Objective To observe the effects of statins on ATP-binding cassette transporter 1(ABCA1) gene expression in neurons and astrocytes.Methods Primary human astrocytes and neuron cell line HCN-2 were incubated with simvastatin and pravastatin at different concentrations and under different conditions.Using RNA isolated from the cultured cells,we performed quantitative PCR to measure the ABCA1 gene expression in astrocytes and neurons.The protein expression of ABCA1 was measured by Western blot.Results The two statins significantly decreased the ABCA1 gene and protein expressions.Compared with pravastatin,simvastatin significantly reduced the expression of ABCA1 in neurons and astrocytes by 95% and 75%,respectively(both P

Objective To observe the effect of Sirt1 on the phosphorylation of Tau protein in neuroblastoma SK-N-SH cell line.Methods We cultured SK-N-SH cells in vitro with adenovirus packaging of Sirt1 and SirtM (Sirt mutant),and then observed the expression of Sirt1 under an inverted fluorescence microscope.The expressions of Sirt1and SirtM were detected by Western blot;t-Tau protein and phosphorylation of Tau protein were detected by Western blot,Real-time PCR,immunohistochemistry and immunofluorescence;and the effect of Sirt1 on SK-N-SH apoptosis was investigated by flow cytometry.Results The t-Tau protein level and its phosphorylation were significantly decreased in Sirt1 and SirtM groups compared with those in control group,and Sirt1 group showed more significantly decreased ser404,thr231 phosphorylation of tau protein and the mRNA level of Tau.Flow cytometry showed that Sirt1 could significantly reduce the apoptosis of SK-N-SH cells compared with the control group.Conclusion Sirt1 can decrease the phosphorylation of Tau protein and reduce the apoptosis of SK-N-SH,which provides an important laboratory basis for studies on Tau protein disease and other neurodegenerative diseases.

Objective To evaluate the relationship between 25-(OH) vitamin D [25-(OH) D] level and peripheral neuropathy in patients with type 2 diabetes mellitus.Methods Eighty patients with type 2 diabetes mellitus were enrolled in this cross-sectional study,including 37 subjects with and 43 without diabetic neuropathy.Anthropometric data was collected and serum levels of 25-(OH) D,HbA1c,blood lipid,and hepatic and renal functions were determined in all patients.Results Serum 25-(OH) D level was significantly lower in patients with diabetic neuropathy compared to those without neuropathy [(12.73 ± 4.68 vs 17.56 ± 5.28) ng/ml,P＜0.01].Logistic regressions demonstrated that vitamin D level was associated with diabetic neuropathy (OR=1.222,95％ CI 1.095-1.364).Conclusions Vitamin D insufficiency is associated with diabetic peripheral neuropathy.25-(OH) D level seems to be an independent risk factor of diabetic neuropathy in patients with type 2 diabetes mellitus.

Objective This study aims to biomechanically analyze a mini-implant at different healing times before loading. Methods Sixty-four mini-implants with (12±1) N·cm insertion torque were placed in the low jaw of eight beagle dogs. The test mini-implants remained in the low jaw for 0, 1, 3, and 8 weeks of bone healing and for an additional 10 weeks under a force of 0.98 N. The unloaded control implants were further divided into four groups (1, 3, 8, and 10 weeks). Maximum removal torque (MRT) testing was performed to evaluate the interfacial share strength of each group. Surface analysis of the removed implants was performed by scanning electric microscope (SEM). Results The MRT for the loading implants at 0, 1, 3, and 8 weeks of healing were 4.10, 4.25, 2.42, and 4.42 N·cm, respectively. During the healing process, the removal torque values of the 3-week implants were significantly lower than those of the other healing groups (P<0.05). The unloaded 3-week implants also had lower removal torques (P<0.05). The implant surface of the 3-week test group showed more fibrous bone. However, the other loading implants had more lamellar-like tissue. Conclusion A stable dangerous period occurred approximately 3 weeks after mini-implant insertion. A 3-week healing is disadvantageous to the stability of the implant. Orthodontics loading occurred immediately or after 1 week as a function of the healing time. The 8-week implant appeared to have a positive effect on peri-implant bone remodeling and implant stability.

Objective: To investigate the role of CD11b agonist leukadherin-1 (LA1) in the development of intestinal inflammation and colitis disease in a mouse model of dextran sulfate sodium (DSS)-induced colitis. Methods: The mouse model of experimental colitis was induced by DSS. Body weight changes and survival status were monitored every day. The length of colons was measured at day 7. Colon tissue sections were stained with hematoxylin and eosin (HE) and observed under an optical microscope for pathological analysis. The percentages of apoptotic cells in colon tissues were observed by TUNEL staining. Myeloperoxidase (MPO) activity was measured with MPO activity detection kit. IL-1β and TNF-α levels were detected by ELISA. Macrophages and TNF-α in colon tissues were observed using immunofluorescence staining and confocal microscopy. Flow cytometry was performed to detect the changes in TLR4 expression on macrophages after stimulating mice with LA1 for 0, 3, 6 and 12 h. Moreover, TLR4 expression was also measured by Western blot after treating bone marrow-derived macrophages (BMDMs) with LA1 for 0, 3, 6 and 12 h. Unpaired t-test was used for statistical analysis. Results: Compared with the DSS group, the LA1+ DSS group presented lower mortality rate, greater body weight and longer colon and the differences between the two groups were statistically significant. Moreover, the LA1+ DSS group showed lighter pathological damages, decreased percentage of apoptotic cells and suppressed MPO activity as compared with those of the DSS group. The number of macrophages and the relative concentrations of IL-1β and TNF-α in colon tissues were lower in the LA1+ DSS group than in the DSS group, and the differences between the two groups were statistically significant. There was no significant difference in the total expression of TLR4 on macrophages before and after LA1 treatment. However, the mean flourscence indensity (MFI) of TLR4 was weaker on the LA1-treated macrophages than on the untreated macrophages. Conclusions LA1 could alleviate the DSS-induced experimental colitis in mice through suppressing the activation of TLR4 pathway on macrophages. This study provided a new insight and theoretical reference for understanding the pathogenesis of inflammatory bowel diseases.