Objective The activation of NMDA receptor plays an important role in the pathophysiological process of hypoxic ischemic brain damage (HIBD). This paper aims at studying the mechanism of the protective effect of NMDA receptor antagonist MK 801 against HIBD. Methods Thirty 7 day old SD rats were randomly assigned into Normal control, HIBD and HIBD+MK 801 groups (n=10 each). The rats in the latter two groups were kept in an environment of 8% O 2 after their right common carotid arteries were ligated. The rats in the HIBD+MK 801 group were injected with 0.3 mg/kg of MK 801 intraperitoneally before hypoxia exposure. All rats were sacrificed by decapitation immediately hypoxia and ischemia (HI). The single cell suspension of each hemisphere was prepared and the mitochondrial membrane potential (△Ψm) and intracellular free calcium ([Ca 2+ ]i) of the brain cell suspension were measured by flow cytometry and fluorescence spectrophometer respectively. Results Compared to the Normal control group, the △Ψm levels of both hemispheres and the right to left △Ψm ratio in the HIBD group decreased significantly and the [Ca 2+ ]i level increased significantly (P< 0.05 or 0.01 ); compared to the HIBD group, the △Ψm level and the right to left △Ψm ratio in the HIBD+MK 801 group increased significantly (P< 0.05 or 0.01 ). There was no difference in the right to left [Ca 2+ ]i ratio between the HIBD and the HIBD+MK 801 groups. Conclusions MK 801 may protect the neonatal brain from hypoxic ischemic damage by improving the brain cell mitochondrial function through the "NMDA receptor other △Ψm" pathway, but not through the "NMDA receptor [Ca 2+ ]i △Ψm" pathway.
Objective This study aims to investigate the interleukin 13 (IL 13) expression in the human mesangial cells (HMC) and its effect on expressions of cytokines synthesized by HMC so as to study the role of IL 13 in the inflammatory process of glomerulonephritis. Methods The HMC were cultured and treated with LPS and/or recombinant human IL 13. The IL 13 mRNA expression and the IL 13 protein level in the cultured HMC were detected by semiquantitative reverse transcription polymerase chain reaction (RT PCR) and enzyme linked immunosorbent assay (ELISA) respectively. The effects of IL 13 on the expressions of proinflammatory cytokines, chemokines and profibrogenic cytokine in the HMC were determined by ribonuclease protection assay (RPA). The cultured HMC without LPS or recombinant human IL 13 stimulation were used as the controls. Results The IL 13 mRNA expression and IL 13 protein were undetected in the controls without stimulation. The IL 13 mRNA expression in the HMC with LPS stimulation was induced as early as 12 hrs after LPS stimulation, reached a peak at 48 hrs and remained high level until 72 hrs. The activation of HMC with LPS resulted in the induction of IL 13 mRNA expression in a dose and time dependent way. The IL 13 protein was induced 24 hrs after LPS stimulation and was further increased with stimulation time. The recombinant IL 13 inhibited TNF α, IL 1α, IL 1β, MCP 1, IL 8 and TGF β1 mRNA expressions were induced by LPS in a dose dependent way. The expressions of TNF α, IL 1α, IL 1β, MCP 1, IL 8, and TGF β1 mRNA were increased after endogenously produced IL 13 was neutralized with anti IL 13 mAb. Conclusions LPS can induce the IL 13 expression in HMC. The mesangial cell derived IL 13 can inhibit the production of proinflammatory cytokines, chemokines, and profibrogenic cytokine synthesized by HMC.
Objective To study the significance of kinetic detection of the PML RARα fusion gene in the treatment of childhood acute promyelocytic leukemia (APL). Methods Ten children with APL were involved in this study. They were administered with all trans retinoic acid (ATRA) alone or with ATRA plus other chemotherapeutic drugs during remission induction, consolidation and maintenance treatments and were followed up. The bone marrow samples were regulary collected for morphological evaluation and PML RARα fusion gene detection (by RT PCR assay). Results The median follow up time was 42 months (ranging from 14 to 156 months). The estimated 5 year disease free survival rate was 56.0 ± 18.5% . Clinical complete remission (CR) was obtained in 9 cases (90%) and 1 case died on the 4th day after ATRA treatment. Of the 9 cases, 4 cases relapsed 14-42 months after CR and 5 cases remained continuous CR. Among the 4 cases with relapse, the PML RARα fusion gene was positive in 2 cases and it converted into positive in another 2 cases. Of the 5 cases with continuous CR, 3 cases with a positive PML RARα fusion gene 24, 42 and 36 months after CR were given salvage therapy. After the salvage treatment, the 3 cases had negative PML RARα fusion gene. Conclusions A continuous negative PML RARα fusion gene may be associated with long term disease free survival. The kinetic detection of PML RARα is important for modifying treatment and for preventing hematological relapse in the treatment of APL.
Objective The nerve growth factor receptor (TrkA) gene is an independent marker of the favourable prognosis of neuroblastoma (NB). High expression of TrkA can not only induce differentiation and inhitit proliferation of NB cells but can also be involved in the regulation of tumor angiogenesis. This study aims to investigate the role of the TrkA gene in human NB angiogenesis. Methods The NB SY5Y cells were named SY5Y TrkA cells and SY5Y Vec cells after being transfected with TrkA gene and PBPSTR1 empty vector respectively, and the NB SY5Y cells without transfection were named the SY5Y cells. Fifteen nude mice were assigned into a Control group, an Empty Vec group an Experiment group (n=5 each). The SY5Y cells of the Control group, the SY5Y Vec cells of the Empty Vec group and the SY5Y TrkA cells of the Experiment group were inoculated. The mice were then sacrificed 50 days after inoculation. The tumor volume was measured; the microvessel density (MVD) of the tumor was evaluated and the expression of vascular endothelial growth factor (VEGF) was determined by RT PCR and immunohistochemistry. Results The tumor volume in the Experiment group ( 0.39 ± 0.02 cm 3 ) was significantly smaller than that of the Control group ( 1.74 ± 0.49 cm 3 ) and also was smaller than the Empty Vec group ( 1.80 ± 0.75 cm 3 ) (P< 0.01 ). The expressions of VEGF mRNA and VEGF protein in the Experiment group were significantly lower than those of both the Control and the Empty Vec groups (P< 0.01 ). The MVD in the Experiment group ( 4.08 ± 4.72% ) was also significantly lower than that of the Control ( 27.21 ± 14.58% ) and Empty Vec groups ( 27.76 ± 14.15% ) (P< 0.01 ). Conclusions Angiogenesis and tumor growth of human NB can be effectively inhibited by the TrkA gene. This experiment provides a theoretical basis for the treatment of NB with anti angiogenesis gene therapy.
Interleukin 8 (IL 8) which is released from inflammatory cells during the ischemia/reperfusion process can cause cell damage. This paper aims at studying whether IL 8 is involved in the brain ischemia/reperfusion injuries in the neonates with hypoxic ischemic encephalopathy (HIE). Methods Serum IL 8 levels were detected using enzyme linked immunoabsorbent assay (ELISA) in 50 neonates with HIE, 20 neonates without HIE but with infectious diseases and 30 normal neonates. Results Serum IL 8 levels in neonates with HIE ( 21.52 ± 9.59 pg/ml ) were significantly higher than those in the normal cases ( 14.43 ± 4.84 pg/ml )(P< 0.01 ). Serum IL 8 levels were related to the severity of HIE. The more severe the HIE, the higher the serum IL 8 levels. However, a significant difference was noted only between the mild and severe HIE cases ( 17.56 ± 6.52 pg/ml vs 26.07 ± 13.83 pg/ml ; P< 0.05 ). After a regular 2 week treatment of HIE, serum IL 8 levels decreased significantly compared with those of before treatment ( 14.53 ± 4.87 pg/ml vs 22.60 ± 7.06 pg/ml ; P< 0.01 ). Serum IL 8 levels in HIE neonates complicated by infectious disease ( 23.97 ± 11.04 pg/ml ) were higher than those in HIE neonates without infections ( 18.38 ± 6.07 pg/ml ) and also higher than those in neonates with infectious disease but without HIE ( 18.22 ± 8.01 pg/ml )(both P< 0.05 ). Conclusions IL 8 appears to be involved in the brain injuries of HIE. The detection of serum IL 8 levels may be of value in the diagnosis of neonatal HIE and in the assessment of its severity. There findings can then be used as guidelines for its treatment.
Energy metabolism of mitochondria plays an important role in hypoxic ischemic encephalopathy (HIE). This study aims to investigate the changes of energy metabolism following hypoxic ischemic brain damage (HIBD) in cortical neurons of newborn rats. Methods Seven day old Wistar rats were randomly assigned into a Sham operation control group (n=6) and a Cerebral hypoxia ischemia (HI) group. The HI group was divided into 10 subgroups of 6 animals, sacrificed respectively at 0, 2, 4, 6, 8, 10, 12, 24, 48 and 72 hrs after HI. The rats in the Sham operation control group were sacrificed at 4 hrs post operatively. The concentrations of PCr, ATP, ADP and AMP in cortical neurons were measured with high performance liquid chromatography (HPLC). Results The concentrations of PCr, ATP and ATP+ADP+AMP decreased immediately after HI and reached a nadir 0-6 hrs after HI ( 51% , 71% and 50% of controls, respectively), returning almost to normal values by 8-12 hrs after HI. Twelve hrs after HI the values again decreased reaching a second nadir by 24-48 hrs post HI ( 58% , 61% , 33% of controls, respectively; P< 0.05 ). Conclusions There is a secondary decrease in high energy phosphates 24-48 hrs after cerebral HI in newborn rats. Changes of energy metabolism may serve as indicators in evaluating the efficacy of intervention for HIBD.
Naloxone as an assist drug has been used to treat neonatal hypoxic ischemic encephalopathy (HIE). However, there is controversy about its therapeutic effect. This study aims to evaluate the effect by Meta analysis. Methods Using the Meta analysis method, 20 case control studies about the effect of naloxone on neonatal HIE were qualitatively and quantitatively analysed, and the combined OR value and 95% confidence interval (CI) of curative effects and side effects were calculated. Results Compared with the routine therapy, the therapy with naloxone can significantly improve clinical symptoms of neonates with HIE(combined OR= 4.89 , 95% CI= 2.59 - 9.21 ). Also, it can significantly shorten the time of respiratory failure (combined OR= 11.09 , 95% CI= 5.13 - 23.98 ), gastro intestine function failure (combined OR= 44.58 , 95% CI= 18.42 - 107.93 ) and circulatory system dysfunction (combined OR= 5.54 , 95% CI= 2.97 - 10.35 ), and increase the survival rate (combined OR= 3.38 , 95% CI 2.01 - 5.71 ). Conclusions The therapy with naloxone can markedly improve the severity and increase the survival rate of neonates with HIE.
The efficacy of β 2 agonist in the treatment of bronchiolitis has been questioned. This study aims to explore the changes of pulmonary function in infants with acute bronchiolitis before and after treatment with nebulized salbutamol. Methods Thirty infants with bronchiolitis were randomly assigned into a Treatment group (nebulized salbutamol, 0.15 mg/kg in 2 ml normal saline; n=16) and a Control group (2 ml normal saline; n=14). Tidal breathing flow volume (TBFV) loops and static respiratory system compliance (Crs) and resistance (Rrs) were measured before nebulization and immediately after nebulizer treatment, and 15 minutes and 30 minutes after treatment. Results A significant improvement in the percentage of tidal volume to peak tidal expiratory flow (%V/PF) was found in the treatment group 30 minutes after nebulization (0.184±0.05 vs 0.13±0.04; P< 0.05 ). Terminal flows/peak expiratory flow (25/PF) and peak tidal expiratory flow (PTEF) of the Treatment group also tended to improve, but there were no differences. There were also significant differences in 25/PF and inspiratory time (Ti) immediately after nebulization between the two groups. Conclusions Salbutamol treatment appears to improve peripheral airway resistance and ventilation in children with acute bronchiolitis.
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Large series of case reports of juvenile polymyositis/dermatomyositis (JPM/JDM) are now seldom found in either Chinese or overseas literature. Clinical and pathological data of 42 cases of JPM/DM, including serum enzymes, electromyography (EMG) and muscular pathology were studied retrospectively. Patients with JPM/JDM manifested muscle weakness, muscle atrophy, elevation of creatine kinase and abnormal EMG with myogenic damage. Children with JDM generally manifested characteristic cutaneous abnormalities. Subcutaneous calcifications were present in some chronic cases of JDM. Muscle biopsy demonstrated immune inflammation in both JPM and JDM cases. The incidence of endomysium inflammatory in patients with JPM was higher than that in patients with JDM ( 70.8% vs 38.9% ) (P< 0.05 ), whereas the incidences of microvasculopathy ( 54.2% vs 94.4% ; P< 0.01 ) and perifascicular atrophy ( 41.7% vs 72.2% ; P< 0.05 ) was lower in JPM compared to JDM. Infiltrates were more frequently seen in JPM. Corticosteroid therapy was effective in most JPM/DM patients. It was concluded that there are some clinical and pathological differences between JPM and JDM. JPM frequently manifests sporadic muscle fibre degeneration, necrosis and endomysium inflammatory, while microvasculopathy and perifascicular atrophy are the characteristic pathology of JDM.
Objective To investigate the effect of adenotonsillectomy or adenoidectomy in the treatment of obstructive sleep apnea syndrome (OSAS) in children with adenoidal hypertrophy. Methods The clinical menifestations and overnight polysomnography findings in 20 children with OSAS secondary to adenoidal hypertrophy (OSAS group) were compared before and after adenotonsillectomy or adenoidectomy and were compared with those in 10 children with adenoidal hypertrophy without OSAS (Control group) admitted to Beijing Children's Hospital at the same period as the OSAS group. Results There was no significant difference in the incidence of the common symptoms between the OSAS group and the Control group. The body mass index, A/n ratio in the neck roentgenography, total sleep time, sleep efficiency, and the proportion of S1, S2 and slow wave sleep (SWS) time and rapid eye movement (REM) time of the OSAS group did not differ from those of the Control group. After adenotonsillectomy or adenoidectomy, the apnea index, apnea hypopnea index of all children with OSAS and obstructive apnea index significantly decreased and the proportion of REM sleep time in the total sleep time significantly increased (P< 0.05 or 0.01 ). Conclusions There are no differences in clinical manifestations, A/n ratio and the sleep architecture between the adenoidal hypertrophy children with and without OSAS. Adenotonsillectomy or adenoidectomy is effective in the treatment of childhood adenoidal hypertrophy with OSAS.
Primary extra nodal lymphoma of bone means the malignant lymphoma presents initially in bones. It is a rare disease of unknown etiology in children. The disorder mainly manifests in localized bone lesions. Bone arthrodynia and localized bone swelling are the most common symptoms, with or without systemic symptoms. Radiologic examinations reveal osteolytic lesions. The histological features are various, and the majority of histology are diffuse large B cell lymphomas. Diagnosis of the disease may be confirmed by bone biopsy. The prognosis of the patients with this disorder is comparatively favorable after general treatment with chemotherapy and radiation therapy.
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