Objective To analyse the serum levels and clinical significance of interleukin-8(IL-8),tumor necrosis factor-α(TNF-α)and high-sensitivity C-reactive protein(hs-CRP)in patients with acute cerebral infarction.Methods 40 cases of patients with a-cute cerebral infarction were enrolled in this study.The degrees of neurological impairment and infarct volumes of these patiens were evaluated,serum levels of IL-8,TNF-αand hs-CRP were detected as well.40 cases of healthy individuals were selected as con-trol.Results The serum levels of IL-8,TNF-αand hs-CRP in patients with acute cerebral infarction were higher than those in the control group,had statistically significant differences(P <0.05).The serum levels of IL-8,TNF-αand hs-CRP in these patients be-gan to rise at the onset of acute cerebral infarction and reached peak in 72 hours,were also correlated with the volumes of infarction and the degrees of neurologic impairment.14 days after onset of acute cerebral infarction,serum levels of these indexes returned to normal.Conclusion The serum levels of IL-8,TNF-α,hs-CRP are significantly elevated in the patients with acute cerebral infarc-tion,which may be correlated with the volumes of infarction and the degree of neurologic impairment,and could be used to guiding clinical treatment and estimating the severity and prognosis of acute cerebral infarction.

OBJECTIVE：To study the e ffects of stilbene glycoside c（TSG）on phosphorylation of Thr 205，Ser404 sites of Tau protein in Aizheimer ’s disease （AD）model mice ，and to investigate the potential anti-AD mechanism of TSG. METHODS ：APP/ PS1/Tau three transgenes （3×Tg-AD）mice were randomly divided into model group ，positive control group （huperzine，0.15 mg/kg），TSG low-dose ，medium-dose and high-dose groups （0.033，0.1，0.3 g/kg），with 6 mice in each group. In addition ，6 C57BL/6J mice were chosen as normal control group. Administration groups were given relevant medicine intragastrically. Model group and normal control group were given equal volume of normal saline intragastrically ，once a day ，for consecutive 60 days. After last medication ，immunofluorescence staining was used to detect Tau protein and phosphorylated Tau protein （Thr205， Ser404 sites） distribution and expression in brain tissue of mice in each group. Western blotting assay was used to detect phosphorylated Tau protein （Thr205，Ser404 sites）expression level in brain tissue of mice in each group. RESULTS ：Compared with normal control group ，the expression of Tau protein，phosphorylated Tau protein （Thr205，Ser404 sites）in 729011126@qq.com the brain tissue of mice were increased in model group ，which were easy to aggregate and distributed more widely ；theirrelative expression were increased significantly （P＜0.01）. Results of Western blotting assay showed that the expression levels of phosphorylat ed Tau protein （Thr205，Ser404 sites）were increased significantly （P＜0.01）. Compared with model group ，the expression of Tau protein ，phosphorylated Tau protein （Thr205，Ser404 sites） in the brain tissue of mice were decreased in positive control group and TSG groups ；aggregation decreased，distribution narrowed and their relative expression were decreased significantly （P＜0.01）. Results of Western blotting assay showed that the expression levels of phosphorylated Tau protein （Thr205，Ser404 sites）were decreased significantly （P＜ 0.01）. Compared with positive control group ，There was no significant difference in the distribution of Tau protein ，phosphorylated Tau protein （Thr205，Ser404 sites）in the brain tissue of mice in TSG groups ；the relative expression were not statistically significant（P＞0.05）；but Western blotting assay showed the expression levels of phosphorylated Tau protein （Thr205 site）in TSG medium-dose and high-dose groups as well as the expression levels of phosphorylated Tau protein （Ser404 site）in TSG groups were decreased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS ：TSG can play an anti-AD effect on AD model mice by down-regulating the expression of phosphorylated Tau protein （Thr205，Ser404 sites）in brain tissue.

OBJECTIVE：To study the regulatory effects of stilbene glucosid e（TSG）on c-Jun N-terminal kinase （JNK）and protein phosphortase 2B（PP2B）in APP/PS1/Tau transgenic dementia （3×Tg-AD）mice，and to explore its potential mechanism of anti-Alzheimer’s disease （AD）. METHODS ：Totally 45 male 3×Tg-AD mice were randomly divided into model group ，positive control group （huperzine A ，0.15 mg/kg），TSG low-dose ，medium-dose and high-dose groups （0.033，0.1，0.3 g/kg），with 9 mice in each group. Another 9 normal male C 57BL/6J mice were included into normal control group. Administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 60 d. Normal control group and model group were given constant volume of normal saline intragastrically. After medication ，Morris water maze experiment was used to test the spatial learning and memory ability of mice in each group ；Nissl staining was used to observe the changes of Nissl bodies in cerebral cortex and hippocampus ；mRNA and protein expressions of JNK and PP 2B were detected by qRT-PCR and Western blotting assay. RESULTS：Compared with normal control group ，the escape latency was significantly prolonged （P＜0.01），the retention time of the original platform quadrant was significantly shortened （P＜ and the times of crossing the platform was significantly reduced in model group （P＜0.01）；the number of Nissl bodies in cerebral cortex and hippocampus was significantly 729011126@qq.com reduced，the staining was slight ；the relative expressions of JNK mRNA and protein were significantly increased （P＜ 0.01），and the relative expressi ons of PP 2B mRNA and protein were significantly decreased （P＜0.01）. Compared with model group ，the escape latency was significantly shortened in positive control group and TSG groups （P＜0.01）；the retention time of the original platform quadrant was significantly prolonged （P＜0.01）；the times of crossing the platform was significantly increased （P＜0.01）；the number of Nissl bodies in cerebral cortex and hippocampus was increased significantly ，the staining was heavy ；the relative expression of JNK protein was significantly decreased（P＜0.05 or P＜0.01），the relative expressions of PP 2B mRNA and protein were significantly increased （P＜0.01）， while the relative expression of JNK mRNA was significantly decreased in TSG high-dose group （P＜0.05）. CONCLUSIONS ：TSG can improve the learning and memory ability and neuronal damage of 3 × Tg-AD mice. The mechanism may be related to down-regulating the transcription and expression of protein kinase JNK ，up-regulating the transcription and expression of protein phosphatase PP 2B.

Objective:To observe the effect of tetrahydroxy stilbene glycoside （TSG） on the expression of glycogen synthase kinase 3β （GSK3β）， cyclic adenosine monophosphate-dependent protein kinase （PKA） and Serine/threonine phosphatase 2A（PP2A） in the brain of amyloid precursor protein/presenilin-1/Tau （APP/PS1/Tau） triple-transgenic mice dementia model. Method:A total of forty-five 8-month-old APP/PS1/Tau transgenic mice were randomly divided into model group， positive control group （Huperzine-A， 0.15 mg·kg^-1）， low， medium and high dose TSG groups （TSG， 0.033，0.1，0.3 g·kg^-1）， with 9 mice in each group， and another nine C5B7L/6J mice of the same age were selected as normal control group. After 60 days of intragastric administration， the general structure of hippocampal neurons was observed by hematoxylin-eosin （HE） staining， immunohistochemical （IHC） was used to detect the expression of PKA protein in the brain of mice in each group， the mRNA expression levels of GSK3β， PKA and PP2A were detected by real time quantitative reverse transcription polymerase chain reaction （Real-time PCR）， and protein expression levels of GSK3β and PP2A were detected by Western blot. Result:Compared with the normal control group， the apoptosis level of neurons in the model group was significantly increased， the protein and mRNA expression levels of GSK3β and PKA were significantly increased （P<0.05， P<0.01）， and the protein and mRNA expression levels of PP2A were significantly decreased （P<0.05， P<0.01）. Compared with the model group， the apoptosis level of neurons in each treatment group was significantly down-regulated， the protein and mRNA expression levels of GSK3β and PKA were significantly down-regulated （P<0.05， P<0.01）， and the protein and mRNA expression levels of PP2A were significantly increased （P<0.05， P<0.01）. Conclusion:The mechanism of TSG in the treatment of Alzheimer's disease （AD） may be related to lowering the transcription and expression of GSK3β and PKA， increasing the transcription and expression of PP2A.

OBJECTIVETo study the changes of serum interleukin-2 (IL-2), interleukin-8 (IL-8) and immunoglobulin (IgG, IgA, IgM) in patients with esophageal cancer, and to probe the relationship between the levels of IL-2, IL-8, IgG, IgA and IgM and the progress of cancer.

METHODSThe serum levels of IL-2 and IL-8 were detected by enzyme-linked immunosorbent assay for 72 case of primary esophageal cancer, 68 advanced esophageal cancer and 120 healthy controls, and the level of immunoglobulin (IgG, IgA, IgM) in patients with esophageal cancer was dynamically observed.

RESULTSThe IL-2 level in patients with early esophageal cancer [(1.69 +/- 0.53) ng/ml] or late esophageal cancer [(1.11 +/- 0.60) ng/ml] was lower than the control group [(2.78 +/- 0.51) ng/ml] (P < 0.01), the late esophageal cancer group was lower than early esophageal cancer group (P < 0.05). The level of IL-8 in patients with early esophageal cancer [(85.48 +/- 6.14) ng/L] or late esophageal cancer [(121.41 +/- 6.22) ng/L] was much higher than the control group [(54.48 +/- 12.20) ng/L] (P < 0.01), the late esophageal cancer group was much higher than early esophageal cancer group (P < 0.01); There was correlation between the levels of IL-2 and IL-8 and the worsen-extent of the tumour in patients with early esophageal cancer or late esophageal cancer. But the level of IgG [(12.23 +/- 2.50) g/L], IgM [(1.60 +/- 0.80) g/L] in the patients with esophageal cancer compared with the level of IgG [(11.65 +/- 3.70) g/L], IgM [(1.46 +/- 0.71) g/L] in the health control group have no significant difference (P > 0.05), the level of IgA [(3.50 +/- 1.10) g/L] in patients with esophageal cancer Compared with the control group [(1.88 +/- 1.08) g/L] has significant difference (P < 0.01), and along with the worsen-extent of the tumor in patients the level of IgA has the increased tendency.

CONCLUSIONThe IL-8 might accelerate the pathogenesis of esophageal cancer, and the IL-2 might restrain. The positive correlation between the level of IgA and the patients with esophageal cancer is observed in this study; the immune maladjustment of IL-2, IL-8 and IgA might be correlative to esophageal cancer, and the IL-2, IL-8 and IgA levels might be an available index for the severity of esophageal cancer, Which may be of some help for clinic practitioners to judge the progress, curative effect and prognosis of the cancer.

Adult ; Aged ; Case-Control Studies ; Esophageal Neoplasms ; blood ; pathology ; Female ; Humans ; Immunoglobulin A ; blood ; Immunoglobulin G ; blood ; Immunoglobulin M ; blood ; Interleukin-2 ; blood ; Interleukin-8 ; blood ; Male ; Middle Aged ; Neoplasm Staging

OBJECTIVEFindings from the previous studies have suggested a relationship between ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP-1) or plasma cell membrane glycoprotein 1 (PC-1) gene single nucleotide polymorphism (K121Q, rs1044498) and genetic susceptibility to obesity. However, such relationship is not reproduced by some currently available studies. In this context, the present study is aimed to quantitatively analyze the association of K121Q variant with obesity in all published case-control studies in European adult populations.

METHODSPublished literature from PubMed, EMBASE, and ISI web of science databases were retrieved. The studies evaluating the association of ENPP1/PC1 gene K121Q polymorphism with obesity were included, in which sufficient data were presented to calculate the odds ratio (OR) with 95% confidence intervals (CIs).

RESULTSTen case-control studies meeting the inclusion criteria identified a total of 24,324 subjects including 11,372 obese and 12,952 control subjects. The meta-analysis results showed a statistically significant association of K121Q with obesity [OR (95%CI): 1.25 (1.04-1.52) P=0.021] under a recessive model of inheritance (QQ vs. KK+KQ) without heterogeneity or publication bias.

CONCLUSIONSThe results from the present study have indicated that ENPP1/PC1 Q121 variant may increase the risk of obesity and that more well-designed studies based on a larger population will be required to further evaluate the role of ENPP1/PC1 gene K121Q polymorphism in obesity and other related metabolic syndromes.

Europe ; epidemiology ; Genetic Predisposition to Disease ; Humans ; Obesity ; epidemiology ; genetics ; Odds Ratio ; Phosphoric Diester Hydrolases ; genetics ; Polymorphism, Genetic ; Pyrophosphatases ; genetics ; Risk Factors