Biomedical subjects

K Yasui

Publications and source records attributed to K Yasui.

At least 217 records · Page 12Linked to original sources

PubMed1994

Collagen fibrils in the odontoblast layer of the rat incisor by scanning electron microscopy using the maceration method.

BACKGROUND: There is not universal agreement on the existence of the extracellular pathway from the pulp along the odontoblast layer to the predentin. METHOD: To confirm this pathway, the architecture of collagen fibrils in the rat incisor dentin and pulp, especially in the odontoblast layer of the lateral (periodontal ligament) sides of the tooth, was demonstrated in the present investigation using scanning electron microscopy of the maceration method for collagen networks. RESULTS: Numerous collagen bundles were observed in the odontoblast layer in the mature odontoblast region which, except for the young odontoblast region, comprises the major portion of the incisor. The collagen bundles went from the pulp, through the odontoblast layer, and were woven into the collagen network of the predentin. The meshwork structure was composed of fine secondary fibrils among these collagen bundles. The surface of the predentin contained many oval-shaped holes which were surrounded by collagen fibrils. Fracturing the dentin longitudinally relative to the dentinal tubules revealed that the arrangement of the collagen fibrils at the surface of the tubules was either circular or oblique. In the young odontoblast region, i.e., the thin portion from the apical end of the incisor where the mineralization of the dentin does not occur and where the height of the odontoblasts was less than 30 microns, many thick bundles composed of thick collagen fibrils ran straight from the pulp to the predentin through the odontoblast layer and fanned out in the collagen network of the predentin. These thick bundles might correspond to the so-called "von Korff fibers." The distribution of collagen fibrils in the pulp was random except on the surface of the blood vessels where the fibrils comprised two sheets of collagen: the inner sheet which coursed longitudinally to the long axis of the vessel, and the outer sheet which ran transversely. CONCLUSION: It was considered that the fluid in the pulp could flow to the predentin along the collagen fibrils through the tight junction between the odontoblasts.

Animals↗

PubMed1994

Neurofilament expression in lens cells of the house shrew, Suncus murinus.

Immunohistochemical analysis demonstrated that lens cells of the laboratory house shrew, Suncus murinus, expressed many intracellular filaments that immunoreacted with pooled monoclonal antibodies against 70-kDa, 160-kDa, and 210-kDa neurofilament triplet proteins. Immunopositive filaments in lens cells first appeared in day 13 embryos, while the invaginating lens placode was thickening, and this immunoreactivity was still present in immature lens fiber cells of the adult animal. Western blot analysis showed that the immunopositive molecule was a low-molecular-weight neurofilament protein that appeared in the neural tissues of this animal. The immunoreactive pattern of lens cells was quite similar to that of neurons, although there were some peculiar aspects. When the cells of the lens vesicle differentiated into the lens epithelium and fibers, immunoreactivity occurred in both, suggesting that the neurofilaments in the lens cells do not directly relate to lens fiber elongation nor to a determinant of the fiber caliber. The strong immunoreactivity in the embryonic lens and weak expression of this protein in the immature lens fiber cells of the adult animal suggest that low-molecular-weight neurofilament protein is transiently expressed in the differentiating lens cells. This may be a common feature of placode-derived cells.

Aging↗

PubMed1994

Apical cell escape from the neuroepithelium and cell transformation during terminal lip fusion in the house shrew embryo.

The house shrew embryo has many cells in the ventricular lumen and on the luminal surface of the fusing terminal lip of the cephalic neural tube. The origin and fate of these cells were studied by means of light and electron microscopy, and by DiI labeling in a whole-embryo culture system. The cells appeared at stage 11A and persisted until stage 12A. Most of the cells seemed to originate from the neuroepithelium, as shown by frequent observations of epithelial cell escape and DiI labeling analysis. The cells on the luminal surface sometimes showed apoptotic features, but were not subjected to phagocytosis. Some of the escaping cells seemed to migrate to the ventral part of the prosencephalic neuropore and insert themselves into it. Others separated from the luminal surface and floated into the lumen. It seems likely that the floating cells either become autolyzed, or else change into macrophage-like cells, the latter alternative being supported by the results of DiI labeling. The macrophage-like cells actively phagocytosed the other degenerating cells and apoptotic bodies. These observations suggest that the apical escape of cells may play an important role in the remodeling of the neural fold during the terminal lip fusion, and that early neuroepithelial cells may have the potential to become cells with vigorous phagocytic activity, like macrophages.

Animals↗

PubMed1994

Analysis of virus-cell binding characteristics on the determination of Japanese encephalitis virus susceptibility.

The susceptibility of fourteen established cell lines to infection with Japanese encephalitis virus (JEV) was assayed using an indirect fluorescent antibody technique. In kinetic studies, the degree of binding and internalization of JEV allowed the identification of high susceptibility and low-susceptibility cells. Scatchard analysis showed that JEV specifically bound to high-susceptibility Vero cells with greater affinity than to low-susceptibility NRK cells. Microinjection of viral genomic RNA into NRK cells induced highly efficient production of viral antigen and infectious virions. A hemagglutinin-inhibiting monoclonal antibody against JEV (MAb 301) inhibited the binding of JEV to the Vero and NRK cells. JEV was found to bind to a 74K molecule present in the membrane fraction of Vero cells and this binding was inhibited by MAb 301. Importantly, the 74K molecule was not detected in the membrane faction of NRK cells. These results suggest that early events in the JEV-cell interaction influence the susceptibility of cells to infection, and in particular suggests that the 74K molecule may be a possible candidate or component of the cellular receptor for JEV.

Animals↗

PubMed1994

Inhibition of myelin formation by HIV-1 gp120 in rat cerebral cortex culture.

To study the role of HIV-1 gp120 in loss of myelin in HIV encephalopathy, the binding of gp120 to various types of neural cells and its effects on myelination were examined in rat primary brain culture. Double-staining of cultured cells with gp120 and specific antibodies for different neural cell types showed that gp120 bound to most of the galactocerebroside (GalC)-positive oligodendrocytes, a small population of type-2-like astrocytes and a few small neurons. Gp120 did not bind to type-1-like astrocytes, most neurons, or to macrophage/microglia. To assay myelination, cells were bathed in a myelination medium containing chick embryo extract and high glucose, with or without gp120. Seven days after the application, myelination in the culture was observed morphologically and by staining with anti-myelin basic protein (MBP) antibody, and was found to be significantly inhibited by the addition of gp120 (50-100 nM). The processes of oligodendrocytes were reduced in length and arborization relative to the control, but MBP production by oligodendrocytes was unaffected. These results show that gp120 can cause a functional disorder of oligodendrocytes and thus could underlie the diffuse loss of myelin sheaths of HIV encephalopathy.

Animals↗

PubMed1994

Regulation of hepatocyte albumin and alpha 1-acid glycoprotein secretion by monokines, dexamethasone, and nitric oxide synthase pathway: significance of activated liver nonparenchymal cells.

To clarify the mechanism involved in regulating the secretion of albumin and alpha 1-acid glycoprotein by rat hepatocytes, we studied hepatocyte culture and cocultures of hepatocyte and liver nonparenchymal cells. The secretion of alpha 1-acid glycoprotein by hepatocytes was stimulated and that of albumin was inhibited by combinations of dexamethasone and monokines, especially by dexamethasone and interleukin-6. The secretion of these proteins was equally inhibited during stimulation by lipopolysaccharide in cocultures. The inhibitory effect of sinusoidal endothelial cells was smaller than that of Kupffer cells. This inhibition was partially abolished by blocking the nitric oxide synthase pathway in cocultured cells and was completely abolished by dexamethasone. In conclusion, the secretion of albumin and alpha 1-acid glycoprotein by hepatocytes was regulated by monokines, dexamethasone, and the inducible nitric oxide synthase pathway in hepatocytes and liver nonparenchymal cells in vitro.

Albumins↗

PubMed1994

Negative control mechanism with features of adaptation controls Ca2+ release in cardiac myocytes.

The central paradox of cardiac excitation-contraction coupling is that Ca(2+)-induced Ca2+ release (CICR), an inherently self-regenerating process, is finely graded by surface membrane Ca2+ current (ICa). By using FPL64176, a novel Ca2+ channel agonist that reduces inactivation of ICa, a rapid negative control mechanism was unmasked at the Ca2+ release level in isolated rat ventricular myocytes. This mechanism terminates CICR independently of the duration of trigger ICa and before the sarcoplasmic reticulum becomes depleted of Ca2+. In its ability to be reactivated by incremental increases in trigger ICa, this mechanism differs from conventional inactivation/desensitization and is similar to the mechanism of increment detection or adaptation described for intracellular Ca2+ release channels. These results indicate that ryanodine receptor adaptation regulates Ca2+ release in cardiac muscle, accounting for or contributing to the graded nature of CICR and, additionally, permitting stores to reload at later times during Ca2+ entry.

Animals↗

PubMed1994

Prognostic values of preoperative and postoperative CEA and CA19.9 levels in pancreatic cancer.

Preoperative serum levels of carcinoembryonic antigen (CEA) and/or carbohydrate antigen 19.9 (CA19.9) were measured in 90 patients with advanced pancreatic cancer. CEA antigen was above the cutoff levels of 5.0 ng/ml in 51% of patients and CA19.9 was above the cutoff limit of 37 U/ml in 87% of patients. High preoperative CEA and CA19.9 levels were related to a poor prognosis of the patients. In multivariate analysis, the hazard rate was significantly higher in the high-CEA group (> 2.5 ng/ml) compared to the low-CEA group (< 2.4 ng/ml). An increase in CEA and/or CA19.9 within 1 month after the operation was also significantly related to the hazard rate. This study reconfirms the prognostic importance of preoperative and postoperative CEA and CA19.9.

CA-19-9 Antigen↗

PubMed1994

Pentoxifylline and CD14 antibody additively inhibit priming of polymorphonuclear leukocytes for enhanced release of superoxide by lipopolysaccharide: possible mechanism of these actions.

Lipopolysaccharide (LPS) primes human polymorphonuclear leukocytes (PMN) for enhanced O2- production in response to stimulation by N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe). Serum factor is essential for priming at lower concentrations of LPS. Complexes of LPS and LPS-binding protein are recognized by CD14 on PMN. We investigated the effects of a monoclonal antibody against CD14 (MY4) and of pentoxifylline (POF), a membrane fluidizer, alone and in combination, on LPS-LPS-binding protein activation of phospholipase D evidenced by increased phosphatidic acid formation. Phosphatidic acid formation and O2- production were inhibited by MY4 and POF. Our results suggest that the actions of these agents occur at an early step in the excitation-response sequence. In the absence of a second stimulus, LPS plus serum caused an increase in the amount of Gi alpha 2 associated with the membrane via CD14. POF, however, had no effect on Gi alpha 2 in the membrane. POF alone significantly changed the affinity (KD) of the fMet-Leu-Phe receptor of PMN (from 25.2 +/- 4.5 nM to 15.2 +/- 2.4 nM [P < 0.01; n = 4]) at 37 degrees C. The differences between the sites of action of MY4 and POF may lead to cooperation by these agents for inhibition of priming by LPS plus serum for enhanced O2- production. Clinical use of the antibody and POF may diminish tissue damage caused by PMN in clinical endotoxic shock.

Adult↗

PubMed1994

Control of cardiac Ca2+ levels. Inhibitory actions of sphingosine on Ca2+ transients and L-type Ca2+ channel conductance.

The naturally occurring second messenger sphingosine (SPH) was examined for its ability to influence cardiac myocyte Ca2+ regulation. SPH inhibited intracellular Ca2+ transients in adult and neonatal rat ventricular myocytes. The inhibition was steeply dose dependent, with complete blockage of the Ca2+ transients occurring in the 20- to 25-mumol/L range. Whole-cell patch clamping revealed substantial inhibition of the L-type Ca2+ channel current (ICa) by SPH. The ability of SPH to block both the Ca2+ transients and ICa was not dependent on protein kinases, since the general protein kinase inhibitor H7 failed to prevent the actions of SPH. The specificity of the effect of SPH was determined in experiments showing that SPH analogues did not produce comparable effects. Neither the naturally occurring ceramide, N-stearoyl SPH, nor the cell-permeant ceramide, N-acetyl SPH, had SPH-like actions on the Ca2+ transients or L-type channel conductances. Caffeine-induced Ca2+ transients were also inhibited by the actions of SPH on cardiac sarcoplamic reticulum Ca2+ release, and the threshold for caffeine-induced Ca2+ release was raised. We conclude that SPH inhibits excitation-contraction coupling in cardiac myocytes by reducing the amount of entering "trigger Ca2+" for Ca(2+)-induced Ca2+ release and by simultaneously raising the threshold of the ryanodine receptor for Ca(2+)-induced Ca2+ release. Consequently, we propose that sphingolipids produced by the sphingomyelin signal transduction pathway could be physiologically relevant regulators of cardiac [Ca2+]i and therefore cardiac contractility.

Animals↗

PubMed1994

[Side effects of interferon on endocrine and respiratory system in 545 cases of chronic hepatitis C].

We investigated the side effects of interferon (IFN) on the endocrine and respiratory system in 545 cases of chronic hepatitis C. Eleven of 494 (2.2%) patients with chronic hepatitis C who were treated with natural or recombinant interferon (IFN) developed thyroid disease while on treatment. Eight patients developed hyperthyroidism and 3 patients developed hypothyroidism. All 11 patients required definitive therapy, who became euthyroid after the therapy. Two patients received nIFN alpha and one patient received rIFN alpha 2b developed diabetes mellitus. Two patients received rIFN alpha 2a and rIFN alpha 2b, respectively, developed interstitial pneumonia 12 weeks and 24 weeks later, respectively. One patient showed positive reaction for RA test and LE factor and positive LE cell, and complained of fever, arthralgia and dry cough. These phenomenon disappeared after the cessation of IFN therapy.

Adult↗

PubMed1994

[Autoimmune disorders in interferon therapy].

Interferons (IFNs) have immunomodulatory properties such as direct increase in the production of pathogen autoantibodies, enhanced cytotoxic T cell and B cell activities, inhibition of T suppressor cell function and induction of HLA class I antigen expression. These actions of IFN induce autoimmune disorders including autoimmune thyroiditis, hemolytic anemia and thrombocytopenia, SLE, rheumatoid arthritis and psoriasis, however, these autoimmune diseases except for autoimmune thyroiditis, are rare among side effects of IFN therapy. Most of the patients showing these autoimmune disorders during IFN treatment have predisposal immunological abnormalities such as positive ANA and antithyroidal autoantibodies. We described here autoimmune disorders during and after IFN treatment among 1023 cases with chronic active type C hepatitis. The cases with SLE, thrombocytopenic purpura, rheumatoid arthritis and psoriasis showed good prognosis after cessation of IFN administration.

Adult↗

PubMed1993

[Percutaneous transhepatic gastrostomy with CT guidance in patients with partial gastrectomy].

Percutaneous transhepatic gastrostomy was performed in two patients, one with partial gastrectomy and Billroth I anastomosis and one with esophageal reconstruction with subtotal stomach, in whom oral feeding was precluded. In both patients, percutaneous gastrostomy with fluoroscopic guidance was impossible since the gastric remnants were small, had a high subcostal position, and were overlain by the transverse colon, lung and left lobe of the liver. The only route available to avoid the overlying bowel and lung was the transhepatic approach. The gastric remnants were punctured with a 22-gauge PTC needle through the left lobe of the liver with CT guidance, and an 8 Fr. Cope-type catheter was fluoroscopically placed in the gastric remnant or the duodenum after tract dilatation over the guide wire. No complications occurred during or after the procedures, and the condition of both patients was greatly improved. Although gastrostomy in patients with partial gastrectomy is thought to be very difficult, percutaneous transhepatic gastrostomy with CT guidance is easy and may be safe since adhesion between the liver and gastric remnant can prevent massive hemorrhage or displacement of the catheters.

Aged↗

PubMed1993

Inhibition of acid secretion in gastric parietal cells by the Ca2+/calmodulin-dependent protein kinase II inhibitor KN-93.

A novel Ca2+/calmodulin-dependent protein kinase II (CaM Kinase II) inhibitor, KN-93 potently inhibits gastric acid secretion from parietal cells. As previously reported (1), treatment of parietal cells with a selective inhibitor of CaM kinase II, KN-62 resulted in the inhibition of cholinergic-stimulated rabbit parietal cell secretion, whereas it failed to inhibit the histamine and forskolin response. In contrast effects of carbachol, histamine and forskolin were significantly inhibited by KN-93 with an IC50 of 0.15, 0.3 and 1 microM, respectively; these effects occurred without any changes in intracellular cyclic AMP and Ca2+ levels. In the present study we investigated the mechanism by which KN-93 acts upon the acid-secreting machinery of gastric parietal cells. Neither redistribution of the proton pump activity nor the morphological transformation were affected by KN-93. The drug only weakly inhibited the H+, K(+)-ATPase activity but strongly dissipated the proton gradient formed in the gastric membrane vesicles and reduced the volume of luminal space. Thus KN-93 acts at pH gradient formation whereas KN-62 acts only at CaM Kinase II.

1-Methyl-3-isobutylxanthine↗

PubMed1993

Significance of pre-S region-defective hepatitis B virus that emerged during exacerbation of chronic type B hepatitis.

A defective form of the hepatitis B virus has been found in a patient with chronic type B hepatitis. Sequence analysis of the viral DNA after polymerase chain reaction amplification revealed a 117-base pair deletion (nucleotides 3129-53, subtype adr). This deletion includes the initiation codon of the pre-S2 region and a newly created in-frame stop codon in the pre-S1 region (nucleotide 3055) located 230 base pairs downstream from the pre-S1 initiation codon. This virus coexisted with the wild-type virus during the exacerbation period, as evidenced by an elevation of serum transaminase levels. It was not detected in the stable period, and the blood chemistry results were normal. We assayed antibodies against the mutation-related region by enzyme immunoassay in serial serum samples to clarify the mechanism of the emergence of this variant virus. Antibodies against the pre-S2 region were negative; however, the antibody response against the pre-S1 epitopes coincided with the appearance of the variant virus. These findings suggest that an activated T-cell and B-cell response had developed against the pre-S1 region during hepatic inflammation in this patient and that, consequently, selection occurred for a pre-S antigen-defective mutant strain of the virus that might be resistant to such an immune response.

Adult↗

PubMed1993

High-level expression of the Japanese encephalitis virus E protein by recombinant vaccinia virus and enhancement of its extracellular release by the NS3 gene product.

Recombinant vaccinia viruses expressing the prM and E genes of the Japanese encephalitis virus (JEV) were constructed by use of synthetic promoters. While the recombinant virus mOJ6-SL, with an optimized vaccinia late-gene promoter, produced a 20-fold elevated level of E protein, as well as an 86-kDa precursor protein in infected cells, no significant quantitative difference was detected between the extracellular or cell-surface E protein produced by mOJ6-SL and those produced by mOJ6 with the 7.5-kDa promoter. However, when the cells were infected with Dengue 2 virus before infection with mOJ6-SL, the amount of the extracellular E protein increased 16-fold. In addition, enhancement of its extracellular release was observed when cells were co-infected with mOJ6-SL and recombinant vaccinia virus expressing the NS3 gene of JEV.

Amino Acid Sequence↗

PubMed1993

Embryonic development of the house shrew (Suncus murinus). II. Embryos at stages 11 and 12 with 13 to 29 pairs of somites, showing limb bud formation and closed cephalic neural tube.

The embryonic development of the laboratory house shrew (Suncus murinus) was observed during the period from 13 to 29 pairs of somites and was compared with that of other mammalian species. This period ranged from 10 to 12 days after fertilization. Embryos were allocated to stages 11A-C and 12A-C according to somitic count. These embryos were characterized by the following features. 1. The curvature of the body became gradually enhanced, changing from a parenthesis-like to a bracket-like shape. 2. The swelling of the future hindlimb bud appeared at stage 11A, while the forelimb bud became apparent at stage 12A. The latter developed rapidly and had exceeded the former in size by the end of stage 12C. 3. The timing of closure of the cephalic neuropores varied, but the order of closure is constant. The prosencephalic neuropore closed later. The caudal neuropore still existed even at the end of stage 12C. 4. In all of the cranial nerve ganglia except for the auditory one, crest-derived cells seemed to contribute to the initial formation, while placodal cells seemed to be involved later. A different pattern of primordial formation was observed between trigeminal/facial and glossopharyngeal/vagal ganglia. 5. By the end of stage 12C, the eye cup and nasal pit began to form, and the endolymphatic appendage also appeared. 6. In the heart, the sinus valves were well developed, and the atrium and ventricle were being divided by the developing interatrial septum I and interventricular septum, respectively. 7. The thyroid primordium was temporarily everted and projected into the pharynx. The internal structure of this protruding thyroid resembled "tuberculum thyroideum" observed in the human embryo.

Animals↗

PubMed1993

Contribution of potassium accumulation in narrow extracellular spaces to the genesis of nicorandil-induced large inward tail current in guinea-pig ventricular cells.

The mechanism of nicorandil-induced large inward tail current (Itail) in single guinea-pig ventricular cells was investigated using the whole-cell patch-clamp technique. In the presence of 0.5-1.0 mM nicorandil, an activator of adenosine 5'-triphosphate (ATP)-sensitive K+ current (IKATP), a depolarization pulse causing a large outward current was followed by a large inward Itail on the repolarization step to the holding potential at -85 mV. The larger the outward current, the greater the Itail. The amplitude of Itail increased as a single exponential function (tau = 74.9 ms) as the duration of preceding depolarization was prolonged. Both the outward current and Itail were inhibited nearly completely after application of glibenclamide (1 microM), a specific blocker of IKATP. Substitution of K+ with Cs+ in both the external and internal solutions resulted in a virtual elimination of Itail. Itail was well preserved under the condition where Ca2+ entry during the preceding depolarization was largely inhibited or where external Na+ was replaced by Li+. A transient positive shift of reversal potential for the net current was observed at the peak of Itail). At 30 mM external K+ concentration, Itail was almost eliminated. From these findings, its is concluded that the Itail is a K+ current associated with an alteration of the K+ equilibrium potential (EK) following a substantial K+ efflux. This EK change is most likely explained by an accumulation of K+ in transverse tubules (T-tubules) since Itail was not induced in atrial cells in which T-tubules are poorly developed.

Adenosine Triphosphate↗