38 research outputs found
Supply Chain Optimisation with Machine Learning and Neural Networks: Applications to Demand Planning, Supply Planning, and Inventory Planning.
Full text linkThis thesis explores the impact of machine learning (ML) on supply chain planning, particularly in demand forecasting, supply planning, and inventory optimisation. By analysing literature on supply chain management, data flow, and the intersection of ML and competitive advantage, the author contextualises the research within a globalised market\u27s demands. Case studies, interviews with industry professionals, and raw data collection provide empirical support for evaluating the research objectives and documenting the integration of ML in supply chain processes.
The findings reveal that optimised ML models, particularly those using model stacking (autoregressors, GRUs, and Random Forests), significantly outperform traditional demand forecasting methods, achieving a 70% MAPE improvement over a 45% benchmark. The integration of advanced techniques like XGBoost further optimised supply and inventory planning. The research concludes that leveraging ML not only enhances forecast accuracy but also strengthens supply chain competitiveness through superior planning outputs.
By critically relating empirical data to literature insights, the author demonstrates that ML-driven approaches enhance supply chain management in a Central European wholesale clothing business. This research validates the transformative potential of advanced data analytics for achieving a competitive edge in the supply chain
Plague outbreaks in prairie-dog colonies associated with El Niño climatic events
Full text linkThe SGS-LTER research site was established in 1980 by researchers at Colorado State University as part of a network of long-term research sites within the US LTER Network, supported by the National Science Foundation. Scientists within the Natural Resource Ecology Lab, Department of Forest and Rangeland Stewardship, Department of Soil and Crop Sciences, and Biology Department at CSU, California State Fullerton, USDA Agricultural Research Service, University of Northern Colorado, and the University of Wyoming, among others, have contributed to our understanding of the structure and functions of the shortgrass steppe and other diverse ecosystems across the network while maintaining a common mission and sharing expertise, data and infrastructure.Colorado State University. Natural Resource Ecology Laboratory; Colorado State University. Department of Forest and Rangeland Stewardship; Colorado State University. Department of Soil and Crop Sciences; Colorado State University. Department of Biology; California State University, Fullerton; United States. Agricultural Research Service; United States. Forest Service. Pawnee National Grasslands; University of Northern Colorado.Plague (Yersinia pestis) was introduced to the western U.S. in the mid-20th century and is a significant threat to the persistence of black-tailed prairie dog (Cynomys ludovicianus) populations. The social, colonial habits of prairie dogs make them particularly susceptible to plague, and many flea species, including known carriers of plague, are associated with prairie dogs or their extensive burrow systems. Mortality during plague epizootics, or outbreaks, is nearly 100% (Cully and Williams 2001; J. Mammal. 82:894), resulting in the extinction of entire colonies. In northern Colorado, prairie dogs exist in metapopulations (Roach et al. 2001, J. Mammal. 82:946), in which colonies naturally isolated by topography, soils and vegetation are connected by dispersal. Dispersal of either infected prairie dogs or plague-resistant reservoir species is hypothesized to spread plague among colonies. Plague outbreaks therefore may disrupt the dynamics of prairie-dog metapopulations and affect regional persistence. In the context of a century of past eradication efforts that have drastically reduced prairie-dog numbers, and increasing agricultural and urban development, plague represents a relatively new and unique threat to prairie dogs and the species that are closely associated with them. Poster presented at the 6th SGS Symposium held on 1/10/03
Application of failure modes and effects analysis to support product in-use information feedback
No full textCharacterizing the target of ivermectin, the glutamate-gated chloride channel, and other insecticide targets as candidate antigens for an anti-mosquito vaccine
Full text linkIncludes bibliographical references.2015 Fall.The latest WHO World Malaria Report estimates that, in 2013, there were 198 million cases worldwide causing 584,000 malaria-related deaths. Current malaria control programs primarily target malaria vectors through the use of long lasting insecticide treated bed nets and indoor residual spraying of pyrethroid-based insecticides. However, pyrethroid resistance is becoming widespread in many An. gambiae populations across Africa (Ranson et al., 2011; Trape et al., 2011). Out of recent efforts to find new vector-targeting interventions with novel modes of action, the endectocide ivermectin (IVM) has arisen as a new candidate to control malaria transmission. IVM, when imbibed by vectors from host-treated blood meals, has proven to efficiently kill or disable An. gambiae s.s. both in the lab and the field (Kobylinski et al., 2010; Sylla et al., 2010). More recently, IVM mass drug administrations in multiple locations across west Africa have been shown to temporarily reduce the proportion of P. falciparum-infected An. gambiae in IVM-treated villages (Kobylinski et al., 2011; Alout et al., 2014). The primary target of IVM is the invertebrate glutamate-gated chloride channel (GluCl) (Cully et al., 1994; Cully et al., 1996; Janssen et al., 2007; McCavera et al., 2009; Janssen et al., 2010; Moreno et al., 2010). The purpose of the first chapter of this thesis was to characterize GluCl from An. gambiae in order to understand the physiological role of GluCl and how IVM may be affecting mosquito physiology. Cloning of the An. gambiae GluCl (AgGluCl) revealed unique splicing sites and products not previously predicted. We expressed AgGluCl clones in Xenopus laevis oocytes to measure its electrophysiological activity in response to glutamate and IVM. We also examined AgGluCl isoform-specific transcript levels across different tissues, ages, blood feeding status and gender and GluCl tissue expression in adult An. gambiae. Given that GluCl can be targeted by drugs found in a blood meal and that GluCl is not expressed in mammals, we wanted to test the efficacy of AgGluCl as a candidate mosquitocidal vaccine antigen. We administered a polyclonal anti-AgGluCl immunoglobulin G (anti-AgGluCl IgG) to An. gambiae mosquitoes through a blood meal or directly into the hemocoel by intrathoracic injections and found it significantly reduced An. gambiae survivorship. By co-administering anti-AgGluCl IgG with a known GluCl agonist, IVM, we discovered anti-AgGluCl IgG reverses the mosquitocidal effects of IVM. Our results describing the mosquitocidal properties of anti-AgGluCl IgG suggest that other neuronal proteins could be used as candidate antigens for a mosquitocidal vaccine. The An. gambiae GABA-gated chloride channel (resistance to dieldrin; AgRDL) is another member of the cys-loop ligand-gated ion channels with a similar structure and physiological function to AgGluCl. The An. gambiae voltage-gated sodium channel (AgVGSC) is the target of dichlorodiphenyltrichloroethane (DDT) and the pyrethroid class of insecticides (Soderlund and Bloomquist, 1989). VGSCs are also the target of multiple classes of spider, scorpion and snail toxins, demonstrating that peptides binding to VGSC extracellular residues can affect channel function (Nicholson, 2007; King et al., 2008; Stevens et al., 2011; Klint et al., 2012). Preliminary results shows that IgG targeting AgRDL or AgVGSC similarly reduce An. gambiae survivorship. Finally we tested anti-AgGluCl IgG against A. aegypti and C. tarsalis to see if this strategy has broad potential across both Anopheline and Culicine mosquitoes. However, blood meals containing anti-AgGluCl IgG had no effect on A. aegypti or C. tarsalis survivorship. We determined that this was due to a barrier in antibody translocation from the blood meal to the hemolymph. Since the IgG target, AgGluCl, is only expressed in the hemocoel, antibody translocation was required for mosquito toxicity
Author response: NADPH oxidase mediates microtubule alterations and diaphragm dysfunction in dystrophic mice
No full textRGS5, a Hypoxia-inducible Apoptotic Stimulator in Endothelial Cells
No full textEndothelial cells rapidly respond to changes in oxygen homeostasis by regulating gene expression. Regulator of G protein signaling 5 (RGS5) is a negative regulator of G protein-mediated signaling that is strongly expressed in vessels during angiogenesis; however, the role of RGS5 in hypoxia has not been fully understood. Under hypoxic conditions, we found that the expression of RGS5, but not other RGS, was induced in human umbilical vein endothelial cells (HUVEC). RGS5 mRNA was increased when HUVEC were incubated with chemicals that stabilized hypoxia-inducible factor-1 alpha (HIF-1 alpha), whereas hypoxia-stimulated RGS5 promoter activity was absent in HIF-1 beta(-/-) cells. Vascular endothelial growth factor (VEGF), which is regulated by HIF-1, did not appear to be involved in hypoxia-induced RGS5 expression; however, VEGF-mediated activation of p38 but not ERK1/2 was increased by RGS5. Overexpression of RGS5 in HUVEC exhibited a reduced growth rate without affecting the cell proliferation. Annexin V assay revealed that RGS5 induced apoptosis with significantly increased activation of caspase-3 and the Bax/Bcl-2 ratio. Small interfering RNA-specific for RGS5, caspase-3 inhibitor, and p38 inhibitor resulted in an attenuation of RGS5-stimulated apoptosis. Matrigel assay proved that RGS5 significantly impaired the angiogenic effect of VEGF and stimulated apoptosis in vivo. We concluded that RGS5 is a novel HIF-1-dependent, hypoxia-induced gene that is involved in the induction of endothelial apoptosis. Moreover, RGS5 antagonizes the angiogenic effect of VEGF by increasing the activation of p38 signaling, suggesting that RGS5 could be an important target for apoptotic therapy.Biochemistry & Molecular BiologySCI(E)EIPubMed19ARTICLE3523436-2344328
Response Gene to Complement 32, a Novel Hypoxia-Regulated Angiogenic Inhibitor
No full textBackground-Response gene to complement 32 (RGC-32) is induced by activation of complement and regulates cell proliferation. To determine the mechanism of RGC-32 in angiogenesis, we examined the role of RGC-32 in hypoxia-related endothelial cell function. Methods and Results-Hypoxia/ischemia is able to stimulate both angiogenesis and apoptosis. Hypoxia-inducible factor-1/vascular endothelial growth factor is a key transcriptional regulatory pathway for angiogenesis during hypoxia. We demonstrated that the increased RGC-32 expression by hypoxia was via hypoxia-inducible factor-1/vascular endothelial growth factor induction in cultured endothelial cells. However, overexpression of RGC-32 reduced the proliferation and migration and destabilized vascular structure formation in vitro and inhibited angiogenesis in Matrigel assays in vivo. Silencing RGC-32 had an opposing, stimulatory effect. RGC-32 also stimulated apoptosis as shown by the increased apoptotic cells and caspase-3 cleavage. Mechanistic studies revealed that the effect of RGC-32 on the antiangiogenic response was via attenuating fibroblast growth factor 2 expression and further inhibiting expression of cyclin E without affecting vascular endothelial growth factor and fibroblast growth factor 2 signaling in endothelial cells. In the mouse hind-limb ischemia model, RGC-32 inhibited capillary density with a significant attenuation in blood flow. Additionally, treatment with RGC-32 in the xenograft tumor model resulted in reduced growth of blood vessels that is consistent with reduced colon tumor size. Conclusions-We provide the first direct evidence for RGC-32 as a hypoxia-inducible gene and antiangiogenic factor in endothelial cells. These data suggest that RGC-32 plays an important homeostatic role in that it contributes to differentiating the pathways for vascular endothelial growth factor and fibroblast growth factor 2 in angiogenesis and provides a new target for ischemic disorder and tumor therapies. (Circulation. 2009;120:617-627.)http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000269051900011&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Cardiac & Cardiovascular SystemsPeripheral Vascular DiseaseSCI(E)PubMed19ARTICLE7617-U14112
Endothelial Cells Require Related Transcription Enhancer Factor-1 for Cell-Cell Connections Through the Induction of Gap Junction Proteins
No full textObjective-Capillary network formation represents a specialized endothelial cell function and is a prerequisite to establish a continuous vessel lumen. Formation of endothelial cell connections that form the vascular structure is regulated, at least in part, at the transcriptional level. We report here that related transcription enhancer factor-1 (RTEF-1) plays an important role in vascular structure formation. Methods and Results-Knockdown of RTEF-1 by small interfering RNA or blockage of RTEF-1 function by the transcription enhancer activators domain decreased endothelial connections in a Matrigel assay, whereas overexpression of RTEF-1 in endothelial cells resulted in a significant increase in cell connections and aggregation. In a model of oxygen-induced retinopathy, endothelial-specific RTEF-1 overexpressing mice had enhanced angiogenic sprouting and vascular structure remodeling, resulting in the formation of a denser and more highly interconnected superficial capillary plexus. Mechanistic studies revealed that RTEF-1 induced the expression of functional gap junction proteins including connexin 43, connexin 40, and connexin 37. Blocking connexin 43 function inhibited RTEF-1-induced endothelial cell connections and aggregation. Conclusion-These findings provide novel insights into the transcriptional control of endothelial function in the coordination of cell-cell connections. (Arterioscler Thromb Vasc Biol. 2012;32:1951-1959.)HematologyPeripheral Vascular DiseaseSCI(E)PubMed2ARTICLE81951-U5233
RTEF-1, an Upstream Gene of Hypoxia-inducible Factor-1 alpha, Accelerates Recovery from Ischemia
No full textThe amount of available hypoxia-inducible factor (HIF)-1 alpha has been considered to be largely a consequence of post-translational modification by multiple ubiquitin-proteasome pathways. However, the role of transcriptional regulation of HIF-1 alpha is less certain, and the mechanisms of transcriptional regulation of HIF-1 alpha require further investigation. Here we report that related transcriptional enhancer factor-1 (RTEF-1), a member of the TEF transcriptional factor family, transcriptionally regulates the HIF-1 alpha gene under normoxic and hypoxic conditions. The expression of HIF-1 alpha mRNA was decreased in endothelial cells in which RTEF-1 was knocked down with siRNA. Sequential deletional analysis of the HIF-1 alpha promoter revealed that the MCAT-like element in the HIF-1 alpha promoter was essential for HIF-1 alpha transcription. Binding of RTEF-1 to the MCAT-like element was confirmed by ChIP. Treatment of endothelial cells with a HIF-1 inhibitor resulted in retardation of RTEF-1-induced proliferation and tube formation. Moreover, increased HIF-1 alpha expression was observed in transgenic mice expressing RTEF-1 under the VE-cadherin promoter (VE-Cad/RTEF-1). VE-Cad/RTEF-1 mice subjected to hindlimb ischemia demonstrated increased levels of HIF-1 alpha, accelerated recovery of blood flow, and increased capillary density compared with littermate controls. These results identify RTEF-1 as a regulator of HIF-1 alpha transcription, which results in up-regulation of HIF-1 alpha and acceleration of recovery from ischemia.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000291719900076&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologySCI(E)PubMed13ARTICLE2522699-2270528
Do youth in sport stay out of court? Insights and recommendations for families, coaches, community groups, sports organisations, and policymakers
No full textIn Aotearoa New Zealand, rugby and rugby league are popular sporting codes, historically and particularly among males. In their 2023 annual reports, New Zealand Rugby reported 147,434 registered participants, while New Zealand Rugby League reported 28,180. Both institutions have also developed equity, diversity and inclusion strategies aimed at nurturing the participation and involvement of women and girls, as well as Māori and Pacific communities. However, while both codes have recorded an increase in female participation, there has been a gradual decline in male participation (Cully, 2023; Radio New Zealand, 2023; Wilson, 2022). This decline in sport participation has also been noted by (former) Principal Youth Court Judge Andrew Becroft, who found that young male offenders are often not involved in sport (Bruce, 2013; Sport NZ, 2018).
This report summarises the findings of a study that examines sports attrition in relation to youth offending. In that study, the author (Clarke, 2012) examined the childhood and youth sporting experiences and illegal activities of five young men aged between 18 and 25 years old.
The aim of this report is to provide insights into how these young men became involved in sport and why they dropped out, how they became involved in crime, and possible links between their sport participation and offending. Their experiences highlight several issues that can be addressed by parents/caregivers, clubs, sport administrators, coaches, community groups, sports organisations, and policymakers.
In course of the study, six key observations were made. For these young men:
1. rugby and or rugby league were their primary and final sporting codes;
2. these sports were or had become ‘just a game’;
3. aggressive coaches diminished their enjoyment and commitment to sport;
4. their parents/caregivers were absent from their sporting lives;
5. their participation in sport and crime was simultaneous; and
6. the collision aspect of rugby and rugby league may have helped to facilitate their offending.
In this document, the names of these young men have been replaced with aliases. To provide the reader with a richer and deeper understanding of the issues, the report features a number of their stories and reflections (edited for readability only). The research methods are briefly outlined in Appendix 1. Sources included in this report are listed in the References section. For a fuller review of the literature and the research analysis refer to the original research document (Clarke, 2012)
