Objective To explore the applied value of urine light chainκ、λand κ/λ ratio test in older people with B cell malignant proliferative disease.Methods Young volunteers, general older patients, kidney failure older patients and older patients with B cell malignant proliferative disease were selected and immunoephe-lometry method was applied to detect the level of urine light chainκ、λ and κ/λ ratio.Result The average levels (mg/L)of urine light chain κand λin older patients with kidney failure group(172.00 ±188.10,111.50 ± 109.32)were higher than that in general older patients group(32.72 ±33.60,15.02 ±15.58).In each of the ol-der patients groups,the levels of urine light chainκandλwere higher than that in young volunteers groups(9.30 ±5.80,4.97 ±2.61).The κ/λ ratios of urine light chain in older patients with kidney failure group(1.59 ± 0.4),general older patients group(2.19 ±0.54)and young volunteers group(1.92 ±0.48)were consistent,how-ever,it was significantly abnormal in older patients with B cell malignant proliferative disease group,the ratio was high inκtype(44.8 ±83.17)and low inλtype(0.06 ±0.08).After effective treatment, κ/λ ratio of urine light chain in older patients with B cell malignant proliferative disease tended to normal.Conclusion The level of u-rine light chainκandλis effected by renal function,but not involved the κ/λ ratio.B cell malignant proliferative disease significantly affects theκ/λratio of urine light chain.Constantly monitoring the change ofκ/λratio of u-rine light chain in older peoples with B cell malignant proliferative disease can reflect the proliferative degree of malignant B cell in vivo.

Objective To observe the effects and study the underlying mechanism of siRNA targeting PARP1 on the proliferation of androgen independent prostate cancer PC3 cell line.Methods Three specific siRNA sequences targeting PARP1 were designed and synthesized.And two sequences which had better interfering effect on the expression of PARP1 were evaluated and selected through lipofectamine transfection,RT-PCR and Western Blot.The effect of PARP1 silencing on the proliferation of PC3 cells was observed with MTS assay and the levels of the phosphorylation of Akt and GSK3β were detected by Western Blot.Results Compared to the blank control group,the transfected group with the negative control sequence had no significant impact on the expression of PARP1,however the transfected group with siRNA-1706,-2003 or-2907 could significantly suppress the mRNA and protein expression of PARP1.The mRNA inhibition rate reached to(52.07 ± 4.65)％,(44.38 ± 9.15)％ and(22.05 ± 6.65)％,respectively;and the protein inhibition rate reached to(86.86 ± 4.94)％,(83.30 ± 7.18)％ and(63.05 ± 10.19)％,respectively.The siRNA-1706 and-2003 could significantly inhibit the proliferation of PC3 cells;the inhibition rate was(38.93 ± 3.87)％ and(34.93 ± 1.21)％.And they also could down-regulate the intracellular levels of phosphorylated Akt and GSK3β in PC3 cells.Conclusion PARP1-targeted siRNA can significantly suppress the expression of endogenous PARP1 and inhibit the proliferation of PC3 cells,which is related to the inhibition of Akt activity and the activation of GSK3 β.

Objective To assess the enhancement characteristic of breast lesions of contrast-enhanced ultrasound (CEUS) in comparison with contrast-enhanced magnetic resonance imaging (MRI).Methods Between August 2011 and March 2013,72 women with 72 lesions were enrolled.All patients underwent ultrasound,CEUS and MRI.The histopathologic results obtained from ultrasound-guided core biopsy or operation excisions were used as the reference standard.CEUS section evaluations were made similar with MRI regarding the size and shape of lesions.Different contrast enhancement patterns including homogeneous/heterogeneous,the tumor areas,the perfusion defect areas,and modality of time-intensity curve were evaluated.Pearson's correlation coefficient,Student's t-tests,and the concordance test were used for evaluation.Results Of the 72 lesions,pathologic examination revealed 56 (77.8％) malignant lesions and 16 (22.2％) benign lesions.The tumor areas measured by CEUS and MRI agreed well,with a correlation of r =0.894,P =0.000.The difference between the two measurements was not significant according to a paired t test (P =0.886).The concordance tests gave a value of the coefficient Kappa =-0.153 (P =0.061),indicating a low concordance between the results obtained with CEUS and those obtained with MRI regarding the enhanced uniformity.There were statistically significant differences in the perfusion defect areas as measured by CEUS and MRI (P =0.01).The CEUS estimates [(0.837 ± 0.827)cm2] were consistently higher than the MRI estimates [(0.576 ± 0.524)cm2].The time-intensity curve patterns between the two groups showed no correlation.Conclusions The enhancement patterns evaluated by CEUS and MRI partly agreed well.There was no direct association between the two methods regarding the enhancement patterns because of the different contrast agent.

[Objective]To study the effect of curcumin on the cholesterol metabolism of nonalcoholic fatty liver disease(NAFLD) cells model induced in vitro and its potential mechanism. [ Methods]The cellmodel of nonalcoholic fatty liver disease(NAFLD) was established by oleic acid and treated with curcumin. The method of oil red O staining was used to observe accumulation of intracellular lipid while the intracellular content of TG, FC and TC was detected by enzymatic method. Meanwhile, the mRNA levels of SR-BΙand HMGCR were detected with qPCR.[ Results] The NAFLD cellmodel was successful y established by culturing with 30 μg·mL-1 oleic acid. After curcumin intervention, TG, FC and intracellular lipid accumulation levels were significantly reduced in NAFLD cellmodel. Meanwhile, curcumin can reduce HMGCR mRNA expression and raise SR-BΙ mRNA expression. [Conclusion] Curcumin can decrease FC level in NAFLD cellmodel and the mechanism might be related with its capacity of restraining endogenous cholesterol biosynthesis and promoting foreign cholesterol transfer into the liver cells for metabolism.

Objective To study the anti-tumor effect and mechanism of bortezomib in primary acute leukemia cells from elderly patients.Methods Primary acute leukemia cells were treated with bortezomib 50-5000 nmol/L for 24-48 h,cell proliferation was analysed by MTT assay; apoptosis of primary acute leukemia cells was observed by fluorescence microscopy and flow cytometry; protein expression of bcl-2 and Bax was detected by Western blot.Results The cell viability was 90 ％ and 70 ％ when leukemia cells were treated with 50 and 5000 nmol/L bortezomib for 24 h,respectively.Meanwhile,cells showed (10.2±2.3) ％ and (13.3±3.3) ％ apoptosis.With prolonged treatment for 48 h,cell viability decreased to 86 ％ and 60 ％,respectively,while the apoptosis rates were increased to(18.4±3.9) ％ and(20.7±3.7) ％.Compared to the control group 0 nmol/L bortezomib,the differences were statistically significant (F =53.76,F =7.74,F =54.49,F =16.94,all P values ＜ 0.05).With the increase of bortezomib concentration,the bcl-2 protein expression was decreased,while Bax was up-regulated.Conclusion Bortezomib can inhibit primary leukemia cells from elderly patients proliferation and induce apoptosis.The mechanism may be associated with the changes in bcl-2 family protein expression.

ObjectiveTo investigate the role of platelet in mouse pulmonary microvascular endothelial cell (PMVEC) injury caused by lipopolysaccharide( LPS)-activated neutrophil.MethodsPMVECs were obtained from pathogen-free C3H/HeN mice of both sexes aged 6-8 weeks weighing 18-25 g according to the method described by Lim YC et al.Platelets and neutrophils were isolated from mouse blood by twice centrifugation and denaity gradient centrifugation respectively.PMVECs were seeded into twelve- or six-well plates ( 1 or 2 ml/well) after 2-5 passages and were randomly divided into 4 groups (n =31 each): group LPS; group platelets (group P);group neutrophils (group N) and group platelets + neutrophils (group PN).Each well contained about 5 × 107/ml platelets and/or 5 × 105/ml neutrophils respectively.PMVECs were incubated with LPS1 μg/ml at 37 ℃ in a 5％ CO2 humidified atmosphere for 1,6,12,18 and 24 h respectively in all 4 groups.The cells were examined with phase contrast microscope for morphological changes and survival condition.Viability rate,apoptotic rate and activation rate of PMVECs were detected by flow cytometry at each time points.ResultsThere was no significant difference in morphology and number of endothelial cells (ECs) among the 4 groups,while the number of activated ECs was significantly increased but the number of living cells decreased in group PN compared with group LPS.The activation rate of ECs was significantly higher after being incubated with LPS for 6-12 h in groups P and N than in group LPS.The viability rate was significantly lower,while the apoptotic rate and activation rate were significantly higher after ECs were incubated with LPS in group PN than in groups LPS,P and N.ConclusionPlatelets play a decisive role in mouse PMVEC injury induced by LPS activated neutrophils.

Objective To observe learning and memory behavior changes of one time cerebral concussion called pure cerebral concussion(PCC)and three times cerebral concussion called multiple cerebral concussion (MCC)after injured 24 days in rats.Methods A metallic pendulum striker device was deployed to duplicate PCC and MCC model in SD rata which were the complete closed head injury model.The animals were divided into PCC and MCC groups at random.One control group was used,each group has eight animals(n=8).One 8-arms radial maze was used to assessed each animal's capabilities,that is,spatial reference memory,working memory,spirited activity and take in food.Results Compared with control group,there were some significance(P＜0.05)in both experiment groups post injury,that was,(1)The food intake decreased,PCC group from the 1st to the 11th day(from 0.00±0.00 to 2.62±1.76)after injury,MCC group from the 1st day to the 24th day(from 0.00±0.00 to 0.75±1.48)after injury.(2)Spirited activity depressed,PCC group on the 1st to the 7th,13rd day(from 4.87±1.24 to 10.0±2.39)after injury,MCC group on the 1st to 8th,22nd day(from 4.25±5.03 to 9.37±4.20)after injury.(3)The spatial reference memory was lower in early then gradually increased,PCC group on the 1 st to 7th day(from 0.50±0.75 to 3.O0±1.06)after injury,MCC group from the 1st to 19th day(from 1.88±2.10 to 2.50±2.44)after injury.(4)The working memory was delaying damaged,PCC group from the 1st to the 6th day and the 10th to the 23rd day(from 0.00±0.00 to 4.25±3.05)after injury,MCC group on the 1～4th,6th,9～13th,15th,16th,19th～22nd day(from 0.25±0.46 to 3.12±2.87)after injury.Conclusion The injured rata'capability of spatial reference memory,working memory,spirited activity and food intake were obviously damaged after CC,and the MCC group's capability of spatial reference memory,spirited activity and food intake was worse than PCC group.

The effect of cholesterol ester transfer protein(CETP) on SR-B1 mRNA expression in mouse liver was investigated.The results demonstrated that CETP transgenic mice showed lower serum total cholesterol and high density lipoprotein-cholesterol levels but higher total cholesterol and cholesterol ester content in liver when compared with wild type mice(P＜0.05).The expression of SR-B1 mRNA in liver of CETP transgenic mice was significantly lower as compared with the control group(P＜0.05).

Objective To explore the signal-to-noise ratio loss (SNR loss) of the people with normal pure-tone audiograms .Methods A group of 10 patients were recruited into the study ,who complained they could not hear speech clearly in the real world environment but had normal pure-tone audiograms ,immittance and word rec-ognition score (WRS) results .The Mandarin hearing in noise test (M-HINT ) was administered to them and the results were compared to the normal ranges published in the journal .Results All of them had SNR loss when noise (speech spectrum) came from front of them ,but 9 patients had SNR loss when noise came from 90 degree left or 90 degree right of them .Conclusion The current study showed the patients had speech hearing loss in the noisy envi-ronment ,regardless of whether they had normal audiograms ,immittance and WRS results .So we should pay atten-tion to such patients and adopt some special tests (eg M-HINT) .It is better for us to communicate and counsel with them .

Objective To study the relationship between Nogo-B and transforming growth factor-β1 (TGF-β1)/Smad2 signaling pathway in mice models of hepatic fibrosis.Methods Twenty four healthy male ICR mice were divided into two groups,with 6 in the control group and 18 in the model group.Mice in the model group were further divided into three subgroups according to different time points:subgroups of 4,8 and 12 weeks,with 6 mice in each subgroup.Hepatic fibrosis of mice was induced by subcutaneous injection of carbon tetrachloride (CCl4).The histopathologic changes of the liver were observed by optical microscope using hematoxylin-eosin and Masson trichrome stainings of the liver tissues.Expressions of Nogo-B,Smad2 and TGF-β1 mRNA and proteins in liver were detected by reverse transcription-polymerase chain reaction (RT-PCR),Western blot and immunohistochemistry assays,respectively.Means among groups were compared by univariate analysis of variance.Results The hepatic fibrosis models were successfully induced by CCl4 injection.The expressions of two subtypes of Nogo-B,Nogo-B1 and Nogo-B2 mRNA in normal livers were 0.140±0.050 and 0.104±0.023,but both significantly increased in the livers of mice in the 12 week model subgroup (1.054±0.040 and 0.500±0.057,F=431.41 and 135.46,respectively; both P＜0.01).The Nogo-B protein was mainly expressed in nonparenchymal cells of the liver,and was hardly expressed in hepatocytes.Linear correlation analysis showed that the expressions of Nogo-B mRNA and proteins were positively correlated with Smad2 and TGF-β1 mRNA and proteins (all P＜0.01),which were considered to participate in the signaling pathway of hepatic fibrosis.Conclusion Nogo-B might play a role in the development and progression of hepatic fibrosis by participating in TGF-β1/Smad2 signaling pathway.