Objective To investigate the relationship of the cytogenetic abnormalities detected by FISH in patients with MM and their clinical features. Methods FISH on bone marrow (BM) cells was performed in 57 enrolled MM patients. Relationships between cytogenetic abnormalities and clinical features were analyzed. Results By statistical analysis , both D13S319 deletion and RB1 deletion were associated with high level of serum LDH (P = 0.024; P = 0.018) and BM plasma cells index (P = 0.027; P = 0.013). 1q21 amplification was significantly associated with high level of LDH (P = 0.030 ) and the occurence of light chain type myeloma (P = 0.023). IgH rearrangement was associated with renal function damage (P = 0.009). There were correlations among D13S319 deletion, RB1 deletion, 1q21 amplification and IgH rearrangement (P<0.01). Conclusion The genetic abnormalities detected by FISH in patients with MM were correlated with various clinical poor prognostic indicators, which can evaluate the condition and prognosis of patients more efficiently.

OBJECTIVE: : To investigate the effect of chlorogenic acid (CGA) on non-enzymatic glycation and oxidation of low density lipoprotein (LDL). METHODS: : The non-enzymatic glycation incubation system of LDL-glucose was established. The contents of early glycation products (Amodori product) and intermediate products (dicarbonyl compound) were determined by ultraviolet-visible spectrophotometry, and the content of advanced glycation end products (AGEs) was determined by fluorescence spectrophotometry. The LDL oxidation incubation system was established. The contents of thiobarbituric acid reactive substances(TBARS) and conjugated diene were determined by ultraviolet-visible spectrophotometry. The tryptophan fluorescence quenching, and the content of lipofuscin, total fluorescence products, active aldehydes and malondialdehyde were determined by fluorescence spectrophotometry, and further verified by three-dimensional fluorescence spectroscopy. RESULTS: : In the LDL glycation experiment, 150 μg/mL and 300 μg/mL CGA inhibited the formation of Amadori product, dicarbonyl compounds and AGEs. In the LDL oxidation experiment, 15 μg/mL and 25 μg/mL CGA inhibited the formation of TBARS effectively; 5 μg/mL and 10 μg/mL CGA inhibited tryptophan fluorescence quenching, and the formation of active aldehydes, malondialdehyde, total fluorescence products, lipofuscin and conjugated diolefine. And the three-dimensional fluorescence spectroscopy showed the same results. CONCLUSIONS : CGA can inhibit non-enzymatic glycation and oxidation of LDL.
Chlorogenic Acid ; pharmacology ; Glycosylation ; drug effects ; Lipoproteins, LDL ; metabolism ; Oxidation-Reduction ; drug effects ; Thiobarbituric Acid Reactive Substances ; analysis