Carisolv对根管微渗漏的影响

目的:建立以亚硝酸钠为示踪物的流体输送模型,探讨Carisolv对根管微渗漏的影响。方法:将70颗离体牙随机分为5组,分别采用Carisolv、2%氯亚明+3%H2O2、2.5%NaclO、5%NaclO(阴性对照)、蒸馏水(阳性对照)预备根管,对根管侧方加压充填后进行桩腔预备,置于模型上,分别于第1、2、4、7、10、15、20、25、30、35、40、45、50、55、60天利用重氮反应检测由冠方向根尖方渗出的亚硝酸钠浓度。采用SPSS11.5软件包对数据进行多因素方差分析。结果:阴性对照组从第1天到第60天均未检测到亚硝酸钠。阳性对照组从第1天就检测到较高浓度的亚硝酸钠,从第1天到第60天亚硝酸钠渗出量显著高于其余4组(P<0.01)。Carisolv组亚硝酸钠渗出量显著低于2%氯亚明+3%H2O2组(P<0.01),与2.5%NaclO组相比,除第25、30、35、40天外,其渗出量均较低(P<0.05)。结论:Carisolv可有效去除玷污层,减少根管微渗漏的发生,达到良好的根管封闭目的。以亚硝酸钠作为示踪物的流体输送模型,可客观、灵敏、准确地评价根管微渗漏。     

Prevention of β-amyloid degeneration of microglia by erythropoietin depends on Wnt1, the PI 3-K/mTOR pathway, Bad, and Bcl-xL

Central nervous system microglia promote neuronal regeneration and sequester toxic β-amyloid (Aβ) deposition during Alzheimer's disease. We show that the cytokine erythropoietin (EPO) decreases the toxic effect of Aβ on microgliain vitro. EPO up-regulates the cysteine-rich glycosylated wingless protein Wnt1 and activates the PI 3-K/Akt1/mTOR/ p70S6K pathway. This in turn increases phosphorylation and cytosol trafficking of Bad, reduces the Bad/Bcl-xL complex and increases the Bcl-xL/Bax complex, thus preventing caspase 1 and caspase 3 activation and apoptosis. Our data may foster development of novel strategies to use cytoprotectants such as EPO for Alzheimer's disease and other degenerative disorders.     

Monoclonal antibody 12D5 inhibits eosinophil infiltration in the brain of Angiostrongylus cantonensis-infected BALB/c mice

Each of BALB/c mice was infected with 50 Angiostrongylus cantonensis larvae. One group of mice received an intraperitoneal injection of 50 μg 12D5 monoclonal antibody (mAb) against a 98 kDa antigen of adult worms at 10 days post-infection (dpi), with a booster injection of 25 μg at 12 dpi. Five mice from each group were sacrificed at 14 dpi for pathological examination and RNA extraction. The infiltration of eosinophils and severity of eosinophilic meningitis were reduced in 12D5 mAb-treated mice compared with the infected mice without 12D5 treatment. The levels of eotaxin mRNA expression in spleen significantly increased and the expression of the Th2-type cytokine IL-5 significantly decreased. However, the expression of IL-4 was not changed. 12D5 mAb can observably enhance the survival rate of infected mice and reduce symptoms of angiostrongyliasis. A. cantonensis infection is a major cause of eosinophilic meningoencephalitis. The results of this study could be helpful for the development of treatment of human angiostrongylosis.     

Bruton tyrosine kinase inhibition is a novel therapeutic strategy targeting tumor in the bone marrow microenvironment in multiple myeloma

Bruton tyrosine kinase (Btk) has a well-defined role in B-cell development, whereas its expression in osteoclasts (OCs) further suggests a role in osteoclastogenesis. Here we investigated effects of PCI-32765, an oral and selective Btk inhibitor, on osteoclastogenesis as well as on multiple myeloma (MM) growth within the BM microenvironment. PCI-32765 blocked RANKL/M-CSF-induced phosphorylation of Btk and downstream PLC-γ2 in OCs, resulting in diminished TRAP5b (ED(50) = 17nM) and bone resorption activity. PCI-32765 also inhibited secretion of multiple cytokines and chemokines from OC and BM stromal cell cultures from both normal donors (ED(50) = 0.5nM) and MM patients. It decreased SDF-1-induced migration of MM cells, and down-regulated MIP1-α/CCL3 in MM cells. It also blocked MM cell growth and survival triggered by IL-6 or coculture with BM stromal cells or OCs in vitro. Importantly, PCI-32765 treatment significantly inhibits in vivo MM cell growth (P < .03) and MM cell-induced osteolysis of implanted human bone chips in SCID mice. Moreover, PCI-32765 prevents in vitro colony formation by stem-like cells from MM patients. Together, these results delineate functional sequelae of Btk activation mediating osteolysis and growth of MM cells, supporting evaluation of PCI-32765 as a novel therapeutic in MM.     

Chronic inflammatory demyelinating polyneuropathy mimicking diabetic neuropathy in a young female with type 2 diabetes mellitus

The presentations of chronic inflammatory demyelinating polyneuropathy (CIDP) overlap with those of diabetic peripheral neuropathy (DPN). We described a young girl with CIDP underlying type 2 diabetes mellitus, presenting with progressive numbness and limb weakness, who was initially misdiagnosed to have DPN. Finally immunosuppressive therapy got good response.     

miR-21 induces cell cycle at S phase and modulates cell proliferation by down-regulating hMSH2 in lung cancer

Purpose

MicroRNAs regulate critical genes associated with lung cancer. Human mutS homolog 2 (hMSH2), one of the core mismatch repair genes, is affected in lung cancer development. The aim of this study is to investigate the role of miR-21 in hMSH2 gene expression and the effect of miR-21 on cell proliferation and cell cycle in lung cancer.

Methods

The targets of miR-21 were predicted by a bioinformatics tool, and hMSH2 was validated as a direct target of miR-21 by luciferase activity assay. MiRNA mimics or inhibitors were used to stimulate or attenuate the effect of endogenous miR-21 on hMSH2 expression. MiR-21 and hMSH2 expressions were assessed with real-time RT-PCR and Western blotting. Cell cycle was determined by flow cytometry, and cell growth was analyzed by MTT assay and real-time cell analysis system.

Results

MiR-21 expression was inversely correlated with hMSH2 expression in human lung cancer cell lines. Further validation showed hMSH2 was directly regulated by miR-21. The up-regulation of miR-21 significantly promoted cell proliferation and revealed a higher proportion of cells at S phase. However, knockdown of miR-21 expression resulted in cell cycle arrest at G2/M phase and inhibited cell proliferation.

Conclusions

These data suggest miR-21 is a key regulator of hMSH2 and modulates cell cycle and proliferation by targeting hMSH2 in human lung cancer.