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Search Results: 1 - 10 of 477414 matches for " Richard A. Levine "
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Comment: On Random Scan Gibbs Samplers
Richard A. Levine,George Casella
Statistics , 2008, DOI: 10.1214/08-STS252B
Abstract: Comment on ``On Random Scan Gibbs Samplers'' [arXiv:0808.3852]
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.
Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity
Fouad Lemtiri-Chlieh, Liangfang Zhao, Drew D Kiraly, Betty A Eipper, Richard E Mains, Eric S Levine
BMC Neuroscience , 2011, DOI: 10.1186/1471-2202-12-126
Abstract: We have performed a detailed electrophysiological characterization of the role of Kal7 in hippocampal synaptic plasticity. We show that loss of Kal7 results in impaired NMDA receptor-dependent LTP and long-term depression, whereas a NMDA receptor-independent form of LTP is shown to be normal in the absence of Kal7.These results indicate that Kal7 is an essential and selective modulator of NMDA receptor-dependent synaptic plasticity in the hippocampus.Dendritic spines are the locus of the majority of excitatory synapses on hippocampal and cortical pyramidal neurons. An abundance of research in the field of synaptic plasticity has demonstrated that dendritic spines display morphological plasticity in response to a myriad of extracellular stimuli [1,2]. These changes are thought to be cellular correlates of the plasticity seen in learning and memory [3]. Importantly, spines have repeatedly been shown to increase in both size and number following the induction of long-term potentiation (LTP) [4-7] and to decrease in size and number following induction of long-term depression (LTD) [8,9]. The ability of dendritic spines to remain labile/plastic is dependent on rearrangement of the actin cytoskeleton which forms the core of each spine [10-12]. This process is dependent on the activity of Rho-GTPases, which are activated by Rho-guanine nucleotide exchange factors (Rho-GEFs) [13]. About a dozen of the 58 Rho-GEFs encoded by the mouse genome are localized to the postsynaptic density (PSD) [14].Among the PSD-localized Rho-GEFs is Kalirin-7 (Kal7), the predominant adult splice variant of the multiply spliced Kalrn gene [15,16]. Kal7 has been repeatedly shown to have a profound effect on dendritic spine density in vitro, with over-expression dramatically increasing spine density and knockdown decreasing spine density [17,18]. More recently, we developed a mouse that cannot produce Kal7 (Kal7KO) and demonstrated that this mouse had decreased hippocampal spine density at baseline
Activated Membrane Patches Guide Chemotactic Cell Motility
Inbal Hecht ,Monica L. Skoge,Pascale G. Charest,Eshel Ben-Jacob,Richard A. Firtel,William F. Loomis,Herbert Levine,Wouter-Jan Rappel
PLOS Computational Biology , 2011, DOI: 10.1371/journal.pcbi.1002044
Abstract: Many eukaryotic cells are able to crawl on surfaces and guide their motility based on environmental cues. These cues are interpreted by signaling systems which couple to cell mechanics; indeed membrane protrusions in crawling cells are often accompanied by activated membrane patches, which are localized areas of increased concentration of one or more signaling components. To determine how these patches are related to cell motion, we examine the spatial localization of RasGTP in chemotaxing Dictyostelium discoideum cells under conditions where the vertical extent of the cell was restricted. Quantitative analyses of the data reveal a high degree of spatial correlation between patches of activated Ras and membrane protrusions. Based on these findings, we formulate a model for amoeboid cell motion that consists of two coupled modules. The first module utilizes a recently developed two-component reaction diffusion model that generates transient and localized areas of elevated concentration of one of the components along the membrane. The activated patches determine the location of membrane protrusions (and overall cell motion) that are computed in the second module, which also takes into account the cortical tension and the availability of protrusion resources. We show that our model is able to produce realistic amoeboid-like motion and that our numerical results are consistent with experimentally observed pseudopod dynamics. Specifically, we show that the commonly observed splitting of pseudopods can result directly from the dynamics of the signaling patches.
Arrhythmia Diagnosis Following an ICD Shock: Comment
Pual A. Levine
Indian Pacing and Electrophysiology Journal , 2002,
Abstract: This case study by Dr. John1 demonstrates the care that one must take in programming an implantable cardioverter defibrillator, the complexity of these patients and the utility of the internal diagnostics in the system to facilitate the physician's understanding of device behavior. Even the single chamber ICDs have SVT discrimination algorithms that can be enabled in an effort to differentiate SVT from VT allowing the device to withhold ATP and shock therapy in the setting of an SVT. Many physicians, myself included, will initially utilize these discriminators in a monitoring mode preferring to deliver unnecessary therapy rather than inappropriately withholding needed therapy. This also provides an opportunity to better understand all the rhythms that may be occurring in a patient, many of which may not have been appreciated prior to the implant. After one or more SVT episodes have occurred and the clinician has a chance to review the stored electrograms (first introduced by Ventritex) along with the response of the device to any discriminators, a decision can be made as to how the ICD prescription might be adjusted. My examination of the stored electrogram documenting the initial atrial fibrillation episode suggests significant irregularity of the ventricular response. As such, had the stability criteria been enabled, it is likely that the system would have appropriately recognized the rhythm as atrial fibrillation and withheld therapy. If the stability criteria had been programmed to the monitoring mode, the retrieved information would have indicated that the diagnosis was supraventricular but therapy was delivered because the discriminator was not active. A further refinement in single chamber and more recent dual chamber ICDs is a feature called morphology discrimination. This would allow the device to separate a rapid irregular ventricular response falling within the VT rate zone associated with atrial fibrillation from polymorphic ventricular tachycardia. Given the complexity of these patients, if atrial fibrillation was hemodynamically compromising, it might be appropriate to not enable any discrimination algorithms. Dr. John indicates that amiodarone was not tolerated and other drugs have both a higher incidence of side effects and lower efficacy rate. If the episodes of atrial fibrillation were not frequent, another option would be to allow the AF to trigger ATP therapy which was arrhythmogenic but then take advantage of the subsequent shock to not only terminated the induced-VT but also terminate the atrial fibrillation as occurred in this cas
Management of the Patient with an Acute Massive Rise in the Capture Threshold.
Paul A. Levine
Indian Pacing and Electrophysiology Journal , 2001,
Abstract: Since the introduction of steroid eluting electrodes, the incidence of an early massive rise in the capture threshold that either exceeds or threatens to exceed the programmed output of the pacemaker has declined but has not totally disappeared1 If a persistent or massive threshold rise is encountered in the days to months post-implant, one consideration is microinstability of the lead. In this setting, there may be a change in the morphology of the pacemaker evoked depolarization on the ECG or a change in the physical location of the lead as assessed with a chest x-ray. Another marker is fluctuations in the capture threshold on repeated assessments at the same office or clinic visit. The options for this problem include an operative procedure to reposition or replace the lead or to closely observe the patient hoping that the lead settles into a secure location. Another potential totally reversible cause is the introduction of an new medication or herb. If the possible explanations for threshold increase cited above have been excluded and the high capture threshold is believed to be due to lead maturation, increasing the output or possible lead replacement or repositioning have been the usual options.
Genetic Analysis of the Early Natural History of Epithelial Ovarian Carcinoma
Bhavana Pothuri,Mario M. Leitao,Douglas A. Levine,Agnès Viale,Adam B. Olshen,Crispinita Arroyo,Faina Bogomolniy,Narciso Olvera,Oscar Lin,Robert A. Soslow,Mark E. Robson,Kenneth Offit,Richard R. Barakat,Jeff Boyd
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010358
Abstract: The high mortality rate associated with epithelial ovarian carcinoma (EOC) reflects diagnosis commonly at an advanced stage, but improved early detection is hindered by uncertainty as to the histologic origin and early natural history of this malignancy.
Allelic Variation on Murine Chromosome 11 Modifies Host Inflammatory Responses and Resistance to Bacillus anthracis
Jill K. Terra,Bryan France,Christopher K. Cote,Amy Jenkins,Joel A. Bozue,Susan L. Welkos,Ragini Bhargava,Chi-Lee Ho,Margarete Mehrabian,Calvin Pan,Aldons J. Lusis,Richard C. Davis,Steven M. LeVine,Kenneth A. Bradley
PLOS Pathogens , 2011, DOI: 10.1371/journal.ppat.1002469
Abstract: Anthrax is a potentially fatal disease resulting from infection with Bacillus anthracis. The outcome of infection is influenced by pathogen-encoded virulence factors such as lethal toxin (LT), as well as by genetic variation within the host. To identify host genes controlling susceptibility to anthrax, a library of congenic mice consisting of strains with homozygous chromosomal segments from the LT-responsive CAST/Ei strain introgressed on a LT-resistant C57BL/6 (B6) background was screened for response to LT. Three congenic strains containing CAST/Ei regions of chromosome 11 were identified that displayed a rapid inflammatory response to LT similar to, but more severe than that driven by a LT-responsive allele of the inflammasome constituent NRLP1B. Importantly, increased response to LT in congenic mice correlated with greater resistance to infection by the Sterne strain of B. anthracis. The genomic region controlling the inflammatory response to LT was mapped to 66.36–74.67 Mb on chromosome 11, a region that encodes the LT-responsive CAST/Ei allele of Nlrp1b. However, known downstream effects of NLRP1B activation, including macrophage pyroptosis, cytokine release, and leukocyte infiltration could not fully explain the response to LT or the resistance to B. anthracis Sterne in congenic mice. Further, the exacerbated response in congenic mice is inherited in a recessive manner while the Nlrp1b-mediated response to LT is dominant. Finally, congenic mice displayed increased responsiveness in a model of sepsis compared with B6 mice. In total, these data suggest that allelic variation of one or more chromosome 11 genes in addition to Nlrp1b controls the severity of host response to multiple inflammatory stimuli and contributes to resistance to B. anthracis Sterne. Expression quantitative trait locus analysis revealed 25 genes within this region as high priority candidates for contributing to the host response to LT.
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