Effects of 1.8mm coaxial micro incision phacoemulsification on corneal endothelial injury and postoperative visual acuity / 国际眼科杂志(Guoji Yanke Zazhi)

AIM:To investigate the effects of 1.8mm coaxial micro incision phacoemulsification on corneal endothelial injury and postoperative visual acuity.METHODS: Totally 145 eyes in 120 patients underwent phacoemulsification from July 2013 to July 2015 were randomly divided into observation group 60 cases (73 eyes) and control group 60 cases (72 eyes).The observation group 60 cases were given 1.8mm coaxial micro incision cataract phacoemulsification operation,while the control group were given traditional 3.2mm coaxial micro incision cataract surgery.The uncorrected visual acuity (UCVA),best corrected visual acuity (BCVA),corneal thickness of incision area,incision width,incision length,macular retinal thickness,surgically induced astigmatism,corneal endothelial cell counts and complications of the two groups were compared.RESULTS: The UCVA and BCVA on 1wk after surgery of the observation group were significantly higher than the control group (t=3.604,7.109;P0.05).CONCLUSION: The 1.8mm micro incision phacoemulsification is helpful to improve the visual acuity of patients with cataract phacoemulsification,which may be related to the reduction of corneal cell injury,enhancement of corneal closure and decrease post-operation corneal original astigmatism.

CXCL12 G801A polymorphism and cancer risk: An updated meta-analysis / 华中科技大学学报（医学）（英德文版）

Many studies have reported the relationship between CXCL12 G801A polymorphism and cancer risk, with conflicting results. In this study, we tried to clarify the possibility that this polymorphism may increase cancer risk by conducting an updated meta-analysis. PubMed and EMbase were searched for case-control studies regarding the association of the gene polymorphism and cancer risk. Data were extracted and odds ratios (ORs) with 95% confidence intervals (95% CIs) were used to assess the strength of the association. Heterogeneity among articles and publication bias was also assessed. Significantly increased risk for cancer was found (A vs. G: OR=1.26, 95% CI=1.13-1.40, P<0.01; AA+AG vs. GG: OR=1.33, 95% CI=1.16-1.52, P<0.01). In subgroup analysis, statistically elevated cancer risk was found in both Asian and Caucasian populations (for Asian, AA+AG vs. GG: OR=1.74, 95% CI=1.22-2.47, P<0.01; for Caucasian, AA+AG vs. GG: OR=1.24, 95% CI=1.09-1.42, P<0.01). Our result indicated that CXCL12 G801A polymorphism is a risk factor for cancer. To validate the finding, further large-size case-control studies are warranted.

CXCL12 G801A polymorphism and cancer risk: An updated meta-analysis / 华中科技大学学报（医学）（英德文版）

Many studies have reported the relationship between CXCL12 G801A polymorphism and cancer risk, with conflicting results. In this study, we tried to clarify the possibility that this polymorphism may increase cancer risk by conducting an updated meta-analysis. PubMed and EMbase were searched for case-control studies regarding the association of the gene polymorphism and cancer risk. Data were extracted and odds ratios (ORs) with 95% confidence intervals (95% CIs) were used to assess the strength of the association. Heterogeneity among articles and publication bias was also assessed. Significantly increased risk for cancer was found (A vs. G: OR=1.26, 95% CI=1.13-1.40, P<0.01; AA+AG vs. GG: OR=1.33, 95% CI=1.16-1.52, P<0.01). In subgroup analysis, statistically elevated cancer risk was found in both Asian and Caucasian populations (for Asian, AA+AG vs. GG: OR=1.74, 95% CI=1.22-2.47, P<0.01; for Caucasian, AA+AG vs. GG: OR=1.24, 95% CI=1.09-1.42, P<0.01). Our result indicated that CXCL12 G801A polymorphism is a risk factor for cancer. To validate the finding, further large-size case-control studies are warranted.

Contribution of protein kinase C to passively sensitized human airway smooth muscle cells proliferation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Airway smooth muscle proliferation plays an important role in airway remodeling in asthma. But little is known about the intracellular signal pathway in the airway smooth muscle cell proliferation in asthma. The objective of this paper is to investigate the contribution of protein kinase C (PKC) and its alpha isoform to passively sensitized human airway smooth muscle cells (HASMCs) proliferation.</p><p><b>METHODS</b>HASMCs in culture were passively sensitized with 10% serum from asthmatic patients, with non-asthmatic human serum treated HASMCs used as the control. The proliferation of HASMCs was examined by cell cycle analysis, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazoliumbromide (MTT) colorimetric assay and proliferating cell nuclear antigen (PCNA) immunofluorescence staining. The effect of PKC agonist phorbol 12-myristate 13-acetate (PMA) and PKC inhibitor Ro-31-8220 on the proliferation of HASMCs exposed to human asthmatic serum and non-asthmatic control serum was also examined by the same methods. The protein and mRNA expression of PKC-alpha in passively sensitized HASMCs were detected by immunofluorescence staining and reverse transcription-polymerase chain reaction.</p><p><b>RESULTS</b>The percentage of S phase, absorbance (value A) and the positive percentage of PCNA protein expression in HASMCs passively sensitized with asthmatic serum were (16.30 +/- 2.68)%, 0.430 +/- 0.060 and (63.4 +/- 7.4)% respectively, which were significantly increased compared with HASMCs treated with control serum [(10.01 +/- 1.38)%, 0.328 +/- 0.034 and (37.2 +/- 4.8)%, respectively] (P < 0.05). After HASMCs were passively sensitized with asthmatic serum, they were treated with PMA, the percentage of S phase, value A and the positive percentage of PCNA protein expression were (20.33 +/- 3.39)%, 0.542 +/- 0.065 and (76.0 +/- 8.7)% respectively, which were significantly increased compared with asthmatic serum sensitized HASMCs without PMA(P < 0.05). After HASMCs passively sensitized with asthmatic serum were treated with Ro-31-8220, the percentage of S phase, value A and the positive percentage of PCNA protein expression were (11.21 +/- 1.56)%, 0.331 +/- 0.047 and (38.8 +/- 6.0)% respectively, which were significantly decreased compared with asthmatic serum sensitized HASMCs without Ro-31-8220 (P < 0.05). The relative ratio of value A of PKC-alpha mRNA and the positive percentage of PKC-alpha protein expression in passively sensitized HASMCs were 1.23 +/- 0.10 and (61.1 +/- 9.4)% respectively, which were significantly increased compared with HASMCs treated with control serum [1.05 +/- 0.09 and (34.9 +/- 6.7)%, respectively] (P < 0.05).</p><p><b>CONCLUSIONS</b>The proliferation of HASMCs passively sensitized with human asthmatic serum is increased. PKC and its alpha isoform may contribute to this proliferation.</p>

The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the effect of the metabolite of leflunomide, A771726,on proliferation and collagen synthesis of hepatic stellate cell (HSC).</p><p><b>METHODS</b>HSC and Kupffer cells were isolated from the rat liver by collagenase IV and pronase perfusion, and purified by density gradient separation. The effects of A771726 on cell proliferation and collagen synthesis were examined by 3H-thymidine and 3H-proline incorporation assays, respectively. The TGF-beta, TNF-alpha and IL-1 levels in Kupffer cell conditioned medium (KCCM) were determined by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>HSC and Kupffer cells in rat liver were well separated. The KCCM of CCl4-injured rats had significant stimulation effect on proliferation and collagen synthesis of HSC in primary culture. Addition of A771726 (0.001-10 micromol/Lein HSC culture stimulated by KCCM significantly inhibited proliferation and collagen synthesis of HSC. Furthermore, the elevated TGF-beta, TNF-alpha and IL-1 levels in KCCM of CCl4-injured rats were significantly reduced in A771726 treatment groups.</p><p><b>CONCLUSION</b>A771726 has markedly inhibitory effect on proliferation and collagen synthesis of HSC and secretion of TGF-beta,TNF-alpha and IL-1 from Kupffer cells.</p>

Effect of melatonin on the expression of nuclear factor-kappa B and airway inflammation in asthmatic rats / 中华儿科杂志

<p><b>OBJECTIVE</b>Nuclear factor-kappa B (NF-kappaB) is a critical transcription factor governing the expression of many cytokines that are involved in the pathogenesis of inflammatory diseases, such as asthma and rheumatoid arthritis. Melatonin (MT), a relatively safe and potent antioxidant which has shown efficacy in several chronic inflammatory models, may inhibit the expression of NF-kappaB and therefore might have a therapeutic use in asthma. This study aimed at observing the effect of MT on the expression of NF-kappaB and airway inflammation in a rat model of bronchial asthma.</p><p><b>METHODS</b>Twenty-four male Sprague-Dawley (SD) rats weighing 120 g to 170 g were randomly divided into three experimental groups (8 in each): (1) Asthmatic group: Rats were immunized on day 1 by intraperitoneal injection of 100 mg ovalbumin (OVA) in 1 ml of saline with 100 mg of alu minum hydroxide. From day 15 the animals were challenged with aerosolized OVA (1% in saline) for 20 minutes per day for 7 consecutive days. (2) MT group: OVA-sensitized rats were injected intraperitoneally with 10 mg/kg MT 30 minutes before each OVA challenge. (3) CONTROL GROUP: OVA for inhalation and MT for intraperitoneal injection was replaced with normal saline (NS). Airway responsiveness to aerosolized acetylcholine of 24 rats was detected six hours after the last challenge. Then the rats were lavaged and total and differentiated leukocytes counts in bronchoalveolar lavage fluid (BALF) were performed after staining with Wright-Giemsa staining. At the same time, levels of nitric oxide (NO) in BALF, inducible nitric oxide synthesis (iNOS) and constitute nitric oxide synthesis (cNOS) in the lung tissues were assessed with the use of nitrate reductase and chemical colorimetry, respectively. The expression of NF-kappaB in the lung tissues was observed by means of immunohistochemical staining.</p><p><b>RESULTS</b>(1) After OVA challenge, there was a significant decrease in airway responsiveness, lymphocytes and eosinophils in BALF in MT group compared with asthmatic group (P < 0.01 respectively); (2) There was a significant decrease in amounts of NO(2)(-)/NO(3)(-) in the BALF and levels of iNOS in the lung tissues in MT group comparing with asthmatic group (P < 0.01 respectively); and the levels of iNOS in the lung tissues was correlated positively with NO(2)(-)/NO(3)(-) in the BALF (P < 0.01), but there were no significant differences in activity of cNOS in any of the groups analyzed. (3) There was a significant increase in expression of NF-kappaB in lung tissues in asthmatic group compared with the other groups (P < 0.01), and so was in MT group compared with control group (P < 0.05).</p><p><b>CONCLUSIONS</b>MT could partially inhibit the expression of NF-kappaB and down-regulate the activity of iNOS in lung tissue, decrease the production of NO in BALF. These data suggest that the inhibitory effect of MT probably play a role in decreasing airway hyperresponsiveness and airway inflammation of asthmatic rats model.</p>

Inhibitory effect of 5-fluorouracil encapsulated by galactosylceramide liposomes on drug resistance and its mechanisms / 中国药理学通报

Aim To study inhibitory effect of 5-fluorouracil encapsulated by galactosylceramide liposomes (5-Fu-GCL)on 5-Fu-resistent HepG_2 cells and its mechanisms. Methods Inhibitory effect of 5-Fu-GCL on established model of 5-Fu-resistant HepG_2 cells was assessed with MTT assay in vitro. The concentration-time course of 5-Fu-GCL in intracellular fluid was detected with high performance liquid chromatography (HPLC). Thymidylic acid synthase (TS) expression was observed with immunohistochemical method,and NO content was determined with chemical method. Results Obvious inhibitory effects of 5-Fu-GCL (75,150,300,600,1200?mol?L-1) on 5-Fu-resistant HepG_2 cells were observed with IC_ 50 of 158.6 ?mol?L-1,far lower than that of free 5-Fu (400.9 ?mol?L-1). 5-Fu-GCL (300 ?mol?L-1) inhibited 5-Fu-resistant HepG_2 cells in a time-dependent manner,and the inhibitory effect of 5-Fu-GCL was stronger than that of free 5-Fu during 12～48 h. Compared with free 5-Fu,5-Fu-GCL (300 ?mol?L-1) increased the content of intracellular fluid in 5-Fu-resistant HepG_2 cells. 5-Fu-GCL(62.5,300,1200 ?mol?L-1) not only inhibited the expression of TS,but also increased the production of NO in 5-Fu-resistant HepG_2 cells,and these effects of 5-Fu-GCL(300,1200 ?mol?L-1) were stronger than those of free 5-Fu. Conclusion 5-Fu-GCL has inhibitory effect on 5-Fu-resistant HepG_2 cells. The effect may be related to the increased concentration of 5-Fu-GCL in intracellular fluid,inhibited expression of TS and increased production of NO.