Humans ; Intestines ; microbiology ; Liver Diseases ; Microbiota

Objective To develop a Scoring System for Academic Conference Papers,in order to achieve real-time paper scoring in large academic conference with the information technology and network.Methods Based on Microsoft.Net technology,an information system Was developed,supporting multimeeting.multi-client and dynamic screen show.Results In this system,the conference inforrnation,meeting name and scoring standards Call be customized;the doctor information,papers information,used time,score detail and dynamic list Can be displayed in the screen.This system has been applied in national ophthalmic conferences several times and gained praise from the organizing committee and judges.Conclusions The scoring system for Academic Conference Papers can significantly improve efficiency,help to promote the standardization of paper scoring,and manifest the open,fair and just principles.It is worth of spreading.

Retina is composed of a heterogeneous population of cell types, each with a unique biological function. Even if the same type of cells, due to genetic heterogeneity will lead to cell function differences. In the past, traditional molecular biological methods cannot resolve variations in their functional roles that arise from these differences, and some cells are difficult to define due to the lack of specific molecular markers or the scarcity of numbers, which hindered the understanding and research of these cells. With the development of biotechnology, single-cell RNA sequencing can analyze and resolve differences in single-cell transcriptome expression profiles, characterize intracellular population heterogeneity, identify new and rare cell subtypes, and more definitely define the characteristics of each cell type. It clarifies the origin, function, and variations in cell phenotypes. Other attributes include pinpointing both disease-related characteristics of cell subtypes and specific differential gene expression patterns, to deepen our understanding of the causes and progression of diseases, as well as to aid clinical diagnosis and targeted therapy.

Objective:Using high-throughput transcriptome sequencing technology to study the differentially expressed genes (DEGs) and related regulatory signaling pathways involved in H1N1 influenza virus infection in primary human retinal pigment epithelial (RPE) cells.Methods:Primary human RPE cells were infected with H1N1 influenza virus for 2 h or 12 h, respectively. Taking H1N1 uninfected cells as a control group, total RNA was extracted, a library was constructed, and transcriptome sequencing was performed. DEGs were screened by DESeq2 software, and DEGs were analyzed by gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway.Results:Compared with the control group, a total of 1830 DEGs were identified in the 2 h H1N1 influenza virus infection group, and 2847 DEGs were identified in the 12 h infection group; 1213 DEGs were identified in the H1N1 influenza virus infection kinetics process (2 h: 12 h). The GO functional annotation analysis of DEGs in the H1N1 influenza virus infection group for 12 h showed that DEGs widely exist in a variety of cellular components and participate in various biological processes such as cellular processes, biological regulation, and metabolic processes. KEGG pathway enrichment analysis showed that DEGs were mainly enriched in the PI3K-Akt signaling pathway, MAPK signaling pathway, cancer MicroRNAs, and cytokine-cytokine receptor interactions in the 2 h H1N1 influenza virus infection group; in the 12 h H1N1 influenza virus infection group, DEGs were mainly enriched in PI3K-Akt signaling pathway, cancer MicroRNAs, AGE-RAGE signaling pathway and immune-inflammatory pathways; during the kinetics of H1N1 influenza virus infection (2 h: 12 h), DEGs were mainly enriched in cytokine-cytokine receptor interaction, TGF-β signaling pathway.Conclusions:Infection with H1N1 influenza virus leads to significant changes in the transcriptome of RPE cells. These data provide scientific reference for elucidating the molecular mechanism of eye infection by respiratory viruses such as influenza virus.

Objective To investigate the effects of form deprivation on the morphology of different types of RGC in mice.Methods Sixty B6.Cg-Tg (Thy1-YFP) HJrs/J transgenic mice were randomly assigned to form-deprived group (n=28) and control group (n=32). The right eyes of mice in the form-deprived group were covered by an occluder for 2 weeks as experimental eyes. The right eyes of mice in the control group were taken as control eyes. Before and 2 weeks after form deprivation, the refraction and ocular biometrics were measured; RGC were stained with Bra3a antibody and counted; the morphology of RGC was reconstructed with Neuroexplore software after immunohistochemical staining. The data was compared among experimental eyes, fellow eyes and control eyes by one-way analysis of variance.Results Two weeks after form deprivation, the axial myopia was observed in the experimental eyes (refraction:F=15.009,P<0.001; vitreous chamber depth:F=3.360,P=0047; ocluar axial length:F=5.011,P=0013). The number of RGC in central retina of the experimental eyes was decreased compared with the fellow eyes and the control eyes (F=4.769,P=0.035). The reconstructed RGC were classified into 4 types according to their dendritic morphology. Form deprivation affected all 4 types of RGC but in a different way. Among them, 3 types of RGC were likely contribute to form vision perception. Form deprivation increased the dendrite branches in these types of ganglion cells. However, form deprivation decreasd dendrite segment numbers in both eyes and the intersection and length insholl analyse type 4 ganglion cells which were morphologically identified as ipRGC.Conclusion Form deprivation distinguishingly affects the morphology of different types of RGC, indicating that form vision and non-form vision play different role in myopia development.

Postzygotic mutations are acquired in normal tissues throughout an individual's lifetime and hold clues for identifying mutagenic factors.Here,we investigated postzygotic mutation spectra of healthy individuals using optimized ultra-deep exome sequencing of the time-series samples from the same volunteer as well as the samples from different individuals.In blood,sperm,and muscle cells,we resolved three common types of mutational signatures.Signatures A and B represent clock-like mutational processes,and the polymorphisms of epigenetic regulation genes influence the pro-portion of signature B in mutation profiles.Notably,signature C,characterized by C＞T transitions at GpCpN sites,tends to be a feature of diverse normal tissues.Mutations of this type are likely to occur early during embryonic development,supported by their relatively high allelic frequencies,presence in multiple tissues,and decrease in occurrence with age.Almost none of the public datasets for tumors feature this signature,except for 19.6％of samples of clear cell renal cell carcinoma with increased activation of the hypoxia-inducible factor 1(HIF-1)signaling pathway.Moreover,the accumulation of signature C in the mutation profile was accelerated in a human embryonic stem cell line with drug-induced activation of HIF-1α.Thus,embryonic hypoxia may explain this novel signature across multiple normal tissues.Our study suggests that hypoxic condition in an early stage of embryonic development is a crucial factor inducing C＞T transitions at GpCpN sites;and indi-viduals'genetic background may also influence their postzygotic mutation profiles.

Reduced levels of retinal dopamine, a key regulator of eye development, are associated with experimental myopia in various species, but are not seen in the myopic eyes of C57BL/6 mice, which are deficient in melatonin, a neurohormone having extensive interactions with dopamine. Here, we examined the relationship between form-deprivation myopia (FDM) and retinal dopamine levels in melatonin-proficient CBA/CaJ mice. We found that these mice exhibited a myopic refractive shift in form-deprived eyes, which was accompanied by altered retinal dopamine levels. When melatonin receptors were pharmacologically blocked, FDM could still be induced, but its magnitude was reduced, and retinal dopamine levels were no longer altered in FDM animals, indicating that melatonin-related changes in retinal dopamine levels contribute to FDM. Thus, FDM is mediated by both dopamine level-independent and melatonin-related dopamine level-dependent mechanisms in CBA/CaJ mice. The previously reported unaltered retinal dopamine levels in myopic C57BL/6 mice may be attributed to melatonin deficiency.
Animals ; Disease Models, Animal ; Dopamine ; Melatonin ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Myopia ; Retina ; Sensory Deprivation