Objective To realize the characteristics of“zheng”differentiation-treatment for hand, foot and mouth disease (HFMD), a new methodology of syndrome differentiation for different stages of HFMD has been explored.
Methods Total of 2 325 cases with HFMD were recorded by distributing them into exterior syndrome stage, interior syndrome stage, severe syndrome stage and recovered syndrome stage, respectively, and the main symptoms and subsidiary symptoms of different stages of HFMD have been observed. The major and minor pathogenesis of HFMD in different stages were obtained, and compared with the “2010 Guideline for the Diagnosis and Treatment of HFMD”.
Results It was found that the major pathogenesis of exterior stage was deifned as“the invation of the wen-evil to the defender of the body with the collaterals got involved”, and the minor as“qi deifciency”;in interior stage,“the fury of Gan-Yang”was the main pathogenesis, and“qi in chaos and qi deifciency”was the minor;in severe syndrome stage,“the damage of heart, liver and lung”was the main pathogenesis, and“qi in chaos”was the minor;and the pathogenesis of recovered stage was“qi-yin deficiency”. Compared with the“2010 Guideline for the Diagnosis and Treatment of HFMD”, it showed that“the obstruction of the fei-pi qi by the mixture of shi-re evil”and“the mixture of shi-re”in vivo was quite dififcult to be explained in completely different context in the general situation; in the severe stage, the TCM clinical characteristics of syndrome differentiation might lose;in the early acute severe cases, the phenomenon that xin-yang and fei-qi almost ran out was dififcult to be observed, then, the line between the severe and the acute severe became vague.
Conclusions The theory of syndrome differentiation by stages of HFMD was reasonable in the actual situation of clinical description on HFMD which was expected to be further tested and widely applied in the“zheng”differentiation-treatment of HFMD in the future.

Objective To investigate the relationship between single nucleotide polymorphisms (SNPs) of the interleukin-4 (IL-4) gene and outcome of hepatitis B virus (HBV) infection in a Chinese Han population.
Methods Total of 501 patients with chronic hepatitis B virus (HBV) infection and 301 controls with self-limiting HBV infection were studied. Three tag SNPs in the IL-4 gene (rs2227284G/T, rs2243283C/G and rs2243288A/G) were genotyped by the Multiplex snapshot technique. The genotype and allele frequencies were calculated and analyzed.
Results The three SNPs showed no significant genotype/allele associations with chronic HBV infection. Overall allele P values were:rs2227284, P=0.655, odds ratio (OR) [95%conifdence interval (CI)]=1.070 (0.793-1.445);rs2243283, P=0.849, OR (95%CI)=0.976 (0.758-1.257);rs2243288, P=0.659, OR (95%CI) = 1.060 (0.818-1.375). Overall genotype P values were: rs2227284, P = 0.771; rs2243283, P = 0.571;rs2243288, P=0.902. There were no statistically signiifcant differences between patients with chronic HBV infection and controls. Haplotypes generated by these three SNPs also had no signiifcant differences between the two groups.
Conclusions The three tag SNPs of IL-4 were not associated with the outcome of HBV infection in the Han Chinese population.

Objective To construct the prokaryotic expression vector pET-32a(+)-C2orf69 and induce the expression of recombinant proteins in vitro. Then the possible effects of recombinant protein on cell proliferation was observed and rabbit-anti-C2orf69 protein polyclonal antibodies was obtained.
Methods Gene fragment of C2orf69 was ampliifed by PCR and then prokaryotic expression plasmid pET-32a(+)-C2orf69 was constructed. Recombinant protein C2orf69 expression was identiifed by SDS-PAGE and Western blot. The white-ear rabbits were immunized with purified recombinant protein C2orf69, and the potency and speciifcity of polyclonal antibody were evaluated by enzyme-linked immunosorbent assay (ELISA) and Western blot. Also, different liver cells were incubated with recombinant protein C2orf69 in vitro.
Results C2orf69 gene fragment was successfully ampliifed, results of gene sequencing were consistent with the sequence in GenBank. Recombinant protein of C2orf69 was successfully induced and expressed. The polyclonal antibody titer was up to 1︰1 280 000 through enzyme-linked immunosorbent assay. Results of cell proliferation showed that the recombinant protein could inhibit the proliferation of different liver cells.
Conclusions The recombinant protein C2orf69 could inhibit the proliferation of different liver cells, and we speculated that it may be a widely roled inhibitor of hepatocyte proliferation. Our experiment showed that the proliferation inhibition of cells may be realized by G1 phase extending and S phase shortening.

Objective To investigate the efficiency of pegylated interferon α therapy for patients with HBeAg-positive chronic hepatitis B (CHB) and explore whether liver histopathological features and other factors might inlfuence HBeAg seroconversion.
Methods Total of 80 HBeAg-positive CHB patients who received liver puncture were treated with pegylated interferonαonce a week for 48 weeks. The rate of HBeAg seroconversion was determined after therapy, and the factors inlfuencing HBeAg seroconversion were analyzed.
Results The rate of HBeAg seroconversion was 30.00％ at the end of treatment. The rate of HBeAg seroconversion gradually increased with the elevation of liver inlfammatory activity (χ2=9.170, P=0.027). But liver ifbrosis has little correlation with the rate of HBeAg seroconversion (χ2=5.917, P=0.116). Except HBeAg, other baseline indexes including gender, age, serum ALT and serum HBV DNA 1evels had no statistical difference between the patients with HBeAg seroconversion and the patients without HBeAg seroconversion. By binary logistic regression analysis, liver inlfammation and HBeAg were inlfuencing factors for HBeAg seroconversion. Conclusions Pegylated interferonαtherapy induces a higher rate of HBeAg seroconversion in HBeAg-positive chronic hepatitis B patients with severe liver inlfammation, so the liver biopsies should be performed in time.

A twenty-eight-year-old male patient with five-day’s fever (the highest body tempreture reached 39.4℃) and 10-hour’s rash (first on face) presented to the department of emergency for “drug rash”, at that time his temperature was 38.6℃. Two hours later, his temperature fell to normal. Then this patient’s entire body rash increased signiifcantly and lasted for 13 hours. Serum measles antibody IgM(+) conifrmed the measles diagnosis. He had received measles vaccine as a baby. Clinicians should be aware of this atypical clinical manifestation of adult measles. If this kind of patients were misdiagnosed as drug rash and given corticosteroid, measles disease may be aggravated. Speciifc serum measles antibody testing may be the only reliable method for differential diagnosis, but the earliest time point for examining the antibodies of measles still needs precise research.

The data of 35 246 patients with intestinal diseases were retrospectively analyzed, 28 cases of cholera patients were screened in 17 years, of which 23 cases had suspicious unclean food history, 10 cases were migrant workers, 8 cases had history of coastal city tour in one week. All of the 28 patients were positive for Vibrio cholerae culture, 19 cases were identiifed as O1 serotype Ogawa and 6 were identiifed as O1 serotype Inaba, 3 were identified as O139. Twenty-three patients were mild, five cases were moderate, patients with severe diseases were not found. It was found in this study that O1 serotype Vibrio cholerae was still dominant, 82%of cholera patients were mild cases. Tourists who had a incompletely heated seafood intake history and migrant people are susceptible to cholera.

Acute pancreatitis in pregnancy (APIP) is rare and the reasons for APIP are biliary disease and congenital or acquired hypertriglyceridemia, which could occur during any trimester but more than 50% cases happened during the third trimester. In this report, one case of a young pregnant woman, a HBV carrier in her 37th week+5 d of gestation, was admitted to Emergency Department due to acute abdominal pain, vomiting and diarrhea. The patient was in antiretroviral treatment with telbivudine from 28 weeks of gestation to prevent mother-to-child transmission of HBV. Laboratory tests demonstrated hypertriglyceridemia, abdominal computed tomography scan revealed peripancreatic edema. Hyperlipidemic pancreatitits was primary diagnosed and the patient was admitted to the intensive care unit. Considering the possible role in the pathogenesis of pancreatitis, telbivudine was interrupted after birth giving. After supportive treatment, her condition gradually improved. Since it is the ifrst description of APIP during treatment with telbivudine, the association between pregnancy, hyperlipidemia, telbivudine and acute pancreatitis has been well investigated.

Treatment of nucleos(t)ide antiviral drugs for decompensated HBV-related cirrhosis can signiifcantly improve the prognosis. But those patients with refractory ascites possibly deteriorate due to the complications of ascites before any beneift from anti-viral drugs could be observed. Therefore, it is important to ifnd a way to help the patients with HBV-related cirrhosis and refractory ascites to receive the full beneifts from antiviral therapy. Peritoneovenous shunt (PVS) using Denver tube enables ascites to continuously bypass into systemic circulation, thereby reducing ascites and albumin input and improving quality of life. We report herein 3 cases of decompensated HBV-related cirrhosis with refractory ascites, PVS using Denver tube was combined with lamivudine for antiviral treatment before and after. Then, ascites was alleviated significantly or disapeared and viral responsed well. All patients achieved a satisfactory long-term survival from 6.7 to 14.7 years. It was suggested that the Denver shunt could be used as an adjuvant method to antiviral drugs for decompensated HBV-related cirrhosis with refractory ascites to help the patients reap the full beneifts and maximize efifcacy of antiviral treatment.

Acute-on-chronic liver failure is a characteristic clinical liver syndrome, which should be differentiated from acute liver failure, acute decompensated liver cirrhosis and chronic liver failure. The pathogenesis of ACLF is not fully understood yet. Viral factors and immune injury have been reported to be the two major pathogenesis. This paper reviewed the researches on the pathogenesis of acute on chronic hepatitis B liver failure in recent years, to provide theoretical basis for prompt and accurate diagnosis and treatment of this syndrome. This would beneift for the prognosis and raise the survival rate of patients.