Intestinal dysmotility symptoms,such as abdominal pain,diarrhea and tenesmus are frequently seen in patients with ulcerative colitis( UC). Interstitial cells of Cajal( ICC)has been accepted as a therapeutic target for gastrointestinal motility disorders and regulation of autophagy might be a potential strategy for various diseases. Study on relationship between intestinal dysmotility in UC and ICC autophagy and the intervention mechanism of related drugs will benefit the controlling of disease activity,relieving of dysmotility symptoms and improving of quality of life in UC patients. In this review article,the possible relationship between intestinal dysmotility in UC and ICC autophagy,as well as the possibility of regulating ICC autophagy as a treatment strategy for UC intestinal dysmotility were summarized.

Objective To explore the effect of schisanhenol on adipokine expression in 3T3-L1 adipocyte and its related mechanism. Methods 3T3-L1 adipocyte was cultured in vitro and induced to differentiation and maturity. Glucokinase was added to culture medium to make an oxidative model. The expression of adipocytokines were detected under the circumstance of different doses and at different time points of schisanhenol. Results The expression of adiponectin, leptin, resistin and visfatin were decreased with the increase of glucokinase concentration. Concentration-dependent inhibition effect was most obvious in leptin (25 mU/ml Glucokinase vs Blank group, t =7.29, P＜0.01). With pretreatment of oxidative stress, the adipocytokines increased as the doses of schisanhenol increased (t=6.31,P＜0.01 in adiponectin;t=5.92, P＜0.01 in leptin; t=3.77, P＜0.05 in resistin; t=3.63,P＜0.05 in visfatin). With the extension of schisanhenol effect, the expression of four adipokines showed the process of first decrease-then increase'. The effects of schisanhenol on adipokines were parallel with the alteration of oxidative stress. Conclusions Schisanhenol increased adipocytokines expression in 3T3-L1 adipocyte by reducing oxidative stress, and the increase of leptin and adiponectin were most obvious, which indicated that schisanhenol could play a role in the treatment of diabetes by Chinese herb wuweizi.

Objective:To evaluate the value of improved pulmonary ultrasonography in the follow-up assessment of lung damage in patients who recovered from corona virus disease 2019(COVID-19).Methods:Twenty-two patients who were cured of COVID-19 in Quanzhou First Hospital from January to May 2020 were randomly selected and divided into 7 mild cases, 12 moderate cases and 3 severe cases according to the first high-resolution CT (HRCT) at admission. Six months after recovery, modified lung ultrasonography and HRCT were used prospectively to assess the lung damage and evaluate the correlation and consistency between the two techniques.Results:①There were significant differences in lung damage between the mild group and the moderate group, severe group (all P<0.05), while there was no significant difference between the moderate group and severe group ( P>0.05). ②There was good consistency between the improved lung ultrasound examination and HRCT (Kappa=0.776, P<0.001). ③There was a positive correlation between the score of improved pulmonary ultrasound examination and HRCT Warrick score ( r=0.755, P<0.001). Conclusions:Improved pulmonary ultrasonography can be used as a priority in the evaluation of pulmonary damage follow-up in patients with COVID-19 recovery, reducing the use of CT, and providing favorable evidence for further clinical management.

SUMO4 Met55Val variation was shown to be related to type 2 diabetes susceptibility and the vascular complications in Asian people. To further examine the related mechanisms, this study was designed to evaluate the association of SUMO4 Met55Val polymorphism with insulin resistance and β cell function in newly diagnosed type 2 diabetic patients in a Chinese population. Four hundred and twenty seven newly diagnosed type 2 diabetic patients were selected for SUMO4 Met55Val polymorphism genotype analysis. All subjects underwent a 75-g oral glucose tolerance test (OGTT) to estimate the insulin sensitivity and β cell function. Anthropometrics and a metabolic profile were used for phenotyping analysis. The results showed that the SUMO4 Met55Val polymorphism was associated with higher insulin resistance (P<0.001) and lower insulin sensitivity (P<0.001). Patients with GG genotype had higher levels of plasma glucose, insulin and C peptide. Insulin sensitivity index (ISI) was closely correlated with body mass index (BMI) in patients with GG genotype in comparison to the counterparts with AG or AA genotype (r= -0.504 vs. r= -0.430 vs. r= -0.340). Multiple regression linear analysis showed that SUMO4 Met55Val polymorphism was an independent determinant for insulin sensitivity (P=0.001), which, along with triglyceride, BMI and sex, could account for 20.1% of the variation in ISI. The result remained the same after adjusting for BMI and sex. No association was found between SUMO4 Met55Val polymorphism and β cell function (all P>0.05). It was concluded that SUMO4 Met55Val variant was associated with increased insulin resistance in Chinese patients with newly diagnosed type 2 diabetes.

The molecular mechanism by which obesity induces insulin resistance is not completely understood. The aim of this study was to determine how lipopolysaccharide-induced tumor necrosis-α factor (LITAF) influenced obesity-induced insulin resistance using a cellular co-culture system. The cells were divided into 3 groups: palmitic acid (PA) stimulation group, LITAF small interfering RNA (siRNA) group and untreated (NC) group. The LITAF siRNA was used for knockdown of LITAF expression in human THP-1 macrophages. The expression levels of LITAF, IRS-2, IRS-2Tyr465, PI3K, and GLUT2 in each group were measured by using quantitative reverse transcriptase real-time polymerase chain reaction and Western blotting. The expression of LITAF was much higher in the PA group than in the siRNA and NC groups (*P<0.05); meanwhile, the expression of IRS-2, IRS-2Tyr465, PI3K, and GLUT2 was much lower in the PA group than in the NC group (*P<0.05); however, IRS-2, IRS-2Tyr465, PI3K, and GLUT2 had much higher expression in the siRNA group than in the PA group (*P<0.05). It is concluded that PA can induce insulin resistance in liver cells and knockdown of LITAF expression can reduce insulin resistance in liver cells, suggesting LITAF may regulate the insulin signal transduction pathway involved in obesity-induced insulin resistance.

Apoptosis ; drug effects ; Hep G2 Cells ; Humans ; Iron Compounds ; adverse effects ; pharmacology ; Nanostructures

To investigate the mechanism and biologic effects of 37 nm magnetic nano FeOx powders (MNPs) on human hepatoma-bearing nude mice. 37 nm MNPs were prepared by coprecipitation methods and then injected into human hepatoma (Bel-7402) bearing-nude mice through the tail vein. After injection of MNPs, the mice were first exposed under static magnetic field and then treated under extremely low frequency altering-electric magnetic field directing to the tumor area. The migration and trafficking of MNPs were determined by MMR. Tumor growth was monitored with calipers every 5 days and tumor volume was calculated on the basis of three-dimensioned measurements. The apoptosis of tumor cells was analyzed by flow cytometry analysis. The expressions of apoptosis-associated proteins Bcl-2, Bax and HSP27 were determined using western-blot analysis. Static magnetic field could direct the migration and trafficking of MNPs to the tumor site with a higher ratio of 98.9%. Extremely Low Frequency Electric-Magnetic Field (EMF) treatment could inhibit the proliferation of tumor cells and prolong the survive time of tumor-bearing mice injected with MNPs. In addition, the survival time of tumor-bearing mice and percentages of prohibition on tumor cell growth were 27.4+/-0.7 days and 37.5+/-0.8% (F = 0.005, P is less than to 0.05), respectively. The results of flow cytometry analyses showed that about 18.1+/-0.6% (F = 0.030, P is less than to 0.05) of tumor cells were induced into early apoptosis. Furthermore, expressions of apoptosis-associated proteins Bcl-2 and Bax were significantly induced by MNPs under EMF treatment. The ratio of Bcl/Bax in both MNPs and EMF treatment group was 0.07+/-0.01, which was much lower than that of control group (0.23+/-0.02) (F = 0.016, P is less than to 0.05). Heat shock protein-27 (Hsp-27) was not significantly induced in different treatment groups. Injection of MNPs with EMF exposure on human hepatoma-bearing nude mice could significantly prolong the survival time, inhibit the tumor proliferation and growth, and induce tumor cells into apoptosis.
Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Biological Products ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Flow Cytometry ; Humans ; Magnetic Fields ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Powders ; Proto-Oncogene Proteins c-bcl-2 ; bcl-2-Associated X Protein

SUMO4 Met55Val variation was shown to be related to type 2 diabetes susceptibility and the vascular complications in Asian people.To further examine the related mechanisms,this study was designed to evaluate the association of SUMO4 Met55Val polymorphism with insulin resistance and βcell function in newly diagnosed type 2 diabetic patients in a Chinese population.Four hundred and twenty seven newly diagnosed type 2 diabetic patients were selected for SUMO4 Met55Val polymorphism genotype analysis.All subjects underwent a 75-g oral glucose tolerance test (OGTT) to estimate the insulin sensitivity and β cell function.Anthropometrics and a metabolic profile were used for phenotyping analysis.The results showed that the SUMO4 Met55Val polymorphism was associated with higher insulin resistance (P＜0.001) and lower insulin sensitivity (P＜0.001).Patients with GG genotype had higher levels of plasma glucose,insulin and C peptide.Insulin sensitivity index (ISI) was closely correlated with body mass index (BMI) in patients with GG genotype in comparison to the counterparts with AG or AA genotype (r=-0.504 vs.r=-0.430 vs.r=-0.340).Multiple regression linear analysis showed that SUMO4 Met55Val polymorphism was an independent determinant for insulin sensitivity (P=0.001),which,along with triglyceride,BMI and sex,could account for 20.1％ of the variation in ISI.The result remained the same after adjusting for BMI and sex.No association was found between SUMO4 Met55Val polymorphism and β cell function (all P＞0.05).It was concluded that SUMO4Met55Val variant was associated with increased insulin resistance in Chinese patients with newly diagnosed type 2 diabetes.

The molecular mechanism by which obesity induces insulin resistance is not completely understood.The aim of this study was to determine how lipopolysaccharide-induced tumor necrosis-α factor (LITAF) influenced obesity-induced insulin resistance using a cellular co-culture system.The cells were divided into 3 groups:palmitic acid (PA) stimulation group,LITAF small interfering RNA (siRNA) group and untreated (NC) group.The LITAF siRNA was used for knockdown of LITAF expression in human THP-1 macrophages.The expression levels of LITAF,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 in each group were measured by using quantitative reverse transcriptase real-time polymerase chain reaction and Western blotting.The expression of LITAF was much higher in the PA group than in the siRNA and NC groups (*P＜0.05); meanwhile,the expression of IRS-2,IRS-2Tyr465,PI3K,and GLUT2 was much lower in the PA group than in the NC group (*P＜0.05); however,IRS-2,IRS-2Tyr465,PI3K,and GLUT2 had much higher expression in the siRNA group than in the PA group (*P＜0.05).It is concluded that PA can induce insulin resistance in liver cells and knockdown of LITAF expression can reduce insulin resistance in liver cells,suggesting LITAF may regulate the insulin signal transduction pathway involved in obesity-induced insulin resistance.

Female ; Hearing Disorders ; etiology ; Hearing Tests ; Humans ; Infant, Newborn ; Male ; Neonatal Screening ; Risk Factors