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An experimental apparatus is described for the investigation of frequency dispersion, and related attenuation, of fluid-saturated rocks under confining pressure and undrained boundary conditions. The forced-oscillation method is performed on cylindrical samples. The measurement of stress and strain under hydrostatic oscillations allows the dynamic bulk modulus to be inferred, while axial oscillations give access to dynamic Young's modulus and Poisson's ratio. We present calibration measurements for dispersion and attenuation on standard materials such as glass, plexiglass, and gypsum. Results show that for strain amplitudes below 10-5, robust measurements can be achieved up to 1 kHz and 1.3 Hz, respectively, for axial and hydrostatic oscillations. A new experimental design of the endplatens (sample holders) allows control of drained or undrained boundary conditions using microvalves. The microvalves were tested on a porous Vosgian sandstone. In addition, numerical modeling confirms that the resonances of the apparatus only affect frequencies above 1 kHz, with little sensitivity to the sample's stiffness.

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The alpha2-adrenoceptors are G-protein-coupled receptors that mediate many of the physiological effects of norepinephrine and epinephrine. Mammals have three subtypes of alpha2-adrenoceptors, alpha2A, alpha2B and alpha2C. Zebrafish, a teleost fish used widely as a model organism, has five distinct alpha2-adrenoceptor genes. The zebrafish has emerged as a powerful tool to study development and genetics, with many mutations causing diseases reminiscent of human diseases. Three of the zebrafish adra2 genes code for orthologues of the mammalian alpha2-adrenoceptors, while two genes code for alpha2Da- and alpha2Db- adrenoceptors, representing a duplicated, fourth alpha2-adrenoceptor subtype. The three different mammalian alpha2-adrenoceptor subtypes have distinct expression patterns in different organs and tissues, and mediate different physiological functions. The zebrafish alpha2-adrenergic system, with five different alpha2-adrenoceptors, appears more complicated. In order to deduce the physiological functions of the zebrafish alpha2-adrenoceptors, we localized the expression of the five different alpha2-adrenoceptor subtypes using RT-PCR, mRNA in situ hybridization, and receptor autoradiography using the radiolabelled alpha2-adrenoceptor antagonist [ethyl-3H]RS-79948-197. Localization of the alpha2A-, alpha2B- and alpha2C-adrenoceptors in zebrafish shows marked conservation when compared with mammals. The zebrafish alpha2A, alpha2Da, and alpha2Db each partially follow the distribution pattern of the mammalian alpha2A: a possible indication of subfunction partitioning between these subtypes. The alpha2-adrenergic system is functional in zebrafish also in vivo, as demonstrated by marked locomotor inhibition, similarly to mammals, and lightening of skin colour induced by the specific alpha2-adrenoceptor agonist, dexmedetomidine. Both effects were antagonized by the specific alpha2-adrenoceptor antagonist atipamezole.

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Twenty-five symptomatic patients of chronic heart failure were subjected to spirometry to detect abnormalities of pulmonary function and to assess the effect of ipratropium bromide in reversing or minimising these abnormalities. All the patients exhibited abnormal pulmonary function manifesting as obstructive (15/25) or restrictive (10/25) ventilatory defect. There was overall improvement in lung functions with ipratropium bromide especially in those with obstructive ventilatory defects and mostly comprised of smokers. Forced expiratory volume in one second increased by 47.7 percent (p < 0.02), forced expiratory volume in one second/forced vital capacity ratio by 14.1 percent (p < 0.001) and maximal voluntary ventilation by 40.6 percent (p < 0.05) in these patients. It is concluded that ipratropium bromide can prove as a promising adjunctive therapeutic intervention in improving quality of life in patients of chronic congestive heart failure who are incapacitated by dyspnoea and have clearly documented ventilatory defects.

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OBJECTIVE: To evaluate the association of silent myocardial ischemia (SMI) with cardiac autonomic neuropathy in asymptomatic diabetic patients. MATERIAL AND METHODS: Two hundred asymptomatic patients of diabetes mellitus were assessed for evidence of cardiac autonomic neuropathy. Of these, 30 (15 males, 15 females; mean age 44.7 +/- 8.8 years) were found to have cardiac autonomic neuropathy. Thirty (30) age and sex matched diabetic patients (mean age 42.4 +/- 7.6 years) who had no evidence autonomic neuropathy were included in the study as control group. Both the groups of patients were evaluated for SMI by 24 hour ambulatory electrocardiographic (ECG) monitoring. RESULTS: Incidence of SMI was significantly higher in patients with autonomic neuropathy 12/30 (40%) compared to those without 3/30 (10%) p < 0.001. Duration of diabetes was more (13 +/- 1.59 years) in patients with autonomic neuropathy compared to the control group (8.66 +/- 1.55 years) p < 0.001. Serum cholesterol and triglyceride levels were significantly higher in patients with autonomic neuropathy in comparison to control group < 0.05 and < 0.01, respectively. There was no difference in the pattern of SMI in the two groups (p = N.S). CONCLUSION: Cardiac autonomic neuropathy predisposes patients with diabetes mellitus to SMI. Twenty four hour ambulatory ECG monitoring provides useful diagnostic information in early detection and evaluation of SMI in asymptomatic diabetic patients.

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