Search Results - (Author, Cooperation:I. Cohen)

2018-02-09

American Physical Society (APS)

0031-9007

1079-7114

Physics

Nuclear Physics

2018-01-12

American Heart Association (AHA)

1942-325X

1942-3268

Medicine

Arrhythmias, Sudden Cardiac Death, Genetic, Association Studies, Genetics

2018-07-19

American Association for the Advancement of Science (AAAS)

2375-2548

Natural Sciences in General

2018-09-25

American Physical Society (APS)

1050-2947

1094-1622

Physics

Quantum information

2011-09-03

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

2011-10-01

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

2013-07-13

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

CD8-Positive T-Lymphocytes/*immunology ; Cation Transport Proteins/genetics/metabolism ; *Cytotoxicity, Immunologic ; Epstein-Barr Virus Infections/*immunology ; Humans ; Killer Cells, Natural/*immunology ; Magnesium/*immunology ; Magnesium Deficiency/*immunology ; NK Cell Lectin-Like Receptor Subfamily K/genetics/*metabolism ; X-Linked Combined Immunodeficiency Diseases/immunology

2014-08-12

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

2011-07-29

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Calcium/immunology ; Cation Transport Proteins/genetics ; Female ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Magnesium/*immunology ; Male ; Phospholipase C gamma/genetics/metabolism ; Second Messenger Systems/*immunology ; T-Lymphocytes/*immunology ; T-Lymphocytopenia, Idiopathic CD4-Positive/genetics/*immunology

0020-1693

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0040-4039

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0040-4039

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

2018-12-21

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Geosciences

Computer Science

Medicine

Natural Sciences in General

Physics

Geochemistry, Geophysics, Physics, Planetary Science

1089-7550

AIP Digital Archive

Physics

The formation of a discharge between a wire and a plane has been simulated numerically through the development of large electron and positive ion number densities. When the number densities grow sufficiently large and equal a new region within the computational model is formed, within which the governing equations of the quasi-neutral region are solved for the common ion and electron number density and electric potential. Results for the temporal development of the quasi-neutral region, radial profiles of charged particle number density, electric potential, and electric field strength from discharge initiation to program termination are described. The quasi-neutral region is shown to develop first off of the discharge axis, above the wire-to-plane gap. Near the quasi-neutral region the electric field strength and electric potential are highly distorted and within the quasi-neutral region are greatly diminished.

Electronic Resource

1089-7674

AIP Digital Archive

Physics

Electrical breakdown of an axisymmetric, atmospheric pressure air gap between a wire and a plane has been investigated for a gap length of 0.5 mm. O− and O−2 have been identified as the negative ions affecting the discharge development in air, besides electrons and positive ions, and have been included in the electrical breakdown model. Five coupled two-dimensional transient partial differential equations describing the discharge evolution in the air gap have been solved using a finite difference algorithm developed earlier. Temporal development of the charged particle number densities, electrostatic potential, electric field, and current at both the electrodes is presented when the wire is negatively biased at 2500 V. The impact of negative ions on gap breakdown has been assessed by comparing the results of analyses with and without negative ions. It is concluded that the negative ions have negligible effect during the early stages of the discharge development. However, as the discharge evolves, the negative ions cause a net loss of electrons from the discharge. The effect is most pronounced away from the discharge axis, where peaks in the electron density occur as breakdown proceeds. Radial spread of discharge and current growth rate are relatively unaffected by the presence of negative ions, but the magnitude of total current at the electrodes has been found to decrease by a decade when the negative ions are present.

Electronic Resource

1524-475X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Fetal rabbit wounds that are sutured show excellent repair without obvious scarring. In contrast, an unsutured wound in a rabbit fetus does not close, and it appears that the process of wound contraction does not occur. Experiments were carried out to illustrate the mechanisms responsible for the noncontraction of open fetal rabbit wounds. Results showed that the lack of wound contraction was not an artifact caused by rapid fetal growth. With regard to the ability of cultured fetal fibroblasts to show cytoplasmic muscle-induced cell contraction, we found that, in cultured fetal fibroblasts, cell contraction was induced by adenosine triphosphate. Contractile abilities of fetal-derived fibroblasts were equivalent to those of adult-derived fibroblasts. The fetal fibroblasts also demonstrated the generation of superior contractile activity when examined in a fibroblast-populated collagen lattice model. Finally, the ability of amniotic fluid to alter wound contraction was addressed by means of the fibroblast-populated collagen lattice in vitro model. Increasing concentrations of amniotic fluid inhibited fetal fibroblast lattice contraction. Therefore, rabbit amniotic fluid contains an inhibitor that may be partially responsible for the noncontraction of fetal rabbit wounds in utero.

Electronic Resource

1524-475X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1524-475X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Open wounds in the fetal rabbit do not heal by contraction and actually expand between 60% and 90% over a period of 5 days. Experiments were carried out to determine whether transforming growth factor-β1 can reduce expansion of open wounds in the fetal rabbit. This study was based on the concept that transforming growth factor-β1 causes differentiation of fibroblasts into contractile fibroblasts or “myofibroblasts.” To test this hypothesis, pregnant New Zealand White rabbits underwent laparotomy and hysterotomy on day 24 of gestation. A circular full-thickness cutaneous wound was made on the back of each fetus. After wounding, either vehicle alone or vehicle with transforming growth factor-β1 was applied topically to the wound site, and each fetus was then returned to the uterus. The hysterotomy and laparotomy were closed in standard fashion. On postoperative day 5, fetuses were harvested by repeat Cesarean section. Wound areas were determined from photographs, calculated as percentage of original wound size, and expressed in square millimeters. In addition, a portion of each wound was fixed and processed for histologic and immunohistochemical analysis. At harvest, the control wounds had expanded by an average of 87% of the original area. In marked contrast, the transforming growth factor-β1-treated wounds had only expanded an average of 16%. Thus, transforming growth factor-β1 significantly decreased the area of the open fetal wounds compared with control (p 〈 0.001). By histologic examination, no significant difference was found between the test group and the control group with regards to inflammation, neovascularization, collagen deposition, elastin content, glycosaminoglycan content, or hyaluronic acid content. Most notably, however, there was an increased density of fibroblasts in the transforming growth factor-β1-treated group. In addition, immunohistochemical staining with an anti-α-smooth muscle actin antibody showed the presence of contractile fibroblasts in the wound margins in the transforming growth factor-β1-treated group but failed to show any positive-staining fibroblasts in the matrices of the control group. These results indicate that open wounds in the fetal rabbit treated in vivo with transforming growth factor-β1 were significantly smaller than control wounds. This process appears to result from the recruitment and differentiation of normal dermal fibroblasts into contractile fibroblasts containing α-smooth muscle actin.

Electronic Resource

1524-475X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Extracellular matrix degradation during dermal wound healing involves multiple levels of regulation by several enzymes of the matrix metalloproteinase family, their activators, and their inhibitors. This study tested the hypothesis that a temporal pattern of interstitial collagenase appearance occurs during normal dermal wound healing, with matrix metalloproteinase-8 originating from neutrophils appearing earlier than the fibroblast-derived matrix metalloproteinase-1. Open (6 mm) full-thickness dermal wounds, which were covered by transparent occlusive dressings, were made in healthy human volunteers (n = 20). Wound fluids from under the dressings were collected daily through day 8, and wound tissue biopsies were obtained on days 0, 2, 4, 14, and 28. Collagenases were extracted from homogenized tissue biopsies for analysis. Samples were analyzed for the presence of matrix metalloproteinase-1 and matrix metalloproteinase-8 by enzyme-linked immunosorbent assays and by collagenase activity assays using purified types I and III collagen as substrates. In addition, tissue inhibitor of metalloproteinases-1 and matrix metalloproteinase-1/tissue inhibitor of metalloproteinases-1 complexes in wound fluids were measured. Results showed a differential temporal pattern of matrix metalloproteinase-1 and matrix metalloproteinase-8 in wound exudates with peak levels of matrix metalloproteinase-8 occurring on day 4 and matrix metalloproteinase-1 peak levels on day 7. Maximal levels in tissue for both enzymes occurred on day 2. At all time points examined, levels of matrix metalloproteinase-8 were statistically higher than matrix metalloproteinase-1 (100-fold to 200-fold). Tissue inhibitor of metalloproteinases-1 levels declined over time, whereas levels of matrix metalloproteinase-1/tissue inhibitor of metalloproteinase-1 complexes increased to a plateau on day 7. This study provides new evidence implicating matrix metalloproteinase-8 as a major collagenase in healing human dermal wounds. It also shows a temporal pattern in the appearance of the matrix metalloproteinases, tissue inhibitor of metalloproteinase-1, and matrix metalloproteinase-1/tissue inhibitor of metalloproteinases-1 complexes, suggesting that a tightly regulated pattern of expression of matrix metalloproteinases and their inhibitors is essential for normal wound healing in humans.

Electronic Resource

1524-475X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

A cotton-bound serine protease inhibitor of elastase (fiber-inhibitor) has been formulated for in vitro evaluation in chronic wound fluid. As a model to understand the properties of the inhibitor in wound dressings, the kinetic profile and in vitro release of the fiber-inhibitor formulation have been examined. The elastase inhibitor N-Methoxysuccinyl-Ala-Ala-Pro-Val-chloromethylketone was modified onto cotton cellulose fibers and assayed as a colloidal system. Amino acid analysis and reversed phase high performance liquid chromatography were compared as semiquantitative methods to assess elastase inhibitor release from the cotton fibers. The kinetics of inhibition was assessed on treated fibers of synthetic dressings such that a colloidal suspension of the fiber-inhibitor and elastase was employed as an assay. A dose–response relationship was observed in the kinetics of substrate hydrolysis catalyzed by three elastases: porcine pancreatic elastase, which was employed to model this approach; human leukocyte elastase; and elastase in human chronic wound fluid. Both freely dissolved and fiber-bound inhibitors were studied. The initial rates of substrate hydrolysis were inversely linear with freely dissolved inhibitor dose. The apparent first order rate constants, kobs, for the elastase-inhibitor complex were calculated from the kinetic profiles. The kobs for inhibitor bound enzyme varied as a function of inhibitor vs. enzyme concentration and based on the order of mixing of substrate, inhibitor and enzyme in the assay. Enzyme inhibition by the fiber-inhibitor was measured as inhibitor concentration at 50% inhibition (I50). I50 values measured from the colloidal assay with fiber-released inhibitor were within the same range to those for freely dissolved inhibitor. Inhibition of elastase activity in chronic wound fluid was observed with 1–5 mg of fiber-inhibitor formulation. This approach constitutes an in vitro assessment of synthetic serine protease inhibitors on fibers and may be employed to evaluate structure vs. function of elastase inhibition in the modified fibers of wound dressing composites.

Electronic Resource