Epigenetic DNA methylation changes in Chronic and Episodic migraine

Background: No valid biomarkers are available to detect among patients who suffer from Episodic (EM) and Chronic migraine (CM) those at greatest risk of develop a Medication Overuse Headache (MOH). Several evidences confirmed that pain vulnerability and attitude to chronic pain sensitivity are heritable via genetic but also epigenetic pathways though changes in DNA expression. Epigenetic mechanisms would have the potential to link early life events, neuro-inflammation and brain plasticity in the aetiology of migraine chronification. Method: The aim of this pilot study was to identify changes in DNA methylation associated with headache chronification comparing controls without headache (HC), episodic migraineurs and patients suffering from MOH. In all selected subjects, genome-wide DNA methylation levels were characterized longitudinally at baseline and during follow-up using the Infinium HumanMethylationEPIC Bead-Chip. Results: A total of 25 patients with MOH were enrolled at baseline (T0), of these 18 completed the 6 months follow up (T3). In the group of EM, 20 patients were enrolled and completed the 6-month follow up (T1). 13 HC subjects were enrolled at T0, and 11 completed study. Comparing MOH vs HC group at T0, none differentially methylated regions (DMRs) reached statistical significance. Nevertheless 29 DMRs had a delta of at least 0.05 in at least one CpG site. One of the most significant CpG site identified was at the chr10:76993892 island, which maps in the COMT (catechol-O-methyltransferase) gene and resulted hypermethylated in MOH. Discussion: These preliminary data suggest a role in MOH of epigenetic processes involved in aberrant immune-inflammatory responses and deregulation of dopaminergic neurotransmission theoretically implied in mechanisms of brain plasticity which control drug addiction and cognitive-emotional processes. However, all these data are preliminary and require replication and validation in a larger sample

Nucleic Acid Sequence-Based Amplification using molecular beacons for quantification of enterovirus RNA

Quantificazione dell'enterovirus RNA mediante Nucleic Acid Sequence-Based Amplification utilizzando sonde molecular beacon

Polyomavirus BK replication in renal transplant recipients: combined monitoring of viremia and VP1 mRNA in urine

Introduction. Human polyomavirus BK (BKV) is worldwide distributed, with a seroprevalence rate of 70–90% in the adults. Following primary infection, BK remains latent in the renourinary tract as the epidemiologically most relevant latency site, and in B cell, brain, spleen and probably other tissues. Reactivation may occur in both immunocompetent subjects and immunocompromised patients. In renal transplantation, in the context of intense immunosuppression, viral replication may determine BKV-associated nephropathy (BKVAN) with interstitial nephritis and/or ureteral stenosis in 1–10% of the patients and leading to graft failure and return to haemodialysis in 30 to 80% of the cases (5). Screening of BKV replication represents the basic strategy to predict early the onset of BKVAN and may allow for earlier intervention with reduced allograft loss (3, 4). Nowadays, replication of BKV is monitored by quantification of BKV-DNA in serum and urine (2). The aim of this study was to evaluated the role of BKV VP1 mRNA in urine as a marker of viral replication in renal transplant recipients

Direct immunofluorescence (DFA) on HEP2 and R-Mix Too for Adenovirus detection

Immunofluorescenza diretta (DFA) su cellule HEP2 e R-Mix Too per la rilevazione degli Adenoviru

Real time RT-PCR assays using cRNA standards for quantification of syncytial respiratory virus type A and B

Quantificazione del virus respiratorio sinciziale di tipo A e B mediante saggi real time RT-PCR con standards a cRN

Quantificazione mediante PCR dell'EBV-DNA da biopsie cutanee di pazienti con linfomi cutanei primitivi (micosi fungoide e sindrome di Sèzary)

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