In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Physical activity is beneficial for cancer survivors, but exercise participation is low in this population. It is therefore important to understand the psychological factors underlying exercise uptake so that more effective interventions can be developed. Social-cognitive theory constructs such as outcome expectancies predict exercise behavior, but self-report measures have several limitations. We examined the associations between implicit (automatic) cognitions and exercise behavior and self-efficacy in endometrial cancer survivors.', 'This was a longitudinal study to examine predictors of exercise behavior in female endometrial cancer survivors who all received an exercise intervention. Participants (N = 100, mean age of 57.0) completed questionnaires to assess self-report exercise-related measures (outcome expectancy and attitudes about and identification with exercise) and reaction time (RT) tasks to assess implicit exercise cognitions (expectancy accessibility, implicit attitudes about exercise, and implicit self-identification with exercise) at baseline and at 2, 4, and 6 months at follow-up. Exercise behavior was measured using accelerometers and self-report. Data were analyzed using linear mixed models.', 'Expectancy accessibility was associated with exercise duration independent of the corresponding self-report measure. Exercise implicit attitudes and self-identification were prospectively associated with exercise self-efficacy only after adjustment for the corresponding self-report measures and baseline self-efficacy. Self-report measures were also associated with study outcomes.\Question: Are self-reported and automatic cognitions associated with exercise behavior in cancer survivors?
Both self-reported cognitions and implicit cognitions may be useful to identify individuals at risk of failing to exercise. Individuals so identified might be provided with a different or more intensive intervention. The data also suggest cognitive targets for intervention. (PsycINFO Database Record

Context: Enterovirus infections are major etiological factors in myocarditis and dilated cardiomyopathy. Using an experimental murine model of this disease, previous studies have shown that myocarditis susceptibility depends upon activation of T lymphocytes expressing the gamma delta T cell receptor (TcR), and that only mouse strains which accumulate gamma delta T cells in the myocardium show apoptosis of myocytes or evidence of dilated cardiomyopathy-like disease. The objective of the present studies is to demonstrate that gamma delta T cells directly induce greater Fas-dependent apoptosis of cultured myocytes than T cells expressing the alpha beta TcR.', 'Bl.Tg.E alpha mice were infected for 7 days with coxsackievirus B3 (CVB3). Hearts were removed and were either formalin-fixed, sectioned and stained with hematoxylin and eosin for inflammation, and using TdT-TUNEL for apoptosis, or were minced and collagenase digested for isolation of gamma delta+ and alpha beta+ T cells using immunomagnetic bead separation. Neonatal cultures of cardiac myocytes were isolated from mice less than 2 days old by collagenase and pancreatin digestion, and were either untreated or infected with virus. Levels of Fas (CD95) were measured using FITC-conjugated hamster anti-mouse Fas monoclonal antibody and flow cytometry. Susceptibility of myocytes to Fas-dependent killing was measured by 51Cr-release by labeled myocytes incubated for 4 h on either 3T3-mock or 3T3-FasL transfected cell monolayers. Killing by T cells was also measured in a 4 h 51Cr-release assay. Fas-dependent and perforin-dependent cytotoxicity was determined by specific blocking using either Fas-Fc or concanamycin A.', 'Virally infected myocyte cultures showed significantly enhanced Fas expression compared to uninfected cells, with maximal upregulation of Fas occurring 18-24 h after virus infection. Both infected and uninfected myocytes were selectively killed by FasL-transfected 3T3 cells but not by mock control cells. Approximately 38% of CD3+ lymphocytes isolated from the heart express the gamma delta TcR with the remainder expressing the alpha beta TcR. Both gamma delta+ and alpha beta+ T cells lysed myocyte targets. Blocking studies indicate that gamma delta+ T cells induced predominantly Fas-mediated killing, while alpha beta+ cell produced more perforin-mediated death, although these effectors were capable of Fas-dependent killing as well.\Question: Do t cells expressing the gamma delta T cell receptor induce apoptosis in cardiac myocytes?
These studies demonstrate that T cells expressing the gamma delta TcR are more effective mediators of myocyte apoptosis than alpha beta+ T cells in vitro and suggests that these effectors may be primarily responsible for myocardial injury associated with dilated cardiomyopathy-like signs during coxsackievirus B3-induced myocarditis.

Context: Valve interstitial cells are active and aggressive players in aortic valve calcification, but their dynamic mediation of mechanically-induced calcific remodeling is not well understood. The goal of this study was to elucidate the feedback loop between valve interstitial cell and calcification mechanics using a novel three-dimensional culture system that allows investigation of the active interplay between cells, disease, and the mechanical valve environment.', 'We designed and characterized a novel bioreactor system for quantifying aortic valve interstitial cell contractility in 3-D hydrogels in control and osteogenic conditions over 14 days. Interstitial cells demonstrated a marked ability to exert contractile force on their environment and to align collagen fibers with the direction of tension. Osteogenic environment disrupted interstitial cell contractility and led to disorganization of the collagen matrix, concurrent with increased αSMA, TGF-β, Runx2 and calcific nodule formation. Interestingly, RhoA was also increased in osteogenic condition, pointing to an aberrant hyperactivation of valve interstitial cells mechanical activity in disease. This was confirmed by inhibition of RhoA experiments. Inhibition of RhoA concurrent with osteogenic treatment reduced pro-osteogenic signaling and calcific nodule formation. Time-course correlation analysis indicated a significant correlation between interstitial cell remodeling of collagen fibers and calcification events.\Question: Does valve interstitial cell tensional homeostasis direct calcification and extracellular matrix remodeling processes via RhoA signaling?

Interstitial cell contractility mediates internal stress state and organization of the aortic valve extracellular matrix. Osteogenesis disrupts interstitial cell mechanical phenotype and drives disorganization, nodule formation, and pro-calcific signaling via a RhoA-dependent mechanism.