Sick sinus syndrome (SSS) is a disease of multiple arrhythmias and symptoms.It has great impact on patients in the quality of life for the symptoms of high incidence.The asynchrony of myocardial electromechanical movement caused by the SSS electrophysiological changes are focused.The ultrasound can not only observe the electrical physiological activity,but also measure the mechanical movement caused by electrophysiological delay.The research progresses of ultrasound in quantitative evaluation of myocardial function in SSS patients was reviewed in this article.

China ; Dental Auxiliaries ; organization & administration ; trends ; Humans

Objective To investigate the infiltration of dendritic cell (DC) in Vocal cord polyp, laryngeal leukopla-kia and glottic squamous cell carcinoma,and to observe laryngeal mucosal lesions of the state of the immune microenviron-ment, and to research significance of DC on the development of glottic squamous cell carcinoma. Methods The infiltration of S-100+and CD83+DC in 20 cases of Vocal cord polyp, 47 cases of laryngeal leukoplakia, 45 cases of glottic squamous cell carcinoma tumor and 20 cases of laryngeal normal mucosa were examined using immunohistochemistry. Results The num-ber of S-100+and CD83+DC were significantly higher in glottic squamous cell carcinoma, laryngeal leukoplakia and vocal cord polyp than that in laryngeal normal mucosa (P<0.05). The number of S-100+and CD83+DC were higher in laryngeal leukoplakia than that in glottic squamous cell carcinoma (P<0.05). The number of S-100+and CD83+DC in mild dysplasia and moderate dysplasia were less than that in severe atypical hyperplasia (P<0.01). In glottic squamous cell carcinoma, S-100+ and CD83+DC with poor-differentiated was significantly less than that with well-differentiated (P < 0.01). Conclu-sion Changes in the number of dendritic cell was found in vocal cord polyp, laryngeal leukoplakia and glottic squamous cell carcinoma, which indicated that there were an abnormal immune status. Changing of dendritic cell in laryngeal mucosa plays an important role in laryngeal cancer development.

Cyclophosphamide (CPA) is the most common alkylating antineoplastic agent, as well as a strong immunosuppressant that is frequently applied to autoimmune diseases and organ transplantation. It is metabolized by cytochrome P450 oxidases (CYPs) to its active metabolite which played a critical role in therapy. CPA has serious and even fatal side effects, and its efficacy and adverse reactions are significantly varied among individuals. In this review, the association of the genetic polymorphisms in the metabolic enzymes and transporters involved in the disposition of CPA with the efficacy and adverse effects of CPA were summarized, thereby providing fundamental reference for further pharmacogenomic study of CPA.
Antineoplastic Agents, Alkylating ; pharmacology ; Cyclophosphamide ; pharmacology ; Humans ; NADPH-Ferrihemoprotein Reductase ; metabolism ; Pharmacogenetics

AIM: To investigate the regulatory effects of nuclear factor-κB ( NF-κB) and activator protein-1 (AP-1) on the expression of ectopic trypsin and proinflammatory cytokines in influenza A virus (IAV)-induced myocardi-tis.METHODS:Male BALB/c mice of 8 weeks old ( n=40) were randomly divided into 4 groups:normal control group ( NC) , infection control group ( IC) , NF-κB inhibitor group ( NI) and AP-1 inhibitor group ( AI) .The mice in NC group and IC group were instilled intranasally with 15μL saline and 40 plaque forming units ( PFU) IAV, respectively.The mice in NI group and AI group were infected intranasally with 40 PFU IAV and injected intraperitoneally with 10 mg/kg NF-κB inhibitor pyrrolidine dithiocarbamate ( PDTC) or 2.5 mg/kg AP-1 inhibitor nordihydroguaiaretic acid ( NDGA) once daily. The mice were euthanized at day 9 after instillation, and the hearts were removed for pathological and biochemical analysis. RESULTS:IAV infection induced significant up-regulation of ectopic trypsin, and proinflammatory cytokines interleukin 6 (IL-6), IL-1βand tumor necrosis factor-α(TNF-α) in the myocardium, and triggered acute myocarditis.PDTC signifi-cantly inhibited NF-κB activation and up-regulation of ectopic trypsin and proinflammatory cytokines, and effectively sup-pressed IAV replication and myocardial inflammatory response (P<0.01).NDGA effectively inhibited AP-1 activity (P<0.01) and mildly suppressed up-regulation of proinflammatory cytokines ( P<0.05) , but had no effects on the expression of ectopic trypsin, IAV replication and the extent of myocarditis ( P>0.05) .CONCLUSION:IAV infection induces up-regulation of ectopic trypsin and proinflammatory cytokines in myocardium predominantly by the activation of NF-κB.AP-1 signaling pathway might be only partially involved in the regulation of proinflammatory cytokines.

Objective To analyze mutations of the STAT3 gene in a patient with hyper-IgE syndrome (HIES).Methods Clinical data were collected and blood samples were obtained from a 14-year-old patient with hyper-IgE syndrome (HIES) and her parents.Genomic DNA was extracted and subjected to PCR for the amplification of the entire encoding and splice sites of the STAT3 gene followed by bidirectional sequencing.Meanwhile,amplified ribosomal DNA restriction analysis was carried out.Results A heterozygous missense mutation A1843G,which caused a K615E substitution,was found in exon 19 encoding the SH2 domain of the STAT3 gene in the patient,but not in either of her parents.The result of amplified ribosomal DNA restriction analysis was consistent with the findings mentioned above.Conclusion The novel K615E missense mutation in the STAT3 gene may contribute to the development of HIES.

The expression of heat shock proteins(HSPs) can protect against acute lung injury(ALI).However,HSPs are restrained from clinical application due to the toxicity of most of the former inductors.Glutamine,which also has the ability to induce the expression of HSPs,can protect against ALI and sepsis,and may serve as a candidate for clinical application.

Objective To investigate the in vivo effects of glutamine(Gln) on inflammatory cytokine release in murine peritoneal macrophages during sepsis. Methods Sixty Kunming mice were randomly divided into sham-operation group(Sham group,n=20),operation control group(Con group,n=20) and Gln-treatment group(Gln group,n=20).Sepsis was induced by cecal ligation and puncture in Gln group and Con group,and Gln(0.75 g/kg) or saline was immediately administered via single tail vein injection.Serum was collected and macrophages were harvested from peritoneal lavage at 6 h in these three groups.Intracellular and serum cytokines of tumor necrosis factor-?(TNF-?),interleukin(IL)-6 and IL-10 were detected by ELISA.The expression of TNF-? mRNA in macrophages was analyzed by RT-PCR,and the expression of heat shock protein(HSP) 72 in macrophages was evaluated by Western blotting. Results Gln group demonstrated significantly lower intracellular TNF-? and IL-6 levels than Con group(P0.05).The serum TNF-? level was significantly lower in Gln group than in Con group(P

Objective To investigate the expression and importance of basic fibroblast growth factor(bFGF)in renal tissue of doxorubicin-induced nephropathy rats,and discuss its possible role in minimal change nephrotic syndrome(MCNS).Methods Fifty male Wistar rats were enrolled in this study.They were randomly divided into normal group(n=10)and nephropathic group(n=40).The nephropathic group was established by a single intraperitoneal injection of doxorubicin 5 mg/kg.The rats of nephropathic group were killed on the 3rd,7th,14th and 28th day and 24 h urinary protein of all rats was measured.Normal group rats were killed on the 28th day.bFGF level in renal tissue was determined with immunohistochemistry assays,and was quantitatively analyzed with color image analysis system.The SPSS 10.0 software was used to obtain t-test of various groups and correlation analysis of 2 variables.Results 1.The 24 h urinary protein of nephropathy rats increased gradually on the 7th,14th and 28th day,and it was greatly higher than that in control group(Pa

Objective To investigate the clinical efficacy of Q-switch 1064 nm wavelength laser combining with microneedle technology for the treatment of melasma.Methods 70 melasma patients were selected in the Out-patient Department of Wuhan General Hospital of Guangzhou Military Command from July 2012 to Sept.2013.The patients were randomly divided into 3 groups:the combining therapy group (patients in this group received Q-switch 1064 nm wavelength laser combining with microneedles technology,the treatment interval was 2 or 3 weeks,and the whole course was 2-6 months);the microneedle group and the Q-switch 1064 nm wavelength laser group.The effect and the adverse reaction were observed and recorded during the treatment,and the reduced area of the pigment patch was also measured to judge the total efficacy after the course.Results The total effective rate was 78.6％ (22/28) in the combining therapy group and 40.0％ (8/20) in the microneedle group,45.5％ (10/22) in the Q-switch 1064 nm wavelength laser group.There were statistically significant differences between the combining therapy group and the other groups (P1 ＜0.05,P2 ＜0.05),without obvious adverse reaction.Conclusions It is significantly better to use American Medlite C6 Q-switch 1064 nm wavelength laser combining with microneedles technology than that of the single use of Q-switch 1064 nm wavelength laser or microneedles in the treatment for the patients with melasma.The method is also simple to handle and suitable for clinical application.