[Analysis of clinical features of secondary benign paroxysmal positional vertigo].

Objective:To analyze the clinical features of secondary benign paroxysmal positional vertigo (BPPV) and provide evidence for its precise diagnosis and treatment. Method:There were 942 patients with vertigo related to BPPV, including 204 patients with primary BPPV, 592 patients with vestibular migraine (VM), 83 patients with Meniere's disease (MD), 48 patients with vestibular neuronitis (VN), and 15 patients with sudden sensorineural hearing loss (SSNHL) accompanied by vertigo.There were 127 patients with BPPV secondary to vertigo in MD, VN, VM, and SSNHL. All patients received otolith repositioning treatment by hand or instrument based on detailed medical history. Secondary BPPV patients are treated according to the principle of diagnosis and treatment of primary BPPV. The incidence of secondary BPPV in each related disease was counted, and the difference between primary and secondary BPPV in gender, age, affected semicircular canal, number of reductions, and vertigo control rate was compared. Result:①The incidence of MD, VN, sudden vertigo, and VM secondary BPPV were 36.1% (30/83), 35.4%(17/48), 33.3% (5/15), and 12.7% (75/592). ②In patients with BPPV secondary to MD, the proportion of multi-semicircular canals involved was higher than that of primary BPPV, the difference was statistically significant (P<0.05), and there was no significant difference in the distribution of semicircular canals involved among the remaining diseases. ③The vertigo control rate of BPPV secondary to MD and VM was lower than that of primary BPPV, and the difference was statistically significant (P<0.05). ④The repositioning time of BPPV secondary to VM (2.88±2.32) and MD (2.53±1.14) was higher than that of primary BPPV (2.37±1.77). The difference was statistically significant (P<0.05). There was no significant difference in the repositioning time between other secondary BPPV and primary BPPV. Conclusion:Common causes of secondary BPPV include MD, VN, SSNHL, and VM. Same as primary BPPV, the secondary BPPV was more common in women and the posterior semicircular canal was most affected. BPPV secondary to MD is more susceptible to multi-semicircular canals involvement than primary BPPV. Detailed medical history combined with targeted examination is conducive to the accurate diagnosis of BPPV. Secondary BPPV can also be treated by manipulation or instrument, however, the effect is worse than primary BPPV. Secondary BPPV should be treated according to the treatment principle of primary disease besides otolith repositioning.

[Effects of allogeneic hematopoietic stem cell transplantation in combination with infusion of endothelial progenitor cells on bone marrow inflammatory injury].

Objective: To explore effects of allogeneic hematopoietic stem cell transplantation (HSCT) in combination with infusion of endothelial progenitor cells (EPC) on bone marrow inflammatory injury. Methods: 6-8 weeks BALB/c (H-2K(d)) mice after lethal dose of irradiation (TBI) were subjected to allogeneic bone marrow transplantation (BMT group) or co-transplantation of EPC (EPC group) . Samples of bone marrow cells of mice in each group on days 7,14,21,28 after transplantation were obtained to detect EPC cultural and cell chimeric rates by flow cytometer. Mice were sacrificed on days 7, 14, 21 and 28 post HSCT to analyze bone marrow pathology by H&E staining, the infiltration of macrophages and neutrophils by Western blot, validation expression levels of inflammatory complexes nlrp1、nlrp6 and its downstream molecules casepase-1 by Q-PCR and Western blot. Results: Cell chimeric rate on day 7 after transplantation in EPC group[ (91.65±2.77) %] was significantly higher than in BMT group[ (83.69±1.26) %]. Alleviated osteomyelitis injury and inflammatory cell infiltration in EPC group were observed when compared with BMT mice. Also significant reductions of the levels of nlrp1、nlrp6、casepase-1 transcription complexes in EPC mice were noted when compared with BMT ones. Conclusion: Co-transplantation of HSC and EPC could alleviate inflammatory cell infiltration and activation of the complex to promote the repair of bone marrow.

[Research advances in pathogenesis of autoimmune hepatitis].

Autoimmune hepatitis (AIH) is liver parenchymal inflammation mediated by the autoimmune response of hepatocytes. Its clinical features include elevation of aminotransferases in serum, presence of various autoantibodies in circulation, hypergammaglobulinemia, and interface hepatitis in liver tissue. Although the etiology and pathogenesis of AIH have not been fully elucidated, a consensus has been reached on the theories of "genetic susceptibility" and "molecular simulation" , and "immunoregulatory disorder" remains a hot research topic for many scholars. This article reviews the research advances in the theories of "genetic susceptibility" , "molecular simulation" , and "immunoregulatory disorder" .

Influence of suppression of CapG gene expression by siRNA on the growth and metastasis of human prostate cancer cells.

This study investigated CapG gene expression in prostate cancer cell lines; in addition, we explored the effects of CapG suppression on DU145 cell growth, and the underlying mechanism with which CapG affects DU145 cell growth and invasiveness. The expression of CapG and 18 related genes in DU145 cells was analyzed by flow cytometry, quantitative polymerase chain reaction (qPCR), CCK8 assay, western blot, and the trans-well assay. DU145 cells were transfected with designed small interfering RNA (siRNA). CapG expression was quantified by qPCR and western blot. DU145 cell proliferation and invasiveness was analyzed using the CCK8, flow cytometric, and trans-well assays. CapG, TMPRSS1, EGFR, ETS-1, ERBB2, AKT, Cyclin D1, P21, Bcl-2, and Bak1 gene and Bcl-2, Cyclin D1, and CapG protein expressions were significantly lower in the siRNA group compared to the negative control group (P < 0.05). The proliferation of CapG siRNA DU145 cells was lower than that of the two control groups, 48 h after transfection. The cell inhibition rate was 24.5, 35.4, and 16,5% at 24, 48, and 72 h, respectively. The growth curve indicated that CapG siRNA DU145 cells showed a significantly slower proliferation rate (P < 0.05). The trans-well assay showed a significant decrease in the migratory and invasive capacities of DU145 cells in the siRNA group (P < 0.05). The suppression of CapG expression caused a significant decrease in the proliferation, invasiveness, and metastasis of DU145 cells. The mechanism with which CapG, with other oncogenes, influences cancer cell cycle remains to be elucidated.