皮鳞癌1号方对人皮肤鳞状癌A431细胞生长的抑制作用

目的:研究皮鳞癌1号方对人皮肤鳞状癌A431细胞生长的抑制作用。方法:以0、5、10、20、40、80μg(生药)/ml皮鳞癌1号方分别作用A431细胞24、48、72 h后,测定光密度并计算细胞增殖抑制率以评价其抑制作用;在显微镜下观察细胞形态学变化;光化学法测定乳酸脱氢酶(LDH)的活性;免疫细胞化学法测定B淋巴细胞瘤2(Bcl-2)蛋白、Bcl-2相关X蛋白(Bax)的表达。结果:5、10、20、40、80μg(生药)/ml皮鳞癌1号方对A431细胞均有抑制作用(P<0.01);5、40μg(生药)/ml皮鳞癌1号方可使A431细胞增殖变缓,细胞出现皱缩,与周围细胞黏附力减弱;5、10、20μg(生药)/ml可明显增强A431细胞LDH活性、Bax表达,减弱Bcl-2表达,降低Bcl-2/Bax的比值(P<0.01)。结论:皮鳞癌1号方对A431细胞的增殖具有一定的抑制作用;可能与促进Bax表达、抑制Bcl-2表达、降低Bcl-2/Bax的比值有关。     

Vascular-specific epicardial adipose tissue in predicting functional myocardial ischemia for patients with stable chest pain

Journal of Thrombosis and Thrombolysis - The relationship between vascular-specific epicardial adipose tissue (vEAT) volume and myocardial ischemia measured by fractional flow reserve (FFR) was not...     

Lipotoxic hepatocyte-derived exosomal miR-1297 promotes hepatic stellate cell activation through the PTEN signaling pathway in metabolic-associated fatty liver disease

BACKGROUNDExosomes play an important role in metabolic-associated fatty liver disease (MAFLD), but the mechanism by which exosomes participate in MAFLD still remain unclear.AIMTo figure out the function of lipotoxic exosomal miR-1297 in MAFLD.METHODSMicroRNA sequencing was used to detect differentially expressed miRNAs (DE-miR) in lipotoxic exosomes derived from primary hepatocytes. Bioinformatic tools were applied to analyze the target genes and pathways regulated by the DE-miRs. Quantitative real-time PCR (qPCR) was conducted for the verification of DE-miRs. qPCR, western blot, immunofluorescence staining and ethynyl-20-deoxyuridine assay were used to evaluate the function of lipotoxic exosomal miR-1297 on hepatic stellate cells (LX2 cells). A luciferase reporter experiment was performed to confirm the relationship of miR-1297 and its target gene PTEN. RESULTSMicroRNA sequencing revealed that there were 61 exosomal DE-miRs (P < 0.05) with a fold-change > 2 from palmitic acid treated primary hepatocytes compared with the vehicle control group. miR-1297 was the most highly upregulated according to the microRNA sequencing. Bioinformatic tools showed a variety of target genes and pathways regulated by these DE-miRs were related to liver fibrosis. miR-1297 was overexpressed in exosomes derived from lipotoxic hepatocytes by qPCR. Fibrosis promoting genes (α-SMA, PCNA) were altered in LX2 cells after miR-1297 overexpression or miR-1297-rich lipotoxic exosome incubation via qPCR and western blot analysis. Immunofluorescence staining and ethynyl-20-deoxyuridine staining demonstrated that the activation and proliferation of LX2 cells were also promoted after the above treatment. PTEN was found to be the target gene of miR-1297 and knocking down PTEN contributed to the activation and proliferation of LX2 cells via modulating the PI3K/AKT signaling pathway.CONCLUSIONmiR-1297 was overexpressed in exosomes derived from lipotoxic hepatocytes. The lipotoxic hepatocyte-derived exosomal miR-1297 could promote the activation and proliferation of hepatic stellate cells through the PTEN/PI3K/AKT signaling pathway, accelerating the progression of MAFLD.     

Dietary Patterns and Chronic Obstructive Pulmonary Disease: A Meta-analysis

Investigation of the relationship between dietary patterns and some chronic noncommunicable diseases has become appealing in nutritional epidemiology. Some studies have reported potential associations between dietary patterns and the risk of chronic obstructive pulmonary disease; however, the results remain conflicting. Thus, we conducted this meta-analysis to pool the results of studies to clarify the associations between dietary patterns and the risk of chronic obstructive pulmonary disease. A literature search of MEDLINE and EBSCO databases was performed to identify relevant studies published from January 1990 up to June 2015. A total of 13 studies met the inclusion criteria and were included in this meta-analysis. The highest category of healthy/prudent dietary patterns when compared with the lowest category was apparently associated with a decreased risk (OR = 0.55; CI: 0.46, 0.66; P < 0.0001). An increase in the risk of chronic obstructive pulmonary disease was shown for the highest compared with the lowest categories of “unhealthy/western-style” dietary patterns (OR = 2.12; CI: 1.64, 2.74; P < (0.0001). The results of this meta-analysis indicate that different dietary pattern may be associated with the risk of chronic obstructive pulmonary disease.     

Advances in neuroimaging for HIV-1 associated neurological dysfunction: clues to the diagnosis, pathogenesis and therapeutic monitoring

Persons with advanced human immunodeficiency virus type one (HIV-1) infection seek medical advice for a wide range of neurological disorders including, but not limited to, peripheral neuropathy, toxoplasmosis, cryptococcal meningitis, cytomegalovirus retinitis progressive multifocal leukoencephalopathy, lymphoma and dementia. The diagnosis of HIV-1-associated dementia (HAD) induced as a direct consequence of HIV infection of the brain comes commonly by exclusion. Diagnostic decisions can often be clouded by concomitant depression, motor impairments, and lethargy that follow debilitating immune suppression and weight loss. Indeed, cognitive, motor and behavior abnormalities underlie a variety of neurological dysfunctions associated with advanced HIV-1 infection. Thus, even combinations of clinical, laboratory and neuroimaging tests [for example, magnetic resonance imaging (MRI), computed tomography (CT), single photon emission computed tomography (SPECT) and positron emission tomography (PET)] often fail to provide conclusive diagnostic information. Nonetheless, the recent development of quantitative MR spectroscopic imaging has improved diagnostic possibilities for HAD. We are pleased to discuss these developments as well as taking a forward look into what will soon be made available to improve neuroimaging diagnostic precision. New MR and SPECT testing are being developed in our laboratories and elsewhere both for animal model systems and in humans with HIV-1 disease. Such tests can facilitate dynamic measures of HIV-1 neuropathogenesis providing information for disease events that even 2 years ago were unattainable.     

Human endostatin gene transfer, either naked or with liposome, has the same inhibitory effect on growth of mouse liver tumor cells in vivo

AIM: To explore a safe and efficient strategy of tumor therapy using anti-angiogenetic agents. METHODS: Endostatin gene with a signal sequence of human IgGgamma chain was amplified by PCR and cloned into pVAX1 plasmid which was the only vector authorized by FDA in clinical trial to construct a recombinant plasmid named as pVAX-sEN. The recombinant plasmid was detected with EcoRI/KpnI and DNA sequencing. BALB/c mice bearing hepatocarcinoma cell line H22 were treated with naked pVAX-sEN or liposome-DNA complex in which the dose of DNA and the ratio of DNA and liposome were different from each other. To compare the efficiency of gene transfection, expression of endostatin at the treated tumor site was assayed with ELISA. To investigate the effect of pVAX1-sEN on hepatocellular carcinoma, pVAX-sEN either naked or in liposome-DNA complex was injected into BALB/c mice bearing H22, then the diameter of tumors was measured, microvessel density was detected by immunohistochemistry, endostatin expression in vivo was assayed at different time points. RESULTS: DNA sequencing showed the endostatin gene with the signal peptide was correctly cloned. In situ gene expression assay indicated that both the ratio of DNA and liposome and the dose of DNA could affect the gene transfection efficiency. Interestingly, naked pVAX-sEN had a similar in situ endostatin expression to pVAX-sEN with liposome. Animal experiments showed that pVAX-sEN together with pVAX-sEN-liposome complex could efficiently suppress the growth of mouse hepatoma cells. CONCLUSION: Naked endostatin plasmid intratumoral injection can get a similar gene transfection efficiency to liposome-DNA complex when used in situ.     

Effects of Ethanol Extract of Radix Sophorae Flavescentis on Activity of Colon Cancer HT29 Cells

This paper mainly studied the inhibitory effect of total ethanol extract of Radix Sophorae Flavescentis on proliferation of colon cancer HT29 cells. By reflux extraction method and with ethanol as extraction solvent, different extracts were obtained at different ethanol concentrations, different solid-liquid ratios, and at different times. And their inhibitory activities against HT29 cells were compared using MTT assay. The experimental results showed that the extraction processes under three conditions can all draw relatively high inhibition rates. The optimum ethanol extraction process conditions were as follows: a solid-liquid ratio of 1:9, 80 min of heat reflux extraction with 95% ethanol.     

基于局部场电位固有模态分量的响应调谐特性研究

局部场电位(LFP)反映了视觉刺激下大脑皮层局部区域神经元集群的响应.LFP响应特征的准确提取,对分析视觉信息的处理机制具有重要意义.本研究针对LFP的非平稳特性,采用具有自适应特征的希尔伯特黄变换,分解LFP固有模态分量,据此研究了大鼠Vl区对刺激光栅空间频率的响应调谐特性,并与多神经元锋电位(MUA)和小波分解提取的Gamma频带进行了对比.结果表明:LFP第二阶固有模态分量对刺激光栅空间频率的调谐特性最强,调谐指数的均值(0.795 1)高于MUA调谐指数(0.631 3)和小波分解调谐指数(0.6646),而且与MUA响应一致率达68.75％.所提出的方法在LFP响应频带特征提取上更有优势.     

DNA hypermethylation of SFRP2 influences the pathology of rheumatoid arthritis through the canonical Wnt signaling in model rats

Abstract

In this work, the expression of secreted frizzled related protein 2 (SFRP2) in rheumatoid arthritis (RA) model rats and the mechanisms of SFRP2 on the RA pathogenesis were investigated. Data suggested that SFRP2 was significantly down-regulated in RA model rats compared with normal control, and overexpression of SFRP2 suppressed the RA pathogenesis and the canonical Wnt signaling in fibroblast-like synovial cells (FLS) from RA model rats, whereas knockdown of SFRP2 got an opposite observation. Interestingly, 5-azadC treatment up-regulated the SFRP2 expression, inhibited the FLS proliferation, suppressed the expression of IL-6 and IL-8 and the fibronectin production, suggesting that the decreased SFRP2 in RA model rats was due to the DNA methylation. Furthermore, DNMT1 knockdown up-regulated the SFRP2 expression, DNMT1 overexpression inhibited the SFRP2, and the quantitative methylation-specific PCR (qMSP) confirmed that the DNMT1 has direct methylation roles for the SFRP2 promoter, leading to a regulation of FLS proliferation and fibronectin expression in RA model rats. In addition, up-regulated MeCP2 was involved in the SFRP2 regulation and the pathogenesis of RA model rats, and MeCP2 and DNMT1 have synergistic inhibition roles in the SFRP2 expression. Combination of DNMT1 and DNA methylation may be a promising treatment strategy for individuals with RA in which SFRP2 is down-regulated.