Comparative study of antegrade and retrograde intramedullary nailing for the treatment of humeral shaft fractures / 中国骨伤

<p><b>OBJECTIVE</b>To compare therapeutic effects between antegrade intramedullary nailing and retrograde intramedullary nailing for the treatment of humeral shaft fractures.</p><p><b>METHODS</b>From March 1999 to October 2006, 105 patients with humeral shaft fractures were treated with locked intramedullary nail and were adequately followed up. There were 82 antegrade nailing and 23 retrograde nailing. The follow-up parameters included operation time, blood loss,fracture healing rate, healing time, complications, Constant-Murley shoulder score and Mayo elbow performance score.</p><p><b>RESULTS</b>The mean follow-up period was 31.2 months. Antegrade intramedullary nailing had significantly less blood loss than that in retrograde intramedullary nailing (P=0.002). The differences in operation time, complications, healing time and bone healing rate between he two groups had no statistical significance. Complications in the antegrade intramedullary nail group included 4 patients with nonunions, 1 patient with radial nerve palsy, and 8 patients with shoulder pains and decrement in shoulder range of motion. Complications in the retrograde intramedullary nail group included 1 patient with radial nerve palsy and 3 patients with iatrogenic fractures. For shoulder joints,the difference in the average Constant-Murley shoulder score between the two groups was statistically significant (P=0.04). For elbow joints, the average postoperative Mayo elbow performance score between these two approaches did not differ significantly.</p><p><b>CONCLUSION</b>Both the antegrade intramedullary nailing and the retrograde intramedullary nailing are good alternatives for the treatment of humeral shaft fractures. Because of higher incidence of iatrogenic fractures, the insertion point of retrograde intramedullary nailing should be carefully prepared. With antegrade insertion, it important to bury the humeral nail below the rotator cuff to prevent the subacromial impingement, and the rotator cuff should be carefully repaired to avoid shoulder pain and improve shoulder function.</p>

Antibiotic-PMMA beads combined with external fixator for treating the infected fracture nonunion / 中国骨伤

<p><b>OBJECTIVE</b>To investigate the effects of antibiotic-PMMA (polymethyl-methacrylate) beads combined with external fixator in treatment of infected fracture nonunion.</p><p><b>METHODS</b>Twenty-two cases of infected fracture-nonunions were reviewed involving 20 male and 2 female with an average age of 34.68 years (ranging 21 to 74 years). The data consisted of 9 cases of tibial fractures, 2 distal fractures of the femur, 6 femoral shaft fractures, 3 intertrochanteric fracture of the femur and 2 humeral shaft fractures. The procedure included thorough debridement to wipe out dead bone and granulation tissue, then antibiotic-PMMA bead chains imbedded into the dead space. One week later, secondary debridement was performed, antibiotic-PMMA bead chains were changed according to result of bacterial culture and susceptibility test, and fractures were stabilized with external fixator. Three months after debridement, antibiotic-PMMA bead chains were taken out and bone graft with autogenous iliac cancellous bone chips was performed.</p><p><b>RESULTS</b>The mean follow-up period was 19.98 months (ranging 15 to 28 months). Infection was controlled in 20 cases. One tibial fracture and 1 intertrochanteric fracture of the femur needed repeated debridement 2 and 3 months after bone grafting respectively,because of infection recurrence and sinus formation. All 22 cases achieved bony union averaged 15.09 weeks after bone grafting with a range of 8 to 24 weeks.</p><p><b>CONCLUSION</b>Thorough debridement, imbedding antibiotic-PMMA bead chains combined with external fixator and staged bone grafting has proven to be effective and simple for treatment of infected fracture nonunion. The antibiotic bead delivers high tissue levels,obliterates dead space, aids bone repair.</p>

Effect of (-)-epigallocatechin-3-gallate and 5-AZA-CdR on expression of X-linked inhibitor of apoptosis protein-associated factor 1 in human leukemia HL-60 and K562 cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the expression of X-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (Xaf1) in human leukemia HL-60 and K562 cells treated with interferon alpha (INFalpha) and the demethylating agent 5-AZA-CdR, and observe the synergetic antitumor effect of Xaf1 inducer and (-)-epigallocatechin-3-gallate (EGCG).</p><p><b>METHODS</b>Human leukemia HL-60 and K562 cells were treated for 48 h with 1000 U/ml INFalpha and different doses of 5-AZA-CdR, and the mRNA expressions of both Xaf1 and XIAP were measured by RT-PCR. The leukemia cells were also treated with the optimal Xaf1 inducer in combination with EGCG, after which flow cytometry was employed to examine the changes in the members of the Bcl-2 family, mitochondrial transmembrane potential and apoptosis.</p><p><b>RESULTS</b>As the dose increased, 5-AZA-CdR dose-dependently up-regulated the mRNA expression of Xaf1 in HL-60 and K562 cells; INFalpha treatment also resulted in increased Xaf1 expression, but 5 micromol/L 5-AZA-CdR showed the most potent effect. Neither INFalpha nor 5-AZA-CdR caused significant changes in XIAP expression. Combined treatment with 5-AZA-CdR and EGCG altered the expressions of Bcl-2 (Bcl-xl) and Bax in HL-60 and K562 cells, decreased the mitochondrial transmembrane potential and induced cell apoposis, and the two agents exhibited obvious synergistic effect.</p><p><b>CONCLUSION</b>INFalpha and 5-AZA-CdR can induce Xaf1 mRNA expressions in HL-60 and K562 cells, and the effect of 5-AZA-CdR was dose-dependent. 5-AZA-CdR and EGCG induces apoptosis of leukemia cells in vitro, and they exhibits obvious synergetic effects.</p>

Effect of dexamethasone on the expression of aquaporin-5 in the lungs of mice with acute allergic asthma / 南方医科大学学报

<p><b>OBJECTIVE</b>To detect the expression of lung aquaporin 5 (AQP5) in mice with acute allergic asthma and the effect of dexamethasone (DEX) treatment on AQP5 expression, and investigate the role of AOP5 in asthma pathogenesis.</p><p><b>METHODS</b>Mouse models of acute allergic asthma were randomly divided into acute asthma group, normal control group and DEX treatment group. The total number of white blood cells, the subpopulations, and the levels of IL-5 and IFN-gamma were detected in the bronchoalveolar larvage fluid (BALF). The lung tissue AQP5 mRNA expression was detected by RT-PCR, and AQP5 distribution by immunohistochemical method.</p><p><b>RESULTS</b>In asthma group, the total white blood cells, eosinophils and IL-5 levels were all significantly higher (P<0.01) and IFN-gamma levels lower than those of the control group (P<0.01). After DEX treatment, the levels underwent a significant reverse change (P<0.05, P<0.01, P<0.01, and P<0.01, respectively). AQP5 mRNA expression in the asthma group was significantly higher than that in the control group (P<0.01), and was significantly lowered with DEX treatment (P<0.01). Extensive inflammatory changes, mucus hypersecrection, several edema and inflammatory cell infitration around the blood vessels were observed in the lung tissue of the mice in the asthma group. The morphological changes of the treatment group were significantly ameliorated. AQP5 protein was detected in the type I alveolar epithelial cells, the airway columnar epithelial cells and the apical membranes of the submucosal gland acinar cells in the control group. Stronger AQP5 protein expression was found in the asthma group.</p><p><b>CONCLUSION</b>AQP5 is over-expressed in mice with acute asthma which is possibly associated with mucus hypersecrection. DEX can inhibit AQP5 expression and ameliorate allergic airway inflammation, edema and mucus hypersecrection.</p>

Promoting male circumcision in China for preventing HIV infection and improving reproductive health / 中华男科学杂志

The incidence of heterosexually transmitted HIV infection is rapidly increasing in China, which reached 44.7% among the HIV-positive patients in 2007. With a view to the reduction of HIV transmission and improvement of reproductive health in the Chinese population, this paper introduces the latest evidence obtained from the international epidemiological studies and randomized controlled clinical trials on the preventive effect of male circumcision (MC) on HIV transmission, and elucidates the cellular and molecular mechanisms of HIV transmission through the foreskin. Four studies published during 1997-2007 demonstrated that the mean prevalences of redundant prepuce and phimosis in 15,109 Chinese males aged 3-23 years in 4 areas of China were 43.90 and 11.55% , respectively, while the rate of MC was only 2.66%. As MC is a simple, inexpensive and highly effective technique in HIV prevention, we appeal to the policy-makers in China to conduct a practical program for promoting MC and enhancing male productive health in combination with other approaches to the prevention of HIV infection. MC for neonates, children, adolescents and adults should be included in the health insurance program, and free and timely MC should be performed for the male adults with the high risk of HIV infection and the normal ones whose wives are HIV-positive. Further investigations should be carried out on the epidemiology of redundant prepuce and phimosis, the acceptance and socio-cultural context of MC and the development of simpler and safer methods for MC.

Identification of genes that are differentially expressed in omental fat of normal weight subjects, obese subjects and obese diabetic patients / 中国应用生理学杂志

<p><b>AIM</b>To identify genes that are differentially expressed in omental fat of normal weight subjects, obese subjects and obese type 2 diabetic patients.</p><p><b>METHODS</b>Using a home-made high-density cDNA microarray, we compared gene expression profile of omental fat from normal weigh subjects, obese subjects and obese type 2 diabetic patients, to identify adipose-specific genes associated with obesity and diabetes.</p><p><b>RESULTS</b>119 and 257 genes were up-regulated in obese patients and obese diabetic patients respectively, while 46 and 58 genes were down-regulated in obese patients and obese diabetic patients respectively. 77 genes, including metabolism related genes (PDK4), and caveolin 2, metallo thionein 1B, were up-regulated in both obese and obese diabetic patients, while 8 genes, including key enzymes in lipid synthesis, such as HMG-CoA synthase, fatty acid synthase and stearoyl-CoA desaturase, were down-regulated in both groups. Another interesting finding was that tyrosine-3-monooxygenase/ tryptophan 5-monooxygenase activation protein theta (YWHAZ), a negative regulator for insulin signal transduction, was up-regulated only in obese diabetic patient, but not in normal-glycemic obese subjects.</p><p><b>CONCLUSION</b>Our study demonstrated that decrease of lipogenesis along with increase of fatty acids oxidation of adipose tissue could be a common cause of insulin resistance in obesity and type 2 diabetes, while functional changes of other genes, such as immune regulation genes,might also be involved in the pathogenesis of obesity and type 2 diabetes. Block of insulin signal transduction might trigger the transition from obesity to diabetes. Further exploration of these genes will greatly help us in the understanding of the pathogenesis of obesity and type 2 diabetes.</p>

Advance of study on mesenchymal stem cell homing--review / 中国实验血液学杂志

Mesenchymal stem cells (MSCs) are non-hematopoietic stem cells possessing multi-differentiation potential, and were widely used in stem cell transplantation, tissue engineering, organ transplantation and immunotherapy, etc. However, the distribution and differentiation of MSCs after reinfusion directly influence their application. In this paper the "homing" characteristics, mechanisms and significance of MSCs were reviewed.

McCune-Albright syndrome: a difficult and complicated case study / 中国当代儿科杂志

McCune-Albright syndrome is a rare G proteins alpha disorder. The disorder is characterized by polyostotic fibrous dysplasia, sexual precocity and hyperpigmented macules. It is caused due to mutations in the gene Gsalpha that incodes the alpha subunit of the trimeric guanosine triphate-binding protein. There is no specific treatment for this syndrome. Treatment is generally symptomatic. This paper reported three cases of McCune-Albright syndrome and reviewed the relevant literatures regarding to the pathogenesis, pathological features, diagnosis and treatment. All three cases presented with a characteristic triad: polyostotic fibrous dysplasia, sexual precocity and hyperpigmented macules and were thus definitely diagnosed with McCune-Albright syndrome.

Construction of Microvessel Angiogenesis Model in Nonobese Diabetic/Severe Combined Immunodeficient Disease Leukemia Mice / 实用儿科临床杂志

Objective To construct microvessel angiogenesis model in nonobese diabetic/severe combined immunodeficient disease(NOD/SCID) leukemia mice.Methods Divided NOD/SCID mice into group A:blank group;group B:endothelial cell(EC) injection group;group C:leukemia model mice with EC injection group.Microvessel density(MVD) in bone marrow was calculated with cnemis slice after immunohistochemistry dyeing.Evaluated leukemia burden in leukemia model mice.Results Bone marrow MVD in group C was significantly more than group B.Microvessels in leukemia mice had disordered branches and irregular cavity.The morphism of vessels was immature.Conclusions Microvessel angiogenesis model in NOD/SCID leukemia mice has been constructed successfully.It can be used in the study of anti-angiogenesis in leukemia and relative researches.

Role of menin in regulation of SOX4 gene expression / 上海第二医科大学学报

Objective To explore the role of menin in regulation of SOX4 gene expression. Methods Reporter gene vectors with SOX4 promoter were constructed,and the influence of menin on SOX4 gene promoter activity was analyzed by dual-luciferase reporter gene assay system.Real-time PCR was employed to detect the expression of SOX4 gene in mef cells of MEN1-/-mice and wild-type mef cells. Results Compared with wild-type mef cells,the SOX4 gene promoter activity was significantly higher in mef cells of MEN1-/-mice.After MEN1 gene was transfected into mef cells of MEN1-/-mice,the SOX4 gene promoter activity significantly descreased.The expression of SOX4 gene in mef cells of MEN1-/-mice was 2.5 time higher than that in wild-type mef cells. Conclusion Menin can inhibit the expression of SOX4 gene.

Experimental study on the mechanism of the apoptosis of leukemic cells induced by valproic acid / 中华儿科杂志

<p><b>OBJECTIVE</b>To overcome the drug-resistance of tumor cells is one of the methods of improving the therapeutic results. Histone deacetylase inhibitors (HDACIs) is a novel class of chemotherapeutic agents which can induce apoptosis of tumor cells. Valproic acid (VPA) is a common drug used in the treatment of epilepsy. It has been shown that VPA has a marked HDACIs effect at the pharmaceutical level, and can induce the differentiation and apoptosis of transformed cells. But the mechanism of its effect has not been clarified. The aim of this study was to investigate the mechanism of VPA in inducing the apoptosis of leukemic cells at molecular level.</p><p><b>METHODS</b>The cell lines U937, Jurkat clone E6 - 1 (Jurkat) and BALL-1 were cultured in RPMI 1640 medium containing 20% calf serum, then divided into three groups (control group, 1 mmol/L VPA group and 1 mmol/L VPA + 1 micromol/L Pan-caspase inhibitor zVAD-fmk group). At 72 hours after the treatment, the cells were double stained with Aunexin and PI (propidium iodide) and then were analyzed with the flow cytometry (FCM) to detect apoptosis. Before and after treatment with VPA the mean fluorescence index (MFI) of Bcl-2, Bax, Bcl-xl and the levels of caspase 8, 9 and 3 were also detected with the FCM. The changes of P(44/42) mitogen activating protein kinase (MAPK) and phosphorylated P(44/42) MAPK were determined by Western blotting.</p><p><b>RESULTS</b>Seventy-two hours after the treatment, 1 mmol/L VPA induced apoptosis of U937 and Jurkat. The apoptotic rate of U937 was (75.78 +/- 4.20)% and that of Jurkat was (53.50 +/- 5.87)% (P < 0.01, vs. control group); zVAD-fmk could fully inhibit the apoptosis of U937, and the apoptotic rate was (2.89 +/- 0.36)%; while it could partly inhibit the apoptosis of Jurkat, and the apoptotic rate was (15.38 +/- 1.40)% (P < 0.01). 1 mmol/L VPA could not induce the apoptosis of BALL-1 which had a high expression level of Bcl-2. The MFI of Bcl-2, Bax and Bcl-xl in these three cell lines did not change significantly with VPA (P > 0.05). After treatment with VPA, the level of caspase 3 in U937 increased from (14.09 +/- 1.19)% to (32.30 +/- 2.47)%, and caspase 8 from (4.58 +/- 1.41)% to (86.47 +/- 3.26)% (P < 0.01), but there was no significant change in caspase 9 [(13.25 +/- 3.11)% and (10.95 +/- 1.30)%]. In Jurkat, the level of caspase 3 increased from (12.01 +/- 1.63)% to (35.56 +/- 0.27)%, and caspase 9 from (13.89 +/- 1.71)% to (75.89 +/- 4.08)% (P < 0.01 for both); no significant change was observed for caspase 8 [(5.94 +/- 1.38)% and (5.44 +/- 0.72)%]. In BALL-1, there was a slight decline in caspase 3 (P < 0.05). With the effect of VPA, levels of P(44/42) MAPK and phosphorylated P(44/42) MAPK decreased in all three cell lines (P < 0.01).</p><p><b>CONCLUSION</b>VPA could induce apoptosis of U937 through the activation of caspase 3 and 8; and it induced the apoptosis of Jurkat involving the activation of caspase 3 and 9. P(44/42) MAPK pathway also plays an important role in this course. VPA induced apoptosis of these cell lines without the alteration of Bcl-2, Bax and Bcl-xl. High level of Bcl-2 could antagonize the effect of VPA.</p>

Inhibiting Effect of Vascular Endothelial Growth Factor Antisense Oligonucleotides on HL60 Cell and HL60/VCR Multidrug Resistance Cell / 实用儿科临床杂志

Objective To explore the effect of vascular endothelial growth factor antisense oligonucleotides(AS-VEGF)on HL60 cell and HL60/VCR multidrug resistance cell and analyze the function of P-gp and the expression of related multidrug resistance genes including Bcl-2,Mcl-1,MDR1,MRP,GST?,TopoⅡ? and TopoⅡ?.Methods A vector AS-VEGF which expressed in eukaryotic cell was established,then transfected the vector into HL60 and HL60/VCR by limposome transfection technology,observed and drew the growth curve by Tapanlan taining,RT-PCR was used to detect the expression of Bcl-2,Mcl-1,MDR1,MRP,GST?,TopoⅡ? and TopoⅡ? in mRNA level after transfected 24 h and 48 h.Western Blot was used to detect the expression of P-gp in proteinum level after transfected 24 h and 48 h.Results The growth of HL60 and HL60/VCR was inhibited by AS-VEGF(1.25 mmol/L).Between HL60 and HL60/VCR,AS-VEGF decreased the expression of MDR1,MRP,GST? and TopoⅡ? but could not influence the expression of Bcl-2,Mcl-1 and TopoⅡ?,and the expression of P-gp was also obviously decreased in 48 h compared with that in 24 h.Conclusions AS-VEGF can inhibite the growth of HL60 and HL60/VCR and reverse multidrug resistance by changing cell microenvironment and the cell membrane correlated protein transportating channel,reduce the cell disintoxicating and the self-repair ability.

Effects of meisoindigo on the expression of globin gene in vitro / 中华儿科杂志

<p><b>OBJECTIVE</b>The pathophysiology of beta-thalassemia is the imbalance of the alpha and non-alpha globin chain which leads to a series of clinical symptoms of hemolytic anemia. Scientists continuously try to explore gene-activated drugs to increase the level of non-alpha globin chain or decrease the level of alpha globin chain in the treatment of beta-thalassemia. To probe into the effects on globin-gene expression of meisoindigo (Me) in cultured erythroid cells derived from peripheral blood, so as to provide the theoretical basis for applying Me in the treatment of beta-thalassemia.</p><p><b>METHODS</b>By using the two-step liquid culture of erythroid progenitor cells and reverse transcription polymerase chain reaction (RT-PCR), and by using alpha mRNA as an inner control, the level of gamma mRNA and beta mRNA in cultured erythroid cells derived from peripheral blood of 11 patients with severe beta-thalassemia and 6 normal volunteers were measured under the effect of different concentration (2.5 micro mol/L, 5 micro mol/L and 10 micro mol/L) of Me.</p><p><b>RESULTS</b>(1) No statistic significance was found in the ratio of beta/alpha mRNA by Me in cultured cells from both normal individuals and beta-thalassemia. (2) Me can significantly increase the ratio of gamma/alpha mRNA and (beta + gamma)/alpha mRNA (that is non-alpha/alpha mRNA) in cultured cells from normal individuals and beta-thalassemia. The ratio of gamma/alpha mRNA was increased 0.31 - 0.45 times and the ratio of non-alpha mRNA/alpha mRNA increased 0.21 - 0.32 times in Me induced cells from normal individuals. No significant result was observed among the different concentrations of Me (2.5 micro mol/L, 5 micro mol/L and 10 micro mol/L) in normal individuals. With the increasing of Me concentrations, the ratios of gamma/alpha mRNA and alpha/alpha mRNA were increased in cultured cells from beta-thalassemia. The ratio of gamma/alpha mRNA was increased 0.33 - 1.17 times and the ratio of non-alpha/alpha mRNA increased 0.25 - 0.89 times in Me induced cells from beta-thalassemia. There was no significant difference between the concentrations of 2.5 micro mol/L and 5 micro mol/L concentration in beta-thalassemia. However, there was significant difference between the concentrations of 10 micro mol/L and the concentrations of 2.5 micro mol/L and 5 micro mol/L in beta-thalassemia. (3) The increase of the ratio of gamma/alpha mRNA and non-alpha/alpha mRNA in beta-thalassemia was higher than that in normal individual with induction by Me with a higher concentration (10 micro mol/L).</p><p><b>CONCLUSION</b>Me can raise the ratio of gamma/alpha mRNA and non-alpha/alpha mRNA in cultured erythroid cells derived from peripheral blood of both normal individual and beta-thalassemia in the level of transcription, which can improve the imbalance of the alpha and non-alpha globin chain. So Me has a latent value in the therapy of beta-thalassemia.</p>