Objective:To investigate the role of heparin-binding protein (HBP) as a predictor of early bacterial infections in patients with traumatic intracerebral hemorrhage.Methods:Patients with traumatic intracerebral hemorrhage admitted to the Emergency Department of the First Hospital of Shanxi Medical University from September 2021 to June 2022 were collected prospectively. Patients with bacterial infection diagnosed by pathogenic examination were classified as the infected group, and those with negative pathogenic examination were classified as the non-infected group. Peripheral blood HBP counts were measured within 48 h of admission, and general information and relevant laboratory tests were collected. The differences of the indicators between the two groups were compared, the receiver operating characteristic (ROC) curve was drawn, the predictive value of the indicators for patients with co-infection was assessed, and the valuable predictors were screened out using multivariate logistic regression analysis.Results:Eighty-five patients [44 males and 41 females, aged (55.09±1.18) years] , were included in the study. Among the patients included in the study, 39 patients had bacterial infection and 46 were non-infected. Patients in the infected group were older , and had more surgeries, higher respiratory rate and injury severity score, and higher levels of HBP [(33.00±3.49) ng/mL vs. (16.27±1.61) ng/mL, P<0.001], leukocytes, and neutrophils [(15.32±3.19) ×10 9/L vs. (6.69±0.57) ×10 9/L, P=0.005] than in the non-infected group, while the Glasgow Coma Scale [(8.72±0.63) vs. (11.37±0.48), P=0.001] was lower than that in the non-infected group, with statistically significant differences (all P<0.05). There was no significant differences in lymphocytes, red blood cells, platelets, calcium, procalcitonin and coagulation indexes between the two groups (all P>0.05). Logistic regression analysis showed that neutrophils ( OR=1.252, 95% CI: 1.075-1.457, P=0.004) and HBP ( OR=1.081, 95% CI: 1.025-1.141, P=0.004) were independent risk factors for infection in patients with traumatic cerebral hemorrhage. The area under ROC curve for HBP of diagnosing early co-infection in patients with traumatic intracerebral hemorrhage was 0.82 (95% CI: 0.71-0.88), the sensitivity was 92.31%, and the specificity was 52.17%. Conclusions:HBP is a valuable predictor of early traumatic intracerebral hemorrhage complicated with bacterial infection in the emergency department, and has a good supplementary value to the existing test indicators.

Objective:To investigate the occurrence and predictors of hypopituitarism after traumatic brain injury (TBI) .Methods:A prospective study was conducted on 185 patients with severe TBI in the Emergency Department of the First Hospital of Shanxi Medical University from Jan. 2020 to May. 2022, of whom 108 were male and 77 were female; age ranged from 18 to 79 years, mean (51.32±9.34) years. Pituitary function was assessed within 3-7 d after the onset of TBI, and the occurrence of hypopituitarism after severe TBI was counted. 41 cases in the hypopituitarism group, 26 males and 15 females, aged (52.76±9.83) years, were divided into the hypopituitarism group (hypopituitarism occurred) and the non-hypopituitarism group (hypopituitarism did not occur) according to whether hypopituitarism occurred. In the non-decompensated group, there were 144 cases, 82 males and 62 females, aged (50.91±9.27) years. The clinical data of the decompensated and non-decompensated groups were compared, and the factors influencing the occurrence of hypopituitarism were analysed, and a logistic prediction model was constructed based on the relevant influencing factors. The value of this model in predicting the occurrence of hypopituitarism after severe TBI was evaluated by using the receiver operating characteristic (ROC) curve.Results:The prevalence of hypopituitarism in the 185 patients with severe TBI in this study was 22.16%; the Glasgow coma scale (GCS) score on admission was lower in the decompensated group than in the non-decompensated group [ (6.36±1.04) vs (7.48±0.59) ], the percentage of hyperbaric oxygen therapy was lower than in the non-decompensated group (21.95% vs 49.31%) , the percentage of intracranial pressure (82.93% vs 49.31%) , midline displacement ≥5 mm (78.05% vs 29.86%) , skull base fracture (34.15% vs. 17.36%) , diffuse cerebral edema (19.51% vs 4.17%) , and serum brain derived neurophic factor (BDNF) . Brain derived neurophic factor (BDNF) was higher than that in the non-reduced group [ (6.35±1.29) ng/ml vs (4.51±1.06) ng/ml], and neuronal-specific enolase (NSE) was higher than that in the non-reduced group [ (33.06±5.42) μg/L vs (23.15±4.97) μg/L]. (4.97) μg/L]. Vascular epithelial growth factor (VEGF) was higher than that in the non-reduced group [ (312.07±24.35) pg/ml vs (226.80±20.96) pg/ml], tumor necrosis factor-α (TNF-α) was higher than that in the non-reduced group [ (281.24±38.91) ng/L vs (186.91) pg/ml], and tumor necrosis factor-α (TNF-α) was higher than that in the non-reduced group (186.55±35.72) ng/L (all P<0.05) . Increased intracranial pressure, midline displacement ≥5 mm, diffuse cerebral edema, serum BDNF, NSE, VEGF, and TNF-α levels were all independent risk factors for the development of hypopituitarism after severe TBI, with admission GCS score and hyperbaric oxygen therapy as protective factors ( P<0.05) ; a logistic prediction model was constructed based on the influencing factors as: Logit ( P) = 5.264-0.880×admission GCS score + 1.618×increased intracranial pressure + 1.941×midline displacement ≥5 mm + 1.289×diffuse cerebral edema+1.306×BDNF+1.426×NSE+1.781×VEGF+1.615×TNF-α-0.758×hyperbaric oxygen therapy; the model predicted the occurrence of severe TBI after the area under the curve (AUC) of hypopituitarism was 0.930 (95% CI 0.883-0.962) , with a predictive sensitivity and specificity of 90.24% and 89.19%, respectively. Conclusions:The incidence of hypopituitarism is higher after severe TBI. Increased intracranial pressure, midline displacement ≥5 mm, diffuse cerebral edema, serum BDNF, NSE, VEGF and TNF-α levels are all used as predictors of hypopituitarism.

In recent years, studies have shown that transplanted neural stem cells (NSCs) help neural tissues regenerate and return to normal through paracrine action rather than just replacing cells. Exosomes are essential paracrine mediators that can participate in cell communication through substance transmission. This review focuses on NSCs regulated by exosomes and their application in treatment of nervous system diseases, in order to provide important references for further research and clinical application of NSCs exosomes..

Objective:To evaluate the effects of different densities of rat cardiac fibroblasts (RCF) subjected to hypothermic hypoxia-reoxygenation on cardiomyocyte injury and intercellular coupling.Methods:RCF was cultured in vitro and divided into 3 groups ( n=12 each) using a random number table method: RCF density 0.5×10 5 cells/ml group (T 0.5 group), RCF density 1.0×10 5 cells/ml group (T 1.0 group), and RCF density 2.0×10 5 cells/ml group (T 2.0 group). The three groups were placed in an anoxic device, into which 95% N 2 + 5% CO 2 was continuously blown at the speed of 5 L/min for 15 min, and then placed in a 4 ℃ refrigerator for 1 h for low temperature treatment.After completion of culture, cells were placed in a incubator containing 95% air + 5% CO 2 at 37 ℃ for 4 h of reoxygenation.After the end of culture, RCF in three groups were indirectly co-cultured with cardiomyocytes of the same density (1.0×10 5 cells/ml) in a Transwell chamber for 16 h, cardiomyocytes were seeded in the lower chamber of Transwell, and RCF were seeded in the upper chamber of Transwell.After the end of co-culture, cardiomyocytes were collected for determination of the cell viability (by CCK8 method), apoptosis rate (by flow cytometry), expression of connexin 43 (Cx43) mRNA (by real-time fluorescence quantitative polymerase chain reaction), and expression of Cx43 and phosphorylated Cx43 (p-Cx43) (by Western blot). Results:Compared with T 0.5 group, the cell viability, apoptosis rate and expression of Cx43, p-Cx43 and Cx43 mRNA were significantly decreased in T 1.0 and T 2.0 groups ( P<0.01). Compared with T 1.0 group, the cell viability, apoptosis rate and expression of Cx43 and p-Cx43 were significantly decreased ( P<0.01), and no significant change was found in expression of Cx43 mRNA in cardiomyocytes in T 2.0 group ( P>0.05). Conclusions:RCF subjected to hypothermic hypoxia-reoxygenation induces cardiomyocyte injury in a density-dependent manner in a certain range, and the mechanism may be related to down-regulation of the expression of Cx43 and reduction of the activity of Cx43.

Objective:To evaluate the effects of different density rat fibroblasts on the expression of conjunctin 43 (Cx43) in cardiomyocytes and cell viability.Methods:Cardiomyocytes and fibroblasts were co-cultured using Transwell, cardiomyocytes were inoculated into the lower chamber of Transwell and fibroblasts into the upper chamber of Transwell.The cells were divided into 3 groups ( n=12 each) by a random number table method: fibroblast density 0.5×10 5 cells/ml group (group C 0.5), fibroblast density 1×10 5 cells/ml group (group C 1), and fibroblast density 2×10 5 cells/ml group (group C 2), with the density of cardiomyocytes 1×10 5 cells/ml in three groups.Cardiomyocytes and fibroblasts were co-cultured for 20 h in three groups.Cardiomyocytes were collected after co-culture for determination of cell viability (by CCK8 method), apoptosis rate (by flow cytometry), and expression of Cx43 mRNA (by quantitative real-time polymerase chain reaction) and expression of Cx43 and phosphorylated Cx43 (p-Cx43) (by Western blot). Results:There was no significant difference in the apoptosis rate of cardiomyocytes among the three groups ( P>0.05). Compared with group C 0.5, the expression of Cx43 protein and mRNA and p-Cx43 was significantly up-regulated in group C 1, the cardiomyocyte viability was significantly increased, and the expression of Cx43 protein and mRNA and p-Cx43 was up-regulated in group C 2 ( P<0.05). Compared with group C 1, the cardiomyocyte viability was significantly increased, and the expression of Cx43 protein and mRNA and p-Cx43 was up-regulated in group C 2 ( P<0.05). Conclusion:Rat fibroblasts up-regulate the expression of Cx43 and enhance the activity of Cx43 in cardiomyocytes and enhance cell viability in a density-dependent manner in a certain range.

Objective:To explore the changes in miR-3195, miR-328-5p, and miR-6867-5p expressions levels and their relationships with the prognosis of patients with traumatic brain injury after hyperbaric oxygen (HBO) therapy.Methods:A total of 124 patients with traumatic brain injury admitted to the First Hospital of Shanxi Medical University from May 2018 to August 2020 were selected as research subjects. According to the scores of Glasgow Outcome Scale (GOS) six months after onset, patients with traumatic brain injury were divided into good prognosis group ( n=75) and poor prognosis group ( n=49). The expression levels of MiR-3195, miR-328-5p, and miR-6867-5p before HBO treatment (T1) and after one month of HBO treatment (T2) were detected by real-time fluorescence quantitative PCR. Receiver operating characteristics (ROC) curve and Logistic regression were used to assess the efficiencies of these three indicators in evaluating the prognosis of patients given HBO therapy for traumatic brain injury and their relationships with prognosis. Results:The Glasgow coma scale(GCS) scores of the good prognosis group were higher than those of the poor prognosis group, and the time from onset to treatment was shorter than that of the poor prognosis group, the differences were statistically significant ( P<0.05). The relative expression levels of miR-3195 at T1 and T2, miR-328-5p at T2, and miR-6867-5p at T1 and T2 in the good prognosis group were lower than those in the poor prognosis group ( P<0.05). The relative expression levels of miR-3195, miR-328-5p, and miR-6867-5p at T2 were all lower than those at T1 in both groups ( P<0.05). The relative expression levels of miR-6867-5p in both groups were all reduced, yet the reduction in the good prognosis group was greater than that in the poor prognosis group ( P<0.05). The areas under the curve (AUC) of miR-3195, miR-328-5p, and miR-6867-5p at T2 were bigger than those at T1, and the differences were all statistically significant ( P<0.05). GCS was an independent protective factor for the prognosis of traumatic brain injury ( P<0.05), while the time from onset to treatment and the expression levels of miR-3195 and miR-6867-5p at T2 were independent risk factors for the prognosis of traumatic brain injury ( P<0.05). Conclusion:The expression levels of miR-3195 and miR-6867-5p are highly related to the prognosis of patients with traumatic brain injury after HBO treatment, while the expression level of miR-328-5p is not related to the prognosis.

Objective:To explore the changes in miR-3195, miR-328-5p, and miR-6867-5p expressions levels and their relationships with the prognosis of patients with traumatic brain injury after hyperbaric oxygen (HBO) therapy.Methods:A total of 124 patients with traumatic brain injury admitted to the First Hospital of Shanxi Medical University from May 2018 to August 2020 were selected as research subjects. According to the scores of Glasgow Outcome Scale (GOS) six months after onset, patients with traumatic brain injury were divided into good prognosis group ( n=75) and poor prognosis group ( n=49). The expression levels of MiR-3195, miR-328-5p, and miR-6867-5p before HBO treatment (T1) and after one month of HBO treatment (T2) were detected by real-time fluorescence quantitative PCR. Receiver operating characteristics (ROC) curve and Logistic regression were used to assess the efficiencies of these three indicators in evaluating the prognosis of patients given HBO therapy for traumatic brain injury and their relationships with prognosis. Results:The Glasgow coma scale(GCS) scores of the good prognosis group were higher than those of the poor prognosis group, and the time from onset to treatment was shorter than that of the poor prognosis group, the differences were statistically significant ( P<0.05). The relative expression levels of miR-3195 at T1 and T2, miR-328-5p at T2, and miR-6867-5p at T1 and T2 in the good prognosis group were lower than those in the poor prognosis group ( P<0.05). The relative expression levels of miR-3195, miR-328-5p, and miR-6867-5p at T2 were all lower than those at T1 in both groups ( P<0.05). The relative expression levels of miR-6867-5p in both groups were all reduced, yet the reduction in the good prognosis group was greater than that in the poor prognosis group ( P<0.05). The areas under the curve (AUC) of miR-3195, miR-328-5p, and miR-6867-5p at T2 were bigger than those at T1, and the differences were all statistically significant ( P<0.05). GCS was an independent protective factor for the prognosis of traumatic brain injury ( P<0.05), while the time from onset to treatment and the expression levels of miR-3195 and miR-6867-5p at T2 were independent risk factors for the prognosis of traumatic brain injury ( P<0.05). Conclusion:The expression levels of miR-3195 and miR-6867-5p are highly related to the prognosis of patients with traumatic brain injury after HBO treatment, while the expression level of miR-328-5p is not related to the prognosis.

Objective:To observe the changes in the expression of microRNAs in ventricular myocardium in a rat model of hypothermic ischemia-reperfusion (I/R).Methods:Healthy clean-grade male Sprague-Dawley rats, aged 2-3 months, weighing 300-400 g, were anesthetized with intraperitoneal chloral hydrate.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O 2-5%CO 2.Sixteen Langendorff-perfused hearts were prepared and divided into 2 groups ( n=8 each) by a random number table method: control group (group C) and hypothermic I/R group (group I/R). The hearts were made globally ischemic for 60 min followed by 30-min hypothermic (4 ℃) reperfusion to establish the model of hypothermic I/R injury.The type and duration of arrhythmia and time of recovery of spontaneous heartbeats were recorded during reperfusion.The rats in group I/R were further divided into low-risk group (I/R-L group) and high-risk group (I/R-H group). The left ventricular myocardium was collected after the end of perfusion for high throughput sequencing to screen the differentially expressed microRNAs, and the reliability of the sequencing results was verified by quantitative real-time polymerase chain reaction.Gene Ontology and KEGG databases were used to analyze the biological regulatory pathways of differentially expressed target genes. Results:Compared with group C, there were 437 up-regulated microRNAs and 242 down-regulated microRNAs in group I/R-L and 419 up-regulated microRNAs and 260 down-regulated microRNAs in group I/R-H.Compared with group I/R-L, 392 microRNAs were up-regulated, and 287 microRNAs were down-regulated in group I/R-H.There were 84 microRNAs with absolute value of fold change ≥2 and significantly differential expression ( P<0.01) among the three groups.Subsequently, 4 microRNAs were randomly selected for validation using quantitative real-time polymerase chain reaction, confirming that the sequencing results were reliable.These differentially expressed target genes were involved in 11 biological processes and 6 KEGG pathways which were related to reperfusion arrhythmia.Potassium ion transmembrane transport and the adrenergic receptor signaling pathway in cardiomyocytes were enriched by the largest number of target genes. Conclusion:The expression of microRNAs in ventricular myocardium changes significantly after heart hypothermic I/R.These differentially expressed microRNAs regulate potassium ion transmembrane transport probably and mainly through the adrenergic receptor signaling pathway in the cardiomyocytes and thus are involved in the occurrence and development of hypothermic I/R arrhythmias.

Objective:To evaluate the relationship between decreased atrial myoelectric conduction and gap junction protein 40 (Cx40) and Cx43 in rats with reperfusion atrial arrhythmia.Methods:Sixteen Langendorff-isolated heart perfusion models were randomly divided into control group (group C) and ischemia-reperfusion group (group IR), with 8 rats in each group.According to whether the atrial arrhythmia occurred after reperfusion, group IR was further divided into reperfusion non-atrial arrhythmia subgroup (group R-NAA) and reperfusion atrial arrhythmia subgroup (group R-AA). Group C was balanced perfusion with K-H solution (37 ℃) for 120 min.In group IR, hearts were perfused with K-H solution (37 ℃) for 30 min, perfusion was then stopped, Thomas solution (4 ℃, 20 ml/kg) was injected to induce cardiac arrest for 60 min, the surrounding of the heart was protected with 4 ℃Thomas solution, and hearts were perfused with Thomas solution (4 ℃, 10 ml/kg) again after 30 min of cardiac arrest and then with K-H solution 37 ℃ for 30 min.At 120 min of equilibration or 30 min of reperfusion, the effective refractory period (ERP) and conduction velocity (CV) of the right atrium were measured, the expression of Cx40 and Cx43 in the right atrial myocardium was detected by Western blot, and ratio of Cx40 to Cx40+ Cx43 and the ratio of Cx43 to Cx40+ Cx43 were calculated.Results:The incidence of reperfusion atrial arrhythmia was 38% in group IR.Compared with group C, ERP was significantly prolonged, CV was decreased, the expression of Cx40 and Cx43 was down-regulated, the ratio of Cx40 to Cx40+ Cx43 was increased, and the ratio of Cx43 to Cx40+ Cx43 was decreased in R-NAA and R-AA groups ( P<0.05). Compared with group R-NAA, ERP was significantly prolonged, CV was decreased, the expression of Cx40 and Cx43 was down-regulated, the ratio of Cx40 to Cx40+ Cx43 was increased, and the ratio of Cx43 to Cx40+ Cx43 was decreased in group R-AA ( P<0.05). Conclusion:The decreased atrial myoelectric conduction may be related to the down-regulation of Cx40 and Cx43 expression in rats with reperfusion atrial arrhythmia.

Objective:To evaluate the changes in the electrical conduction of ventricular myocardium during hypothermic ischemia-reperfusion (I/R) in rats with arrhythmia.Methods:Healthy clean-grade adult male Sprague-Dawley rats, aged 2-3 months, weighing 200-300 g, were studied.The hearts were removed and retrogradely perfused with oxygenated K-H solution in a Langendorff apparatus. Sixteen isolated hearts were divided into 2 groups ( n=8 each) using a random number table method: normal control group (group C) and hypothermic I/R group (group I/R). In group C, the heart was perfused with K-H solution at 37 ℃ for 120 min.In group I/R, the heart was perfused with K-H solution at 37 ℃ for 30 min, and then perfusion was stopped, cardiac arrest was induced through injecting Thomas solution (4 ℃), the area around the heart was protected with low temperature (4 ℃) Thomas solution, and hearts were perfused with 4 ℃ Thomas solution at 30 min after cardiac arrest and with 37 ℃ K-H solution for 30 min staring from 60 min after cardiac arrest.The rats in group I/R were further divided into high-risk subgroup (I/R-H subgroup) and low-risk subgroup (I/R-L subgroup). The time of spontaneous recovery of heart beat and development of arrhythmia were recorded.At the end of reperfusion, the atrioventricular conduction 2∶1 block point (2∶1B) and ventricular electrical conduction velocity (CV) were measured and recorded by program-controlled electrical stimulation. Results:Compared with group C, CV and 2∶1B were significantly decreased in IR-L and IR-H subgroups ( P<0.05). Compared with IR-L subgroup, the time for restoration of spontaneous heart beat was significantly prolonged, the incidence of ventricular fibrillation and arrhythmia score were increased, and CV and 2∶1B were decreased in IR-H subgroup ( P<0.05). Conclusion:The electrical CV of ventricular myocardium is decreased during hypothermic I/R, which may be the mechanism of reperfusion-induced ventricular arrhythmia in rats with arrhythmia.