Keywords: myocardial infarction, recurrent stroke, risk factors of stroke s u m m a r y Background: Recurrent stroke is often devastating, and can cause severe disability or death. Risk factors associated with recurrent strokes unrelated to atrial fibrillation have been well identified; however, it remains to be further elucidated whether the risk factors for recurrent stroke are the same in young as in older patients. Methods: Data from 1017 stroke patients unrelated to atrial fibrillation were retrospectively reviewed. Risk factors analyzed included sex, smoking history, previous history of ischemic stroke or transient ischemic attack, hypertension, diabetes mellitus, coronary atherosclerotic heart disease, and previous myocardial infarction. All patients were followed up via telephone 1 year after their initial strokes. Logistic regression was used to assess the associations between the various factors and risk of recurrent stroke events. Results: Predictive independent risk factors of recurrent stroke in older men included previous history of myocardial infarction [odds ratio (OR), 6.761; 95% confidence interval (CI), 1.030e44.371], ischemic stroke or transient ischemic attack (OR, 2.496; 95% CI, 1.567e3.976), diabetes mellitus (OR, 1.986; 95% CI, 1.223e3.227), and coronary atherosclerotic disease (OR, 1.733; 95% CI, 1.010e2.974). In young men, hypertension (OR, 1.709; 95% CI, 1.104e2.645), coronary atherosclerotic heart disease (OR, 1.812; 95% CI, 1.129e2.911), and previous history of ischemic stroke or transient ischemic attack (OR, 2.317; 95% CI, 1.580e3.397) were independent risk factors of recurrent strokes. Conclusion: The predictive independent risk factors of recurrent stroke differ between young and older stroke patients. Our findings may help guide the prevention of recurrent strokes.
The early diagnosis and treatment of sepsis are of particular importance to patient survival. To obtain novel biomarkers that serve as prompt indicators of sepsis, the current study screened the differentially expressed micrornas (deMs) that were associated with sepsis susceptibility. The correlation between the elucidated DEMs and the inflammatory response was also examined. The present study included 40 patients with sepsis and 40 healthy controls. rna-sequencing technology and bioinformatics analysis were applied to screen the deMs between the two cohorts. The expression of these deMs was subsequently verified by performing reverse transcription-quantitative Pcr (rT-qPcr). in addition, il-6, il-21, c-X-c motif chemokine ligand-8 (cXcl8) and monocyte chemoattractant protein-1 (McP-1) levels, along with T-cell death-associated gene 8 (TdaG8) and toll-like receptor 4 (Tlr4) mrna expression levels were assessed. The association between microrna (miRNA/miR)-3663-3p and the secretion of various proinflammatory cytokines or TdaG8 and Tlr4 mrna expressions were subsequently evaluated by linear correlation analysis. The results revealed 305 deMs (P<0.05; fold change >2) between patients with sepsis and healthy controls. among these, the top 18 up-and downregulated mirnas were selected for RT-qPCR verification. In addition, the serum content of IL-6, il-21, cXcl8 and McP-1, and the expression of TdaG8 and TLR4 mRNAs were significantly increased in patients with sepsis compared with healthy controls. Moreover, in patients with sepsis, a positive correlation was identified between miR-3663-3p and the secretion of inflammatory cytokines or TdaG8 and Tlr4 mrna expression. a positive correlation was also elucidated between TdaG8 and Tlr4 mrna expression and proinflammatory cytokine/chemokine secretion. Receiver operating characteristic curve analysis of mir-3663-3p expression, il-6, il-21, cXcl8 and McP-1 secretion and TdaG8 and Tlr4 mrna expression demonstrated that mirna analysis may be invaluable for the diagnosis of sepsis. collectively, the results determined that mir-3663-3p may be a potentially powerful diagnostic and predictive biomarker of sepsis and that the combined and simultaneous detection of several biomarkers, including proteins, mirnas and mrna may be a reliable approach for the fast diagnosis and early identification of sepsis.
Sepsis serves as a leading cause of admission to and death of patients in the intensive care unit (icu) and is described as a systemic inflammatory response syndrome caused by abnormal host response to infection. adipose-derived mesenchymal stem cells (adScs) have exhibited reliable and promising clinical application potential in multiple disorders. However, the function and the mechanism of adScs in sepsis remain elusive. in the present study, the crucial inhibitory effect of adSc-derived hydroxy-carboxylic acid receptor 1 (Hcar1) on sepsis was identified. reverse transcription quantitative-Pcr determined that the mrna expression of Hcar1 was reduced while the mrna expression of Toll-like receptor 4 (Tlr4), major histocompatibility complex class ii (MHc ii), nod-like receptor family pyrin domain containing 3 (nlrP3), and the levels of interleukin-1β (il-1β), tumor necrosis factor-α (TnF-α), interleukin-10 (il-10), and interleukin-18 (il-18) were enhanced in the peripheral blood of patients with sepsis. The expression of Hcar1 was negatively correlated with Tlr4 (r=-0.666), MHc ii (r=-0.587), and nlrP3 (r=-0.621) expression and the expression of Tlr4 was positively correlated with nlrP3 (r=0.641), il-1β (r=0.666), TnF-α (r=0.606), and il-18 (r=0.624) levels in the samples. receiver operating characteristic (roc) curve analysis revealed that the area under the roc curve (auc) of Hcar1, Tlr4, MHc ii and nlrP3 mrna expression was 0.830, 0.853, 0.735 and 0.945, respectively, in which nlrP3 exhibited the highest diagnostic value, and the auc values of il-1β, il-18, TnF-α, and il-10 were 0.751, 0.841, 0.924 and 0.729, respectively, in which TnF-α exhibited the highest diagnostic value. a sepsis rat model was established by injecting lipopolysaccharide (lPS) and the rats were randomly divided into 5 groups, including a normal control group (nc group; n=6), a sepsis model group (lPS group; n=6), an adSc transplantation group (l + M group; n=6), a combined Hcar1 receptor agonist group [l + Hcar1 inducer (Gi) + M group; n=6], and a combined Hcar1 receptor inhibitor group [l + Hcar1 blocker (Gk) + M group; n=6]. Hematoxylin and eosin staining determined that adScs attenuated the lung injury of septic rats and adSc-derived Hcar1 enhanced the effect of adScs. The expression of Hcar1, Tlr4, MHc ii, nlrP3, il-1β, il-18 and TnF-α levels were suppressed by adScs and the effect was further induced by adSc-derived Hcar1. However, adSc-derived Hcar1 induced the levels of anti-inflammatory factor IL-10. The negative correlation of Hcar1 expression with Tlr4, MHc ii, and nlrP3 expression in the peripheral blood and lung tissues of the rats was then identified. It is thus concluded that ADSC-derived Hcar1 regulates immune response in the attenuation of sepsis. adSc-derived Hcar1 may be a promising therapeutic strategy for sepsis.
Objective: To study the influence of bone marrow mesenchymal stem cells (MSCs) transplantation on hypoxic pulmonary hypertension (HPH) in rats. Methods: MSCs in SD rats were separated, cultivated, identified in vitro, and labeled by the green fluorescence protein (GFP) adenovirus. Healthy male SD rats were randomly divided into four groups: normal control group (NC group) and HPH group, with eight rats in each group respectively; HPH + mesenchymal stem cell transplantation group (MSCs group) and HPH + vascular endothelial growth factor + mesenchymal stem cell transplantation group (VEGF + MSCs group), with twenty-four rats in each group respectively. In this experiment, intermittent normobaric hypoxia was employed to establish the pulmonary hypertension rat models, with stem cells transfected and transplanted. The mean pulmonary artery pressure (mPAP) was observed in rats to calculate the right ventricular hypertrophy index (RVHI); the morphological changes of pulmonary arterioles in each group of rats were observed under the microscope; the distribution and manifestation of MSCs fluorescently labeled by adenovirus transfection were observed in pulmonary arterioles under the fluorescence microscope at the set time points of 7 d, 14 d and 28 d after the transplantation of stem cells. Results: For NC group, the mPAP (mmHg) was 15.5 ± 1.5 at 28 d, while the mPAP in HPH, MSCs and VEGF + MSCs groups were 26.1 ± 1.9, 21.6 ± 2.7 and 20.1 ± 2.9 respectively which were apparently higher than that in NC group (p < .01). Compared with HPH group (p < .01), the mPAP was obviously decreased in MSCs and VEGF + MSCs groups. There was no significant difference between MSCs and VEGF + MSCs groups. At 28 d, RVHI for NC group was 0.28 ± 0.02, while the RVHI in HPH, MSCs and VEGF + MSCs groups were 0.43 ± 0.07, 0.34 ± 0.03 and 0.35 ± 0.01 respectively which were apparently higher than that in NC group (p < .01). In comparison with HPH group, RVHI was significantly decreased in MSCs and VEGF + MSCs groups (p < .05). There was no significant difference between MSCs and VEGF + MSCs groups. For HPH group, at 28 d, pulmonary arterioles were apparently thickened, with luminal stenosis & obliteration and incomplete endothelial cells. Compared with HPH group, pulmonary arterioles in MSCs group became thinning, with the lumen unobstructed and the integrity of endothelial cells improved. The changes in the manifestation of MSCs and VEGF + MSCs groups were not significant. Conclusions: The transplantation of MSCs can improve the remodeling of pulmonary arterioles to partially reverse the progress of HPH; the combined transplantation of VEGF and MSCs doesn't improve the effect of MSC transplantation.
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