PubMed Health⌕ Search

Biomedical subjects

C Nucci

Publications and source records attributed to C Nucci.

At least 19 recordsLinked to original sources

Prevalence of blindness and low vision in an Italian population: a comparison with other European studies.

AIM: The scientific literature contains recent data on the prevalence of blindness and low vision for a few European countries, but most of these studies have been focused exclusively on the elderly sector of the populations. The purpose of the present study was to provide age-specific estimates of the prevalence and causes of visual loss in an Italian population aged 40 years and over. METHODS: In total, 847 of the 1,200 citizens >40 years of age (70.6%) in the island community of Ponza underwent complete standardized ophthalmological examinations. Visual acuity (VA) was measured using a standard logarithmic chart. World health organization (WHO) definitions of blindness and low vision were adopted (respectively, VA>1.3 logMAR or a visual field <10 degrees around central fixation, and VA >0.5 to 1.3 logMAR or a visual field <20 degrees around central fixation). Prevalence rates based on presenting VAs were also calculated. RESULTS: The overall best-corrected prevalence rates were 0.6% (presenting, 0.8%) for better eye blindness, 2.1% (presenting, 6.7%) for better eye low vision, 1.8% (presenting, 2.6%) for monocular blindness, 5.0% (presenting, 11.2%) for monocular low vision. Cataract, glaucoma, degenerative myopia, and AMD were the main causes of better eye visual loss. CONCLUSION: Age-specific prevalence rates in Ponza are fairly consistent with those for other European countries with similar socio-economic conditions and public healthcare systems. A substantial percentage of visual losses remains uncorrected despite the availability of potentially curative therapy. Greater emphasis needs to be placed on educating the public regarding the importance of good vision.

Adult↗

Incidence of visual loss in the Ponza Eye Study, Italy.

AIM: To study the incidence of visual loss over a 12-year period in the survivors of an original cohort aged 40 years or older at baseline. METHODS: Visual acuity (VA) was measured by means of a standardized logMAR chart. World Health Organization definition of blindness and low vision was adopted (respectively, best-corrected VA >1.3 logMAR or a visual field <10 degrees around central fixation, and best-corrected VA >0.5-1.3 logMAR or a visual field <20 degrees around central fixation). Moreover, binocular visual loss incidence (VA>0.5 logMAR) was calculated in a 'healthy' group who had uncorrected VA of 0.0 logMAR or better in both eyes at baseline and absence of eye diseases. RESULTS: Of the 584 eligible survivors, 411 (70.7%) had a 12-year follow-up visit. The overall incidence figures were as follows: best-corrected binocular blindness (0.7%), binocular low vision (3.9%), monocular blindness (2.7%), and monocular low vision (5.0%), respectively. The results for presenting VAs were 1.2, 9.5, 4.2, and 15.3%. Figures for uncorrected, best-corrected, and presenting binocular visual loss incidence in the 'healthy' group were respectively 12.7, 0.9, and 3.7%. CONCLUSION: The discrepancy between the ideal and real situations that emerges from this study has important implications for health-care planning. Over a period of 12 years, a substantial percentage of 'healthy' subjects will have to seek medical care. Incident visual loss was caused mainly by untreated cataract, glaucoma, myopia, and age-related macular degeneration.

Adult↗

Direct costs of glaucoma and severity of the disease: a multinational long term study of resource utilisation in Europe.

BACKGROUND: Resource utilisation and direct costs associated with glaucoma progression in Europe are unknown. As population progressively ages, the economic impact of the disease will increase. METHODS: From a total of 1655 consecutive cases, the records of 194 patients were selected and stratified by disease severity. Record selection was based on diagnoses of primary open angle glaucoma, glaucoma suspect, ocular hypertension, or normal tension glaucoma; 5 years minimum follow up were required. Glaucoma severity was assessed using a six stage glaucoma staging system based on static threshold visual field parameters. Resource utilisation data were abstracted from the charts and unit costs were applied to estimate direct costs to the payer. Resource utilisation and estimated direct cost of treatment, per person year, were calculated. RESULTS: A statistically significant increasing linear trend (p = 0.018) in direct cost as disease severity worsened was demonstrated. The direct cost of treatment increased by an estimated 86 for each incremental step ranging from 455 euro per person year for stage 0 to 969 euro per person year for stage 4 disease. Medication costs ranged from 42% to 56% of total direct cost for all stages of disease. CONCLUSIONS: These results demonstrate for the first time in Europe that resource utilisation and direct medical costs of glaucoma management increase with worsening disease severity. Based on these findings, managing glaucoma and effectively delaying disease progression would be expected to significantly reduce the economic burden of this disease. These data are relevant to general practitioners and healthcare administrators who have a direct influence on the distribution of resources.

Adult↗

SEM evaluation of canal wall dentine following use of Mtwo and ProTaper NiTi rotary instruments.

AIM: To compare using scanning electron microscopy (SEM) root canal walls following instrumentation in vitro with two different rotary NiTi instruments. The hypothesis was that no difference should be observable between the experimental groups in terms of debris on canal walls and surface morphology. METHODOLOGY: Twenty-four single-rooted human teeth were selected. Two types of NiTi instruments were used, Mtwo (Sweden & Martina, Padova, Italy) and ProTaper (Dentsply Maillefer, Ballaigues, Switzerland). Irrigation for both groups was performed after each instrument change with 5% NaOCl, 3% H2O2 and 17% EDTA solutions. Three different areas (coronal, middle and apical thirds) of the root canal were evaluated using SEM. The canal wall of each sample was assessed and compared using a predefined scale of four parameters, namely, smear layer, pulpal debris, inorganic dentine debris, surface profile. Data were analysed statistically using the Kruskal-Wallis test (anova). RESULTS: A statistically significant difference (P < 0.01) was found between the apical third and the middle and coronal thirds for both groups. No difference was observable between instrumentation groups. In the apical third canal walls were often contaminated by inorganic debris and by smear layer. In the apical third, the surface profile was affected by uninstrumented regions, comprising dentine depressions and grooves in which predentine was still visible. CONCLUSION: Both instruments produced a clean and debris-free dentine surfaces in the coronal and middle thirds, but were unable to produce a dentine surfaces free from smear layer and debris in the apical third. The presence of deep grooves and depression on dentine walls in the apical third may well explain the presence of less-instrumented areas.

Chelating Agents↗

Multifaceted roles of nitric oxide in the lateral geniculate nucleus: from visual signal transduction to neuronal apoptosis.

The lateral geniculate nucleus (LGN) is the thalamic relay of retinal inputs to the visual cortex. It contains a rich array of brain terminals, which modulate the visual signals to the cortex. Several data have documented that beside cholinergic, GABA-nergic, istaminergic, serotoninergic, and glutamatergic signals, the LGN contains also fibers and interneurons expressing the enzyme that produces nitric oxide (NO). Here, we review the documented physiological roles of NO in the transmission of visual inputs to the cortex and in the processes of activity-dependent refinement of LGN connections. Moreover we focus on the recently suggested role of NO in processes of neurotoxicity in the LGN. Particular relevance is given to studies documenting that, through an excitotoxic cascade, NO triggers apoptosis in the LGN of new-born rats deprived of vision in one eye. Data are also discussed on a possible role of NO in the mechanisms of LGN neuronal loss induced by glaucoma. We believe that a better understanding of the role of NO in the LGN may contribute to discover new experimental strategies for the treatment of degenerative ophthalmic diseases.

Animals↗

Apoptosis in the mechanisms of neuronal plasticity in the developing visual system.

Visual experience during early postnatal life is essential for normal development of synaptic connections in the visual system. In fact, altered visual experiences such as monocular deprivation (MD) or abnormal visual stimulation (e.g. strabismus, anisometropia) during this period disrupt the physiologic organization of the visual pathway, leading to loss of visual responses in cortical neurons and reduction in visual acuity of the affected eye, so that it becomes amblyopic. The authors review the main functional and morphologic changes induced by altered visual experiences in the developing visual system and focus on the recent discovery that MD induces apoptotic cell death in the lateral geniculate nucleus of newborn rats. Particular attention is given to the authors' studies documenting that, during development, MD leads retinal terminals to release excessive glutamate in the lateral geniculate nucleus where it elevates nitric oxide and causes DNA fragmentation. The latter event is known to activate poly-(ADP-ribose) polymerase, which in turn may trigger apoptosis. Better understanding of the mechanisms underlying the morphologic changes induced by altered visual experiences during development may open new venues for studying novel neuroprotective strategies for amblyopia and, more generally, for the treatment of ophthalmic diseases associated with neuronal apoptosis.

Amblyopia↗

Microbiological comparative study of isolates of Edwardsiella tarda isolated in different countries from fish and humans.

It is difficult to use tissue culture assays to investigate adherence and other properties of Edwardsiella tarda because the organism is invasive and produces a potent hemolysin. We therefore relied on polymerase chain reaction (PCR) to determine the occurrence of genes for enterotoxins (LT-I, EAST-1), Shiga toxin (Stx-1, Stx-2), cytotoxic necrotizing factors (CNF-1, CNF-2), aerobactin, invasion plasmid of enteroinvasive Escherichia coli, EPEC adherence factor (EAF), intimin (Eae), enterohemolysin (EntHly) and hemolysin (Hly) in 53 isolates of E. tarda from humans and fish from several countries. All isolates were negative for all genes investigated by PCR. Adhesion to and invasion of HeLa cells were determined by using the unusually short incubation time of 1h or 30 min. All isolates adhered and invaded in these tests. Finally, a random amplified polymorphic DNA (RAPD) test distinguished, with a few exceptions, isolates of human and fish origin.

Animals↗

Apoptosis in the dorsal lateral geniculate nucleus after monocular deprivation involves glutamate signaling, NO production, and PARP activation.

In mammals, visual experience during early postnatal life is critical for normal development of the visual system. Here we report that monocular deprivation for 2, 7, and 14 consecutive days causes p53 accumulation, cell death, and progressive loss of neurones in the dorsal lateral geniculate nucleus (dLGN) of newborn rats and these are prevented by NMDA and non-NMDA glutamate receptor antagonists, and by L-NAME, an inhibitor of nitric oxide synthesis. Monocular deprivation also increases dLGN levels of citrulline, the coproduct of nitric oxide synthesis, and this, as well as cell death and neuronal loss, is abolished by antagonists of glutamate receptors and by L-NAME. Finally, poly-(ADP-ribose) polymerase (PARP) knock-out mice appear to be protected from monocular deprivation-induced cell death. In conclusion, during early postnatal development of the rat visual system monocular deprivation causes excitotoxic, nitric oxide-mediated, cell death in the dLGN that appears to be apoptotic and also requires activation of PARP.

Animals↗

The gene encoding DRAP (BACE2), a glycosylated transmembrane protein of the aspartic protease family, maps to the down critical region.

We applied cDNA selection methods to a genomic clone (YAC 761B5) from chromosome 21 located in the so-called 'Down critical region' in 21q22.3. Starting from human fetal heart and brain mRNAs we obtained and sequenced several cDNA clones. One of these clones (Down region aspartic protease (DRAP), named also BACE2 according to the gene nomenclature) revealed a striking nucleotide and amino acid sequence identity with several motifs present in members of the aspartic protease family. In particular the amino acid sequences comprising the two catalytic sites found in all mammalian aspartic proteases are perfectly conserved. Interestingly, the predicted protein shows a typical membrane spanning region; this is at variance with most other known aspartic proteases, which are soluble molecules. We present preliminary evidence, on the basis of in vitro translation studies and cell transfection, that this gene encodes a glycosylated protein which localizes mainly intracellularly but to some extent also to the plasma membrane. Furthermore DRAP/BACE2 shares a high homology with a newly described beta-secretase enzyme (BACE-1) which is a transmembrane aspartic protease. The implications of this finding for Down syndrome are discussed.

Amino Acid Sequence↗

Imbalance in corneal redox state during herpes simplex virus 1-induced keratitis in rabbits. Effectiveness of exogenous glutathione supply.

A significant decrease in the antioxidant glutathione (GSH) was found in the corneal tissue of rabbits with Herpes Simplex 1 (HSV-1)-induced keratitis. Such a decrease was due to a loss of the reduced species, since no increase in its oxidized form was observed. Topical administration of purified GSH was able to reduce the virus titre in corneal tissue and, at the same time, was effective in reducing the severity and progression of keratitis and conjunctivitis. This effect was paralleled by a partial recovery in the corneal GSH content. In vitro experiments performed on HSV-1 infected corneal-derived rabbit cells showed that exogenous GSH reduced virus titre in the supernatant of infected cells. These results are in agreement with our previous findings that an oxidative environment, due to GSH depletion, is necessary for virus replication and suggest that topical GSH treatment could be considered as complementary therapy in HSV-1-induced keratitis.

Animals↗

Ocular changes associated with Giardia lamblia infection in children.

BACKGROUND: The protozoan disease giardiasis can cause ocular complications, including "salt and pepper" retinal changes. METHODS: Ophthalmic examinations were performed in 141 children (mean age 4.7 (SD 2.0) years) with active or past giardiasis diagnosed on the basis of microscopic examination of stool specimens or duodenal secretions--53 were newly diagnosed and untreated (group A), 50 had active infections in spite of metronidazole therapy (group B), and 38 had been successfully treated, with negative stool specimens for 1-3 years (group C). 300 children with no evidence of giardiasis were used as controls. RESULTS: Salt and pepper retinal changes (with normal electroretinographic findings) were diagnosed in 28 (19.9%) of the patients with giardiasis (11 from group A, 10 from group B, and seven from group C), including five pairs of siblings. In all subgroups, the children with retinal changes were consistently younger than those with normal retinas. In eight cases, the lesions could be visualised only with direct ophthalmoscopy. CONCLUSION: Our findings indicate that asymptomatic, non-progressive retinal lesions are particularly common in younger children with giardiasis. This risk does not seem to be related to the severity of the infection, its duration, or the use of metronidazole but may reflect a genetic predisposition.

Adolescent↗

Electro-oculography in pigment dispersion syndrome.

Clinical data and the common embryological origin of the pigment epithelium of the iris and retinal pigment epithelium suggest that the latter may be involved in the pigment dispersion syndrome (PDS). In our study functional changes of the retinal pigment epithelium were evaluated by electro-oculography in 10 PDS patients, 10 patients with chronic open-angle glaucoma (COAG) and 10 normal subjects. The mean dark-trough latency and Arden ratio for the PDS group were significantly lower than those of the COAG and control groups. Analysis of the Arden ratios based on the Kruskall-Wallis test revealed that 30% of the PDS values were subnormal with respect to the control group mean -1 SD. These results indicate primary involvement of the retinal pigment epithelium in PDS.

Adult↗

N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptor antagonists protect from apoptosis induced in the lateral geniculate nucleus of rabbits exposed to the dark.

Mono or binocular deprivation, during early postnatal development, produces dramatic effects on the anatomy and physiology of the visual system. Here we report that dark exposure induces apoptotic cell death in the lateral geniculate nucleus (LGN) of adult rabbit and this may be related to activation of N-methyl-D-aspartate (NMDA) and non-NMDA subtypes of glutamate receptors. In situ DNA fragmentation (TUNEL) was observed in the LGN of rabbits exposed to dark for 48 h. Morphological changes were confirmed on hematoxylin-eosin stained brain tissue coronal sections. Systemic treatment with CGP 040116 or MK 801, two NMDA receptor antagonists, and with GYKI 52466, a non-NMDA receptor antagonist, prevented in situ DNA fragmentation and nuclear chromatin marginalization and condensation. In no instance was apoptosis seen in rabbits kept under a normal light-dark cycle. Our findings indicate that glutamate, acting on NMDA and non-NMDA receptors, may be involved in the mechanisms of apoptotic cell death induced in the LGN of adult rabbits exposed to darkness.

Animals↗

N omega-nitro-L-arginine methyl ester prevents apoptosis induced in the lateral geniculate nucleus by light deprivation in adult rabbit.

Exposure of adult rabbits to darkness for 48 h produces bilateral DNA fragmentation in the lateral geniculate nucleus as revealed in brain sections by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labelling (TUNEL) technique, suggesting an apoptotic type of cell death. In agreement with the latter deduction, light microscopy assessment of the morphological characteristics showed marginalization and condensation of nuclear chromatin, typical features of apoptosis. These effects were abolished by systemic administration of N omega-nitro-L-arginine methyl ester, an inhibitor of nitric oxide (NO) synthesis, whereas the D isomer was ineffective. In conclusion, the present data demonstrate that light deprivation for 48 h produces apoptosis in the lateral geniculate nucleus of rabbit and suggest that NO might be involved.

Animals↗

Nitric oxide enhances amino acid release from immature chick embryo retina.

Nitric oxide (NO) was investigated for its ability to induce amino acid release from immature chick retina. The production of endogenous NO by activation of NO synthase after stimulation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptor caused a significant increase in basal release of gamma-aminobutyric acid (GABA) and glutamine, whereas a more modest increase in the glutamate release was also observed. The exposure of chick retina from 9-day-old embryos to NO-generating compounds, S-nitroso-N-acetylpe-nicillamine (SNAP) and sodium nitroprusside (SNP) produced a dose dependent increase in GABA, glutamine, and glutamate release. This effect was reduced by about 80% by haemoglobin. These results indicate that NO has a stimulatory effect on amino acid release from chick embryo immature retina. However, this effect does not appear to involve a cGMP-related mechanism because 8-bromo-cGMP, a stable analogue of cGMP, failed to affect spontaneous amino acid release and because zaprinast did not enhance NMDA-stimulated release. In conclusion, our present observations may account for a role of NMDA-mediated events in the biochemical maturation under depolarizing conditions.

Amino Acids↗