tbuckley/cabot-search huggingface dataset:
Sources of Sodium in US Adults From 3 Geographic Regions
Authors: Lisa J. Harnack, Mary E. Cogswell, James M. Shikany, Christopher D. Gardner, Cathleen Gillespie, Catherine M. Loria, Xia Zhou, Keming Yuan, Lyn M. Steffen
Journal: Circulation (2017)

Most US adults consume excess sodium. Knowledge about the dietary sources of sodium intake is critical to the development of effective reduction strategies.A total of 450 adults were recruited from 3 geographic locations: Birmingham, AL (n=150); Palo Alto, CA (n=150); and the Minneapolis-St. Paul, MN (n=150), metropolitan areas. Equal numbers of women and men from each of 4 race/ethnic groups (blacks, Asians, Hispanics, and non-Hispanic whites) were targeted for recruitment. Four record-assisted 24-hour dietary recalls were collected from each participant with special procedures, which included the collection of duplicate samples of salt added to food at the table and in home food preparation.Sodium added to food outside the home was the leading source of sodium, accounting for more than two thirds (70.9%) of total sodium intake in the sample. Although the proportion of sodium from this source was smaller in some subgroups, it was the leading contributor for all subgroups. Contribution ranged from 66.3% for those with a high school level of education or less to 75.0% for those 18 to 29 years of age. Sodium inherent to food was the next highest contributor (14.2%), followed by salt added in home food preparation (5.6%) and salt added to food at the table (4.9%). Home tap water consumed as a beverage and dietary supplement and nonprescription antacids contributed minimally to sodium intake (<0.5% each).Sodium added to food outside the home accounted for ≈70% of dietary sodium intake. This finding is consistent with the 2010 Institute of Medicine recommendation for reduction of sodium in commercially processed foods as the primary strategy to reduce sodium intake in the United States.URL: http://www.clinicaltrials.gov. Unique identifier: NCT02474693.
Abstract 19177: Calpain Inhibition Stabilizes Cytoskeletal Protein Expression in Chronically Ischemic Myocardium of Hypercholestrolemic Swine
Authors: Brittany A Potz, Sharif A Sabe, Benedikt J Braun, Richard T Clements, Anny Usheva, Frank W Sellke
Journal: Circulation (2016)

Introduction: In the setting of myocardial ischemia, calpain inhibition has been found to increase myocardial blood flow and vessel density and improve oxidative stress in myocardial tissue. Calpai...
Characterization of drug responses of mini patient-derived xenografts in mice for predicting cancer patient clinical therapeutic response
Authors: Feifei Zhang, Wenjie Wang, Yuan Long, Hui Liu, Jijun Cheng, Lin Guo, Rongyu Li, Chao Meng, Shan Yu, Qingchuan Zhao, Shun Lu, Lili Wang, Haitao Wang, Danyi Wen
Journal: Cancer Communications (2018)

Patient-derived organoids and xenografts (PDXs) have emerged as powerful models in functional diagnostics with high predictive power for anticancer drug response. However, limitations such as engraftment failure and time-consuming for establishing and expanding PDX models followed by testing drug efficacy, and inability to subject to systemic drug administration for ex vivo organoid culture hinder realistic and fast decision-making in selecting the right therapeutics in the clinic. The present study aimed to develop an advanced PDX model, namely MiniPDX, for rapidly testing drug efficacy to strengthen its value in personalized cancer treatment.We developed a rapid in vivo drug sensitivity assay, OncoVee® MiniPDX, for screening clinically relevant regimens for cancer. In this model, patient-derived tumor cells were arrayed within hollow fiber capsules, implanted subcutaneously into mice and cultured for 7 days. The cellular activity morphology and pharmacokinetics were systematically evaluated. MiniPDX performance (sensitivity, specificity, positive and negative predictive values) was examined using PDX as the reference. Drug responses were examined by tumor cell growth inhibition rate and tumor growth inhibition rate in PDX models and MiniPDX assays respectively. The results from MiniPDX were also used to evaluate its predictive power for clinical outcomes.Morphological and histopathological features of tumor cells within the MiniPDX capsules matched those both in PDX models and in original tumors. Drug responses in the PDX tumor graft assays correlated well with those in the corresponding MiniPDX assays using 26 PDX models generated from patients, including 14 gastric cancer, 10 lung cancer and 2 pancreatic cancer. The positive predictive value of MiniPDX was 92%, and the negative predictive value was 81% with a sensitivity of 80% and a specificity of 93%. Through expanding to clinical tumor samples, MiniPDX assay showed potential of wide clinical application.Fast in vivo MiniPDX assay based on capsule implantation was developed-to assess drug responses of both PDX tumor grafts and clinical cancer specimens. The high correlation between drug responses of paired MiniPDX and PDX tumor graft assay, as well as translational data suggest that MiniPDX assay is an advanced tool for personalized cancer treatment.
Abstract 19547: FOXO3 Genotype Strongly Impacts Coronary Heart Disease Mortality in Three Populations
Authors: Bradley J Willcox, Brian J Morris, Gregory J Tranah, Randi Chen, Kamal H Masaki, Qimei He, D. Craig Willcox, Richard Allsopp, Stefan Moisyadi, Leonard W Poon, Beatriz Rodriguez, Anne B Newman, Tamara B Harris, Steven R Cummings, Yongmei Liu, Neeta Parimi, Daniel S Evans, Timothy A Donlon
Journal: Circulation (2015)

The G allele of the FOXO3 SNP rs2802292 has a strong, consistently replicated protective association with longevity. We investigated the effect of FOXO3 genotype on coronary heart disease (CHD) mortality - a major cause of mortality worldwide. We genotyped DNA collected in 1991-93, at Exam 4 of the Honolulu Heart Program (HHP), from 3,584 American males of Japanese ancestry aged 71-93 years. Study participants were followed for up to 9 years for CHD mortality and for up to 11 years in a replication cohort - the Health Aging and Body Composition (Health ABC) study. Health ABC is a prospective observational study of 3,075 well functioning, community-dwelling, male and female, white and black Americans, aged 70-79 years at baseline. Cox proportional hazards models demonstrated that Americans of Japanese, white and black ethnicity who were G allele carriers had a combined risk reduction of 31% for CHD mortality (HR = 0.69; 95% CI, 0.58-0.82; P =0.00002). Reduction in risk of death from CHD was 38% in Japanese, 24% in whites and 29% in blacks. This finding remained virtually unchanged when included in a multivariable model of common CHD risk factors. We subsequently assessed the contribution of FOXO3 genotype, relative to other common risk factors, to CHD mortality in these populations by estimating population attributable risk (PAR). In the Americans of Japanese ancestry, PAR for the TT (non-protective) genotype was high, at 24%, equivalent to hypertension (24%), and greater than diabetes (21%), hypercholesterolemia (12%) and ever smoking (6%). PAR for FOXO3 genotype was lower at 9% and 3% in white and black Americans, respectively, principally due to lower prevalence of the TT (risk) genotype. We subsequently measured C-reactive protein (CRP) in a population subsample, and found lower blood CRP levels in G allele carriers ( P &lt;0.05), suggesting a potential link to inflammation. In conclusion, the G allele of the FOXO3 SNP rs2802292 has a major protective effect on CHD mortality, possibly related to lower blood levels of inflammation. The findings support further research on potential mechanisms and point to FoxO3 as a potential target therapeutic target.
Outcome reporting bias in trials: a methodological approach for assessment and adjustment in systematic reviews
Authors: Jamie J Kirkham, Douglas G Altman, An-Wen Chan, Carrol Gamble, Kerry M Dwan, Paula R Williamson
Journal: BMJ (2018)

Systematic reviews of clinical trials aim to include all relevant studies conducted on a particular topic and to provide an unbiased summary of their results, producing the best evidence about the benefits and harms of medical treatments. Relevant studies, however, may not provide the results for all measured outcomes or may selectively report only some of the analyses undertaken, leading to unnecessary waste in the production and reporting of research, and potentially biasing the conclusions to systematic reviews. In this article, Kirkham and colleagues provide a methodological approach, with an example of how to identify missing outcome data and how to assess and adjust for outcome reporting bias in systematic reviews.
Razia Sultana Mir
Authors: Sabuhi Gard
Journal: BMJ (2018)

Razia Sultana Mir was born in Multan in British India (now in Pakistan), the youngest of five siblings. Determined to become a doctor at a young age, she would recount how she would take a “tonga” to Nishtar Medical College and Hospital in the southern Punjab every day in the punishing heat, in order to study for her five year MBBS degree.

Razia was named after Razia Sultana, the first female sultan of Delhi (from 1236 to 1240). She definitely lived up to her name and was a pioneer, not only during her 40 year career as a GP in the NHS, but by overcoming extreme prejudice as a junior doctor in Scotland in the 1960.

In 1965 she had …
Post-operative vital signs: How often is too often?
Authors: Kristen Filson, Colleen Atherholt, Meredith Simoes, Michael DiPalma, Susheela John, Robin Reynolds, Joanne McGovern
Journal: Journal of Clinical Oncology (2018)

210 Background: Current protocol for post-operative patients admitted to medical-surgical/telemetry units from post anesthesia care units states vital signs are taken every 15 minutes for 1 hour, every 30 minutes for 2 hours and then, every 4 hours for 24 hours. To date, published evidence-based research regarding the frequency and duration of vital signs to safely monitor post-operative patients is limited. The goal is to determine best practice in post-operative vital sign monitoring to ensure safe patient care. The purpose of this review is to determine what frequency and duration of vital signs is required to identify a deviation greater than 20% of patient baseline to ensure safe post-operative monitoring of patients. Methods: A total of 742 post-operative patients’ charts were evaluated. A time frame in which vital signs deviated greater than 20% from patient baseline was established from the data collected. A chart was created depicting these results; listing the total deviations by individual vital sign and time frame. Results: Results show blood pressure and heart rate are the vital signs that have the greatest deviation from baseline followed by pulse-oximetry. Temperature deviations are widespread, while changes in respiratory rate are seen within the first hour. When looking at specific percentages, it was noted that 65% of the total patients reviewed had a 20% deviation from their baseline vital signs. Blood pressures made up 50% of those deviations, while heart rates made up 45%. A total of 27% of the deviations occurred 4-8 hours after admission, 13% of deviations occurred 8-12 hours after admission, 9% of deviations occurred 1.5 hours after admission, and 7% of deviations occurred 12-16 hours after admission. Conclusions: Based on these results, the best times to take post-operative vitals to ensure deviations are detected are: every 15 minutes for 30 minutes upon admission, 1.5 hours after admission, 4 hours after admission, and then every 4 hours for 20 hours. Findings indicate vital signs can safely be taken less frequently in post-operative patients admitted to medical-surgical/telemetry units.
The costs of breast cancer care: Patient-reported experiences and preferences for transparency.
Authors: Rachel Adams Greenup, Christel Rushing, Laura Fish, Terry Hyslop, Jeffrey M. Peppercorn, Stephanie B. Wheeler, Yousuf Zafar, Evan Myers, Eun-Sil Shelley Hwang
Journal: Journal of Clinical Oncology (2018)

207 Background: Despite the recognized side effect of financial toxicity after cancer, treatment decisions for breast cancer rarely include the costs of care. We sought to determine women’s experiences with breast cancer treatment costs, and their preferences for cost transparency at diagnosis. Methods: Women ≥18 years old with a history of breast cancer completed an 88-question electronic survey based on validated or published items. Descriptive statistics and regression analysis were used. Results: In total, 607 women with stage 0-III breast cancer participated. Median age at diagnosis was 49.6 years. Median time from diagnosis was 6.7 years (range 0.1-37.1). The majority had private (70%) insurance or Medicare (25%), and reported an annual household income ≥$74,000. 43% reported considering costs in treatment decisions. Median reported out-of-pocket (OOP) costs were $3,500; 25% reported OOP costs ≥$8,000, 10% reported OOP costs ≥$18,000 and 5% reported OOP costs ≥$30,000. 15.5% reported significant to catastrophic financial burden. Bilateral mastectomy +/- reconstruction vs lumpectomy (OR 1.9, p 0.03), greater stage at diagnosis (stage 3 vs 0, OR 3.9, p &lt; 0.01), and discussion of costs during the clinical encounter (OR 2.3, p &lt; 0.01) were associated with a higher risk of financial harm. Women who reported discussing costs were more likely to be stage 2 or 3 (56% vs 40%, p = 0.02), less likely to be depressed (24% vs 30%, p = 0.03), and had less insurance coverage (trend p = 0.02) compared to those who did not. Older age (OR 0.95, p &lt; 0.01), increasing household income (overall p &lt; 0.001), better insurance coverage (OR 0.5, p &lt; 0.001), and longer time since diagnosis (OR 0.65, p &lt; 0.001) was associated with a decreased risk of financial harm. 78% of participants never discussed costs with their cancer team. 79% preferred cost transparency prior to embarking on care, and 40% preferred that doctors consider costs when making recommendations. Conclusions: Many women with breast cancer reported significant financial burden related to their care, and the vast majority preferred knowing costs at diagnosis. Cost transparency may improve the quality of preference-sensitive treatment decisions and reduce the risk of financial harm.
Herpes simplex virus (HSV) pneumonia in the non-ventilated immunocompromised host: Burden and predictors
Authors: Roberto Luzzati, Pierlanfranco D'Agaro, Annalisa Busca, Cristina Maurel, Fulvia Martellani, Chiara Rosin, Ludovica Segat, Giuseppe Gatti, Marta Mascarello, Marco Confalonieri
Journal: Journal of Infection (2018)
Early CTC decline as a biomarker of response to treatment in castration-resistant prostate cancer (CRPC): Analysis of the COU-AA-301 and IMMC38 trials.
Authors: David Lorente, David Olmos, Joaquin Mateo, Diletta Bianchini, George Seed, Penelope Flohr, Mateus Crespo, Ines Figueiredo, Susana Miranda, Kurt Baeten, Tim Pitfield, Arturo Molina, Thian Kheoh, Robert Thomas Mccormack, Howard I. Scher, Johann Sebastian De Bono
Journal: Journal of Clinical Oncology (2015)

5014 Background: Circulating tumor cell counts (CTC) are prognostic in CRPC. Baseline (BL) CTC ≥ 5 CTCs/7.5mL are associated with worse prognosis. A post-treatment 30% decline in CTC has been associated with improved survival (OS) (Olmos et al, 2009). We investigated the value of 30% declines in CTC after 4 and 12 weeks (wks) of treatment in the COU-AA-301 (abiraterone) and IMMC-38 (chemotherapy) trial datasets. This is the first time %CTC decline has been evaluated in phase III CRPC clinical trials. Methods: CTC of patients (pts) were determined (CellSearch). Pts with BL CTCs ≥5 and valid counts at Wk 4/Wk 12 (IMMC38) or Cycle 2/Cycle 4 Day 1 (COU-AA-301) were evaluated. CTC response was defined as a ≥30% decline in CTC relative to BL (30%CTCresp). Association of 30%CTCresp with OS was evaluated with Cox regression in uni- and multivariable (MV) analysis with ECOG, LDH, ALP, Alb, Hb, BL CTC and PSA as covariates (continuous). C-index was calculated to determine the performance of the MV model with and without 30%CTCresp as a covariate. Results: 439 pts (326 in COU-301 and 113 in IMMC38) were analyzed. Median BL CTC was 18.5 in COU-301 and 23 in IMMC38. OS in pts with 30%CTCresp at Wk 4 was significantly better in COU-AA-301 and IMMC-38 datasets (Table). BL CTC (continuous) and 30%CTCresp at Wk4 were independently associated with OS in MVA in both datasets. C-index of the MV model improved from 0.677 to 0.712 (COU-AA-301) and from 0.747 to 0.800 (IMMC-38) after including 30%CTCresp. Equivalent results were acquired when evaluating 30%CTCresp at Wk 12. Conclusions: BL CTC and 30% CTC falls are independently associated with OS in in CRPC pts treated with abiraterone and chemotherapy. Adding CTC response improved the performance of the MV model. A 30% decline in CTCs from BL as early as 4 wks post-treatment may be a valid biomarker of response to treatment in CRPC. 30% CTC decline at 4 weeks and survival. N(%) OS (m) HR (95%CI) p-value COU-AA-301 326 11.6 (10.3-13) 30% CTC Decline 208 (64%) 14.4 (13.2-15.5) - No 30% CTC Decline 118 (36%) 7.9 (6.8-9) 0.4 (0.3-0.6) <0.001 IMMC-38 113 11.2 (9.7-12.6) 30% CTC Decline 75 (66%) 12.3 (8.2-16.3) - No 30% CTC Decline 38 (34%) 6.8 (4.4-9.2) 0.5 (0.3-0.8) 0.001
Reduced Opioid Marketing Could Limit Prescribing Information for Physicians—Reply
Authors: Scott E. Hadland, Magdalena Cerdá, Brandon D. L. Marshall
Journal: JAMA Internal Medicine (2018)

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Abstract 17161: Inflammatory Serine Protease Inhibition Attenuates Myocyte Apoptosis and Cardiac Dysfunction via Intervention of Peroxisome Proliferator-activated Receptor Gamma-induced Lipotoxicity and Inflammation in High Fat Diet-induced Diabetic Cardiomyopathy
Authors: Kunal Sikder, Amrita Sarkar, Sanket Kumar Shukla, Aimee Abbott, Domenica Carrier, Carlos Barbery, Richard Pestell, Khadija Rafiq
Journal: Circulation (2016)

Background: Diet consisting of high percentage of fat induces lipotoxicity, leading to type II diabetes and diabetic cardiomyopathy (DCM). The mechanism by which high fat diet (HFD) mediated lipoto...
Role of MEL-18 Amplification in Anti-HER2 Therapy of Breast Cancer
Authors: Jeong-Yeon Lee, Hyeong-Seok Joo, Hee-Joo Choi, Sora Jin, Hyung-Yong Kim, Ga-Young Jeong, Hee Woon An, Mi Kyung Park, Seung Eun Lee, Wan-Seop Kim, Taekwon Son, Kyueng-Whan Min, Young-Ha Oh, Gu Kong
Journal: JNCI Journal of the National Cancer Institute (2018)

Resistance to HER2-targeted therapy with trastuzumab still remains a major challenge in HER2-amplified tumors. Here we investigated the potential role of MEL-18, a polycomb group gene, as a novel prognostic marker for trastuzumab resistance in HER2-positive (HER2+) breast cancer.The genetic alteration of MEL-18 and its clinical relevance were examined in multiple breast cancer cohorts including METABRIC (n = 1,980), TCGA (n = 825), and our clinical specimens (n = 213, trastuzumab-treated HER2+ cases). MEL-18 amplification was validated by fluorescence in situ hybridization (FISH) analysis. The MEL-18 effect on trastuzumab response was confirmed by in vitro cell viability assays and an in vivo xenograft experiment (n = 7 per group). Gene expression microarray and receptor tyrosine kinase array were performed to identify the trastuzumab resistance mechanism by MEL-18 loss. All statistical tests were two-sided.MEL-18 was exclusively amplified in approximately 30-50% of HER2+ breast tumors and was associated with a favorable clinical outcome (disease-free survival: P = .02 in HER2+ cases, METABRIC; P = .04 in patients receiving trastuzumab). In MEL-18-amplified HER2+ breast cancer, MEL-18 depletion induced trastuzumab resistance by increasing ADAM sheddase-mediated ErbB ligand production and receptor heterodimerization. MEL-18 epigenetically silenced ADAM10/17 expression in cooperation with polycomb-repressive complex (PRC) 1 and PRC2. Combination treatment with an ADAM10/17 inhibitor and trastuzumab could overcome MEL-18 loss-mediated trastuzumab resistance in vivo (BT474/shMEL-18 xenograft: trastuzumab, mean [SD] tumor volume = 406.1 [50.1] mm3, vs trastuzumab + GW280264 30 mg/kg, mean [SD] tumor volume = 68.4 [15.6] mm3, P < .001). Consistently, trastuzumab-treated patients harboring concomitant MEL-18 amplification and low ADAM17 expression showed prolonged relapse-free survival (P = .02 in our cohort, n = 213).MEL-18 serves to prevent ligand-dependent ErbB heterodimerization and trastuzumab resistance, suggesting MEL-18 amplification as a novel biomarker for HER2+ breast cancer.