OBJECTIVEBy means of observing the clinical development of asymptomatic chronic HBsAg carriers (AsC) to explore the clinical rule of development of chronic hepatitis B (CHB) to liver cirrhosis (LC) to hepatocellular carcinoma (HCC) and to seek effective method for blocking the procedure.

METHODSAsCs were selected from health examination according to the diagnostic standard from the National Program for Prevention and Treatment of Viral Hepatitis, by periodical or non-periodical conventional examination of liver diseases, mixed infection of HCV was excluded. A 16-year systematic observation on clinical process of HBV infection series was completed.

RESULTSIn the 217 AsCs observed, 21 cases (9.68%) with the HBsAg negatively converted, the average year negative conversion rate being 0.58%, among them, 13/21 cases (61.9%) had production of anti-HBs antigen; 20 cases were clinically cured; 1 case transferred to HCC; 124 cases (57.14%) remained asymptomatic carriers; 73 transferred to chronic liver disease, showing a tendency of gradually developing from CHB to LC to HCC, the year transferring rate from AsC to LC and HCC being 1.04% and 0.40%, respectively. Fifteen patients died of liver diseases, in which one died of severe CHB, 3 of LC and 11 of HCC.

CONCLUSIONDifferent clinical end-results may reveal in AsCs according to their age and regulation on immune response to HBV. Few of the HCC and LC patients were HBeAg (e+) positive, they often reveal HBeAg (e-) negative or anti-HBe positive. HCC always develops on the basis of liver fibrosis or cirrhosis, which are the prophase of HCC, and patients with liver fibrosis or cirrhosis are the high risk group of developing HCC. HCC is not only the terminal pathologic stage of hepatopathy, but also one of the most important factors that causes death of chronic hepatopathy. From the viewpoint of integrative medicine in typing hepatopathy to observe the clinical speciality of AsC developing to CHB, LC and HCC, it is considered that the degree of blood stasis is in accordance with the development of hepatopathy.

Carcinoma, Hepatocellular ; virology ; Carrier State ; virology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Hepatitis B Surface Antigens ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; virology ; Liver Neoplasms ; virology ; Male ; Medicine, Chinese Traditional

Objective: To explore the clinical effects of expanded forehead flaps in repairing midfacial defects. Methods: From January 2003 to December 2018, 19 patients with midfacial defects were admitted to our unit, including 8 males and 11 females, aged 7 to 52 years. One cylindrical expander with rated capacity ranged from 100 to 170 mL was placed in the forehead of patients in the first stage of expansion, and the total water injection volume was about 2 times of the rated capacity of the expander during 1 to 2 months. The area of midfacial defects was 4 cm×2 cm to 9 cm×5 cm after resection in the second stage surgery. Expanded forehead flaps with vascular pedicle of supratrochlear vessels or frontal branch of superficial temporal vessels were used to repair the midfacial defects, with flap size ranging from 5 cm×2 cm to 16 cm×6 cm. The donor sites were closed by direct suturing. Three weeks later, the pedicle was divided. The complications, blood supply after flap transfer and pedicle division, and the treatment effects during follow-up were observed. Results: Among the patients, flaps of 11 patients had vascular pedicle of supratrochlear vessels; flaps of 8 patients had vascular pedicle of frontal branch of superficial temporal vessels. All the flaps survived with no complications and good blood supply after flap transfer and pedicle division. During the follow-up of 6 to 12 months after the third stage surgery of pedicle division of 12 patients, no lower eyelid ectropion occurred, the appearance of the flaps was similar to the surrounding tissue with no swelling. Conclusions The application of expanded forehead flaps can not only repair the defects but also effectively avoid the complication of lower eyelid ectropion, which is a promising method in repairing midfacial defects.

Objective To investigate the effects of salidroside(Sal)on mitochondrial autophagy in ischemic cardiomyopathy(ICM)rats by modulating the PTEN-induced kinase 1(PINK1)/E3 ubiquitin ligase(Parkin)signaling pathway.Methods Thirty SD rats were randomly divided into control group,model group,low-dose Sal group,high-dose Sal group,mitochondrial autophagy inhib-itor(Mdivi-1)group and high-dose Sal+Mdivi-1 group,with five rats in each group.The ICM rat model was established.The left ventricular ejection fraction(LVEF),left ventricular fractional short-ening(LVFS),left ventricular end-diastolic diameter(LVIDd)and left ventricular end-systolic diam-eters(LVIDs)were analyzed.Enzyme-linked immunosorbent assay(ELISA)was used to detect serum levels of lactate dehydrogenase(LDH),cardiac troponin Ⅰ(cTnⅠ),creatine kinase(CK)and N-terminal pro-brain natriuretic peptide(NT-proBNP).Hematoxylin and eosin(HE)staining was performed to observe pathological changes in myocardial tissue,and transmission electron microscopy was used to examine mitochondrial structure.The levels of reactive oxygen species(ROS),malondialdehyde(MDA)and superoxide dismutase(SOD)were measured.Western blot analysis was conducted to determine the expression levels of microtubule-associated protein light chain 3(LC3),Beclin1,p62,PINK1 and Parkin in myocardial tissue.Results Compared with the control group,the model group showed more severe myocardial tissue and mitochondrial damage.The LVEF,LVFS,SOD and p62 levels in the model group were significantly lower than those in the control group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels were significantly higher(P＜0.05).Compared with the model group,the low-dose and high-dose Sal groups exhibited reduced myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the low-dose and high-dose Sal groups were significantly higher than those in the model group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly lower(P＜0.05).Compared with the model group,the Mdivi-1 group showed more severe myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the Mdivi-1 group were significantly lower than those in the model group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly higher(P＜0.05).Compared with the low-dose Sal group,the high-dose Sal group demonstrated further improvement in myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the high-dose Sal group were significantly higher than those in the low-dose Sal group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly lower(P＜0.05).Mdivi-1 significantly inhibited mitochondrial autophagy and suppressed the activation of the PINK1/Parkin signaling pathway and the improvement in cardiac function induced by Sal(P＜0.05).Conclusion Sal may improve myocardial injury in ICM rats by activating the PINK1/Parkin signaling pathway and promoting mitochondrial autophagy.

Objective To investigate the effects of salidroside(Sal)on mitochondrial autophagy in ischemic cardiomyopathy(ICM)rats by modulating the PTEN-induced kinase 1(PINK1)/E3 ubiquitin ligase(Parkin)signaling pathway.Methods Thirty SD rats were randomly divided into control group,model group,low-dose Sal group,high-dose Sal group,mitochondrial autophagy inhib-itor(Mdivi-1)group and high-dose Sal+Mdivi-1 group,with five rats in each group.The ICM rat model was established.The left ventricular ejection fraction(LVEF),left ventricular fractional short-ening(LVFS),left ventricular end-diastolic diameter(LVIDd)and left ventricular end-systolic diam-eters(LVIDs)were analyzed.Enzyme-linked immunosorbent assay(ELISA)was used to detect serum levels of lactate dehydrogenase(LDH),cardiac troponin Ⅰ(cTnⅠ),creatine kinase(CK)and N-terminal pro-brain natriuretic peptide(NT-proBNP).Hematoxylin and eosin(HE)staining was performed to observe pathological changes in myocardial tissue,and transmission electron microscopy was used to examine mitochondrial structure.The levels of reactive oxygen species(ROS),malondialdehyde(MDA)and superoxide dismutase(SOD)were measured.Western blot analysis was conducted to determine the expression levels of microtubule-associated protein light chain 3(LC3),Beclin1,p62,PINK1 and Parkin in myocardial tissue.Results Compared with the control group,the model group showed more severe myocardial tissue and mitochondrial damage.The LVEF,LVFS,SOD and p62 levels in the model group were significantly lower than those in the control group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels were significantly higher(P＜0.05).Compared with the model group,the low-dose and high-dose Sal groups exhibited reduced myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the low-dose and high-dose Sal groups were significantly higher than those in the model group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly lower(P＜0.05).Compared with the model group,the Mdivi-1 group showed more severe myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the Mdivi-1 group were significantly lower than those in the model group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly higher(P＜0.05).Compared with the low-dose Sal group,the high-dose Sal group demonstrated further improvement in myocardial and mitochondrial damage.The LVEF,LVFS,SOD,LC3Ⅱ/LC3I,Beclin1,PINK1 and Parkin levels in the high-dose Sal group were significantly higher than those in the low-dose Sal group,while the LVIDd,LVIDs,LDH,cTnⅠ,CK,NT-proBNP,ROS,MDA and p62 levels were significantly lower(P＜0.05).Mdivi-1 significantly inhibited mitochondrial autophagy and suppressed the activation of the PINK1/Parkin signaling pathway and the improvement in cardiac function induced by Sal(P＜0.05).Conclusion Sal may improve myocardial injury in ICM rats by activating the PINK1/Parkin signaling pathway and promoting mitochondrial autophagy.

OBJECTIVE To investigate the improvement effects of azithromycin on bronchopulmonary dysplasia （BPD） in neonatal rats based on hypoxia-inducible factor-1α（HIF-1α）/HIF-2α/vascular endothelial growth factor （VEGF） pathway. METHODS Sixty newborn SD rats were randomly divided into negative control group （NC）， BPD group， azithromycin group and budesonide group （positive control）， with 15 rats in each group. Rats in NC group were given normal breathing air， while rats in other three groups were exposed to high-concentration oxygen for 14 days to establish BPD rat models. After successful modeling， rats in azithromycin group were intraperitoneally injected with azithromycin 200 mg/kg， and rats in budesonide group were atomized with budesonide 1.5 mg/kg once a day for 14 consecutive days， while rats in BPD group and NC group were not treated. Pathological changes of lung tissue， radial alveolar count and mean alveolar intercept of rats were observed in each group. The white blood cell count in bronchoalveolar lavage fluid （BALF） and the levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， IL-1β， superoxide dismutase （SOD）， catalase （CAT） and malondialdehyde （MDA） were detected； mRNA and protein expressions of VEGF， HIF-1α， HIF-2α were also detected. RESULTS Compared with NC group， the lung tissue in BPD group was obviously damaged； the white blood cell count， average alveolar intercept and the levels of TNF-α， IL-6， IL-1β and MDA were significantly increased； the radial alveolar count， SOD and CAT levels， the relative expressions of VEGF， HIF-1α， HIF-2α mRNA and protein were significantly decreased （P＜0.05）. Compared with BPD group， the changes of the above indexes in azithromycin group and budesonide group were significantly reversed （P＜0.05）. CONCLUSIONS Azithromycin can obviously improve the symptoms of BPD in rats， reduce inflammation and oxidative stress， and exert lung protection， the mechanism of which may be realized by activating HIF-1α/HIF-2α/VEGF pathway.