RESUMEN
Background@#Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. @*Results@#Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. @*Conclusions@#Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.
RESUMEN
Background@#Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. @*Results@#Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. @*Conclusions@#Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.
RESUMEN
Objective@#In Korea, many hospitals have recently changed the process of internal medicine management in the emergencydepartment (ED) because of reduced manpower, raising concerns regarding the decreased quality of medicalcare. The process of medical management in the ED was streamlined to resolve the reduced manpower. Thus, this studycompared the pneumonia treatment effectiveness before and after the process changes. @*Methods@#This study included patients who were diagnosed with pneumonia in the ED and hospitalized from January2014 to December 2016. They were divided into two groups based on before and after the changes. The disease severity,management adequacy, and prognosis were compared using the initial quick sequential organ failure assessmentscore (qSOFA), systemic inflammatory response syndrome criteria (SIRS), CURB-65 score, door-to-antibiotic time(DAT), length of stay (LOS), hospitalization period (HP), and in-hospital mortality, were collected retrospectively from themedical records. @*Results@#The qSOFA, SIRS, and CURB-65 scores did not differ between the two groups. The median (interquartilerange) DAT, LOS, and HP were reduced after the process changes: DAT (160.0 minutes [111.0-230.0] vs. 120.0 minutes[74.0-175.0], P<0.001), LOS (7.6 hours [4.8-15.8] vs. 4.7 hours [3.2-6.8], P<0.001), and HP (9.0 days [6.0-16.0] vs. 8.0days [5.0-15.0], P=0.011). On the other hand, the in-hospital mortality was similar in the two groups (14.1% vs. 11.2%,P=0.162). @*Conclusion@#The DAT, LOS, and HP decreased after the process changes, but the in-hospital mortality did not worsen.This shows that pneumonia management in the ED was not compromised, but rather improved, after the changes.
RESUMEN
Obesity has been known as an independent risk factor for stroke. Effects of high-fat diet (HFD)-induced obesity on neuronal damage in the somatosensory cortex of animal models of cerebral ischemia have not been studied yet. In this study, HFD-induced obesity was used to study the impact of obesity on neuronal damage/loss and microgliosis in the somatosensory cortex of a gerbil model of 5-min transient forebrain ischemia. We used gerbils fed normal diet (ND) and HFD and chronologically examined microgliosis (microglial cell activation) by ionized calcium-binding adapter molecule 1 (Iba-1) immunohistochemistry. In addition, we examined neuronal damage or death by using neuronal nuclear protein (NeuN, a neuronal marker) immunohistochemistry and Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. We found that ischemia-induced microgliosis in ND-fed gerbils was increased from 2 days post-ischemia; however, ischemia-mediated microgliosis in HFD-fed gerbils increased from 1 day post-ischemia and more accelerated with time than that in the ND-fed gerbils. Ischemia-induced neuronal death/loss in the somatosensory cortex in the ND-fed gerbils was apparently found at 5 days post-ischemia. However, in the HFD-fed gerbils, neuronal death/loss was shown from 2 days post-ischemia and progressively exacerbated at 5 days post-ischemia. Our findings indicate that HFD can evoke earlier microgliosis and more detrimental neuronal death/loss in the somatosensory cortex after transient ischemia than ND evokes.