Search results for "Cyst"

showing 10 items of 1960 documents

Changes of homocysteine and related compounds in Down syndrome

2011

Settore BIO/10 - BiochimicaHomocysteineDown's syndrome
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Plasma Cysteine and Homocysteine concentrations in pregnant and nonpregnant women with controlled folate intake

2010

Settore BIO/10 - BiochimicaPregnat womenCysteineHomocysteine
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Blood lipid, homocysteine, uric acid and vitamins in clinically stable Multiple Sclerosis patients

2008

A decrease of antioxidants, of neuroprotective and immunoregulatory vitamins and an increase of total-Homocysteine, Cholesterol, HDL-cholesterol, and of cellular stress markers [1] was reported in patients affected by Multiple Sclerosis. Recently, considering their unreliability, mainly due to the variability of the samples investigated, the attention focused on clinical relapse that results associated to a decrease of Uric acid and an increase of Cholesterol and stress markers. Aim. To identify the biochemical status during Multiple Sclerosis (MS) in a phase of clinical stability (PCS), we compared the blood levels of Urico acid (UA), Folic acid (FA), vitamins B12, A, and E, total-Homocyst…

Settore BIO/10 - BiochimicaSettore MED/26 - NeurologiaHomocysteineSclerosis Multiple
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SEARCH OF MUTATIONS IN CFTR GENE AND IN GENES ENCODING CFTR INTERACTORS IN PATIENTS BEARING ATYPICAL CISTIC FIBROSIS

2011

Settore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaCFTR CYSTIC FIBROSIS
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Elevated cerebrospinal fluid and plasma homocysteine levels in ALS

2012

Background: Numerous recent evidence suggests that homocysteine (HC), a putative risk factor for stroke and coronary artery disease [1,2], could play a role in the physiopathology of several neurodegenerative disorders, such as Alzheimer’s Parkinson’s diseases and amyotrophic lateral sclerosis (ALS) [3,4,5]. HC, an aminoacid involved in the methionine metabolism, acts as a neurotoxin through several mechanisms, including free radicals and cytosolic accumulation, mitochondrial dysfunctions, activation of apoptotic pathways, and excitotoxic aminoacid-mediated damage [5]. A recent report showed that plasma HC levels were significantly elevated in ALS, and in particular in those patients with a…

Settore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaHomocysteine; ALS;ALSHomocysteine
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Hsp27 and Hsp60 in human submandibular salivary gland: Quantitative patterns in healthy and cancerous tissues with potential implications for differe…

2021

Tumors of the submandibular salivary gland (SMG) are uncommon but sufficiently frequent for the physician to consider them in routine examinations and for the pathologist to be prepared to differentiate them from other tissue abnormalities. However, scarcity of specimens makes training difficult, a situation compounded by the lack of accepted universal diagnostic guidelines. Furthermore, there is little information on the chaperone system (CS) of the gland, despite the increasing evidence of its participation in carcinogenesis as a biomarker for diagnosis and patient follow up, and in the mechanisms by which the tumor cells thrive. We are investigating this aspect of various tumors, and her…

Settore BIO/17 - IstologiaMalePathologymedicine.medical_specialtyHistologyCarcinogenesisAdenoid cystic carcinomaSubmandibular GlandHsp27 Hsp60 Pleomorphic adenoma Submandibular salivary glandAdenoid cystic carcinomamedicine.disease_causeDiagnosis DifferentialMitochondrial ProteinsPleomorphic adenomaHsp27Biomarkers TumormedicineHumansHeat-Shock ProteinsSalivary glandbiologySettore BIO/16 - Anatomia Umanabusiness.industryChaperonin 60Cell BiologyGeneral Medicinemedicine.diseaseNeoplasm ProteinsSubmandibular Gland Neoplasmsmedicine.anatomical_structurebiology.proteinBiomarker (medicine)ImmunohistochemistryChaperone systemFemaleDifferential diagnosisbusinessCarcinogenesisMolecular ChaperonesActa Histochemica
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Identification and validation of novel molecules obtained by integrated computational and experimental approaches for the readthrough of PTCs in CF c…

2014

Cystic Fibrosis patients with nonsense-mutation in h-CFTR gene generally make virtually no CFTR protein and thus often have a more severe form of CF. Ataluren (PTC124) was suggested to induce read-through of premature but not normal termination codons. Despite the promising results there is not a general consensus on the mechanism of its action (protein stabilization or codon read-through) and its efficacy, the identification of new PTC124 analogues and the study of the mechanism of action may led to a new strategy for the development of a pharmacologic approach to the cure of CF.

Settore BIO/18 - GeneticaCystic Fibrosis CFTR Readthrough Stop CodonSettore CHIM/06 - Chimica Organica
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PTC124 derivatives as a novel approach to improve the readthrough of premature stop codons in the CFTR gene.

2011

Background Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). Approximately 10% (worldwide) of patients have in-frame nonsense mutations (UAA, UAG or UGA class I mutations) in the CF trans-membrane regulator (CFTR) gene that result in premature stop codons (PTCs) in the messenger RNA (mRNA) generating truncated CFTR protein responsible for a severe CF phenotype. Pharmacological approaches have been proposed to directly overcome PTCs. Ataluren (PTC124) a small molecule that mimics the activity of aminoglycosides has been suggested to allow PTCs readthrough and to partially restore the protein function. However, des…

Settore BIO/18 - GeneticaCystic fibrosis Nonsense mutation PTC124Settore CHIM/06 - Chimica OrganicaPTC124 Cystic fibrosis.
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COMBINING TRANSLATION READTHROUGH INDUCING DRUGS AND NONSENSE MEDIATED DECAY PATWHAY INHIBITION TO THE CFTR RESCUE IN CYSTIC FIBROSIS CELL MODEL SYST…

2021

Nonsense mutations affect 10% of patients with cystic fibrosis and produce a premature termination codon in CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) mRNA causing early termination of translation and leading to lack of CFTR function. A potential therapy for nonsense mutations provides the use of small molecules able to overcome the premature stop codon (PTC) by a readthrough mechanism that lead to synthesis a complete CFTR protein. Despite the good results obtained from this approach, TRIDs efficiency is considerably reduced by the poor amount of target transcript, that is the mRNA containing the PTC. The readthrough, indeed, does not occur on the totality of target transcr…

Settore BIO/18 - GeneticaReadthrough Stop mutations PTC CFTR Cystic Fibrosis TRIDsSettore CHIM/06 - Chimica Organica
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X CONVENTION OF INVESTIGATORS IN CYSTIC FIBROSIS.

2012

Background Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). Approximately 10% (worldwide) of patients have in-frame nonsense mutations (UAA, UAG or UGA class I mutations) in the CF trans-membrane regulator (CFTR) gene that result in premature stop codons (PTCs) in the messenger RNA (mRNA) generating truncated CFTR protein responsible for a severe CF phenotype. Pharmacological approaches have been proposed to directly overcome PTCs. Ataluren (PTC124) a small molecule that mimics the activity of aminoglycosides has been suggested to allow PTCs readthrough and to partially restore the protein function. However, des…

Settore BIO/18 - GeneticaSettore CHIM/06 - Chimica OrganicaCystic fibrosis PTC124 Nonsense mutation
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