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Objectives Successful treatment of acute coronary syndrome (ACS) relies on its rapid recognition. It is unclear whether the accepted presentation of chest pain applies to different ethnic groups. We thus examined potential ethnic variations in ACS symptoms and clinical care outcomes in white, South Asian and Chinese patients. Design Cross-sectional survey. Setting Participants were hospitalised at 1 of 12 Canadian centres across four provinces. Participants 1334 patients with ACS (630 white; 488 South Asian; 216 Chinese). Main outcome measures ACS presentation symptoms (classic/typical midsternal pain/discomfort with or without radiation to the left neck, shoulder or arm) were assessed by self-report. Clinical care outcomes (time to emergency room [ER] presentation, cardiac catheterisation; receipt of cardiac catheterisation, percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]) were obtained by health record audit. Results The mean age of the sample was 62 years and 30% had ST-elevation myocardial infarction (STEMI). The most common presenting symptom was midsternal pain/discomfort of any intensity regardless of ethnic status. Yet, a substantial proportion of patients reported atypical symptoms (33% white, 19% South Asian, 20% Chinese; p<0.006). After adjustment for age, sex, education, current smoking, extent of coronary artery disease, presence of diabetes or chronic kidney disease and STEMI vs non-STEMI/unstable angina, South Asians were more likely to present with at least moderate intensity midsternal pain/discomfort (adjusted OR [AOR] 1.44; 95% CI 1.05 to 1.98), whereas Chinese were less likely to present with radiating symptoms (AOR 0.53; 95% CI 0.38 to 0.74) compared with whites. South Asians with atypical pain (relative to those with midsternal pain/discomfort) took significantly longer to present to the ER (p=0.037), and were less likely to receive PCI (p=0.008) or CABG (p=0.041). Conclusions Atypical presentations were associated with greater delays in arrival to the emergency department and reduced invasive cardiovascular care in South Asians. [ABSTRACT FROM AUTHOR]

Purpose: The pro-inflammatory effects of kinins are mediated by two bradykinin receptors: BRI and BR2. The aim of this study was to evaluate the expression profile of kinin receptor genes by an estimation of mRNA levels in human nasal polyps (NP) and normal mucosa (NM). Material and Methods: BRI and BR2-dependent genes differentially transcribed in NP were investigated using oligonucleotide microarray technology. The mRNA copy number of BR1, BR2 and TIMP1 genes was assessed by QRT-PCR. Thirty six eosinophilic (ENP), 17 neutrophilic nasal polyps (NNP) and 28 NM samples were included into the study. Results: Among 92 genes encoding proteins involved in signal transduction via B1 and B2 kinin receptors TIMP1 was found to be 2,63-fold higher in the NP than in NM. Increased TIMP1 gene expression was proved by QRT-PCR (p=0,003). Moreover two genes: FOS and PTGSI presented higher (3,82- and 4,27-fold, respectively) expression in NM compared to NP tissues. In QRT-PCR analysis insignificantly higher expression of gene encoding BR1 in ENP [2564 mRNA copies/µg RNA (22-32863)] compared with NM [1426 copies mRNA (15-27995)] was found, mRNA expression for the BR2 in ENP [9872 copies mRNA (19-244832)] was insignificantly higher than in NM [5753 copies (46-199658)]. BR2 mRNA was the predominant transcript in most NP and NM samples followed by BR1 mRNA (p<0.01). There was a positive correlation between the expression of BR1 and BR2 in the ENP (r=0,91; p<0,01) and NNP (r=0,6; p<0,01). Conclusions: We did not document any changes in the expression profile of kinin receptors in the analyzed groups, which may suggest that kinin receptors do not make an important contribution in the etiology of NP. [ABSTRACT FROM AUTHOR]

Purpose: The object of the study was to assess the expression of tile genes encoding TNFα and its receptors (TNF-R1 and TNF-R2) in patients with nasal polyps (NP), Material and methods: The number of the mRNA copies was assessed by QRT-PCR in RNA extracts from 16 eosinophilic (ENP) and 5 neutrophilic nasal polyps (NNP), and 9 normal mucosa (NM) samples. The expression of corresponding proteins was demonstrated using immunohistochemistry. Results: The mean level of mRNA copies for YNFα in ENP (82229c/µg) was not significantly higher when compared with controls (74869c/µg). NNP demonstrated significantly lower mean TNFα gene expression (7021c/µg) than the controls (p<0.05). A statistically higher mRNA TNFα copy number in ENP than in NNP was also revealed (p<0,01). A noticeably lower mRNA expression of TNF-R1 in ENP and NNP was seen as compared to the control group (10198c/µg vs. 30749c/µg, p<0.05 and 3440c/µg vs. 30749c/µg: p<0,05 respectively). In ENP the mean TNF-R2 mRNA copy number was markedly higher than in NNP (185c/µg vs. 7.6c/µg, p<0.05), TNF-R2 mRNA level did not differ significantly between ENP and the control group (185c/µg vs. 469c/µg). TNF-R1 expression was significantly higher than TNF-R2 at the mRNA (p<0.01) and protein (p<0.05) level both in ENP and NNP. No significant correlations in proteins expression were detected between ENP and NNP. Conclusions: TNF-R1 has been identified to be a prevalent form of the TNFα receptor in nasal polyps which may reflect the apparent dominance of this form in TNFα signalling. The findings raise the possibility that the eosinophils from NP may influence biological responses through TNFα-dependent mechanisms. The differences between ENP and NNP relating to TNFα and the expression of its receptors may reflect the distinct character of those diseases. [ABSTRACT FROM AUTHOR]

Background: More than 60% of new strokes each year are "mild" in severity and this proportion is expected to rise in the years to come. Within our current health care system those with "mild" stroke are typically discharged home within days, without further referral to health or rehabilitation services other than advice to see their family physician. Those with mild stroke often have limited access to support from health professionals with stroke-specific knowledge who would typically provide critical information on topics such as secondary stroke prevention, community reintegration, medication counselling and problem solving with regard to specific concerns that arise. Isolation and lack of knowledge may lead to a worsening of health problems including stroke recurrence and unnecessary and costly health care utilization.The purpose of this study is to assess the effectiveness, for individuals who experience a first "mild" stroke, of a sustainable, low cost, multimodal support intervention (comprising information, education and telephone support)--"WE CALL" compared to a passive intervention (providing the name and phone number of a resource person available if they feel the need to)--"YOU CALL", on two primary outcomes: unplanned-use of health services for negative events and quality of life.Method/design: We will recruit 384 adults who meet inclusion criteria for a first mild stroke across six Canadian sites. Baseline measures will be taken within the first month after stroke onset. Participants will be stratified according to comorbidity level and randomised to one of two groups: YOU CALL or WE CALL. Both interventions will be offered over a six months period. Primary outcomes include unplanned use of heath services for negative event (frequency calendar) and quality of life (EQ-5D and Quality of Life Index). Secondary outcomes include participation level (LIFE-H), depression (Beck Depression Inventory II) and use of health services for health promotion or prevention (frequency calendar). Blind assessors will gather data at mid-intervention, end of intervention and one year follow up.Discussion: If effective, this multimodal intervention could be delivered in both urban and rural environments. For example, existing infrastructure such as regional stroke centers and existing secondary stroke prevention clinics, make this intervention, if effective, deliverable and sustainable.Trial Registration: ISRCTN95662526. [ABSTRACT FROM AUTHOR]