Objective To investigate altered levels and clinical significance of serum miR-133a in patients with acute coronary syndrome ( ACS ) and stable coronary artery disease ( SCAD ) .Methods Retrospective study.Serum miR-133a levels were determined by TaqMan quantitative reverse-transcription PCR assay in 64 ACS, 62 SCAD patients who were admitted to Jinling Hospital from October 2011 to October 2012 and 70 normal controls who had contemporaneously visited Jinling Hospital for routine examination .The ACS and SCAD patients were diagnosed according to the European Society of Cardiology guidelines .Serum lipid/lipoprotein profiles , myonecrosis biomarkers and Gensini scores were also analyzed .The area under curve ( AUC) and 95%confidence interval ( CI) were calculated using ROC analyses .The odds ratio ( OR) and 95%CI were calculated using the multivariate logistic regression analyses .Results Compared with the controls [ΔCt:1.00 ±0.05], serum miR-133a levels were significantly increased in both ACS [ΔCt:2.34 ±0.24] (t=6.059, P<0.001) and SCAD [ΔCt:1.45 ±0.13] (t=3.265, P=0.001) patients.The miR-133a levels in ACS patients were significantly higher than in SCAD patients (t=3.133, P=0.002). Serum miR-133a were positively correlated with levels of creatine kinase MB ( CK-MB) ( r=0.402, P<0.001), cardiac troponin I (cTNI) (r=0.410, P=0.001) and Gensini scores (r=0.438, P<0.001). ROC curve analyses showed that the AUC of miR-133a for differentiating coronary artery disease (CAD) and controls was 0.717 (95%CI:0.645-0.788, P<0.001) and the AUC for differentiating ACS and SCAD was 0.667 (95% CI:0.573-0.761, P=0.001).Logistic regression analyses revealed that high miR-133a levels were closely associated with the presence of ACS ( OR=6.00, 95% CI:1.93 -18.67, P=0.002) and SCAD (OR=2.81, 95%CI:1.03-7.68, P=0.044), and also had statistical significance for differentiating ACS and SCAD (OR=2.13, 95% CI:1.20-3.78, P=0.010), after adjustment for the age, gender and serum lipid/lipoprotein levels.Conclusions Serum miR-133a levels were significantly elevated in CAD patients, and ACS patients exhibited the more significant increase .Serum miR-133a may be function as the potential biomarker for the disease assessment and judgement .

[Objective] To explore the mechanism of fever in damp- heat syndrome. [Methods] Hyperlipemia rabbit models were established by feeding fatty - sweet diet. After the injection of endotoxin, the secretion of tumor necrosis factor and interleukin 1 was observed in rabbit model (Group A) and compared with normal rabbits (Group B) . [ Results] The peak of tumor necrosis factor and interleukin 1 secretion was decreased and the decline was slow in Group A. [ Conclusion ] The damp - heat syndrome in seasonal febrile disease is not merely a simple addition of damp and heat, but a result of retention and interaction of the two factors.

Objective To investigate the effect of human epidermal growth factor receptor-2 (HER2) silenced by lentivirus-mediated RNA interference (RNAi) on the growth of SKOV-3 ovarian cancer,and to explore the value of radioimmunoimaging in monitoring the biotherapy of RNAi.Methods The ovarian cancer cell line SKOV-3 was infected with lentivirus-mediated HER2-short hairpin (sh) RNA expression vector and scrambled control lentivirus vector,respectively.Both infected cells were inoculated into nude mice to establish two ovarian cancer xenograft models:knock down 1 (KD1) group and normal control (NC) group.The uninfected SKOV-3 xenograft model served as blank control (CON) group.The tumor formation rate,tumor generation time and tumor size at different time points were measured.The expression of HER2 protein was measured by immunohistochemistry.1n Ⅰ-Herceptin was injected before radioimmunoimaging,and the T/B ratios were acquired.One-way analysis of variance and the least significant difference (LSD)-t test were performed with SPSS 17.0.Results All mice models were constructed successfully (100％,15/15).The average time of tumor generation was (4.583±0.520) d,(4.567±0.284) d and (6.023±0.316) d in CON,NC and KD1 groups,respectively(F=13.946,P＜0.01).The tumor formation time of KD1 group was significantly longer than the other two groups (t=4.557,4.608,both P＜0.01),respectively.On the 28th day after the tumor cell implantation,the tumor size was significantly different among the three groups (F=26.343,P＜0.01).The tumor mass was (0.614±0.135) g,(0.558±0.190) g and (0.120±0.489) g in CON,NC and KD1 groups,respectively (F=225.026,P＜0.01).Both the tumor size (t=7.125,4.759) and tumor mass (t=19.158,16.977) of KD1 group were significantly less than those of CON and NC groups (all P＜0.01),respectively.Immunohistochemical results showed that the HER2 protein expression was inhibited in the KD1 group.The tumor could be visualized clearly on radioimmunoimaging at different time points.The T/B ratio of the KD1 group (0.208-4.427) was significantly lower than those of the other two groups at any intervals (0.576-5.508,0.640-5.695; F=9.197-39.375,all P＜0.05).Conclusions The growth of SKOV-3 could be inhibited remarkably by lentivirus-mediated HER2-siRNA.Radioimmunoimaging with 1nI-Herceptin might positively correlate with the expression of HER2 protein,which might have potential for monitoring the biotherapy of RNAi targeting HER2.

Progesterone has nongenomic effects on inducible nitric oxide synthase (iNOS), which is mediated by mitogen activated protein kinase (MAPK) pathways. This effect is supposed to have some potential association with asymptomatic gonococcal infections in women by immunological depression. In this study, polymorphonuclear leukocytes (PMNs) challenged by gonococci were used to study the nongenomic effects of progesterone. The activation of iNOS was assessed by measuring [(3)H] L-arginine converses to [(3)H] L-citrulline, and the activity of MAPK was detected by Western blot. It was found that the activity of iNOS and the yields of NO were enhanced significantly in gonococci-challenged PMNs compared with the controls (P<0.01). Progesterone could repress the activation of iNOS through P38MAPK pathway within PMNs (P<0.05), which could be blocked by SB203580 (P<0.01), but not by actinomycin D (P>0.05). It was also found subsequently that in the serum specimens collected from gonococci-infected but asymptomatic women, the progesterone level was higher than that in women with severe symptoms (P<0.01). Moreover, the yield of NO had an inverse correlation with progesterone. With these results it suggested that the rapid nongenomic effects of progesterone may inhibit iNOS activation and NO yields mediated by P38MAPK pathways, which were supposed to be concerned with asymptomatic women infected with gonococci.

Objective To investigate the relationship between serum levels of homocysteine (HCy) and adiponectin (APN) in patients with type 2 diabetes mellitus(T2DM).Methods 65 patients with T2DM (diabetes mellitus group) and 25 healthy controls (control group) matched in the age and sex were recruited in the study.Serum HCy,APN,fasting plasma glucose (FPG),fasting insulin (FINS),total cholesterol (TC) and triglyceride (TG) were simultaneously measured.The homeostatic model assessment for insulin resistance(HOMA-IR) was calculated according to FPG and FINS.All the serum indicators were compared between the two groups.Results Serum level of HCy in T2DM group was (15.74 ± 2.76) μmol/L,which was significantly higher than (6.98 ± 1.94) μmol/L in the healthy control group (t =16.88,P ＜ 0.01).The serum level of APN in T2DM group was (8.14 ± 2.70) mg/L,which was significantly lower than (16.10 ± 1.93)mg/L in the healthy control group (t =13.44,P ＜ 0.01).Serum levels of FPG,HOMA-IR,TC,TG in T2DM group were significantly higher than those in the healthy control group (t =10.62,17.49,6.30,7.52,P ＜ 0.05).Serum level of APN in HCy ≥ 15μmol/L group was significantly decreased compared with HCy ＜ 15μmol/L group.Serum level of HCy was negatively correlated with APN in T2DM group after the influence of FPG,HOMA-IR,TG,TC were corrected in the partial correlation analysis.Conclusion In T2DM group,serum level of HCy was increased,but serum level of APN was decreased,serum HCy was negatively correlated with APN,higher serum level of HCy and lower serum level of APN are related with the process of insulin resistance and T2DM.

Objective To evaluate the distribution and significance of IgG subclasses of anti-cyclic cirullinated peptide antibody (anti-CCP) in sera from patients with rheumatoid arthritis (RA).Methods A total of 83 patients with RA at the Department of Endocrinology of Taizhou Hospital , 51 disease controls and 50 healthy controls during the period from August 2012 to June 2013 were enrolled.The total serum IgG and IgG subclasses of anti-CCP antibodies were detected by antigen specific enzyme linked immune-sorbent assay( ELISA ).The prevalence and relative amount of IgG subclasses were calculated and compared.Statistical analysis was performed by χ2 test and Kruskal-Wallis H test.Results The positive rates of IgG subclasses of anti-CCP were anti-IgG 71.1%(59/83), anti-IgG1 78.3%(65/83), anti-IgG2 26.5%(22/83), anti-IgG3 60.2%(50/83), anti-IgG4 74.7%(62/83) respectively.The diagnostic value of anti-CCP-IgG1, anti-CCP-IgG3 and anti-CCP-IgG4 alone or combined (AUC =0.818-0.901),compared with anti-CCP-IgG(AUC=0.857), had no significant difference(Z=0.028-0.045,P>0.05).The DAS28 score of anti-CCP-IgG1(DAS28 =6.5), and anti-CCP-IgG4(DAS28 =6.5)positive in patients with RA were significantly higher than those in negative groups (DAS28=4.5,4.6)(U=396.0,427.5,P<0.01).The T28(T28=4.0,4.0)and SW28(SW28=4.0,4.0) results of CCP-IgG1and CCP-IgG4 positive in patients with RA were significantly higher than those in negative groups (T28=3.0,3.0,SW28 =3.0,3.0)(U=377.5,406.0,255.5,286.5,P<0.05).Conclusions The distribution of IgG subclasses of anti-CCP in sera from patients with RA was predominantly anti-CCP-IgG1, anti-CCP-IgG3 and anti-CCP-IgG4 associated with RA disease activity.However , whether joint detection of IgG subclasses can replace conventional anti -CCP is questionable.

Objective To observe the changes of serum ferritin and 25-(OH) vitamin D3 in patients with diabetic cranial neuropathy.Methods There were 50 patients without diabetic Cranial neuropathy,46 patients with diabetic cranial neuropathy,and 40 cases of normal control group.The changes of serum ferritin and 25-hydroxy vitamin D3 were observed in each group.The correlation between two indexes and the correlation with diabetic cranial neuropathy were analzyzed.Results The serum ferritin levels in diabetic group and diabetic neuropathy group were significantly higher than those in normal control group (P ＜ 0.01),and its level in patients with diabetic cranial neuropathy [(687.54 ± 65.38)ng/ml] was significantly higher than that of patients without diabetic cranial neuropathy [(497.28 ± 46.39) ng/ml,P ＜0.01].The serum 25-(OH) vitamin D3 levels in the diabetic group and diabetic neuropathy group were lower than those in the control group (P ＜ 0.01),and its level in patients with diabetic cranial neuropathy [(26.45 ± 8.93)nmol/l] was significantly less than that of patients without diabetic cranial neuropathy [(37.19-± 9.74)nmol/L,P ＜ 0.01].Serum ferritin levels were positively correlated with 25-(OH) vitamin D3 (r =-0.59,P ＜ 0.01).Multivariate unconditional Logistic regression analysis showed that diabetic neuropathy was negatively correlated with 25-(OH) vitamin D3 (P ＜ 0.05).Conclusions The increases of serum ferritin and 25-(OH) vitamin D3 are closely related to the occurrence and development of diabetic cranial neuropathy,which provides the theoretical basis for clinical intervention therapy.

The cDNA of Insulin-like growth factor binding protein 3 was subcloned into a eukaryotic secretory expression vector pSectagA to construct pSectag-IGFBP3. Human renal cell carcinoma (RCC) 786-0 cells were transfected with pSectag-IGFBP3 using lipofectamine 2000. After 48 h, the secretory IGFBP-3 was tested and identified by western blotting. Meanwhile, Annexin V-EGFP stain was used to analyze the apoptosis of 786-0 cells induced by IGFBP-3. Secretory IGFBP-3 protein could express successfully in the 786-0 cells and the expressed IGFBP-3 directly displayed an apoptotic effect on the host cells. This work provides a basis for further study on the apoptosis-inducing mechanism of IGFBP-3 and the development of a new anti-tumor drug.
Apoptosis ; drug effects ; Base Sequence ; Carcinoma, Renal Cell ; metabolism ; pathology ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; genetics ; secretion ; Kidney Neoplasms ; metabolism ; pathology ; Molecular Sequence Data ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; physiology ; Transfection ; Tumor Cells, Cultured

Objective:To compare the effects of laparoscopic and surgical catheterization on catheter-related complications and microinflammation in uremic peritoneal dialysis (PD) patients.Methods:According to different catheterization methods, 98 uremic patients who were scheduled to undergo peritoneal dialysis in the First People's Hospital of Jiande from January 2014 to March 2019 were divided into group A (38 cases), group B (60 cases). Laparoscopic catheterization was used in group A, and incision catheterization was used in group B. Surgical parameters, catheter complications, microinflammation and survival rate of early catheterization were observed in the two groups.Results:The operation time of group A was (35.00±3.14)min, which was shorter than that of group B [(50.00±5.17)min], and the operation cost of group A was (5 800.0±318.9)CNY, which was higher than that of group B [(3 400.0±297.4)CNY], and the visual analogue score (VAS) of group A was (2.33±0.31)points, which was lower than that of group B [(3.25±0.49)points], there were statistically significant differences between the two groups ( t=11.540, 9.317, 10.328, 36.578, all P<0.05). The incidence of catheter-related complications in group A was 10.53%(4/38), which was significantly lower than 28.33%(17/60) in group B (χ 2=4.383, P<0.05). There were no statistically significant differences in high-sensitivity C-reactive protein (hs-CRP), interleukin-6(IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels between group A and group B before catheterization (all P>0.05). After catheterization, the levels of hs-CRP, IL-6 and TNF-alpha in group B were (12.52±3.75)mg/L, (12.02±3.76)ng/L, (15.92±5.72)ng/L, respectively, which were higher than those in group A [(9.63±2.36)mg/L, (9.11±3.54)ng/L, (13.41±5.61)ng/L] ( t=4.244, 4.081, 4.510, all P<0.05). After 2 months of follow-up, the survival rate of dialysis tube technique was 89.47%(34/38) in group A and 71.67%(43/60) in group B, there was statistically significant difference between the two groups (χ 2=4.382, P<0.05). Conclusion:Application of laparoscopic catheterization in uremic PD patients has satisfactory effect, light pain, fewer complications, mild inflammation and high survival rate of early catheterization technology, which is worthy of clinical promotion.

Pentraxin 3 (PTX3) was identified as a marker of the inflammatory response and overexpressed in various tissues and cells related to cardiovascular disease. Honokiol, an active component isolated from the Chinese medicinal herb Magnolia officinalis, was shown to have a variety of pharmacological activities. In the present study, we aimed to investigate the effects of honokiol on palmitic acid (PA)-induced dysfunction of human umbilical vein endothelial cells (HUVECs) and to elucidate potential regulatory mechanisms in this atherosclerotic cell model. Our results showed that PA significantly accelerated the expression of PTX3 in HUVECs through the IkappaB kinase (IKK)/IkappaB/nuclear factor-kappaB (NF-kappaB) pathway, reduced cell viability, induced cell apoptosis and triggered the inflammatory response. Knockdown of PTX3 supported cell growth and prevented apoptosis by blocking PA-inducted nitric oxide (NO) overproduction. Honokiol significantly suppressed the overexpression of PTX3 in PA-inducted HUVECs by inhibiting IkappaB phosphorylation and the expression of two NF-kappaB subunits (p50 and p65) in the IKK/IkappaB/NF-kappaB signaling pathway. Furthermore, honokiol reduced endothelial cell injury and apoptosis by regulating the expression of inducible NO synthase and endothelial NO synthase, as well as the generation of NO. Honokiol showed an anti-inflammatory effect in PA-inducted HUVECs by significantly inhibiting the generation of interleukin-6 (IL-6), IL-8 and monocyte chemoattractant protein-1. In summary, honokiol repaired endothelial dysfunction by suppressing PTX3 overexpression in an atherosclerotic cell model. PTX3 may be a potential therapeutic target for atherosclerosis.
Apoptosis/drug effects ; Atherosclerosis/chemically induced/*drug therapy/immunology/pathology ; Biphenyl Compounds/chemistry/isolation & purification/*pharmacology ; C-Reactive Protein/*genetics/immunology ; Down-Regulation/drug effects ; Drugs, Chinese Herbal/chemistry/isolation & purification/*pharmacology ; Human Umbilical Vein Endothelial Cells ; Humans ; I-kappa B Kinase/*immunology ; Lignans/chemistry/isolation & purification/*pharmacology ; Magnolia/chemistry ; Palmitic Acid ; Protein-Serine-Threonine Kinases/*immunology ; Serum Amyloid P-Component/*genetics/immunology ; Signal Transduction/drug effects