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Peter Klüfers – One of the best experts on this subject based on the ideXlab platform.
Metal chelation by the common 2-amino-2-deoxy-, 2-N-acetylamino-2-deoxy-, and 2-deoxy-hexosesDalton Transactions, 2010Co-Authors: Thomas Schwarz, David Heß, Peter KlüfersAbstract:
The chelating properties of the common aldohexoses D-glucose, D-mannose, and D-galactose are characteristically modified in 2-substituted derivatives. The 2-amino-2-deoxy-aldohexoses provide mono- and bis-metallisable anionic ligands after their reaction with metal probes of the PdIIN2 type (N2 = bidentate nitrogen ligand). The 2-amino function reliably participates in metal binding of the, mostly pyranoidic, carbohydrate chelators. Acetylation of the amino function yields the biologically important 2-N-acetylamino-2-deoxy-hexoses (GlcNAc, ManNAc, and GalNAc). On reaction with the palladium probe, the metal-binding properties of the deprotonated acetylamino function depends on the steric requirements introduced by the acetyl residue which is forced into a coplanar arrangement with the chelate ring. In the two 2-deoxy-aldohexoses, 2-deoxy-arabino-D-hexose (the 2-deoxy derivative of both D-glucose and D-mannose, ‘2-deoxy-glucose’) and 2-deoxy-lyxo-D-hexose (‘2-deoxy galactose’), the 2-position cannot contribute to metal binding. As a result, furanose-1,3 chelation becomes an important metal-binding mode. Due to the decreased acidity of the 2-deoxy-glycose’s 1-hydroxy function, monometallation also takes place at the pyranose’s 3,4-site.
Charles L. Wilson – One of the best experts on this subject based on the ideXlab platform.
Control of Decay of Apple and Citrus Fruits in Semicommercial Tests with Candida saitoana and 2-Deoxy-D-GlucoseBiological Control, 2001Co-Authors: Ahmed El-ghaouth, Joseph L. Smilanick, G. Eldon Brown, Antonio Ippolito, Charles L. WilsonAbstract:
Abstract Efficacy of a combination of Candida saitoana and 0.2% 2-deoxy- d -glucose as a treatment for the biological control of postharvest diseases of apple and citrus fruits was determined in semicommercial tests. The combination of C. saitoana and 0.2% 2-deoxy- d -glucose was more effective in controlling decay of ‘Rome’ and ‘Empire’ apples than C. saitoana alone, and the level of control was comparable or superior to that provided by the synthetic fungicide thiabendazole, depending on the variety used. In orange (‘Washington’ navel, ‘Hamlin’, and ‘Valencia’) and ‘Eureka’ lemon trials, the combination of C. saitoana and 0.2% 2-deoxy- d -glucose was also superior to C. saitoana for controlling decay, and the control level was equal to imazalil, especially on early-season fruits. On late-season ‘Washington’ navel orange and ‘Eureka’ lemon fruits, the combination of C. saitoana and 0.2% 2-deoxy- d -glucose was superior in controlling decay than C. saitoana alone, but control was significantly less than with imazalil. These results indicate the reliability and efficacy of the combination of C. saitoana and 2-deoxy- d -glucose for the control of postharvest diseases of apple and citrus fruits. Further tests under commercial conditions are needed to confirm these results.
Improved Control of Apple and Citrus Fruit Decay with a Combination of Candida saitoana and 2-Deoxy-D-Glucose.Plant disease, 2000Co-Authors: Ahmed El-ghaouth, Joseph L. Smilanick, Michael Wisniewski, Charles L. WilsonAbstract:
ABSTRACT A combination of Candida saitoana with 0.2% 2-Deoxy-D-Glucose to control decay of apple, lemon, and orange fruit was evaluated. Growth of C. saitoana in vitro was reduced by 2-Deoxy-D-Glucose; however, in apple wounds, the yeast grew as well in the presence of 2-Deoxy-D-Glucose as in its absence. When applied to fruit wounds before inoculation, the combination of C. saitoana with 0.2% 2-Deoxy-D-Glucose was more effective in controlling decay of apple, orange, and lemon caused by Botrytis cinerea, Penicillium expansum, and P. digitatum than either C. saitoana or the application of a 0.2% solution of 2-Deoxy-D-Glucose alone. Increasing the concentration of 2-Deoxy-D-Glucose from 0.2 to 0.5% did not improve control significantly. The combination of C. saitoana with 0.2% 2-Deoxy-D-Glucose was also effective against infections established up to 24 h before treatment. When applied within 24 h after inoculation, the combination of C. saitoana with 0.2% 2-Deoxy-D-Glucose was very effective in controlling…
Hachiro Nakagawa – One of the best experts on this subject based on the ideXlab platform.
Bilateral lesions of the hypothalamic suprachiasmatic nucleus eliminated sympathetic response to intracranial injection of 2-Deoxy-D-Glucose and VIP rescued this response.Brain research bulletin, 1996Co-Authors: Katsuya Nagai, Nobuo Nagai, Akira Niijima, Hiroshi Hibino, Soo-jin Chun, Kimiko Shimizu, Hachiro NakagawaAbstract:
Abstract We previously found that bilateral lesions of the suprachiasmatic nucleus abolished hyperglycemic response to intracranial injection of 2-deoxy- d -glucose in rats. Because the hyperglycemia due to 2-deoxy- d -glucose was shown to be dependent on the functions of the adrenal medulla and sympathetic nervous system, the effect of bilateral lesions of the suprachiasmatic nucleus on changes in the nervous activity of sympathetic efferents to the adrenal after intracranial injection of 2-deoxy- d -glucose was examined in rats. It was found that bilateral lesions of the nucleus eliminated the increase in nerual activity of the sympathetic efferent that occurred after the injection of 2-deoxy- d -glucose. Because the suprachiasmatic nucleus posseses neurons containing a vasoactive intestinal polypeptide-like substance, the effects of vasoactive intestinal polypeptide and 2-deoxy- d -glucose, administered alone or in combination, on the sympathetic activity were examined in intact control rats and in rats with bilateral lesions of the suprachiasmatic nucleus. It was found that in the normal control rats, vasoactive intestinal polypeptide alone increased the sympathetic activity, whereas it dramatically enhanced the sympathetic response to 2-deoxy- d -glucose. However, in rats with bilateral lesions of the suprachiasmatic nucleus, vasoactive intestinal polypeptide alone elicited no increase in the nervous activity of the sympathetic efferents to the adrenal, but combined administration of vasoactive intestinal polypeptide and 2-deoxy- d -glucose caused an increase in the nervous activity of sympathetic efferents to the adrenal. These findings suggest that the suprachiasmatic nucleus is involved in the enhancement of sympathetic activity caused by intracranial injection of 2-deoxy- d -glucose, and that neurons containing a vasoactive intestinal polypeptide-like substance in the suprachiasmatic nucleus play an important role in the sympathetic enhancement that occurs after intracranial injection of 2-deoxy- d -glucose. This role might be a permissive and facilitative one.
mazindol enhances glucose uptake by rat skeletal muscleEuropean Journal of Pharmacology, 1994Co-Authors: Katsuya Nagai, Nobuo Nagai, Yasushi Isojima, Shunji Itoh, Nobuaki Okumura, Hachiro NakagawaAbstract:
The pharmacological action of mazindol (5-hydroxy-5-p-chlorophenyl-2,3-dihydro-5-imidazo[2,1-a]isoindol) was examined by studying its effect on glucose uptake by rat tissues using radiolabelled 2-Deoxy-D-Glucose. The following results were obtained. (1) The rate constant (Ki) of net tissue 2-Deoxy-D-Glucose uptake increased in the cerebral cortex (4.7-fold, P < 0.05), the hypothalamus (4.6-fold, P < 0.05), heart (4.0 fold, P < 0.05) and skeletal muscles (gastrocnemius, 5.7-fold, P < 0.01; soleus, 4.7-fold, P < 0.05), but not in epididymal adipose tissue in vivo 90 min after intragastric administration of mazindol (20 mg/kg). (2) This increase in Ki values of net tissue 2-Deoxy-D-Glucose uptake was not observed after addition of mazindol to the diet (40 mg/100 g of diet) for 4 days. (3) Mazindol (16.7 ng/ml to 16.7 μg/ml) stimulated 2-Deoxy-D-Glucose transport into sarcolemmal vesicles of the gastrocnemius muscle in vitro (1.6–1.8-fold, P < 0.05) and this stimulation was blocked by cytochalasin B (10 μM). These findings suggest that mazindol stimulates glucose transport into skeletal muscles by acting on glucose transporters in the sarcolemmal membrane, and suggest that mazindol may stimulate glucose transport into the brain and heart by a similar mechanism.