Publications by authors named "Candito M"

The tympanic membrane (TM), is a thin tissue lying at the intersection of the outer and the middle ear. TM perforations caused by traumas and infections often result in a conductive hearing loss. Tissue engineering has emerged as a promising approach for reconstructing the damaged TM by replicating the native material characteristics.

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The biocompatibility and the antioxidant activity of barium titanate (BaTiO) and lithium niobate (LiNbO) were investigated on a neuronal cell line, the PC12, to explore the possibility of using piezoelectric nanoparticles in the treatment of inner ear diseases, avoiding damage to neurons, the most delicate and sensitive human cells. The cytocompatibility of the compounds was verified by analysing cell viability, cell morphology, apoptotic markers, oxidative stress and neurite outgrowth. The results showed that BaTiO and LiNbO nanoparticles do not affect the viability, morphological features, cytochrome c distribution and production of reactive oxygen species (ROS) by PC12 cells, and stimulate neurite branching.

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A cochlear implant (CI) is an electronic device that enables hearing recovery in patients with severe to profound hearing loss. Although CIs are a successful treatment for profound hearing impairment, their effectivity may be improved by reducing damages associated with insertion of electrodes in the cochlea, thus preserving residual hearing ability. Inner ear trauma leads to inflammatory reactions altering cochlear homeostasis and reducing post-operative audiological performances and electroacoustic stimulation.

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Sensorineural hearing loss (SNHL) affects the inner ear compartment and can be caused by different factors. Usually, the lack, death, or malfunction of sensory cells deputed to transduction of mechanic-into-electric signals leads to SNHL. To date, the therapeutic option for patients impaired by severe or profound SNHL is the cochlear implant (CI), a high-tech electronic device replacing the entire cochlear function.

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Sensorineural hearing loss due to aging, noise exposure, trauma or drug ototoxicity is irreversible because cochlear hair cells and neurons cannot regenerate. Recently, therapeutic strategies involving nanoparticles have been developed as innovative drug delivery systems. Thermodynamically stable liquid crystalline nanoparticles based on the polar lipid glycerol monooleate (GMO NP, cubosomes), nontoxic and able to encapsulate both hydrophilic and hydrophobic compounds, were produced and tested for biocompatibility in an immortalized Organ of Corti derived cell line (OC-k3), through cell viability and cytomorphological assays, and Western blot expression profiles of apoptotic markers.

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Cis-diamminedichloridoplatinum (II) (cisplatin) is a chemotherapeutic drug currently prescribed for the treatment of many types of human cancer, but its use is associated with numerous adverse effects, one of which is ototoxicity. Cisplatin-induced hearing loss is mainly attributed to oxidative stress, but recent data suggest that inflammation could be the trigger event leading to inner ear cell death through endoplasmic reticulum (ER) stress, autophagy, necroptosis, and then intrinsic apoptosis. In this review, we look at the molecular targets of cisplatin, and the intracellular pathways underlying its ototoxicity.

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Cochlear implants, the only way to recover from severe/profound hearing loss, may cause adverse effects, among which reactions to silicone materials coating implant electrodes, leading to apoptosis and necrosis of spiral ganglion cells. Our aim was to evaluate whether three polydimethylsiloxane (PDMS) compounds (hexadimethylsiloxane, octamethyltrisiloxane, decamethylcyclopentasiloxane) used in silicone rods could exert toxic effects on an in vitro neuronal cell model (PC12). Cell viability, morphology and mRNA expression levels of apoptotic markers were evaluated on PC12 cells at different PDMS dilutions up to 6 days of exposure.

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Neural tube defects (NTDs) are severe congenital malformations due to failure of neural tube formation in early pregnancy. The proof that folic acid prevents NTDs raises the question of whether other parts of homocysteine (Hcy) metabolism may affect rates of NTDs. This French case-control study covered: 77 women aged 17-42 years sampled prior to elective abortion for a severe NTDs (cases) and 61 women aged 20-43 years with a normal pregnancy.

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Background: Folic acid supplementation reduces the occurrence of neural tube defects (NTDs); however, it is not clear whether it protects against teratogenic effects of antiepileptic drugs.

Methods: We report the cases of four pregnant women receiving valproic acid therapy, who all had NTD-affected offspring, despite periconceptional 5 mg/day of folic acid supplementation (cases), and investigated homocysteine metabolism, linked with folate metabolism. Their plasma homocysteine, folates, and vitamin B6 and B12 results were compared with values of two other women, who were also receiving valproic acid and folic acid complement, but who had normal pregnancies (valproic acid controls), and values of 40 pregnant women who had normal pregnancies and were not receiving any therapy (controls without therapy).

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Introduction: Decompression sickness with cerebral ischemic lesions occurs even in divers who have not committed any technical error. This study sought to determine whether an acquired or inborn thrombophilic factor might be involved.

Methods: 44 divers with ischemic medullar lesions (36 men, 8 women, mean age 39.

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Background: Elevated plasma homocysteine levels are associated with increased risk of vascular disease and of congestive heart failure (CHF), with a relationship between homocysteine values and disease severity. Hyperhomocysteinemia is a risk factor for cardiac dysfunction. In this study, the predictive value of elevated homocysteine levels was investigated in the prognosis of ischemic and non-ischemic CHF.

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Nutritional factors and comedications are among the postulated causes of fatigue, a highly prevalent symptom in the multiple sclerosis (MS) population, with serious impact on patients' quality of life. Deficiency of carnitine may play a role by reducing energy production through fatty acid oxidation and numerous MS therapies can induce fatigue syndrome. The aim of this prospective open-labelled study was to collect and study serum carnitine levels in MS patients with and without disease-modifying treatment-induced fatigue syndrome.

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While receiving lamotrigine, a patient pregnant with triplets suffered a double fetal neural tube defect. Plasma homocysteine, folate, vitamins B12 and B6 (pyridoxal phosphate), and red cell folate levels were measured in samples while she was receiving folic acid therapy for 1 month during the second trimester of pregnancy. Some mutations were sought, involved in homocysteine metabolism and linked with the folate metabolism.

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Unlabelled: In divers with a vascular disease in decompression sickness, who have not committed any technical error, thrombophilic risk factors were sought. Six cases of confirmed divers, without diving technical error, were investigated. Thrombophilic screening included proteins C, S, antithrombin III, and factor VIII assays, and circulating antibodies, Factor V Leiden, and mutation G20210A mutation in Factor II gene research.

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Methylenetetrahydrofolate reductase polymorphism (MTHFR C677T) is an established determinant of homocysteine plasma level (t-Hcys) while its association with coronary artery disease (CAD) seems to be more limited. In contrast, the association of the substitutions A2756G of methionine synthase (MTR), A66G of methionine synthase reductase (MTRR) and C776G of transcobalamin (TCN) to both t-Hcys and CAD needs to be evaluated further. The objective was to evaluate the association of these polymorphisms with t-Hcys and CAD in a French population.

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The number of consultant clinical chemists (NCCC) in the 15-nation European Union (EU) (Austria, Belgium, Denmark, Finland, France, Germany, Greece, Ireland, Italy, Luxembourg, The Netherlands, Portugal, Spain, Sweden, United Kingdom) has been ascertained. These data were analysed in relation to several established national parameters, including demographics, gross domestic product (GDP), cost of healthcare, cost of in vitro diagnostic (IVD) testing and the number of physicians and pharmacists. Large differences in the population-corrected costs of IVD testing (range approximately 2.

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Electrocortical effects of long duration exercise on cognitive function were investigated by analyzing P300 amplitude and latency changes during a 3-h cycling exercise. P300 components were measured in 12 well-trained cyclists and blood glucose, cortisol, insulin, glycerol, and free fatty acids (FFAs) epinephrine and norepinephrine were analyzed. Results indicated that P300 components were affected by exercise with a temporary increase in amplitude between the 1st and the 2nd hour and an increase in latency after 2 h of exercise concomitant with some hormonal changes, including an increase in cortisol and epinephrine and a decrease in blood glucose.

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Periconceptional folic acid supplementation reduces the frequency of embryological neural tube defects (NTD). This fact led the USA to fortify grain products with folic acid (140 microg/100 g) starting in January 1998, with a resultant decrease in the incidence of NTD. Folate deficiency is thus confirmed to be a risk factor for NTD.

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One-carbon metabolism is under the influence of folate, vitamin B12 and genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR 677 C --> T and 1298 A --> C), of methionine synthase (MTR 2756 C --> G), methionine synthase reductase (MTRR 66 A --> G) and transcobalamin (TCN 776 C --> G). The pathogenesis of neural tube defect (NTD) may be related to this metabolism. The influence of the MTHFR 677 C --> T polymorphism reported in The Netherlands and Ireland can be questioned in southern Italy, France and Great Britain.

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Moderate hyperhomocysteinaemia (HHcy) and the homozygous mutation C677T in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene are associated with increased risk of recurrent pregnancy loss. This HHcy is currently reported as a consequence of folate rather than of vitamin B12-deficient status. We describe one case of recurrent early pregnancy loss with HHcy caused by B12 deficiency.

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Accelerated atherosclerosis is common in diabetes mellitus, although its extent is not always related to its strong association with classical cardiovascular risk factors. Diabetic patients, especially with type 2 diabetes, are prone to cardiovascular disease which is the leading cause of death in this population. Recent clinical studies among general population have shown that an even mild increase of homocysteinemia play an important role in the progression of atherosclerosis, either in coronary or peripheral arteries.

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