Objective To analyze the clinical and laboratory features of patients with mild and severe HFMD to identify early predictive or diagnostic markers for severe cases. Methods Samples of feces, nasopharyngeal-swab specimens, peripheral blood, serum and cerebral spinal lfuid were collected. Postmortem pathological examination was conducted on 2 dead patients with complication due to neurogenic pulmonary edema. Reverse transcription-polymerase chain-reaction (RT-PCR), culture and isolation of enterovirus 71 (EV71) were performed to detect EV71 infection. Both univariate and multivariate logistic analysis were used to identify factors associated with severe cases. Results EV71 was mainly responsible for HFMD. In this study, 5 isolated EV71 strains belonged to C4 gene subtype. Compared with mild patients, EV71-RNA detection rate was higher and CoxA16 detection rate was lower among severe patients (P < 0.01). Inlfammatory cell inifltration in the lung, cardiac and liver tissues were mild by postmortem pathological examination. It was found that body temperature, vomitting, limb tremor, neutrophil, blood glucose and EV71 infection were significantly related to the severe cases by univariate logisticanalysis. However, after multivariate logistic regression analysis, only vomiting (OR 16.1, CI 2.3-110.5,P < 0.01) and limb tremor (OR 117.6, CI 13.8-1004.5,P < 0.01) were signiifcantly and independently correlated with the severe cases. Conclusions EV71 was mainly responsible for HFMD, particularly for severe cases. Vomiting and limb tremor were predictive markers for severe cases.

Objective To observe the application of continuous renal replacement therapy(CRRT) and heparin anticoagulation in patients with HFRS, and to explore a more suitable anticoagulant strategy. MethodsEighty-five severe-type patients (severe group) and 71 critical-type patients (critical group) were enrolled in this study. The frequency of CRRT was compared between the two groups; the frequency of CRRT treated with and without heparin anticoagulation and the frequency of hemorrhage and channel blood clotting induced by the two anticoagulant strategies were observed. ResultsThe frequency of CRRT in the critical group was higher than thatin the severe group (P<0.001). The frequency of CRRT initiated during the overlapping phases in the critical group was signiifcantly higher than that of the severe group (P=0.032). The total times of CRRT was 103, and 70 of them were treated with heparin anticoagulation. The frequencies of hemorrhage induced by heparin anticoagulation and no heparinization were 16 and 0, respectively, and the frequencies of channel blood clotting were 2 and 4, respectively. Conclusions CRRT has been used extensively in the critical-type patients with HFRS. The heparin anticoagulation and no anticoagulant strategies should be used more rationally in patients treated with CRRT, according to the clinical characteristics of the disease.

Objective A diagnostic model was established to discriminate infectious diseases from non-infectious diseases. Methods The clinical data of patients with fever of unknown origin (FUO) hospitalized in Xiangya Hospital Central South University, from January, 2006 to April, 2011 were retrospectively analyzed. Patients enrolled were divided into two groups. The ifrst group was used to develop a diagnostic model: independent variables were recorded and considered in a logistic regression analysis to identify infectious and non-infectious diseases (αin= 0.05, αout= 0.10). The second group was used to evaluate the diagnostic model and make ROC analysis. Results The diagnostic rate of 143 patients in the ifrst group was 87.4%, the diagnosis included infectious disease (52.4%), connective tissue diseases (16.8%), neoplastic disease (16.1%) and miscellaneous (2.1%). The diagnostic rate of 168 patients in the second group was 88.4%, and the diagnosis was similar to the ifrst group. Logistic regression analysis showed that decreased white blood cell count (WBC < 4.0×109/L), higher lactate dehydrogenase level (LDH > 320 U/L) and lymphadenectasis were independent risk factors associated with non-infectious diseases. The odds ratios were 14.74, 5.84 and 5.11 (P≤ 0.01) , respectively. In ROC analysis, the sensitivity and speciifcity of the positive predictive values was 62.1% and 89.1%, respectively, while that of negative predicting values were 75% and 81.7%, respectively (AUC = 0.76,P = 0.00). Conclusions The combination of WBC < 4.0×109/L, LDH > 320 U/L and lymphadenectasis may be useful in discriminating infectious diseases from non-infectious diseases in patients hospitalized as FUO.

Objective To observe the biological function of human 3-hydroxyisobutyrate dehydrogenase (HIBADH). Methods Human 3-hydroxyisobutyrate dehydrogenase (HIBADH, 3-hydroxy-2-methyl propanoate: NAD+oxidoreductase) recombinant protein was expressed inE. coli BL21,and puriifed by Ni+ column. The special antisera was obtained from rabbits immunized by this purified antigen. On the distribution of HIBADH, it was found that HIBADH over-expressed in the injured liver cells when serious hepatitis occurred. The phenomenon was conifrmed in the animal models of SD rats with acute liver cell injury induced by CCl4, but this phenomenon did not exist in the models induced by endotoxin combined with galactosamine. Further more, HIBADH’s overexpression in liver cells will induce cell necrosis through the pathway of oxidative stress. Results When the liver cells injured by drug or other chemical materials, HIBADH will be compensationally over-expressed for the deifciency of energy, so liver cells can make enough ATP through brand-chain amino acid catabolism. However, the overexpression of HIBADH will be harmful for liver cells through the product of much more active oxygens which will induce the cell necrosis. Conclusions HIBADH over-expression is a signal of the liver cell metabolism injury, and it can aggravate the liver cell injury through oxidative stress.

Objective To study the mutual relationship between anti-HBx and IL-10, IL-12 or soluble Fas (sFas) in sera of patients with chronic HBV infection and to explore the importance of anti-HBx detection as well as its role in the development of chronic HBV infection. Methods Total of 90 cases with chronic HBV infection were randomly selected, including 10 of asymptomatic carriers (ASC), 28 of chronic hepatitis B (CHB), 26 of liver cirrhosis (LC) and 26 patients of hepatocellular carcinoma (HCC). Their clinical data and blood samples were collected, and serum was prepared and stored at-73℃. Anti-HBx was detected with an indirect ELISA established in our earlier research, and levels of IL-10, IL-12 and Fas were determined with commercial double-antibody sandwich ELISA kits. The mutual relationship between anti-HBx and IL-10, IL-12 or sFas in serum were analyzed with the software SPSS 20.0. Results All levels of IL-10, IL-12 and sFas in peripheral blood showed a rising trend with development of chronic HBV infection. The levels of IL-10 in ASC, CHB, LC and HCC groups were13.93 ± 14.40 ng/L, 39.38 ± 20.77 ng/L, 69.06 ± 46.37 ng/L and 62.82 ± 23.42 ng/L, respectively, levels of IL-12 in the 4 groups were15.64 ± 23.04 ng/L, 68.50 ± 23.14 ng/L, 76.83 ± 12.82 ng/L and 83.74 ± 24.88 ng/L, respectively, and levels of sFas were 58.17 ± 77.42 ng/L, 179.88 ± 104.36 ng/L, 249.22 ± 107.80 ng/L and 252.98 ± 87.65 ng/L, respectively. Twenty-seven out of90 patients showed a positive result for anti-HBx detection, including 1 in ASC, 4 in CHB, 12 in LC and 10 in HCC group. The levels of IL-10, IL-12 and sFas were higher in anti-HBx pos-itive group than in negative group. Statistical analysis demonstrated signiifcant differences of IL-10 and IL-12 between the two groups (P < 0.05), but the differences of sFas had no statistical signiifcance (P = 0.094). ConclusionsAnti-HBx antibody is not protective, and is closely related to IL-10, IL-12 and sFas. It may be an important serum indicator for aggravation from chronic hepatitis B to liver cirrhosis or hepatocellular carcinoma in patients with chronic HBV infection.

Objective The cellular apoptosis susceptibility (CAS) protein plays a regulatory role in the induction of cell death in tumor cells. The objective of this study was to investigate the association of the expression of CAS protein with HBV infection in the development of HCC. Methods The expression level of CAS was measured with immunohistochemistry. The occurrence of HBsAg, HBeAg and HBV DNA in HCC were concurrently examined with immunohistochemistry and in situ hybridization, respectively. Results The results showed that the CAS protein was detected in 86% (43/50), 70% (7/10), 15% (3/20) and none (0/20) of livers from patients with HCC, cholangiocarcinoma, cirrhosis and hepatitis, respectively. Furthermore, the level of CAS protein was higher in poorly differentiated tumors than moderately or well differentiated HCC. Interestingly, the CAS was stained significantly stronger in HBV-infected HCC than in non-HBV infected tissues (P < 0.01). Conclusions The expression of CAS is facilitated by HBV infection in HCC, suggesting that CAS might be a prognostic marker and a putative therapeutic target for HCC.

Objective To investigate the occurrence of basal core promoter (BCP) and pre-C mutations in patients with hepatitis B virus (HBV) infection in Gansu Province, China, and to analyze the correlation of HBV mutation and HBV genotype with primary hepatocellular carcinoma (HCC). Methods PCR-RFLP was applied to detect HBV subgenotypes, and the presence of the pre-C and BCP mutations in 62 patients with HCC, 70 patients with hepatitis B induced liver cirrhosis (LC) and 90 patients with chronic hepatitis B (CHB). Results In HCC patients, genotype C was the major genotype (70.97%). The pre-C mutation was found in 59.68%, 31.43% and 16.67% patients with HCC, LC and CHB, respectively. The frequency of BCP mutations was signiifcantly different between patients with HCC, LC and CHB (74.19%, 51.43% and 37.78%, respectively;χ2=30.727, 19.540, respectively,P < 0.01). Patients in HCC group had a higher incidence of pre-C as well as BCP mutations compared to the other groups. The prevalence of pre-C and BCP mutations was signiifcantly higher in patients with genotype C1 (44.32% and 69.32%, respectively) compared to patients with other subgenotypes (P < 0.05). Conclusions The incidence of pre-C and BCP mutations increases with disease progression. Pre-C and BCP mutations frequently occur in patients with genotype C1. HBV genotype C, pre-C mutations and BCP mutations are closely related to the occurrence of HCC.