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F Bellini

Publications and source records attributed to F Bellini.

At least 37 records · Page 2Linked to original sources
PubMed1990

Signalling mechanism in the lysophosphatidylserine-induced activation of mouse mast cells.

Lysophosphatidylserine (0.1-1 microM) elicits histamine release in isolated mouse peritoneal mast cells. The effect becomes manifest after a lag of 30 s and reaches completion in 5 min. Maximal activity is observed when serine is in L-configuration. As shown by the activity of a lysophosphatidylserine analogue lacking the OH group in C2 position of glycerol, conversion into phosphatidylserine is not required. When 32PO4-labeled mast cells are challenged 2-5 min with lysophosphatidylserine, the labeling of phosphatidate, phosphatidylinositol and phosphatidylcholine is increased. When [3H]arachidonate-labeled mast cells are used, lysophosphatidylserine increases the appearance of isotopic diacylglycerol and phosphatidate. Like the secretory response, these effects are independent of the presence of extracellular Ca2+. Incubations in the presence of [3H]glycerol show that lysophosphatidylserine does not activate the de novo synthesis of phospholipids. In agreement with a participation of phosphoinositidase C in the action of lysophosphatidylserine, we observe accumulation of inositol phosphates in [3H]inositol labeled mast cells incubated in the presence of Li+. The results suggest that lysophosphatidylserine delivers its stimulus to mast cells, by the activation of phosphoinositide-dependent signalling mechanism.

Acylation↗
PubMed1990

Genetic differences in cystic fibrosis patients with and without pancreatic insufficiency. An Italian collaborative study.

To determine the number and frequency of mutations that occur at the cystic fibrosis locus (CF), we have examined the allele and haplotype frequencies of eight polymorphic DNA markers linked to CF in 163 Italian patients who were sub-divided according to their clinical presentations. The distribution of haplotypes for the tightly linked polymorphisms KM.19 and XV-2c differ significantly between patients with and those without pancreatic insufficiency. The haplotype found most commonly in CF chromosomes occurs much more frequently in pancreatic insufficient than in pancreatic sufficient patients. Among the 19 pancreatic sufficient patients, 6 (31.6%) show at least one copy of the rare KM.19 = 1, XV-2c = 2 haplotype, as against 16 of 138 patients (11.6%) with pancreatic insufficiency. In addition, only 5 pancreatic sufficient patients (26.3%) are homozygous for the common 2.1 haplotype, as compared with 88 patients (63.8%) with pancreatic insufficiency. These findings support the hypothesis of allelic heterogeneity at a single locus in CF and suggest that different mutations underlie the presence or absence of pancreatic insufficiency in this disorders.

Alleles↗
PubMed1989

Juvenile nephronophthisis associated with new skeletal abnormalities, tapetoretinal degeneration and liver fibrosis.

This report concerns a boy presenting renal disease with tubulointerstitial nephropathy which suggests familial juvenile nephronophthisis, hepatosplenomegaly due to congenital hepatic fibrosis, tapetoretinal degeneration, probable endocrine involvement and congenital skeletal abnormalities. The associations presented in this paper have not previously been reported.

Abnormalities, Multiple↗
PubMed1988

Activation of phosphoinositide hydrolysis by nerve growth factor and lysophosphatidylserine in rat peritoneal mast cells.

Histamine secretion in rat peritoneal mast cells stimulated by nerve growth factor requires a synergistic signal delivered by lysophosphatidylserine. To study the signal-transducing system activated by these compounds, phospholipid metabolism has been investigated in these cells. Phospholipid labeling with 32PO4 reveals a 5-9-fold stimulation of phosphatidic acid, phosphatidylinositol and phosphatidylcholine synthesis. Increased synthesis of phosphatidylinositol is also monitored using [3H]inositol incorporation. When [3H]inositol-labeled mast cells are incubated in the presence of Li+, nerve growth factor and lysophosphatidylserine enhance the accumulation of inositol monophosphate, inositol bisphosphate and inositol trisphosphate. Similar to the induced histamine release, accumulation of inositol phosphates (a) does not occur when the two agonists are added separately; (b) is inhibited when lysophosphatidyl-L-serine is replaced by lysophosphatidyl-D-serine; and (c) is enhanced in the presence of extracellular Ca2+. The data suggest that the interactive stimulus of nerve growth factor and lysophosphatidylserine is transmitted through the polyphosphoinositide-phospholipase C system.

Animals↗
PubMed1988

Increase in muscular pain threshold following low frequency-high intensity peripheral conditioning stimulation in humans.

The effects of low frequency-high intensity transcutaneous and intramuscular electrical nerve stimulation (TENS and IENS, respectively) on ipsilateral muscular pain threshold were studied in healthy volunteers. The combined effects of TENS (or IENS) and vibration as well as the effects of TENS applied to contralateral regions were also investigated. Muscular pain threshold was evaluated by the subjects' verbal reports in response to electrical stimulation (wire electrodes) of the vastus medialis muscle and by the appearance of blink response (startle reaction) without habituation. TENS was generally applied to the skin overlying the same muscle, and in some instances to the skin overlying the contralateral vastus medialis or triceps muscle. IENS was performed through the same electrodes used for inducing muscular pain. Vibration was applied to the tendon of ipsilateral quadriceps femoris muscle. TENS consistently induced marked and long-lasting elevations of ipsilateral muscular pain threshold. Comparable results were obtained by IENS. TENS and vibration performed simultaneously induced increases in muscular pain threshold, which were greater than those obtained with each individual conditioning stimulation. TENS proved to be capable of enhancing muscular pain threshold even when applied to contralateral regions; however, these effects were smaller and of shorter duration. The results provide evidence that low frequency-high intensity TENS (or IENS) are effective in raising muscular pain threshold and support the hypothesis that this type of stimulation brings supraspinal control systems into action through the activation of group III afferent fibres.

Adult↗
PubMed1988

Effects of heterotopic ischemic pain on muscular pain threshold and blink reflex in humans.

Ischemic pain was induced in the left arm of 6 healthy volunteers using a modification of the submaximal effort tourniquet test. Its effects on both muscular pain threshold (determined in the vastus medialis muscle by means of electrical stimulation) and on the 2nd component of the blink reflex (R2) were investigated in the contralateral body side. Muscular pain threshold increased (peak value during ischemic pain) and maintained significantly higher values for 60 min. R2 response decreased while its latency increased; these variations appeared during ischemic pain and reached a maximum soon after the end of ischemia, still remaining significant for 15 min. The results support the suggestion that the analgesic effects of heterotopic noxious stimulation in humans are subserved by supraspinal inhibitory mechanisms.

Adult↗
PubMed1988

Autacoid properties of lysophosphatidylserine.

The hypothesis of this study is summarized in Fig. 6. Phosphatidylserine due to distribution in the internal side of plasma membrane is prevented to react with the extracellular environment. When injury to cell occurs, phospholipid asymmetry is lost and the exposed phosphatidylserine becomes a signal of cell damage. Phosphatidylserine may activate defense reactions while it is still anchored to plasma membrane (Zwaal, 1978; Tanaka and Schroit, 1983). Alternatively, the soluble lysophosphatidylserine is generated, ready to diffuse and transmit the information of tissue damage to other cells. In this sequence of events, lysophosphatidylserine becomes an autacoid, originated from a membrane phospholipid. In rodents, lysophosphatidylserine seems specifically devoted to activate mast cells. The role of these cells in the regulation of the immune reactions and in tissue repair has been advocated (Dexter et al., 1981). The lysophosphatidylserine-induced mast cell activation has been shown in vivo and in vitro in a variety of rodent species (mouse, rat, gerbil, hamster). It may occur through a direct effect or through the participation of synergistic endogenous compounds. Structure-activity relationships in the action of lysophosphatidylserine show that the effect on mast cells is linked to a definite molecular organization. Determinants of the mast cell activation are the free amino group and the carboxyl group of the serine. Support to the general hypothesis of this study originates from the observation that active lysophosphatidylserine is generated within a population of leukocytes, the cells migrating in areas of wounded tissue (Mietto et al., 1987). Production of lysophosphatidylserine can be anticipated in pathological situations associated with extensive cell death (tumor growth, graft rejection, burns). At present, the observations on lysophosphatidylserine are confined to rodent mast cells. Other histamine-secreting cells (e.g., the human basophil) are unresponsive to this phospholipid (Kolster et al., 1987). Among the endogenous compounds interacting with lysophosphatidylserine, nerve growth factor seems of particular interest (Bruni et al., 1982). The synergism with lysophosphatidylserine has been confirmed in other laboratories (Sugiyama et al., 1985; Pearce and Thompson, 1986; Mazurek et al., 1986). The concerted effects by these two compounds on mast cells is in line with current opinion on the participation of nerve growth factor in the regulation of inflammatory and immune reactions (Mietto et al., 1987; Weskamp and Otten, 1987).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Age-dependent changes in the mechanisms controlling prolactin secretion and phosphatidylinositol turnover in male rats: effect of phosphatidylserine.

The present study was undertaken in order to better characterize the functional state of anterior pituitary gland in young and old rats by using prolactin secretion and incorporation of radioactive phosphate into phosphatidylinositol (PI) as markers. The in vitro incorporation of radiolabeled phosphate into anterior pituitary PI was significantly (p less than 0.01) greater in young (3-5 months) than in aged (24-25 months) male Sprague-Dawley rats. No significant difference was found in the incorporation by pituitary tissue of 32P into phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Also, the extent of prolactin secretion from isolated pituitary was significantly greater in young than in aged rats, while the prolactin pituitary content was significantly higher in aged animals. In vitro dopamine (DA) decreased the incorporation of 32P into PI, both in young and old pituitary glands, and inhibited prolactin secretion into the incubation medium. Brain cortex-phosphatidylserine (BC-PS), a pharmacologically active purified phospholipid, capable of stimulating the dopaminergic system in the hypothalamus and of decreasing prolactin secretion both in humans and rats in vitro and in vivo, inhibited the incorporation of labeled phosphate into PI of pituitary glands from either young or old rats, but did not alter the prolactin secretion from the glands incubated in vitro. Baseline prolactin plasma levels did not differ significantly between young and old rats either when blood was collected from the trunk after decapitation or underwent sampling from chronically cannulated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1987

Reparative processes in aged brain.

Endogenous neurotrophic factors have been proposed to play an important role in degenerative diseases and aging. In aged rats, neurotrophic activity induced by partial lesion of nigro-striatal pathways seems to be lower compared to young rats when assayed in vitro on cultured mesencephalic dissociated neuronal cells. In parallel experiments, we could also observe an age-dependent delay in spontaneous recovery of striatal tyrosine hydroxylase activity after lesion. Both experimental evidences suggest a low-potential neuroplasticity in aged rats. Nevertheless, the aging brain seems to be responsive to pharmacological manipulation. Long-term phosphatidylserine treatment has been shown to maintain the integrity of neuronal structures altered by the aging process. Putative mechanisms of action underlying these effects are presented.

Aging↗
PubMed1987

Rapidly growing yolk sac tumor of the ovary in a lactating patient.

A case of yolk sac tumor of the ovary exceptional for its size and rapid development is here presented and discussed. The patient was feeding her baby delivered only two months earlier. Hormonal influences of pregnancy and lactation might have played an important role in the progression of this neoplasm.

Adult↗
PubMed1986

Synthesis and activity profiles of atrial natriuretic peptide (ANP) analogs with reduced ring size.

Three deletion analogs of the atrial natriuretic peptide, [desGly-120]-ANP(103-126), [desLeu119, desGly120]ANP(103-126) and [desGly118,120,-desLeu119]-ANP(103-126), were synthesized by the solid-phase method. Successive elimination of the non-functional residues in positions 120-118 of the peptide sequence resulted in a progressive potency reduction in the rabbit aorta assay, in the bioassay monitoring suppression of aldosterone secretion from bovine zona glomerulosa cells and in a binding assay based on displacement of radioiodinated ANP(101-126) from bovine zona glomerulosa cell membranes. The fact that the deletion analogs showed quantitatively different relative potencies in each of the three in vitro assay systems was interpreted as further evidence in support of the existence of two or more classes of ANP receptors or binding sites.

Adrenal Glands↗
PubMed1986

Inhibition of protein kinase activity by apomorphine.

The effect of apomorphine (1-20 microM) on protein kinase activity was studied in extracts from rat peritoneal mast cells and brain tissue. Apomorphine inhibited the cyclic AMP-dependent and the calcium-plus phosphatidylserine-dependent protein kinase activity with an IC50 between 1 and 6 microM, depending on the tissue and on the protein kinase involved. This effect might explain previous results on the apomorphine-induced inhibition of histamine release in rat peritoneal mast cells.

Animals↗
PubMed1984

Role of the plasma membrane in the mechanism of cholesterol efflux from cells.

In order to investigate the role of the plasma membrane in determining the kinetics of removal of cholesterol from cells, the efflux of [3H]cholesterol from intact cells and plasma membrane vesicles has been compared. The release of cholesterol from cultures of Fu5AH rat hepatoma and WIRL-3C rat liver cells to complexes of egg phosphatidylcholine (1 mg/ml) and human high-density apolipoprotein is first order with respect to concentration of cholesterol in the cells, with half-times (t 1/2) for at least one-third of the cell cholesterol of 3.2 +/- 0.6 and 14.3 +/- 1.5 h, respectively. Plasma membrane vesicles (0.5-5.0 micron diameter) were produced from both cell lines by incubating the cells with 50 mM formaldehyde and 2 mM dithiothreitol for 90 min. The efflux of cholesterol from the isolated vesicles follows the same kinetics as the intact, parent cells: the t 1/2 values for plasma membrane vesicles of Fu5AH and WIRL cells are 3.9 +/- 0.5 and 11.2 +/- 0.7 h, respectively. These t 1/2 values reflect the rate-limiting step in the cholesterol efflux process, which is the desorption of cholesterol molecules from the plasma membrane into the extracellular aqueous phase. The fact that intact cells and isolated plasma membranes release cholesterol at the same rates indicates that variations in the plasma membrane structure account for differences in the kinetics of cholesterol release from different cell types. In order to investigate the role of plasma membrane lipids, the kinetics of cholesterol desorption from small unilamellar vesicles prepared from the total lipid isolated from plasma membrane vesicles of Fu5AH and WIRL cells were measured. Half-times of cholesterol release from plasma membrane lipid vesicles of Fu5AH and WIRL cells were the same, with values of 3.1 +/- 0.1 and 2.9 +/- 0.2 h, respectively. Since bilayers formed from isolated plasma membrane lipids do not reproduce the kinetics of cholesterol efflux observed with the intact plasma membranes, it is likely that the local domain structure, as influenced by membrane proteins, is responsible for the differences in t 1/2 values for cholesterol efflux from these cell lines.

Animals↗