[Analysis of Bacterial Communities and Antibiotic Resistance Genes in the Aquaculture Area of Changli County].

In order to understand the distribution of microorganisms and various antibiotic resistance genes in the aquaculture area of Changli County, Qinhuangdao, high-throughput sequencing technology was used in this study. We utilized 16S rDNA gene sequencing and metagenome sequencing methods to analyze the seawater, sediment, and gut contents of the local fish Synechogobius hasta in the aquaculture area in spring. The results showed that Proteobacteria, Firmicutes, and Bacteroidota were the dominant bacteria in seawater; and Proteobacteria, Crenarchaeota, Acidobacter, and Actinobaciota were rich in the sediment; whereas Proteobacteria, Cyanobacteria, Firmicutes, and Bacteroidota were in relatively high abundance in fish gut contents. The microbial diversity of sediment samples was the most abundant, followed by seawater samples, and the microbial diversity of fish intestinal contents was the lowest. Moreover, the microbial diversity of similar samples was relatively similar, and the microbial diversity of different types of samples was quite different. For samples at different sites, there were significant differences between seawater samples at each site, and there were small differences between sediment samples at each site, and some sediment sample groups did not have significant differences in microbial composition. In all sample groups, five ß-lactam antibiotic resistance genes (blaOXA-325, cepS, blaCARB-20, blaOXA-55, and blaTRU-1) and four aminoglycoside antibiotic resistance genes[aac(6')-IIb, amrA, aac(6')-Ie-aph(2″)-Ia, and aph(3')-Vc] were detected. There was also a certain correlation between antibiotic resistance genes and microbial communities.

Efficacy and mechanism of anti-vascular endothelial growth factor drugs for diabetic macular edema patients.

BACKGROUND: Diabetes is a serious public health concern in China, with 30% of patients developing retinopathy, and diabetic macular edema (DME) having the biggest impact on vision. High blood glucose level can cause retinal cell hypoxia, thus promoting vascular endothelial growth factor (VEGF) formation and increasing vascular permeability, which induces DME. Moreover, cell hypoxia can accelerate the rate of apoptosis, which leads to the aging of patients. In severe cases, optic cell apoptosis or retinal fibrosis and permanent blindness may occur. AIM: To investigate and compare the efficacy, mechanism, and differences between two anti-VEGF drugs (Compaq and ranibizumab) in DME patients. METHODS: Ninety-six patients with DME who attended our hospital from April 2018 to February 2020 were included and randomly divided into two groups (Compaq group and ranibizumab group). The groups received vitreal cavity injections of 0.5 mg Compaq and 0.5 mg ranibizumab, respectively, once a month. The best corrected visual acuity (BCVA), intraocular pressure (IOP), macular retinal thickness (CMT), macular choroidal thickness (SFCT), foveal no perfusion area (FAZ), superficial capillary density, deep capillary density, treatment effect, and adverse reactions were compared before and after treatment and between the two groups. RESULTS: Before treatment and 1-mo post-treatment, there was no statistically significant difference in the estimated BCVA in both groups (P > 0.05). BCVA decreased in the Compaq group 3 mo after treatment, and the difference was statistically significant (P < 0.05). Before treatment, and 1 mo and 3 mo post-treatment, there was no statistically significant difference in the estimated IOP in either group (P > 0.05). Before treatment and 1-mo post-treatment, there was no statistically significant difference in the estimated CMT, SFCT, or FAZ in either group (P > 0.05). CMT and SFCT values decreased in the Compaq group 3 mo post-treatment, and the difference was statistically significant (P < 0.05). Before treatment, and 1 mo and 3 mo post-treatment, there were no statistically significant differences in vascular density in the shallow or deep capillary plexi of the fovea, parafovea, or overall macular area between the two groups (P > 0.05). Marked efficient, effective, and invalid rates were 70.83% and 52.08%, 27.08% and 39.58%, and 2.08% and 8.33% in the Compaq and ranibizumab groups, respectively. The differences between the two groups were statistically significant (P < 0.05). CONCLUSION: Anti-VEGF drugs can effectively improve CMT and SFCT, without affecting microcirculation, thus providing an effective and safe treatment for patients with DME.

PDIA3-regulted inflammation and oxidative stress contribute to the traumatic brain injury (TBI) in mice.

Traumatic brain injury (TBI) is a leading cause of death and disability throughout the world. However, the molecular mechanism contributing to TBI still remains unclear. Protein disulfide isomerases (PDI) are a family of redox chaperones, which catalyze formation or isomerization of disulfide bonds in proteins. PDIA3, a critical member of PDI family, is a multi-functional protein, playing critical roles in modulating inflammation, apoptosis and oxidative stress under various kinds of disease conditions. Nevertheless, its regulatory effects on TBI have far from to be known. In the present study, we attempted to explore the modulation of neuroinflammatory responses by PDIA3 and its contribution to oxidative stress and cell death after TBI in the wild type (PDIA+/+) and PDIA3 knockout (PDIA3+/+) C57BL/6 mice. Results here suggested that PDIA3 expression was markedly up-regulated in the late trauma human brain tissues, which was verified in the PDIA3+/+ mice at 24 h after TBI. PDIA-/- provided significant improvements in cognitive impairments and contusion volume induced by TBI. Apoptosis in brain samples was also alleviated in TBI mice with PDIA3 deficiency. Significantly, PDIA3-/- mitigated neuroinflammation after TBI in mice, as evidenced by the reduced expression of pro-inflammatory factors interleukin (IL)-6, tumor necrosis factor-α (TNF-α) and IL-1ß, while the enhanced anti-inflammatory regulator IL-10. These anti-inflammatory activities by PDIA3-/- were associated with the decrease in phosphorylated nuclear factor kappa B (NF-κB)/p65. PDIA3-/- mice following TBI showed attenuated oxidative stress, as proved by the restored superoxide dismutase (SOD) and glutathione (GSH) activities, and the down-regulated malondialdehyde (MDA) levels in brain samples. These effects regulated by PDIA3 were confirmed in OGDR-treated astrocytes. Collectively, these data demonstrated a detrimental role of PDIA3 in regulating TBI, providing an effective therapeutic target for TBI treatment in future.

[Signal pathway in apoptosis of K562 cells induced by STI571].

This study was aimed to investigate the effect of tyrosine kinase inhibitor (STI571) on growth and proliferation of K562 cells by using microarray method, the changes of gene expression in the process of K562 cell apoptosis induced by STI571 and the mechanism of K562 cell apoptosis. The gene microarray probes were prepared by RD-PCR technique, then the microarray of gene expression map was constructed; the morphologic changes of K562 cells were observed under phase-contrast microscopy before and after treatment with STI571; the apoptosis of K562 cells treated with STI571 was assayed by MTT method; the expression level of genes was analyzed by self-made microarray. The results indicated that after the treatment of STI571 for 24 hours, in K562 cells appeared major morphological changes, which included nuclear shrinkage, membrane bleb and scattered apoptotic bodies. DNA gel electrophoresis also showed that the typical "DNA ladder" phenomena existed in the treated group. After hybridization, detection and analysis with microarray method, expression of 9 genes significantly down-regulated and expression of 4 genes up-regulated. These differentially expressed genes included cell cycle related genes, cell metabolizing pathway related genes, signal transduction and transcription regulation related genes and antiapoptosis genes. It is concluded that STI571 can effectively inhibit the K562 cell growth and induce K562 cell apoptosis. The genes screened from this microarray offer new information for exploration of pathogenesis of K562 cell malignant transformation and shows abundant potential targets for the treatment of CML.