[Abstract ] Objective C reactive protein (CRP), an in-flammatory maker, increased significantly among diabetes mellitus and other metabolic diseases.Meanwhile, adiponectin plays a vital role in anti-atherogenic, anti-inflammatory and anti-diabetic poten-tials.Further, it decreased in diabetes mellitus.To investigate the effects of C-reactive protein in the expression of high-molecular-weight adiponectin ( HMWA) and adiponectin multimerization. Methods The fully differentiated 3T3-L1 cells were respectively treated with 50μg/mL CRP for 0 h、6 h、12 h and 24 h , and different doses of CRP with 0μg/mL、5μg/mL、25μg/mL、50μg/mL for 24 h.The expres-sion of HMWA was further detected by Western blot.Additionally,
the mRNA expressions of adiponectin assembly related genes ( Ero1-L、DsbA-L、ERp44 ) were detected by Real time PCR after 50μg/mL CRP treatment for 24 h. Results After 24 h treatment, 25μg/mL CRP and 50μg/mL CRP resulted in a substantial reduction ( [70 ±7]%vs [44 ±7]%, P<0.05) while 5μg/mL CRP revealed no change.With the dose of 50μg/mL CRP treated, the ex-pression of HWMA were both inhibited after the 12 h and 24 h CRP treatment ([71 ±6]%vs [48 ±11]%, P<0.05), but for the 6 h CRP treatment group, HWMA remained unchanged.Additionally, CRP inhibited Ero1-L(86 ±10)%and DsbA-L(72 ±6)%gene expression and upregulated the expression of ERp44(141 ±23)%. Conclusion CRP decreases HMWA expression in a dose and time-dependent manner and inhibits the multimerization of adiponectin, thus weaken the benefits of adiponectin in diabetes.

Objective There are few researches for the serum betatrophin level and diabetic nephropathy (DN) recently.The aim of this study was to investigate the change of serum betatrophin level and the correlation of serum betatrophin and urinary albumin-to-creatintine ratio (UACR) in patients with type 2 diabetes mellitus (T2DM).Methods A total of 150 Chinese subjects from Mar 2013 to Jul 2016 were enrolled in the study, including 90 patients with type 2 diabetes and 60 healthy controls.According to the level of UACR, the diabetic patients were divided into two groups:normal UACR group (UACR<30 mg/g, n=60) and abnormal UACR group(UACR>30 mg/g, n=30).Serum betatrophin was measured by enzyme linked immunosorbent assay (ELISA).UACR was measured by turbidimetric inhibition immune assay.Blood glucose blood lipid were measured simultaneously.Results The serum betatrophin level was significantly higher in abnormal UACR group than that in normal UACR group[677.37±59.02 vs 486.13±41.22 pg/mL, P<0.05];Serum betatrophin level in T2DM patients was positively correlated with age (r=0.246), waist hip ratio (WHR) (r=0.240), fasting blood glucose (FPG) (r=0.234), 2 hour plasma glucose (2hPG) (r=0.363), glycosylated hemoglobin (HbA1c) (r=0.346), fasting insulin (FINS) (r=0.249), insulin resistance index (HOMA-IR) (r=0.309), blood urea nitrogen (BUN) (r=0.223), creatinine (CREA) (r=0.277) and UACR (r=0.244) (P<0.05),and negatively correlated with glomerular filtration rate (GFR) (r=0.308) (P<0.01).Serum betatrophin level in normal UACR group was positively correlated with age, HbA1c and UACR (P<0.05);Serum betatrophin level in abnormal UACR group was positively correlated with WHR (r=0.504), 2hPG (r=0.600), HbA1c (r=0.449), HOMA-IR (r=0.395) (P<0.05).The WHR, HbA1c, HOMA-IR and GFR were the influential factors of the serum betatrophin level.Conclusion The level of serum betatrophin was significantly increased in T2DM patients with albuminuria, which suggests that the betatrophin might play an important role in the pathogenesis of DN.

Objective To detect serum oxytocin and highly sensitive C-reactive protein (hs-CRP) levels in obese and type 2 diabetes mellitus(T2DM) subjects and investigate the relationships between serum oxytocin levels and hs-CRP, glycolipid metabolism, insulin resistance and pancreas β cell function. Methods A total of 176 subjects were enrolled in the study, including 88 patients with newly-diagnosed type 2 diabetes ( T2DM) and 88 subjects with normal glucose tolerance(NGT). NGT and T2DM groups were further divided each into normal weight (NW) and obese(OB) subgroups. Obesity was defined as body mass index(BMI)≥25 kg/ m2 according to the WHO-Western Pacific Region diagnostic criteria (2000). 75g oral glucose tolerance test ( OGTT) was performed in all subjects. Fasting plasma glucose ( FPG), 2 h postprandial plasma glucose (2hPG), fasting insulin ( FINS), 2h postprandial serum insulin(2hINS), HbA1C and lipids were also determined. Insulin resistance and pancreas β-cell function were determined by homeostasis model assessment ( HOMA-IR, HOMA-β). Highly sensitive C-reactive protein(hs-CRP) level was determined by chemiluminescence immunoassay and fasting serum oxytocin level was determined by ELISA. Results Serum oxytocin level was lower in T2DM group than that in NGT group(P<0. 01), while serum hs-CRP level was higher in T2DM group than that in NGT group(P<0. 01). The level of serum oxytocin in subjects with obesity was also lower than that in subjects with NW in both NGT and T2DM groups [7. 16(6. 45-8. 82) vs 7. 98(7. 03-9. 17) ng/ L and 9. 23(8. 16-10. 36) vs 9. 86(8. 77-12. 06) ng/ L, P<0. 05]. The level of serum hs-CRP in subjects with obesity was higher than that in subjects with NW in both NGT and T2DM groups [0. 99(0. 25-1. 97) vs 0. 54(0. 19-0. 91) mg/ L and 3. 47(1. 63-6. 20) vs 1. 65(0. 81-3. 81) mg/ L, P<0. 05]. Serum oxytocin level was negatively correlated with hs-CRP, BMI, WC, WHR, HbA1C , FPG, 2hPG, FINS, 2hINS, total cholesterol, triglycerides, LDL-C and HOMA-IR, while was positively correlated with HOMA-β(P<0. 05). Subjects within the upper serum hs-CRP tertile had lower level of oxytocin when compared to subjects in the middle or lower serum hs-CRP tertiles(P<0. 05 ). Conclusion Serum oxytocin level was decreased in subjects with type 2 diabetes as well as with obesity. Serum oxytocin level was closely correlated with inflammation, glycolipid metabolism, insulin resistance, and pancreas β cell function. It may play an important role in the pathogenesis of obesity and T2DM.

ObjectiveTo evaluate the local failure and the impact on survival by prospectively comparing involved field radiotherapy (IFRT) and elective nodal irradiation (ENI) in combination with concurrent chemotherapy for locally advanced non-small cell lung cancer ( LA-NSCLC ).Methods LANSCLC patients were treated with 2 cycles of carboplatin ( AUC =5 - 6,d1 ) combined with paclitaxel ( 175mg/m2 ),followed assessment without distant metastasis,then randomized into IFRT (45 patients) or ENI (54 patients) arm.IFRT included primary tumor,ipsilateral hilar and positive mediastinal lymph nodes;ENI included the primary lesion,ipsilateral hilar,hilateral mediastinal lymph node drainage and bilateral supraclavicular area.The prescription dose was given as high as possible with V20 ≤35％ and spinal cord dose ≤50 Gy,combined weekly paclitaxel 40 mg/m2 concurrent chemotherapy.The Kaplan-Meier method was used to estimate survival data and the log-rank method was used to test distribution of survival time between arms.ResultsThe follow-up rate was 99％.49,29 and 17 patients were followed-up for 1-,2-and 3-year,respectively.More patients from group IFRT received ＞60 Gy than ENI (49％ vs.26％,x2 =5.59,P =0.018 ).The local failure rates were 29％ and 36％,respectively ( x2 =0.46,P =0.497 ).The 1-,2-and 3-year local tumor progression-free survival rates were 76％,69％,65％ and 80％,53％,49％ ( x2 =0.74,P =0.389),respectively; the 1-,3-and 5-year overall survival rates were 80％,41％,33％ and 69％,32％,13％ (x2 =3.97,P =0.046),respectively.There were no significant differences in acute and late toxicities between the arms ( x2 =3.910 - 0.155,P =0.142 - 0.925 ).ConclusionsIFRT improved radiation dose and survival rate and did not increase the failure of elective lymph node region compared with ENI.The toxicities were no differences between IFRT and ENL Further investigation with big size sample is warranted.

Objective: To explore the mechanisms of vascular endothelial growth factor receptor 2 (VEGFR2) expression regulated by recombinant human erythropoietin (rh-EPO) in a premature rat model of periventricular white matter damage. Methods: Sprague-Dawley rats aged three days were randomly divided into five groups: sham group without hypoxia-ischemia (HI), HI group (HI with saline administration), HI+erythropoietin (EPO) group, HI+erythropoietin receptor (EPOR) antagonist group and HI+EPO+EPOR antagonist group. Rat pups were either subjected to permanent ligation of the right common carotid artery and 6% O₂+94% N₂ for two hours (HI) or sham operated and exposed to normal air (sham). After the operation, rats in the HI+EPOR antagonist and HI+EPO+EPOR antagonist groups received a single intraventricular injection of EPOR antagonist (5 μl). Four hours after the operation, rats in the HI+EPO and HI+EPO+EPOR antagonist groups received a single intraperitoneal injection of rh-EPO (5 U/g). Western-blot was performed to detect EPOR, phosphorylated EPOR (p-EPOR), extracellular regulated protein kinases (ERK) and phosphorylated ERK (p-ERK) at 60 and 90 minutes after the models were established successfully, and also used to analyze the expression of VECFR2 on day 2 and 4. Analysis of variance and SNK test were used as statistical methods. Results: At 60 and 90 minutes after model establishment, the expression of EPOR protein in rat brain tissues was increased in HI (1.717±0.206 and 1.416±0.242), HI+EPO (2.557±0.222 and 2.111±0.159) and HI+EPO+EPOR antagonist (1.547±0.170 and 1.452±0.250) groups as compared with that in sham group (1.095±0.182 and 0.751±0.136), that in HI+EPO group was higher than that in HI and HI+EPO+EPOR antagonist groups, and that in HI+EPOR antagonist group (1.088±0.160 and 1.020±0.174) was lower than that in HI group. All differences were statistically significant (F=30.154 and 20.265, both P<0.05). The expressions of p-EPOR, p-ERK and VEGFR2 in the five groups were consistent with the expression of EPOR, and the differences were also statistically significant (all P<0.05). In addition, the expression of VEGFR2 in HI+EPO+EPOR antagonist group was lower than that in HI group on day 4 (1.053±0.118 vs 1.439±0.074, F=54.248, P<0.05). No statistically significant difference in ERK expression was found among all groups at 60 or 90 minutes after modeling (F=1.117 and 0.734, both P>0.05). Conclusions ERK signaling pathways will be affected by EPO binding to EPOR. As a result, VEGFR2 expression was increased leading to enhanced angiogenesis in a premature rat model of periventricular white matter damage.