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Biomedical subjects

G Biagini

Publications and source records attributed to G Biagini.

At least 109 records · Page 6Linked to original sources

Osteoconduction exerted by methylpyrrolidinone chitosan used in dental surgery.

Surgical wounds from wisdom tooth avulsions were medicated with freeze-dried methylpyrrolidinone chitosan, a gel-forming resorbable biopolymer obtained from crab chitosan by chemical modification. Methylpyrrolidinone chitosan promoted osteoconduction and the space left after avulsion was filled with newly formed bone tissue, which conferred desirable mechanical and physiological characteristics to the healed would site. Morphological evidence obtained from biopsies confirmed the radiographic data. Methylpyrrolidinone chitosan was progressively depolymerized by lysozyme and was no longer detected 6 months after surgery. None of the 10 patients reported adverse effects over one year of observation.

Bone Regeneration↗

Osteoconductive properties of methylpyrrolidinone chitosan in an animal model.

Bone defects were surgically produced in the tibiae of rabbits and medicated with freeze-dried methylpyrrolidinone chitosan. Histological observations 60 d after surgery showed a considerable presence of neoformed bone tissue, as opposed to controls, originating from the pre-existing bone as well as from the periosteum. The cationic nature and the chelating ability of the methylpyrrolidinone chitosan apparently favoured mineralization. Endosteal-periosteal and bone marrow osteoblast-like precursors, stimulated by growth factors entrapped in the coagulum-polysaccharide mixture, gave rise to intramembranous bone formation. The ultrastructural examination evidenced that bone osteoid was followed by mineralization of the tissue.

Animals↗

Indole-pyruvic acid treatment reduces damage in striatum but not in hippocampus after transient forebrain ischemia in the rat.

The effects of treatment with indole-pyruvic acid, an endogenous metabolite of tryptophan converted into kynurenic acid in the brain, were studied in rats after transient forebrain ischemia induced by the 4-vessel occlusion procedure. The histological analysis showed a significant protective effect of indole-pyruvic acid treatment on striatal ischemic lesions assessed by the extent of regional atrophy and the area of neuronal disappearance 14 days after ischemia. Striatal neurons were labelled by dopamine and adenosine 3':5' monophosphate regulated phosphoprotein-32 immunoreactivity. Conversely, increased neuronal loss, regional atrophy and glial fibrillary acidic protein immunoreactivity, an index of post-injury astroglial activation, were observed in the hippocampal formation, especially the CA3 field, of indole-pyruvic acid-treated rats when compared with vehicle-treated ischemic rats. The treatment with indole-pyruvic acid did not produce any improving effects in a test assessing short-term impairments after transient ischemia (motor test score at 24 h and 48 h post-ischemia). Furthermore, no significant effects of indole-pyruvic acid treatment were found on performance in water T-maze studied at 7 and 14 days post-ischemia. The opposite effects of indole-pyruvic acid on ischemic lesion in different brain regions may be related to its multiple neurochemical actions in the brain. The protective effect of indole-pyruvic acid on ischemic damage in striatum may be due to its conversion into kynurenic acid, a broad spectrum glutamate receptor antagonist. At hippocampal level, where glutamate receptor antagonists have been proved ineffective in the present lesion model, indole-pyruvic acid-induced changes in monamine availability may lead to a worsening of neuronal damage.

Animals↗

Effects of polyamine synthesis blockade on neuronal loss and astroglial reaction after transient forebrain ischemia.

Polyamines and ornithine decarboxylase, the polyamine biosynthetic enzyme, have been demonstrated to increase in the early phase of several types of brain lesion. However, their role in the pathogenesis of tissue damage is still debated. In the present paper the effects of treatments with alpha-difluoromethylornithine, a suicide inhibitor of ornithine decarboxylase, have been investigated in a model of transient forebrain ischemia. Three treatment schedules were used: alpha-difluoromethylornithine treatment was either started 3 hr before and repeated 1 hr after the insult, or started at the time of the insult and continued for 3 or 7 days after post-ischemic reperfusion. The rats were sacrificed 4 hr, 7 or 40 days after reperfusion, respectively. The acute experiment demonstrated that alpha-difluoromethylornithine can reduce the increase of glial fibrillary acid protein immunoreactivity, an early marker of astroglial reaction, in ischemic striatum. Subchronic and chronic alpha-difluoromethylornithine treatments induced a worsening of the morphological outcome of the ischemic lesion. In caudate-putamen a trend for an increase of the area of neuronal loss was present after both treatments. In the hippocampal formation, a significant increase in the severity of neuronal lesion was observed in the mildly lesioned CA3 field. In addition, other alterations of lesioned tissue were observed in alpha-difluoromethylornithine-treated animals, including increases of non-neuronal cells at 7 and especially 40 days post-lesion in striatum and CA3 hippocampal field. In conclusion, present data indicate that ornithine decarboxylase activation after ischemic lesion is a crucial factor for survival of mildly lesioned neurons and proper tissue reaction to the ischemic lesion. The experiment on acute alpha-difluoromethylornithine treatment suggests that these effects may be, at least in part, related to putrescine-induced activation of astroglial cells in the early post-lesion period.

Animals↗

L-deprenyl increases GFAP immunoreactivity selectively in activated astrocytes in rat brain.

L-deprenyl is a selective inhibitor of monoamine oxidase (MAO) B, an enzyme predominantly localized in astrocytes. We have investigated the effect of treatment with L-deprenyl (0.25 mg kg-1 day-1) on glial fibrillary acidic protein (GFAP) immunoreactivity (IR) after lesioning the rat striatum with an injection cannula. No effect of drug treatment on GFAP IR was found in unlesioned striata. A significant increase (p < 0.01 vs saline treated rats) in GFAP IR was found in the tissue surrounding the lesion in striata of rats treated with L-deprenyl for 4 days after the lesion. When post-treated for 42 days, however, L-deprenyl no longer increased GFAP IR although reactive astrocytes were still present in the lesioned area. These results suggest that L-deprenyl can enhance the activation of astrocytes during a critical time-period following a striatal injury.

Animals↗

Cultured human trophoblast cells reproduce the initial events of placental biology.

OBJECTIVE: The objective of this study was to determine whether cultured trophoblast cells shared the same morphological and biological properties observed in trophoblast, in vivo. STUDY DESIGN: Trophoblast cells from human term placenta were cultured, morphologically, biochemically and immunochemically monitored for as long as 30 days. RESULTS: Single cells progressively aggregated and fused into a syncytio, the Ca2+ and the Ca(2+)-ATPase activity drooped, and the 72 kDa collagenase (MMP-2) was consistently expressed. CONCLUSIONS: Term placenta trophoblast cultures can be viewed and used as a model system mimicking morphological and biochemical events of placenta biology and differentiation.

Calcium↗

Changes in membrane fluidity and Na+/K(+)-ATPase activity during human trophoblast cell culture.

The human placenta plays an essential role in embryo development, in particular regulating the transport of ions, nutrients and immunoglobulins from the maternal to the fetal circulation. Trophoblast organization into a syncytial layer involves structural and functional steps that may be monitored and elucidated by in vitro studies. The structural stages by which the syncytial trophoblast is formed are not yet understood. In order to clarify the mechanism of trophoblast development, we studied the morphological characteristics of the syncytial trophoblast formation in culture and the functional changes (transport properties and membrane microviscosity) accompanying the structural modifications. By using both 5-nitroxystearate and 16-nitroxystearate as spin labels, we observed an initial increase in membrane order over 0-24 h of culture, which can be associated with two events: recovery of cell membranes from trypsin and initial aggregation of cytotrophoblasts. The similar behaviour of the order parameters determined with both probes indicates that membrane order changes both inside and in the outer part of the lipid bilayer. The subsequent decrease in membrane order observed at 36-48 h might be related to the process of cellular fusion. The increase in sodium/potassium pump activity in the first 24 h of culture might be an expression of cell recovery following trypsin treatment. The subsequent decrease might represent an adaptive mechanism by which metabolic energy is mainly used for morphogenetic changes.

Cells, Cultured↗

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↗

Effects of dentin surface treatments on the shear bond strength of Vitrabond.

The influences of nine dentin surface treatments were evaluated on the shear bond strength of a new light-cured glass-ionomer cement (GIC) and on the SEM morphology of the treated dentin surfaces. The following treatments were performed: saline solution (control), NaOCl, acidic glycine, EDTA, malic acid, malic acid plus glycine, polyacrylic acid, tannic acid, and neutral+acidic oxalate solutions. Buccal dentin surfaces were polished with #320-grit abrasive paper, treated with one of the chemicals, washed, and air-dried. Cylindrical GIC samples were then applied to the dentin surface, stored in 100% humidity, and tested after 24 h. SEM observations demonstrated no effect of saline or NaOCl treatment on the smear layer but its complete removal with exposure of collagen fibrils after malic or malic acid plus glycine treatment. Partial removal of the smear layer occurred following glycine treatment and with tannic or polyacrylic acids. Complete removal of the smear layer was seen after EDTA or pyruvic acid treatment. Oxalate treatment produced a layer of crystals, which completely covered the dentin surface. Shear bond strength of GIC was significantly increased only by treatment with the oxalate solutions.

Dental Bonding↗

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↗

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↗

Placental villi-decidua interactions in normal and hypertensive pregnancies: a morphological quantitative study.

The decidual response to the implantation of the embryo is characterized by physical modifications to the uterine wall, with proliferation of the stromal cells which later change into decidual cells. We performed associated morphological and morphometrical studies to assess how the placental villi and decidua intersect, both in normal terminal pregnancy and in hypertensive patients in whom microenvironmental modifications induced by hypertension may cause significant alterations in mother-fetus relationships. In placentas of hypertensive women our morphometric analyses showed a higher number of chorionic villi-decidua interactions (p less than 0.05) with a more clumped distribution (p less than 0.05) and a smaller surface area of single interaction (p less than 0.001), in association with a higher number (p less than 0.005), and greater areas (p less than 0.01) of decidual cells. These data demonstrate how the placenta can enhance mother-fetus contacts impaired as the result of a hypertensive condition.

Chorionic Villi↗

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↗

In vitro growth of periodontal fibroblasts on treated cementum.

The aim of the present study was to assess the ability in vitro of phosphoric and citric acids, applied on human root cementum, to neutralize noxious plaque and calculus and to allow the growth of human gingival fibroblasts. Fibroblasts grown on cementum treated with phosphoric acid appeared typically elongated and aligned parallel to the root surface. Fibroblasts grown on cementum treated with citric acid, in both normal and periodontally diseased teeth, lost their elongated shape, acquiring polygonal borders with irregular cytoplasmic extrusions, and the cell density was significantly lower. These findings suggest that phosphoric acid cleaning of both normal and diseased root surfaces may result in an oriented, high rate of fibroblastic growth with more effective periodontal cellular proliferation than that observed after citric acid treatment.

Cell Division↗

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↗

Wound management with N-carboxybutyl chitosan.

In patients undergoing plastic surgery, donor sites were treated with soft pads of freeze-dried N-carboxybutyl chitosan to promote ordered tissue regeneration. Compared to control donor sites, better histoarchitectural order, better vascularization and the absence of inflammatory cells were observed at the dermal level, whilst fewer aspects of proliferation of the malpighian layer were reported at the epidermal level. Accordingly, N-carboxybutyl chitosan leads to formation of regularly organized cutaneous tissue and reduces anomalous healing.

Adult↗