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Biomedical subjects

Andrew Docherty

Publications and source records attributed to Andrew Docherty.

6 recordsLinked to original sources
PubMed2006

Asymptotic analysis of collision-induced timing shifts in return-to-zero quasi-linear systems with predispersion and postdispersion compensation.

An asymptotic method for calculating the collision-induced frequency and timing shifts for quasi-linear pulses in return-to-zero, wavelength-division multiplexed systems with predispersion and postdispersion compensation is developed. Predictions of the asymptotic theory agree well with quadrature and direct numerical simulations. Using this theory, computational savings of many orders of magnitude can be realized over direct numerical simulations.

Journal Article↗
PubMed2005

Calculation, characterization, and application of the time shift function in wavelength-division-multiplexed return-to-zero systems.

We calculate the time shift function for collisions of pairs of pulses in different channels in a prototypical return-to-zero wavelength-division-multiplexed system with dispersion management and precompensation and postcompensation. Once the time shift function is known, the impairments that are due to collision-induced timing jitter can be rapidly determined. We characterize the shape of this function and determine how it scales with the initial pulse separation in time and with channel separation in wavelength. Finally, we apply it to the calculation of the worst-case time shift.

Journal Article↗
PubMed2004

Reduction of collision-induced timing shifts in dispersion-managed quasi-linear systems with periodic-group-delay dispersion compensation.

Periodic-group-delay (PGD) dispersion-compensation modules were recently proposed as mechanisms to alleviate collision-induced timing shifts in dispersion-managed (DM) systems. Frequency and timing shifts in quasi-linear DM systems with PGDs were obtained, and it is shown that significant reductions are achieved when even a small fraction of the total dispersion is compensated for by PGDs.

Journal Article↗
PubMed2003

Treatment of hypertensive patients with coexisting coronary arterial disease.

Despite clear guidelines and an array of available antihypertensive medications, patients with hypertension and coronary artery disease are often inadequately treated. New data from HOPE, LIFE, and ALLHAT underscores the importance of blood pressure reduction for patients with coronary artery disease. Despite our improved understanding of the mechanism by which the various classes of antihypertensive medications achieve their effect, it remains the case that blood pressure reduction remains more important than the medication used to achieve the reduction. For most patients with coronary artery disease, combination therapy will be required to achieve a target blood pressure of less than 140/80. When tolerated, this therapy should include a beta-blocker and ACE inhibitor, both of which are of prognostic benefit for patients with coronary artery disease. There are also attractions in choosing calcium antagonists because of their efficacy in controlling anginal symptoms (Dihydropyridine calcium channel blockers if already on a beta-blocking agent and rate-limiting calcium channel blockers if beta blockers are contraindicated). Thiazide diuretics have proven themselves effective again in the ALLHAT study and are likely to be an integral part of treatment for the great majority of patients with coronary artery disease.

Antihypertensive Agents↗
PubMed2002

Pulmonary hypertension secondary to left ventricular dysfunction: the role of nitric oxide and endothelin-1 in the control of pulmonary vascular tone.

1. Using an in vivo model of pulmonary hypertension (PHT) secondary to left ventricular dysfunction (LVD), the pulmonary arterial response to the nitric oxide synthase (NOS) blocker L-NAME (30 micromol.min(-1) i.v.) and the subsequent responses to cumulatively administered endothelin-1 (ET-1) (0.001 -- 4 nmol.kg(-1) i.v.) or big ET-1 (0.1 -- 2.0 nmol.kg(-1) i.v.) were studied. Additionally, the effect of the non-selective ET-1 receptor antagonist, SB209670, was investigated. 2. Eight weeks after coronary artery ligation or sham operation, rabbits demonstrated increased mean pulmonary arterial pressure (PAP) accompanied by right ventricular hypertrophy. 3. Blockade of NOS caused a greater increase in basal PAP (increased by 7.7 +/- 1.1 mmHg c.f. 3.8 +/- 1.0 mmHg in controls, P<0.05) and uncovered a greater pulmonary pressor response to exogenous ET-1 in rabbits with PHT (increased by 10.2 +/- 2.3 mmHg c.f. 4.9 +/- 1.0 mmHg in controls, P<0.05). 4. Big ET-1 evoked a pulmonary pressor effect, in both groups of rabbits, that was increased following blockade of NOS and was more potent in rabbits with PHT. 5. The non-selective ET-1 receptor antagonist, SB209670, reduced basal PAP (from 16.9 mmHg to 15.9 mmHg, P < 0.05) in rabbits with PHT and blocked the response to ET-1 in the presence of L-NAME. 6. In conclusion, the results demonstrate that basal NO activity masks a pulmonary pressor response to exogenously administered ET-1. An increased responsiveness to ET-1 was shown in the pulmonary arterial bed of rabbits with PHT secondary to LVD, implicating a pathophysiological role for ET-1 in this model.

Animals↗