The aim of this study to determine the cutoff point of telomere length and association with blood glucose and lipid profile among Minangkabau ethnic women. This cross-sectional study was conducted in Padang City, Indonesia using a sample of 116 Minangkabau ethnicity women aged between 40-55 years. The blood sample analysis using O'Callaghan and Fenech's technique to measure telomere length, fasting blood glucose and lipid profile analysis from blood venous. Data analysis using Pearson correlation and then continued for known cut off point by Hosmer-Lemeshow test. Data were processed using Stata version 14.2 (Stata Corporation). The results showed there is no correlation between blood glucose and profile lipid (total cholesterol, LDL, HDL, and triglycerides) with telomere length of Minangkabau ethnicity women (p>0.05). Based on receiver operating characteristic (ROC) curve analysis, we obtained a cutoff point for telomere length is 385 bp with 53% sensitivity, 55% specificity and an accuracy of 58.2%. Blood glucose and lipid profile do not have correlation because of telomere length cause of many factors. This analysis confirmed there is no correlation blood glucose and profile lipid with telomere length of Minangkabau ethnicity women. Cut off point for predicted telomere length is 385 bp.

Purpose:The pur pose of this study was to deter mine the optimal dur ation of long-term video-EEG monitoring (VEEG) in patients with epilepsy. The response time of medical staff to seizures was also evaluated from the viewpoint of safety of the monitoring. Methods: We estimated the optimal duration of VEEG from the seizure onset pattern. We retrospectively investigated all VEEG sessions performed in our department during the period between June 2005 and July 2016. Sessions with no seizures and with only non-epileptic seizures were excluded. Using 91 sessions from 69 patients, information on the onset time and response time of medical staff to seizures was collected. Results: The median duration from the start of VEEG to the first seizure was 2 days. Seventy-seven percent of first seizures occurred within 3 days of VEEG. The median duration from the first seizure to the third seizure was 2 days. Eighty percent of third seizures occurred within 3 days of the first seizure. There was no significant diurnal distribution of seizure occurrence. Medical staff did not respond to 20% of generalized seizures and 69% of focal seizures. The overlooking of generalized seizures occurred mainly during the hours of 1-2 pm and 8-9 pm but there was no significant diurnal pattern in overlooking generalized and focal seizures.Conclusion：Based on these findings, we suggest that VEEG can be terminated when no seizure occurs within 4 days after onset. In our VEEG protocol, in which all antiepileptic drugs were discontinued before the start of a session, there was no diurnal pattern of seizure occurrence. This is the first study investigating the diurnal pattern of overlooking seizures by medical staff during VEEG. Since there was no diurnal pattern to the overlooking, medical staff should pay equal, 24-hour attention to patients on VEEG.

In experimental animals, the induction of isoproterenol which is a synthetic of catecholamine, can cause acute myocardial infarction where the pathophysiology and morphology are the same as myocardial infarction in humans. Isoproterenol induction will increase oxidative stress, which will damage the enzyme dimethylarginine dimethylaminohydrolase (DDAH), thus causing asymmetric dimethylarginine (ADMA) levels to increase in circulation. Increased levels of ADMA will inhibit the activity of the enzyme nitric oxide synthase, which results in decreased nitric oxide resulting in endothelial damage. This study aims to determine the effect of Ramipril on asymmetric dimethylarginine (ADMA) levels in rats (Rattus norvegicus) Wistar strain with acute myocardial infarction. Eighteen male Wistar rats (150-250 g) were randomly allocated into three groups: negative control group, positive control, and treatment group. The treatment group was pretreated with Ramipril at dose 3 mg/kg BW orally for seven days. Acute myocardial infarction was induced in positive control groups and treatment groups by subcutaneous injection of isoproterenol (85 mg/kg BW) for two consecutive days. Twenty-four hours after the last administration, rats from all groups were anesthetized and sacrificed for blood sample collection to evaluate the level of Asymmetric Dimethylarginine with Enzym-linked Immunosorbent Assay (ELISA) method. The result showed that ADMA levels were increased in the treatment group after pretreated with Ramipril. This study concluded that pretreatment with Ramipril increased ADMA concentration in acute myocardial infarction rats induced by isoproterenol.