WordNet

street name for lysergic acid diethylamide (同)back breaker, battery-acid, dose, dot, Elvis, loony toons, Lucy in the sky with diamonds, pane, superman, window pane, Zen
any of various water-soluble compounds having a sour taste and capable of turning litmus red and reacting with a base to form a salt
having the characteristics of an acid; "an acid reaction"

PrepTutorEJDIC

酸性の / 酸味のある,すっぱい(sour) / (言葉・態度などが)厳しい,しんらつな / 酸 / すっぱいもの / 《俗》=LSD

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1. 胎児の酸塩基の生理学 fetal acid base physiology
2. 神経管欠損予防のための葉酸 folic acid for prevention of neural tube defects
3. 疾患予防におけるビタミン補給 vitamin supplementation in disease prevention
4. 胃酸分泌の生理学 physiology of gastric acid secretion
5. バルプロ酸中毒 valproic acid poisoning

English Journal

Probing conformational changes in lipoxygenases upon membrane binding: fine-tuning by the active site inhibitor ETYA.

Di Venere A, Nicolai E, Ivanov I, Dainese E, Adel S, Angelucci BC, Kuhn H, Maccarrone M, Mei G.Author information Department of Experimental Medicine and Surgery, Tor Vergata University of Rome, Via Montpellier 1, 00133 Rome, Italy.AbstractLipoxygenases (LOXs) are lipid-peroxidizing enzymes that are involved in the metabolism of polyunsaturated fatty acids. Their biological activity includes a membrane binding process whose molecular details are not completely understood. The mechanism of enzyme-membrane interactions is thought to involve conformational changes at the level of the protein tertiary structure, and the extent of such alterations depends on the degree of structural flexibility of the different LOX isoforms. In this study, we have tested the resilience properties of a plant and a mammalian LOX, by using high pressure fluorescence measurements at different temperatures. The binding of LOXs to the lipid bilayer has been characterized using both large and giant unilamellar vesicles and electron transfer particles (inner mitochondrial membranes) as model membranes. The data indicate that the degree of LOXs' flexibility is strictly dependent on the two distinct N- and C-terminal domains that characterize the 3D structure of these enzymes. Furthermore, they demonstrate that increasing the rigidity of protein scaffolding by the presence of an active site ligand impairs the membrane binding ability of LOXs. These findings provide evidence that the amphitropic nature of LOXs is finely tuned by the interaction of the substrate with the residues of the active site, suggesting new strategies for the design of enzyme inhibitors.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jan;1841(1):1-10. doi: 10.1016/j.bbalip.2013.08.015. Epub 2013 Sep 3.
Lipoxygenases (LOXs) are lipid-peroxidizing enzymes that are involved in the metabolism of polyunsaturated fatty acids. Their biological activity includes a membrane binding process whose molecular details are not completely understood. The mechanism of enzyme-membrane interactions is thought to inv
PMID 24012824

Arachidonic acid closes innexin/pannexin channels and thereby inhibits microglia cell movement to a nerve injury.

Samuels SE, Lipitz JB, Wang J, Dahl G, Muller KJ.Author information Neuroscience Program, University of Miami, Miami, Florida, 33136, USA.AbstractPannexons are membrane channels formed by pannexins and are permeable to ATP. They have been implicated in various physiological and pathophysiological processes. Innexins, the invertebrate homologues of the pannexins, form innexons. Nerve injury induces calcium waves in glial cells, releasing ATP through glial pannexon/innexon channels. The ATP then activates microglia. More slowly, injury releases arachidonic acid (ArA). The present experiments show that ArA itself reduced the macroscopic membrane currents of innexin- and of pannexin-injected oocytes; ArA also blocked K(+) -induced release of ATP. In leeches, whose large glial cells have been favorable for studying control of microglia migration, ArA blocked glial dye-release and, evidently, ATP-release. A physiological consequence in the leech was block of microglial migration to nerve injuries. Exogenous ATP (100 µM) reversed the effect, for ATP causes activation and movement of microglia after nerve injury, but nitric oxide directs microglia to the lesion. It was not excluded that metabolites of ArA may also inhibit the channels. But for all these effects, ArA and its non-metabolizable analog eicosatetraynoic acid (ETYA) were indistinguishable. Therefore, ArA itself is an endogenous regulator of pannexons and innexons. ArA thus blocks release of ATP from glia after nerve injury and thereby, at least in leeches, stops microglia at lesions.
Developmental neurobiology.Dev Neurobiol.2013 Aug;73(8):621-31. doi: 10.1002/dneu.22088. Epub 2013 Jun 18.
Pannexons are membrane channels formed by pannexins and are permeable to ATP. They have been implicated in various physiological and pathophysiological processes. Innexins, the invertebrate homologues of the pannexins, form innexons. Nerve injury induces calcium waves in glial cells, releasing ATP t
PMID 23650255

Mechanism of inhibition of tubuloglomerular feedback by CO and cGMP.

Ren Y, D'Ambrosio MA, Garvin JL, Wang H, Carretero OA.Author information Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA.AbstractTubuloglomerular feedback (TGF) is a mechanism that senses NaCl in the macula densa (MD) and causes constriction of the afferent arteriole. CO, either endogenous or exogenous, inhibits TGF at least in part via cGMP. We hypothesize that CO in the MD, acting via both cGMP-dependent and -independent mechanisms, attenuates TGF by acting downstream from depolarization and calcium entry into the MD cells. In vitro, microdissected rabbit afferent arterioles and their MD were simultaneously perfused and TGF was measured as the decrease in afferent arteriole diameter. MD depolarization was induced with ionophores, while adding the CO-releasing molecule-3 to the MD perfusate at nontoxic concentrations. CO-releasing molecule-3 blunted depolarization-induced TGF at 50 μmol/L, from 3.6±0.4 to 2.5±0.4 µm (P<0.01), and abolished it at 100 μmol/L, to 0.1±0.1 μm (P<0.001; n=6). When cGMP generation was blocked by guanylyl cyclase inhibitor LY83583 added to the MD, CO-releasing molecule-3 no longer affected depolarization-induced TGF at 50 μmol/L (2.9±0.4 versus 3.0±0.4 µm) but partially inhibited TGF at 100 μmol/L (to 1.3±0.2 μm; P<0.05; n=9). Experiments using eicosatetraynoic acid and indomethacin suggest arachidonic acid metabolites do not mediate the cGMP-independent effect of CO. We then added the calcium ionophore A23187 to the MD, which caused TGF (4.1±0.6 μmol/L); A23187-induced TGF was inhibited by CO-releasing molecule-3 at 50 μmol/L (1.9±0.6 μmol/L; P<0.01) and 100 μmol/L (0.2±0.5 μmol/L; P<0.001; n=6). We conclude that CO inhibits TGF acting downstream from depolarization and calcium entry, acting via cGMP at low concentrations, but additional mechanisms of action may be involved at higher concentrations.
Hypertension.Hypertension.2013 Jul;62(1):99-104. doi: 10.1161/HYPERTENSIONAHA.113.01164. Epub 2013 May 6.
Tubuloglomerular feedback (TGF) is a mechanism that senses NaCl in the macula densa (MD) and causes constriction of the afferent arteriole. CO, either endogenous or exogenous, inhibits TGF at least in part via cGMP. We hypothesize that CO in the MD, acting via both cGMP-dependent and -independent me
PMID 23648700

Japanese Journal

Measurement of Lipid Hydroperoxides by the Ferric-Xylenol Orange Method (2) Application to Lipoxygenase Assay

Fukuzawa Kenji,Sano Masumi,Akai Kaori [他],Morishige Junichi,Tokumura Akira,Jisaka Mituo
Journal of nutritional science and vitaminology 55(1), 92-98, 2009-02-00
… The amounts of 15-S-hydroperoxyeicosa-5,8,10,14-tetraenoic acid (15-HPETE) produced by 15-LOX-2 measured by UV absorption at 237nm attributed to the conjugated diene, coincided with the results of our FOX method measuring absorbance at 610nm. … Furthermore, our method was applicable to assaying the inhibitory effect of 5,8,11,14-eicosatetraynoic acid (ETYA) on SLOX activity using LA and EYPC as substrates. …
NAID 110007110606

Effects of Arachidonic Acid on ATP-Sensitive K^+ Current in Murine Colonic Smooth Muscle Cells

Jun Jae Yeoul,Yeum Cheol Ho,Park Yoo Whan [他],JANG In Youb,KONG In Deok,SIM Jae Hoon,SO Insuk,KIM Ki Whan,YOU Ho Jin
The Japanese journal of pharmacology 90(1), 81-87, 2002-09-01
… The effects of arachidonic acid (AA) and the mechanism through which it modulates ATP-sensitive K<sup>+</sup> … Superoxide dismutase and metabolic inhibitors (indomethacin and nordihydroguaiacretic acid) of AA did not affect the AA-induced inhibition. … Eicosatetraynoic acid, a nonmetabolizable analogue of AA, inhibited the K<sub>ATP</sub> …
NAID 130000078451