ABSTRACT
Objective To understand the epidemiological characteristics and variation of H3N2 influenza virus hemagglutinin (HA) gene in Changzhou from 2017 to 2018. Methods Throat swab specimens of the influenza-like cases were collected from Changzhou Influenza Monitoring Sentinel Hospital from April 2017 to March 2018. RNA was extracted from the specimens for influenza diagnosing and genotyping using real-time RT-PCR．H3N2 positive samples were isolated, and extracted RNA was used for amplification, sequencing and phylogenetic analysis of HA gene. Results From April 2017 to March 2018, 28 strains of influenza A (H3N2) virus were isolated. After gene sequencing, a phylogenetic tree was constructed. It was found that all of the strains belonged to Group3C.2a, which was similar to the vaccine strain A/Hong Kong/4801/2014. The HA amino acid sequence difference was analyzed and compared between the H3N2 influenza virus strains isolated in Changzhou and the vaccine strain A/Hong Kong/4801/2014. It was found that the epidemic strain isolated in Changzhou was in the HA epitope (A-E) region. Ten amino acid site mutations in the HA epitope (A-E) region and two amino acid site mutations in the stem region of HA antigen were found. Conclusion From April 2017 to March 2018, the influenza virus H3N2 prevalent in Changzhou was distributed on the same evolutionary branch with the vaccine strain A/Hong Kong/4801/2014 (group 3C.2a), rendering the popular trend of one subgroup. However, some amino acid sites of the HA epitope had variations, suggesting that mutations may occur, which may affect the immune effect of the vaccine. Monitoring needs to be strengthened in the future work.
ABSTRACT
Thirty eight patients with type 2 diabetes mellitus (T2DM) signed with the Lingering Garden Subdistrict Community Health Service Center of Suzhou Gusu District from October to December 2015 were enrolled in the study. The patients were classified as low risk group (n=3), moderate risk group (n=11), high risk group (n=21) and extremely high risk group (n=3) according to risk stratification of the JADE program based on estimated glomerular filtration rate (eGFR) and risk factors [obesity, dyslipidemia, hypertension, diabetic retinopathy, urinary protein creatinine ratio, foot disease, glycosylated hemoglobin A1c(HbA1c), fasting plasma glucose(FPG) or non fasting plasma glucose]. The patients were managed by a team consisting of general practitioners, general nurses and specialists; the individualized management was implemented with reduction of controllable risk factors and complications as the goal. After one year of management (March 2016 to February 2017) the indicators of T2DM were evaluated. The results showed that the TC, LDL-C, FPG and HbA1c levels were significantly improved in both moderate and high risk groups (P<0.05); the TC, LDL-C and FPG levels in the extremely high risk group were also significantly improved (P<0.05).
ABSTRACT
BACKGROUND:Numerous diseases like cardiac hypertrophy and intervertebral disc degeneration are known to be implicated in the changes of mechanical stress acting on surrounding tissues or cells, and autophagy contributes to the pathogenesis of these diseases. OBJECTIVE:To review the effects of mechanical factors on autophagy in different tissues and the underlying molecular mechanisms, thereby providing references for the research of autophagy and the prevention and treatment of related diseases. METHODS:A search of Web of Science and PubMed databases was performed for the literatures addressing the effects of mechanical factors on autophagy using the English keywords ofautophagy, mechanicaland the articles were summarized systematically. Finally, 52 literatures were enrolled according to the inclusion and exclusion criteria. RESULTS AND CONCLUSION:Mechanical factors make great effects on autophagy of various cells, such as myocardial cells, endothelial cells, chondrocytes and skeletal muscle cells. Autophagy is a self-protective reaction, and the mechanical stress of physiological conditions induces autophagy to maintain cellhomeostasis, normal function and survival. The mechanism of autophagy induced by mechanical stress may involve PI3K-AKT-mTOR, oxygen free radical, AKT-FoxO and other pathways, and the definite mechanism needs to be further studied.