Stop Ischemic Event to the Brain: Screening Risk Factors of Cerebrovascular Stenosis in Coronary Artery Disease Patients.

OBJECTIVES: In this study, we investigated the difference in risk factors between the 2 diseases, aiming to further clarify who needs to do ischemic cerebrovascular disease (ICVD)-related screening among coronary artery disease (CAD) patients. METHODS: Clinical data of 326 patients with first-episode CAD from June 1, 2017, to July 31, 2020, in the Chinese PLA General Hospital were retrospectively reviewed. Outcomes, including clinical features and laboratory examination, were taken. Features related to ICVD including the extension of intracranial arterial (internal carotid artery intracranial segment, middle cerebral artery M1 segment, anterior cerebral A1 segment, vertebrobasilar artery intracranial segment, posterior cerebral artery P1 segment) and carotid arterial (internal carotid artery extracranial segment, common carotid artery, subclavian artery) stenosis were detected. Risk factors for the occurrence of ICVD in patients with CAD were analyzed. RESULTS: Among patients with the onset of CAD, in comparison of the nonstenosis and stenosis of intracranial artery subgroups, there were statistical differences in the onset age, hypertension, and duration of hypertension as well as the biochemical indicators, including high-density lipoprotein and glycosylated hemoglobin. In addition, statistical differences were detected in the onset age as well as the biochemical indicators, including glycosylated hemoglobin and blood glucose serum protein, along with the difference in the degree of cardiovascular stenosis. CONCLUSIONS: The onset age of CAD was shown to serve as a vital risk factor for ICVD. The primary prevention of ICVD in patients with CAD should lay more emphasis on the management of hypertension and diabetes.

Intermittent hypoxia is involved in gut microbial dysbiosis in type 2 diabetes mellitus and obstructive sleep apnea-hypopnea syndrome.

BACKGROUND: Obstructive sleep apnea (OSA)-hypopnea syndrome (OSAHS) has been recognized as a comorbidity of type 2 diabetes mellitus (T2DM); more than half of T2DM patients suffer from OSAHS. Intermittent hypoxia (IH) plays an important role in metabolic diseases, such as obesity and OSAHS, through various mechanisms, including altering the gut microecological composition and function. Therefore, it is important to study the role of gut microbiota in T2DM patients with OSAHS, which has a high incidence and is prone to several complications. AIM: To assess whether IH is involved in altering the fecal microbiome in T2DM patients with OSAHS. METHODS: Seventy-eight participants were enrolled from Henan Province People's Hospital and divided into healthy control (HC, n = 26), T2DM (n = 25), and T2DM + OSA (n = 27) groups based on their conditions. The fecal bacterial DNA of the research participants was extracted and subjected to 16S ribosomal RNA sequencing. The clinical indices, such as insulin resistance index, homocysteine (HCY) concentration, and the concentrations of inflammatory factors in the peripheral blood, were assessed and recorded. RESULTS: Group T2DM + OSA had the highest apnea-hypopnea index (AHI) (2.3 vs 3.7 vs 13.7), oxygen desaturation index (0.65 vs 2.2 vs 9.1), HCY concentration (9.6 µmol/L vs 10.3 µmol/L vs 13.81 µmol/L) and C-reactive protein (CRP) concentrations (0.3 mg/L vs 1.43 mg/L vs 2.11 mg/L), and lowest mean oxygen saturation (97.05% vs 96.6% vs 94.7%) among the three groups. Twelve and fifteen key differences in amplicon sequence variants were identified when comparing group T2DM + OSA with groups T2DM and HC, respectively. We found progressively decreased levels of Faecalibacterium, Eubacterium, and Lachnospiraceae, and an increase in the level of Actinomyces, which strongly correlated with the HCY, CRP, fasting plasma glucose, and hemoglobin A1c concentrations, AHI, mean oxygen saturation, and insulin resistance index in group T2DM + OSA (P < 0.05). CONCLUSION: For T2DM patients with OSAHS, IH may be involved in selective alterations of the gut microbiota, which may affect the pathophysiological development of T2DM and DM-related complications.

Gut microbiota and metabolic syndrome.

Metabolic syndrome (MetS) describes a set of risk factors that can eventually lead to the occurrence of cardiovascular and cerebrovascular disease. A detailed understanding of the MetS mechanism will be helpful in developing effective prevention strategies and appropriate intervention tools. In this article, we discuss the relationship between the clinical symptoms of MetS and differences in the gut microbial community compared with healthy individuals, characterized by the proliferation of potentially harmful bacteria and the inhibition of beneficial ones. Interactions between gut microbiota and host metabolism have been shown to be mediated by a number of factors, including inflammation caused by gut barrier defects, short-chain fatty acids metabolism, and bile acid metabolism. However, although we can clearly establish a causal relationship between gut microbial profiles and MetS in animal experiments, the relationship between them is still controversial in humans. Therefore, we need more clinical studies to augment our understanding of how we can manipulate the gut microbiota and address the role of the gut microbiota in the prevention and treatment of MetS.

Association of gene polymorphisms in ABO blood group chromosomal regions and menstrual disorders.

This study aimed to investigate whether single nucleotide polymorphisms (SNPs) located near the gene of the ABO blood group play an important role in the genetic aetiology of menstrual disorders (MDs). Polymerase chain reaction-ligase detection reaction technology was used to detect eight SNPs near the ABO gene location on the chromosomes in 250 cases of MD and 250 cases of normal menstruation. The differences in the distribution of each genotype, as well as the allele frequency in the normal and control groups, were analysed using Pearson's χ2 test to search for disease-associated loci. SHEsis software was used to analyse the linkage disequilibrium and haplotype frequencies and to inspect the correlation between haplotypes and the disease. Compared with the control group, the experimental group exhibited statistically significant differences in the genotype distribution frequencies of the rs657152 locus of the ABO blood group gene and the rs17250673 locus of the tumour necrosis factor cofactor 2 (TRAF2) gene, which is located downstream of the ABO gene. The allele distribution frequencies of rs657152 and rs495828 loci in the ABO blood group gene exhibited significant differences between the groups. Dominant and recessive genetic model analysis of each locus revealed that the experimental group exhibited statistically significant differences from the control group in the genotype distribution frequencies of rs657152 and rs495828 loci, respectively. These results indicate that the ABO blood group gene and TRAF2 gene may be a cause of MDs.

PPAR-γ agonist pioglitazone prevents apoptosis of endothelial progenitor cells from rat bone marrow.

Selective peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist affects the functions of endothelial progenitor cells (EPCs). This study explores the effect of selective PPAR-γ agonist, pioglitazone, on EPC apoptosis. The cells were cultured and identified via the double staining method in a medium containing different concentrations of pioglitazone. EPC apoptosis was detected by flow cytometry. On Day 7, EPCs engulfed DiL-ac-LDL and FITC-UEA-1, and showed yellow fluorescence in a laser-scanning confocal microscope. EPC apoptosis inhibition was maximal at 50 µmol/L. The ability of pioglitazone to prevent EPC apoptosis may be mediated by the PI3K/Akt signal pathway. The use of thiazolidine two ketone (TZD) to reduce EPC apoptosis may have some potential in treating vascular diseases.

Association of serum uric acid with different levels of glucose and related factors.

BACKGROUND: Previous studies have demonstrated that serum uric acid (UA) is an independent predictor of incident type 2 diabetes mellitus (T2DM) in general populations. This study aimed to investigate specific characteristics of UA and its relationship between UA and blood glucose and other risk factors in the Chinese population. METHODS: A total of 946 subjects were included in this study. UA, glucose, insulin, fractional excretion of UA (FEua), creatinine clearance rate (Ccr), hemoglobin A1c (HbA1c), fructosamine (FA), blood pressure and lipids were studied and also reexamined after the patients underwent two weeks of combined therapeutics. RESULTS: UA levels were the highest in subjects with impaired glucose regulation (IGR), followed by subjects with normoglycemia (NGT) and finally by subjects with T2DM. The level of the 2-hour postprandial insulin and the area under the curve for insulin (AUCins) showed a similar tendency. The UA levels initially increased with increasing fasting blood glucose (FBG) and postprandial blood glucose (PPBG) levels, up to 7 mmol/L and 10 mmol/L, respectively, and thereafter decreased at higher FBG and PPBG levels. Compared with subjects in the lower serum UA quartile, subjects in the upper quartile of serum UA levels had higher weights, triglyceride levels, and creatinine levels as well as lower Ccr and FEua levels. Compared with women's group, UA levels were higher, and FEua levels were lower in men's group. Sex, body mass index (BMI), mean arterial blood pressure (MAP), serum triglycerides (TG), FA and Ccr were independent correlation factors of UA. UA decreased and FEua increased after the patients underwent a combined treatment. CONCLUSIONS: UA increased initially and then decreased as glucose levels increased from NGT to IGR and T2DM. Compared with NGT and T2DM, IGR subjects had higher SUA levels, which related to its high levels of insulin. Under T2DM, male gender, BMI, MAP, Ccr, TG and FA are independent correlation factors of UA. Glucose-lowering, antihypertensive, lipemia-regulating combined treatments were of advantage to decline of SUA of T2DM.

[Changes of cerebral hemodynamics in patients with virus encephalitis].

OBJECTIVE: To explore the changes of cerebral hemodynomics in patients with virus encephalitis (VE). METHODS: Within the initial 24 h and 21 days after admission, respectively, the patients with acute VE (n=38) suspected to result from viral infections were examined with serial transcranial Doppler ultrasound (TCD) for measurements of the systolic flow velocity (Vs), mean blood velocity (Vm) and the pulsatility index (PI) in the middle, anterior and posterior cerebral arteries (MCA, ACA, PCA) and the basilar artery (BA). RESULTS: TCD showed normal findings in 11 and abnormal findings in 27 patients, with a positivity rate of 71%. The Vms were significantly elevated in MCA, ACA, PCA, vertebral artery and BA during the acute phase of VE compared with that of the 30 normal control subjects (P<0.001-0.05). The PIs were significantly increased in MCA, PCA and BA (P<0.001). CONCLUSION: TCD findings indicate the presence of cerebral vasospasm in VE during the acute phase.