Intensive blood pressure control reduces macrovascular and microvascular complications in diabetic patients.A goal blood pressure of

A total of 473 patients of diabetic nephropathy (DN) with normal serum creatinine were recruited.Blood routine,blood lipids and urine albumin/creatinine ratio (UACR) were measured.They were divided into microalbuminuria group (DN1,n =246 ) and macroalbuminuria group (DN2,n =227 ).The white blood cell (WBC) count,monocyte count and CRP significantly increased with the progression of DN in the DN2 group versus those in the DNI group [ (6.8 ± 1.7 ) × 109/L vs.(6.3 ± 1.5 ) × 109/L,(0.49±0.23) ×109/Lvs.(0.32 ±0.21) ×109/L,(4.1 ±1.1)mg/Lvs.(1.7±0.3) mg/L,all P＜ 0.05].According to multiple linear regression analysis,WBC,monocyte,low density lipoproteincholesterol and lymphocyte were found to be independent influencing factors for the elevation of UACR.

Objective To investigate the specific silencing of connective tissue growth factor (CTGF) in a nude mouse keloid model,using RNA interference (RNAi) technique,and to provide the basis for gene therapy of keloid.Methods The nude mouse keloid model was established,and then transfected in vivo with well-amplifiating plasmid.The mRNA expression levels of CTGF mRNA and type Ⅰ collagen mRNA were detected with reverse transcription-polymerase chain reaction (RT-PCR).The distribution and protein expression levels of CTGF and type Ⅰ collagen were determined quantitatively using immunohistochemistry.Results The expression of CTGF at mRNA and protein levels was decreased in the experiment group,and the expression of type Ⅰ collagen at mRNA and protein levels was also decreased after transfection,as compared with negative control group and blank group,with significant difference between groups (P＜0.05).Moreover,the expression of type Ⅰ collagen and CTGF was positively correlated (r=0.979).Conclusions Keloid type Ⅰ collagen can be decreased through in vivo inhibiting CTGF expression.The transfection of CTGF gene in vivo may have effects on type Ⅰ collagen generation,and thus inhibit the keloid growth.

Objective To evaluate the efficacy and safety of short-term sensor-augmented insulin-pump (SAP) therapy for poorly controlled patients with type 1 diabetes mellitus (T1DM).Methods Sixty T1DM patients with glycosylated hemoglobin (HbA1c)>9.0% were randomly assigned to 2 groups treated with SAP or multiple daily insulin injection ( MDI) for 6 days, then all patients converted to MDI therapy. Results Compared with MDI group and before therapy, the mean blood glucose concentration ( MBG) , SD of blood glucose, mean amplitude of glycemic excursion ( MAGE) and 24-h area under curve at 10.0 ( AUC10.0 ) levels in SAP group significantly decreased after 6-day therapy ( compared with MDI group:t=1.761,P=0.028, t=2.569,P=0.037, t=2.712,P=0.020, t=2.985,P=0.014, compared with before therapy:t=3.128,P=0.006, t=2.689,P=0.024, t=2.966,P=0.013, t=3.076,P=0.009);while there was no difference in 24-h area under curve at 3.9 (AUC3.9) between groups (P>0.05).After 1 month follow-up HbA1c levels decreased in SAP group (t=2.344,P=0.023) and were significantly lower than those in MDI group (t=1.844, P=0.035).There was no difference in daily insulin dosage, fasting C peptide (FCP) and postprandial 2h C peptide (2hCP) between two groups (P>0.05).Age (t=2.125, P=0.012) and SAP therapy (t=3.376, P=0.009) were independently correlated with the HbA1c after 1 month.Conclusion Short-term SAP therapy is effective and safe for poorly controlled T1DM patients with rapid glucose lowering and glycemic excursions reduction.

Objective To compare the accuracy of the original-mirror alignment algorithm and a landmark-indepen-dent method in constructing the midsagittal plane(MSP)of the cone beam computed tomography in patients with facial deformities,so as to provide a theoretical basis for symmetric analysis.Methods The study was approved by the hospi-tal ethics committee.Cone beam computed tomography data of 30 patients with facial deformities were obtained,and the output was saved in DICOM format.The scan data were imported into Mimics 21.0;after segmentation,three-dimension-al(3D)skull models were reconstructed.Furthermore,the 3D scan data of skulls were transformed into mirror skull models using Geomagic Studio 2014 reverse engineering software.The MSP of each skull was generated using both the original-mirror alignment algorithm and the landmark-independent method.Original-mirror alignment algorithm:the original skull model and its mirror model were combined,and the new data to calculate the MSP(S1)of the original data in Geomagic Studio 2014 were obtained.Landmark-independent method:the following anatomical landmarks were deter-mined using Mimics 21.0:nasion(N),crista galli(CG),sella(S),basion(Ba),vomer(V),posterior nasal spine(PNS),in-cisive foramen(IF),and anterior nasal spine(ANS).The MSP(S2)of best fit was then found by minimizing the mean square distance of these eight anatomical landmarks to a plane in Geomagic Studio 2014.The results of the S1 and S2 models constructed using the original-mirror alignment algorithm and the landmark-independent method,respectively,were scored subjectively by five senior maxillofacial surgeons,and a paired t-test was performed for the two groups.The internal consistency analysis was performed based on secondary experiments to verify the repeatability of the expert evaluation method.Results The average scores of the S1 and S2 models were 65.73 and 75.90,respectively.The aver-age score of the model constructed using the landmark-independent method was significantly higher than that of the model constructed using the original-mirror alignment algorithm(P＜0.01).Furthermore,the results of the internal con-sistency analysis showed that the expert evaluation method had good reliability and validity.Conclusion In patients with facial deformities,the MSP constructed using the landmark-independent method is superior to that constructed us-ing the original-mirror alignment algorithm.This study provides a theoretical basis for maxillofacial symmetry analysis in clinical settings and is clinically feasible.

OBJECTIVE To observe the anti-inflammatory mechanism of Sanhuang gel on rat model of auricle acne and its possible mechanism with p38MAPK signaling pathway as the entry point. METHODS Sixty-two male Wistar rats were divided into blank group and modelling group. The modeling group replicated the experimental animal model of acne(application of 100% oleic acid+subcutaneous injection of Propionibacterium acnes), and 2 rats were randomly selected for HE staining after 21 days. The remaining rats were randomly divided into model group, positive control group(Vitamin A cream 1.48 g·d−1 ), Sanhuang gel high, medium and low-dose group(1.1, 0.568, 0.3 g·d−1 ). They were administered for 8 weeks, and observed on the 7, 14 and 28 day of treatment. The right auricle tissues were collected, and the histopathological changes were observed by HE stain. The mRNA expressions of p38MAPK, MKK3 and MKK6 were detected by RT-PCR. The protein expressions of MCP-1, HMGB1 and α-SMA in auricle tissues were detected by IHC and Western blotting. RESULTS Compared with blank group, the epidermis of auricular tissue in model group was severely keratinized, inflammatory cell infiltration was obvious, mRNA levels of p38MAPK, MKK3, MKK6 and protein expression levels of MCP-1, HMGB1 and α-SMA were increased(P<0.05). After drug therapy intervention, auricle apparent score at different time points in each treatment group was improved to varying degrees. The mRNA levels of p38MAPK, MKK3, MKK6 and protein levels of MCP-1, HMGB1 and α-SMA in Sanhuang gel high-dose and medium-dose groups and positive control group were decreased(P<0.05), while in Sanhuang gel low-dose group, the expressions of MKK3 mRNA and MCP-1, HMGB1 protein were decreased(P<0.05), the expression of p38MAPK, MKK6 mRNA and α-SMA protein decreased not significantly. CONCLUSION The mechanism of the effect of Sanhuang gel on the inflammatory response of rat compound acne animal model may be related to its intervention of p38MAPK protein feedback regulation signaling pathway and inhibition of MCP-1, HMGB1 and α-SMA expression.