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Lewis J.D.,University of Pennsylvania | Habel L.A.,Kaiser Permanente | Quesenberry C.P.,Kaiser Permanente | Strom B.L.,University of Pennsylvania | And 9 more authors.
JAMA - Journal of the American Medical Association | Year: 2015

Importance Studies suggest pioglitazone use may increase risk of cancers. Objective To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. Design, Setting, and Participants Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193 099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236 507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. Main Outcomes and Measures Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193 099 persons in the bladder cancer cohort, 34 181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100 000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95%CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6%among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95%CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95%CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95%CI, 1.16-1.71). Crude incidences of prostate and pancreatic cancer in pioglitazone users vs nonusers were 453.3 vs 449.3 and 81.1 vs 48.4 per 100 000 person-years, respectively. No clear patterns of risk for any cancer were observed for time since initiation, duration, or dose. Conclusions and Relevance Pioglitazone use was not associated with a statistically significant increased risk of bladder cancer, although an increased risk, as previously observed, could not be excluded. The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality. © 2015 American Medical Association. All rights reserved. Source


Phillips W.A.,University of Stirling | Clark A.,University of Edinburgh | Silverstein S.M.,Rutgers Biomedical and Health science
Neuroscience and Biobehavioral Reviews | Year: 2015

A broad neuron-centric conception of contextual modulation is reviewed and re-assessed in the light of recent neurobiological studies of amplification, suppression, and synchronization. Behavioural and computational studies of perceptual and higher cognitive functions that depend on these processes are outlined, and evidence that those functions and their neuronal mechanisms are impaired in schizophrenia is summarized. Finally, we compare and assess the long-term biological functions of contextual modulation at the level of computational theory as formalized by the theories of coherent infomax and free energy reduction. We conclude that those theories, together with the many empirical findings reviewed, show how contextual modulation at the neuronal level enables the cortex to flexibly adapt the use of its knowledge to current circumstances by amplifying and grouping relevant activities and by suppressing irrelevant activities. © 2015 Elsevier Ltd. Source


Silverstein S.M.,Rutgers Biomedical and Health science | Rosen R.,New York Eye and Ear Infirmary of Mount Sinai
Schizophrenia Research: Cognition | Year: 2015

Although visual processing impairments are common in schizophrenia, it is not clear to what extent these originate in the eye vs. the brain. This review highlights potential contributions, from the retina and other structures of the eye, to visual processing impairments in schizophrenia and high-risk states. A second goal is to evaluate the status of retinal abnormalities as biomarkers for schizophrenia. The review was motivated by known retinal changes in other disorders (e.g., Parkinson's disease, multiple sclerosis), and their relationships to perceptual and cognitive impairments, and disease progression therein. The evidence reviewed suggests two major conclusions. One is that there are multiple structural and functional disturbances of the eye in schizophrenia, all of which could be factors in the visual disturbances of patients. These include retinal venule widening, retinal nerve fiber layer thinning, dopaminergic abnormalities, abnormal ouput of retinal cells as measured by electroretinography (ERG), maculopathies and retinopathies, cataracts, poor acuity, and strabismus. Some of these are likely to be illness-related, whereas others may be due to medication or comorbid conditions. The second conclusion is that certain retinal findings can serve as biomarkers of neural pathology, and disease progression, in schizophrenia. The strongest evidence for this to date involves findings of widened retinal venules, thinning of the retinal nerve fiber layer, and abnormal ERG amplitudes. These data suggest that a greater understanding of the contribution of retinal and other ocular pathology to the visual and cognitive disturbances of schizophrenia is warranted, and that retinal changes have untapped clinical utility. © 2015 The Authors. Source


Therrien M.,University of Maine, United States | Byham-Gray L.,Clinical Nutrition | Denmark R.,Rutgers Biomedical and Health science | Beto J.,Loyola University
Journal of Renal Nutrition | Year: 2014

Objective: The objective of this study was to compare the characteristics and dietary intake of Second National Research Question (SNRQ) participants to the Women's Health Initiative-Dietary Modification (WHI-DM) Trial group and to compare the dietary intake of both groups to relevant reference norms. Design: The study design was a secondary analysis of data collected from the SNRQ and from the WHI-DM Trial. Subjects: SNRQ participants were adult women on dialysis (n = 248) from U.S. dialysis facilities. WHI-DM Trial participants (n = 48,836) were postmenopausal, 50- to 79-year-old women from 40 U.S. clinical centers. Methods: The 1-sample t test, χ2, and Wilcoxon signed-rank test were used to compare the SNRQ participants to the WHI-DM group and to compare the dietary intake of both to nutrition reference norms. Differences were considered significant at a 2-tailed P ≤ .01. Main Outcome Measure: Dietary intake was defined as dietary energy intake (DEI), dietary protein intake (DPI), fiber, fat, saturated fat, sodium, potassium, phosphorus, fruits, and vegetables. Results: Characteristics including age, race, weight, educational level, and cardiovascular disease differed between the SNRQ and WHI-DM groups (P < .001). SNRQ participants had lower DEI, DPI, fiber, fat, saturated fat, potassium, sodium, phosphorus, fruit, and vegetable intake than WHI-DM women (P < .001). Dietary intake of SNRQ hemodialysis (HD) and peritoneal dialysis (PD) patients differed significantly from reference norms (P < .001) except for phosphorus intake in PD patients (P = .03). WHI-DM women had higher intakes of fat and saturated fat and lower intakes of fiber, fruit, and vegetables than recommended in reference norms for the general population. Conclusion: Dietary intake differed significantly between SNRQ participants and the WHI-DM group. Dietary intake of the SNRQ participants, except for phosphorus intake in PD patients, differed significantly from relevant reference norms. © 2014 National Kidney Foundation, Inc. Source


Hafer J.F.,University of Massachusetts Amherst | Hafer J.F.,The New Motion | Brown A.M.,Rutgers Biomedical and Health science | deMille P.,Sports Rehabilitation and Performance Center | And 2 more authors.
Journal of Sports Sciences | Year: 2015

Abstract: Many studies have documented the association between mechanical deviations from normal and the presence or risk of injury. Some runners attempt to change mechanics by increasing running cadence. Previous work documented that increasing running cadence reduces deviations in mechanics tied to injury. The long-term effect of a cadence retraining intervention on running mechanics and energy expenditure is unknown. This study aimed to determine if increasing running cadence by 10% decreases running efficiency and changes kinematics and kinetics to make them less similar to those associated with injury. Additionally, this study aimed to determine if, after 6 weeks of cadence retraining, there would be carryover in kinematic and kinetic changes from an increased cadence state to a runner’s preferred running cadence without decreased running efficiency. We measured oxygen uptake, kinematic and kinetic data on six uninjured participants before and after a 6-week intervention. Increasing cadence did not result in decreased running efficiency but did result in decreases in stride length, hip adduction angle and hip abductor moment. Carryover was observed in runners’ post-intervention preferred running form as decreased hip adduction angle and vertical loading rate. © 2014, © 2014 Taylor & Francis. Source

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