Evaluation of respiratory parameters at presentation as clinical indicators of the respiratory localization in dogs and cats with respiratory distress

OBJECTIVE: To describe clinical respiratory parameters in cats and dogs with respiratory distress and identify associations between respiratory signs at presentation and localization of the disease with particular evaluation between the synchrony of abdominal and chest wall movements as a clinical indicators for pleural space disease. Design - Prospective observational clinical study. SETTING: Emergency service in a university veterinary teaching hospital. ANIMALS: Cats and dogs with respiratory distress presented to the emergency service between April 2008 and July 2009. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The following parameters were systematically determined at time of admission: respiratory rate, heart rate, temperature, type of breathing, movement of the thoracic and abdominal wall during inspiration, presence of stridor, presence and type of dyspnea, and results of thoracic auscultation. Abdominal and chest wall movement was categorized as synchronous, asynchronous, or inverse. Diagnostic test results, diagnosis, and outcome were subsequently recorded. Based on the final diagnoses, animals were assigned to 1 or more of the following groups regarding the anatomical localization of the respiratory distress: upper airways, lower airways, lung parenchyma, pleural space, thoracic wall, nonrespiratory causes, and normal animals. One hundred and seventy-six animals (103 cats and 73 dogs) were evaluated. Inspiratory dyspnea was associated with upper airway disease in dogs and expiratory dyspnea with lower airway disease in cats. Respiratory noises were significantly associated and highly sensitive and specific for upper airway disease. An asynchronous or inverse breathing pattern and decreased lung auscultation results were significantly associated with pleural space disease in both dogs and cats (P<0.001). The combination is highly sensitive (99%) but not very specific (45%). Fast and shallow breathing was not associated with pleural space disease. Increased or moist pulmonary auscultation findings were associated with parenchymal lung disease. CONCLUSIONS: Cats and dogs with pleural space disease can be identified by an asynchronous or inverse breathing pattern in combination with decreased lung sounds on auscultation.

Underneath the cerclage: an ex vivo study on the cerclage-bone interface mechanics

Cerclages regain interest due to a rising number of periprosthetic fractures. The contact distribution at the circumferential cerclage-bone interface is still unknown. Local interface pressure depends on the amount of contact area. Cortical damage at the interface would provoke cerclage loosening. Therefore, the contact area, the bone pressure along the interface and the cortical resistance underneath loaded cerclages were determined in an ex vivo model.

Relationship of horse owner assessed respiratory signs index to characteristics of recurrent airway obstruction in two Warmblood families

REASONS FOR PERFORMING STUDY: The horse owner assessed respiratory signs index (HOARSI-1-4, healthy, mildly, moderately and severely affected, respectively) is based on owner-reported clinical history and has been used for the investigation of recurrent airway obstruction (RAO) genetics utilising large sample sizes. Reliable phenotype identification is of paramount importance in genetic studies. Owner reports of respiratory signs have shown good repeatability, but the agreement of HOARSI with an in-depth examination of the lower respiratory tract has not been investigated. OBJECTIVES: To determine the correlation of HOARSI grades 3/4 with the characteristics of RAO and of HOARSI-2 with the characteristics of inflammatory airway disease. Further, to test whether there are phenotypic differences in the manifestation of lung disease between families. METHODS: Seventy-one direct offspring of 2 RAO-affected Warmblood stallions (33 from the first family, 38 from the second) were graded as HOARSI-1-4 and underwent a clinical examination of the respiratory system, arterial blood gas analysis, endoscopic mucus scoring, cytology of tracheobronchial secretion (TBS) and bronchoalveolar lavage fluid (BALF), and clinical assessment of airway reactivity to methacholine chloride. RESULTS: HOARSI-3/4 animals in clinical exacerbation showed signs consistent with RAO: coughing, nasal discharge, abnormal lung sounds and breathing pattern as well as increased numbers of neutrophils in TBS and BALF, excessive mucus accumulation and airway hyper-responsiveness to methacholine. HOARSI-3/4 horses in remission only had increased amounts of tracheal mucus and TBS neutrophil percentages. Clinical phenotypes were not significantly different between the 2 families. CONCLUSIONS AND CLINICAL RELEVANCE: HOARSI reliably identifies RAO-affected horses in our population.

Metformin inhibits human androgen production by regulating steroidogenic enzymes HSD3B2 and CYP17A1 and complex I activity of the respiratory chain

Metformin is treatment of choice for the metabolic consequences seen in polycystic ovary syndrome for its insulin-sensitizing and androgen-lowering properties. Yet, the mechanism of action remains unclear. Two potential targets for metformin regulating steroid and glucose metabolism are AMP-activated protein kinase (AMPK) signaling and the complex I of the mitochondrial respiratory chain. Androgen biosynthesis requires steroid enzymes 17α-Hydroxylase/17,20 lyase (CYP17A1) and 3β-hydroxysteroid dehydrogenase type 2 (HSD3B2), which are overexpressed in ovarian cells of polycystic ovary syndrome women. Therefore, we aimed to understand how metformin modulates androgen production using NCI-H295R cells as an established model of steroidogenesis. Similar to in vivo situation, metformin inhibited androgen production in NCI cells by decreasing HSD3B2 expression and CYP17A1 and HSD3B2 activities. The effect of metformin on androgen production was dose dependent and subject to the presence of organic cation transporters, establishing an important role of organic cation transporters for metformin's action. Metformin did not affect AMPK, ERK1/2, or atypical protein kinase C signaling. By contrast, metformin inhibited complex I of the respiratory chain in mitochondria. Similar to metformin, direct inhibition of complex I by rotenone also inhibited HSD3B2 activity. In conclusion, metformin inhibits androgen production by mechanisms targeting HSD3B2 and CYP17-lyase. This regulation involves inhibition of mitochondrial complex I but appears to be independent of AMPK signaling.

A prospective study of the impact of air pollution on respiratory symptoms and infections in infants

Rationale: There is increasing evidence that short-term exposure to air pollution has a detrimental effect on respiratory health, but data from healthy populations, particularly infants, are scarce. Objectives: To assess the association of air pollution with frequency and severity of respiratory symptoms and infections measured weekly in healthy infants. Methods: In a prospective birth cohort of 366 infants of unselected mothers, respiratory health was assessed weekly by telephone interviews during the first year of life (19,106 total observations). Daily mean levels of particulate matter (PM10), nitrogen dioxide (NO2), and ozone (O3) were obtained from local monitoring stations. We determined the association of the preceding week's pollutant levels with symptom scores and respiratory tract infections using a generalized additive mixed model with an autoregressive component. In addition, we assessed whether neonatal lung function influences this association and whether duration of infectious episodes differed between weeks with normal PM10 and weeks with elevated levels. Measurements and Main Results: We found a significant association between air pollution and respiratory symptoms, particularly in the week after respiratory tract infections (risk ratio, 1.13 [1.02-1.24] per 10 μg/m(3) PM10 levels) and in infants with premorbid lung function. During times of elevated PM10 (>33.3 μg/m(3)), duration of respiratory tract infections increased by 20% (95% confidence interval, 2-42%). Conclusions: Exposure to even moderate levels of air pollution was associated with increased respiratory symptoms in healthy infants. Particularly in infants with premorbid lung function and inflammation, air pollution contributed to longer duration of infectious episodes with a potentially large socioeconomic impact.