Objective To observe the transformation features of children with complete atrioventricular block(CAVB), and to improve the diagnosis and treatment of this disease.Methods Seventeen children with primary diagnosis of CAVB were reviewed by retrospective and follow-up study and the clinical characteristics, treatment schemes and prognosis were evaluated.Results Four cases of congenital CAVB lived normally without obvious symptoms in the tracing period from 6 months to 9 years;1 case had the onset of Adams-Stokes syndrome induced by diarrhea;3 cases of the CAVB caused by virus myocarditis turned into sinus rhythm after comprehensive therapy;2 cases persistently presented with the CAVB Complicated with enlarged heart;1 case gave up treatment after deterioration, and one case died.Three cases of temporary CAVB after the open heart operation turned to sinus rhythm in transitory time, while other two cases presented with permanent CAVB and treated with epicardium pacemaker,among whom one had the pacemaker replaced for one time in the 8-year follow-up,and the follow-up of other cases were intermitted.Conclusions The congenital CAVB in the study group with normal QRS interphase and no obvious symptom might not require treatment but follow-up is needed. While infants with heart malformation and wide QRS wave could not endure the low ventricular rhythm are in high risk. Virus myocarditis induced CAVB children tend to present the Adams-Stokes syndrome, and require effective treatments. Partial cases of the CAVB caused by open heart operation may turn to normal sinus rhythm in 2-4 weeks after surgery. cases has persistent CAVB for over 4 weeks, or Adams-Stokes syndrome onset after the surgery demand epicardium pacemaker treatment.

There are many progresses in the therapy of MM with ASCT. ASCT improves the ratio of CR,EFS and OS,compared with conventional chemotherapy.Myeloma patients with renal failure or old age also can be candidate for ASCT.Tandem autologous transplantation improves the ratio of CR. Its impact to long-term EFS and OS still need to be judged.To improve conditional project,to choose suitable time,and- toselect consolidation schedule can boost therapeutic effect.

OBJECTIVE: To establish the method to analyze γ-hydroxybutyric acid (GHB) and its precursors 1,4-butanediol (1,4-BD) and gamma-butyrolactone (GBL) in urine through LC-MS/MS and provide evidence for related cases. METHODS: GHB-d6 and MOR-d3 were used as the internal standard. The urine sample was separated by LC after protein precipitation with methanol. The electrospray ion source was for ionization. Each compound was detected through multiple-reaction monitoring (MRM) mode. RESULTS: The limits of detection of GHB and its precursors 1,4-BD and GBL were 0.1, 0.1 and 2 μg/mL. The accuracy was 87.6%-98.1%. The intra-day and inter-day precisions were less than 15% and matrix effects were higher than 80%. CONCLUSION The method is high sensitive, simple, rapid, specific and with high reliability. This study has provided technical support and basic data for forensic cases involving GHB.
4-Butyrolactone/urine* ; Butylene Glycols/urine* ; Chromatography, Liquid ; Forensic Sciences ; Humans ; Hydroxybutyrates/urine* ; Mass Spectrometry ; Reproducibility of Results ; Tandem Mass Spectrometry

Antineoplastic Agents ; therapeutic use ; Diagnosis, Differential ; Female ; Histiocytosis, Langerhans-Cell ; metabolism ; pathology ; Humans ; Interferons ; therapeutic use ; Leukemia, Mast-Cell ; metabolism ; pathology ; Mastocytosis, Cutaneous ; metabolism ; pathology ; Mastocytosis, Systemic ; diagnostic imaging ; drug therapy ; metabolism ; pathology ; Middle Aged ; Proto-Oncogene Proteins c-kit ; metabolism ; Radiography ; Radionuclide Imaging ; Spleen ; pathology ; surgery ; Splenectomy ; Tryptases ; metabolism

Objective To investigate the role of basophils in the imbalance of Th 1/Th2 response in mouse models of collagen-induced arthritis(CIA).Methods 4-6-weeks old C57/BL6 mice were immunized with collagen at multiple points on the back and foot twice (0 and 3 weeks) to establish a mouse model of collagen-induced arthritis.Blood samples were collected before the first immunization and 1, 3, 6 and 9 weeks after immunization , and cells from lymph nodes were collected.Flow cytometry and ELISA were employed to detect the levels of basophils and IL-4, and the joint swelling was scored.Results Mouse model of CIA was successful established .The ratio of IL-4/IFN-γof the CIA group was significantly lower than that in the mice before CIA modeling and the control group , indicating a Th2-dominant response .At the same time, the peripheral basophils counting and percentage of IL-4 positive basophils of the CIA group were significantly higher than those of the control group .While, the IL-4/IFN-γratio of the CIA group was significantly higher than that of the control group , indicating a Th1-dominant response .The peripheral basophils counting of the CIA group was slightly lower than that of the control group .Conclusion Basophils may participate in the development of CIA in mouse models through affecting the imbalance of Th 1/Th2 response.

BackgroundEndostatin (ES) is currently the strongest endogenous angiognesis inhibitor,and it can inhibit the occurrence of neovascularization.Various studies demonstrated that the poly RGD sequence can enhance the function of the ES gene.ObjectiveThis study was to evaluate the use of gene therapy of modified ES for alkaline burn-induced corneal neovascularization (CNV).MethodsOne hundred and two clean SD rats were randomly divided into the normal control group,the pCI empty vector group,the pCI-ES group,and the pCI-RGDRGDES group.Corneal neovascularization models were established by placing a piece of 3 mm filter paper with 1 mol/L NaOH at the central cornea for 40 seconds.3 μg of the pCI blank vector,ES-tranfected pCI blank vector,or RGDRGD-ES-transfected pCI vector was injected into the superior bulbar conjunctiva after the alkali burn twice at 1-week intervals.Area of CNV and edema of the cornea in the various groups of rats were examined daily under the slit lamp biomicroscope.1,4,7 and 14 days after operation,the rats were sacrificed by the excessive anesthesia method and corneal tissues were obtained to evaluate pathological changes.The expression of CD34 in vascular endothelial cells was detected by immunochemistry to calculate the corneal neovascular density.The expressions of VEGF mRNA and Flk-1 protein in the corneas were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.The use and maintenance of animals followed the Statement of ARVO.Results Seven to fourteen days after corneal alkali-burning,the corneal neovascular area was smaller in the pCI-ES group and pCI-RGDRGD-ES group compared with the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and nevascular area in the pCI-RGDRGD-ES group was smaller than that in the pCI-ES group (P＜0.05).The expression level of CD34 was significantly lower in the pCI-ES group and pCI-RGDRGD-ES group than that in the normal control group and pCI blank vector group (P＜0.05,P＜0.01 ),and the expression level of CD34 was further declined in the pCI-RGDRGD-ES group compared with the pCI-ES group (P＜0.05 ).Compared with the normal control group and pCI vector group,the expressions of the Flk-1 protein and VEGF mRNA were decreased in the pCI-ES group and pCI-RGDRGD-ES group on the fourth day after corneal alkali-burning (P＜0.01,P＜0.05 ),and those in the pCI-RGDRGD-ES group were less than the pCI-ES group (P＜ 0.05,P＜ 0.05 ).Conclusions Subconjunctival injection of both ES and modified RGDRGD-ES genes result in significant suppression of CNV in vivo,and modified RGDRGD-ES appears to be more effective than native ES.The main mechanism of ES in inhibiting neovascularization is to downregulate the expression of VEGF and Flk-1.

Objective To evaluate the clinical impact of 18F-FDG PET/CT on patients with suspected cervical cancer recurrence. Methods Fifty-one cervical cancer patients, clinically suspected to have tumor recurrence during follow-up, underwent 18F-FDG PET/CT examination. 18 F-FDG PET/CT results were compared with those of conventional images, as referred to histopathology or clinical follow-up. Impacts of 18F-FDG PET/CT were evaluated based on documented changes of clinical management. Results In total, 43 patients were found to have positive lesions by 18F-FDG PET/CT, in which 40 were true recurrence,but 2 were pelvic abscess and 1 was radiation enterocolitis. Other 8 patients were found negative by 18F-FDG PET/CT and confirmed by pathology or follow-up. In patient-based analyses, the sensitivity, specificity, and accuracy of 18F-FDG PET/CT for the detection of tumor recurrence were 100% (40/40), 72. 73% (8/11),and 94.12% (48/51) respectively. In 7 patients, the clinical management was changed due to 18F-FDG PET/CT findings. Conclusion 18F-FDG PET/CT is an efficient tool for determining the recurrence of cervical cancer and instructing the clinical management.

The genes of maltooligosyl trehalose synthase (MTSase) and maltooligosyl trehalose tetrahydrolase(MTHase) from Sulfolobus solfataricus ATCC 35092 were amplified using PCR. The expression plasmids, pTrc99a-MTSase and pTrc99a-MTHase, were constructed by inserting these two DNA fragments into E. coli expression vector pTrc99a. The specific activity of MTSase and MTHase in E. coli BL21(DE3) at optimal fermentation conditions reached 31.3U/g (wet cell) and 403U/g (wet cell), respectively. The biotransformation of partially hydrolyzed starch to trehalose catalyzed by MTSase and MTHase was carried out at 75℃ and pH 5.0. The highest yield of trehalose (ca. 53.6%) was gained when the original starch concentration was 15%(w/v) and the DE value was 10.

NMDA-induced excitotoxicity cause severe neuronal damage including apoptosis and necrosis. The present study was aimed to evaluate the proportion of NMDA-induced apoptosis of rat cortical neurons and discover signal transduction mechanism. Caspase inhibitor and lactate dehydrogenase (LDH) assay were used to study the NMDA-induced apoptosis. To explore the involved signal pathways, the primary culture of rat cortical neurons were pretreated by the inhibitors of three MAPK pathways, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. With 2 h of NMDA treatment, cellular apoptosis was measured by caspase-3 activity, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) and Annexin V staining. The results showed that: (1) Caspase-dependent apoptosis accounted for 22.49% in NMDA-induced neuronal death; (2) Pretreatment with p38 MAPK inhibitor SB203580 (10 μmol/L) significantly decreased NMDA-mediated caspase-3 activity by 30.43% (P < 0.05). However, ERK inhibitor PD98059 (20 μmol/L) or JNK inhibitor SP600125 (20 μmol/L) did not influence caspase-3 activity; (3) Pretreatment with SB203580 significantly reduced the number of NMDA-induced TUNEL-positive cells by 33.10% (P < 0.05). PD98059 (20 μmol/L) or SP600125 (20 μmol/L) did not show obvious effect; (4) Pretreatment with SB203580 (10 μmol/L) significantly reduced the number of NMDA-induced early apoptotic neurons by 55.56% (P < 0.05). Also, SP600125 (20 μmol/L) significantly decreased the amount of late apoptotic/dead cells by 67.59% (P < 0.05). There was no effect of PD98059 (20 μmol/L). These results indicate that: (1) NMDA induces neuronal apoptosis besides necrosis; (2) p38 MAPK, but not JNK and ERK, is involved in NMDA-induced neuronal apoptosis, and inhibition of the apoptotic signaling pathway contributes to neuroprotection; (3) JNK activation might contribute to NMDA-induced neuronal necrosis rather than apoptosis.
Animals ; Anthracenes ; pharmacology ; Apoptosis ; Caspase 3 ; metabolism ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; Imidazoles ; pharmacology ; JNK Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; MAP Kinase Signaling System ; N-Methylaspartate ; pharmacology ; Neurons ; cytology ; Primary Cell Culture ; Pyridines ; pharmacology ; Rats ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors

Osteoarthritis (OA) is a complex chronic progressive disease attacked by biological and mechanical factors and a result from the anabolic and catabolic imbalance in chondrocyte, subchondral bone and extracellular matrix(ECM). Etiology and pathological of OA are not yet entirely clear. The degradation and destruction of collagen II caused by matrix metalloproteinase -13 (MMP-13) is considered the core factor in the occurrence and development of OA. The research of MMP-13 inhibitor provide ideas and methods for the treatment of OA. In this article,the role and determination of MMP-13 in OA and the development prospect of MMP-13 inhibitor in the treatment of OA research progress were reviewed.
Animals ; Collagen ; metabolism ; Humans ; Matrix Metalloproteinase 13 ; analysis ; physiology ; Matrix Metalloproteinase Inhibitors ; therapeutic use ; Osteoarthritis ; drug therapy ; etiology