RESUMO
In humans and dogs, especially brachycephalics, enlargement of the esophageal hiatus and insufficiency have been correlated with decreased lower esophageal sphincter pressure and increased frequency of gastroesophageal reflux. In cats, it has been suggested that gastroesophageal reflux occurs frequently with upper airway obstruction, including brachycephalics. Therefore, the purpose of the study was to determine whether the esophageal hiatal cross-sectional surface area (EH-CSA) differs between brachycephalic and nonbrachycephalic cats. Clinical records and CT images of cats that underwent thoracic, abdominal, and entire skull CT at multiple centers between January 2015 and September 2022 were retrospectively reviewed. Esophageal hiatal parameters (EH-CSA, EH-long axis diameter, and EH-short axis diameter) and craniometric indices (cranial index, skull index, and facial index) were measured by using multiplanar reconstruction, and the correlation of craniometry with EH-CSA was investigated. Ninety-eight cats (group 1: 42 brachycephalic cats and group 2: 56 nonbrachycephalic cats) were included. Esophageal hiatal cross-sectional surface area in brachycephalic cats was significantly larger than that in nonbrachycephalic cats. The EH-CSA significantly increased with the craniometric indices tending to increase with brachycephalism. The present study contributes to the veterinary literature by providing the EH-CSA as anatomical evidence that could likely correlate to gastroesophageal reflux predisposition in brachycephalic cats.
RESUMO
Endocrine-disrupting chemicals (EDC) are defined as environmental compounds that produce adverse health manifestations in mammals by disrupting the endocrine system. Benzophenone-1 (2,4-dihydroxybenzophenone, BP1) and nonylphenol (NP), which are discharged from numerous industrial products, are known EDC. The aim of this study was to examine the effects of BP1 and NP on proliferation and metastasis of MCF-7 human breast cancer cells expressing estrogen receptors (ER). Treatment with BP1 (10â»5-10â»7 M) and NP (10â»6-10â»7 M) promoted proliferation of MCF-7 cells similar to the positive control 17 -beta-estradiol (E2). When ICI 182,780, an ER antagonist, was co-incubated with E2, BP1, or NP, proliferation of MCF-7 cells returned to the level of a control. Addition of BP1 or NP markedly induced migration of MCF-7 cells similar to E2. To elucidate the underlying molecular mechanisms produced by these EDC, alterations in transcriptional and translational levels of proliferation and metastasis-related markers, including cyclin D1, p21, and cathepsin D, were determined. Data showed increase in expression of cyclin D1 and cathepsin D and decrease in p21 at both transcriptional and translational levels. However, BP1- or NP-induced alterations of these genes were blocked by ICI 182,780, suggesting that changes in expression of these genes may be regulated by an ERα-dependent pathway. In conclusion, BP1 and NP may accelerate growth of MCF-7 breast cancer cells by regulating cell cycle-related genes and promote cancer metastasis through amplification of cathepsin D.