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M Zoli

Publications and source records attributed to M Zoli.

At least 127 records · Page 7Linked to original sources
PubMed1992

Feeding and drinking responses to neuropeptide Y injections in the paraventricular hypothalamic nucleus of aged rats.

Neuropeptide Y (NPY), a peptide of the pancreatic polypeptide family, exerts a potent stimulatory action on eating when injected into the paraventricular hypothalamic nucleus (PVN) in rats. Several NPY-containing systems are altered with advancing age, and aged rodents develop anorexia and a modified daily cycle pattern of feeding. These findings suggest that a relationship may exist between the aging-related anorexia and the reduced function of NPY-containing systems projecting to the PVN. In the present study eating and drinking behavior in satiated or fasted young (3 months) and aged (24 months) rats have been investigated over 22 h after NPY injection into the PVN. The levels of NPY immunoreactivity (IR) in PVN were also evaluated by means of semiquantitative immunocytochemistry. NPY injections into PVN increased food and water consumption in both young and aged satiated rats 30, 90 and 240 min after injection. However, the feeding and drinking responses elicited by 0.05, 0.10 and 1.0 nmol of NPY were significantly attenuated in the aged rats when compared to young rats. In aged rats, 24 h of food and water deprivation produced significant increase of food consumption measured at 30, 90 min and 22 h, which was equivalent to that induced by 1.0 nmol NPY injection. Administration of 1.0 nmol NPY in PVN did not further increase the 24 h deprivation effect on feeding in both groups of rats, but enhanced drinking in deprived young rats. This effect was not present in aged rats. In addition, aged rats showed a stronger response to 24 h deprivation than to 1.0 nmol NPY administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

Defective methionine metabolism in cirrhosis: relation to severity of liver disease.

A block in the transsulfuration pathway has previously been suggested in cirrhosis on the basis of increased fasting methionine concentrations, decreased methionine elimination and low levels of methionine end products. To date, methionine elimination has never been studied under controlled steady-state conditions, and the relation of the severity of liver disease to impaired methionine metabolism has not been clarified. We measured methionine plasma clearance in 6 control subjects and in 12 patients with cirrhosis during steady-state conditions obtained by a primed, continuous methionine infusion. In the presence of high-normal fasting methionine concentrations (range = 14 to 69 mumol.L-1 in controls and 26 to 151 mumol.L-1 in cirrhotic patients), methionine plasma clearance was reduced in cirrhotic patients (2.25 +/- S.D. 0.43 ml.sec-1 vs. 2.86 +/- S.D. 0.43 ml.sec-1 in controls; p less than 0.05), whereas methionine half-life was increased (282 +/- 90 min vs. 187 +/- 25 min in controls; p less than 0.05). Fasting methionine significantly correlated with methionine clearance. The infused methionine was not degraded to urea to any significant extent in cirrhotic patients, whereas a threefold increase in urinary urea nitrogen excretion rate was observed in controls. Similarly, taurine concentrations significantly increased both in plasma and in the urine in controls but not in cirrhotic patients. In cirrhotic patients methionine plasma clearance significantly correlated with galactose elimination capacity (r = 0.818) and with the Child-Pugh score (rs = -0.795). The study supports a major role of impaired liver cell function in the reduced metabolism of methionine and decreased formation of methionine end products that occur in cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of S-adenosyl-L-methionine administration on plasma levels of sulphur-containing amino acids in patients with liver cirrhosis.

An impaired transsulphuration pathway has been described in patients with liver cirrhosis. The defective metabolic step is located at the site of S-adenosyl-L-methionine (SAMe) formation from methionine. In a placebo-controlled study, we measured the fasting plasma levels of sulphur-containing amino-acids in cirrhotic patients with hypermethioninemia and/or severe hepatocellular failure, during treatment with exogenous SAMe (1.2 g i.v. for 3 days, followed by an oral administration of 1.2 g for an additional 30 days; 8 cases) or saline and placebo tablets (8 cases). All subjects were initially treated during hospital admission, and completed the oral study as out-patients. In patients given SAMe, long-term treatment doubled the plasma concentration of the secondary sulphur-containing amino acid cystine (from 36 [SD 18] mumol.l(-1) to 67 [36]) and taurine (from 42 [13] mumol.l(-1) to 89 [33]), which were on average low-normal at baseline, without any change in the concentration of methionine, of neutral amino acids, and of polyamines. No changes in plasma amino acids were observed in the control group. Two-factor, repeated measures of analysis of variance revealed differences between SAMe- and placebo-treated patients, consistent with an effect of long-term SAMe administration on secondary sulphur-containing amino acids. The potential therapeutic advantage of such treatment remains to be determined in clinical studies.

Journal Article↗
PubMed1992

Polyamine plasma levels and liver regeneration following partial hepatic resection in man.

Polyamines (putrescine, spermidine, and spermine) are widely distributed in animal and vegetal tissues, where their intracellular concentration strictly correlates with normal and pathological cell growth and protein synthesis. By means of a sensitive HPLC technique, the fasting plasma concentrations of polyamines were measured serially in 11 patients who underwent partial hepatic resection because of focal liver lesions. Samples were obtained before surgery and over the next 6 months, during hepatic regeneration. Liver volume was also measured by ultrasound on the basis of the 3 maximum diameters of the liver. From 2 to 4 weeks after surgery, plasma putrescine increased by a maximum of 78%, and spermidine by approximately 50%. No changes were observed in spermine levels. The spermidine/spermine ratio nearly doubled during liver regeneration. The volume of the liver decrease from 1505 [SD 236] ml to 743 [151] ml after resection, and returned to nearly normal values after 6 months (1231 [100] ml, p < 0.05 vs. basal values). The liver regeneration rate was highest 2-4 weeks after resection, and declined thereafter, when prevailing polyamine concentrations returned to normal. These data show that liver regeneration is accompanied by a significant increase in fasting putrescine and spermidine concentrations, which might be biochemical signals of active liver cell regeneration.

Adult↗
PubMed1992

Neuronal plasticity and ageing processes in the frame of the 'Red Queen Theory'.

On the basis of the morphofunctional evidence obtained in old brains of humans and mammals the present hypothesis has been introduced. This hypothesis states that neuronal plasticity can be used either to compensate for neuronal degeneration or to store new information. Thus, in pathological ageing the marked rate of degeneration has fully exhausted the already reduced plasticity capability of neural networks. In this way marked impairments of memory trace formation take place in pathological ageing conditions such as Alzheimer's disease. The essence of this hypothesis is that a competition for the available plasticity exists between the compensatory responses to ageing-induced degeneration and the processes necessary for memory trace formation. We have called this hypothesis the 'Red Queen Theory', an analogy borrowed from Lewis Carroll's book Through the Looking Glass. Thus, in ageing, processes responsible for plasticity must be forced to run at the highest possible rate to maintain the morphofunctional substrate of the existing networks as well as to allow the formation of new memory traces.

Aging↗
PubMed1992

Central mechanisms subserving the impaired growth hormone secretion induced by persistent blockade of NMDA receptors in immature male rats.

Recently, we have reported in immature female rats that short-term blockade of glutamate receptors of the N-methyl-D-aspartic acid (NMDA) subtype by the noncompetitive antagonist MK-801 induced a reduction of growth rate, basal and stimulated growth hormone (GH) release and plasma somatomedin C levels. In the present study, we investigated in immature male rats the mechanism(s) through which agonists and antagonists of glutamate receptors affect GH secretion. In 21-day-old male rats, administration of MK-801 (0.2 mg/kg i.p.b.i.d.) for 10 days induced a significant impairment of growth rate, which was unrelated to a significant reduction of food intake. GH secretion from anterior pituitary fragments of MK-801-treated rats was not significantly reduced under basal conditions but was significantly less under stimulation by 40 mM K+. Incubation of dispersed pituitary cells of 31-day-old rats with N-methyl-aspartic acid (1 and 100 microM), alone or associated with MK-801 (1 microM) did not change GH secretion. Semi quantitative densitometric analysis of hypothalami of MK-801-treated rats evidenced a clearcut decrease in the intensity of GHRH-like immuno-reactivity (LI) staining in the median eminence (ME), whereas no difference was observed in the ME-somatostatin (SS)-LI. Finally, GHRH mRNA but not SS-mRNA, evaluated by slot-blot hybridization, was reduced in the hypothalamus of MK-801-treated rats. These and our previous data would demonstrate that NMDA glutamate receptors play an important role in the neuroendocrine control of GH secretion in the rat, and suggest an action mediated by GHRH-secreting neurons.

Animals↗
PubMed1992

Beta-human chorionic gonadotropin and alpha-fetoprotein in central and peripheral venous blood of patients with testicular tumors.

From January 1989 to June 1991, 18 patients ranging in age from 19 to 41 (mean 34) years with testicular tumor were examined. 14 patients had seminoma (11 typical and 3 spermatocytic) and 4 patients had a mixed form (2 seminoma + embryonal tumor and 2 seminoma + teratocarcinoma). Serum levels of beta-human chorionic gonadotropin and alpha-fetoprotein from peripheral venous blood and from spermatic venous vessel were evaluated in every patient. All patients with seminoma and in a patient with mixed tumor (seminoma + embryonal tumor) the markers were regular. The increase of the markers was found in the peripheral and in spermatic blood of 3 patients (2 seminoma + embryonal carcinoma and 1 seminoma + teratocarcinoma). For these reasons the values of spermatic vessels are an important confirmation of the level of peripheral markers.

Adult↗
PubMed1992

Siagoside selectively attenuates morphological and functional striatal impairments induced by transient forebrain ischemia in rats.

BACKGROUND AND PURPOSE: Transient forebrain ischemia induced in rats by the four-vessel occlusion method is known to produce severe neural damage in the hippocampus and striatum and a behavioral syndrome the major symptom of which is a working memory deficit. Recent evidence suggests that monosialogangliosides can ameliorate postischemic symptoms. Our purpose was to study the effect of siagoside, the inner ester of GM1 ganglioside, on some behavioral and morphological impairments induced by four-vessel occlusion in rats. METHODS: Rats were injected daily with 5 mg/kg i.p. siagoside starting 4 hours after the cerebral ischemia. After 14 days the rats were tested for working memory in a water T maze or scored for apomorphine-induced stereotypy. The rats were killed 21 days after the cerebral ischemia. Histological and computer-assisted morphometric analyses were performed on cresyl violet-stained brain sections, which were graded according to a neuropathologic score, and on sections stained with a monoclonal antiserum against dopamine and cyclic adenosine-3',5'-monophosphate-regulated phosphoprotein, a marker for striatal dopaminoceptive neurons. RESULTS: Siagoside treatment reduced the stereotypy score induced by low doses of apomorphine and the extent of striatal lesions but did not affect the working memory deficit or the extent of hippocampal lesions. CONCLUSION: Daily siagoside treatment after acute cerebral ischemia attenuates some morphological and functional deficits related to striatal damage. These effects can be interpreted as a selective protective action on striatal neural populations or as a modulatory action on neural systems involved in striatal control. These data are consistent with preliminary clinical reports showing that monosialogangliosides enhance motor recovery after acute ischemic stroke.

Animals↗
PubMed1992

Regional and cellular distribution within the rat prostate of two mRNA species undergoing opposite regulation by androgens.

We have investigated, by in-situ hybridization histochemistry, the distribution within the rat ventral prostate of the mRNAs for sulphated glycoprotein-2 (SGP-2) and ornithine decarboxylase (ODC; EC 4.1.1.17), two proteins that appear to be inversely regulated by androgens in this organ, in that the level of SGP-2 mRNA is lowered, while the activity of ODC is enhanced by the latter hormones. Low-magnification autoradiograms of whole ventral prostate sections showed that, in intact animals, the SGP-2 transcript was only detectable in restricted areas and not diffused evenly throughout the section. Reciprocally, the ODC transcript was not detectable in areas where the SGP-2 transcript was detected, but appeared distributed uniformly in the remaining parts of the section. The effect of castration on the levels of the two mRNAs was evaluated by a semiquantitative analysis of autoradiograms from whole ventral prostate sections using an autoimmune image analyser. Four days after castration, SGP-2 mRNA increased by about 11-fold, while ODC mRNA decreased by fivefold. The distribution of the two mRNAs among the different cell types, studied by treating the slides with photographic emulsion and counterstaining, showed that both were expressed exclusively in the epithelial luminal cells of the ducts. Furthermore, each of the two mRNAs preferentially accumulated in a cell population which was morphologically distinct while accumulation of the other was negligible. SGP-2 mRNA was mostly found in cuboidal epithelial cells and ODC mRNA in columnar epithelial cells. Castration caused a dramatic accumulation of SGP-2 and a decrease in ODC mRNAs in the cells of the columnar epithelium 4 days later.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗
PubMed1992

Anthropometric assessment of the nutritional status of patients with liver cirrhosis in an Italian population.

A poor nutritional status has repeatedly been described in advanced liver cirrhosis, but the exact prevalence of the defect and its relation to the aetiology and severity of liver disease in the Italian population are only partly known. Anthropometric measurements were carried out in 200 patients with cirrhosis (135 M, 65 F). Liver disease was related to alcohol abuse in 77 cases, but most patients had stopped alcohol for at least 6 months before study. In comparison to a normal elderly Italian and to an age-matched North-American population, 5 to 45% of male patients with cirrhosis and 10 to 30% of females had signs of malnutrition, the proportion being variable according to the test used. Male patients showed a remarkable reduction in muscle mass (30-45% of patients, mainly in the presence of moderate-to-severe or severe liver failure), whereas female patients showed a more remarkable reduction of fat stores (15-30% of cases), with advancing liver failure, and a less severe reduction in muscle mass. No direct effect of alcohol was demonstrated in this selected population.

Adipose Tissue↗
PubMed1992

Oral BCAA supplementation in cirrhosis with chronic encephalopathy: effects on prolactin and estradiol levels.

The effects of oral BCAA supplementation on fasting levels of prolactin and estradiol were retrospectively analyzed in frozen plasma samples of patients with cirrhosis and chronic hepatic encephalopathy, taking part in a 3-month randomized, double-blind trial. Twenty-five patients had received 0.24g of BCAA per kg body weight, 24 had received an equinitrogenous amount of casein, in addition to a diet providing 0.7-1.0 g/kg of protein. Thirty-eight were males, 11 post-menopausal women. Fasting prolactin did not show any change in the BCAA group, where mental state significantly improved. In the casein group plasma prolactin increased by nearly 50% during the 3-month period. Similarly, estradiol concentrations were unchanged during BCAA supplementation, and increased during casein treatment. The analysis of variance demonstrated significant differences between the 2 treatments. Liver function tests and nutritional parameters (albumin, transferrin, urinary creatinine) supported a superiority of BCAA over casein. These data suggest that the favorable effects of BCAA on mental state are not mediated by changes in cerebral neurotransmission, but are due mainly to maintained liver function, possibly related to improved nutrition.

Administration, Oral↗
PubMed1991

Corticosterone treatment counteracts lesions induced by neonatal treatment with monosodium glutamate in the mediobasal hypothalamus of the male rat.

The effects of glucocorticoids on monosodium glutamate-induced neurotoxicity in the neonatal basal hypothalamus were studied by means of semiquantitative immunocytochemistry for tyrosine hydroxylase, growth hormone releasing factor and luteinizing hormone releasing hormone. Neonatal monosodium glutamate treatment induced a marked decrease in tyrosine hydroxylase immunoreactive neurons in the arcuate nucleus and growth hormone releasing factor immunoreactive nerve terminals in the median eminence. These effects were significantly antagonized by the coadministration of corticosterone. Corticosterone alone had no effect on the parameters studied. No significant change in luteinizing hormone releasing hormone immunoreactivity in the median eminence was detected after any treatment. These results demonstrate that corticosterone, possibly acting via type II corticosterone receptors which are highly enriched in the arcuate neurons, can exert a protective action on glutamate-induced neurotoxicity.

Animals↗
PubMed1991

Differential ontogenetic expression and regulation of proenkephalin and preprosomatostatin mRNAs in rat caudate-putamen as studied by in situ hybridization histochemistry.

Specific oligonucleotide probes and in situ hybridization histochemistry were used to study the ontogeny and regulation of the mRNAs for proenkephalin A and preprosomatostatin in rat brain. In adult brain the most intense hybridization signal for the proenkephalin A mRNA was in caudate putamen, nucleus accumbens and olfactory tubercle. By contrast, the hybridization signal for preprosomatostatin mRNA was more diffusely scattered throughout the brain, with high signals in the neocortex, olfactory bulb and hippocampal formation. Studies of the ontogeny of these mRNAs revealed a different pattern of ontogenetic expression and differential regulation by dopaminergic input. The mRNA for preposomatostatin reached the highest level within the first postnatal week, whereas proenkephalin A mRNA progressively increased throughout the entire period studied. In addition the proenkephalin A mRNA showed a medial to lateral gradient in 2-day-old rat striatum which disappeared with increasing age, whereas preprosomatostatin mRNA increased in most brain areas in fairly uniform fashion with increasing age. Treatment of newborn rats with 6-hydroxydopamine increased the expression of proenkephalin A mRNA by 1.6 fold but had no effect on the expression of preprosomatostatin mRNA. The 6-hydroxydopamine-induced change in proenkephalin A mRNA expression was not observed until postnatal day 32, indicating that enkephalin-containing neurons of the developing striatum are relatively insensitive to dopamine input and that they cannot compensate for the neonatal lesion, despite the fact that the insult was given in a period of high plasticity of the neural tissue.

Aging↗
PubMed1991

Decrease in mRNA levels but not in the density of D2 dopamine receptors in rat striatum after transient forebrain ischemia.

D2 dopamine receptor mRNA was analyzed by in situ hybridization histochemistry in rat striatum 7 days after transient forebrain ischemia. A patchy disappearance of the D2 receptor mRNA was observed in the dorsolateral striatum. In the same area, a disappearance of D1 binding sites occurred in the absence of significant changes in D2 receptor density. These results suggest that, although D2 receptors seem to be apparently unaffected after forebrain ischemia, a long-lasting impairment of their neosynthesis may be present in striatal D2 dopaminoceptive neurons.

Animals↗
PubMed1991

Changes in striatal mu and delta opioid receptors after transient forebrain ischemia: a quantitative autoradiographic study.

Transient forebrain ischemia induces specific changes in several neurochemical markers in the dorsolateral striatum. In the present paper, the density and distribution of mu and delta opioid receptors were analyzed in rat striatum 7 days after 30 min forebrain ischemia using the 4-vessel occlusion model. A marked (about 70%) decrease in the density of both opioid receptor subtypes was found in the dorsolateral striatum overlapping the areas of histological damage and of D1 dopamine receptor disappearance. Moreover, the density of delta opioid receptors and of the diffuse mu opioid receptors was also affected (30% decrease) in the ventromedial striatum, an area which is substantially spared by the ischemic lesion. In contrast, the striatal patches of mu opioid receptors were not affected in the ventro-medial striatum and were preserved to a large extent in the area of lesion, although their area and receptor density resulted markedly reduced. The impairment of both opioid receptor subtypes suggests that opiate systems, like dopaminergic systems, are involved in the neurochemical changes observed in the striatum after transient forebrain ischemia.

Animals↗
PubMed1991

Selective reduction of glucocorticoid receptor immunoreactivity in the hippocampal formation and central amygdaloid nucleus of the aged rat.

Hippocampal cell loss during aging has been related to the toxic effects of corticosterone on this cell population. It is not known which receptor mediates corticosterone cytotoxicity. At least two types of receptors for corticosterone have been recognized in the rat brain, type I (corticosterone preferring receptor, CR) and type II (glucocorticoid receptor, GR). In the present study the possible changes in GR immunoreactivity (IR) in various tel- and diencephalic regions of the aged rat have been investigated using immunocytochemistry coupled with computer-assisted image analysis. Male Sprague-Dawley rats of 3, 12 and 24 months of age were used (n = 5/group). A selective decrease of GR-IR was observed in the CA1 hippocampal field and central amygdaloid nucleus of the 24-month-old with respect to both 3- and 12-month-old rats. While in the former region GR-IR decrease was paralleled by a decrease of IR field area, no age-related decrease of GR-IR profile number was detected in central amygdaloid nucleus. A significant decrease of GR-IR and IR field area was also observed in the dentate gyrus of 24- vs 12-month-old rats but not vs 3-month-old rats. The analysis of adjacent sections stained with Cresyl violet showed a pattern of age-related changes (decrease of neuronal profiles in CA1 field pyramidal layer and dentate gyrus granular layer, and no change in the central amygdaloid nucleus of aged rats) which paralleled the observed changes in GR-IR in the same areas. This study provides evidence that GR are selectively decreased in the hippocampal formation and in the central amygdaloid nucleus of the aged rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗