Macro and Micronutrient Substances intake Against Stunting in Toddlers. Stunting is a cumulative process and is caused by insufficient intake of nutrients or recurrent infectious diseases or both. Stunting can also occur before birth and is caused by very poor nutritional intake during pregnancy, eating patterns that are very lacking, low quality of food in line with the frequency of infectious diseases so that it can inhibit growth (UNICEF, 2012). This type of research was descriptive analytic. The study design was cross-sectional consisting of 58 samples of toddlers 24-59 months in the work area of Sumber Urip Health Center Rejang Lebong Regency in 2018. Data were collected in the form of nutritional status data TB/U using microtoice tools, energy intake, macro and micronutrients using questionnaires 2x24 hour recall. Toddlers 24-59 months who experienced stunting were 17 people (29.3%) and normal ones were 41 people (70.7%). The incidence of stunts was largely due to a lack of energy intake, and zinc. The results of this study indicate that there was a significant relationship between energy intake, macronutrients, and zinc with the incidence of stunting in infants.
Bladder stone is a relatively common disease of childhood in West Sumatra with an incidence of 8.3/100,000 population per year. We have studied 87 cases with a peak age of onset of 2-4 years and a male/female ratio of 12:1. The majority of these are from poor families with a diet low in protein and phosphate. Diarrhoea is common. The composition of the stones is primarily ammonium acid urate. Patients with sterile urine have shown significantly higher levels of urinary ammonia than controls, and only approximately 50% of patients' urine were infected. This is consistent with excretion of a high acid load, due both to an acidogenic rice diet and diarrhoea, combined with a low level of phosphate. This condition was once endemic in Europe but is now confined to a belt of countries from the Balkans through Asia.
Background: Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor which maintains cellular homeostasis in response to hypoxia. It can trigger apoptosis while stimulating angiogenesis process and decrease neurological deficit after an ischemic stroke. Up until now, this protein complex has not been widely investigated especially in stroke patient. Objective: Here, we examined the potential of HIF-1α as a marker for neuroplasticity process after ischemic stroke. Methods: Serum HIF-1α were measured in acute ischemic stroke patients. National Institute of Health Stroke Scale (NIHSS) were assessed on the admission and discharge day (between days 7 and 14). Ischemic stroke divided into 2 groups: large vessel disease (LVD, n ¼ 31) and small vessel disease (SVD, n ¼ 27). Statistical significances were calculated with Spearman rank test. Results: A total of 58 patients, 31 with large artery atherosclerosis LVD and 27 with small vessel disease (SVD) were included in this study. HIF-1α level in LVD group was 0.5225 AE 0.2459 ng/mL and in SVD group was 0.3815 AE 0.121 ng/mL. HIF-1α was higher (p ¼ 0.004) in LVD group than in SVD group. The initial NIHSS score in LVD group was 15.46 AE 2.61 and discharge NIHSS score was 13.31 AE 3.449. Initial NIHSS score in SVD group was 6.07 AE 1.82 and the discharge NIHSS was 5.703 AE 1.7055. In both SVD and LVD group, HIF-1α were significantly correlated with initial NIHSS (both p < 0.001) and discharge NIHSS (p < 0.0383 r ¼ 0.94, p < 0.001, r ¼ 0.93, respectively). Conclusions: HIF-1α has a strong correlation with NIHSS and it may be used as predictor in acute ischemic stroke outcome.
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