Background Gut microbiota has been suggested to play a role in stroke patients. Nevertheless, little is known about gut microbiota and the clinical indexes in stroke patients. Methods Total of 30 cerebral ischemic stroke (CI) patients and 30 healthy control were enrolled in this study and the fecal gut microbiota was profiled via Illumina sequencing of the 16S rRNA V1-V2. The National Institutes of Health Stroke Scale (NIHSS) were used to quantify stroke severity and modified Rankin scale (mRS) to assess outcome for CI patients. The correlations between the clinical indexes and microbiota were evaluated. Results Though the microbial α-diversity and structure is similar between CI patients and healthy controls, the gut microbiota of CI patients had more short chain fatty acids producer including Odoribacter , Akkermansia, Ruminococcaceae_ UCG_005 and Victivallis . We also found that the special microbes were correlation with serum index, such as norank_O _ _Mollicutes_RF9 , Enterobacter , Ruminococcaceae _UCG-002 were negative correlation with LDL (r = − 0.401, P < 0.01), HDL (r = − 0.425, P < 0.01) and blood glucose (r = − 0.439, P < 0.001), while the HDL was significantly positive correlation with the genus Ruminococcus _1 (r = 0.443, P < 0.001). The Christensenellaceae _R-7_group and norank_f_ Ruminococcaceae was significantly positive correlation with NIHSS1M (r = 0.514, P < 0.05; r = 0.449, P < 0.05) and mRS (r = 0.471, P < 0.05, r = 0.503, P < 0.01), respectively. On the other hand, the genus Enterobacter was significantly negative correlation with NIHSS1M (r = 0.449, P < 0.05) and mRS (r = 0.503, P < 0.01). Conclusions This study suggests that CI patients showed significant dysbiosis of the gut microbiota with enriched short chain fatty acids producer, including Odoribacter , Akkermansia . This dysbiosis was correlation with the outcomes and deserves further study. Electronic supplementary material The online version of this article (10.1186/s12866-019-1552-1) contains supplementary material, which is available to authorized users.

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BackgroundMental arithmetic has been verified inducing cerebral and cardiovascular responses. However, the mechanism and sequential responses are still ambiguous. This study aims to reveal the mechanism of cardiovascular and autonomic responses and the related scalp positions that regulate the autonomic nerves system (ANS) during MA task.Methods34 healthy male subjects aged between 19 and 27 years old (mean age 23.6 ± 2.3 years) were recruited in. Electrocardiogram, impedance cardiography, beat-to-beat blood pressure and electroencephalography were measured simultaneously and continuously during the experiments. And the analysis of time–frequency, approximate entropy and Pearson correlation coefficient were adopted. For statistical comparison, paired t test is utilized in the study.ResultsThe results showed that mental arithmetic task increased heart rate (from 72.35 ± 1.88 to 80.38 ± 2.34), blood pressure (systolic blood pressure: from 112.09 ± 3.23 to 126.79 ± 3.44; diastolic blood pressure: from 74.15 ± 1.93 to 81.20 ± 1.97), and cardiac output (from 8.71 ± 0.30 to 9.68 ± 0.35), and the mental arithmetic induced physiological responses could be divided into two stages, the first stage (10–110 s) and late stage (150–250 s). The high frequency power component (HF) of HRV decreased during MA, but the normalized low frequency power component (nLF) and LF/HF ratio of HRV increased only at the late stage. Moreover, during first stage, the correlations between approximate entropy of electroencephalography at Fp2, Fz, F4, F7 and the corresponding time–frequency results of HF were significant. During the late stage, the correlations between approximate entropy of electroencephalography at Fp2, Fz, C3, C4 and the corresponding nLF was significant.ConclusionsOur results demonstrated that (1) mental stress induces time-dependent ANS activity and cardiovascular response. (2) Parasympathetic activity is lower during mental arithmetic task, but sympathetic nerve is activated only during late stage of mental arithmetic task. (3) Brain influences the cardiac activity through prefrontal and temporal cortex with the activation of ANS during mental arithmetic.