The Experts below are selected from a list of 56556 Experts worldwide ranked by ideXlab platform
Hiroshi Wada - One of the best experts on this subject based on the ideXlab platform.
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Histamine-induced cyclic AMP accumulation in type-1 and type-2 astrocytes in primary culture
European Journal of Pharmacology, 1991Co-Authors: Akiharu Kubo, Naoyuki Inagaki, Hiroyuki Fukui, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine-induced cyclic AMP (cAMP) accumulation was studied in purified primary cultures of type-1 and type-2 astrocytes from neonatal rat brain. Histamine induced remarkable cAMP accumulation in type-1 astrocytes in a dose-dependent manner (EC50 = 1.2 × 10−5 M, Emax = 1100% of control). In contrast, histamine had no significant effect on cAMP accumulation in type-2 astrocytes. Famotidine, an H2-Antagonist, dose-dependently inhibited histamine-induced cAMP accumulation in type-1 astrocytes (Ki = 3 × 10−8 M), but mepyramine (10−6 M), an H1-Antagonist, had no effect. Dimaprit and impromidine, H2-agonists, stimulated cAMP accumulation, but 2-pyridylethylamine, an H1-agonist, did not stimulate it nor augment the H2-agonist-induced cAMP accumulation. These results indicate that (1) histamine induces cAMP accumulation in type-1 astrocytes but not in type-2 astrocytes, and that (2) histamine-induced cAMP accumulation in type-1 astrocytes is mediated by H2-receptors without significant augmentation via H1-receptors.
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Histamine-induced inositol phosphate accumulation in type-2 astrocytes
Biochemical and Biophysical Research Communications, 1991Co-Authors: Hiroki Kondou, Naoyuki Inagaki, Hiroyuki Fukui, Yutaka Koyama, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine elicited dose-dependent accumulation of [3H]inositol phosphates in type-2 astrocytes, but not in type-1 astrocytes. The ED50 was about 2.4×10−6M and the maximal response was obtained at 10−4M. This response was dose-dependently inhibited by H1-Antagonists, mepyramine and D- and L-chlorpheniramine. Furthermore, D- and L-chlorpheniramine showed stereoselectivity in the inhibition. On the other hand, an H2-Antagonist, famotidine, and an H3-Antagonist, thioperamide, did not inhibit the response. These results indicate that histamine stimulates accumulation of inositol phosphates in type-2 astrocytes via H1-receptors.
Chen-hsiung Liao - One of the best experts on this subject based on the ideXlab platform.
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The histological maturity of regenerating mucosa of healed duodenal ulcer and ulcer recurrence after treatment with H2-Antagonist.
The American journal of gastroenterology, 1990Co-Authors: S. Pan, Chen-hsiung LiaoAbstract:We investigated the relationship between the histological maturity of regenerating mucosa of healed duodenal ulcer and ulcer recurrence, after treatment with an H2-Antagonist. Duodenal ulcer patients were given H2-Antagonists (either cimetidine or famotidine) for 4 wk of therapy. Fifty-two (77.6%) of the 67 patients were healed endoscopically. The histological state of the regenerating mucosa of healed duodenal ulcer was divided into three categories: good, fair, and poor patterns. Of the 52 healed patients, 15 achieved a good histological pattern. None of these 15 patients had a recurrence 3 months later. However, nine of the 37 patients with a fair or poor pattern of regenerating mucosa had a recurrence 3 months after healing (p = 0.034). We concluded that a duodenal ulcer should be treated until the regenerating mucosa of the healed ulcer reaches a good histological pattern, so as to prevent the recurrence of the ulcer.
Naoyuki Inagaki - One of the best experts on this subject based on the ideXlab platform.
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Histamine-induced cyclic AMP accumulation in type-1 and type-2 astrocytes in primary culture
European Journal of Pharmacology, 1991Co-Authors: Akiharu Kubo, Naoyuki Inagaki, Hiroyuki Fukui, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine-induced cyclic AMP (cAMP) accumulation was studied in purified primary cultures of type-1 and type-2 astrocytes from neonatal rat brain. Histamine induced remarkable cAMP accumulation in type-1 astrocytes in a dose-dependent manner (EC50 = 1.2 × 10−5 M, Emax = 1100% of control). In contrast, histamine had no significant effect on cAMP accumulation in type-2 astrocytes. Famotidine, an H2-Antagonist, dose-dependently inhibited histamine-induced cAMP accumulation in type-1 astrocytes (Ki = 3 × 10−8 M), but mepyramine (10−6 M), an H1-Antagonist, had no effect. Dimaprit and impromidine, H2-agonists, stimulated cAMP accumulation, but 2-pyridylethylamine, an H1-agonist, did not stimulate it nor augment the H2-agonist-induced cAMP accumulation. These results indicate that (1) histamine induces cAMP accumulation in type-1 astrocytes but not in type-2 astrocytes, and that (2) histamine-induced cAMP accumulation in type-1 astrocytes is mediated by H2-receptors without significant augmentation via H1-receptors.
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Histamine-induced inositol phosphate accumulation in type-2 astrocytes
Biochemical and Biophysical Research Communications, 1991Co-Authors: Hiroki Kondou, Naoyuki Inagaki, Hiroyuki Fukui, Yutaka Koyama, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine elicited dose-dependent accumulation of [3H]inositol phosphates in type-2 astrocytes, but not in type-1 astrocytes. The ED50 was about 2.4×10−6M and the maximal response was obtained at 10−4M. This response was dose-dependently inhibited by H1-Antagonists, mepyramine and D- and L-chlorpheniramine. Furthermore, D- and L-chlorpheniramine showed stereoselectivity in the inhibition. On the other hand, an H2-Antagonist, famotidine, and an H3-Antagonist, thioperamide, did not inhibit the response. These results indicate that histamine stimulates accumulation of inositol phosphates in type-2 astrocytes via H1-receptors.
Hiroyuki Fukui - One of the best experts on this subject based on the ideXlab platform.
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Histamine-induced cyclic AMP accumulation in type-1 and type-2 astrocytes in primary culture
European Journal of Pharmacology, 1991Co-Authors: Akiharu Kubo, Naoyuki Inagaki, Hiroyuki Fukui, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine-induced cyclic AMP (cAMP) accumulation was studied in purified primary cultures of type-1 and type-2 astrocytes from neonatal rat brain. Histamine induced remarkable cAMP accumulation in type-1 astrocytes in a dose-dependent manner (EC50 = 1.2 × 10−5 M, Emax = 1100% of control). In contrast, histamine had no significant effect on cAMP accumulation in type-2 astrocytes. Famotidine, an H2-Antagonist, dose-dependently inhibited histamine-induced cAMP accumulation in type-1 astrocytes (Ki = 3 × 10−8 M), but mepyramine (10−6 M), an H1-Antagonist, had no effect. Dimaprit and impromidine, H2-agonists, stimulated cAMP accumulation, but 2-pyridylethylamine, an H1-agonist, did not stimulate it nor augment the H2-agonist-induced cAMP accumulation. These results indicate that (1) histamine induces cAMP accumulation in type-1 astrocytes but not in type-2 astrocytes, and that (2) histamine-induced cAMP accumulation in type-1 astrocytes is mediated by H2-receptors without significant augmentation via H1-receptors.
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Histamine-induced inositol phosphate accumulation in type-2 astrocytes
Biochemical and Biophysical Research Communications, 1991Co-Authors: Hiroki Kondou, Naoyuki Inagaki, Hiroyuki Fukui, Yutaka Koyama, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine elicited dose-dependent accumulation of [3H]inositol phosphates in type-2 astrocytes, but not in type-1 astrocytes. The ED50 was about 2.4×10−6M and the maximal response was obtained at 10−4M. This response was dose-dependently inhibited by H1-Antagonists, mepyramine and D- and L-chlorpheniramine. Furthermore, D- and L-chlorpheniramine showed stereoselectivity in the inhibition. On the other hand, an H2-Antagonist, famotidine, and an H3-Antagonist, thioperamide, did not inhibit the response. These results indicate that histamine stimulates accumulation of inositol phosphates in type-2 astrocytes via H1-receptors.
Akira Kanamura - One of the best experts on this subject based on the ideXlab platform.
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Histamine-induced cyclic AMP accumulation in type-1 and type-2 astrocytes in primary culture
European Journal of Pharmacology, 1991Co-Authors: Akiharu Kubo, Naoyuki Inagaki, Hiroyuki Fukui, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine-induced cyclic AMP (cAMP) accumulation was studied in purified primary cultures of type-1 and type-2 astrocytes from neonatal rat brain. Histamine induced remarkable cAMP accumulation in type-1 astrocytes in a dose-dependent manner (EC50 = 1.2 × 10−5 M, Emax = 1100% of control). In contrast, histamine had no significant effect on cAMP accumulation in type-2 astrocytes. Famotidine, an H2-Antagonist, dose-dependently inhibited histamine-induced cAMP accumulation in type-1 astrocytes (Ki = 3 × 10−8 M), but mepyramine (10−6 M), an H1-Antagonist, had no effect. Dimaprit and impromidine, H2-agonists, stimulated cAMP accumulation, but 2-pyridylethylamine, an H1-agonist, did not stimulate it nor augment the H2-agonist-induced cAMP accumulation. These results indicate that (1) histamine induces cAMP accumulation in type-1 astrocytes but not in type-2 astrocytes, and that (2) histamine-induced cAMP accumulation in type-1 astrocytes is mediated by H2-receptors without significant augmentation via H1-receptors.
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Histamine-induced inositol phosphate accumulation in type-2 astrocytes
Biochemical and Biophysical Research Communications, 1991Co-Authors: Hiroki Kondou, Naoyuki Inagaki, Hiroyuki Fukui, Yutaka Koyama, Akira Kanamura, Hiroshi WadaAbstract:Abstract Histamine elicited dose-dependent accumulation of [3H]inositol phosphates in type-2 astrocytes, but not in type-1 astrocytes. The ED50 was about 2.4×10−6M and the maximal response was obtained at 10−4M. This response was dose-dependently inhibited by H1-Antagonists, mepyramine and D- and L-chlorpheniramine. Furthermore, D- and L-chlorpheniramine showed stereoselectivity in the inhibition. On the other hand, an H2-Antagonist, famotidine, and an H3-Antagonist, thioperamide, did not inhibit the response. These results indicate that histamine stimulates accumulation of inositol phosphates in type-2 astrocytes via H1-receptors.
