3 research outputs found
A Study of Relationship between Leader Behaviors and Subordinate Job Expectancies: A Path-Goal Approach
This study investigates relationship between leader behavior (directive, supportive, participative and achievement-oriented) of corporate managers and subordinates’ job expectancies using House (1974) Path-goal model of leadership. The results reveal thatleader behavior affects subordinates’ job expectancies. The situational factors (task structure, role ambiguity, stress, need for autonomy, locus of control, need for achievement and perception about abilities) affect subordinates’ job expectancies (I&II).While subordinates’ attributes/characteristics (age, gender, qualification, rank, experience and length of service under the current supervisor) do not affect job expectancies (I&II) except for rank/position and expectancy-II. Path goal theory predicts that directive leader behavior will be more effective for the subordinates with high need for achievement because directive leader through clarifying path guides subordinates. Similarly, participative leader behavior is also effective as heconsults with subordinates in setting, clarifying and achieving goals. The results of this study reveal that there is an inverse relationship between subordinates’ job expectancy (I&II). According to Yukl (2006), for subordinates with high need for autonomy,participative leader behavior will increase the intrinsic valence of work
Investigating the managerial practices' effect on Employee-Perceived Service Quality with the moderating role of supportive leadership behavior
Identification of new susceptibility loci for type 2 diabetes and shared etiological pathways with coronary heart disease
To evaluate the shared genetic etiology of type 2 diabetes (T2D) and coronary heart disease (CHD), we conducted a genome-wide, multi-ancestry study of genetic variation for both diseases in up to 265,678 subjects for T2D and 260,365 subjects for CHD. We identify 16 previously unreported loci for T2D and 1 locus for CHD, including a new T2D association at a missense variant in HLA-DRB5 (odds ratio (OR) = 1.29). We show that genetically mediated increase in T2D risk also confers higher CHD risk. Joint T2D–CHD analysis identified eight variants—two of which are coding—where T2D and CHD associations appear to colocalize, including a new joint T2D–CHD association at the CCDC92 locus that also replicated for T2D. The variants associated with both outcomes implicate new pathways as well as targets of existing drugs, including icosapent ethyl and adipocyte fatty-acid-binding protein.D.S. has received support from NHLBI, NINDS, Pfizer, Regeneron Pharmaceuticals, Genentech, and Eli Lilly. Genotyping in PROMIS was funded by the Wellcome Trust, UK, and Pfizer. Biomarker assays in PROMIS have been funded through grants awarded by the NIH (RC2HL101834 and RC1TW008485) and Fogarty International (RC1TW008485). The RACE study has been funded by NINDS (R21NS064908), Fogarty International (R21NS064908), and the Center for Non-Communicable Diseases (Karachi, Pakistan). B.F.V. was supported by funding from the American Heart Association (13SDG14330006), the W.W. Smith Charitable Trust (H1201), and the NIH/NIDDK (R01DK101478). J.D. is a British Heart Foundation Professor, European Research Council Senior Investigator, and NIHR Senior Investigator. V.S. was supported by the Finnish Foundation for Cardiovascular Research. S. Ripatti was supported by the Academy of Finland (251217 and 255847), the Center of Excellence in Complex Disease Genetics, the European Union’s Seventh Framework Programme projects ENGAGE (201413) and BioSHaRE (261433), the Finnish Foundation for Cardiovascular Research, Biocentrum Helsinki, and the Sigrid Juselius Foundation. The Mount Sinai IPM Biobank Program is supported by the Andrea and Charles Bronfman Philanthropies. S. Anand is supported by grants from the Canada Research Chair in Ethnic Diversity and CVD and from the Heart and Stroke Michael G. DeGroote Chair in Population Health, McMaster University. Data contributed by Biobank Japan were partly supported by a grant from the Leading Project of the Ministry of Education, Culture, Sports, Science and Technology, Japan. We thank the participants and staff of the Copenhagen Ischemic Heart Disease Study and the Copenhagen General Population Study for their important contributions. The CHD Exome+ Consortium was funded by the UK Medical Research Council (G0800270), the British Heart Foundation (SP/09/002), the UK NIHR Cambridge Biomedical Research Centre, the European Research Council (268834), the European Commission’s Framework Programme 7 (HEALTH-F2-2012-279233), Merck, and Pfizer. PROSPER has received funding from the European Union’s Seventh Framework Programme (FP7/2007-2013) under grant agreement HEALTH-F2-2009-223004