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Biomedical subjects

M Sala

Publications and source records attributed to M Sala.

At least 127 records · Page 7Linked to original sources
PubMed1989

Histamine as a central modulator of rat intestinal transit.

Histamine (HA) injected i.c.v. to rats inhibited intestinal propulsion in linear relation to the log of the administered doses (in the range from 20-100 micrograms/rat). In the same dose range HA also induced a dose-related analgesic effect (tail-flick test). The dose of HA maximally active by the i.c.v. route (100 micrograms/rat) showed neither of these effects when injected i.v. or i.p. HA-induced intestinal inhibition and analgesia were antagonized competitively by i.c.v. mepyramine (10 micrograms/rat), an H1 receptor antagonist, whereas cimetidine (10 micrograms/rat), an H2 receptor antagonist, had no effect. Repeated i.c.v. injections of HA resulted in tachyphylaxis of both intestinal inhibition and analgesia. Pretreatment with i.c.v. naloxone (20 micrograms/rat) antagonized the antipropulsive effect of HA in a noncompetitive fashion, but did not affect its antinociceptive action. The relevance of the central histaminergic system in the modulation of gastrointestinal motility and its relationship with the opioid system are discussed.

Analgesia↗
PubMed1989

Multi-center study of a new technique for measuring free thyroxin in serum.

In a multi-center trial we evaluated the accuracy of a new assay kit for free thyroxin (T4), the Behring free T4 RIAgnost, in 1036 subjects: 379 normal subjects, 536 patients with thyroid dysfunction, and 121 subjects with no thyroid dysfunction but with conditions that potentially could interfere with the assay. The kit combines immunoextraction and the use of a modified tracer. Although some limitations remained in using a direct assay method for free T4 in certain nonthyroid conditions, this test was superior to one based on the use of a T4 analog. This kit seems to be very accurate for the diagnosis of untreated thyroid pathologies.

Adolescent↗
PubMed1988

Differences in the DNA adducts formed in cultured rabbit and rat dermal fibroblasts by benzo(a)pyrene and (-)benzo(a)pyrene-7,8-diol.

Benzo(a)pyrene (BaP) is highly carcinogenic in rats but is without effect in rabbits when administered s.c. The possibility that BaP-DNA adducts could be responsible for this species difference was investigated by comparing BaP-deoxyribonucleoside adducts formed in dermal fibroblast cultures from Wistar rats and New Zealand rabbits. Treatment with [G-3H]BaP (1.2 microM) for 6, 24, and 48 h produced an essentially qualitative species-specific difference. Over 95% of the DNA adducts in the rabbit dermal cell cultures were derived from anti-BaPDE; the major BaP adduct formed (90%) was (+)-anti-BaPDE-deoxyguanosine. This adduct was formed at very low levels in the rat dermal fibroblasts (7%). These cells contained a large proportion of (+/-)-r-7,t-8-dihydroxy-c-9,10-oxy-7,8,9,10-tetrahydrobenzo(a)pyrene (syn-BaPDE)-DNA adducts (45%) and over 48% of other, unidentified, BaP-DNA adducts. Cells treated with (-)-BaP-7,8-diol (1.2 microM) produced almost exclusively (greater than 99%) (+)-anti-BaPDE-deoxyguanosine in rabbit cells, while the rat cells did not form this product. These results suggest that adducts other than anti-BaPDE-deoxyguanosine may be involved in rat s.c. BaP carcinogenesis; the preferential formation of (+)-anti-BaPDE-deoxyguanosine by rabbit dermal fibroblasts does not directly correlate with the resistance of rabbit dermis to tumor formation.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1988

Supraspinal cerebral areas involved in morphine's intestinal inhibition and analgesia.

To explore the neuroanatomical pathways involved in mediating the antipropulsive effect and analgesia of morphine (M) in the periaqueductal gray matter (PAG), we examined the influence of the vagus nerve and the role of serotonergic neurotransmission. M-induced inhibition of intestinal transit was unaffected by subdiaphragmatic vagotomy. In contrast, electrolytic lesions in the raphe magnus nucleus (NRM) and pretreatment with a selective neurotoxin (5,6-DHT, 15 micrograms/rat) in the same region, both significantly reduced M-induced inhibition of intestinal transit. Analgesia was only slightly affected. p-CPA pretreatment (100 mg/kg IP) induced the same results. Finally some other central brain regions were found to be sensitive to M's intestinal inhibition and analgesia such as the mid-line thalamus, the dorsal and lateral hypothalamus, and the bulbar reticular formation. Negative results were obtained for frontal cortex, caudate and amygdala. Some considerations are put forward about the existence in the central nervous system of selective areas involved in intestinal modulation and their relation with those mediating pain transmission.

Analgesia↗
PubMed1988

Splanchnic exchange of amino acids after amino acid ingestion in patients with chronic renal insufficiency.

Splanchnic exchange (net uptake or release) of amino acids (AAs) was evaluated by measuring arterial-hepatic venous differences for AAs and hepatic blood flow in patients with chronic renal insufficiency (CRI) and control subjects before and for 70 min after the ingestion of an AA mixture simulating an animal protein meal. In CRI after AA ingestion, splanchnic exchange area for total nonessential AAs (NEAAs) is increased 135% over control subjects because of an augmented escape of proline, glutamate, serine, glycine, alanine, and cyst(e)ine; contrarily, glutamine shows an increased splanchnic uptake. Splanchnic exchange area for total essential AAs (EAAs) is increased only by 67% over controls because of a higher escape of threonine, isoleucine, phenylalanine, and histidine. Abnormalities in arterial areas for AAs parallel those in splanchnic areas except for glutamine and isoleucine. Data indicate that in CRI, at least for 70 min after an AA meal, splanchnic organs metabolize abnormally ingested AAs and export an increased and unbalanced bulk of AAs, severely affecting postprandial arterial profile of AAs.

Adult↗
PubMed1988

Glycosylation of four acute-phase glycoproteins secreted by rat liver cells in vivo and in vitro. Effects of inflammation and dexamethasone.

We have studied the role of the liver in the relative increase of Concanavalin A (Con A)-reactive molecular forms of various positive rat acute-phase glycoproteins (APGPs) occurring in serum during inflammation. Secretion media of hepatocytes isolated from inflamed rats showed a 2 to 5-fold increase of the total amounts of four APGPs studied in comparison to secretion media of control hepatocytes. These changes were in analogy with those observed for corresponding sera, except for alpha 1-antitrypsin. All the different Con A-reactive molecular forms were present in the media, with exception of the most reactive form of ceruloplasmin. In vitro and in vivo, dexamethasone augmented the secretion of three APGPs, and especially of the Con A-most reactive forms. The in vitro effect of dexamethasone--augmented secretion of Con A-reactive molecular forms of alpha 1-acid glycoprotein and haptoglobin--was comparable with the results obtained for hepatocytes isolated from inflamed rats. In vivo, dexamethasone treatment resulted in an even higher increase of the serum concentration of the Con A-most reactive forms of both APGPs than experimental inflammation did. Although an extrahepatic contribution cannot be excluded, these results suggest that alterations in the Con A reactivity of APGPs as observed during the acute-phase of inflammation have their origin in the liver. A change in the Con A reactivity of glycoprotein indicates a modulation of its glycosylation. Since dexamethasone can affect these changes in vivo and in vitro, glucocorticoids most probably are involved in the regulation of the glycosylation of the APGPs during biosynthesis in the liver.

Acute-Phase Proteins↗
PubMed1987

Further investigations on neurotensin as central modulator of intestinal motility in rats.

Previous studies have shown that neurotensin (NT) administered intracerebroventricularly (i.c.v.) to rats provokes an inhibition of intestinal propulsion linearly related to the log of administered doses. In the present study it is demonstrated that, in contrast to morphine, repeated i.c.v. administrations of NT (2.5 nmol/rat/day) did not result in tolerance to the intestinal effect. Naloxone (Nx) administered i.c.v. fully antagonized the intestinal inhibition of i.c.v. morphine, but did not significantly alter the NT effect. However, centrally administered thyrotropin-releasing hormone (TRH) inhibited NT-induced (but not morphine-induced) intestinal inhibition. Direct microinjections of NT into the periaqueductal gray matter (PAG) produced complete inhibition of intestinal propulsion when the microinjections were localized in the dorsal portion. Finally, subdiaphragmatic vagotomy totally abolished the inhibition induced by NT into the PAG, while morphine was not affected. Some considerations are put forward concerning the existence in the central nervous system of a peptidergic pathway modulating intestinal function.

Animals↗
PubMed1987

Hemoglobin transition in the anuran Pelodytes punctatus.

In the anuran Pelodytes punctatus the larval hemoglobin produces five electrophoretic bands. In the premetamorphic period, two other bands appear which are typical of the adult. They gradually substitute the larval bands completely as in other anurans. The pathway of the hemoglobin shift indicates that the synthesis of the adult fractions does not depend on the thyroid hormones for its activation, whereas the disappearance of the larval fractions depends on the destruction of the "larval" red blood cell line. As in other species of anurans which are considered primitive, the hemoglobinic change of Pelodytes punctatus starts earlier and develops slower than in other more evolved anurans. In normal developing specimens of Pelodytes punctatus the change in the hemoglobin fractions occurs very slowly and finishes 4 weeks after the metamorphosis, whereas in "hibernated" specimens the rate of change is higher and it ends earlier, probably as a consequence in the retarded larvae, of the increased sensibility of the hemopoietic tissues to the metamorphosis factors.

Aging↗
PubMed1987

Morphological transformation in three mammalian cell systems following treatment with 6-nitrochrysene and 6-nitrobenzo[a]pyrene.

Two nitroaromatics, 6-nitrobenzo[a]pyrene (6-N-BaP) and 6-nitrochrysene (6-N-CRY), and the corresponding parent hydrocarbons, benzo[a]pyrene (BaP) and chrysene (CRY), were studied in in vitro transformation assays with Syrian hamster embryo (SHE) cells, BALB/3T3 and C3H10T1/2 mouse cell lines. The three cell systems showed different sensitivities to the transforming effects of the chemicals studied, SHE cells being the most efficient, followed by 3T3 cells and the last being C3H10T1/2 cells. In the SHE cell system all compounds were active. Considering the concentrations (in microM) and the transformation frequency BaP was the most active, followed by 6-N-BaP, 6-N-CRY and CRY. In the BALB/3T3 standard assay and in the C3H10T1/2 assay only BaP was clearly active. When used as initiators 6-N-BaP and 6-N-CRY were inactive in the C3H cell system. In conclusion 6-N-BaP appears less active in in vitro systems than the parent compound BaP; 6-N-CRY is probably negative since it is questionable in vitro and negative in mouse skin.

Animals↗
PubMed1987

Genotype-dependent leaf senescence in maize : inheritance and effects of pollination-prevention.

Objective of research was (a) to evaluate the influence of pollination-prevention on various metabolic parameters of the two maize inbreds B73 and B14A and their F1, and (b) to gain information on the inheritance of leaf senescence, in response to pollination-prevention. The results show that the visual pattern of leaf senescence, in response to prevention of ear pollination, contrasts markedly between the two inbred lines. Relative to control plants, prevention of ear pollination, causes a premature senescence in B73 and B73 x B14A plants, while leaves of unpollinated B14A remain green and similar in appearance to pollinated controls. Furthermore, prevention of ear pollination induces a sizable reduction of dry matter accumulation of all above-ground material and changes in various metabolic parameters. An accumulation of sucrose in the leaves of unpollinated B73 and B73 x B14A plants is correlated with the development of premature senescence. Finally, the genetic analysis supports suggestions that a single dominant gene is responsible for the differences observed, in the visual pattern of leaf senescence, in response to prevention of ear pollination.

Journal Article↗
PubMed1986

Intestinal effect and analgesia: evidence for different involvement of opioid receptor subtypes in periaqueductal gray matter.

Periaqueductal gray matter (PAG) has been shown to be one of the sites in the central nervous system where microinjections of morphine strongly inhibit intestinal transit. To investigate the nature of opioid receptor populations involved in this central effect, selective opioid agonists, FK 33824 for mu, DALA for delta, dynorphin for kappa and tentatively beta-endorphin for epsilon, were microinjected in all PAG areas previously identified as morphine-sensitive for intestinal inhibition. The PAG-induced inhibition of intestinal transit appears to be mediated mainly by mu receptors and possibly by epsilon receptors. kappa and delta receptors seem not to be involved.

Analgesia↗
PubMed1986

In vitro and in vivo activity of 12-O-3-N-dansylamino TPA.

Dansyl-TPA, a fluorescent TPA analogue, which is a label with a high affinity for C3H/10T1/2 cells and induces 3H-choline release from these cells (Tran et al. Nouv. J. Chim 1984, 8, 751-757), has been studied for in vitro promoting activity in the same cell line initiated by a carcinogen MNNG and in vivo short-term mouse skin tests. In vitro, dansyl-TPA expresses transforming effect in its own (without MNNG pretreatment) as well as increases the production of transformed foci in MNNG-treated cells. In in vivo skin tests, dansyl-TPA displays lower effects than TPA on mouse skin. These results indicate a low promoting potential of dansyl-TPA.

Animals↗
PubMed1986

Activity and secretion of sialyltransferase in primary monolayer cultures of rat hepatocytes cultured with and without dexamethasone.

Monolayers of hepatocytes attached on collagen-coated dishes were cultured for 20-24 h and were found suitable to study the activity and secretion of CMP-N-acetylneuraminate:asialo-alpha 1-acid glycoprotein sialyltransferase. A progressive increase of sialyltransferase activity in the culture medium was observed during incubation of the hepatocytes. After 24 h 34-48% of the total sialyltransferase activity of the hepatocyte incubation system was present in the medium. The enzyme activity present in the medium was soluble in nature and could not be stimulated by Triton X-100. The secretion of the enzyme was stimulated about twofold by dexamethasone. The activity of sialyltransferase in the hepatocytes was also increased by dexamethasone. The Km of either hepatocyte or medium sialyltransferase for CMP-sialic acid was only slightly changed by dexamethasone, whereas the Vmax was increased about twofold. The secretion of sialyltransferase could be inhibited partially by the anti-microtubular agent colchicine. The dexamethasone-induced increase of the sialyltransferase activity in cells and media could be eliminated by inclusion of alpha-amanitin in the culture media at 0 h. The inhibiting effect of alpha-amanitin was only partially expressed when the drug was added 4 h after the addition of dexamethasone to the media. The results suggest that isolated rat hepatocytes actively secrete sialyltransferase and that the increase in the sialyltransferase activity in cells and media owing to the synthetic glucocorticosteroid dexamethasone results from increased synthesis of the enzyme molecule. It is supposed that in the intact rat the increased levels of the enzyme activity in serum observed in inflammation may originate from an induction of the synthesis of sialyltransferase in the hepatocytes of rat liver by the increased levels of circulating corticosteroids.

Amanitins↗
PubMed1985

Lack of effect of deflazacort, a novel glucocorticoid, on basal and TRH-stimulated prolactin and thyrotropin levels in healthy subjects.

The possible relationship between cortisol inhibition induced by deflazacort, a new glucocorticoid, and impairment of prolactin (PRL) and thyrotropin (TSH) secretion in healthy volunteers has been investigated. In 8 healthy subjects deflazacort pretreatment partly inhibited cortisol secretion but did not affect basal or TRH-stimulated secretion of PRL and TSH in comparison to placebo. After dexamethasone, there was the anticipated complete suppression of cortisol secretion, no change in PRL secretion, either in basal conditions or after TRH, and significant inhibition of the TSH response to TRH. No significant change in GH, aldosterone or renin secretion was observed after deflazacort or dexamethasone.

Adult↗
PubMed1985

Cerebral sites of central action of dermorphin on intestinal motility in the rat.

Dermorphin (DM), microinjected at 0.4 nmoles/rat into various sites of the periaqueductal gray matter (PAG), provokes complete inhibition of intestinal propulsion always coupled with full analgesia and catalepsy. When electrolytic lesions were made in the raphe magnus nucleus (NRM) a slight but significant reduction of intestinal inhibition evoked by DM into the PAG was observed. In contrast, pretreatment into the NRM 10 days before DM with a selective antiserotoninergic agent (5,6 DHT 15 microgram/rat), did not influence intestinal inhibition. As expected, both lesions reduced DM-induced analgesia but catalepsy was not affected. DM-induced inhibition of intestinal transit was therefore unaffected by subdiaphragmatic vagotomy. Finally, some other central brain regions were found sensitive to DM for the above effects such as the lateral and medial hypothalamus and mid-line thalamus. Negative results were obtained for the supraoptic nuclei and postero-medial cortical amygdaloid nucleus. Some considerations are put forward about the existence in the central nervous system of selective areas involved in intestinal modulation and their relationship with those mediating other opiate behavioural effects.

Amygdala↗