Objective To explore the relationship between serum levels of interferon-inducible protein-10 (IP-10), interferon-γ (IFN-γ) and hepatic inflammatory reaction, disease progression in patients with severe hepatitis B (SHB). Methods Sera of 40 patients with SHB at time of admission,at the beginning of single plasma exchange (PE), at time of PE completion and 5 days after PE. The SHB patients were divided into improved group and aggravated group. And 20 patients with chronic hepatitis B (CHB) and 20 healthy controls were enrolled in this study. Serum levels of IP-10, IFN-γand tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). Results The serum levels of IP-10 in patients with SHB and CHB on admission were (683.6 174.6)ng/L and (216.1 102.9)ng/L, respectively, which were notably higher than those in healthy controls [(107.6 55.8)ng/L F=9.036, both P＜0. 01],and those in patients with SHB was significantly higher than that in patients with CHB (P＜0. 01). The serum level of IFN-γ in patients with SHB and CHB on admission were (19. 8 8. 8) ng/L and (16. 7 7. 8) ng/L,respectively, which were significantly higher than those in healthy controls [(2.6 1.2) ng/L F=9. 288, both P＜0. 01]. The serum level of IP-10 and IFN-γ were both positively correlated with TNF α (r=0. 366 and r=0. 365, respectively;P＜0.05) and both negatively correlated with prothrombinase activity (r=-0.401 and r=-0.350, respectively;P＜0.05), but not correlated with serum total bilirubin(r=0. 223 and r=0. 219, respectively;P＞0.05). The serum level of IP-10 and IFN-γ were positively correlated ( r= 0. 602 ; P= 0. 000 ). On day 5 after PE, serum level of IP-10 in patients with SHB was significantly decreased compared with that'in patients before PE (t= 8. 947, P＜0.01 in improved group;t=4. 121, P＜0.05 in aggravated group) and that in aggravated group was significantly higher than improved group (t=7.862, P＜0.01). But serum level of IFN-γ was not decreased significantly (t=0. 491, P＞0.05). Conclusions IP-10 and IFN-γ are involved in the hepatic immunopathological mechanism. Serum level of IP-10 is correlated with the severity of hepatic inflammatory injury and IP-10 could reflect the progression and development of disease in patients with SHB.

Hepatogenous diabetes (HD) is a common complication of end-stage liver disease, and many studies have confirmed its adverse effect on prognosis. In recent ten years, a great number of studies have been conducted on the pathogenesis of HD and some progress has been made. This article reviews the research advances in the pathogenesis of HD, in order to provide a reference for the diagnosis and treatment of HD by clinicians.

Both diabetes mellitus and liver cirrhosis have high incidence rate and mortality rate around the world, and in recent ten years, scholars in China and globally have conducted many studies on the association between diabetes mellitus and liver cirrhosis. This article systematically reviews the advances in the basic and clinical research on the influence of diabetes mellitus on liver cirrhosis and its complications and summarizes possible mechanisms. The results show that diabetes mellitus can accelerate the process of liver fibrosis, increase the risk of complications and progression to liver cancer in patients with liver cirrhosis, and reduce their survival rate.

With the wide application of nucleos(t)ide analogues (NAs) in antiviral therapy for chronic hepatitis B (CHB), the side effects of NAs after long-term use have attracted more and more attention from clinicians and patients. In recent years, an increasing number of studies have reported muscle injury in CHB patients treated with NAs, and we have gained a deeper understanding of the incidence rate, pathogenesis, and treatment of muscle injury. This article reviews the incidence rate, related factors, clinical manifestations, pathogenesis, management, and prevention and treatment of muscle injury associated with NAs.

OBJECTIVE: To analyze the clinical phenotype of a Chinese pedigree affected with Tuberous sclerosis complex (TSC) and explore pathogenic mutations of TSC1 and TSC2 gene. METHODS: Unique clinical phenotypes，the results of imaging, examination of the proband and special family history, collectively, made the constellation of features of TSC. Genomic DNA was obtained from six affected and eight unaffected members of the family and potential mutations of the TSC1 and TSC2 genes were detected by PCR-amplification of the exons and exon-intron boundaries and direct sequencing. A total of 150 normal unrelated individuals were used as controls. RESULTS: Genetic analysis documented the presence of a heterozygous mutation, c.1781_1782delTG (p.Val594GlyfsX11), in the exon 15 of TSC1 gene within all the patients of the family. This mutation was not observed in the eight unaffected family members or in the 150 unrelated control subjects from the same population , or the Human Gene Mutation Database (HGMD) and had completely co-segregated with the disease phenotype in the family. CONCLUSION The c.1781_1782delTG mutation of TSC1 gene may be responsible for the tuberous sclerosis complex in this family. The data presented in the present study are of significance to clinicians, as well as genetic counselors, and may provide new clues for molecular diagnosis of this disease．.
DNA Mutational Analysis ; Humans ; Mutation ; Pedigree ; Tuberous Sclerosis ; genetics ; Tuberous Sclerosis Complex 1 Protein ; genetics ; Tuberous Sclerosis Complex 2 Protein

OBJECTIVETo determine the risk factor of HCC in Guizhou.

METHODSA group case-control study design was conducted between 762 cases and 798 controls in Guizhou province. The main related-factors were analyzed with unconditional logistic regression model and evaluated by odds ratio (OR) and 95% confidence interval (95% CI).

RESULTSThere are significant differences between cases and controls in regarding to cigarette smoking 210 (27.6%),non-alcoholic fatty liver disease 336 (44.1%), alcoholic liver disease 245 (32.2%), family history of HCC 141 (16.5%), alcohol consumption 300 (39.4%), HBV infection 436 (57.2%), pickled food 290 (38.1%), and economic status 5 years ago 420 (55.1%) in cases,and cigarette smoking 116 (14.5%),non-alcoholic fatty liver disease 160 (20.1%), alcoholic liver disease 101 (12.7%), family history of HCC 40 (5.0%), alcohol consumption 180 (22.6%), HBV infection 82 (10.3%), pickled food 225 (28.2%), and economic status 5 years ago 647 (81.1%) in controls, with OR of each variable was 3.520, 2.464, 4.330, 2.219, 2.451, 19.245, 6.212, 0.174 respectively, P less than 0.01.

CONCLUSIONHBV infection and pickled food were the most common risks for HCC in Guizhou. Alcohol consumption excessively and cigarette smoking may increase the risk too.

Adult ; Aged ; Aged, 80 and over ; Alcohol Drinking ; Carcinoma, Hepatocellular ; epidemiology ; etiology ; Case-Control Studies ; China ; epidemiology ; Feeding Behavior ; Female ; Hepatitis B ; epidemiology ; Humans ; Liver Neoplasms ; epidemiology ; etiology ; Male ; Middle Aged ; Risk Factors ; Young Adult

The plasmodium of Physarum polycephalum is a suitable eukaryotic cell for cell cycle investigation, but there is no compatible transient expression system for the plasmodium. Using the promoter and terminator of ardC actin of Physarum polycephalum substituted the CMV IE and SV40 polyA of plasmid pDsRedl-N1, using cassette PardC-MCS-DsRed1-TardC substituted the cassette PardC-hph-TardC of plasmid pTB38, we constructed plasmids pXM1 and pXM2 for transient expression of red fluorescent protein (RFP) in Physarum polycephalum respectively. After reconstituting the transcription elongation factor homologous gene (pelf1) of Physarum polycephalum into the pXM2, we generated a plasmid pXM2-pelf1. After the plasmid pXM1, pXM2 and pXM2-pelf1 were electroporated into the plasmodium of Physarum polycephalum, we observed optimum RFP and PELF1-RFP expression under fluoroscope and confocal microscope between 24-48 h after electroporation, and found that ELF1-RFP expression was accumulated in nucleus of microplasmodium, the optimum electroporation parameters were 40 V/cm electric field, 1 ampere current, and 70 micros electric shock time. The results suggest that this expression system is qualified for transient expression of specific protein in plasmodium of Physarum polycephalum.
Actins ; genetics ; metabolism ; Electroporation ; Luminescent Proteins ; biosynthesis ; genetics ; Physarum polycephalum ; genetics ; metabolism ; Plasmids ; genetics ; metabolism ; Transcriptional Elongation Factors ; genetics

Objective: To analyze the clinical phenotype of a Chinese pedigree affected with Tuberous sclerosis complex(TSC) and explore pathogenic mutations of TSC1 and TSC2 gene. Methods: Unique clinical phenotypes, the results of imaging, examination of the proband and special family history, collectively, made the constellation of features of TSC.Genomic DNA was obtained from six affected and eight unaffected members of the family and potential mutations of the TSC1 and TSC2 genes were detected by PCR-amplification of the exons and exon-intron boundaries and direct sequencing.A total of 150 normal unrelated individuals were used as controls. Results: Genetic analysis documented the presence of a heterozygous mutation, c. 1781_1782delTG (p.Val594GlyfsX11), in the exon 15 of TSC1 gene within all the patients of the family. This mutation was not observed in the eight unaffected family members or in the 150 unrelated control subjects from the same population , or the Human Gene Mutation Database(HGMD)and had completely co-segregated with the disease phenotype in the family. Conclusions The c. 1781_1782delTG mutation of TSC1 gene may be responsible for the tuberous sclerosis complex in this family. The data presented in the present study are of significance to clinicians, as well as genetic counselors, and may provide new clues for molecular diagnosis of this disease.

In recent years， there has been a deeper understanding of the role and mechanisms of common inflammatory cytokines in the development and progression of liver cirrhosis， such as interleukin-1β， interleukin-6， interleukin-10， interleukin-17， tumor necrosis factor-α， interferon-γ， and C-reactive protein， and significant achievements have also been made in the research on the association of these inflammatory cytokines with disorder of glucose metabolism and pancreatic islet dysfunction. This article reviews the role of inflammatory cytokines in patients with liver cirrhosis and their impact on disorder of glucose metabolism and pancreatic islet dysfunction， in order to provide a theoretical basis for clarifying the pathogenesis of hepatogenous diabetes and performing the clinical management of the disease.