspecific pathways that play a role in determining contractility or mass may have significant and independent effects on prognosis and treatment of weakness acquired in the intensive care unit (ICU). ICU-acquired weakness encompasses each of critical illness polyneuropathy and critical illness myopathy and is characterized by axonal nerve degeneration, muscle myosin loss leading to profound muscle weakness. It may be identified in
Hollow silica and silica-boron nano/microparticles for contrast-enhanced ultrasound to detect small tumors
Authors: Alexander Liberman, H. Paul Martinez, Casey N. Ta, Christopher V. Barback, Robert F. Mattrey, Yuko Kono, Sarah L. Blair, William C. Trogler, Andrew C. Kummel, Zhe Wu
Journal: Biomaterials (2012)
Elderly patients are dying after surgery because of poor care, review says
Authors: S. Mayor
Journal: BMJ (2010)

Only a third of elderly patients who died in UK hospitals within 30 days of undergoing surgery were considered to have received good care, warns an expert review of more than 800 cases by the National Confidential Enquiry into Patient Outcome and Death (NCEPOD), published this week.

The NCEPOD survey looked at the hospital care given to patients over the age of 80 who had had surgery and died within 30 days—most of whom had undergone emergency surgery. NCEPOD identified 1756 cases and sent out questionnaires concerning these. The hospitals returned 820 sets of case notes and 1120 surgical, 957 anaesthetic, and 283 organisational questionnaires.

The reviewers …
Prison Rape and Suicide
Authors: James W. Wiggs
Journal: JAMA (1989)

<h3>To the Editor.—</h3> In reading the article entitled "Suicide Mortality in the Maryland State Prison System, 1979 Through 1987," by Salive et al,<sup>1</sup>I was surprised to discover that the characteristics of inmates who committed suicide did not address the major issue of whether any of them had been subject to homosexual rape. All of the features characteristic of heterosexual rape, which is justly condemned, apply to homosexual rape, with the addition that in the prison environment the man who is raped by homosexual attack has no way to escape further rapes by the same gang. This must have an influence on the incidence of suicide; it is unfortunate that the study was done without addressing this major issue.
The effect of losartan on hemoglobin concentration and renal outcome in diabetic nephropathy of type 2 diabetes
Authors: A. Mohanram, Z. Zhang, S. Shahinfar, P.A. Lyle, R.D. Toto
Journal: Kidney International (2007)

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can decrease hemoglobin, causing anemia and this may be an independent risk factor for chronic kidney disease progression. We studied the relationship between a decline in hemoglobin and outcome in 1513 patients with type 2 diabetes and kidney disease by a post hoc analysis of the RENAAL Study (Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan) with an average follow-up of 3.4 years. The relationship between baseline and year-1 hemoglobin and treatment on end-stage renal disease (ESRD) and ESRD or death was evaluated using multivariate Cox models (covariates: baseline hemoglobin, proteinuria, serum albumin, serum creatinine, and year-1 hemoglobin). Compared with placebo, losartan treatment was associated with a significant decrease of hemoglobin, with the largest between-group difference at 1 year. After adjustment, there were significant relative risk reductions for losartan compared with placebo for ESRD and for ESRD or death regardless of the baseline hemoglobin even in those patients with a baseline hemoglobin below 120 g l(-1). Hence, the renoprotective properties of losartan were maintained despite a significant lowering of the hemoglobin concentration.
Excellence in healthcare is celebrated at The BMJ Awards 2014
Authors: A. Rimmer
Journal: BMJ (2014)

Projects to improve survival after cardiac arrests that occur outside hospitals, to spot chronic lung disease, and to reduce pressure on hospital emergency services scooped the top prizes at The BMJ Awards 2014 last night.

The awards, sponsored by the Medical and Dental Defence Union of Scotland (MDDUS), took place at the Westminster Park Plaza Hotel, London, and was hosted by the broadcaster Gyles Brandreth. Other winners included a team providing training in keyhole surgery in Tanzania and a trial of treatment for HIV positive babies and children in developing countries.

The Lifetime Achievement Award went to Iain Chalmers, co-founder of the Cochrane Collaboration and coordinator of the James Lind Initiative, for his contribution to improving …
Changes in airway responsiveness and β‐ and α‐adrenergic receptors in the lungs of guinea pigs with experimental asthma
Authors: S. Motojima, T. Yukawa, T. Fukuda, S. Makino
Journal: Allergy (1989)

The effects of inhaled allergen on airway responsiveness and on beta- and alpha-1-adrenergic receptors on lung membrane were investigated in guinea pigs. After measuring the respiratory threshold to histamine (RT-HIS), one group of guinea pigs passively sensitized for ovalbumin was challenged by allergen inhalation (challenged group). Measurement of the RT-HIS 24 h following challenge revealed a significant decrease from 687 micrograms/ml (mean, n = 16) to 407 micrograms/ml (P less than 0.05). In addition the RT-HIS 24 h after challenge was also significantly lower in the challenged group than in controls (n = 9, P less than 0.05). The density of beta-adrenergic receptors on the lung membrane of the challenged group was 594 +/- 32 (mean +/- SE) fmol/mg protein (n = 11) compared with 712 +/- 24 fmol/mg protein (n = 9) in the controls, a statistically significant difference (P less than 0.05). A significant correlation was found between the RT-HIS and density of beta-adrenergic receptors. From these results, we concluded that the exaggerated airway responsiveness 24 h after allergen challenge is in part due to a decrease in the density of beta-adrenergic receptors. There was no difference in the density of alpha-1-adrenergic receptors nor a significant correlation between the RT-HIS and the number of alpha-1-adrenergic receptors in the challenged vs. the control groups.
Doctors blame untested policies for financial crisis in the NHS
Authors: Zosia Kmietowicz
Journal: BMJ (2006)

Doctors at the BMA's annual meeting of representatives in Belfast have blamed the government for the financial crisis in the NHS, saying that it has taken a record amount of money away from the care of patients and “squandered” it on unproved reforms.

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James Johnson, the BMA's chairman, addresses the annual representative meeting in Belfast last week

Credit: MARK PEARCE/PACEMAKER INTERNATIONAL/BMA NEWS

“This financial crisis has nothing …

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Pyruvate carboxylase is critical for non–small-cell lung cancer proliferation
Authors: Katherine Sellers, Matthew P. Fox, Michael Bousamra, Stephen P. Slone, Richard M. Higashi, Donald M. Miller, Yali Wang, Jun Yan, Mariia O. Yuneva, Rahul Deshpande, Andrew N. Lane, Teresa W.-M. Fan
Journal: Journal of Clinical Investigation (2015)

Anabolic biosynthesis requires precursors supplied by the Krebs cycle, which in turn requires anaplerosis to replenish precursor intermediates. The major anaplerotic sources are pyruvate and glutamine, which require the activity of pyruvate carboxylase (PC) and glutaminase 1 (GLS1), respectively. Due to their rapid proliferation, cancer cells have increased anabolic and energy demands; however, different cancer cell types exhibit differential requirements for PC- and GLS-mediated pathways for anaplerosis and cell proliferation. Here, we infused patients with early-stage non-small-cell lung cancer (NSCLC) with uniformly 13C-labeled glucose before tissue resection and determined that the cancerous tissues in these patients had enhanced PC activity. Freshly resected paired lung tissue slices cultured in 13C6-glucose or 13C5,15N2-glutamine tracers confirmed selective activation of PC over GLS in NSCLC. Compared with noncancerous tissues, PC expression was greatly enhanced in cancerous tissues, whereas GLS1 expression showed no trend. Moreover, immunohistochemical analysis of paired lung tissues showed PC overexpression in cancer cells rather than in stromal cells of tumor tissues. PC knockdown induced multinucleation, decreased cell proliferation and colony formation in human NSCLC cells, and reduced tumor growth in a mouse xenograft model. Growth inhibition was accompanied by perturbed Krebs cycle activity, inhibition of lipid and nucleotide biosynthesis, and altered glutathione homeostasis. These findings indicate that PC-mediated anaplerosis in early-stage NSCLC is required for tumor survival and proliferation.
Vitamin B_12 Deficiency after Gastric Surgery
Authors: Anne E. Sumner
Journal: Annals of Internal Medicine (1996)

Letters1 December 1996Vitamin B12 Deficiency after Gastric SurgeryAnne E. Sumner, MD, Janet L. Abrahm, MD, and Sally P. Stabler, MDAnne E. Sumner, MDMedical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19129.Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104.University of Colorado Health Sciences Center, Denver, CO 80262.Search for more papers by this author, Janet L. Abrahm, MDMedical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19129.Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104.University of Colorado Health Sciences Center, Denver, CO 80262.Search for more papers by this author, and Sally P. Stabler, MDMedical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19129.Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104.University of Colorado Health Sciences Center, Denver, CO 80262.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-11-199612010-00014 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Our investigation confirms the known metabolic consequences of gastric surgery using the most sensitive available tests—measurement of serum methylmalonic acid and total homocysteine levels—to determine vitamin B12 deficiency. We did not determine the cause of vitamin B12 deficiency but agree with Drs. Murthy and Visweswaraiah that achlorhydria, intestinal blind-loop syndromes, and histamine-2 antagonist therapy could have caused some of the malabsorption. Histamine-2 antagonists are frequently prescribed and available over the counter. We did not test for food protein-bound cobalamin absorption. A limitation of all vitamin B12-absorption tests is that they only measure malabsorption at the time of the ... Author, Article, and Disclosure InformationAuthors: Anne E. Sumner, MD; Janet L. Abrahm, MD; Sally P. Stabler, MDAffiliations: Medical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19129.Philadelphia Veterans Affairs Medical Center, Philadelphia, PA 19104.University of Colorado Health Sciences Center, Denver, CO 80262. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1996Volume 125, Issue 11 Page: 937-938 Keywords Folic acid Inpatients Nursing homes Outpatients Over the counter drugs Proteins Specificity Standardized tests Surgery Vitamin B12 deficiency ePublished: 15 August 2000 Issue Published: 1 December 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Antioxidant Effects of Statins via <i>S</i> -Nitrosylation and Activation of Thioredoxin in Endothelial Cells
Authors: Judith Haendeler, Jörg Hoffmann, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Circulation (2004)

Background— HMG-CoA reductase inhibitors (statins) are lipid-lowering drugs that also exert pleiotropic vasculoprotective effects via activation of the endothelial NO synthesis. NO induces S -nitrosylation of target proteins. S -Nitrosylation of the antioxidant enzyme thioredoxin was recently shown to enhance its activity, thereby reducing intracellular reactive oxygen species. Therefore, we investigated whether statins may exert an antioxidant activity in endothelial cells via S -nitrosylation of thioredoxin. Methods and Results— Statins dose- and time-dependently increased the overall level of S -nitrosylated proteins in endothelial cells (atorvastatin 0.1 μmol/L, 206±30% increase; simvastatin 1 μmol/L, 214±19% increase; mevastatin 1 μmol/L, 191±10% increase). The increased S -nitrosylation was blocked by an NO-synthase inhibitor and mevalonate. Moreover, S -nitrosylation of thioredoxin was also significantly augmented after atorvastatin treatment. The atorvastatin-mediated increase in S -nitrosylation was associated with an enhanced enzymatic activity of thioredoxin (atorvastatin, 157±9% increase). This resulted in a significant reduction of intracellular reactive oxygen species within the endothelial cells. In contrast, in endothelial cells overexpressing a thioredoxin construct in which the S -nitrosylation acceptor amino acid cysteine 69 was replaced by serine [TRX(C69S)], atorvastatin did not activate the redox-regulatory activity of thioredoxin. Moreover, overexpression of the non-nitrosylatable thioredoxin TRX(C69S) abolished atorvastatin-mediated reduction of reactive oxygen species. Conclusions— Here, we demonstrate a novel antioxidant mechanism by which statins reduce reactive oxygen species in endothelial cells. Statin-mediated S -nitrosylation of thioredoxin enhanced the enzymatic activity of thioredoxin, resulting in a significant reduction in intracellular reactive oxygen species.
Peripartum Cardiomyopathy Due to Myocarditis
Authors: Kenneth R. Melvin, Peter J. Richardson, Eckhardt G. J. Olsen, Kieran Daly, Graham Jackson
Journal: New England Journal of Medicine (1982)

PRIMARY myocardial disease that develops during the course of pregnancy is a rare but exacting diagnostic problem. The variation in the time of onset of this disease from the second trimester of pregnancy until well into the puerperium has led to debate regarding terminology.1 , 2 We refer to peripartum cardiomyopathy as the new presentation of primary myocardial disease during pregnancy or in the first five months after pregnancy.In the evaluation of patients with peripartum cardiomyopathy it is necessary to exclude or identify myocarditis immediately because of the important therapeutic implications. We have included endomyocardial biopsy in the diagnostic workup of . . .
An Outbreak of Type A Botulism Associated with a Commercial Cheese Sauce
Authors: John M. Townes
Journal: Annals of Internal Medicine (1996)

Background: Although botulism is rare, recognition of a possible case of this illness represents a public health emergency. To prevent more cases, prompt investigation must be done to determine whether illness is linked to a commercial product or restaurant. Botulism can masquerade as other illnesses, and seemingly unlikely foods can harbor botulinum toxin. Objective: To confirm the diagnosis and determine the cause and extent of an outbreak of botulism associated with food served at a delicatessen. Design: Retrospective cohort study of patrons of the delicatessen; laboratory analysis of food, serum samples, and stool samples; and traceback of implicated food. Setting: Community in Georgia. Participants: Patrons of the delicatessen. Main Outcome Measures: Botulinum toxin in food, serum, or stool and Clostridium botulinum in food and stools. Results: 8 of 52 patrons (15%) met the case definition for botulism. In 4 of the 8 patrons, an illness other than botulism was initially diagnosed. Five of the 8 were hospitalized, and 1 died. Stool cultures from 4 patrons yielded type A C. botulinum, and two serum samples contained botulinum toxin. All ill persons ate food from the delicatessen on 1 October 1993. Of the 22 persons who ate at the delicatessen that day, all 8 ill persons but none of the 14 well persons ate a potato stuffed with meat and cheese sauce. An open can of cheese sauce contained type A botulinum toxin and yielded C. botulinum on culture. Cheese sauce experimentally inoculated with C. botulinum spores became toxic after 8 days at a temperature of 22 °C (room temperature). Conclusions: A commercial, canned cheese caused a botulism outbreak. This product readily becomes toxic when contaminated by C. botulinum spores and left at room temperature. Mild botulism caused by unusual vehicles may be misdiagnosed. Botulism should be included in the differential diagnosis of persons with signs or symptoms of acute cranial nerve dysfunction.