Medial prefrontal cortex oxytocin mitigates epilepsy and cognitive impairments induced by traumatic brain injury through reducing neuroinflammation in mice.

Traumatic brain injury (TBI) is a major risk factor to develop epilepsy and cognitive impairments. Neuropeptide oxytocin has been previously evidenced to produce antiepileptic effects. However, the involvement of central oxytocin in TBI-induced epileptic status and cognitive dysfunctions is not fully elucidated. In this study, we aim to investigate the role of oxytocin on a TBI model followed by seizure induction to clarify whether the epilepsy and cognitive deficits could be mitigated by oxytocin. TBI was established by weight drop and epileptic behaviors were induced by pentylenetetrazole (PTZ) injection in mice. Moreover, oxytocin was microinjected into the medial prefrontal cortex (mPFC) to observe the effects on the epilepsy and cognition. The blood-brain barrier (BBB) function and the neuroinflammation were measured by Evans Blue staining and enzyme-linked immunosorbent assays, respectively. Mice exposed to TBI demonstrate increased vulnerability to PTZ-mediated seizures and cognitive disturbances with a decrease in peripheral and brain oxytocin levels. Additionally, TBI reduces oxytocin, disrupts the BBB permeability and triggers neuroinflammation in mPFC in PTZ-treated mice. Intra-mPFC oxytocin simultaneously mitigates epilepsy and cognitive impairments. Finally, oxytocin restores BBB integrity and reduces mPFC inflammation in PTZ-treated TBI mice. These findings showed that intra-mPFC oxytocin suppressed the seizure vulnerability and cognitive deficits in TBI mice. The normalization of BBB integrity and inhibition of neuroinflammation may be involved in the antiepileptic and cognition-improved effects of oxytocin, suggesting that targeting inflammatory procedure in mPFC may decrease the risk to develop epilepsy and cognitive impairments in individuals previously experienced TBI.

Factors Influencing Post-Stroke Cognitive Impairment in Patients with Type 2 Diabetes Mellitus.

Objective: Type 2 diabetes mellitus (T2DM) and ischemic stroke, which are common diseases among older people, are closely related to cognitive impairment. This study aims to investigate the influencing factors of post-stroke cognitive impairment (PSCI) in patients with T2DM. Methods: We enrolled 161 patients with T2DM who experienced acute ischemic stroke and were hospitalized in the Department of Neurology, Jinan Central Hospital, Shandong, China. Cognitive function was evaluated with the Montreal Cognitive Assessment scale. According to the results, patients were divided into three groups-the cognitively normal group, mild cognitive impairment group, and severe cognitive impairment group. We analyzed general demographic data, laboratory information, imaging data, the results of neuropsychological evaluation, and clinical features as well as influencing factors of PSCI in these patients and established a prediction model. Results: The three groups of patients were significantly different in terms of age, education level, course of diabetes mellitus (DM), recurrent cerebral infarction (RCI), and other factors. RCI, course of DM, and glycated hemoglobin (HbA1c) were independent risk factors of PSCI in patients with T2DM, with odds ratio (95% confidence interval): 7.17 (2.09, 30.37), 5.39 (2.40, 14.59), and 3.89 (1.66, 10.04), respectively, whereas female, senior high school, serum albumin were protective factors: 0.28 (0.07, 0.95), 0.05 (0.01, 0.21), 0.20 (0.08, 0.42), respectively. Furthermore, we constructed a prediction model using sex, age, education level, RCI, DM course, HbA1c and serum albumin and obtained a receiver operating characteristic (ROC) curve. The area under the ROC curve is 0.966, suggesting the significant association of these influencing factors with PSCI in patients with T2DM. Conclusion: In this study, the occurrence of PSCI in patients with T2DM was related to RCI, course of DM, and HbA1c, among other factors. Attention to influencing factors is needed in these patients for early diagnosis and timely intervention of cognitive impairment.

The Clinical Value of High-Quality Nursing in Concurrent Radiotherapy and Chemotherapy after Glioma Surgery and Its Influence on the Stress Indicators Cor, ACTH, and CRP.

OBJECTIVE: The purpose of this study is to explore the clinical value of high-quality nursing in concurrent radiotherapy and chemotherapy after glioma surgery and its influence on the stress indicators such as cortisol (Cor), adrenocorticotrophic hormone (ACTH), and C-reactive protein (CRP). METHODS: A total of 94 glioma patients diagnosed and treated in our hospital were randomly divided into a research group and a control group, with 47 cases in each group. Both groups of patients were given concurrent radiotherapy and chemotherapy. On this basis, patients in the control group were given basic care, while patients in the research group were given a combination of basic care and high-quality care. The nursing satisfaction and adverse reactions of the two groups were compared. The pain degree and the levels of stress indicators Cor, ACTH, and CRP at different time points were compared between the two groups. The sleep quality, bad mood, and quality of life before and after nursing were compared between the two groups. RESULTS: After nursing, the nursing satisfaction of the research group (95.74%) was higher than that of the control group (80.85%), and the difference between the two groups was statistically significant (X 2 = 11.678, P < 0.05). There was no significant difference between patients in the Visual Analogue Scale (VAS) score and the levels of stress indicators Cor, ACTH, and CRP at the T1 time point between the two groups (P > 0.05). With the passage of time, the levels of Cor and ACTH of the two groups showed an upward trend. At T4, the increased levels of Cor and ACTH in the research group were less than those in the control group, and the difference was statistically significant (P < 0.05). The VAS scores and CRP levels of the two groups showed an upward trend at T1 and T2 and a downward trend at T3 and T4. And, at T4, the decrease in CRP level of the research group was greater than that in the control group, and the difference was statistically significant (P < 0.05). Before nursing, there was no statistically significant difference between two groups of patients in the time to fall asleep, sleep time, number of awakenings, SAS score, self-rating depression scale (SDS) score, quality of life index scores, and total scores (P > 0.05). After nursing, the time to fall asleep and the number of awakenings in the two groups of patients showed an upward trend, and the increase in the control group was higher (P < 0.05). The sleep time of the two groups showed a downward trend, and the degree of decline in the control group was higher (P < 0.05). After nursing, the SAS score and SDS score of the two groups of patients decreased ( ∗ P < 0.05), and the decrease in the research group was more obvious (# P < 0.05). After nursing, the scores of all indicators of the quality of life and the total score of the two groups increased and the score of the research group increased more significantly (P < 0.05). After nursing, the control group had 5 cases of gastrointestinal reactions, 7 cases of bone marrow suppression, 6 cases of leukopenia, 6 cases of thrombocytopenia, and 10 cases of dizziness and nausea. In the research group, there were 1 case of gastrointestinal reaction, 2 cases of bone marrow suppression, 1 case of leukopenia, 1 case of thrombocytopenia, and 2 cases of dizziness and nausea. The difference between the two groups was statistically significant (P < 0.05). CONCLUSION: Glioma patients are given high-quality care during the course of concurrent radiotherapy and chemotherapy, which can reduce the pain and bad mood of the patient, reduce the stress response of the patient, and improve the quality of sleep and the quality of life of the patient, thereby improving nursing satisfaction and patients compliance, reducing adverse reactions, and having a good prognosis.

LncRNA-UCA1 inhibits the astrocyte activation in the temporal lobe epilepsy via regulating the JAK/STAT signaling pathway.

This article aimed to reveal the mechanism of long noncoding RNA (lncRNA) urothelial cancer-associated 1 (UCA1) regulated astrocyte activation in temporal lobe epilepsy (TLE) rats via mediating the activation of the JAK/STAT signaling pathway. A model of TLE was established based on rats via kainic acid (KA) injection. All rats were divided into the Sham group (without any treatments), KA group, normal control (NC; injection with empty vector) + KA group, and UCA1 + KA group. The Morris water maze was used to test the learning and memory ability of rats, and the expression of UCA1 in the hippocampus was determined by quantitative real time polymerase chain reaction (qRT-PCR). Surviving neurons were counted by Nissl staining, and expression levels of glial cells glial fibrillary acidic protein (GFAP), p-JAK1, and p-STAT3 and glutamate/aspartate transporter (GLAST) were analyzed by immunofluorescence and Western blot analysis. A rat model of TLE was established by intraperitoneal injection of KA. qRT-PCR and fluorescence analyses showed that UCA1 inhibited astrocyte activation in the hippocampus of epileptic rats. Meanwhile, the Morris water maze analysis indicated that UCA1 improved the learning and memory in epilepsy rats. Moreover, the Nissl staining showed that UCA1 might have a protective effect on neuronal injury induced by KA injection. Furthermore, the immunofluorescence and Western blot analysis revealed that the overexpression of UCA1 inhibited KA-induced abnormal elevation of GLAST, astrocyte activation of the JAK/STAT signaling pathway, as well as hippocampus of epilepsy rats. UCA1 inhibited hippocampal astrocyte activation and JAK/STAT/GLAST expression in TLE rats and improved the adverse reactions caused by epilepsy.