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Biomedical subjects

M Zoli

Publications and source records attributed to M Zoli.

230 records · Page 13Linked to original sources
PubMedDate not supplied

Receptor-receptor interactions as an integrative mechanism in nerve cells.

Several lines of evidence indicate that interactions among transmission lines can take place at the level of the cell membrane via interactions among macromolecules, integral or associated to the cell membrane, involved in signal recognition and transduction. The present view will focus on this last subject, i.e., on the interactions between receptors for chemical signals at the level of the neuronal membrane (receptor-receptor interaction). By receptor-receptor interaction we mean that a neurotransmitter or modulator, by binding to its receptor, modifies the characteristics of the receptor for another transmitter or modulator. Four types of interactions among transmission lines may be considered, but mainly intramembrane receptor-receptor interactions have been dealt with in this article, exemplified by the heteroregulation of D2 receptors via neuropeptide receptors and A2 receptors. The role of receptor-receptor interactions in the integration of signals is discussed, especially in terms of filtration of incoming signals, of integration of coincident signals, and of neuronal plasticity.

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IgA antibodies to dietary antigens in liver cirrhosis.

Antibodies to dietary antigens (ovalbumin, beta-lactoglobulin, casein) have been detected by a micro-ELISA test in 47-50% of serum samples from patients with alcoholic liver cirrhosis, in 27-36% with non-alcoholic cirrhosis (HBV-related, autoimmune and primary biliary) and in 50-70% of cirrhotic patients with portacaval shunt. Dietary antibodies were mainly confined to the IgA class (90%). In patients with chronic active hepatitis dietary antibodies showed a low positivity (11%), similar to that of subjects with alcohol abuse without liver injury and of healthy subjects. Dietary antibodies were significantly associated with portal hypertension (evaluated on the presence of esophageal varices and/or ascites) both in alcoholic and non-alcoholic cirrhosis. The absence of dietary antibodies in the duodenal juice of cirrhotic patients positive for serum antibodies confirms that the intestinal mucosa is normal or slightly altered in liver cirrhosis. Unlike cirrhotics, untreated celiac patients showed a high prevalence of dietary antibodies also in the duodenal juice (55%).

Adult↗
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Reduced growth hormone releasing factor (GHRF)-like immunoreactivity and GHRF gene expression in the hypothalamus of aged rats.

Growth hormone releasing factor-like immunoreactivity (GHRF-LI) and GHRF mRNA levels were evaluated in the hypothalamus of aged (24 months) and young (3 months) rats by semiquantitative immunocytochemistry and slot blot hybridization technique, respectively. Simultaneous detection of reduced GHRF-LI and GHRF mRNA levels in aged rats as compared to young counterparts demonstrates the existence in aged rats of an impaired function of GHRF-producing neurons.

Aging↗
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Age-related alterations in tanycytes of the mediobasal hypothalamus of the male rat.

By means of semiquantitative immunocytochemistry, possible age-related changes in dopamine and cyclic AMP-regulated phosphoprotein mr 32 (DARPP-32) and glial fibrillary acidic protein (GFAP) immunoreactivities (IR) were investigated in tanycytes of the arcuate nucleus. These two markers showed opposite changes during aging. DARPP-32 IR decreased by around 70%, whereas GFAP IR increased by around 300% in 24-month-old vs. 3-month-old rats. These changes were accompanied by a progressive loss in the number of tanycytes, measured by counting of their long processes in the arcuate nucleus. No significant age-related change was observed either in GFAP IR in astrocytic populations of the mediobasal hypothalamus or in tyrosine hydroxylase IR in dopaminergic neurons of the dorsal arcuate nucleus. These observations indicate that the tanycytic population of the arcuate nucleus undergoes important modifications during aging, which include cell loss, impairment in the intracellular signalling cascade linked to DARPP-32, and hypertrophy. These changes may be related to the alterations in the neuroendocrine systems known to occur during aging.

Aging↗
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Neurochemical alterations but not nerve cell loss in aged rat neostriatum.

Numerical changes in the overall neostriatal neuronal population have been investigated by morphometric analysis of Nissl-stained and glucocorticoid receptor-immunoreactive neurons. Number and staining intensity of various chemically-identified nerve cell populations were analysed by means of immunocytochemistry coupled with computer-assisted image analysis. Three- and 24-month-old male Sprague-Dawley rats were used. No change in the number of Nissl-stained, glucocorticoid receptor-, dopamine and adenosine 3':5'-monophosphate-regulated phosphoprotein- and enkephalin-immunoreactive neurons and a 50% decrease of neuropeptide Y-immunoreactive neurons were observed in the aged rat. In our preparations, the glucocorticoid receptor antibody stains around 90% of the neostriatal neurons, the dopamine and adenosine 3':5'-monophosphate-regulated phosphoprotein and enkephalin antibodies label 25-35% and the neuropeptide Y antibody stains only 1% of neostriatal neurons. In the same preparations a significant decrease in the intensity of immunostaining was observed for enkephalin-, dopamine and adenosine 3':5'-monophosphate-regulated phosphoprotein- and neuropeptide Y-immunoreactive neuronal cell bodies and tyrosine hydroxylase-immunoreactive nerve terminals in the aged rat. In the case of neuropeptide Y- and dopamine and adenosine 3':5'-monophosphate-regulated phosphoprotein-immunoreactive neurons, the changes in the intensity of immunostaining were differentially compartmentalized within neostriatum, suggesting selective vulnerability of striatal subregions to ageing processes. In conclusion, these data indicate that no significant age-related neuronal cell loss occurs in neostriatum. On the other hand, a generalized decrease in the levels of peptide transmitters and molecules related to dopamine transmission is observed in aged rat neostriatum, possibly resulting in the known age-related deficits of neostriatally-controlled behaviours.

Aging↗
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Distribution of dopamine-immunoreactive neurons and their relationships to transmitter and hypothalamic hormone-immunoreactive neuronal systems in the rat mediobasal hypothalamus. A morphometric and microdensitometric analysis.

A morphometric and microdensitometric characterization of the dopamine neurons of the mediobasal hypothalamus and their relationships with several other chemically identified systems, including putative tyrosine hydroxylase-positive/dopamine-negative neurons, was carried out after visualization of dopamine content by both immunocytochemistry and the Falck-Hillarp technique. Quantitative assessment of co-existence demonstrated that more than 95% of dopamine-immunoreactive neurons also contained tyrosine hydroxylase immunoreactivity and more than 90% of growth hormone-releasing factor-immunoreactive neurons also contained tyrosine hydroxylase immunoreactivity. Morphometric and densitometric analysis of dopamine, tyrosine hydroxylase and growth hormone-releasing factor-immunoreactive neurons in the arcuate nucleus showed that dopamine/tyrosine hydroxylase-containing and growth hormone-releasing factor/tyrosine hydroxylase-containing neuronal populations are two largely segregated cell groups with specific localization in the arcuate region, rostrocaudal extension and tyrosine hydroxylase-immunoreactivity content. Morphometric characteristics of dopamine-immunoreactive neurons were shown to be equivalent to those of catecholamine fluorescent cell bodies in the arcuate region. In addition, a cell group lacking detectable catecholamine fluorescence in normal animals but accumulating L-DOPA after peripheral loading was identified and characterized from a morphometric standpoint in the ventral premammillary nucleus. Quantitative analysis of nerve terminal co-distribution in the median eminence revealed significant correlations between dopamine and other transmitter or neurohormone systems, such as gamma-aminobutyric acid, galanin, luteinizing hormone-releasing hormone, in specific subregions of the palissade zone. These data point to discrete subregions of the median eminence, which have been called 'medianosomes', as main sites of interactions between transmitter-identified nerve terminal systems in the control of hypothalamic hormone release.

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Subunit and region-specific decreases in nicotinic acetylcholine receptor mRNA in the aged rat brain.

We have investigated possible changes in the mRNA levels for several alpha and beta subunits of the nicotinic acetylcholine receptor (nAChR) and the level of binding for nicotinic ligands in 7- to 32-month-old rats. Alpha4 and beta2, and to a lesser extent alpha6 and beta3, mRNA levels showed decreases between 20 and 30% at 29 months of age which in some areas reached 50% at 32 months of age. Alpha7 showed a small increase from 7 to 14 months and then a progressive decrease from 14 to 32 months down to the 7-month levels. 3H-epibatidine binding did not significantly change from 7 to 32 months of age in rat tel- and diencephalon. Binding in the substantia nigra was exceptional in that it showed a significant decrease starting from 23 months of age. 125I-alpha-bungarotoxin binding showed a pattern of change which roughly paralleled that of alpha7 mRNA. These findings show that an alteration in some steps of nAChR biosynthesis takes place during aging, which may be related to functional changes in nicotinic transmission.

Aging↗
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Overview of randomized clinical trials of oral branched-chain amino acid treatment in chronic hepatic encephalopathy.

BACKGROUND: The role of oral branched-chain amino acid supplements in the prevention and treatment of chronic hepatic encephalopathy is not yet established, and conflicting opinions are expressed in authoritative textbooks. We aimed to review and pool the published controlled studies by means of meta-analytical techniques. METHODS: A computerized search of published papers identified nine studies, controlled against placebo, energy, alimentary proteins, or casein. Their quality score was calculated according to the protocol of Chalmers. The value of the portal-systemic encephalopathy index was chosen as main outcome, because of lack of more significant clinical outcomes. To cope with differences in trial design and data presentation, individual data were requested to authors. RESULTS: After 18 months, we received the individual data of only two studies, thus precluding any meta-analysis. Two studies, accounting for over 60% of total enrolled patients, were in favor of branched-chain amino acids. Their quality score was much better than that of the remaining seven negative small studies, carrying a significant risk of type II error. CONCLUSIONS: Based on the results of the two largest, long-term studies, the use of oral branched-chain amino acids in the prevention and treatment of chronic encephalopathy may only be proposed for patients with advanced cirrhosis, intolerant to alimentary proteins. Large, multicenter, long-term studies, considering more important clinical outcomes, are needed to provide definite answers to an aged question.

Adult↗
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Nerve cell clusters in dorsal striatum and nucleus accumbens of the male rat demonstrated by glucocorticoid receptor immunoreactivity.

Glucocorticoid receptor-immunoreactive nerve cells have been analysed in the dorsal striatum and nucleus accumbens of the rat by means of a monoclonal antibody against rat liver glucocorticoid receptor. Glucocorticoid receptor immunoreactivity was present in the nuclei of the vast majority of the striatal nerve cells. The analysis of sections stained with glucocorticoid receptor antibody and cresyl violet showed that around 90% of the entire striatal neuronal population contained glucocorticoid receptor immunoreactivity. By means of the double immunoperoxidase technique evidence was provided that somatostatin- and choline acetyltransferase-immunoreactive nerve cells in the striatum do not contain glucocorticoid receptor immunoreactivity. The density of glucocorticoid receptor-immunoreactive nerve cells in the grey matter and the presence of clusters of glucocorticoid receptor-immunoreactive nerve cells have been investigated in three fields located in the medial and central dorsal striatum and nucleus accumbens at the coronal level A 8620 microns according to the König and Klippel atlas using computer-assisted image analysis. Every aggregate containing three or more glucocorticoid receptor-immunoreactive nerve cells, which had an intercenter distance less than the mean diameter (10-11 microns) of the striatal cells, was considered an island. A higher density of both glucocorticoid receptor-immunoreactive nerve cell nuclei and islands was found in the nucleus accumbens with respect to dorsal striatal areas. The most frequent island formed consisted of three to ten nerve cells both in dorsal striatum and nucleus accumbens. Furthermore, some nucleus accumbens islands contained up to 100 nerve cells, whereas in the dorsal striatum the maximum number of glucocorticoid receptor-immunoreactive nerve cells per island ranged from 50 to 60. The present procedure proved to be a sensitive method to reveal clusters of chemically identified structures and provided evidence for a basic cytoarchitectonic organization of the dorsal striatum and nucleus accumbens of the rat. This paper also demonstrated that the vast majority, but not all, striatal nerve cells contained glucocorticoid receptor immunoreactivity, and thus may be under the control of circulating glucocorticoids. In fact, only small transmitter-identified neuronal populations, such as somatostatin- and choline acetyltransferase-immunoreactive nerve cells, were devoid of glucocorticoid receptor immunoreactivity.

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Distribution of glutamic acid decarboxylase messenger RNA-containing nerve cell populations of the male rat brain.

The distribution of glutamic acid decarboxylase (GAD) mRNA was investigated throughout the rat brain by means of in situ hybridization. Hybridization was carried out with a 35S-radiolabeled cRNA probe transcribed from a cDNA from cat occipital cortex and cloned in a SP6-T7 promoter-containing vector. Fixed tissue sections were hybridized with 35S GAD probe (0.6 kb length). Signal was detected by means of film or emulsion autoradiography. The autoradiograms were semiquantitatively evaluated by means of computer-assisted image analysis. The results obtained with this evaluation were correlated with the results of the semiquantitative analysis of GAD immunoreactivity performed by Mugnaini and Oertel. Specific labeling was only observed in neuronal cell bodies, whereas no labeling was found over neuropil, glial and endothelial cells. The highest labeling was found in the bulbus olfactorius (internal plexiform and granular layers) and in the caudal magnocellular nucleus of the hypothalamus. Strong labeling was observed in the Purkinje layer of the cerebellar cortex, the interpeduncular nucleus, the interstitial nucleus of Cajal, the nucleus of Darkschewitsch and the suprachiasmatic nucleus. Intermediate or low levels of GAD mRNA were present in various brain nuclei, where gamma-aminobutyric acid (GABA)-containing cell bodies had been observed with other techniques. Interestingly, a low level of GAD mRNA was found in the caudate-putamen and nucleus accumbens, where the vast majority of nerve cells is known to contain GAD immunoreactivity. Only a poor correlation was found between the present semiquantitative measurements of GAD mRNA content and previous analyses of the number of GAD-immunoreactive cell bodies. The present study demonstrates that there exists a differential regional expression of GAD mRNA. The comparison with cell counts performed by immunocytochemistry suggests that some brain areas, such as caudate-putamen and nucleus accumbens, contain a large number of GAD-immunoreactive cell bodies which express a low level of GAD mRNA. The opposite seems to be true for other nuclei, such as the globus pallidus, the zona reticulata of the substantia nigra and the inferior collicle, where few GAD-immunoreactive cell bodies contain high levels of GAD mRNA. In conclusion, the present study gives a low magnification map of GAD mRNA levels in the adult male rat brain. Marked biochemical heterogeneities may be present among GABA neuronal populations based on their expression of GAD mRNA. The comparison between the present in situ hybridization and previous immunocytochemical studies suggests that there may exist at least two populations of GABA neurons in the brain, having high and low levels respectively of both GAD mRNA and GAD enzyme.

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Thyroid involvement in patients with active inflammatory bowel diseases.

Previous studies have documented an association between systemic diseases and disorders of the thyroid gland, expressed by an enlargement of the thyroid and by the presence of anti-thyroid antibodies. Chronic inflammatory bowel diseases (IBD, ulcerative colitis and Crohn's disease) may also present a multi-organ involvement, including the biliary tree, joints and uvea. To detect a possible subclinical thyroid involvement, thyroid volume and function were assessed in 31 patients with IBD in active phase and in 50 control subjects. Thyroid volume was calculated by ultrasonography on the basis of the three maximum diameters of the 2 lobes. A blood sample was taken to determine free thyroid hormones, TSH, and anti-thyroid antibodies. In patients with IBD, thyroid volume was increased on average by 35%, and the prevalence of thyroid enlargements (antero-posterior diameter > 20 mm) was 3 times higher (45% vs 16%). Free thyroxine was increased by nearly 50%, but only 10% of patients had anti-thyroid antibodies. Alterations of thyroid volume and function are present in IBD, even in the absence of clinically-detectable thyroid disease. The association of IBD with thyroid disorders, as well as the involvement of various organs, confirms the view that IBD is a systemic disease.

Adult↗
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Transient spontaneous regression of hepatocellular carcinoma.

We report on 2 patients with liver cirrhosis and biopsy-proven hepatocellular carcinoma who underwent spontaneous regression. In 1 case the tumor became undetectable at ultrasonography, while, in the other, the liver lesions decreased in size and showed inner calcifications. In both patients, alpha-fetoprotein, which was high at first diagnosis, returned to normal values. After a tumor-free period of 4 years and 17 months, respectively, liver cancer reappeared and patients died from complications. We advance the hypothesis that tumor regression, when it occurs in cirrhotic patients, is always transient, with chronic liver disease being the oncogenic triggering factor.

Aged↗