Gallein

Iron gallein elastic method---a substitute for Verhoeff's elastic tissue stain.[Pubmed:60801]

Stain Technol. 1976 Jul;51(4):213-7.

A method for staining elastic fibers in formalin fixed, paraffin embedded sections is described. After deparaffinizing and dehydration, sections are stained for 30 minutes in a solution prepared by mixing equal parts of 1% Gallein dissolved in ethylene glycol and absolute alcohol (1:4), and 1.16% aqueous ferric chloride in 1% hydrochloric acid. The sections are washed in water and then differentiated in 2% ferric chloride for 2 minutes. After washing in water, the sections are counterstained with a variant of Van Gieson's picric acid-acid fuchsin for 1 minute. The results are similar to Verhoeff's elastic stain with elastic fibers staining black. An advantage to this staining procedure is that visually controlled differentiation is not necessary.

Staining myelin in brain with gallein: a new method.[Pubmed:73233]

Stain Technol. 1977 Sep;52(5):261-4.

A procedure is described in which Gallein, mordant violet 25, C.I. 45445, is used to demonstrate myelinated nerve fibers in animal brain. Specimens are fixed in 10% neutral buffered formalin and processed in a routine manner. Microsections are stained in an iron Gallein solution with subsequent differentiation in 0.25% oxalic acid and 0.1% sodium carbonate solutions that avoid overdifferentiation. Methyl green is used to demonstrate other tissue elements. Myelin is stained deep violet, as are erythrocytes, with neuronal cell bodies and microglia shades of green. The staining procedure requires 30 minutes.

Phosphoinositide 3-kinase-dependent antagonism in mammalian olfactory receptor neurons.[Pubmed:21209212]

J Neurosci. 2011 Jan 5;31(1):273-80.

Phosphoinositide signaling, in particular, phosphoinositide 3-kinase (PI3K) signaling, has been implicated in mediating inhibitory odorant input to mammalian olfactory receptor neurons (ORNs). To better understand this phenomenon we investigated PI3K-dependent inhibition between single odorant pairs. The concentration-dependent inhibition of the response of native rat ORNs to octanol by citral is PI3K dependent; blocking PI3K activity with the beta and gamma isoform-specific inhibitors AS252424 (5-[5-(4-fluoro-2-hydroxy-phenyl)-furan-2-ylmethylene]-thiazolidine-2,4-dione) and TGX221(7-methyl-2-(4-morpholinyl)-9-[1-(phenylamino)ethyl]-4H-pyrido [1,2-a]pyrimidin-4-one) eliminated or strongly reduced the inhibition. Interestingly, blocking PI3K also changed the apparent agonist strength of the otherwise noncompetitive antagonist citral. The excitation evoked by citral after blocking PI3K, could be suppressed by the adenylate cyclase III (ACIII) blockers MDL12330A (cis-N-(2-phenylcyclopentyl)-azacyclotridec-1-en-2-amine hydrochloride) and SQ22536 [9-(tetrahydro-2-furanyl)-9H-purin-6-amine], indicating that citral could also activate ACIII, presumably through the canonical olfactory receptor (OR). The G-protein G(beta)gamma subunit blockers suramin (8,8'-[carbonylbis[imino-3,1-phenylen ecarbonylimino(4-methyl-3,1-phenylene)carbonylimino]]bis-1,3,5-naphthalenetrisulf onic acid), Gallein (3',4',5',6'-tetrahydroxyspiro[isobenzofuran-1(3H),9'-(9H)xanthen]-3-one), and M119 (cyclohexanecarboxylic acid [2-(4,5,6-trihydroxy-3-oxo-3H-xanthen-9-yl)-(9CI)]) suppressed citral's inhibition of the response to octanol, indicating that the activation of PI3K by citral was G-protein dependent, consistent with the idea that inhibition acts via the canonical OR. Lilial similarly antagonized the response to isoamyl acetate in other ORNs, indicating the effect generalizes to at least one other odorant pair. The ability of methyl-isoeugenol, limonene, alpha-pinene, isovaleric acid, and isosafrole to inhibit the response of other ORNs to IBMX (3-isobutyl-1-methylxanthine)/forskolin in a PI3K-dependent manner argues the effect generalizes to yet other structurally dissimilar odorants. Our findings collectively raise the interesting possibility that the OR serves as a molecular logic gate when mammalian ORNs are activated by natural, complex mixtures containing both excitatory and inhibitory odorants.

Small molecule disruption of G protein beta gamma subunit signaling inhibits neutrophil chemotaxis and inflammation.[Pubmed:18006643]

Mol Pharmacol. 2008 Feb;73(2):410-8.

G protein betagamma subunit-dependent signaling is important for chemoattractant-dependent leukocyte chemotaxis. Selective small molecule targeting of phosphoinositide 3-kinase (PI3-kinase) gamma catalytic activity is a target of interest for anti-inflammatory pharmaceutical development. In this study, we examined whether small-molecule inhibition of Gbetagamma-dependent signaling, including Gbetagamma-dependent activation of PI3-kinase gamma and Rac1, could inhibit chemoattractant-dependent neutrophil migration in vitro and inflammation in vivo. Small-molecule Gbetagamma inhibitors suppressed fMLP-stimulated Rac activation, superoxide production, and PI3-kinase activation in differentiated HL60 cells. These compounds also blocked fMLP-dependent chemotaxis in HL60 cells and primary human neutrophils. Systemic administration inhibited paw edema and neutrophil infiltration in a mouse carrageenan-induced paw edema model. Overall, the data demonstrate that targeting Gbetagamma-regulation may be an effective anti-inflammation strategy.

Gallein is a G protein βγ (Gβγ) subunit signalling inhibitor. Gallein disrupts the interaction of Gβγ subunits with the PI3Kγ. Anticancer agent. Gallein used as a red dye, an acid-base indicator and as a detection reagent for phosphates.

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