Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99


Search Results: 1 - 10 of 1701 matches for " Beth Levine "
All listed articles are free for downloading (OA Articles)
Page 1 /1701
Display every page Item
The Baetylus Theorem—The Central Disconnect Driving Consumer Behavior and Investment Returns in Wearable Technologies  [PDF]
James A. Levine
Technology and Investment (TI) , 2016, DOI: 10.4236/ti.2016.73008
Abstract: The Wearable Technology market may increase fivefold by the end of the decade. There is almost no academic investigation as to what drives the investment hypothesis in wearable technologies. This paper seeks to examine this issue from an evidence-based perspective. There is a fundamental disconnect in how consumers view wearable sensors and how companies market them; this is called The Baetylus Theorem where people believe (falsely) that by buying a wearable sensor they will receive health benefit; data suggest that this is not the case. This idea is grounded social constructs, psychological theories and marketing approaches. A marketing proposal that fails to recognize The Baetylus Theorem and how it can be integrated into a business offering has not optimized its competitive advantage. More importantly, consumers should not falsely believe that purchasing a wearable technology improves health.
A Five-Step Strategy to Combine Data Sources from Multiple Wearable Sensors  [PDF]
James A. Levine
Technology and Investment (TI) , 2017, DOI: 10.4236/ti.2017.81003
Abstract: With the multitude of non-communicating wearable sensors, there is an urgent need to better combine wearable data streams in order to improve human health and well-being. A five-step process is proposed. The first step is to specify the human behavior that the data set will address. The second step is to critically assess primary measurement that allows the behavioral goal to be addressed. After this, other streams can be integrated in a hierarchical fashion based on their accuracy, precision and relevance. The third step is to perform a hierarchical synthesis of the multiple data streams. In the fourth step, the multiple data streams are integrated for practical use; we propose achieving this with wearable computers. The final step is that system retraining occurs, via Artificial Intelligence, so that an integrated wearable system can be individualized. A case study of Type 1 diabetes is used: this analysis and the proposed solutions illustrate the need for an urgent interdisciplinary debate to advance useful methods for combining data from divergent wearable sensors. Wearable fully integrated systems, programmed with Artificial Intelligence, will enable data from multiple wearable sensors to be optimized to improve individual well-being.
The Application of Wearable Technologies to Improve Healthcare in the World’s Poorest People  [PDF]
James A. Levine
Technology and Investment (TI) , 2017, DOI: 10.4236/ti.2017.82007
Abstract: Wearable technologies could be influential for improving healthcare in underserved areas. Wearable sensors are straightforward to develop, have low production costs and the methods for processing high volumes of data are advanced. Here we examine the application of wearable technology for improving health in three poverty-related scenarios. The first is for diabetes prevention in Mexico City. The second is for medical care in the Kibera slum in Nairobi and the third is for the delivery of “health kits” to refugees. The analysis affirms that investment is worthwhile in mass scalable wearable technologies directed at the half of the world’s population who live in poverty.
The CD40-Autophagy Pathway Is Needed for Host Protection Despite IFN-Γ-Dependent Immunity and CD40 Induces Autophagy via Control of P21 Levels
Jose-Andres C. Portillo,Genevieve Okenka,Erin Reed,Angela Subauste,Jennifer Van Grol,Katrin Gentil,Masaaki Komatsu,Keiji Tanaka,Gary Landreth,Beth Levine,Carlos S. Subauste
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0014472
Abstract: Autophagy degrades pathogens in vitro. The autophagy gene Atg5 has been reported to be required for IFN-γ-dependent host protection in vivo. However, these protective effects occur independently of autophagosome formation. Thus, the in vivo role of classic autophagy in protection conferred by adaptive immunity and how adaptive immunity triggers autophagy are incompletely understood. Employing biochemical, genetic and morphological studies, we found that CD40 upregulates the autophagy molecule Beclin 1 in microglia and triggers killing of Toxoplasma gondii dependent on the autophagy machinery. Infected CD40?/? mice failed to upregulate Beclin 1 in microglia/macrophages in vivo. Autophagy-deficient Beclin 1+/? mice, mice with deficiency of the autophagy protein Atg7 targeted to microglia/macrophages as well as CD40?/? mice exhibited impaired killing of T. gondii and were susceptible to cerebral and ocular toxoplasmosis. Susceptibility to toxoplasmosis occurred despite upregulation of IFN-γ, TNF-α and NOS2, preservation of IFN-γ-induced microglia/macrophage anti-T. gondii activity and the generation of anti-T. gondii T cell immunity. CD40 upregulated Beclin 1 and triggered killing of T. gondii by decreasing protein levels of p21, a molecule that degrades Beclin 1. These studies identified CD40-p21-Beclin 1 as a pathway by which adaptive immunity stimulates autophagy. In addition, they support that autophagy is a mechanism through which CD40-dependent immunity mediates in vivo protection and that the CD40-autophagic machinery is needed for host resistance despite IFN-γ.
Transformational Leadership in Planning Curricula  [PDF]
Beth Nagy, David J. Edelman
Current Urban Studies (CUS) , 2014, DOI: 10.4236/cus.2014.23020
Abstract: Planners are expected to be ethical, advancing socially-responsible citizenship-based practices. They must also have a keen understanding of the implications of top-down policy decisions on communities. A Planner is a public servant. Public servants require a mastery of techniques for community engagement: involving a wide range of people in making decisions, an ability to work with the public and articulate planning issues to a wide variety of audiences, as well as the ability to function as a facilitator when community interests conflict. These skills call for a theoretical foundation in transformational leadership, but students will not learn transformational leadership unless the curriculum deliberately teaches and models it. This research considers the intersection of three major themes in the pedagogy of Planning: sustainable communities, transformational leadership, and community engagement. The intersection, a critical Planning pedagogy, should be a guiding principle of all Planning curricula. Although this is a case study, and its findings limited to one program, the framework can be explored as a means to examining transformational leadership as a means to advancing socially-responsible citizenship-based practices in Planning curricula.
Susceptibility to Dental Caries and the Salivary Proline-Rich Proteins
Martin Levine
International Journal of Dentistry , 2011, DOI: 10.1155/2011/953412
Abstract: Early childhood caries affects 28% of children aged 2–6 in the US and is not decreasing. There is a well-recognized need to identify susceptible children at birth. Caries-free adults neutralize bacterial acids in dental biofilms better than adults with severe caries. Saliva contains acidic and basic proline-rich proteins (PRPs) which attach to oral streptococci. The PRPs are encoded within a small region of chromosome 12. An acidic PRP allele (Db) protects Caucasian children from caries but is more common in African Americans. Some basic PRP allelic phenotypes have a three-fold greater frequency in caries-free adults than in those with severe caries. Early childhood caries may associate with an absence of certain basic PRP alleles which bind oral streptococci, neutralize biofilm acids, and are in linkage disequilibrium with Db in Caucasians. The encoding of basic PRP alleles is updated and a new technology for genotyping them is described. 1. Introduction Dental caries is the dissolution of the enamel and dentin in pits, fissures, and interdental regions of the teeth, eventually spreading to buccal and lingual surfaces. Since the release of “Oral Health in America: A Report of the Surgeon General” in May 2000, efforts have not advanced dental caries prevention, its risk of development, or its early detection [1]. Worse, the severity of caries has since been increasing in all socioeconomic groups [2]. Public preventive measures such as water fluoridation are not universally available, few rural populations have access to fluoridated water, and fluoridated dentifrices are only effective if the teeth are brushed regularly. Dental caries is the commonest chronic infectious disease of childhood in the United States affecting 28% of the population [3]. Childhood caries is a major reason for hospital visits [4], and it may destroy the deciduous dentition disproportionately in disadvantaged ethnic and socioeconomic groups [5]. A better means of identifying and protecting these children needs to be developed [6], but a simple method of identifying such individuals a priori at birth has proved elusive [7]. Dental caries is caused by bacterial acids within a dentally adherent biofilm (plaque) in the presence of dietary carbohydrate especially sucrose [8]. Nevertheless, the same intake of sucrose by different individuals or populations results in large disparities in caries severity. The mean number of teeth with caries in 12-year-old children from 47 different countries increases by about one decayed, missing, or filled tooth (DMFT) for every 25?g of sugar
A systems view of Drosophila segmentation
Mike Levine
Genome Biology , 2008, DOI: 10.1186/gb-2008-9-2-207
Abstract: One of the most intensively studied processes in animal development is the division of the embryonic Drosophila epidermis (ectoderm) into visible segments, a process that lays the foundations for the segmented structure of the adult insect. Segmentation is governed by a program of sequential gene expression that is one of the best-defined genetic cascades in animal development [1]. It is put into motion by three maternal gene regulatory proteins - Bicoid, Hunchback and Caudal - which specify an initial 'pre-segmentation' pattern along the anterior-posterior axis, while the anterior and posterior ends of the body are specified independently by the localized activation of the maternal receptor tyrosine kinase Torso. The principal target genes of these maternal factors in the embryo's genome are known as gap genes, as their lack leads to gaps in the body pattern. The gap genes, such as Krüppel, Knirps and Giant, encode sequence-specific transcriptional repressors. The interplay of the maternal factors and the gap repressors constitutes one of the leading paradigms for the combinatorial control of gene expression in development. These regulatory factors bind to the enhancers of the segmentation genes to produce precisely positioned on/off repeating transverse stripes of expression for each gene, foreshadowing the subdivision of the embryo into a repeating series of body segments. The segmentation genes typically have highly complex enhancers, with multiple binding sites for each gene regulatory protein.Detailed descriptions of individual parts of the Drosophila segmentation process have been available for many years, but Segal and colleagues [2] have recently taken a systems approach to segmentation by developing a comprehensive quantitative thermodynamics-based model in an attempt to describe the regulation of segmentation-gene expression in the early embryo. This analysis was made possible by two recent advances in understanding Drosophila segmentation. First, computa
Tamoxifen stimulates arachidonic acid release from rat liver cells by an estrogen receptor-independent, non-genomic mechanism
Lawrence Levine
BMC Cancer , 2003, DOI: 10.1186/1471-2407-3-24
Abstract: Rat liver cells were radiolabelled with arachidonic acid. The release of [3H] arachidonic acid after various times of incubation of the cells with tamoxifen was measured.Tamoxifen, at micromolar concentrations, stimulates arachidonic acid release. The stimulation is rapid and is not affected by pre-incubation of the cells with actinomycin or the estrogen antagonist ICI-182,780.The stimulation of AA release by tamoxifen is not mediated by estrogen receptor occupancy and is non-genomic.Clinically, breast cancer chemoprevention by tamoxifen has been attributed to its antiestrogenic properties [1-3]. Tamoxifen also has been shown to prevent cancer in animal studies by a mechanism of action that is based, in part, on its antiestrogenic activity [1,4]. However, at μM levels, tamoxifen releases arachidonic acid (AA) from rat liver cells [5]. This ability to release AA, a molecule whose multiple bioactivities [6] include induction of apoptosis [7], suggests a mechanism for cancer prevention that does not require metabolism by cyclooxygenase [8]. I suggest that AA release from cells may be a part of a mechanism by which tamoxifen prevents cancer.Tamoxifen has several biological effects, some of which may be beneficial. It also has unfavorable effects, especially its estrogenic activity on the uterus [1,2]. One of the many activities associated with perturbation of the plasma membrane and/or release of AA may mediate some of these biological effects.The C-9 rat liver cell line was purchased from the American Type Culture Collection (Manassas, VA, USA). The cells were maintained in Eagle's minimum essential medium (MEM) supplemented with 10% fetal bovine serum. [3H] AA (91.8 Ci/mmol) was obtained from NEN Life Science Products, Inc. (Boston, MA, USA). ICI-182,780 was purchased from Tocris Cookson, Inc. (Ballwin, MO, USA). All other reagents were from Sigma Chemical Co. (St. Louis, MO, USA).Two days prior to experiments, the rat liver cells were treated with 0.25% trypsin-EDTA
Tamoxifen and the Rafoxifene analog LY117018: their effects on arachidonic acid release from cells in culture and on prostaglandin I2 production by rat liver cells
Lawrence Levine
BMC Cancer , 2004, DOI: 10.1186/1471-2407-4-49
Abstract: Rat liver, rat glial, human colon carcinoma and human breast carcinoma cells were labelled with [3H] arachidonic acid. The release of the radiolabel from these cells during incubation with tamoxifen and the raloxifene analog LY117018 was measured. The prostaglandin I2 produced during incubation of the rat liver cells with μM concentrations of tamoxifen and the raloxifene analog was quantitatively estimated.Tamoxifen is about 5 times more effective than LY117018 at releasing arachidonic acid from all the cells tested. In rat liver cells only tamoxifen stimulates basal prostaglandin I2 production and that induced by lactacystin and 12-O-tetradecanoyl-phorbol-13-acetate. LY117018, however, blocks the tamoxifen stimulated prostaglandin production. The stimulated prostaglandin I2 production is rapid and not affected either by preincubation of the cells with actinomycin or by incubation with the estrogen antagonist ICI-182,780.Tamoxifen and the raloxifene analog, LY117018, may prevent estrogen-independent as well as estrogen-dependent breast cancer by stimulating phospholipase activity and initiating arachidonic acid release. The release of arachidonic acid and/or molecular reactions that accompany that release may initiate pathways that prevent tumor growth. Oxygenation of the intracellularly released arachidonic acid and its metabolic products may mediate some of the pharmacological actions of tamoxifen and raloxifene.The successful treatment and prevention of estrogen-dependent breast cancer in women by tamoxifen is attributed to its estrogen receptor (ER) occupancy [reviewed in [1,2]]. In the N-nitrosomethylurea (NMU) induced breast cancer model in rats, tumor growth is estrogen dependent and tamoxifen is considerably more effective than raloxifene [3]. In the dimethylbenzanthracene (DMBA)-induced model in rats, in which tumor growth is predominantly dependent on prolactin for growth, tamoxifen and raloxifene show effective anti-tumor action.Tamoxifen and raloxifene h
Statins stimulate arachidonic acid release and prostaglandin I2 production in rat liver cells
Lawrence Levine
Lipids in Health and Disease , 2003, DOI: 10.1186/1476-511x-2-1
Abstract: The statins, by inhibiting HMG-CoA reductase activity, reduce cholesterol and isoprenoid synthesis [1]. They are being used primarily in the prevention of atherosclerosis [2,3]. They have proven to be beneficial in preventing stroke [4] and may increase bone formation [5] and lower the risk of dementia [6]. Some of the benefits in patients with myocardial infarction are independent of cholesterol levels. Statins also inhibit cellular proliferation and induce apoptosis of tumor cells [7]. Essential fatty acids have several properties similar to the statins [8,9] and Das [10] has suggested that "essential fatty acids and their metabolites may serve as second messengers of the actions of statins."Statins affect prostaglandin (PG) production. Mevastatin or lovastatin, at 25 μM, induce PGI2 production and cyclooxygenase (COX)-2 in human aorta smooth muscle cells [11]. Mevalonate and geranylgeranyl-pyrophosphate block these stimulations implicating the cholesterol biosynthetic pathway in this up-regulation. However, fluvastatin down-regulates rather than up-regulates COX-2 expression in human umbilical vein endothelial cells [12] and lovastatin reduces PGI2 production in bovine endothelial cells, human skin fibroblasts and arterial smooth muscle cells [13].I observed that in rat liver cells, the statins stimulate the release of an essential fatty acid, arachidonic acid (AA) and stimulate production of its metabolite, PGI2. These stimulations are independent of HMG-CoA reductase activity as measured by the lack of any suppression by mevalonate.The release of AA from rat liver cells after 6 h incubation with mevastatin, lovastatin and simvastatin is shown in Fig. 1. An extract of the pharmaceutical product Lipitor? also significantly stimulates AA release (data not shown). The release of AA as a function of time in the presence of 50 μM lovastatin or simvastatin is shown in Fig. 2. Stimulation by lovastatin and simvastatin is observed after as little as 15 min incubation wi
Page 1 /1701
Display every page Item

Copyright © 2008-2017 Open Access Library. All rights reserved.