Since August 1983 I had an uninterrupted career in different teaching and research positions with 5 different Universities in Asia, Europe and America. I published more than 50 peer reviewed articles in different reputed journals and contributed significantly to the field of ocular Physiology and Pharmacology. I graduated with Doctor of Veterinary Medicine (DVM) degree in 1982 from Bangladesh Agricultural University. I was awarded University Prize for securing First position in the First Class and appointed as a Lecturer in the Department of Physiology and Pharmacology the following year. During the tenure of my lectureship position I completed MSc in Pharmacology degree in 1985, again with distinction and secured First Class.  I was promoted to Assistant professor in 1987 and worked in that position until Sept. 1990. In 1990 I was awarded Commonwealth Scholarship by the Association of Universities in the United Kingdom to do my PhD in Pharmacology. Strictly speaking this was the start of my research career. I completed PhD in 1994 from the University of Glasgow, UK and because of my outstanding contribution in research I was immediately offered Postdoc position and worked for this University until 2001. During this period I had an outstanding achievement in establishing an experimental model, the perfused intact eye system to study ocular drugs. I published a number of manuscripts utilizing this model system with significant contribution to the field.   In 2001 I was invited by the School of Optometry of the Hong Kong Polytechnic University to help them establish an Ocular Pharmacology laboratory and appointed me as a Research Fellow and Visiting Lecturer. I worked there until June 2005. During this period I was able to adapt the intact eye preparation to record multifocal ERG and this was the first in vitro ERG record in the world. In this position I taught Pharmacology and Physiology to the optometry students. In June 2005 I moved to the United States of America and since then I have been working as Assistant Professor including my present position at the University of Arizona. During this time I established a second model system, the primary culture of nonpigmented ciliary epithelial cells. I published a large number of peer reviewed papers in many reputed journals with significant contribution to ocular physiology and pharmacology research. My notable scientific contributions are:(1) development of arterially perfused eye preparation and primary culture of nonpigmented ciliary epithelium (NPE) and lens epithelium. These experimental platforms played pivotal roles in the discoveries and in studying many aspects of ocular physiology and pharmacology, including retinal electrophysiology, signal transduction mechanisms involved in ion transport, aqueous humor secretion and drug transport by the NPE, and ion transport functions of the lens.  (2) Discovery that Src tyrosine kinases regulate Na,K-ATPase activity in the NPE and in the lens epithelium. I was the pioneer in showing how receptors, and Src family tyrosine kinases interact to regulate Na,K-ATPase activity. Additionally, I showed how activation of certain G protein-coupled receptors speeds up active Na-K transport while different receptors slow down the process. Different receptors appear to couple to different tyrosine kinase members of the Src family (SFKs). (3) Discovery of a role for transient receptor potential vanilloid 4 (TRPV4) in ocular lens. Here I discovered a novel TRPV4 channel-dependent mechanism for SFK activation in the lens epithelium. This discovery enabled scientists to understand how TRPV4 activates a feedback loop mechanism that includes hemichannel opening, ATP release, and a cAMP increase, all of which lead eventually to SFK activation and increased Na,K-ATPase activity. (4) Discovery of interaction between TRPV4 and connexin 50 hemichannels that constitute a unique remote-control signaling mechanism in the lens. I showed that injury to a remote area of the lens fiber mass or changes in hydrostatic pressure (HP) of lens cells can initiate a signaling response in the surface epithelium. In structural context of the lens, the epithelial cells have specialized to make TRPV4 channel a critical component of the remote control mechanism to influence Na,K-ATPase activity. (5) Discovery of two independently operated sense and respond feedback control systems that maintain normal hydrostatic pressure or ion/water or volume homeostasis of the lens. One feedback control system is sensed by TRPV4 in response to swelling (increased volume) or increased HP of the lens initiating a multicomponent signaling cascade that ultimately activates Na,K-ATPase. Activation of Na,K-ATPase in turn helps the lens return to its normal volume or hydrostatic pressure. The other feedback control system is sensed by TRPV1 in response to lens shrinkage (decreased volume) or decreased HP of the lens cells initiating a multicomponent signaling mechanism that ultimately activate Sodium-Potassium-Chloride Cotransporter 1 (NKCC1). Activation of NKCC1 in turn helps the lens return to its normal volume or hydrostatic pressure. These discoveries are published in many high impact scientific journals, including, British Journal of Pharmacology, European Journal of Pharmacology, American Journal of Physiology, Journal of Cellular Physiology, The Journal of Pharmacology and Experimental Therapeutics,