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Sana Hireche Omar Bouaziz Djahida Djenna Sabrina Boussena Rachida Aimeur Rachid Kabouia El Hacène Bererhi 《Tropical animal health and production》2014,46(2):467-473
A cross-sectional study was carried out to estimate prevalence of Chlamydophila spp. antibodies and to investigate risk factors associated with chlamydial infection in 552 ewes between March 2011 and January 2012 in the province of Constantine. Anti-Chlamydophila antibodies were detected using an indirect enzyme-linked immunosorbent assay kit in 24.5 % of examined sera. Of the herds, 70.4 % had at least one seropositive animal. A pretested structured questionnaire was administered in order to collect information on individual animal health and herd management practices. Chi-square analysis and multivariable logistic regression model were used to identify risk factors related to Chlamydophila seropositivity. Univariable analysis revealed 17 variables with p?<?0.25 that were offered to the multivariable logistic regression model which in turn identified 12–23 months age group (OR?=?5.903, 95 % CI (OR)?=?1.690; 20.618) and not using disinfectants (OR?=?2.099, 95 % CI (OR)?=?1.314; 8.065) as risk factors for Chlamydophila spp. seropositivity. Moreover, occurrence of stillbirth problem (OR?=?3.682, 95 % CI (OR)?=?1.825; 7.430) and 5–10 % mortality rate in young lambs (OR?=?2.584, 95 % CI (OR)?=?1.058; 6.310) were significantly associated with seropositivity to Chlamydophila spp. On the other hand, availability of veterinary service was identified as a protective factor (OR?=?0.161, 95 % CI (OR)?=?0.051; 0.511). 相似文献
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Holm TM Habashi JP Doyle JJ Bedja D Chen Y van Erp C Lindsay ME Kim D Schoenhoff F Cohn RD Loeys BL Thomas CJ Patnaik S Marugan JJ Judge DP Dietz HC 《Science (New York, N.Y.)》2011,332(6027):358-361
Transforming growth factor-β (TGFβ) signaling drives aneurysm progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit this signaling cascade are in clinical trials. TGFβ can stimulate multiple intracellular signaling pathways, but it is unclear which of these pathways drives aortic disease and, when inhibited, which result in disease amelioration. Here we show that extracellular signal-regulated kinase (ERK) 1 and 2 and Smad2 are activated in a mouse model of MFS, and both are inhibited by therapies directed against TGFβ. Whereas selective inhibition of ERK1/2 activation ameliorated aortic growth, Smad4 deficiency exacerbated aortic disease and caused premature death in MFS mice. Smad4-deficient MFS mice uniquely showed activation of Jun N-terminal kinase-1 (JNK1), and a JNK antagonist ameliorated aortic growth in MFS mice that lacked or retained full Smad4 expression. Thus, noncanonical (Smad-independent) TGFβ signaling is a prominent driver of aortic disease in MFS mice, and inhibition of the ERK1/2 or JNK1 pathways is a potential therapeutic strategy for the disease. 相似文献
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Habashi JP Doyle JJ Holm TM Aziz H Schoenhoff F Bedja D Chen Y Modiri AN Judge DP Dietz HC 《Science (New York, N.Y.)》2011,332(6027):361-365
Angiotensin II (AngII) mediates progression of aortic aneurysm, but the relative contribution of its type 1 (AT1) and type 2 (AT2) receptors remains unknown. We show that loss of AT2 expression accelerates the aberrant growth and rupture of the aorta in a mouse model of Marfan syndrome (MFS). The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm progression in the mice; full protection required intact AT2 signaling. The angiotensin-converting enzyme inhibitor (ACEi) enalapril, which limits signaling through both receptors, was less effective. Both drugs attenuated canonical transforming growth factor-β (TGFβ) signaling in the aorta, but losartan uniquely inhibited TGFβ-mediated activation of extracellular signal-regulated kinase (ERK), by allowing continued signaling through AT2. These data highlight the protective nature of AT2 signaling and potentially inform the choice of therapies in MFS and related disorders. 相似文献
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Habashi JP Judge DP Holm TM Cohn RD Loeys BL Cooper TK Myers L Klein EC Liu G Calvi C Podowski M Neptune ER Halushka MK Bedja D Gabrielson K Rifkin DB Carta L Ramirez F Huso DL Dietz HC 《Science (New York, N.Y.)》2006,312(5770):117-121
Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder. 相似文献
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