Obesity increases the risk of renal involvement in children with Henoch-Schönlein purpura.

UNLABELLED: The main aim of this study was to evaluate the relationship between obesity and renal involvement in children with Henoch-Schönlein purpura (HSP). A retrospective study of 141 pediatric patients with HSP was conducted in our hospital. The clinical data of all patients were collected from the electronic medical record management system from January 2010 to June 2014. The possible risk factors of renal involvement, especially obesity, were analyzed using univariate and multivariate analyses. Renal involvement occurred in 45/141 of the patients. A univariate analysis showed that an age more than 7 years at onset, persistent purpura, obesity, time from symptoms onset to diagnosis more than 14 days, and decreased C3 all increased the risk of renal involvement in HSP. The forward stepwise logistic regression analysis indicated obesity (odds ratio (OR) 4.43, 95 % confidence interval (CI) 1.896 to 10.358), age more than 7 years at onset (OR 2.81, 95 % CI 1.142 to 6.907), and persistent purpura (OR 2.57, 95 % CI 1.119 to 5.909) were independent risk factors for renal involvement. CONCLUSIONS: Our results show that obesity can increase the hazard of renal involvement in children with HSP and reconfirm that older age at onset and persistent purpura are the independent risk factors for renal involvement. WHAT IS KNOWN: • There have been some reports that obesity was associated with the development of renal injury. • It is not clear whether obesity can increase the risk of renal involvement in children with HSP. What is New: • The main finding of this study is that obesity can increase the hazard of renal involvement in children with HSP.

[Risk factors for recurrent pneumonia in children: a case-control study].

OBJECTIVE: To study the risk factors for recurrent pneumonia in children without underlying diseases. METHODS: A case-control study was conducted in 106 children with recurrent pneumonia (case group) and 106 age, gender- and weight-matched children with pneumonia but no recurrence (control group). The children in both groups had no underlying disease. The risk factors for recurrent pneumonia were investigated by the Chi-Square analysis and the multivariate logistic regression model. RESULTS: The Chi-Square analysis showed that the percentages with the history of wheezing, allergy (food or medicine) and eczema and the percentage of transient neutropenia in the case group were significantly higher than those in the control group. The multivariate logistic regression analysis showed that the wheezing history (OR=13.387, 95% CI: 5.541-32.343), allergic history (food or medicine) (OR=4.267, 95% CI: 2.081-8.751) and transient neutropenia (OR=3.606, 95% CI: 1.806-7.202) were the independent risk factors of recurrent pneumonia. CONCLUSIONS The wheezing history, allergic history and transient neutropenia may increase the risk of recurrence of pneumonia in pneumonic children without underlying diseases.

Magnet-targeted delivery of bone marrow-derived mesenchymal stem cells improves therapeutic efficacy following hypoxic-ischemic brain injury.

Stem cell transplantation may represent a feasible therapeutic option for the recovery of neurological function in children with hypoxic-ischemic brain injury; however, the therapeutic efficacy of bone marrow-derived mesenchymal stem cells largely depends on the number of cells that are successfully transferred to the target. Magnet-targeted drug delivery systems can use a specific magnetic field to attract the drug to the target site, increasing the drug concentration. In this study, we found that the double-labeling using superparamagnetic iron oxide nanoparticle and poly-L-lysine (SPIO-PLL) of bone marrow-derived mesenchymal stem cells had no effect on cell survival but decreased cell proliferation 48 hours after labeling. Rat models of hypoxic-ischemic brain injury were established by ligating the left common carotid artery. One day after modeling, intraventricular and caudal vein injections of 1 × 105 SPIO-PLL-labeled bone marrow-derived mesenchymal stem cells were performed. Twenty-four hours after the intraventricular injection, magnets were fixed to the left side of the rats' heads for 2 hours. Intravoxel incoherent motion magnetic resonance imaging revealed that the perfusion fraction and the diffusion coefficient of rat brain tissue were significantly increased in rats treated with SPIO-PLL-labeled cells through intraventricular injection combined with magnetic guidance, compared with those treated with SPIO-PLL-labeled cells through intraventricular or tail vein injections without magnetic guidance. Hematoxylin-eosin and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining revealed that in rats treated with SPIO-PLL-labeled cells through intraventricular injection under magnetic guidance, cerebral edema was alleviated, and apoptosis was decreased. These findings suggest that targeted magnetic guidance can be used to improve the therapeutic efficacy of bone marrow-derived mesenchymal stem cell transplantation for hypoxic-ischemic brain injury. This study was approved by the Animal Care and Use Committee of The Second Hospital of Dalian Medical University, China (approval No. 2016-060) on March 2, 2016.

Effects of 11beta-hydroxysteroid dehydrogenase inhibitor on body weight and glucose tolerance in Sprague-Dawley rats fed with a high-fat diet.

OBJECTIVE: Many studies have shown that glucocorticoids play a crucial role in the development of obesity and insulin resistance. This study investigated the therapeutic effects of long-term inhibition of glucocorticoid activity on obesity and insulin resistance. METHODS: Four-week-old male Sprague-Dawley (SD) rats were randomly fed with a high-fat diet (fat content accounting for 20% of total calorie) (control group, n=8) or with a high-fat diet along with glycyrrhetic acid (GE, 800 mg/L), an inhibitor of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) for 24 weeks (GE-treated group, n=9). The body weights and the amount of food intake were monitored weekly and daily, respectively. After 24 weeks of GE treatment, oral glucose tolerance tests were performed. Blood glucose was measured by glucose oxidase method. The levels of plasma glucocorticoids, insulin and leptin were measured with radioimmunoassay. The levels of serum cholesterol and triglyceride were determined with an automatic measuring analyzer. RESULTS: The food intake amount decreased significantly in the GE-treated group from 6 weeks and body weight gain was markedly less from 8 weeks after GE administration compared with the control group. After 24 weeks of treatment, the plasma levels of leptin and insulin in GE-treated rats were significantly reduced compared with the control group. The serum levels of cholesterol and triglyceride decreased markedly compared with the control group and the levels of blood glucose were significantly lower 15, 30, 60 and 120 minutes after oral glucose load in the GE-treated group compared with the control group. CONCLUSIONS: Long-term GE treatment may contribute to resisting diet-induced obesity and insulin resistance.

[Effects of leptin and insulin on leptin receptors mRNA expression in human hepatocellular HepG2 cells].

OBJECTIVE: To study the leptin receptor isoforms regulation by leptin and insulin. METHODS: Human hepatocellular carcinoma cells of the line HepG2 were cultured in DMEM containing 10% FBS in six-well plate and were incubated for 24 hours in serum-free medium containing 0, 10(-9), 10(-8), 10(-7), and 10(-6) mol/L of human leptin or insulin. Using the semi-quantitative RT-PCR technique, the mRNA expressions of long (OB-Rb) and short (OB-Ra: OB-R219.3) leptin receptor isoforms were measured. RESULTS: OB-Rb and OB-R219.3 mRNAs were expressed in this cell line. Leptin of the concentrations of 10(-7) approximately 10(-6) mol/L significantly inhibited the OB-Rb mRNA expression, with the maximum decrease (by 43%) at the concentration of 10(-6) mol/L. Similarly the mRNA expression of OB-R219.3 was also markedly reduced in cells treated with leptin of the concentrations of 10(-8) approximately 10(-6) (mol/L), with the maximum inhibition (by 49%) at the concentrations of 10(-6) mol/L. Insulin showed no effect on OB-Rb and OB-R219.3 mRNAs expression in HepG2 cell. CONCLUSION: In HepG2 cells, leptin down-regulates the expressions of OB-Rb and OB-R219.3 mRNAs, and insulin has no effect on OB-Rb and OB-R219.3 mRNAs, which contributes at least partly to an understanding of the mechanism of leptin resistance in vivo and suggests that leptin-induced receptor down-regulation may be relevant to leptin resistance at sites of peripheral action.

The application of nasal synchronized intermittent mandatory ventilation in primary apnea of prematurity.

We aimed to evaluate the efficacy of nasal synchronized intermittent mandatory ventilation (nSIMV) in preterm infants with primary apnea of prematurity (AOP). Forty-four preterm infants with AOP were divided into the nSIMV group or nasal continuous positive airway pressure (nCPAP) group. Clinical symptoms, signs and blood gas results following nSIMV or nCPAP were compared between the two groups. Infants receiving nSIMV had a greater reduction in apneic spells and a greater decrease in bradycardia than those receiving nCPAP. Compared with the nCPAP group, the nSIMV group had a lower incidence of respiratory support failure (9.1% vs. 27.3%; p<0.05), a lower incidence of hypercarbia (4.5% vs. 18.2%; p<0.05) and a lower incidence of gastrointestinal complications (4.5% vs. 13.6%; p<0.05). This study showed that nSIMV was more effective in respiratory support in preterm infants with AOP.

[Effects of D-limonene on leukemia cells HL-60 and K562 in vitro].

To investigate the effects of D-limonene (D-L) on the cell growth and apoptosis in HL-60, K562 cells and to elucidate its mechanism, the influence of D-L on proliferation of HL-60 and K562 cells was determined by propidium iodide assay, the expression levels of mutant p53, bcl-2, bax gene were detected by cell morphological analysis, flow cytometry and immunohistochemistry staining, the D-L-inducing HL-60 and K562 cell apoptosis in vitro was observed systematically. The results showed that D-L inhibited HL-60 and K562 cell growth in a dose- and time-dependent manner with the IC50 of 0.75 mmol/L similarly, D-L induced apoptosis of HL-60 and K562 cells, and expression of bcl-2 gene was down regulated by D-L in a concentration-dependent manner in HL-60 cells. The bcl-2, mutant type of p53 genes were down regulated while bax gene was up regulated by D-L in a concentration-dependent manner in K562 cells. It is concluded that D-L can inhibit proliferation and induce apoptosis of HL-60 and K562 cells. The bcl-2, mutant type of p53 and bax may be involved in the gene regulation of D-L-induced apoptosis.

Effects of leptin and dexamethasone on long and short leptin receptor mRNA.

BACKGROUND: Leptin exerts its effects by using both long (OB-Rb) and short (OB-Ra) receptors. Although leptin resistance or insensitivity is reported to be a cause of human obesity, there have not been enough studies to clarify regulation of leptin receptors. METHODS: The authors studied leptin receptor regulation by leptin and dexamethasone in the human hepatocellular carcinoma cell (HepG2). Using a quantitative RT-PCR technique, the authors demonstrate expression of OB-Ra and OB-Rb mRNA after the incubation for 24 h with leptin or dexamethasone at various concentrations (10(-9)-10(-6) M). RESULTS: Leptin (10(-7)-10(-6) M) significantly inhibited expression of OB-Rb mRNA, with maximum inhibition (43% of control) at 10(-6) M. Expression of OB-R219.1 and OB-R219.3, two short isoforms of leptin receptor, were also reduced in cells treated with leptin most remarkably at 10(-7) M for OB-R219.1 (44% of the control) and at 10(-6) M for Ob-R219.3 (49% of the control). In contrast, dexamethasone (10(-8)-10(-6) M) significantly increased OB-Rb mRNA levels, with a maximum increase (204% of the control) at 10(-7) M, and OB-R219.1 and OB-R219.3 mRNA expression was also markedly increased at 10(-9)-10(-6) M. The peak values were 254% of the control for OB-R219.1 and 246% of the control for OB-R219.3 at 10(-7) M. CONCLUSIONS: In HepG2 cells, leptin inhibits and dexamethasone increases OB-Ra and OB-Rb mRNA expression. It is suggested that glucocorticoids as well as leptin itself contribute to regulatory effects of leptin through changes in gene expression of leptin receptors.