Objective To investigate the molecular mechanisms for the development of cardiac hypertrophy in hypertension,the present study provided the differential protein expression analysis of hypertrophied heart at differ- ent stages in spontaneously hypertensive rats (SHR).Methods The profiles of protein expression of left ventricu lar myocardium in SHR and its normotensive control Wistar-Kyoto (WKY) rats at the age of 4 and 20 weeks were analyzed with two-dimensional gel electrophoresis (2-DE) in combination with matrix assisted laser desorption ioniza- tion-time of flight (MALDI-TOF-TOF) mass spectrometry.Results Although the blood pressure of SHR was normal at 4 weeks age,hypertrophy of the left ventricle had already developed.The expression pattern in the hy- pertrophic myocardium was found 27 modulated proteins,20 of which were identified.These proteins are involved in reactions of energy metabolism,mitoehondrial oxidative phosphorylation and oxidative stress,etc.The expres- sion of 13 proteins was significantly changed in SHR rats at early stage prior to the development of sustained hyper- tension,while the expression changes of other 7 proteins occurred only at late stage in SHR rats when the blood pressure was significantly elevated.Conclusions lncrease in glycolysis and decrease in oxidation of fatty acid and glucose was shown in the hypertrophied myocardium from early stage in SHR prior to the development of hyperten sion.The significant changes in protein expression of the mitochondrial electron transport chain and antioxidative molecules support the hypothesis that oxidative stress promotes and accelerates the development of hypertensive car- diac hypertrophy.

Objective To explore the effect of nitric oxide (NO) on ?-aminobutyric acid B receptor (GABA_BR) subunits during recurrent febrile seizures (FS).Methods Twenty-four Sprague-Dawley rats aged 21 days were randomly divided into 4 groups: control group (37.0 ℃ water,n=8), FS group (45.2 ℃ water,n=8), FS + SNP group (45.2 ℃ water,n=8), FS+L-NMMA group (45.2 ℃ water,n=8). FS rats were induced 10 times in a warm-water bath, once every 2 days. The plasma level of NO was detected by the spectrophotometer. The expressions of GABA_BR subunit mRNA and c-fos gene were examined by in situ hybridization. The expressions of GABA_BR subunit and Fos protein were observed by immunohistochemistry. Results The plasma level of NO increased in FS + SNP group while decreased in FS+L-NMMA group compared with that in FS group. The expressions of GABA_BR_2 were down-regulated in FS+SNP group, while GABA_BR_1 hardly changed compared with those in FS group. In FS+L-NMMA group, both the expression of GABA_BR_2 and GABA_BR_1 up regulated compared with those in FS group. The expressions of c-fos gene and Fos protein were significantly enhanced after recurrent FS. SNP elevated the expressions of c-fos gene and Fos protein, while L-NMMA down regulated the expressions of them.Conclusion NO may play a regulatory role through modulating GABA_BR function in the pathogenesis of recurrent FS.

Objective To explore the influence of ?-aminobutyric acid B receptor(GABA_BR)on carbon monoxide (CO)/heme oxygenase(HO-1)system during recurrent febrile seizures (FS).Methods Sprague-Dawley rats aged 21 days were randomly divi- ded into 4 groups:control group and FS group,FS+baclofen group,FS+phaclofen group.FS in rats were induced 10 times in a bath of warm water, once every 2 days.The plasma level of CO was detected by the dual wave lengh spectrophotometer;the expressions of GABA_BR and HO-1 mRNA were examined by insitu hybridization;the expressions of GABA_BR and HO-1 protein were observed by immunohistochemistry.Results The plasma level of CO increased in FS+baclofen group,while decreased in FS+phaclofen group compared with FS group.The expressions of GABA_BR and HO-1 upregulated in FS+baclofen group,while decreased in FS+phaclofen group compared with FS group.There were significant difference (All P

Objective To explore the underlying relationship between hyperglycemic factors in type 2 diabe- tes.Methods Fifty seven type 2 diabetes with obesity (DM-OB)and 64 without obesity(DM-NOB)were recruited. Age,body mass index(BMI),hemoglobin A1c (HbA1c),homeostasis model assessment-2 insulin resistance (HO- MA-IR),high-sensitivity C-reactive protein (hsCRP),fasting plasma glucose,postprandial plasma glucose (PPG), postprandial glucose excursion(PPGE),lipid profile,blood pressure were determined.Results DM-OB subjects had significantly higher HOMA-IR,BMI,DBP,TC,hsCRP,HbAlc,LDL-C when compared with DM-NOB sub- jects.Pearson correlation analysis,in DM-OB subjects,BMI,FBG,FPG,HOMA-IR,hs-CRP were all the posi- tive relative factors(P all

Objective:To explore the pathogenesis of multiple organ dysfunction syndrome(MODS)with respect to the bal- ance of Th1/Th2.Methods:Eighteen healthy male minipigs,weighing 22-30 kg,were randomly divided into two groups: MODS group and control group.Double-hit method including hemorrhagic shock and endotoxiemia was used to establish the porcine MODS model.The peripheral vein blood samples were collected at different time-points(before bloodletting,before en- dotoxin injection,1 h,24 h,48 h and 72 h after endotoxin injection)in the two groups.The spleen samples were collected after death of the animals.Plasma levels of IFN-?and IL-4 were detected by enzyme-linked immunosorbent assay(ELISA).Real- time PCR was used to detect the expression of IFN-?,IL-4,T-bet and GATA-3 mRNA(The latter 2 were the key transcription factors associated with Th1/Th2 response)in the spleen samples.Results:The plasma levels of IFN-?and IL-4 quickly reached the peak values 1 h after the endotoxin injection,then the level of IFN-?decreased quickly.The ratio of IFN-?/IL-4 was signifi- cantly lower than the baseline value 72 h after endotoxin injection(P=0.000).The ratio of IFN-?/IL-4 mRNA in MODS group was obviously lower than that in the control group(P=0.020);the ratio of T-bet/GATA-3 was also lower in MODS group (P=0.038).Conclusion:The shift from Th1 to Th2 occurs in the progress of MODS.

Aneurysm ; complications ; therapy ; Cardiac Catheterization ; instrumentation ; Child ; Heart Septal Defects, Ventricular ; complications ; therapy ; Humans ; Septal Occluder Device

Objective To investigate the association between the glycated albumin to glycated hemoglobin (GA/A1c) ratio and carotid plaque. Methods Type 2 diabetic (T2DM) patients in endocrine inpatient department of Sichuan Provincial People′s Hospital were chosen whose clinical data were collected. Results Of the recruited 154 T2DM patients , GA/HbA1c ratio was negatively correlated with BMI , blood uric acid and was positively correlated with age, HCY, FBG, PBG, left carotid IMT and right carotid IMT. In terms of carotid plaque, GA, GA/HbA1c ratio and HCY were higher in carotid plaque positive patients than those without carotid plaque. The results of logistic regression analysis showed that GA/HbA1c ratio was significantly associated with the presence of carotid plaque (P=0.008). Conclusions GA/HbA1c ratio was positively correlated with the presence of carotid artery IMT in T2DM This suggests that GA/HbA1c ratio will serve as a useful clinical marker for predicting diabetic cardiovascular complications.

It has been reported that lysophosphatidic acid (LPA) at its lower concentrations prevents apoptosis induced by serum-deprivation in cultured cortical neurons when LPA is added into the cultural medium with serum withdrawal. The present study was designed to investigate whether LPA could also block the apoptosis induced by beta-amyloid peptide fragment 31-35 (AbetaP31-35) in cultured cortical neurons by using techniques of DNA fragmentation electrophoresis, HO33342 staining, and TUNEL examinations. The results showed that pretreatment of LPA suppressed the AbetaP31-35-induced apoptosis only when LPA was applied to the cultured neurons with lower concentrations (1-10 micromol/L) and especially, with a preceding time of 12-24 h before the AbetaP31-35 exposure. These facts imply that LPA also acts as a neuroprotective factor against AbetaP31-35-induced apoptosis, though the mechanism underlying the protective action in this case may be more complex than that involved in the serum deprivation-induced apoptosis.
Amyloid beta-Peptides ; antagonists & inhibitors ; Animals ; Animals, Newborn ; Apoptosis ; drug effects ; physiology ; Cells, Cultured ; Cerebral Cortex ; pathology ; Lysophospholipids ; pharmacology ; Mice ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Peptide Fragments ; antagonists & inhibitors

OBJECTIVETo elaborate the role of quantitative magnetic resonance imaging (MRI) parameters in the evaluation of treatment response in malignant tumors.

DATA SOURCESData cited in this review were obtained mainly from PubMed in English from 1999 to 2014, with keywords "dynamic contrast-enhanced (DCE)-MRI," "diffusion-weighted imaging (DWI)," "microcirculation," "apparent diffusion coefficient (ADC)," "treatment response" and "oncology."

STUDY SELECTIONArticles regarding principles of DCE-MRI, principles of DWI, clinical applications as well as opportunity and aspiration were identified, retrieved and reviewed.

RESULTSA significant correlation between ADC values and treatment response was reported in most DWI studies. Most quantitative DCE-MRI studies showed a significant correlation between K trans values and treatment response. However, in different tumors and studies, both high and low pretreatment ADC or K trans values were found to be associated with response rate. Both DCE-MRI and DWI demonstrated changes in their parameters hours to days after treatment, showing a decrease in K trans or an increase in ADC associated with response in most cases.

CONCLUSIONSCombinations of quantitative MRI play an important role in the evaluation of treatment response of malignant tumors and hold promise for use as a cancer treatment response biomarker. However, validation is hampered by the lack of reproducibility and standardization. MRI acquisition protocols and quantitative image analysis approaches should be properly addressed prior to further testing the clinical use of quantitative MRI parameters in the assessment of treatments.

The effect of lysophosphatidic acid (LPA), with a wide range of its different concentrations, upon cultured mouse cortical neurons was assessed by electrophoresis of DNA fragments, HO33342 and TUNEL stainings, and also by ultrastructural examination at times. The results showed that administration of LPA at lower concentrations (0.1-30 micromol/L) dose-dependently protected cortical neurons from apoptosis that was induced by deprivation of serum from the cultural medium, while 50 micromol/L or higher concentrations of LPA failed to show this effect; and moreover, the concentrations higher than 50 micromol/L induced apoptosis in neurons cultured in serum-containing complete medium. These results suggest that a moderate concentration of LPA may play as a survival factor in apoptotic cortical neurons, while an excessive level of LPA induces apoptosis in neurons cultured in complete medium.
Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Cerebral Cortex ; cytology ; Culture Media, Serum-Free ; Lysophospholipids ; pharmacology ; Mice ; Neurons ; cytology