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Traumatic central nervous system injury can cause imbalance in intestinal microenvironmental homeostasis by disrupting intestinal barrier function, while the disturbed intestinal microenvironment can react on the central nervous system and aggravate the secondary injury of it. A large number of studies suggest that the intestinal barrier plays an important role in the pathophysiological process of traumatic central nervous system injury and can be an important target for the action of central nervous system injury. This paper reviews the structural and functional changes of intestinal microbial, chemical, mechanical and immune barriers after traumatic central nervous system injury and their bidirectional interaction with the central nervous system, summarizes the possible mechanisms leading to the disruption of intestinal barrier, including malnutrition, ischemia-reperfusion injury, inflammatory response and the release of neurotransmitters and hormones, to provide theoretical basis and new ideas for the development of research on the intestinal microenvironment after traumatic central nervous injury.

This paper summarized the meticulous nursing in fluid management of a patient with chronic heart failure. Meticulous nursing interventions of fluid management including limiting salt intake, patterns of fluid intake, usage of diuretics, monitoring of body weight and urine volume, edema care, psychological care and exercise guidance. Meticulous nursing of fluid management was carried out to make an active participation in self-management, and improve the cardiac function and quality of life. (本文总结1例慢性心力衰竭患者容量管理的精细化护理经验。针对患者进行限盐、液体摄入方式、利尿剂应用方式、体质量及尿量监测、水肿护理、心理干预、运动指导等精细化容量管理方式, 使患者主动积极参与自我管理, 改善患者心功能, 提高患者生活质量。)

Age-related neurodegenerative diseases is increasing with the aggravation of global aging. Studies show that neurodegenerative diseases could be prevented or delayed by intermittent fasting (IF) regulating metabolic pathways, and the mechanism of action may be associated with improved mitochondrial function and metabolic homeostasis by IF. Mitochondrial dysfunction is an early marker of brain aging and neurodegeneration. These suggest that IF, mitochondria, and neurodegenerative diseases may be closely correlated. We reviewed the improvement effects of IF on neurodegenerative diseases, the important role of mitochondria in neurodegenerative diseases, the regulation of IF on mitochondrial function, and the effects of excessive calorie intake on neurons and mitochondrial function, and summarized that IF could improve mitochondrial function, while excessive calorie intake could damage the neurons and mitochondrial function. Future research could continue to focus on the mechanism of action and metabolism signal pathway of IF improving neurodegenerative diseases, which may be favorable to the determination of the proper window period for intervention, and the development of alternative targeted drug therapy, thereby assisting clinical application of IF.

Objective To investigate the effect of miR-200c-5p on malignant proliferation of human colorectal cancer cell line SW480. Methods Human colorectal cancer cell line SW480 was transfected with miR-200c-5p mimic/inhibitor and negative control agent respectively. The expression of miR-200c-5p was detected by qPCR, and the effects of miR-200c-5p on the proliferation activity and clonogenesis ability of colorectal cancer cells were detected by CCK-8 and foci formation experiment. Bioinformatics methods were used to analyze the differential target genes and related pathways of miR-200c-5p in human colorectal cancer. Results Transient transfection with miR-200c-5p mimic/inhibitor succeeded in high/low expression of miR-200c-5p (P＜0.05). The proliferation of cells with high expression of miR-200c-5p was significantly inhibited as compare to that of controls(P＜0.05). The clone-formation rate of miR-200c-5p cells with high expression was significantly lower than that of untransfected cells, while the clone-formation rate of miR-200c-5p cells with low expression was the opposite (P＜0.05). CXCL10, the target gene of miR-200c-5p, was significantly up-regulated in colorectal cancer, while C2orf72, ZC3H12C and DST were significantly down-regulated. The most significant KEGG pathways were “melanoma”, “microRNAs in cancer” and “bladder cancer”. Conclusions miR-200c-5p inhibits the proliferation and clonal formation of human colorectal cancer cell line SW480, which is related to the occurrence and progression of colorectal cancer.

Polycystic ovary syndrome (PCOS) is an endocrine disorder with reproductive dysfunction and abnormal metabolic syndrome. However, its etiology is unknown yet. Androgen hypersecretion is one of the main features of PCOS. It has been found that PCOS has various effects on the offspring in reproductive, metabolic and nervous systems, including:increasing secretion of gonadotropin-releasing hormone and luteinizing hormone, ovarian morphological changes and abnormal secretion of sex hormones, leading to disorders of lipid and glucose metabolism, and increasing the risks of depression and autism. However, there is still lack of direct evidence, and more studies should be conducted on the underlying mechanism in future.