OBJECTIVE:To explore risk factors for the death in HIV/AIDS patients suffering from myelosuppression during highly active antiretroviral therapy(HAART)treatment. METHODS:The historical cohort study method was used to choose 735 in-patients from Nanning Forth People's Hospital during Jan. 2011 to Jul. 2015. Univariate and multivariate Logistic regression analy-sis were used to show the risk factors for the death. RESULTS:Of 735 cases,there were 648 survival cases and 87 dead cases, with mortality of 11.8%. Univariate Logistic analysis showed that:male,elder,higher total bilirubin,lower creatinine clearance, lower CD4+T cell count in baseline,combined more opportunistic infection,combined more myelosuppressive drugs,thrombocyto-penia,lower hemoglobin were the risk factors for the death of HIV patients with myelosuppression in HARRT treatment,while route of HIV infection,HAART treatment A including Zidovudine,weight were the protective factors. Multivariate Logistic regres-sion analysis showed male,elder,higher total bilirubin,lower creatinine clearance,lower CD4+ T cell count in baseline,com-bined more opportunistic infection,combined more myelosuppressive drugs,thrombocytopenia,lower hemoglobin were the risk factors for the death of HIV patients with myelosuppression in HARRT treatment too. CONCLUSIONS:Pertinence treatment and control methods for HIV/AIDS with myelosuppression in HARRT treatment should be taken to reduce the mortality in the future.

Objective To illustrate the features of soman induced signal transducers and activators of transcription (STATs) gene and protein expressions in cell line PC 12 . Methods The expression levels of STAT1, 3 and 5 mRNAs and protein in PC 12 cells were detected by semi quantitative RT PCR and Western blotting. PC 12 cells at 5～8 passages were randomly divided into 5 groups: control, intoxication groups for 2, 6, 12 and 24 h respectively. The products were sequenced by Sanger's double strand DNA sequence determination. Results The expression levels of STAT1, 3 and 5 mRNAs and proteins increased in PC 12 cell at 2 h and reached the highest at 12 h, then decreased at 24 h, but they were still higher than those of the control. The sequences of amplification products by RT PCR were the same to those in GenBank. Conclusion Soman intoxication can enhance the expression of STATs in PC 12 cells. STAT genes may possibly play an important role in brain injury.

Objective To investigate the effect of soman on the Janus kinases (JAKs) expression in cell line PC 12 . Methods The PC 12 cell was used in these experiments and treated with soman at a concentration of 20 ?mol/L . RT PCR and Western blotting were employed to detect the mRNA and protein expressions of JAK1, JAK2 and JAK3 at the time points of 0, 6, 12 and 24 h. The products were sequenced by Sanger's double strand DNA sequence determination. Results The expression levels of JAK1, JAK2 and JAK3 mRNAs and proteins increased at 2 h, reached the highest at 12 h and decreased at 24 h, but they were still higher than those of the control. It was shown that the sequences of amplification products by RT PCR were the same to corresponding ones in GenBank. Conclusion Soman intoxication enhances the expression of Janus kinases in PC 12 cells. JAKs genes may play an important role in brain injury due to soman intoxication.

Objective To investigate the effects of anticholinergic antidote and rhodosin on the brain injury induced by soman intoxication combined with hypobaric hypoxia in rats. Methods A total of 72 Wistar rats were divided into 4 groups: hypoxia control (HC), hypoxia plus soman (HS), hypoxia plus soman plus anticholinergic antidote (HSAA), and hypoxia plus soman plus anticholinergic antidote plus rhodosin (HSAAR). The animals after soman intoxication (72 ?g/kg) were placed in a hypobaric (62 kPa) apparatus for hypoxic exposure for 48 h. Rats were sacrificed for brain tissue detachment at the time points of 12, 24, and 48 h. Evans blue (EB) content and PLA 2 activity were detected biochemically. CaM concentration was determined by radioimmuno assay. Results Compared with the rats in HC, soman induced significant increases of brain EB, PLA 2, and CaM at 12, 24, and 48 h in HS. Elevated EB, PLA 2, and CaM induced by hypoxia and soman intoxication in rats in group HSAA were obviously attenuated by anticholinergic antidote. More significant decreases of brain EB, PLA 2, and CaM were found in rats in group HSAA. Conclusion Both anticholinergic antidote and anticholinergic antidote plus rhodosin have the preventive effect on rat brain damage induced by soman intoxication combined with hypoxia.

Objective:To evaluate the quantitative diagnostic value of controlled attenuation parameter (CAP) in health checkup groups with asymptomatic nonalcoholic fatty liver disease.Methods:A multicenter prospective study was conducted among Chinese individuals undergoing regular health checkups; a total of 173 subjects were investigated. Human body indexes such as height, weight, and blood pressure were measured, and complete blood count, liver function, blood lipid, FibroScan, and MRI-PDFF examinations were performed. Correlation between MRI-PDFF and CAP was described using Spearman′s and Pearson′s coefficients. Diagnostic efficacy of the CAP was evaluated using the subject work characteristic curve and the area under this curve, and the optimal cut-off value was determined according to the Youden index.Results:The average age and body mass index of the subjects were 45.0±10.5 years and 25.8±4.0 kg/m 2, respectively. A linear correlation was found between CAP and lg transformed magnetic resonance imaging-based proton density fat fraction results (Pearson′s coefficient 0.772, P<0.001). When optimized for ≥90% sensitivity, the CAP cutoff for staging ≥S1 steatosis was 244 dB/m. Conclusions:The CAP result was significantly correlated with the liver fat fraction measured by MRI-PDFF, and capable of differentiating steatosis grades. CAP can be used as a tool for screening fatty liver in health checkup groups.

Objective To explore the clinical features and risk factors of poor prognosis in neonatal necrotizing enterocolitis(NEC).Methods A retrospective study was carried out in the infants with NEC admitted to 6 cooperative hospitals in Guangdong Province between January 2005 and December 2014.The clinical features and risk factors of poor prognosis in preterm and full-term infants diagnosed NEC,early onset and late onset NEC were analyzed.Results A total of 449 cases who met the criteria were admitted during the study time.The mortality was 23.6％ (106/449 cases),of which the preterm group was 24.6％ (58/238 cases) while the full-term group was 22.7％ (48/211 cases),the early onset group was 22.1％ (45/204 cases) while the late onset group was 24.3％ (57/235 cases).The median number of NEC onset in preterm group was 11 d after birth while the number of the full-term group was 6 d.Full-term infants who diagnosed NEC were more likely to manifest themselves as abdominal distension (52.1％ vs.42.0％,x2 =4.597,P =0.032),vomiting(36.5％ vs.17.2％,x2 =21.428,P =0.000) and bloody stool(30.3％ vs.21.4％,x2 =4.653,P =0.031);but in the onset of NEC,preterm infants more likely to have feeding intolerance (21.0％ vs.12.8％,x2=5.309,P =0.021).The early onset group of full-term NEC was much common in twins or multiplets(9.4％ vs.1.1％,x2 =6.226,P =0.013),which rate of surgical therapy was much higher (41.0％ vs.27.0％,P =0.036) and the breast-feeding rate before NEC was lower than the late onset group(14.5％ vs.32.6％,x2 =9.500,P =0.002),the differences were statistically significant.The gestational age and birth weight were bigger in the early onset group of preterm NEC[(33.8 ±2.5) weeks vs.(32.2 ±2.8) weeks,t =4.261,P =0.000;(2.1 ±0.5) kg vs.(1.7 ± 0.5) kg,t =4.735,P =0.000)],but length of stay was shorter than the late onset group (18.0 d vs.26.5 d,P =0.000).Logistic regression analysis showed that the risk factors of poor prognosis of full-term NEC were shock,peritonitis and sepsis;while risk factors of poor prognosis of preterm NEC were small for gestational age infant,pulmonary hemorrhage,shock,intestinal perforation and sepsis;the risk factors of poor prognosis of the early onset group of full-term NEC was shock;while those of the late onset group were shock and peritonitis;the risk factors of poor prognosis in the early onset group of preterm NEC were shock and sepsis,while those in the late onset group were pulmonary hemorrhage,shock,intestinal perforation and sepsis.Conclusions Compared to the preterm NEC,the onset time of full-term NEC was earlier and the clinical manifestations were more typical.Early identification and management of shock,peritonitis,intestinal perforation,sepsis and pulmonary hemorrhage can reduce the risk of poor prognosis of neonate NEC.