Expression of Peripheral Blood DCs CD86, CD80, and Th1/Th2 in Sepsis Patients and Their Value on Survival Prediction.

Objective: To explore the expression of peripheral blood dendritic cells (DCs) CD86, CD80, and Th1/Th2 in patients with sepsis and their value on survival prediction. Methods: 118 patients with sepsis from January 2019 to December 2020 were selected, According to the prognosis, the patients were divided into the death group (n = 46) and survival group (n = 72). The general data and pathogen division of the two groups were collected, and the levels of peripheral blood DCs CD86, CD80, and Th1/Th2; APACHE II score; inflammatory factor (procalcitonin (PCT)); and cell growth chemokine (GRO) were compared between the two groups heparin-binding protein (HBP) and myocardial enzyme indexes (creatine kinase (CK), creatine kinase isozyme (CK-MB), and lactate dehydrogenase (LDH)) to explore the relationship between CD86, CD80, Th1/Th2, and various serological indexes and the evaluation value of prognosis. Results: 124 strains of pathogenic bacteria were isolated from 118 patients, including 78 strains of gram-negative bacteria (62.90%), 31 strains of Gram-positive bacteria (25.00%), and 15 strains of fungi (12.10%). The scores of CD86, CD80, Th1, Th2, Th1/Th2, and APACHE II in the dead group were higher than those in the surviving group, and the difference was statistically significant (P < 0.05). PCT, GRO-α, HBP, LDH, CK-MB, and CK levels of patients in death group were higher than those in survival group, and the difference was statistically significant (P < 0.05). The levels of peripheral blood DCs CD86, CD80, and Th1/Th2 were positively correlated with PCT, GRO-α, HBP, LDH, CK-MB, and CK (P < 0.05). ROC curve analysis showed that the AUC of the combined detection of DCs CD86, CD80, and Th1/Th2 in peripheral blood was 0.951, which was higher than 0.882, 0.883, and 0.734 of single index (P < 0.05). Conclusion: All patients with sepsis have immune imbalance, and the peripheral blood CD86, CD80, and Th1/Th2 of the dead patients are higher than those of the survivors. The combined detection of these three indicators has the highest predictive value for the prognosis of patients.

Downregulation of interleukin-6 and C-reactive protein underlies a novel inhibitory role of microRNA-136-5p in acute lower extremity deep vein thrombosis.

Deep vein thrombosis (DVT) comprises a critical and common health condition with high incidence, mortality, and long-term adverse sequelae. Several differentially expressed microRNAs (miRNAs) have emerged as promising prognostic markers in DVT. The present study intended to explore the functional relevance of miR-136-5p in acute lower extremity DVT (LEDVT). Rat models of acute LEDVT were established and miR-136-5p expression was altered by agomir or antagomir to assess its effects. In addition, in vitro gain- and loss-experiments, prior to exposure to CoCl2, were performed to investigate effects of miR-136-5p on human umbilical vein endothelial cell (HUVEC) apoptosis and levels of interleukin-6 (IL-6) and C-reactive protein (CRP). miR-136-5p was downregulated, whereas IL-6 and CRP were elevated in acute LEDVT patients. Notably, miR-136-5p was confirmed to target both IL-6 and CRP. Overexpression of miR-136-5p led to reduced length, weight, and ratio of weight to length of the venous thrombus. Furthermore, overexpressed miR-136-5p downregulated the expression of IL-6 and CRP, consequently inhibiting HUVEC apoptosis. Conjointly, our data indicate that the overexpression of miR-136-5p has the potential to bind to the 3'-UTR in the mRNAs for IL-6 and CRP and mitigate acute LEDVT, which provides a basis for new therapeutic targets in acute LEDVT treatment.

MicroRNAs let-7b/i suppress human glioma cell invasion and migration by targeting IKBKE directly.

We demonstrated that IKBKE is overexpressed in human gliomas and that the downregulation of IKBKE markedly inhibits the proliferative and invasive abilities of glioma cells, which is consistent with the results reported by several different research groups. Therefore, IKBKE represents a promising therapeutic target for the treatment of glioma. In the present study, we verified that the microRNAs let-7b and let-7i target IKBKE through luciferase assays and found that let-7b/i mimics can knock down IKBKE and upregulate E-cadherin through western blot analysis. Moreover, the expression levels of let-7b/i were significantly lower in glioma cell lines than that in normal brain tissues, as determined by quantitative real-time PCR. Furthermore, let-7b/i inhibit the invasion and migration of glioma cells, as determined through wound healing and Transwell assays. The above-mentioned data suggest that let-7b/i inhibit the invasive ability of glioma cells by directly downregulating IKBKE and indirectly upregulating E-cadherin.