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Biomedical subjects

S Lupo

Publications and source records attributed to S Lupo.

At least 19 recordsLinked to original sources
PubMed2005

Adrenomedullin plasma concentrations in patients with retinitis pigmentosa.

PURPOSE: To evaluate the relationship between retinitis pigmentosa (RP) and plasma adrenomedullin (ADM) levels. METHODS: Blood samples were obtained from a group of 40 consecutive patients with RP matched with 35 healthy subjects (HS) as control. We carried out a complete ophtalmological examination. The study group included 26 patients with RP and 14 patients with syndromic RP. Plasma ADM levels were determined in duplicate with a specific radioimmunoassay method. RESULTS: In the HS plasma ADM levels were 13.7 +/- 6.1 pg/mL. The mean of plasma ADM concentrations in all patients with RP (23.4 +/- 10.7 pg/mL) was significantly (P < 0.0001) higher than that of HS. Moreover, in the syndromic RP patients, plasma ADM levels (28.6 +/- 14.35 pg/ml) were higher than those of HS and RP patients (P < 0.0017). CONCLUSION: The increase of plasma ADM levels in RP patients may be a response to photoreceptor damage.

Adrenomedullin↗
PubMed2004

Inter-nerves and intra-nerve conduction heterogeneity in CMTX with Arg(15)Gln mutation.

OBJECTIVE: In X-linked Charcot-Marie-Tooth disease (CMTX), electrophysiological and histopathological studies have suggested either a demyelinating or an axonal polyneuropathy. We report a CMTX family with a striking heterogeneity of nerve conductions between and within nerves. METHODS: Two men and one woman have been studied by conduction velocities, sural nerve biopsy with morphometry (one man) and DNA analysis. RESULTS: In both men motor conduction velocities were slowed in the demyelinating range, conduction velocity differences among nerves in the same subject varied from 13 to 24 m/s, and distal median compound muscle action potential (CMAP) amplitudes were 3-5 times reduced compared to ulnar CMAPs. Abnormal area reduction or excessive temporal dispersion of proximal CMAP was present in at least two nerves in all patients. Sural nerve biopsy showed reduction of large myelinated fibres, cluster formations, occasional onion bulbs. Teased fibres study revealed short internodes for fibre diameter, enlarged Ranvier nodes but no evidence of segmental demyelination and remyelination. DNA analysis showed an Arg(15)Gln mutation in connexin32 gene in all patients. CONCLUSIONS: In this family conduction slowing and segmental conduction abnormalities, in absence of morphological evidence of de-remyelination, may be related to short internodes, widened Ranvier nodes and the specific effect of the mutation. The occurrence in some CMTX patients of a non uniform involvement between and within nerves, as in acquired demyelinating neuropathies, should be kept in mind to avoid misdiagnoses.

Adult↗
PubMed2004

Macrophagic myofasciitis: an infantile Italian case.

Macrophagic myofasciitis is a recently identified inflammatory myopathy mostly described in adult French patients complaining of arthro-myalgias and fatigue. It is probably due to intramuscular injection of aluminium-containing vaccines and is characterized by a typical muscular infiltrate of large macrophages with aluminium inclusions. We report a 1-year-old Italian child presenting irritability, delayed motor development, hyperCKemia (up to 10 times the normal value), and typical features of macrophagic myofasciitis on muscle biopsy. The child recovered fully after steroid therapy. Macrophagic myofasciitis is a new treatable cause of motor retardation and hyperCKemia in children, and is probably more common than reported. Diagnosis requires a high index of suspicion and can be missed if biopsy is performed outside the vaccination site.

Aluminum↗
PubMed2001

Anti-GD1a antibodies from an acute motor axonal neuropathy patient selectively bind to motor nerve fiber nodes of Ranvier.

Acute motor axonal neuropathy (AMAN) is associated with high titer anti-GD1a antibodies. We have found that very high titer IgG anti-GD1a antibodies (Ab) from one AMAN patient selectively bind to motor, but not sensory, nerve nodes of Ranvier. Binding is abolished by preadsorption with GD1a. Sera negative for Ab do not immunostain motor and sensory nerve roots. We have also found that botulinum toxin A (BTA), which binds to GD1a, stains both motor and sensory nerve nodes of Ranvier. Our results strongly support the pathogenetic role of anti-GD1a antibodies in AMAN. Why BTA also binds to sensory fibers still remains to be elucidated, although the different size of BTA and its specificity to other gangliosides present in sensory axons might represent important factors.

Acute Disease↗
PubMed2001

Endophytic fungi from flowers, capsules and seeds of Eucalyptus globulus.

The main goal of this work was to detect whether Cytospora chrysosperma and Fusicoccum eucalypti are present as endophytes of symptomless hypocotyls, cotyledons, flowers, capsules, peduncles of flowers in order to interpret an earlier finding of their presence in seeds, seedling stems and twigs of E. globulus. Segments from these organs as well as from bark and the xylem from flower peduncles were surface-sterilized and plated on 2% malt-agar. All plates were incubated at 24 degrees C for six weeks or more depending on the growth rate of fungi. C. chrysosperma was asymptomatically present in flowers, capsules, hypocotyls, cotyledons and peduncles. F. eucalypti was isolated from asymptomatic flowers and capsules. It is probable that C. chrysosperma spreads during seed germination colonizing seedling stems through hypocotyl and cotyledon.

Journal Article↗
PubMed1997

Tyrosine is involved in protection from oxidative stress in Saccharomyces cerevisiae.

The phenotypic characterization of a Saccharomyces cerevisiae mutant unable to grow under agitated conditions is presented here. When this strain was incubated under aerobic conditions, it did not grow and the viability of the culture decreased. The loss in viability was prevented by the addition of antioxidants or chelating agents to the medium, indicating that this mutant was unable to withstand the oxidative stress generated by aerobic metabolism. This strain was complemented with plasmids from a yeast genomic library. The transformants that were obtained carried plasmids harbouring the TYR1 gene, which codes for one of the enzymes involved in tyrosine biosynthesis. A monogenic S. cerevisiae tyr1 mutant obtained from the Yeast Genetic Stock Center showed higher sensitivity to hydrogen peroxide than a TYR1 strain. This sensitivity was reverted when this strain was complemented with the TYR1 gene. Considering these results, we propose that tyrosine plays a role in the protection against oxidative stress.

Cloning, Molecular↗
PubMed1996

A comparison of time to exhaustion at VO2 max in élite cyclists, kayak paddlers, swimmers and runners.

A recent study has shown the reproducibility of time to exhaustion (time limit: tlim) at the lowest velocity that elicits the maximal oxygen consumption (vVO2 max). The same study found an inverse relationship between this time to exhaustion at vVO2 max and vVO2 max among 38 élite long-distance runners (Billat et al. 1994b). The purpose of the present study was to compare the time to exhaustion at the power output (or velocity) at VO2 max for different values of VO2 max, depending on the type of exercise and not only on the aerobic capacity. The time of exhaustion at vVO2 max (tlim) has been measured among 41 élite (national level) sportsmen: 9 cyclists, 9 kayak paddlers, 9 swimmers and 14 runners using specific ergometers. Velocity or power at VO2 max (vVO2 max) was determined by continuous incremental testing. This protocol had steps of 2 min and increments of 50 W, 30 W, 0.05 m s-1 and 2 km-1 for cyclists, kayak paddlers, swimmers and runners, respectively. One week later, tlim was determined under the same conditions. After a warm-up of 10 min at 60% of their vVO2 max, subjects were concluded (in less than 45 s) to their vVO2 max and then had to sustain it as long as possible until exhaustion. Mean values of vVO2 max and tlim were respectively equal to 419 +/- 49 W (tlim = 222 +/- 91 s), 239 +/- 56 W (tlim = 376 +/- 134 s), 1.46 +/- 0.09 m s-1 (tlim = 287 +/- 160 s) and 22.4 +/- 0.8 km h-1 (tlim = 321 +/- 84 s), for cyclists, kayak paddlers, swimmers and runners. Time to exhaustion at vVO2 max was only significantly different between cycling and kayaking (ANOVA test, p < 0.05). Otherwise, VO2 max (expressed in ml min-1 kg-1) was significantly different between all sports except between cycling and running (p < 0.05). In this study, time to exhaustion at vVO2 max was also inversely related to VO2 max for the entire group of élite sportsmen (r = -0.320, p < 0.05, n = 41). The inverse relationship between VO2 max and tlim at vVO2 max has to be explained, it seems that tlim depends on VO2 max regardless of the type of exercise undertaken.

Adolescent↗
PubMed1989

Mechanism of toxicity of an experimental bidentate phosphine gold complexed antineoplastic agent in isolated rat hepatocytes.

SK&F 104524 (bis-[1,2 bis(diphenylphosphino)-ethane]gold(l) lactate) [( Au(dppe)2]+) is an experimental antineoplastic agent that is hepatotoxic in vivo in the dog as well as highly cytotoxic to isolated canine hepatocytes in vitro. Preliminary studies in isolated dog hepatocytes have indicated that [Au(dppe)2]+ causes an increase in hepatocyte respiration and a decrease in cellular ATP. The purpose of the present investigation was to characterize [Au(dppe)2]+-induced cytotoxicity and biochemical lesions in the intact cell and to correlate these changes with mitochondrial function. The uptake of [14C][Au(dppe)2]+ by rat hepatocytes was rapid, reaching a maximum by 30 min. [Au(dppe)2]+ was distributed throughout the hepatocyte and associated rapidly with mitochondria, nuclei, cytosol and cellular membranes. [Au(dppe)2]+ caused cell lethality in a concentration-dependent fashion; although 5 microM did not cause any changes in lactic dehydrogenase leakage, 20 microM produced 100% cell death by 120 min. [Au(dppe)2]+ also caused concentration-dependent bleb formation of the hepatocyte plasma membrane, increased oxygen consumption and loss of ATP within 30 min. ATP loss was associated with transient increases in AMP and ADP and a profound drop in the ATP/ADP ratio and energy charge. Total nucleotides (adenine and xanthine nucleotides) remained constant. The pattern of glutathione depletion coincided with that of lactic dehydrogenase leakage. Electron microscopy of hepatocytes exposed to [Au(dppe)2]+ for 30 min revealed depletion of glycogen granules and marked swelling of mitochondria. In isolated rat liver mitochondria, [Au(dppe)2]+ caused a stimulation of state 4 respiration and loss of the respiratory control ratio. [Au(dppe)2]+ also relieved the oligomycin-induced inhibition of state 3 (ADP-stimulated) respiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Toxicity of H2-receptor antagonists to isolated rat hepatocytes: structure-activity relationships.

Oxmetidine is a potent and specific antagonist of the histamine H2-receptor. Oxmetidine is also cytotoxic to isolated rat hepatocytes through inhibition of mitochondrial oxidative phosphorylation. The purpose of this investigation was to test a variety of H2-receptor antagonists that are structural analogs of oxmetidine in an attempt to identify a critical structural component or a physicochemical property of the molecule which may be responsible for cytotoxicity. Six histamine receptor H2-antagonists were tested. The minimum drug concentrations that caused 100% cell death (leakage of intracellular lactate dehydrogenase and loss of intracellular potassium) ranged from 0.87 to 22.50 mM for the analogs tested. At toxic concentrations, two of the least potent analogs, SK&F 92909 and SK&F 9205A both caused a rapid decrease in hepatocyte O2 consumption and ATP content which occurred before any evidence of cell injury. The potency of these molecules as cytotoxicants to isolated hepatocytes did not correlate with their potency as histamine H2-receptor antagonists whereas there was a significant correlation between increasing potency and increasing octanol/water partition coefficients. These data suggest that lipid solubility may be a key factor in the cytotoxicity of this class of drugs to isolated rat hepatocytes.

Animals↗
PubMed1988

Sjögren's syndrome: clinical, cytological, histological and colposcopic aspects in women.

Sjögren's syndrome, characterized by a progressive alteration of the exocrine glands which ultimately results in their atrophy, has the highest incidence among females. The main etiopathogenetic mechanism is autoimmunological. The symptomatology is made up of symptoms depending on an altered glandular secretion and mucosal dryness. Dyspareunia and pruritus, due to vaginal and vulvar dryness, are quite common symptoms. Few studies have considered the clinical and histological consequences of Sjögren's syndrome in the external female genitalia. In the present study 26 women (mean age 46 years) affected by Sjögren's syndrome were examined by means of a series of tests including gynecological examination exam, colposcopic inspection and cervical biopsy. All the patients showed a particular dryness a series of tests including gynecological examination failed to evidence malign cells and, in 15% of the subjects, showed an estrogenic insufficiency in various degrees. The colposcopic inspection revealed dystrophic processes resulting in the atrophy of the cervico-vaginal mucosa in 50% of the cases. The histological findings of the cervical biopsies evidenced the presence of a chronic cervicitis in 10% of the cases.

Adult↗
PubMed1987

In vivo and in vitro hepatotoxicity and metabolism of acetaminophen in Syrian hamsters.

The purpose of this investigation was to correlate the in vitro and in vivo toxicity of the hepatotoxicant, acetaminophen. Hamsters were pretreated with either phenobarbital (70 mg/kg) or 3-methylcholanthrene (20 mg/kg) or an appropriate vehicle for 3 days. In non-pretreated hamsters, single doses of acetaminophen (200-400 mg/kg i.p.) caused elevations in serum alanine aminotransferase and sorbitol dehydrogenase activities in a dose-related manner. 3-Methylcholanthrene significantly potentiated, while phenobarbital significantly reduced acetaminophen-induced elevations in serum liver enzyme activities. Both phenobarbital and 3-methylcholanthrene significantly reduced acetaminophen plasma T1/2 while only 3-methylcholanthrene increased APAP clearance. Phenobarbital pretreatment increased the urinary excretion of APAP-glucuronide. Exposure of isolated hepatocytes to acetaminophen (0.01-2.0 mM) resulted in concentration-related decreases in hepatocyte viability. Cells from 3-methylcholanthrene-pretreated hamsters were more markedly susceptible to acetaminophen toxicity than cells isolated from non-induced animals. Hepatocytes isolated from phenobarbitol pretreated animals were slightly but significantly more susceptible to acetaminophen toxicity than cells from control animals. Hepatocytes isolated from 3-methylcholanthrene pretreated animals had increased formation of an acetaminophen-glutathione conjugate compared to control. Pre-treatment with either phenobarbital or 3-methylcholanthrene enhanced glucuronidation of acetaminophen in vitro. These data demonstrate a lack of correlation between in vivo hepatotoxicity and in vitro cytotoxicity in that phenobarbital pre-treatment protected hamsters from acetaminophen-induced liver toxicity, but failed to protect hepatocytes exposed to acetaminophen in vitro.

Acetaminophen↗
PubMed1986

Cadmium toxicity in the isolated perfused rat liver.

Isolated perfused livers from male and female Sprague-Dawley rats were exposed to cadmium chloride (50 and 200 microM). Acute hepatotoxicity was investigated by measuring cadmium-induced changes in bile flow, urea synthesis and alanine aminotransferase (ALT) leakage. Cadmium-induced lipid peroxidation was estimated by formation of conjugated dieners and thiobarbituric acid (TBA) reactants. Cadmium, at both concentrations, caused a rapid decrease in bile flow (within 40 min) and complete cholestasis within 70 min exposure in livers perfused from both male and female rats. Cadmium exposure (50 and 200 microM) also resulted in the leakage of ALT into the perfusate within 60 min. In contrast, exposure of isolated rat hepatocytes to as high as 500 microM cadmium did not result in enzyme leakage until 180 min exposure. Sex differences in cadmium-induced cholestasis and ALT leakage were not observed at these concentrations. Malondialdehyde was not detected in the perfusate nor were conjugated dienes detected in liver tissue following 90 min cadmium exposure. These data demonstrate that the isolated perfused rat liver (IPRL) is a sensitive system in which to study chemically induced hepatotoxicity. Cadmium rapidly causes functional alterations and cellular damage in perfused livers from both male and female rats. Cadmium-induced liver injury was apparently not related to lipid peroxidation.

Alanine Transaminase↗