Search PubMed⌕ Search

Biomedical subjects

M Cirillo

Publications and source records attributed to M Cirillo.

At least 73 records · Page 4Linked to original sources
PubMed1994

Urinary sodium to potassium ratio and urinary stone disease. The Gubbio Population Study Research Group.

The relation was investigated of urinary sodium to potassium ratio in first morning voided urine (spot urine) to urinary stone disease in 3,625 men and women aged 25 to 74 years participating in the baseline examination of the Gubbio Population Study. History of urinary stone disease (excretion of stone, and/or radiographic or ultrasonic evidence of urinary stone, and/or operation for urinary stone removal) was reported by 127 individuals (3.50%). Prevalence of urinary stone disease was lower in women than in men (2.59 and 4.58%, P < 0.001) and positively related to age (P < 0.001). Compared to nonstone formers, stone formers (N = 127) had higher urinary sodium to potassium ratio (P < 0.01), with similar plasma potassium and sodium concentration. In both sexes, urinary stone disease was positively related (P < 0.001) to sodium to potassium ratio: quartile analysis of this ratio showed that prevalence of stone formers in quartile 4 compared to quartile 1 was 3.33 times higher in women (P < 0.005, 95% confidence interval 1.36/8.60) and 2.71 times higher in men (P < 0.004, 95% confidence interval 1.35/5.93). In multiple logistic regression, urinary stone disease was significantly related to age, sex, and urinary sodium to potassium ratio (P < 0.01), controlled for other possible confounders, with or without exclusion of stone formers with plasma creatinine > 1.20 mg/dl. In an alternative model, with urinary sodium to potassium ratio not included, urinary stone disease was positively related to urinary sodium to creatinine ratio (P < 0.001) and weakly (P = 0.079) related inversely to urinary potassium to creatinine ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

A history of salt.

The medical history of salt begins in ancient times and is closely related to different aspects of human history. Salt may be extracted from sea water, mineral deposits, surface encrustations, saline lakes and brine springs. In many inland areas, wood was used as a fuel source for evaporation of brine and this practice led to major deafforestation in central Europe. Salt played a central role in the economies of many regions, and is often reflected in place names. Salt was also used as a basis for population censuses and taxation, and salt monopolies were practised in many states. Salt was sometimes implicated in the outbreak of conflict, e.g. the French Revolution and the Indian War of Independence. Salt has also been invested with many cultural and religious meanings, from the ancient Egyptians to the Middle Ages. Man's innate appetite for salt may be related to his evolution from predominantly vegetarian anthropoids, and it is noteworthy that those people who live mainly on protein and milk or who drink salty water do not generally salt their food, whereas those who live mainly on vegetables, rice and cereals use much more salt. Medicinal use tended to emphasize the positive aspects of salt, e.g. prevention of putrefaction, reduction of tissue swelling, treatment of diarrhea. Evidence was also available to ancient peoples of its relationship to fertility, particularly in domestic animals. The history of salt thus represents a unique example for studying the impact of a widely used dietary substance on different important aspects of man's life, including medical philosophy.

Africa↗
PubMed1994

New bileaflet bioprosthesis: early and mid term results.

A new bovine pericardial bioprosthesis (AMB bioprosthesis) with a bileaflet geometry was designed and developed, with the aim of achieving uniform stress distribution within the prosthesis. The ultimate goal was to limit tissue degeneration to a minimum by attaining optimum fluid dynamics, thereby obtaining an extended clinical durability. The two-leaflet, dome-shaped geometry with a central hinge allowed a very low profile, low ventricular projection in the mitral position, large effective orifice area and low gradients. The design of the thin Delrin stent and the centrally crossing bridge was developed using finite element analysis. Pre-clinical laboratory investigations showed very low trans-valvular gradients and no mechanical or tissue failure after 400 million cycle accelerated wear test. The final model of the prosthesis was manufactured by Baxter-Edwards CVS Division and tested in sheep with good results for up to five months. A limited clinical trial was started in January 1990 and stopped one year later encompassing 12 aortic and six mitral implants. The patients were followed clinically and by echocardiography three, six and 12 months, and four years after surgery. Mean gradients were 4 mmHg in the mitral and 10 mmHg in the aortic position with only minimum regurgitation and no tissue failure. We conclude that early and mid term results with this new pericardial bioprosthesis appear to be favorable and intend to closely monitor further outcome within the limited patient population.

Animals↗
PubMed1993

Regulation of Ca2+ transport by platelet-derived growth factor-BB in rat vascular smooth muscle cells.

The present study investigates the effects of platelet-derived growth factor (PDGF) isoform BB (PDGF-BB) on cytosolic Ca2+ concentration ([Ca2+]i), Ca2+ transport, and Ca2+ pools in rat vascular smooth muscle (VSM) cells. VSM cells from thoracic aorta of Milan normotensive rats were enzymatically dispersed, cultured in 10% serum medium, and made quiescent by 72 hours in 0.3% serum medium. [Ca2+]i, Ca2+ influx, Ca2+ efflux, and exchangeable cell Ca2+ pool were evaluated by ratiometric fluorescent and radioisotope techniques. Ca2+ transport showed time-dependent changes during stimulation with PDGF-BB. The initial early responses to this peptide were transient rise in [Ca2+]i, a 30% decrease in Ca2+ influx, and a 3.6-fold increase in the rate constant for active Ca2+ efflux. Stimulation of Ca2+ efflux and inhibition of Ca2+ influx were associated with a substantial 30% reduction in the cell Ca2+ pool. This initial stimulation of Ca2+ efflux is concomitant with Ca2+ mobilization into the cytosol and is due to activation of Na(+)-independent Ca2+ efflux via the Ca2+ pump. After a 10-minute stimulation, Ca2+ influx returned to the basal value, whereas Ca2+ efflux remained 2.2-fold above control values, leading to a decline in [Ca2+]i below basal levels and a further decrease in the cell Ca2+ pool. Nearly half of this late Ca2+ efflux appears to be driven by Na(+)-Ca2+ exchange, as evidenced by its external Na+ dependence. After a 120-minute stimulation with PDGF-BB, nifedipine-sensitive Ca2+ influx is increased 37% above basal levels, and Ca2+ efflux remains elevated. During prolonged stimulation by PDGF-BB, both Ca2+ influx and efflux are stimulated, resulting in a new intracellular Ca2+ homeostasis marked by the recovery of the cell Ca2+ pool but a lowered [Ca2+]i. These final events coincide with the initiation of cell proliferation in VSM cells by PDGF-BB.

Animals↗
PubMed1993

Calcium-mediated intracellular acidification and activation of Na(+)-H+ exchange in adrenal glomerulosa cells stimulated with potassium.

Intracellular pH (pHi) regulation by Na(+)-H+ exchange is important in cellular responses to hormones and growth factors, particularly those which raise cytosolic Ca2+ (Cai). Since elevation of Cai occurs when adrenal glomerulosa cells are stimulated by angiotensin II (Ang II) and high external K+ (Ko), we evaluated the relationship of Na(+)-H+ exchange to calcium movement particularly during high Ko stimulation of bovine glomerulosa cells. Inhibition of Na(+)-H+ exchange by dimethylamiloride markedly reduced aldosterone secretion in response to 8 mM Ko. This high Ko stimulation was accompanied by a rise in dimethylamiloride-sensitive Na+ influx and pHi acidification which was extracellular Ca2+ (Cao) dependent. High Ko also produced a rise in Ca2+ influx, Cai levels and Ca2+ efflux at 37 C. However, at 4 C, Ca2+ influx remained intact, but Ca2+ efflux and cellular acidification were inhibited. In contrast, Ang II produced protein kinase C (PKC) activation accompanied by a Na(+)-H+ exchange-dependent rise in pHi which was independent of Cao. After PKC depletion by phorbol ester pretreatment, Ang II also produced a Cao-dependent cell acidification as with high Ko. Thus, Na(+)-H+ exchange is activated by both Ang II and high Ko but by different mechanisms. High Ko stimulation induces an enhanced cellular acidification, whereas Ang II induces alkalinization driven by PKC activation of the antiporter. These findings suggest that a physiological role of Na(+)-H+ exchange may be, in part, to counteract the acidification produced by enhanced active Ca2+ efflux (via Ca2+ pumping) during both high Ko and Ang II stimulation of aldosterone secretion.

Aldosterone↗
PubMed1993

Early and late effects of angiotensin-II on Ca2+ fluxes in bovine adrenal zona glomerulosa cells.

Previous studies have yielded conflicting results concerning the effects of angiotensin-II (Ang II) on Ca2+ fluxes in adrenal zona glomerulosa (ZG) cells. The present study was designed to investigate the kinetics and dose-dependency of Ang II-mediated changes in Ca2+ influx and efflux in cultured bovine ZG cells. At a high (10 nM) Ang II concentration, cytosolic Ca2+ (Cai) shows a peak-plateau response for the first 15 min, with small Cai transients commonly observed with longer stimulations. At 50 pM Ang II, more sustained Cai changes were elicited, typically consisting of Cai oscillations. The underlying changes in Ca2+ influx and efflux were studied. The early modifications of Ca2+ influx after 2 min of agonist stimulation were biphasic, with uptake increased by 90% between 1-100 pM Ang II and inhibited by 30% at 10 nM Ang II. Furthermore, high (10 nM) Ang II doses inhibited extracellular K(+)-stimulated Ca2+ influx. After 30 min of Ang II stimulation, the later dose response of Ca2+ influx was of similar magnitude but shifted to the left, showing a maximal influx at 10 pM Ang II and a modest enhancement at 10 nM. Basal Ca2+ efflux followed a two-compartment exponential decay, reflecting rapid Ca2+ displacement from extracellular sites (k1) and active Ca2+ transport (k2). A high (10 nM) Ang II concentration induced a transient large increase (130%) in k2 during the initial phase of Ang II stimulation, which returned to basal values within 10 min. A low (50 pM) Ang II concentration induced a small sustained increase (30%) in k2. A 10-nM Ang II concentration markedly reduced the exchangeable Ca2+ pool, as Ca2+ mobilized from intracellular stores into the cytosol was rapidly extruded, while Ca2+ influx was inhibited. A more physiological (50 pM) concentration of Ang II did not significantly alter the total exchangeable Ca2+ pool due to modest stimulation of both Ca2+ efflux and influx. In summary, the initial transient Cai response to high Ang II results from a large Ca2+ mobilization combined with inhibition of Ca2+ influx, which does not allow for the refilling of Ca2+ stores. At later times, small increases in Ca2+ influx allow for the eventual recovery of exchangeable cell Ca2+ and an enhanced elevation in Cai. At low Ang II concentrations, stimulation of both Ca2+ influx and efflux are concurrent and maintained, allowing for a sustained increase in Cai with little change in exchangeable cell Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II↗
PubMed1993

Can overnight urine replace 24-hour urine collection to measure urinary calcium in epidemiologic studies?

The present study investigated whether overnight urine collection can replace 24-hour urine collection to measure urinary calcium (Ca) excretion in healthy individuals. One hundred healthy men (age 25-74 years) on their usual diet participated in the present study as part of an ongoing epidemiological population-based survey. Two separate bags (daytime and overnight bags) were given together with instructions to collect a complete 24-hour urine sample divided in to the daytime and the overnight specimen. Urinary Ca was analyzed by atomic absorption spectrophotometry and creatinine by the picric acid colorimetric method. Overnight urinary Ca was correlated to daytime (r = 0.618, p < 0.0001) and 24-hour urinary Ca (r = 0.891, p < 0.0001). In the 17 men found to have hypercalciuria (24-hour urinary Ca > or = 7.5 mmol), the overnight urinary Ca averaged 4.44 +/- 0.29 mmol/12 h (mean +/- SEM, range 2.35-6.38 mmol/12 h), indicating that an overnight urinary Ca of < 2.35 mmol/12 h (< 60% of the overnight urinary Ca distribution) ruled out the possibility of finding hypercalciuria in 24-hour urine. Fourteen of the seventeen hypercalciuric men had overnight urinary Ca in the upper 20% of the distribution (> or = 3.25 mmol/12 h). Hypercalciuria was found in 14 of the 19 men (73.7%) with an overnight urinary Ca of > or = 3.25 mmol/12 h, but only in 3 of the 81 men (3.7%) with an overnight urinary Ca of < 3.25 mmol/12 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Hematocrit, blood pressure, and hypertension. The Gubbio Population Study.

Baseline data from the Gubbio Population Study in north central Italy were used to investigate the relation of hematocrit to blood pressure and hypertension among 2,809 men and women aged 25-74 years. Independent of gender, age, and other confounders, the hypertensive group had a higher hematocrit than the nonhypertensive group (p less than 0.001). In comparison with the untreated hypertensive group, the hypertensive group being treated with diuretics or with other drugs only had similar mean hematocrit levels despite significantly lower blood pressures. Hematocrit was positively correlated with systolic pressure (r = 0.085, p less than 0.01 and r = 0.264, p less than 0.001 for men and women, respectively) and diastolic pressure (r = 0.214, p less than 0.001 and r = 0.266, p less than 0.001). In both sexes, whether or not the treated hypertensive group was included, age-adjusted prevalence of hypertension and average blood pressure were higher for persons in higher quintiles of hematocrit (p less than 0.001). The association of hematocrit with blood pressure and hypertension was significant and independent of several confounders. The regression coefficient of blood pressure on hematocrit ranged between 0.410 and 0.620 mm Hg per unit of hematocrit for systolic pressure and between 0.371 and 0.581 for diastolic pressure, depending on gender and whether the treated hypertensive group was included in multiple regression analysis. Based on exponentiation of the multiple logistic coefficient, prevalence of hypertension was at least two times greater for persons whose hematocrit levels were higher by 10 units.

Adult↗
PubMed1992

The Gubbio data. Epidemiology and pathophysiology. Gubbio Study Research Group.

The relation between the maximal velocity of red blood cell sodium-lithium countertransport and blood pressure/hypertension has been studied in 2,748 men and women aged 25-74 years who participated in the 1983-85 baseline examination of the Gubbio Population Study, an epidemiologic investigation performed in a hill town of north central Italy. Men had a higher sodium-lithium countertransport velocity than women at all ages, and, in both sexes, a higher velocity was observed at successive ages. Hypertensives of both sexes had a higher sodium-lithium countertransport velocity than normotensive individuals, the difference remaining significant after control for age, body mass index and plasma uric acid concentration. Individuals with high sodium-lithium countertransport velocity had significantly greater prevalence of hypertension in both sexes. The data show the existence of a cross-sectional association between sodium-lithium countertransport velocity and hypertension in general population. Prospective study of the Gubbio population is now in progress to investigate the relation between baseline sodium-lithium countertransport velocity, its change over the years and the incidence of hypertension.

Adult↗
PubMed1991

Sodium transport kinetics in erythrocytes and inside-out vesicles from Milan rats.

This paper describes the kinetics of the Na(+)-K+ pump and the Na(+)-K(+)-Cl- cotransport in sodium-loaded erythrocytes and of the Na(+)-K(+)-Cl- cotransport in erythrocyte inside-out vesicles (IOV) from Milan hypertensive (MHS) and normotensive (MNS) rats in order to evaluate the possible role of intracellular factor(s). In intact erythrocytes, no difference was detectable in the Na(+)-K+ pump kinetics between the two strains while the apparent affinity (Km) of Na(+)-K(+)-Cl- cotransport for internal sodium was significantly greater and the maximal rate of sodium transport lower in MHS when compared with MNS rats. IOV, which are depleted of cytoskeleton, showed a bumetanide-sensitive potassium- and chloride-dependent sodium uptake. However, the erythrocyte differences in Na(+)-K(+)-Cl- cotransport activity and the Km between strains disappeared in IOV, suggesting tha the altered sodium transport of MHS erythrocyte might be due to some intracellular factor or a membrane skeleton protein abnormality.

Animals↗