Cyclooxygenase-2 Signalling Pathway in the Cortex is Involved in the Pathophysiological Mechanisms in the Rat Model of Depression

Background: In several mammals, subfertility or infertility associated with endometritis was reported. Although there have been studies about endometritis in bitches, the pathophysiological mechanisms are not completely known.Aim: This study aimed to evaluate the immunohistochemical expression of Cyclooxygenase 2 (COX2) in clinically healthy bitches with normal uterine tissue and bitches with endometritis.Methods: Forty-eight mixed breed bitches in diestrus were used. Uterine biopsies were collected for diagnosis [normal endometrium (n = 15; NE), cystic endometrial hyperplasia (n = 1), atrophy (n= 2), acute endometritis (n = 9; AE), subacute endometritis (n = 7; SE), and chronic endometritis (n = 14; CE)]. Immunostaining and quantification of positively stained cells was performed on full-thickness uterine biopsies. Data were analyzed by the GLIMMIX procedure of SAS.Results: COX2 immunostaining was scattered and restricted to cells in the stroma in bitches with NE. However, in bitches with endometritis, strong staining was observed in the luminal epithelium, glandular epithelium, and stromal cells. Staining was also observed in inflammatory cells localized in the stroma as well as inside of the glands. The percentage of COX2 positive stromal cells in bitches with AE, SE, and CE was significantly higher compared with NE (p < 0.005). In addition, the percentage of COX2 positive stromal cells in bitches with SE, and CE was significantly lower compared with AE (p < 0.003).Conclusion: COX2 could be involved in the pathophysiological mechanisms producing endometritis without the presence of cystic endometrial hyperplasia in bitches. However, further researches on this topic are required. Keywords: Bitch, COX2, Endometritis, Immunohistochemical.

Download Full-text

Cyclooxygenase-2 Mediates Hyperbaric Oxygen Preconditioning in the Rat Model of Transient Global Cerebral Ischemia

Stroke ◽

10.1161/strokeaha.110.604421 ◽

2011 ◽

Vol 42 (2) ◽

pp. 484-490 ◽

Cited By ~ 63

Author(s):

Oumei Cheng ◽

Robert P. Ostrowski ◽

Bihua Wu ◽

Wenwu Liu ◽

Chunhua Chen ◽

...

Keyword(s):

Cerebral Ischemia ◽

Hyperbaric Oxygen ◽

Rat Model ◽

Cyclooxygenase 2 ◽

Global Cerebral Ischemia ◽

Transient Global Cerebral Ischemia ◽

Hyperbaric Oxygen Preconditioning

Download Full-text

Schistosomiasis-associated pulmonary arterial hypertension: a systematic review

European Respiratory Review ◽

10.1183/16000617.0089-2019 ◽

2020 ◽

Vol 29 (155) ◽

pp. 190089 ◽

Cited By ~ 3

Author(s):

Daniela Knafl ◽

Christian Gerges ◽

Charles H. King ◽

Marc Humbert ◽

Amaya L. Bustinduy

Keyword(s):

Systematic Review ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Transforming Growth Factor ◽

Meta Analysis ◽

Signalling Pathway ◽

Pathophysiological Mechanisms ◽

Clinical Registries ◽

Life Threatening ◽

Pulmonary Arterial

Schistosomiasis-associated pulmonary arterial hypertension (Sch-PAH) is a life-threatening complication of chronic hepatosplenic schistosomiasis. It is suggested to be the leading cause of pulmonary arterial hypertension (PAH) worldwide. However, pathophysiological data on Sch-PAH are scarce. We examined the hypothesis that there are pronounced similarities in pathophysiology, haemodynamics, and survival of Sch-PAH and idiopathic PAH (iPAH).This systematic review and meta-analysis was registered in the PROSPERO database (identifier CRD42018104066). A systematic search and review of the literature was performed according to PRISMA guidelines for studies published between 01 January 1990 and 29 June 2018.For Sch-PAH, 18 studies evaluating pathophysiological mechanisms, eight studies on haemodynamics (n=277), and three studies on survival (n=191) were identified. 16 clinical registries reporting data on haemodynamics and survival including a total of 5792 patients with iPAH were included for comparison. Proinflammatory molecular pathways are involved in both Sch-PAH and iPAH. The transforming growth factor (TGF)-β signalling pathway is upregulated in Sch-PAH and iPAH. While there was no difference in mean pulmonary artery pressure (54±17 mmHg versus 55±15 mmHg, p=0.29), cardiac output (4.4±1.3 L·min−1versus 4.1±1.4 L·min−1, p=0.046), and cardiac index (2.6±0.7 L·min−1·m−2versus 2.3±0.8 L·min−1·m−2, p<0.001) were significantly higher in Sch-PAH compared to iPAH, resulting in a lower pulmonary vascular resistance in Sch-PAH (10±6 Woods units versus 13±7 Woods units, p<0.001). 1- and 3-year survival were significantly better in the Sch-PAH group (p<0.001).Sch-PAH and iPAH share common pathophysiological mechanisms related to inflammation and the TGF-β signalling pathway. Patients with Sch-PAH show a significantly better haemodynamic profile and survival than patients with iPAH.

Download Full-text