Background FIZZ1 is a newly found protein associated with pulmonary inflammation. It has been shown to involve in proliferation of pulmonary arterial vascular smooth cells, contriction of vascular vessels, and stimulation of fibroblasts. Objective This study was designed to investigate the expression of FIZZ1 in atherosclerotic plaque of C57BL/6J ApoE-/-mice and the role of FIZZ1 on the proliferation of vascular smooth muscle cells obtained from aorta. Methods Nine C57BL/6J ApoE-/-mice were fed with high fat diet and nine C57BL/6J wild type mice with normal chow for 24 weeks. All mice were euthanized and the aortas were collected. HE stain histological examination and FIZZ1 immunohistochemistry were used in vivo study. In vitro, smooth muscle cells were treated with normal saline (control groups) or recombinate FIZZ1 at different concentrations (final concentration 3?10-6, 9?10-6, 2.7?10-5 mmol/L) respectively. The proliferation of smooth muscle cells were detected by MTT. Results After 24 weeks of high fat diet treatment, large atherosclerotic plaques were found in aortic root of ApoE-/-mice. FIZZ1 was found in atherosclerotic plaques of C57BL/6J ApoE-/-mice, however, no FIZZ1 was expressed in the arteries of C57BL/6J wild type mice. Cell culture study showed FIZZ1 promoted the proliferation of smooth muscle cells in a dose dependent manner(P

Background Found in Inflammatory Zone 1(FIZZ1)is a newly found protein associated with pulmonary inflammation.We previously had reported its role in the development of atherosclerosis,but its detailed mechanism has not been explored.Objective This study was designed to delineate the effect of FIZZ1 on the expression of scavenger receptor(SR-A)in vascular smooth muscle cells(VSMC)scavenger receptor(SR-A)induced by ox-LDL.Methods Smooth muscle cells were treated with ox-LDL(20 mg/L)or cocultured with recombinate FIZZ1 at different concentration(final concentration 3?10-6,9?10-6,2.7?10-5 mmol/L).The expression of SR-A of smooth muscle cell was detected by flow cytometry and laser confocal microscopy.Results SR-A positive expression was found in VSMCs treated with ox-LDL after 24 hours,which were located mainly in cell membrane by laser confocal microscopy.FIZZ1 significantly accentuate the LDL induced increases in SR-A positive rate in VSMC in a dose dependent manner(P

Aesthetics of science is truly present.But only those people who have ability to appreciate the beautiful can comprehend the aesthetics of science.Aesthetics of science is a senior pattern of aesthetics.Aesthetics of science can arouse people to explore knowledge and truth.Aesthetics of science bring first light of morning to medical science education which has lots of beautiful material.Recognizing aesthetics of science in medical science education is helpful to cultivating the higher quality persons with ability of medicine and training aesthetic accomplishment.

Objective To observe the variation of plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG),a biomarker of oxidative DNA damage,in patients with Alzheimer's disease (AD) versus vascular dementia (VaD),and to investigate the important role and the difference of oxidative DNA damage in the initiation and development of AD and VaD.Methods 35 AD patients,28 VaD patients and 23 age and sex matched normal controls were enrolled in this study.Plasma 8-OHdG was measured by an enzyme-linked immunosorbent assay (ELISA) method.Cognition function in AD and VaD patients was measured by Mini-Mental State Examination (MMSE).Results There were significant differences in plasma 8-OHdG concentrations among AD,VaD and control groups [(601.8±266.0) ng/L,(1748.0±665.6)ng/L,(352.0±94.5)ng/L,respectively,P＜0.001].Plasma 8-OHdG was significantly higher in VaD group than in control group (P＜0.05).While,there was no significant difference in plasma 8OHdG concentration between AD group and control group (P＞0.05).Plasma 8-OHdG was significantly higher in VaD group than in AD group (P＜0.05).Plasma 8-OHdG levels were positively related with age in AD,VaD and control groups (r=0.661,0.702,0.719,respectively,all P％0.01).No correlations were found between plasma 8-OHdG concentration and education level among the three groups (all P＞0.05).AD and VaD patients were subgrouped according to the risk factors including gender,smoking,hypertension,diabetes,hyperlipidemia.There were no significant differences in plasma 8-OHdG level between the subgroups (all P＞ 0.05).After adjusting for sex,age,education level,smoking,hypertension,hyperlipidemia and diabetes,logistic regression analysis showed that the probability of high plasma 8-OHdG level was higher in VaD group than in AD and control groups.Plasma 8-OHdG level had a negative correlation with MMSE score in VaD group (r=-0.592,P＜0.01),while no correlation was found between plasma 8-OHdG level and MMSE score in AD group (r =-0.122,P＞ 0.05).Conclusions There is significant oxidative DNA damage in VaD patients.Plasma oxidative DNA damage is more serious in VaD patients than in AD patients and healthy people.Plasma 8-OHdG level,a oxidative DNA damage biomarker,has a significant correlation with the degree of cognition impairment in VaD patients.

Objective Making the fusion protein of IgG-binding peptide with enhanced green fluorescent protein(EGFP) and determining its bioactivity.Methods The enhanced green fluorescent protein(EGFP) gene was cloned into pEZZ 18 vector containing ZZ peptide gene to construct expression vector pSpA-EGFP-His.The fusion protein was expressed in E.coliDH5? and its bioactivity was detected by competitive ELISA and fluorescence properties.Results The fusion protein migrated at approximately 42kD in SDS-PAGE,which correspond to the theoretical molecular weight.The spectra of SpA-EGFP fusion protein was similar to what was reported.SpA-EGFP competed with SpA-Peroxidase to bind IgG.Conclusion The plasmid pSpA-EGFP-His correctly expressed in E.coli.The fusion protein retains the bifunctional effects of EGFP and IgG-binding activity.

Objective To sum up main syndrome differentiation points of liver depression and spleen asthenia syndrome of chronic hepatitis B(CHB).Methods Logistic regression and discriminant analysis were used for analysis of symptoms,tongue and pulse of liver depression and spleen asthenia syndrome,liver depression syndrome and spleen asthenia syndrome.Results The symptoms selected by logistic regression of liver depression and spleen asthenia syndrome were:abdominal distention or pain,lassitude,poor appetite,loose stool,hypochondriac pain or discomfort and tense pulse;while that selected by discriminant analysis were:abdominal distention or pain,lassitude,loose stool and yellowish fur.Conclusion Main syndrome differentiation points of liver depression and spleen asthenia syndrome of CHB include hypochondriac pain or discomfort,abdominal distention or pain,lassitude,poor appetite and loose stool.Logistic regression and discriminant analysis are feasible for analysis of main diagnosis points of liver depression and spleen asthenia syndrome of CHB.

Objective To investigate the mechanisms of metformin (Met) for protecting H9C2 myocardial cells damage induced by saturated fatty acids (palmitic acid,PA) in rats.Methods Rat H9C2 myocardial cell lines in blank control group,PA group and three different concentrations of metformin and PA combination groups were cultured for 24 h.Then Western blot was adopted to detect the protein expression of nuclear factor κB p65 (NFκB p65),intercellular cell adhesion molecule-1 (ICAM1),phosphorylated inhibitor of nuclear factor κB (p-IκBα) and phosphorylated adenosine monophosphate activated protein kinase(p-AMPK);the quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of nuclear factor of nuclear factor κB(NFκB),chemokine (C-C motif) ligand 2 (CCL2) andintercellular cell adhesion molecule-1(ICAM1).Results Compared with the control groups,the protein expression of NFκB p65,p-IκBα and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the protein expression of NFκB p65,IκBα and ICAM1 in the Met+PA combination groups was decreased in various degrees with the Met concentration increase (all P<0.05),while the protein expression of p-AMPK was significantly risen with the Met concentration increase (all P<0.05).Compared with the control group,the mRNA expression of CCL2 and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the mRNA expression of CCL2 and ICAM1 in the Met+PA combination groups was decreased (P<0.05).Conclusion Met can alleviate H9C2 myocardial cellular damage caused by saturated fatty acid inducing increase of CCL2 and ICAM1 expression.

Heart Failure ; diagnosis ; therapy ; Humans ; MicroRNAs ; Vascular Remodeling

Background Gene encoding optineurin (OPTN) is a causative gene for glaucoma and amyotrophic lateral sclerosis,with a more expression in retina.Our previous study isolated OPTN-interacting proteins and identified that the gene encode the basic leucine zipper (bZIP) transcription factor neural retina leucine (NRL) zipper,a causative gene for retinitis pigmentosa,and further study demonstrated the interaction between OPTN and NRL proteins in nuclei of cultured HeLaS3 cells.Objective This study was to determine the protein binding site of OPTN necessary for NRL binding.Methods A deletion series of OPTN-expression plasmids were constructed and co-expressed with hemagglutinin (HA)-tagged NRL in HeLaS3 cells,respectively.The cytoplasmic and nuclear fractions were used to perform co-immunoprecipitate (CoIP) and Western blot with anti-tag antibodies.Results In the nuclear fractions of cells transfected with the del1 st,del2nd or del3rd plasmid,a band of coimmunoprecipitated HA-labelled NRL (HA-NRL) was detected.However,the del4th plasmid did not produce a band.The NRL band was not found in cytoplasmic fractions from transfected cells with any of the deletion plasmids or with the whole-length OPTN plasmid.Conclusions The protein binding site of OPTN necessary for NRL binding is determined.This result demonstrates the binding of Flag-OPTN and HA-NRL in HeLaS3 cells.A series of partial-deletion OPTN plasmids demonstrated that the tail region (423-577 amino acids) of OPTN was necessary for binding with NRL.

Objective To summarize the MSCT signs and the key points of differential diagnosis of sclerosing mesenteritises (SM) which were misdiagnosed by clinical and CT,to reduce the misdiagnosis rate.Methods Clinical and MSCT data of 23 misdiagnosed SM patients were analyzed retrospectively.The misdiagnosed diseases,misdiagnosed causes,and differential diagnosis were analyzed.Results SM were mainly misdiagnosed as tumor and infective inflammation.The main causes of misdiagnosis and differential diagnostic features were listed as follows.(1)SM didn't have specific clinical manifestations.(2)The density of the adipose tissue in mesentery increasedmisty mesentery.A clear demarcation between the lesion and the surrounding normal fatty tissue could be differentiated from infective inflammation.(3)The mass-like false capsule had space-occupying effect of displacement of the surrounding structures.However, the blood vessels were encapsulated by the mass-like false capsule with fat ring around, which could be differentiated from fat-containing tumors.(4)The soft mass was formed at the root of the mesentery.The fat halo sign and mild enhancement of the mass can be differentiated from lymphoma and carcinoid.Conclusion SM is easily misdiagnosed both in clinical practice and medical imaging.Recognition of differential diagnostic features of MSCT can reduce the misdiagnosis rate.