Epidermodysplasia verruciformis (EV)-type human papillomavirus (HPV) DNA have been detected by PCR in squamous cell carcinomas (SCC) from both organ transplant recipients (OTR) and immunocompetent individuals. Their role in skin cancer remains unclear, and previous studies have not addressed whether the viruses are transcriptionally active. We have used in situ hybridization to investigate the transcriptional activity and DNA localization of HPV. EV-HPV gene transcripts were demonstrated in four of 11 (36%) OTR SCC, one of two (50%) IC SCC, and one of five (20%) OTR warts positive by PCR. Viral DNA co-localized with E2/E4 early region gene transcripts in the middle or upper epidermal layers. Non-EV cutaneous HPV gene transcripts were demonstrated in one of five (20%) OTR SCC and four of 10 (40%) OTR warts. In mixed infections transcripts for both types were detected in two of six (33%) cases. Our results provide evidence of EV-HPV gene expression in SCC; although only a proportion of tumors were positive, the similarly low transcriptional activity in warts suggests this is an underestimate. These observations, together with emerging epidemiological and functional data, provide further reason to focus on the contribution of EV-HPV types to the pathogenesis of cutaneous SCC.
Patients and clinicians sometimes take coping with chronic pain primarily as a process of gaining more control over pain. An alternate approach might include helping the pain sufferer to discriminate parts of their situation that can be effectively controlled from those that cannot. When faced with situations that do not yield to attempts at direct control patients may gain better results from leaving those situations as they are and investing their efforts elsewhere. This study was designed to examine this type of expanded view of coping with pain, a view that includes both attempts at control and acceptance. 200 adults seeking treatment for chronic pain were the subjects of this investigation. They completed a number of self-report inventories including a measure called the Brief Pain Coping Inventory, an inventory assessing accepting responses to pain as well as pain management responses standardly targeted by cognitive-behavioral treatment methods. Preliminary results showed that the BPCI yields scores with adequate temporal consistency and validity. Further results showed that a number of the responses assessed by the BPCI were reliable predictors of patient functioning. In general less frequent struggling to control pain, fewer palliative and avoidant coping responses, and more explicit persistence with activity despite acknowledged pain were associated with less depression and anxiety and greater life functioning. These results demonstrate that, in some instances, attempts at avoidance and control of chronic pain may be less helpful compared with a willingness to experience pain and focus on functioning.
BackgroundThe genetic basis of the autoimmune disease type 1 diabetes (T1D) has now been largely determined, so now we can compare these findings with emerging genetic knowledge of disorders and phenotypes that have been negatively or positively associated with T1D historically. Here, we assessed the role in T1D of variants previously reported to be associated with atopic diseases and epithelial barrier function, profilaggrin (), and those that affect the expression levels of the proinflammatory cytokines tumour necrosis factor (TNF)-α, interleukin (IL)-1β, interferon (IFN)γ and IL-18.MethodsWe genotyped single nucleotide polymorphisms (SNPs): − 105/rs28665122 in SELS or SEPS1 (selenoprotein), three single nucleotide polymorphisms in IL18 (−105/rs360717, + 183/rs5744292 and + 1467/rs574456) and R501X/rs61816761 in FLG, the major locus associated with atopic dermatitis and predisposing to asthma, in a minimum of 6743 T1D cases and 7864 controls.ResultsNo evidence of T1D association was found for any of the SNPs we genotyped at FLG, SELS or IL18 (p ≥ 0.03), nor with haplotypes of IL18 (p = 0.82). Review of previous T1D genome-wide association results revealed that four (human leucocyte antigen (HLA), gasdermin B/ORM1 (Saccharomyces cerevisiae)-like/gasdermin B/, GSDMB/ORMDL3/GSDMA and IL2RB) of ten loci recently reported to be associated with asthma were associated with T1D (p≤0.005).ConclusionsThese results show that there are shared genetic associations for atopy-related traits and T1D, and this might help in the future to understand the mechanisms, pathways and environmental factors that underpin the rapid rise in incidence of both disorders in children. Copyright © 2011 John Wiley & Sons, Ltd.
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