Objective To investigate the application of SIEMENS Ysio DR amplification in the radiation dose reduction. Methods Totally 160 patients with similar heights and body shapes were divided equally into A,B,C and D groups,and then underwent radiological examinations with SIEMENS Ysio DR from September 2014 to May 2016.A and B groups went through right hand AP oblique examination with the same kV while different mAs, and C and D groups had chest posteroanterior examination with different kV and the same mAs. Image quality was regulated with the amplification coefficient, and then evaluated with double-blind method by two senior radiologists.Statistical analysis was executed over the values of mAs in A and B groups and those of kV in C and D groups. Results A group had the mAs value being(2.26 ±0.16)mAs, which was significantly different from that of B group [(4.05±0.19)mAs] (P<0.05);while C group had kV value being (104.79±6.39)kV, which was statistically different from that of D group [(83.48±3.67)kV] (P<0.05). Satisfactory image were obtained by regulation with amplication coefficient.There was no obvious difference between the image quality in either A and B groups or C and D groups(P>0.05).Based on the principle that low mAs resulted in low radiation dose and high kV lead to low effective dose,A group had the radiation dose lower than those of B group,and C group had the effective dose lower than those of D group. Conclusion SIEMENS Ysio DR has the photographing parameters regulated according to different sites and the amplification coefficient for enhancing image quality, which decreases X-ray radiation dose and effective dosage with the diagnosis results unaffected.

The DNA fragments of ag85b、esat-6、hsp65、mpb64 and ag85b-esat-6、hsp65-esat-6、mpb64-esat-6 were amplified by PCR and SOE technique.These seven fragments were inserted into pCDNA3.1(+)vector to construct recombinant plasmids pCA、pCE6、pCH、pCM、pCAE、pCHE and pCME.The seven plasmids were transfected into SP2/0 cell in vitro to detect the expression of target genes.BALB/c mice were intramuscularly vaccinated with the seven plasmids and the control vector pCDNA3.1(+)and PBS respectively.The serum antibodies and the spleen lymphocyte proliferation(SLP)and secreted IFN～? of spleen were tested.The results of indirect ELISA showed the levels of antibodies in all recombinant plasmids groups were significantly higher than the two control groups(P

Our previous results have demonstrated that insulin reduces myocardial ischemia/reperfusion (MI/R) injury and increases the postischemic myocardial functions via activating the cellular survival signaling, i.e., phosphatidylinositol 3-kinase (PI3-K)-Akt-endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) cascade. However, it remains largely controversial whether c-Jun NH2-terminal kinase (JNK) is involved in the effects of insulin on MI/R injury. Therefore, the aims of the present study were to investigate the role of JNK, especially the cross-talk between JNK and previously expatiated Akt signaling, in the protective effect of insulin on I/R myocardium. Isolated hearts from adult Sprague-Dawley rats were subjected to 30 min of regional ischemia and followed by 2 or 4 h of reperfusion (n=6). The hearts were pretreated with PI3-K inhibitor LY294002, or phosphorylated-JNK inhibitor SP600125, respectively, then perfused retrogradely with insulin, and the mechanical functions of hearts, including the heart rate (HR), left ventricular developed pressure (LVDP) and instantaneous first derivation of left ventricular pressure (+/-LVdp/dt(max)) were measured. At the end of reperfusion, the infarct size (IS) and apoptotic index (AI) were examined. MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with the control group, insulin treatment in MI/R rats exerted protective effects as evidenced by reduced myocardial IS [(28.9 +/- 2.0)% vs (45.0 +/- 4.0) %, n=6, P<0.01], inhibited cardiomyocyte apoptosis [decreased AI: (16.0 +/- 0.7) % vs (27.6 +/- 1.3) %, n=6, P<0.01] and improved recovery of cardiac systolic/diastolic function (including LVDP and +/-LVdp/dt(max)) at the end of reperfusion. Moreover, insulin resulted in 1.7-fold and 1.5-fold increases in Akt and JNK phosphorylation in I/R myocardium, respectively (n=6, P<0.05). Inhibition of Akt activation with LY294002 abolished, and inhibition of JNK activation with SP600125 enhanced the cardioprotection by insulin, respectively. And the abolishment by LY294002 could be partly converted by SP600125 pretreatment. In addition, SP600125 also decreased the Akt phosphorylation (n=6, P<0.05). These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect.
Animals ; Apoptosis ; Heart ; Insulin ; metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Myocardial Infarction ; Myocardial Ischemia ; Myocardial Reperfusion Injury ; Myocardium ; Myocytes, Cardiac ; Nitric Oxide Synthase Type III ; Phosphatidylinositol 3-Kinase ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; Signal Transduction

Objective:To explore the application effect of early warning model of chemotherapy complications in nursing care of non-small cell lung cancer during chemotherapy.Methods:By using convenient sampling method, 106 patients with non-small cell lung cancer treated by chemotherapy in the Thoracic Surgery Department of the First Affiliated Hospital of Zhengzhou University from January 2016 to February 2019 were selected as the study objects. According to the time of admission, they were divided into the control group ( n=52) and the observation group ( n=54) . The control group was given routine nursing care during chemotherapy, while the observation group was given nursing care through early warning model of chemotherapy complications during chemotherapy. Hamilton Anxiety Scale (HAMA) , Hamilton Depression Scale (HAMD) and European Organization for the Research and Treatment of Cancer QLQ-C30 (EORTCQLQ-C30) were used to compare the intervention effect of the two groups, and the incidence of complications during chemotherapy was counted. Results:The total incidence of complications was 26.92% (14/52) in the observation group and 46.15% (24/52) in the control group, the difference was statistically significant (χ 2=4.147, P<0.05) . Three months after the intervention, HAMA (9.87±4.25) and HAMD (15.54±3.58) in the observation group were lower than those in the control group; the differences were statistically significant ( t=4.738, 8.296; P<0.05) . The functional score, symptom score, overall quality of life score and single measurement item score of the observation group were higher than those of the control group with statistical differences ( P<0.05) . Conclusions:During chemotherapy for non-small cell lung cancer, nursing through the early warning model of chemotherapy complications can reduce the incidence of chemotherapy complications, alleviate the negative emotions of patients, and improve the quality of life, which is worthy of clinical application.

Objective To study the Th17/Treg (regulatory T cells) immunoregulation in patients coinfected with TB and HIV before and after HAART( highly active anti-retroviral therapy).Methods 10 HIV cases coinfected with TB ( HIV/TB group) and 10 cases infected with HIV only ( HIV group) received HAART.PBMCs were stained and immunophenotyping of Th17( IL-17 expressing T cells) and CD4 + CD25 +T cells (Treg) were analysed by flow cytometry.Results The pre-treatment patients tended to have lower Th17 cells and higher Tregs cells compared to post-treatment( 1.90％ ± 0.9％ vs.4.65％ ± 1.48％,16.48％ ±4.91％ vs.8.29％ ± 3.13％ respectively).The percentage of IL-17 before and after HAART were 1.90 ± 0.9％ vs.4.65 ± 1.48％ respectively in HIV/TB group patients ( P ＜ 0.01 ).The difference between the percentage of IL-17 before and after HAART in the HIV/TB group and the HIV group were 2.65 ± 1.62％ vs.0.67％ ± 0.46％ respectively (P ＜0.01 ).IL-17 expressing T cells were increased faster after HAART in the former group than the latter.The percentage of Treg before and after HAART were 16.48％ ±4.91％ vs.8.29％ ± 3.13％ respectively in HIV/TB group ( P ＜ 0.01 ).The difference between the percentage of Treg before and after HAART in the HIV/TB group and the HIV group were 8.91％ ±4.82％ vs.2.63％ ± 2.34％ respectively ( P ＜ 0.01 ).Treg were decreased more rapidly after HAART in the former than the latter.Conclusions TB and HAART both had an effect on the Th17/Treg ratio of HIV/ TB co-infected patients,which can cause increased Th17 expression,the later plays a pro-inflammatory role.TB and HAART can decrease Treg expression and enhance anti-inflammation response.The fact that Th17/Treg disorder are more likely to exist in patients with HIV/TB co-infection after HAART for one month suggests a potential role for Th17/Treg imbalance leading to tuberculosis-associated immune reconstitution inflammatory syndrome during patients receiving HAART period.

OBJECTIVE: To compare the levels of short-chain fatty acids in enterobacteria-related metabolites in feces between infants with cholestatic hepatopathy and healthy infants. METHODS: Thirty infants with cholestatic hepatopathy were enrolled in this study as the disease group, while 30 healthy infants were enrolled as the control group. Fecal specimens were collected from the disease group before and after treatment and from the control group. Gas chromatography was used to quantitatively determine the content of short-chain fatty acids in the feces of both groups including acetic acid, propionic acid, butyric acid, isobutyric acid, and isovaleric acid. RESULTS: There were no significant differences in the concentrations of acetic acid and propionic acid between the control and disease groups before and after treatment, as well as no significant changes in the two markers in the disease group after treatment (P>0.05). The disease group had a significantly increased concentration of butyric acid after treatment (P<0.05). The concentrations of isobutyric acid and isovaleric acid in the control group were significantly higher than those in the disease group before and after treatment (P<0.05). CONCLUSIONS Intestinal protein metabolites in infants with cholestatic hepatopathy are significantly different from those in healthy infants, whereas there is no significant difference with respect to carbohydrate metabolites.
Acetates ; Butyric Acid ; Enterobacteriaceae ; Fatty Acids, Volatile ; Feces ; Humans ; Infant

This study was aimed to explore whether bortezomib can sensitize HL-60 cells to TNF-related apoptosis-inducing ligand (TRAIL) and to investigate its possible mechanism. The HL-60 cells were treated by different concentrations of TRAIL combined with subtoxic concentration of bortezomib. The proliferative inhibition of treated HL-60 cell was analysed by MTT assay. The cell apoptosis was determined by flow cytometry with Annexin V/PI double staining and the expression of caspase-8 was detected by Western blot. The results showed that the subtoxic concentration of bortezomib combined with 10 ng/ml of TRAIL enhanced apoptosis of HL-60 cells, as compared with TRAIL used alone; the expression of caspase-8 increased correspondingly. It is concluded that subtoxic concentration of bortezomib can sensitize HL-60 cells to TRAIL and its mechanism may be related to upregulation of caspase-8 expression.
Apoptosis ; drug effects ; Boronic Acids ; pharmacology ; Bortezomib ; Caspase 8 ; metabolism ; HL-60 Cells ; Humans ; Pyrazines ; pharmacology ; TNF-Related Apoptosis-Inducing Ligand ; pharmacology

This study was aimed to investigate the expression characteristics of two transcriptional factors in Ikaros family, Ikaros and Helios isoforms and their mechanism, as well as their correlation with clinical parameters, which play important roles in transcriptional regulation of hematopoiesis. Expression of Ikaros and Helios isoforms in a total of 163 patients with leukemia and correlations between Ikaros and Helios isoforms were analyzed by PCR. The results showed that different expression patters of Ikaros and Helios isoforms existed in leukemia patients, that is, Ikaros isoform (Ik-6) was predominantly expressed in acute lymphoblastic leukemia (ALL) with BCR/ABL fusion gene, while Helios isoform (He-i) was overexpressed in T-cell ALL patients. The results of cloning and sequencing demonstrated that the isoforms of Ikaros and Helios had different genetic alterations. The statistical correlation between these two isoforms not was found in this study, although interaction between Ikaros and Helios has been reported. It is concluded that although Ikaros and Helios belong to the same family with similar structure of zinc fingers, their isoforms have different expression profile, specific genetic alterations, and different clinical relevance in patients with leukemia. The connection and interaction between Ik-6 and He-i needs further research.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Female ; Gene Expression Profiling ; Humans ; Ikaros Transcription Factor ; genetics ; metabolism ; Leukemia ; genetics ; metabolism ; Male ; Middle Aged ; Protein Isoforms ; genetics ; metabolism ; Young Adult

OBJECTIVETo study the correlation between polyoma virus load and hemorrhagic cystitis after allogeneic stem cells transplantation for prevention of hemorrhagic cystitis.

METHODSBlood and urine specimens were collected from 40 healthy persons, 40 patient with stem cells transplantation and 20 cases complicated with hemorrhagic cystitis for determination of VP1 gene of polyomaviruses BK virus (BKV)/Jamestown Canyon virus (JCV) and simian virus 40 (SV40) by polymerase chain reaction (PCR) and EvaGreen stain fluorescence quantitative assay.

RESULTSIn the peripheral blood, all genes of BKV/JCV and SV40 were negative, while BKV gene in urine and blood from healthy persons and patient with stem cells transplantation was 15% (6/40) and 100% (40/40), respectively. The gene of JCV was positive in 10% (4/40) and 12% (5/40), the gene of SV40 was negative.

CONCLUSIONGenes of BKV and JCV was detectable in urine specimens of healthy persons and there was a correlation between the load of polyomavirus and incidence of hemorrhagic cystitis.

Capsid Proteins ; genetics ; Cystitis ; diagnosis ; etiology ; virology ; DNA, Viral ; blood ; genetics ; urine ; Hematopoietic Stem Cell Transplantation ; adverse effects ; Hemorrhage ; diagnosis ; etiology ; virology ; Humans ; Polymerase Chain Reaction ; methods ; Polyomavirus ; genetics ; growth & development ; Polyomavirus Infections ; complications ; virology ; Viral Load

Objective Epidemiological studies have suggested that alcohol drinking is closely associated with di-verse tumor development, but fewer laboratory studies or mechanism analysis is made. Our study aims to explore the effect of alcohol on the tumorigenicity and metastasis of breast cancer in nude mice in vivo and on the malignant behavior in vitro, and whether it is related to endoplasmic reticulum stress ( ERS) . Methods We first established the nude mouse model of breast cancer with chronic alcohol consumption (2%) and to detect the effects of ethanol on tumor growth and metastasis. We also observed the changes of malignant biological behavior of EO771 cells in cell culture induced by chronic alcohol treatment (0. 2%) using MTT, Transwell and soft agar tests, and detect the expression of ROS and ERS marker, i. e. p?eIF2a, Bip, and XBP1?s. Results The in vivo experiment showed that alcohol drinking enhanced the growth and metasta?ses of breast cancer in nude mice. The in vitro test showed that chronic exposure to ethanol also promoted the cell prolifera?tion and migration ability, increased the ROS expression, activated ERS pathway, and enhanced the expression of p?eIF2a, Bip and XBP1?s. Conclusions Alcohol drinking may promote the malignant behavior of breast cancer cells through endo?plasmic reticulum stress.