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Biomedical subjects

C Yamamoto

Publications and source records attributed to C Yamamoto.

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

Immune response of tonsillar lymphocytes to Haemophilus parainfluenzae in patients with IgA nephropathy.

The pathogenesis of IgA nephropathy (IgAN) is unclear. We have previously shown glomerular deposition of Haemophilus parainfluenzae (HPI) antigens and the presence of IgA antibody against HPI antigens in patients with IgAN. We examined the immune response to HPI antigens in tonsillar lymphocytes from patients with IgAN. Lymphocytes isolated from the palatine tonsils of 13 IgAN patients and 16 patients with chronic tonsillitis but without renal disease were used as controls. We examined lymphocyte proliferation and production of IgA antibody against HPI antigens by measuring thymidine uptake and IgA antibody in culture supernatants after lymphocyte incubation with HPI antigens. Patients with IgAN showed a significantly higher stimulation index to HPI antigens (thymidine incorporation in tonsillar lymphocytes with HPI/thymidine incorporation in unstimulated tonsillar lymphocytes) than controls (P < 0.002). Lymphocytes from patients with IgAN also showed a significantly higher level of IgA antibody and IgA1 antibody against HPI antigens in culture supernatants than lymphocytes from controls (P = 0.0002 and P = 0.004, respectively). Our results suggest that HPI antigens stimulate tonsillar T and B lymphocytes in patients with IgAN and that an immune response to HPI antigens may play a role in the pathogenesis of this disease in some cases.

Adolescent↗
PubMed2000

Synthesis of immunoglobulins against Haemophilus parainfluenzae by tonsillar lymphocytes from patients with IgA nephropathy.

BACKGROUND: We previously demonstrated glomerular deposition of Haemophilus parainfluenzae (HP) antigens and the presence of IgA antibody against HP antigens in patients with IgA nephropathy (IgAN). In this report we examine the synthesis of immunoglobulins against HP antigens in tonsillar lymphocytes from patients with IgAN. METHODS: We used tonsillar lymphocytes isolated from the palatine tonsils of 15 patients with IgAN and 16 patients with chronic tonsillitis but without renal disease. We examined lymphocyte proliferation and production of IgA, IgG, and IgM antibodies against HP antigens by measuring thymidine uptake and concentrations of these antibodies in culture supernatants after lymphocyte incubation with HP antigens by ELISA. RESULTS: Lymphocytes from patients with IgAN showed a significantly higher stimulation index (SI) on exposure to HP antigens (thymidine incorporation in tonsillar lymphocytes exposed to HP (c.p.m.)/ thymidine incorporation in unstimulated tonsillar lymphocytes (c.p.m.)) than did controls (P=0. 0015). Lymphocytes from patients with IgAN also showed a significantly higher IgA SI (concentrations of IgA against HP antigens in supernatants from HP-stimulated lymphocytes/IgA against HP antigens in supernatants from unstimulated tonsillar lymphocytes) than did controls (P=0.0004). We found positive correlations between concentrations of IgA and IgG antibodies, between IgA and IgM antibodies, and between IgG and IgM antibodies against HP antigens after HP stimulation. CONCLUSIONS: Our results suggest that HP antigens stimulate tonsillar T and B lymphocytes in patients with IgAN and that these patients have polyclonal activation of lymphocytes against HP antigens, with isotype switching of antibody production from IgM to IgA.

Adolescent↗
PubMed2000

[Toxicity of cadmium and lead on vascular cells that regulate fibrinolysis].

Cadmium and lead are heavy metals that cause vascular lesions such as atherosclerosis and hypertension. Toxicity of cadmium and lead on the regulation of fibrinolysis by vascular-composing cells was investigated using a cell culture system. It was found that cadmium promotes the synthesis of plasminogen activator inhibitor-1 (PAI-1) whereas lead inhibits the synthesis of tissue plasminogen activator (t-PA) in vascular endothelial cells; consequently, both heavy metals reduced fibrinolytic activity in the liquid phase. The responses of endothelial cells to cadmium and lead were different from those to other heavy metals and the release of the fibrinolytic proteins from vascular smooth muscle cells and fibroblasts was perturbed by cadmium and lead in different manners. In conclusion, the present study showed that cadmium and lead exhibit their toxicity on fibrinolysis regulated by vascular cells in different manners among cell types and the individual cell types respond to cadmium and lead in different manners with respect to the release of fibrinolytic proteins.

Cadmium↗
PubMed2000

Enantioseparations using cellulose tris(3,5-dichlorophenylcarbamate) during high-performance liquid chromatography with analytical and capillary columns: potential for screening of chiral compounds.

The appropriate selection of the mobile phase facilitated the use cellulose tris(3,5-dichlorophenylcarbamate (CDCPC) as a chiral stationary phase (CSP) during high-performance liquid chromatography (HPLC). A preliminary evaluations of this material indicated its very high chiral resolving ability toward many analytes of different chemical and pharmacological groups. Some chemicals and drugs containing two centers of chirality were also successfully resolved into all possible stereoisomers. The applicability of CDCPC for enantioseparations in capillary liquid chromatography was also shown giving promising prospects for the screening of novel biologically active compounds (which may be also synthesized based on combinatorial strategies) for their enantiomeric composition.

Carbamates↗
PubMed1999

Chiral recognition of cellulose tris(5-fluoro-2-methylpheylcarbamate) toward (R)- and (S)-1, 1'-bi-2-naphthol detected by negative ion fast-atom bombardment mass spectrometry

Chiral recognition between cellulose tris(5-fluoro-2-methylphenylcarbamate) (MW > 120,000) as a host compound and (R,S)-1,1'-binaphthol (MW 286) as a guest compound was investigated by fast-atom bombardment mass spectrometry (FAB-MS). The use of negative ion FAB-MS made it possible to obtain a very simple mass spectrum of the guest compound with a high signal-to-noise ratio. Additionally, when nitrophenyl octyl ether, which has no OH group, was utilized as matrix, chiral recognition between the host and the guest compounds was unequivocally detected. Copyright 1999 John Wiley & Sons, Ltd.

Journal Article↗
PubMed1999

Adult and geriatric normative data and validation of the profile of mood states.

The Profile of Mood States (POMS; McNair, Lorr, & Droppleman) is widely used to assess mood states. However, the utility of the POMS has been restricted by the lack of normative data from the general population. We report on our adult (N = 400) and geriatric (N = 170) POMS standardization samples. Both groups were age-, gender-, and race-stratified according to 1990 census data. We also report on convergent and discriminant validity of POMS scales, using a multitrait, multimethod paradigm.

Adolescent↗
PubMed1999

Contribution of P-glycoprotein to bunitrolol efflux across blood-brain barrier.

In this study, we investigated the mechanism of the blood-brain barrier (BBB) transport of bunitrolol (BTL), as a model of beta-blocker, in vivo and in vitro. In order to define the contribution of P-glycoprotein (P-gp) to the active efflux of BTL from brain to blood, we examined the in vivo brain distribution of BTL in mdr1a(-/-) mice with a disrupted mdr1a gene. After intravenous administration of BTL to mdr1a(-/-) mice, the brain concentration and Kp value of BTL were significantly increased as compared with those in mdr1a(+/+) mice. Next, the contribution of the mdr1a P-gp to in vitro uptake of BTL was compared in LV500 cells and L cells (mouse mdr1a-expressing cells and host cells, respectively). The intracellular accumulations of [3H]vinblastine and BTL by LV500 cells were lower than those by L cells, but were significantly increased by verapamil, a P-gp inhibitor. Furthermore, the BTL uptake by KB-VJ300 cells, which express human P-gp, was also significantly lower than that by KB host cells, and was increased by verapamil. The steady-state uptake of BTL by LLC-GA5-COL300 cells, expressing human P-gp, was significantly increased in the presence of 20 microM cyclosporin A (another P-gp inhibitor), which had no effect in the LLC-PK1 host cells. On the other hand, the steady-state intracellular accumulation of BTL by MBEC4 cells, which express mdr1b P-gp instead of mdr1a P-gp, was not significantly changed in the presence of verapamil. This finding suggested that BTL is not a good substrate for mdr1b P-gp. In conclusion, our results suggest that BTL is transported from brain to blood by mdr1a P-gp in mice and by MDR1 in humans, and this presumably accounts for the low brain distribution of BTL.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Cycloprodigiosin hydrochloride, a new H(+)/Cl(-) symporter, induces apoptosis in human and rat hepatocellular cancer cell lines in vitro and inhibits the growth of hepatocellular carcinoma xenografts in nude mice.

The effects of cycloprodigiosin hydrochloride (cPrG-HCl), a new H(+)/Cl(-) symporter, were examined in liver cancer cell lines in vitro and in vivo. In the in vitro MTT assay, cPrG-HCl inhibited the growth of 6 liver cancer cell lines (Huh-7, HCC-M, HCC-T, dRLh-84, and H-35, hepatocellular carcinoma; HepG2, hepatoblastoma) in a dose- and time-dependent manner. The 50% inhibitory concentrations (IC(50)) at 72 hours' treatment for liver cancer cell lines were 276 to 592 nmol/L, while that for isolated normal rat hepatocyte was 8.4 micromol/L. The cPrG-HCl treatment of Huh-7 cells induced apoptosis as confirmed by the appearance of a subG(1) population, intranucleosomal DNA fragmentation, and chromatin condensation. cPrG-HCl raised the pH of acidic organelles and lowered pHi (below pH 6.8). In addition, the apoptosis in Huh-7 cells induced by cPrG-HCl was strongly suppressed when the cells were cultured with imidazole, a cell-permeable base. In the in vivo assay, nude mice bearing subcutaneous xenografted Huh-7 cells received 2 weeks of treatment with cPrG-HCl (1 or 10 mg/kg/d) subcutaneously. This treatment significantly inhibited tumor growth compared with the control after 8 days. The control mice were treated with 1% dimethylsulfoxide (DMSO) in saline (vehicle). A histopathological examination using the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) method showed apoptosis in the treated tumor cells. No pathological changes were observed in any organs, and the serum alanine transaminase levels remained within normal limits. These results suggest that cPrG-HCl may be useful for the treatment of hepatocellular carcinoma.

Animals↗
PubMed1999

Down-regulation of TGF-beta receptors in human colorectal cancer: implications for cancer development.

Many colorectal cancer cells are resistant to the anti-proliferative effects of transforming growth factor-beta (TGF-beta). TGF-beta also acts as paracrine factor from cancer cells on their mesenchymal cells. The aim of this study was to examine the expression of TGF-beta and its receptors in human colorectal cancer tissue and determine any relationship with cancer growth. In situ hybridization and Northern blot hybridization detection of TGF-beta1, type I and type II receptor mRNA and immunohistochemical staining of TGF-beta1 were performed using 11 human colorectal adenomas, 22 colorectal cancers and ten normal colorectal mucosas as control. TGF-beta receptor mRNAs were expressed mainly by normal colorectal epithelial cells and adenoma. However, mRNAs for TGF-beta receptors were only faintly, if at all, expressed in eight of 22 human colorectal cancers. In addition, intense signals of TGF-beta1 mRNA and the protein were detected in all colorectal cancers. TGF-beta receptor mRNAs and TGF-beta1 protein were also distributed in fibroblasts and endothelial cells in the interstitium. Moreover, Smad 4 protein was translocated to nucleus in primarily cultured adenoma cells, but not in cancer cells after TGF-beta stimulation. The escape of human colon cancer from TGF-beta-mediated growth inhibition by down-regulation of TGF-beta receptors as well as the effects of TGF-beta on stroma formation and angiogenesis indicate a possible role for TGF-beta in the progression of colon cancer in an intact host.

Adenoma↗
PubMed1999

Physical and psychological improvements after phase II cardiac rehabilitation in patients with myocardial infarction.

We have designed a new 4-week hospitalized phase II cardiac rehabilitation program. The purpose of the present study is to clarify whether the physical and psychological status of patients with myocardial infarction (MI) improves after participation in our program. Twenty-nine patients (27 males, two females) with acute MI who enrolled in the 4-week hospitalized phase II rehabilitation program were assessed. All patients enrolled in this study had received coronary interventions. The rehabilitation consisted of exercise training, education and counseling. We evaluated the physical and psychological status of the patients before and just after the program, and at a 6-month follow up. The physical status was assessed by exercise tolerance measured by the peak oxygen consumption and anaerobic threshold, frequency of exercise, and serum concentrations of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, and low-density lipoprotein-cholesterol. The psychological status was assessed by the Spielberger state-trait anxiety inventory questionnaire (STAI) and the self-rating questionnaire for depression (SRQ-D). Thirty-four patients (27 men, seven women) with MI who did not participate in our rehabilitation program served as a control group. After participation in our rehabilitation program, exercise tolerance and the serum lipid profiles of the patients were improved compared with those before rehabilitation. These parameters had improved significantly 6 months after rehabilitation. The STAI anxiety score was improved significantly and the SRQ-D depression score tended to be improved just after the rehabilitation program. Regular physical activity was continued even 6 months after the completion of the program. Our hospitalized phase II cardiac rehabilitation program improved the management of cardiac risk factors and the psychological status in patients with MI. This comprehensive program may contribute to the secondary prevention of MI as well as the recovery of physical and psychological activities.

Adult↗
PubMed1999

[A study of factors relating to aggravation of patients with pulmonary Mycobacterium avium complex disease--with special reference to malnutrition].

We examined physical and blood statuses of 24 patients with pulmonary M. avium complex disease who entered our hospital from April 1993 to March 1997. Ten patients (41.7%) were diagnosed as primary infection type and 14 patients (58.3%) as secondary infection type. Twenty-four patients were classified to the following two groups: Group A was 14 patients who converted to MAC negative within six months after the admission and group B was 10 patients who continued to excrete MAC for more than six months after the admission. We made a comparison between group A and group B as to the results of physical and blood examinations on admission. Mean value of %IBW in group B was significantly lower (group B:74.4 +/- 8.9%, group A:82.9 +/- 12.7%, p < 0.05) than that of group A. The level of serum albumin in group B was significantly lower (group B: 3.39 +/- 0.53 g/dl, group A: 3.99 +/- 0.45 g/dl, p < 0.01) than that of group A. ChE in group B was significantly lower (group B: 321.2 +/- 94.5 IU/l, group A: 442.9 +/- 148.4 IU/l, p < 0.05) than that of group A. Group B was nutritionally depleted than group A. In conclusion, these findings suggested that nutritional support should be taken into consideration in combination with conventional chemotherapy in treating chronic, intractable MAC disease.

Aged↗
PubMed1999

[Haemophilus parainfluenzae and IgA nephropathy].

IgA nephropathy (IgAN) was first reported by Berger in 1968, and characterized by diffuse IgA deposition in the mesangium. Patients with IgAN have usually episodic macroscopic hematuria accompanied with pharyngitis, gastroenteritis, bronchitis, or sinusitis. These findings suggest that IgAN is an immune-complex disease resulting from a poorly controlled mucosal immune response to environmental antigens to which the patient was chronically exposed. We reported the glomerular deposition of the outer membrane of Haemophilus parainfluenzae (OMHP) antigens and the presence of IgA antibody against OMHP in the sera of patients with IgAN. These suggest that Haemophilus parainfluenzae plays a role in the aetiology of this disease. This study was conducted to determine whether OMHP antigens induced immunohistologically evident glomerular deposition of IgA and C3 in C3H/HeN mice. Female C3H/HeN mice (4 weeks old) received intraperitoneal injection (HP-IP group), and oral administration (HP-PO group) of OMHP antigens. The control group similarly received intraperitoneal injection of PBS, and oral intake of ordinary water. The mice were sacrificed at 10, 20, 30, 40, 50 weeks after the start of the experiment. The HP-IP group showed glomerular deposition of IgA, C3 and OMHP antigens, glomerular changes (Mesangial hypercellularity and increase in mesangial matrix) after 20 weeks. The HP-PO group showed only mild deposition of IgA, and mild increase in mesangial matrix. These results suggest that OMHP antigens play a role in the glomerular deposition of IgA and C3 in C3H/HeN mice. This is the first use of OMHP antigens to establish an active model of IgAN.

Animals↗
PubMed1998

Distribution and properties of kainate receptors distinct in the CA3 region of the hippocampus of the guinea pig.

To characterize the nature of kainate (KA) receptors distinct in the CA3 region of the hippocampus, properties of depolarizations induced by pulses of KA or AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) applied to dendrites of CA3 neurons with micropipettes were studied in thin transverse slices of the guinea pig hippocampus. KA induced depolarizations at negligible latencies only when administered to the most proximal dendritic areas. The depolarization was unaffected by tetrodotoxin or by a decrease in Ca2+ and an increase in Mg2+ concentrations. The declining slope of the KA-induced depolarization was significantly slower than that of the AMPA-induced depolarization. In comparison with the AMPA-induced depolarization, the KA-induced depolarization was much less susceptible to antagonists such as 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX) and 1-(4-aminophenyl)-4-methyl-7, 8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI52466). 6, 7,8,9-Tetrahydro-5-nitro-1H-benz[g]indole-2,3-dione-3-oxime (NS-102) and (2S,4R)-4-methylglutamate (SYM 2081) were without effects. The threshold concentration of pressure-ejected KA to induce depolarizations was about 200 nM. Excitatory postsynaptic potentials elicited by mossy fiber stimulation were more potently suppressed by CNQX than by GYKI52466. These results indicate that receptors responsible for the slow KA depolarization in the CA3 region of the hippocampus are not AMPA receptors but KA receptors. They are localized in the most proximal part of the apical dendrite and distinct from those observed in primary cultures of hippocampal neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1998

Immunolocalization of transforming growth factor beta during wound repair in rat retina after laser photocoagulation.

BACKGROUND: Scatter photocoagulation induces regression of retinal neovascularization, but the mechanism of its therapeutic effect is incompletely understood. To elucidate the mechanism of therapeutic effect of photocoagulation is the main focus of our research. We have already demonstrated basic fibroblast growth factor (bFGF) immunolocalization during retinal wound repair following laser photocoagulation. Transforming growth factor beta (TGF beta) reportedly inhibits endothelial cell growth and bFGF-induced cell proliferation in vitro. In the present study, we evaluated the immunohistochemical localization of TGF-beta 1 and -beta 2 during wound repair in the rat retina following laser photocoagulation. METHODS: Krypton laser photocoagulation was performed on the eyes of pigmented rats. The eyes were then enucleated on day 1, 3, 7, 14, 28 or 56 following the photocoagulation and enrolled into the analysis of immunohistochemical localization of TGF-beta 1 and -beta 2. RESULTS: Immunoreactivity for TGF-beta 1 and -beta 2 was present in the ganglion cell layer and photoreceptor outer segments of the normal adult rat retina. The cytoplasm of RPE cells at the photocoagulated lesion showed intense TGF-beta 1 and -beta 2 immunoreactivity on day 3 after laser photocoagulation. Macrophages that migrated into the lesion lacked positive staining for TGF-beta 1 and -beta 2. TGF-beta immunoreactivity in RPE cells continued to be upregulated for more than 1 month compared with that in normal RPE cells. Controls did not exhibit any positive staining. CONCLUSION: An elevated expression of TGF-beta immunoreactivity for a longer period of time than bFGF was observed in RPE cells at the photocoagulated lesion in vivo. In the late phase of retinal wound repair, TGF-beta may inhibit cell proliferation induced by mitogens, introduce an end stage of cellular events, and induce extracellular matrix induction.

Animals↗
PubMed1998

Expression of basic fibroblast growth factor and its receptor mRNA in retinal tissue following ischemic injury in the rat.

BACKGROUND: Our purpose was to determine the time-dependent changes of expression of basic fibroblast growth factor (bFGF) and its receptor in pressure-induced retinal ischemia in rats. METHODS: Retinal ischemia was induced in Wistar rats by increasing the intraocular pressure to 110 mmHg for 45 min by cannulation into the eyes. At the end of the ischemic period, reperfusion of the retinal vasculature was confirmed. Localization of bFGF and FGF receptor-1 (FGF-R) mRNAs were evaluated by in situ hybridization at various times after reperfusion. The reverse-transcription polymerase chain reaction (RT-PCR) method was used to detect the expression of bFGF and FGF-R mRNA in the sensory retina. RESULTS: In normal sensory retina, bFGF and FGF-R mRNAs were observed in the ganglion cell layer and inner nuclear layer. bFGF gene expression in the sensory retina increased within 24 h, particularly at 6-12 h. FGF-R gene expression increased earlier than that of bFGF. By RT-PCR, expression of bFGF gene reached a peak at 6-24 h, and FGF-R reached a peak at 3-12 h. These RT-PCR results are comparable to those of in situ hybridization. CONCLUSIONS: These results demonstrate that transient retinal ischemia leads to the induction of bFGF mRNA synthesis, and suggest that bFGF has a protective role, e.g., a defense mechanism for the sensory retina.

Animals↗
PubMed1998

Properties of depolarization-induced suppression of inhibitory transmission in cultured rat hippocampal neurons.

Properties of depolarization-induced suppression of inhibitory transmission ("DSI") in cultured rat hippocampal neurons were examined, by recording inhibitory postsynaptic currents (IPSCs) evoked by single presynaptic neurons. In about 40% of the inhibitory synapses, transient suppression of IPSCs was induced by applying a depolarizing pulse (to 0 mV, > 2 s) to the postsynaptic neuron, which was identified to be gamma-aminobutyric acid dependent (GABAergic) in some pairs, and to be glutamatergic in some other pairs. This depolarization-induced suppression of IPSCs, "DSI", was Ca2+ dependent, and was associated with an increase in the paired-pulse ratio. Phorbol esters had an occluding effect on DSI when applied to the bath solution, but not to the pipette solution used for the postsynaptic neuron. Application of the opioid receptor antagonist naloxone had no effect on DSI. The present study demonstrates that a pair of cultured hippocampal neurons can exhibit DSI similar to that previously reported to occur in hippocampal slices; this suggests that a dissociated cell culture system can provide a useful model system for the study of DSI. Furthermore, it was found that inhibitory neurons, in addition to excitatory ones, can induce DSI, and that a process sensitive to phorbol esters, but not activation of opioid receptors, is involved in DSI.

Animals↗
PubMed1998

Calcitonin gene-related peptide affords gastric mucosal protection by activating potassium channel in Wistar rat.

BACKGROUND & AIMS: Calcitonin gene-related peptide (CGRP) protects the gastric mucosa against injurious stimuli in various experimental models. The underlying mechanism could be the increase in gastric mucosal blood flow (GMBF). A number of endogenous vasodilators exert their effects through the activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels on vascular smooth muscle. The present experiments were performed to elucidate whether CGRP increases GMBF through the activation of KATP channels and whether the channels are involved in the protection by CGRP of gastric mucosa. METHODS: GMBF was determined by the hydrogen-clearance technique in male Wistar rats. Mucosal lesions were produced by intragastric superfusion with 0.15N HCland 15% ethanol for 40 minutes. Effects of an agonist (Y-26763, intra-arterially) and an inhibitor (glibenclamide, intravenously) of KATP channels were tested. RESULTS: Y-26763 increased GMBF, which was abolished by glibenclamide, and a CGRP-induced increase in GMBF was attenuated by glibenclamide. Macroscopic and microscopic lesions were exacerbated by human CGRP-(8-37) (a CGRP-1 receptor antagonist; intra-arterially) and glibenclamide but were ameliorated by exogenous CGRP (intra-arterially). CONCLUSIONS: CGRP protects the gastric mucosa against ulcerogenic stimuli, at least in part, through the activation of KATP channels in rats.

Animals↗