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The aim of the present study was to investigate the alterations in thoracic aortic vasomotor function in rats with chronic heart failure (CHF) post myocardial infarction (MI), and then explored the possible mechanism of pathological changes. Male Sprague-Dawley rats were divided into sham and CHF groups randomly. The CHF model group of rats was generated by ligating the left anterior descending artery. In sham-operated rats the ligation was placed but not tightened. A total of 20 rats underwent either sham-operated (n=8) or surgery for MI (n=12). All sham-operated rats survived the surgical procedure and the post-surgical period, whereas total mortality among MI-rats was 25% (3 out of 12). Only MI-rats with infarct-size >30% of the left ventricle (LV) were included for analysis (8 out of 9). Ten weeks after surgery, rats were anaesthetized for hemodynamic measurements, which contains systolic pressure, diastolic pressure, left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), LV+dp/dt(max) and LV-dp/dt(max). After that hearts were rapidly excised and weighed. Myocardial infarct size was determined by triphenyltetrazolium chloride (TTC) staining method. Isolated thoracic artery ring preparations were studied in a wire-myograph. The arterial constrictive responses to KCl, CaCl2, phenylephrine (PE), and caffeine and the arterial diastolic responses to acetylcholine (ACh) were recorded by the Multi Myograph System. To explore the possible mechanism, nitric oxide synthase (NOS) inhibitor N-nitrl-L-arginine methylester (L-NAME) and non-selective cyclooxygenase (COX) inhibitor indomethacin (Indo) were used. The results obtained were as follows: (1) CHF group showed an increased contraction response to KCl (5-100 mmol/L) and PE (1x10(-8)-3x10(-4) mol/L), and a reduced endothelium-dependent relaxation response to ACh (1x10(-12)-1x10(-4) mol/L) compared with those observed in sham group (P<0.01, P<0.05); (2) In the presence of L-NAME (1 mmol/L), the endothelium-dependent cumulative contractions to ACh (1x10(-7)-1x 10(-4) mol/L) was significantly enhanced in CHF group (P<0.05), and this effect was reversed by pretreatment with Indo (10 mumol/L); (3) In CHF group, the vessels incubated with Indo (10 mumol/L) showed an increased vasodilation induced by ACh (1x10(-12)-1x10(-4) mol/L) (P<0.05); (4) In the Ca(2+)-free K-H solution, calcium-dependent contraction curves induced by CaCl2 (1x10(-4)-3x10(-2) mol/L) in CHF group significantly shifted to the left compared with sham group (P<0.05); while the vascular contraction induced by caffeine (30 mmol/L) had no significant changes. These findings suggest that thoracic arteries of rats with CHF have endothelial dysfunction, and the contribution of endothelial dilation and contraction was significantly altered in CHF rats. The mechanism could be partly associated with the increased endothelium-dependent contracting factors by COX pathway, or the increased extracellular Ca(2+) influx through voltage-operated channels, thus leading to elevated vasoconstriction.

Objective: To examine serum concentration of interleukin-18 (IL-18) and IL-18 mRNA expression in peripheral blood mononuclear cells (PBMCs) in children with primary nephrotic syndrome (PNS) and explore the possible role of IL-18 in steroid-resistant nephrotic syndrome (SRNS)., Methods: Sixty-six children with newly diagnosed PNS, including 39 cases of steroid sensitive nephrotic syndrome (SSNS) and 27 cases of SRNS, were enrolled. Forty healthy children were used as a normal control group. Blood samples were collected before and 8 weeks after glucocorticoid treatment. Serum concentration of IL-18 was measured using ELISA. IL-18 mRNA expression in PBMCs was detected by the RT-PCR method. The amount of 24-hr urine protein was measured by the biuret method. Serum contents of total cholesterol (T-Ch), triglyceride (TG), low density lipoprotein (LDL), total protein (TP), and albumin (Alb) were measured by the automatic biochemistry analyzer., Results: Serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SSNS and the SRNS groups were significantly higher than those in the normal control group before treatment (P< 0.05). The SRNS group had increased serum protein concentration of IL-18 and IL-18 mRNA expression in PBMCs compared with the SSNS group before treatment (P< 0.05). Serum LDL content in the SRNS group was also significantly higher than that in the SSNS group before treatment (P< 0.05). After treatment, serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SRNS group were significantly higher than those in the SSNS and the normal control groups (P< 0.05). Serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SSNS group were significantly reduced after treatment, but the alterations of IL-18 were not observed in the SRNS group after treatment., Conclusions: SRNS was associated with increased serum IL-18 concentration and IL-18 mRNA expression in PBMCs. Over-production of IL-18 may play a role in the development of SRNS.

Objective: To study serum concentration and mRNA expression of interleukin-13 (IL-13) in children with steroid-responsive nephrotic syndrome (SRNS) and the effect of methylprednisolone pulse therapy (MPT) on IL-13 expression., Methods: Twenty-eight children with SRNS were enrolled in this study. Serum protein level of IL-13 was measured using ELISA and IL-13 mRNA expression in peripheral blood mononuclear cells (PBMC) was detected with RT-PCR before MPT, 2 and 5 days after MPT, and 2 weeks after disappearance of proteinuria following MPT. Twenty-four urinary protein was measured with the biuret assay. Twenty healthy children were used as controls., Results: Serum IL-13 levels (38.48 +/- 13.01 pg/mL vs 5.18 +/- 2.71 pg/mL) and PBMC IL-13 mRNA expression (1.31 +/- 0.23 vs 0.36 +/- 0.07) before MPT in SRNS patients were significantly higher than in the controls. After 5 days of MPT and 2 weeks after disappearance of proteinuria following MPT, serum IL-13 levels (15.33 +/- 7.81 and 5.35 +/- 2.12 pg/mL respectively) and PBMC IL-13 mRNA expression (0.89 +/- 0.26 and 0.33 +/- 0.08 respectively) were significantly reduced (P < 0.01). Serum IL-13 levels and PBMC IL-13 mRNA expression in SRNS patients 2 weeks after disappearance of proteinuria following MPT were reduced to control levels, but remained at a higher level than controls 5 days after MPT. A positive correlation was found between serum levels of IL-13 and 24-hour urinary protein in SRNS patients before (r=0.75, P < 0.01) and after 2 and 5 days of MPT (r=0.68, r=0.71 respectively; P < 0.05)., Conclusions: Serum IL-13 levels and PBMC IL-13 mRNA expression in children with SRNS increase. MPT can inhibit the expression of protein and mRNA of IL-13 in these patients.

Response of water quality to agricultural cultivation was investigated for the Liangwanghe River catchment of Fuxianhu Lake region in Yunnan Province of China. Two typical tillage lands-the rice-wheat rotation (R-W) and the tobacco-pea (T-P) rotation were selected and monitored. Groundwater quality and water quality of Liangwanghe River were monitored simultaneously, as well as the farmland cultivation situation at that time. It was found that cultivation activities, such as transplanting, base fertilizer applying, top dressing, draining would cause apparent elevation of concentrations of TP, PO4(3-)-P, TN, NO3(-)-N and NH4(+)-N of groundwater in a short time period. Nutrients adsorption by crops during different bearing periods has an obvious relationship to the change of contents of TP, PO4(3-)-P, TN, NO3(-)-N, and NH4(+)-N in groundwater in a long time scale. When the crops are in a peak demand for nutrients, contents of nutrients in groundwater were found to reduce obviously, and contents of nutrients may rise for other crop conditions. Contents of TP and PO4(3-)-P of Liangwanghe River for full cultivation periods were found to be 5.8% and 21.7% lower than those for partial cultivation periods, while contents of TN, NH4(+)-N and NO3(-)-N for full cultivation periods were found to be 11.5%, 242.6% and 9.55% higher than those for partial cultivation periods.

Objective: Progressive muscular dystrophy (PMD) is characterized by muscle fiber necrosis, regeneration, and endomysial fibrosis. Although absence of dystrophin and subsarcolemmic protein has been known as the cause of muscle fiber degeneration, pathogenesis of interstitial fibrosis is still unknown. The aim of this study was to investigate the role of connective tissue growth factor (CTGF) in PMD and its relationship with muscular fibrosis., Methods: Immunological localization of CTGF was examined in frozen muscle specimens obtained via biopsy from 8 patients with Duchenne muscular dystrophy (DMD), 2 patients with Becker muscular dystrophy (BMD), 6 patients with congenital muscular dystrophy (CMD) and 6 cases with normal muscle by immunohistochemistry, double immunofluorescence and Western blot analysis., Results: The results of immunohistochemistry and double immunofluorescence showed that CTGF was positive only in vessels of normal muscle. Both immunohistochemistry and Western blot analysis showed that CTGF expression was distinctly increased in dystrophy muscles of PMD than that in normal muscles. In dystrophy muscle, marked immunostaining of CTGF was not only observed in vascular walls, but also strongly expressed in the cytoplasm and nuclei of regenerating muscle fibers, and also immunolocalized in the muscle fiber sarcolemma of non-regenerating fibers. Double labeling with antibodies against CTGF and CD68 demonstrated that CTGF was expressed in some macrophages and some macrophage infiltrated necrotic fibers. CTGF was strongly expressed in endomysial and perimysial connective tissues of dystrophy muscles of patients with DMD, CMD and FCMD. Double immunolabeling revealed that most activated fibroblasts in perimysium and endomysium were positive for CTGF, but not all of connective tissues were co-localized with CTGF. Older cases with FCMD showed poor or no expression of CTGF in advanced fibrosis., Conclusion: CTGF may play a role in the pathogenetic process of muscular dystrophy, and CTGF may be important for muscle repair and fibrosis.