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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with sensitizer is a potential method to reverse TRAIL-resistance in tumor cells. Rhein (RH) is a monomer extracted from Chinese herbs that has been reported to show anti-tumor effects in a variety of tumor cells, but the role of RH in TRAIL-induced anti-tumor effects in bladder cancer cells has not been reported. In this study, we found that the combined treatment of a non-toxic concentration of RH with TRAIL significantly inhibited the proliferation and induced apoptosis in both TRAIL sensitive and resistant bladder cancer cell lines. Furthermore, we found that RH promoted bladder cancer cell apoptosis by up-regulating DR5 expression. Our findings provide potential value in the clinical treatment of bladder cancer.

Background The epidemiology and economic burden of hospitalized community-acquired pneumonia (CAP) children due to MP is still poorly understood. This study aimed to investigate the dynamic changes of Mycoplasma pneumoniae pneumonia (MPP) in children in a general hospital. Methods A total of 2011 CAP children aged 1-16 years hospitalized at Peking University Third Hospital from 2017 to 2019 were enrolled by cross-sectional study for the retrospective analysis of the clinical data mainly including seasonal distribution of MPP, hospital stay, severity, complications, use of flexible bronchoscopy, and hospitalization costs. The dynamic changes of CAP and MPP children within 3 consecutive years and the differences between the MPP group and non-MPP groups were compared. Results The proportion of CAP children among hospitalized children was 32.4%, 38.5%, and 39.5% in 2017, 2018, and 2019, respectively, showing an upward trend (P 0.05). Conclusions The proportions of severe pneumonia, complications, and use of flexible bronchoscopy as well as the hospitalization days and costs are higher in MPP children. General hospitals should develop integrated clinical quality control programs for MPP children, so as to optimize the allocation of medical resources.

BACKGROUND: This study aimed to assess the underlying causes and outcomes of acute peritoneal dialysis (APD) and the complications of PD procedure in preterm neonates with acute kidney injury (AKI). METHODS: A retrospective study of 21 preterm neonates who underwent APD in a neonatal intensive care unit (NICU) in Peking University Third Hospital between 2016 and 2019 was conducted. The demographic, clinical, biochemistry, and PD procedure­-related information of the neonates was analyzed. RESULTS: Of the 21 preterm neonates, the average gestational age (GA) was 28.9±2.6 weeks, and the average birth weight was 1,226.7±495.3 g, and included 5 (23.8%) low-birth-weight infants (LBWIs), 7 (33.3%) very LBWIs (VLBWIs), and 9 (42.9%) extremely LBWIs (ELBWIs). The major underlying causes for APD were asphyxia (66.7%, n=14) and twin-twin transfusion syndrome (47.6%, n=10). PD procedure-related complications mainly involved inadequate drainage (n=5, 23.8%) and drainage infections (n=2, 9.5%). The median duration of PD was 3 days (range, 1 hour–20 days). Compared to pre-PD, blood urea nitrogen (BUN) and serum K(+) levels were significantly decreased post-PD (P

BACKGROUND: Children with vitamin A, D, and E deficiency are susceptible to respiratory infections. However, the correlations between the levels with Mycoplasma pneumoniae pneumonia (MPP) and patient MPP occurrence is still unclear. This study aims to measure and compare the serum levels in severe (sMPP) and non-severe MPP (nsMPP) and to investigate the correlations between their levels and the occurrence of MPP. METHODS: A total of 122 children were enrolled, including 52 sMPP and 70 nsMPP aged 0–15 years old in 2015–2018. The serum levels of vitamins A, D, and E were measured and compared, and two-category logistic regression was used for correlation analysis of vitamins A, D, and E levels with nsMPP and sMPP. RESULTS: The age was older (7.12 vs. 4.01 y, P=0.002) in the sMPP samples than that in the nsMPP samples. Vitamin A deficiency was present in both the nsMPP and sMPP samples; its level was significantly lower (0.15±0.06 vs. 0.19±0.07, P=0.0193) in the sMPP serum than that in the nsMPP serum. Vitamins E and D in the sMPP samples were significantly lower (vitamin E 7.43±1.55 vs. 8.22±2.22, P=0.0104; vitamin D 23.08±11.0 vs. 32.07±19.2, P=0.0007) than that in the nsMPP group; both sMPP and nsMPP did not show a deficiency of vitamins E and D. Logistic regression analysis revealed that vitamin A deficiency was significantly (OR 0.001, 95% CI: 0.001–0.334, P=0.009) associated with sMPP, and vitamin A supplementation could reduce the incidence of sMPP. In ≥6 y sMPP, the incidence of vitamin A deficiency was 62.5%, while

OBJECTIVE: To establish and evaluate an ovalbumin (OVA)-induced bronchial asthma model in mice with intrauterine growth retardation (IUGR), and to explore the molecular mechanism of relationship between IUGR and asthma. METHODS: A total of 16 pregnant BALB/c female mice were divided into a low-protein diet group (n=8) and a normal-protein diet group (n=8), which were fed with low-protein (8%) diet and normal-protein (20%) diet respectively. The neonatal mice were weighed 6 hours after birth. Sixteen male neonatal mice with IUGR were randomly chosen from the low-protein diet group and enrolled in the IUGR group, and 16 male neonatal mice from the normal-protein diet group were enrolled in the control group. Blood samples were collected from the mice in both groups for testing of blood glucose. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum insulin level. The mice in the control group were randomized into a control + PBS group and a control + OVA group (n=8 each). The mice in the IUGR group were randomized into an IUGR + PBS group and an IUGR + OVA group (n=8 each). Six-week-old mice in the control + OVA and IUGR + OVA groups were subjected to intraperitoneal injection of 2 mg/mL OVA for sensitization and aerosol inhalation of 1% OVA for challenge. Mice in the control + PBS group and the IUGR + PBS group were treated with an equivalent amount of PBS. ELISA was used to determine serum IgE level in the mice in each group. Bronchoalveolar lavage fluid (BLF) was collected from the mice in each group for cell counting. The lung tissue of the mice in each group was stained with hematoxylin and eosin to observe pathological changes. RESULTS: The body weight at 6 hours after birth was significantly lower for neonatal mice in the low-protein diet group compared with those in the normal-protein diet group (P < 0.01). The IUGR group had a significantly lower serum insulin level than the control group (P < 0.01). The IUGR + PBS group had a significantly lower IgE level than the control + PBS group (P < 0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had a significantly increased IgE level, and the IgE level was significantly higher in the IUGR + OVA group than in the control + OVA group (P < 0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had significantly increased counts of leukocytes, eosinophils, lymphocytes, and macrophages in the BLF (P < 0.01). The pulmonary alveoli of OVA-induced IUGR mice showed massive inflammatory cell infiltration and damage of intercellular continuity. Meanwhile, airway epithelial cell proliferation, bronchial wall thickening, bronchial lumen narrowing, and massive inflammatory cell infiltration around the bronchi and the vascular wall were observed. CONCLUSIONS: An OVA-induced bronchial asthma model has been successfully established in the mice with IUGR induced by low-protein diet, which provides a basis for further study of the molecular mechanism of relationship between IUGR and airway inflammation.

OBJECTIVE: To investigate the physical development, incidence of common respiratory diseases, and motor development during infancy in preterm infants with bronchopulmonary dysplasia (BPD). METHODS: A retrospective analysis was performed on the clinical features and infantile outcomes of preterm infants with BPD who were admitted to the neonatal intensive care unit between January 2012 and December 2015. Preterm infants without BPD were used as controls who were admitted to the neonatal intensive care unit during the same period and had similar gestational age and birth weight. Physical development, number of hospital stays, the incidences of pneumonia and wheezing, and motor development during infancy were compared between the two groups. RESULTS: Compared with the control group, BPD infants had a significantly higher incidence of extrauterine growth retardation at discharge (48% vs 41%; P < 0.05); BPD infants were more susceptible to pneumonia, wheezing, eczema and rhinitis; BDP infants also had a significantly higher number of readmissions due to respiratory tract infection (P < 0.05). BPD infants had a significantly smaller head circumference than the control group at corrected ages of 3, 6, and 12 months (P < 0.05). BPD infants had significantly delayed gross, fine, and overall motor development than the control group at corrected ages of 6 and 9 months (P < 0.05). CONCLUSIONS: Infants with BPD are susceptible to extrauterine growth retardation at discharge. Their head circumference growth is relatively slow. They are susceptible to pneumonia and wheezing during infancy. Moreover, they have delayed motor development when compared with those without BPD at corrected ages of 6 and 9 months.

A female infant was admitted to the hospital due to perioral cyanosis two hours after birth. The infant was born at the gestational age of 35 weeks by cesarean section with a birth weight of 2 400 g. Physical examination revealed wry mouth to the left side while crying, small auricles, and high palatal arch; fibrolaryngoscopy suggested bilateral vocal cord paralysis; echocardiography suggested ventricular septal defect; single nucleotide polymorphism testing showed 22q11.21 microdeletion. Therefore, the infant was given a definite diagnosis of asymmetric crying facies syndrome accompanied by 22q11.21 microdeletion. After 8-month follow-up, the infant still had asymmetric crying facies with presence of growth retardation.

Individuals with intrauterine growth retardation (IUGR) are prone to insulin resistance, whereas the underlying molecular mechanisms remain unclear. In this study, we investigated if the PI3K/Akt signaling pathway in skeletal muscle tissues involves insulin resistance in IUGR offsprings, particularly ones with catch-up growth. An IUGR rat model was established by feeding rats an isocaloric (30.50 Kcal/g) diet containing 8% protein (low-protein diet) from day 1 of pregnancy until the birth of their pups. Glucometabolic parameters were measured and compared. Quantitative PCR and western blot were performed to assess mRNA and protein expression changes of the PI3K/Akt related signals in skeletal muscle tissues. Pearson analysis was used to assess the correlation of the PI3K/Akt signaling level and catch-up growth with the insulin resistance index (IRI). The values of fasting plasma glucose, fasting insulin and IRI were significantly higher, whereas insulin sensitivity index was significantly lower in IUGR offsprings than those in the controls. The PI3K mRNA and protein levels as well as the phospho-AktSer473 levels were significantly lower in IUGR offsprings compared to the controls. Reductions of GLUT4 as well as increases of PTEN and nuclear fractional PPARγ were detected in IUGR offsprings. Catch-up growth IUGR rats were positively correlated with insulin resistance and underwent more remarkable alterations of the PI3K, PTEN and GLUT4 expressions. Our results demonstrated that rats born IUGR developed insulin resistance later in life, which was likely mediated by reductions of the PI3K/Akt related signaling activities, particularly in those with excess catch-up growth.

Autoclave is widely used in the food processing industry. This article expounds a way of heat recovery system. The aim of the system is that after heat exchanging the water energy recycle use. The article also discusses the economic efficiency of the recycling use system, so as to improve the comprehensive benefits of food production enterprises, and to protect the natural environment.

Motion control technology has become the key technology of mechatronics. This paper first introduces the general scheme of motion control technology, through the practical application of the system needs analysis, the development of specific technical implementations.

The forklift is the research object, for the reason of its large application quantities, high fuel consumption and bad emission. It is the important research direction of the energy saving of forklift to improve the working state of engine by means of hybrid technology. Based on the study of energy distribution, the schemes of parallel and series hybrid systems are evaluated, according to their fuel consumption, equipped power of working components and working parameters. The parallel hybrid system with the capacitor as energy accumulator and the project of energy regeneration with hydraulic motors are explored in detail, combining theoretical analysis. Finally, the energy regeneration,with hydraulic motor, is presented and synthetically evaluated.

A direct temperature control method for electric heating dryers was proposed in order to obtain satisfactory control effect. The controller of analog compound orthogonal neural network used a direct adaptive control method. Simulation results show that this controller has higher speed performance and smaller overshoot than a PID controller. It is suitable for the control of uncertain objects and provides a novel approach for the control of uncertain systems.

The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-β-hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P

To investigate the complications of twin-twin transfusion syndrome (TTTS) in preterm infants and to analyze the clinical conditions and prognosis of cardiac abnormalities in TTTS recipients.A retrospective analysis was performed on the clinical data of 17 pairs of preterm infants with TTTS born between June 2009 and December 2012.Compared with the recipients, the donors had significantly lower body weights (1.4±0.6 kg vs 1.9±0.6 kg; P0.05). With treatment during pregnancy, cardiac complications were found in 14 cases, and brain injuries in 12 cases. The proportion of recipients with cardiac abnormalities (60%) was higher than that of donors (24%). Among 10 recipients who had cardiac complications, cardiac abnormalities mainly included valve thickening, stenosis, or atresia (50%).Among preterm infants with TTTS, the recipients are more susceptible to complications of valvular heart disease and cardiomyopathy. Fetal echocardiography, evaluation of cardiac function, and treatment should be performed for recipients as early as possible to improve the prognosis.

The mechanisms responsible for the cardioprotective effect of hydrogen sulfide (H(2)S) are unclear. The present study was designed to examine whether H(2)S could regulate hyperhomocysteinemia (HHcy)-induced cardiomyocytic endoplasmic reticulum (ER) stress. A rat model of HHcy was produced, and H9c2 cells (rat embryonic heart-derived cell line) were cultured. The plasma homocysteine was measured by using HPLC. Plasma H(2)S concentration and myocardial H(2)S production were measured with a sulfide-sensitive electrode. Confocal immunofluorescent analysis for cardiomyocytic C/EBP homologous protein (CHOP) was performed. Glucose-regulated protein 78 (GRP78), CHOP, and caspase 12 expressions by myocardial tissues and cleaved caspase 12 and p-eIF2alpha expressions by H9c2 cells were detected with Western blotting. The results showed that methionine overload induced HHcy, resulting in a marked cardiomyocytic ER stress, whereas endogenous production of H(2)S was reduced in rats with HHcy. H(2)S supplementation, however, decreased expressions of ER stress-associated proteins, including GRP78, CHOP, and caspase 12, by myocardial tissues in vivo. The inhibition of endogenous H(2)S production further enhanced cardiomyocytic ER stress, but H(2)S supplementation effectively antagonized the H9c2 cell CHOP, cleaved caspase 12 and p-eIF2alpha expressions induced by Hcy, thapsigargin, or tunicamycin in vitro. The results suggest that H(2)S can attenuate cardiomyocytic ER stress in HHcy-induced cardiomyocytic injury.

Objective— We explored the effect of hydrogen sulfide (H 2 S) on atherosclerotic progression, particularly on intracellular adhesion molecule-1 (ICAM-1) in apolipoprotein-E knockout (apoE −/− ) mice and human umbilical vein endothelial cells (HUVECs). Methods and Results— ApoE −/− mice were treated with sodium hydrosulfide (NaHS) or DL-propargylglycine (PPG); HUVECs were pretreated with NaHS. Compared with control mice, apoE −/− mice showed decreased plasma H 2 S level and aortic H 2 S production but increased plasma ICAM-1 and aortic ICAM-1 protein and mRNA. Compared with apoE −/− mice, apoE −/− +NaHS mice showed increased plasma H 2 S level, but decreased size of atherosclerotic plaque and plasma and aortic ICAM-1 levels, whereas apoE −/− +PPG mice showed decreased plasma H 2 S level but enlarged plaque size and increased plasma and aortic ICAM-1 levels. NaHS suppressed ICAM-1 expression in tumor necrosis factor (TNF)-α–treated HUVECs. NaHS inhibited IκB degradation and NF-κB nuclear translocation in HUVECs treated with TNF-α. Conclusions— The vascular CSE/H 2 S pathway was disturbed in apoE −/− mice. H 2 S exerted an antiatherogenic effect and inhibited ICAM-1 expression in apoE −/− mice. H 2 S inhibited ICAM-1 expression in TNF-α-induced HUVECs via the NF-κB pathway.

The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats.Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-beta- hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed.In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P0.01) in association with the elevated SO2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDXtreated rats, lung tissues and plasma SO2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCT-treated rats (P0.01). In contrast, with the use of a SO2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels.Endogenous SO2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.

To investigate the modulatory effect of sodium hydrosulfide on lung tissue-oxidized glutathione and total antioxidant capacity in the development of hypoxic pulmonary hypertension (HPH).After 21 d of hypoxia, the mean pulmonary artery pressure was measured by cardiac catheterization. The plasma H2S level and production of H2S in the lung tissues were determined by using a spectrophotometer. The lung homogenates were assayed for total antioxidant capacity (T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione and malonaldehyde by colorimetry. The mRNA level of SOD was analyzed by real-time PCR, and the SOD expression was detected by Western blotting.In the hypoxia group, the plasma H2S concentration and H2S production in the lung was significantly decreased compared with the control group (187.2+/-13.1 vs 299.6+/-12.4 micromol/L; 0.138+/-0.013 vs 0.289+/-0.036 nmol x mg(-1) x min(-1), P0.01). The administration of sodium hydrosulfide could reduce the mean pulmonary artery pressure by 31.2% compared with the hypoxia group (P0.01). Treatment with sodium hydrosulfide decreased GSSG, and the T-AOC level of the lung tissues was enhanced compared with the hypoxia group (P0.05). There were no significant changes in the lung tissue SOD mRNA level, protein level, and its activity among the 3 groups.Oxidative stress occurred in the development of HPH and was accompanied by a decrease in the endogenous production of H2S in the lung tissues. H2S acted as an antioxidant during the oxidative stress of HPH partly as a result of the attenuated GSSG content.

To study the modulatory effect of hydrogen sulfide (H(2)S) on oxidative stress in the development of pulmonary hypertension induced by hypoxia.Twenty male Wistar rats were randomly divided into control group (n=6), hypoxic group (n=6) and hypoxia+NaHS group (n=8). Hypoxic challenge was performed everyday for 21 days. NaHS solution was injected intra-peritoneally everyday before hypoxic challenge for rats in the hypoxia+NaHS group. After 21 days of hypoxia, the mean pulmonary artery pressure(mPAP) was measured by cardiac catheterization. The weight ratio of right ventricle to left ventricle+septum [RV/(LV+SP)] was also measured. The lung homogenates were assayed for total antioxidant capacity(T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione (GSH), malondialdehyde(MDA) and hydroxy radical(*OH), and the SOD mRNA levels were assayed by real time polymerase chain reaction.After three weeks of hypoxic disposure, hypoxic hypertension and vascular remodeling developed. Compared with the control group, the mPAP[(23.7+/-2.2) mm Hg vs (16.3+/-3.7) mm Hg,P0.01] and the weight ratio of RV/(LV+SP) increased (P0.01), but lung tissue T-AOC was decreased by 21.4% (P0.01).But GSSG was increased by 68.5% (P0.01) as compared with those of the control rats. However, compared with those of the hypoxic group, the mPAP in rats of hypoxia+NaHS group was decreased [(16.3+/-2.8) mm Hg vs (23.7 +/-2.2) mm Hg]. Administration of NaHS increased T-AOC by 18.8% (P0.05) but eliminated GSSG by 23.2% (P0.05) in rats of hypoxia+NaHS group as compared with the hypoxic group. There were no significant changes in lung tissue SOD mRNA level and its capacity among the three groups.Hydrogen sulfide acted as antioxidant during the oxidative stress of hypoxic pulmonary hypertension, and the mechanism was partly through attenuating the content of GSSG.