Search

In order to understand the quality of local sorghum in Chongqing and provide theoretical and applied guidance for the development of local sorghum industry, 12 main sorghum varieties in Chongqing were collected in the experiment. The physical and chemical components of the two main sorghum varieties in the northeast and northwest were measured and analyzed by principal component analysis, and their components and uses were correlated. At the same time, the digestibility of sorghum starch was determined to screen out the anti-digestible sorghum varieties. The results showed that there were significant differences in the physical and chemical properties of 16 sorghum varieties (P

The present study was undertaken to examine the hemodynamic state using the latest ultrasound biomicroscopy (UBM) technique and to investigate the effect of local shear stress on the development of atherosclerosis in the constrictive collar-treated carotid arteries of apolipoprotein E-deficient ([apoE.sup.-/-]) mice. Fifty-six male [apoE.sup.-/-] mice fed a high-lipid diet were divided into an interventional group (n = 48) and the control group (n = 8). Constrictive and nonconstrictive collars were placed around the carotid artery of the mice in the interventional group and the control group, respectively. The carotid lumen diameters and flow velocities were measured by UBM, and shear stress in the lesion region was calculated. Histopathology and electron microscopy were performed to observe the morphological changes in the carotid artery. In the region proximal to the constrictive collar, shear stress was significantly reduced 2 days after collar placement and remained low over time compared with the baseline level. In contrast, within the constrictive collar region, shear stress was increased significantly. Although endothelial permeability was enhanced in both regions, monocyte chemotaxis protein-1 (MCP-l) expression, macrophage infiltration, and atherosclerotic lesions were more prominent in the region proximal to the constrictive collar. Moreover, increased MCP-1 expression was observed as early as 2 days after constrictive collar placement, which preceded the morphological changes of the vessel wall. In conclusion, UBM offers a noninvasive and reliable technique for measuring shear stress in [apoE.sup.-/-] mice. Persistent low shear stress promotes endothelial permeability and enhances MCP-1 expression and macrophage recruitment, which were essential in the pathogenesis of atherosclerosis in [apoE.sup.-/-] mice. atherosclerosis; apolipoprotein E-deficient mice; shear stress; endothelial permeability; monocyte chemotaxis protein-1 doi: 10.1152/ajpheart.00308.2009.

To establish an animal model with disruptions of atherosclerotic plaques, 96 male apolipoprotein E knockout (apo[E.sup.-/-]) mice were randomly divided into stress, lipopolysaccharide (LPS), stress+LPS, and control groups (n = 24 each). All mice were fed a high-fat diet throughout the experiment, and carotid atherosclerotic lesions were induced by placement of a constrictive perivascular collar. Four weeks after surgery, mice in the LPS and stress+LPS groups were intraperitoneally injected with LPS (1 mg/kg twice per week for 8 wk). Eight weeks after surgery, mice in the stress and stress+LPS groups were treated with intermittent physical stress (electric foot shock and noise stimulation) for 4 wk. Morphological analysis revealed a plaque disruption rate of 16.7% in control, 34.8% in LPS, 54.2% in stress, and 60.9% in stress+LPS groups. The disruption rates in stress and stress+LPS groups were both significantly higher than those of controls (P = 0.007 and P = 0.002, respectively). Luminal thrombosis secondary to plaque disruption was observed only in the stress+LPS group. Both stress and LPS stimulation significantly decreased fibrous cap thickness and increased macrophage and lipid contents in plaques. Moreover, the combination of stress and LPS stimulation further lowered cap thickness and enhanced accumulation of macrophages and expression of inflammatory cytokines and matrix metalloproteinases. Stress activated the sympathetic nervous system, as manifested by increased blood pressure and flow velocity. Plasma fibrinogen levels were remarkably elevated in the stress and stress+LPS groups. In conclusion, stress- and LPS-costimulated apo[E.sup.-/-] mice provide a useful model for studies of plaque vulnerability and interventions. atherosclerosis; inflammation; hemodynamics

The human neonate is at a higher risk for hypoglycemia-induced neuronal injury than other pediatric and adult patients. Repetitive and profound neonatal hypoglycemia can result in severe neurologic sequelae, of which the mechanisms was not elucidated by hitherto. Moreover, no reliable animal model of brain injury induced by neonatal hypoglycemia is available in order to carry out more research. Therefore, we tried to induce neonatal hypoglycemia in newborn rats by fasting and insulin injection, and then examined the neuronal degeneration after repetitive hypoglycemic insults by Fluoro-Jade B (FJB) staining. Experimental animals were randomly divided into four groups: insulin-treated rats with short hypoglycemia, insulin-treated rats with prolonged hypoglycemia, fasted rats, and control rats. Insulin injection and fasting both could induce consistent hypoglycemia in newborn rats. But from FJB staining results, only in insulin-treated rats with prolonged hypoglycemia could extensive neurodegeneration be detected. We can conclude that FJB staining is a useful method of marking neuronal degeneration in neonatal rats following hypoglycemic brain damage. Repetitive and profound neonatal hypoglycemia can result in extensive neurodegeneration, and it seems that neurons of the cortex, dentate gyrus of the hippocampus, the thalamus, and the hypothalamus are more vulnerable to hypoglycemic insult in newborn rats. Repetitive and profound insulin-induced hypoglycemia in newborn rats can establish a reliable animal model of brain injury resulting from neonatal hypoglycemia. [ABSTRACT FROM AUTHOR]

The article analyzes the variation in prolactin (PRL) exon 2 in geese and the genetic effects of the variation using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP).

Aim: To explore the relationship between gene polymorphisms of vascular endothelial growth factor (VEGF) and retinopathy of prematurity (ROP)., Methods: Literature materials related to gene polymorphisms of VEGF and ROP in PubMed, EMBASE, Cochrane and CBM database were retrieved. These materials were screened according to inclusion and exclusion standards. Patients diagnosed with ROP in clinic were regarded as control group and ROP patients who were in treatment were regarded as observation group. The indexes in two groups were matched except birth weight (BW), gender and gestational weeks. Meta5.1 was used to analyze the relationship between gene polymorphisms of VEGF and ROP., Results: Four random control tests (RCT) were included in this research, including 2611 patients. Meta analysis results showed that VEGF affected ROP, having statistical significance. The combined ratio was 0.44 (95%CI, 0.07, 0.80), 0.42 (95%CI, 0.09, 0.74) and 0.75 (95%CI, 0.02, 1.49), respectively. Carrying +405 allele might increase the premature infants' risk of having ROP., Conclusion: ROP may be related to its carrying of +405 allele. Large-scale, multi-factor RCT researches are still needed in order to identify the relation between VEGF and ROP.

Objective: Caveolin-1 (Cav-1) may positively or negatively influence the development of atherosclerosis, depending on the cell type and the metabolic pathways regulated by this protein. We investigate the effects of Cav-1 on cholesterol efflux in RAW264.7 infected with AdPPARgamma1 and whether Cav-1 could attenuate established atherosclerotic lesions in PPARgamma1-treated apoE-deficient mice., Methods and Results: Compared with AdGFP control, PPARgamma1 and Cav-1 were constitutively overexpressed in AdPPARgamma1-infected RAW264.7 cells, which stimulated cholesterol efflux to apolipoprotein A-I. Using a small interfering RNA approach (Cav-1-siRNA) we achieved an efficient and specific knockdown of caveolin-1 expression (80%), which resulted in a remarkable reduction of cholesterol efflux in RAW264.7 cells . Moreover, PPARgamma1-treated Cav-1-siRNA RAW264.7 cells showed more ability to stimulate cholesterol efflux than Cav-1-siRNA RAW264.7 cells, but far less than control-siRNA RAW264.7 cells and PPARgamma1-treated RAW264.7 cells. In addition, 40-week-old apoE-deficient mice fed a Western-type diet and infected for 4 weeks with AdPPARgamma1 showed induced Cav-1 expression in aortic vascular endothelial cells, smooth muscle cells and macrophages, as well as attenuated established atherosclerotic lesions., Conclusions: PPARgamma1 gene therapy could induce Cav-1 expression and enhance cholesterol efflux and attenuate atherosclerosis in apoE-deficient mice., (Copyright 2009 S. Karger AG, Basel.)

This study was carried out to test the hypothesis that Tongxinluo (TXL) as a Chinese herbal medicine enhances stability of vulnerable plaque dose dependently via lipid-lowering and anti-inflammation effects, similar to a high-dose simvastatin therapy. After abdominal aortic balloon injury, 75 rabbits were fed a 1% cholesterol diet for 10 wk and were then divided into five groups for 8-wk treatment: control group, low-dose TXL group, moderate-dose TXL group, high-dose TXL group, and high-dose simvastatin group. At the end of week 16, an adenovirus containing p53 was injected into the abdominal aortic plaques. Two weeks later, plaque rupture was induced by pharmacological triggering. The incidence of plaque rupture in all treatment groups (14.3%, 7.1%, 7.7%, and 7.1%) was significantly lower than that in control group (73.3%; P>0.01). TXL dose-dependently lowered serum lipid levels and inhibited systemic inflammation. Corrected acoustic intensity and fibrous cap thickness of the aortic plaques were significantly increased, whereas plaque area, plaque burden, vulnerable index, and expression of oxidized low-density lipoprotein (ox-LDL) receptor 1, matrix metalloproteinase 1 (MMP-1), MMP-3, tissue inhibitor of MMP 1, and NF-kappaB in plaques were markedly reduced in all treatment groups when compared with the control group. Similar to high-dose simvastatin group, high-dose TXL group exhibited a low serum level of low-density lipoprotein cholesterol and ox-LDL, a low expression level of systemic and local inflammatory factors and a low plaque vulnerability index, with no differences in the incidence of plaque rupture among all treatment groups. TXL dose-dependently enhances the stability of vulnerable plaques and prevents plaques from rupture. Simvastatin and TXL offer similar protection in terms of lipid-lowering, anti-inflammation, and antioxidation effects.

This study aims to develop a new animal model of vulnerable plaques and investigate the potential mechanisms of exogenous p53-induced plaque instability. Forty rabbits underwent aortic balloon injury, were fed a 1% cholesterol diet for 10 weeks and then normal chow for 6 weeks. Rabbits were divided into Ad5-CMV.p53-treated group (n = 16), Ad5-CMV.lac Z-treated group (n = 16) and blank control group (n = 8). Under the guidance of intravascular ultrasound, a 50-microl suspension of adenovirus containing p53 or lac Z was injected into the largest plaque of the first two groups, respectively, and these rabbits received pharmacological triggering 2 weeks later. In 76.9% of rabbits with p53 transfection, plaque rupture was found, which was significantly (P < 0.05) higher than that in the Ad5-CMV.lac Z-treated plaques (23.1%), or blank controls plaques (0%). Increased apoptotic cells, and subsequently, decreased vascular smooth muscle cells and collagen content, enhanced intima macrophage accumulation, increased C-reactive protein (CRP) and matrix metalloproteinases staining and high serum levels of high sensitive CRP (hs-CRP) and monocyte chemoattractant protein-1 (MCP-1) were observed in Ad5-CMV.p53-treated rabbits. However, a binary logistic regression model revealed that hs-CRP concentration rather than apoptosis rate played an independent role in plaque rupture with an odds ratio as 1.314 (95% CI: 1.041-1.657, P = 0.021), and there were high positive correlations between inflammatory biomarkers (hs-CRP or MCP-1) and apoptosis (R(2) = 0.761, and R(2) = 0.557, respectively, both P < 0.01). Intraplaque injection of p53 gene provides a safe and effective method for inducing plaque vulnerability in rabbits. The destabilizing effect of p53 overexpression is mediated mainly through apoptosis-enhanced inflammation rather than cell apoptosis itself.

Objective: Angiotensin converting enzyme 2 (ACE2) efficiently hydrolyses the potent vasoconstrictor angiotensin II to vasodilative angiotensin (1-7). We hypothesized that ACE2 overexpression may inhibit inflammation response in atherosclerotic plaque by degrading Ang II into Ang-(1-7)., Methods: Atherosclerosis (AS) plaques were induced in the abdominal aorta of 38 rabbits by endothelial injury and atherogenic diet for 3 months. Rabbits were then underwent injection of a recombinant adenovirus (2.5 x 10(9) pfu/ml) carrying a murine ACE2 gene (Ad-ACE2) through a catheter into the abdominal aortic segments rich in plaques (n = 19) or injection of a control vector Ad-EGFP (n = 19). One month later, all rabbits were sacrificed and plaques from aortic segments were analyzed., Results: ACE2 expression in aortic tissues of the Ad-ACE2 group were confirmed by immunohistochemistry. Macrophage infiltration (13.6% +/- 4.2% vs. 23.6% +/- 6.9%, P < 0.01) and MCP-1 expression (13.2% +/- 0.4% vs. 25.0% +/- 7.4%, P < 0.01) were significantly reduced in Ad-ACE2 group compared to Ad-EGFP group., Conclusions: Overexpression of ACE2 inhibited atherosclerotic plaque inflammation response in hypercholesterolemic rabbits.

Peroxisome proliferator-activated receptor-gamma1 (PPARgamma1) is an important transcription factor involved in atherosclerosis progression. Thus, PPARgamma1 appears to be an interesting gene therapeutic target to favorably affect atherosclerosis development. The present study was carried out to test the hypothesis that PPARgamma1 gene therapy may attenuate and stabilize atherosclerotic plaques in apolipoprotein E-knockout mice. The recombinant adenovirus carrying mouse PPARgamma1 cDNA (AdPPARgamma1) was constructed and AdPPARgamma1 (5 x 10(8) PFU) or AdGFP (5 x 10(8) PFU), diluted to a total volume of 200 mul, was injected into the tail vein of mice (40 weeks of age and fed a high-fat diet) in two intervention groups (n = 20 each). Mice (n = 20) injected with phosphate-buffered saline (PBS) served as vehicle controls. The results showed that 4-week treatment with AdPPARgamma1 attenuated atherosclerotic lesions, although the overall mRNA levels of CD36 were increased in the AdPPARgamma1 group. Moreover, PPARgamma1 gene overexpression stabilized atherosclerotic plaques as shown by the reduced depositions of lipids and macrophages and increased contents of smooth muscle cells and collagen within the plaques. In addition, marked upregulation of the mRNA levels of cholesterol efflux-related molecules such as liver X receptor alpha and ATP-binding cassette transporter A1 in liver, and downregulation of matrix metalloproteinase-9, human tissue factor, CD40, CD40 ligand, tumor necrosis factor-alpha, monocyte chemoattractant protein-1, vascular cell adhesion molecule-1, macrosialin, class A scavenger receptor, and macrophage migration inhibitory factor in aorta, were demonstrated in AdPPARgamma1-treated animals. In contrast, there was no significant difference in aforementioned parameters between the AdGFP and PBS groups. In conclusion, overexpression of the PPARgamma1 gene exerts beneficial effects in attenuating atherosclerosis progression and stabilizes vulnerable plaques. Thus, PPARgamma1 might offer a promising gene therapeutic target against atherosclerosis.

Objective: To study the effects of amiloride, an inhibitor of urokinase, on pathological and pathophysiological changes of chronic obstructive pulmonary disease (COPD) model, and to investigate the role of urokinase plasminogen activator system components in the pathogenesis of COPD., Methods: Healthy Wistar rats (n = 24) were randomly divided into a control group, a model group and an amiloride group. After 7 weeks, lung function measurements were performed. The total and different white blood cell counts of bronchoalveolar lavage fluid (BALF) were determined, and collagen deposition of lung sections was observed by picrosirius staining. The expressions of u-PA, u-PAR and PAI-1 in bronchial lung tissues were examined by immunohistochemical analysis., Results: In the model group the expiratory resistance (Re) was significantly higher than that of the control group and the amiloride group, while forced expiratory volume in the 0.3 s/forced expiratory capacity (FEV(0.3)/FVC%) and peak expiratory flow (PEF) were significantly lower than those of the other two groups. Significant increase in total white blood cells and percentage of neutrophils and macrophages in BALF was found in the model group as compared to the control group and the amiloride group. The collagen deposition, mainly type I collagen, in airway walls was significantly increased in the model group. The levels of u-PA, u-PAR and PAI-1 in the model group [(0.166 +/- 0.010), (0.158 +/- 0.024), (0.171 +/- 0.012), respectively] were significantly higher than those in the control group [(0.137 +/- 0.015), (0.122 +/- 0.009), (0.144 +/- 0.005), respectively] and the amiloride group [(0.126 +/- 0.004), (0.120 +/- 0.010), (0.122 +/- 0.004), respectively]. F values were 32.463, 4.094, 79.562 respectively, and all P < 0.001. Moreover, u-PAR protein level was positively correlated with neutrophils in BALF in the model group (r = 0.754, P = 0.031)., Conclusion: Administration of u-PA inhibitor-amiloride significantly alleviated airway inflammation and the pathological changes in COPD rats, suggesting that the u-PA system components are key mediators regulating the inflammatory reaction and tissue remodeling in the pathological process of COPD.

Objective: To investigate the effect of PPARgamma1 gene overexpression on caveolin-1 mRNA and protein expressions in a murine macrophage cell line Raw264.7., Methods: Replication-deficient recombinant adenovirus expression vector of PPARgamma1 was constructed using the AdEasy system. Raw264.7 cells were randomly treated as follows: P group (PPARgamma1 gene overexpression), T group (Troglitazone 40 micromol/L in DMSO), PT group (PPARgamma1 gene overexpression and Troglitazone) and control group. Changes of PPARgamma1 and caveolin-1 at mRNA and protein levels were investigated., Results: Caveolin-1 expression can be detected by RT-PCR in Raw264.7, by immunocytochemistry method in cell and nuclear membrane but not by immunoblotting at protein level. Caveolin-1 expression at mRNA and protein levels in Raw264.7 were significantly higher in P, T and PT groups compared to control group and the expression was also significantly higher in PT group than that in P group and T group (P < 0.05). PPARgamma expression was significantly increased in PT group and P group where remained unchanged in T group compared to control group., Conclusion: PPARgamma1 overexpression can upregulate caveolin-1 expression in macrophages. Troglitazone upregulated caveolin-1 expression in the absence of increased PPARgamma1 expressions at mRNA and protein levels.