tbuckley/cabot-search huggingface dataset:
Sevoflurane Preconditioning Attenuates Myocardial Ischemia/Reperfusion Injury via Caveolin-3–Dependent Cyclooxygenase-2 Inhibition
Authors: Jianli Zhao, Feng Wang, Yanqing Zhang, Liyuan Jiao, Wayne Bond Lau, Lili Wang, Baojiang Liu, Erhe Gao, Walter J. Koch, Xin-Liang Ma, Yajing Wang
Journal: Circulation (2013)

Background— The inhaled anesthetic sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (MI/R) injury via mechanisms involving AMP-activated protein kinase (AMPK) and caveolin-3 (Cav-3). However, the relative contributions of AMPK and Cav-3 to sevoflurane preconditioning (SF-PreCon)–mediated cardioprotection and their precise underlying mechanisms of action remain incompletely understood. Methods and Results— SF-PreCon (consisting of 3 cycles of 15-minute exposure to 2% sevoflurane before 30 minutes of MI) decreased MI/R injury in wild-type mice (caspase-3 activity, −29.1%; infarct size, −20.2%; and left ventricular end diastolic pressure, −33.8%). In cardiac-specific AMPKα2 dominant-negative overexpressing mice, the cardioprotective effect of SF-PreCon was largely retained (caspase-3 activity, −26.7%; infarct size, −16.7%; and left ventricular end-diastolic pressure, −25.9%; P &lt;0.01). In contrast, SF-PreCon failed to significantly protect Cav-3 knockout mice against MI/R injury ( P &gt;0.05). SF-PreCon significantly decreased MI/R-induced superoxide generation in wild-type (−43.6%) and AMPK dominant-negative overexpressing mice (−35.5%; P &lt;0.01) but not in Cav-3 knockout mice. SF-PreCon did not affect nicotinamide adenine dinucleotide phosphate oxidase expression but significantly inhibited cyclooxygenase-2 expression in wild-type (−38.7%) and AMPK dominant-negative overexpressing mice (−35.8%) but not in Cav-3 knockout mice. Conclusions— We demonstrate for the first time SF-PreCon mediates cardioprotection against MI/R injury via caveolin-3–dependent cyclooxygenase-2 inhibition and antioxidative effects.
The University of Illinois Plan for Expanding Medical Education
Authors: William J. Grove
Journal: JAMA (1969)

The State of Illinois Plan for increasing health services 1 to the citizenry evolved as a result of a growing intensity of economic, social, and population pressures. There is no need to detail these pressures here, as they have been recounted in a series of reports 2-6 that have alerted the public and their legislators to the need for change.  The University of Illinois' plans for increasing health care for the citizens of the state includes expansion of all its health professions, colleges, and schools. This report, however, will describe only those proposals relating more directly to medical education.  The volume of physicians services delivered to a given area can be increased by: (1) increasing the number of physicians in the area (through increased production, retention, or in-migration); (2) increasing the number of years of productive service of each physician; and (3) increasing the efficiency of the physician.  The University
Prenatal Genetic Diagnosis: Current Status
Authors: Michael T. Mennuti
Journal: New England Journal of Medicine (1977)

In this issue of the Journal Mahoney et al. report the diagnosis of Duchenne's muscular dystrophy with use of fetal plasma obtained during fetoscopy. This advance is notable because it adds to the growing list of genetic disorders amenable to prenatal diagnosis and further illustrates the use of fetoscopy and fetal-blood sampling. It also typifies the collaborative effort required for the development of methods for prenatal diagnosis and the complicated nature of such investigations.Prenatal genetic diagnosis is unusual in clinical medicine in that critical decisions are based on laboratory diagnosis without physical examination of the patient. Fetoscopy offers the . . .
Making progress with competing interests
Authors: R. Smith
Journal: BMJ (2002)

Papers p 1391 

The BMJ and other journals are making progress with managing the problem of competing interests (or conflicts of interest, as most journals call them). Today we take two further steps forward by posting on our website the competing interests of editors, our editorial board, and our group executive (http://bmj.com/aboutsite/competing_interests.shtml) and by publishing a study we have conducted that shows that readers' reactions to research are strongly influenced by statements of competing interests.1 We still, however, have some way to go to the fully transparent world that is desirable.

The history of medical journals and conflict of interest might be cruelly summarised as lots of rhetoric and not much action. The International Committee of Medical Journal Editors produced a policy on conflicts of interest as long ago as 1993,2 but several studies have shown that such conflicts are rarely declared in most journals—despite good evidence that most authors have them.3–7 The international committee strengthened its policy in 2001 by stating that journals should declare the exact role of sponsors (often pharmaceutical companies) in studies and decline to publish studies where the sponsors controlled the decision on publication. 8 9 This policy too has yet to be widely implemented.7

At the BMJ all authors and reviewers of original articles, editorials, and most other material are asked to complete competing interests forms, and declarations of …
The Summerland Disaster.
Authors: R J Hart, J O Lee, D J Boyles, N R Batey
Journal: BMJ (1975)

The reception, admission, and subsequent management of casualties from the Summerland fire are described. A senior member ofthe staff assessed priorities and direceted casualties to different prearranged teams, and a nurse was allocated to each patient to aid continuity of treatment and documentation. Though regular revision and discussion of major accident procedures with all members of the hospital staff and co-ordination with other rescue workers is helpful expensive rehearsals are of limited value in a civilian incident.
Beta-adrenergic agonists increase lung liquid clearance in anesthetized sheep.
Authors: Y Berthiaume, N C Staub, M A Matthay
Journal: Journal of Clinical Investigation (1987)

We did experiments to determine whether beta-adrenergic agonists increase lung liquid clearance in anesthetized ventilated adult sheep and, if so, whether the increase is mediated by beta receptors and what mechanism is involved. We instilled 100 ml of autologous serum either alone or with a beta-adrenergic agonist (terbutaline, 10(-5) M, or epinephrine, 5.5 X 10(-6) M) into one lower lobe. After 4 h both terbutaline and epinephrine increased lung liquid clearance. The increase in lung liquid clearance was inhibited when propranolol (a beta blocker) or amiloride (a sodium channel blocker) was added to the terbutaline. Increased clearance was not explained by changes in pulmonary hemodynamics, pulmonary blood flow, or lung lymph flow. We conclude that beta-adrenergic agonists increase lung liquid clearance in anesthetized intact adult sheep. This increase is mediated through beta receptors and probably depends on increased active transport of sodium across the alveolar barrier.
HLA-Mismatched Renal Transplantation without Maintenance Immunosuppression
Authors: Tatsuo Kawai, A. Benedict Cosimi, Thomas Richard Spitzer, Nina Ellen Tolkoff-Rubin, Manikkam Suthanthiran, Susan L. Saidman, Juanita Shaffer, Frederic Ira Preffer, Ruchuang Ding, Vijay Sharma, Jay Alan Fishman, Bimalangshu Dey, Dicken S.C. Ko, Martin Hertl, Nelson B. Goes, Waichi Wong, Winfred Woodrow Williams, Robert Barnes Colvin, Megan Sykes, David H. Sachs
Journal: New England Journal of Medicine (2013)

Five patients with end-stage renal disease received combined bone marrow and kidney transplants from HLA single-haplotype mismatched living related donors, with the use of a nonmyeloablative preparative regimen. Transient chimerism and reversible capillary leak syndrome developed in all recipients. Irreversible humoral rejection occurred in one patient. In the other four recipients, it was possible to discontinue all immunosuppressive therapy 9 to 14 months after the transplantation, and renal function has remained stable for 2.0 to 5.3 years since transplantation. The T cells from these four recipients, tested in vitro, showed donor-specific unresponsiveness and in specimens from allograft biopsies, obtained after withdrawal of immunosuppressive therapy, there were high levels of P3 (FOXP3) messenger RNA (mRNA) but not granzyme B mRNA.
Development of the formalin-inactivated hepatitis A vaccine, VAQTATM from the live attenuated virus strain CR326F
Authors: Marcy E. Armstrong, Paula A. Giesa, Joseph P. Davide, Francine Redner, Julie A. Waterbury, Audrey E. Rhoad, Robert D. Keys, Philip J. Provost, John A. Lewis
Journal: Journal of Hepatology (1993)
Detection of Gp210 autoantibodies in primary biliary cirrhosis using a recombinant protein containing the predominant autoepitope
Authors: Flora Tartakovsky, Howard J. Worman
Journal: Hepatology (1995)

Autoantibodies against nuclear pore membrane glycoprotein gp210 have been identified in between 10% and 25% of patients with primary biliary cirrhosis (PBC). These antibodies may be useful in diagnosing PBC and in identifying subgroups of patients. Because previous detection procedures relied on the need to purify hydrophobic proteins and perform immunoblotting, the aim of the present study was to develop a simple assay to detect gp210 autoantibodies. A recombinant polypeptide containing glutathione-S-transferase (GST) fused to the region of gp210 that contains its predominant autoepitope(s) was expressed in bacteria. This fusion protein was purified by glutathione-Sepharose chromatography and used in an enzyme-linked immunosorbent assay (ELISA). The ELISA was reproducible in detecting gp210 autoantibodies in serum samples from patients with PBC. Compared with immunoblotting, the ELISA was 93% sensitive and 96% specific for the detection of gp210 autoantibodies. In conclusion, autoantibodies against gp210 can be easily and reliably detected in patients with PBC by an ELISA that uses a purified recombinant polypeptide.
Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes
Authors: Diwakar R. Pattabiraman, Crystal McGirr, Konstantin Shakhbazov, Valerie Barbier, Keerthana Krishnan, Pamela Mukhopadhyay, Paula Hawthorne, Ann Trezise, Jianmin Ding, Sean M. Grimmond, Peter Papathanasiou, Warren S. Alexander, Andrew C. Perkins, Jean-Pierre Levesque, Ingrid G. Winkler, Thomas J. Gonda
Journal: Blood (2014)
Reduction in Lipopolysaccharide-Induced Thrombocytopenia by Triflavin in a Rat Model of Septicemia
Authors: Joen-Rong Sheu, Wei-Chung Hung, Ching-Hsiang Wu, Ming-Chieh Ma, Ya-Chen Kan, Chien-Huang Lin, Ming-Shyan Lin, Hsiung-Ning Luk, Mao-Hsiung Yen
Journal: Circulation (1999)

Background —Thrombocytopenia frequently occurs early in the course of Gram-negative bacterial infections. Triflavin, an Arg-Gly-Asp–containing disintegrin, has been suggested to interfere with the interaction of fibrinogen with the glycoprotein IIb/IIIa complex. The present study was undertaken to determine whether triflavin could prevent thrombocytopenia in lipopolysaccharide (LPS)-treated rats. Methods and Results —In this study, 51 Cr-labeled platelets were used to assess blood and tissue platelet accumulation after LPS challenge. The administration of LPS (4 mg/kg IV bolus) for 4 hours induced a reduction in radiolabeled platelets in blood and an obvious accumulation of platelets in liver. Triflavin (500 μg/kg) but not GRGDS (20 mg/kg) significantly prevented the alteration of radiolabeled platelet distribution in blood and liver when induced by LPS. Furthermore, triflavin but not GRGDS markedly suppressed the elevation in plasma thromboxane B 2 concentration within the 4-hour period of LPS administration. In LPS-treated rats, the 5-hydroxytryptamine level was lower in the blood and higher in the liver compared with levels in normal saline–treated rats. Pretreatment with triflavin (500 μg/kg) significantly reversed the 5-hydroxytryptamine concentration in blood and liver of LPS-treated rats. In histological examinations and platelet adhesion assay, triflavin markedly inhibited the adhesion of platelets to subendothelial matrixes in vivo and in vitro. Conclusions —The results indicate that triflavin effectively prevents thrombocytopenia, possibly through the following 2 mechanisms: (1) Triflavin markedly inhibits platelet aggregation, resulting in decreased thromboxane A 2 formation. (2) It inhibits the adhesion of platelets to subendothelial matrixes, thereby leading to a reversal in the distribution of platelets in blood and liver in LPS-treated rats.
STATE INSURANCE AND THE POOR LAW COMMISSION
Authors: J. H. Keay
Journal: BMJ (1910)

Vomiting: as in a large measure the comfort of the patient depends upon the amount of vomiting, I have followed -my after-results closely.At first sight they do not appear good, but it must be remembered that most of ihese patients swallow'some blood, and in my experience this is practically always vomited.Then, as the majority of the vomiting takes place before complete consciousness is established, the patient knows little or nothing about itt -In only one case was treatment for the vomiting Of the oases on whom these observations were made- Vomited.Did not Vomit.77 per cent. 23 per cent.Of the patients who vomited- 30 per cent.vomited ... ... Once.27.5 per cent.vomited ... ... Twice. 25per cent.vomited ... ... Three times. 5per cent.vomited .Four times.2.5 per cent.vomited .Five times. 5per cent.vomited ... ... Six times.*5 per cent.; vomiting lasted over twelve hours.*One case vomited for twenty-four hours, and required special treatment. CONCLUSIONS.From the foregoing remarks it will be seen that patients anaesthetized by this method are easily given open ether for operations on the throat and nose.The chief difficulty met with is excessive secretion, which I have never seen unless adrenalin-had been used.This excessive secretion has only followed the use of strong and never the use of weak (1 in 5,000 and under) adrenalin.The method of using the post-nasal plug has been described at length; having once tried it on a suitable case, no one, I am sure, would ever be without it.Another point I wish to emphasize is the reflex effeots occasionally met with in submucous resections.From my
Decreasing mitochondrial fission diminishes vascular smooth muscle cell migration and ameliorates intimal hyperplasia
Authors: Li Wang, Tianzheng Yu, Hakjoo Lee, Dawn K. O'Brien, Hiromi Sesaki, Yisang Yoon
Journal: Cardiovascular Research (2015)

Vascular smooth muscle cell (VSMC) migration in response to arterial wall injury is a critical process in the development of intimal hyperplasia. Cell migration is an energy-demanding process that is predicted to require mitochondrial function. Mitochondria are morphologically dynamic, undergoing continuous shape change through fission and fusion. However, the role of mitochondrial morphology in VSMC migration is not well understood. The aim of the study is to understand how mitochondrial fission contributes to VSMC migration and provides its in vivo relevance in the mouse model of intimal hyperplasia. In primary mouse VSMCs, the chemoattractant PDGF induced mitochondrial shortening through the mitochondrial fission protein dynamin-like protein 1 (DLP1)/Drp1. Perturbation of mitochondrial fission by expressing the dominant-negative mutant DLP1-K38A or by DLP1 silencing greatly decreased PDGF-induced lamellipodia formation and VSMC migration, indicating that mitochondrial fission is an important process in VSMC migration. PDGF induced an augmentation of mitochondrial energetics as well as ROS production, both of which were found to be necessary for VSMC migration. Mechanistically, the inhibition of mitochondrial fission induced an increase of mitochondrial inner membrane proton leak in VSMCs, abrogating the PDGF-induced energetic enhancement and an ROS increase. In an in vivo model of intimal hyperplasia, transgenic mice expressing DLP1-K38A displayed markedly reduced ROS levels and neointima formation in response to femoral artery wire injury. Mitochondrial fission is an integral process in cell migration, and controlling mitochondrial fission can limit VSMC migration and the pathological intimal hyperplasia by altering mitochondrial energetics and ROS levels.
Interleukin-11 promotes T cell polarization and prevents acute graft-versus-host disease after allogeneic bone marrow transplantation.
Authors: G R Hill, K R Cooke, T Teshima, J M Crawford, J C Keith, Y S Brinson, D Bungard, J L Ferrara
Journal: Journal of Clinical Investigation (1998)

Administration of IL-11 prevented lethal graft-versus-host disease (GVHD) in a murine bone marrow transplant (BMT) model (B6 --> B6D2F1) across MHC and minor H antigen barriers (survival at day 50: 90 vs 20%, P < 0.001). Surpisingly, IL-11 administration polarized the donor T cell cytokine responses to host antigen after BMT with a 50% reduction in IFNgamma and IL-2 secretion and a 10-fold increase in IL-4. This polarization of T cell responses was associated with reduced IFNgamma serum levels and decreased IL-12 production in mixed lymphocyte cultures (MLC). In addition, IL-11 prevented small bowel damage and reduced serum endotoxin levels by 80%. Treatment with IL-11 also reduced TNFalpha serum levels and suppressed TNFalpha secretion by macrophages to LPS stimulation in vitro. IL-11 thus decreased GVHD morbidity and mortality by three mechanisms: (a) polarization of donor T cells; (b) protection of the small bowel; and (c) suppression of inflammatory cytokines such as TNFalpha. We conclude that brief treatment with IL-11 may represent a novel strategy to prevent T cell-mediated inflammatory processes such as GVHD.
Specific IgE to reindeer epithelium in Finnish reindeer herders
Authors: K. Reijula, L. Halmepuro, M. Hannuksela, E. Larmi, J. Hassi
Journal: Allergy (1991)

Reindeer herding is a major source of living for more than 4200 inhabitants in northern Finland. To determine the prevalence of allergic symptoms among reindeer herders clinical examinations and skin prick tests (SPT) with nine inhalant allergens were performed in 211 randomly selected men from 21 to 69 (mean 45) years. Specific IgE antibodies to reindeer epithelium (RE) and total serum IgE were evaluated in 99 herders, five persons who handled reindeer leather indoors, 21 atopic patients with cow allergy and another 20 subjects with specific IgE to other inhalant allergens. Positive SPT to RE was detected in one and specific IgE by using enzyme allergosorbent test (EAST) (≥ 0.8 PRU/ml) in seven herders. Specific IgE to RE was also demonstrated in one control. Using RAST inhibition a patient with cow allergy did not show cross‐reactivity between cow and RE while another patient did. Thus, RE should be included in the allergy test panel when hypersensitivity to RE is suspected.
Haemoptysis with a normal chest radiograph: how concerned should we be?
Authors: G. L Colice
Journal: Thorax (2009)

In this issue of Thorax ( see page 854 ), Thirumaran and colleagues describe their experience with a consecutive group of patients evaluated for haemoptysis who had a normal chest radiograph.1 Over a 4-year period these investigators identified 270 patients who were evaluated for this problem. They made two important observations. First, they found that 26 of the 270 patients (9.6%) had respiratory tract malignancies as the cause of the haemoptysis. Of these 26 respiratory tract malignancies, 20 were non-small cell lung cancer (NSCLC) and 2 were small cell lung cancer. Secondly, they performed both fibreoptic bronchoscopy (FOB) and chest CT on the majority of the 270 patients evaluated. Overall, at least 269 FOBs and 257 CTs were performed to diagnose these 22 lung cancers. These observations lead to a series of fundamentally important questions for doctors to consider.

Why should haemoptysis with a normal chest radiograph be a concern? Haemoptysis can be massive and life-threatening, by causing either airway compromise or haemodynamic insufficiency. Fortunately, haemoptysis is rarely massive. I work in a busy Intensive Care Unit (ICU; 19 beds and >1500 admissions per year) in a large urban hospital (907 beds and about 47 000 admissions per year) and we see probably only 1–2 cases of massive, life-threatening haemoptysis per year. In the study by Thirumaran et al , of the 275 episodes of haemoptysis, none was massive; the majority were described as simply streaks of bleeding. Although doctors should be aware of the risk of massive haemoptysis, most cases of haemoptysis represent minor bleeding which stops spontaneously. The real concern about haemoptysis with a normal chest radiograph is understanding the cause. As Thirumaran and colleagues point out, haemoptysis should be considered a possible signal of an underlying serious illness, particularly lung cancer. Doctors should not be lulled into believing that …
Combination antibiotic susceptibility testing in CF: disappointing clinical results
Authors: J Holme
Journal: Thorax (2005)

▴ Aaron SD, Vandemheen KL, Ferris W, et al . Combination antibiotic susceptibility testing to treat exacerbations of cystic fibrosis associated with multiresistant bacteria: a randomised, double-blind, controlled clinical trial. Lancet2005;366:463–71 [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] Patients with cystic fibrosis (CF) are often colonised with multiresistant organisms. In vitro data suggest that bactericidal activity may result from antibiotic synergy even if species are resistant to individual agents on routine resistance testing. Simultaneously testing the bactericidal activity of two or more antibiotics (multiple combination bactericidal antibiotic testing, MCBT) is one approach that has been suggested to … [1]: {openurl}?query=rft.jtitle%253DLancet%26rft.stitle%253DLancet%26rft.aulast%253DAaron%26rft.auinit1%253DS.%2BD.%26rft.volume%253D366%26rft.issue%253D9484%26rft.spage%253D463%26rft.epage%253D471%26rft.atitle%253DCombination%2Bantibiotic%2Bsusceptibility%2Btesting%2Bto%2Btreat%2Bexacerbations%2Bof%2Bcystic%2Bfibrosis%2Bassociated%2Bwith%2Bmultiresistant%2Bbacteria%253A%2Ba%2Brandomised%252C%2Bdouble-blind%252C%2Bcontrolled%2Bclinical%2Btrial.%26rft_id%253Dinfo%253Adoi%252F10.1016%252FS0140-6736%252805%252967060-2%26rft_id%253Dinfo%253Apmid%252F16084254%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1016/S0140-6736(05)67060-2&link_type=DOI [3]: /lookup/external-ref?access_num=16084254&link_type=MED&atom=%2Fthoraxjnl%2F60%2F11%2F915.atom [4]: /lookup/external-ref?access_num=000231022300027&link_type=ISI