tbuckley/cabot-search huggingface dataset:
MicroRNA-26a regulates insulin sensitivity and metabolism of glucose and lipids
Authors: Xianghui Fu, Bingning Dong, Yan Tian, Philippe Lefebvre, Zhipeng Meng, Xichun Wang, François Pattou, Weidong Han, Xiaoqiong Wang, Fang Lou, Richard Jove, Bart Staels, David D. Moore, Wendong Huang
Journal: Journal of Clinical Investigation (2015)

Type 2 diabetes (T2D) is characterized by insulin resistance and increased hepatic glucose production, yet the molecular mechanisms underlying these abnormalities are poorly understood. MicroRNAs (miRs) are a class of small, noncoding RNAs that have been implicated in the regulation of human diseases, including T2D. miR-26a is known to play a critical role in tumorigenesis; however, its function in cellular metabolism remains unknown. Here, we determined that miR-26a regulates insulin signaling and metabolism of glucose and lipids. Compared with lean individuals, overweight humans had decreased expression of miR-26a in the liver. Moreover, miR-26 was downregulated in 2 obese mouse models compared with control animals. Global or liver-specific overexpression of miR-26a in mice fed a high-fat diet improved insulin sensitivity, decreased hepatic glucose production, and decreased fatty acid synthesis, thereby preventing obesity-induced metabolic complications. Conversely, silencing of endogenous miR-26a in conventional diet-fed mice impaired insulin sensitivity, enhanced glucose production, and increased fatty acid synthesis. miR-26a targeted several key regulators of hepatic metabolism and insulin signaling. These findings reveal miR-26a as a regulator of liver metabolism and suggest miR-26a should be further explored as a potential target for the treatment of T2D.
Abstract P315: Association of Marital Status with Health Care Use among Hispanic/Latino Adults: Results from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL)
Authors: Veronica Y Womack, Peter De Chavez, Frank J Penedo, Patricia Gonzalez, Lizette Ojeda, Robert Ostfeld, Jianwen Cai, Linda C Gallo, Aida Giachello, Martha L Daviglus, Mercedes Carnethon
Journal: Circulation (2014)

Background: Sociocultural factors have been linked to health care seeking among Latino adults. A supportive social context may encourage proactive steps leading to health maintenance, including healthcare seeking. Objective: To explore the cross-sectional association of marital status with annual health care provider visits among Hispanic/Latino adults ages 18-74 with and without chronic diseases. Methods: Participants from HCHS/SOL Sociocultural Ancillary Study with measures of social support, marital status, and health care use were included in the analysis (n=3,401). Marital status was self-reported. Health care use was defined as whether the participant saw a health care provider in the past twelve months. Weighted multiple logistic regression models were used to examine the associations of marital status with healthcare use, after adjusting for covariates. Results: On average, participants were 40 years old , 83% were currently married, and 73% had at least one health care provider visit in the past twelve months. Analyses were stratified by gender and the findings were null in men, therefore only the findings in women are reported. Among Hispanic/ Latino women with chronic diseases, individuals who were married were more likely to have an annual health care provider visit than those who had never married. However, this association no longer remained significant after adjustment. Among Latino women without chronic diseases, individuals who were married were less likely to have an annual health care provider visit than those who were never married. Conclusion: Marital status is associated with health care use among Hispanic/Latino women without chronic diseases. Future research should assess whether marianismo, a culture specific gender role characterized by self-sacrifice and prioritization of familial needs, influences marital status’ association with preventive health care utilization among Latino women.
Patient Management After Noninvasive Cardiac Imaging
Authors: Rory Hachamovitch, Benjamin Nutter, Mark A. Hlatky, Leslee J. Shaw, Michael L. Ridner, Sharmila Dorbala, Rob S.B. Beanlands, Benjamin J.W. Chow, Elizabeth Branscomb, Panithaya Chareonthaitawee, W. Guy Weigold, Szilard Voros, Suhny Abbara, Tsunehiro Yasuda, Jill E. Jacobs, John Lesser, Daniel S. Berman, Louise E.J. Thomson, Subha Raman, Gary V. Heller, Adam Schussheim, Richard Brunken, Kim A. Williams, Susan Farkas, Dominique Delbeke, Uwe J. Schoepf, Nathaniel Reichek, Stuart Rabinowitz, Steven R. Sigman, Randall Patterson, Carolyn R. Corn, Richard White, Ella Kazerooni, James Corbett, Sabahat Bokhari, Josef Machac, Erminia Guarneri, Salvador Borges-Neto, John W. Millstine, James Caldwell, James Arrighi, Udo Hoffmann, Matthew Budoff, Joao Lima, James R. Johnson, Barbara Johnson, Mariya Gaber, Julie A. Williams, Courtney Foster, Jon Hainer, Marcelo F. Di Carli
Journal: Journal of the American College of Cardiology (2012)
NUP98–HMGB3: a novel oncogenic fusion
Authors: A Petit, C Ragu, V Della-Valle, M J Mozziconacci, M Lafage-Pochitaloff, G Soler, C Schluth, I Radford, C Ottolenghi, O A Bernard, V Penard-Lacronique, S P Romana
Journal: Leukemia (2009)
Cross-resistance to ON01910.Na among drug-resistant human tumor cell lines
Authors: Adrian Preda, Takao Ohnuma, Jian-Dong Jiang, James F. Holland, E. Premkumar Reddy
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4707 

The benzyl styryl sulfone analog ON 01910.Na (1910) is a novel anticancer agent that inhibits CDK1 and PDGFR, and is currently in Phase 1 trials. The objective of the present study was to evaluate whether human cells in culture, which were made resistant to various anticancer agents exhibited any cross-resistance to 1910. 1910’s cell kill effects were exposure time-dependent. Thus, in Daudi lymphoma cells IC50s were 750, 220 and 130 nM after 24 , 48 and 72 hr exposure at 37° respectively. Tumor cells were exposed to graded concentrations of drug for 72 hr and then subjected to sulforhodamine B assay (Skehan). Degrees of resistance were determined as a ratio of IC50 of drug resistant cells vs. parent cells. 10,000-fold methotrexate-resistant MOLT ALL cells were more sensitive to 1910 (relative resistance 0.56). 200-fold doxorubicine-resistant MCF-7/DOX breast cancer cells, 200-fold vinblastine-resistant KB/VBL laryngeal tumor cells and 2,500-fold trimetrexate-resistant MOLT ALL cells were as sensitive to 1910 as the respective parent cell lines. 20-fold vincristine-resistant Daudi /MDR20 lymphoma cells which overexpress P-gp, 120-fold etoposide-resistant HEK-293/pcDNA3.1-MRP1cells which overexpress MRP1, 140-fold mitoxantrone-resistant HEK-293/ABCG2 cells, which carry mutant form of ABCG2 were all 1910-sensitive. 1910 had a minor cross-resistance (2.6-fold) to 34-fold cisplatin-resistant Bel7404/CP20 hepatoma cells and (2.1 fold) to 24-fold flavopiridol-resistant MCF-7/FLV1,000 cells. Attempts were made to develop 1910-resistance in Daudi cells by continuous or pulse exposure to 1910. For continuous exposure the initial drug concentration was 25 nM or IC10 concentration. After recovery of population cell growth, drug concentration was gradually increased. After nearly 2 yrs of experiment cells were finally able to grow avidly in the presence of 400 nM of drug. Attempts to increase the drug to higher concentrations were met with cell death. For pulse exposure cells were exposed to 100 nM or IC50 drug concentration for 3 days, after which cells were washed free of drug and were allowed to grow. Finally, cells could be retrieved from 3,000 nM for 3 days exposure. After recovery of cell growth the degree of resistance was found to be only 2 fold for both modes of exposure. These data show that 1910 is not a MDR1 or MRP1 substrate drug, not cross-resistant to many of drug-resistant tumor cells, and has unique characteristic of not making tumor cells resistant to the drug. All of these characteristics are considered favorable as a novel anticancer agent. (We thank Drs. Michael Gottesman and Susan Bates/Robert Robey for allowing us to examine their drug-resistant cell lines. Supported by the T.J. Martell Foundation and by Onconova Therapeutics, Inc.)
Ebola Vaccines Tested in Humans, Monkeys
Authors: Brian Vastag
Journal: JAMA (2004)

disease.” Indeed, there are signs that most individuals have not panicked—they have not even resorted to depriving themselves of T-bones and hamburgers. In the first week of January, a Gallup Poll reported that only 17% of those polled said they had cut back on meat consumption because of mad cow concerns. Only 6% thought the mad cow situation in the United States was a “crisis,” 28% said it was a “major problem,” 53% said it was a “minor problem,” and 12% said it was “not a problem” at all. Hueston said if individuals want to be especially cautious but still enjoy beef, they might opt for steaks and roasts, which tend to come from young cows, rather than ground products, which are often from older animals. Eating beef from older animals is riskier because mad cow disease takes years to develop.
Thalidomide Approved for Erythema Nodosum Leprosum
Authors: Stuart L. Nightingale
Journal: JAMA (1998)

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Concurrence of autoantibodies to bullous pemphigoid antigens and desmoglein 3: analysis of pathogenic and nonpathogenic antibodies
Authors: S. Ono, M. Tanioka, H. Tanizaki, A. Fujisawa, H. Koga, T. Hashimoto, K. Kamiya, Y. Aoyama, K. Iwatsuki, Y. Miyachi
Journal: British Journal of Dermatology (2013)

Journal Article Concurrence of autoantibodies to bullous pemphigoid antigens and desmoglein 3: analysis of pathogenic and nonpathogenic antibodies Get access S. Ono, S. Ono Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan Search for other works by this author on: Oxford Academic Google Scholar M. Tanioka, M. Tanioka Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan Miki Tanioka. E‐mail: mtanioka@kuhp.kyoto-u.ac.jp Search for other works by this author on: Oxford Academic Google Scholar H. Tanizaki, H. Tanizaki Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan Search for other works by this author on: Oxford Academic Google Scholar A. Fujisawa, A. Fujisawa Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan Search for other works by this author on: Oxford Academic Google Scholar H. Koga, H. Koga Department of Dermatology, Kurume University School of Medicine, and Kurume University Institute of Cutaneous Cell Biology, Fukuoka, Japan Search for other works by this author on: Oxford Academic Google Scholar T. Hashimoto, T. Hashimoto Department of Dermatology, Kurume University School of Medicine, and Kurume University Institute of Cutaneous Cell Biology, Fukuoka, Japan Search for other works by this author on: Oxford Academic Google Scholar K. Kamiya, K. Kamiya Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Aoyama, Y. Aoyama Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Search for other works by this author on: Oxford Academic Google Scholar K. Iwatsuki, K. Iwatsuki Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Miyachi Y. Miyachi Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 168, Issue 6, 1 June 2013, Pages 1357–1360, https://doi.org/10.1111/bjd.12143 Published: 01 June 2013
Abstract MP85: Mediterranean Diet and Incidence of Stroke in the California Teachers Study
Authors: Ayesha Z Sherzai, Huiyan Ma, Pamela Horn-Ross, Alison J Canchola, Jenna Voutsinas, Joshua Z Willey, Yian Gu, Nikolaos Scarmeas, Dean Sherzai, Leslie Bernstein, Mitchell S Elkind, Sophia S Wang
Journal: Circulation (2015)

Introduction: A Mediterranean diet (MeDi) has been associated with a reduced incidence of cardiovascular and neurodegenerative diseases, and overall mortality, in several prospective studies. There is limited data, however, regarding the relationship between MeDi and stroke, and in particular, stroke subtypes. We hypothesized that MeDi would be associated with reduced total, ischemic, and hemorrhagic stroke incidence. Methods: The California Teachers Study comprises 133,478 women who enrolled in 1995 and have been continuously followed. Using linked California state hospitalization data and national death records from 1996-2011, incident strokes were identified and validated. Socio-demographic and medical risk factor data were collected from the baseline questionnaire. Diet was assessed using a food-frequency questionnaire in 113,547 women. The Mediterranean diet emphasizes plant-based foods, mono-unsaturated fats, fish and moderate alcohol intake. We used the MeDi adherence score, a nine point scale, which has been used and validated in prior studies. A higher score on the 0-9 scale represents increased adherence. Multivariable Cox proportional-hazard models adjusted for socio-demographic factors including age, ethnicity, socioeconomic status, moderate-to-strenuous physical activity, total calorie intake, body mass index, cigarette smoking, menopausal and hormonal status and vascular risk factors were used to assess the association (hazard ratios and 95% confidence intervals, HR 95% CI) between MeDi score and risk of stroke and stroke subtypes. Results: A total of 104,268 participants were eligible for the analysis (mean age 52 ± 13.9 years, 87.4% white, 4.6% Hispanic, 3.2% Asian and 2.1% black). The MeDi score distribution was: 0-2 (16.1%), 3 (18.2%), 4 (21.4%), 5 (20.1%), and 6-9 (24.3%). During follow-up, 3165 stroke events occurred (2270 ischemic ; 895 hemorrhagic). In the multivariable model, compared to those in the lowest MeDi score quintile (score 0-2), those in the fourth quintile (score 5: HR 0.86, 95% CI 0.75-0.98) and highest quintile (score 6 - 9: HR 0.83, 95% CI 0.73-0.95) were at lower risk of stroke (p for trend 0.009). For ischemic stroke, those in the third (HR 0.84, 95% CI 0.72-0.97), fourth (0.85, 95% CI 0.73-0.98), and highest quintile (HR 0.82, 95% CI 0.70-0.95) were all at reduced risk (p for trend 0.02). There was no association with hemorrhagic stroke. Discussion: Adherence to the Mediterranean diet is associated with decreased risk of total and ischemic stroke incidence among the participants of the California Teachers Study.
Mutations in RAB27A cause Griscelli syndrome associated with haemophagocytic syndrome
Authors: Gaël Ménasché, Elodie Pastural, Jérôme Feldmann, Stéphanie Certain, Fügen Ersoy, Sophie Dupuis, Nico Wulffraat, Diana Bianchi, Alain Fischer, Françoise Le Deist, Geneviève de Saint Basile
Journal: Nature Genetics (2000)
Glucagon Response to Oral Glucose Challenge in Type 1 Diabetes: Lack of Impact of Euglycemia
Authors: Caroline K. Kramer, Carla A. Borgoño, Paula Van Nostrand, Ravi Retnakaran, Bernard Zinman
Journal: Diabetes Care (2013)

OBJECTIVE Previous studies have demonstrated aberrant glucagon physiology in the setting of type 1 diabetes (T1D) but have not addressed the potential impact of ambient glycemia on this glucagon response. Thus, our objective was to evaluate the impact of euglycemia versus hyperglycemia on the glucagon response to an oral glucose challenge in T1D. RESEARCH DESIGN AND METHODS Ten adults with T1D (mean age 56.6 ± 9.0 years, duration of diabetes 26.4 ± 7.5 years, HbA1c 7.5% ± 0.77, and BMI 24.1 kg/m(2) [22.6-25.4]) underwent 3-h 50-g oral glucose tolerance tests (OGTTs) on two separate days at least 24 h apart in random order under conditions of pretest euglycemia (plasma glucose [PG] between 4 and 6 mmol/L) and hyperglycemia (PG between 9 and 11 mmol/L), respectively. RESULTS Glycemic excursion on the OGTT was similar between the euglycemic and hyperglycemic tests (P = 0.72 for interaction between time postchallenge and glycemic setting). Interestingly, glucagon levels increased in response to the OGTT under both glycemic conditions (P < 0.001) and there were no differences in glucagon response between the euglycemic and hyperglycemic days (P = 0.40 for interaction between time postchallenge and glycemic setting). In addition, the incretin responses to the OGTT (glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, glucagon-like peptide-2) were also not different between the euglycemic and hyperglycemic settings. CONCLUSIONS In patients with T1D, there is a paradoxical increase in glucagon in response to oral glucose that is not reversed when euglycemia is achieved prior to the test. This abnormal glucagon response likely contributes to the postprandial hyperglycemia in T1D irrespective of ambient glycemia.
Epirubicin for breast cancer may cause considerable venous sclerosis
Authors: Paula Bolton Maggs, Aileen Flavin
Journal: BMJ (2005)

The use of the adjuvant epirubicin for breast cancer in the United Kingdom has increased since initial data from the national epirubicin adjuvant trial (NEAT) were presented in 2003.1 Two women, aged 53 and 55 years, developed pain and restriction of movement of the arm due to venous sclerosis after having infusions of epirubicin. They both had grade 3 invasive ductal carcinoma and had had surgery and axillary node dissection followed by eight courses of adjuvant chemotherapy using the epirubicin, cyclophosphamide, methotrexate, and fluorouracil regimen. This includes four cycles of …
Current Concepts on the Pathogenesis of Type 1 Diabetes—Considerations for Attempts to Prevent and Reverse the Disease
Authors: Mark A. Atkinson, Matthias von Herrath, Alvin C. Powers, Michael Clare-Salzler
Journal: Diabetes Care (2015)

It may be considered unusual to consider a period of three decades “historical.” Yet, the evolution for our understanding of the natural history and pathogenesis of type 1 diabetes has been greatly advanced by a vast number of studies aimed at validating a model (1), proposed by the late Dr. George Eisenbarth in 1986 (2). As a result of this work, the majority of current conventional wisdom portrays type 1 diabetes as a T cell–mediated autoimmune disease involving the specific destruction of insulin-producing pancreatic β-cells.

In this model, persons destined to develop type 1 diabetes are assumed to begin life with a full cadre of β-cells. However, a “triggering” insult, likely environmental, initiates a process involving the recruitment of antigen-presenting cells. Antigen-presenting cells sequester self-antigens released by injured β-cells, followed by their transport to pancreatic lymph nodes where they are subsequently presented to autoreactive T cells. These T cells, rogue constituents brought to life due to genetically driven failures of thymic deletion (i.e., central tolerance) combined with defects in mechanisms designed to induce peripheral immune tolerance, come into play (3). This toxic duo, imparting lack-of-tolerance formation, again in the context of genetic susceptibility, allows for migration of self-reactive T cells to islets, mediating β-cell killing and promoting further inflammation (4). When 85–90% of pancreatic β-cells meet their demise, symptoms of the disease occur. In the final stage of the model, the autoimmune process ends with the complete elimination of β-cells.

While this concept still forms the prevailing intellectual dogma for the majority of individuals associated with diabetes care and research today, a series of recent observations has challenged multiple aspects of this long-standing model (5). Many of these evolving concepts will be presented in this Perspective, with a discussion of how our understanding of models of type 1 diabetes pathogenesis …
Abstract 13235: Reentrant Sources in Persistent AF Are Located in Regions with Specific Spatial Patterns of Fibrosis
Authors: Sohail Zahid, Patrick M Boyle, Peter Malamas, Fijoy Vadakkumpadan, Remi Dubois, Edward J Vigmond, Michel Haissaguerre, Meleze Hocini, Pierre Jais, Hubert Cochet, Natalia A Trayanova
Journal: Circulation (2014)

Introduction:  Fibrosis is associated with increased risk of persistent atrial fibrillation (psAF), but it remains unknown how the specific distribution of fibrosis determines the preferential locations of atrial reentrant sources (RSs).   Hypothesis:  We hypothesized that RSs in psAF patients persist in fibrotic regions with distinct spatial characteristics that can be quantitatively assessed.   Methods:  Late Gadolinium Enhancement LGE-MRI and noninvasive electrocardiographic imaging (ECGI) data were acquired from patients with psAF. Patient specific, biophysically accurate atrial models were developed from images (Fig A). A dynamic pacing protocol was used to induce psAF in models. Locations of persistent RSs in simulations (reentries lasting >2s) were compared to ECGI data to validate each model. Then, at each point in the model atria, we computed local spatial metrics for the volume within a 2.5 mm radius: fibrosis density (proportion of LGE tissue by volume), fibrosis clustering (diffuse or patchy) by Moran’s I, and complexity of fibrosis pattern by Shannon entropy.   Results:  In all patient-specific models, persistent RS locations were the same as those detected by ECGI (within 2 cm of each other, as in Fig B). At such locations, fibrosis characteristics were distinct from those in the rest of the atria (p 0.6, clustering > 0.8, and complexity > 0.8 occupied only 3.25% of atrial volume (Fig D), suggesting that a limited amount of tissue had the specific fibrosis pattern that favored RS persistence.   Conclusion:  Persistent RSs in psAF are harbored by fibrotic regions with distinct spatial characteristics. Identifying such regions can help determine the optimal targets for ablation of psAF.
AML1–ETO downregulates the granulocytic differentiation factor C/EBPα in t(8;21) myeloid leukemia
Authors: Thomas Pabst, Beatrice U. Mueller, Nari Harakawa, Claudia Schoch, Torsten Haferlach, Gerhard Behre, Wolfgang Hiddemann, Dong-Er Zhang, Daniel G. Tenen
Journal: Nature Medicine (2001)