Images in rheumatology. Hemorrhagic schwannoma with purely cystic appearance in the shoulder.
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Aged↗
Biomedical subjects
H Koda
Publications and source records attributed to H Koda.
Possible contribution of protein kinase C in the effects of histamine on the visceral nociceptor activities in vitro.
To clarify the possible contribution of protein kinase C activation in histamine-induced excitation and sensitization of the heat response of testicular polymodal receptors, the effects of staurosporine, a protein kinase C inhibitor, and phorbol 12,13-dibutyrate, a protein kinase C activating phorbol ester, were studied in visceral polymodal receptors. Single polymodal receptor activities were recorded in vitro from testis-spermatic nerve preparations obtained from deeply anesthetized dogs (pentobarbital sodium, 30 mg/kg, i.v.). Histamine (10 microM)-induced excitation and facilitation of the heat response of polymodal receptors were both suppressed by staurosporine (1 microM), suggesting that activation of protein kinase C is involved in both these effects of histamine. Application of phorbol 12,13-dibutyrate (0.1 microM) mixed with histamine increased the histamine-induced excitation, whereas a 5 min application of phorbol 12,13-dibutyrate before histamine suppressed it. These results suggest that phorbol 12,13-dibutyrate-activated protein kinase C has inactivation as well as activation effects on the intracellular cascade connected to histamine receptors, and that the former has a slower time course.
Animals↗
Potentiation and suppression of the histamine response by raising and lowering the temperature in canine visceral polymodal receptors in vitro.
It is well known that itch and inflammatory pain are enhanced when tissue is warmed, while they are suppressed when tissue is cooled. To see whether these changed sensations are based on the changed response of sensory receptors, the temperature dependency of the excitation of polymodal receptors induced by histamine, which plays an important role both in itch and inflammatory pain, was studied. Single nerve activities of polymodal receptors were recorded from canine testis-spermatic nerve preparations in vitro. Raising the temperature from 34 to 40 degrees C, a temperature below the threshold for the heat response of polymodal receptors, facilitated the histamine-induced nerve discharge to 268% of that at 34 degrees C, while lowering the temperature to 28 degrees C decreased it to 25%. Facilitation of the histamine response was also observed in the noxious temperature range (48 and 51 degrees C). These results suggest that the potentiation of the histamine-induced sensation by increasing the tissue temperature, as well as its suppression by lowering tissue temperature, can be explained by a temperature-dependent response of peripheral sensory receptors to histamine. However, the suppression of itch by noxious heat reported by Bickford (Bickford, R.G., Experiments relating to the itch sensation, its peripheral mechanism, and central pathways, Clin. Sci. Incorp. Heart, 3 (1937) 377-386) cannot be explained by the noxious heat-induced facilitation of the peripheral receptor response reported in this paper.
Animals↗
A novel endogenous inhibitor of phenoloxidase from Musca domestica has a cystine motif commonly found in snail and spider toxins.
Phenoloxidase inhibitor (POI), found in the hemolymph of housefly pupae, is a novel dopa-containing and cystine-rich peptide that competitively inhibits phenoloxidase with a Ki in the nanomolar range. [Tyr32]POI is a potential precursor molecule also found in the hemolymph that may be posttranslationally oxidized to the dopa-containing peptide after creation of a rigid structure. By employing both a solid-phase peptide synthesis system based on a 9-fluorenylmethoxycarbonyl strategy and a specific air oxidation technique to ensure correct folding, we have been able to synthesize [Tyr32]POI. The synthetic [Tyr32]POI was confirmed to be identical to the native [Tyr32]POI by coelution high-performance liquid chromatography analysis and by enzymatic analysis using the phenoloxidase inhibition assay. To determine the disulfide pairings within the peptides, a series of enzyme hydrolyses and partial reduction/alkylation steps were performed. Three cystine pairs (Cys11-Cys25, Cys18-Cys29, and Cys24-Cys36) were determined by identification of the resulting peptides. The disulfide pairings of the two adjacent Cys residues (Cys11-Cys25 and Cys24-Cys36) were unambiguously assigned by comparing the derived fragments with the two possible isomers synthesized through a novel disulfide-linking technique. The arrangement of the disulfide bridges in POI was found to be topologically identical to those found for several peptides within the inhibitor cystine knot structural family. Although these peptides share a low primary sequence homology and display a diversity of biological functions, they nonetheless share similarities in their cystine motifs and tertiary structure. The tertiary structure model of POI, which was derived through molecular dynamics and energy minimization studies using restraints with determined disulfide connectivities, suggests that POI is a new class member of the inhibitor cystine-knot structural family.
Amino Acid Sequence↗
Antagonistic effect of N-methyltyramine on alpha2-adrenoceptor in mice.
We examined the effect of N-methyltyramine (NMT) on alpha2-adrenoceptor. NMT (10(-8)-10(-3) M) inhibited the binding of [3H]p-aminoclonidine to alpha2-adrenoceptor dose-dependently. However, the IC50 value for NMT (5.53 x 10(-6) M) was higher than that for RX821002, an alpha2-adrenoceptor antagonist (1.07 x 10(-8) M). RX821002 (5 mg/kg, i.p.) inhibited hypermotility induced by scopolamine (8 mg/kg, s.c.) in male ddY mice. NMT (20 or 100 mg/kg, i.p.) was found to have a dose-dependent inhibitory effect similar to that of RX821002. These findings indicate that NMT has the properties of an alpha2-adrenoceptor antagonist. However, the affinity of NMT for alpha2-adrenoceptor is weaker than that of RX821002.
Adrenergic alpha-2 Receptor Antagonists↗
Evidence that protein kinase C activation is involved in the excitatory and facilitatory effects of bradykinin on canine visceral nociceptors in vitro.
The involvement of protein kinase (PK) C activation in the effects of bradykinin (BK) on peripheral nociceptors, polymodal receptors, was examined using canine testis-spermatic nerve preparations in vitro. Phorbol 12,13-dibutyrate 0.1 microM, which activates PKC, suppressed the BK-induced excitation when applied for 3-5 min prior to BK application, but facilitated it when applied simultaneously with BK. Neither effect was induced by an inactive phorbol ester, 4alpha-phorbol 12, 13-didecanoate, demonstrating that both effects were mediated through the activation of PKC. In addition, staurosporine 1 microM, a PK inhibitor, suppressed both BK-induced excitation and facilitation of the heat response of testicular polymodal receptors without influencing on-going activities and the heat response itself. These results suggest that PKC activation is involved in the excitatory and facilitatory effects of BK on peripheral nociceptors.
Adaptation, Physiological↗
Retinoic acid-stimulated liver stellate cells suppress the production of albumin from parenchymal cells via TGF-beta.
We studied a cell-cell interaction via transforming growth factor-beta (TGF-beta ) between liver stellate cells (SCs) and parenchymal cells (PCs) using co-cultures of rat primary SCs and PCs. Both TGF-beta added exogenously to the culture medium, and TGF-beta produced endogenously from SCs after stimulation with retinoic acid (RA), suppressed the production and secretion of albumin from PCs. This effect occurred at the translational level, but not at the transcriptional level; TGF-beta, as well as SC culture medium conditioned by RA, did not affect the albumin mRNA levels, but decreased the biosynthesis of [35-S]methionine-labeled albumin without altering its post-translational degradation rate. These results suggest that TGF-beta generated from SCs facilitates the development of liver cirrhosis not only by inducing the production of fibrotic components from SCs, but also by impairing the function of the surrounding PCs.
Albumins↗
[A case of Evans's syndrome with antiphospholipid antibody syndrome].
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Anemia, Hemolytic, Autoimmune↗
Excitation and sensitization of the heat response induced by a phorbol ester in canine visceral polymodal receptors studied in vitro.
To clarify the possible involvement of protein kinase (PK) C activation in the excitation and sensitization of polymodal receptors (PMRs), the effects of phorbol 12,13-dibutyrate (PDBu) on PMRs were studied in canine testis-spermatic nerve preparations in vitro. Application of PDBu (10(-7), 10(-6), AND 10(-5) M) for 5 min evoked a significant increase in the ongoing activity of the PMRs within 15 min. PDBu (10(-8) to 10(-5) M) significantly augmented the subsequent heat responses of the PMRs. Staurosporine (10(-6) M), a PK inhibitor, attenuated the effect of PDBu on heat responses. These data suggest that activation of PKC contributes to the activities of PMRs.
Alkaloids↗
Myxolipoma mimicking a cystic tumor.
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Aged↗
Opposite effects of increased intracellular cyclic AMP on the heat and bradykinin responses of canine visceral polymodal receptors in vitro.
To clarify the validity of the long standing hypothesis that effects of E series prostaglandin (PG)S are mediated by cyclic AMP (cAMP), we studied the effects of increases in intracellular cAMP on the heat and bradykinin responses of testicular polymodal receptors. Polymodal receptor activities were recorded in vitro from testis-spermatic nerve preparations excised from dogs anesthetized with pentobarbital (30 mg/kg, i.v.). Increases in intracellular cAMP induced by either forskolin (5 or 10 microM), an adenylyl cyclase activator, or a mixture of dibutyryl cAMP (20-100 microM), a membrane permeable cAMP analog, and 3-isobutyl-1-methyl xanthine (20-100 microM), an inhibitor of the cAMP degrading enzyme, significantly augmented the response to heat (42-48 degrees C). In contrast, these substances failed to facilitate the response to bradykinin (0.1 or 1 microM) and instead suppressed it. Dideoxyforskolin (10 microM), an inactive analog of forskolin, had no effects on both the heat and bradykinin responses. These results demonstrate that an increase in intracellular cAMP induces opposite effects on the heat and bradykinin responses. Possible involvement of intracellular cAMP in the facilitatory effects of PGE2 on both responses was discussed in connection with the PGE receptor subtypes involved in the sensitization of the bradykinin and heat responses.
Animals↗
EP receptor subtypes implicated in the PGE2-induced sensitization of polymodal receptors in response to bradykinin and heat.
1. Our previous studies, in which we used in vitro canine testispermatic nerve preparations, showed that prostaglandin E2 (PGE2) augments both bradykinin (BK)- and heat-induced discharges of polymodal receptors. However, the PGE2 concentration required to augment the BK responses were 100 times lower than those necessary for the heat responses, suggesting that different receptors are involved in these phenomena. We studied which receptors for E series of prostaglandins (EP receptors) were responsible, using the antagonist and agonists for three subtypes of EP receptors. 2. PGE2-induced augmentation of the BK responses was unaffected when treated with an antagonist for the EP1 receptor, AH6809. 3. An agonist for the EP3 receptor, M&B28767, at > or = 10 nM, significantly augmented the BK responses in a concentration-dependent manner that mimics the PGE2-induced effect. An agonist for the EP1 receptor, 17-phenyl trinor PGE2 (17-phen PGE2), at the high concentrations of 0.1 and 1 microM, augmented the BK responses in two and four of nine cases tested, respectively. However, this augmentation was not suppressed by the antagonist for the EP1 receptor, AH6809. In addition, an agonist for the EP2 receptor, butaprost, did not affect the BK responses even when applied at 10 microM. 4. In contrast, butaprost at > or = 10 nM significantly augmented the heat responses in a concentration-dependent manner. M&B28767 and 17-phen PGE2, respectively, augmented the heat responses at higher concentrations of 100 nM and 1 microM. 5. These results indicate that the EP3 and EP2 receptor subtypes are differentially implicated in the respective PGE2-induced augmentation of BK responses and heat responses of polymodal receptors.
Alprostadil↗
H1-receptor-mediated excitation and facilitation of the heat response by histamine in canine visceral polymodal receptors studied in vitro.
1. We examined excitation and the facilitatory effect on the heat responses induced by histamine in visceral polymodal receptors with the use of the canine testis-spermatic nerve preparation in vitro. 2. The proportion of units that showed excitation (> 10 impulses 1 min after application of histamine was initiated) increased roughly with higher concentrations of histamine: 7% at 1 microM, 26% at 10 microM, 79% at 100 microM, and 61% at 1,000 microM. The discharge rate also increased with the concentration. 3. Histamine (100 and 1,000 microM) responses > 0.5 imp/s were observed only in units with conduction velocities (CVs) of < or = 10 m/s, but not in those with CVs faster than 10 m/s. On average, histamine-induced discharges were significantly greater in units with CVs of < or = 10 m/s at all concentrations > or = 10 microM. Thus units studied in this experiment were empirically divided into slow-CV (< or = m/s) and fast-CV (> 10 m/s) groups. 4. Histamine significantly facilitated the heat responses of the slow-CV group from 10 microM, and also facilitated the fast-CV group from 100 microM. This sensitizing effect was observed irrespective of the precedent histamine-induced excitation. The magnitude of sensitization tended to increase with an increase in histamine concentration. 5. For studying the histamine receptor subtype involved in excitation and facilitation, we used D-chlorpheniramine maleate (5 microM) (an H1 receptor antagonist), famotidine (20 microM) (an H2 receptor antagonist), and thioperamide maleate (20 microM) (an H3 receptor antagonist). The magnitude of histamine-induced excitation of the slow-CV group was significantly suppressed by the H1 receptor antagonist but not by other antagonists. 6. The facilitatory effect of histamine on the heat response was also suppressed by the H1 receptor antagonist in both slow- and fast-CV groups. 7. These results strongly suggested that both excitation and facilitation of the heat response induced by histamine are mediated through the H1 receptor.
Animals↗
Multiple endocrine neoplasia type 1 presenting as insulinoma, gastrinoma, and postbulbar duodenal ulcers: report of a case.
We report herein the unusual case of a 55-year-old man with multiple endocrine neoplasia type 1 presenting as hyperparathyroidism, hyperpituitarism, insulinoma, and gastrinoma with postbulbar duodenal ulcers. The patient was referred to our hospital for further investigations of nephrolithiasis, acromegaly, and hematemesis. Laboratory studies showed high serum levels of calcium, parathyroid hormone, growth hormone, insulin, gastrin, and prolactin. Computed tomography of the cranial cavity demonstrated an enlargement of the serra turcica and swelling of two parathyroid glands in the neck. Computed tomography and angiography of the abdomen also showed a mass in the head of the pancreas. Endoscopy demonstrated reflux esophagitis, erosive gastritis, and multiple postbulbar duodenal ulcers. We diagnosed this patient as having multiple endocrine neoplasia type 1, with concomitant lesions of the pituitary gland, parathyroid glands, and islet cells of the pancreas. Following excision of the two enlarged parathyroid glands, his serum calcium and parathyroid hormone levels fell to within the normal range. Thereafter, a total gastrectomy was performed to alleviate the frequent bleeding from the upper gastrointestinal tract. However, resection of the pancreatic mass could not be performed owing to severe inflammation around the duodenum, probably induced by the postbulbar duodenal ulcers.
Adenoma↗
Influence of histamine on the bradykinin response of canine testicular polymodal receptors in vitro.
Effects of histamine on the testicular polymodal receptors were studied in vitro using canine testis-spermatic nerve preparations. Histamine induced distinct increase in the discharge rate in 6 out of 17 units tested (high responders), while it only weakly excited the remaining 11 units (low responders). The bradykinin response of low responders tended to be slightly facilitated by pretreatment with histamine, while that of high responders tended to be suppressed. Significant correlation was observed between the magnitude of histamine-induced discharges and the magnitude of change in the bradykinin responses.
Animals↗
Inhibition of oxidation of low-density lipoprotein with red wine.
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Adult↗
Possible involvement of the EP2 receptor subtype in PGE2-induced enhancement of the heat response of nociceptors.
Prostaglandin E2 augments bradykinin- and heat-induced discharges of polymodal receptors as studied in vitro preparations. Our previous study revealed the involvement of the EP3 receptor subtype in the PGE2 induced enhancement of the BK response [Brain Res. 632 (1993) 321-324]. The agonist for EP2 (butaprost; 10(-8) M) significantly augmented heat responses, but did not augment the BK responses at concentrations from 10(-8) to 10(-5) M; however, the agonist for EP3 (M&B28767) or EP1 (17-phenyl-trinor-PGE2) at 10(-7) M did not affect the heat responses. These findings indicate the involvement of the EP2 receptor subtype in the augmenting effect of PGE2 on heat responses.
Alprostadil↗
Histamine-induced sensitization of the heat response of canine visceral polymodal receptors.
In elucidating the possible involvement of histamine (His) in hyperalgesia to heat, the effects of His on the heat response of testicular polymodal receptors were studied in vitro in canine testis-spermatic nerve preparations. His (100 and 1000 microM) induced discharges > 0.5 impulses/s (high-responders) in about one third of units tested. His (> or = 10 microM) facilitated the heat response irrespective of whether His alone induced substantial excitation, and the magnitude of facilitation at 100 microM did not differ between high- and low-responders (His-induced discharges < or = 0.5 impulses/s). Conduction velocity of high-responders at 100 microM (2.2 +/- 0.9 m/s, n = 5) was slower on average than that of low-responders (12.9 +/- 1.6 m/s, n = 9). The sensitizing effect of His reported in this paper suggests that His plays a role in hyperalgesia.
Animals↗