RESUMEN
There are approximately 1.3 million cases of neonatal sepsis reported worldwide with deaths occurring more commonly in preterm and low-weight newborns. Neonatal sepsis is the third major cause of neonatal deaths resulting in 203,000 deaths per year. It is divided into two subtypes based on time of occurrence: early-onset neonatal sepsis (ENS), occurring within the first 72 hours of birth usually due to perinatal risk factors, and late-onset neonatal sepsis (LOS) usually occurring after the first week of life and up to 28th day of life. There are many complications associated with neonatal sepsis including septic shock, multiple organ failure, and death. It is vital for clinicians to know the signs and symptoms of neonatal sepsis in order to diagnose it early. Preventive measures, early diagnosis, appropriate antibiotic administration, timely supportive management, and the establishment of efficient management are vital in the prevention of severe complications or death. In this review, we aim to provide the most up-to-date information regarding risk factors, pathophysiology, signs and symptoms, diagnosis, and treatment of neonatal sepsis. We discuss the maternal and neonatal risk factors involved in the pathogenesis of neonatal sepsis and the signs and symptoms of early and late neonatal sepsis. We focus on the different pathogens involved and the markers used in the diagnosis and treatments available for each.
RESUMEN
Cerebral ischemia-reperfusion (C I/R) accelerates neuronal injury through the overproduction of reactive oxygen species due to mitochondrial dysfunction. Hesperidin has cerebroprotective effects due to its antioxidant and anti-apoptotic nature against oxidative damage caused by C I/R. The blood-brain barrier also limits the hesperidin passage into the cerebral region due to its poor bioavailability. Current research included analysis of binding energy, hesperidin inhibitory constant on inflammatory cytokines (TNF α, IL 6) and apoptotic protein (caspase 3), hesperidin nanoparticles prepared, and investigation of their defense against C I/R rats. Binding energy and IC50 of hesperidin on pathological proteins using AutoDoc. 1.5.6 and PyRx in silico tools were compared with thalidomide. The fabrication method was engaged in the preparing of nano-hesperidin, characterized by SEM assessment. Bilateral common carotid artery occlusion technique has been used in experimental rats to cause C I/R. Nano-hesperidin cerebroprotective activity was assessed by differing infarction magnitude, oxidative stress parameters, TNF α and IL 6, and hippocampal histopathology with rats treated with unformulated hesperidin. Hesperidin found stronger binding strength and IC50 was relative to thalidomide on TNF α, IL 6, and caspase 3. Nano-hesperidin with a size of 100-500 nm was shown in a uniform nano-size and spherical form. Nano-hesperidin-treated rats showed significantly increased glutathione (p < 0.00***), catalase (p < 0.01**), and total protein (p < 0.001***), and decreased cerebral infarction size, TNF α (p < 0.01**), IL 6 (p < 0.01**), and malondialdehyde (p < 0.05*), compared with hesperidin-treated ischemic rats. Therefore, hesperidin nanoparticles may confer protection to the neurons against ischemic injury compared with hesperidin treatment.
