Introduction: Acute brain injury caused by cerebral ischemia, either due to stroke or ischemic hypoxic-ischemic encephalopathy (HIE), represents a major neurological cause of death and disability worldwide. Neuronal cell injury has been shown to correlate with a significant increase in neuron-specific enolase (NSE) levels in in vitro studies. This study aims to measure NSE levels in the blood serum of rats with HIE. Methods: This study used an experimental post-test design in which occlusion of the right common carotid artery (CCA) was performed on Wistar rats, which were then placed in a hypoxic chamber and reperfused after 60 minutes (treatment group). Neurological scores were collected over the first 24 hours. After 48 hours, experimental animals were sacrificed and their serum NSE levels were measured using ELISA. Statistical analysis using a T-test was performed for independent samples. Results: A total of 16 male rats were included in the study. Neurological scores indicated that all HIE group rats experienced hemiparesis to varying degrees. NSE levels in the treatment group were significantly higher than in the control group (p < 0.05). The mean NSE level in the treatment group was higher than that in the other group. Conclusion: Consistent with in vitro studies, we found that NSE was higher in the HIE rat model than in controls. These data support future studies to assess the fitness of serum NSE as a biomarker of brain damage.

Hypoxic-ischemic encephalopathy (HIE) brain injury is one of the leading causes of death and disability worldwide. Nerve growth factor (NGF) is a neurotrophin that plays an important role in the natural repair and regeneration of nerves, but the previous study regarding NGF level after brain injury is still scant. This study aims to determine NGF levels in male Wistar rat models that received right Common Carotid Artery (CCA) occlusion.  This study used an experimental and control design conducted in July-August 2021 at the Stem Cell Research and Development Center, Universitas Airlangga. The right CCA occlusion was performed on the Wistar mouse model in the treatment group, then placed in a hypoxic chamber and reperfusion after 60 minutes. Observations of neurology scores were carried out in the first 24 hours.  After 2x24 hours the animal was sacrificed for serum NGF level measurement using the ELISA method. Statistical analysis using t-test for independent sample.  A total of 16 male rats participated in the study.  Eight rats in the treatment group were put into hemiparesis at different levels according to observations of neurological scores.  Statistically meaningful differences in NGF levels were found in the treatment group compared to controls (P<0.05). Average NGF levels in the treatment group were higher than in the controls.  NGF levels in mice with HIE were higher than the control group, which indicates the body's natural mechanism for neuron protection following ischemic hypoxic events.

Background: Serum lactate was a biomarker implemented to estimate the prognosis in children suffered from status epilepticus (SE). Brain neuroimaging may demonstrate the site area, range of neuronal impairment and ischemic injury. This study aims to evaluate the correlation between long-lasting serum lactate with brain imaging abnormality reflected on Magnetic Resonance Imaging (MRI) in children suffered from SE. Method: This prospective analytical research was conducted from June-November 2018 in children with SE. Serum lactate were collected on 24 hours following SE, and brain MRI was carried out within a period of 7-14 days after SE terminated. Abnormal MRI was categorized as Hypoxic Ischemic Encephalopathy (HIE) grade I to III. Statistical analysis with Kruskal Wallis was applied to calculate the details. Results: Forty two SE subjects were enrolled, 85.7% boys, with a mean age of 59.29 months and mostly with the diagnosis of encephalitis (47.6%). Elevated serum lactate levels were found in 71.4% of patients and about 47.8% had abnormal MRI images in the form of HIE Grade I. Mean serum lactate level in HIE grade I, II, III was 1.69 mmol/L, 3.32 mmol/L, 3.48 mmol/L respectively. Two patients were death and 28.6% had a life with neurological deficit. There was a significant correlation (p=0.021) between long-lasting serum lactate level and abnormal brain MRI. Conclusion: In children suffered from SE, HIE grade I is the most neuroimaging pattern obtained, and long-lasting serum lactate was considered to correlate with abnormal brain MRI.

To investigate the effect of intracerebral adipose neural stem cell transplantation in the inflammatory process after brain HI. The study used 16male Wistar rats aged 2 months which were randomly divided into the following group: Ischemia-Reperfusion group (IR, n=8) and ANSC-treated group (IR+ANSC, n=8). IR was performed by right common carotid artery occlusion for 2 hours, hypoxia procedure for 1 hour and reperfusion.  ANSC was prepared from rats adipose tissue and processed in Laboratory. ANSC was inserted intracerebally after hypoxia procedure and after 48 hours the blood sample were analyzed by using ELISA. T-test for independent samples was used for statistial analysis. There were no significant differences in the TNF-α level between the IR group and IR+ANSC group. There were statistically significant difference in IL-10 level between groups (P< 0.05). Intracerebral ANSC transplantation cannot reduce TNF-α expression and increase IL-10 expression in brain ischemia induced by CCA ligation and hypoxia.

Brain abscess is a local infection within the brain parenchyma. Predisposing factors include cyanotic congenital heart disease (CHD). Identification of risk factors for mortality is important to determine the prognosis. A case-control study of children with cyanotic CHD associated with brain abscess was conducted in the pediatric ward of a hospital from January 2016 to December 2020. Data were collected from medical records with the case to controls ratio of 1:3.07. A total of 61 children were evaluated, 46 children survived and 15 children non-survived. From 11 risk factors evaluated, 6 risk factors had a significant different of mortality risk included the level of hemoglobin (p=0.07), leukocyte (p=0.063), Neutrophil-to-lymphocyte ratio (NLR) (p<0.001), peripheral oxygen saturation (SpO2) (p=0.00), multiple abscesses (p=0.008), brain abscess diameter (p<0.001). Multivariate logistic regression analyses revealed significant risk factors for mortality in cyanotic CHD children with brain abscesses were NLR (OR 13.62, 95%CI 2.123-87.319, p=0.006); SpO2 (OR 1.5, 95% CI 1.25-2, p=0.04); brain abscess diameter (OR 7.61, 95%CI 1.064-54.434, p=0.043). NLR, brain abscess diameter, and SpO2 were the risk factors in increasing mortality in cyanotic CHD children with brain abscess. The prevention of abscess cerebral development and cyanotic CHD management are needed to reduce the mortality.