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Biomedical subjects

H Yanagida

Publications and source records attributed to H Yanagida.

At least 37 records · Page 2Linked to original sources
PubMed2000

Temperature-sensitive gating of cation current in guinea pig ileal muscle activated by hyperpolarization.

The temperature dependence of hyperpolarization-activated current (I(h)) was investigated in freshly isolated guinea pig ileal smooth muscle cells, using the nystatin-perforated whole cell recording technique. Hyperpolarizing pulses (-50 to -120 mV) from -40 mV evoked time-dependent inward rectifying currents with a reversal potential of -33 mV and a slow activation time course well approximated by a single exponential. The properties of these currents, such as steady-state variables, dependence on external K, modification by norepinephrine, and blockade by Cs or ZD-7288, coincide well with those of the "classical" I(h) discovered in the sinoatrial node. Raising the temperature (range: 22-33 degrees C) accelerated the activation time course of this I(h) and shifted its 50% activation potential positively (12 mV/10 degree) with much less change in the maximum conductance. Based on a simple closed-open model, this can be explained by a high temperature dependence of the opening rate constant (temperature coefficient: 3.4). The activation profile of reconstructed I(h) at 36 degrees C suggests that a considerable overlap could occur between the ranges of I(h) activation and physiological membrane potential.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Heparin-binding EGF-like growth factor is expressed by mesangial cells and is involved in mesangial proliferation in glomerulonephritis.

Heparin-binding epidermal growth factor-like growth factor (HB-EGF), a new member of the EGF family, is mitogenic for several types of cells, through binding to cell surface heparan sulphate proteoglycans. This study has attempted to delineate HB-EGF expression by mesangial cells and to identify its role in experimental and human glomerulonephritis. Rat mesangial cells, cultured in the presence of phorbol acetate, hydrogen peroxide, interleukin-1beta, and tumour necrosis factor-alpha, expressed HB-EGF mRNA. Recombinant HB-EGF stimulated rat mesangial cells to proliferate and to express types I and III collagen. In the rat anti-Thy-1.1 nephritis, glomerular HB-EGF mRNA was up-regulated and peaked at days 5-7; its expression at the protein level in the glomerulus was prominent at days 5-10. By immunofluorescence, HB-EGF was positive predominantly in the mesangial area of renal tissues from 23 of 45 patients with various types of human glomerulonephritis, showing a significant correlation with the grade of mesangial proliferation; there was no staining in tissues from patients with minimal change nephrotic syndrome and normal kidney tissues. These data provide the evidence that HB-EGF is synthesized and expressed by mesangial cells and stimulates mesangial cell proliferation and collagen synthesis in vitro. HB-EGF is a potential mediator in mesangial cell proliferation and matrix expansion in experimental and human glomerulonephritis.

Animals↗
PubMed1999

Immunocytochemical localization of a cell adhesion molecule, integrin alpha5beta1, in nerve growth cones.

It is well-known that nerve growth cones, the growing tips of nerves, play a central role in determining the direction taken by regenerating peripheral nerves though neurotropism and contact guidance. In order to identify the molecules expressed on growth cones that are responsible for contact guidance, we investigated the possible involvement of integrins as sensors for the extracellular matrix. In cultured rat PC-12i cells and chick dorsal root ganglion cells, we found that integrin alpha5beta1 was concentrated in the filopodia and central regions of the growth cones. These integrin alpha5beta1-rich regions corresponded well with the sites where the growth cones came into contact with and adhered to the extracellular matrix. Integrin alpha5beta1 has been reported to bind with fibronectin in the extracellular matrix. When examined by triple staining and confocal laser scanning microscopy, we found that the distribution of integrin alpha5beta1 in the growth cones was very similar to that of actin filaments. Integrin alpha5beta1 was also expressed by Schwann cells. On immuno-electron microscopy, integrin alpha5beta1 was also identified in regenerating axons in vivo. These results suggest that integrin alpha5beta1 expressed on growth cones may function as a sensor for the extracellular matrix and Schwann cells, and thus mediate functionally important interactions in the development and regeneration of peripheral nerves.

Actin Cytoskeleton↗
PubMed1999

Electroencephalographic responses to the formalin test in rats.

The formalin test is an animal model of persistent pain. Although biphasic behavioral responses to formalin injection have been well described, the significance of the biphasic time course of the pain behaviors has not been established. To explore the significance of the behavioral responses to the formalin injection, we measured and analyzed cortical electroencephalogram (EEG) during the formalin tests in rats. Formalin was injected subcutaneously in the hindpaw of freely moving rats, and behavioral responses were visually counted and recorded. Results were compared with a control group which received saline injection. Neocortical EEG was recorded from implanted dural surface electrodes and analyzed using a Fast Fourier Transformation. Formalin produced biphasic pain behaviors with a transient pause between two phases. Cortical EEG recordings showed a biphasic change; a vigilant pattern (a low amplitude high frequency activity) followed by a non-vigilant pattern (a high amplitude low frequency activity), showing a good correlation with apparent arousal states of rats. Observed discrepancies between pain behaviors and EEG-measured vigilance stages included (1) a vigilant EEG pattern persisted during the transient pause of pain behavior, and (2) pain behaviors persisted even after non-vigilant EEG pattern became dominant. The results of the current study showed that there are temporal discrepancies between the pain behaviors and EEG-measured vigilance during the formalin test in rats. The temporal relationship between the 'pain' behaviors and nociception per se may not be as solid as believed.

Animals↗
PubMed1999

A reaction kinetics model of water sonolysis in the presence of a spin-trap.

The time development of the concentration of a spin-trapped OH radical was studied by electron spin resonance at various sound intensities and various 5,5-dimethyl-1-pyrroline N-oxide (DMPO) concentrations in water sonolysis. The lifetime of the spin-trapped OH radical was also studied, and factors governing sonolysis are discussed. We found that the production of spin-trapped OH radical increases with increasing ultrasound intensity. The lifetime of a spin-trapped OH radical decreases linearly with increase in sonication time. This result suggests that an unknown scavenger is produced by ultrasound. Based on the above results, we suggested a model of the reaction kinetics and estimated the production rate of OH radical from this model.

Journal Article↗
PubMed1999

Coexpression of CD9 augments the ability of membrane-bound heparin-binding epidermal growth factor-like growth factor (proHB-EGF) to preserve renal epithelial cell viability.

BACKGROUND: Transfection of renal epithelial cells (NRK 52E) with membrane-associated heparin-binding epidermal growth factor-like growth factor (proHB-EGF) increased renal epithelial cell survival by promoting cell-cell and cell-extracellular matrix interactions. ProHB-EGF has been shown to form a complex in the plasma membrane with the tetraspanin CD9, an interaction that significantly increases the effectiveness of proHB-EGF as a juxtacrine mitogenic agent. METHODS: We examined whether the coexpression of proHB-EGF and CD9 would increase renal epithelial cell survival. CD9 was stably transfected into NRK 52E cells, either alone (NRKCD9) or together with proHB-EGF (NRKboth). RESULTS: Juxtacrine mitogenic activity of NRKCD9 was no different than in cells transfected with vector alone (NRKvector), but was increased by NRKboth; juxtacrine mitogenic activity by NRKboth was twofold greater than when proHB-EGF was transfected alone (NRKproHB-EGF). When grown in 10% fetal calf serum, growth rates were similar among all transfectants. However, in 1% fetal calf serum, NRKproHB-EGF grew 50% faster than NRKvector or NRKCD9, and NRKboth grew 20% to 50% faster than NRKproHB-EGF at one, two, and three days of culture. NRKproHB-EGF attachment to plastic substratum at one, two, and three hours was 250% greater than that of NRKvector, and NRKboth was 20% to 30% greater than that of NRKproHB-EGF. Coating plates with either poly 2-hydroxyethyl methacrylate or the GRGDTP peptide prevented normal cell-extracellular matrix attachment, and NRKvector or NRKCD9 failed to attach or form cell-cell attachments. NRKproHB-EGF exhibited 300% and NRKboth exhibited 600% greater cell viability under these conditions. Expression of type I and type III collagen mRNA was enhanced similarly in NRKproHB-EGF and NRKboth, but the expression of beta1 integrin was up-regulated only in NRKboth. CONCLUSIONS: Coexpression of proHB-EGF and CD9 may render the renal epithelial cells more resistant to disruption of cell-cell and cell-matrix interactions and could accelerate the re-establishment of these attachments.

Animals↗
PubMed1999

[Clinical evaluation of serum cytokine from patients with collagen diseases].

PURPOSE: Systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS) are characterized by an imbalance of cytokine production. To clarify the relationship between the profile of cytokines and the pathophysiology of systemic autoimmune diseases, we estimated the cytokine levels in sera from patients with several systemic autoimmune diseases. METHOD: Serum cytokine levels in patients with unclassified connective tissue diseases were measured using ultrasensitive specific enzyme-linked immunosorbent assay (ELISA). RESULT: These patients were diagnosed using the established category by further examinations within a 2-year period. Sera from patients with SLE contained higher titers of IL-10, and equal levels of IFN gamma and TNF alpha compared with those of normal controls. Patients with progressive systemic sclerosis (PSS) showed lower titers of IL-10 and higher titers of IFN gamma and TNF alpha in their sera than those of healthy controls. Seronegative rheumatoid arthritis (snRA) patients had a higher amount of IL-10 and TNF alpha, equivalent level of IFN gamma in their sera compared to those of controls. Moreover, patients with Sjögren's syndrome (SS) showed higher titers of IL-10 and TNF alpha, and an equivalent level of IFN gamma in their sera compared to healthy volunteers. CONCLUSION: Based on these findings, for the differential diagnosis of patients with systemic autoimmune diseases such as SLE, PSS, snRA and SS, it may be useful to measure the levels of cytokines such as IL-10, IFN gamma, and TNF alpha in their sera.

Autoimmune Diseases↗
PubMed1998

Seroma with fibrous capsule formation requiring a surgical resection after a modified radical mastectomy: report of a case.

Seroma formation is the most common complication of a modified radical mastectomy for breast cancer. Although various management or risk factors for seroma formation have been previously reported, little has been published concerning seromas with fibrous capsule formation which ultimately require a surgical resection. We herein present a case who developed a seroma with a fibrous capsule after a modified radical mastectomy for breast cancer, in spite of an uneventful intraoperative and postoperative course. The seroma was refractory to all conventional treatments, and thus finally required a surgical resection.

Axilla↗
PubMed1998

The NMDA-receptor antagonist ketamine abolishes neuropathic pain after epidural administration in a clinical case.

A 14-year-old male patient developed severe right limb pain after traumatic sciatic nerve injury. His pain was diagnosed as neuropathic pain (complex regional pain syndrome, type II). He did not respond to any conventional therapy for limb pain including non-steroidal antiinflammatory drugs, antidepressants, anticonvulsants, continuous epidural administration of local anesthetics and psychotherapy. Following continuous epidural administration of a very low dose of ketamine, an N-methyl-D-aspartic acid (NMDA) receptor antagonist, 25 microg/kg per h for 10 days, complete pain relief was obtained without any side-effects. There has been no recurrence of pain for 8 months after discontinuation of epidural ketamine. The symptoms related to dysfunction of the sympathetic nervous system still remained after complete pain relief. We discuss pain mechanisms, pain relief and the use of ketamine in this case.

Adolescent↗
PubMed1998

Postsynaptic enhancement by motilin of muscarinic receptor cation currents in duodenal smooth muscle.

We have investigated a potential role of motilin in amplifying the postsynaptic muscarinic responses in the rabbit duodenal smooth muscle cells, using the whole cell variant of patch-clamp technique. Stimulation of motilin receptors by exogenously applied motilin (1 nM) resulted in a large increase in carbachol (CCh)-induced atropine-sensitive cation current (ICCh) at threshold concentrations of CCh (0.3-1 microM) at 30 degrees C. This potentiation was abolished in the presence of a specific blocker of motilin receptor (GM109) and was attenuated with increased concentrations of either motilin or CCh, being virtually absent with maximally effective concentrations of these agonists. Motilin failed to potentiate ICCh when the ambient temperature was reduced to 20 degrees C or if the cation current had been directly activated by internal perfusion with guanosine 5'-O-(3-thiotriphosphate) (50 microM) bypassing the muscarinic receptor. These results suggest that some biochemical processes, such as enzymatic reactions, might be involved in the motilin-induced potentiation and that its site of action might be the muscarinic receptor and/or associated G proteins.

Animals↗
PubMed1998

Potentiating actions of lanthanum on ACh-induced cation current in guinea-pig ileal smooth muscle cells.

Potentiating actions of external lanthanum (La3+) on muscarinic receptor-activated nonselective cation current (Icat) were investigated in myocytes dissociated from the longitudinal muscle layer of guinea-pig ileum, with a whole-cell variant of the patch clamp technique. Icat was dissected from other membrane currents by loading Cs-aspartate into the cell. Application of submilimolar concentrations of La3+ following 300 microM ACh into the bath caused a dose-dependent increase in the amplitude of Icat. The apparent Kd value for this increase was 190 microM, with a cooperativity factor of 1.7. La(3+)-induced increase in Icat amplitude was not associated with either changes in the reversal potential of Icat or altered sensitivity of muscarinic receptor to ACh, and paralleled by the conductance increase of Icat, the maximum of which (Gmax) occurred at about 1 mM La3+. Voltage-jump experiments revealed that the rate of current relaxation at hyperpolarizing potentials was greatly reduced in the presence of La3+, and correspondingly the steady state activation curve shifted toward more negative potentials. Divalent cations such as Cd2+ or Ni2+, which have been known to block Icat, antagonized the augmentative effect of La3+ on Icat in a competitive fashion, suggesting that the site of their actions might be similar. Furthermore, single Icat activities induced by internal perfusion of GTP gamma S (100 microM) was also greatly enhanced by external addition of 1 mM La3+. Under current clamp conditions, 1 mM La3+ blocked spontaneous Ca2+ spike activities, but was almost without effect on the membrane depolarization induced by ACh. In contrast, milimolar concentrations of Cd2+ and Ni2+ abolished both Ca2+ spike activities and ACh-induced depolarization. Potential importance of La3+ as a tool to investigate the external Ca(2+)-dependence of Icat has been discussed.

Acetylcholine↗
PubMed1997

[Clonal deletion and clonal anergy as the mechanism of self-tolerance induction].

In the immune system, it is most important to discriminate self from nonself and to acquire and maintain the unresponsiveness to self antigens, self-tolerance. Recently, the transgenic animals provides the evidence of the mechanism of self-tolerance induction. Self-tolerance is established mainly by elimination, clonal deletion, and functional inactivation, clonal energy, of the autoreactive T cells and B cells. Clonal deletion and clonal anergy are involved not only in the central tolerance, in thymus or bone marrow, but also in the peripheral tolerance. The failure of self-tolerance involves the induction of auto-immune disease.

Animals↗
PubMed1997

[An imbalance between Th1 and Th2-like cytokines in patients with autoimmune diseases--differential diagnosis between Th1 dominant autoimmune diseases and Th2 dominant autoimmune diseases].

An imbalance between T helper cell (Th)1 and Th2-like cytokines has been described in several autoimmune diseases. Organ specific autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel diseases (IBD) are caused by Th1 dominant immune responses. On the contrary, systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome(SS) are characterized by Th2 dominant imbalance of cytokine production. It might be useful for differential diagnosis among patients with various autoimmune diseases such as SLE, SS, IBD, and MS to measure the serum levels of cytokines such as IL-10, IFN gamma, and TNF alpha using ultrasensitive enzyme-linked immunosorbent assay system.

Animals↗
PubMed1996

IL-10 suppresses cell surface CD23/Fc epsilon RII expression, not by enhancing soluble CD23 release, but by reducing CD23 mRNA expression in human monocytes.

To examine a possible involvement of interleukin-10 (IL-10) in CD23/Fc epsilon RII expression in human monocytes, effects of IL-10 on the cell surface CD23 expression, soluble CD23 (sCD23) release, and CD23 type b mRNA expression were investigated. IL-10 suppressed IL-4-induced surface CD23 expression on monocytes in a dose-dependent manner, and this effect was completely neutralized by anti-IL-10 antibody. The suppressive effect of IL-10 on surface CD23 expression was not due to enhancement of sCD23 release from the cell surface because no increase in sCD23 in culture supernatant was detected after incubation with IL-10. Instead, the effect of IL-10 seemed to be exerted at the transcriptional level since IL-4-induced expression of CD23 type b mRNA was significantly reduced when IL-10 was present. Although IL-4 induced surface CD23 expression on both monocytes and B cells, the suppressive effect of IL-10 was observed only on monocytes, which underscores different regulatory mechanisms for CD23 expression between the two cell types.

B-Lymphocytes↗
PubMed1995

Enhanced production of transforming growth factor-beta (TGF-beta) during autologous mixed lymphocyte reaction of systemic sclerosis patients.

Systemic sclerosis (SSc) is characterized by systemic fibrosis and microvascular lesions. As TGF-beta is suggested to be related to skin fibrosis, we examined the production of TGF-beta from peripheral mononuclear cells (MNC) of SSc patients. Since anti-TGF-beta neutralizing antibody improved the defective proliferative response in autologous mixed lymphocyte reaction (AMLR) of SSc patients, TGF-beta was thought to participate in the decreased AMLR of SSc patients. Greater amounts of TGF-beta in the active as well as in the latent forms were produced during AMLR of SSc patients than that of normal subjects. It was suggested that TGF-beta excessively produced from the MNC of SSc patients might play a major role in the fibrosis of the patients during AMLR-like in vivo responses.

Adult↗
PubMed1994

Localization of Rabphilin-3A on the synaptic vesicle.

Rabphilin-3A is a putative target protein for Rab3A small GTP-binding protein which is implicated in neurotransmitter release. Rabphilin-3A is expressed mainly in brain, but its subcellular localization remains to be clarified. Immunohistochemical analysis has revealed that Rabphilin-3A is most abundant in the synaptic area of the rat cerebellum, retina, and neuromuscular junction. Ultrastructural analysis of the neuromuscular junction using the immunogold method indicates that Rabphilin-3A is localized on the synaptic vesicle. Subcellular fractionation analysis of rat brain has shown that Rabphilin-3A is most highly concentrated in the purified synaptic vesicle fraction. These results indicate that Rabphilin-3A is localized on the synaptic vesicle in the presynapse.

Adaptor Proteins, Signal Transducing↗