Objective To study the effects of α-melanocyte-stimulating hormone (α-MSH) on excessive inflammatory response of patients to traumatic brain injury (TBI) so as to prevent against the development of the secondary injury by observing the changes of α-MSH level in the serum of patients with TBI,and the relationships of the levels of serum α-MSH with the severity of TBI,and with the levels of tumor necrosis factor-α (TNF-α).Methods A total of 48 patients with acute TBI were divided into three groups according to GCS score:severe group with GCS 3-8 (n =18),moderate group with GCS 9-12 (n =16),and mild group with GCS 13-15 (n =14).Ten healthy volunteers were recruited as a control group.The blood samples were collected within 24 h and 3 d,5 d,7 days after injury.The concentrations of α-MSH and TNF-α in the separated serum were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA).All variables were presented as ((x)±s).Repeated measures and analysis of variance and further multiple comparisons were carried out to compare variables.When necessary,the Student's t test was utilized.Pearson correlation analyses were performed to determine the correlations between variables.Results The serum α-MSH levels in the three TBI groups were lower than that in the control group (P ＜ 0.05).And the severer injury was,the lower α-MSH level was.The lowest α-MSH levels dropped to the trough on the 3rd day or the 5th day after TBI [severe group:(9.65 ±4.21) pg/mL,moderate group:(10.69 ±4.30) pg/mL,mild group:(18.89 ±7.19) pg/mLvs.control:(45.67 ± 10.95) pg/mL].While the serum TNF-α levels in three TBI groups were higher than that in the control group (P ＜ 0.05),and the TNF-α level was higher in the severer group.The peak values of TNF-α in the three TBI groups reached on the 3rd day after TBI [severe group:(37.24 ± 18.28) pg/mL,moderate group:(26.19 ±6.78) pg/mL,mild group:(18.60 ±7.83) pg/mL vs.control:(10.74 ± 1.71) pg/ mL].There were negative correlations between the levels of serum α-MSH and TNF-α at four intervals.Conclusions In patients with TBI,the serum levels of α-MSH decreased,and the lowest levels of α-MSH dropped to the trough on the 3rd day or the 5th day after TBI.While the levels of TNF-α increased,and the peak values reached on the 3rd day after TBI.And as the injury was more severe,these changes were more significant.There were negative correlations between the serum α-MSH levels and TNF-α levels in general.

Objective To detect the variations of the serum α-MSH and TNF-α in multiple-trauma patients and discuss their role in severity of casualties.Methods Fifty casualties were divided into two groups for study.There were 30 casualties with moderate severe trauma(ISS 16 ～ 25 point)and 20 patients with extreme severe trauma(ISS ＞ 25 point),and another 15 healthy subjects were enrolled as controls.The blood samples were obtained within 24 hours,and 3 days,5 days,7 days after admission.The serum levels of α-MSH and TNF-α in casualties with multiple injuries were determined by using enzyme-linked immunosorbent double antibody sandwich method(ELISA).The data were expressed in((x)± s),and analyzed with chi-square test and repetitive measures of ANOVA by using SPSS 13.0 package.P value less than 0.05 indicated statistical significance Results The serum α-MSH levels of casualties within 24 hours,and 3 days,5 days,7 days after injury in the two groups were much lower than those in the control group (P ＜ 0.01),while the serum TNF-α levels of casualties were much higher than those in the control group (P ＜0.01).The serum α-MSH levels of casualties with extreme severe traumawere lower,and the TNF-αlevels of casualties with extreme severe trauma were higher than those in patients with moderate severe trauma(P ＜0.01,respectively).There were negative correlations between two biomarkers 24 hours,5d and 7d after injury.Conclusions In casualties,the serum levels of α-MSH decreased and the serum levelsof TNF-α increased,and the degrees of changes were closely depended on the severity of trauma,the more severe the more significant changes.There was a negative correlation between two biomarkers.

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.

Aspirated pneumonia is common in coma, poor ability of swallowing reflex, glottal uncoordinated move-ments, pharyngeal lesions or foreign body stimulation in patients,in which can cause ARDS, infectious shock, etc. Based on the rapid progression of the disease, without treating in time may lead to adverse prognosis, especially in multiple organ dysfunction such as craniocerebral injury is very dangerous.

Objective To investigate the electrophysiological characteristics of myocardium after hypothermic ischemia-reperfusion (I/R) in rats with different degrees of arrhythmia using an in vitro experiment.Methods Healthy clean-grade male Sprague-Dawley rats,aged 2-3 months,weighing 300-400 g,were used in this study.The rats were sacrificed after anesthesia,and their hearts were rapidly excised.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 occurrence and duration of arrhythmia and time of recovery of spontaneous heartbeat were recorded during reperfusion.The rats in group I/R were further divided into low-risk group (I/R-L group,ventricular arrhythmia score≤3 points) and high-risk group (I/R-H group,ventricular arrhythmia score＞3 points) according to the arrhythmia score.Monophasic action potential amplitude (MAPA),monophasic action potential (MAP) duration at 50％ and 90％ repolarization (MAPDs0 and MAPD90) and maximum ascending velocity (Vmax) of phase 0 in the endocardium,myocardium and epicardium of the left ventricular anterior wall were recorded at 30 min of equilibration (T0) and 15 and 30 min of reperfusion (T1,2).The effective refractory period (ERP) and ventricular fibrillation threshold (VFT) of the left ventricle were measured by programmed electrical stimulation,and the ERP/MAPD90 ratio was calculated.Results Compared with the baseline at T0,MAPA in the three layers was significantly decreased,and MAPD50 and MAPD90 were prolonged at T1,2 in I/R-L and I/R-H groups,and V in the three layers was decreased at T1,2 in I/R-H group (P＜0.05).MAPD50 and MAPD90 in the three layers were significantly shorter at T2 than at T1 in I/R-L and I/R-H groups (P＜0.05).Compared with group C,MAPDs0,MAPDg0 and ERP in the three layers were significantly prolonged at T1,2,the ERP/MAPDg0 ratio was decreased,and VFT was increased in I/R-L and I/R-H groups (P ＜ 0.05).Compared with I/R-L group,the duration of arrhythmia and MAPD90 and ERP in the three layers were significantly prolonged at T2,the ERP/MAPDg0 ratio was decreased,and VFT was increased in group I/R-H (P＜0.05).Conclusion Myocardial depolarization is inhibited,repolarization duration is prolonged,and electrophysiological stability is decreased after hypothermic I/R in the rats with arrhythmia,and the prolongation of myocardial repolarization and decrease in electrophysiological stability are more obvious in the rats at high risk of arrhythmia.

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 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.

Objective:To determine the changes in the expression of myocardial miRNA and the target genes in the rats with hypothermic ischemia-reperfusion (I/R) arrhythmia.Methods:Clean-grade healthy male Sprague-Dawley rats, aged 2-3 months, weighing 300-400 g, were anesthetized, the chest was opened, and the heart was taken to establish an isolated heart perfusion model.Six successfully perfused isolated hearts were divided into 2 groups ( n=3 each) using a random number table method: control group (group C) and heart I/R group (IR group). The model of hypothermic global I/R injury was established by interrupting perfusion for 60-min followed by 30-min reperfusion in chloral hydrate-anesthetized rats.The arrhythmia score was recorded during reperfusion.High-throughput sequencing was used to identify the differentially expressed miRNAs in two groups.The RNAhybrid and miRanda databases were used to predict the target genes of mRNA regulated by the differentially expressed miRNAs, and the enrichment for target genes was performed by Gene Ontology and KEGG databases, and the miRNAs closely related to arrhythmia and with higher expression were selected to carry out the real-time polymerase chain reaction detection. Results:The results of high-throughput sequencing showed that there were 7 differentially expressed miRNAs (novel-miR-17, novel-miR-19, novel-miR-30, novel-miR-43, rno-miR-122-5p, novel-miR-16 and rno-miR-429) in group IR as compared with group C. There were 4 miRNAs that were closely related to arrhythmia and had higher expression: the expression of novel-miR-17, novel-miR-30 and rno-miR-122-5p was significantly up-regulated, and the expression of rno-miR-429 was down-regulated in group IR when compared with group C ( P<0.05). The miRNA-mRNA correlation analysis revealed that GJA1 gene was the target of novel-miR-17. Conclusion:Myocardial novel-miR-17 is involved in the occurrence of hypothermic I/R arrhythmia probably by acting on GJA1 gene in rats.

Objective: To understand the differences in physical indices, physical functions, and physical fitness among primary school students of De’ang and Han nationalities in the De’ang community, and to provide a reference for the healthy development of the physique of children and adolescents. Methods: The cluster sampling method was used to select the test data of height, weight, vital capacity, 50 meter running, seated forward flexion, and 1 minute skipping rope of 2 493 De’ang and Han pupils in five complete primary schools in Mangshi, Dehong Prefecture. Differences in each indices were compared between groups. Results: For physical indicators: height in boys in 8,9 and 11 year old group, girls in 7 and 8 year old group, were significantly higher in Han nationality,weight among Han boys of 9 years old was higher than Deang nationality; For physical function indicators: vital capacity of girls 11 years old group and 12 years old group, boys 9 years old group, 10 years old group, 12 years old group, children of Han nationality were higher than Deang peers. For physical fitness indicators: in 50 m running, Han boys of 8,9,10 and 12 year old,as well as Han girls of 8 year old were higher than age matched peers of De’ang nationality;For seated forward flexion, Han boys of 11 years old and girls of 9 years old, were lower than Deang; in 1 min skipping, Han boys of 9,10,11 and 12 year old,as well as Han girls of 9 and 10 year old, were lower than the De’ang nationality. Conclusion Unbalanced development of physical fitness is observed among primary school students of De’hong and Han nationality, with significant differences in physical, functional and fitness indices.