ABSTRACT
Vitamin D deficiency/insufficiency not only results in disorders of skeletal system, but may also be associated with other nonskeletal diseases.Therefore, measurement of 25 -hydroxyvitamin D has received more and more attentions.Common methods for 25-hydroxyvitamin D testing include vitamin D binding protein -based competitive assays, immunoassays, high performance liquid chromatography (HPLC), and liquid chromatography -tandem mass spectrometry(LC -MS/MS).Vitamin D binding protein-based assays and immunoassays can be performed on automated chemistry analyzers,permitting an easy and quick measurement with high throughput.However, significant variability exists among various assays.They cannot separate 25 -hydroxyvitamin D3 and D2 either.HPLC method can separate D3 and D2,but the sensitivity and specificity are not as good as mass spectrometry.LC-MS/MS is more specific and sensitive and it can measure D3 and D2 individually.However, the methodology is more complicated and its throughput is relatively low.Also, it requires special instrument and operators who need additional training.In addition,most LC-MS/MS methods are developed and validated by individual laboratories,so the standardization of the method is an urgent problem to be solved.Although the specificity of LC -MS/MS method is high, some metabolites may still interfere with the assay.The reference interval of 25 -hydroxyvitamin D is still controversial and how to establish gender -and age-specific reference intervals remains debatable.Besides 25-hydroxyvitamin D,whether its metabolites and free 25-hydroxyvitamin D should be measured is still questionable.Although 25-hydroxyvitamin D testing is primarily used for the diagnosis and treatment of skeletal diseases, epidemiological studies suggest that vitamin D deficiency /insufficiency may be related to the development and prognosis of nonskeletal diseases.However, more evidence is needed in order to determine the causal relationship between them and the mechanism.
ABSTRACT
PurposeTo explore the relationship between expression of apoptosis-modulating proteins and chemotherapeutic efficacy in acute leukemia. MethodsImmunocytochemical method was used to detect the expression of Bcl-2、Bcl-XL、Bax and Bak in 36 cases of acute leukemia including previously untreated/ drug-sensitive group and refractory/relapse group. ResultsThe average positive cell rates of Bcl-2 and Bcl-XL in refractory/relapse group were (41.68 ± 14.39) % and (35.96 ± 9.95 ) %, while the rates in previously untreated/drug-sensitive group were (15.64 ± 8.51 )% and (12.91 ± 8.63 )%. Statistical analysis showed the average positive cell rates of Bcl-2 and Bcl-XL in refractory/relapse group were higher than those in previously untreated/drug-sensitive group (P ＜ 0.01 ). There was no significant difference in average positive cell rates of Bax and Bak between refractory/relapse group (25.28 ± 15.49) %, (15.53 ± 10.64) % and previously untreated/drug-sensitive group (21.55 ± 12.58)%, (13.23 ± 8.36)%. The Logistic regression of expression of Bd-2 、Bcl-XL、Bax and Bak to complete remission rate (CR) of 36 cases of acute leukemia showed that Bcl-XL was the most risk factor in reducing the CR.ConclusionsBcl-2 and Bcl-XL might play important roles in multi-drug resistance of acute leukemia and Bcl-XL was more important than Bcl-2.
ABSTRACT
Purpose To explore the Relationship between expression of apoptosis-modulating proteins amdmultidrug resistance in K562/VCR cells. Methods Irnmunocytochemical methol and western blot wereused to analyze the expression of apoptosis-modulating proteins (Bcl - 2, Bcl-XL, Bax, Bak ) in multidrugresistant cell line K562/VCR and drugsensitive cell line K562. Results The positive cell rates ofapoptosis-suppressing protein Bcl-2 and Bcl-XL in K562/VCR were (40.0 ± 8.0) % and (60.0 ± 10.0) % .While the rates in K562 were (1.0 ± 0.3) % and (20.0 ± 4.0) %. There was significant difference in thepositive cell rates of Bcl - 2 and Bcl - XL between K562/VCR and K562 ( n = 3, P ＜ 0.05 ). It was alsofound there was no significant difference in expression of Bax between K562/VCR and K562. Furthemore,Bak was not expressed in both K562/VCR and K562 or the expression was very low. Conclusions Wesuggest that Bcl-2 and Bcl-XL play important roles in multidrug resistance in K562/VCR, while Bax and Bakmight not be important.