[Medical computer programming for active diagnosis of glaucoma].
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The lipidemic pattern has been evaluated in 40 systematically trained subjects and in 43 subjects of same age and BMI sedentary ones. The mean CT concentration of active subjects was not different from that of the sedentary group, whereas HDL-C was significantly higher and TG significantly lower, CT/HDL-C was significantly lower in active subjects. The obtained results show that systematic physical activity, even if not at agonistic level, can induce antiatherogenic modifications of the lipidemic pattern.
A behaviorally-oriented activities therapy program was designed and implemented with adolescents who manifested problems in school, at home, and with peers. Baseline measures for target behaviors were taken within the activities therapy program and, after a behavioral analysis, specific techniques were chosen to remediate problems. Techniques employed included: contingency contracting, assertiveness training, relaxation training, and cognitive restructuring. Evaluation of the effectiveness of each program was performed through daily measurement of the frequency of the occurrence of the target behaviors. Three case studies are presented which are illustrative of the range of programs which can be successfully implemented with this population.
BACKGROUND Acute myocardial infarction (AMI) reflects inherited susceptibility and inflammatory remodeling, but the cellular contexts linking genetic risk to disease remain unclear. MATERIAL AND METHODS We integrated a meta-transcriptome-wide association study (TWAS) with a human cardiac single-nucleus RNA-sequencing atlas contained 11 individuals (5 AMI and 6 donor) to identify genetics-informed cellular programs. Composite program states were defined by global score quartiles. A fixed 5-gene panel was evaluated for nucleus-level endocardial low-transcriptional-state (Endo_LTS) vs endocardial high-transcriptional-state (Endo_HTS) discrimination within the AMI endocardium using 5-fold leave-1-patient-out cross-validation. Functional follow-up used CRIM1 silencing in hypoxia-treated human induced pluripotent stem cell (hiPSC)-derived endocardial endothelial-like cells and complementary peripheral blood analyses. RESULTS The endocardium exhibited the most prominent infarction-associated increase in TWAS-anchored program activity, with expansion of program-high states and higher CytoTRACE scores. A consensus 5-gene panel (RPS8, PLEC, CFDP1, CRIM1, TNS2) was identified. Among 2163 AMI endocardial nuclei from 5 patients, the state classifier included 364 Endo_LTS and 751 Endo_HTS nuclei; 1048 Endo_MTS nuclei were excluded. Pooled out-of-fold ROC-AUCs ranged from 0.665 to 0.831. The panel also showed discriminatory value in an independent peripheral-blood AMI-vs-control cohort. CRIM1 was prioritized as a candidate linked to the remodeling program. CRIM1 silencing attenuated ACTA2/alpha-SMA, vimentin, LDHA, CCL2, and VEGFA and partially restored CD31, whereas TGF-ß remained elevated. CONCLUSIONS These findings identify a genetics-informed endocardial inflammatory remodeling state in AMI and define a 5-gene surrogate of its activated state. CRIM1 is prioritized as a candidate linked to selected inflammatory, metabolic, and structural outputs. Persistent TGF-b elevation after CRIM1 silencing argues against a simple linear regulatory model and indicates that further mechanistic validation is required.