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In wireless ad hoc networks, nodes cooperatively form a network without any infrastructure such as a BS/AP (base station or access point). The widely-used contention-based MAC protocol, IEEE 802.11b, is inefficient in multi-hop networks due to the hidden and exposed terminal problems. The most popular schedule-based MAC protocol, TDMA (time division multiple access), is difficult to implement in an ad hoc network due to the lack of infrastructure. The contribution of this paper is to provide the community novel and efficient MAC (medium access control) protocols (i.e., a collision resolution protocol) for a wireless ad hoc network without a centralized infrastructure. We propose two new MAC protocols (one distributed algorithm and one cluster-based algorithm) that use a collision resolution scheme for a network with a single BS/AP. We first compare the performance of our distributed algorithm with our cluster-based algorithm. Then, we compare our algorithm that performs better (i.e., our cluster-based algorithm) to TDMA in a two-hop network. The simulation results illustrate that our cluster-based algorithm provides higher throughput and lower delay than TDMA in a two-hop network.
Insulin resistance is an important risk factor in the
development of cardiovascular diseases such as hypertension and
atherosclerosis. However, despite its importance, the specific role
of insulin resistance in the etiology of these diseases is poorly understood.
At the same time, ethanol (ETOH) is a potent vasoconstrictor that primarily
induces down regulation of mitogen activated protein kinases (MAPKs) which could
exacerbate insulin resistance and possibly lead to cardiovascular diseases. This
article describes how chronic ETOH exposure interferes with insulin signaling
in hypertensive vascular smooth muscle cells (HVSMCs) which leads to the
alteration of MAPKs, the major signaling molecules. Elevated (50 - 800 mM)
chronic exposure (24 hr) of HVSMCS to ETOH prior to insulin stimulation
decreased insulin-induced ERK 1/2 (MAPKs) and AKT expression. Similar
experiments were conducted using normotensive cells from rat. These cells
showed reductions in insulin-induced ERK 1/2 phosphorylation as well, but only
at higher concentrations of ETOH (400 - 800 mM). These alterations in insulin signaling
could provide an alternative molecular mechanism that may increase the risk of
insulin resistance, thus increasing the possibility of cardiovascular diseases.