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Search Results: 1 - 10 of 211566 matches for " William N Rom "
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Role of Oxidants in Interstitial Lung Diseases: Pneumoconioses, Constrictive Bronchiolitis, and Chronic Tropical Pulmonary Eosinophilia
William N. Rom
Mediators of Inflammation , 2011, DOI: 10.1155/2011/407657
Abstract: Oxidants such as superoxide anion, hydrogen peroxide, and myeloperoxidase from activated inflammatory cells in the lower respiratory tract contribute to inflammation and injury. Etiologic agents include inorganic particulates such as asbestos, silica, or coal mine dust or mixtures of inorganic dust and combustion materials found in World Trade Center dust and smoke. These etiologic agents are phagocytosed by alveolar macrophages or bronchial epithelial cells and release chemotactic factors that recruit inflammatory cells to the lung. Chemotactic factors attract and activate neutrophils, eosinophils, mast cells, and lymphocytes and further activate macrophages to release more oxidants. Inorganic dusts target alveolar macrophages, World Trade Center dust targets bronchial epithelial cells, and eosinophils characterize tropical pulmonary eosinophilia (TPE) caused by filarial organisms. The technique of bronchoalveolar lavage in humans has recovered alveolar macrophages (AMs) in dust diseases and eosinophils in TPE that release increased amounts of oxidants in vitro. Interestingly, TPE has massively increased eosinophils in the acute form and after treatment can still have ongoing eosinophilic inflammation. A course of prednisone for one week can reduce the oxidant burden and attendant inflammation and may be a strategy to prevent chronic TPE and interstitial lung disease. 1. Introduction Gaseous and particulate air pollutants activate inflammatory cells to release oxidants such as superoxide anion, hydrogen peroxide, and hydroxyl radicals [1]. Oxidants damage proteins, lipids, DNA forming nitrotyrosine, 4-OH-2-nonenal, and 8-OHdeoxyguanosine, and single strand breaks [2]. Oxidants from macrophages and bronchial epithelial cells cause inflammation leading to injury and fibrosis [3]. These events are particularly important to the upper airways leading to asthma and constrictive bronchiolitis and to the lower respiratory tract where exogenous oxidants can activate macrophages to release endogenous oxidants, attract other inflammatory cells, and injure the delicate walls of the peripheral respiratory bronchioles and alveolar sacs [4]. The respiratory tract is a target organ for cigarette smoke, inorganic dusts (asbestos, silica, and coal), PM2.5, and World Trade Center dust contributing to asthma, COPD, fibrosis, and constrictive bronchiolitis [5]. Oxidants in the lung can be from endogenous sources since air pollutants activate neutrophils, alveolar macrophages, eosinophils, and epithelial cells. Antioxidants include superoxide dismutase and glutathione
Preneoplastic lesions of the lung
Alissa K Greenberg, Herman Yee, William N Rom
Respiratory Research , 2002, DOI: 10.1186/rr170
Abstract: Lung cancer is the leading cause of cancer deaths worldwide [1] and the number of cases continues to increase. Smoking is the primary cause in the great majority of these cases. In Asia, particularly China, smoking rates continue to increase. Despite advances in therapy, the overall survival rate for lung cancer patients remains only 15%. This poor survival is probably due to the relatively advanced stage of disease at diagnosis. To date, screening trials have had no significant impact on survival [2]. Screening can detect small (2–3 mm in size), asymptomatic nodules, but even these nodules may already be malignant, and therefore late in the course of the disease. Tumor cells have been found in the peripheral blood and bone marrow of patients with lung cancer of all sizes and stages [3,4].If lung cancer could be identified earlier – at a preneoplastic stage, before angiogenesis, invasion and micrometastases can occur – we might have a greater chance of improving survival. At this point, we have little information about possible progenitor lesions. Which lesions are preneoplastic? How and why do they progress? Is there any treatment that can prevent progression? Advances in molecular biology and microdissection techniques, and greater understanding of genetic changes involved in malignant transformation will aid in answering some of these questions. Advances in computerized tomography (CT), bronchoscopy and genomics technology raise the possibility that we may be able to detect these early lesions in vivo. Therefore, if preneoplastic lesions can be defined, and if appropriate therapies can be found, screening may then significantly improve survival.To define preneoplastic lesions, we need to understand the molecular events that occur during bronchogenic carcinogenesis. Carcinogenesis is thought to be a multistep process consisting of the accumulation of gene mutations. Preneoplastic lesions may be morphological phenotypes of the different steps in this progression fr
Redefinition of the Terminus of the Middle America Trench  [PDF]
Román Alvarez
International Journal of Geosciences (IJG) , 2013, DOI: 10.4236/ijg.2013.44070
Abstract:

The terminus of the Middle America Trench has been traditionally represented as an arc, concave towards the continent. Tres Marías Islands are located at the terminus of the Middle America Trench in western Mexico, and their location is not only intriguing but also a key to the re-construction of the position of Baja California peninsula before separation from the North America plate. Previous re-constructions suggested various places around the location of Tres Marías Islands for the position of the tip of the peninsula, and several converge to a position that invades the area occupied by the islands, offering no explanation for the overlap. Before peninsular separation from North America, the Guadalupe trench followed a smooth curve; recreating the position of this paleo-trench yields a baseline for fixing the position of the peninsula, as well as the original position of the Tres Marías Islands fragment. A new tectonic view of the structure of the Middle America Trench terminus is proposed, replacing the traditional arc representation with a series of en echelon blocks, the northernmost terminates at the Tres Marías Escarpment. The long sides of the blocks correspond to previously identified geological faults in the Bahía de Banderas region, while their offshore continuation is supported by topographic observations. As a test of this model I show the corresponding re-construction of the position of Baja California prior to separation from the North America plate and the positional evolution of the peninsula and the Tres Marías fragment from Chron 4n.2 (7.90 Ma) to Chron 3n.4 (5.12 Ma).

NF-kappaB in Lung Tumorigenesis
Zhenjian Cai,Kam-Meng Tchou-Wong,William N. Rom
Cancers , 2011, DOI: 10.3390/cancers3044258
Abstract: The development of lung cancer in humans can be divided into three steps: initiation, promotion and progression. This process is driven by alterations in related signal transduction pathways. These pathways signal the aberrant activation of NF-kappaB, a transcription factor that regulates the expression of genes important for lung tumorigenesis. Our current knowledge about the role of the NF-kappaB signaling pathway in the development of lung cancer has been bolstered by animal models demonstrating the connection between K-ras and tobacco induced lung transformation with NF-kappaB. Activation of downstream genes leads to cell proliferation, inhibition of apoptosis, angiogenesis, inflammation, invasion, and metastasis.
Sputum-Based Molecular Biomarkers for the Early Detection of Lung Cancer: Limitations and Promise
Connie E. Kim,Kam-Meng Tchou-Wong,William N. Rom
Cancers , 2011, DOI: 10.3390/cancers3032975
Abstract: Lung cancer is the leading cause of cancer deaths, with an overall survival of 15% at five years. Biomarkers that can sensitively and specifically detect lung cancer at early stage are crucial for improving this poor survival rate. Sputum has been the target for the discovery of non-invasive biomarkers for lung cancer because it contains airway epithelial cells, and molecular alterations identified in sputum are most likely to reflect tumor-associated changes or field cancerization caused by smoking in the lung. Sputum-based molecular biomarkers include morphology, allelic imbalance, promoter hypermethylation, gene mutations and, recently, differential miRNA expression. To improve the sensitivity and reproducibility of sputum-based biomarkers, we recommend standardization of processing protocols, bronchial epithelial cell enrichment, and identification of field cancerization biomarkers.
Southward Migration of Magmatic Activity in the Colima Volcanic Complex, Mexico: An Ongoing Process  [PDF]
Román Alvarez, Vsevolod Yutsis
International Journal of Geosciences (IJG) , 2015, DOI: 10.4236/ijg.2015.69085
Abstract: The Colima Volcanic Complex trends in a nearly N-S direction in western Mexico, and one of itsstructures, Colima volcano, is the most historically active volcano in the country. Immediately to theN, there is another volcanic center called El Cántaro volcano, whose activity started around 1.7 Ma in its N portion and migrated to the S in various episodes. Volcanic activity migrated further south, from El Cántaro to the Colima Volcanic Complex where the southernmost manifestation, Hijos del Volcán domes, is located on the south slope of Fuego volcano. The above date appears to mark initiation of the rather continuous volcanic activity in the area. It has been noted that these volcanic manifestations lie on, or near the Rivera-Cocos inland plate boundary. Colima’s Fuego volcano is also the closest to the Middle America Trench, among the polygenetic volcanoes in Mexico. We submit that the anomalous location of volcanism in this area originates in an anomalous subduction process of the Rivera and Cocos plates and evoke a tectonic model, proposed elsewhere, to support the idea. Modeling gravimetric and aeromagnetic data we locate the magma chambers of the Fuego (active) and Nevado (extinct) volcanoes within a 65 mGals negative Bouguer anomaly elongated in a nearly N-S direction. The corresponding aeromagnetic map displays a magnetic high over the southern portion of the Fuego volcano edifice. We found two additional, associated structures whose anomalies have not been previously reported, which appear to follow the southward magmatic migration pattern. One of them is a collapse structure with a circular topographic expression, and the southernmost is a low-density intrusion ~1 km below sea level, associated with a moderate topographic bulge at the surface that we interpret as a magma body. Five lines cross the anomalies; gravimetric and magnetic fields are concurrently modeled along them to locate the magmatic bodies. In addition to the 2-D models we perform 3-D gravimetric and magnetic inversions. For each field a 3-D mesh is built under the area occupied by the Colima Volcanic Complex, the volume elements are then assigned density or magnetic susceptibility values and their surface contributions in various points are evaluated. The process is
Multiple strand displacement amplification of mitochondrial DNA from clinical samples
Samantha Maragh, John P Jakupciak, Paul D Wagner, William N Rom, David Sidransky, Sudhir Srivastava, Catherine D O'Connell
BMC Medical Genetics , 2008, DOI: 10.1186/1471-2350-9-7
Abstract: DNA was isolated from clinical samples and sent to NIST. Samples were amplified by PCR and those with no visible amplification were re-amplified using the Multiple Displacement Amplificaiton technique of whole genome amplification. All samples were analyzed by mitochip for mitochondrial DNA sequence to compare sequence concordance of the WGA samples with respect to native DNA. Real-Time PCR analysis was conducted to determine the level of WGA amplification for both nuclear and mtDNA.In total, 19 samples were compared and the concordance rate between WGA and native mtDNA sequences was 99.995%. All of the cancer associated mutations in the native mtDNA were detected in the WGA amplified material and heteroplasmies in the native mtDNA were detected with high fidelity in the WGA material. In addition to the native mtDNA sequence present in the sample, 13 new heteroplasmies were detected in the WGA material.Genetic screening of mtDNA amplified by WGA is applicable for the detection of cancer associated mutations. Our results show the feasibility of this method for: 1) increasing the amount of DNA available for analysis, 2) recovering the identical mtDNA sequence, 3) accurately detecting mtDNA point mutations associated with cancer.It is often the case that an insufficient quantity of DNA can be isolated from clinical specimens and controls for full genome analysis. The quantity of DNA is particularly limited in patient tumor specimens, most notably in early tumors with limited mass and therefore, insufficient DNA may be available to perform the multiple analyses required for full genome screening [1-4]. Whole genome amplification (WGA) methods have been developed to solve the problem of insufficient quantities of DNA [5,6]. Using these technologies, investigators have been successful in applying genome scanning technologies to patient cohort samples collected years ago that are not recoverable by other means [7]. WGA is useful for amplification of DNA from stored histolo
Pedigree Analysis in Criollo Limonero
Villasmil-Ontiveros,Yenen; Aranguren-Méndez,José; Román,Rafael; Isea,William; Contreras,Gloria; Zambrano,Sunny; Jordana,Jordi;
Revista Científica , 2008,
Abstract: in order to continue the genetic program for the conservation of the criollo limonero population, a study was carried out to evaluate the genetic variability of this local breed. for this purpose, 2552 genealogical records from the criollo herd at the carrasquero local station (inia) located at playa bonita, mara county, north of zulia state-venezuela, during the 1985-2003 period were used. global inbreeding of the herd (fh) and animal inbreeding were determined; in addition, average of relatedness (ar), probabilities of gene origin, number of founders (nf), effective number of founders (fe), effective ancestors number (fa), genome founders number (ng ) and number of founders explaining 50% (f50) of the genetic variability. for the year 2003 fh was 0.35%, whereas ar, nf, fe, fa, ng and f50 were 3.4%, 386, 63.5, 38, 27.71 and 18 respectively. even though ar showed a high relationship among the individuals in the herd, fh did not have a significant increase. for this reason, mates should be planned carefully in order to avoid related mates. probabilities of gene origin suggest that genetic variation has decreased in this population due to a bottleneck effect and genetic drift, without increasing inbreeding. an important genetic diversity exists in this population which should be preserved, given the importance of this genetic resource for the region and the country.
Aspectos clínico epidemiológicos del síndrome coronario agudo: Hospital "Abel Santamaría Cuadrado", 2006-2007
Cruz Ledesma,Bernardo; Delgado Rodríguez,Ariel E; Pastrana Román,Irene C; Brown Sotolongo,Carlos; Quintero Pérez,William;
Revista de Ciencias M??dicas de Pinar del R?-o , 2009,
Abstract: a prospective, longitudinal and descriptive study was carried out aimed at characterizing the clinical-epidemiological aspects of the acute coronary syndrome at "abel santamaria" university hospital, pinar del rio during july 1st 2006 to june 30th 2007. the universe of the study was constituted by 1 784 patients admitted at the intensive coronary care unit and the sample included 300 diagnosed with coronary acute syndrome. data were collected from the clinical records of the patients and the following variables were analyzed: age, sex, race, interval of time between the onset of the pain and admission in the emergency unit, type of the acute coronary event and complications. epi info-6 was used as a statistical package to the control of data and statistical analysis. the informed consent was requested to the patients. the disease prevailed in caucasian, 60 years old or older men. being acute unstable angina with electrocardiographic changes was the coronary syndrome mostly diagnosed, followed by acute myocardial infarction. most of the patients attended to the hospital before the 6 hours of the onset of the precordial pain. the heart failure, malignant ventricular arrhythmias and the atrioventricular block were the most frequent complications and the ones provoking a greater mortality rate.
Chemoprevention of Lung Cancer: Prospects and Disappointments in Human Clinical Trials
Alissa K. Greenberg,Jun-Chieh Tsay,Kam-Meng Tchou-Wong,Anna Jorgensen,William N. Rom
Cancers , 2013, DOI: 10.3390/cancers5010131
Abstract: Decreasing the risk of lung cancer, or preventing its development in high-risk individuals, would have a huge impact on public health. The most effective means to decrease lung cancer incidence is to eliminate exposure to carcinogens. However, with recent advances in the understanding of pulmonary carcinogenesis and the identification of intermediate biomarkers, the prospects for the field of chemoprevention research have improved dramatically. Here we review the most recent research in lung cancer chemoprevention—focusing on those agents that have been investigated in human clinical trials. These agents fall into three major categories. First, oxidative stress plays an important role in pulmonary carcinogenesis; and therefore, antioxidants (including vitamins, selenium, green tea extracts, and isothiocyanates) may be particularly effective in preventing the development of lung cancer. Second, inflammation is increasingly accepted as a crucial factor in carcinogenesis, and many investigators have focused on anti-inflammatory agents, such as glucocorticoids, NSAIDs, statins, and PPARγ agonists. Finally, the PI3K/AKT/mTOR pathway is recognized to play a central role in tobacco-induced carcinogenesis, and inhibitors of this pathway, including myoinositol and metformin, are promising agents for lung cancer prevention. Successful chemoprevention will likely require targeting of multiple pathways to carcinogenesis—both to minimize toxicity and maximize efficacy.
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