Research on the correlation of immunity in patients with chronic insomnia.

Purpose: To investigate the changes in immunity and clinical infection events among patients with chronic insomnia. Materials and methods: Forty-two patients with chronic insomnia (age = 64.44 ± 10.53) and 47 normal controls (age = 67.08 ± 7.822) were selected to determine differences in data, such as complete blood counts (CBCs), biochemical indices, lymphocyte subsets, immunoglobulin (Ig), complement C3 and C4 and interleukin-6 (IL-6), as well as to compare the incidence of clinical infection between the two groups. Results: There were significant differences in erythrocyte, hemoglobin, hematocrit, albumin, globulin, creatinine, IgG, IgG/IgM ratio, CD4+ T-lymphocytes, CD19-lymphocytes, CD4+/CD8+ ratio, platelet/lymphocyte ratio, CD19/CD3 ratio, and clinical infection events between the chronic insomnia group and the control group (p < 0.05). There was no significant difference in neutrophil, lymphocyte, monocyte, and platelet counts; lymphocyte subsets CD8+ T and CD56+; platelet-to-lymphocyte ratio (PLR); neutrophil-to-lymphocyte ratio (NLR); complement C3; complement C4; IgM; IgA; and IL-6 between the experimental group and their controls (p > 0.05). The systolic and diastolic blood pressures of the chronic insomnia group did not vary widely from those of the controls (p > 0.05). Conclusion: Patients with chronic insomnia have immunological abnormalities, characterized by a higher incidence of clinical infection.

The Association Between Insomnia and Atherosclerosis: A Brief Report.

Aim: The objective of the study was to clarify the occurrence of atherosclerosis in patients with insomnia. Methods: A total of 60 patients with insomnia and 58 patients in a control group were selected to measure blood glucose, blood lipids and other biochemical and physiological indicators. Brachial-ankle pulse wave velocity (baPWV) was measured to assess arterial stiffness, and color Doppler ultrasound was used to examine carotid artery intima-media thickness (CIMT) and plaque incidence. These indicators were used to determine the occurrence and degree of carotid atherosclerosis, and to compare the differences between the two groups. Results: While there was no significant difference in biochemical or physiological indicators between the two groups (P > 0.05), the baPWV, CIMT, and incidence of carotid plaque in the insomnia group were higher than the control group. In addition, the baPWV, CIMT, and incidence of carotid plaque in the chronic insomnia group were higher than that in the short-term insomnia group. Multiple linear regression analysis was carried out to analyze the effects of insomnia, systolic blood pressure, blood glucose, triglycerides, cholesterol, BMI, age and low-density lipoprotein on atherosclerosis. The results showed that increased CIMT was significantly correlated with insomnia in atherosclerosis group (R2=0.27 on the left, R2=0.37 on the right, P < 0.001). Conclusion: Insomnia correlated with increased arterial stiffness and carotid atherosclerosis, and as the duration of insomnia prolongs, the correlation between them became more obvious.

Regulatory effects of miR-146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice.

The study aims to explore how microRNA-146a/b (miR-146a/b) regulates the function of endothelial progenitor cells (EPCs) in acute ischemic stroke in mice. Eighty male SPF C57BL/6J mice were evenly divided into the model-6 h, model-12 h, model-24 h (mice suffered from middle cerebral artery occlusion [MCAO] for 6 h, 12 h and model-24 h) and normal groups. EPCs were transfected and assigned into the control, MCAO, MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. The qRT-PCR was used to detect miR-146a/b expression in EPCs. Expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were detected using western blotting. Cell proliferation and migration of EPCs were testified using CCK-8 assay and scratch test, respectively. Angiogenesis ability of EPCs was observed under microscope. MiR-146a and miR-146b expressions were lower in the model groups than the normal group. There were up-regulated TRAF6 and IRAK1 expressions in the model-6 h, model-12 h and model-24 h groups compared with the normal group. And there were down-regulated TRAF6 and IRAK1 expressions in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups than in the MCAO group. Compared with the control group, the proliferation, migration and angiogenesis ability of EPCs were significantly lower in the MCAO group, but higher in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. Besides, the miR-146a/b group showed more enhancement than the MCAO-miR-146a and MCAO-miR-146b groups. MiR-146a/b could down-regulate the TRAF6 and IRAK1 expressions and promote proliferation, migration and angiogenesis ability of EPCs, which was important for recovery of patients with hyperacute ischemic stroke.

Synergistic effects of sorafenib in combination with gemcitabine or pemetrexed in lung cancer cell lines with K-ras mutations.

K-ras is currently accepted as the most frequently mutated oncogene in non-small cell lung cancer (NSCLC, including squamous carcinoma, adenocarcinoma, and large cell carcinoma). NSCLC patients with the K-ras mutation appear to be refractory to the majority of systemic therapies. In the present study, the in vitro antitumor effects and correlated molecular mechanisms of sorafenib combined with gemcitabine or pemetrexed were explored in the K-ras mutation-positive NSCLC A549 cell line. Sorafenib was seen to exhibit dose-dependent growth inhibition in the A549 cells, while sorafenib combined with pemetrexed demonstrated a greater synergism compared with sorafenib combined with gemcitabine. Sorafenib arrested the cell cycle at the G1 phase, while gemcitabine and pemetrexed caused arrest at the S phase. The molecular mechanism of this synergism was due to the downstream signalling pathways, which were efficiently suppressed by sorafenib, therefore increasing the incidence of the entry of the chemotherapeutic drugs into the apoptotic pathways. Moreover, sorafenib and pemetrexed demonstrated stronger synergism, demonstrating that inhibiting the Ras/Raf/Mek/Erk and Ras/PI3K/Akt pathways concurrently may achieve improved antitumor effects.