The oxygen therapy.

Oxygen (O(2)) is a vital element. Shortage of O(2) results in deranged metabolism and important changes in vascular tone with opposite effects on the systemic and pulmonary circulation. During hypoxemia, oxidative stress exposes the organism to a sort of accelerated senescence as well as to several acute untoward effects.

Relationship between renal function and physical performance in elderly hospitalized patients.

Chronic kidney disease (CKD) is increasingly recognized as a cause of worsening physical functioning in older patients. The Short Physical Performance Battery (SPPB) is highly reliable in older populations, but no data on older hospitalized patients with different degrees of kidney function are available. We aimed at testing the association between estimated glomerular filtration rate (eGFR) and SPPB, either global score (range 0-12) or its individual components (muscle strength, balance, and walking speed, each ranging from 0 to 4), in a sample of older hospitalized patients.

Prognostic significance of the short physical performance battery in older patients discharged from acute care hospitals.

We investigated the prognostic role of the Short Physical Performance Battery (SPPB) in elderly patients discharged from the acute care hospital. Our series consisted of 506 patients aged 70 years or more enrolled in a multicenter collaborative observational study. We considered three main outcomes: 1-year survival after discharge, functional decline, and hospitalization during follow-up.

Angiotensin II type 1 receptor, but no type 2 receptor, interferes with the insulin-induced nitric oxide production in HUVECs.

Objective: Two subtypes of angiotensin II (ATII) receptor have been defined on the basis of their differential pharmacological and biochemical properties: ATII-type1 receptors (AT(1)-R) and ATII-type2 receptors (AT(2)-R). It has been hypothesized that part of the protective effects on the cardiovascular system of AT(1)-R blockers is mediated by an ATII-mediated overstimulation of AT(2)-R. We hypothesized that the inhibition of AT(1)-R has a stronger impact on insulin-induced nitric oxide (NO) production than ATII-mediated overstimulation of AT(2)-R.