Based on the results of oral glucose tolerance test( OGTT )and the levels of 1-h plasma glucose ( 1 hPG),793 subjects were classified into three groups:583 with NGTN ( normal 1 hPG in OGTT),127 with NGT1 H( higher 1 hPG in OGTT) and 83 with IGT( impaired glucose tolerance).NGT1H group had large waist circumference,higher body mass index,fasting plasma glucose( FPG),triglyceride,and lower high density lipoprotein-cholesterol than those of NGTN group.NGT1 H group had higher homeostasis model assessment insulin index ( 1.2 ± 0.6),lower homeostasis model assessment β3 ( HOMA-β ) (4.5 ± 0.7 ) and insulinogenic index (2.1 ±0.7) than those of NGTN group(0.5 ±0.6,4.8 ±0.7,2.7 ±0.9,respectively,all P ＜0.05 ).HOMA-β of NGT1 H group was higher than that of IGT group(4.5 ±0.7 vs.4.4 ±0.6,P ＜0.05 ).The results indicate that 1 hPG in OGTT may identify a condition of glucose metabolic abnormalities characterized by insulin resistance and reduced β-cell function.

A cross-section study was designed to investigate clinical utility of lipid measures for prediction of insulin resistance(IR).A total of 793 healthy volunteers were divided to IR group or non-IR group based on the value of HOMA-IR.Area under receiver operating characteristic curve(ROC)found that TG/HDL-C was more related with IR in comparison with other lipid ratios,and could be used as a measure in predicting IR.

Aged ; Coal Mining ; Electrocardiography ; Heart Rate ; physiology ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; physiopathology

Aged ; Arrhythmias, Cardiac ; diagnosis ; physiopathology ; Coal Mining ; Electrocardiography ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; complications ; physiopathology

Type 2 diabetes is a hypermetabolic disease characterized with disorders of glucose/lipid metabolism, absolute or relative lack of insulin, and can induce skeletal muscle atrophy. Hyperglycemia, hyperlipidemia, insulin resistance, and abnormal release of inflammatory factors can lead to abnormal signal transduction in skeletal muscle, thus make protein synthesis and degradation imbalance and eventually causing muscle atrophy. Under normal conditions, insulin-like growth factor 1 (IGF-1)/insulin can activate phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT). AKT not only increases protein synthesis through mammalian target protein of rapamycin (mTOR), but also phosphorylates forkhead box O (FoxO) transcription factor and then inhibits the transcription of several ubiquitin ligases (such as MAFbx/atrogin-1 and MuRF1), or autophagy related genes. The weakened IGF-1/PI3K/AKT pathway in type 2 diabetes is an important factor leading to skeletal muscle atrophy. Studies have shown that the commonly used anti-type 2 diabetic drugs have different effects in regulating the synthesis and degradation of skeletal muscle protein. Studies reported that drugs with effect of anti-diabetic muscle atrophy include thiazolidinediones, glucagon-like peptide analogs, glucose-sodium cotransporter 2 inhibitors, etc.; drugs that are still in controversial or even promote skeletal muscle atrophy include metformin, and some sulfonylurea or non-sulfonylurea insulin secretagogues. This article overviewed and analyzed the currently commonly used drugs for type 2 diabetes and summarized the related mechanisms, with the aim to provide references for the rational applications of drugs for type 2 diabetes.

Wound healing is a complex and highly regulated process to maintaining the skin barrier function. Wounds of diabetic patients are hard or even not healing. Non-healing diabetic foot ulcers can lead to lower-extremity amputations. Diabetic wound healing problem is the main complication that leads to high disability rate of diabetes and can threaten the lives in severe cases. The healing of skin wounds requires the synergy of multiple factors to restore the injured skin to its barrier function. The mechanisms that cause it difficult to heal diabetic wounds are complex, including oxidative stress, chronic inflammation, decreased neovascularization, peripheral neuropathy, and imbalance of extracellular matrix accumulation and remodeling. This review classifies mechanisms of diabetic wound healing and provides a reference for its further research.

OBJECTIVESTo explore whether the angiotensin I -converting enzyme (ACE) I/D (insertion/ deletion) polymorphism is associated with the susceptibility to high altitude pulmonary edema (HAPE) in the Han Chinese.

METHODSOne hundred and forty-seven HAPE-p (HAPE patients) and 193 HAPE-r (HAPE resistants) were enrolled from the Yushu earthquake reconstruction workers in Qinghai province where the altitude is over 3 500 m above sea level. Blood samples were collected from each of the HAPE-p and HAPE-r groups. Information about physiological phenotypes was obtained via fieldwork investigation. The ACE-I/D polymorphism in HAPE-p and HAPE-r was detected by polymerase chain reaction (PCR).

RESULTSThe SaO2 was significantly lower while HR was significantly higher in HAPE-p group than those in HAPE-r group. The genotype frequencies of ACE-I/D for II, ID, DD in HAPE-r and HAPE-p groups were 0.430, 0.446, 0.124 and 0.435, 0.469, 0.095, respectively, the allelic frequencies of I and D were 0.650, 0.350 and 0.670, 0.330, respectively. The OR of ID, DD and D alleles relative to II for HAPE was 0.961 (0.610-1.514), 1.322 (0.634-2.758) and 1.080 (0.783-1.489). There was no significant difference of the genotypic and the allelic frequencies in ACE-I/D polymorphism between HAPE-p and HAPE-r groups.

CONCLUSIONSThere is no relation between ACE-I/D polymorphism and HAPE in the Han Chinese.

Alleles ; Altitude ; Asian Continental Ancestry Group ; genetics ; Case-Control Studies ; Gene Frequency ; Genotype ; Humans ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Genetic ; Pulmonary Edema ; genetics

Objective To investigate the protein expression of stanniocalcin 1 (STC1) in papillary thyroid carcinoma (PTC) in gerontal patients versus non-gerontal subjects,and its relationship with clinicopathological features.Methods The protein expression levels of STC1 in PTC,nodular goiter and normal thyroid tissues in the gerontal patients versus non-gerontal subjects were detected by immunohistochemistry.The protein expressions of STC1 were detected by Western blotting.Results The protein expression of STC1 in gerontal patients was higher in PTC than in nodular goiter and normal thyroid tissues (60.9％ vs.30.0％,15.0％,P＜0.05 or 0.01).The relative expression of STC1 protein in gerontal patients was higher in PTC than in nodular goiter and normal thyroid tissues [(0.647 ± 0.076) vs.(0.280 ± 0.039),(0.248 ± 0.065),F =9.965 and 1.143,both P＜0.01].STC1 protein expression had no correlations with age,gender,tumor diameter and tumor position in patients (P＜0.05),while it was associated with tumor lymph node metastasis and clinical stage (P＜0.05).There was no significant difference in above indexes between the elderly and non-elderly patients with papillary thyroid carcinoma (F=0.007,P=0.934).Conclusions STC1 protein may be associated with the development of papillary thyroid carcinoma,and it may has a some reference value in differentiating benign from malignant thyroid neoplasms and in predicting the prognosis of thyroid carcinomas.

Purpose The diagnosis of adult onset Still's disease (AOSD) is usually difficult due to the lack of specific clinical manifestation.This paper summarizes the manifestations of 18F-FDG PET/CT in adult onset Still's disease and investigates the value of PET/CT in diagnosis and differential diagnosis of AOSD.Materials and Methods Fiftyfour patients who was diagnosed as AOSD were selected and underwent 1 8F-fluorodeoxyglueosepositron emission tomography/computed tomography (18F-FDG PET/CT).The clinical features,laboratory examination and the maximum standard uptake value (SUVmax) of liver,spleen,bone marrow,lymph node were collected.Then the main PET/CT manifestations of patients with AOSD,the influence factor of SUVmax and correlation between SUVmax and laboratory indexes were analyzed.Results FDG accumulation occurred mainly in bone marrow (88.89％;SUVmax:3.91 ± 1.16),spleen (79.63％,SUVmax:3.24±0.89) and lymph node (77.78％;SUVmax:3.83± 1.97).FDG accumulation can also occurred in joints,parotid gland,submandibular gland,pleural and other organs.Compared with the nonglucocorticoid group,SUVmax of the spleen,bone marrow and lymph node were significantly decreased in the glucocorticoid group with or without fever (P＜0.05),whereas the SUVmax of liver,spleen,bone marrow and lymph node between the two glucocorticoid groups were not statistically different (P＞0.05).The SUVmax of liver,spleen,bone marrow and lymph node between two groups with or without disease-modifying anti-rheumatic drugs were not statistically different (P＞0.05).Correlation analysis showed that spleen SUVmax and lactate dehydrogenase,bone marrow SUVmax and C reactive protein were weakly correlated (r=0.33 and 0.30,P＜0.05).Conclusion The main manifestations of 18F-FDG PET/CT of AOSD are FDG accumulation in spleen,bone marrow and lymph nodes.Glucocorticoid can reduce the SUVmax.18F-FDG PET/CT can help to rule out malignancy,guide biopsy and assist in definite diagnosis of AOSD.

AIM To investigate the protective effect of polydatin on ischemia-reperfusion (I-R) injury in cardiac muscle and the possible mechanism. METHODS Langendorff technique was used to make I-R injury in rats. Male Sprague-Dawley rats were randomly divided into control, model, polydatin(25, 50 and 75 μmol·L-1), glibenclamide(Gli, 10 μmol·L-1)+polydatin(50 μmol·L-1), 5-hydroxydecanoate(5-HD, 100 μmol·L-1)+polydatin(50 μmol·L-1), and atractyloside (Atr, 20 μmol·L-1)+polydatin(50 μmol·L-1) groups. The hearts in control group were perfused with K-H solution for 110 min. Model group hearts were subjected to 30 min no-flow global ischemia followed by 60 min of reperfusion. The hearts in 3 polydatin groups were perfused with K-H solution containing different concentrations of polydatin for 10 min before I-R. The hearts in Gli+polydatin and 5-HD+polydatin groups were perfused with K-H solution containing Gli or 5-HD for 5 min firstly, then perfused with K-H solution containing both polydatin and Gli or 5-HD for 10 min before I-R. The hearts in Atr+polydatin group were perfused with K-H solution containing polydatin for 10 min before I-R and perfused with K-H solution containing Atr for 15 min after I-R. The cardiac function, including left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximal rates of rise and decline of left ventricular pressure (±dp/dtmax), and coronary flow (CF), were recorded before, after 30 min no-flow global ischemia and, during 60 min reperfusion. Myocardial infarct size was assessed using 2, 3, 5-triphenyltetrazolium chloride method and myocardial ultrastructure was observed via transmission electron microscope after 60 min reperfusion. RESULTS There were no significant differences in cardiac functional parameters between control and model groups in pre-ischemia condition. Compared with model group, polydatin promoted a better recovery of cardiac function after I-R in a concentration-dependent manner. After 60 min of reperfusion, the values of LVDP, ±dp/dtmax and CF in polydatin groups were much higher, but LVEDP was lower than those in model group. Polydatin (50 μmol·L-1) also significantly reduced myocardial infarct size and relieved the I-R injury of myocardial ultrastructure. The protective effects of polydatin (50 μmol·L-1) on LVDP, LVEDP, ±dp/dtmax and CF, as well as the inhibitory effect on infarct size after I-R were abolished by Gli, 5-HD and Atr. CONCLUSION Polydatin has protective effect against I-R injury in rat hearts, which may be related with the opening of ATP-sensitive potassium channel located in both cell membrane and mitochondrial membrane, as well as inhibition of mitochondrial permeability transition pore opening.