Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ (DCIS), psoriasin was identified as one of the most abundant transcripts. We have previously shown that psoriasin was induced by reactive oxygen species (ROS). Moreover, the downregulation of psoriasin by short hairpin RNA (shRNA) led to the reduced expression of VEGF and inhibited tumour Our data suggest that psoriasin expression in mammary epithelial cells leads to increased endothelial cell proliferation in a paracrine manner through RAGE. Psoriasin may therefore play a role in breast cancer progression by promoting oxidative stress response and angiogenesis.
What is already known about this topic:Serum levels of cytokines and chemokines in psoriasis patients have been analysed with contradictory results.
What does this study add:We identified markedly increased serum levels of EGF and IL-1Ra in psoriasis patients compared with matched controls. None of these cytokines were correlated to the severity of the disease (PASI) or decreased with phototherapy, suggesting that sources other than lesional skin contribute to the production of these cytokines which provide a potential mechanism linking psoriasis with its extracutaneous co-morbidities.
SummaryBackground The psoriatic plaques present a complex expression profile, including high levels
Chemokines may contribute to the systemic inflammation that is linked to the increased risk of co-morbidities in patients with psoriasis. The aim of this study was to investigate circulating chemokines in patients with psoriasis and their relationship to disease severity. Analysis of plasma levels of chemokines in patients with psoriasis before narrowband ultraviolet B (UVB) therapy revealed increased expression of Th1-associated CXCL9 and -10, Th2-associated CCL17 and CCL22, and Th17-associated CCL20. CCL20 correlated with disease severity. UVB therapy reduced skin symptoms, but did not affect the chemokine levels in plasma. Anti-CD3 and anti-CD28-mediated activation of peripheral blood mononuclear cells (PBMCs) caused a higher secretion of Th2 cytokine interleukin (IL)-13 by PBMCs from patients with psoriasis than from healthy controls. The sustained high expression of inflammatory chemokines is a potential link to systemic inflammation in psoriasis. UVB therapy may be a more effective treatment of local rather than systemic inflammation.
Background and Objectives: The prevalence of back pain and its effect on function and health-related quality of life across three levels of lower limb amputation secondary to trauma or tumour was studied. Study design: Cross-sectional survey. Methods: Forty-six lower limb amputees, aged 19-78 years, participated. The Roland Morris disability questionnaire (RMDQ) and the short form 36 health survey (SF-36) were used. Results: Participants reported more back pain after amputation than before (p < 0.001). There was a significant association between back pain daily or several times/week and severe or moderate disability reporting on the RMDQ (p ¼ 0.003). On the SF-36, the group as a whole scored significantly lower in health-related quality of life with regard to physical functioning, role physical, bodily pain, general health, social functioning and the physical component summary (PCS), and significantly higher in the mental component summary (MCS) compared to normative Swedish data. When all three levels of amputation were compared, no statistically significant differences were found in the RMDQ or SF-36 results. Conclusions: There was a high prevalence of back pain after amputation. Almost all participants having back pain daily or several times per week reported severe or moderate disability on the RMDQ. The group as a whole scored significantly lower for health-related quality of life in the PCS and significantly higher in the MCS compared to normative Swedish data.
Clinical relevanceThe high prevalence of back pain, and the significant association between back pain daily or several times per week and severe or moderate disability on the RMDQ, and the negative correlation between RMDQ and SF-36, may have clinical relevance with regard to rehabilitation and follow-up of lower limb amputation.
The endogenous fibrinolytic system and the ability of the endothelium to release tissue-plasminogen activator (t-PA) play a pivotal role to protect humans from atherothrombotic events. We have recently reported that the decreased capacity for t-PA release in hypertension is restored with chronic blood pressure lowering. Thus, we explored if acute blood pressure lowering has the same effect. The capacity for acute t-PA release was investigated in the perfused-forearm model during stimulation by intra-arterial substance P 8 pmol/min in hypertensive subjects. The procedure was then repeated during acute blood pressure lowering (n = 9) induced by sodium nitroprusside (SNP) infusion or during placebo infusion (n = 3). SNP lowered mean arterial pressure from 108.6 (2.6) to 83.0 (2.6) (mean and SEM) mmHg (P < 0.001). Substance P induced significant increase in t-PA release during both high- and low-pressure conditions (P < 0.01, ANOVA). Peak t-PA release rate was 199 (77) and 167 (41) (mean and SEM) ng/min/l tissue, and accumulated t-PA release was 2,395 (750) and 2,394 (473) ng, during high- and low-pressure conditions, respectively. t-PA release and hemodynamic responses were almost identical during high- and low-pressure conditions (P = ns, for all). Acute blood pressure lowering does not restore stimulated t-PA release from the endothelium in hypertensive subjects. These findings are in contrast to previously described effects of chronic blood pressure treatment. Although data need to be confirmed in a larger study, they suggest that high blood pressure decreases the cellular t-PA pool rather than interferes with release mechanisms of the protein.
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