Thyroid hormone insensitive syndrome is an inherited disease characterized by decreased target tissue responsiveness to thyroid hormone. Most cases are due to thyroid hormone receptor β gene mutation. Two novel types of thyroid hormone insensitive syndrome were recently identified, which are caused by gene mutations of MCT8, a specific thyroid hormone transporter, and SBP2 in the synthesis of deiodinase.

Turner Syndrome (TS) is a common X sex chromosome abnormality syndrome. Its main clinical features are growth retardation and germinal aplasia. The study found that the incidence of thyroid abnormalities in patients with TS was higher than that in the general population. This article reviews the clinical features and mechanisms of thyroid abnormalities in patients with TS.

Objective To investigate the effect of transverse incision surgery for epicanthoplasty with double eyelid fold reconstruction. Design Retrospective case series. Participants 103 patients with epicanthus. Method Transverse incision was applied for epicanthoplasty in all patients, and incorporated with double eyelid fold reconstruction. Patients were followed up 3-6 months. Main Outcome Measures Size of lacrimal caruncle, length of palpebral fissure, inner canthic diameter and scarring degree. Results Lacrimal caruncle was revealed 3/4 merous in 21 cases, 2/3 merous in 56 cases, 1/2 merous in 8 cases. Extent of palpebral fissure was 30-31mm in 5 cases, 28-29 mm in 69 cases, 26-27 mm in 11 cases. Inner canthic diameter was 32-33mm in 61 cases, 30-31 mm in 23 cases, 29 mm in 1 case. The scarring was little in 56 cases, obviously in 29 cases. Epicanthus relapsed in 2 cases. 16 cases lost follow-up. Conclusion Transverse incision surgery for epicanthoplasty with double eyelid fold reconstruction has less tissue damage and minimal scarring produced at the medial cantha. It is a simple and reliable surgical approach for correction of epicanthus.

Objective To investigate the changes of serum stromal cell‐derived factor‐1α (SDF‐1α) in patients with diabetic peripheral neuropathy (DPN) and the influence of mouse never growth factor (MNGF) on the levels of serum SDF‐1α. Methods 180 patients with type 2 diabetes (T2DM ) were divided into T2DM with DPN (DPN group ,n=92) and T2DM without DPN (T2DM group ,n=88). 90 healthy people were select as normal control (NC group). DPN group was divided into 47 cases of MNGF treatment (A) subgroup and 45 cases of basic treatment (B) subgroup. The levels of serum SDF‐1αwere measured using ELISA method. The relationships between the levels of serum SDF‐1αand SOD ,TGF‐β1 , hsC‐RP ,and GAP‐43 were analyzed. After treatment ,the levels of serum SDF‐1α in A and B subgroups were compared. Results Compared with NC group [(0.91 ± 0.37)μg/L] ,the levels of serum SDF‐1αin T2DM and DPN group were higher [(2.58 ± 0.58) μg/L and(1.71 ± 0.43)μg/L ,respectively ,P<0.05 or P<0.01]. The levels of SDF‐1αwere positively correlated with FPG ,HbA1 c ,TGF‐β1 and hsC‐RP ,and negatively correlated with SOD in T2DM group. The levels of SDF‐1αwere positively correlated with TG and TGF‐β1 ,and negatively correlated with course of disease ,FPG ,HbA1 c ,SOD ,hsC‐RP ,GAP‐43 , MMCV ,PMCV ,MSCV and PSCV in DPN group. SDF‐1α levels were significantly increased after treatment with MNGF in subgroup A [(1.75 ± 0.39) vs (2.09 ± 0.45)μg/L ,P<0.05]. There were no significant difference of SDF‐1αlevels after treatment in subgroup B [(1.67 ± 0.48) vs (1.71 ± 0.51)μg/L , P>0.05] .Multiple stepwise regression analysis showed that HbA1c ,hsC‐RP and PSCV were the independent factors related with the levels of SDF‐1αin DPN patients. Conclusion The levels of serum SDF‐1αin DPN patients are lower than in T2DM patients without DPN. MNGF may increase the level of serum SDF‐1α.

Objective To explore the level of angiopoietin‐like protein 4 (ANGPTL4) in patients with early chronic kidney disease (CKD ) in diabetes and the influence of pioglitazone on the level. Methods 92healthypeoplewithnormalglucosetolerancewereselectedasthecontrols(NCgroup).89 newly diagnosed T2DM were selected (T2DM group ). 90 cases of CKD group were divided into pioglitazone (PGZ) and glimepiride (GLI) treated subgroups ,45 cases in each subgroup. After treatment , serum ANGPTL4 levels were observed in CKD group. Results There were significant differences in serum ANGPTL4 levels among NC ,T2DM and CKD groups [(34.8 ± 4.75) vs (31.1 ± 3.65) vs (27.1 ± 3.52)ng/ml ,P<0.05 or P<0.01]. ANGPTL4 level was positively correlated with SOD ,TG (r=0.635 , 0.526 ,P< 0.05 or P< 0.01) ,and negatively correlated with BMI ,FPG ,HbA1c ,hsC‐RP ,UAlb/Cr , VEGF ,FIns ,HOMA‐IR (r= -0.502 ,-0.624 ,-0.542 ,-0.520 ,-0.538 ,-0.566 ,-0.576 ,-0.509 ,P< 0.05 or P < 0.01 ). In PGZ subgroup after treatment ,ANGPTL4 levels were significantly increased and UAlb/Cr significantly decreased [(31.51 ± 3.87 ) vs (27.60 ± 3.58 )ng/ml ,P < 0.05 ;(88.50 ± 8.90 ) vs (116.20 ± 10.30 )mg/24 h ,P < 0.01 ]. In GLI subgroup after treatment ,there were no significant difference in FPG and HbA1 c as compared with PGZ subgroup but ANGPTL4 levels have no significant differences after treatment ,and UAlb/Cr decreased [(27.20 ± 3.54 ) vs (26.60 ± 3.48 )ng/ml ,P > 0.05 ;(99.70 ± 12.80 ) vs (122.40 ± 13.10 )mg/24 h ,P < 0.05]. HbA1 c ,FIns ,UAlb/Cr were the independent related factors influencing ANGPTL4 of CKD patients. Conclusion Serum ANGPTL4 has a lower level in CKD patients. PGZ is effective in treating CKD. This role is associated with the increase of serum ANGPTL4.

Objective To explore the mechanism of the interaction between sulfur dioxide(SO2) and bovine serum albumin (BSA). Methods The spectrum characteristic of the interaction between SO2 and BSA was studied by fluorescence quenching spectrum and three dimensional fluorescence spectrum. Results The binding constants and thermodynamic parameters of SO2 with BSA were calculated at different temperatures. The quenching mechanism of BSA by SO2 was determined,the result showed that it did not belong to dynamic quenching but belonged to static quenching,which produced the complex. The hydrophobic interaction and electrostatic force played a main role in the binding of SO2 with BSA and only about one binding site occurred in the reaction. There was a certain influence to the conformation of BSA after adding SO2. Conclusion The quenching reaction of BSA by SO2 was weak. SO2 dissolved in body fluid easily and then SO32-and HSO3-are generated in vivo.

Objective To establish a method of isolating and purifying islets from Wistar rat, and to evaluate the biological characters of the isolated and purified islets. Methods The pancreases were surgically removed from adult Wistar rats, carefully minced with scissors as small as possible prior to incubation in 0.9 mg/ml collagenase (Sigma, type Ⅴ) for 10~17min at 37℃. The digested tissue was filtered through a 60 apertures/cm~2 metal sieve and washed with 10% fetal bovine sera (FBS) in Hank’s solution. Purification was performed using Dextran discontinuous density gradient centrifugation to separate the contents of the postcollagenase pellets. Islet samples were stained with DTZ staining for identification. The viability of the purified islet was determined by acridine orange/propidium iodide (AO/PI) double staining. The in vitro function was assayed by different densities of glucose incubating islets for 45min, respectively. Insulin secretion in the supernatant was assayed by radioimmunoassay. Islets were transplanted under the kidney capsule into recipient SD rats that had been rendered diabetic by injecting streptozotocin 50mg/kg, so as to evaluate the in vivo function of islets. Results The islets were recovered between the 11% and 22% Dextran layers, and between the 11% and 1640 layers. The average number of isolated islets was 2181?14 per rat pancreas. After a discontinuous Dextran density gradient purification, about 1826?24 islets were obtained from per rat pancreas, with an average purity over 95%. Islets showed good response to glucose and high efficiency to invert hyperglycemia 7-10d after transplantation. Conclusion These results showed that the digestion methods and purification procedure which we have developed could provide islets from rats for transplantation studies. The biological characters of islets harvested by our method were very well.

Background:Hepatic veno-occlusive disease( HVOD) is a disease characterized by hepatomegaly,jaundice, ascites,weight gain and lack of effective treatment currently. Our prophase research showed that ligustrazine had therapeutic effect on Sedum aizoon induced HVOD in mice. Aims:To investigate the mechanism of therapeutic effect of ligustrazine on Sedum aizoon induced HVOD in mice. Methods:A total of 115 mice were randomly divided into 4 groups:mice in group A were intragastrically administrated with 30 mg·kg-1 ·d-1 Sedum aizoon to induce HVOD and served as model group;mice in group B were given 30 mg·kg-1 ·d-1 Sedum aizoon + 100 mg·kg-1 ·d-1 ligustrazine and served as low dose ligustrazine intervention group;mice in group C were given 30 mg·kg-1 ·d-1 Sedum aizoon + 200 mg·kg-1 ·d-1 ligustrazine and served as high dose ligustrazine intervention group;mice in group D were given 30 mg·kg-1 ·d-1 PBS and served as normal control group. After 30 days,all the mice were sacrificed. HE staining and Masson staining were performed for histological examination. The mRNA and protein expressions of tissue factor(TF),nuclear factor(NF)-κBp65 and early growth response factor( Egr)-1 in liver tissue were determined by RT-PCR and Western blotting, respectively. Results:HE staining and Masson staining histological examination showed that ligustrazine could obviously ameliorate the pathological injury of liver tissue in HVOD mice. Compared with group D,the mRNA and protein expressions of TF,NF-κBp65,Egr-1 were significantly increased in group A( P < 0. 05). After intervention with ligustrazine,the mRNA and protein expressions of TF,NF-κBp65,Egr-1 were significantly decreased( P < 0. 05), especially in group C,and no significant differences were found between group C and group D(P > 0. 05). Conclusions:Ligustrazine has therapeutic effect on HVOD,the possible mechanism is that ligustrazine could interrupt the activation of coagulation system by reducing the expression of TF via down regulating the expressions of NF-κBp65 and Egr-1,especially in high dose ligustrazine group.