Objective To explore the effects of impaired glucose metabolism and impaired blood lipoprotein metabolism on heart rate variability(HRV) in aged male hypertension patients and to have an insight into the correlation between the years of impaired glucose metabolism and the patients’ HRV. Methods 120 male subjects were divided into three groups: simple hypertension patients (group A, 40 people), hypertension patients with diabetes mellitus (group B, 40 people), and hypertension patients with diabetes mellitus and impaired blood lipoprotein metabolism (group C, 40 people). All subjects had 24h recordings of ECG. The data of HRV time domain were collected and analyzed to gain an insight into the effects of the impaired glucose metabolism and impaired blood lipoprotein metabolism on patients’ HRV. In group C, patients were divided into normal TC subgroup and high TC subgroup according to the index of TC (TC

Objective:To determine the derivative chromosome 9 by the method of detecting the ASS gene,and to explore the relationship between the deletion of derivative chromosome 9 and the efficacy and prognosis of the chronic myeloid leukemia (CML)patients. Methods:The materials of 34 CML patients with positive BCR-ABL fusion gene whose ASS genes were detected were retrospectively analyzed. All patients were treated with Extra-signal (ES)probe to detect the derivative chromosome 9.All patients were divided into two groups according to whether they carried the derivative chromosome 9.The blastic phase or the accelerated phase rates in two groups were compared by using Fisher exact probability. Results:All patients were detected by FISH (BCR-ABL ES probe),and all the BCR-ABL fusion signals were positive.6 of 34 patients were found the deletion of ASS gene, among them 1 case blonged to chronic phase,and 5 cases developed into blastic phase or accelerated phase. In the patients without ASS gene deletion,there were 22 cases in chronic phase,and 6 cases in plastic phase or accelerate phase,there was significant difference of blastic phase rate/accelated phase rate between them (P<0.05).A total of 26 patients were treated with tyrosine kinase inhibitors (TKI).5 of 26 patients belonged to the ASS gene deletion group,1 of 5 patients treated with TKI got molecular remission,4 of 5 patients developed into blastic phase or accelerated phase.21 of 26 patients belonged to the group without ASS gene deletion,and among them,19 cases got molecular remission,2 cases developed into plastic phase or accelerated phase after treatment of TKI,there was significant difference between them (P < 0.05 ). 6 patients were treated with traditional chemotherapy (hydroxyurea,interferon);1 of 6 patients belonged to the ASS gene deletion group,finally developed into the blastic phase or accelerated phase;5 of 6 patients belonged to the group without ASS gene deletion,2 cases got the hematological remission,and 3 patients developed into blastic phase or accelerated phase after treatment,and there was no significant difference of blastic phase rate/ accelerated phase rate between them (P > 0.05 ). Conclusion:The CML patients with derivative chromosome 9 (ASS gene deletion)prone to get disease progression, and have a higher proportion in the blastic phase or accelerated phase patients.Derivative chromosome 9 is related to the bad treatment efficacy of TKI and the poor prognosis of CML.

Objective:To study the inductive effect of recombinant MUC1-MBP fusion protein combined with R848 on the immune activity of T cells in the mice,and to provide experimental basis for searching the suitable adjuvants of recombinant MUC1-MBP fusion protein.Methods:A total of 21 C57BL/6 mice were randomly divided into control group(treat with normal saline),MUC1-MBP+R848 group (treated with MUC1-MBP+R848),and MUC1-MBP+baillus calmette guerin(BCG) group(treated with MUC1-MBP+BCG)(n=7).After immunized for 4-7 d,the spleen tissue was taken and the spleen indexes of the mice in various groups were measured;the stimmulus index(SI) of the mice was detected by lymphocyte proliferation response;the levels of tumor necrosis factor-γ(TNF-γ) and interleukin-4(IL-4) were detected by ELISA method;the proprotions of T lymphocyte subsets in spleen cells were analyzed by flow cytometry.Results:Compared with control group,the spleen indexes,SI,and TNF-γ levels of the mice in MUC1-MBP+ R848 and MUC1-MBP+BCG groups were significantly increased (P<0.05 or P<0.01);the indexes metioned above of the mice in MUC1-MBP+ R848 were higher than those in MUC1-MBP+BCG group;the IL-4 levels had no significant difference(P>0.05).Compared with control group,the proprotions of CD3+T,CD4+T,and CD8+ T cells of the mice in MUC1-MBP+ R848 group and MUC1-MBP+BCG group were significantly increased(P<0.05 or P<0.01).Conclusion:Both MUC1-MBP fusion protein combined with R848 and BCG can induce the Th1 type of immune activity in the mice,and R848 is the potential candidate adjuvant for MUC1-MBP.

Objective To observe the effects of Hedysari Polysaccharide (HPS) on the expressions of TSP-1 and PDGF-B in the retina of diabetic rats;To discuss the protective effect and possible mechanism on diabetic retinopathy. Methods The diabetic model was established by intraperitoneal injection of streptozotocin. 50 male SPF Wistar rats were randomly divided into 5 groups:model group, calcium dobesilate group, and HPS high-, medium-, and low-dose group, extra 10 rats were set as the normal group, 10 rats in each group. Each administration group was given relevant medicine for gavage, while model group and normal control group were given same amount NS for gavage, once a day for 8 weeks. The mRNA and protein expression of TSP-1 and PDGF-B were detected by qRT-PCR and immunohistochemistry. The retinal structure was observed by HE staining. Results HE staining showed that each layer of the retina of the model group was clear and complete, but the outer nucleus layer became looser, thinner and more disorderly, and the number of ganglion cells decreased slightly; the administration groups were improved markedly compared with the model group. Compared with the normal control group, the mRNA level and protein expression of retina TSP-1 on the model group dramatically dropped (P<0.01), and those of PDGF-B strikingly increased (P<0.01);Compared with the model group, the mRNA level and protein expression of retina TSP-1 on alladministration groups rose (P<0.05, P<0.01), and those of PDGF-B went down (P<0.01); Compared with all other administration groups, there was statistical significance in the mRNA level and protein expression of retina TSP-1 and PDGF-B on HPS high-dose group (P<0.05, P<0.01). Conclusion HPS may prevent the angiogenesis and proliferation in diabetic retinopathy process through adjusting the content of TSP-1 and PDGF-B in retina of diabetic rats so as to protect the retina.

Objective To investigate MRI features of metanephric adenoma(MA). Methods The retrospective analysis was performed on 6 adult patients that were scanned by regular, DWI and dynamic-enhancement MRI two weeks before surgery and diagnosed with MA pathologically after surgery. MRI features of lesions were observed. The signal intensities of lesions and contralateral normal renal cortex and medulla were respectively measured in plain scan, cortex, parenchyma and delayed phase. The enhancement magnitudes were calculated and the ADC values of lesions were measured. The differences of the signal intensity and enhancement magnitude were assessed by paired-sample t test among renal cotex, medulla and lesions. Results All lesions in MA were single and solid masses. Four cases occurred in the right kidney and two cases in the left kidney. The maximum diameters of the lesions ranged from 21 to 79 mm and the mean value was(41 ± 20)mm. Five cases were round or oval, while one case was irregular. The signal intensity in five cases was slightly lower in T2WI than the renal parenchyma, while one case was slightly higher than the renal parenchyma. The hyperintentsity of DWI and hypointensity of ADC were seen in all cases. The mean ADC value was(0.759 ± 0.211) × 10-3mm2/s. Hemorrhage were seen in two cases. Necrosis was present in one case and the capsules were seen in two cases. No scar, fat and swollen lymph nodes was seen in all cases . There was no statistical significance of the signal intensity between lesions measure in the plain scan and normal renal parenchyma(P>0.05). After adminstrating contrast materials, all lesions shown persistently mild to moderate enhancement . The siganl intensities of lesions measured in three phases after enhancement were signifcantly lower than those of the renal cortex(P<0.05). No significant differences of the signal intensity measured in cortex and medulla phase between lesions and normal renal medulla was present(P>0.05). But the signal intensities of leisons in delayed phases were significantly lower than thoseof renal medulla(P<0.05). Except from the difference of enhanced magnitude in cortex phase between lesions and normal medulla, significant differences were present between leisons and normal renal parenchyma(P<0.05). Conclusion MRI manifestations of MA show certain distinction, including, dominantly solid lesions, relatively lower signal intensity of lesions than that of renal cortex, slowly persistent enhancement, high signal on DWI and low signal on ADC.

OBJECTIVETo investigate the changes of aldehyde dehydrogenase 2 (ALDH2) expression in H O inducedcardiomyocytes oxidative stress injury.

METHODSCultured H9C2 cardiomyocytes were exposed to H O -inducedoxidative stress and the effects of the ALDH2 agonist Alda-1 and ALDH2 inhibitor Daidzin were tested on the stress level ofthe exposed cells. MTT colorimetric assay was used to assess the cell viability after the treatments. The oxidative stress level inthe myocardial cells was detected using DHE fluorescence staining, and the activity and protein level of ALDH2 were detectedwith spectrophotometry and Western blotting.

RESULTSCompared with normal control cells, Alda-1 treatment did notsignificantly affect the cell viability, oxidative stress level, or ALDH2 activity and protein level. H O exposure significantlylowered the cell activity and ALDH2 activity and protein expression and increased the oxidative stress level; Alda-1 treatmentobvious antagonized the effects of H O . Blocking ALDH2 with Daidzin produced similar effects to H O exposure on theviability, oxidative stress level, and ALDH2 activity and expression in the myocardial cells.

CONCLUSIONSH O exposure lowersthe activity and reduces the protein expression of ALDH2 in cardiomyocyte H9C2 cells, and activation of ALDH2 can alleviateH O -induced oxidative stress in the cells.