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Biomedical subjects

V Calabrese

Publications and source records attributed to V Calabrese.

At least 37 records · Page 2Linked to original sources
PubMed2000

A modified retrosigmoid approach for direct exposure of the fundus of the internal auditory canal for hearing preservation in acoustic neuroma surgery.

OBJECTIVE: This is a clinical report on a modified retrosigmoid approach with direct exposure of the fundus of the internal auditory canal for hearing preservation in acoustic neuroma surgery. STUDY DESIGN: Retrospective case review. SETTING: Tertiary referral center of an ear, nose, and throat department in a public hospital. PATIENTS: One hundred fifty consecutive procedures were reviewed, including 61 males and 89 females with an age range of 13 to 69 years and a mean age of 47 years. There were 15 patients with tumor occupying solely the internal auditory canal and 135 patients with extension into the cerebellopontine angle with an extrameatal diameter of up to 52 mm and a mean of 11.5 mm. INTERVENTION: The retrosigmoid approach included a wide craniotomy, a perimeatal petrous bone removal up to the blue line of the labyrinth, and a direct exposure of the fundus at the orifices of the facial and cochlear nerves. The quadrant of the superior vestibular nerve remained unexposed. MAIN OUTCOME MEASURES: Hearing was measured according to the American Academy of Otolaryngology-Head and Neck Surgery criteria for reporting results of hearing preservation and by comparison with the preoperative level. Facial nerve function was measured using the House-Brackmann grading. The radicality of tumor removal was investigated with mid- to long-term magnetic resonance imaging (MRI). RESULTS: Measurable hearing was preserved in 45.3%, and in 32.4% of these cases, it was within 15 dB/15% discrimination. Grade 1 or 2 facial function was preserved in 85.3%. MRI follow-up revealed a 3.3% tumor residual or regrowth in the complete series. No residual tumor was found at the 3-year MRI in the last series of patients operated on with direct control of the fundus. CONCLUSIONS: This modified retrosigmoid approach permits the direct exposure of the facial and cochlear quadrants of the fundus. This allows tumor dissection under direct visual control. Removing the tumor from the vestibular quadrant of the fundus is done blindly in a minority of cases and carries a minimal risk of residual tumor. This technique requires only conventional equipment and skills of neurotology.

Adolescent↗
PubMed2000

NO synthase and NO-dependent signal pathways in brain aging and neurodegenerative disorders: the role of oxidant/antioxidant balance.

Nitric oxide and other reactive nitrogen species appear to play several crucial roles in the brain. These include physiological processes such as neuromodulation, neurotransmission and synaptic plasticity, and pathological processes such as neurodegeneration and neuroinflammation. There is increasing evidence that glial cells in the central nervous system can produce nitric oxide in vivo in response to stimulation by cytokines and that this production is mediated by the inducible isoform of nitric oxide synthase. Although the etiology and pathogenesis of the major neurodegenerative and neuroinflammatory disorders (Alzheimer's disease, amyothrophic lateral sclerosis, Parkinson's disease, Huntington's disease and multiple sclerosis) are unknown, numerous recent studies strongly suggest that reactive nitrogen species play an important role. Furthermore, these species are probably involved in brain damage following ischemia and reperfusion, Down's syndrome and mitochondrial encephalopathies. Recent evidence also indicates the importance of cytoprotective proteins such as heat shock proteins (HSPs) which appear to be critically involved in protection from nitrosative and oxidative stress. In this review, evidence for the involvement of nitrosative stress in the pathogenesis of the major neurodegenerative/ neuroinflammatory diseases and the mechanisms operating in brain as a response to imbalance in the oxidant/antioxidant status are discussed.

Aging↗
PubMed2000

Biochemical studies of a natural antioxidant isolated from rosemary and its application in cosmetic dermatology.

Oxidative damage to DNA, RNA, proteins and cell membranes occurs when the cellular concentration of reactive oxygen species exceeds the capacity of the cell to eliminate them. Aerobic prokaryotic and eukaryotic organisms have developed a set of cell defense systems to mitigate the damaging effects of reactive oxygen species. Epithelial surfaces contain antioxidants that could be expected to provide a defence against environmental stress caused by reactive oxygen and nitrogen species. Skin, which has a highly differentiated and complex structure, is particularly vulnerable to free radical damage because of its contact with oxygen and with other environmental stimuli. Fruit and vegetables contain several classes of compounds that when ingested can potentially contribute to endogenous modulation of antioxidant defences. The purpose of this study was to investigate the effectiveness of a natural extract derived from rosemary to protect free radical-induced skin damage. We provide evidence that an alcoholic extract of rosemary leaves, Rosm1, is endowed with strong antioxidant activity and, as evaluated by both in vitro and in vivo systems, is capable of inhibiting oxidative alterations to skin surface lipids. The present study provides a preclinical perspective on the interface between the biochemical properties of a natural extract isolated from rosemary leaves, a better understanding of the endogenous antioxidant potential of skin and the real validity of natural antioxidant biotechnology in antiaging skin management.

Adolescent↗
PubMed1999

Formation of propionate after short-term ethanol treatment and its interaction with the carnitine pool in rat.

Organic acidurias are genetic disorders of mitochondrial metabolism that lead to the accumulation in tissues and biological fluids of organic acids. It has been demonstrated that interaction of carnitine with the cellular CoA pool, through the production of acyl-carnitines, is potentially critical for maintaining normal cellular metabolism under conditions of impaired acyl-CoA use and that exposure of humans and other mammals to ethanol effects leads to impairment of mitochondrial function. The aim of the present study was to evaluate the role of ethanol on urinary excretion of short-chain organic acids and endogenous carnitines in rats. The data reported show that ethanol significantly increases urinary excretion of propionate, methylmalonate, as well as free acetate, butyrate, pyruvate, lactate, and beta-hydroxybutyrate. Furthermore, the increased formation of propionate and methylmalonate was dependent on the dose of ethanol; did not require the metabolism of ethanol, as was shown in experiments with pyrazole treatment of ethanol rats; and appears to be mediated by beta-adrenergic mechanisms because propranolol almost completely suppresses propionate accumulation. Alcohol administration also increased excretion of specific acyl-carnitines, corresponding to the accumulating acyl groups, whereas excretion of free carnitine was significantly reduced, with respect to control values. The data presented indicate that the short-term ethanol administration is associated with increased excretion of selected organic acids. This study suggests that endogenous carnitine pool might play a role against the deleterious effects of accumulating short-chain organic acids.

Acids, Acyclic↗
PubMed1999

Effects of L-carnitine on the formation of fatty acid ethyl esters in brain and peripheral organs after short-term ethanol administration in rat.

A study was undertaken in rats to evaluate the effects of short-term oral ethanol administration on the levels of fatty acid ethyl esters (FAEE) in brain and peripheral organs in the presence and absence of pretreatment with L-carnitine. Administration of ethanol to rats for seven days resulted in fatty acid ethyl ester formation, particularly in the heart and brain, but also in the kidney and liver. FAEE generation was associated with a significant increase of GSH transferase activity. Treatment with L-carnitine significantly reduced both FAEE and GSH transferase activity, and these effects were associated with a significant decrease in alcohol blood concentrations. The present evidence supports the hypothesis that fatty acid ethyl esters could be mediators involved in the production of alcohol-dependent syndromes. Administration of L-carnitine through an increment in lipid metabolism and turnover, and by the modulation of cellular antioxidant enzymes, greatly reduces these metabolic abnormalities supporting its potential usefulness as a pharmacological tool in alcoholism management.

Alcohol Drinking↗
PubMed1999

Absence of response to early transcranial magnetic stimulation in ischemic stroke patients: prognostic value for hand motor recovery.

BACKGROUND AND PURPOSE: Transcranial magnetic stimulation (TMS) has been proposed as a prognostic tool in stroke patients. Most of the previous studies agree in considering the presence of motor-evoked potentials (MEPs) in the first days after a stroke as an indicator of good outcome. In the present study, we have assessed the prognostic value of the absence of response to early TMS on hand motor recovery in stroke patients with complete hand palsy at onset due to ischemia in the area of the middle cerebral artery. METHODS: Fifteen patients submitted to TMS within 48 hours of stroke onset (defined as day 1) and again after 1 year. They were also evaluated clinically on day 1 by a scale derived from the Medical Research Council (MRC) and by the National Institutes of Health (NIH) stroke scale; they were reevaluated by the same scales and by Barthel Index on day 365. RESULTS: On day 1, all the patients had complete hand palsy and no response to TMS; their NIH scores showed great variability. After 1 year, 6 of 15 patients regained small and prolonged MEPs, together with a very poor and not functionally useful motor recovery. NIH scores were significantly improved. Barthel Index scores showed large interindividual differences and were not correlated with MRC scores. CONCLUSIONS: We conclude that in patients with complete hand palsy, the absence of response to TMS in the first hours is predictive of absent or very poor, not useful, hand motor recovery.

Adult↗
PubMed1999

An ex vivo biochemical model to study the antioxidant clinical properties of cosmetic products in human antiaging skin care.

It is generally accepted that lipid peroxides play an important role in the pathogenesis of free radical-induced cellular injury and that endogenous thiols are vital in cellular defense against oxidative stress. The purpose of this study was to investigate in cultured human skin fibroblasts the effect of oxidative stress on the synthesis of heat shock protein (HSP70) and on the sulfhydryl group content in the absence and presence of alpha-tocopherol as an antioxidant compound. The interesting observation emerging from this study was a marked increase in malonaldehyde and fluorescent peroxide levels associated with a significant thiol depletion and induction of HSP70 stress proteins observed in primary cultures of normal human skin fibroblasts subjected to heat shock or incubated with hydrogen peroxide. These changes were significantly reduced in the presence of alpha-tocopherol. Our findings suggest a correlation between the mechanisms of oxidative stress, antioxidants and HSP70 induction, which can be assessed to evaluate either the perturbation of skin oxidant/antioxidant balance or the protection afforded by antioxidant test compounds.

3,4-Methylenedioxyamphetamine↗
PubMed1999

Biochemical studies on a novel antioxidant from lemon oil and its biotechnological application in cosmetic dermatology.

It is generally accepted that lipid peroxides play an important role in the pathogenesis of free radical-induced cellular injury and that antioxidants such as glutathione, ascorbic acid and alpha-tocopherol are vital in cellular defense against endogenous and exogenous oxidants. The purpose of this study was to investigate the effectiveness of a natural compound, derived from lemon oil extract, in controlling free radical-induced lipid peroxidation and tissue damage in the skin. We provide evidence that a compound isolated from lemon oil, which we have called Lem1, is endowed with a strong antioxidant activity and that it is capable of inhibiting free radical-mediated reactions, evaluated by both in vitro and in vivo biochemical systems. The present study aims to give a preclinical perspective on the biochemical properties of Lem1, a natural compound, as well as to provide a better understanding of the endogenous antioxidant potential of skin and the real validity of a natural antioxidant biotechnology in the antiaging management of the skin.

Adolescent↗
PubMed1999

Oxidative stress and antioxidants at skin biosurface: a novel antioxidant from lemon oil capable of inhibiting oxidative damage to the skin.

Atmospheric pollutants are an important source of oxidative and nitrosative stress both to terrestrial plants and to animals. Skin, which has a highly differentiated and certainly complex organizational structure, is particularly vulnerable to free radical damage because of its contact with oxygen and with other environmental stimuli. Fruit and vegetables contain several classes of compounds that when ingested can potentially contribute to antioxidant defenses. In the present study we employed a novel gas chromatographic method to assess the antioxidant properties of a natural compound isolated from lemon oil, which we have called Lem1. We provide experimental evidence that Lem1 is endowed with a strong antioxidant activity and that it is capable of inhibiting free radical-mediated reactions, as evaluated in vitro and in vivo. The present study extends our previous findings and demonstrates that topical application of Lem1 in healthy volunteers significantly increases the antioxidative potential of skin biosurface, thus highlighting the effectiveness of a natural antioxidant biotechnology in the antiaging management of skin.

Administration, Topical↗
PubMed1998

Effect of nitric oxide synthase induction on the expression of mitochondrial respiratory chain enzyme subunits in mixed cortical and astroglial cell cultures.

In the present study we evaluated the effects of NO synthase (NOS) induction on the regulation of cytochrome c oxidase (CO) and F0F1-ATPase subunit expression in astroglial and mixed cortical cell cultures. In mixed cortical cell cultures, 18 h of treatment with lipopolysaccharide (LPS, 0.1 microgram/mL) plus interferon-gamma (INF-gamma, 10 U/mL) caused an increase of mRNAs for CO-I, F0F1-ATPase 6 and also for iNOS at 20 DIV. The induction of both CO-I and F0F1-ATPase 6 was abolished by the NOS inhibitor N-monomethyl-L-arginine (NMMA) or by the enzymatic scavenger superoxide dismutase/catalase (SOD/CAT). In primary astroglial cell cultures, treatment for 18 h with increasing concentrations of LPS and INF gamma, produced an increase in the amount of mitochondrial encoded CO-I and -II subunits, with no significant modifications of nuclear encoded subunit IV. An increase was also observed at level of transcription for CO-I and -II, and F0F1-ATPase 6 mRNAs. These effects were abolished by addition of NMMA or SOD/CAT. mRNA induction of CO-I was higher in mixed cortical than in astroglial cell cultures while that of F0F1-ATPase 6 was similar in both cell types. These results suggest that the expression of mitochondrial encoded subunits (CO-I, CO-II and F0F1-ATPase 6) is up-regulated in response to oxygen and NO reactive species. The activity of cytochrome c oxidase decreased after LPS/INF gamma treatment in both astroglial and mixed cortical cultures. The activity of ATP synthase was unmodified, while ATP content drastically decreased after LPS/INF gamma treatment, in both astroglial and mixed cortical cultures. The enzymatic activities of catalase and Mn-SOD (mitochondrial) showed a significant increase after LPS/INF gamma treatment, which was abolished by NMMA.

Animals↗
PubMed1998

Stress proteins and SH-groups in oxidant-induced cellular injury after chronic ethanol administration in rat.

It is generally agreed that lipid peroxides play an important role in the pathogenesis of ethanol-induced cellular injury and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. It has been observed that oxidative stress induces the synthesis of the 70-kDa family of heat-shock proteins (HSPs). Induction of HSPs represents an essential and highly conserved cellular response to a variety of stressful stimuli. In the present study we measured in various brain areas and in liver the intracellular levels of HSP70 proteins, sulfhydryl groups and the antioxidant enzyme status after chronic administration of mild intoxicating doses of ethanol to rats. Expression of HSP70 in response to alcohol administration was particularly high in the hippocampus and striatum. In these brain areas, the increase in HSP70 protein levels occurred in absence of significant changes of antioxidant enzyme activities and was correlated with a marked depletion of intracellular bound thiols and with a decreased susceptibility to lipid peroxidation. Lower levels of HSP70 induction were found in cortex and cerebellum and were associated to decreases in SOD and CAT enzyme activities, with a lower depletion of protein bound thiols and with an increased susceptibility to lipid peroxidation. This study agrees with our previous results performed on acute alcohol intoxication and supports the hypothesis that HSP70 induction protects the different brain areas against oxidative stress.

Animals↗
PubMed1998

Long-term ethanol administration enhances urinary ultraweak luminescence and age-dependent modulation of redox in central and peripheral organs of the rat.

Numerous experimental evidence sustains a pathogenic role for oxidative stress in aging. Acute and chronic ethanol metabolism is also known to be associated with oxidative perturbation of cellular oxidant/antioxidant balance. In the present work we investigated the effects of 25 months of ethanol consumption on the antioxidant defense system in different organs of rats, in comparison with normal and aged animals. We show that aged rats underwent a significant perturbation of the antioxidant defense system, as indicated by depletion of reduced glutathione content, increases in oxidized glutathione and free radical-induced urinary luminescence associated with a decrease of glutathione reductase and increase of glutathione transferase activities. These modifications, observed particularly in the liver and brain, were enhanced by long-term alcohol exposure. Our results indicate that increased glutathione transferase activity and decreased glutathione reductase activity, followed by thiol depletion, are important factors sustaining a pathogenic role for oxidative stress in aging and in all situations where age-correlated changes occur. They also reinforce the oxidative potential of toxic compounds, such as ethanol intoxication.

Administration, Oral↗
PubMed1998

Long-term ethanol administration enhances age-dependent modulation of redox state in central and peripheral organs of rat: protection by metadoxine.

Evidence is accumulating that intermediates of oxygen reduction may be associated with the development of alcoholic disease. In addition, free radical-induced perturbation of the oxidant/antioxidant balance in cells is widely recognized as the main causative factor of age-related disorders. In the present work, we investigated the effects of 25 months of ethanol consumption on the antioxidant defense system in different organs of rat in comparison with normal aging, in the absence and presence of treatment with metadoxine, an ion pair composed of pirrolidone carboxylate and pyridoxine. We demonstrate that aged rats underwent a significant perturbation of the antioxidant defense system, as indicated by depletion of reduced glutathione (GSH) content, and increases in oxidized GSH and free radical-induced luminescence associated with a decrease of GSH reductase and an increase of GSH transferase activities. These modifications, observed particularly in the liver and brain with respect to other organs, were enhanced by long-term alcohol exposure, and interestingly, significantly reduced after metadoxine supplementation. Our results indicate that increased GSH transferase activity and decreased GSH reductase activity, followed by thiol depletion, are important factors sustaining a pathogenic role for oxidative stress in aging and in all situations where age-correlated changes occur. Administration of metadoxine greatly reduces these metabolic abnormalities. This evidence supports the pharmacological potential of metadoxine in the management of alcoholic disturbances.

Aging↗
PubMed1998

Increased cerebrospinal fluid and plasma levels of ultraweak chemiluminescence are associated with changes in the thiol pool and lipid-soluble fluorescence in multiple sclerosis: the pathogenic role of oxidative stress.

The pathogenesis of multiple sclerosis (MS), the major neurological disease of young adults in the western world, is still poorly understood and no effective therapy to block MS is yet available. It is generally accepted that reactive oxygen species have a major role in the mediation of cell damage and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. Modification of the cellular oxidant/antioxidant balance has been involved in the neuropathogenesis of several diseases, e.g., stroke, Parkinson's disease, Alzheimer's disease and physiological aging. An increasingly important area of antioxidant defense is based on sulfhydryl chemistry, owing to the role of sulfhydryl groups in the function of macromolecular structures such as enzymes and cellular membranes. The chemical composition of human cerebrospinal fluid (CSF) is considered to reflect brain metabolism and in the present study we provided experimental evidence of a decrease in sulfhydryl groups and increased content of products of lipid peroxidation, such as ultraweak chemiluminescence and liposoluble fluorescence, which we found higher in the CSF and plasma of MS patients than in controls, pointing out the role of oxidative stress in the pathogenesis of MS.

Adult↗
PubMed1997

Cysteine-induced enhancement of lipid peroxidation in substantia nigra: comparative effect with exogenous administration of reduced glutathione.

It is generally accepted that reactive oxygen species have a major role in the mediation of cell damage and that free sulphydryl (SH) groups are vital in cellular defence against endogenous or exogenous oxidants. Modification of cellular oxidant/antioxidant balance has been involved in the neuropathogenesis of several diseases, e.g., stroke, Parkinson's disease, Alzheimer's disease and physiological ageing. An increasingly important area of antioxidant defence is based on sulphydryl chemistry, owing to the role of SH groups in the function of macromolecular structures such as enzymes and cellular membranes. Thiols, however, may themselves generate deleterious free radicals, and thionyl radicals, which have been demonstrated to originate in biological systems through enzymatic reactions of different peroxidases, by reacting with molecular oxygen or hydrogen peroxide are able to promote reactions of oxidatives stress. In the present study we provide experimental evidence suggesting a selective effect of cysteine in promoting reactions of oxidative stress in the brain areas of substantia nigra and septum, but not in other areas. In contrast, exogenous administration of reduced glutathione led to a significant decrease of lipoperoxidation in the brain areas of cortex and hippocampus, associated to selective changes in the endogenous pool of thiols.

Animals↗
PubMed1996

Nuclear DNA strand breaks during ethanol-induced oxidative stress in rat brain.

Free radical-mediated oxidative damage has been implicated in the pathophysiological mechanisms of apoptosis. In this study we report that statistically significant strand breaks were induced primarily in the hippocampus and cerebellum during chronic, and not acute, ethanol treatment. Damage to DNA observed in hippocampus and cerebellum was also correlated with significant modification in the activities of mitochondrial respiratory complexes I and IV and with a significant increase in lipid peroxidation products. This finding lends support to the fact that hippocampus and cerebellum are brain areas particularly vulnerable to redox changes induced by alcohol intoxication, suggesting lower threshold levels of ethanol tolerance.

Animals↗
PubMed1996

Stress proteins and SH-groups in oxidant-induced cell damage after acute ethanol administration in rat.

It is generally accepted that lipid peroxides play an important role in the pathogenesis of ethanol-induced cellular injury and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. It has been observed that oxidative stress induces the synthesis of the 70-kDa family of heat-shock proteins (HSPs). Furthermore, induction of HSPs represents an essential and highly conserved cellular response to a variety of stressful stimuli. In the present study, we measured the intracellular levels of HSP 70 proteins after administration of mild intoxicating and grossly intoxicating doses of ethanol to rats. Our results demonstrate that elevated doses of ethanol induce HSP in various brain areas, namely, cerebellum, hippocampus, and to a lesser extent, striatum or liver. Induction of HSP 70 protein was correlated with a marked depletion of intracellular bound thiols and a decrease in lipid peroxidation measured as MDA formation. These studies support the hypothesis that a redox mechanism may be involved in the heat-shock signal pathway.

Alanine Transaminase↗