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INTERLEUKIN-7 DIFFERENTIALLY REGULATES THE ACTIVATION, PROLIFERATION, AND HOMING OF T-CELLS: IMPLICATIONS FOR IMMUNOTHERAPY
Title
INTERLEUKIN-7 DIFFERENTIALLY REGULATES THE ACTIVATION, PROLIFERATION, AND HOMING OF T-CELLS: IMPLICATIONS FOR IMMUNOTHERAPY.
Creator
Kittipatarin, Christina, Khaled, Annette, University of Central Florida
Abstract / Description
Interleukin-7 (IL-7) is an essential lymphocyte growth factor required for the survival and proliferation of mature T-cells. As a therapeutic agent, IL-7 has the potential to restore T-cell numbers following immune depletion and to promote immunity against cancers. While the survival function of IL-7 is well established, less is known about how it supports T-cell expansion, a critical feature of the immune response. To study the biological effects of IL-7 on T-cell growth, we developed an in...
Show moreInterleukin-7 (IL-7) is an essential lymphocyte growth factor required for the survival and proliferation of mature T-cells. As a therapeutic agent, IL-7 has the potential to restore T-cell numbers following immune depletion and to promote immunity against cancers. While the survival function of IL-7 is well established, less is known about how it supports T-cell expansion, a critical feature of the immune response. To study the biological effects of IL-7 on T-cell growth, we developed an in vitro culture technique to expand T-cells ex vivo. A significant finding from our studies is that IL-7 did not induce the expansion of all T-cells, indicating that there are inherent differences in the response of individual T-cell subsets to IL-7. Culture with high doses of IL-7 (>150 ng/ml) preferentially expanded CD8 T-cells, but lead to the dramatic loss of CD4 T-cells which favored growth in lower dosages of IL-7 (<10 ng/ml). This effect was due to the regulation of LCK, a kinase predominantly associated with the CD4 co-receptor. We found that transgenic expression of the CD4 co-receptor onto CD8 T-cells promoted their growth in lower concentrations of IL-7. Conversely, inhibition of LCK activity in CD4 T-cells restored their responsiveness to high doses of IL-7 as indicated by the activation of the transcription factor STAT5, in a manner similar to CD8 T-cells. Interestingly, not all CD8 T-cells expanded in high doses of IL-7 and this effect was specific to CD8 T-cells that expressed an activated memory phenotype. We found that IL-7 promoted the proliferation of CD8 T-cells through Cdc25A, a phosphatase required for cell cycle progression. Expression of a constitutively active Cdc25A could maintain T-cell survival and proliferation in the absence of IL-7, demonstrating that Cdc25A is a crucial transducer of IL-7 growth signals. Inhibition of Cdc25A was sufficient to decrease proliferation and down-regulate the expression of activation/ memory markers on CD8 T-cells in the presence of IL-7. Upon further study, we identified a novel role for IL-7 through Cdc25A in the regulation of CD62L, an adhesion molecule required for lymph node entry. Culture with high doses of IL-7 down-regulated the expression of CD62L, suggesting that high doses of IL-7 could affect the ability of T-cells to enter or re-enter the lymph nodes. Collectively, our findings demonstrate that IL-7 administration at the supraphysiological doses currently used in the clinical trials could have a negative impact on the growth of CD4 T-cells and the homing of CD8 T-cells to the lymph nodes, effects which can impede the generation of an effective immune response.
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Date Issued
2010
Identifier
CFE0003372, ucf:48449
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0003372
AN ADAPTIVE MULTIOBJECTIVE EVOLUTIONARY APPROACH TO OPTIMIZE ARTMAP NEURAL NETWORKS
Title
AN ADAPTIVE MULTIOBJECTIVE EVOLUTIONARY APPROACH TO OPTIMIZE ARTMAP NEURAL NETWORKS.
Creator
Kaylani, Assem, Georgiopoulos, Michael, University of Central Florida
Abstract / Description
This dissertation deals with the evolutionary optimization of ART neural network architectures. ART (adaptive resonance theory) was introduced by a Grossberg in 1976. In the last 20 years (1987-2007) a number of ART neural network architectures were introduced into the literature (Fuzzy ARTMAP (1992), Gaussian ARTMAP (1996 and 1997) and Ellipsoidal ARTMAP (2001)). In this dissertation, we focus on the evolutionary optimization of ART neural network architectures with the intent of optimizing...
Show moreThis dissertation deals with the evolutionary optimization of ART neural network architectures. ART (adaptive resonance theory) was introduced by a Grossberg in 1976. In the last 20 years (1987-2007) a number of ART neural network architectures were introduced into the literature (Fuzzy ARTMAP (1992), Gaussian ARTMAP (1996 and 1997) and Ellipsoidal ARTMAP (2001)). In this dissertation, we focus on the evolutionary optimization of ART neural network architectures with the intent of optimizing the size and the generalization performance of the ART neural network. A number of researchers have focused on the evolutionary optimization of neural networks, but no research has been performed on the evolutionary optimization of ART neural networks, prior to 2006, when Daraiseh has used evolutionary techniques for the optimization of ART structures. This dissertation extends in many ways and expands in different directions the evolution of ART architectures, such as: (a) uses a multi-objective optimization of ART structures, thus providing to the user multiple solutions (ART networks) with varying degrees of merit, instead of a single solution (b) uses GA parameters that are adaptively determined throughout the ART evolution, (c) identifies a proper size of the validation set used to calculate the fitness function needed for ART's evolution, thus speeding up the evolutionary process, (d) produces experimental results that demonstrate the evolved ART's effectiveness (good accuracy and small size) and efficiency (speed) compared with other competitive ART structures, as well as other classifiers (CART (Classification and Regression Trees) and SVM (Support Vector Machines)). The overall methodology to evolve ART using a multi-objective approach, the chromosome representation of an ART neural network, the genetic operators used in ART's evolution, and the automatic adaptation of some of the GA parameters in ART's evolution could also be applied in the evolution of other exemplar based neural network classifiers such as the probabilistic neural network and the radial basis function neural network.
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Date Issued
2008
Identifier
CFE0002212, ucf:47907
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0002212
THE SHEDDASE ACTIVITY OF ADAM10/ADAM17 ON CXCL16 INCREASES PROLIFERATION AND SURVIVAL OF COLORECTAL CANCER CELLS
Title
THE SHEDDASE ACTIVITY OF ADAM10/ADAM17 ON CXCL16 INCREASES PROLIFERATION AND SURVIVAL OF COLORECTAL CANCER CELLS.
Creator
Talton, Tamu, von Kalm, Laurance, University of Central Florida
Abstract / Description
CXCL16 is an interferon-inducible chemokine of the CXC-subfamily and functions as an adhesion molecule, when membrane bound, and a chemoattractant when soluble. Upregulation of cell associated CXCL16 (cCXCL16) in colorectal cancer is associated with increased tumor infiltrating lymphocytes and good prognosis. ADAM10 and ADAM17 are metalloproteinases responsible for cleaving CXCL16, releasing soluble CXCL16 (sCXCL16) and contributing to proliferation and migration of mesangial cells, in kidney...
Show moreCXCL16 is an interferon-inducible chemokine of the CXC-subfamily and functions as an adhesion molecule, when membrane bound, and a chemoattractant when soluble. Upregulation of cell associated CXCL16 (cCXCL16) in colorectal cancer is associated with increased tumor infiltrating lymphocytes and good prognosis. ADAM10 and ADAM17 are metalloproteinases responsible for cleaving CXCL16, releasing soluble CXCL16 (sCXCL16) and contributing to proliferation and migration of mesangial cells, in kidney inflammatory disease. We hypothesize that cCXCL16 is a substrate for ADAM10 and ADAM17 cleavage in colorectal cancer, releasing sCXCL16, which mediates cell proliferation. To this end, we first identified CXCL16 in the human colon carcinoma cell line, RKO, by immunohistochemistry. cCXCL16 was found in the membrane, cytoplasm and nucleus. We treated RKO, in vitro, with an inflammatory cytokine mix containing 1.4 nM rhIFN³, 2.0 nM rhTNFα and 2.0 nM rhIL1² to increase the cleavage of cCXCL16 to sCXCL16. Overnight incubation with the cytokine mix significantly (P=.004) increased the release of sCXCL16 compared to normal conditions. To confirm that a metalloproteinase is responsible for the cleavage of cCXCL16, we used a broad spectrum metalloproteinase inhibitor, GM6001, in combination with inflammatory stimulation, in cell culture. We assayed the supernatant using ELISA for sCXCL16. GM6001 at 100 ¼M decreased sCXCL16 to levels indistinguishable from the background. Using siRNA, we knocked down the expression of ADAM10 and ADAM17, independently, to determine if the activity of each on cCXCL16 was mediated by inflammatory stimulation. It was shown that ADAM10 constitutively cleaved cCXCL16, and ADAM17 cleavage activity was induced by inflammatory stimulation. To determine if sCXCL16 increased colorectal cancer cell (CRC) proliferation through ligand-receptor binding, we treated cells with a range of rhCXCL16 from 3.125-100 ng/mL. rhCXCL16 did not increase RKO proliferation at doses up to 100 ng/mL. We used GM6001, to inhibit the cleavage of cCXCL16 into sCXCL16 then performed an ATPase assay and 6 day cell cycle analysis, under inflammatory stimulation. Increased cleavage of cCXCL16 induced by inflammatory stimulation with the cytokine mix containing 1.4 nM rhIFN³, 2.0 nM rhTNFα and 2.0 nM rhIL1², increased RKO proliferation and reduced apoptosis. We conclude that ADAM10 and ADAM17 cleavage of cCXCL16 to sCXCL16 is increased by ADAM17 activation with inflammatory stimulation. The cleavage of the extracellular portion from cCXCL16 is associated with increased proliferation and decreased apoptosis of colorectal cancer cells.
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Date Issued
2011
Identifier
CFE0003587, ucf:48909
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0003587
THE RESPONSE OF SATELLITE GLIAL CELLS TO P2X7 RECEPTOR ACTIVATION
Title
THE RESPONSE OF SATELLITE GLIAL CELLS TO P2X7 RECEPTOR ACTIVATION.
Creator
Kursewicz, Christina D, Lambert,Stephen, University of Central Florida
Abstract / Description
Satellite glial cells (SGCs) surround the cell bodies of neurons of the peripheral nervous system, including those of the sensory ganglia. Their close apposition to the neuronal soma allows for bi-directional communication between neurons and SGCs, which are thought to regulate neuronal activity. After nerve injury, SGCs in the dorsal root ganglia contribute to neuropathic pain. Although the mechanisms are not fully understood, SGCs show increased coupling via gap junctions, and communicate...
Show moreSatellite glial cells (SGCs) surround the cell bodies of neurons of the peripheral nervous system, including those of the sensory ganglia. Their close apposition to the neuronal soma allows for bi-directional communication between neurons and SGCs, which are thought to regulate neuronal activity. After nerve injury, SGCs in the dorsal root ganglia contribute to neuropathic pain. Although the mechanisms are not fully understood, SGCs show increased coupling via gap junctions, and communicate with the neuron via bi-directional purinergic signaling after nerve injury. The increased coupling between SGCs and neurons may have implications for chronic pain following peripheral nerve injury. In vivo studies suggest that injury through the administration of capsaicin to the sensory nerve endings causes SGCs to be activated and proliferate. We have shown that capsaicin treatment in an in vitro co-culture of sensory neurons and SGCs increased the expression of the proliferation marker, Ki-67 in the glia. Here, we examine whether purinergic signaling plays a role in the promotion of SGC proliferation.
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Date Issued
2017
Identifier
CFH2000172, ucf:45960
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFH2000172
IDENTIFICATION OF SMALL MOLECULES THAT INHIBIT PROSTATE CANCER CELL PROLIFERATION
Title
IDENTIFICATION OF SMALL MOLECULES THAT INHIBIT PROSTATE CANCER CELL PROLIFERATION.
Creator
Zelaya, Rainel, Chakrabarti, Ratna, University of Central Florida
Abstract / Description
Prostate cancer is the second most often diagnosed cancer and internationally the sixth foremost cause of cancer death in males, as of 2011. Within the United States it is the most common form of cancer in men with 186,000 new cases and with an overall 28,600 deaths in 2008, and it is the second leading kind of cancer-related death in men. The widespread threat that prostate cancer poses against men across the globe cannot be understated, and its initiation and progression must be understood...
Show moreProstate cancer is the second most often diagnosed cancer and internationally the sixth foremost cause of cancer death in males, as of 2011. Within the United States it is the most common form of cancer in men with 186,000 new cases and with an overall 28,600 deaths in 2008, and it is the second leading kind of cancer-related death in men. The widespread threat that prostate cancer poses against men across the globe cannot be understated, and its initiation and progression must be understood in order to truly comprehend its implicated risks and possible forms of treatment. As its name implies, prostate cancer is a form of cancer that develops in the prostate gland located in the male reproductive system. Its progress starts when standard semen-secreting prostate gland cells mutate into cancer cells. Although its developments may start at the prostate gland, cancer cells may metastasize to other parts of the body through circulation systems such as the lymph nodes. The main sites of metastasis for prostate cancer include the adrenal gland,the bones, the liver and the lungs. Although there are treatments available for prostate cancer, there is no definitive cure. The primary goal of this project was to find an alternative form of treatment, which is what will be necessary to combat this cancer.
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Date Issued
2014
Identifier
CFH0004595, ucf:45228
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFH0004595
Identification and Functional Characterization of a Long Non-coding RNA associated with Prostate Cancer
Title
Identification and Functional Characterization of a Long Non-coding RNA associated with Prostate Cancer.
Creator
Hasan, Md Faqrul, Chakrabarti, Ratna, Zhao, Jihe, Zhang, Shaojie, University of Central Florida
Abstract / Description
Prostate cancer is the most common cancer in men in the western world. Although early stage prostate cancer is treatable late stage, more specifically, metastatic and drug resistant prostate cancers are mostly incurable. The failure of current treatments obligates the research community to explore novel areas in prostate cancer biology and find better therapeutic targets. Emerging evidences show that non-coding RNAs specifically long non-coding RNAs (lncRNAs) play regulatory roles in various...
Show moreProstate cancer is the most common cancer in men in the western world. Although early stage prostate cancer is treatable late stage, more specifically, metastatic and drug resistant prostate cancers are mostly incurable. The failure of current treatments obligates the research community to explore novel areas in prostate cancer biology and find better therapeutic targets. Emerging evidences show that non-coding RNAs specifically long non-coding RNAs (lncRNAs) play regulatory roles in various cellular processes and are frequently dysregulated in cancer including prostate cancer. These aberrantly expressed lncRNAs mostly with unexplored genetic information may drive cancer progression. Previous studies done in our laboratory showed a tumor suppressor role of a cluster of small non-coding RNAs or microRNA (miRNA) miR-17-92a in PC-3 prostate cancer cells. To learn the underlying mechanism, transcriptome analysis with or without expression of miR-17-92a was conducted in our laboratory. RNA-sequencing data analysis identified reduced expression of a set of lncRNAs and oncogenes, and up regulation of several tumor suppressor genes upon expression of miR-17-92a cluster miRNAs. One of the down regulated intergenic lncRNAs, PAINT (Prostate Cancer Associated Intergenic Non-coding Transcript) (LINC00888), was selected for determining its functional role in prostate cancer. TCGA and GEO profiles analyses revealed up regulation of PAINT in prostate tumors with higher Gleason Scores, in highly aggressive metastatic prostate cancer cell lines, and upon androgen deprivation therapy of prostate cancer cells. This observation was supported by our studies on expression analysis of PAINT in prostate tumor tissues using RNA in-situ hybridization in tissue microarrays (TMA) containing tissues from different stages of prostate cancer and normal prostate tissues, which showed higher expression of PAINT in prostate cancer tissues compared to normal tissues. Furthermore, late stage (stage III and stage IV) prostate tumors showed significant overexpression of PAINT compared to early stage (stage II) prostate cancer tissues. We examined the functional relevance of PAINT in promoting tumor progression next using different prostate cancer cell lines. Silencing of PAINT using siRNAs showed decreased cell proliferation, reduced S-phase progression and activation of pro-apoptotic proteins PARP and Caspase-3. Silencing of PAINT also showed decreased cell migration and increased expression of the epithelial marker, E-cadherin while reduced expression of mesenchymal markers Slug and Vimentin. Ectopic expression of PAINT reversed the effects observed upon silencing of PAINT. Increased cell proliferation, cell cycle progression and cell migration were noted in prostate cancer cells overexpressing PAINT. Additionally, cancer promoting phenotype such as larger colony formation and higher expression of mesenchymal marker Slug, was detected upon overexpression of PAINT. Our study also determined the therapeutic benefit of inhibition of expression showing an increased sensitivity of metastatic prostate cancer cells to the chemotherapeutic agent docetaxel (DTX) and selective Aurora kinase inhibitor VX-680. Taken together, our study establishes an oncogenic function of PAINT, its clinical relevance as a marker for advanced stage prostate cancer and its potential as a therapeutic target for metastatic prostate cancer.
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Date Issued
2019
Identifier
CFE0007466, ucf:52681
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0007466
TIMP-1 ACTIVATES A UNIQUE CARDIAC STEM CELL POPULATION, CD63+ve/C-KIT+ve, THEREBY ENHANCING CARDIAC DIFFERENTIATION, AND PROTECTS THE HEART FROM ADVERSE CARDIAC REMODELING FOLLOWING MYOCARDIAL INFARCTION
Title
TIMP-1 ACTIVATES A UNIQUE CARDIAC STEM CELL POPULATION, CD63+ve/C-KIT+ve, THEREBY ENHANCING CARDIAC DIFFERENTIATION, AND PROTECTS THE HEART FROM ADVERSE CARDIAC REMODELING FOLLOWING MYOCARDIAL INFARCTION.
Creator
Abdelli, Latifa, Singla, Dinender, Cheng, Zixi, Parthasarathy, Sampath, Jewett, Mollie, University of Central Florida
Abstract / Description
We previously demonstrated that embryonic stem (ES) cells over-expressing tissue inhibitor of metalloproteinase-1 (TIMP-1) have increased potential to engraft and differentiate into cardiac myocytes following transplantation into the infarcted heart. However, the ability of TIMP-1 to activate endogenous stem cells and enhance their differentiation into cardiac regenerative cell types is still unknown. We postulate that TIMP-1 may additionally activate a stem cell population that enhances...
Show moreWe previously demonstrated that embryonic stem (ES) cells over-expressing tissue inhibitor of metalloproteinase-1 (TIMP-1) have increased potential to engraft and differentiate into cardiac myocytes following transplantation into the infarcted heart. However, the ability of TIMP-1 to activate endogenous stem cells and enhance their differentiation into cardiac regenerative cell types is still unknown. We postulate that TIMP-1 may additionally activate a stem cell population that enhances cardiac cell type differentiation in the infarcted myocardium. To prove this hypothesis, we isolated c-kit+ve cells from four weeks old C57BL/6 mice and cultured them in vitro in presence of ES conditioned media (ESCM), ES-TIMP-1-CM or TIMP-1. Our immunostaining data validate the existence of a novel CD63+ve/c-kit+ve cells. When treated with TIMP-1, these cells showed significantly (p(<)0.05) increased proliferation and differentiation into cardiac myocytes, vascular smooth muscle cells, and endothelial cells. Western blot analysis revealed significantly (p(<)0.05) increased expression of CD63, phosphorylated and total ?-catenin proteins. Furthermore, our RT-PCR data showed increased cardiac gene expression (GATA-4, Mef2C, and Nkx-2.5) when compared to ESCM and control cells. Based on the in vitro findings, we investigated the effect of intramyocardial delivery of TIMP-1 on endogenous CD63+ve/c-kit+ve cells following myocardial infarction (MI). C57BL/6 and TIMP-1 KO mice underwent coronary artery ligation followed by intramyocardial delivery of 20(&)#181;l of culture media (CC), ESCM, ES-TIMP-1-CM or TIMP-1. Subsequent immunohistochemistry analysis demonstrated the presence of a CD63+ve/c-kit+ve cell population within the peri-infarct area and confirmed intramyocardial delivery of ES-TIMP-1-CM or TIMP-1 significantly (p(<)0.05) enhanced their proliferation. Percentage of CD63+ve/c-kit+ve cells was significantly (p(<)0.05) lower in TIMP-1 KO mice compared to C57BL/6 animals. RT-PCR analysis revealed TIMP-1 KO animals expressed significantly less CD63 and TIMP-1 mRNAs compared to C57BL/6 mice. Activated CD63+ve/c-kit+ve cells were also able to differentiate into major cardiac cell types as previously shown in vitro. The differentiation potential of these cells was however higher in C57BL/6 mice compared to TIMP-1 KO mice. We also demonstrate that CD63+ve/c-kit+ve cells differentiation is regulated by CD63/?-catenin pathway in vivo. Additionally, we provide evidence that TIMP-1 protects the heart from adverse cardiac remodeling through inhibition of cardiac apoptosis and fibrosis leading to significantly (p(<)0.05) improved contractile function. Collectively, our data show TIMP-1 plays a dual protective role in the MI heart. It activates a unique stem cell population, CD63+ve/c-kit+ve, which proliferates and differentiates into functional myocytes, smooth muscle cells and endothelial cells mediated through CD63/?-catenin pathway. TIMP-1 also protects the heart from adverse cardiac remodeling. Increased cardiac regeneration and inhibition of adverse cardiac remodeling consequently lead to restored cardiac function. ?
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Date Issued
2015
Identifier
CFE0005750, ucf:50108
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0005750
IRANIAN NUCLEAR PROGRAM: DOMESTIC IMPLICATIONS
Title
IRANIAN NUCLEAR PROGRAM: DOMESTIC IMPLICATIONS.
Creator
Serrano, Manuel A, Sadri, Houman, University of Central Florida
Abstract / Description
The intent for this thesis is to explain and inform the process of the Iranian Nuclear Program throughout the last decades. The stand of the Islamic Republic of Iran has brought very delicate issues and confrontations to the international community. This thesis discusses the history of key countries that play an important part into developing the Iranian nuclear program. These countries being the United States, Israel, Russia and other countries part of the UN Security Council. This thesis...
Show moreThe intent for this thesis is to explain and inform the process of the Iranian Nuclear Program throughout the last decades. The stand of the Islamic Republic of Iran has brought very delicate issues and confrontations to the international community. This thesis discusses the history of key countries that play an important part into developing the Iranian nuclear program. These countries being the United States, Israel, Russia and other countries part of the UN Security Council. This thesis also attempts to analyze and focuses on the domestic policies the government of Iran and its people have interacted with the nuclear deal. The nuclear deal between the UN Security Council members and the Islamic Republic of Iran have shown an array of acceptance and rejection within, specially, the United States, Arab countries in the region and Israel. The implementations of the solution to future confrontation are probably the main ideal to a healthy international community who can adapt to new measures and policies to a safer world. Using classical realist theory, based on Hans J. Morgenthau realist theory, the Iranian nuclear program could be explained with a different perspective. There are other international relations theories that could help explaining Iran's government behavior and how it interacts with the international community. Iran's move in the past years has shown progress towards the international community and has lowered the potential military action against Iran. Some countries like Israel continue on the dissatisfaction against the nuclear deal signed by Iran and the UN Security Council member countries. This thesis will show the behavior the country of Iran has had towards other countries based on their domestic policy.
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Date Issued
2016
Identifier
CFH2000137, ucf:45961
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFH2000137
The Effects of Phosphatidylserine on Reaction Time and Cognitive Function Following an Exercise Stress
Title
The Effects of Phosphatidylserine on Reaction Time and Cognitive Function Following an Exercise Stress.
Creator
Wells, Adam, Hoffman, Jay, Fragala, Maren, Stout, Jeffrey, University of Central Florida
Abstract / Description
Phosphatidylserine (PS) is an endogenously occurring phospholipid that has been shown to have cognition and mood enhancing properties in humans, possibly through its role as an enzyme co-factor in cellular signal transduction. Specifically, PS has been identified as activator of classical isoforms of protein kinase C, an enzyme known to be involved in the growth and differentiation of neural cells, and is therefore thought to play a role in the protection of neurons.The purpose of this study...
Show morePhosphatidylserine (PS) is an endogenously occurring phospholipid that has been shown to have cognition and mood enhancing properties in humans, possibly through its role as an enzyme co-factor in cellular signal transduction. Specifically, PS has been identified as activator of classical isoforms of protein kinase C, an enzyme known to be involved in the growth and differentiation of neural cells, and is therefore thought to play a role in the protection of neurons.The purpose of this study was to examine the effects of supplementation with PS and caffeine on measures of cognition, reaction time and mood prior to and following an exercise stress. Twenty, healthy, resistance trained males (17) and females (3) (mean (&)#177; SD; age: 22.75 (&)#177; 3.27 yrs; height: 177.03 (&)#177; 8.44cm; weight: 78.98 (&)#177; 11.24kg; body fat%: 14.28 (&)#177; 6.6), volunteered to participate in this randomized, double-blind, placebo-controlled study. Participants were assigned to a PS group (400mg/day PS; 100mg/day caffeine, N=9) or PL (16g/day Carbs, N=11) delivered in the form of 4 candy chews identical in size, shape and color. Subjects performed an acute bout of full body resistance exercise, prior to (T1) and following 14 days of supplementation (T2). Measures of reaction time (Dynavision(&)#174; D2 Visuomotor Training Device), cognition (Serial Subtraction Test, SST), and mood (Profile of Mood States, POMS) were assessed immediately before and following resistance exercise in both T1 and T2. Data was analyzed using two-way ANCOVA and repeated measures ANOVA.Supplementation with 400mg PS and 100mg caffeine did not have a significant impact upon measures of reaction time or cognition between groups at baseline or following acute resistance exercise. However, there was a non-significant trend to the attenuation of fatigue between groups, following acute resistance exercise (p = 0.071). Interestingly, our data suggests that acute resistance exercise alone may improve cognitive function.Although more research is necessary regarding optimal dosage and supplementation duration, the current findings suggest that supplementation 400mg/day PS with 100mg/day caffeine may attenuate fatigue following acute resistance exercise. It is possible that the lack of significance may be the result of both an inhibition of the PS activated pathway and a withdrawal effect from caffeine.
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Date Issued
2012
Identifier
CFE0004457, ucf:49325
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0004457
INDIA AND CHINA SPACE PROGRAMS: FROM GENESIS OF SPACE TECHNOLOGIES TO MAJOR SPACE PROGRAMS AND WHAT THAT MEANS FOR THE INTERNATIONAL COMMUNITY
Title
INDIA AND CHINA SPACE PROGRAMS: FROM GENESIS OF SPACE TECHNOLOGIES TO MAJOR SPACE PROGRAMS AND WHAT THAT MEANS FOR THE INTERNATIONAL COMMUNITY.
Creator
BHOLA, GAURAV, HANDBERG, ROGER, University of Central Florida
Abstract / Description
The Indian and Chinese space programs have evolved into technologically advanced vehicles of national prestige and international competition for developed nations. The programs continue to evolve with impetus that India and China will have the same space capabilities as the United States with in the coming years. This will present new challenges to the international community in spheres civilian, to space and military applications and their residual benefits.
Date Issued
2009
Identifier
CFE0002745, ucf:48156
Format
Document (PDF)
PURL
http://purl.flvc.org/ucf/fd/CFE0002745