Objective To observe if endothelial progenitor cells (EPCs) and bone marrow mesenchymal stem cells (BMSCs) could home to the injured region and study the effect of BMSCs-derived EPCs on traumatic brain injury (TBI) in rats.Methods BMSCs were isolated from 3-month-old SD male rats weighing 150 g,and induced to EPCs.EPCs were identified by surface markers CD133,CD34 and FLK-1.A total of 120 female adult SD rats were divided into 3 groups (n =40 each) according to the random probability table method:EPCs group,BMSCs group and 3T3 cells group.The model of moderate to severe TBI was induced by the fluid percussion device.All the cells (i.e.EPCs,BMSCs and 3T3 cells) were injected with BrdU before transplantation to the tail vein of rats.On days 2,7,14 and 28 after transplantation,rat neurological function was evaluated using the modified neurological severity score (mNSS),and injured brain tissue was harvested to detect CD34 and brain-derived neurotrophic factor (BDNF) positive cell density using the immunohistochemistry method.Sry-positive cells were evaluated using the fluorescence in situ hybridization (FISH).Results The positive rate of CD133,CD34 and Flk-1 was 52％,33％ and 38％,indicating BMSCs differentiation towards an EPCs phenotype.On days 7,14 and 28 after transplantation,the mNSS in EPCs group [(10.2 ± 1.5),(8.7 ± 1.0) and (4.9 ± 1.0) points] and in BMSCs group [(10.8 ± 1.7),(10.1 ± 1.7),and (7.2 ± 1.3) points] were lower than that in 3T3 cells group [(12.4 ± 1.5),(1 1.7 ± 1.8),(10.3 ± 1.5) points] (P ＜ 0.05).On 14 and 28 days after transplantation,BrdU-positive CD34 and BDNF in EPCs group were significantly more than those in BMSCs group (P ＜ 0.05).Instead,there were no positive cells in 3T3 cells group.The method of Sry probe to trace the transplanted cells could detect more positive cells compared to the BrdU labeling method.Conclusion Both BMSCs and EPCs can home to the injured region,but EPCs have much better therapeutic effect.

Objective To explore the changing rule and clinical significance of the abnormal cortical secretion resulted from traumatic brain injury (TBI). Methods The serums from 55 TBI patients and 13 normal persons were collected to measure the level of secreting total cortisol (Cor) , adrenocorticotropin (ACTH) and corticosteroid-binding-globulin (CBG) by using radioimmunoactive assay and chemiluminescent immunometric assay. In the meantime, the free cortisol (FC) and free cortisol index (CI) were calculated by using Coolen formula. Results CBG maintained stable, while Cor and other hormones were increased significantly with the severity of TBI. Surgical operation could release the stress partially without disturbing the secretion of hormone. The more quickly the serum hormone decreased, the better prognosis the patients would have. The lower level of Cot could result in poorer prognosis. Conclusions TBI can result in a higher level of Cor as well as other hormones in the serum. The prognosis is poor in patients with a persistent high or low level of Cor. It should be cautious to supply large volume of cortisol at the early phase of TBI.

Objective To evaluate the correlation of the baseline clinical and laboratory test index with death,and to discuss the independent risk factors for long-term prognosis in elderly HIV/ AIDS patients who had accepted highly active antiretroviral therapy (HAART).Methods 1671 cases of HIV/AIDS patients were included in retrospective cohort study,divided into death group (183 cases) and non-death group (1488 cases) according to HIV/AIDS related death event,and followed up for 2 days to 120 months,an average of 427 days.Results During the period of followup,the proportion of male (12.45％) was higher than that of women (6.9％) in death group(x2 =10.42,P＜0.01).The mortality ratio of the WHO stage Ⅲ and Ⅳ was higher than that of the WHO stage Ⅰ and Ⅱ (x2 =18.67,P＜0.01).The mortality ratio was significantly higher in HIV/AIDS patients with baseline CD4+ T lymphocyte cell ＜100 cells/mm3 than ＞100 cells/mm3 (x2 =52.59,P＜0.01).The platelet (PLT),hemoglobin (HB),and blood glucose levels were lower in death group than in non-death group (P ＜ 0.05),but serum creatinine (SCR) and AST (aspartate aminotransferase) levels were higher than that in the non-death group (P＜0.05).There was no significantly differences between the death group and the non-death group in the index of white blood cell (WBC),blood urea nitrogen (BUN),total cholesterol (CH),triglyceride (TG),alanine aminotransferase (ALT) and total bilirubin (TB) levels (all P＞ 0.05).Multiple logistic regression analysis revealed that the WHO stage (OR=0.777,95％ CI:0.612～0.987,P＜0.05) and the baseline level of CD4+ T lymphocytes cell (OR=1.345,95％ CI:1.089～1.662,P＜0.01) were independent risk factors for long-term outcomes in elderly HIV/AIDS patients.Conclusions The WHO stage and baseline CD4+ T lymphocyte cell level are the independent risk factors for long-term prognosis in HIV/AIDS patients over 60 years of age.Early discovery and early beginning HAART can effectively improve the prognosis of elderly HIV/AIDS patients.

Objective To investigate the protective effect of hypoxia-inducible factor-1α(HIF-1 α) on the neurovascular unit in rats with traumatic brain injury (TBI).Methods The fluid percussion model was applied to induce TBI in rats.A total of 600 rats were divided into sham operation group,TBI group,TBI + HIF-1 α silence group and TBI + control virus group according to the random number table,with 150 rats in each.Virus-mediated HIF-1 α silence gene and control virus were delivered 24 h before the fluid percussion injury.After 3,7 and 14 d,brain injury area and morphological changes in injured region were detected by HE staining,expressions of vascular endothelial cell markers (vWF) and HIF-1 α were detected by Western blot method,and expressions of vascular endothelial growth factor (VEGF),matrix metalloproteinase-9 (MMP-9),tumor necrosis factor-α (TNF-α),interleukin 6 (IL-6) and nuclear factor-κB (NF-κB) in peripheral blood and brain tissue were detected by ELISA method.Rat neural function was dynamically assessed using the modified neurological severity score (mNSS).Results (1) Brain injury area and edema area in TBI + HIF-1 α silence group were higher than those in TBI group at all time points (P ＜ 0.05).(2) Compared with sham operation group and TBI + control virus group,expression of HIF-1α in TBI group gradually increased and remained high at 7 and 14 d postinjury (P ＜ 0.05).Compared with TBI group,expression of vWF in TBI + HIF-1αsilence group decreased at all time points (P ＜ 0.05) and inhibited angiogenesis.(3) TBI + HIF-lα silence group versus TBI group showed remarkably decreased VEGF at all time points,increased expressions of TNF-α,IL-6 and NF-κB at all time point,and increased expression of MMP-9 at 7 and 14 d postinjury (all P ＜0.05).(4) TBI + HIF-1α silence group versus TBI group showed significant difference in mNSS at 7 and 14 d postinjury (all P ＜ 0.05).Conclusions After TBI,high expression of HIF-1αcan facilitate vascular formation and inhibit inflammatory reaction related factor expression,inducing the mitigation of brain edema and brain injury.Therefore,promoting HIF-1α expression may become a new means to improvement of neurovascular function after TBI.

Objective To investigate the epidemiological characteristics and therapeutic strategies of patients infected with hepatitis C virus (HCV)genotype 6 in Guangxi area.Methods Serum samples were collected from 150 patients with serologic HCV RNA positive in Guangxi, China. Reverse transcription nested polymerase chain reaction (PCR)was employed to amplify HCV NS5B fragments and the DNA products were sequenced.The sequences obtained were compared with the sequences deposited in GenBank to construct a phylogenetic tree.Among the patients who accomplished 48-week treatment of interferon plus ribavirin and 24-week follow-up after stopping medication,10 cases were infected with genotype 6a and 28 cases with genotype 1 HCV.The virological responses were evaluated at week 4,week 12,week 24 of treatment and week 24 after the end of the treatment.Results Among all recruited 150 cases,21 (14.0%)cases were HCV genotype 6 including two subtypes 6a (n = 20 )and 6d (n = 1 ). Genotype 6 HCV mainly affected intravenous drug users, especially with age of ≤ 40 years old. Phylogenetic tree showed that there was very close evolutionary distance between HCV 6 strains of Guangxi and Hongkong,China strains (Y12083,DQ 480515)and Vietnam strain (EU246930).All of 10 HCV genotype 6a patients who completed 48 weeks of antiviral therapy achieved sustained virological response (SVR).The rate of SVR was higher than that of genotype 1 patients,but without statistically different significance (10/10 vs 75 .0%,P >0.05).Conclusion HCV genotype 6 in Guangxi area mainly affects young intravenous drug users with age of ≤ 40 years old,which has high homology with Hongkong,China and Vietnam standard strains.Patients with HCV 6 genotype infection treated with interferon plus ribavirin for 48 weeks usually achieve favorable SVR.

Objective To investigate the relationship between carotid intima-media thickness (IMT) and coronary atherosclerosis plaque through coronary CT angiography (CTA) in asymptomatic individuals.Methods Two hundred and fifty cases with CTA screened were selected in asymptomatic individuals,and according to the inspection result they were divided into no plaque group (detection of no coronary atherosclerosis plaque,180 cases) and plaque group (detection of coronary atherosclerosis plaque,70 cases).All cases were checked carotid IMT with B-ultrasonic.Results ANOVAs analysis showed that age and body mass index (BMI) had significant correlation with coronary atherosclerosis plaque (P ＜ 0.05).x2 test was used to show the smoking and family history of coronary heart disease had significant correlation with coronary atherosclerosis plaque (P ＜ 0.05).Univariate Logistic regression analysis showed that carotid IMT,systolic pressure,diastolic pressure,low density lipoprotein cholesterol,fasting serum glucose and creatinine had significant correlation with coronary atherosclerosis plaque (P ＜ 0.05).Multifactor Logistic regression analysis showed that carotid IMT had correlation with coronary atherosclerosis plaque (P ＜ 0.05).Conclusion There is significant relationship between carotid IMT and coronary atherosclerosis plaque in asymptomatic individuals.

Objective:To compare the similarities and differences of clinical characteristics of human immunodeficiency virus (HIV)-negative and HIV-positive patients with talaromycosis marneffei (TSM).Methods:The clinical data of 175 inpatients diagnosed with TSM in First Affiliated Hospital of Guangxi Medical University from May 2012 to April 2019 were retrospectively analyzed. The patients were divided into HIV-positive group and HIV-negative group according to the results of HIV confirmation test. The clinical manifestations, laboratory examination indicators (white blood cell count, hemoglobin, albumin, CD4 + T lymphocyte count and C-reactive protein (CRP)) between the two groups were compared. Mann-Whitney U test and chi-square test were used for statistical analysis. Results:Among 175 TSM patients, 85 were HIV-positive and 90 were HIV-negative patients. The main clinical manifestations of fever and lymphadenopathy in the HIV-positive group and HIV-negative group were 71 (83.53%) cases and 73 (81.11%) cases, 50 (58.82%) cases and 47 (52.22%) cases, respectively, and there were both no statistical differences ( χ2=0.175 and 0.771, respectively, both P>0.05), while respiratory symptoms, weight loss and subcutaneous masses were 62 (72.94%) cases and 81 (90.00%) cases, 73 (85.88%) cases and 56 (62.22%) cases, one (1.18%) case and 16 (17.78%) cases, respectively, the differences were all statistically significant ( χ2=8.514, 12.630 and 13.737, respectively, all P<0.01). Hemoglobin in HIV-positive group and HIV-negative group were 90.50 (77.00, 113.95) g/L and 88.65 (72.85, 99.93) g/L, respectively. The difference was statistically significant ( Z=2.023, P=0.043). The ratios of albumin<30 g/L, CRP>10 mg/L in the two groups were 69.41%(59/85) and 60.00%(54/90), 94.37%(67/71) and 94.19%(81/86), respectively, and the differences were both not statistically significant ( χ2=1.693 and 0, respectively, both P>0.05). The ratios of cases with white blood cell counts >10×10 9/L and CD4 + T lymphocyte count<50/μL in the positive and negative groups were 3.53%(3/85) and 81.11%(73/90), 80.77%(63/78) and 1.75%(1/57), respectively, the differences were both statistically significant ( χ2=107.095 and 82.467, respectively, both P<0.01). Conclusions:In TSM patients, HIV-negative with subcutaneous masses, and increased white blood cell counts are common. Decreased body weight and CD4 + T lymphocyte count<50/μL in HIV-positive patients are more common than HIV-negative patients.

Traumatic brain injury is always associated with hemorrhage and coagulopathy, leading the occurrence of anemia, platelet function inactivation, platelet and coagulation factor consumptive reduction. Theoretically, transfusion therapy should be given to supplement the missing component in an appropriate range. However, whether the transfusion therapy can improve the prognosis of patients with traumatic brain injury, and the indications of transfusion, have been the focus of academic debate for a long time. This article reviews the latest progress of transfusion therapy in traumatic brain injury, and provides reference for better guidance of transfusion in clinical treatment.

BACKGROUND:Previous studies have indicated that ulinastatin can inhibit RANKL-induced osteoclastogenesis on RAW264.7 cells and also lower matrix metal oproteinase-9 expression and activity. However, it remains be unclear whether ulinastatin has the intervention effect on polymethyl methacrylate (PMMA)-induced MC3T3-E1 mouse preosteoblast apoptosis or not. ＜br> OBJECTIVE:To explore the intervention role of ulinastatin on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis and its effects on type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression. ＜br> METHODS:MC3T3-E1 mouse preosteoblasts at passages 6 and 7 were divided into four groups:blank group (only cultured MC3T3-E1 mouse preosteoblast), PMMA-induced group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension), low dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+500 U/mL ulinastatin) and high dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+5 000 U/mL ulinastatin). MTT method was adopted to detect the proliferation activity of proliferative activity of MC3T3-E1 mouse preosteoblast;alizarin red staining method was used to observe mineralization nodules of MC3T3-E1 mouse preosteoblast among different groups;the change of apoptosis rate for MC3T3-E1 cells was detected by flow cytometry analysis;semi-quantitative RT-PCR was taken to analyze type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression level in MC3T3-E1 mouse preosteoblasts among different groups. ＜br> RESULTS AND CONCLUSION:Compared with the blank group, PMMA significantly inhibited the proliferation activity of MC3T3-E1 mouse preosteoblast (P＜0.05), and however significantly promoted cells apoptosis (P＜0.05). After addition of different concentrations of ulinastatin (500, 5 000 U/mL), the proliferation activity of MC3T3-E1 mouse preosteoblasts significantly raised (P＜0.05), and cells apoptosis rate significantly decreased (P＜0.05), showing the dose and time-dependent relation. Type I col agen and osteocalcin mRNA expression levels both significantly decreased after co-culture in PMMA group compared with the blank group (P＜0.05), matrix metal oproteinase-2 mRNA expression level, however, significantly increased (P＜0.05). After intervention with 5000 U/mL ulinastatin, type I col agen and osteocalcin mRNA expression levels both significantly increased, while matrix metal oproteinase-2 mRNA expression level significantly decreased (P＜0.05). PMMA group showed no obvious mineralization nodules. Yet, mineralization nodules were formed in the blank group, high and low dose ulinastatin groups. These results indicate that ulinastatin could have the inhibitory effect on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis, and it could promote type I col agen and osteocalcin mRNA expression and yet suppress matrix metal oproteinase-2 mRNA expression.

Objective To study the effect of simvastatin (SIM) on the expression of neuron specific enoalse (NSE) in rat brain and serum after traumatic brain injury (TBI), and therapeutic effects of SIM on TBI thereof. Methods A total of 90 Sprague-Dwalye (SD) rats aged 8 weeks were randomly divided into sham TBI group, control group and treatment group (n=30). The TBI model was established in control group and treatment group by using Feeney method. Rats in treatment group were fed SIM 10 mg/kg in the evening pre-injury and in every evening post-injury while those in control group were fed the same dose of starch at the same time. Blood samples (3 mL) were collected from carotid atrery in three groups, then rats were sacrificed and brains were collected at different time points (3 h, 12 h, 24 h, 3 d, 7 d and 14 d post-injury). The serum ex-pressions of NSE were detected by ELISA method. The NSE expressions in hippocampal area CA3 were detected with immu-nohistochemistry. Results (1) In control group, the serum NSE level was significantly increased at 3 h after injury, reached the peak at 3 d, and was still higher than that of sham injury group at 14 d. In treatment group, the serum NSE level was in-creased 3 h after injury, reached the peak at 24 h, decreased after 3 d, and was near the sham injury group at 14 d after inju-ry, but was significantly lower than that of control group. (2) Immunohistochemical detection showed that the NSE optical density values in hippocampal area CA3 area were decreased at 3 h after injury in control group. The optical density values reached the lowest level between 3 d to 7 d and were still significantly lower than those of sham injury group at 14 d. In treat-ment group the optical density value was decreased at 3 h after injury, reached the lowest level between 12 h to 24 h and re-bounded significantly at 7 d, then at 14 d up to the level of sham injury group. Conclusion SIM can promote the decrease of serum NSE level in TBI rats and increase the NSE expression of hippocampal neurons of injured side, showing protective effects on neuronal damage after traumatic brain injury.