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The only therapeutic options currently used are invasive procedures by surgery or transcatheter intervention. However, no approved drug has shown prophylactic or therapeutic effectiveness. Selleck AZD-5462 Conventional diagnostic imaging is currently the best method for detecting, measuring, and assisting in the treatment of calcification. However, these common imaging modalities are unable to detect early subclinical stages of disease at the level of microcalcifications; therefore, the vast majority of patients are diagnosed when macrocalcifications are already established. In this review, we unravel the current knowledge of how innate and adaptive immunity regulate cardiovascular calcification; and put forward differences and similarities between vascular and valvular disease. Additionally, we highlight potential immunomodulatory drugs with the potential to target calcification and propose avenues in need of further translational inquiry. PURPOSE The objective of this study was to objectivize if the cardiovascular therapeutic changes performed during hospitalization of older patients with hypertension and/or heart failure (HF), were maintained in ambulatory 3 month after hospitalization. METHODS This is a longitudinal study conducted in a geriatric unit. Patients over 65 years with hypertension and/or HF, who had at least one change in cardiovascular medicaton during hospitalization, and who accepted the 3-month follow-up were included in the longitudinal study. At admission, during hospitalization and 3 months after hospitalization data concerning cardiovascular medication were collected. RESULTS During hospitalization, 142 (73.6%) patients had at least one change in hypertension and/or HF medication. Overall, 249 changes were performed. Forty-one patients received follow-up at 3 months. At 3 months, therapeutic changes were maintained by 48.8% of the general practitioners (n=20 patients). For the rest, 41.5% of the patients had benefited from new therapeutic changes (28 changes for 10 patients) and 9.7% of the general practitioners (n=4 patients) had restored the initial prescription before hospitalization. CONCLUSIONS Medication review performed by geriatricians and pharmacists during hospitalization resulted in 249 changes. These changes aimed at limiting iatrogenic disease, by reducing overtreatment and potentially inappropriate prescriptions. Difficulties in the patient care continuity between the hospital and ambulatory setting have been identified. Sudden cardiac death in young is seen as a dramatic phenomenon requiring knowledge of its impact. We aim to study the epidemiological characteristics of sudden cardiac ischemic death in young, and to discuss his involvement in the occurrence of death. We performed a retrospective cohort study using autopsy data from the department of forensic medicine of the University Hospital of Fattouma Bourguiba, Monastir-Tunisia. A review of all autopsies performed during 23 years was done. In each case, clinical information and circumstances of death were obtained. We have included all sudden death in persons aged between 1 year and 35 years for the male and from one year to 45 years for female. We collected 312 cases of sudden death during the studied period. The collected data were processed using SPSS 20. The significance level was set at 0.05. Thirty-two cases of cardiac ischemic sudden death have been collected. Myocardial infarction was the second cause of sudden death in young patients. There was a male predominance. The most affected subjects were aged between 25-45 years. The death occurred more frequently at rest. Coronary artery disease has been discovered in twenty-four cases (75%). The myocardial infarction occurred on healthy coronary arteries in eight cases. An anomalous course of coronary arteries, in particular myocardial bridging, was found in eight cases (25%). Toxicological screening was negative in all cases. Identifying epidemiological characteristics of sudden cardiac ischemic death in this population is important for guiding approaches to prevention that must be based on dietary hygienic measures and the control of cardiovascular risk factors. An atrial septal aneurysm (ASA) is a rare but well recognized entity characterized by saccular deformity of the atrial septum that bulges into the right or left atrium. Diagnosis can be established using transthoracic and transesophageal echocardiography. Although this abnormality is considered clinically benign, it has been independently associated with systemic or cerebral embolism. We present a unique case of isolated atrial septal aneurysm complicated by digital ischemia in a 51 years old woman. Dnmt1, Dnmt3a and Dnmt3b are main genes encoding DNA methyltransferases (Dnmts) which catalyze DNA methylation and regulate gene expression without changing DNA sequence. Our previous study disclosed that double knockout of Dnmt1 and Dnmt3a in forebrain excitatory neurons impaired synaptic plasticity and led to hippocampus-dependent learning and memory deficits, however the underlying synaptic mechanisms remain uncertain. In this study, we selectively knocked down the expression of Dnmt1 and Dnmt3a in primary cultured hippocampal neurons derived from embryonic Dnmt1,3a2flox/2flox mice by transfection with Cre-expressing virus, to study the effect of Dnmts and mediated DNA methylation on synaptogenesis and synaptic function. We found that the hippocampal neurons at 15 days in vitro (DIV15) exhibited similar size of cell body, but longer dendrites with reduced number of branches and lower density of excitatory synapses formation after virus-mediated Dnmt1 and Dnmt3a deletion. Supportively, cultured neurons with Dnmt1 and Dnmt3a deficiency displayed reduced frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs), indicating that both pre- and post-synaptic dysfunction are involved. In addition, our Ca2+-image study with Rhod-3AM revealed suppression of glutamate-evoked elevation of cytoplasmic [Ca2+] after Dnmt1 and Dnmt3a deletion. Altogether our findings provide new evidence that normal expression of Dnmt1 and Dnmt3a in hippocampal neurons are essential for excitatory synaptogenesis and synaptic function.

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