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Background: The articularis genus muscle pulls the suprapatellar pouch upwards when the knee joint is extended, preventing mechanical impingement of the joint capsule which theoretically could cause anterior knee pain. However, few anatomical studies have addressed this muscle. Here we present the precise morphology of articularis genus. Materials and methods: A total of 22 (13 male and 9 female) adult cadavers with no pathological conditions in the knee joints were examined during educational dissection at Nagoya City University Medical School in 2012. After exclusion of 4 joints due to their flexion contracture, 40 knee joints (18 right and 22 left) were analysed. We performed statistical analysis on anatomical laterality and the difference of sizes among lateral, medial and central branches and studied the correlation of the length and area of the articularis genus muscle to the length and cross-section area of the femur. Results and Conclusions: The average number of branches of the deep layer of the articularis genus muscle was 2.7 ± 0.5, the mean length of all branches was 5.4 ± 1.3 cm and the mean area of all branches was 5.5 ± 2.6 cm². There was no significant correlation between the length and area of the articularis genus muscle to the length and cross-section area of the femur. There was no significant laterality in central, medial and lateral branches; however we found that the medial branch was statistically longer and larger than the lateral branch on either knee. This could be contributing to prevention of lateral dislocation of the patella. (Folia Morphol 2014; 73, 3: 309–313)
We investigated the cyclooxygenase (COX) isoforms as well as prostaglandin E receptor EP subtypes responsible for acid-induced gastric HCO3- secretion in rats and EP receptor-knockout (-/-) mice. Under urethane anesthesia, a chambered stomach (in the presence of omeprazole) was perfused with saline, and HCO3-secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Mucosal acidification was achieved by exposing the stomach for 10 min to 50 or 100 mM HCl. Acidification of the mucosa increased the secretion of HCO3- in the stomach of both rats and WT mice, in an indomethacin-inhibitable manner. The acid-induced gastric HCO3- secretion was inhibited by prior administration of indomethacin and SC-560 but not rofecoxib in rats and mice. Acidification increased the PGE2 content of the rat stomach, and this response was significantly attenuated by indomethacin and SC-560 but not rofecoxib. This response was also attenuated by ONO-8711 (EP1 antagonist) but not AE3-208 (EP4 antagonist) in rats and disappeared in EP1 (-/-) but not EP3 (-/-) mice. PGE2 increased gastric HCO3- secretion in both rats and WT mice, and this action was inhibited by ONO-8711 and disappeared in EP1 (-/-) but not EP3 (-/-) mice. These results support a mediator role for endogenous PGs in the gastric response induced by mucosal acidification and clearly indicate that the enzyme responsible for production of PGs in this process is COX-1. They further show that the presence of EP1 receptors is essential for the increase in the secretion of HCO3- in response to mucosal acidification in the stomach.
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