Children can represent complex social status hierarchies: Evidence from Indonesia.

Children's ethnicity-status associations are often studied in societies where one ethnic group possesses status across multiple dimensions, such as political influence and wealth. This study examined children's (6-12 years) and adults' representations of more complex hierarchies in Indonesia (N = 341; 38% Native Indonesian, 33% Chinese Indonesian, and 27% other ethnicities; 55% female, 36% male; 2021-2022), a society where ethnic groups hold distinct forms of status (on average, Native Indonesians have political influence; Chinese Indonesians have wealth). By 6.5 years, children associated Native Indonesians with political influence and Chinese Indonesians with wealth. Intersectional analyses indicated that ethnicity-status associations were stronger for male than female targets. Children of all ethnicities preferred Chinese Indonesians and preferences were predicted by wealth judgments.

Clinical and Psychosocial Profiles of Asian Immigrants Who Repeatedly Attempt Suicide: A Mixed-Method Study of Risk and Protective Factors.

BACKGROUND: Persons who repeatedly attempt suicide comprise a highly distressed population that warrants the understanding of risk and protective factors in assessment and treatment. There is a dearth of literature on Asian immigrants' suicidal behavior. AIMS: The study aimed to capture the clinical and psychosocial profiles of Asian immigrants who made repeated suicide attempts. METHOD: We utilized retrospective chart reviews (n = 44) and in-person interviews (n = 12) in two urban public hospitals. RESULTS: The study samples shared major suicide risk factors identified in studies of other populations. Participants of the interview sample suffered from a pervasive sense of hopelessness stemming from social isolation, self-stigma, feelings of failure in their life roles, and perceptions of rejection by their families. Conversely, psychological well-being--feeling cared for and able to reciprocate care for others--appeared to be a protective factor for participants who improved in their functioning and recovery. CONCLUSION: The study lays the groundwork for further research on suicide risk and protective factors.

Regional fractionation and dominant frequency in persistent atrial fibrillation: effects of left atrial ablation and evidence of spatial relationship.

AIMS: The aim was to study regional fractionation and dominant frequency (DF) to determine if any relationship exists between the two parameters and also to assess the impact of limited left atrial ablation. METHODS AND RESULTS: Patients undergoing catheter ablation of persistent AF using three-dimensional navigation were studied. Regional left atrial electrograms were analysed in the frequency domain by assessing DF and organization index (OI), and for degree of fractionation [using complex fractionated electrograms (CFE)-mean] before and after circumferential pulmonary vein and left atrial roof ablation. Twenty-three patients with persistent AF were studied. After ablation, global CFE-mean increased [100 ± 5 to 147 ± 11 ms (P= 0.0003)], DF decreased [6.1 ± 0.2 to 5.3 ± 0.2 Hz (P= 0.0003)], and OI was unchanged [0.27 ± 0.01 to 0.26 ± 0.02, (P= 0.70)]. Comparing sites close to and distant from ablation lines, percentage change in CFE-mean was 94 ± 10 vs. 37 ± 6% (P< 0.0001), DF change was -13 ± 3 vs.-12 ± 2% (P= 0.98), and OI change was 3 ± 6 vs. 10 ± 5% (P= 0.75), respectively. There was modest correlation between CFE-mean and DF points prior to ablation (r = -0.33, P< 0.0001) which was reduced following left atrial ablation (r = -0.24, P= 0.005). CONCLUSIONS: Left atrial ablation reduces global left atrial DF and decreases the degree of fractionation. Complex fractionated electrograms-mean and DF appear to share only modest spatial correlation and are affected to different extents by ablation, suggesting that they are either separate entities or reflect different components of the same substrate.

Changes in the sociocultural reality of chinese immigrants: challenges and opportunities in help-seeking behaviour.

INTRODUCTION: This paper uses findings from a larger study to present a nuanced depiction of the interplay of informal and formal help-seeking processes of a sample of Chinese immigrants in their mental healthcare in New York City. METHOD: Thirty one participants who were receiving mental health treatment were interviewed with regard to their experiences preceding their suicide attempt. Their narratives were coded for thematic analysis. FINDINGS: Acculturation difficulties, inaccessibility to services and stigma associated with mental illness were major obstacles in the participants' help-seeking process, which was consistent with other studies of immigrants of ethnic minority groups in the USA. In addition, the findings showed how changes in this sample of Chinese immigrants' socio-cultural reality disrupted familiar help-seeking pathways, and perpetuated and amplified the aforementioned stressors. Issues of human connection, immigrants' resiliency and missed opportunities were also identified as potential resources to modify cultural stigmas and help-seeking behaviour. CONCLUSION: There are varied socio-cultural factors that need to be considered in mental health outreach services in immigrant communities.

Soluble, platelet-bound, and total P-selectin as indices of platelet activation in congestive heart failure.

BACKGROUND: Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF. OBJECTIVE: To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHF patients-compared to 'disease controls' and 'healthy controls'-and to assess their prognostic value in CHF. METHODS: We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel 'platelet lysate' assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometry-in 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) <50%). Levels were compared with 50 healthy controls and 70 'disease controls' (patients with coronary artery disease with normal left ventricular systolic function). RESULTS: CHF patients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P>0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340-535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up. CONCLUSIONS: Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in 'disease controls' indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.

Soluble CD40 ligand, platelet surface CD40 ligand, and total platelet CD40 ligand in atrial fibrillation: relationship to soluble P-selectin, stroke risk factors, and risk factor intervention.

BACKGROUND: Abnormal levels of soluble CD40 ligand (sCD40L) have been reported in patients with hypertension, coronary artery disease, diabetes mellitus, heart failure, and stroke, all of which are conditions that are associated with nonvalvular atrial fibrillation (AF). We hypothesized the following: (1) CD40 ligand (CD40L)-related indexes (ie, platelet surface expressed CD40L, the soluble fragment of CD40L [sCD40L], and the total amount of CD40L per platelet [pCD40L]) are elevated in patients with AF compared to control subjects; (2) these indexes correlate with soluble P-selectin (sP-selectin), which is an established platelet marker; and (3) these indexes differentiate "high-risk" from "low-risk" subjects. METHODS: We performed a case-control study of 121 AF patients, 71 "disease control subjects," and 56 "healthy control subjects." Peripheral venous levels of platelet surface-expressed CD40L were analyzed by flow cytometry, while levels of sCD40L, pCD40L, and sP-selectin were measured by enzyme-linked immunosorbent assay. RESULTS: AF patients had significantly higher sCD40L levels compared to healthy control subjects (p = 0.042), with no difference in platelet surface CD40L and pCD40L levels. A positive correlation was noted between levels of sCD40L and pCD40L, and not with sP-selectin. CD40L-related indexes failed to distinguish between high-risk and low-risk AF patients. AF patients receiving optimal antithrombotic therapy had significantly lower pCD40L levels (p < 0.001) compared to control subjects. Optimized AF management also resulted in significant reductions in the levels of sCD40L (p = 0.023) and pCD40L (p < 0.001). CONCLUSION: CD40L-related indexes are not useful in the risk stratification of AF patients, and abnormal sCD40L levels can be reduced by intense multifactorial risk management. While there is a significant, albeit modest, excess of platelet activation in AF patients (as measured by sCD40L levels) compared to healthy control subjects, this is not in excess of that seen in patients with underlying cardiovascular diseases.

Platelet surface CD62P and CD63, mean platelet volume, and soluble/platelet P-selectin as indexes of platelet function in atrial fibrillation: a comparison of "healthy control subjects" and "disease control subjects" in sinus rhythm.

OBJECTIVES: The aim of this work was to comprehensively study the role of platelets in atrial fibrillation (AF), in relation to the underlying cardiovascular diseases and type of AF, and to analyze the effect of antithrombotic treatment on different aspects of platelet activation. BACKGROUND: Platelet activation is present in nonvalvular AF, but there is debate whether this is due to AF itself and/or to underlying cardiovascular diseases. METHODS: A total of 121 AF patients were compared with 65 "healthy control subjects" and 78 "disease control subjects" in sinus rhythm. Platelet activation was assessed using 4 different aspects of platelet pathophysiology: 1) platelet surface expression of CD62P (P-selectin) and CD63 (a lysosomal glycoprotein) (by flow cytometry); 2) mean platelet volume (MPV) (by flow cytometry); 3) plasma levels of soluble P-selectin (sP-selectin, enzyme-linked immunoadsorbent assay); and 4) total amount of P-selectin per platelet (pP-selectin) ("platelet lysis" assay). RESULTS: Both AF patients and "disease control subjects" had higher levels of CD62P (p < 0.001), CD63 (p < 0.001), and sP-selectin (p < 0.001) compared with "healthy control subjects," with no difference between AF patients and "disease control subjects." Patients with permanent AF had higher levels of sP-selectin (p = 0.014) and MPV (p = 0.025) compared with those with paroxysmal AF. The presence of AF independently affected the levels of CD62P expression, while "high-risk" AF patients (CHADS score > or =2) had higher levels of CD62P compared with those with "low risk." Introducing warfarin resulted in a reduction of pP-selectin (p = 0.013). CONCLUSIONS: There is a degree of excess of platelet activation in AF compared with "healthy control subjects," but no significant difference between AF patients and "disease control subjects" in sinus rhythm. Platelet activation may differ according to the subtype of AF, but this is not in excess of the underlying comorbidities that lead to AF. Platelet activation in AF may be due to underlying cardiovascular diseases, rather than due to AF per se.

Elevated platelet microparticle levels in nonvalvular atrial fibrillation: relationship to p-selectin and antithrombotic therapy.

BACKGROUND: Platelet microparticles (PMPs), are procoagulant membrane vesicles that are derived from activated platelets, the levels of which are elevated in patients with hypertension, coronary artery disease (CAD), diabetes, and stroke, all of which are conditions that lead to (and are associated with) atrial fibrillation (AF). We hypothesized the following: (1) PMP levels are elevated in patients with AF compared to levels in both healthy control subjects (ie, patients without cardiovascular diseases who are in sinus rhythm) and disease control subjects (ie, patients with hypertension, CAD, diabetes or stroke, but who are in sinus rhythm); (2) PMP levels correlate with levels of soluble P-selectin (sP-selectin) [a marker of platelet activation]; and (3) PMP levels are related to the underlying factors in patients with AF that contribute to the overall risk of stroke secondary to AF. METHODS: We performed a case-control study of 70 AF patients, 46 disease control subjects and 33 healthy control subjects. Peripheral venous levels of PMP and sP-selectin were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively. RESULTS: Both AF patients and disease control subjects had significantly higher levels of PMPs (p < 0.001) and sP-selectin (p = 0.001) compared to healthy control subjects, but there was no difference between AF patients and disease control subjects. There was no difference in PMP levels between patients with paroxysmal and permanent AF (p = 0.581), and between those receiving therapy with aspirin and warfarin (p = 0.779). No significant correlation was observed between PMP and sP-selectin levels (p = 0.463), and the clinical characteristics that contribute to increased stroke risk in patients with AF. On stepwise multiple regression analysis in the combined cohort of AF patients plus disease control subjects, the presence/absence of AF was not an independent determinant of PMP and sP-selectin levels. CONCLUSION: There is evidence of platelet activation (ie, high PMP and sP-selectin levels) in AF patients, but this is likely to be due to underlying cardiovascular diseases rather than the arrhythmia per se.

Platelet activation in acute, decompensated congestive heart failure.

BACKGROUND: Congestive heart failure (CHF) is associated with increased risk of venous thromboembolism, stroke and sudden death. This may be related to abnormalities of thrombogenesis and platelet activation. A comprehensive assessment of platelet (dys)function in acute decompensated heart failure (AHF) is lacking, and we hypothesised that such patients would show greater abnormalities in platelet indices, compared to stable CHF and healthy controls. METHODS: We measured soluble P-selectin (sP-sel, by ELISA); platelet surface P-selectin (CD62P%G) and CD63%G expression by flow cytometry; and platelet structural indices [mean platelet volume (MPV), mean platelet mass (MPM) and mean platelet component (MPC)] in 22 patients with AHF (pre- and posttreatment), who were compared to 68 patients with stable congestive heart failure (CHF, all with left ventricular ejection fraction (LVEF) <50%) and 23 healthy controls. RESULTS: There were significant differences between the 3 study groups in MPV (p<0.001), MPC (p=0.001), platelet surface P-selectin (CD62P%G, p<0.0001) and platelet surface CD63P%G (p=0.017). On post-hoc analyses, AHF patients had higher platelet surface P-selectin (CD62P%G) compared to stable CHF patients and healthy controls (Tukey's test, all p<0.05), whilst CD63%P was similarly high in both disease groups, compared to healthy controls. Platelet surface P-selectin (p=0.032), CD63 (p=0.024) and CD40L (p=0.024) were significantly reduced following treatment of AHF, though platelet morphology and sP-sel levels were not significantly changed. CONCLUSION: AHF patients demonstrate some abnormalities of platelet activation compared to stable CHF patients and healthy controls. These platelet abnormalities are modified by treatment, raising the possibility that platelets may partly contribute to the pathophysiology of adverse complications associated with AHF.

Platelet adhesion in atrial fibrillation.

BACKGROUND: Increased platelet activation has been reported in nonvalvular atrial fibrillation (AF) but it remains unclear whether or not this is due to the underlying cardiovascular diseases, clinical subtype of AF and the influence of anti-thrombotic therapy. METHODS: Platelet adhesion in AF patients was assessed using a 'platelet adhesion assay', and compared to both 'healthy controls' and 'disease controls' (patients with hypertension, coronary artery disease, diabetes or stroke but in sinus rhythm). RESULTS: AF patients on no anti-thrombotic treatment (N=20) had increased platelet adhesion compared to 'healthy controls' (N=57) (p=0.044). Initiating treatment with both aspirin and warfarin resulted in significant reduction in platelet adhesion in AF patients (p=0.014 and 0.019 respectively). AF patients on optimal anti-thrombotic therapy (N=98) had no significant difference in platelet adhesion compared to 'healthy controls' and 'disease controls' (p=0.312). Platelet adhesion failed to distinguish between 'high-risk' (i.e. CHADS score > or = 2) and 'low-risk' (i.e. CHADS score < 2) AF patients (p=0.352). Amongst the clinical parameters that contribute to increased stroke risk in AF, platelet adhesion was only correlated with age (r=0.215, p=0.034), and not with other stroke risk factors. There was no significant difference in platelet adhesion between paroxysmal and permanent AF (p=0.618). CONCLUSION: There is a significant, albeit weak, excess of platelet adhesion in AF patients on no anti-thrombotic therapy compared to 'healthy controls'. In optimally treated AF patients, platelet adhesion is not different to both 'healthy' and 'disease controls'. It is possible that abnormal platelet adhesion does not significantly contribute to the increased risk of stroke and thromboembolism that persists despite anti-thrombotic treatment in AF or in identifying 'high-risk' AF patients.

Raised leptin concentrations among South Asian patients with chronic heart failure.

BACKGROUND: The disease presentation of chronic heart failure (CHF) is considered to progress with metabolic deterioration, underlined by changes in adipose associated hormones (adipocytokines). However, little is known about ethnic variations of adipocytokines amongst CHF patients, in particular South Asians, who are at an increased risk of CHF. METHODS: Using a cross-sectional study, South Asians (n=106) and Caucasians (n=105) living in the UK were compared by CHF status. We investigated ethnic differences in adipocytokines (leptin, adiponectin, tumor necrosis factor (TNF)alpha), and their association with CHF. Patients with mild to moderate CHF were recruited from heart failure clinics (47 Caucasian, 54 South Asian), and compared to healthy controls. Metabolic parameters (including insulin resistance using HOMA modelling), echocardiography and brain natriuretic peptide (BNP) were measured amongst patients and healthy controls, and compared across and within ethnic groups. RESULTS: Mean (log transformed) plasma leptin concentrations were highest amongst South Asian patients, being 5.25% (95%CI: 1.50-9.02) higher than Caucasian patients (P=0.007), and similarly raised with respect to controls (P< or =0.04). Indices of insulin resistance were higher amongst CHF patients compared with controls, with no ethnic variation. In addition to age, female gender and body-mass index, levels of leptin were also associated with South Asian ethnicity (P<0.001), insulin resistance (P=0.02), smoking habit (P=0.01) and HDL cholesterol (P=0.004). Levels of adiponectin showed no ethnic variation, but were associated with CHF and a previous history of myocardial infarction (P<0.001). On multivariate regression analysis of patients and healthy controls, CHF was independently associated with smoking habit, adiponectin and insulin resistance (all P<0.01). CONCLUSION: Metabolic abnormalities are present in CHF, which in turn, are influenced by ethnicity. The role of adipocytokines in CHF pathophysiology and prognosis merits further study.

Platelets and heart failure.

Heart failure is associated with increased risk of venous thromboembolism, stroke, and sudden death. Platelet abnormalities have been well described in heart failure but the significance of platelets in contributing to the thromboembolic complications of heart failure remains uncertain. Furthermore, the role of antiplatelet agents in heart failure remains unclear. This review will focus on platelet activation and the role of platelet dysfunction in heart failure, with particular regard to pathophysiology and outcome. The effects of heart failure therapeutics on platelet function and antiplatelet therapy in heart failure will also be discussed.

Virchow's triad revisited: blood constituents.

An update of Virchow's triad for thrombogenesis can be considered by reference to abnormalities in the endothelium/endocardium ('abnormal vessel wall'), abnormalities of haemorhelogy and turbulence at bifurcations,atheroma at vessel wall ('abnormal bloodflow') and abnormalities in platelet as well as the coagulation and fibrinolytic pathways ('abnormal blood constituents'). The constituents of the blood are many and varied, but soluble coagulation factors (such as fibrinogen and tissue factor) and cells (such as platelets)are clearly important. Clearly, 'a continuum exists between health, 'statistically' increased haemostatic abnormalities in prothrombotic or hypercoagulable states and 'overtly' increased clotting in acute thrombosis.Thus, the patients with the highest levels of the markers appear to be the highest risk of disease progression,and if so, a panel of 'high risk' blood constituent indices (platelet and coagulation markers) may potentially give a composite score of risk, and may be a useful tool in predicting subjects at highest risk. Further longitudinal studies are clearly required. There is no doubt that Virchow would be impressed on how his classical triad has expanded to encompass the wide range of pathophysiological processes leading to thrombogenesis.