Coupling of respiratory and sympathetic activities in rats submitted to chronic intermittent hypoxia

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

On the long standing issue of an R phi(2) coupling between gravity and a massless free scalar field

Using 2-body trees on a flat space background, it is shown that the actions A[g, φ] = (Latin small letter esh) d4x√-g [(R/2K) + (1/2)(gμν ∂μφ∂νφ + λRφ2)] and Ā[ḡ, φ̄] = (Latin small letter esh) d4x√ - ḡ [(R̄/2k) + (1/2) ḡμν∂μφ̄∂ νφ] describe the same theory at the tree-level in this case. We also demonstrate the quantum equivalence (at one-loop) of the barred and unbarred systems for λ == -1/6 (conformal coupling).

Future e(+)e(-) colliders' sensitivity to Hb(b)over-bar coupling and CP violation

A complete analysis of the sensitivity to new Hbb̄ couplings from the process e+e- → bb̄vv̄ at the next generation of linear colliders was performed. These new couplings were predicted by many extensions of the Standard Model. The results are comparable to the study performed previously where a global fit analysis for L=500 fb-1 and √s=500 GeV resulted in a relative accuracy of 2.2% in the gHbb Yukawa coupling.

Coupling between respiratory and sympathetic activities as a novel mechanism underpinning neurogenic hypertension

Enhanced sympathetic outflow to the heart and resistance vessels greatly contributes to the onset and maintenance of neurogenic hypertension. There is a consensus that the development of hypertension (clinical and experimental) is associated with an impairment of sympathetic reflex control by arterial baroreceptors. More recently, chronic peripheral chemoreflex activation, as observed in obstructive sleep apnea, has been proposed as another important risk factor for hypertension. In this review, we present and discuss recent experimental evidence showing that changes in the respiratory pattern, elicited by chronic intermittent hypoxia, play a key role in increasing sympathetic activity and arterial pressure in rats. This concept parallels results observed in other models of neurogenic hypertension, such as spontaneously hypertensive rats and rats with angiotensin II–salt-induced hypertension, pointing out alterations in the central coupling of respiratory and sympathetic activities as a novel mechanism underlying the development of neurogenic hypertension.