Abundant oral microorganisms constitute a complex microecosystem within the oral environment of the host, which plays a critical role in the adjustment of various physiological and pathological states of the oral cavity. In this study, we demonstrated that variations in the “core microbiome” may be used to predict carcinogenesis.

A diabetes-specific formula may improve acute-term glycemic control in severe acute ischemic stroke patients.

Cigarette smoking could have certain effects on gut microbiota. Some pioneering studies have investigated effects of active smoking on the microbiome in local segments of the digestive tract, while active smoking-induced microbiome alterations in the whole digestive tract have not been fully investigated. Here, we developed a rat model of active smoking and characterized the effects of active smoking on the microbiota within multiple regions along the digestive tract. Blood glucose and some metabolic factors levels, the microbial diversity and composition, relative abundances of taxa, bacterial network correlations and predictive functional profiles were compared between the control group and active smoking group. We found that active smoking induced hyperglycemia and significant reductions in serum insulin and leptin levels. Active smoking induced region-specific shifts in microbiota structure, composition, network correlation and metabolism function along the digestive tract. Our results demonstrated that active smoking resulted in a reduced abundance of some potentially beneficial genera (i.e. Clostridium, Turicibacter) and increased abundance of potentially harmful genera (i.e. Desulfovibrio, Bilophila). Functional prediction suggested that amino acid, lipid, propanoate metabolism function could be impaired and antioxidant activity may be triggered. Active smoking may be an overlooked risk to health through its potential effects on the digestive tract microbiota, which is involved in the cause and severity of an array of chronic diseases.

Background and Objective: The effects of the combination of naloxone and edaravone on acute cerebral infarction (ACI), a severe cerebrovascular disease, have seldom been referred. This study aimed to assess the therapeutic effects of naloxone combined with edaravone on elderly ACI patients. Materials and Methods: A total of 176 ACI patients were randomly divided into control and experimental groups (n = 88) to be administered with edaravone and naloxone combined with edaravone, respectively for 2 weeks. Neurological function was evaluated by the National Institute of Health Stroke Scale (NIHSS) score. Living ability was assessed with the Barthel score. The levels of serum inflammatory factors and related markers were measured. Results: The total effective rate of the experimental group (92.05%) exceeded that of the control group (72.73%) (p<0.05). Two weeks after treatment, cerebral infarction volume and NIHSS score significantly declined and Barthel score rose in both groups, especially in the experimental group (p<0.05). Interleukin-6 (IL-6), IL-8, tumor necrosis factor-", C-reactive protein, matrix metalloproteinase-9, neuron-specific enolase, S100B, ubiquitin carboxy-terminal hydrolase L1, homocysteine, Fibulin-5, thromboxane B2 and 6-keto-prostaglandin F1" levels reduced in both groups, being lower in the experimental group (p<0.05). Superoxide dismutase and vascular endothelial growth factor levels increased in both groups, which were higher in the experimental group (p<0.05). Conclusion: Naloxone combined with edaravone exerts obvious therapeutic effects on ACI by inhibiting inflammatory cascade and platelet aggregation, reducing cerebral infarction volume, endothelial cell adhesion and blood viscosity, promoting angiogenesis and improving neurological function and daily living ability.