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1.
Journal of Experimental Hematology ; (6): 478-481, 2016.
Article in Chinese | WPRIM | ID: wpr-360063

ABSTRACT

<p><b>BACKGROUND</b>The false positive in conventional syphilis serological test was found in patients with multiple myeloma (MM).</p><p><b>OBJECTIVE</b>To investigate the relationship between the M-protein of patients with MM and the false positive in conventional syphilis serologic test.</p><p><b>METHODS</b>The M-protein of 68 MM cases was typed with immunofixation electrophoresis and 68 cases of MM were screened with non-specific and specific syphilis serologic tests, then the samples with syphilic serological positive were chosen and confirmed with immonobloting test, finally the relationship between M protein of MM and the false positive of syphilis serological test were analysed.</p><p><b>RESULTS</b>Four out of 68 cases showed the positive in syphilis serological test and further were confimed to be false positive by immunoblotting test, the false positive rate was nearly 6%. The M-protein of MM patients in our hospital mostly possessed IgG, κ type, followed by IgA, κ type, light chain κ type. In general, κ : λ = 2.4 : 1. Among samples of 4 cases with syphilis serological positive 2 cases were of IgG and κ type, 1 case was of IgG, λ type, another 1 case was IgA, κ type.</p><p><b>CONCLUSION</b>The M-protein of IgG and IgA types in MM patients results in syphilis serological false positive reaction. The clinicians and laboratorial technicians should pay a great attention to screen the MM patients for the false positive syphilis serological test so as to avoid the misdiagnosis and subsequent embarassment.</p>


Subject(s)
Humans , Diagnostic Errors , False Positive Reactions , Immunoglobulin A , Classification , Immunoglobulin G , Classification , Multiple Myeloma , Diagnosis , Myeloma Proteins , Metabolism , Syphilis , Diagnosis , Syphilis Serodiagnosis
2.
Chinese Journal of Otorhinolaryngology Head and Neck Surgery ; (12): 504-508, 2009.
Article in Chinese | WPRIM | ID: wpr-245894

ABSTRACT

<p><b>OBJECTIVE</b>To investigate whether down-regulation of Twist1 could change sensitivity of nasopharyngeal carcinoma cell line HNE1 to taxol.</p><p><b>METHODS</b>HNE1 cells were transfected with the small interfering RNA (siRNA) expression vector pSuppressor-Retro-Si-Twist, containing the short hairpin RNA (shRNA) sequence targeting the Twist gene-coding region by Fugene 6. Positive clones were then selected in Neomycin (400 microg/ml) for 21 days. The low expressions of Twist1 were examined by real-time reverse-transcription polymerase chain reaction (RT-PCR) and Western blot. Drug sensitivity of si-Twist1 HNE1 to taxol was determined by Annexin V-fluorescein isothiocyanate( FITC)/propidium lodide (PI) double-labeled flow cytometry and detection of DNA ladder. The Effect of Twist1 inactivation on HNE1 cell proliferation was observed by MTT assay and flow cytometry.</p><p><b>RESULTS</b>Annexin V- FITC-PI assay showed that apoptosis ratio was 40.2% in si-Twist HNE1 after treated with 10 ng/ml taxol, significantly higher than that in the control siRNA group 24.3%. The deference had statistic meaning. After the re-expression of HNE1, apoptosis ratio was 44.80% +/- 4.80% (x +/- s) in low Twist1 protein expression group and that was 27.00% +/- 2.91% in high expression group. The deference had statistic meaning (t = 4.374, P = 0.049). Real time PCR test revealed apoptosis protein bcl-2 expression in si-Twist HNE1 was 0.28 +/- 0.05, significantly lower than that in the control siRNA HNE1 (0.57 +/- 0.08, t = 6.710, P = 0.021), nevertheless, significant bax and bcl-XL changes were not observed (t = 2.000, P = 0.184 and t = 1.502, P = 0.272). MTT and FCM showed that down-regulation of Twist1 did not alter cell proliferation rate (P>0.05).</p><p><b>CONCLUSIONS</b>Down-regulation of Twist1 could increase drug sensitivity of nasopharyngeal carcinoma cell line HNE1 to taxol by inducing apoptosis. These results suggested that Twist1 may be a promising treatment target for nasopharyngeal carcinoma therapy.</p>


Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Down-Regulation , Gene Expression Regulation, Neoplastic , Nasopharyngeal Neoplasms , Drug Therapy , Nuclear Proteins , Genetics , Paclitaxel , Pharmacology , RNA Interference , RNA, Small Interfering , Twist-Related Protein 1 , Genetics
3.
Acta Academiae Medicinae Sinicae ; (6): 329-335, 2007.
Article in Chinese | WPRIM | ID: wpr-229979

ABSTRACT

<p><b>OBJECTIVE</b>To explore the relationship between genetic polymorphisms of C-344T in the promoter region and K173R in the exon 3 of aldosterone synthase gene (CYP11B2) and the incidence of essential hypertension in a northern Chinese Han population.</p><p><b>METHODS</b>We conducted a case-control study including 182 hypertensive patients and 189 healthy controls in Harbin newspaper office and assayed the genotypes of C-344T and K173R using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and direct sequencing technology.</p><p><b>RESULTS</b>The distributions of C-344T and K173R genotype frequencies in men and women were in accordance with the Hardy-Weinberg equilibrium. The differences of C-344T allele and genotype as well as K173R allele frequency distributions between hypertensive patients and healthy controls were not statistically significant in men and women and pooled population (P > or = 0.05). The difference of K173R genotype frequency distribution reached borderline significance (P = 0.0500) and was more pronounced in women (P = 0.0038) according to the dominant mode of inheritance. Moreover, the magnitude of this mode of inheritance was more remarkable after the confounding factors were adjusted. K173R statistically correlated with the systolic hypertension in women.</p><p><b>CONCLUSION</b>The CYP11B2 K173R polymorphism correlates with the susceptibility of essential hypertension in the northern Chinese Han population.</p>


Subject(s)
Female , Humans , Male , Asian People , Case-Control Studies , Cytochrome P-450 CYP11B2 , Genetics , Genetic Association Studies , Genetic Predisposition to Disease , Hypertension , Genetics , Polymorphism, Genetic
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