Objective To investigate the low hemoglobin density (low haemoglobin density,LHD) and red blood cell volume distribution width (red blood cell volume distribution width,RDW) in iron deficiency anemia (iron-deficiency anemia,IDA)in children with the value of diagnosis and treatment.Methods From February 2016 to May 2017,in the Second People's Hospital of Longgang District in Shenzhen City,86 cases of children with iron deficiency anemia for IDA group,and 120 cases of healthy children (as the control group) at the same time were confirmed.Blood routine of children with IDA were detected before and after treatment hemoglobin concentration and the results were analyzed statistically.Results 120 cases of healthy children in the peripheral blood LHD value was 2.74 ％ ± 0.90 ％ and the boy was 3.07 ％ ± 0.81％,higher than that of 2.26 ％ ± 0.69 ％ of the girls.Between them,there was statistically significant difference (t=3.815,P＜0.05).The value of RDW was 12.37 ％ ± 2.84 ％,12.09 ％ ± 2.80 ％ for the boys and 12.56 ％ ± 2.87 ％ for the girls,there was no statistically significant difference between the them (t=0.517,P＞0.517).Before treatment,86 cases of children with IDA LHD and RDW values in peripheral blood were 30.67 ％ ± 20.12 ％ and 16.62 ％ ± 3.27 ％,significantly higher than the control group,the difference was statistically significant between (t=4.025 ～ 4.025,P＜0.05 ～ 0.01),and there was no statistically significant difference between male and female children (t =0.761 ～ 0.917,P＞ 0.05).After treatment L HD and RDW values were 10.65 ％ ± 8.92 ％ and 14.02 ％ ± 2.93 ％,significantlylower than before the treatment,between them was statistically significant difference (t=2.912～9.675,P＜0.05).Conclusion Children with iron deficiency anemia treatment before the LHD and RDW values significantly elevated in the blood,significantly decreased after treatment,the LHD and RDW values for diagnosis and treatment of children with iron deficiency anemia dynamic monitoring has certain application value,worthy of popularization and application.

Objective To observe the effects of creatine phosphate sodium on heart function and B -type natriuretic peptide in patients combination with ischemic cardiomyopathy and intractable heart failure .Methods 70 cases of coronary heart disease combined with ischemic cardiomyopathy and intractable heart failure were randomly ( with the random number table ) divided into the control group ( n=33) and the creatine phosphate sodium treatment group (n=37).The control group treated with conventional therapy (digitalis,diuretics,vasodilator,ACEI,et al) ten days;the treatment group with creatine phosphate sodium treatment on the basis of conventional therapy .The symp-tom,sign of the heart failure patients of the two groups before and after treatment were observed .NYHA cardiac func-tional grading were estimated.Echocardiography was used to detect left ventricular end -systolic diameter(LVESD), left ventricular end diastolic diameter ( LVEDD ) and left ventricular ejection fraction ( LVEF ); amino terminal pro brain natriuretic peptide (NT-proBNP) tested by laboratory of the two groups.Drug treatment for 10 days,the chan-ges of the indicators before and after treatment were observed .Results After treatment , compared with the control group[(50.63 ±4.67) mm,(61.30 ±4.58) mm].LVESD,LVEDD of the creatine phosphate sodium treatment [(47.16 ±4.30)mm,(57.92 ±4.30)mm]significantly decreased(t=5.73,4.96,all P<0.01),LVEF[(40.57 ± 4.51)%,(37.63 ±4.53)%]increased significantly(t =5.53,P<0.01).After ten days of treatment levels of NT-proBNP decreased in both two groups [(1 659.±248.18) pg/mL,1 899.3 ±205.45] than before treatment [2 043.46 ±217.04,(2 105.46 ±239.09)pg/mL](t=3.23,3.64,all P<0.05),and the decrease degree of the creatine phosphate sodium treatment group was more obvious than those of the control group (t=4.11,P<0.05). Conclusion Creatine phosphate sodium can improve the cardiac function and left ventricular ejection fraction of ischemic cardiomyopathy and intractable heart failurepatients ,enhance the clinical symptoms of patients .

Objective To investigate the effect of gene silencing of Y-box binding protein-1(YB-1) by RNA interference on the proliferation and migration in prostate cancer cells lines PC-3 cells .Methods YB-1 siRNAs(pGenesil-1-YB-1-1 and pGenesil-1-YB-1-2) were synthesized and transfected into cloned into the the PC-3 cells by liposome .The expressions of YB-1 were measure by RT-PCR and Western blotting .The proliferation and migration were respectively detected by MTT and Transwell method . Results ThemRNA and protein expressions of YB-1 were significantly decreased by pGenesil-1-YB-1-1 and pGenesil-1-YB-1-2 (P<0 .05) ,compared with the control group ,the inhibition ratio of mRNA expression was 36 .23% and 39 .42% respectively and the inhibition ratio of protein expression was 41 .56% and 55 .33% respectively .The proliferation and migration were significantly decreased by pGenesil-1-YB-1-1 and pGenesil-1-YB-1-2(P<0 .05) .Conclusion YB-1 gene silencing by RNA interference inhibits the proliferation and migration in prostate cancer cells lines PC-3 cells .

Objective To investigate the effect of hydrogen sulfide (H2S) on the cholesterol efflux and ATP-binding cassette transporter A1 (ABCA1) expression in foam cells .Methods RAW 264 .7 macrophages were incubated with oxidized low density lipoprotein to induce foam cells .Foam cells were incubated with H2S donor sodium hydrosulfide .Cholesterol efflux from macropha-ges was tested by labed cholesterol .The cellular levels of free cholesterol (FC) ,cholesterol ester (CE) and total cholesterol (TC) were measured by high performance liquid chromatography assays .The mRNA and protein expressions of ABCA1 were detected by Real-time PCR and Western blot .Results Compared with the foam cells ,the rates of cholesterol efflux were significantly in-creased ,the levels of TC ,FC ,CE and CE/TC ratio were significantly decreased(P<0 .05) and expression of ABCA1 was signifi-cantly increased by treatment with H2S in dose-and time-dependent manner(P<0 .05) .Conclusion H2S up-regulates of expres-sion ABCA1 and promotes cholesterol efflux in RAW 264 .7 macrophage-derived foam cells .

Ammonia toxicity has been generally accepted as one of the classic theories of the pathogenesis of hepatic encephalopathy (HE). Ammonia induces changes in neurological system energy metabolism, oxidative stress, mitochondrial permeability transition (MPT), GABA and Glutamatergic neurotransmission, intracellular signal transduction and Aquaporin 4 (AQP4) expression, astrocyte swelling is another important consequence of ammonia neurotoxicity. This article reviewed the role of these factors in the mechanism of HE and ammonia toxicity.

Objective To estimate the clinical value of thinprep cytologic test (TCT) in screening cervical lesion. Methods 4234 TCT samples were interpreted according to the Besthesda System (TBS), 272positive cases (ASC-US or above) were taken colposcopic examination and biopsy. Results The coincidence of the results between TCT and biopsy in low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), squamous cell carcinoma (SCC), adenocarcinoma (AC) were 85.71%(12/14), 100 % (20/20), 75 % (3/4) and 100 % (2/2), respectively. The positive rates of over ASC-H by TCT and of over CIN Ⅰ by biopsy were 23.16 % (63/272) and 24.26 % (66/272), respectively. There is no difference between two positive rates (x2 = 0.868, P = 0.581). Conclusion TCT and histopathological diagnosis had a high coincidence, a combination of both can greatly enhance HSIL and cervical cancer and reduce the incidence of missed diagnosis. TCT would be a rapid and convenient method for screening cervical cancer.

Objective To study the mechanism of RING finger protein 34 ( RNF34 ) involved in innate immunity . Methods Recombinant PCR was used and transient expression of the plasmid was achieved in HEK 293T cells.The cells were stimulated with Sendai virus ( SeV) or N-RIG-Ⅰfor the indicated time while luciferase activity was observed using the dual-luciferase reporter assay kit .Results We constructed the plasmid pcDNA 3-Flag-RNF34 and its three mutations .The study found that when stimulated by SeV , RNF34 could inhibit the activity of NF-κB and IFN-βmore significantly than RNF34-ΔFYVE, RNF34-ΔCID and RNF34-ΔRING.We also found that RNF 34 and its three mutants had similar inhibitory effect when the activation of NF-κB and IFN-βwas stimulated by the N-RIG-Ⅰ.Conclusion RNF34 negatively regulates innate immunity by acting on the RIG-Ⅰ-MAVS signaling pathway .

Objective To investigate the effect and its mechanism of diazoxide on the blood-brain barrier (BBB) of rats after cerebral ischemia/reperfusion (I/R) injury.Methods Sixty Wistar rats were randomly divided into sham operation group,I/R group,and diazoxide pretreatment groups of low,middle,large dose (5,10,20 mg/kg).The I/R models of rats were performed to undergo middle cerebral artery embolism by thread.BBB permeability was estimated by Evans blue (EB) dyeing,transmission electron microscope (TEM) was used to observe the modification of interendothelial tight junction (TJ) of capillaries.The expression of aquaporin-4 (AQP4) in every rat brain tissues was detected by immunity histochemistry technique.Results (1) Compared to sham operation group,the permeability extent of EB were significantly increased by I/R,which was distinctly attenuated in middle and large dose of diazoxide pretreatment rats,while no obvious changes were found between I/R and low dose groups.(2) TEM showed that TJ of the brain tissue opened after I/R injury and no significant opening of TJ was observed in middle and large dose of diazoxide preconditioning groups.(3) Compared to sham operation group,the expression of AQP4 in the brain tissue of the I/R group was apparently increased (P ＜0.01).Compared to I/R group,the expression of AQP4 was apparently increased in middle and large dose pretreatment groups (P ＜ 0.01),and there were no obvious difference between low dose group and the I/R group.Conclusions Preconditioning of ischemia/reperfusion injury with diazoxide protects the blood-brain barrier,which may due to keep the TJ closed and decrease expression of AQP4 protein.

Objective To investigate the effects of remote ischemic postconditioning (RIPoC) on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods One hundred and twenty-eight male adult SD rats weighing 200-250 g were randomly divided into 4 groups ( n =32 each):sham operation group (group S),group I/R,group I/R + RIPoC and remote I/R group (group RI/R ).Global cerebral I/R was induced by four-vessel occlusion.Group I/R + RIPoC received 3 cycles of 15 min reperfusion followed by 15 min ischemia in bilateral femoral arteries at the beginning of cerebral reperfusion.The rats were sacrificed at 24 and 48 h of cerebral reperfusion,and brains were removed for determination of neuronal apoptosis (by TUNEL method) in hippocampal CA1 region and the parietal cortex,Bcl-2 and Bax expression (by Western blot) in hippocampal CA1 region.The superoxide dismutase (SOD) and catalase (CAT) activity and malondialdehyde (MDA) content in hippocampal CA1 region and the parietal cortex were also measured at 48 h of cerebral reperfusion.Morris water maze task was used to test the learning and memory function at 4 d of cerebral reperfusion,and the rats were sacrificed at 7 d of cerebral reperfusion,and brains were removed for determination of neuronal density in hippocampal CAl region and the parietal cortex.Results Cerebral I/R significantly increased the number of apoptotic neurons and MDA content,upregulated Bcl-2 and Bax expression,decreased neuronal density,SOD and CAT activity and learning and memory function in group I/R as compared with group S.RIPoC significantly attenuated these cerebral I/R-induced changes.Conclusion RIPoC could protect brain against global cerebral I/R-induced injury,and the mechanism may be related to inhibiting lipid peroxidation,regulating the balance between Bcl-2 and Bax and inhibiting apoptosis.

[ABSTRACT]AIM:ToinvestigatetheeffectofmiR-155-specificsiRNAaloneorincombinationwithcytosinear-abinoside (Ara-C) on the growth and apoptosis of Burkitt lymphoma Raji cells .METHODS: miR-155-specific siRNA and/or Ara-C were used to treat the cells .Quantitative real-time polymerase chain reaction was used to detect the expres-sion of miR-155.The growth of the cells was analyzed by CKK-8 assay.The cell apoptosis was determined by flow cytome-try.RESULTS:The miR-155 expression level of the cells transfected with miR-155 siRNA was significantly lower than that in the 2 control groups .Ara-C or miR-155 siRNA alone inhibited the growth of Raji cells in a dose-depend manner . miR-155 siRNA combined with Ara-C produced more inhibition of cell proliferation (P<0.05).After treatment for 48 h, the apoptotic rate of Raji cells in miR-155 siRNA+Ara-C group [(38.4 ±1.4)%] was higher than that in Ara-C group [(16.5 ±0.3)%] and miR-155 siRNA group [(14.6 ±0.3)%], with statistically significant difference (P<0.05). The expression of caspase-3 in Ara-C+miR-155 siRNA group was increased significantly as compared with Ara-C group and miR-155 siRNA group.CONCLUSION:miR-155-specific siRNA enhances the chemosensitivity of Raji cells to Ara-C by inducing apoptosis through the caspase-3 pathway .