Nursing Presentations (UMKC)
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Items in this collection are the scholarly output of the School of Nursing faculty, staff, and students, either alone or as co-authors, and which may or may not have been published in an alternate format.
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Item Biomedical Tissue Engineering - Where We Go in the Future(2010-03) Bonewald, Lynda F.; Brotto, Marco; Day, Delbert E.; Detamore, Michael S.; Johnson, Mark L. (Mark Louis); Leon-Salas, Walter D. (Walter Daniel); University of Missouri (System); Missouri Life Sciences Summit (2010: University of Missouri--Kansas City)Researchers and entrepreneurs examine breakthroughs in tissue engineering and regeneration that enhance healing, remodeling, and recovery.Item Hyperthermia Induces Functional and Molecular Modifications in Cardiac, Smooth and Skeletal Muscle Cells(2010-03) Romero, Sandra; Hall, Todd; Touchberry, Chad; Elmore, Chris; Silswal, Neerupma; Parelkar, Nickil; Baker, Kendra; Loghry, Michael; Rizk, Hatem Ibrahim; Mo, Chenglin; Brotto, Leticia; Leon-Salas, Walter D. (Walter Daniel); Wacker, Michael J.; Andresen, Jon; Brotto, Marco; University of Missouri (System); Missouri Life Sciences Summit (2010: University of Missouri--Kansas City)Hyperthermia is used for the treatment of a number of diseases, including muscle injuries, inflammations, tendinitis, and osteoarticular disorder. More recently, hyperthermia has been used as an adjuvant in cancer treatment. Only two studies have shown that hyperthermia leads to hypertrophy in in-vitro models of cardiac and skeletal muscle cells. Functional, biochemical and molecular mechanisms of hyperthermia-induced hypertrophy in muscles remain largely undiscovered. We investigated the effects of mild heat shock (HS) on C2C12 skeletal, HL-1 cardiac and AR-75 smooth muscle cells. Mild HS (20 min 43ºC) induced increases in the cell area in all muscle cells tested. C2C12 cells are a well-accepted model of skeletal muscle fibers, and were selected for complementary studies. First, to biochemically confirm an increase in protein synthesis we measured and found an increase of ~6% in total protein content 24 hrs after HS. Second, we examined potential modifications in calcium (Ca) homeostasis regulation by measuring intracellular Ca. We detected a lower resting level of intracellular Ca and smaller and longer caffeine-induced Ca transients in C2C12 muscle cells 24 hrs after HS. Next, to search for molecular mechanisms involved with HS-induced hypertrophy and calcium homeostasis modifications, mRNA from C2C12 muscle cells was analyzed at different time points after HS (0, 1, 2, and 24 hrs). We used an ABI Step One Plus RT2 PCR Array System and a custom-built 96 gene array. We report for the first time that the expression of key heat-shock, hypertrophy/ metabolic, and Ca+2 signaling genes were altered after HS. Hsp70 and Hsp72 genes were highly expressed (211-1829 fold change) after HS. Also, Myh7 (MHC-I), Myh6, Srf, Ppp3r1 and Pck1 were up-regulated by 2-6 fold change compared with control cells.. Furthermore, a reduction in the expression of RyR and Trdn genes was observed (2- 3.6 fold change) with an associated increase in the expression of IP3R genes (2-4 fold change). These results indicate that hyperthermia modulates not only heat-shock related and hypertrophy genes, but also genes involved with metabolism, apoptosis repression, calcium homeostasis and signaling, and cell homeostasis. Our studies offer an initial exploration of the functional, biochemical and molecular mechanisms that may help explain the beneficially adaptive effects of hyperthermia on muscle function. Our studies shall also prove useful for the refinement of a specific device (EM-Stim) to be employed for the treatment of muscle and bone diseases (See poster by Hatem et al). Importantly, our studies have potential translational applications. By learning how to more precisely use hyperthermia to control specific genes that can improve or treat muscle injuries, musculoskeletal, and cardiovascular diseases, the ensuing benefits shall be unmistakable. Our short and long-term goals are: i) optimize our protocols; ii) test HS in animal models; iii) manipulate expression of promising genes of interest in vitro and in in-vivo animal models; iv) initiate clinical studies to fully translate from the bench to the bed-side.Item Skeletal Muscle - Bone Crosstalk Regulating Osteocyte Function [abstract](2010-03) Lara, Nuria; Karabilo, Julia; Hall, Todd; Wacker, Michael J.; Andresen, Jon; Brotto, Marco; Bonewald, Lynda F.; Johnson, Mark L. (Mark Louis); University of Missouri (System); Missouri Life Sciences Summit (2010: University of Missouri--Kansas City)Osteocytes are thought to be the primary cell in bone that responds to mechanical loading and the traditional view is that skeletal muscle's role relative to bone is in the application of those loads. We have hypothesized that muscle cells can exert influences on bone through the production of endocrine like factors that alter the behavior of bone cells. To test this hypothesis we have cultured MLO-Y4 osteocyte like cells in the presence of conditioned media (CM) from C2C12 differentiated muscle cell cultures, a myogenic cell line that closely represents adult mammalian skeletal muscle cells. We have observed that muscle cell CM causes increased dendrite lengthening and decreased cell body area similar to previously reported effects of fluid flow shear stress (FFSS) applied to the MLO-Y4 osteocytic cells. We next determined whether muscle cell CM could alter the regulation of early biochemical signaling pathways that are known to be activated by FFSS. The addition of 10% muscle cell CM during the application of FFSS for 2 hours resulted in a potentiation of Akt signaling activation by FFSS on MLO-Y4 osteocytic cells. Erk1/2 activation in response to FFSS is normally transient in MLO-Y4 cells reaching a peak at 15 minutes and declining by 2 hours; however, in the presence of 10% CM there was a sustained activation at 2 hours. These data are consistent with the production of a factor(s) by skeletal muscle cells that can modulate the function of the bone osteocytes and their response to loading. The identification of this factor could lead to the development of new paradigms or agents to treat diseases of low bone mass such as osteoporosis and muscle related diseases such as sarcopenia.Item An Electro-magnetic cell stimulator [abstract](2010-03) Rizk, Hatem Ibrahim; Mo, Cheng L.; Leon-Salas, Walter D. (Walter Daniel); Hall, Todd; Wacker, Michael J.; Brotto, Marco; University of Missouri (System); Missouri Life Sciences Summit (2010: University of Missouri--Kansas City)A device to stimulate bone and muscle cell growth and possibly for treatment of bone and muscle injuries is presented. The device, called EStim, generates electric and magnetic pulses at programmable intervals. This device will also be used to study the crosstalk between bone and muscle cell growth. In a human or animal body, muscles and bones are intimately interrelated and the loss of activity in one of them affects the other. This interrelation is especially evident in persons with bone fractures. While the bone is healing, the muscles loose mass due to lack of exercise. Furthermore, when skeletal muscles are not exercised, bone mass decreases. In these situations, muscle mass can be partially maintained if externally stimulated by applying repetitive electric pulses. The EStim has been designed to generate electric pulses of different frequencies and amplitudes to stimulate muscle growth. It also generates magnetic pulses to stimulate bone growth. This dual stimulation is a unique feature of the EStim and makes it a promising device in the treatment of bone fractures or for muscle stimulation. Besides this clinical application, the EStim is being used to study the crosstalk at the cellular level between muscle and bone cells. A line of C2C12 cells is being used to test the effects of the electric and magnetic pulses on cell growth. Variables such as pulse repetition, field strength and rest period duration have been evaluated. Initial results show that electric stimulation induces cell hypertrophy similar to the ones observed in heat shock experiments (see abstract by Romero et al). The EStim device consists of three sections: the controller, the high-voltage generation unit and the high-current generation unit. The controller is built around the MSP430 low-power microcontroller. It handles communication with a host computer to change settings or to perform tests. Settings such as pulse repetition, pulse width, number of pulses, rest time between pulses, and magnetic field strength can be changed by the user. The controller also monitors the battery voltage and the maximum pulse current. As a safety measure, pulse generation is stopped if the current through the probe exceeds a preset value. The high-voltage generation unit consists of a boost converter that is able to generate voltages up to 40 V and an H-bridge that allows the generation of biphasic or monophasic electric pulses. The high-current unit consists of a buck converter able to generate currents up to 10 A. These large currents are used to generate magnetic fields of up to 10 mT. This device will be used to better understand the interplay between bones and muscles. Ultimately, our goal is test this device in animals and humans to fully realize its applications on musculoskeletal injuries and diseases.