Objective To study the feasibility of the treatment of tubule pregnancy by interventional technique. Methods By using Seldinger′s method, 40 cases of tubule pregnancy received superselective angiography of uterine artery,followed by perfusion of methotrexate (MTX) through the catheter and embolization of uterine artery with gelatin sponge. The concentration of serum ? HCG, the change of pelvic cavity, and the open condition of oviduct were regularly monitored postoperatively. Results Angiographic findings of tubule pregnancy were classified into 3 types. Type Ⅰ, no abnormal vascular appearance were found in 3 cases (7.5%). Type Ⅱ, patchy vascular staining of villi in parauterine area was observed in 4 cases (10.0%). Type Ⅲ, a round vascular staining of villi surrounded by small blood vessels in parauterine area occurred in 33 cases (82.5%). The cure rate in total 40 cases achieved 97.5% (39/40). After treatment, the mean time that the serum ? HCG concentration returned to normal was (7.66?2.01) d and the mean time that the menstruation returned to normal was (29.78?7.14) d. In 21 cases who hoped their fertility remaining intact, the oviduct were verified open by hysterosalpingography (HSG) in 20 cases, the open rate was 95.24%. Conclusion The treatment of tubule pregnancy by interventional technique was proved no harmful effect to reproductive organs and would expect to preserve fertility. This method could resolve the difficult problem of celiac hemorrhage which making conservative treatment impossible and internal hemorrhage happened in the course of traditional conservative therapy leading to treatment failure finally. This method might be a new conception and a choice to treat tubal pregnancy through artery.

This study was aimed to investigate the effect of bortezomib alone or combined with arsenic trioxide on the apoptosis of Jurkat cells and expression of livin mRNA. The Jurkat cells were cultured and treated with different concentrations of bortezomib, arsenic trioxide or their combination for 24 hours. Then, the expression of livin mRNA was detected by RT-PCR, the cell proliferation was analyzed with MTT assay and flow cytometry. The results showed that 5 - 25 nmol/L bortezomib could effectively inhibit Jurkat cells in a dose-dependent manner, the group of bortezomib combined with arsenic trioxide showed more inhibitory effect on Jurkat cells than the effect of bortezomib alone or arsenic trioxide alone on Jurkat cells. The expression of livin mRNA in Jurkat cells decreased in a dose-dependent manner after treated with bortezomib, which was downregulated significantly after combined treatment. It is concluded that bortezomib and arsenic trioxide can induce apoptosis by inhibiting the expression of livin mRNA in Jurkat cells. The combination of bortezomib with arsenic trioxide displays a synergistic effect.
Adaptor Proteins, Signal Transducing ; genetics ; metabolism ; Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Boronic Acids ; administration & dosage ; pharmacology ; Bortezomib ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; metabolism ; Jurkat Cells ; Neoplasm Proteins ; genetics ; metabolism ; Oxides ; pharmacology ; Pyrazines ; administration & dosage ; pharmacology ; RNA, Messenger ; genetics

Objective To evaluate the visual improvement of therapeutic plasma exchange (TPE) for refractory optic neuritis (ON) patients in acute phase.Methods Seventy-five affected eyes from 44 refractory ON patients with severe visual defect or resistance to high-dose intravenous methylprednisolone (IVMP) therapy,who were admitted to The Chinese PLA General Hospital between January 2015 and August 2016,were recruited and received TPE therapy.Among these patients,11 were male and 33 were female;the average age was 39.1 ± 13.9;31 patients had two affected eyes,13 patients had one affected eye.The course of the disease on the group of patients were more than 2 weeks,and the visual acuity worsened for more than 10 days and continued to deteriorate.TPE treatment was performed on all of the patients.BCVA was recorded before and 24 h after treatment,and the visual function was scored using visual outcome scale (VOS).At the same time,the adverse reactions of TPE treatment were observed.The paired t-test was used to compare the VOS before and after treatment.The correlation between VOS before and after treatment was analyzed by Linear-by-Linear correlation analysis.Results Among 75 affected eyes,the post-therapy VOS 3.89 ±2.13 was significantly improved from pre-therapy VOS 5.56± 1.69 (t=6.77,P＜0.001).Forty-eight of 75 eyes were improved at lease 1 score of VOS,the overall rate of visual improvement was 64.0％.Especially among the eyes with initial vision of light perception,an improved rate of 82.4％ was presented.75.0％ in those eyes with initial vision of count fingers and 67.7％ in no light perception.Linear-by-Linear correlation analysis showed a significant linear correlation between the scores of VOS before and after TPE treatment (r=0.398,P=0.01).During the course of TPE treatment,5 patients had mild adverse reactions such as low calcium reaction and allergic reaction and were well controlled after treatment.Conclusion Using TPE to treat refractory ON in acute phased can improve the visual function of patients.

OBJECTIVE To explore the protective effects and mechanisms of Ginsenoside Rg1 (Rg1) on H2O2-induced hippocampal neurons aging in vitro. METHODS The primary culture hippo-campal neurons(7 d)were randomly placed into six groups:normal control group,H2O2(200 μM)treat-ment group,and H2O2+Rg1(1,5 and 10μM)groups.The neurons were with Rg1(1,5 and 10 μmol·L-1) for 6h. H2O2(200 μmol·L-1) was added to the medium and incubate for 18 h. The Dihydroethidium (DHE) staining was performed for ROS production assessment. The LDH release and Hoechst 33258 were performed to examine the neuronal damage and apoptosis. The immunoblot was used to deter-mine the expression of β-Gal,NOX2,p22phox,p47phox,NLRP-1,ASC and Caspase-1 in hippocampal neurons.The ELISA was performed to detect the levels of IL-1β and IL-18 released in the supernatant in hippocampal neurons.RESULTS Rg1(5 and 10 μmol·L-1)significantly reduced the ROS production, attenuated H2O2-induced neuronal damage and apoptosis (P<0.05, P<0.01). The immunoblot results showed that Rg1(5 and 10 μmol·L-1)treatment significantly decreased the expression of β-Gal,NOX2, p22phox,p47phox,NLRP-1,ASC and Caspase-1 in hippocampal neurons(P<0.05,P<0.01).Additionally, Rg1(5 and 10 μmol·L-1)treatment significantly decreased IL-1β and IL-18 release in the supernatant. CONCLUSION The protective effect of Rg1 in H2O2-induced hippocampal neurons aging may be due to inhibit NOX2-NLRP1 activation.

OBJECTIVE: To explore the characteristics of autopsy cases of anaphylactic shock induced by cephalosporins and provide the evidences in forensic medicine. METHODS: Twenty cases of anaphylactic shock induced by cephalosporins were collected from April 2005 to August 2009 in judicial expertise center of China Medical University, and the characteristics of the cases were analyzed retrospectively. RESULTS: The age of decedents ranged from 40 to 60 years. Ninety percent of cases were from local medical centers and private clinics. The symptoms of the shock appeared 30 s-150 min after the administration of the drug, and death occurred 10 min-210 min after the appearance of the shock symptoms. In all cases, various degrees of eosinophil infiltration were observed in trachea and the lungs. Serum IgE detected by ELISA method was normal value in 14 cases. CONCLUSION In fatal anaphylactic cases, little specific findings are detected during postmortem and microscope examination. For this reason, the determination of cause of death in these cases requires comprehensive analysis combined with clinic information and excludes other diseases leading to the sudden death.
Adolescent ; Adult ; Anaphylaxis/pathology* ; Anti-Bacterial Agents/adverse effects* ; Autopsy ; Cause of Death ; Cephalosporins/adverse effects* ; Child ; Child, Preschool ; Drug Hypersensitivity/pathology* ; Edema/pathology* ; Female ; Forensic Pathology ; Humans ; Immunoglobulin E/blood* ; Infant ; Infusions, Intravenous ; Larynx/pathology* ; Lung/pathology* ; Male ; Middle Aged ; Retrospective Studies ; Trachea/pathology* ; Young Adult

BACKGROUNDIn our previous study, we found that DAZAP2 was the most significantly down regulated gene when differential screening of complementary DNA (cDNA) chips were used to analyze mRNA isolated from bone marrow mononuclear cells from newly diagnosed multiple myeloma (MM) patients without anticancer treatment. In this study, we observed DAZAP2 mRNA and protein expression in the mononuclear cells from MM bone marrow and investigated its role in the pathogenesis of MM.

METHODSThe full-length cDNA of DAZAP2 was cloned and sequenced from mononuclear cells from human bone marrow. The nucleotide and amino acid sequences of DAZAP2 were analyzed using the ClustalW program. A dendrogram was constructed by multiple sequence alignment using ClustalW and amino acid sequence identity/similarity was derived based on comparisons attained using the MegAlign software. The recombinant pEGFP expression vector was constructed and the confocal microscopy was used for the localization of the DAZAP2 protein in transfected COS7 cells. The expression of DAZAP2 mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and the expression level of DAZAP2 protein was detected by Western blotting analysis in MM samples.

RESULTSDAZAP2 proteins of vertebrates is highly conserved in evolution. It contains a proline-rich region, several potential SH2 and SH3 domain-binding motifs and a possible protein kinase C (PKC) phosphorylation site. We showed by confocal microscopy that the DAZAP2 protein predominantly resides in the cytoplasm with a discrete pattern of punctuated distribution. The expression of DAZAP2 was not detected in 24 of 36 MM samples by semi-quantitative RT-PCR. In contrast, DAZAP2 expression was detected in all 30 normal controls. The expression level of DAZAP2 protein was assayed by Western blotting analysis, showing a robust down-regulation in MM patients (P < 0.001) that matched with the results of the RT-PCR.

CONCLUSIONSDAZAP2 is downregulated in MM samples and it may be a signal molecule in MM cells. DAZAP2 is involved in the pathogenesis of MM and could be used as a genetic marker for MM.

Adult ; Aged ; Amino Acid Sequence ; Blotting, Western ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Molecular Sequence Data ; Multiple Myeloma ; etiology ; metabolism ; RNA, Messenger ; analysis ; RNA-Binding Proteins ; analysis ; chemistry ; genetics

OBJECTIVETo explore the level of serum uric acid (UA) in children with obstructive sleep apnea/hypopnea syndrome (OSAHS).

METHODBetween Sep. 2008 and Mar. 2010, 138 children with OSAHS were enrolled in study group. Sixty-five children with accessory auricle or ptosis of upper lid were enrolled into the control group. Furthermore, according to apnea/hypopnea index (AHI) or obstructive apnea index (OAI) the study group was further divided into three subgroups (mild, moderate and severe group). At last, the study group and control group were divided into two groups according to the body mass index (BMI), separately. The fasting serum UA level was compared among the different groups. Then the correlation between the serum UA level and AHI, BMI, oxygen desaturation index, least arterial oxygen saturation (LSaO(2)) and the percentage of total sleep time with arterial oxygen saturation < 0.92 was also analyzed in OSAHS children with or without overweight and obesity respectively.

RESULTThe difference of serum UA level between the study group and control group (z = -0.443), and the difference among the three groups (χ(2) = 1.241) was not significant(P > 0.05). The serum UA level in overweight and obese children [study group, 273.0 (238.3 - 357.3); control group, 298.0 (253.0 - 336.0)] was significantly higher than that in children with normal BMI [study group, 246.5(215.8 - 300.0); control group, 266.0 (224.0 - 303.3)] (z = -2.084, -2.214, P < 0.05). That serum UA level did not correlate with the above index of OSAHS was observed in children with or without overweight and obesity in study group (P > 0.05).

CONCLUSIONFindings of higher serum UA level were not observed in children with OSAHS. There was no correlation between serum UA level and the above indices of OSAHS. The serum UA level in overweight and obese children was significantly higher than that in children with normal BMI.

Case-Control Studies ; Child ; Child, Preschool ; Humans ; Sleep Apnea, Obstructive ; blood ; Uric Acid ; blood

Objective To explore the effect of point Neiguan(PC6) electroacupuncture pretreatment on nitric oxide (NO), nitric oxide synthase (NOS) and mitochondrial membrane potential by determining NO, NOS and mitochondrial membrane potential in rats with myocardial ischemia/reperfusion injury (MIRI).Method Forty male SD rats were randomized to sham operation, ischemia/reperfusion model, point Neiguan electroacupuncture and point Huantiao(GB30) electroacupuncture groups, 10 rats each. The model was made by coronary artery ligation. Before model making, electroacupuncture was given to the point Neiguan electroacupuncture and point Huantiao electroacupuncture groups, 20 min/d for a total of 7 d. T wave value in ECG leadⅡ was measured before and after model making. Myocardial pathomorphological changes were examined by HE staining. Serum NO and NOS contents were measured by a colorimetric nitrate reductase assay. Cardiomyocyte mitochondrial membrane potential was determined by fluorescence techniques.Result Serum NO and NOS contents and mitochondrial membrane potential decreased significantly in the model group compared with the sham operation group (P<0.05). Serum NO and NOS contents increased significantly in the point Neiguan electroacupuncture group compared with the model, sham operation and point Huantiao electroacupuncture groups (P<0.01,P<0.05). Mitochondrial membrane potential increased significantly in the point Neiguan electroacupuncture group compared with the model, point Huantiao electroacupuncture and sham operation groups (P<0.01,P<0.05). There was no statistically significant difference in mitochondrial membrane potential between the model and point Huantiao electroacupuncture groups (P>0.05). Conclusion Point Neiguan electroacupuncture pretreatment has a preventive protecting effect on MIRI rats. It produces a protecting effect on myocardium by increasing the NO content, strengthening NOS activity, reducing a decrease in cardiomyocyte mitochondrial membrane potential and inhibiting apoptosis.

Adult ; Deep Brain Stimulation ; methods ; Female ; Humans ; Tardive Dyskinesia ; therapy

This study aimed to identify the type of carnitine palmitoyltransferase 2 (CPT2) gene mutation in the child with carnitine palmitoyltransferase II (CPT II) deficiency and her parents and to provide the genetic counseling and prenatal diagnosis for the family members. As the proband, a 3-month-old female baby was admitted to the hospital due to fever which had lasted for 8 hours. Tandem mass spectrometric analysis for blood showed an elevated plasma level of acylcarnitine, which suggested CPT II deficiency. The genomic DNA was extracted from peripheral blood of the patient and her parents. Five exon coding regions and some intron regions at the exon/intron boundaries of the CPT2 gene were analyzed by PCR and Sanger sequencing. Amniotic fluid was taken from the mother during the second trimester, and DNA was extracted to analyze the type of CPT2 gene mutation. Sanger sequencing results showed that two mutations were identified in the CPT2 gene of the proband: c.886C>T (p.R296X) and c.1148T>A (p.F383Y), which were inherited from the parents; the second child of the mother inherited the mutation of c.886C>T (p.R296X) and showed normal acylcarnitine spectrum and normal development after birth. It is concluded that the analysis of CPT2 gene mutations in the family suggested that the proband died of CPT II deficiency and that the identification of the mutations was helpful in prenatal diagnosis in the second pregnancy.
Carnitine O-Palmitoyltransferase ; deficiency ; genetics ; Female ; Humans ; Infant ; Metabolism, Inborn Errors ; diagnosis ; genetics ; Mutation ; Prenatal Diagnosis