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Institution

University at Buffalo

EducationBuffalo, New York, United States
About: University at Buffalo is a education organization based out in Buffalo, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 33773 authors who have published 63840 publications receiving 2278954 citations. The organization is also known as: UB & State University of New York at Buffalo.


Papers
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Journal ArticleDOI
TL;DR: Biocompatible ferrofluid containing dye-functionalized magnetite nanoparticles that can serve as fluorescent markers enable optical tracking of basic processes at the cellular level combined with magnetophoretic manipulation and should be of substantial value to researchers engaged in both fundamental and applied biomedical research.
Abstract: A method is presented for the preparation of a biocompatible ferrofluid containing dye-functionalized magnetite nanoparticles that can serve as fluorescent markers. This method entails the surface functionalization of magnetite nanoparticles using citric acid to produce a stable aqueous dispersion and the subsequent binding of fluorescent dyes to the surface of the particles. Several ferrofluid samples were prepared and characterized using Fourier transform infrared spectroscopy (FTIR), X-ray photoelectron spectroscopy (XPS), thermogravimetric analysis (TGA), BET surface area analysis, transmission electron microscopy (TEM), and SQUID magnetometry. In addition, confocal fluorescence microscopy was used to study the response of the fluorescent nanoparticles to an applied magnetic field and their uptake by cells in vitro. Results are presented on the distribution of particle sizes, the fluorescent and magnetic properties of the nanoparticles, and the nature of their surface bonds. Biocompatible ferrofluids ...

396 citations

Book ChapterDOI
TL;DR: Their increased production seems to accompany most forms of tissue injury, and the formation of free radicals has been implicated in a multitude of disease states ranging from inflammatory/immune injury to myocardial infarction and cancer.
Abstract: The occurrence of reactive oxygen species (ROS), termed as prooxidants, is a characteristic of normal aerobic organisms. The term “reactive oxygen species” collectively denotes oxygen-centered radicals such as superoxide (O2·-)and hydroxyl (·OH), as well as nonradical species derived from oxygen, such as hydrogen peroxide (H2O2), singlet oxygen (1ΔgO2) and hypochlorous acid (HOC1). Radical reactions are central to the maintenance of homeostasis in biological systems. Radical species perform a cardinal role in many physiological processes such as cytochrome P450-mediated oxidative transformation reactions, a plethora of enzymic oxidation reactions, oxidative phosphorylation, regulation of the tone of smooth muscle, and killing of microorganisms.1–3 Excessive generation of free radicals can have deleterious biological consequences.4–6 Organisms are equipped with an armamentarium of defense systems, termed antioxidants in order to safeguard them against the onslaught of ROS.1–3,7 When the generation of prooxidants overwhelms the capacity of antioxidant defense systems oxidative stress ensues. This can cause tissue damage leading to pathophysiological events. ROS play a pivotal role in the action of numerous foreign compounds (xenobiotics). Their increased production seems to accompany most forms of tissue injury.4,5 Whether sustained and increased production of ROS is a primary event in human disease progression or a secondary consequence of tissue injury has been discussed.5,6 Whatever may be the case, the formation of free radicals has been implicated in a multitude of disease states ranging from inflammatory/immune injury to myocardial infarction and cancer.

396 citations

Journal ArticleDOI
TL;DR: These findings, together with other converging lines of evidence, suggest that deficient pallidal inhibition may be etiologically related to tic and movement disorders.

395 citations

Journal ArticleDOI
TL;DR: The purpose of this paper is to discuss statistical considerations associated with the evaluation of such early detection programmes, and to examine problems associated with screening programmes where an individual is examined periodically.
Abstract: SIUMMARY It is assumed that a chronic disease progresses from a pre-clinical state to a clinical state. If an individual, having pre-clinical disease, participates in an early detection programme, the disease may be detected in the pre-clinical state. The potential benefit of a screening programme is related to the lead time gained by early diagnosis. A stochastic model is developed for early detection programmes which leads to an estimate of the mean lead time as a function of observable variables. An investigation is also made of a non-progressive disease model in which individuals in a pre-clinical state may not necessarily advance to the clinical state. At the present time special diagnostic procedures are available for early detection of some chronic diseases. For example, chest X-rays have long been used to detect tuberculosis. Currently, there are many public health programmes to detect women having cancer of the uterine cervix by using Papanicolaou smears; other programmes designed to test for glaucoma and diabetes are in wide use. An especially interesting programme for early detection of breast cancer using soft tissue X-rays, mammography, is now being conducted by the Health Insurance Plan of Greater New York; see Shapiro, Strax & Venet (1967). The aim of all such programmes is to detect the disease earlier than it normally would be detected, the motivation being that earlier detection may result in a cure or better prognosis. Unfortunately, with only a few exceptions we know of no chronic disease in which unambiguous evidence has been coLlected showing that early detection has resulted in significantly improved prognosis. Even in cancer of the uterine cervix, the results are not without question, because the survival rate had been increasing before the widespread introduction of the Papanicolaou smear. It is the purpose of this paper to discuss statistical considerations associated with the evaluation of such early detection programmes. Attention is confined to screening programmes where an individual is examined only once. In a future paper, we shall examine problems associated with screening programmes where an individual is examined periodically. It will be assumed that a person having a particular chronic disease can be regarded as

394 citations

Journal ArticleDOI
TL;DR: It is postulate that oxidative stress in thermal‐stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes, decreased calcification, and the initiation of cell death via apoptosis and necrosis, the cellular foundation of thermal stress‐induced coral bleaching.
Abstract: The declining health of coral reefs worldwide is likely to intensify in response to continued anthropogenic disturbance from coastal development, pollution, and climate change. In response to these stresses, reef-building corals may exhibit bleaching, which marks the breakdown in symbiosis between coral and zooxanthellae. Mass coral bleaching due to elevated water temperature can devastate coral reefs on a large geographical scale. In order to understand the molecular and cellular basis of bleaching in corals, we have measured gene expression changes associated with thermal stress and bleaching using a complementary DNA microarray containing 1310 genes of the Caribbean coral Montastraea faveolata. In a first experiment, we identified differentially expressed genes by comparing experimentally bleached M. faveolata fragments to control non-heat-stressed fragments. In a second experiment, we identified differentially expressed genes during a time course experiment with four time points across 9 days. Results suggest that thermal stress and bleaching in M. faveolata affect the following processes: oxidative stress, Ca2+ homeostasis, cytoskeletal organization, cell death, calcification, metabolism, protein synthesis, heat shock protein activity, and transposon activity. These results represent the first medium-scale transcriptomic study focused on revealing the cellular foundation of thermal stress-induced coral bleaching. We postulate that oxidative stress in thermal-stressed corals causes a disruption of Ca2+ homeostasis, which in turn leads to cytoskeletal and cell adhesion changes,

394 citations


Authors

Showing all 34002 results

NameH-indexPapersCitations
Rakesh K. Jain2001467177727
Julie E. Buring186950132967
Anil K. Jain1831016192151
Donald G. Truhlar1651518157965
Roger A. Nicoll16539784121
Bruce L. Miller1631153115975
David R. Holmes1611624114187
Suvadeep Bose154960129071
Ashok Kumar1515654164086
Philip S. Yu1481914107374
Hugh A. Sampson14781676492
Aaron Dominguez1471968113224
Gregory R Snow1471704115677
J. S. Keller14498198249
C. Ronald Kahn14452579809
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202388
2022363
20212,772
20202,695
20192,527
20182,500