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E Agostoni

Publications and source records attributed to E Agostoni.

At least 37 records · Page 2Linked to original sources
PubMed2001

Electrical resistance and ion diffusion through mesothelium.

(1) Since phospholipids (PHL) added on the luminal side of specimens of parietal pericardium of rabbits decrease diffusional permeability (P) to Na+, but not to Cl-, P to Rb+, a cation with hydrated radius similar to that of Cl- was measured. P(Rb+) was 13.1 (+/-1.1, S.E.)x10(-5) cm/sec and it was not decreased by PHL. This suggests that PHL decrease size of intercellular "pores" of mesothelium, and restrict diffusion of solutes with radius>0.2 nm. (2) Electrical resistance (Re) of pericardium specimens was measured without PHL, with PHL, and after mesothelium was scraped away, to obtain Re of connective tissue and, thus, to compute Re of mesothelium. Re of connective tissue was 1.0+/-0.2 Omega cm(2); Re of mesothelium was 10.1+/-0.6 and 12.3+/-0.9 Omega cm(2) without and with PHL, respectively. The fraction of electrical current carried by Na+ indicates that Na+ diffusion through mesothelium without PHL is nearly free. (3) Re of cultured mesothelial cell monolayers of rat visceral pleura was 6.1+/-0.2 Omega cm(2), i.e. smaller than that of specimen mesothelium; it did not increase with PHL. P(Na+) of cultured mesothelial cell monolayers was 20.0x10(-5) cm/sec, i.e. greater than that of specimen mesothelium.

Animals↗
PubMed2000

Macromolecule transfer through mesothelium and connective tissue.

Diffusional permeability (P) to inulin (P(in)), albumin (P(alb)), and dextrans [70 (P(dx 70)), 150 (P(dx 150)), 550 (P(dx 550)), and 2, 000 (P(dx 2,000))] was determined in specimens of parietal pericardium of rabbits, which may be obtained with less damage than pleura. P(in), P(alb), P(dx 70), P(dx 150), P(dx 550), and P(dx 2, 000) were 0.51 +/- 0.06 (SE), 0.18 +/- 0.03, 0.097 +/- 0.021, 0. 047 +/- 0.011, 0.025 +/- 0.004, and 0.021 +/- 0.005 x 10(-5) cm/s, respectively. P(in), P(alb), and P(dx 70) of connective tissue, obtained after removal of mesothelium from specimens, were 10.3 +/- 1.42, 2.97 +/- 0.38, and 2.31 +/- 0.16 x 10(-5) cm/s, respectively. Hence, P(in), P(alb), and P(dx 70) of mesothelium were 0.54, 0.20, and 0.10 x 10(-5) cm/s, respectively. Inulin (like small solutes) fitted the relationship P-solute radius for restricted diffusion with a 6-nm "pore" radius, whereas macromolecules were much above it. Hence, macromolecule transfer mainly occurs through "large pores" and/or transcytosis. In line with this, the addition of phospholipids on the luminal side (which decreases pore radius to approximately 1.5 nm) halved P(in) but did not change P(alb) and P(dx 70). P(in) is roughly similar in mesothelium and capillary endothelium, whereas P to macromolecules is greater in mesothelium. The albumin diffusion coefficient through connective tissue was 17% of that in water. Mesothelium provides 92% of resistance to albumin diffusion through the pericardium.

Animals↗
PubMed1999

Identification and characterization of a new member of the gas3/PMP22 gene family in C. elegans.

The Gas3/PMP22 protein family is characterized by tetraspan transmembrane proteins. The gas3/PMP22 gene is highly expressed in Schwann cells of the peripheral nervous system, and different alterations of this gene are associated with hereditary demyelinating neuropathies, such as the Charcot-Marie-Tooth type 1A, the Dejerine-Sottas syndrome and the Hereditary Liability to Pressure Palsies (HNPP).Here, we report on the identification of at least one member of the Gas3/PMP22 family in the nematode C. elegans (C01C10.1b). C01C10.1b shares 36% of identical amino acids with the human Gas3/PMP22 and is characterized by four hydrophobic putative transmembrane domains. It lacks the typical N-linked glycosylation consensus in the first extracellular loop. C01C10.1b is transcribed as an operon downstream to the gene C01C10.1a, which encodes for a putative tetraspan protein with less conserved homology with the Gas3/PMP22 family. Interestingly, C01C10.1a contains three N-glycosylation sites at the C-terminus. Both genes are expressed in different nematode developmental stages and in the adults. The characterization of one member of the gas3/PMP22 family in C. elegans gives the opportunity to use this model organism to investigate the role of gas3/PMP22 in the regulation of cell proliferation and differentiation and its relation to the hereditary neurodegenerative diseases in humans.

Amino Acid Sequence↗
PubMed1999

Rho-dependent regulation of cell spreading by the tetraspan membrane protein Gas3/PMP22.

Gas3/PMP22 plays a crucial role in regulating myelin formation and maintenance, and different genetic alterations in gas3/PMP22 are responsible for a set of human peripheral neuropathies. We have previously demonstrated that Gas3/PMP22 could regulate susceptibility to apoptosis in NIH3T3 cells but not in REF 52 cells. In this report we demonstrate that when the apoptotic response triggered by gas3/PMP22 was counteracted by Bcl-2 coexpression, morphological changes were observed. Time-lapse analysis confirmed that Gas3/PMP22 can modulate cell spreading, and this effect was strengthened after inhibition of phosphoinositide 3-kinase. Using the active form of the small GTPase RhoA, we have been able to dissect the different Gas3/PMP22 biological activities. RhoA counteracted the Gas3/PMP22-dependent morphological response but was unable to neutralize the apoptotic response. Treatment of NIH3T3 cells with cytotoxic necrotizing factor 1, which activates endogenous Rho, also counteracted Gas3/PMP22-mediated cell shape and spreading changes. Treatment of REF 52 cells, which are unresponsive to Gas3/PMP22 overexpression, with the C3 exoenzyme, inhibiting Rho activity, renders REF 52 cells responsive to Gas3/PMP22 overexpression for cell shape and spreading changes. Finally, assembly of stress fibers and focal adhesions complexes, in response to lysophosphatidic acid-induced endogenous Rho activation, was impaired in Gas3/PMP22-overexpressing cells. We hypothesize that cell shape and spreading regulated by Gas3/PMP22 through the Rho GTPase might have an important role during Schwann cells differentiation and myelinization.

3T3 Cells↗
PubMed1999

Chronic axonal sensory and autonomic polyneuropathy without motor involvement: a new 'chronic inflammatory neuropathy?'.

We report the case of a woman with axonal sensory and autonomic neuropathy lasting several months who improved in association with steroid administration. During the course of her disease and in the follow-up, the patient underwent repeated cerebrospinal fluid (CSF) examinations, neurophysiological somatic, autonomic nervous system studies and sural nerve biopsy. Clinical and laboratory assessments demonstrated the occurrence of a monophasic, chronic sensory and autonomic neuropathy. A sural nerve biopsy suggested an axonopathy. After a progressive worsening of symptoms lasting about 6 months, steroid treatment was started and within 6 months a complete recovery, with normalization of the CSF findings, was observed. Although the 'chronic inflammatory neuropathies' are still debated entities, the features of this chronic, exclusively sensory and autonomic neuropathy are new, and the occurrence of a high protein level in the CSF, together with the favorable outcome associated with steroid treatment, suggests that our case might be another variant in this debated area.

Autonomic Nervous System Diseases↗
PubMed1999

Equivalent radius of paracellular "pores" of the mesothelium.

Diffusional permeability (P) to water (P(w)), Cl(-) (P(Cl(-))), and mannitol (P(man)) was determined in specimens of rabbit parietal pericardium without and with phospholipids added on the luminal side, as previously done with sucrose and Na(+). P to the above-mentioned molecules and to Na(+) (P(Na(+))) was also determined after mesothelium was scraped away from specimens. P(w), P(Cl(-)), P(Na(+)), and P(man) of connective tissue were the following (x10(-5) cm/s): 73.1 +/- 7.3 (SE), 59.5 +/- 4.5, 41.7 +/- 3.4, and 23.4 +/- 2.4, respectively. From these and corresponding data on integer pericardium, P(w), P(Cl(-)), P(Na(+)), and P(man) of mesothelium were computed. They were the following: 206, 17.9, 9.52, and 3.93, and 90.2, 14.4, 4.34, and 1.75 x 10(-5) cm/s without and with phospholipids, respectively. As previously found for P to sucrose, P to solutes is smaller in mesothelium than in connective tissue, although the latter is approximately 35-fold thicker; instead, P(w) is higher in mesothelium, suggesting marked water diffusion through cell membrane. Equivalent radius of paracellular "pores" of mesothelium was computed with two approaches, disregarding P(w). The former, a graphical analysis on a P-molecular radius diagram, yielded 6.0 and 1.7 nm without and with phospholipids, respectively. The latter, on the basis of P(man), P to sucrose, and function for restricted diffusion, yielded 7.8 and 1. 1 nm, respectively.

Animals↗
PubMed1998

Mechanical coupling and liquid exchanges in the pleural space.

The pleural space provides the mechanical coupling between lung and chest wall: two views about this coupling are reported and discussed. Information on volume, composition, thickness, and pressure of the pleural liquid under physiologic conditions in a few species is provided. The Starling pressures of the parietal pleura filtering liquid into pleural space, and those of the visceral pleura absorbing liquid from the space are considered along with the permeability of the mesothelium. Information on the lymphatic drainage through the parietal pleura and on the solute-coupled liquid absorption from the pleural space under physiologic conditions and with various kinds of hydrothorax are provided.

Age Factors↗
PubMed1998

Diffusional permeability of rabbit mesothelium.

Diffusional permeability (P) to sucrose (Psuc) and Na+ (PNa+) was determined in specimens of rabbit sternal parietal pericardium, which may be obtained without stripping. Specimens were mounted in an Ussing apparatus with 3H-labeled sucrose and 22Na+ in a luminal (L) or interstitial (I) chamber. Psuc was 2.16 +/- 0.44 for L-->I and 2.63 +/- 0.45 (SE) x 10(-5) cm/s for I-->L, i.e., approximately 10 times smaller than that previously obtained in stripped specimens of pleura despite the similarity of intercellular junctions in pericardium and pleural mesothelium of various species. These findings suggest that previous Psuc was overestimated because stripping damages the mesothelium. PNa+ (x10(-5) cm/s) was 7.07 +/- 0.71 for L-->I and 7.37 +/- 0.69 x 10(-5) cm/s for I-->L. Measurements were also done with phospholipids, which are adsorbed on the luminal side of mesothelium in vivo. With phospholipids in L, Psuc was 0.75 +/- 0.10 and 0.65 +/- 0.08 and PNa+ was 3.80 +/- 0.32 and 3.76 +/- 0.15 x 10(-5) cm/s for L-->I and I-->L, respectively, i. e., smaller than without phospholipids. With phospholipids in I (where they are not adsorbed), Psuc (2.33 +/- 0.42 x 10(-5) cm/s) and PNa+ (7.01 +/- 0.45 x 10(-5) cm/s) were similar to those values without phospholipids. Hence, adsorbed phospholipids decrease P of mesothelium. If the mesothelium were scraped away from the specimen, Psuc of the connective tissue would be 13.2 +/- 0.76 x 10(-5) cm/s. Psuc of the mesothelium, computed from Psuc of the unscraped and scraped specimens, corrected for the effect of unstirred layers (2. 54 and 19.4 x 10(-5) cm/s, respectively), was 2.92 and 0.74 x 10(-5) cm/s without and with phospholipids, respectively. Hence, most of the resistance to diffusion of the pericardium is provided by the mesothelium.

Animals↗
PubMed1997

Effect of adrenaline and alpha-agonists on net rate of liquid absorption from the pleural space of rabbits.

Indirect evidence supporting a solute-coupled liquid absorption from the pleural space of rabbits has recently been provided; moreover, the beta 2-adrenoceptor agonist terbutaline has been found to increase this absorption. In this study the effect of adrenaline and alpha-adrenoceptor agonists on net rate of liquid absorption (Jnet) from albumin Ringer hydrothoraces of various sizes has been determined in anaesthetized rabbits. In hydrothoraces with adrenaline (5 x 10(-6) M) the relationship between Jnet and volume of liquid injected was displaced upwards by 0.09 ml h-1 relative to that in control hydrothoraces (P < 0.01). This displacement did not occur with lower adrenaline concentrations or after pretreatment with the beta-blocker propranolol. Hence, this increase in Jnet is mediated by stimulation of beta-receptors. It seems to be caused by an increase in solute-coupled liquid absorption, since beta-agonists inhibit lymphatic activity while, at relatively high concentrations, they may increase active transport. Conversely, the strong stimulation of lymphatic alpha-receptors that should occur with adrenaline after beta-blockade may fail to increase lymphatic drainage, because it has been shown that the increase in contraction frequency of lymphatics may be balanced by the decrease in their stroke volume. Arterial blood pressure during the hydrothoraces with adrenaline was unchanged. In hydrothoraces with the alpha 2-agonist clonidine (5 x 10(-6) M; a less potent agent than adrenaline) the slope of the relationship between Jnet and volume injected increased by 26% (P < 0.01), while its origin did not change. This increase in slope did not occur with a lower clonidine concentration or after pretreatment with the alpha-blocker phentolamine. Hence, it is caused by stimulation of alpha 2-receptors, which probably lead to an increase in lymphatic drainage related to liquid load. In hydrothoraces with the alpha 1-agonist phenylephrine (5 x 10(-6) or 10(-7) M) Jnet was simlar to control values.

Absorption↗
PubMed1996

cec-1, a soma-specific chromobox-containing gene in C. elegans.

The chromo domain is a phylogenetically conserved sequence motif which was identified as a region of homology between the repressor protein Pc and the heterochromatin constitutive protein HP1 of Drosophila. The specific function of the chromo domain is not yet understood, but it seems to be required for protein-protein interactions in chromatin-associated complexes. Here, we present a new chromobox-containing gene from Caenorhabditis elegans (cec-1). It encodes a nuclear protein that is present in all somatic cells from the 50- to 80-cell stage on throughout development and in adult animals. No cec-1 protein was detected in the cells of early embryos, in germ cells, and in their precursor cells Z2 and Z3. cec-1 mRNA, however, is already present in all the blastomeres of early embryos. Immunolocalization experiments revealed a homogeneous distribution of CEC-1 within interphase nuclei, while during mitosis CEC-1 seems to dissociate from the condensing chromosomes. The expression pattern of the cec-1 gene suggests that it may represent a new regulatory gene in C. elegans.

Amino Acid Sequence↗
PubMed1996

Effect on phloridzin on net rate of liquid absorption from the pleural space of rabbits.

Previous indirect findings have suggested the occurrence of solute-coupled liquid absorption from the pleural space, consistent with Na(+)-K(+)-ATPase on the interstitial side plus a Na(+)-H+ and CI(-)-HCO3- double exchange on the luminal side of the pleural mesothelium. To assess whether Na(+)-glucose cotransport also operates on the luminal side, the relationship between net rate of liquid absorption from the right pleural space (Jnet) and volume of liquid injected into this space (0.5, 1 or 2 ml) was determined in anaesthetized rabbits during hydrothoraces with phloridzin (10(-3)M) or with phloridzin plus 4-acetamido-4'-isothiocyanatostilbene-2, 2'-disulphonic acid (SITS; 1.5 x 10(-4)M). The relationship obtained during hydrothoraces with phloridzin was displaced downwards by 0.09 ml h-1 relative to that in control hydrothoraces (P < 0.01). The decrease in Jnet was similar in hydrothoraces of various sizes. The relationship obtained in hydrothoraces with phloridzin plus SITS was displaced downwards by 0.16 ml h-1 relative to that in control hydrothoraces (P < 0.01), i.e. the decrease in Jnet was similar to the sum (0.17 ml h-1) of the decreases in Jnet produced individually by phloridzin and by SITS (0.08 ml h-1). The decrease in Jnet was similar in hydrothoraces of differing size. The above findings are consistent with the occurrence of Na(+)-glucose cotransport on the luminal side of the pleural mesothelium, operating simultaneously with the double exchange also under physiological conditions.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1995

Beta-agonist activation of an amiloride-insensitive transport mechanism in rabbit pleura.

The beta-agonist terbutaline increases the net rate of liquid absorption from hydrothoraces with albumin-Ringer solution: since beta-agonists decrease lymphatic drainage, the effect of terbutaline seems due to an increase in solute-coupled liquid absorption, (Zocchi et al. 1994 Respir. Physiol. 97:347-356). In this research we determined in anesthetized rabbits the rate of volume change in albumin-Ringer hydrothoraces of different size with amiloride plus terbutaline, and compared it with that previously obtained in hydrothoraces with amiloride alone. The net rate of liquid absorption was 0.09 ml/h greater (P < 0.01) with amiloride plus terbutaline than with amiloride alone. This indicates that terbutaline activates an amiloride-insensitive mechanism of Na+ transport. The increase in net rate of liquid absorption produced by terbutaline persisted with bumetanide 10(-6) M and SITS 10(-4) M, disappeared almost completely with bumetanide 10(-5) M, and completely with furosemide 10(-3) M. These findings suggest that the mechanism activated by terbutaline, when the amiloride-sensitive mechanisms of the pleura have been blocked, is a Na(+)-K(+)-2 Cl- or Na(+)-Cl- symport little sensitive to bumetanide.

Amiloride↗
PubMed1994

Effects of beta-adrenergic blockade or stimulation on net rate of hydrothorax absorption.

We determined in anesthetised rabbits the net rate of liquid absorption (NRLA) from Ringer or 1% albumin-Ringer hydrothoraces with the beta-blocker propranolol (or nadolol) or the beta-agonist terbutaline. The beta-blocker reduced NRLA by 38% in 2 ml Ringer hydrothoraces, and did not change it in 2 ml albumin-Ringer hydrothoraces; hence, with beta-blocker NRLA became similar in both kinds of hydrothorax (0.31 +/- 0.02 ml/h). Terbutaline decreased NRLA by 25% in 2 ml Ringer hydrothoraces, and increased it by 29% in 2 ml albumin-Ringer hydrothoraces; hence, with terbutaline NRLA became similar in both kinds of hydrothorax (0.40 +/- 0.02 ml/h), and 25% higher than with beta-blocker. Because beta-adrenoreceptor activity inhibits lymphatic smooth muscles and may increase Na+ transport in epithelia, these results suggest that: (1) pleural mesothelium is provided with beta-receptors, which increase Na+ transport and seem activated by protein dilution, (2) beta-receptors of the pleural lymphatics are essentially silent with and without protein dilution, (3) the lymphatic drainage produced by smooth muscle activity is smaller than the increase in solute-coupled liquid absorption caused by mesothelium beta-receptors.

Absorption↗
PubMed1993

Active Na+ transport and coupled liquid outflow from hydrothoraces of various size.

The net rate of liquid flow and Na+ flux across the pleura was determined in anesthetised rabbit during hydrothoraces 0.5 to 5 ml in size, without and with amiloride. In the hydrothoraces with amiloride the net liquid flow and Na+ flux reversed when the volume injected approached zero. This indicates that the active Na+ transport and the consequent liquid absorption occur also under physiological conditions. The difference between the data obtained without and with amiloride provides the net solute-coupled liquid outflow and active Na+ efflux. These parameters increased linearly with the hydrothorax size up to 2 ml (0.39 ml/h and 54 muEq/h, respectively), and then levelled off. The linear relationship allowed their extrapolation to physiological conditions: 0.15 ml/h (0.07 ml.h-1.kg-1) and 21 muEq/h (0.1 muEq.h-1.cm-2). The increase in these parameters with the hydrothorax size seems due to the protein dilution caused by the Ringer injection, because it did not occur if Ringer was added with albumin to keep the protein concentration in the pleural liquid similar to that under physiological conditions.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1993

Preimplantation development of the mammalian embryo.

The bases for the differentiation of an adult individual are founded during the early development of the mammalian embryo before its implantation in the uterus. After the first cleavage, which is under maternal genome control, the segmentation continues under the control of the embryonic genome. At this time polarization and flattening of the blastomeres and the formation of specialized junctions among them, characterize the foundation of two different cell populations. These will give rise to the inner cell mass and the trophectoderm, which are finally segregated during cavitation. The last step of the preimplantation development is the blastocyst hatching from the zona pellucida, that prevented the implantation until now. During the preimplantation period the embryo may be exposed to environmental chemicals via mother genital fluid and teratogenic effects have been reported during this period. Even if the differentiation of the blastomeres begins very early in the development, the embryo seems to conserve its developmental plasticity, suggesting that the mechanisms of this teratogenicity are eventually to be found at DNA level.

Abnormalities, Drug-Induced↗
PubMed1992

Liquid volume, Na+ and mannitol concentration in a hypertonic mannitol-Ringer hydrothorax.

In anesthetised rabbits with a 2 ml hypertonic mannitol-Ringer hydrothorax in the right space 30 mM/L mannitol were required for an unchanged volume of the hydrothorax after 60 min. [Na+] in the pleural liquid 10, 30 and 60 min after this hydrothorax was 8, 7 and 5 mEq/L, respectively, lower (P less than 0.01) than the initial one and that in a Ringer-hydrothorax. This seems due to the active transport of Na+ out of the pleural space followed by little water because of the osmotic pressure exerted by mannitol. This finding provides further evidence for an active transport without using inhibitors, and implies that the mesothelium offers an appreciable resistance to small solute diffusion. Mannitol concentration, measured at corresponding times from the activity of labeled mannitol, was 76, 68 and 56%, respectively, of the initial one (24.5 mM/L). From 30 to 60 min 6.5 microM of mannitol left the right space mainly by diffusion. The diffusional permeability of the mesothelium was indirectly assessed from the diffusional outflux of mannitol, the surface of the pleural space, and an estimate of mannitol concentration in the interstitium next to the mesothelium: it is smaller than that found in vitro.

Animals↗
PubMed1991

Electrolyte transport across the pleura of rabbits.

The amounts of Na+ and Cl- in the right pleural space of anesthetized rabbits were determined 10 and 60 min after a 2 ml hydrothorax with the following solutions: Ringer, Ringer with an inhibitor of the Na(+)-Cl- coupled transport or of the Na+/K+ pump, Ringer with gluconate instead of Cl- or with methylglucamine instead of Na+. During the 10-60 min period: (a) with Ringer Na+ and Cl- decreased (P less than 0.01) along with an iso-osmotic liquid absorption, (b) with disulfonic-stilbene (0.1 mM), amiloride (0.7 mM), acetazolamide (0.1 mM), or ouabain (0.5 mM) Na+ did not change and Cl- decreased less (P less than 0.01) than with Ringer. With gluconate-Ringer or methylglucamine-Ringer the liquid flow reversed: in the former case Cl- and, to a smaller extent, Na+ increased (P less than 0.01); in the latter only Na+ increased (P less than 0.01). These findings suggest: (1) the occurrence of a Na+/H+ and Cl-/HCO3- double exchange on the serosal side and of a Na+/K+ pump on the interstitial side of the pleural mesothelium; (2) a slow efflux from the pleural space of gluconate or methylglucamine relative to the corresponding influx of Cl- or Na+, respectively; this drags liquid into the space by osmotic gradient.

Acetazolamide↗