Background Platelet activation and aggregation are critical in the pathogenesis of acute ischemic stroke (AIS). Circulating platelet microparticles (PMPs) and platelet parameters are biological markers of platelet function in AIS patients, however, their associations with stroke subtypes and infarct volume remain unknown. Methods We recruited 112 AIS patients including large artery atherosclerosis (LAA) and small artery occlusion (SAO) subtypes, and 35 controls in this study. Blood samples were collected at admission and after antiplatelet therapy. The levels of circulating PMPs and platelet parameters [mean platelet volume (MPV), platelet count (PC), plateletocrit (PCT) and platelet distribution width (PDW)] were determined by flow cytometry and hematology analysis, respectively. Infarct volume was examined at admission by magnetic resonance imaging. Results (1) The levels of circulating PMPs and MPV were significantly elevated in AIS patients when compared with healthy controls; (2) The level of circulating PMPs, but not platelet parameters, was decreased after antiplatelet therapy in AIS patients; (3) The infarct volume in LAA subtype was larger than that in SAO subtype. Notably, circulating PMP level was positively correlated with the infarct volume in LAA subtype. No association with infarct volume in either AIS subtype was observed for platelet parameters; (4) According to the regression analysis, circulating PMPs was an independent risk factor for the infarct volume in pooled AIS patients after adjustments of other impact factors (hypertension and diabetes). Conclusions Our results suggest that circulating PMP level is associated with cerebral injury of AIS, which offers a novel evaluation parameter for AIS patients.

Background Atherosclerosis is the primary cause of coronary artery disease (CAD), and stearoyl‐CoA desaturase (SCD) is associated with atherosclerosis. However, the associations between variants of SCD and CAD have not yet been decided. Methods This study analyzed SCD rs41290540 single‐nucleotide polymorphism (SNP) in the 3′‐untranslated region for an association with a risk of CAD among the Chinese Han population. CAD patients and controls were genotyped for SNP rs41290540 in SCD by SNaPshot. The binding affinity of miR‐498 to rs41290540 was determined by a luciferase assay, and SCD expression was assessed using Western blot. Results A total of 969 CAD patients and 1,095 control subjects were involved in this study. The SCD rs41290540CC genotype is associated with a decreased risk of CAD compared with the AA genotype. Furthermore, the CC genotype is associated with lower serum total cholesterol (TC). Western blot analysis demonstrated that miR‐498 suppressed the expression of SCD. A luciferase assay confirmed that rs41290540 A>C variation in the SCD 3′UTR inhibits miR‐498 binding. Conclusion This study demonstrates that the SCD rs41290540 may be associated with a decreased risk of CAD, lower serum TC, and decreased miR‐498 binding.

Circulating progenitor cells and stromal-derived factor-1alpha (SDF-1α) have been suggested to participate in tissue repair following ischemic injury. However, the predictive role of circulating CD133+CD34+ progenitors and plasma SDF-1α in ischemic stroke (IS) patients remains unknown. In this study, we recruited 95 acute IS patients, 40 at-risk subjects and 30 normal subjects. The NIH stroke scale (NIHSS), infarct volume and carotid intima-media thickness (IMT) were determined at day 1 and the modified rankin scale (mRS) of functional outcome was assessed at day 21. The levels of circulating CD133+CD34+ cells and plasma SDF-1α were determined by flow cytometry and enzyme-linked immunosorbent assay, respectively. Our data showed that: 1) The levels of CD133+CD34+ cells were lower in at-risk subjects and IS patients at admission (day 1) when compared to normal controls. 2) The day 1 level of CD133+CD34+ cells varied in IS subgroups and inversely correlated with NIHSS and carotid IMT. The level of SDF-1α inversely correlated with NIHSS and infarct volume. 3) The increment rates of circulating CD133+CD34+ cells and plasma SDF-1α within the first week were correlated. 4) Patients with a higher level of CD133+CD34+ cells at day 7 had a low mRS. The increase rate of CD133+CD34+ cells in the first week was inversely associated with mRS. In conclusion, our findings demonstrate that the circulating CD133+CD34+ progenitor cells and plasma SDF-1α can be used as predictive parameters for IS severity and outcome.

BackgroundAtherosclerosis is the leading etiologic factor of Atherosclerotic Cerebral Infarction (ACI). Previous studies have shown that thrombin activatable fibrinolysis inhibitor (TAFI) may play an important role in the occurrence of acute cerebral infarction, and the levels of TAFI are affected by several single nucleotide polymorphisms (SNPs) located in the regulatory and coding regions of the gene encoding TAFI. The present study aimed to determine whether polymorphisms (TAFI –2345 2G/1G, –1690 A/G, –438 A/G, +1583 A/T) of the TAFI gene were associated with ACI in a Han Chinese population.MethodsThe variant genotypes were identified by restriction fragment length polymorphism (RFLP) and allele-specific polymerase chain reactions (AS-PCR) in 225 patients with ACI and 184 age-matched healthy individuals.ResultsThere was a significant difference in the genotype and allele frequencies of TAFI –2345 2G/1G and −1690 A/G polymorphisms between the ACI and control subjects. Further stratification analysis by gender revealed that the presence of the –438 AA genotype and the A allele conferred a higher risk of developing ACI in male patients (p < 0.05). Haplotype analysis demonstrated that four haplotypes of TAFI are significantly associated with ACI.ConclusionsOur study provides preliminary evidence that the TAFI –2345 2G/1G and –1690 A/G polymorphisms are associated with ACI susceptibility in a Han Chinese population.

The thymus, the central immune organ in mammals, plays an important role in immune defense. Porcine reproductive and respiratory syndrome virus (PRRSV) infection in piglets can cause thymus injury and immunosuppression. However, the mechanisms of thymus injury remain unknown. This study was aimed at investigating the specific manifestations of thymus injury through the construction of a PRRSV-infected piglet model and histopathological observation. In this study, fourteen 40-day-old PRRSV-free piglets were randomly divided into two groups, eleven of which were intramuscularly injected with 3 mL of PRRSV WUH3 virus suspension (106 PFU /mL) in the infection group, and three of which were sham-inoculated with 3 mL of RPMI-1640 medium in the control group. Clinical necropsy and samples collection were performed on day 8 after artificial infection. With the Illumina platform, the transcriptomes of piglet thymus tissues from infected and control piglets were sequenced to explore the relationships of differentially expressed genes (DEGs) and signaling pathways with thymus injury. The immune organs of PRRSV-infected piglets were severely damaged. The histopathological findings in the thymus indicated that PRRSV infection was associated with a large decrease in lymphocytes, cell necrosis and cell apoptosis; an increase in blood vessels and macrophages; thymic corpuscle hyperplasia; and interstitial widening of the thymic lobules. The transcriptomic analysis results revealed that the Gene Ontology functions of DEGs were enriched primarily in biological processes such as angiogenesis, regulation of angiogenesis and positive regulation of cell migration. Moreover, greater numbers of blood vessels and macrophages were observed in the thymus in PRRSV-infected than control piglets. KEGG pathway enrichment analysis revealed that the DEGs were significantly enriched in the Toll-like receptor signaling pathway, chemokine signaling pathway, IL-17 signaling pathway and TNF signaling pathway. The expression of TLR8, IRF5, the chemokines CCL2, CCL3L1 and CCL5; and their receptors CCR1, CCR2 and CCR5 was significantly up-regulated in PRRSV infection, thus suggesting that these cytokines were associated with the pathological processes of thymus injury.