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7. Unravelling processes of alliance capability development: longitudinal processual insights from an emerging country multinational enterprise

Author

Pereira, V, Patnaik, S, Roohanifar, M, Baliga, R, Pereira, V, Patnaik, S, Roohanifar, M, and Baliga, R

Abstract

Purpose: The purpose of this paper is to explore and unbundle the complex processes underpinning development of alliance capabilities, particularly in the context of emerging country multinational enterprises. More specifically, this paper focuses on how firms internalize and translate knowledge generated from experiences gained by participating in international collaborations. Design/methodology/approach: The authors adopt an exploratory case study approach to undertake in-depth processual analysis of alliance capability development in an Indian biopharmaceutical company. The authors focused their analysis on the initial four international alliances the company formed and identified key elements pertaining to alliance capabilities that the company internalized and those that it could not, as this was key in understanding alliance capability. Findings: The research shows that based on experiences from previous alliances, the Indian organization was able to overhaul its negotiation and governance designing processes and practices as well as made robust changes to its internal communication and coordination practices. Interestingly, the company organization, however, did not make any significant changes to its processes and practices regarding partner selection. Practical implications: The results from our study can be used by managers to develop processes and practices when it comes to developing alliance capabilities. Originality/value: The paper is novel, as it addresses two specific gaps in the nascent alliance capability literature. First, it provides insights on how different constituent elements/aspects of alliance capability actually develop and integrate within the organizational system over time, and in the process, the paper identifies that some aspects are better internalized as compared to other aspects. Second, by focusing the attention on an Indian biopharmaceutical company, the authors attempt to address a gap in alliance capability development researc

Published
2021

9. Metabolic Syndrome in Heart Failure: Friend or Foe?

Author

Arcopinto M., Schiavo A., Salzano A., Bossone E., D'Assante R., Marsico F., Demelo-Rodriguez P., Baliga R. R., Cittadini A., Marra A. M., Arcopinto, M., Schiavo, A., Salzano, A., Bossone, E., D'Assante, R., Marsico, F., Demelo-Rodriguez, P., Baliga, R. R., Cittadini, A., and Marra, A. M.

Subjects
Heart Failure, Metabolic Syndrome, Survival Rate, Prognosi, Risk Factor, Insulin resistance, Morbidity, Global Health, Risk stratification, Human
Abstract

The interplay between metabolic syndrome (MetS) and heart failure (HF) is intricate. Population studies show that MetS confers an increased risk to develop HF and this effect is mediated by insulin resistance (IR). However, obesity, a key component in MetS and common partner of IR, is protective in patients with established HF, although IR confers an increased risk of dying by HF. Such phenomenon, known as "obesity paradox," accounts for the complexity of the HF-MetS relationship. Because IR impacts more on outcomes than MetS itself, the former may be considered the actual target for MetS in HF patients.

Published
2019

12. In vitro Fab display: a cell-free system for IgG discovery

Author

Stafford, R. L., primary, Matsumoto, M. L., additional, Yin, G., additional, Cai, Q., additional, Fung, J. J., additional, Stephenson, H., additional, Gill, A., additional, You, M., additional, Lin, S.-H., additional, Wang, W. D., additional, Masikat, M. R., additional, Li, X., additional, Penta, K., additional, Steiner, A. R., additional, Baliga, R., additional, Murray, C. J., additional, Thanos, C. D., additional, Hallam, T. J., additional, and Sato, A. K., additional

Published
2014
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14. Scleroderma and related disorders: 223. Long Term Outcome in a Contemporary Systemic Sclerosis Cohort

Author

Nihtyanova, S., primary, Ong, V., additional, Black, C., additional, Denton, C., additional, Lutalo, P., additional, Shattles, W., additional, Jones, H., additional, Nouri, R., additional, Hepburn, A., additional, Chard, M., additional, Horwood, N., additional, Lynn, M., additional, Duke, O., additional, Kiely, P., additional, Zouita, L., additional, Davies, U., additional, Hughes, R., additional, Lloyd, M., additional, Nikitorowicz Buniak, J., additional, Shiwen, X., additional, Abraham, D., additional, Stratton, R., additional, Hugle, T., additional, Schuetz, P., additional, Daikeler, T., additional, Tyndall, A., additional, Matucci-Cerinic, M., additional, Walker, U. A., additional, van Laar, J. M., additional, Pauling, J. D., additional, Flower, V., additional, McHugh, N., additional, Liu, S., additional, Leask, A., additional, Aden, N., additional, Khan, K., additional, Hoyles, R., additional, Bhagat, S., additional, Drummond, T., additional, Goh, C., additional, Busch, R., additional, Hall, F., additional, Meyer, P., additional, Moinzadeh, P., additional, Krieg, T., additional, Hellmich, M., additional, Brinckmann, J., additional, Neumann, E., additional, Mueller-Ladner, U., additional, Kreuter, A., additional, Dumitresco, D., additional, Rosenkranz, S., additional, Hunzelmann, N., additional, Binai, N., additional, Huegle, T., additional, van Laar, J., additional, Sonnylal, S., additional, Tam, A., additional, Norman, J., additional, de Crombrugghe, B., additional, Chighizola, C. B., additional, Luigi Meroni, P., additional, Coghlan, G., additional, Newton, F., additional, Derrett-Smith, E. C., additional, Dooley, A., additional, Baliga, R., additional, Hobbs, A., additional, MacAllister, R., additional, Futema, M., additional, Pantelidis, P., additional, Renzoni, E., additional, Schreiber, B. E., additional, Coghlan, G. J., additional, Wells, A. U., additional, Welsh, K., additional, Fonseca, C., additional, Ponticos, M., additional, Wells, A., additional, Guillevin, L., additional, Schwierin, B., additional, Rosenberg, D., additional, Silkey, M., additional, Parapuram, S., additional, Shi-wen, X., additional, Nihtyanova, S., additional, Ahmed Abdi, B., additional, and Xu, S., additional

Published
2011
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16. Scleroderma and Related Disorders [202-212]: 202. Multi-Centre Audit of Treatment of Interstitial Lung Disease in Systemic Sclerosis with IV Cyclophosphamide

Author

Yazdani, R., primary, Abhishek, A., additional, Fiona, P., additional, Lim, K., additional, Regan, M., additional, Lanyon, P., additional, Khan, K., additional, Hoyles, R. K., additional, Shiwen, X., additional, Derrett-Smith, E., additional, Abraham, D., additional, Denton, C. P., additional, Ottewell, L., additional, Walker, K., additional, Griffiths, B., additional, Ali Nazarinia, M., additional, Abbasi, N., additional, Karimi, A., additional, Amiri, A., additional, Derrett-Smith, E. C., additional, Baliga, R., additional, Dooley, A., additional, Shi-Wen, X., additional, Stretton, K., additional, Shukla, S., additional, Hall, F., additional, Nandagudi, A., additional, Kingsley, G., additional, Scott, D., additional, Stratton, R., additional, Leask, A., additional, Guillevin, L., additional, Krieg, T., additional, Schwierin, B., additional, Rosenberg, D., additional, Silkey, M., additional, Matucci-Cerinic, M., additional, Jones, H., additional, Bou-Gharios, G., additional, So, P., additional, Renzoni, E., additional, Denton, C., additional, and Wells, A., additional

Published
2010
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29. Neuregulins promote survival and growth of cardiac myocytes. Persistence of ErbB2 and ErbB4 expression in neonatal and adult ventricular myocytes.

Author

Zhao, Y Y, Sawyer, D R, Baliga, R R, Opel, D J, Han, X, Marchionni, M A, and Kelly, R A

Abstract

Neuregulins (i.e. neuregulin-1 (NRG1), also called neu differentiation factor, heregulin, glial growth factor, and acetylcholine receptor-inducing activity) are known to induce growth and differentiation of epithelial, glial, neuronal, and skeletal muscle cells. Unexpectedly, mice with loss of function mutations of NRG1 or of either of two of their cognate receptors, ErbB2 and ErbB4, die during midembryogenesis due to the aborted development of myocardial trabeculae in ventricular muscle. To examine the role of NRG and their receptors in developing and postnatal myocardium, we studied the ability of a soluble NRG1 (recombinant human glial growth factor 2) to promote proliferation, survival, and growth of isolated neonatal and adult rat cardiac myocytes. Both ErbB2 and ErbB4 receptors were found to be expressed by neonatal and adult ventricular myocytes and activated by rhGGF2. rhGGF2 (30 ng/ml) provoked an approximate 2-fold increase in embryonic cardiac myocyte proliferation. rhGGF2 also promoted survival and inhibited apoptosis of subconfluent, serum-deprived myocyte primary cultures and also induced hypertrophic growth in both neonatal and adult ventricular myocytes, which was accompanied by enhanced expression of prepro-atrial natriuretic factor and skeletal alpha-actin. Moreover, NRG1 mRNA could be detected in coronary microvascular endothelial cell primary cultures prepared from adult rat ventricular muscle. NRG1 expression in these cells was increased by endothelin-1, another locally acting cardiotropic peptide within the heart. The persistent expression of both a neuregulin and its cognate receptors in the postnatal and adult heart suggests a continuing role for neuregulins in the myocardial adaption to physiologic stress or injury.

Published
1998

30. PROFESSOR SUHAS V. PATANKAR ON HIS 60TH BIRTHDAY.

Author

Chai, J. C., Baliga, R. B., Karki, K. C., Kelkar, K. M., Radmehr, A., Minkowycz, W . J., and Sparrow, E. M.

Subjects
*FLUID dynamics
Abstract

Profiles Suhas V. Patankar, a professor on computational fluid dynamics and president of the Innovative Research Inc. in India. Educational background; Career highlights of Patankar; Contributions in the field of computational fluid dynamics.

Published
2001
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32. Medical therapy for rheumatic heart disease: Is it time to be proactive rather than reactive?

Author

Rajamannan, N. M., Antonini-Canterin, F., Luis Moura, Zamorano, J. L., Rosenhek, R. A., Best, P. J. M., Lloyd, M. A., Rocha-Gonçalves, F., Chandra, S., Alfieri, O., Lancellotti, P., Tornos, P., Baliga, R. R., Wang, A., Bashore, T., Ramakrishnan, S., Spargias, K., Shuvy, M., Beeri, R., Lotan, C., Suwaidi, J. A., Bahl, V., Pierard, L. A., Maurer, G., Nicolosi, G. L., Rahimtoola, S. H., Chopra, H. K., Pandian, N. G., Rajamannan, Nm, Antonini Canterin, F, Moura, L, Zamorano, Jl, Rosenhek, Ra, Best, Pj, Lloyd, Ma, Rocha Goncalves, F, Chandra, S, Alfieri, Ottavio, Lancellotti, P, Tornos, P, Baliga, Rr, Wang, A, Bashore, T, Ramakrishnan, S, Spargias, K, Shuvy, M, Beeri, R, Lotan, C, Suwaidi, Ja, Bahl, V, Pierard, La, Maurer, G, Nicolosi, Gl, Rahimtoola, Sh, Chopra, K, and Pandian, Ng

Subjects
Causality, Risk Factors, Rheumatic Heart Disease, Animals, Humans, Mitral Valve Stenosis, Aortic Valve Stenosis, Comorbidity, Article
Abstract

Rheumatic Heart Disease (RHD) is well known to be an active inflammatory process which develops progressive calcification and leaflet thickening over time. The potential for statin therapy in slowing the progression of valvular heart disease is still controversial. Retrospective studies have shown that medical therapy is beneficial for patients with calcific aortic stenosis and recently for rheumatic valve disease. However, the prospective randomized clinical trials have been negative to date. This article discusses the epidemiologic risk factors, basic science, retrospective and prospective studies in valvular heart disease and a future clinical trial to target RHD with statin therapy to slow the progression of this disease. Recent epidemiological studies have revealed the risk factors associated with valvular disease include male gender, smoking, hypertension and elevated serum cholesterol and are similar to the risk factors for vascular atherosclerosis. An increasing number of models of experimental hypercholesterolemia demonstrate features of atherosclerosis in the aortic valve (AV), which are similar to the early stages of vascular atherosclerotic lesions. Calcification, the end stage process of the disease, must be understood as a prognostic indicator in the modification of this cellular process before it is too late. This is important in calcific aortic stenosis as well as in rheumatic valve disease. There are a growing number of studies that describe similar pathophysiologic molecular markers in the development of rheumatic valve disease as in calcific aortic stenosis. In summary, these findings suggest that medical therapies may have a potential role in patients in the early stages of this disease process to slow the progression of RHD affecting the valves. This review will summarize the potential for statin therapy for this patient population.

34. Clinical quiz

Author

Boineau Fg, Chesney Rw, John E. Lewy, and Baliga R

Subjects
03 medical and health sciences, medicine.medical_specialty, 0302 clinical medicine, Nephrology, business.industry, Pediatrics, Perinatology and Child Health, Toxicity, Medicine, 030212 general & internal medicine, 030204 cardiovascular system & hematology, business, Dermatology
Published
1988
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