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Publications (21)135 Total impact
Article: G-Protein-Coupled Receptor Kinase Interacting Protein-1 Mediates Intima Formation by Regulating Vascular Smooth Muscle Proliferation, Apoptosis, and Migration[Show abstract] [Hide abstract]
ABSTRACT: OBJECTIVE: The G-protein-coupled receptor kinase interacting protein-1 (GIT1) is a scaffold protein that is important for phospholipase Cγ and extracellular signal-regulated kinase 1/2 signaling induced by angiotensin II and epidermal growth factor. Because GIT1 regulates signaling by several vascular smooth muscle cell (VSMC) growth factors, we hypothesized that intima formation would be inhibited by GIT1 depletion.Approach and Results-Complete carotid ligation was performed on GIT1 wild-type and knockout (KO) mice. We compared changes between GIT1 wild-type and KO mice in carotid vascular remodeling, VSMC proliferation, and apoptosis in vivo and in vitro. Our data demonstrated that GIT1 deficiency significantly decreased intima formation after carotid ligation as a result of both reduced VSMC proliferation and enhanced apoptosis. To confirm the effects of GIT1 in vitro, we performed proliferation and apoptosis assays in VSMC. In mouse aortic smooth muscle cells (MASM), we found that the growth rate and [3H]-thymidine incorporation of the GIT1 KO MASM were significantly decreased compared with the wild-type MASM. Cyclin D1, which is a key cell cycle regulator, was significantly decreased in GIT1 KO cells. Serum deprivation of GIT1 KO MASM increased apoptosis 3-fold compared with wild-type MASM. Treatment of rat aortic smooth muscle cells with GIT1 small interfering RNA impaired cell migration. Both phospholipase Cγ and extracellular signal-regulated kinase 1/2 signaling were required for GIT1-dependent VSMC proliferation and migration, whereas only phospholipase Cγ was involved in GIT1-mediated VSMC apoptosis. CONCLUSIONS: GIT1 is a novel mediator of vascular remodeling by regulating VSMC proliferation, migration, and apoptosis through phospholipase Cγ and extracellular signal-regulated kinase 1/2 signaling pathways.Arteriosclerosis Thrombosis and Vascular Biology 02/2013; 33(5). DOI:10.1161/ATVBAHA.112.300966 · 5.53 Impact Factor
Article: Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat[Show abstract] [Hide abstract]
ABSTRACT: Cardiac fibrosis is a hallmark of heart disease and plays a vital role in cardiac remodeling during heart diseases, including hypertensive heart disease. Hexarelin is one of a series of synthetic growth hormone secretagogues (GHSs) possessing a variety of cardiovascular effects via action on GHS receptors (GHS-Rs). However, the role of hexarelin in cardiac fibrosis in vivo has not yet been investigated. In the present study, spontaneously hypertensive rats (SHRs) were treated with hexarelin alone or in combination with a GHS-R antagonist for 5 wk from an age of 16 wk. Hexarelin treatment significantly reduced cardiac fibrosis in SHRs by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content and reducing mRNA and protein expression of collagen I and III in SHR hearts. Hexarelin treatment also increased matrix metalloproteinase (MMP)-2 and MMP-9 activities and decreased myocardial mRNA expression of tissue inhibitor of metalloproteinase (TIMP)-1 in SHRs. In addition, hexarelin treatment significantly attenuated left ventricular (LV) hypertrophy, LV diastolic dysfunction, and high blood pressure in SHRs. The effect of hexarelin on cardiac fibrosis, blood pressure, and cardiac function was mediated by its receptor, GHS-R, since a selective GHS-R antagonist abolished these effects and expression of GHS-Rs was upregulated by hexarelin treatment. In summary, our data demonstrate that hexarelin reduces cardiac fibrosis in SHRs, perhaps by decreasing collagen synthesis and accelerating collagen degradation via regulation of MMPs/TIMP. Hexarelin-reduced systolic blood pressure may also contribute to this reduced cardiac fibrosis in SHRs. The present findings provided novel insights and underscore the therapeutic potential of hexarelin as an antifibrotic agent for the treatment of cardiac fibrosis.AJP Heart and Circulatory Physiology 07/2012; 303(6):H703-11. DOI:10.1152/ajpheart.00257.2011 · 4.01 Impact Factor
Article: EVI1 Acts as an Inducible Negative-Feedback Regulator of NF-kappa B by Inhibiting p65 Acetylation[Show abstract] [Hide abstract]
ABSTRACT: Inflammation is a hallmark of many important human diseases. Appropriate inflammation is critical for host defense; however, an overactive response is detrimental to the host. Thus, inflammation must be tightly regulated. The molecular mechanisms underlying the tight regulation of inflammation remain largely unknown. Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zinc finger transcription factor, plays important roles in normal development and leukemogenesis. However, its role in regulating NF-κB-dependent inflammation remains unknown. In this article, we show that EVI1 negatively regulates nontypeable Haemophilus influenzae- and TNF-α-induced NF-κB-dependent inflammation in vitro and in vivo. EVI1 directly binds to the NF-κB p65 subunit and inhibits its acetylation at lysine 310, thereby inhibiting its DNA-binding activity. Moreover, expression of EVI1 itself is induced by nontypeable Haemophilus influenzae and TNF-α in an NF-κB-dependent manner, thereby unveiling a novel inducible negative feedback loop to tightly control NF-κB-dependent inflammation. Thus, our study provides important insights into the novel role for EVI1 in negatively regulating NF-κB-dependent inflammation, and it may also shed light on the future development of novel anti-inflammatory strategies.The Journal of Immunology 05/2012; 188(12):6371-80. DOI:10.4049/jimmunol.1103527 · 5.36 Impact Factor
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ABSTRACT: Lung injury, whether induced by infection or caustic chemicals, initiates a series of complex wound-healing responses. If uncontrolled, these responses may lead to fibrotic lung diseases and loss of function. Thus, resolution of lung injury must be tightly regulated. The key regulatory proteins required for tightly controlling the resolution of lung injury have yet to be identified. Here we show that loss of deubiquitinase CYLD led to the development of lung fibrosis in mice after infection with Streptococcus pneumoniae. CYLD inhibited transforming growth factor-β-signalling and prevented lung fibrosis by decreasing the stability of Smad3 in an E3 ligase carboxy terminus of Hsc70-interacting protein-dependent manner. Moreover, CYLD decreases Smad3 stability by deubiquitinating K63-polyubiquitinated Akt. Together, our results unveil a role for CYLD in tightly regulating the resolution of lung injury and preventing fibrosis by deubiquitinating Akt. These studies may help develop new therapeutic strategies for preventing lung fibrosis.Nature Communications 04/2012; 3:771. DOI:10.1038/ncomms1776 · 10.74 Impact Factor
Article: Activation of Epidermal Growth Factor Receptor Is Required for NTHi-Induced NF-κB-Dependent Inflammation[Show abstract] [Hide abstract]
ABSTRACT: Inflammation is a hallmark of many serious human diseases. Nontypeable Haemophilus influenzae (NTHi) is an important human pathogen causing respiratory tract infections in both adults and children. NTHi infections are characterized by inflammation, which is mainly mediated by nuclear transcription factor-kappa B (NF-κB)-dependent production of proinflammatory mediators. Epidermal growth factor receptor (EGFR) has been shown to play important roles in regulating diverse biological processes, including cell growth, differentiation, apoptosis, adhesion, and migration. Its role in regulating NF-κB activation and inflammation, however, remains largely unknown. In the present study, we demonstrate that EGFR plays a vital role in NTHi-induced NF-κB activation and the subsequent induction of proinflammatory mediators in human middle ear epithelial cells and other cell types. Importantly, we found that AG1478, a specific tyrosine kinase inhibitor of EGFR potently inhibited NTHi-induced inflammatory responses in the middle ears and lungs of mice in vivo. Moreover, we found that MKK3/6-p38 and PI3K/Akt signaling pathways are required for mediating EGFR-dependent NF-κB activation and inflammatory responses by NTHi. Here, we provide direct evidence that EGFR plays a critical role in mediating NTHi-induced NF-κB activation and inflammation in vitro and in vivo. Given that EGFR inhibitors have been approved in clinical use for the treatment of cancers, current studies will not only provide novel insights into the molecular mechanisms underlying the regulation of inflammation, but may also lead to the development of novel therapeutic strategies for the treatment of respiratory inflammatory diseases and other inflammatory diseases.PLoS ONE 11/2011; 6(11):e28216. DOI:10.1371/journal.pone.0028216 · 3.53 Impact Factor
Article: G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart[Show abstract] [Hide abstract]
ABSTRACT: G-protein-coupled receptor (GPCR)-kinase interacting protein-1 (GIT1) is a multi-function scaffold protein. However, little is known about its physiological role in the heart. Here we sought to identify the cardiac function of GIT1. Global GIT1 knockout (KO) mice were generated and exhibited significant cardiac hypertrophy that progressed to heart failure. Electron microscopy revealed that the hearts of GIT1 KO mice demonstrated significant morphological abnormities in mitochondria, including decreased mitochondrial volume density, cristae density and increased vacuoles. Moreover, mitochondrial biogenesis-related gene peroxisome proliferator-activated receptor γ (PPARγ) co-activator-1α (PGC-1α), PGC-1β, mitochondrial transcription factor A (Tfam) expression, and total mitochondrial DNA were remarkably decreased in hearts of GIT1 KO mice. These animals also had impaired mitochondrial function, as evidenced by reduced ATP production and dissipated mitochondrial membrane potential (Ψ(m)) in adult cardiomyocytes. Concordant with these mitochondrial observations, GIT1 KO mice showed enhanced cardiomyocyte apoptosis and cardiac dysfunction. In conclusion, our findings identify GIT1 as a new regulator of mitochondrial biogenesis and function, which is necessary for postnatal cardiac maturation.Journal of Molecular and Cellular Cardiology 07/2011; 51(5):769-76. DOI:10.1016/j.yjmcc.2011.06.020 · 5.22 Impact Factor
Article: Direct relationship between levels of TNF-alpha expression and endothelial dysfunction in reperfusion injury.[Show abstract] [Hide abstract]
ABSTRACT: We previously found that myocardial ischemia/reperfusion (I/R) initiates expression of tumor necrosis factor-alpha (TNF) leading to coronary endothelial dysfunction. However, it is not clear whether there is a direct relationship between levels of TNF expression and endothelial dysfunction in reperfusion injury. We studied levels of TNF expression by using different transgenic animals expressing varying amounts of TNF in I/R. We crossed TNF overexpression (TNF(++/++)) with TNF knockout (TNF(-/-)) mice; thus we have a heterozygote population of mice with the expression of TNF "in between" the TNF(-/-) and TNF(++/++) mice. Mouse hearts were subjected to 30 min of global ischemia followed by 90 min of reperfusion and their vasoactivity before and after I/R was examined in wild type (WT), TNF(-/-), TNF(++/++) and TNF heterozygote (TNF(-/++), cross between TNF(-/-) and TNF(++/++)) mice. In heterozygote TNF(-/++) mice with intermediate cardiac-specific expression of TNF, acetylcholine-induced or flow-induced endothelial-dependent vasodilation following I/R was between TNF(++/++) and TNF(-/-) following I/R. Neutralizing antibodies to TNF administered immediately before the onset of reperfusion-preserved endothelial-dependent dilation following I/R in WT, TNF(-/++) and TNF(++/++) mice. In WT, TNF(-/++) and TNF(++/++) mice, I/R-induced endothelial dysfunction was progressively lessened by administration of free-radical scavenger TEMPOL immediately before initiating reperfusion. During I/R, production of superoxide (O(2) (.-)) was greatest in TNF(++/++) mice as compared to WT, TNF(-/++) and TNF(-/-) mice. Following I/R, arginase mRNA expression was elevated in the WT, substantially elevated in the TNF(-/++) and TNF(++/++) mice and not affected in the TNF(-/-) mice. These results suggest that the level of TNF expression determines arginase expression in endothelial cells during myocardial I/R, which is one of the mechanisms by which TNF compromises coronary endothelial function in reperfusion injury.Archiv für Kreislaufforschung 07/2010; 105(4):453-64. DOI:10.1007/s00395-010-0083-6 · 5.96 Impact Factor
Article: Vinpocetine inhibits NF-kappa B-dependent inflammation via an IKK-dependent but PDE-independent mechanism[Show abstract] [Hide abstract]
ABSTRACT: Inflammation is a hallmark of many diseases, such as atherosclerosis, chronic obstructive pulmonary disease, arthritis, infectious diseases, and cancer. Although steroids and cyclooxygenase inhibitors are effective antiinflammatory therapeutical agents, they may cause serious side effects. Therefore, developing unique antiinflammatory agents without significant adverse effects is urgently needed. Vinpocetine, a derivative of the alkaloid vincamine, has long been used for cerebrovascular disorders and cognitive impairment. Its role in inhibiting inflammation, however, remains unexplored. Here, we show that vinpocetine acts as an antiinflammatory agent in vitro and in vivo. In particular, vinpocetine inhibits TNF-alpha-induced NF-kappaB activation and the subsequent induction of proinflammatory mediators in multiple cell types, including vascular smooth muscle cells, endothelial cells, macrophages, and epithelial cells. We also show that vinpocetine inhibits monocyte adhesion and chemotaxis, which are critical processes during inflammation. Moreover, vinpocetine potently inhibits TNF-alpha- or LPS-induced up-regulation of proinflammatory mediators, including TNF-alpha, IL-1beta, and macrophage inflammatory protein-2, and decreases interstitial infiltration of polymorphonuclear leukocytes in a mouse model of TNF-alpha- or LPS-induced lung inflammation. Interestingly, vinpocetine inhibits NF-kappaB-dependent inflammatory responses by directly targeting IKK, independent of its well-known inhibitory effects on phosphodiesterase and Ca(2+) regulation. These studies thus identify vinpocetine as a unique antiinflammatory agent that may be repositioned for the treatment of many inflammatory diseases.Proceedings of the National Academy of Sciences 05/2010; 107(21):9795-800. DOI:10.1073/pnas.0914414107 · 9.81 Impact Factor
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ABSTRACT: Growth hormone-releasing peptides (GHRP) and ghrelin are synthetic and natural ligands of growth hormone secretagogue receptor (GHSR) respectively and are shown to exert protective actions on cardiac dysfunction. Because ghrelin has been reported to inhibit proinflammatory responses in human endothelium and GHSR has been identified in blood vessels, we hypothesized that GHRP could alleviate the development of atherosclerosis (As). Atherosclearosis was induced by a short period (4 days) of vitamin D(3) and chronic (three months) intragastric feeding of high fat emulsion (containing 0.5% propylthiouracil) in adult SD rats. Some As rats received chronic hexarelin (a variant of GHRP) injection (SC BID, 30 days) and normal rats received placebo as control. Significant atherosclerosis developed in animals fed with the emulsion. Serum total cholesterol and LDL-c increased, and HDL-c and aortic nitric oxide (NO) decreased significantly in As group. Hexarelin suppressed the formation of atherosclerotic plaques and neointima, partially reversed serum HDL-c/LDL-c ratio and increased the levels of serum NO and aortic mRNAs of eNOS, GHSR and CD36 in As rats. Hexarelin also decreased [(3)H]-TdR incorporation in cultured vascular smooth muscle cell (VSMC) and calcium sedimentation in aortic wall. Furthermore, foam cell formation induced by ox-LDL was decreased by hexarelin. In conclusion, hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in rats, possibly through upregulating HDL-c/LDL-c ratio, vascular NO production and downregulating the VSMC proliferation, aortic calcium sedimentation and foam cell formation. These novel anti-atherosclerotic actions of hexarelin suggest that the peptide might have a clinical potential in treating atherosclerosis.Peptides 11/2009; 31(4):630-8. DOI:10.1016/j.peptides.2009.11.007 · 2.61 Impact Factor
Article: Role of Ca2+/Calmodulin-Stimulated Cyclic Nucleotide Phosphodiesterase 1 in Mediating Cardiomyocyte Hypertrophy[Show abstract] [Hide abstract]
ABSTRACT: Cyclic nucleotide phosphodiesterases (PDEs) through the degradation of cGMP play critical roles in maintaining cardiomyocyte homeostasis. Ca(2+)/calmodulin (CaM)-activated cGMP-hydrolyzing PDE1 family may play a pivotal role in balancing intracellular Ca(2+)/CaM and cGMP signaling; however, its function in cardiomyocytes is unknown. Herein, we investigate the role of Ca(2+)/CaM-stimulated PDE1 in regulating pathological cardiomyocyte hypertrophy in neonatal and adult rat ventricular myocytes and in the heart in vivo. Inhibition of PDE1 activity using a PDE1-selective inhibitor, IC86340, or downregulation of PDE1A using siRNA prevented phenylephrine induced pathological myocyte hypertrophy and hypertrophic marker expression in neonatal and adult rat ventricular myocytes. Importantly, administration of the PDE1 inhibitor IC86340 attenuated cardiac hypertrophy induced by chronic isoproterenol infusion in vivo. Both PDE1A and PDE1C mRNA and protein were detected in human hearts; however, PDE1A expression was conserved in rodent hearts. Moreover, PDE1A expression was significantly upregulated in vivo in the heart and myocytes from various pathological hypertrophy animal models and in vitro in isolated neonatal and adult rat ventricular myocytes treated with neurohumoral stimuli such as angiotensin II (Ang II) and isoproterenol. Furthermore, PDE1A plays a critical role in phenylephrine-induced reduction of intracellular cGMP- and cGMP-dependent protein kinase (PKG) activity and thereby cardiomyocyte hypertrophy in vitro. These results elucidate a novel role for Ca(2+)/CaM-stimulated PDE1, particularly PDE1A, in regulating pathological cardiomyocyte hypertrophy via a cGMP/PKG-dependent mechanism, thereby demonstrating Ca(2+) and cGMP signaling cross-talk during cardiac hypertrophy.Circulation Research 09/2009; 105(10):956-64. DOI:10.1161/CIRCRESAHA.109.198515 · 11.09 Impact Factor
Article: Feed-forward signaling of TNF-alpha and NF-kappa B via IKK-beta pathway contributes to insulin resistance and coronary arteriolar dysfunction in type 2 diabetic mice[Show abstract] [Hide abstract]
ABSTRACT: We hypothesized that the interaction between tumor necrosis factor-alpha (TNF-alpha)/nuclear factor-kappaB (NF-kappaB) via the activation of IKK-beta may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. To test this hypothesis, endothelium-dependent (ACh) and -independent (sodium nitroprusside) vasodilation of isolated, pressurized coronary arterioles from mLepr(db) (heterozygote, normal), Lepr(db) (homozygote, diabetic), and Lepr(db) mice null for TNF-alpha (db(TNF-)/db(TNF-)) were examined. Although the dilation of vessels to sodium nitroprusside was not different between Lepr(db) and mLepr(db) mice, the dilation to ACh was reduced in Lepr(db) mice. The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected. The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice. Lepr(db) mice showed an increased insulin resistance, but NaSal improved insulin sensitivity. The protein expression of TNF-alpha and NF-kappaB and the protein modification of phosphorylated (p)-IKK-beta and p-JNK were greater in Lepr(db) mice, but NaSal attenuated TNF-alpha, NF-kappaB, p-IKK-beta, and p-JNK in Lepr(db) mice. The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Lepr(db) compared with mLepr(db) mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Lepr(db) mice. MG-132 or the neutralization of TNF-alpha reduced superoxide production in Lepr(db) mice. In conclusion, our results indicate that the interaction between NF-kappaB and TNF-alpha signaling induces the activation of IKK-beta and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes.AJP Heart and Circulatory Physiology 05/2009; 296(6):H1850-8. DOI:10.1152/ajpheart.01199.2008 · 4.01 Impact Factor
Article: G-Protein-Coupled Receptor Kinase Interacting Protein-1 Is Required for Pulmonary Vascular Development[Show abstract] [Hide abstract]
ABSTRACT: The G-protein-coupled receptor kinase interacting protein-1 (GIT1) is a multidomain scaffold protein that participates in many cellular functions including receptor internalization, focal adhesion remodeling, and signaling by both G-protein-coupled receptors and tyrosine kinase receptors. However, there have been no in vivo studies of GIT1 function to date. To determine essential functions of GIT1 in vivo, we generated a traditional GIT1 knockout mouse. GIT1 knockout mice exhibited approximately 60% perinatal mortality. Pathological examination showed that the major abnormality in GIT1 knockout mice was impaired lung development characterized by markedly reduced numbers of pulmonary blood vessels and increased alveolar spaces. Given that vascular endothelial growth factor (VEGF) is essential for pulmonary vascular development, we investigated the role of GIT1 in VEGF signaling in the lung and cultured endothelial cells. Because activation of phospholipase-Cgamma (PLCgamma) and extracellular signal-regulated kinases 1/2 (ERK1/2) by angiotensin II requires GIT1, we hypothesized that GIT1 mediates VEGF-dependent pulmonary angiogenesis by modulating PLCgamma and ERK1/2 activity in endothelial cells. In cultured endothelial cells, knockdown of GIT1 decreased VEGF-mediated phosphorylation of PLCgamma and ERK1/2. PLCgamma and ERK1/2 activity in lungs from GIT1 knockout mice was reduced postnatally. Our data support a critical role for GIT1 in pulmonary vascular development by regulating VEGF-induced PLCgamma and ERK1/2 activation.Circulation 04/2009; 119(11):1524-32. DOI:10.1161/CIRCULATIONAHA.108.823997 · 14.95 Impact Factor
Article: Synergistic induction of nuclear factor-κB by transforming growth factor-β and tumour necrosis factor-α is mediated by protein kinase A-dependent RelA acetylation[Show abstract] [Hide abstract]
ABSTRACT: The TGF-beta (transforming growth factor-beta) pathway represents an important signalling pathway involved in regulating diverse biological processes, including cell proliferation, differentiation and inflammation. Despite the critical role for TGF-beta in inflammatory responses, its role in regulating NF-kappaB (nuclear factor-kappaB)-dependent inflammatory responses still remains unknown. In the present study we show that TGF-beta1 synergizes with proinflammatory cytokine TNF-alpha (tumour necrosis factor-alpha) to induce NF-kappaB activation and the resultant inflammatory response in vitro and in vivo. TGF-beta1 synergistically enhances TNF-alpha-induced NF-kappaB DNA binding activity via induction of RelA acetylation. Moreover, synergistic enhancement of TNF-alpha-induced RelA acetylation and DNA-binding activity by TGF-beta1 is mediated by PKA (protein kinase A). Thus the present study reveals a novel role for TGF-beta in inflammatory responses and provides new insight into the regulation of NF-kappaB by TGF-beta signalling.Biochemical Journal 01/2009; 417(2). DOI:10.1042/BJ20080781 · 4.78 Impact Factor
Article: Differential regulation of Streptococcus pneumoniae-induced human MUC5AC mucin expression through distinct MAPK pathways.[Show abstract] [Hide abstract]
ABSTRACT: Human epithelial mucin, the major glycoprotein component of mucus, plays a critical role in host innate defense response against invading microbes by facilitating the mucociliary clearance. Excess mucin production, however, overwhelms the mucociliary clearance, resulting in not only defective mucosal defense but also conductive hearing loss in the middle ear and mucus obstruction in the airway. Indeed, mucus overproduction is a hall-mark of otitis media (OM) and chronic obstructive pulmonary diseases (COPD). Thus, tight regulation of mucin production plays an important role in maintaining an appropriate balance between beneficial and detrimental outcomes. We previously reported that Streptococcus pneumoniae (S. pneumoniae) up-regulates MUC5AC mucin expression via a positive MAPK ERK1/2 and a negative JNK1/2 signaling pathway. However, the signaling components including the up-stream activators and the down-stream transcription factors involved in these two path-ways remain largely unknown. In the present study, we showed that positive regulation of MUC5AC mucin expression by ERK1/2 is dependent on Ras-Raf-1 signaling pathway, whereas the negative regulation of MUC5AC expression by JNK1/2 is dependent on MEKK3. Moreover, transcriptional factor AP-1 acts as a key regulator for both of the positive and negative regulation of MUC5AC mucin expression as evidenced by mutagenesis analysis of two AP-1 sites in the promoter region of human MUC5AC mucin gene. Ras-Raf1-ERK1/2-dependent AP-1 activation positively regulates MUC5AC mucin induction by S. pneumoniae, whereas MEKK3-JNK1/2-dependent AP-1 activation negatively regulates it. Therefore, our data unveiled a novel signaling mechanism underlying the tight regulation of MUC5AC mucin induction by S. pneumoniae and may lead to the development of new therapeutic strategy for reducing mucus overproduction in both OM and COPD.American Journal of Translational Research 01/2009; 1(3):300-11. · 3.23 Impact Factor
Article: Role of TNF-α-induced reactive oxygen species in endothelial dysfunction during reperfusion injury[Show abstract] [Hide abstract]
ABSTRACT: We hypothesized that neutralization of TNF-alpha at the time of reperfusion exerts a salubrious role on endothelial function and reduces the production of reactive oxygen species. We employed a mouse model of myocardial ischemia-reperfusion (I/R, 30 min/90 min) and administered TNF-alpha neutralizing antibodies at the time of reperfusion. I/R elevated TNF-alpha expression (mRNA and protein), whereas administration of anti-TNF-alpha before reperfusion attenuated TNF-alpha expression. We detected TNF-alpha expression in vascular smooth muscle cells, mast cells, and macrophages, but not in the endothelial cells. I/R induced endothelial dysfunction and superoxide production. Administration of anti-TNF-alpha at the onset of reperfusion partially restored nitric oxide-mediated coronary arteriolar dilation and reduced superoxide production. I/R increased the activity of NAD(P)H oxidase and of xanthine oxidase and enhanced the formation of nitrotyrosine residues in untreated mice compared with shams. Administration of anti-TNF-alpha before reperfusion blocked the increase in activity of these enzymes. Inhibition of xanthine oxidase (allopurinol) or NAD(P)H oxidase (apocynin) improved endothelium-dependent dilation and reduced superoxide production in isolated coronary arterioles following I/R. Interestingly, I/R enhanced superoxide generation and reduced endothelial function in neutropenic animals and in mice treated with a neutrophil NAD(P)H oxidase inhibitor, indicating that the effects of TNF-alpha are not through neutrophil activation. We conclude that myocardial ischemia initiates TNF-alpha expression, which induces vascular oxidative stress, independent of neutrophil activation, and leads to coronary endothelial dysfunction.AJP Heart and Circulatory Physiology 10/2008; 295(6):H2242-9. DOI:10.1152/ajpheart.00587.2008 · 4.01 Impact Factor
Article: Tumor Suppressor Cylindromatosis Acts as a Negative Regulator for Streptococcus pneumoniae -induced NFAT Signaling[Show abstract] [Hide abstract]
ABSTRACT: Gram-positive bacterium Streptococcus pneumoniae is an important human pathogen that colonizes the upper respiratory tract and is also the major cause of morbidity and mortality worldwide. S. pneumoniae causes invasive diseases such as pneumonia, meningitis, and otitis media. Despite the importance of pneumococcal diseases, little is known about the molecular mechanisms by which S. pneumoniae-induced inflammation is regulated, especially the negative regulatory mechanisms. Here we show that S. pneumoniae activates nuclear factor of activated T cells (NFAT) signaling pathway and the subsequent up-regulation of inflammatory mediators via a key pneumococcal virulence factor, pneumolysin. We also demonstrate that S. pneumoniae activates NFAT transcription factor independently of Toll-like receptors 2 and 4. Moreover, S. pneumoniae induces NFAT activation via both Ca(2+)-calcineurin and transforming growth factor-beta-activated kinase 1 (TAK1)-mitogen-activated protein kinase kinase (MKK) 3/6-p38alpha/beta-dependent signaling pathways. Interestingly, we found for the first time that tumor suppressor cylindromatosis (CYLD) acts as a negative regulator for S. pneumoniae-induced NFAT signaling pathway via a deubiquitination-dependent mechanism. Finally, we showed that CYLD interacts with and deubiquitinates TAK1 to negatively regulate the activation of the downstream MKK3/6-p38alpha/beta pathway. Our studies thus bring new insights into the molecular pathogenesis of S. pneumoniae infections through the NFAT-dependent mechanism and further identify CYLD as a negative regulator for NFAT signaling, thereby opening up new therapeutic targets for these diseases.Journal of Biological Chemistry 06/2008; 283(18):12546-54. DOI:10.1074/jbc.M710518200 · 4.60 Impact Factor
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ABSTRACT: Abnormal growth of cardiac fibroblasts is critically involved in the pathophysiology of cardiac hypertrophy/remodeling. Hexarelin is a synthetic growth hormone secretagogue (GHS), which possesses a variety of cardiovascular protective activities mediated via the GHS receptor (GHSR), including improving cardiac dysfunction and remodeling. The cellular and molecular mechanisms underlying the effect of GHS on cardiac fibrosis are, however, not clear. In this report, cultured cardiac fibroblasts from 8-day-old rats were stimulated with ANG II or FCS to induce proliferation. The fibroblast proliferation and DNA and collagen synthesis were evaluated utilizing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, (3)H-thymidine incorporation, and (3)H-proline incorporation. The level of mRNA of transforming growth factor (TGF)-beta was evaluated by RT-PCR, and the active TGF-beta1 release from cardiac fibroblasts was evaluated by ELISA. The level of cellular cAMP was measured by radioimmunoassay. In addition, the effects of 3,7-dimethyl-l-propargylxanthine (DMPX; a specific adenosine receptor A(2)R antagonist) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; a specific A(1)R antagonist) were tested. It was found that incubation with 10(-7) mol/l hexarelin for 24 h 1) inhibited the ANG II-induced proliferation and collagen synthesis and the 5% FCS- and TGF-beta-induced increase of DNA synthesis in cardiac fibroblast and 2) reduced ANG II-induced upregulation of TGF-beta mRNA expression and active TGF-beta1 release from fibroblasts. Hexarelin increased the cellular level of cAMP in cardiac fibroblasts. DMPX (10(-8) mol/l) but not DPCPX abolished the effect of hexarelin on cardiac fibroblast DNA synthesis. It is concluded that hexarelin inhibits DNA and collagen synthesis and proliferation of cardiac fibroblasts through activation of both GHSR and A(2)R and diminishment of ANG II-induced increase in TGF-beta expression and release.AJP Heart and Circulatory Physiology 12/2007; 293(5):H2952-8. DOI:10.1152/ajpheart.00004.2007 · 4.01 Impact Factor
Article: TNF-alpha contributes to endothelial dysfunction by upregulating arginase in ischemia/reperfusion injury[Show abstract] [Hide abstract]
ABSTRACT: We tested whether tumor necrosis factor (TNF)-alpha increases arginase expression in endothelial cells as one of the primary mechanisms by which this inflammatory cytokine compromises endothelial function during ischemia-reperfusion (I/R) injury. Mouse hearts were subjected to 30 minutes of global ischemia followed by 90 minutes of reperfusion and their vasoactivity before and after I/R was examined in wild-type (WT), tumor necrosis factor knockout (TNF-/-), and TNF 1.6 (TNF++/++) mice. In WT mice, dilation to the endothelium-dependent vasodilator ACh was blunted in I/R compared with sham control. L-arginine or arginase inhibitor NOHA restored NO-mediated coronary arteriolar dilation in WT I/R mice. O2(-) production was reduced by eNOS inhibitor, L-NAME, or NOHA in WT I/R mice. In TNF-/- mice, I/R did not alter Ach-induced vasodilation and O2(-) production compared with sham mice. The increase in arginase expression that occurs during I/R in WT mice was absent in TNF-/- mice. Arginase expression was confined largely to the endothelium and independent of inflammatory cell invasion. Arginase activity was markedly lower in TNF-/-, but higher in WT I/R than that in WT sham mice. Our data demonstrate TNF-alpha upregulates expression of arginase in endothelial cells, which leads to O2(-) production then induces endothelial dysfunction in I/R injury.Arteriosclerosis Thrombosis and Vascular Biology 07/2007; 27(6):1269-75. DOI:10.1161/ATVBAHA.107.142521 · 5.53 Impact Factor
Article: Anti-LOX-1 rescues endothelial function in coronary arterioles in atherosclerotic ApoE knockout mice[Show abstract] [Hide abstract]
ABSTRACT: We hypothesized that atherosclerosis inhibits NO-mediated endothelium-dependent dilation of coronary arterioles through interaction of ox-LDL with its receptor, LOX-1, through the production of O2ÿ- in endothelial cells. We assessed the role of ox-LDL in endothelial dysfunction in a murine model of atherosclerosis (ApoE KO mice). Coronary arterioles from WT control and ApoE KO mice were isolated and pressurized without flow. Although dilation of vessels to endothelium-independent vasodilator SNP was not altered between ApoE KO and WT mice, dilation to the endothelium-dependent agonist, ACh was reduced in ApoE KO versus WT mice. Impaired vasodilation to ACh in ApoE KO mice is partially restored by NAD(P)H oxidase inhibitor, apocynin or DPI. Messenger RNA expression for NAD(P)H oxidases was higher in ApoE KO mice than that in WT and anti-LOX-1 treated ApoE KO mice. Anti-LOX-1, given in vivo, restored NO-mediated coronary arteriolar dilation in ApoE KO mice, but did not affect the endothelium-dependent vasodilation in controls. These results suggest that ox-LDL impairs endothelium-dependent NO-mediated dilation of coronary arterioles by activation of a signaling cascade involving LOX-1 and NAD(P)H oxidase expression.Arteriosclerosis Thrombosis and Vascular Biology 05/2007; 27(4):871-7. DOI:10.1161/01.ATV.0000259358.31234.37 · 5.53 Impact Factor
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ABSTRACT: We hypothesized that the inflammatory cytokine tumor necrosis factor-alpha (TNF) produces endothelial dysfunction in type 2 diabetes. In m Lepr(db) control mice, sodium nitroprusside and acetylcholine induced dose-dependent vasodilation, and dilation to acetylcholine was blocked by the NO synthase inhibitor N(G)-monomethyl-L-arginine. In type 2 diabetic (Lepr(db)) mice, acetylcholine- or flow-induced dilation was blunted compared with m Lepr(db), but sodium nitroprusside produced comparable dilation. In Lepr(db) mice null for TNF (db(TNF-)/db(TNF-)), dilation to acetylcholine or flow was greater than in diabetic Lepr(db) mice and comparable to that in controls. Plasma concentration of TNF was significantly increased in Lepr(db) versus m Lepr(db) mice. Real-time polymerase chain reaction and Western blotting showed that mRNA and protein expression of TNF and nuclear factor-kappaB were higher in Lepr(db) mice than in controls. Administration of anti-TNF or soluble receptor of advanced glycation end products attenuated nuclear factor-kappaB and TNF expression in the Lepr(db) mice. Immunostaining results show that TNF in mouse heart is localized predominantly in vascular smooth muscle cells rather than in endothelial cells and macrophages. Superoxide generation was elevated in vessels from Lepr(db) mice versus controls. Administration of the superoxide scavenger TEMPOL, NAD(P)H oxidase inhibitor (apocynin), or anti-TNF restored endothelium-dependent dilation in Lepr(db) mice. NAD(P)H oxidase activity, protein expression of nitrotyrosine, and hydrogen peroxide production were increased in Lepr(db) mice (compared with controls), but these variables were restored to control levels by anti-TNF. Advanced glycation end products/receptor of advanced glycation end products and nuclear factor-kappaB signaling play pivotal roles in TNF expression through an increase in circulating and/or local vascular TNF production in the Lepr(db) mouse with type 2 diabetes. Increases in TNF expression induce activation of NAD(P)H oxidase and production of reactive oxidative species, leading to endothelial dysfunction in type 2 diabetes.Circulation 02/2007; 115(2):245-54. DOI:10.1161/CIRCULATIONAHA.106.650671 · 14.95 Impact Factor
Top Journals
Chinese Academy of Medical SciencesPeping, Beijing, China
University of Rochester
Rochester, New York, United States
- Department of Microbiology and Immunology
University Center RochesterRochester, Minnesota, United States
Peking Union Medical College HospitalPeping, Beijing, China
University of Missouri
Columbia, Missouri, United States
- • Department of Internal Medicine
- • Department of Medical Pharmacology and Physiology
Texas A&M University
College Station, TX, United States
- Department of Veterinary Physiology & Pharmacology


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You can now invite anyone to meet at your favorite Starbucks.
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46 year old man | Fenton, MO, USA | Seeking women 40-50 within 50 miles of Crestwood, MO
I have an open heart and I'm not afraid to use it!
I am kind of burnt out on the bar scene and would really love to find that special someone to share life?s joys with. I am looking for an honest woman with a big heart. I love to love and I love to be loved. I am a good family man; I cherish my relationship with my daughter and my granddaughter as well as my parents and siblings.
Camping , Coffee and conversation , Cooking , Dining out , Movies/Videos , Music and concerts , Nightclubs/Dancing , Playing sports , Travel/Sightseeing , Watching sports , Wine tasting
Baseball, Billiards / Pool, Bowling, Cycling, Football, Golf, Running, Skiing, Swimming, VolleyBall, Walking / Hiking, Weights / Machines
I exercise 3-4 times per week.
I would love to visit Ireland, Napa Valley, and Hawaii, but somehow I always end up on a beach in the Caribbean so far. I have become a red wine enthusiast, so I love going to wineries or any nice bar/restaurant with a good wine list.
My favorite food is lobster or king crab legs. I love seafood. I am not a picky eater though. I can always find something on a menu to appeal to me. Sushi has become one of my favorite things to eat lately, so healthy and delicious. :)
I enjoy spending time outdoors. Especially in the spring and fall. I like to do anything on the water. I also enjoy golfing, camping, fishing. I'm not a fanatic about these things, just like to do them. I also enjoy playing sand volleyball.
Just finishing up Angels and Demons... any suggestions on what to read next?
Z{{Cta}} {{#if HasMoreInfo}} ?{{CtaSecondary}} {{/if}}
|What he is looking for
|6'0" (182cms)
|5'1" (154cms) to 5'11" (180cms)
|Body type:
|Athletic and toned
|Slender, About average, Curvy, Athletic and toned
|No preference
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|No Way, Occasionally
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I work for a large company here in town. I have been with them for almost 20 years now and I really like what I do. I have a good job with good people.
|$100,001 to $150,000
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|Yes, and they live away from home
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Finally completed my Bachelors degree, thinking about going for my Masters

subset: commoncrawl


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Pro-Russia rebels and commander flee Slavyansk in Ukraine
Published on Jul 5, 2014 3:27 PM
KIEV (AFP) - Ukraine's interior minister said on Saturday that most pro-Russian rebels and their top commander had fled their main eastern stronghold in what would be Kiev's biggest success of the nearly three-month campaign.
"This morning, intelligence reported that Girkin (Igor Strelkov) and a substantial part of the rebels had fled Slavyansk," Interior Minister Arsen Avakov said in reference to the industrial city of nearly 120,000 which the insurgents captured on April 6.
Ukraine alleges that Strelkov is a colonel in Russia's military intelligence unit know as the Chief Intelligence Directorate (GRU). Both Strelkov and Moscow deny any GRU link despite Western claims that the Kremlin is covertly funding and arming the uprising to destabilise Kiev's new pro-European leaders and retain control over over Russia-speaking eastern regions of Ukraine.
Avakov said in a Facebook post that the militias were fleeing to Gorlivka - a city of 260,000 about 50 kilometre southeast of Slavyansk that also remains largely under the militias' control.
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I Love Your ShopStyle: Soft Vanilla
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Chocolate is super delicious, but sometimes I'm in the mood for soft vanilla. Actually, ssandra's serene ensemble put me in the mood. Everything she chose is understated in color but pops in silhouette. I love the batwing top against the slim gray jeans. The yellow accents provide just enough oomph without messing with the calmness. Om.


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Whatever happened to Starship Exeter?
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February 3 2011, 12:04 AM
Admiral Buzzkill
Fleet Admiral
Re: Whatever happened to Starship Exeter?
USS Intrepid wrote:
Expo67 wrote:
Harlan Ellison and his commentary was never meant to be as such. He is a straight-shooter and he speaks his mind. He cuts through the BS and gets right to the point. Better those admirable and direct qualities than just beating around the bush.
I make no judgment on Ellison's qualities one way or the other. I was merely making an observation.
As in an actual observation, not a sideways swipe at someone I dislike.
Oh, I'm all for offending those who deserve it.
Admiral Buzzkill
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We don't know about you, but when we were 10, our idea of the ultimate in a cool look was a direct copy of Olivia Newton John at the end of Grease. A cropped leather jacket with big lapels? Big, teased hair? A sulky "yeah, so what" sneer? All present and correct for the pre-teen who wants to look like they might have an ounce of rebellion in them. Grrr.
And at 34 years old, Kate Moss has discovered this look, too. No matter she's the woman who pioneered edgy British fashion, and is held up as a natural style icon for the world to see. No, when the going gets tough, it's good to see that even Kate digs out her old videos for inspiration. [Photo: WireImage]


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...building hybrid clouds that can support any device from anywhere
Happy New Year to all private cloud architecture fans. OK, so I'm a little late with that. The private cloud architecture blog has been on hiatus for the last couple of months due to unforeseen and someforeseen reasons. The good news is that the blog drought is over and this year is going to be a banner year for the Private Cloud Architecture blog.
Two big pieces of news to start off the year:
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Tom Tom Shinder email@example.com Principal Knowledge Engineer, SCD iX Solutions Group Follow me on Twitter: http://twitter.com/tshinder Facebook: http://www.facebook.com/tshinder
Go Social with Private Cloud Architecture! Private Cloud Architecture blog Private Cloud Architecture Facebook page Private Cloud Architecture Twitter account Private Cloud Architecture LinkedIn Group Private Cloud TechNet forums TechNet Private Cloud Solution Hub Private Cloud on the TechNet Wiki


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Actor Brad Pitt hit in the face at Maleficent premiere
Published on May 29, 2014 2:15 PM
Hollywood (Reuters) - A man struck actor Brad Pitt in the face while he was signing autographs at the Hollywood premiere of a film starring partner Angelina Jolie, police said on Wednesday.
Pitt, a Golden Globe-winning actor, was at the premiere of Maleficent, at the El Capitan Theater in Hollywood, California, when the man leaped over a fence and hit him, said Sergeant Leonard Calderon of the Los Angeles Police Department.
Pitt was not seriously hurt and authorities quickly subdued the man, who was arrested for misdemeanor battery and remained in police custody on Wednesday night, Calderon said.
"The officers who were handling him said it looked like it was intentional, but at this point, it remains to be determined," Calderon said.
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text: Mother of Ronaldo's baby 'wants to see son' Ronaldo girlfriend may sue over 'nude' shots Kardashian plays down Ronaldo rumors Ronaldo, Kardashian 'spotted together' Mom of Ronaldo son was 'broke waitress' Ronaldo's baby son 'rushed to hospital' Ronaldo 'mistaken for Jersey Shore star' Ronaldo's girlfriend denies rumors Ronaldo 'names baby after himself' Ronaldo 'paid baby's mother £10m' Ronaldo on date after son's birth? Sister: 'Ronaldo happy about fatherhood' There's bad news, but there's good news too... Don't you wish you could be a fly on the wall? Radcliffe 'wants to look like Ronaldo' Ronaldo invites Kardashian to World Cup? Kardashian, Ronaldo "in daily contact" Ronaldo 'wins Kardashian from Bridge' Ronaldo accepts "substantial" libel damages Ronaldo named Armani underwear model Magician: 'I injured Cristiano Ronaldo' Hilton 'rejects' Ronaldo's romance hopes Ronaldo 'blanks ex-girlfriend Gallardo' Ronaldo's mom: 'Paris is just a friend' Paris Hilton reflects on Ronaldo fling Ronaldo 'investigated for attacking teenager' Ronaldo: 'Hilton is a really cool girl' Ronaldo 'pulls three girls' in LA bar Hilton 'will visit Ronaldo in Madrid' Ronaldo 'in love' with model ex Hilton: 'I'm getting to know Ronaldo' Hilton: 'I'm just friends with Ronaldo' Ronaldo 'boasts over Hilton fling' Hilton's ex 'furious' over Ronaldo fling Ronaldo 'spends evening with Hilton' Your afternoon helping of Cristiano Cristiano's at it again! R Kelly 'a real inspiration for Ronaldo' You can't beat a bit of Cristiano Model 'wants to bed Ronaldo'


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Corn Pepper Sausage Skillet
4 May 2010
|Italian pork sausage/Bulk pork sausage
|12 Ounce
|Chopped pepper
|1 Cup (16 tbs) (Green Or Red)
|Chopped onion
|1 Cup (16 tbs)
|Whole kernel corn/1 package of 16 ounces frozen whole kernel corn, thawed
|3 Cup (48 tbs) (Fresh)
|Garlic salt
|1⁄2 Teaspoon
|1⁄4 Teaspoon
|Chili powder
|1⁄4 Teaspoon
|Ground cumin
|1⁄4 Teaspoon
Crumble sausage into heavy 10-inch skillet or heavy foil pan.
Add green pepper and onion.
Place skillet, on covered grill, over medium-hot briquets about 15 minutes or until meat is browned, stirring once or twice.
Remove from grill; carefully drain off fat.
Stir in corn, garlic salt, pepper, chili powder and cumin; mix well.
Cover skillet with foil.
Grill, on covered grill, over medium-hot coals, 10 minutes longer or until heated through.
Garnish with tomato halves spread with cream cheese; top with parsley sprig.
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Corn Pepper Sausage Skillet Recipe


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hge new to me. Bruiser in hospital
- I took Bruiser to the vet this Tues and told him Bruiser has diarhea and blood in his stool. He gave usw an antibiotic and sent us home. Now after bleeding out his rectum he's back at the vet hospital being treated for HGE. I'm very worried.
- —Guest Patty
My 8yr old White German Shepard is....
- Still hanging on! On 5/21 I took my dogs to the beach, Sonny was very happy & active, swimming & running around with my 2 other dogs, no signs that something was wrong at all. Later he was displaying Extremely Strange Behavior! He then disappeared for 4 hrs. When he returned he seem as if he had been poisoned! After rushing him to the ER I was told that he had possibly suffered a heat stroke!!! They also mentioned Addisons Disease, Parvo & HGE??? Now he is on day 3 @ the vet! I have never witnessed or seen anything so horrible & the onset was almost immediate. I really am praying that he comes home soon. He is still unable to eat but is drinking water & is very responsive to his treatment, however we do not know how long it will take for him to fully recover & now that I know he is susceptible to this disease again... I WILL NEVER TAKE MY DOG BACK TO THE BEACH!!! The Dr believes that it was something he contracted from ingesting salt water containing parasites!
- —Guest Arlene
HGE episodes with my pet
- My Lil Dog Sparky had HGE in May. We took him home from the dog hospital on the 11 of may. HGE retured on the 22 of May. I hope some day they find out what causes this. Sparky had barely enough recovery before it came back. He is right now still at the vets. But doing good.
- —Guest Denise
- My black lab came down with this. didnt see any blood, but could smell it. he was dehydrated, lathargic, would not eat anything, even his favorite foods. my vet started iv immediatly, ran test , x ray. his kedneys were shutting down. it came back hge, which she(my vet suspected) he is home after three days of iv;s and meds. he gets 1/2 chicken breast two times a day.i inheirted this dog when my brother passed away, sure am glad i didnt loose him.
- —Guest lAURA kELSEY rANEY
Da-Budha Recovery
- My 13 yr old chow w/HGE. Look for any dead animals in yard & remove animal droppings. Spray yard with mix 1 cup bleach per gal of water. Toss all dog food, treats, old bones, & wash bowls, hard floors with 1 part bleach 9 parts water. Wash all bedding. Use only dog foods that include prebiotics or probiotics...or...add it to your pet's food. I use Flora Source for myself as it has 22 strands of healthy bacteria which prevent bad bacteria's from overtaking the digestive system. My husband and I have Crohn's disease. It works! I believe this to be the exact equivalent as Crohn's in humans. It is most likely due to a bad bacterial explosion in the dog's system. Do not let your dog near any dead animals or let them dig in your compost pile; dig up old bones, etc...Do NOT give your dog suspicious foods! If it can make you sick, it can just as easily make them sick. Stress just lowers the immunity and makes them more susceptible to HGE. Use metal food bowls instead of plastic. Make SURE y
- —Guest Valerie Orlando
hge pdsa
- Everyone be very allert. After noticing vomiting and no diarrhea we took our 7 month old to pdsa hospital. We were told Jo starve her for 24 hours and that doctor is not going to have a look at her before this is done. We waited. She didn't stop vomiting. Kept ringing and asking them saying its not normal. Eventuality, took her in myself saying its emergency. They gave her medication to stop vomiting. It did for sometime, but then started again. She still didn't drink. The very next day we took her in again. They injected her and told us to go home again. But nothing had changed. She was vomiting once, and had a normal poo. The 3rd morning we took her in again saying we are not taking her home, she wasn't very week, could still jump on our bed. Pdsa kept her over nigh. However, they said she is not improving. When I saw her at this hospital I was in shock. My dog was just crying, not moving, not reacting. They advised me to put her to sleep. We did. Why they didn't look at her earlier
- —Guest guest
My Cavalier had it twice
- My Cavalier King Charles Spaniel is currently at the vet's on a drip with this condition for the second time. She had it first when she was about 4 years old, very sudden onset of bloody vomiting and runny bloody stools, very listless, no interest in food. Because I got her to the vet for treatment quickly she recovered quickly. I was told that as she had it once it was a good possibility she would get it again. I have just returned from the emergency vets tonight having taken her in and she is hospitalised on a drip with a second bout of HGE aged 7 years. As she has had it before I knew the signs so she has received immediate treatment and I am hoping that she will pull through again this time - I am told that with prompt treatment most dogs survive this condition. Knowing the signs and quick treatment are the key to beating this condition. HGE is also not contagious which is a godsend as I have 2 other dogs.
- —Guest CavvieOwner
Do NOT wait to go to the vet
- Please, please go to your vet asap if your dog had multiple episodes of diarrhea or vomiting! My dog is very, very lucky to have survived this rare disease - only because I was able to monitor the symtomes.
- —Guest guest
- My dog who weights only 3 LBS full grown vomited 5 times at 9am on mothers day n she had 2 episodes of diarrhea but there was no blood in her diarrhea. She had no energy n didn't want to eat or drink. Due to her size the doctor said if I would have waited to bring her in I could have lost her. She lost 4 oz in 8 hours n for her weight size that is a lot for her to loose.
- —Guest Amie
- My dog who weights only 3 LBS full grown vomited 5 times at 9am on mothers day n she had 2 episodes of diarrhea but there was no blood in her diarrhea. She had no energy n didn't want to eat or drink. Due to her size the doctor said if I would have waited to bring her in I could have lost her. She lost 4 oz in 8 hours n for her weight size that is a lot for her to loose.
- —Guest Amie
Hemorrhagic GastroEnteritis
- my 12 year old collie, had been sick the night before with bile, but it hadn't stopped her stealing a piece of steak. But next day she started to reach small amounts of CLEAR SLIMY Fluid, tried to get her to drink which she then vomitted up like a water cannon, she was clingy, wimpering, and took on the praying position so took her off to the emergency vets, who said it was poss just a tummy upset, came home, she vomitted badly went into the garden and passed a huge pool of blood, the clour and consistency of Tomatoe ketcup. Straight back to the vets, who diagonossed HGE, My girl is not insured and as I know what I am doing the vet was happy for me to bring her home and do the job of the IV Drip. which meant syringing 2,5 ml into her mouth every 20 mins for the next 12 hours, by morning she had stopped crying and no more blood loss (although plenty during the night) and has actually asked for food, only a teaspoon, every 2 hrs of chicken and rice. important, get to vets imediantly.
- —Guest RebHayter
HGE currently
- My daisy is currently at the vet on IVF. Luckily for me she was at my parents and began to throw up blood and have bloody diarrhea. She became lethargic and was foaming at the mouth. Had she not been at my parents I probably would have lost her. My vet sad had we waited till morning to bring her in she would have passed away. She is not out of the woods yet but they say she is doing better. Take your dog in immediately if they begin to show any of these signs.
- —Guest Sarah
Hits fast, lots of blood
- 5 yrs old male Lhasa Apso threw up early yesterday afternoon. He had good stool that morning. By 8pm, he had bad diarrhea, was drooling excessively, still vomiting. By 2am, he was unable to hold his bowels and the stool was more blood than anything else. (explosive!) Blood was bright red and I was in a panic. Rushed him to the vet at 7am. My vet, knew exactly what it was, having seen many cases treated my dog with antibiotics and IV drip. The dehydration is the real problem. Its a day later, I just picked him up. He's doing much better though seems very tired from the episode. He's wagging his tail, and eating a little. He's on a bland diet for a few days along with meds to help soothe and heal his belly. The vet said she never heard of this until she moved from the north to the south. (We're in FL). I know its not uncommon to see blood in dog stool. This is something different. Get your dog to the vet asap. They decline fast once you notice the obvious symptoms.
- —Guest Ali
- I have a beautiful 3 year old Aussie that developed diarrhea on a Friday morning, I took her dog food away and gave her hamburger and rice. By Saturday morning she was doing much better. Sunday morning she started to vomit and after about 3 bowel movements It looked like solid blood. There were also small amounts of blood in her vomit. I found a vet that would see her (it was Sunday). She treated her with fluids and antivomiting shot and antibotics and also sent several medications home, both shots (she wont take a pill) and pills that I can mix in her food when she is eating. She is much better today. I would suggest to anyone to take your pet to the vet right away for frequent vomiting and diarrhea. My girl was just slightly dehydrated but it had only been about 6 hours. They can go down hill fast if not treated.
- —Guest Rhonda
My Beagle hit suddenly with HGE
- My 3 yr old Beagle Bowie had a diagnosed episode of Colitis a month ago which was loose and semi bloody stools. But now exactly 1 month later he is in the hospital with HGE. It came on suddenly within 24 hrs and started off with loose stools and within hours just blood running out of him. He had symptoms of tender abdomen and listlessness that quickly became foam vomiting at the mouth and blood in stools. No obstructions were found no parasites and no adrenal gland disease. He is on IV fluids and other medications as well as being tested for other conditions. For now they say it's HGE. I'm so glad I followed my intuition and rushed him to the ER because he would not have made it through the night. This sickness is quick and deadly so immediate attention is a must. $2000 dollars later and he's still not out of the woods but he's my everything so I will spare no expense until he's at home.
- —Guest Fina


text:
Listed below are NYIT's degree programs located at the Manhattan campus, in New York City. Click on the major in which you are interested to find out more!
NYIT-Abu Dhabi Honors Graduates in the Class of 2015
Police Officers Compete in NYIT's Cast Iron Chef Event
NYIT Engineering Degree Program Approved for United Arab Emirates
NYIT and NUPT To Co-Host Teaching and Learning Conference in China
New NYITCOM Physicians Celebrate at Hooding Ceremony


text:
Padres keep Bell, lose game in Arizona
"I admit, I was bummed out a bit when I wasn't traded," said Bell of July 31. "But I felt better by the time I went to bed that night."
Bell said he wasn't surprised that the Padres placed him on waivers. But he was surprised by the reaction, even from some of his younger teammates.
"A lot of people inside here didn't know what waivers meant," said Bell. "Some thought that if you went on waivers you were automatically gone. I had to explain it to some of the younger players. Almost every player is placed on waivers at some time. You're just not supposed to hear about it. It's supposed to be kept a secret."
And while Bell was dealing with the trade and waiver issues, his father's open-heart surgery to repair an aneurysm was twice delayed before being completed Tursday. Jim Bell is resting comfortably in a Round Rock, Tex., hospital.
On top of all that, the pitcher's daughter Jordyn suffered a ruptured ear drum last week.
Padres blanked
Arizona scored four in the first Friday night as five of the first six Diamondbacks batters got hits against Padres starter Wade LeBlanc. Although Padres catcher Nick Hundley was charged with two throwing errors in the inning, all four runs were earned.
"I don't know if I've ever seen a first inning like that," said LeBlanc, who had won his two previous starts. "There isn't a whole lot more to say.
"A couple balls that weren't hit hard found holes."
Meanwhile, the Padres were shut out for only the second time in the second half and the first time in 21 games. Both teams had nine hits.
"The difference was they bunched their hits in the first," said Padres manager Bud Black. "We couldn't get the hit to break through and keep the innings going."


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These are so easy to hang up in the limbs where the squirrels can't get to them. The birds love them, though they are a little messy but other birds come along & eat what falls on the ground. They're really nice in the winter when food sources are scarce.
Pros: attracts a variety of birds
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Should I play Skyrim again? Haven't played in 1 1/2 yrs and got no DLC or mods
Wait nvm I don't remember but I think I downloaded a couple mods. How do I find out if I did or not? Also should I download official HD texture pack or from mods?
Try not playing the non-terrible version of it called Morrowind
"HE are genius, firstly." - ASlaveObeys
Oakland510_ posted...
I guess I wanted to try out different classes as well as having a "perfect" game and I screwed up a good amount of times.
No such thing as classes in Skyrim, and no such thing as a "perfect" game.
Fight Science with Wood
http://gifs.gifbin.com/072010/1280303569_walmart-moonwalk.gif http://img32.imageshack.us/img32/8299/0341551001256026444.gif
TimePharaoh posted...
Try not playing the non-terrible version of it called Morrowind
If the OP can't keep a single game on Skyrim going for wanting to change his character he has no hope for it in Morrowind. Where your decisions actually mean something.
i5-2500k @ 4.5Ghz | H100 | Z77 Sabertooth | GTX 670 AMP! | 16GB G.Skill Ares | Samsung 830 128GB | 4GB Storage | HX650 | 650D
classes don't matter at all in skyrim. you can be a vampire mage Nord or a heavy armor two-handed weapon wood elf if you want and be just as good at it as any other race.. nothing matters.
Stop taking exactly what I'm saying and repeating it as if its exactly what I said because it is. -Cryptospuridium
Do people not make their own minds up any more?
Oakland510_ posted...
cody4783 posted...I question why you would keep restarting it. o.O
I think there are a lot of games that are better when you let go of this idea of wanting to play a "perfect game", not missing anything, and building the perfect character. I used to be like that , but a game like Skyrim is actually much more enjoyable if you just play it. My suggestion is to not even go online to check out where to find optimal items or how to craft them and what not. You will just end up bored, overpowered, stressed (from trying not to miss out on anything) and the sense of adventure and exploration quickly fades once you go and check online guides.
This is not an online competitive game anyway, I am not sure why people seem to be so obsessed with making the most effective character. Imo, just go for something you enjoy. I made the mistake of going for a known overpowered build, and the constant instant headshot 1-hit kill playstyle that I had to endure the rest of the game did not really make it enjoyable. I would have been better off using much less powerful, but much more fun magic for example.
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I guess I'll just wait for the DLC sales before I fully invest time in this game again. Also can you dudes answer my other questions?
Skyrim with mods is awesome. So much better than the base game. I've got about 20-ish running right now and the visuals and sounds are so immersive. I don't want to sound shallow, but Morrowind just doesn't cut it anymore for me. It was great when it was released but it has aged a lot as all games do.
It's funny, I can play all the old school 2D games (NES,SNES ect.) with no problem, but with 3D rpgs, I want modern visual/audio immersion. Sure, a lot of things were better with Morrowind, but overall it's showing too much age, even with mods, for me to give another serious run through of it. Hopefully the next game will incorporate some of Morrowind's best features (hand placed loot, less hand holding ect.) with the next game.
I know, I know... casual. peasant ect. Guilty as charged. Don't care. I've been gaming for almost 30 years now... labels don't really bother me.
"Even if you go by the cheapest price the game has ever been anywhere, psn+ would still be cheaper by at least 3 fold". DemonDog on psn+ vs. Steam
Oakland510_ posted...
Since it's been a long time how can I tell if I downloaded the official hd texture pack? I think I remember I downloaded it but it says I don't. I think I downloaded a mod or two, how do I find if I did or not?
Do you have Nexus? Are you running off of Steam? If you answered yes to both of those questions, start up Nexus and run the game. It should detect everything you have downloaded and update the ones you have as needed. If you don't have Nexus/Steam for Skyrim, I have no idea..
"Even if you go by the cheapest price the game has ever been anywhere, psn+ would still be cheaper by at least 3 fold". DemonDog on psn+ vs. Steam


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The biggest Ganesh Chaturthi attraction in the western suburbs is the Andhericha Raja at Veera Desai Road. The pandal organisers are known for introducing innovative themes for their pandal every year. This year too, they have a special theme; they have planned to replicate Tipu Sultan's magnificent Mysore palace. The 4,500 sq. ft pandal is being designed by artists Dharmesh Shah and Raju Sawla and the eight-and-a-half feet idol is scheduled to arrive on Saturday.
The speciality of the Bal Gopal Mitra Mandal in Vile Parle is that since the last seven years, the Ganesha idols and the decorations have been created using eco-friendly materials. 'Peshwa' is a tag that goes well with their idol as the manner in which they orchestrate the entire festival is grand. Apart from the eco-friendly decorators and their 14ft idol, there's another aspect, which is just as unique—the social message imparted through the event. The decorations at the pandal are built around various socially-conscious ideas that appeal to the masses. This year too, the organisers have a special message to share, but we will have to wait until the D-day arrives, as the organisers are not willing to disclose it yet.
The 15-year-old Sham Nirmal Mitra Mandal at Narsing Lane, Malad (W), is popular for its interestingly themed Ganesha idols. Every year, the mandal brings a plain Ganesha idol, which the volunteers (including children) decorate. The themes for the previous years include materials like shells, walnuts, Cadbury Gems, popcorn, Kurkure, tea-coffee-sugar, Polo mints, marbles, Mumbai bhel, dry fruits, among several others. The idol is decked up with such fun material, and is done entirely by the volunteers, without any professional help. This year, the theme for Ganesha Chaturthi is 'sports' and the mandal plans to use approximately 4,000 miniature-sized decorations, which include cricket bats, footballs, tennis rackets, etc.


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Woofer: When twitter's 140 character isn't enough
If your having trouble getting your point across on twitter in 140 characters or less then a new service has been launched to meet your verbose writing style.
Called Woofer, the spoof twitter micro-blogging website will offer its "wooferers" 1,400 characters instead of the paltry 140 to say the same thing just 10 times as long.
Just like the real twitter you can see the trending topics which are called "Popular woofs" and check out other woofer users.
Created purely for fun rather than having altruistic tendencies to take over the world, according to the chaps behind it you can woof it seems until you're in the dog house.


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Petition To Add Star Wars: Clone Wars To NetflixFeb 14, 2014 News 7 comments
Seeing that Star Wars: The Clone Wars is getting added to Netflix, it seems a bit unfair that it's predecessor doesn't. So I've decided to change that...
Supreme Chancellor/ Co- Founder: RC-100NICK
Vice Chancellor/ Founder: Delta289
grand admiral /(LONEWOLF) AKA shadowdude100
Canon, what is it? Yes it is a type of artillery fixture however it has another meaning. "To understand canon and continuity, the overall Star Wars saga should be looked at as a set of stories written by many different people which "document\" past "events." Although some stories are more reliable than others, they all are looked upon as part of the overall "history." It should also be remembered that all of these stories are simply that-stories. There are numerous errors that inevitably arise between the stories simply because different authors have their own ways of telling the story and may not have the time and resources to perfectly align the details."- Wookieepedia. Different types of canon are present. In Star Wars canon, the highest level of canon is the 6 films made by George Lucas, the next level of cannon includes Tv Series such as the 2 Clone Wars series one made by Dave Filloni and the other by Genndy Tartakovsky. Last but not least, the next level of canon is the Novels and Comics written and published by various authors and companies.
In Tolkien's franchise, the concept of Canon is a little more complex, for the subject is still being debated. Naturally, the highest canon material is works published by J. R. R. Tolkien and his son, Christopher Tolkien. "I would draw some of the great tales in fullness, and leave many only placed in the scheme, and sketched. The cycles should be linked to a majestic whole, and yet leave scope for other minds and hands, wielding paint and music and drama ." - J.R.R Tolkien. From 2001 to 2003, film maker, Peter Jackson released 3 films depicting his interpretation of The Lord Of the Rings trilogy. Certain events that Jackson cut out or re-wrote in his interpretation sparked controversy amongst some fans of the series. The biggest issue was that in Jackson's interpretation of The Return Of The King in 2003, depicted the Shire a happy and un-touched place after the destruction of the one ring. In Tolkien's book, when Frodo returns from destroying the ring, the Shire is in ruins, industrialized, and secretly under the control of Saruman. Despite the differences, Jackson's films are loved and enjoyed and will continue to be enjoyed for years to come.
The goal of this group, The Alliance To Restore Canon, is to compile and discuss contradictions with canon in various sci-fi and fantasy franchises. Not to criticize the franchises but to simply make note of the contradictions and ask "how does this contradict? Why does this contradict? Is it an accident or on purpose? Is it directly from the franchise or one of the many independent authors?". So again, we are not criticizing the franchises, just wondering why these contradictions exist and why have they not been fixed. Something as simple as deeming it uncanon can fix a contradiction. Like the 2008 Clone Wars series for example, George Lucas has not yet officially declared the series canon and whether or whether not the series will re-write existing canon entirely or simply add to the time- line that had been established before 2008.
At the moment, the Alliance To Restore Canon is mostly made up of star wars fans, but we are open to other sci-fi and fantasy series so if you have found contradictions in other franchises and feel as if your not being heard, don't be afraid to join. All are welcome and all are treated with respect.
Seeing that Star Wars: The Clone Wars is getting added to Netflix, it seems a bit unfair that it's predecessor doesn't. So I've decided to change that...
With the Expanded Universe hierarchy now eliminated, the opportunity has arisen to bring back what has been reticoned, however this requires a little...
The clusterfunk that is the Star Wars Timeline is going to be cleaned up a bit and YOUR favorite EU stories may be thrown in the proverbial trash.
The 23 year reign of Dark Horse Comic will soon be at an end come 2015. Read the article for more information.
Crucial release information: Please Read* Crucial release information: Please Read* Crucial release information: Please Read
Lucas is the reason the were not allowed to use Alpha 17 as Anakin's clone and the crew had to create Rex. Lucas said it would stray to far from cannon from the 2004 series. The Clone Wars crew pretty much has to get approval from Lucas to do almost anything.
But its a bit exaggerated which is why I Don't like it, since the Republic win EVERY battle Its not as good as the old one.
The early episodes with few characters and ships is because the animation department had poor techniques to produce models for the show which is why they reused a lot of them over and over again. The newer episodes have more characters and ships because they have improved their animation. Recent space battles have been filled with many of the CIS ships and a few more classes of Republic ships.
The show is not about the good guys always winning, it's about the Republic being destroyed by Corruption from within and Sidious and Dooku creating the Republic's downfall and Anakin's fall to the Darkside.
did you also notice that every battle that doesnt have some special ship in it is always ventors vs munificients?
yeah.. since when does the CIS use 50 munificents in every battle? and nothing else.. its total tosspot!
what does Tosspot mean? XD sorry yank over here
Wikipedia says: 'Tosspot is a British slang insult, which can mean, depending on the context, a drunkard, a masturbator, or an objectionable person'
I didn't know it meant wanker too!
thank you. if u need to know any yankee slang, im your guy
reading the little paragraph at the top, i support this fully. i is one of the overzealous nerds who hates the canonical contradictions. such as ahsoka. anakin was made a knight ( the minimum requirement for a padawaan)roughly 3 months before coruscant. ahsoka comes in about 4 months in at best. anakin cannot have an apprentice. malevalence, also false. mandolorians did not have a dutches, especially a pasifist one, despite the fact that the large majority of the population was farmers,
there was no dutchess, and the deathwatch had been disbanded during this period of time. i could go on, but you dont want me too.
and that was the greatest tv show, and was that ssissi tiin?
welcome to the group!
uhhhh i dont know much about moddb (i actually joined just to comment on thrawn's revenge) so excuse me if i seem stupid and dont know how to join or if its controled by others.
Right side of the page, go down till yo see 'join this group'
Promote Alliance to Restore Canon (ARC) on your homepage or blog by selecting a button and using the embed code provided (more).


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Club competitions
National team competitions
Every second week leading up to EuroBasket 2013, fibaeurope.com's undercover expert ranks the 24 teams headed for Slovenia. Join the discussion on facebook now.This week Russia and Serbia begin their trip back to the top.
Disclaimer: These rankings in no way reflect any official ranking system. They are purely subjective and are intended to be viewed as such.
In Marc Gasol Spain have the best defender in the NBA regular season and in Serge Ibaka the second-best shot blocker. Good luck breaking through this front court.
Eight teams left in the NBA play-offs and two of them are led by Frenchmen. Joakim Noah has resembled a stock truck, loading the Bulls onboard and taking them one step closer to their final destination.
Andrea Trinchieri has announced that anything short of a podium finish would be a disappointment. Who are we to doubt him - especially when he claims to be bringing Vasilis Spanoulis along for the ride.
Mindaugas Kuzminskas and the Lavrinovic brothers have hit double figures in the first three games of the best-of-seven LKL Finals, providing more options in a crowded Lithuanian front court.
Eurocup: Check. EuroChallenge: Check: Euroleague: Pending. Russian teams have dominated basketball competitions in Europe this year with the Russians on the verge of an impressive treble.
No chance of Slovenian players becoming worn out prior to summer with all NBA-based national team players already finished for the season. Erazem Lorbek has also been quiet in the Euroleague play-offs for Barcelona. Will be hoping to change that this weekend.
Nenad Krstic is aging like a fine wine, making the All-Euroleague team for a second consecutive season, whilst CSKA and national teammate Milos Teodosic made the second team.
Bojan Dubljevic and Milko Bjelica are both expected to go deep into the ACB play-offs with their respective teams, but for a number of other key national team players, an elongated period on the sidelines awaits them.
Ante Tomic has had a breakthrough season for Barcelona, earning himself a post spot on the All-Euroleague team posting career-high stats to be the only Barcelona player to make the team.
No Turkish teams are going to be making the trip to London this season for the EuroLeague Final Four and no Turkish players are remaining in the NBA playoffs.
Dennis Schroeder is touted as a first-round NBA draft selection and should be an automatic pick for the national team come summer. Meanwhile, Tim Olhbrecht has helped take the Rio Grande Valley Vipers to a D-League title.
Finally some positive news for the Azzuri! Marco Belinelli is putting in some of his biggest offensive performances of the season for the Bulls in the NBA play-offs whilst Luigi Datome has been voted Player of the Season in the Serie-A League.
Yotam Halperin is a shining light for Israeli prospects, playing a key role for Bayern in their opening game of the Beko BBL play-offs. However, one man does not maketh the team, hence the one place dropping.
Mirza Teletovic failed to feature in the NBA play-offs as the Brooklyn Nets became victims of the Bulls in the first round whilst Igokea failed to back up their ABA regular season top placing, getting knocked out in the ABA Final Four semis.
Drew Sullivan shone on the home front this season - taking the Leicester Riders to UK glory with a game-high 24 points in the gold medal game. Could have a bigger presence this summer following the withdrawal of Luol Deng.
With many new faces expected to be on board this time round for F.Y.R. of Macedonia keep an eye out for sharp-shooting point guard Aleksandar Kostoski. has been tearing it up domestically this season for Kumanovo, scoring 20.7 points-a-game.
Perhaps expect some new names in the Finnish squad this summer with only two current national team players - Mikko Koivisto and Matti Nuutinen - making it to the gold-medal series of the Korisliiga.
Is Dirk Bauermann going to bring a clean slate to the Polish national team? The way the Polish play-offs are progressing, do not be surprised to see some new faces in red and white in Slovenia.
EuroChallenge club Sodertalje Kings have come out on top of the Swedish Basketligan this season, meaning that more players than just Dino Pita from amongst their ranks may be in line for national team honours this summer.
Ukraine's top scorer during the qualification campaign, Sergiy Gladyr - one of the few Ukrainians playing outside of their home borders - is about to have his season cut short in Spain with Fuenlabrada well outside the play-off cut-off line.
Concern for the Latvian backcourt with both Janis Blums and Janis Strelnieks failing to make an impact in the play-offs of their respective competitions. Some strong performances from Davis Bertans in the ABA Final Four goes some way to even the ledger.
Zaragoza is play-off bound in the ACB League and Sam Van Rossom has been at the forefront of their success, consistently playing over 20 minutes a night throughout May.
CEZ Nymburk may be having something of a forgettable season as a whole, but on an individual note Petr Benda - the Czech's top scorer during qualification - has been solid under the hoops shooting at over 60% from the field in the Czech domestic league.
Giorgi Shermadini will be anticpating his trip to London this weekend as part of the Olympiacos setup. However, do not expect the big man to make too much of an impact with his input of the bench throughout the season at best minimal.


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The City Council is currently undertaking a review of Ward Forums as part of a wider look at the way we engage with local people to make sure that the mechanisms we use are as effective as possible and use our resources in the best way. A report will be expected to be considered by Cabinet within the next few months and this report will be publically available. The review aims to ensure that future meetings are well planned, publicised and attended and fit within a broader approach to engagement.
Ward Forums are a way of taking a closer look at the places where we live and making life in our neighbourhoods better together.
They are an important way for local people to get involved and get things done on their doorstep and are organised by the council to enable the public to stake a claim for changes to happen locally.
The forums meet regularly between 7.00pm - 9.00pm, except St. Michael's (6.00pm - 8.00pm) and Upper Stoke (6.30pm - 8.30pm). They meet in local venues and are led by one of the three councillors who represent each of the 18 wards on Coventry City Council.
The forums also include other people who care about local neighbourhoods - council staff, police, community and voluntary groups - and that's why we want people like you, people who can talk about life on your doorstep and the things that matter most to your community.
It's easy to get involved - just turn up on the night and we'll make sure you feel welcome.
Details and a full list of the next meetings in your area:
If you are not sure which ward you live in you can check using our "Who is your Councillor?" search. It will also give you the names and contact details for your local councillors.
Please complete this online form to register/amend your details so you can be updated about Ward Forums Meetings.
Email: firstname.lastname@example.com
Tel: 024 7683 3049The Council House


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Krasovic: What happened to Antonio Gates?
Blocking failures led to five of the six sacks of Rivers. Four of those five were one-one-one victories by Ravens rushers: Edge rusher Paul Kruger, who has become Baltimore's top sacker since succeeding Jarrett Johnson, bull-rushed Jeromey Clary and got to Rivers in 2.4 seconds to end San Diego's first drive; Terrell Suggs, rushing from the edge, beat Michael Harris (2.5) for his second sack since returning from a torn Achilles; notching his first two sacks of the season, 3-4 end Arthur Jones (2.6. 2.3) blew past Rex Hadnot, making his first start this year for the injured Tyronne Greene. A clever zone blitz allowed Ellerbe (2.3) to halt San Diego's second drive, and rookie Courtney Upshaw (4.6) picked up a coverage sack.
Every week, the Chargers should tell Antwan Barnes the Ravens are the opponent. One year after registering four sacks against his former team, Barnes won several rushes against Baltimore's ponderous tackles. The play before Rice devastated the Chargers, Barnes knocked the ball from Joe Flacco for a 9-yard loss. "I don't think they'll be focusing only on me," Barnes said on Friday. Maybe next time.