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Biomedical subjects

H Ichikawa

Publications and source records attributed to H Ichikawa.

At least 343 records · Page 19Linked to original sources

The effects of several pharmacologic agents upon postischemic recovery.

Using an isolated working rat heart model, the effects of DL-verapamil, ryanodine, gabexate mesilate (FOY), recombinant human superoxide dismutase (RH-SOD), and coenzyme Q10 upon myocardial protection were evaluated. Under conditions of normothermic ischemia, all these compounds, except RH-SOD, when added to the St. Thomas' cardioplegic solution at an optimal concentration, showed beneficial effects upon functional recovery and enzyme leakage. In contrast, the above compounds, except ryanodine and FOY, failed to improve the protective properties of the St. Thomas' cardioplegic solution under conditions of hypothermic ischemia. Our results indicate that calcium overload via the calcium channel and calcium-induced calcium release from sarcoplasmic reticulum (SR) may contribute to the onset of ischemic-reperfusion injury. However, under conditions of hypothermic ischemia, calcium-induced calcium release from SR plays a dominant role in calcium overload. Furthermore, intracellular calcium overload may activate proteases and result in the acceleration of myocardial injury.

Animals↗

Harmful effects of inotropic agents on myocardial protection.

Using an isolated working rat heart model, the pretreatment effects of positive inotropic agents on ischemia-reperfusion injury were investigated. The experiment consisted of (1) working control perfusion; (2) working perfusion with isoproterenol (I), milrinone (M), a combination of these drugs (I + M) and dibutyl-cyclic adenosine monophosphate (DB) followed by ischemic arrest for 33 minutes at 37 degrees C or 150 minutes at 20 degrees C and Langendorff reperfusion; and (3) working perfusion. Under conditions of normothermic ischemia, percent recoveries of postischemic cardiac output (mean +/- standard error of the mean) in the I, M, I + M, and DB groups were 37.8% +/- 12.7%, 61.3% +/- 3.1%, 0%, and 53.1% +/- 5.2%, respectively. Under conditions of hypothermic ischemia, the percent recoveries in I + M and DB groups were 10.9% +/- 7.9% and 29.8% +/- 9.5%; they were all significantly lower than that in the control group. The addition of diltiazem or ryanodine at several concentrations and lowering of the Ca2+ concentration in the St. Thomas' cardioplegic solution did not prevent I + M-induced injury. Our data suggest that pretreatment by I + M aggravated ischemia-reperfusion injury, and adjustments in Ca2+ concentration were not sufficient to prevent that injury.

Animals↗

Neuropeptide Y- and substance P-like immunoreactivities in the guinea pig parotid gland.

These immunoreactivities were examined by double immunofluorescence, which demonstrated that many nerve fibres around the glandular acini and blood vessels contain neuropeptide Y and substance P. It appears that these substances may coexist in nerve fibres around acini, but that there may be two populations of fibres containing these peptides around the blood vessels.

Animals↗

New metabolites of thiabendazole and the metabolism of thiabendazole by mouse embryo in vivo and in vitro.

Thiabendazole [2-(4'-thiazolyl)benzimidazole; TBZ], a teratogen in ICR mice, is known to be mainly metabolized to 5-hydroxy-TBZ (5-OH-TBZ) and its conjugates in domestic and laboratory animals. Besides the known metabolites of TBZ, 4-hydroxy-TBZ and 2-acetylbenzimidazole (ABI) were identified as new metabolites of TBZ in the urine of F344 rats and ICR mice. 5-OH-TBZ and ABI, as well as TBZ, were found in the embryos of ICR mice given TBZ orally on day 10 of gestation. In the whole-embryo culture system, 5-OH-TBZ and ABI in the medium, and TBZ, 5-OH-TBZ and ABI in the embryo were detected after 24 hr of culture in 25 or 50 micrograms TBZ ml. However, the amount of metabolites in the embryo in vitro was very small compared with that detected in vivo, whereas the amount of TBZ was comparable. Furthermore, the mouse embryo homogenate, at organogenesis, metabolized TBZ to 5-OH-TBZ or ABI. The specific activity required by this homogenate to form 5-OH-TBZ or ABI was less than 1/1000 of that of the liver microsomal fraction. The results suggested that mouse embryos at organogenesis could metabolize TBZ, although most of the metabolites in the embryo in vivo came from the dam.

Animals↗

[A case report of siblings with hemolytic uremic syndrome from whose stool E. coli O157:H7 was isolated].

We experienced siblings of hemolytic uremic syndrome which occurred following diarrhea and bloody stool. They were immediately treated with dipyridamole and aspirin, and recovered from hemolytic uremic syndrome in about two weeks. E. coli O157:H7 (verotoxin producing E. coli) which is recently thought to be related to the pathogenesis of hemolytic uremic syndrome was isolated in their stool cultures on admission. As far as we know, this is the first case in Japan from which stool E. coli O157:H7 was detected. Moreover, we reported clinical effectiveness of genomic investigation utilizing polymerase chain reaction method for verotoxin coding region in a rapid diagnosis of this bacterial infection.

Child, Preschool↗

Ontogeny of cholinergic ganglionic cells which take up L-3,4-dihydroxyphenylalanine and contain vasoactive intestinal polypeptide in the mouse tongue.

During the prenatal development of the mouse tongue, the intralingual ganglion was investigated histochemically and immunohistochemically for acetylcholinesterase (AChE) activity, the capacity to take up L-3,4-dihydroxyphenylalanine (L-DOPA) and vasoactive intestinal polypeptide (VIP)-like immunoreactivity. AChE-positive cells were first observed at gestational day 12, and AChE-positive neurons which take up L-DOPA were found at gestational day 14, while VIP-like immunoreactive neurons were not seen until gestational day 16. The present results suggested that the cholinergic neurons within the mouse tongue can take up L-DOPA from gestational day 14 and synthesize VIP from gestational day 16.

Acetylcholinesterase↗

Systematized keratotic nevus with finger contracture.

A case of systematized keratotic nevus which is a peculiar form of epidermal nevus is reported. The present case is rare because of the dysfunction of incomplete flexion of fingers by systematized keratotic nevus. Furthermore, it involved mixed clinical and histological changes of epidermal nevus from fingers to elbow. An operation with full-thickness skin graft was undertaken.

Adult↗

[The effects of calcium concentration of reperfusion solution upon myocardial protection].

The effects of several calcium concentrations in reperfusion solution were studied. Experimental time course was as followed: 20 min working perfusion, 3 min cardioplegic infusion with St. Thomas cardioplegic solution (STS) followed by global ischemia for 30 min at 37.5 degrees C, 15 min early Langendorff reperfusion with reperfusion solution and 5 min late reperfusion with Krebs Henseleit bicarbonate buffer [( Calcium] = 2.5 mM), followed by 20 min working perfusion. Percent recoveries of aortic flow at the Ca concentration of 0, 0.1, 0.6, 1.2, 1.8, 2.5 mM were 0, 14 +/- 1, 43 +/- 4, 64 +/- 3, 55 +/- 2, 59 +/- 1 (%), respectively. Our data indicated that reperfusion solution with less than 1.2 mM calcium reduced the protective properties of STS.

Animals↗

[The effects of magnesium concentration in reperfusion solution upon myocardial protection].

Experimental time course was as follows: 20 min working perfusion, 3 min cardioplegic infusion with St Thomas Cardioplegic Solution followed by global ischemia for 35 min at 37.5 degrees C, 15 min first Langendorff reperfusion with reperfusion solution (RS) with various concentrations of Mg and 5 min second reperfusion with KHBB, followed by 20 min working. Cardiac functions were measured during pre and post working perfusion and CK leakage were measured during reperfusion. Percent recoveries of aortic flow at the Mg concentration of 0, 0.6, 1.2, 3.0, 6.0, 12 mM were 21 +/- 5, 22 +/- 3, 48 +/- 2, 37 +/- 4, 28 +/- 3, 15 +/- 3 (%) (mean +/- SEM), respectively. Our data indicated that 1.2 mM Mg of RS possessed protective properties with bell shaped dose response characteristics.

Animals↗

[Chemoembolization with degradable starch microspheres for liver metastases of colorectal cancer].

Transcatheter chemoembolization using degradable starch microspheres (DSM) was performed in 17 patients with liver metastases of colorectal cancer. DSM, 45 microns in diameter, which are easily degraded by serum amylase, and therefore obstruct arterial blood flow temporarily at the arteriolar capillary bed. DSM mixed with mitomycin C were administered through the catheter introduced by Seldinger's method in 13 cases, and through subcutaneously implanted drug delivery system (Port-A-Cath) in 4 cases. The treatment was repeated 5 times on the average at intervals of 2 to 4 weeks. The therapeutic effect of this chemoembolization was evaluated by the change in tumor size measured by angiography or computed tomography. Tumor regression of over 50% was observed in 9 of 17 cases (53%). Elevated serum CEA levels (greater than 10 ng/ml) decreased in 10 of 15 cases (67%). One-year survival rate was 48% in 17 cases, and among them it was 100% in 7 cases with the extent of several liver metastases (H2). Extrahepatic metastasis was observed in 3 of 17 cases (18%) before the treatment, and in 8 cases (47%) after the treatment. Abdominal pain occurred in 36% of the cases by the administration of DSM, but the pain disappeared within 2 hours. No major side effects such as bone marrow suppression or hepatotoxicity were observed. Our results suggest that chemoembolization using DSM is effective and safe in the treatment of liver metastases from colorectal cancer.

Carcinoembryonic Antigen↗

Electron microscopic visualization of actin filaments in the early embryo of Drosophila melanogaster: the use of phalloidin and tropomyosin.

Various specimen preparations for thin-section electron microscopy were tested to better preserve and visualize actin filaments in the cortex of the early embryos of Drosophila melanogaster. When embryos were treated with phalloidin prior to fixation, many actin filaments were observed in their cortex comparable to the staining with fluorescently labeled phalloidin in light microscopy. Then we used various fixatives containing phalloidin. As far as we examined, actin filaments were best preserved in the specimen fixed with 2.5% glutaraldehyde, 2% paraformaldehyde in 0.1 M sodium phosphate buffer or in 0.1 M PIPES buffer (1 mM EGTA and 1 mM MgCl2) containing 10 microM phalloidin and 0.1% saponin. When embryos were glycerinated and then treated with tropomyosin before fixation, actin filaments were well visualized as thicker, uniform-sized filaments, though the number of filaments decreased probably owing to glycerination. This suggests that, like heavy meromyosin and its subfragment-1, this protein may protect actin filaments from being disrupted by chemical fixation. Using these improved fixation procedures, we successfully examined the distribution of actin filaments in the Drosophila embryo cortex during cellularization. These methods may be applicable to stabilize labile actin filaments in other types of cells.

Actin Cytoskeleton↗

In vitro transposition of transposon Tn3.

Transposition of the ampicillin-resistant transposon Tn3 was reproduced in vitro using the Escherichia coli cell extract. In this cell-free system, we used plasmid DNA carrying mini-Tn3 as donor and phage lambda DNA as target and assayed for ampicillin-resistance transducing phages formed by cointegration of these DNA molecules. Ampicillin-resistance transducing phages, which were obtained by in vitro packaging of lambda DNA after the in vitro transposition reaction, were formed only in the presence of Tn3 transposase. The reaction required mini-Tn3 with the proper sequence and orientation of the terminal inverted repeats of Tn3. The reaction also required DNA synthesis but not RNA synthesis by E. coli RNA polymerase.

Ampicillin Resistance↗

Aversive taste stimuli increase CGRP levels in the gustatory insular cortex of the rat.

Calcitonin gene-related peptide-like immunoreactivity (CGRP-IR) was surveyed immunohistochemically in the insular cortex of the rat, and the levels of insular cortical CGRP-IR were measured with the radioimmunoassay method following intraoral stimulation with various taste stimuli. CGRP-IR was localized in nerve fibers within the agranular and dysgranular insular cortices. The CGRP-IR levels in the rostral (gustatory) part of the insular cortex were increased significantly by strongly aversive taste stimuli such as quinine hydrochloride and conditioned taste stimuli (NaCl and sucrose) which animals had been taught to avoid. The results suggest that CGRP in the gustatory insular cortex is concerned with rejection or avoidance behaviors to aversive taste stimuli.

Animals↗

Tn3 transposition immunity is conferred by the transposase-binding domain in the terminal inverted-repeat sequence of Tn3.

A series of mutant terminal inverted repeats (IRs), having 2 bp substitutions at various sites within the 38-bp IR sequence of the ampicillin-resistance transposon Tn3, were tested for transposition immunity to Tn3. Mutations within region 1-10 in the IR did not affect transposition immunity, while mutations within region 13-38 inactivated the immunity function. These two regions corresponded to domain A which was not bound specifically by Tn3 transposase and to domain B which was bound by the transposase, respectively. This indicates that specific binding of transposase to domain B within the IR sequence is responsible for transposition immunity.

Ampicillin Resistance↗

Two domains in the terminal inverted-repeat sequence of transposon Tn3.

Tn3 and related transposons have terminal inverted repeats (IR) of about 38 bp that are needed as sites for transposition. We made mini-Tn3 derivatives which had a wild-type IR of Tn3 at one end and either the divergent IR of the Tn3-related transposon, gamma delta or IS101, or a mutant IR of Tn3 at the other end. We then examined both in vivo transposition (cointegration between transposition donor and target molecules) of these mini-Tn3 elements and in vitro binding of Tn3-encoded transposase to their IRs. None of the elements with an IR of gamma delta or IS101 mediated cointegration efficiently. This was due to inefficient binding of transposase to these IR. Most mutant IR also interfered with cointegration, even though transposase bound to some mutant IR as efficiently as it did to wild type. This permitted the Tn3 IR sequence to be divided into two domains, named A and B, with respect to transposase binding. Domain B, at positions 13-38, was involved in transposase binding, whereas domain A, at positions 1-10, was not. The A domain may contain the sequence recognized by some other (e.g., host) factor(s) to precede the actual cointegration event.

Base Sequence↗