Insulin resistance in children with nephrotic syndrome with long-term glucocorticoid treatment and its intervention / 中华实用儿科临床杂志

Objective To investigate children with nephrotic syndrome (NS) receiving long-term glucocorticoid treatment while monitoring insulin resistance(IR) index,and analyze the influencing factors,and to observe the efficacy of metformin for preventing glucocorticoid-induced obesity and diabetes mellitus type 2.Methods A total of 32 cases including 20 boys and 12 girls with mean age of 7.6 years old(2 to 14 years old),were diagnosed as NS.All children undergoing long-term treatment of prednisone ＞ 1 mg/(kg · d) for at least 3 months.The height,body weight and body mass index(BMI) were monitored.The concentrations of serum insulin and C-peptide were determined by radioimmunoassay,the concentrations of serum HbA1 c were determined by high performance liquid chromatography,and the levels of fasting glucose,cholesterol and triglyceride were measured with an automatic measuring analyzer (American ABBO TT CCX-Ⅱ).The homeostasis model assessment-estimated insulin resistance(HOMA-IR) was calculated;When HOMA-IR ＞ 3.5,the patients were given metformin treatment for 12 weeks while supervising their height,weight,fasting blood glucose levels monthly.Results Out of 32 cases of NS with long-term use of prednisone,23 cases had HOMAIR ＞ 3.5 (72％).Thus,IR group included 23 patients,and non-IR (NIR) group had 9 patients.There were significant differences between 2 groups in BMI,age,prednisone dosage and the levels of triglyceride (TG) (all P ＜ 0.05).After 12 weeks of metformin treatment,the HOMA-IR (5.24 ± 1.82 vs 2.54 ± 1.09,P ＜ 0.01),HbA1 c levels [(6.36 ±0.82)％ vs(5.39 ±0.51)％,P ＜0.05],BMI[(27.42 ±6.12) kg/m2 vs(22.72 ±5.48) kg/m2,P ＜0.01],and TG levels[(2.03 ± 1.10) mmol/L vs(1.45 ±0.48) mmol/L,P＜0.05] were significantly reduced.Conclusions Older children with long-term use of glucocorticoid may easily lead to IR.Therefore,monitoring the HOMA-IR and early administration of mefformin is helpful for prevention and treatment of glucocorticoid-induced obesity and diabetes mellitus type 2.

Risk factors for recurrent pneumonia in children: a case-control study / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the risk factors for recurrent pneumonia in children without underlying diseases.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p>

Effects of 11beta-hydroxysteroid dehydrogenase inhibitor on body weight and glucose tolerance in Sprague-Dawley rats fed with a high-fat diet / 中国当代儿科杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>Long-term GE treatment may contribute to resisting diet-induced obesity and insulin resistance.</p>

Effects of D-limonene on leukemia cells HL-60 and K562 in vitro / 中国实验血液学杂志

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.

Construction and Identification of Lentiviral-Mediated RNA Interference Vector of Rat Suppressors of Cytokine Signaling 3 Gene / 实用儿科临床杂志

Objective To study the construction of the lentiviral-mediated RNA interference(RNAi) vector targering rat suppressors of cytokine signaling 3(SOCS3) gene.Methods Three target sequences were selected by on-line designer software on Ambion according to rat SOCS3 mRNA sequence(NM053565),the complementary DNA contained both sense and antisense oligonucleotides were designed and synthesized.After annealing,these double strands DNA were cloned to pRNA-Lenti-green fluorescent protein(GFP),which contained U6 promoter and GFP.The resulting Lentiviral vector containing SOCS3 shRNA was named pRNA-Lenti-SOCS3-GFP.After the rat glioma cells(C6)were transduced with the constructed 1entiviral vectors,real-time polymerase chain reaction was used to evaluate the level of SOCS3 expression(including siRNA1 group,siRNA2 group,siRNA3 group,vacuity group and siRNA-Negative group).The pRNA-Lenti-SOCS3-GFP and Lentivector Pakaging plasmid mix were cotransfected into 293T to package Lentivirus particles.Culture supematant was harvested,then the virus titer was determined by serial dilution assay.Results The SOCS3 mRNA sequence was successfully cloned to pRNA-Lenti-GFP,which was proved by PCR and DNA sequence.Compared with control group,the SOCS3 mRNA expressions were obviously suppressed in all 3 experimental groups,especially the expression rate in siRNA1 group was reduced by 80%.The Lentiviral particle titer was determined by serial dilution assay with 1.0?1010 TU?L-1.Conclusion The lentiviral-mediated RNAi vector of rat SOCS3 gene has been constructed successfully,this may provide a potential tool for studying and treating SOCS3-related diseases.