tbuckley/cabot-search huggingface dataset:
Abstract P209: Which Comes First, Type 2 Diabetes (T2DM) or Hypertension?
Authors: Kazuko Masuo, Gavin W Lambert
Journal: Circulation (2014)

Objectives: It is well demonstrated that there is a higher prevalence of hypertension (HT) in patients with type 2 diabetes (T2DM) than non-DM individuals as well as higher prevalence of DM in HT than normotensives (NT). However, it has not been clarified which of DM or HT leads to other, and what mechanisms may play a major role. Methods: In the present study, we compared neurohormonal parameters in the following 4 groups in weight loss (WL) program with a mild calorie restriction and exercise over 12 weeks; 53 obese NT without DM, 44 NT with T2DM, 68 HT without DM, and 43 HT with T2DM. HT and T2DM were all diagnosed in the last 3 months and none had medications. At entry period, the 4 groups were strictly matched in BMI and in BP. They were measured BMI, total body fat-mass, waist/hip ratio (W/H), BP, PR, HbA 1c , fasting glucose, insulin (HOMA-IR), norepinephrine (NE) and leptin (LEP) at entry, 4 and 12 weeks. Results: At entry, fat-mass was greater in subjects with T2DM than non-DM in both NT and HT and HT had slightly greater fat-mass than NT, although BMI were strictly matched in the 4 study groups. HbA 1c in T2DM was greater than non-DM, and slightly greater in HT than NT. Fasting insulin was greater in HT and T2DM than NT or non-DM, and HOMA-IR was slightly greater in HT than NT and significantly greater in T2DM than non-DM. LEP was similar between NT and HT, but it was greater in T2DM than non-DM. (HbA 1c , HT with T2DM&gt;NT with T2DM&gt;&gt;HT without DM&gt;NT without DM; Insulin, HT with T2DM&gt;NT with T2DM&gt;&gt;HT without DM&gt;NT without DM; NE, HT with T2DM&gt;&gt;HT without DM≥NT with T2DM&gt;&gt;NT without DM; LEP, HT with T2DM≈NT with T2DM&gt;&gt;HT without DM&gt;NT without DM). WL over 12 wks in HT and T2DM were smaller than those in NT or non-DM. At 12 weeks, in HT groups regardless of T2DM, percent (%) decreases in plasma NE and BP, and reductions in HbA 1c were smaller than those in NT groups, although reductions in fat-mass and leptin were similar. In T2DM groups regardless of BP levels at entry, reductions in BMI, BP, HbA 1c , HOMA-IR and NE were smaller than those in non-DM group. In the 4 groups, reductions in plasma NE was observed at first followed by reductions in HOMA-IR, HbA 1c, BMI and BP over 12 weeks. Conclusions: These findings demonstrate that insulin resistance (IR) may play an important role on the onset of T2DM and high plasma NE appears to cause HT. HT had resistance to normalized high plasma NE and %reductions in NE, and T2DM had resistance to normalize IR and sympathetic overactivity. We previously reported that high plasma NE could predict future weight gain and BP elevation, and high NE preceded IR in non-obese subjects. Taken together, sympathetic overactivity observed in high NE may cause obesity and HT, and then IR seems to start with weight gain leading T2DM, suggesting that HT may lead to T2DM with this mechanisms.
Comparison of single-dose and escalating-dose regimens of donor lymphocyte infusion for relapse after allografting for chronic myeloid leukemia
Authors: F. Dazzi, R. M. Szydlo, C. Craddock, N. C. P. Cross, J. Kaeda, A. Chase, E. Olavarria, F. van Rhee, E. Kanfer, J. F. Apperley, J. M. Goldman
Journal: Blood (2000)
Potential association of specific Candida parapsilosis genotypes, bloodstream infections and colonization of health workers' hands
Authors: D. Delfino, F. Scordino, I. Pernice, C. Lo Passo, R. Galbo, A. David, I. Barberi, G. Criseo, A. Cascio, O. Romeo
Journal: Clinical Microbiology and Infection (2014)
Association of Erythrodermic Cutaneous T-Cell Lymphoma, Superantigen-Positive Staphylococcus aureus, and Oligoclonal T-Cell Receptor Vβ Gene Expansion
Authors: Clotilde M. Jackow, Jennifer C. Cather, Vicki Hearne, Arisa T. Asano, James M. Musser, Madeleine Duvic
Journal: Blood (1997)
Mortality Among Injured Children Treated at Different Trauma Center Types
Authors: Chethan Sathya, Aziz S. Alali, Paul W. Wales, Damon C. Scales, Paul J. Karanicolas, Randall S. Burd, Michael L. Nance, Wei Xiong, Avery B. Nathens
Journal: JAMA Surgery (2015)

IMPORTANCE Trauma is the leading cause of death among US children.Whether pediatric trauma centers (PTCs), mixed trauma centers (MTCs), or adult trauma centers (ATCs) offer a survival benefit compared with one another when treating injured children is controversial.Ascertaining the optimal care environment will better inform quality improvement initiatives and accreditation standards.OBJECTIVE To evaluate the association between type of trauma center (PTC, MTC, or ATC) and in-hospital mortality among young children (5 years and younger), older children (aged 6-11 years), and adolescents (aged 12-18 years). DESIGN, SETTING, AND PARTICIPANTSIn this retrospective cohort study, injured children aged 18 years or younger who were hospitalized in the United States from January 1, 2010, to December 31, 2013, were observed for the duration of their admission until discharge or death.We included patients with an Abbreviated Injury Score of 2 or greater in at least 1 body region.Random-intercept multilevel regression was used to evaluate the association between center type and in-hospital mortality after adjusting for confounders.Stratified analyses in young children, older children, and adolescents were performed.We conducted secondary analyses limited to patients with severe injuries (Injury Severity Score Ն25).Both analyses were performed between January 1 and August 31, 2014.Data were derived from 252 US level I and II trauma centers voluntarily participating in the American College of Surgeons adult or pediatric Trauma Quality Improvement Program. MAIN OUTCOME AND MEASUREIn-hospital mortality. RESULTSWe identified 175 585 injured children.Crude mortality rates were 2.3% for children treated at ATCs, 1.8% for children treated at MTCs, and 0.6% for children treated at PTCs.After adjustment, children had higher odds of dying when treated at ATCs (odds ratio [OR], 1.57; 95% CI, 1.15-2.14)and MTCs (OR, 1.45; 95% CI, 1.05-2.01)compared with those treated at PTCs.In stratified analyses, young children had higher odds of death when treated at ATCs vs PTCs (OR, 1.78; 95% CI, 1.05-3.40),but there was no association between center type and mortality among older children (OR, 1.17; 95% CI, 0.65-2.11)and adolescents (OR, 1.23; 95% CI, 0.82-1.85).Results were similar in analyses of severely injured children: those treated at ATCs (OR, 1.75; 95% CI, 1.25-2.44)and MTCs (OR, 1.62; 95% CI, 1.15-2.29)had higher odds of death when compared with those treated at PTCs. CONCLUSIONS AND RELEVANCEInjured children treated at ATCs and MTCs had higher in-hospital mortality compared with those treated at PTCs.This association was most evident in younger children and remained significant in severely injured children.Quality improvement initiatives geared toward ATCs and MTCs are required to provide optimal care to injured children.
A Manual of Selected Biochemical Methods, as Applied to Urine, Blood and Gastric Analysis.
Authors: Frank Pell Underhill
Journal: JAMA (1922)

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
Abstract 1609: Proline-directed kinase signaling in human hepatocellular carcinomas developed on non-fibrotic liver
Authors: Saïd Taouji, Kristen Leong, Lee A. Beausang, Daniela Arma, Violaine Moreau, Charles Balabaud, Paulette Bioulac-Sage, Jessica Zucman-Rossi, Martin Latterich, Jean Rosenbaum, Eric Chevet
Journal: Cancer Research (2014)

Abstract Ten to 40% hepatocellular carcinoma (HCC) arise on non-cirrhotic liver, including 5% on non-fibrotic liver (nfHCC). These tumors provide an interesting model for the analysis of the hepatocarcinogenesis pathways without the confounding factors associated with cirrhosis. Carcinogenesis has been often associated with the deregulation of phosphorylation-dependent signaling pathways. Quantitative phosphoproteomics recently allowed us to unravel the specific activation of proline-directed kinases (PDK) in nfHCC. Our aim was then to use medium throughput analytical tools (Alphascreen® and AMMP®) to evaluate the activation status of PDK dependent signaling pathways in a series of nfHCC samples. We have used a phosphoproteomics set comprising surgical samples from nfHCC (METAVIR F0 or F1) and samples of histologically normal livers. Proteins were extracted and analyzed for the activation status of select signaling pathways such as MAPK using both Alphascreen® and AMMP® technologies. Because MAPK are prototypic PDKs and are deregulated in many cancers, we analyzed their activation in a series of 25 nfHCC as compared to 6 non-tumor samples and found an overall increased activity in nfHCC samples. Moreover the phosphorylation status of Calnexin, a MAPK substrate found in the phosphoproteomics analysis was monitored and compared in nfHCC samples. In conclusion, we have identified phosphopeptide signatures in human samples of nfHCC that led to the identification of a deregulated PDK-dependent network in those tumors. The elucidation of the functional causes and consequences of such deregulation is ongoing. Citation Format: Saïd Taouji, Kristen Leong, Lee A. Beausang, Daniela Arma, Violaine Moreau, Charles Balabaud, Paulette Bioulac-Sage, Jessica Zucman-Rossi, Martin Latterich, Jean Rosenbaum, Eric Chevet. Proline-directed kinase signaling in human hepatocellular carcinomas developed on non-fibrotic liver. [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 1609. doi:10.1158/1538-7445.AM2014-1609
Abstract 13566: Pitavastatin Regulates mTOR Complex 1 Signaling Through Inhibition of Rheb in T Cells
Authors: Kazuko Tajiri, Nobutake Shimojo, Satoshi Sakai, Tomoko Machino-Ohtsuka, Kyoko Imanaka-Yoshida, Michiaki Hiroe, Taizo Kimura, Akira Sato, Kazutaka Aonuma
Journal: Circulation (2014)

Accumulated evidence has shown that statins have anti-inflammatory and immunomodulatory effects; however, the mechanism has not been fully elucidated. Here we report that pitavastatin inhibited mTOR complex 1 (mTORC1) activity by inhibiting the farnesylation of the small GTPase Rheb in murine T cells. As a result of The 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibition, statins regulate the biosynthesis of cholesterol and isoprenoid farnesylpyrophosphate (farnesyl-PP) that mediates the farnesylation and membrane association of Rheb. Pitavastatin-treated T cells failed to differentiate into T helper (Th)1 and Th17 cells, and this failure was rescued by adding farnesyl-PP. Pitavastatin and a farnesyltransferase inhibitor affected the transcription of T-bet and RORγT which have critical roles in the development of Th1 and Th17 cells respectively. In a mouse model of experimental autoimmune myocarditis, a CD4+ T cell-mediated disease, pitavastatin treatment ameliorated the pathophysiological severity of myocarditis associated with reduced Th1 and Th17 responses and mTORC1 signaling. We conclude that statins reduce the inflammatory functions and pathogenic activity of T cells through inhibition of mTORC1 signaling, and that this pathway may be a potential therapeutic target for Th1- and Th17-related diseases.
Abstract 2613: Wnt/β-catenin signaling mediates the anti-tumor activity of three ginsenoside derivatives in lung cancer
Authors: Xiuli Bi
Journal: Cancer Research (2014)

Abstract In previous publication, the anti-tumor activity of 25-hydroxyprotopanaxadiol (25-OH-PPD), a natural compound isolated from fruits of Panax ginseng, has been studied. In the current study, we investigated the anti-tumor activity of three derivatives synthesized from 25-OH-PPD, namely xl, 1c, and 8b, respectively. All three compounds significantly inhibited the growth of human lung cancer cells in vitro, while having lesser effect on the growth of normal primary muscle cells. In vivo, oral administration of three compounds could significantly inhibit the growth of xenograft tumors without affecting body weight. Further mechanistic study demonstrated that these compounds could decrease the expression levels of β-catenin and its downstream targets Cyclin D1, CDK4, and c-myc in A549 cells. Taken together, the results suggested that the anti-tumor activity exerted by these 25-OH-PPD derivatives is partially through β-catenin mediated signaling pathway in lung cancer cells, a finding that could potentially translate into a chemotherapeutic strategy for the treatment of lung cancer. Note: This abstract was not presented at the meeting. Citation Format: Xiuli Bi. Wnt/β-catenin signaling mediates the anti-tumor activity of three ginsenoside derivatives in lung cancer. [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 2613. doi:10.1158/1538-7445.AM2014-2613
A radiation hybrid transcript map of the mouse genome
Authors: Philip Avner, Thomas Bruls, Isabelle Poras, Lorraine Eley, Shahinaz Gas, Patricia Ruiz, Michael V. Wiles, Rita Sousa-Nunes, Ross Kettleborough, Amer Rana, Jean Morissette, Liz Bentley, Michelle Goldsworthy, Alison Haynes, Eifion Herbert, Lorraine Southam, Hans Lehrach, Jean Weissenbach, Giacomo Manenti, Patricia Rodriguez-Tome, Rosa Beddington, Sally Dunwoodie, Roger D. Cox
Journal: Nature Genetics (2001)
New Studies Illuminate Brain DisordersCDC Director Invites Participation in Disease Control and PreventionMISCELLANEA MEDICANew Studies Illuminate Brain DisordersCDC Director Invites Participation in Disease Control and PreventionMISCELLANEA MEDICA
Authors: J Stephenson
Journal: JAMA (1999)

LOS ANGELES—The Society of Neuroscience’s annual meeting offers a scientific smorgasbord of new research findings about the brain and nervous system. The most recent meeting was no exception, with reports on areas ranging from the etiology of narcolepsy through the potential of nicotinelike drugs to enhance memory to a possible link between an infectious agent and Alzheimer disease (AD).
A simple validated method for predicting the risk of hospitalization for worsening of heart failure in ambulatory patients: the Redin‐SCORE
Authors: Jesús Álvarez‐García, Andreu Ferrero‐Gregori, Teresa Puig, Rafael Vázquez, Juan Delgado, Domingo Pascual‐Figal, Luis Alonso‐Pulpón, José R. González‐Juanatey, Miguel Rivera, Fernando Worner, Alfredo Bardají, Juan Cinca
Journal: European Journal of Heart Failure (2015)

Prevention of hospital readmissions is one of the main objectives in the management of patients with heart failure (HF). Most of the models predicting readmissions are based on data extracted from hospitalized patients rather than from outpatients. Our objective was to develop a validated score predicting 1-month and 1-year risk of readmission for worsening of HF in ambulatory patients.A cohort of 2507 ambulatory patients with chronic HF was prospectively followed for a median of 3.3 years. Clinical, echocardiographic, ECG, and biochemical variables were used in a competing risk regression analysis to construct a risk score for readmissions due to worsening of HF. Thereafter, the score was externally validated using a different cohort of 992 patients with chronic HF (MUSIC registry). Predictors of 1-month readmission were the presence of elevated natriuretic peptides, left ventricular (LV) HF signs, and estimated glomerular filtration rate (eGFR) <60 mL/min/m(2) . Predictors of 1-year readmission were elevated natriuretic peptides, anaemia, left atrial size >26 mm/m(2) , heart rate >70 b.p.m., LV HF signs, and eGFR <60 mL/min/m(2) . The C-statistics for the models were 0.72 and 0.66, respectively. The cumulative incidence function distinguished low-risk (<1% event rate) and high-risk groups (>5% event rate) for 1-month HF readmission. Likewise, low-risk (7.8%), intermediate-risk (15.6%) and high-risk groups (26.1%) were identified for 1-year HF readmission risk. The C-statistics remained consistent after the external validation (<5% loss of discrimination).The Redin-SCORE predicts early and late readmission for worsening of HF using proven prognostic variables that are routinely collected in outpatient management of chronic HF.
Stringency of Rate Control in Patients with Atrial Fibrillation and Heart Failure: Data of the Rate Control Efficacy in Permanent Atrial Fibrillation: a Comparison between Lenient versus Strict Rate Control II (RACE II) Study
Authors: Bart A. Mulder, Jan G. Tijssen, Hans L. Hillege, A. Marco Alings, Maarten P. Van den Berg, Harry J. Crijns, Ype S. Tuininga, Hessel F. Groenveld, Dirk J. Van Veldhuisen, Isabelle C. Van Gelder
Journal: Circulation (2010)
Chemotherapeutic Characterization in Mice of 2-Amino-9-β-D-ribofuranosylpurine-6-sulfinamide (Sulfinosine), a Novel Purine Nucleoside with Unique Antitumor Properties
Authors: Thomas L. Avery, Rick A. Finch, Karen M. Vasquez, Saeed Radparvar, Naeem B. Hanna, Ganapathi R. Revankar, Roland K. Robins
Journal: Cancer Research (1990)

Abstract  In preclinical investigations performed in mice, 2-amino-9-β-d-ribofuranosyl purine-6-sulfinamide (sulfinosine), a novel derivative of 6-thioguanosine (6TGR), was active against six solid tumors and four strains of experimental leukemia. Sulfinosine penetrated the central nervous system more readily than did 6TGR and, when given repeatedly, was much more effective in the treatment of L1210 leukemia, being curative for some mice. Other findings of major interest to us were the different dosing characteristics of sulfinosine and 6TGR, the divergent efficiencies of the two drugs in generating cellular resistance, and the activity of sulfinosine against experimental leukemias refractory to 6TGR and other experimental or clinically used chemotherapeutic agents. The chemotherapeutic characterization of sulfinosine that evolved from these studies suggests that this agent may have unique properties that deserve clinical consideration. Both the dosing characteristics of the drug and its pronounced activity against thiopurine-resistant experimental leukemia favor the possibility that sulfinosine could be used to advantage in the treatment of human leukemia unresponsive to 6-mercaptopurine or 6-thioguanine.
Primary Endpoint Results of the EVOLVE Trial
Authors: Ian T. Meredith, Stefan Verheye, Christophe L. Dubois, Joseph Dens, Jean Fajadet, Didier Carrié, Simon Walsh, Keith G. Oldroyd, Olivier Varenne, Seif El-Jack, Raul Moreno, Anita A. Joshi, Dominic J. Allocco, Keith D. Dawkins
Journal: Journal of the American College of Cardiology (2012)
Anatomy of an Illness as Perceived by the Patient. Reflections on Healing and Regeneration.
Authors: Norman Cousins
Journal: Annals of Internal Medicine (1980)

The premise of Norman Cousins's enormously influential work is that the human mind is capable of promoting the body's capacity for combating illness and healing itself even when faced with a seemingly hopeless medical predicament. The author recounts his personal experiences while working in close collaboration with his doctor to overcome a crippling and supposedly irreversible disease, and illustrates the life-saving and ultimately life-prolonging benefits to be gained by taking responsibility for one's own well-being. Cousins's story is inspirational reading for anyone contending with a serious illness.
Anthracycline Type during Induction Associated with Outcome in Pediatric t(8;21) and Inv(16) AML
Authors: Henrik Hasle, Jonas Abrahamsson, Evelina S De Bont, Valerie de Haas, Barbara De Moerloose, Erik Forestier, Shau Yin Ha, Jesper Heldrup, Kirsi Jahnukainen, Ólafur G Jónsson, Birgitte Lausen, Josefine Palle, Ardine Reedijk, Kadri Saks, Bernward Zeller
Journal: Blood (2014)
Abstract 15923: CaMKII Links ER Stress Signaling in Pressure Overload-Induced Left Ventricular Hypertrophy and Failure
Authors: Guangming Cheng, Lin Zhao, Lei Chen, Xing Chen, Arash Davani, Anweshan Samanta, Magdy Girgis, Harold Elias, Yanjuan Yang, Robert J Vincent, Jeryl Hauptman, Buddhadeb Dawn
Journal: Circulation (2014)

Introduction: Recent evidence indicates that the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays a key role in pathogenesis of cardiac hypertrophy and failure. The cytosolic calcium resulting from endoplasmic reticulum (ER) also involves CaMKII. However, the molecular connection between ER stress and LV hypertrophy remains unclear. Hypothesis: We hypothesized that CaMKII serves as the molecular link between ER stress and LV hypertrophy. Methods: We used mice with genetic deletion of C/EBP Homologous Protein (CHOP), a mediator of ER stress. Transverse aortic constriction (TAC) or sham surgeries were performed in age-matched male CHOP knockout (KO) mice and controls to induce pressure overload. Serial echocardiography was performed prior to (baseline, BSL) and weekly after TAC. Mice were sacrificed after 6 weeks for measurement of heart weight, morphometry, histology, and protein assays. Separate groups of CHOP KO and control mice were sacrificed at 2 weeks after TAC for protein assays. Results: Pressure overload resulted in progressive LV dysfunction (Figure) and hypertrophy in control mice compared with baseline. At 6 wks after TAC these adverse effects of pressure overload were significantly attenuated in CHOP KO mice as evidenced by greater LV EF (Figure) and smaller LV mass compared with controls. Compared with control hearts, phosphorylation of CaMKII was significantly reduced in CHOP KO hearts at 2 and 6 weeks after TAC (Figure). The phosphorylation of eIF2α, a signaling molecule upstream of CHOP in the ER stress pathway was significantly increased in CHOP KO hearts after TAC compared with control mice (Figure). Conclusion: Genetic deletion of CHOP attenuates LV hypertrophy and dysfunction induced by pressure overload; and CaMKII serves as a link between ER stress and hypertrophic signaling. Potential modulation of CaMKII and CHOP signaling may be used to ameliorate LV hypertrophy in patients with cardiovascular diseases.