Organizational challenges of community associations:applying nonprofit research to real-world problems

Can voluntary and nonprofit research be helpful for local community associations (CAs) seeking to respond to organizational challenges and problems? This paper builds on a study of an organizational crisis in an English CA to explore this question. The events which precipitated and prolonged the crisis seemed inexplicable to outside observers. Yet the study found that much of what occurred could be explained in the light of earlier theories and research. The paper concludes that voluntary and nonprofit scholarship, as well as generic organizational theories, has the potential to be helpful for community association members and activists in anticipating and responding to organizational problems. But scholars need to do more to disseminate existing research findings; to make them accessible and to adapt them to the distinctive needs and real world problems of community associations.

Footballers and social media ‘Faux Pas’:the Football Association’s cash cow?

Reflects on the increasing scope for irresponsible comments made on social media sites to attract civil or criminal penalties, and how such remarks by professional footballers have generated significant amounts of revenue for the Football Association (FA). Reviews the range of social media "faux pas" committed by footballers, the large fines imposed by the FA Regulatory Commission and why these constitute a useful "cash cow".

On Integral Means for Fractional Calculus Operators of Multivalent Functions

2000 Mathematics Subject Classification: Primary 30C45, Secondary 26A33, 30C80

Monocyte subpopulation counts and associations with left ventricular ejection fraction post ST elevation myocardial infarction

Background: Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to plaque instability and rupture. Little is known about the role of the three phenotypically and functionally different monocyte subpopulations in determining ventricular remodelling following ST elevation myocardial infarction (STEMI). Mon1 are the ‘classical’ monocytes with inflammatory action, whilst Mon3 are considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited within the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Transthoracic 2D echocardiography was performed within 7 days and at 6 months post infarct to assess ventricular volumes, mass, systolic, and diastolic functions as well as strain and strain rate. Results: Using linear regression analysis higher counts for Mon1, and lower counts for Mon2 and Mon3 were significantly associated with the baseline left ventricular ejection fraction (LVEF) within 7 days post infarct (table 1). At 6 months post STEMI lower counts of Mon2 remained positively associated with a decrease in LVEF at completion of remodelling (p=0.002). Conclusion: Peripheral monocytes of all three subsets correlate with LVEF after a myocardial infarction. High counts of the inflammatory Mon1 are associated with the reduced baseline ejection fraction post infarction. After remodelling, the convalescent ejection fraction was independently predicted by monocyte subpopulation 2. As lower counts depicted negative ventricular remodelling, this suggests a possible myofibroblast deposition and angiogenesis role for the newly described intermediate monocyte subpopulation Mon2 as opposed to the previously anticipated inflammatory role.

Monocyte subpopulation counts and TNF alpha associations with clinical outcome post ST elevation myocardial infarction

Background Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to its instability and rupture. Although peripheral monocytosis has been related to poor clinical outcome post ST elevation myocardial infarction (STEMI), only scarce information is available of mechanisms of this association. Tumour necrosis factor alpha (TNFα) is a key cytokine in the acute phase inflammatory response, and it is predominantly produced by inflammatory macrophages. Little is known about TNFα association with circulating monocyte subpopulations post STEMI. Method A total of 142 STEMI patients (mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited with blood samples obtained within first 24 hours from the onset and on day 10-14. Peripheral blood monocyte subpopulations were enumerated and characterized using flow cytometry after staining for CD14, CD16 and CCR2 and were defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Plasma levels of TNFα were measured by enzyme-linked immunosorbent assay (ELISA, Peprotec system, UK). Major adverse cardiac events (MACE), defined as recurrent STEMI, new diagnosis of heart failure and death were recorded at follow up, mean of 164±134 days. Results TNFα levels were significantly higher 24 hours post STEMI, compared to day 14 (paired t-test, p <0.001) with day 1 levels weakly correlated with total monocyte count as well as Mon1 (Spearman’s correlation, r=0.19, p=0.02 and r=0.22, p=0.01, respectively). There was no correlation between TNFα and Mon2 or Mon3 subpopulations. TNFα levels were significantly higher in patients with a recorded MACE (n=28, Mann-Whitney test, p<0.001) (figure 1).⇓

Monocyte subset counts associations with left ventricular systolic function post ST elevation myocardial infarction

Background: Monocytes are implicated in the initiation and progression of theatherosclerotic plaque contributing to plaque instability and rupture. Little is knownof the role played by the 3 phenotypically and functionally different monocytesubpopulations in determining ventricular remodeling following ST elevation my-ocardial infarction (STEMI). Mon1 are "classical" inflammatory monocytes, whilstMon3 are considered reparative with fibroblast deposition ability. The function ofthe newly described Mon2 is yet to be elucidated. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treatedwith percutaneous revascularization were recruited within the first 24 hours. Pe-ripheral blood monocyte subpopulations were enumerated and characterizedusing flow cytometry after staining for CD14, CD16 and CCR2. Phenotypi-cally, monocyte subpopulations are defined as: CD14+CD16-CCR2+ (Mon1),CD14+CD16+CCR+ (Mon2) and CD14lowCD16+CCR2- (Mon3) cells. Transtho-racic 2D echocardiography was performed within 7 days and 6 months post infarctto assess ventricular volumes, mass, systolic, and diastolic functions. Results: Using linear regression analysis higher counts for Mon1, and lowercounts for Mon2 and Mon3 were significantly associated with the baseline leftventricular ejection fraction (LVEF) within seven days post infarction. At 6 monthspost STEMI lower counts of Mon2 remained positively associated with decreasedLVEF (p value= 0.002).Monocyte subsets correlation with LVEFMonocytes mean florescence Baseline left ventricular Left ventricular ejectionintensity (cells/μl) ejection fraction (%) fraction (%) at 6 months post infarctβ-value P-valueβ-value P-valueTotal Mon0.31 P<0.001 0.360.009Mon 10.019 0.020.070.62Mon 2−0.28 0.001 −0.420.002Mon 3−0.27 0.001 −0.180.21 Conclusion: Peripheral monocytes of all three subsets correlate with LVEF af-ter a myocardial infarction. High counts of the inflammatory Mon1 are associatedwith reduction in the baseline LVEF. Post remodelling, the convalescent EF wasindependently predicted by monocyte subpopulation 2. As lower counts depictednegative ventricular remodeling, this suggests a reparative role for the newly de-scribed Mon2, possibly via myofibroblast deposition and angiogenesis, in contrastto an anticipated inflammatory role.

Formal professional relationships between general practitioners and specialists: possible associations with patient health and pharmacy costs

This article investigates whether the strength of formal professional relationships between general practitioners (GPs) and specialists (SPs) affects either the health status of patients or their pharmacy costs. To this end, it measures the strength of formal professional relationships between GPs and SPs through the number of shared patients and proxies the patient health status by the number of comorbidities diagnosed and treated. In strong GP–SP relationships, the patient health status is expected to be high, due to efficient care coordination, and the pharmacy costs low, due to effective use of resources. To test these hypotheses and compare the characteristics of the strongest GP–SP connections with those of the weakest, this article concentrates on diabetes—a chronic condition where patient care coordination is likely important. Diabetes generates the largest shared patient cohort in Hungary, with the highest traffic of specialist medication prescriptions. This article finds that stronger ties result in lower pharmacy costs, but not in higher patient health statuses. Key points for decision makers • The number of shared patients may be used to measure the strength of formal professional relationships between general practitioners and specialists. • A large number of shared patients indicates a strong, collaborative tie between general practitioners and specialists, whereas a low number indicates a weak, fragmented tie. • Tie strength does not affect patient health—strong, collaborative ties between general practitioners and specialists do not involve better patient health than weak, fragmented ties. • Tie strength does affect pharmacy costs—strong, collaborative ties between general practitioners and specialists involve significantly lower pharmacy costs than weak, fragmented ties. • Pharmacy costs may be reduced by lowering patient care fragmentation through channelling a general practitioner’s patients to a small number of specialists and increasing collaboration between general practitioner and specialists. • Limited patient choice is financially more beneficial than complete freedom of choice, and no more detrimental to patient health.