1.A model for quantitative cigarette smoking and response of airways to cigarette smoke in guinea pigs.
Jian-rong SHI ; Li-ben FANG ; Xiao-hong MAO ; Qiu-huo YANG
Journal of Zhejiang University. Medical sciences 2003;32(4):310-314
OBJECTIVETo establish an animal model for quantitative cigarette smoking and to determine the acute response of airways to cigarette smoke in guinea pigs.
METHODSThe device for inhaling quantitative cigarette smoking was made, which was double pass and single-direction with the minimum dead space. The changes of airway resistance(R(L))and dynamic lung compliance(Cdyn) in guinea pigs exposed to compound air consisting of 75% cigarette smoke and 25% oxygen were observed. Exudation of Evans blue in pulmonary vessels was also determined after consecutive inhalation of 60 ml smoke.
RESULTThe R(L) increased from the baseline of (0.21+/-0.05) cmH(2)O x ml(-1) x s to (0.37+/-0.13) cmH(2)O x ml(-1) x s after 10 consecutive breaths of cigarette smoke exposure(P<0.01). The Cdyn decreased to (61+/-19)% of baseline at the ninth to eleventh breaths (P<0.01). The exudations of Evans blue significantly increased in all measured parts of the airways such as lower trachea, main bronchi, proximal intrapulmonary airways and distal intrapulmonary airways (P<0.01).
CONCLUSIONThe model established in this study is useful for measuring the acute responses of airways induced by cigarette smoke in guinea pigs. Acute inhalation of cigarette smoke decreases dynamic lung compliance, increases airway resistance and vascular permeability of pulmonary vessels in guinea pigs.
Airway Resistance ; Animals ; Capillary Permeability ; Female ; Guinea Pigs ; Lung Compliance ; Male ; Models, Animal ; Smoking ; adverse effects
2.The Effet of Nifedipine on the Blood Pressure, Water and Cation Balance of the Lens in Spontaneous Hypertensive Rats.
Kyu Ryong CHOI ; Ae Kyung JUN ; Mi Ae PARK ; Byung Chae CHO
Journal of the Korean Ophthalmological Society 1989;30(4):509-510
In systemic hypertension, capillary resistance is highly elevated and' contractility of vascular smooth muscle is elevated. This is due to increased calcium uptake into the sarcoplasmic reticulum of the vascular smooth muscle. Recently, nifedipine, an antihypertensive medication which inhibits calcium uptake into the vascular smooth muscle is commonly used. It decreases the contractility of the vascular smooth muscle and causes the vessels to relax, which in turn lowers the blood pressure. In 1987, according to Rodriguez-Sargent et al. the increased incidence of cataract in Dahl-salt sensitive rats(DSR) was due to increasd water and sodium contents and decreased potassium content. In this investigative study on hypertension, the water, Sodium and potassium contents in Spontaneous Hypertensive Rats(SHR) were measured. After treatment with nifedipine in SHR, we observed decreased blood pressure along with the changes in water, sodium and potassium contents of the lenses. The following results were obtained from our experiments. 1. In normal SDR, The blood pressure did not decrease with nifedipine injection. 2. After 3-7 days of nifedipine injection bidaily, the blood pressure of SHR did not decrease. 3. After 2 weeks of nifedipine injection bidaily, the blood pressure of the SHR decreased slightly and after 4 weeks of nifedipine injection bidaily, the blood pressure of SHR decreased significantly. 4. Water and sodium contents of SHR were higher than that of SDR and the potassium content was similar to that of SDR. 5. The elevated water and sodium contents of SHR decreased along with decrease of blood pressure, and after 2 weeks of nifedipine injection, showed similar level as the contents of SDR lenses. 6. Potassium contents of SHR lenses showed no change were similar to SDR lines except the 4 weeks nifedipine injection group which showed higher potasslum contents.
Animals
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Blood Pressure*
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Calcium
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Capillary Resistance
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Cataract
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Hypertension
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Incidence
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Muscle, Smooth, Vascular
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Nifedipine*
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Potassium
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Rats*
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Sarcoplasmic Reticulum
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Sodium
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Water*
3.Genomic Basis for Methicillin Resistance in Staphylococcus aureus.
Keiichi HIRAMATSU ; Teruyo ITO ; Sae TSUBAKISHITA ; Takashi SASAKI ; Fumihiko TAKEUCHI ; Yuh MORIMOTO ; Yuki KATAYAMA ; Miki MATSUO ; Kyoko KUWAHARA-ARAI ; Tomomi HISHINUMA ; Tadashi BABA
Infection and Chemotherapy 2013;45(2):117-136
Since the discovery of the first strain in 1961 in England, MRSA, the most notorious multidrug-resistant hospital pathogen, has spread all over the world. MRSA repeatedly turned down the challenges by number of chemotherapeutics, the fruits of modern organic chemistry. Now, we are in short of effective therapeutic agents against MRSA prevailing among immuno-compromised patients in the hospital. On top of this, we recently became aware of the rise of diverse clones of MRSA, some of which have increased pathogenic potential compared to the classical hospital-associated MRSA, and the others from veterinary sources. They increased rapidly in the community, and started menacing otherwise healthy individuals by causing unexpected acute infection. This review is intended to provide a whole picture of MRSA based on its genetic makeup as a versatile pathogen and our tenacious colonizer.
Adenosine
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Chemistry, Organic
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Chromatography, Micellar Electrokinetic Capillary
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Clone Cells
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Colon
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England
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Fruit
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Humans
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Methicillin
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Methicillin Resistance
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Methicillin-Resistant Staphylococcus aureus
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Sprains and Strains
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Staphylococcus
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Staphylococcus aureus
4.Angiopoietin-1 variant, COMP-Ang1 attenuates hydrogen peroxide-induced acute lung injury.
So Ri KIM ; Kyung Sun LEE ; Seoung Ju PARK ; Kyung Hoon MIN ; Ka Young LEE ; Yeong Hun CHOE ; Sang Hyun HONG ; Gou Young KOH ; Yong Chul LEE
Experimental & Molecular Medicine 2008;40(3):320-331
Reactive oxygen species (ROS) play a crucial role in acute lung injury. Tissue inflammation, the increased vascular permeability, and plasma exudation are cardinal features of acute lung injury. Angiopoietin-1 (Ang1) has potential therapeutic applications in preventing vascular leakage and also has beneficial effects in several inflammatory disorders. Recently developed COMP-Ang1 is more potent than native Ang1 in phosphorylating tyrosine kinase with immunoglobulin and EGF homology domain 2 receptor in endothelial cells. However, there are no data on effects and related molecular mechanisms of COMP- Ang1 on ROS-induced acute lung injury. We used hydrogen peroxide (H2O2)-inhaled mice to evaluate the effect of COMP-Ang1 on pulmonary inflammation, bronchial hyper-responsiveness, and vascular leakage in acute lung injury. The results have revealed that VEGF expression, the levels of IL-4, TNF-alpha, IL-1 beta, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in lungs, the levels of hypoxia-inducible factor-1alpha (HIF-1 alpha) and NF-kappa B in nuclear protein extracts, phosphorylation of Akt, and vascular permeability were increased after inhalation of H2O2 and that the administration of COMP-Ang1 markedly reduced airway hyper-responsiveness, pulmonary inflammation, plasma extravasation, and the increases of cytokines, adhesion molecules, and VEGF in lungs treated with H2O2. We have also found that the activation of HIF-1a and NF-kappa B and the increase of phosphoinositide 3-kinase activity in lung tissues after H2O2 inhalation were decreased by the administration of COMP-Ang1. These results suggest that COMP-Ang1 ameliorates ROS-induced acute lung injury through attenuating vascular leakage and modulating inflammatory mediators.
Acute Lung Injury/chemically induced/complications/*drug therapy/metabolism
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Administration, Inhalation
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Airway Resistance/drug effects
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Animals
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Bronchial Hyperreactivity/drug therapy/etiology
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Bronchoalveolar Lavage Fluid
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Capillary Permeability/*drug effects
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Cytokines/antagonists & inhibitors
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Female
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Hydrogen Peroxide/adverse effects
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Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors
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Intercellular Adhesion Molecule-1/metabolism
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Mice
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Mice, Inbred BALB C
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NF-kappa B/antagonists & inhibitors
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Pneumonia/*drug therapy/etiology
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Recombinant Fusion Proteins/*administration & dosage
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Vascular Cell Adhesion Molecule-1/metabolism