Background The study examines the expression and function of hypoxia-inducible gene 2 (HIG2) in hepatocellular carcinoma (HCC) tissues and cells. Methods Forty patients with HCC were included in the study. Bioinformatic analysis was used to analyze the clinical relevance of HIG2 expression in HCC tissue samples. Immunohistochemistry was employed to determine the expression of target proteins in tumor tissues. Hepatic HepG2 and SMMC-7721 cells were transfected with HIG2 -targeting siRNA with Lipofectamine 2000. qRT-PCR was carried out to determine gene expression levels, while Western blotting was used to determine protein expression. A CCK-8 assay was performed to detect proliferation of cells, while migration and invasion of cells were studied by Transwell assay. Flow cytometry was carried out to detect surface markers and effector molecules in Nature killercells, as well as the killing effect of NK cells. Results HIG2 expression was upregulated in HCC. Silencing of HIG2 suppressed HCC cell migration and invasion. The killing effect of NK cells on HCC cells was enhanced after HIG2 was silenced in HCC cells. Conditioned media from HIG2 -silenced SMMC-7721 cells inhibited the phenotype and function of NK cells. HCC cells with silenced expression of HIG2 modulated the activity of NK cells via STAT3. HIG2 promoted the evasion of HCC cells from killing by NK cells through upregulation of IL-10 expression. Conclusion The study demonstrates that HIG2 activates the STAT3 signaling pathway in NK cells by promoting IL-10 release by HCC cells, thereby inhibiting the killing activity of NK cells, and subsequently promoting the recurrence and metastasis of HCC.

The current study aimed to analyze the clinical characteristics of severe fever with thrombocytopenia syndrome (SFTS) and to explore the risk factors of critical patients. From 2016 to 2018, we collected the hospitalized diagnosed cases with SFTS in Jinan infectious disease hospital of Shandong University and analyzed by the descriptive epidemiological method. According to the prognosis, they were divided into general group and severe group. The epidemiological characteristics, clinical features, and laboratory indexes of these 2 groups of patients were compared and analyzed at the first visit. The risk factors related to the severity of the disease were analyzed by univariate Logistic regression. In total, 189 cases of SFTS were treated during the period and 33 deaths occurred in the severe group, with the fatality rate of 17.46%. The patients’ age (χ2 = 8.864, P < .01), ALT (Z = −2.304, P = .03), AST (Z = −3.361, P < .01), GLU (t = −4.115, P < .01), CK (Z = −3.964, P < .01), CK-MB (Z = −2.225, P = .03), LDH (Z = −3.655, P < .01), α-HBDH (Z = −2.040, P = .04), APTT (t = −3.355, P < .01), BUN (Z = −2.040, P = .04), Cr (Z = −3.071, P = .01), and D-dimer (Z = −2.026, P = .04) in the severe group were higher than that in the normal group, but the blood platelet (PLT) counts were significantly lower (Z = −2.778, P < .01) than that in the normal group. With the neuropsychiatric symptoms (OR = 24.083, 95% CI = 6.064–95.642), skin bleeding point (OR = 30.000, 95% CI = 6.936–129.764), multiple organ dysfunction (OR = 34.048, 95% CI = 7.740–149.782), past medical history (OR = 3.792, 95% CI = 1.284–11.200), and fasting glucose elevation (OR = 1.359, 95% CI = 1.106–1.668) could predict the severity of the SFTS. In summary, the abnormality of the laboratory index, the special clinical manifestations, and the past medical history of SFTS patients were the important basis for judging the patient's serious condition.

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Epilepsy is a common complex neurological disorder, and some forms are resistant to drug treatment. The HCN1/HCN2 genes encode hyperpolarization-activated cyclic nucleotide-gated channels, which play important roles in the electrophysiology of neurons. We investigated the association between HCN1/HCN2 variants and drug resistance or the risk of genetic generalized epilepsies (GGEs). We used matrix-assisted laser desorption/ionization time-of-flight mass spectrometry to assess nine variants of HCN1/HCN2 in 284 healthy participants and 483 GGEs (279 drug-responsive, 204 drug-resistant). Frequencies of HCN2 rs7255568 and rs3752158 G alleles differed in GGEs and in controls (P = .039, P = .027, respectively). The frequency of HCN2 haplotype (CAC) was higher in patients than controls (P = .046). The frequency of the HCN1 rs10462087 CC+CT genotype was lower in patients with childhood absence epilepsy (CAE) than controls (P = .047). Rs7255568 was associated with the risk of CAE (P = .028) and juvenile myoclonic epilepsy (JME) (P = .02). Rs3752158 was associated with the risk of generalized tonic-clonic seizures, JME, and febrile seizures (all P < .05). The frequency of the HCN2 haplotype (CAC) was higher in patients with JME (P = .015) and in those with febrile seizures (P = .024) than in controls. No significant association was found between HCN1/HCN2 alleles, genotypes or haplotypes, and drug resistance in patients. After Bonferroni's multiple comparisons correction, only the HCN2 rs3752158 C allele and GC+CC genotype frequencies in patients with JME were higher than those in controls (19.2% vs 11.6%, odds ratio (OR) = 1.71, 95% CI = 1.18-2.32), P = .004 < 0.05/9; 36% vs 22.2%, OR = 1.62(1.18-2.23), P = .003 < 0.05/9). Our study suggests that HCN2 rs3752158 is involved in the susceptibility to JME.

The aim of the present study was to investigate the prevalence rate of hepatitis C virus (HCV) infection in human immunodeficiency virus (HIV)-positive individuals and to study the infection status of HCV RNA in HIV-infected individuals who did not have anti-HCV antibodies in the Guangxi province of China, in order to provide basis for screening and clinical treatment of hepatitis C in future. Data were collected from patients recruited via a questionnaire. Between August 2008 and January 2009, 300 HIV-infected individuals were randomly selected from various HIV monitoring points in Liuzhou and Qinzhou (Guangxi, China). In addition, 41 patients with only hepatitis C were recruited from a hospital clinic (First Affiliated Hospital of Guangxi Medical University, Nanning, China). HCV antibodies in patient serum samples were detected by ELISA. HCV RNA expression was detected using nested polymerase chain reaction (PCR), HCV RNA levels in the serum were evaluated using quantitative fluorescence PCR, and HCV genotypes were confirmed using restriction fragment length polymorphism. The infection rate of HCV in the HIV-infected people was 48.67%. The anti-HCV positive rate differed between routes of disease transmission: Anti-HCV positive rate was 63.7% among drug users, 34.96% among sex-transmitted persons and 1.37% among other persons. In the anti-HCV-negative group, the HCV RNA-positive rate was 26.62%. In the anti-HCV-positive group, HCV RNA positive rate was 78.08%. HCV RNA level of HIV/HCV coinfected patients was higher than those infected with HCV alone, and there was no difference of anti-HCV-positive rate among different levels of HCV RNA. HCV genotypes of HIV/HCV coinfected persons showed diversity across Guangxi, and the predominant ones were the 1b and mixed subtypes. The predominant HCV genotypes were 6a, mixed subtypes and 3b amongst patients that contracted HCV via drug use-related routes of transmission. The patients with HCV transmission routes other than drug-related routes possessed 1b and 1a+1b genotypes. In conclusion, there was a large proportion of HIV infected persons with mixed HCV infection in the Guangxi province of China. The present results show that 26.62% of HCV-infected persons will be fail to be diagnosed with hepatitis C virus coinfection if we simply use ELISA to detect HCV antibody. The predominant HCV genotypes were 1b, mixed, 6a and 3b in HIV/HCV coinfected persons.