The spread of COVID-19 is accelerating. At present, there is no specific antiviral drugs for COVID-19 outbreak. This is a multicenter retrospective cohort study of patients with laboratory-confirmed COVID-19 infection pneumonia from 3 hospitals in Hubei and Guangdong province, 141 adults (aged !18 years) without ventilation were included. Combined group patients were given Arbidol and IFN-a2b, monotherapy group patients inhaled IFN-a2b for 10e14 days. Of 141 COVID-19 patients, baseline clinical and laboratory characteristics were similar between combined group and monotherapy group, that 30% of the patients leucocytes counts were below the normal range and 36.4% of the patients experienced lymphocytopenia. The duration of viral RNA of respiratory tract in the monotherapy group was not longer than that in the combined therapy group. There was no significant differences between two groups. The absorption of pneumonia in the combined group was faster than that in the monotherapy group. We inferred that Arbidol/IFN-2 b therapy can be used as an effective method to improve the COVID-19 pneumonia of mild patients, although it helpless with accelerating the virus clearance. These results should be verified in a larger prospective randomized environment.

Aberrant glycosylation of proteins has major implications for human diseases. To determine whether protein glycosylation contributes to the pathogenesis of Parkinson’s disease (PD), a mouse model of PD was established by injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Induction of PD-like features was verified by assessing motor impairment and confirming reductions in biological markers, including dopamine, 5-hydroxytryptamine and tyrosine hydroxylase, as well as the aggregation of α-synuclein. Altered glycosylation was detected using biotinylated agaracus bisporus lectin, which specifically binds exposed Gal-(β-1,3)-GalNAc linked to glycoproteins. Subsequent lectin affinity chromatography coupled with mass spectrometry revealed enhanced glycosylation of microtubule-associated protein 6 (MAP6) in PD mice as compared to healthy controls. In situ dual co-immunofluorescence analysis and immunoblotting confirmed that MAP6 is glycosylated with Gal-(β-1,3)-GalNAc oligosaccharides, which in turn alters the distribution and structure of MAP6 complexes within neurons. This is the first study to described MAP6 as a glycoprotein containing Gal-(β-1,3)-GalNAc oligosaccharides and to show that hyperglycosylation of MAP6 is strongly associated with the pathogenesis of PD. These findings provide potentially valuable information for developing new therapeutic targets for the treatment of PD as well as reliably prognostic biomarkers.

Background/Aims: Distribution of Hepatitis C virus (HCV) genotypes vary geographically and may associate with the mode of transmission. Little is known about the molecular epidemiology of HCV infection in Guangzhou, China. Methods: A cross-sectional survey included 561 subjects with chronic HCV infection registered at Nanfang Hospital, Southern Medical University, was performed. All residents were invited for a questionnaire interview to collect information about their personal status and commercial blood donation history. Results: A total of 463 chronic hepatitis C (CHC) patients were finally enrolled. Among the 463 samples, 426 were characterized by partial core-E1 sequences and classified into 7 subtypes: 1b (n=263, 61.7%), 6a (n=86, 20.2%), 2a (n=26, 6.1%), 3b (n=26, 6.1%), 3a (n=22, 5.2%), 6u (n=2, 0.5%), and 4a (n=1, 0.2%). Analysis of genotype-associated risk factors revealed that blood donation and transfusion were strongly associated with subtypes 1b and 2a, while genotype 3b and 6a were more frequent in intravenous drug users. Conclusions: Phylogeographic analyses demonstrated that the distribution of HCV genotypes in Guangzhou is complex. Interestingly, 6a has become a local endemic in Guangzhou and may be the second source region to disseminate 6a to other provinces.

The present study aimed to determine whether HepG2 can induce epithelial-mesenchymal transition (EMT) via angiotensin II (AngII) simulation. The expression levels of EMT markers vimentin and E-cadherin in cancer tissues and adjacent tissues of patients with hepatocellular carcinoma (HCC) were detected by immunohistochemistry. In addition, HepG2 cells were stimulated with AngII, and the gene and protein expression levels of vimentin and E-cadherin were measured by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively, whereas cell migration and invasion were assessed using Transwell assays. The AngII inhibitor Ang1-7 and the Ang1-7 inhibitor A779 were added to the system to further evaluate AngII-induced EMT. Compared with that in normal tissue, the expression level of vimentin in HCC tissue was increased, whereas that of E-cadherin was decreased. EMT occurred 48 h following AngII stimulation. The transcription level of E-cadherin in HepG2 cells was decreased, whereas that of vimentin was increased. In addition, the migration and invasion abilities of the cells were increased simultaneously. Ang1-7 partly inhibited AngII-induced EMT. When stimulated at an appropriate time, HepG2 cells have the ability to undergo EMT.

Background ADP/ATP translocase 1 (ANT1) is involved in the exchange of cytosolic ADP and mitochondrial ATP, and its defection plays an important role in mitochondrial pathogenesis. To reveal an etiological implication of ANT1 for Parkinson’s disease (PD), a neurodegenerative disorder, a mouse model treated with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine and neuroblastoma cell model induced by 1-methyl-4-pehny1-pyridine were utilized in this study. Results The tissue-specific abundance in ANT1 in mouse brains was accessed using the analysis of Western blot and immunohistochemistry. Down-regulated soluble ANT1 was found to be correlated with PD, and ANT1 was associated with PD pathogenesis via forming protein aggregates with α-synuclein. This finding was confirmed at cellular level using neuroblastoma cell models. ANT1 supplement in neuronal cells revealed the protective roles of ANT1 against cytotoxicity caused by MPP+. Protein interaction assay, coupled with the analysis of LC-MS/MS, silver-stained SDS-PAGE and Western blot against anti-ANT1 antibody respectively, illustrated the interaction of ANT1 with α-synuclein using the expressed α-synuclein as a bite. Additionally, a significant increasing ROSs was detected in the MPP+-treated cells. Conclusions This study indicated that ANT1 was a potentially causative factor of PD, and led to neuropathogenic injury via promoting the formation of protein aggregates with α-synuclein. This investigation potentially promotes an innovative understanding of ANT1 on the etiology of PD and provides valuable information on developing potential drug targets in PD treatment or reliable biomarkers in PD prognostication.