Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 37 records · Page 2Linked to original sources

PubMed1996

(+/-)-tamsulosin, an alpha 1A-adrenoceptor antagonist, inhibits the positive inotropic effect but not the accumulation of inositol phosphates in rabbit heart.

The influence of (+/-)-tamsulosin, a selective alpha 1A-adrenoceptor antagonist, on the positive inotropic effect and the accumulation of inositol phosphates that are induced via alpha 1-adrenoceptors was studied in comparison with that of another alpha 1A-adrenoceptor ligand oxymetazoline in the rabbit ventricular myocardium. Phenylephrine elicited a concentration-dependent positive inotropic effect via alpha 1-adrenoceptors in the presence of either (+/-)-bupranolol or S(-)-timolol. The mode of antagonism induced by (+/-)-tamsulosin on the effect of phenylephrine was dependent or the concentration applied: (+/-)-tamsulosin at 1 and 3 nM acted in a competitive manner, the slope of the regression line of the Schild plot being unity and the pA2 value being 9.12; at 10 nM, it shifted further the concentration-response curve to the right without affecting the maximal response but the slope became less than unity. At 100 nM and higher, it suppressed the maximal response to phenylephrine. (+/-)-Tamsulosin effectively antagonized the positive inotropic effect of phenylephrine even after inactivation of alpha 1B-adrenoceptors by treatment with chlorethylclonidine, which is an indication that the (+/-)-tamsulosin-sensitive subtype belongs to a class resistant to chlorethylclonidine. (+/-)-Tamsulosin, over the range of concentrations at which it antagonized the positive inotropic effect mediated by alpha 1-adrenoceptors, did not affect the accumulation of [3H]inositol phosphates that was induced by 10 microM phenylephrine. Oxymetazoline antagonized the positive inotropic effect of phenylephrine in a competitive manner without affecting the accumulation of inositol monophosphate induced by phenylephrine. These results indicate that the positive inotropic effect, mediated via (+/-)-tamsulosin- and oxymetazoline-sensitive subtype of alpha 1-adrenoceptors, is exerted by a subcellular mechanism that is independent of the accumulation of inositol phosphates.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1996

Significantly increased frequency of the apolipoprotein E epsilon 4 allele in elderly non-demented leprosy patients.

Apolipoprotein E (apo E) genotypes in 350 leprosy patients were examined and compared with those of 870 age-matched controls. The allelic frequencies of the apo E gene did not differ between demented patients with leprosy and controls. However, the frequency of apo E epsilon 4 allele was significantly higher in non-demented leprosy patients than in controls (P < 0.001). Of special interest is that the prevalence of E3/4 genotype in non-demented leprosy patients increased significantly with age, being 14.1%, 24.4%, and 28.3% in the 60s, 70s, and 80s, respectively (P < 0.05). These data suggest that apo E epsilon 4 is not a risk factor for senile dementia in elderly leprosy patients, and there exist factors to overcome the risk of apo E4 in leprosy patients.

Age Distribution↗

PubMed1996

Methoxamine-induced inhibition of the positive inotropic effect of endothelin via alpha1-adrenoceptors in the rabbit heart.

The influence of methoxamine on the positive inotropic effect of endothelin was assessed in the isolated rabbit ventricular myocardium. Methoxamine by itself elicited a positive inotropic effect and it simultaneously inhibited the positive inotropic effects of endothelin-1 and endothelin-3 without affecting the acceleration of the hydrolysis of phosphoinositide that was induced by the endothelin isopeptides. By contrast, the positive inotropic effects induced by elevation of concentration of external Ca2+ ions, by Bay k 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5- carboxylate), by dihydroouabain and by forskolin were unaffected by methoxamine. The inhibitory action of methoxamine was abolished by alpha1-adrenoceptor antagonists, such as prazosin, WB 4101 (2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane hydrochloride) and (+/-)-tamsulosin; and it was inhibited to a lesser extent by chlorethylclonidine. In addition, methoxamine did not modify the specific binding of [125I]endothelin-3 to ventricular membrane fraction. These results indicate that methoxamine antagonizes the positive inotropic effect of endothelin isopeptides at the level of the signal-transduction process, subsequent to acceleration of the hydrolysis of phosphoinositide, via activation of alpha1-adrenoceptors in the rabbit ventricular myocardium.

Adrenergic alpha-Agonists↗

PubMed1996

Chronic dexamethasone administration decreases noradrenaline-stimulated, but not serotonin-stimulated, phosphoinositide metabolism in the rat brain.

The present study was undertaken to investigate the effects of chronic administration of dexamethasone on the noradrenaline- and serotonin-stimulated (5-HT-stimulated) phosphoinositide metabolism in hippocampus and frontal cortex of the rat brain. For determination of phosphoinositide metabolism, slices from selected regions of the rat brain (hippocampus or frontal cortex) were loaded with myo- [3H] inositol and stimulated with the agonists (noradrenaline or 5-HT) in the presence of LiCl (7.5 mM). Administration of dexamethasone (1 mg/kg/day) every 2nd day for 14 days markedly reduced the noradrenaline-stimulated phosphoinositide metabolism in the rat hippocampus (IP1: 60% of the control value). In the rat frontal cortex, the noradrenaline-stimulated phosphoinositide metabolism was less depressed by the chronic administration of dexamethasone (IP1: 84% of the control value). However, the chronic administration of dexamethasone did not affect the 5-HT-stimulated phosphoinositide metabolism in the rat brain. The binding characteristics of alpha 1 -adrenoceptors and 5-HT2A receptors were unaffected by the chronic treatment with dexamethasone. These results indicate that chronic administration of dexamethasone induces regional and neurotransmitter-specific changes of phosphoinositide metabolism in rat brain. The results suggest that the reduction of noradrenaline-stimulated phosphoinositide metabolism is due to modification of the intracellular signal transduction system.

Animals↗

PubMed1996

Altered synthesis of interferon-gamma and expression of interferon-gamma receptor by peripheral blood mononuclear cells from patients with IgA nephropathy and non-IgA proliferative glomerulonephritis.

Previously we reported disease-specific interaction between interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) in patients with IgA nephropathy (IgAN), suggesting the existence of unusual T cell behavior in this disease. In the present study, we investigated characteristic synthesis of interferon-gamma (IFN-gamma) and expression of IFN-gamma receptor (IFN-gamma R) in the peripheral blood mononuclear cells (PBMC) from patients with IgAN and other chronic proliferative glomerulonephritis (PGN). Heparinized peripheral blood samples were obtained from 38 patients with chronic mesangial proliferative glomerulonephritis (CGN; including 24 with IgA nephropathy) and 20 healthy controls. PBMC were isolated by gradient centrifugation and fragments were cultured in Iscove's modified Dulbecco's medium (IMDM) supplemented with 10% fetal calf serum (FCS) for 72 hr. IFN-gamma concentrations in supernatants were evaluated by the enzyme-linked immunosorbent assay (ELISA). Other parts of PBMC pellets were reacted with anti-human IFN-gamma R monoclonal antibody and FITC-labeled anti-mouse second antibody for analysis of IFN-gamma R expression on these cells by FACScan. The remaining PBMC were fractionated into CD4+ T cells, CD8+ T cells, B cells, NK, cells and macrophages using the MACS cell sorting system. The isolated cells were evaluated for IFN-gamma or IFN-gamma R mRNA expression by the semiquantitative RT-PCR method. In vitro IFN-gamma synthesis was enhanced in patients with CGN, and NK cells were revealed to be responsible for such enhancement. On the other hand, the expression of IFN-gamma R on macrophages was suppressed in CGN patients. These results suggest that impairment of regulation of the IFN-gamma system might be involved in the development of CGN.

Antigens, CD↗

PubMed1996

Complications of childhood Sjögren syndrome.

UNLABELLED: Sjögren syndrome (SS) is a common disorder in adults and involves both glandular and extraglandular systems. We report here four cases of childhood SS complicated by chronic thyroiditis, interstitial nephritis or sweat gland inflammation. Additionally, in one of these cases, the central nervous system was involved. All of these complications are common in adult cases. CONCLUSION: Childhood SS is a systemic "ductilitis" or "exocrinopathy" with complications which are commonly observed in adult cases.

Acidosis, Renal Tubular↗

PubMed1996

Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC.

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.

Acute Disease↗

PubMed1996

Cardiac alpha(1)-adrenoceptors that regulate contractile function: subtypes and subcellular signal transduction mechanisms.

Activation of alpha(1)-adrenoceptors as well as endothelin (ET) and angiotensin II (Ang II) receptors in cardiac muscle is coupled to acceleration of the hydrolysis of phosphoinositide (PI), with resultant production of inositol 1,4,5-trisphosphate (IP(3)) and diacylglycerol. There is an excellent correlation between the extent of acceleration of the PI hydrolysis and the positive inotropic effect (PIE) under most experimental conditions after the administration of a-adrenoceptor agonists, ET and Ang II in the rabbit ventricular muscle. The PIE of the alpha-adrenoceptor agonists, ET and Ang II is associated with a negative lusitropic effect and an increase in the sensitivity of myofilaments to Ca(2)+ ions. The PIE can be selectively inhibited by inhibitors of protein kinase C (PKC) such as staurosporine, NA 0345 and H-7, with little effect on the PI hydrolysis and the PIE of isoproterenol and Bay k 8644. Surprisingly, an activator of PKC, phorbol 12,13-dibutyrate (PDBu), selectively and more completely inhibited the PIE and acceleration of PI hydrolysis induced by the alpha-adrenoceptor agonists as well as by ET and Ang II in the rabbit. These receptor agonists consistently cause intracellular alkalinization by activation of Na+-H+ exchange, while the effects on membrane ion channel activities are divergent. For example, alpha-adrenoceptor agonists cause monophasic prolongation of the action potential, the time course of which coincides well with that of the PIE, while ET and Ang II produce a biphasic change in action potential duration, i.e., the long-lasting prolongation preceded by a transient abbreviation. Alpha-adrenoceptor agonists scarcely affect I(ca), whereas ET elicits a biphasic alteration of the current. In addition, the potassium current, I(K1), is markedly suppressed by alpha-adrenoceptor agonists, but this effect is not revealed with Ang II under the same experimental condition. These results indicate that the effects of alpha(1)-adrenoceptor stimulation are partially shared by those of FT and Ang II receptor activation in the heart. Approximately 60% of the total population of alpha(1)-adrenoceptors in the rabbit ventricle are composed of alpha(1A) subtype, which is susceptible to chlorethylclonidine (CEC) and is predominantly responsible for the alpha(1)-mediated PIE and PI hydrolysis. The remaining fraction that belongs to alpha(1A) subtype is further subclassified into the WB 4101-sensitive (partly coupled to PI hydrolysis) and the niguldipine-sensitive (PI hydrolysis-unrelated) subtypes.

Animals↗

PubMed1996

Increase of HLA-DR-positive natural killer cells in peripheral blood from patients with IgA nephropathy.

Previous in vivo and in vitro studies have presented various abnormalities of cellular immunity in patients with IgA nephropathy (IgAN). In the present study, we described increased expression of HLA-DR antigens on peripheral natural killer cells (NK cells) in relation to altered cytokine interactions. The numbers of HLA-DR expressing NK cells were enumerated by two-color flow cytometry and found to be significantly increased in patients with IgAN. Peripheral blood mononuclear cells were then fractionated into pure NK cells by a magnetic cell-sorting system and analyzed concerning expression of messages of interleukin (IL)-2, IL-4, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). Among the four cytokines, only the IFN-gamma message was significantly increased in patients' NK cells. Furthermore, intensity of the IFN-gamma message in NK cells showed positive correlation with the percentage of HLA-DR-positive NK cells from the same patient. Then we assayed serum levels of IL-2, IL-12, and IFN-gamma by enzyme-linked immunosorbent assay (ELISA) and the levels of IL-12 and IFN-gamma showed positive correlations with HLA-DR expression on NK cells. Creatinine clearance of the patients was reevaluated 36 months later, and patients with high HLA-DR on NK cells tended to show faster deterioration of renal function than patients with lower HLA-Dr expression. On the basis of these findings, we suggested that HLA-DR-positive NK cells in patients with IgAN form an "activated" population that produces IFN-gamma, and this unique cell population may be maintained by multiple factors and be involved in the development and progression of IgAN.

Adult↗

PubMed1996

Superoxide dismutase activity in human glomerulonephritis.

Superoxide dismutase (SOD) in renal tissue biopsy specimens obtained from patients with immunoglobulin A nephropathy (13 cases) and non-immunoglobulin A mesangial proliferative glomerulonephritis (nine cases) was studied at the protein level by an enzyme-linked immunosorbent assay method and at the mRNA level by the reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Total SOD activity in the tissue supernatant was measured by applying an electron paramagnetic resonance/spin trapping method. Normal renal tissues obtained from kidneys removed for malignancies (six cases) were included as healthy controls. The copper and zinc form of SOD (Cu,Zn-SOD) activity at both the protein and mRNA levels was lower in the moderately or severely damaged tissues compared with that in the normal or mildly damaged tissues. On the other hand, manganese SOD (Mn-SOD) values at either the protein level or the mRNA level did not differ significantly between control and patient samples. In the histochemical study using a polyclonal rabbit anti-Cu,Zn-SOD antibody, the staining intensity for Cu,Zn-SOD antigen was lower in the areas with advanced histologic damage than in the intact tissues. A follow-up study showed that renal function deterioration was proportionately slower in patients whose SOD activity was within the range of healthy tissue levels at the time of biopsy. Our data suggest that a lower level of SOD activity, whether as a cause or a consequence of the disease process, might induce a decrease in the scavenger reaction of superoxide (O2-) thus causing the tissue to become more vulnerable to oxidative stress.

Adult↗

PubMed1996

Effects of endothelin-1 on [Ca2+]i-shortening trajectory and Ca2+ sensitivity in rabbit single ventricular cardiomyocytes loaded with indo-1/AM: comparison with the effects of phenylephrine and angiotensin II.

In most mammalian species, activation of myocardial endothelin as well as alpha1-adrenergic and angiotensin receptors leads to an increase in contractile function and myocardial cell hypertrophy, in association with acceleration of PI hydrolysis and with resultant production of IP3 and diacylglycerol. Therefore, these receptors may share a common intracellular signal transduction process in cardiac regulation. Although the pathophysiological relevance of endothelin- and angiotensin-mediated signal transduction has been postulated to play a key role in the progress of congestive heart failure, the details of the regulation are still controversial. We carried out experiments to further study the regulation induced by activation of these receptors. In spite of a wide range of species-dependent variation among mammals in the induction of the cardiotonic effect via these receptors, there is an excellent correlation between the extent of acceleration of PI hydrolysis and the positive inotropic effect (associated with a negative lusitropic effect) of the respective receptor agonists under most experimental conditions in rabbit ventricular myocardium. In isolated rabbit ventricular cardiomyocytes loaded with indo-1/AM, activation of these receptors elicited a very similar changes in the relationship between [Ca2+]i and cell shortening: the [Ca2+]i-shortening trajectory was shifted mainly upwards and the relationship of peak shortening vs peak [Ca2+]i was shifted to the left, an indication that the PIE of these agonists is consistently associated with an increase in [Ca2+]i and in the sensitivity of myofilaments to Ca2+ ions under the same experimental condition. Pieces of evidence in biochemical and pharmacological analyses imply that the products of PI hydrolysis, namely diacylglycerol and subsequent activation of protein kinase C, might play a crucial role in the regulation of cardiac function that is induced upon activation of endothelin, angiotensin and alpha-adrenergic receptors in the rabbit ventricular myocardium.

Angiotensin II↗

PubMed1996

Expression of inducible-NOS in human glomerulonephritis: the possible source is infiltrating monocytes/macrophages.

Nitric oxide (NO) is a biological mediator which is synthesized from L-arginine by a family of nitric oxide synthases (NOS). In this paper, we have studied the expression of the inducible NO synthase (iNOS) in the tissues of the human kidney at the mRNA level by RT-PCR assay and at the protein level by an immunohistochemistry technique using a specific anti-macrophage NOS monoclonal antibody. Biopsied renal tissues from patients with IgA nephropathy (IgAN; 28 cases) and with non-IgA mesangial proliferative glomerulonephritis (PGN;12 cases), and normal renal tissues obtained from kidneys removed for malignancies (11 cases) were included in this experiment. iNOS message was present in about 73% tissues from IgAN and PGN patients, which was supported by histochemical findings and the iNOS positive cells were predominantly in the tubulointerstitial areas where infiltration of monocytes/macrophages was abundant. The iNOS positive tissues were also strongly positive for CD14, INF-gamma and TNF-alpha mRNA expression. In our in vitro study, iNOS expression was found only in cytokines (INF-gamma and TNF-alpha) stimulated monocytes/macrophages but not in lymphocytes and neutrophils. Normal renal tissues did not show any iNOS expression either at the mRNA level or at the protein level in this study. Clinical and histological data showed that decreased renal function and tubulointerstitial damage were greater in the iNOS expressing patients. This study demonstrates that there is some in vivo induction for iNOS expression, likely to be mediated by cytokines, for local NO production that might be involved in the initiation and/or progression of mesangial proliferative glomerulonephritis.

Base Sequence↗

PubMed1996

Effects of cyclopiazonic acid and ryanodine on cytosolic calcium and contraction in vascular smooth muscle.

1. In smooth muscle, both Ca2+ release from the sarcoplasmic reticulum (SR) and Ca2+ influx across the plasma membrane are responsible for the increase in the cytosolic Ca2+ level ([Ca2+]i). To understand further the role of SR on smooth muscle contraction, the effects of an inhibitor of the SR Ca2+ pump, cyclopiazonic acid (CPA 10 microM), an inhibitor of the Ca(2+) -induced Ca2+ release, ryanodine, (10 microM), and an activator of the Ca(2+) -induced Ca2+ release, caffeine (20 mM), on [Ca2+]i and contractile force were examined in the ferret portal vein loaded with a photoprotein, aequorin. 2. CPA induced a small increase in the aequorin signal reaching a maximum at 7 min. Several minutes after the increase in the aequorin signal, muscle tension increased reaching a maximum at 21.5 min. In contrast, ryanodine changed neither the aequorin signal nor contraction. In the presence of ryanodine, caffeine induced a sustained increase in the aequorin signal and transient contraction. After washing ryanodine and caffeine, the aequorin signal and muscle tone returned to their respective control levels. After treatment with ryanodine and caffeine, the second addition of caffeine was almost ineffective whereas CPA still increased the aequorin signal and muscle tension. 3. In the presence of external Ca2+, noradrenaline (NA, 10 microM) induced a transient increase followed by a sustained increase in the aequorin signal and sustained contraction. In contrast, KCl (70 mM) induced sustained increases in the aequorin signal and sustained contraction. In Ca(2+) -free solution, NA induced a small transient increase in the aequorin signal and a small transient contraction. These changes were inhibited in the presence of CPA or on pretreatment of the muscle with ryanodine and caffeine. These results suggest that CPA or ryanodine and caffeine depleted Ca2+ in SR. High K+ was ineffective in the absence of external Ca2+. 4. In the presence of external Ca2+ and CPA, NA and high K+ induced larger aequorin signals than in the absence of CPA, whereas the magnitude and shape of the contractions did not change. In contrast, pretreatment with ryanodine and caffeine did not have such an effect. In the muscle pretreated with ryanodine and caffeine, CPA changed the responses to high K+ and NA in a similar manner to that in the muscle without the pretreatment with ryanodine and caffeine. 5. Dissociation of contraction from [Ca2+]i as measured with aequorin suggests that NA and high K+ increase Ca2+ in two compartments: a compartment containing contractile elements (contractile compartment) and another compartment unrelated to contractile elements (non-contractile compartment). Because CPA augmented the stimulant-induced increase in aequorin signal without changing contraction, the non-contractile compartment may be located near the SR and the CPA-sensitive SR Ca2+ pump may regulate the Ca2+ level in this compartment. However, because CPA changed neither the magnitude nor shape of the contractions in the presence of external Ca2+, the SR Ca2+ pump may have little effect on regulation of Ca2+ level in the contractile compartment. Furthermore, the release of Ca2+ from SR seems to have little effect on the increase in the contractile Ca2+ because ryanodine and caffeine changed neither the aequorin signals nor contractions induced by NA and high K+ in the presence of external Ca2+ in the ferret portal vein.

Adrenergic alpha-Agonists↗

PubMed1996

Ca2+ sensitizer Org-30029 reverses acidosis- and BDM-induced contractile depression in canine myocardium.

Effects of the Ca2+ sensitizer N-hydroxy-5,6-dimethoxy-benzo[b]thiophene-2-carboximidamide hydrochloride (Org-30029) on the myocardial contractile depression induced by acidosis and 2,3-butanedione monoxime (BDM) were investigated in aequorin-loaded canine ventricular myocardium. The peak Ca2+ transient-peak force relation during administration of Org-30029 (10(-4) to 10(-3) M) was shifted to the left and upward compared with the relation for elevation of the extracellular Ca2+ concentration ([Ca2+]o) (2.5-12.5 mM). Acidosis (pH 6.6) depressed the force with a small increase in the peak Ca2+ transient. BDM (3 mM) depressed the force with no change in the peak and duration of the Ca2+ transient, indicating that BDM may inhibit selectively the cross-bridge interaction. During acidosis or in the presence of BDM, elevation of [Ca2+]o increased the peak Ca2+ transient to the same extent as that in the control, but the force was inhibited. In contrast, Org-30029 increased the force to a level equivalent to the control with a slight change in the peak Ca2+ transient. In addition, during acidosis, Org-30029 (10(-3) M) increased the force in association with a slight decrease in the peak Ca2+ transient. Thus Org-30029 can reverse the myocardial contractile depression induced by a decrease in the Ca2+ sensitivity of myofilaments, as occurs in pathophysiological situations such as acidosis in cardiac ischemia. Org-30029 may exert the Ca(2+)-sensitizing effect by an increase in the affinity of troponin C for Ca2+ and by a direct action on the cross-bridge interaction.

Acidosis↗

PubMed1996

Involvement of interleukin-4 and soluble CD23 in hypersynthesis of immunoglobulins A and E in patients with IgA nephropathy.

To determine the cytokines responsible for the increase in production of IgA in patients with IgA nephropathy (IgAN), the roles of interleukin-4 (IL-4) and soluble CD23 (sCD23) were examined. Peripheral blood mononuclear cells (PBMCs) and serum were obtained from 24 patients with IgAN and 14 patients with non-IgA proliferative glomerulonephritis. Twenty healthy adults served as controls. Concentrations of IgA and IgE in 10-day culture supernatants of PBMCs were measured by the sandwich ELISA method. Levels of sCD23 and activities of IL-4 in 4-day (96-hour) culture supernatants and serum were measured by ELISA and bioassay, respectively. Activities of IL-4 both in culture supernatants and serum were significantly elevated in patients with IgAN compared with controls (1.26 +/- 0.53 vs. 0.68 +/- 0.37 U/ml in culture supernatants, p < 0.05; 1.35 +/- 1.34 vs. 0.89 +/- 0.82 U/ml in serum, p < 0.05). Levels of sCD23 in IgAN patients' serum were also significantly elevated (521.7 +/- 514.9 vs. 173.0 +/- 166.2 U/ml, p < 0.01). In vitro IgA and IgE synthesis were suppressed by anti-IL-4 monoclonal antibody (mAb) only when the antibody was added on the day when the culture was started (day 0). No suppression of IgA or IgE synthesis was observed when the antibody was added on day 4. IgE but not IgA synthesis was suppressed by anti-CD23 mAb when added on both days 0 and 4. Serum levels of IgE showed positive correlations with serum activities of IL-4 and with levels of serum sCD23. It is concluded that IL-4 and sCD23 might play decisive roles in in vitro and in vivo hyperproduction of IgA and IgE in patients with IgAN, and that sCD23 seemed to control IgE but not IgA synthesis through a unique pathway.

Adult↗

PubMed1996

Incontinentia pigmenti and Behçet's disease: a case of impaired neutrophil chemotaxis.

We describe a patient with incontinentia pigmenti who developed the clinical picture of intestinal Behçet's disease. Diagnosis of Behçet's disease was base on a recurrent genital and oral ulcer and a positive HLA-B51. Impaired neutrophil chemotactic activity and an elevated plasma IL-6 level were found. Chromosomal study revealed no abnormality in the patient or her family. We discuss the possibility that there are common immunological abnormalities in the two syndromes.

Adult↗

PubMed1996

Production of antibody against calmodulin which is a protein with poor antigenicity.

Calmodulin (CaM), a Ca(2+)-binding protein, is a multifunctional modulator mediating the calcium regulation of a large number of intracellular enzyme systems. Because of its highly conserved structure, it has been difficult to produce anti-CaM antibody. We describe here a simplified method for production of this antibody. BALB/c mice were immunized with a polymerized CaM, and the serum was prepared and tested for the presence of anti-CaM antibody by immunoblot analysis. The serum obtained from the immunized mice was shown to contain anti-CaM antibody. Immunoblot analysis proved that a 500-fold diluted serum was able to recognize both types of CaM with a polymerized form and monomer form. The method developed in this study may be applicable to a wide range of proteins for enhancement of antigenicity.

Animals↗

PubMed1996

Failure of smooth muscle cells treated with collagenase to respond to Bordetella heat-labile toxin.

HLT, bordetella heat-labile toxin, caused a release of radioactivity from cultured smooth muscle cells (SMC) previously labeled with [14C]arachidonic acid, and from membrane preparations from the labeled SMC. HLT, however, failed to induce release from primary SMC prepared by treatment with an enzyme solution containing collagenase and elastase. When cultured SMC were treated with the enzyme solution, their susceptibility to HLT was reduced more significantly than that of untreated cells. SMC also lost their susceptibility, after treatment with collagenase alone, but not with elastase, in a dose-dependent manner. These data suggest that collagen on the SMC surface might play an important role in HLT activity.

Animals↗