Objective To investigate the optimal index of serum lipids to predict insulin resistance(IR) in subjects with normal fasting plasma glucose(FPG).Methods In Nor 2003-11 the 1002 subjects with FPG

Relationship between blood pressure and insulin resistance was analyzed in 839 non hypertensive subjects (fasting plasma glucose

Nine hundred and two subjects were divided into combined hyperlipidemia group, hypertriglyceridemia group, hypercholesteremia group, isolated low high-density-lipoprotein group and normal group. The results suggested that insulin resistance may be accompanied with hyperlipidemia and hypertrigly-ceridemia.

Objective To summarize the clinical experience about therapy for ear keloid by local injection of triamcinolone acetonide acetate combined with surgical resection to control the growth of keloid. Methods After 3~4 times injecting the triamcinolone acetonide ac-etate,the keloid was removed by surgery,some edge of keloid skin was kept and sutured without tension. Results The patients were followed up for 6~24 months,all of 31 ears were primary healing, 26 ears were cured, 4 ears were effective,only one ear was invalid,the effective cure rate was about 96. 8%. Conclusion Local injection with triamcinolone acetonide acetate combined with surgical resection can treat ear keloid.

Objective To investigate the role ofglutamic acid decarboxylase autoantibody(GAD-Ab)and protein tyrosine phosphatase autoantibody(IA-2A) in postpartum follow-up of gestational diabetes mellitus (GDM).MethodsGAD-Ab,IA-2A,insulin and glucose metabolism index were measured in 82subjects with normal glucose tolerance (control group) and 84 patients with GDM(GDM group) during 24 to 28 weeks in pregnancy,postpartum 6 to 12 weeks and 2 years.GDM group was divided into antibodies positive group (GAD-Ah or IA-2A were positive) with 18 cases and antibodies negative group (GAD-Ab and IA-2A was negative) with 66 cases.Results Homeostasis model insulin resistance index (HOMA-IR) in GDM group was higher than that in control group (3.87 ± 2.17 vs.2.31 ± 0.52,P ＜ 0.05 ).Homeostasis β -cell function index (HBCI) and 30 min net increment of insulin/30 min net increment of glucose ( △ I30/△ G30) in GDM group were lower than those in control group[206.38 ± 138.06 vs.422.43 ± 228.93 and (20.16 ±11.38) mU/mmol vs.(26.54 ±24.30) mU/mmol,P ＜0.05].The numbers who had the family history of diabetes mellitus and the used of insulin for treatment in antibodies positive group were higher than those in antibodies negative group[ 83.3％ (15/18) vs.28.8％ (19/66) and 77.8％ ( 14/18 ) vs.30.3％ (20/66) ],HOMA-IR,△ I30/ △ G30 and HBCI in antibodies positive group were lower than those in antibodies negative group [3.20±0.84 vs.4.02±0.36,(16.81 ±2.91) mU/mmol vs.(21.55± 11.11) mU/mmol and 124.95 ± 5.03 vs.217.43 ± 115.64,P＜ 0.01 ].Fasting plasma glucose (FPG),2 hours postprandial glucose (2hPG)and glycosylated hemoglobin (HbA1c) in antibodies positive group were higher than those in antibodies negative group during postpartum 6 to 12 weeks and 2 years [postpartum 6 to 12 weeks: (8.20 ±3.11)mmol/L vs.(5.39 ±0.76) mmol/L,(15.22 ±7.29) mmol/L vs.(8.15 ± 1.93) mmol/L,(7.26 ± 1.04)％ vs.(5.88 ±0.41)％ ;postpartum 2 years: (8.91 ±2.80) mmol/L vs.(4.93 ±0.66) mmol/L,(15.75 ±7.87)mmol/L vs.(7.85 ± 1.79) mtmol/L,(7.18 ± 1.22)％ vs.(5.64 ± 0.32 )％,P ＜ 0.01].△ I30/ △ G30 and HBCI were significantly decreased in antibodies positive group postpartum 2 years.No change of the above parameters in antibodies negative group was found.The occurrence rate of type 1 diabetes mellitus (T1DM) was 16.7％(3/18) and 33.3％(6/18) postpartum 6 to 12 weeks and 2 years in antibodies positive group,there was no T1DM in antibodies negative group.ConclusionsWomen with GDM are partly associated with T1DM.Requiring insulin therapy during pregnancy and GAD-Ab or IA-2A positive have considerable risk for developing T1DM.It is also an important predictor to GDM after parturition.

The clinical data of 5 cases of fulminant type 1 diabetes mellitus were analyzed retrospectively.This disease was characterized by abrupt onset and severe diabetic ketoacidosis.The mean duration from the appearance of hyperglycemic symptoms to first hospital visit was 3.4 days.The mean plasma glucose level was 47.7 mmol/L,but the mean value of HbA_(1C) level was 6.8% at first visit.The mean fasting serum C-peptide was 40.0 pmol/L,and mean serum postprandial C-peptide was 68.0 pmol/L at onset.β-cell function did not recover after 3-26 months of follow-up.

Objective To explore the efficiency of continuous glucose monitoring system(CGMS) and blood glucose self-monitoring (SMBG)in evaluating blood glucose excursion in type 1 diabetes mellitus (T1DM) complicated with pregnancy. Methods Twenty-five patients having suffered from T1DM complicated with pregnancy were selected randomly during June 2012 to July 2015. All subjects underwent blood glucose monitoring by CGMS and SMBG for 72 h, including the data of blood glucose before meal, 2 h post-meal blood glucose (2hBG) and blood glucose at 2:00 AM. Results The level of the highest blood glucose in CGMS was significantly higher than that in SMBG:(10.60 ± 2.11) mmol/L vs. (7.50 ± 1.18) mmol/L, P<0.01. The level of the lowest blood glucose in CGMS was significantly lower than that in SMBG:(3.60 ± 1.06) mmol/L vs. (4.50 ± 1.15) mmol/L, P<0.01. The level of mean blood glucose in CGMS and SMBG had no significant difference:(7.20 ± 1.18) mmol/L vs. (7.30 ± 1.15) mmol/L, P>0.05. The rate of hypoglycemia(blood glucose<3.3 mmol/L) in CGMS was 4.6%, and in SMBG was 1.9%. Through adjusting the treatment by CGMS, the blood glucose before meal, 2hBG and blood glucose at 2:00 AM at 49-72 h were significantly lower than that at 0-24 h (P<0.05). Conclusions Compared with SMBG, CGMS has a relatively larger blood glucose monitoring range and can sensitively evaluate blood glucose excursion, CGMS provides a scientific basis to develop a more rational and effective strategies for controlling diabetes.

Objective To study the proliferation of human skin fibroblast and synthesis of extracellular matrix which were regulated by LATS1-YAP pathway. Methods They were divided into three groups:control groups, LATS1 siRNA intervention group and YAP siRNA treatment group. Using LATS1 siRNA transferred human skin fibroblasts cell lines HS27 in LATS1 siRNA intervention group, and using YAP siRNA transferred HS27 in YAP siRNA treatment group. Expression of LATS1,YAP and collageⅠwere detected by western-blot 48 h later, and the activity of HS27 cells was determined by MTT. Results Compared with control group,expression of LATS1 protein decreased while expression of YAP protein and collagenⅠprotein increased 48 h after LATS1 siRNA transfection. Expression of LATS1 protein remains un-changed and expression of YAP protein and collagenⅠprotein decreased 48 h after YAP siRNA transfection. Conclusion LATS1-YAP pathway could regulate proliferation of human skin fibroblast and synthesis of extracellular matrix. It provides a potential therapeutic targets for skin wound repair and cicatrization.

BACKGROUND:Temporomandibular joint osteoarthritis can cause severe pain,which significantly affects the patient's quality of life and psychological health.Studies have found that medical ozone can effectively alleviate pain due to temporomandibular joint osteoarthritis,but its analgesic effect and mechanism are still unclear. OBJECTIVE:To explore the effects of medical ozone on pain relief in temporomandibular joint osteoarthritis and the potential mechanisms. METHODS:Twenty-four Sprague-Dawley rats were randomly divided into four groups(n=6 per group):control group,model group,air group,and medical ozone group.A sodium iodate-induced rat model of temporomandibular joint osteoarthritis was established in all groups except for the control group.After 1 week of modeling,rats in the air group and medical ozone group were injected with clean air and medical ozone,respectively,in the temporomandibular joint.The injection frequency for the air group and medical ozone group was once a week for three times in total.The von Frey mechanized pain measurement technique was used to assess the mechanical pain threshold of the temporomandibular joint in rats before and 28 days after modeling.ELISA was utilized to detect interleukin-1β in both serum and temporomandibular joint fluid at 28 days after modeling.Histopathologic changes of the temporomandibular joint were evaluated through hematoxylin-eosin staining.Additionally,the expression levels of hypoxia-inducible factor 1α and cyclooxygenase 2 in the temporomandibular joint were analyzed using immunohistochemistry. RESULTS AND CONCLUSION:Compared with the control group,the mechanical pain thresholds of the temporomandibular joint in the model group were decreased at 1,3,7,14,21,and 28 days after modeling(P<0.01);and compared with the model and air groups,the mechanical pain thresholds of the temporomandibular joint in the medical ozone group were increased at 28 days after modeling(P<0.01).Compared with the control group,the level of interleukin 1β in the serum and joint fluid of rats in the model group was elevated(P<0.01);compared with the model and air groups,the level of interleukin 1β in the serum and joint fluid of rats in the medical ozone group was decreased(P<0.01).Hematoxylin-eosin staining results showed derangement and degeneration of the cartilage structure in the model group and the air group,while the derangement of the cartilage structure in the medical ozone group was less than that in the model group and the air group.Immunohistochemical staining showed that the expression of hypoxia-inducible factor 1α and cyclooxygenase 2 in the temporomandibular joints of rats in the model group was elevated compared with that in the control group(P<0.01);the expression of hypoxia-inducible factor 1α and cyclooxygenase 2 in the temporomandibular joints of rats in the medical ozone group was decreased compared with that in the model group and the air group(P<0.01,P<0.05).These findings suggest that medical ozone can alleviate the pain caused by osteoarthritis of the temporomandibular joints in Sprague-Dawley rats by reducing the expression of hypoxia-inducible factor 1α,interleukin 1β,and cyclooxygenase 2.