Sunday, February 16, 2020

Business School Networking Refelction Essay Example | Topics and Well Written Essays - 250 words

Business School Networking Refelction - Essay Example I conducted my research prior to attending the simulation. I checked the websites about networking simulations. I also managed to play one of the online networking simulations prior to this one. This helped me prepare well before the actual test. I wrote my weaknesses from the prior simulation and tried to work on them before we went for the class simulation. During the conversation I was able to interact with Mr. Schiff managing Director of BIDCO Company. He told me that networking is not about whom you are but what people say you are. Our tutor Mr. Tom also told me that networking is critical and building relationships is the catalyst for a successful business. In addition to this, my friend Claire told me that if I was to succeed I would need to continually connect with new people and cultivate emerging relationships and leverage my network. I took all these conversations as very important. During this time I built my confidence and gained courage in the field of business. In the end I learnt that networking is all about cultivating a win-win situation by accelerating professional development and seeking new career

Sunday, February 2, 2020

The Case of the Off-Rhythm Bongo Player Essay Example | Topics and Well Written Essays - 2000 words

The Case of the Off-Rhythm Bongo Player - Essay Example As explained by Jason Bardi reports from the Scripps Institute, "calcium is a second messenger and regulates many different intracellular processes, including gene expression within cells." (Bardi, 2004) and "the transfer or spread of this excitability to a neuronal network, manifested as electro-graphic and clinical seizures, occurs via synaptic transmission." (Wellmer J, Su H, Beck H, Yaari Y and Eur J Neurosci, 2002) The effect on ion channels and effect on threshold are distinctive in the sense that "native calcium channels have been classified by both their electrophysiological and pharmacological properties and are generally divided into low-threshold (T-types) and high threshold (L-, N-, P/Q- and R-types). The L-, N-, P/Q- and R-type channels typically activate at membrane potentials near -30 mV and display diverse kinetic, voltage-dependent and pharmacological properties.1 The availability of specific pharmacological agents targeting the high threshold channels has permitted elucidation of many of their physiological functions. The T-type calcium channels describe a class of molecules that transiently activate at relatively negative potentials (-60 mV) and for which a general lack of high-affinity selective blockers has made their exact physiological contributions lag behind those of the high-voltage activated isoforms" (Snutch, 2005) The effect on Bado's muscles including the aching, twitching and tingling fingers is based on how the calcium mediates constriction and relaxation of blood vessels. This includes those excitable cells which controls the nerve impulses like those occurring in his twitching fingers. More definitively explained by Jane Higdon of the Linus Pauling Institute at Oregon University, calcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones, such as insulin. Excitable cells, such as skeletal muscle and nerve cells, contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell that release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy for muscle contraction. (Higdon, 2003) As explained in the following afflictions, cell excitability and effects on the skeletal muscle are discussed: a) Hyperkalemia: "In acute hyperkalemia, the ratio of intracellular to extracellular K+ is decreased. The gap between the resting membrane potential to the excitability threshold is decreased and the nerve conduction is initiated more easily. If this continues it progresses to weakness of muscles. Gradual hyperkalemia, as in