tbuckley/cabot-search huggingface dataset:
Prevalence and Trends in Obesity Among US Adults, 1999-2000
Authors: Katherine M. Flegal
Journal: JAMA (2002)

The prevalence of obesity and overweight increased in the United States between 1978 and 1991. More recent reports have suggested continued increases but are based on self-reported data.To examine trends and prevalences of overweight (body mass index [BMI] > or = 25) and obesity (BMI > or = 30), using measured height and weight data.Survey of 4115 adult men and women conducted in 1999 and 2000 as part of the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the US population.Age-adjusted prevalence of overweight, obesity, and extreme obesity compared with prior surveys, and sex-, age-, and race/ethnicity-specific estimates.The age-adjusted prevalence of obesity was 30.5% in 1999-2000 compared with 22.9% in NHANES III (1988-1994; P<.001). The prevalence of overweight also increased during this period from 55.9% to 64.5% (P<.001). Extreme obesity (BMI > or = 40) also increased significantly in the population, from 2.9% to 4.7% (P =.002). Although not all changes were statistically significant, increases occurred for both men and women in all age groups and for non-Hispanic whites, non-Hispanic blacks, and Mexican Americans. Racial/ethnic groups did not differ significantly in the prevalence of obesity or overweight for men. Among women, obesity and overweight prevalences were highest among non-Hispanic black women. More than half of non-Hispanic black women aged 40 years or older were obese and more than 80% were overweight.The increases in the prevalences of obesity and overweight previously observed continued in 1999-2000. The potential health benefits from reduction in overweight and obesity are of considerable public health importance.
A gene-based recessive diplotype exome scan discovers FGF6, a novel hepcidin-regulating iron-metabolism gene
Authors: Shicheng Guo, Shuai Jiang, Narendranath Epperla, Yanyun Ma, Mehdi Maadooliat, Zhan Ye, Brent Olson, Minghua Wang, Terrie Kitchner, Jeffrey Joyce, Peng An, Fudi Wang, Robert Strenn, Joseph J. Mazza, Jennifer K. Meece, Wenyu Wu, Li Jin, Judith A. Smith, Jiucun Wang, Steven J. Schrodi
Journal: Blood (2019)
Intestinal Transplant-Associated Thrombotic Microangiopathy: Histopathological Review. a Single Center Experience
Authors: Javier Checa, Óscar Javier Blanco Núñez, Estefania Pérez-López, Mónica Cabrero, Ana A. Martín, Daniel Rivera, Alejandro Avendaño Pita, Antonio velasco Guardado, Miguel Alcoceba, Luis Miguel Chinchilla Tábora, Dolores Caballero, Lucia Lopez Corral
Journal: Blood (2018)
Adjunctive Intermittent Pneumatic Compression for Venous Thromboprophylaxis
Authors: Yaseen M. Arabi, Fahad Al-Hameed, Karen E.A. Burns, Sangeeta Mehta, Sami J. Alsolamy, Mohammed S. Alshahrani, Yasser Mandourah, Ghaleb A. Almekhlafi, Mohammed Almaani, Ali Al Bshabshe, Simon Finfer, Zia Arshad, Imran Khalid, Yatin Mehta, Atul Gaur, Hassan Hawa, Hergen Buscher, Hani Lababidi, Abdulsalam Al Aithan, Sheryl A.I. Abdukahil, Jesna Jose, Lara Y. Afesh, Abdulaziz Al-Dawood
Journal: New England Journal of Medicine (2019)

Whether adjunctive intermittent pneumatic compression in critically ill patients receiving pharmacologic thromboprophylaxis would result in a lower incidence of deep-vein thrombosis than pharmacologic thromboprophylaxis alone is uncertain.
Service Costs of Caring for Adolescents With Mental Illness in a Rural Community, 1993–2000
Authors: E. Costello
Journal: American Journal of Psychiatry (2007)

Objective: Costs of treating child psychiatric disorders fall on educational, primary care, juvenile justice, and social service agencies as well as on psychiatric services. The authors estimated multiagency mental health costs by integrating service unit costs with utilization rates in an 11-county area. Using psychiatric diagnoses made independently of service use records, the authors calculated costs across agencies as well as the extent of unmet need for psychiatric care. Method: Annual parent and child reports were used to measure mental health care needs and units of service across 21 types of settings for the population-based Great Smoky Mountain Study sample of 1,420 adolescents from ages 13 to 16. Unit costs for services were generated from information from service providers and records. The authors calculated costs overall, costs by type of service, and costs by diagnosis. Results: Average annual costs per adolescent treated were $3,146. Juvenile justice and inpatient/residential facilities accounted for well over half of the total costs. Costs for youths with two or more diagnoses were twice as much as costs of those with a single disorder. Among adolescents with service needs, 66.9% received no services. Public health insurance was associated with higher rates of specialty mental health care than either private insurance or no insurance. Conclusions: Annual costs across all services were three to four times greater than recent health insurance estimates alone. Many costs for adolescents with mental health problems were borne by agencies not designed primarily to provide psychiatric or psychological services. Only one in three adolescents needing psychiatric care received any mental health services.
High-Risk Cytogenetics in Newly Diagnosed Multiple Myeloma: Prognostic Relevance of Co-Segregations and Analysis of the Role of Double Versus Single Autotransplantation
Authors: Nicoletta Testoni, Giulia Marzocchi, Lucia Pantani, Gaia Ameli, Luca Dozza, Maria Teresa Petrucci, Francesco Di Raimondo, Francesca Patriarca, Monica Galli, Vittorio Montefusco, Barbara Gamberi, Claudia Crippa, Donatella Iolanda Vincelli, Massimo Offidani, Carolina Terragna, Katia Mancuso, Serena Rocchi, Pieter Sonneveld, Mario Boccadoro, Michele Cavo
Journal: Blood (2017)
Higher Incidence of Graft Rejection in Non-Sibling Fully Matched Related Donor Stem Cell Transplants for Thalassemia Major: A Cautionary Note
Authors: Anu Korula, Fouzia N., Anup Devasia, Uday Prakash Kulkarni, Kavitha M Lakshmi, Eunice Sindhuvi Edison, Aby Abraham, Alok Srivastava, Biju George, Vikram Mathews
Journal: Blood (2018)
Continuation of Statin Therapy in Patients with Presumed Infection
Authors: Peter S Kruger, Meg L Harward, Mark A Jones, Christopher J Joyce, Karam M Kostner, Michael S Roberts, Bala Venkatesh
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

In patients on prior statin therapy who are hospitalized for acute infections, current literature is unclear on whether statins should be continued during their hospitalization.To test the hypothesis that continuation of therapy with statins influences the inflammatory response to infection and that cessation may cause an inflammatory rebound.Prospective randomized double-blind placebo-controlled trial of atorvastatin (20 mg) or matched placebo in 150 patients on preexisting statin therapy requiring hospitalization for infection.The primary end point was progression of sepsis during hospitalization. At baseline, the rate of severe sepsis was 32% in both groups. Compared with baseline, the odds ratio for severe sepsis declined in both groups: 0.43 placebo and 0.5 statins (Day 3) versus 0.14 placebo and 0.12 statins (Day 14). The rate of decline of severe sepsis was similar between the groups (odds ratio 1.17 [0.56-2.47], P = 0.7 Day 3; 0.85 [0.21-3.34], P = 0.8 Day 14). IL-6 and C-reactive protein declined in both groups with no statistically significant difference (P = 0.7 and P = 0.2, respectively). An increase in cholesterol occurred in the placebo group (P < 0.0001). Most patients were not critically ill. Hospital mortality was 6.6%, with no difference between the groups (6 [8%] of 75 statin group; 4 [5.3%] of 75 placebo group; P = 0.75).This study does not support a beneficial role of continuing preexisting statin therapy on sepsis and inflammatory parameters. Cessation of established statin therapy was not associated with an inflammatory rebound. Clinical trial registered at the Australian New Zealand Clinical Trials Registry (ACTRN 12605000756628).
P035 Occupational physical workload and development of anti-collagen type II antibodies in rheumatoid arthritis: results from the swedish EIRA population-based case-control study
Authors: E Pertsinidou, P Zeng, B Brynedal, VA Manivel, L Klareskog, M Mullazehi, S Saevarsdottir, C Bengtsson, L Alfredsson, J Rönnelid
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Career situation of first and presenting author</h3> Young investigator. <h3>Introduction</h3> Separate studies have previously observed an association between exposure to physical workload (PW) and risk of developing rheumatoid arthritis (RA). Levels of antibodies against collagen type II (CII), which are associated with HLA-DRB*01 and *03 are transiently elevated at the time of RA diagnosis. PW might impose mechanical stress on the articular cartilage where CII is the main constituent, leading to immune activation and production of anti-CII antibodies. <h3>Objectives</h3> We hypothesize that exposure to PW would associate more strongly with anti-CII positive RA than with anti-CII negative RA. <h3>Methods</h3> Data involving 2916 incident RA cases and 5130 controls from the Swedish Epidemiological Investigations in Rheumatoid Arthritis (EIRA) population-based case-control study were analysed. Information on exposure to PW was collected through questionnaires. The odds ratios (OR) with 95% CI of developing anti-CII positive RA or anti-CII negative RA was calculated using logistic regression. <h3>Results</h3> The OR observed for the association between different types of PW and anti-CII positive RA ranged from 1.2 (0.8–1.8) to 1.7 (1.5–3.1). The OR for the association between PW and anti-CII negative RA ranged from 1.3 (1.1–1.4) to 1.6 (1.4–1.8). No statistically significant difference was observed between the OR for anti-CII positive RA and anti-CII negative RA (all p-values&gt;0.10). Moreover, stratification for HLA-DRB*01 and *03 did not yield any statistical differences. <h3>Conclusions</h3> We found no evidence suggesting an association between PW and elevated anti-CII levels at the time of diagnosis. <h3>Acknowledgements</h3> We thank the investigators and participants from the EIRA study. The authors also thank Marie-Louise Serra and Lena Nise for data collection. <h3>Disclosure of Interest</h3> None declared.
Review of US Medical School Finances, 1993-1994
Authors: J L Ganem, R L Beran, J K Krakower
Journal: JAMA (1995)

THIS ANNUAL financial review of the 126 US medical schools accredited by the Liaison Committee on Medical Education (LCME) reports revenues and expenditures for fiscal year 1993-1994 and identifies patterns in the financing of medical education during the past 3 years. To display recent patterns in medical school financing amid the current economic climate, we chose 1991-1992 as the base year. The review also highlights changes in student financial aid during a 3-year period and differences in the funding of public and private medical schools for fiscal year 1993-1994. <h3>DATA SOURCES AND CHARACTERISTICS</h3> For the 1993-1994 fiscal year, all 126 LCME-accredited US medical schools responded to the LCME's Part I-A annual financial questionnaire (AFQ). For the same fiscal year, 125 accredited US medical schools reported their financial aid information on the LCME Part I-B student financial aid questionnaire. This analysis used data derived from the results of these questionnaires. Where
Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines—2016 revision
Authors: Jan L. Brożek, Jean Bousquet, Ioana Agache, Arnav Agarwal, Claus Bachert, Sinthia Bosnic-Anticevich, Romina Brignardello-Petersen, G. Walter Canonica, Thomas Casale, Niels H. Chavannes, Jaime Correia de Sousa, Alvaro A. Cruz, Carlos A. Cuello-Garcia, Pascal Demoly, Mark Dykewicz, Itziar Etxeandia-Ikobaltzeta, Ivan D. Florez, Wytske Fokkens, Joao Fonseca, Peter W. Hellings, Ludger Klimek, Sergio Kowalski, Piotr Kuna, Kaja-Triin Laisaar, Désirée E. Larenas-Linnemann, Karin C. Lødrup Carlsen, Peter J. Manning, Eli Meltzer, Joaquim Mullol, Antonella Muraro, Robyn O'Hehir, Ken Ohta, Petr Panzner, Nikolaos Papadopoulos, Hae-Sim Park, Gianni Passalacqua, Ruby Pawankar, David Price, John J. Riva, Yetiani Roldán, Dermot Ryan, Behnam Sadeghirad, Boleslaw Samolinski, Peter Schmid-Grendelmeier, Aziz Sheikh, Alkis Togias, Antonio Valero, Arunas Valiulis, Erkka Valovirta, Matthew Ventresca, Dana Wallace, Susan Waserman, Magnus Wickman, Wojtek Wiercioch, Juan José Yepes-Nuñez, Luo Zhang, Yuan Zhang, Mihaela Zidarn, Torsten Zuberbier, Holger J. Schünemann
Journal: Journal of Allergy and Clinical Immunology (2017)
Karl Ernst Schmidt
Authors: Bruce Dougan
Journal: BMJ (2019)

Karl Ernst Schmidt was born in Ronneburg, Thuringia, Germany, on 10 September 1916. I was his friend, and it is with great sadness that I report his death at the age of 102 years, in Yeovil Hospital.

I am not qualified to write about his long career in medicine in general and psychiatry in particular—others …
Abstract P5-10-14: MicroRNAs as biomarkers and therapeutic adjuvants for the prognosis and treatment of drug-resistant breast cancers
Authors: Y-F Chang, S Panneerdoss, B Zoghi, A Pertsemlidis, M Rao
Journal: Cancer Research (2012)

Abstract Intrinsic and acquired resistance to antineoplastic agents continues to be a major clinical impediment to successful treatment of cancer in general, and breast cancer in particular. For example, about 40% of ER-positive breast tumors fail to respond to tamoxifen therapy, and of those that initially respond many will eventually develop resistance. Similarly, taxanes used as a first-line chemotherapy agent will have a response rate of 50%, which comes down to 20–30% in second- or third-line chemotherapy; nearly half of the treated subjects do not respond to it and suffer side effects. These facts underscore the importance of understanding the mechanism of resistance, which is crucial for better management of breast cancer. Unfortunately, in spite of extensive inquiry in this field, little is known about the key molecules/signaling pathways that regulate this phenomenon. Recently, we have discovered that small non-coding RNAs, i.e. microRNA (miRNAs), may play a critical role in mediating drug resistance in breast cancers. We have identified miRNAs that are differentially expressed between chemoresistant and sensitive breast cancer cells. Specifically, we have combined a high-throughput screening platform with a library of chemically synthesized inhibitors for all known human miRNAs and identified specific miRNA that selectively sensitize/de-sensitize drug-resistant breast cancer cells to either tamoxifen or trastuzumab (herceptin), drugs that are commonly used as a first line treatment for ER-positive and Her2-positive breast cancers, respectively. Interestingly, we identified 10 and 12 miRNA inhibitors that sensitized resistant cells to tamoxifen and trastuzumab, respectively. Interestingly, expression of cognate miRNA/s that sensitize resistant tumors to drug-induced cell death in our screen was found to be lower in relapsed (drug resistant) metastatic breast cancer patients compared to normal matched control. In addition to tumor tissues, the levels of sensitizer miRNA/s in the blood sera of relapsed metastatic breast cancer patients was found to be dramatically lower than that of normal healthy individual. These findings are significant as it suggests that miRNAs can be efficiently detected in blood serum and therefore, can be used as a potential biomarker for predicting treatment outcomes. In addition, miRNAs may provide novel therapeutic tools for the treatment of drug-resistant breast cancers. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P5-10-14.
Abstract 2351: The novel potential of palbociclib (CDK4/6 inhibitor) in the treatment of triple-negative breast cancer
Authors: Yuka Asano, Shinichiro Kashiwagi, Wataru Goto, Katsuyuki Takahashi, Tsutomu Takashima, Satoru Noda, Naoyoshi Onoda, Shuhei Tomita, Kosei Hirakawa, Masaichi Ohira
Journal: Cancer Research (2017)

Abstract Background: The effectiveness of palbociclib (CDK4/6 inhibitor) for estrogen receptor positive breast cancer has been demonstrated by large-scale clinical studies, with the drug garnering attention as a key drug for breast cancer subtypes with endocrine sensitivity in the future. According to PALOMA-3 trial, palbociclib has been demonstrated to contribute to the extension of progression-free survival in patients with advanced hormone receptor-positive and HER2-negative metastatic breast cancer after endocrine therapy. On the other hand, in the case of triple-negative breast cancer (TNBC), luminal AR (LAR) related to androgen signaling is believed to have endocrine activity. Previous clinical data revealed that palbociclib shows high sensitivity in luminal breast cancer cell lines with endocrine activity, with effectiveness also expected in LAR. In this study, we created TNBC cell lines that forcibly express AR and examined the effectiveness of palbociclib for TNBC. Materials and Methods: MCF-7 and T-47D were used as luminal breast cancer cell lines, while MDA-MB-231 and BT-549 were used as TNBC cell lines. In addition, we created TNBC cell lines that forcibly express AR, called AR-MDA-MB-231, by the transfection of pEGFP-C1-AR Plasmid Vector using Lipofectamine® 3000 Reagent. We confirmed the expression of AR by qRT-PCR as well as Western blotting and examined the impact of palbociclib on proliferation as well as apoptosis of breast cancer cell lines. Results: AR was found to have been expressed only in luminal breast cancer cell lines but not TNBC cell lines. It was confirmed that AR was expressed in AR-MDA-MB-231 which are stable cell lines with the properties of LAR. In a CCK assay, palbociclib showed high sensitivity in AR-MDA-MB-231 as in luminal breast cancer cell lines. Furthermore, in an apoptosis assay using FACS and cell cycle assay, apoptosis was induced in AR-MDA-MB-231 and cell cycle arrest at the G1S check point was confirmed. Conclusion: palbociclib (CDK4/6 inhibitor) showed effectiveness for TNBC cell lines that compulsively express AR, suggesting it may be one treatment option for TNBC in the future. Note: This abstract was not presented at the meeting. Citation Format: Yuka Asano, Shinichiro Kashiwagi, Wataru Goto, Katsuyuki Takahashi, Tsutomu Takashima, Satoru Noda, Naoyoshi Onoda, Shuhei Tomita, Kosei Hirakawa, Masaichi Ohira. The novel potential of palbociclib (CDK4/6 inhibitor) in the treatment of triple-negative breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2351. doi:10.1158/1538-7445.AM2017-2351
A stemness screen reveals C3orf54/INKA1 as a promoter of human leukemia stem cell latency
Authors: Kerstin B. Kaufmann, Laura Garcia-Prat, Qiang Liu, Stanley W. K. Ng, Shin-Ichiro Takayanagi, Amanda Mitchell, Erno Wienholds, Peter van Galen, Christian A. Cumbaa, Mike J. Tsay, Chiara Pastrello, Elvin Wagenblast, Gabriela Krivdova, Mark D. Minden, Eric R. Lechman, Sasan Zandi, Igor Jurisica, Jean C. Y. Wang, Stephanie Z. Xie, John E. Dick
Journal: Blood (2019)
Evaluation of magnetic nanoparticle of irinotecan for personalized treatment of colorectal cancer
Authors: A.V. Singh
Journal: Annals of Oncology (2019)

Background: Cancer, a heterogeneous disease is caused by genetic and epigenetic mutation. Irinotecan was indicated for treatment of colorectal cancer either alone or in combination with other chemotherapeutic drug. Due to associated toxicity, irinotecan was less explored in cancer therapy research. In recent years, magnetic nanoparticles (MNPs) were well explored for different biomedical applications including targeted drug delivery. Methods: We hypothesized that the anticancer activity of irinotecan would improve when attached to the surface of MNPs. Magnetic nanoparticles were developed using in house developed method. Fourier transform infrared (FT-IR) spectra and scanning electron microscopy (SEM) were recorded to characterize the irinotecan MNPs. In Vitro and in vivo evaluations were perfomed to assess the feasibility of this novel formulation using colon cancer cell lines. Results: Irinotecan MNPs were successfully developed with an average diameter of the magnetic core of 22 ± 5 nm and the thickness of the shell is around 7 ± 4 nm. Using colon cancer culture (HT-29 cells), we evaluated the effects of MNPs on cancer cell viability and apoptosis. Treatment of cancer cells with the irinotecan MNPs caused a greater decrease in cell viability and a higher rate of apoptosis compared with treatment using free irinotecan. Conclusions: Although further clinical study is needed, the targeted uptake of irinotecan MNPs by colon cancer cells associated with their ability to eliminate and prevent further cancer cell growth indicates its potential for targeted and personalized cancer therapy with lower toxicity in patients with colon cancer. Legal entity responsible for the study: Akhilesh Vikram Singh. Funding: Has not received any funding. Disclosure: The author has declared no conflicts of interest.
Retinoic Acid–Related Orphan Receptor C Regulates Proliferation, Glycolysis, and Chemoresistance via the PD-L1/ITGB6/STAT3 Signaling Axis in Bladder Cancer
Authors: Dalong Cao, Zihao Qi, Yangyang Pang, Haoran Li, Huyang Xie, Junlong Wu, Yongqiang Huang, Yao Zhu, Yijun Shen, Yiping Zhu, Bo Dai, Xin Hu, Dingwei Ye, Ziliang Wang
Journal: Cancer Research (2019)

Retinoic acid-related orphan receptor C (RORC) is a member of the nuclear orphan receptor family and performs critical regulatory functions in cell proliferation, metastasis, and chemoresistance in various types of malignant tumors. Here we showed that expression of RORC is lost in tumor tissues of bladder cancer patients. Enhanced expression of RORC suppressed cell proliferation and glucose metabolism and increased cisplatin-induced apoptosis in vitro and in vivo. RORC bound the promoter region of programmed death ligand-1 (PD-L1) and negatively regulated PD-L1 expression. PD-L1 directly interacted with integrin β6 (ITGB6) and activated the ITGB6/FAK signaling pathway. RORC prevented the nuclear translocation of STAT3 via suppression of the PD-L1/ITGB6 signaling pathway, which further inhibited bladder cell proliferation and glucose metabolism and increased cisplatin-induced apoptosis. These findings reveal that RORC regulates bladder cancer cell proliferation, glucose metabolism, and chemoresistance by participating in the PD-L1/ITGB6/STAT3 signaling axis. Moreover, this new understanding of PD-L1 signaling may guide the selection of therapeutic targets to prevent tumor recurrence. SIGNIFICANCE: These findings suggest that RORC-mediated regulation of a PD-L1/ITGB6/FAK/STAT3 signaling axis in bladder cancer provides several potential therapeutic targets to prevent tumor progression.