tbuckley/cabot-search huggingface dataset:
Severe hypoglycemia was associated with increased risk for adverse clinical outcomes in type 2 diabetes
Authors: Rozalina Grubina, Steven A. Smith
Journal: Annals of Internal Medicine (2011)

ACP Journal Club15 February 2011Severe hypoglycemia was associated with increased risk for adverse clinical outcomes in type 2 diabetesRozalina Grubina, MD, Steven A. Smith, MDRozalina Grubina, MDMayo Clinic, Rochester, Minnesota, USA (R.G., S.A.S.)Search for more papers by this author, Steven A. Smith, MDMayo Clinic, Rochester, Minnesota, USA (R.G., S.A.S.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-154-4-201102150-02013 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationZoungas S, Patel A, Chalmers J, et al. Severe hypoglycemia and risks of vascular events and death. N Engl J Med. 2010;363:1410-8. https://pubmed.ncbi.nlm.nih.gov/20925543Clinical Impact RatingsGIM/FP/GP: Neurology: References1 Bonds DE, Miller ME, Bergenstal RM, et al. The association between symptomatic, severe hypoglycaemia and mortality in type 2 diabetes: retrospective epidemiological analysis of the ACCORD study. BMJ. 2010;340:b4909. [PMID: 20061358] Google Scholar2 Miller ME, Bonds DE, Gerstein HC, et al. The effects of baseline characteristics, glycaemia treatment approach, and glycated haemoglobin concentration on the risk of severe hypoglycaemia: post hoc epidemiological analysis of the ACCORD study. BMJ. 2010;340:b5444. [PMID: 20061360] Google Scholar3 American Diabetes Association. Executive summary: Standards of medical care in diabetes—2010. Diabetes Care. 2010;33 Suppl 1:S4-10. [PMID: 20042774] Google Scholar Author, Article, and Disclosure InformationAuthors: Rozalina Grubina, MD; Steven A. Smith, MDAffiliations: Mayo Clinic, Rochester, Minnesota, USA (R.G., S.A.S.)This article was published at Annals.org on 1 February 2011. Previousarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySevere Hypoglycemia and Risk of Subsequent Cardiovascular Events: Systematic Review and Meta-Analysis of Randomized Controlled Trials 15 February 2011Volume 154, Issue 4Page: JC2-13KeywordsCardiovascular disease riskCreatinineGlucoseHypoglycemiaInsulinMyocardial infarctionRenal diseasesRetinopathySystolic pressureType 2 diabetes ePublished: 15 February 2011 Issue Published: 15 February 2011 Copyright & PermissionsCopyright © 2011 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Neutrophil Apoptosis in the Acute Respiratory Distress Syndrome
Authors: GUSTAVO MATUTE-BELLO, W. CONRAD LILES, FRANK RADELLA, KENNETH P. STEINBERG, JOHN T. RUZINSKI, MECHTHILD JONAS, EMIL Y. CHI, LEONARD D. HUDSON, THOMAS R. MARTIN
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Little is known about neutrophil (PMN) apoptosis in the acute respiratory distress syndrome (ARDS). We uses morphologic criteria to count apoptotic PMN in bronchoalveolar lavage fluid (BAL) of 35 patients on Days 1, 3, 7, 14, and 21 of ARDS and 13 patients on Days 1 and 3 of risk for ARDS. We found that the proportion of apoptotic PMN in BAL was low throughout the course of ARDS. There was no significant difference between the percentage of apoptotic PMN in patients at risk and patients with established ARDS or between patients who lived (2.4%) and patients who died (1.8%). When normal human PMN were incubated in ARDS BAL, a significantly lower proportion became apoptotic (50 +/- 4%), as compared with PMN incubated in lavage fluid from normal volunteers (76 +/- 7%, p < 0.05). This antiapoptotic effect of ARDS BAL was blocked by immunodepleting BAL of G-CSF and GM-CSF. We conclude that the proportion of apoptotic PMN recovered from the lungs of patients with ARDS is low throughout the course of ARD S. Furthermore, BAL from patients with ARDS prolongs survival of normal human PMN in vitro, and this effect is partially mediated by G-CSF and GM-CSF.
Paroxysmal Ventricular Fibrillation in Two Patients with Hypomagnesemia
Authors: HENRY S. LOEB, RAYMOND J. PIETRAS, ROLF M. GUNNAR, JOHN R. TOBIN
Journal: Circulation (1968)

Paroxysmal ventricular fibrillation unassociated with heart block occurred in two patients with hypomagnesemia. In neither patient were other causes of the arrhythmia apparent. Temporary transvenous pacing successfully suppressed the episodes after drug therapy failed. Prolongation of the Q-T interval was a prominent electrocardiographic feature in both patients and is postulated to have resulted from a loss of intracellular potassium secondary to hypomagnesemia.
Obesity and respiratory infection in children.
Authors: B H Hutchinson-Smith
Journal: BMJ (1971)

pital as a day centre, but financed from hospital revenue.In a paper by us and C. M. Hyland3 the case was put that a day ward should not be provided by the hospital service to make up for the deficiencies of the welfare services, but should highlight these deficiencies so that they can be remedied.De Martino' stressed that as long as the finance of the National Health Service is divided into hos- pital, general practitioner, and local author- ity services, it is essential that the hospital service should spend its money only to per- form a hospital function.We wish to draw the attention of those in the specialty of geriatric medicine to the fallacious reasoning and inherent dangers of the Department of Health's current method of financing day hospital running costs, which will penalize the smaller and busier day hospital with a high turnover at the expense of the larger day centre type of day hospital.-Weare, etc.,
Cerebrovascular response to acute hypocapnic and eucapnic hypoxia in normal man
Authors: William Shapiro, Albert J. Wasserman, James P. Baker, John L. Patterson
Journal: Journal of Clinical Investigation (1970)

Alterations in human cerebral blood flow and related blood constituents were studied during exposure to acute hypoxia. Observations were made during serial inhalation of decreasing O(2) concentrations with and without maintenance of normocarbia, during 8 min inhalation of 10% O(2), and after hyperventilation at an arterial P(O2) of about 40 mm Hg. In the range of hypoxemia studied, from normal down to arterial P(O2) of about 40 mm Hg, the magnitude of the cerebral vasodilator response to hypoxia appeared to be largely dependent upon the coexisting arterial CO(2) tension. The mean slope of the increase in cerebral blood flow with decreasing arterial O(2) tension rose more quickly (P < 0.05) when eucapnia was maintained when compared with the slope derived under similar hypoxic conditions without maintenance of eucapnia. When 12 subjects inhaled 10% oxygen, cerebral blood flow rose to more than 135% of control in four whose mean decrease in arterial CO(2) tension was - 2.0 mm Hg. The remaining eight had flows ranging from 97 to 120% of control, and their mean decrease in CO(2) tension was - 5.1 mm Hg. When mean arterial P(O2) was 37 mm Hg, hyperventilation was carried out in 10 subjects. Arterial P(O2) increased insignificantly, arterial P(CO2) declined from 34 to 27 mm Hg (P < 0.05), and cerebral blood flow which had been 143% of control decreased to 109%, a figure not significantly different from control.These data demonstrate the powerful counterbalancing constrictor effects of modest reductions in CO(2) tension on the vasodilator influence of hypoxia represented by arterial P(O2) reductions to about 40 mm Hg. Indeed, mild hyperventilation completely overcame the vasodilator effect provided by an arterial O(2) tension as low as 40 mm Hg. The effects of hypoxia on the control of the cerebral circulation must be analyzed in terms of the effects of any associated changes in CO(2) tension.
PMO-121 Osteopontin promotes natural killer T (NKT) cell accumulation in nonalcoholic steatohepatitis (NASH)
Authors: E Liaskou, L C Claridge, R Younis, H Shah, J Shaw, Y H Oo, Z Mi, P C Kuo, A Canbay, D H Adams, A M Diehl, W K Syn
Journal: Gut (2012)

<h3>Introduction</h3> Progressive steatohepatitis is characterised by increased inflammatory cell infiltration. Osteopontin (OPN) is a cytokine intricately associated with immune-cell accumulation, and we reported that NKT cells accumulate to promote hepatic injury in NASH. We hypothesise that OPN promotes NASH progression by supporting NKT migration across hepatic sinusoidal endothelium. <h3>Methods</h3> Mice were fed chow or methionine-choline deficient (MCD) diet to induce NASH. After 4 weeks, mice were sacrificed; severity of disease assessed by serum aminotransferase (AST), liver OPN quantified by QRTPCR and immunohistochemistry, blood OPN measured by ELISA. In separate studies, MCD-fed mice were treated with sham or OPN aptamers, and FACS used to quantify liver NKTs. Primary human hepatic sinusoidal endothelial cells (HSEC) were stimulated with recombinant (r)OPN (0–1000 ng/ml), with or without TNFa (20 ng/ml)+IFNg (100 ng/ml), and expression of adhesion molecules (ICAM1, VCAM1) and chemokines (CXCL9, 10, 11, 16) assessed. To assess lymphocyte migration, lymphocytes were perfused over rOPN—or vehicle-treated-HSEC, with or without TNFa+IFNg. In separate experiments, TNFa+IFNg stimulated-HSEC were treated with OPN aptamers or blocking antibodies, and total lymphocyte adhesion recorded. Human NASH livers were immunostained for OPN, plasma measured for OPN, and liver NKT numbers from normal or NASH-cirrhotic patients quantified by FACS. <h3>Results</h3> In mice, MCD-induced NASH upregulated expression of liver OPN by threefolds (p&lt;0.05), blood OPN by twofolds (p&lt;0.05), increased liver CD4 by 2.2-fold, and NKT cells by threefold (p&lt;0.05). MCD-fed mice treated with OPN aptamers accumulated fewer CD4 and NKT cells (p&lt;0.05), and exhibited attenuated injury (ALT: twofold reduction; p&lt;0.02). rOPN induced expression of ICAM-1, VCAM-1 and CD31 on human HSEC, enhanced lymphocyte recruitment under conditions of flow (40%), and amplified recruitment ability of TNFa+IFNg stimulated HSEC (20%), while OPN neutralisation with RNA-aptamers reduced lymphocyte recruitment by 50% (all p&lt;0.05). OPN effects were mediated via CD44, a<sub>v</sub>b<sub>3</sub>, ICAM1, VCAM1, and CXCL16. In humans, liver and plasma OPN was significantly upregulated in NASH; livers from NASH-cirrhosis harboured twofolds more CD4 and threefolds more NKT cells (p&lt;0.05) than normal. <h3>Conclusion</h3> Liver and plasma OPN levels are upregulated during steatohepatitis in mice and humans, and promote liver NKT accumulation. OPN neutralisation significantly reduces lymphocyte subset recruitment and liver injury, suggesting that OPN is a promising anti-inflammatory target in steatohepatitis. <h3>Competing interests</h3> None declared.
Cell Patterning: Patterned Three‐Dimensional Encapsulation of Embryonic Stem Cells using Dielectrophoresis and Stereolithography (Adv. Healthcare Mater. 3/2013)
Authors: Piyush Bajaj, Daniel Marchwiany, Carlos Duarte, Rashid Bashir
Journal: Advanced Healthcare Materials (2013)

The integration of dielectrophoresis (DEP) with stereolithography (SL) apparatus for the spatial patterning of cells on custom-made gold micro-electrodes is reported by Rashid Bashir and co-workers on page 450. After patterning, the cells are encapsulated in poly (ethylene glycol) diacrylate (PEGDA) hydrogels of different stiffnesses. This robust and flexible in vitro platform can enable various applications in stem cell differentiation and tissue engineering by mimicking elements of the native 3D in vivo cellular micro-environment.
Abstract 3215: Role of pterostilbene on proliferation, invasion, and migration in ovarian and uterine cancer cells
Authors: Gina Lowe, Wei Wen, Cai Roberts, James Finlay, Carlotta Glackin, Ernest Han, Thanh H. Dellinger
Journal: Cancer Research (2014)

Abstract PURPOSE: To determine the functional effects of the resveratrol analog, pterostilbene (PTE), and its potential adjuvant role with cisplatin, in ovarian and uterine cancer cells. EXPERIMENTAL DESIGN: The human ovarian cancer cell lines (OVCAR8, SKOV3) and uterine cancer cell lines (HEC1A, ECC1) were obtained from ATCC, and grown according to standard protocols using recommended media. Standard proliferation (MTT) and migration assays were performed in routine fashion, with or without PTE +/- cisplatin treatment. For the in-vitro Cell Proliferation Assay, different concentrations of cisplatin (3 - 50 μM), pterostilbene (PTE) (30 - 500 μM), or both in combination were added for 72 hours. Cell migration was assayed using 24-mm diameter chambers with 8-μm pore filters, with or without treatment of PTE and cisplatin, and migrated cells were counted using Image-pro program. A synergistic analysis from the MTT assay results was calculated via the CompuSyn for Windows computer program based on the combination index (CI) theorem of Chou-Talalay, to determine the presence of synergy between cisplatin and PTE. RESULTS: PTE reduces proliferation in OVCAR8, SKOV3, HEC1A, and ECC1 cells, and its anti-proliferative effect approaches that of cisplatin. Addition of PTE to cisplatin potentiates the anti-proliferative effects of cisplatin in HEC1A, ECC1, SKOV3, and OVCAR8 cells. The combined effect of PTE and cisplatin is synergistic in OVCAR8 cells based on synergy calculations (CI&amp;lt;1). PTE reduces cell migration in HEC1A and OVCAR8 cells, and its addition to cisplatin treatment improves the anti-migratory effect. CONCLUSIONS: Pterostilbene, a resveratrol analog with improved bioavailability, reduces proliferation and migration in ovarian and uterine cancer cells, and potentiates the anti-proliferative and anti-migratory effects of cisplatin, thus presenting as an attractive non-toxic alternative for potential adjuvant chemotherapy in ovarian and uterine cancer. Citation Format: Gina Lowe, Wei Wen, Cai Roberts, James Finlay, Carlotta Glackin, Ernest Han, Thanh H. Dellinger. Role of pterostilbene on proliferation, invasion, and migration in ovarian and uterine cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3215. doi:10.1158/1538-7445.AM2014-3215
Putting the Patient in Patient Safety
Authors: William M. Sage
Journal: JAMA (2002)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Pfizer's open data policy should include trials of off-label uses, say critics
Authors: Z. Kmietowicz
Journal: BMJ (2013)

A commitment from the pharmaceutical giant Pfizer to extend access to the data it holds on drug trials in patients has been criticised for excluding studies of unlicensed uses.

On 4 December Pfizer announced that it was updating its clinical trial access policy, claiming that the move would “simplify and broaden access to information gathered in Pfizer-sponsored clinical trials.”1

From 1 January 2014, the company said, researchers will be able to apply to access anonymised, patient level data of approved or discontinued products posted on clinicaltrials.gov 24 months after trials have been completed.

But the doctor and author of Bad Pharma , Ben Goldacre, said that excluding off-label studies from transparency was “a senseless loophole.”

He said that so far Pfizer had been fined for promoting unlicensed uses …
Supplying Clotting Factors From Hematopoietic Stem Cell–derived Erythroid and Megakaryocytic Lineage Cells
Authors: Michel Sadelain, Alex Chang, Leszek Lisowski
Journal: Molecular Therapy (2009)

Systemically distributed proteins such as clotting factors have been traditionally expressed from muscle or liver to achieve therapeutic, long-term expression. As long-lived cell capable of generating an abundant progeny, hematopoietic stem cells (HSCs) also merit consideration for this purpose. To be clinically relevant, this approach would require that hematopoietic cells be capable of expressing high levels of functional, secreted proteins, that the risk of insertional oncogenesis be minimized, and that sufficient stem cell engraftment be achieved following minimally invasive conditioning. Recent reports demonstrate the feasibility of expressing either factor IX (FIX) or factor VIII (FVIII) in erythroblasts and platelets using lineage-restricted vectors, resulting in effective treatments in mouse models of hemophilia. The erythroid system is especially powerful in providing high protein output, yielding FIX levels approaching 1 micro g/ml per vector copy in the plasma of long-term hematopoietic chimeras, a secretion level that vastly outperforms any other current mammalian constitutive or long-terminal repeat (LTR)-driven vector system. These early but promising studies raise the prospect of further developing these strategies for clinical investigation.
A genome-wide association study of metabolic traits in human urine
Authors: Karsten Suhre, Henri Wallaschofski, Johannes Raffler, Nele Friedrich, Robin Haring, Kathrin Michael, Christina Wasner, Alexander Krebs, Florian Kronenberg, David Chang, Christa Meisinger, H-Erich Wichmann, Wolfgang Hoffmann, Henry Völzke, Uwe Völker, Alexander Teumer, Reiner Biffar, Thomas Kocher, Stephan B Felix, Thomas Illig, Heyo K Kroemer, Christian Gieger, Werner Römisch-Margl, Matthias Nauck
Journal: Nature Genetics (2011)
The Economics of Financing Medicare
Authors: Katherine Baicker, Michael E. Chernew
Journal: New England Journal of Medicine (2011)

The pressure the Medicare program puts on the federal budget has been much discussed, but financing Medicare also has broader implications for the economy. Medicare expenditures currently account for 15% of federal spending and 3.6% of the total gross domestic product (GDP).1 Moreover, Medicare spending grew an average of about 2.5 percentage points faster than the GDP from 1975 through 2008,2 consuming a rapidly increasing share of the country's total resources.Health care services provided to Medicare beneficiaries are paid for by a combination of dedicated taxes and general revenues — in addition to the care financed by supplemental plans . . .
Abstract 1447: An unbiased screen for Nm23-H1 interacting proteins identifies the cytoskeletal crosslinking protein Ezrin
Authors: Jean-Claude A. Marshall, Joshua Collins, Ming Zhou, Timothy Veenstra, Chand Khanna, Patricia Steeg
Journal: Cancer Research (2011)

Abstract We hypothesized that Nm23-H1 may suppress metastasis through binding and inactivation of proteins that promote aggressive behavior. An unbiased survey of Nm23-H1 binding proteins was conducted in a 4T1 murine mammary carcinoma model system. Flag tagged Nm23-H1 and its mouse variant, -M1, were transfected into 4T1 mouse mammary cancer cells. Clonal lines were inoculated into the number four mammary fat pad of mice and allowed to grow for 10 days prior to excision due to size of the primary tumor. Mice were then imaged weekly for the remainder of the experiment, 8 weeks to follow the metastatic spread of the 4T1 cells from each group. Primary tumor size was unaffected by over-expression of Nm23-H1 or -M1. Histological examination revealed a 75% decrease in liver metastasis by Nm23-H1 or -M1 over-expression (P &amp;lt; 0.001). To characterize Nm23-H1/M1 binding proteins, Flag tagged Nm23 from both H1 and M1 clones were immunoprecipitated (IP) from in vitro cell lines as well as isolated primary tumors, lymph nodes, spleen and liver tissue after verification of metastasis by histological examination of the tissue. Mass spectrometry analysis of IP samples from cell lines and primary tumors showed 99 proteins of interest including Ezrin. Co-IP of Ezrin and Nm23-H1/M1 has been confirmed using both Nm23 and Ezrin as the IP antibodies, implicating Ezrin as a potential binding partner of NM23-H1 and M1. Ezrin belongs to a family of widely expressed proteins known as ERMs which have been described to link the actin cytoskeleton to membrane signaling pathways. To rule out potential interaction due to F-actin, cells were exposed to latrunculin B and co-IP of Nm23-H1 and Ezrin was again verified, indicating that the Ezrin and Nm23-H1/M1 interaction is not due to F-actin binding. To further elucidate this interaction plasmid constructs expressing either the N terminal FERM domain or C terminal F-actin binding domain of Ezrin coupled to GFP were constructed. Co-IP showed a binding of Nm23-H1 to the N terminal domain of Ezrin. In addition the expression of the N terminal overcame the motility and invasive inhibitory phenotype of Nm23-H1 expression in both 4T1 and MDA-MB-231 cells. The data identify a novel interaction of the metastasis suppressor Nm23-H1 and the cytoskeletal linker Ezrin. Suppression of metastasis by Nm23-H1 may be due, in part, to the abrogation of a pro-invasive function of the N-terminus of Ezrin. 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 1447. doi:10.1158/1538-7445.AM2011-1447