tbuckley/cabot-search huggingface dataset:
5-lipoxygenase expression in dendritic cells generated from CD34+ hematopoietic progenitors and in lymphoid organs
Authors: Rainer Spanbroek, Markus Hildner, Dieter Steinhilber, Norbert Fusenig, Kozo Yoneda, Olof Rådmark, Bengt Samuelsson, Andreas J.R. Habenicht
Journal: Blood (2000)
Abstract P103: Patterns of Childhood Obesity and Relation to Middle-Age Sleep Apnea Risk: The Bogalusa Heart Study
Authors: TIAN HU, Suzanne Bertisch, Wei Chen, Jeanette Gustat, Larry Webber, Shengxu Li, Kirk Pak, Sathanur Srinivasan, Gerald Berenson, Lydia Bazzano
Journal: Circulation (2014)

Background: Patients with obesity have high risk of obstructive sleep apnea (OSA); however, the relationship between childhood obesity and later OSA risk is unknown. Methods: We prospectively examined the association between changes in overweight/obesity status in childhood and subsequent OSA in 823 middle-aged adults free of cardiovascular diseases at baseline and who had at least 2 measures of body mass index (BMI) between 4 and 18 yrs old (1974-) and responded to the Berlin Questionnaire in 2010. Childhood overweight/obesity was defined as age and gender specific BMI ≥85 th percentile based on 2000 CDC Growth Charts. Four groups were generated based on change in obesity status from the earliest to most recent visit in childhood: persistent normal weight, incident overweight (from normal to overweight), weight loss (from overweight to normal), and persistent overweight. Based on Berlin Questionnaire, high-risk OSA was defined as any 2 of the following: obesity or hypertension, persistent snoring symptoms, and persistent daytime sleepiness. Persistent snoring was defined as snoring on ≥3 nights/week, snoring louder than talking or very loud, and breathing pauses on ≥3 nights/week; and persistent daytime sleepiness was defined as feeling tired ≥3 days/week after sleeping, feeling tired during time awake ≥3 days/week, and falling asleep while driving. Results: Mean age was 42 yrs and mean BMI was 31.0 kg/m 2 in adulthood. Of the total, 43% were male, and 34% were African-American. There were 604, 68, 39, and 112 persons in the persistent normal weight, incident overweight, weight loss, and persistent overweight groups, respectively. Median time between measures of BMI in childhood was 5 yrs (IQR: 5 yrs) across the 4 groups. Over an average of 35 years follow-up from childhood to adulthood (IQR: 1 yr), 326 (38%) participants had high-risk of OSA. In multivariate log-linear regression models, compared to participants in persistent normal weight group, those in persistent overweight, incident overweight, and weight loss groups had 1.80 (95% CI: 1.48, 2.19), 1.61 (1.22, 2.12), and 1.28 (0.89, 1.87) times higher risk of OSA, after adjustment for age, gender, race, educational level, leisure-time physical activity, regular drinking, and current smoking. The persistent overweight group had significantly higher risk of persistent snoring symptoms than persistent normal group (RR: 1.39; 95% CI: 1.12, 1.73). Results were not statistically significant for persistent daytime sleepiness among the groups. Conclusions: Persistent overweight or change from normal weight to overweight in childhood was associated with a higher risk of OSA in middle age, while weight loss during childhood did not have higher risk of OSA in adulthood compared to their counterparts in the persistent normal weight group.
Does Intracoronary Thrombus Influence the Outcome of High Risk Percutaneous Transluminal Coronary Angioplasty? Clinical and Angiographic Outcomes in a Large Multicenter Trial fn1fn1This study was suppported by a grant from Centocor, Inc.
Authors: M.Musa Khan, Stephen G. Ellis, Frank V. Aguirre, Harlan F. Weisman, Nancy M. Wildermann, Robert M. Califf, Eric J. Topol, Neal S. Kleiman
Journal: Journal of the American College of Cardiology (1998)
Abstract 04: Fried Food Consumption and Genetic Predisposition to Obesity
Authors: Qibin Qi, Audrey Chu, Jae Kang, Majken Jensen, Gary Curhan, Pasquale Louis, Immaculata De Vivo, Andrew Chan, Hyon Choi, Rulla Tamimi, Paul Ridker, David Hunter, Walter Willett, Eric Rimm, Daniel Chasman, Frank Hu, Lu Qi
Journal: Circulation (2014)

Background: Fried food consumption has been associated with obesity; little is known about whether genetic background modifies this association. Methods: We analyzed interactions between a genetic risk score (GRS) based on 32 BMI-associated variants and fried food consumption on body mass index (BMI) and obesity in 9623 women from the Nurses’ Health Study (NHS) and 6379 men from the Health Professionals Follow-up Study (HPFS) and in a replication cohort of 21426 women from the Women’s Genome Health Study (WGHS). Results: An interaction between fried food consumption and the GRS on BMI was identified in both NHS and HPFS (P for interaction≤0.001). Among participants in the highest tertile of the GRS, the differences in BMI between individuals who consumed fried foods ≥4times/week and those consumed &lt;1time/week amounted to 1.0 in women and 0.7 kg/m2 in men, whereas the corresponding differences were 0.5 and 0.4 kg/m2 in the lowest tertile of the GRS. The gene-diet interaction was replicated in the WGHS (P for interaction&lt;0.001). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.2, 1.6, and 2.4 kg/m2 for fried food consumption&lt;1, 1-3 and ≥4times/week (P for interaction&lt;0.001) (Figure); and the odds ratios (95% CI) for obesity per 10 risk alleles were 1.60 (1.38-1.84), 2.13 (1.74-2.60) and 2.65 (2.08-3.39) across the three categories of consumption (P for interaction=0.002). In addition, we found that the individual variants in genes highly expressed or known to act in the central nervous system showed significant interactions, with the FTO variant showing the strongest result (P for interaction&lt;0.001). Conclusion: Fried food consumption may interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.
Chile approves emergency contraception pill
Authors: Emily Russell
Journal: BMJ (2001)

After two months of heated debate the Chilean health ministry has given the go-ahead to the distribution in Chile of emergency contraception after accepting that the drug is a form of contraception, rather than abortion.

Since the decision, the Public Health Institute has authorised the Chilean pharmaceutical firm Silesia to manufacture and supply the drug levonorgestrel under the brand name Postinal. The drug will be administered in two doses of 75 m g to be taken 12 hours apart.

The step …
NHS modernisation teams announced
Authors: Linda Beecham
Journal: BMJ (2000)

The health secretary has announced some of the members of the modernisation teams which will carry forward the five challenges for the NHS set out by the prime minister last week.

There will be six teams, each tackling a different area.

The partnership team includes John Hutton, minister of state, Department of Health (chairman); Christine Hancock, general secretary, Royal College of Nursing; Dr Ian Bogle, chairman, BMA council; Jo Williams, president, Association of …
Association of the New York State Marriage Equality Act With Changes in Health Insurance Coverage
Authors: Gilbert Gonzales
Journal: JAMA (2015)

When states recognize same-sex marriage, some workplaces are required to offer employer-sponsored health insurance (ESI) to married same-sex couples. 1 Research found laws establishing domestic partnerships for lesbian, gay, bisexual, and transgender (LGBT) populations increased health insurance coverage for lesbian women. 2 On July 24, 2011, New York State began licensing same-sex marriages under the state's Marriage Equality Act, and at least 12 280 marriage licenses were issued to same-sex couples in the following 18 months. 3 This study investigated the association between legalizing same-sex marriage in New York and changes in health insurance coverage in men and women.
Synergistic induccion of apoptosis in human breast cancer cells by proteasome and histone deacetylase inhibitors
Authors: Josep Domingo-Domenech, Marian Tapia, Pere Gascon, Joan Albanell, Oriol Bachs, Marta Bosch
Journal: Cancer Research (2006)

4694  Objective: Histone deacetylase inhibitors (HDACi) are a new class of anticancer agents which have shown to cause growth arrest, differentiation and/or apoptosis of many tumor cells. Previous studies have implicated acetylases and deacetylases in the regulation of the antiapoptotic transcription factor NF-κB. We hypothesize that proteasome inhibition will disrupt NF-κB activitation induced by HDACi and sensitize breast cancer cells to apoptosis. Material and Methods: Breast cancer cell lines (MDA-MB-231, BT474 and MCF-7) were treated with HDAC inhibitors (Trichostatin A -TSA- or Suberoylanilide hydroxamic acid -SAHA-), proteasome inhibitor (MG132) or both drugs simultaneously. BAY-11-7085 was used for selective NF-κB inhibition. Cell viability and apoptosis were tested by MTT Assay, Annexin V and caspase-3 activity. NF-κB activity was determinated by reporter gene expression and DNA binding assays. Expression of cell cycle regulatory and apoptosis related molecules, as well as phosphorylation of p38 and JNK were analysed by immunobloting. Results: HDACi induced breast cancer cell death in a dose dependent maner. SAHA and TSA significantly enhanced NF-κB dependent reporter gene transcription and DNA binding. These effects were inhibited by BAY 11-7085 and MG132. Co-expossure of cells to minimally toxic concentrations of MG132 plus HDACi resulted in a striking increase in cell death, caspase activitation and apoptosis. These events were associated with the up-regulation of p21 and p27, the down-regulation of Bcl-2 and cyclin D1, PARP cleavage and induction of the stress related kinases JNK and p38. Finally, pharmacologic interruption of NF-κB pathway by BAY 11-7085 mimicked the actions of proteasome inhibitor in promoting HDACi-induced cell death. Conclusion: Proteasome inhibition increased the efficacy of HDACi-induced apoptosis of breast cancer cell lines suggesting that the interruption of the NF-κB cytoprotective pathway induced by HDACi plays a key role in this phenomenom. Our data suggests that combined treatment of proteasome and HDAC inhibitors may represent a novel treatment strategy for breast cancer.
Direct Reprogramming
Authors: Eduardo Marbán, Eugenio Cingolani
Journal: JAMA (2015)

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
984. Fetal Administration of Lentiviral Vectors and the Potential for Germ Cell Transduction in Rhesus Monkeys (Macaca mulatta)
Authors: Chang I. Lee, Daniel F. Jimenez, Donald B. Kohn, Alice F. Tarantal
Journal: Molecular Therapy (2004)

Our prior studies have shown that the HIV-1-derived lentiviral vector can efficiently deliver transgenes into cells of multiple organ systems in rhesus monkey fetuses (Macaca mulatta) when delivered using systemic and organ-targeting approaches. In this study, we have focused on the potential for germ-line transduction post-fetal gene delivery when using the HIV-1-derived lentiviral vector expressing the enhanced green fluorescent protein (EGFP) under the control of the cytomegalovirus (CMV) promoter (HIV/VSV-G/CMV/EGFP; 107 infectious particles/fetus). Rhesus monkey fetuses (N=21) were administered lentiviral vector supernatant intraperitoneal (IP) at 50 days gestation, or using an intrapulmonary (N=24; 55-90 days gestation), intramyocardial (N=6; 60 days gestation), or yolk sac route (N=6; 25 days gestation) (term 165±10 days). Tissue harvests were performed near term or 3 months postnatal age. Genomic DNA obtained from collected sections of gonads was analyzed for vector sequences. Results indicated that higher EGFP copies per 50,000 cells were detected in fetal (4,464.9±1,485.7) or infant (43,442.7±31,833.8) ovaries compared to fetal (56.7±27.4) or infant (947.6±599.1) testes with IP administration. Germ cells, surrounding stromal cells, and the surface epithelium were then individually isolated from formalin-fixed tissue sections using laser capture microdissection, and re-analyzed for vector sequences. Vector sequences were detected in female fetal (2.5±1.7 EGFP copies/copy e-globin) or infant (0.5±0.5 EGFP copies/copy e-globin) germ cells, whereas no vector sequences were detected in male germ cells. For the ovarian surface epithelium, 0.7±0.4 to 2.2±1.7 EGFP copies/copy e-globin were detected in both age groups, whereas no or 0.8±0.8 EGFP copies/copy -globin were observed in males. Limited copies (<0.02 EGFP copies/copy e-globin) were detected in surrounding stromal cells of females, whereas no vector sequences were detected in males. There was no evidence of gene transfer to germ cells using any of the other routes of administration. The results of these studies suggest that the HIV-1-derived lentiviral vector may have a higher likelihood of transducing germ cells in vivo in female fetuses when administered IP at a defined period in gestation and when compared to male fetuses. These findings contrast results with direct organ-targeting gene transfer approaches (e.g., intrapulmonary, intramyocardial, intra-yolk sac), where no evidence of germ cell gene transfer was shown to occur.
Chronic Appendicitis from the Viewpoint of an Internist
Authors: Harry Wald Bettmann
Journal: Annals of Internal Medicine (1928)

Article1 December 1928Chronic Appendicitis from the Viewpoint of an InternistHARRY WALD BETTMANN, M.D.HARRY WALD BETTMANN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-2-6-509 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe literature on chronic appendicitis has continued to grow during the past ten years. It has finally established certain truths. One such truth is that chronic appendicitis is in no way to be confounded with recurrent appendicitis. Recurrent appendicitis at the time it is observed is in reality an attack of acute or subacute appendicits. In general we know that the more nearly the clinical picture resembles an acute attack the more sure the diagnosis and the more certain the curative results of an operation. Per contra, we know that the more chronic the condition, the less typical the picture... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cincinnati*Read before the American College of Physicians, New Orleans Meeting, March 8, 1928. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byChronic appendicitisCecopexy as an adjunct to appendectomy in some operations on the appendixThe Spastic Colon*HARRY GAUSS, M.D. 1 December 1928Volume 2, Issue 6Page: 509-517KeywordsAppendicitis ePublished: 1 December 2008 Issue Published: 1 December 1928 PDF downloadLoading ...
Abstract 13577: A Selective SGLT2 Inhibitor Early Resolutes Metabolic and Arterial Disturbances in Type-2 Diabetics With Coronary Artery Disease
Authors: Tatsuaki Murakami, Sumio Mizuno
Journal: Circulation (2014)

Introduction:  Diabetes mellitus is thought to be highly involved in complex metabolic and atherothrombogenic disturbances, but the effective therapies in patients with type-2 diabetes mellitus have not been established.   Hypothesis:  We assessed hypothesis a selective SGLT2 (Sodium Glucose co-Transporter 2) inhibitor, a recently developed antidiabetic agent, promptly reverses complex metabolic and atherothrombogenic disturbances in patients with type-2 diabetes mellitus.   Methods:  Type-2 diabetic patients with stable coronary artery disease were randomized to group-SG where they received antidiabetic therapy with a selective SGLT2 inhibitor for 2 weeks, or to group-C where they continued therapy without an inhibitor against SGLT2. We quantified flow-mediated endothelium-dependent dilatation of brachial artery after 5 minutes forearm occlusion (FMD), and intima-media thickness of brachial artery (IMT) using high-resolution ultrasonography. Changes in FMD, IMT, and other practical metabolic variables from the baseline through the follow-up point were compared between the 2 groups.   Results:  All the patients in group-SG (n=10) manifested good compliance to the treatment and improvements in metabolic variables represented by blood glucose, systolic blood pressure, body weight, and high sensitive CRP (mg/dL: from 0.15±0.07 to 0.11±0.04, p=0.01), while those in group-C (n=10) showed no improvement. FMD (%) increased after medication in group-SG (from 3.5±1.3 to 4.8±1.8, p=0.01), while it remained unchanged in group-C (from 3.4±1.3 to 3.5±1.9, p=0.82). IMT (mm) decreased after medication in group-SG (from 0.34±0.08 to 0.31±0.06, p=0.04), while it remained unchanged in group-C (0.35±0.08 to 0.36±0.05, p=0.88). Changes of FMD or IMT in group-SG did not correlate to those of blood glucose (FMD: r=0.09, p=0.89, IMT: r=0.13, p=0.78).   Conclusions:  These results indicate selective inhibition of SGLT2 in diabetic patients early improves metabolic status and furthermore improves arterial status independent of reversal for glycemic status, which may have novel potential benefit of a selective SGLT2 inhibitor for management of progressive metabolic and atherothrombogenic disturbances in type-2 diabetics with coronary artery disease.
Use of Breast Reconstruction After Mastectomy Following the Women's Health and Cancer Rights Act
Authors: Amy K Alderman, Yongliang Wei, John D Birkmeyer
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Revascularization for Unprotected Left Main Stem Coronary Artery Stenosis
Authors: David P. Taggart, Sanjay Kaul, William E. Boden, T. Bruce Ferguson, Robert A. Guyton, Michael J. Mack, Paul T. Sergeant, Richard J. Shemin, Peter K. Smith, Salim Yusuf
Journal: Journal of the American College of Cardiology (2008)
Abstract 584: NVP-BEZ235 decreases mutant p53 and downregulates miR-23a-24-27a to inhibit metastasis in breast cancer cells
Authors: Dongsheng Wang, Qin Du, Binfeng He, Yibin Deng, Xiaolan Guo
Journal: Cancer Research (2014)

Abstract Nearly half of human cancers harbor TP53 mutations, which are predominantly through missense mutations that result in accumulation of mutant p53 proteins in cancer cells. More and more findings indicate that the mutant p53 proteins acquire gain-of-function abilities to promote carcinogenesis, metastasis, tumor recurrence and chemoresistance. TP53 mutations are the most frequent genetic alterations in breast cancer, observed in 30% of breast carcinomas, especially the triple negative breast cancer (TNBC),which most easily metastasizes and confers chemoresistance. Therefore targeting TP53 mutation in breast cancer might be another promising approach of therapeutics. Our previous investigation showed that the AKT-mTOR dual inhibitor, NVP-BEZ235(called BEZ235 thereafter), could inhibit AKT-mTOR pathway activation, most interestingly mutant p53 was significantly reduced with BEZ235 treatment(unpublished data). In this study, three TNBC cell lines MDA-MB-231, MDA-MB-436, MDA-MB-468 as TP53 mutation group and MCF-7 as control were employed with BEZ235 treatment at different dosages and time points. We found that AKT-mTOR signaling pathway were highly activated in these TNBC cells but were inhibited obviously after BEZ235 treatment; most importantly, mutant p53 in these TNBC cells decreased significantly, but rare changes were detected in MCF-7 cells with BEZ235 treatment. Interestingly, we found miR-23a-24-27a cluster was about 2 fold upregulation in TNBC cells after BEZ235 treatment while exploring the decline of p53 by detecting microRNAs expression in those cell lines. To address whether BEZ235 could affect the metastasis ability of TNBC cells, cell invasion assay Transwell was used to measure the invasiveness of TNBC cells with BEZ235, and we observed that BEZ235 could inhibit the metastasis of TNBC cells, on the other hand miR-23a-24-27a cluster mimics could also induce the inhibition of metastasis in TNBC cells. Our results suggest that BEZ235 might target mutant p53 accumulation and downregulate miR-23a-24-27a cluster to inhibit the metastasis abilities of triple negative breast cancer cells, which might provide an important direction to further study the breast cancer harboring mutant p53, and also have promising therapeutic benefits for cancer patients carrying such p53 mutations. Citation Format: Dongsheng Wang, Qin Du, Binfeng He, Yibin Deng, Xiaolan Guo. NVP-BEZ235 decreases mutant p53 and downregulates miR-23a-24-27a to inhibit metastasis in breast 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 584. doi:10.1158/1538-7445.AM2014-584