instruction:
Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
question:
Cadherins are calcium-dependent cell-to-cell adhesion glycoproteins playing a critical role in the formation and maintenance of normal tissue architecture. In normal mammary gland, E-cadherin is expressed by luminal epithelial cells, while P-cadherin is restricted to myoepithelial cells. Changes in the expression of classical E- and P-cadherins have been observed in mammary lesions and related to mammary carcinogenesis. P-cadherin and E-cadherin expressions were studied in a series of feline normal mammary glands, hyperplastic/dysplastic lesions, benign and malignant tumours by immunohistochemistry and double-label immunofluorescence.', 'In normal tissue and in the majority of hyperplastic/dysplastic lesions and benign tumours, P-cadherin was restricted to myoepithelial cells, while 80% of the malignant tumours expressed P-cadherin in luminal epithelial cells. P-cadherin expression was significantly related to high histological grade of carcinomas (p <0.0001), tumour necrosis (p = 0.001), infiltrative growth (p = 0.0051), and presence of neoplastic emboli (p = 0.0401). Moreover, P-cadherin positive carcinomas had an eightfold likelihood of developing neoplastic emboli than negative tumours. Cadherins expression profile in high grade and in infiltrative tumours was similar, the majority expressing P-cadherin, regardless of E-cadherin expression status. The two cadherins were found to be co-expressed in carcinomas with aberrant P-cadherin expression and preserved E-cadherin.
answer:
Is aberrant P-cadherin expression associated to aggressive feline mammary carcinomas?


question:
Regular physical activity is an effective non-pharmacological therapy for prevention and control of hypertension. However, the underlying mechanisms are not fully understood. Accumulating evidence shows that the elevated vascular tone in hypertension is a consequence of the 'ion channel remodelling' that occurs during sustained high BP. The present study investigated the effects of aerobic exercise on the electrical remodelling of L-type Ca(2+) (Cav 1.2) and large-conductance Ca(2+) -activated K(+) (KCa 1.1) channels in mesenteric arteries (MAs) from spontaneously hypertensive rats (SHRs).", 'SHRs and normotensive (Wistar-Kyoto) rats were subjected to aerobic training or kept sedentary, and vascular mechanical and functional properties were evaluated.', 'Exercise did not affect the heart weight, but reduced the heart rate and body weight in SHR. In mesenteric arterial myocytes, exercise normalized the increased Cav 1.2 and KCa 1.1 current density in SHRs. Exercise also ameliorated the increased open probability and mean open time of the single KCa 1.1 channel in hypertension. The isometric contraction study revealed that both nifedipine (Cav 1.2 channel blocker) and NS11021 (KCa 1.1 channel activator) induced concentration-dependent vasorelaxation in MAs precontracted with noradrenaline. Exercise normalized the increased sensitivity of tissues to nifedipine and NS11021 in SHR. Furthermore, protein expression of the Cav 1.2 α1C -subunit together with the KCa 1.1 α- and β1-subunit was significantly increased in SHRs; and exercise ameliorated these molecular alterations in hypertension.
answer:
Does chronic exercise normalize changes in Cav 1.2 and KCa 1.1 channels in mesenteric arteries from spontaneously hypertensive rats?


question:
Monitoring of respiratory mechanics during ventilator treatment in paediatric intensive care is currently based on pressure and flow measurements in the ventilator or at the Y-piece. The characteristics of the tracheal tube will modify the pressures affecting the airways and alveoli in an unpredictable manner. The dynostatic algorithm (DSA), based on a one-compartment lung model, calculates the alveolar pressure during on-going ventilation. The DSA is based on accurate measurement of tracheal pressure. The purpose of this study was to test the validity of the DSA in a paediatric lung model and to apply the concept in an observational clinical study in children.', 'We validated the DSA in a paediatric lung model with linear, nonlinear pressure flow and frequency-dependent characteristics by comparing calculated dynostatic (alveolar) pressures with directly measured alveolar pressures in the model and proximal plateau pressure with maximum alveolar pressure. Sixty combinations of ventilation modes, positive end expiratory pressures, inspiratory : expiratory ratios, volumes and frequencies were studied. A 0.25-mm fibreoptic pressure transducer in the tube lumen was used in combination with volume and flow from ventilator signals. Clinical measurements were performed in eight patients during anaesthesia and postoperative ventilator treatment.', 'In the lung model we found a correlation coefficient between calculated and measured alveolar pressure of 0.93-0.99 with root mean square median values of 1 cm H2O. Distal plateau pressure agreed well with maximum alveolar pressure. In the clinical situation, the algorithm provided a breath-by-breath display of the volume-dependent lung compliance and the temporal course of alveolar pressure during uninterrupted ventilation.
answer:

Does the dynostatic algorithm accurately calculate alveolar pressure on-line during ventilator treatment in children?