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Search Results: 1 - 10 of 226152 matches for " James L. Kreindler "
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On Preventing the Extinction of the Physician-Scientist in Pediatric Pulmonology
Ronald C. Rubenstein,James L. Kreindler
Frontiers in Pediatrics , 2014, DOI: 10.3389/fped.2014.00004
Abstract: While the founders of Pediatric Pulmonology recognized the necessity of research as a vital part of the developing sub specialty, the field has struggled to develop and maintain physician-scientists and investigators. The clinical growth in Pediatric Pulmonology has resulted in significant challenges in career development faced by physician-scientists who aim to establish or maintain independent investigative programs. Such challenges may only be overcome with changes in how both trainees and established physician-scientists in Pediatric Pulmonology are supported.
Ectopic Cdx2 Expression in Murine Esophagus Models an Intermediate Stage in the Emergence of Barrett's Esophagus
Jianping Kong,Mary Ann Crissey,Shinsuke Funakoshi,James L. Kreindler,John P. Lynch
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018280
Abstract: Barrett's esophagus (BE) is an intestinal metaplasia that occurs in the setting of chronic acid and bile reflux and is associated with a risk for adenocarcinoma. Expression of intestine-specific transcription factors in the esophagus likely contributes to metaplasia development. Our objective was to explore the effects of an intestine-specific transcription factor when expressed in the mouse esophageal epithelium. Transgenic mice were derived in which the transcription factor Cdx2 is expressed in squamous epithelium using the murine Keratin-14 gene promoter. Effects of the transgene upon cell proliferation and differentiation, gene expression, and barrier integrity were explored. K14-Cdx2 mice express the Cdx2 transgene in esophageal squamous tissues. Cdx2 expression was associated with reduced basal epithelial cell proliferation and altered cell morphology. Ultrastructurally two changes were noted. Cdx2 expression was associated with dilated space between the basal cells and diminished cell-cell adhesion caused by reduced Desmocollin-3 mRNA and protein expression. This compromised epithelial barrier function, as the measured trans-epithelial electrical resistance (TEER) of the K14-Cdx2 epithelium was significantly reduced compared to controls (1189 Ohm*cm2 ±343.5 to 508 Ohm*cm2±92.48, p = 0.0532). Secondly, basal cells with features of a transitional cell type, intermediate between keratinocytes and columnar Barrett's epithelial cells, were observed. These cells had reduced keratin bundles and increased endoplasmic reticulum levels, suggesting the adoption of secretory-cell features. Moreover, at the ultrastructural level they resembled “Distinctive” cells associated with multilayered epithelium. Treatment of the K14-Cdx2 mice with 5′-Azacytidine elicited expression of BE-associated genes including Cdx1, Krt18, and Slc26a3/Dra, suggesting the phenotype could be advanced under certain conditions. We conclude that ectopic Cdx2 expression in keratinocytes alters cell proliferation, barrier function, and differentiation. These altered cells represent a transitional cell type between normal squamous and columnar BE cells. The K14-Cdx2 mice represent a useful model to study progression from squamous epithelium to BE.
Secondhand smoke inhibits both Cl- and K+ conductances in normal human bronchial epithelial cells
Amy N Savitski, Clementina Mesaros, Ian A Blair, Noam A Cohen, James L Kreindler
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-120
Abstract: Tobacco use is a worldwide epidemic accounting for 3% of the world's morbidity and mortality at a cost of tens of billions of U.S. dollars annually [1]. Even in the United States of America, where smoking rates have declined over the last 4 decades, the prevalence of smoking among adults and teenagers remains approximately 22-24%, meaning that more than 66,000,000 people smoke regularly [1,2]. The wide prevalence of smoking means that many children and adults are exposed to SHS. A recent study released by the Social Climate Survey of Tobacco from the Mississippi State University http://socialclimate.org/ webcite suggested that more than 40% of American children are exposed to secondhand smoke (SHS). This exposure is a significant risk factor for respiratory diseases, including lower airways infections, chronic rhinosinusitis, middle ear infection, and asthma in adults [3], as well as asthma and more severe respiratory syncytial virus (RSV) infection in children [4,5]. These diseases, while clearly multifactorial, all share a component of impaired mucociliary clearance (MCC) and mucus retention.Maintenance of normal MCC in the respiratory tract depends on salt and water transport by respiratory epithelial cells. MCC is disrupted when epithelial salt and water transport is abnormal, as in cystic fibrosis (CF). Previous studies from our and others' laboratories demonstrated that components of cigarette smoke inhibited chloride (Cl-) secretion in polarized epithelia [6-8]. Mainstream cigarette smoke inhibited both CFTR expression and function both in vitro in immortalized cell lines and in vivo where nasal potential difference measurements were consistent with inhibition of Cl- transport similar to that seen in cystic fibrosis [9]. These findings led us to hypothesize that SHS may have similar effects on epithelial Cl- transport.To test this hypothesis, we designed a system for in vitro exposure of mature, well-differentiated human bronchial epithelial cells (HBECs) to
Tobacco Smoke Mediated Induction of Sinonasal Microbial Biofilms
Natalia Goldstein-Daruech,Emily K. Cope,Ke-Qing Zhao,Katarina Vukovic,Jennifer M. Kofonow,Laurel Doghramji,Bernardo González,Alexander G. Chiu,David W. Kennedy,James N. Palmer,Jeffery G. Leid,James L. Kreindler,Noam A. Cohen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015700
Abstract: Cigarette smokers and those exposed to second hand smoke are more susceptible to life threatening infection than non-smokers. While much is known about the devastating effect tobacco exposure has on the human body, less is known about the effect of tobacco smoke on the commensal and commonly found pathogenic bacteria of the human respiratory tract, or human respiratory tract microbiome. Chronic rhinosinusitis (CRS) is a common medical complaint, affecting 16% of the US population with an estimated aggregated cost of $6 billion annually. Epidemiologic studies demonstrate a correlation between tobacco smoke exposure and rhinosinusitis. Although a common cause of CRS has not been defined, bacterial presence within the nasal and paranasal sinuses is assumed to be contributory. Here we demonstrate that repetitive tobacco smoke exposure induces biofilm formation in a diverse set of bacteria isolated from the sinonasal cavities of patients with CRS. Additionally, bacteria isolated from patients with tobacco smoke exposure demonstrate robust in vitro biofilm formation when challenged with tobacco smoke compared to those isolated from smoke na?ve patients. Lastly, bacteria from smoke exposed patients can revert to a non-biofilm phenotype when grown in the absence of tobacco smoke. These observations support the hypothesis that tobacco exposure induces sinonasal biofilm formation, thereby contributing to the conversion of a transient and medically treatable infection to a persistent and therapeutically recalcitrant condition.
IL-17RA Is Required for CCL2 Expression, Macrophage Recruitment, and Emphysema in Response to Cigarette Smoke
Kong Chen, Derek A. Pociask, Jeremy P. McAleer, Yvonne R. Chan, John F. Alcorn, James L. Kreindler, Matthew R. Keyser, Steven D. Shapiro, A. McGarry Houghton, Jay K. Kolls, Mingquan Zheng
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0020333
Abstract: Chronic Obstructive Pulmonary Disease (COPD) is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and in vivo Th17, but not Th1, cell differentiation via the aryl hydrocarbon receptor. Smoke exposed IL-17RA?/? mice failed to induce CCL2 and MMP12 compared to WT mice. Remarkably, in contrast to WT mice, IL-17RA?/? mice failed to develop emphysema after 6 months of cigarette smoke exposure. Taken together, these data demonstrate that cigarette smoke is a potent Th17 adjuvant and that IL-17RA signaling is required for chemokine expression necessary for MMP12 induction and tissue emphysema.
Design of a Solar Tracker System for PV Power Plants
Tiberiu Tudorache,Liviu Kreindler
Acta Polytechnica Hungarica , 2010,
Abstract: This paper deals with the design and execution of a solar tracker systemdedicated to the PV conversion panels. The proposed single axis solar tracker deviceensures the optimization of the conversion of solar energy into electricity by properlyorienting the PV panel in accordance with the real position of the sun. The operation of theexperimental model of the device is based on a DC motor intelligently controlled by adedicated drive unit that moves a mini PV panel according to the signals received from twosimple but efficient light sensors. The performance and characteristics of the solar trackerare experimentally analyzed.
The Discrete Agglomeration Model: Equivalent Problems  [PDF]
James L. Moseley
Applied Mathematics (AM) , 2012, DOI: 10.4236/am.2012.311236
Abstract: In this paper we develop equivalent problems for the Discrete Agglomeration Model in the continuous context.
Mood assessment via animated characters: An instrument to access and evaluate emotions in young children  [PDF]
Katharina Manassis, Sandra Mendlowitz, Annie Dupuis, David Kreindler, Charles Lumsden, Suneeta Monga, Carly Guberman
Open Journal of Psychiatry (OJPsych) , 2013, DOI: 10.4236/ojpsych.2013.31A010
Abstract: Objective: Mood Assessment via Animated Characters (MAAC) is a novel, computer-based instrument to improve assessment and communication about feelings in young children with internalizing distress. Well-validated assessment instruments are lacking for those under age eight years. Method: Children ages 4 - 10 years with primary diagnosis of anxiety disorder (n = 74; 33 boys, 41 girls) or no diagnosis (n = 83; 40 boys, 43 girls) completed MAAC for 16 feelings. Those 8 - 10 years also completed standardized measures of internalizing symptoms. Results: MAAC’s emotions clustered into positive, negative, fearful, and calm/neutral factors. Clinical children rated themselves less positive (difference score -3.18; p = 0.002) and less calm/neutral (difference score -2.06; p = 0.04), and explored fewer emotions spontaneously (difference score = -2.37; p = 0.02) than nonanxious controls. Older children’s responses correlated with scores on several standardized measures. Conclusions: MAAC appears to be highly engaging, with clinical utility in the assessment of young anxious children. Applications in other populations are considered for future study.
Comparison On Sensorless Control Of Synchronous Motors
Annals of Dunarea de Jos , 2002,
Abstract: The paper compares two different methods for speed and position estimation in AC permanent magnet synchronous motors vector control applications. The first method implies two observer blocks — one for the speed, and the other for the electrical position, using the voltage equations in the (d,q) reference frames. The second method estimates the same variables starting from the calculation of instantaneous reactive power. The tests have proved excellent behaviour in steady state (method 1) as well as in transient state (method 2). The implementation has been made on the 16 bits fixed-point DSP - TMS320F240 from Texas Instruments.
Uptake of Cystatin by Melanoma Cells in Culture  [PDF]
Lauren Deady, James L. Cox
CellBio (CellBio) , 2013, DOI: 10.4236/cellbio.2013.22008

The cystatins are a super family of cysteine protease inhibitors which are ubiquitous in their biologic occurrence. Cystatin C, a type II cystatin, is primarily a secreted protein found in most biological fluids. Besides acting as inhibitors of cathepsin, the cystatins have been found to have some non-inhibitor related functions and multiple physiological roles. Much interest has been generated for the cystatins as metastasissuppressor-like proteins, as they have been shown to inhibit metastasis for multiple cancer types. The sites and actions of the cystatins related to tumor suppressor actions are still unclear, however. In this work, we have examined the uptake of cystatin by metastatic melanoma cells in culture. Our results indicate cystatin uptake is mediated by a non-canonical endocytotic pathway in B16 murine melanoma cells.

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