Perilipin2 inhibits the replication of hepatitis B virus deoxyribonucleic acid by regulating autophagy under high-fat conditions

BACKGROUND Chronic hepatitis B virus(HBV)infection is often associated with increased lipid deposition in hepatocytes.However,when combined with non-alcoholic fatty liver disease or hyperlipidemia,it tends to have a lower HBV deoxyribonucleic acid(DNA)load.The relationship between lipid metabolism and HBV DNA replication and its underlying mechanisms are not well understood.AIM To investigate the relationship between lipid metabolism and HBV DNA replication and its underlying mechanisms.METHODS 1603 HBsAg-seropositive patients were included in the study.We first explored the relationship between patients'lipid levels,hepatic steatosis,and HBV DNA load.Also,we constructed an HBV infection combined with a hepatic steatosis cell model in vitro by fatty acid stimulation of HepG2.2.15 cells to validate the effect of lipid metabolism on HBV DNA replication in vitro.By knocking down and overexpressing Plin2,we observed whether Plin2 regulates autophagy and HBV replication.By inhibiting both Plin2 and cellular autophagy under high lipid stimulation,we examined whether the Plin2-autophagy pathway regulates HBV replication.RESULTS The results revealed that serum triglyceride levels,high-density lipoprotein levels,and hepatic steatosis ratio were significantly lower in the HBV-DNA high load group.Logistic regression analysis indicated that hepatic steatosis and serum triglyceride levels were negatively correlated with HBV-DNA load.Stratified analysis by HBeAg showed significant negative correlations between HBV-DNA load and hepatic steatosis ratio in both HBeAgpositive and HBeAg-negative groups.An in vitro cell model was developed by stimulating HepG2.2.15 cells with palmitic acid and oleic acid to study the relationship between HBV-DNA load and lipid metabolism.The results of the in vitro experiments suggested that fatty acid treatment increased lipid droplet deposition and decreased the expression of cell supernatant HBsAg,HBeAg,and HBV DNA load.Western blot and polymerase chain reaction analysis showed that fatty acid stimulation significantly induced Plin2 protein expression and inhibited the expression of hepatocyte autophagy proteins.Inhibition of Plin2 protein expression under fatty acid stimulation reversed the reduction in HBsAg and HBeAg expression and HBV DNA load induced by fatty acid stimulation and the inhibition of cellular autophagy.Knocking down Plin2 and blocking autophagy with 3-methyladenine(3-MA)inhibited HBV DNA replication.CONCLUSION In conclusion,lipid metabolism is a significant factor affecting HBV load in patients with HBV infection.The in vitro experiments established that fatty acid stimulation inhibits HBV replication via the Plin2-autophagy pathway.

Treatment of lower part of glenoid fractures through a novel axillary approach:A case report

BACKGROUND Based on the location and size of the fracture block,open reduction and internal fixation can be employed or assisted for shoulder arthroscopy in the treatment of glenoid fractures.However,the treatment of lower part of glenoid fractures through a novel axillary approach has not been reported so far.CASE SUMMARY A 22-year-old right-handed man was transferred to our outpatient clinic because of right shoulder injury during a traffic accident.X-ray examination after admission suggested the fracture of the lower part of the right glenoid and an ipiselial proximal humeral fracture.Three-dimensional(3D)computed tomography(CT)further suggested that the size of the fracture block of the lower part of the right glenoid was 3.4 mm×16.2 mm.The patient was diagnosed as the fracture of the lower part of the glenoid,also known as bony Bankart lesion without shoulder dislocation.After general anesthesia,the patient was surgically treated with the open reduction internal fixation through a novel axillary approach.3D CT and shoulder joint function were reexamined at 12 mo of followup,showing acceptable recovery.CONCLUSION This case report describes a novel axillary approach adopted in an open reduction with cannulated screw and wire anchor internal fixation.After a follow-up for more than 12 mo,3D CT and shoulder joint function examinations display a good recovery.

Acute neck tendonitis with dyspnea:A case report

BACKGROUND Longus colli tendinitis(LCT)with dyspnea is a relatively less-reported condition in the literature,and physicians should be aware of its existence.Misdiagnosis of this condition may cause unnecessary treatment for dyspnea.CASE SUMMARY Herein,we report the case of a 40-year-old man with acute neck tendonitis.The patient presented to the pneumology department clinic with a complaint of acute neck tendonitis with dyspnea.An emergency cervical magnetic resonance examination was performed,and the preliminary diagnosis was“acute longus cervicalis tendinitis.”After aggressive medical treatment,the symptoms obviously improved.CONCLUSION LCT is a self-limiting disease that usually improves after three to seven days of conservative treatment following a definite diagnosis.However,owing to its insidious onset and complex clinical manifestations,most relevant personnel are not fully understood.The definite diagnosis of LCT is based on a comprehensive understanding of the triad,rare symptoms,and the clear identification of cervical 1 and 2 levels calcification and prevertebral edema by medical imaging examination,especially magnetic resonance imaging and computed tomography.

GRP78 upregulation-induced increase in cisplatin sensitivity of SPCA1 lung cancer cells

Background Glucose regulated protein 78 （GRP78）, an endoplasmic reticulum （ER） chaperone, plays a critical role in chemotherapy resistance in a variety of cancers. In this study, we investigated the up-regulation of GRP78 induced by A23187 and its association with the chemotherapeutical sensibility to cisplatin in human lung cancer cell line SPCAI. Methods SPCA1 cells were pretreated with A23187 at different concentrations. The expression of GRP78 at the mRNA level was analyzed by RT-PCR; the expression of GRP78 at the protein level was determined by Western blotting and immunofluorescence assay. Cell survival was determined by MTT assay. Cell apoptosis was analyzed by flow cytometry. Results The expression of GRP78 at both the mRNA and protein levels was obviously induced by A23187 in SPCA1 cells, with an elevation of GRP78 by 2.1-fold at the mRNA level and by 3.8-fold at the protein level compared to the control. There was a dose-dependent response. Survival curve analysis demonstrated that A23187 induction caused a significant reduction of survival for the cells subjected to cisplatin treatment （P 〈0.05）. After treatment by cisplatin, the percentage of apoptotic cells in the A23187 pretreated group increased about three fold compared with the control group （（27.53!-4.32）% vs. （9.25＋3.64）%, P 〈0.05）. Conclusions A23187 treatment was fairly effective for the induction of GRP78 in SPCA1 cells at both the mRNA and protein levels. To a certain extent, GRP78 up-regulation by A23187 was associated with the enhancement of drug sensitivity to cisplatin in human luncl cancer cell line SPCAI.