332 research outputs found
Erratum: Corrigendum to “Procalcitonin and community-acquired pneumonia (CAP) in children” (Clinica Chimica Acta (2015) 451(Part B) (215–218) (S0009898115004404) (10.1016/j.cca.2015.09.031))
The authors regret that the authors’ names in the original article appear, as reported, in the wrong form, which follows: Bivona Giulia, Agnello Luisa, Scazzone Concetta, Lo Sasso Bruna, Bellia Chiara, Ciaccio Marcello. The correct form is: Giulia (first name) Bivona (last name), Luisa (first name) Agnello (surname), Concetta (first name) Scazzone (surname), Bruna (first name) Lo Sasso (surname), Chiara (first name) Bellia (surname), Marcello (first name) Ciaccio (last name). The authors would like to apologise for any inconvenience caused
Rip-1 controlla l’espressione delle caspasi in cellule MDA-MB231 trattate con PTHrP[38-94]-amide
Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells
It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes encoding for apoptosis factors and caspases. Employing a combination of conventional and semi-quantitative multiplex PCR techniques, antisense oligonucleotide (asODN) transfections, proliferation/invasion assays and protein analyses, here we report that PTHrP treatment induces the up-regulation of Bcl-xS, Bad and Rip1 and switches-on the expression of caspase-2, -5, -6, -7 and -8 in MDA-MB231 cells. Moreover, we demonstrate for the first time that asODN-induced under-expression of Rip1 can lead to a more pronounced up-regulation of some caspases due, at least in part, to JNK inactivation, thus providing a new example of factor involved in the transcriptional regulation of the apoptotic enzymes
Rip-1 regulation of caspase expression in PTHrP [38-94]-treated MDA-MB231 breast cancer cells
Effect of vitamin supplementation on hyperhomocysteinemia and cardiovascular risk reduction
Homocysteine is a sulfur-containing aminoacid produced during methionine metabolism. Since 1969 the relationship
between altered homocysteine metabolism and both coronary and peripheral atherotrombosis has been known; in
recent years, experimental evidence has shown that elevated plasma concentrations of homocysteine are associated
with an increased risk of atherosclerosis and cardiovascular ischemic events. Several mechanisms by which elevated
homocysteine concentrations impair vascular function have been proposed, including impairment of endothelial
function, production of reactive oxygen species and consequent oxidation of low-density lipoproteins. Folate and B
vitamins, required for remethylation of homocysteine to methionine, are the most important dietary determinants of
homocysteinemia and daily supplementation typically lowers plasma homocysteine concentrations. Recently, largescale
intervention trials have been conducted to determine whether lowering homocysteine concentrations through B
vitamins supplementation can decrease cardiovascular risk in healthy subjects or improve survival in patients with
coronary heart disease. Some of these trials found no significant beneficial effects of combined treatment with folate
and vitamin B12, with or without vitamin B6, in spite of significant homocysteine lowering. In conclusion, it is still unclear
whether decreasing plasma concentrations of homocysteine through diet or vitamin supplementation may be
paralleled by a reduction in cardiovascular risk
Studio delle fitocenosi sul materiale di riporto nei pressi dell'imbocco del traforo del Gran Sasso (Assergi-Abruzzo). Approccio metodologico ed analisi floristica.
Nell'ambito di un ampio progetto di monitoraggio biologico del Gran Sasso (Abruzzo), si è avviato lo studio della successione primaria in atto sul materiale di riporto situato presso l'imbocco del traforo del Gran Sasso (Assergi). Uno studio di questo genere risulta nuovo per l'ambiente montano appenninico, sia da un punto di vista conoscitivo che metodologico. Dopo un'indagine floristica preliminare, sono state impiantate 4 aree permanenti per il rilevamento periodico di dati floristici e vegetazionali. Dai risultati finora ottenuti è emerso per questi siti l'importante ruolo colonizzatore delle specie mediterranee e di alcuni elementi endemici e boreali provenienti da ambienti di alta quota. Tale fenomeno si discosta da quanto conosciuto per la Regione Mediterranea in cui il ruolo colonizzatore è svolto per lo più da elementi ad ampia distribuzione
Polimorfismo del gene ACE:gene della longevità o fattore di rischio nella patologia ipertensiva
Negli ultimi decenni l’allungamento della vita media ha stimolato un particolare interesse nello studio dei processi dell’invecchiamento e nella ricerca di possibili geni coinvolti nella longevità. In particolare i centenari dimostrano di avere una prevalenza minore di malattie cardiovascolari e dei fattori di rischio ad essa correlati. L’enzima di conversione dell’angiotensina (ACE), presente in tutte le cellule endoteliali, gioca un ruolo essenziale nel mantenimento dell’omeostasi del flusso vascolare, regolando sia la produzione del vasocostrittore angiotensina II sia inattivando la bradichinina. In particolare alcuni studi hanno riportato una possibile correlazione tra il polimorfismo Inserzione/Delezione (I/D) localizzato all’interno dell’introne 16 del gene ACE e la patologia ipertensiva nonché un suo possibile ruolo nella longevità.
Lo studio è stato condotto su 200 soggetti di età >90 anni provenienti dalla Regione Sardegna, 123 pazienti ipertesi (24-76 anni) e 112 soggetti normotesi (30-65 anni). Il polimorfismo (I/D) è stato tipizzato mediante PCR; gli amplificati di 490bp (allele I) e di 190bp (allele D) sono stati visualizzati su gel di agarosio al 2%.
I nostri risultati mostrano una frequenza del genotipo D/D maggiore nei soggetti ipertesi rispetto ai soggetti normotesi (49% vs 36%, P = 0.027) e maggiore nel gruppo dei centenari sia rispetto ai soggetti ipertesi che normotesi ( 52% vs 49%, P = 0.016; 52% vs 36% , P < 0.01 ) .
Sebbene il ruolo del gene ACE nel processo della longevità e nella patogenesi delle malattie cardiovascolari rimanga controverso, il nostro studio suggerisce una possibile associazione tra longevità e varianti alleliche di geni coinvolti nella patogenesi dell’ipertensione
Explainable artificial intelligence advances breath analysis for monitoring Crohn’s disease
Breath analysis has emerged as a promising tool for non-invasive disease monitoring, particularly for tracking ongoing disease, due to its reproducibility and accessibility. One of the disorders that can be investigated through breath analysis is inflammatory bowel disease, such as Crohn’s disease. While many studies address this disease epidemiologically, at present a comprehensive understanding of biomarkers that can differentiate the metabolic responses between male and female patients is still missing. In this study, we explore significant biomarkers in classifying male and female body response with Crohn’s disease using explainable artificial intelligence. By leveraging a public dataset, we apply an AI-based algorithm to analyze the volatile organic compounds present in exhaled breath, which impact gender classification. Our data-driven approach not only identifies key endogenous biomarkers, but also provides interpretability in understanding patterns useful to reveal a differentiated metabolic response and develop personalized clinical treatment. The results highlight the potential of AI in advancing breath analysis for personalized monitoring of Crohn’s disease and improving gender-specific medicine
Standardized measurement of circulating vitamin D [25(OH)D] and its putative role as a serum biomarker in Alzheimer's disease and Parkinson's disease
The current review provides an overview on the development of 25(OH)D measurement standardization tools over the last three decades and clarifies whether there is a role as a serum biomarker for vitamin D in neurological diseases. In the past, a lack of internationally recognized 25(OH)D reference measurement procedures and reference standard materials led to unstandardized serum total 25(OH)D results among research and clinical care laboratories. The vitamin D Standardization Program (VDSP) has been introduced in 2010 to address this problem, however, vitamin D External Quality Assessment Scheme (DEQAS) reports still show substantial sample- to- sample variability. Further, immunoassays, which are mainly used in clinical care laboratories, display analytical issues, including matrix-effects interferences, which cannot be overcome by the standardization process. Hence, liquid chromatography-tandem mass spectrometry (LC/MS-MS) methods should be used to measure 25(OH)D. Low vitamin D serum levels have been found in patients affected by Alzheimer's disease and Parkinson's disease, suggesting a role for vitamin D as a serum biomarker in these diseases. However, few studies reported 25(OH)D standardized results, thus, no clear evidence on the potential role of 25(OH)D serum levels in these diseases exists
- …
