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Carbonate weathering and the CO 2 consumption in karstic area are extensive affected by anthropogenic activities, especially sulfuric and nitric acids usage in the upper-middle reaches of Wujiang River, China. The carbonic acid would be substituted by protons from sulfuric and nitric acids which can be reduce CO 2 absorption. Therefore, The goal of this study was to highlight the impacts of sulfuric and nitric acids on carbonate dissolution and the associated deficit of CO 2 uptaking during carbonate weathering. The hydrochemistries and carbon isotopic signatures of dissolved inorganic carbon from groundwater were measured during the rainy season (July; 41 samples) and post-rainy season (October; 26 samples). Our results show that Ca 2 + and Mg 2 + were the dominant cations (55.87–98.52%), and HCO 3 – was the dominant anion (63.63–92.87%). The combined concentrations of Ca 2 + and Mg 2 + commonly exceeded the equivalent concentration of HCO 3 − , with calculated [Ca 2 + + Mg 2 + ]/[HCO 3 − ] equivalent ratios of 1.09–2.12. The mean measured groundwater δ 13 C DIC value (− 11.38‰) was higher than that expected for carbonate dissolution mediated solely by carbonic acid (− 11.5‰), and the strong positive correlation of these values with [SO 4 2 − + NO 3 − ]/HCO 3 – showed that additional SO 4 2 − and NO 3 − were required to compensate for this cation excess. Nitric and sulfuric acids are, therefore, suggested to have acted as the additional proton-promoted weathering agents of carbonate in the region, alongside carbonic acid. The mean contribution of atmospheric/pedospheric CO 2 to the total aquatic HCO 3 – decreased by 15.67% (rainy season) and 14.17% (post-rainy season) due to the contributions made by these acids. The annual mean deficit of soil CO 2 uptake by carbonate weathering across the study area was 14.92%, which suggests that previous workers may have overestimated the absorption of CO 2 by carbonate weathering in other karstic areas worldwide. [ABSTRACT FROM AUTHOR]

Abstract: Epidemiological data indicate an increasing incidence of asthma in the obese individuals recent decades, while very little is known about the possible association between them. Here, we compared the roles of adipocyte-derived factors, including leptin, adiponectin and resistin on proliferation, wound repair and apoptosis in human bronchial epithelial cells (HBECs) which play an important role in the pathogenesis of asthma. The results showed that exogenous globular adiponectin (gAd) promoted proliferation, cell-cycle and wound repair of HBECs. This effect may be relevant to Ca2+/calmodulin signal pathway. Besides, gAd inhibited apoptosis induced by ozone and release of lactate dehydrogenase (LDH) of HBECs via regulated adipoR1 and reactive oxygen species. No effects of leptin or resistin on proliferation, wound repair and apoptosis of HBECs were detectable. These data indicate that airway epithelium is the direct target of gAd which plays an important role in protecting HBECs from mechanical or oxidant injuries and may have therapeutic implications in the treatment of asthma. [Copyright &y& Elsevier]

Abstract: To investigate abnormalities of cystic fibrosis transmembrane conductance regulator (CFTR) expression in chronic inflammatory airway diseases and its regulation mechanisms, the present study was designed to observe the expression of CFTR, CFTR chloride current and the possible relevant signal pathways in in vitro and in vivo bronchial epithelium by using real-time PCR, immunofluorescence, Western blot and whole cell patch-clamp. The results demonstrated that CFTR staining was decreased in rat airway epithelium under ozone stress. Ozone stress also down-regulated CFTR protein and mRNA expression and CFTR chloride current in cultured human bronchial epithelial cells (HBEC). STAT1 signal pathway was checked to investigate the signal mechanism. It was found that pretreatment with STAT1 inhibitor attenuated the down-regulated CFTR expression induced by ozone stress. We also observed that ozone stress accelerated the phosphorylation of STAT1 in HBEC, which could be influenced by some signaling molecules related to the early transduction of cellular stress. Furthermore, reactive oxygen species inhibitors N-acetylcysteine and nitric oxide synthase inhibitor aminoguanidine increased the expression of CFTR. Ozone stress could down-regulate the expression of CFTR and decrease CFTR chloride current in HBEC. The signal mechanism which referred to cascade events in cells included early oxidative stress signal transmission molecules, and subsequently transcription modulator STAT1. [Copyright &y& Elsevier]

Abstract: In the present study, we investigated the effects of vasoactive intestinal peptide (VIP) on wound healing of bronchial epithelium. Wound healing of the mechanical damaged human bronchial epithelial cells (HBEC) was observed in the absence or presence of VIP. Effects of VIP on chemotactic migration, cell proliferation of HBEC were also tested. HBEC chemotaxis was assessed by the blind well chamber technique, the cell cycle was determined by flow cytometry, and cell proliferation was determined by measuring the expression of proliferating cell nuclear antigen Ki67. Effects of VIP on epithelial E-cadherins protein and mRNA were also measured by immunohistochemistry and RT-PCR. The results showed that VIP accelerated the recovery of wound area of HBEC. VIP increased the migration and proliferation of HBEC, and these effects were blocked by a VPAC1 receptor antagonist. VIP also increased the expression of E-cadherin mRNA and protein in HBEC, suggesting that protective effects of VIP on wound healing may be related to its ability to increase the expression of E-cadherin. In conclusion, VIP has protective effects against human bronchial epithelial cell damage, and the beneficial effects of VIP might be mediated, at least in part, by VPAC1, and associated with increased expression of E-cadherin. [Copyright &y& Elsevier]

Abstract: The present study was designed to investigate the role of bombesin receptor subtype 3 (BRS-3) in airway wound repair. The results showed that: (1) There was few expression of BRS-3 mRNA in the control group. In contrast, the expression of BRS-3 mRNA was gradually increased in the early 2 days, and peaked on the fourth day, and then decreased in the ozone-stressed AHR animal. BRS-3 mRNA was distributed in the ciliated columnar epithelium, monolayer columnar epithelium cells, scattered mesenchymal cells and Type II alveolar cells; (2) The wound repair and proliferation of bronchial epithelial cells (BECs) were accelerated in a concentration-dependent manner by BRS-3 activation with P3513, which could be inhibited by PKA inhibitor H89. The study demostrated that activation of BRS-3 may play an important role in wound repair of AHR. [Copyright &y& Elsevier]

Abstract: Respiratory syncytial virus (RSV) infection causes bronchiolitis in infants and children, which is an important risk factor for the development of chronic asthma. To probe the underlying mechanisms that RSV infection increases the susceptibility of asthma, this present study was designed to establish a RSV persistent infection animal model by cyclophosphamide (CYP) pretreatment that more closely mimic human RSV infection. CYP is an immunosuppressant, which induced deficiency in cellular and humoral immunity. Pulmonary RSV titers, airway function and peptidergic innervation were measured on 7d, 28d, 42d and 60d postinfection. The results showed that during RSV persistent infection, the lungs of RSV-inoculated animals pretreated with CYP showed higher RSV titers and exhibited obvious chronic inflammation. The results also showed that protein gene product 9.5 (PGP9.5), substance P (SP) and calcitonin gene-related peptide (CGRP)-immunoreactive fibers increased and vasoactive intestinal peptide (VIP)-immunoreactive fibers decreased during RSV persistent infection. These results demonstrate that RSV persistent infection induces significant alterations in the peptidergic innervation in the airways, which may be associated with the development of altered airway function. [Copyright &y& Elsevier]

Abstract: We previously reported that vasoactive intestinal peptide (VIP) promoted synthesis of phosphatidylcholine (PC) in alveolar type II (ATII) cells. But the intracellular mechanism for this effect was unknown. In this work, we investigated the intracellular signal transduction pathway for VIP promoted synthesis of PC, the major lipid component of pulmonary surfactant (PS), by using an antagonist of VIP receptors, inhibitor of protein kinase C (PKC) and antisense oligonucleotides (AS-ODN) for c-fos oncogene. Our results showed that: ① [D-P-Cl-Phe(6)-Leu(17)]-VIP (10−6 mol/l), an antagonist of VIP receptors, could decrease the quantity of [3H] choline incorporation, microsomal choline-phosphate cytidylyltransferase (CCT) mRNA expression and CCT activity induced by VIP (10−8 mol/l) in cultured lung explants to the control levels; ② VIP (10−8 mol/l) upregulated c-Fos protein expression in ATII cells. AS-ODN for c-fos oncogene (9×10−6 mol/l) could block the elevation of [3H] choline incorporation, microsomal CCT mRNA expression and CCT activity induced by VIP in cultured lung explants and in ATII cells; ③ H7 (10−5 mol/l), a PKC inhibitor could also reduce VIP induced [3H] choline incorporation, microsomal CCT mRNA expression and CCT activity in cultured lung explants and in ATII cells. These results demonstrated that VIP receptors, PKC and c-Fos protein played important roles in the signaling pathway through which VIP promoted the synthesis of PC. [Copyright &y& Elsevier]