Search PubMed⌕ Search

Biomedical subjects

N Maeda

Publications and source records attributed to N Maeda.

At least 253 records · Page 14Linked to original sources
PubMed1997

Beta-estradiol protects hippocampal CA1 neurons against transient forebrain ischemia in gerbil.

Beta-estradiol has been considered to be a neurotrophic agent, but its in vivo effect on gerbils with transient forebrain ischemia has not yet been demonstrated. In the first set of the present experiments, we infused beta-estradiol at a dose of 0.05 or 0.25 microg/day for 7 days into the lateral ventricles of normothermic gerbils starting 2 h before 3-min forebrain ischemia. Beta-estradiol infusion at a dose of 0.25 microg/day prevented significantly the ischemia-induced reduction of response latency time as revealed by a step-down passive avoidance task. Subsequent light and electron microscopic examinations showed that pyramidal neurons in the hippocampal CA1 region as well as synapses within the strata moleculare, radiatum and oriens of the region were significantly more numerous in gerbils infused with beta-estradiol than in those receiving saline infusion. Beta-estradiol at a dose of 1.25 microg/day was ineffective and occasionally increased the mortality of experimental animals. Since the total brain content of exogenous beta-estradiol at 12 h after forebrain ischemia was estimated to be less than 145 ng, the second set of experiments focused on the neurotrophic action of beta-estradiol at concentrations around 100 ng/ml in vitro. Beta-estradiol at concentrations of 1-100 ng/ml facilitated the survival and process extension of cultured hippocampal neurons, but it did not exhibit any significant radical-scavenging effects at the concentration range. On the other hand, 100 microg/ml of beta-estradiol, even though failing to support hippocampal neurons in vitro, effectively scavenged free radicals in subsequent in vitro studies, as demonstrated elsewhere. These findings suggest that beta-estradiol at a dose of 0.25 microg/day prevents ischemia-induced learning disability and neuronal loss at early stages after transient forebrain ischemia, possibly via a receptor-mediated pathway without attenuating free radical neurotoxicity.

Animals↗
PubMed1997

Using a reference point and videokeratography for intraoperative identification of astigmatism axis.

PURPOSE: To estimate the misalignment of the astigmatism axis caused by intraoperative identification of the axis without using reference points. SETTINGS: Osaka University Medical School, Suita, Japan. METHODS: This study included 38 eyes of 19 patients with no ocular pathology except refractive error and 32 eyes of 16 patients with cataract. A point was marked on the nasal conjunctiva, on the "intraoperative" horizontal axis as estimated by the examiner using a surgical microscope while the patient lay on the operating table in the supine position. Videokeratography was performed with the patient seated, and the degree of axial misalignment was determined by measuring the angle between the conjunctival mark and the horizontal axis identified on the video image. RESULTS: Mean axial misalignment for all patients was 4.4 degrees +/- 2.8 (SD), which could theoretically cause about a 15% loss of surgical effect. The maximal misalignment was 14 degrees, which would correspond to a 48% loss of astigmatic correction. CONCLUSION: The results of this study suggest that intraoperative identification of the astigmatism axis without using reference points may reduce the surgical effect because of axis misalignment. The use of a reference point and preoperative videokeratography may increase the accuracy of identification of the astigmatism axis.

Adult↗
PubMed1997

Severe myoclonic epilepsy in infancy: evolution of seizures.

Changes in seizure type of severe myoclonic epilepsy (SME) in infancy were reviewed retrospectively in 14 patients (11 males and 3 females) who were followed-up to the age of 7 years or more. The observation period ranged from 5 to 16 years with a mean of 10 years. During the follow-up, three or four types of seizures were seen per patient, but the pattern of appearance and disappearance of each seizure type varied considerably among the patients. Tonic-clonic convulsion, either generalized or unilateral, was seen most consistently through the entire course, and it continued to the end of follow-up in 11 patients (79%). On the contrary, myoclonic seizure, complex partial seizure, and atypical absence often disappeared and reappeared repeatedly during the course. In SME, seizure symptoms varied widely among patients in comparison with other neurological symptoms, and the most consistent core seizure type was tonic-clonic convulsions.

Child↗
PubMed1997

Detection of alterations in the levels of neuropeptides and salivary gland responses in the non-obese diabetic mouse model for autoimmune sialoadenitis.

The salivary glands of non-obese diabetic (NOD) mice and BALB/c controls were evaluated for the stimulatory effects of the following neuropeptides; substance P (SP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY). Injection of either of the three neuropeptides in combination with the muscarinic-cholinergic agonist pilocarpine increased saliva flow rates in BALB/c mice while there was no observable augmentation to flow rates in pre-diabetic or diabetic NOD mice. Small increases in protein content of the stimulated saliva were observed in the BALB/c group of animals with the injection of any of the above neuropeptides in combination with pilocarpine. In pre-diabetic NOD animals, only VIP and NPY increased the protein content-ratio above pilocarpine alone. Radioimmunoassay determination of neuropeptide concentrations in the submandibular and parotid glands revealed reduced levels of SP with diabetes onset as compared with pre-diabetic NOD or BALB/c mice. The levels of NPY were similar between BALB/c and NOD animals except in the pre-diabetic parotid gland where NPY concentrations were 1.3-fold greater. On the other hand, VIP concentrations were substantially reduced in the submandibular gland of NOD mice, while in the parotid gland neuropeptide levels were evaluated 3.8-fold relative to BALB/c controls. Immunohistochemical staining of the parotid and submandibular glands for SP revealed primarily ductal cell staining which was reduced with diabetes onset in NOD animals. These findings further define the sialoadenitis observed in NOD mice to be due, in part, to a general loss of neurotransmitter responsiveness on the part of salivary gland cells.

Animals↗
PubMed1997

Effects of chronic isoproterenol treatment or submandibular and sublingual ablation on microflora of mouse tooth surfaces.

BALB/cA mice were examined for the effects of chronic isoproterenol treatment or submandibular-sublingual gland ablation on the natural patterns of oral bacterial colonization on tooth surfaces. Indigenous microflora on the tooth surfaces of BALB/cA mice was relatively simple. The predominant bacterial groups were Enterobacteriaceae (45.9%), enterococci (29.4%) and staphylococci (15.7%). Isoproterenol, which resulted in the induced synthesis of proline-rich proteins, caused a decrease in the total cultivable bacteria on the tooth surfaces. The proportion of Enterobacteriaceae in the isoproterenol-treated mice decreased, although the proportion of other bacterial groups increased. Salivary gland ablation, which caused the loss of mucins in saliva, showed essentially the same number of total bacteria as the control. Salivary gland ablation resulted in a decrease in the proportion of Enterobacteriaceae, while the proportion of Gram-positive rods and staphylococci increased.

Adrenergic beta-Agonists↗
PubMed1997

Hyaluronidase activity in human pus from which Streptococcus intermedius was isolated.

Hyaluronidase (HAase) activity was detected in both a human pus sample and the culture supernatant of the only bacterial isolate from the pus, Streptococcus intermedius, using a zymographic technique. The optimum pH range for HAase activity was similar for both samples. Although the bands showing the strongest HAase activity of these samples differed from each other with respect to molecular size, both samples were equally inhibited by an antiserum raised against HAase of S. intermedius. These results suggest that S. intermedius may produce HAase in vivo as well as in vitro, and that this enzyme and/or its fragments may play an important role in host tissue degradation.

Adult↗
PubMed1997

Induction of specific cytotoxic T lymphocytes against autologous brain tumor by crossreactive allo-tumor cell stimulation.

Cytotoxic T lymphocytes (CTL) against autologous malignant brain tumor were generated in peripheral blood lymphoid cells (PBL) prepared from a patient with a malignant brain tumor by stimulation of the cultured PBL for 7 days with attenuated crossreactive malignant melanoma (MM2) cells pretreated with mitomycin C. The crossreactive MM2 cells were effective for antigen stimulation for CTL induction in place of autologous glioblastoma cells, which are difficult to expand in culture. The optimal ratio between nylon wool-passed T lymphocytes and nylon wool-adherent accessory cells to induce CTL in the patient's PBL was found to be 25 to 1. In vitro-activated CTLs induced by MM2 were cytotoxic not only to MM2, but also to the autologous tumor cells in an HLA class I-restricted manner, and their surface phenotype was found to be CD3+ and CD8+. CTL therapy using cross-reactive allogeneic tumor cells as the stimulator could be clinically valuable to treat malignant brain tumors.

Aged↗
PubMed1997

Spatially and temporally regulated modification of the receptor-like protein tyrosine phosphatase zeta/beta isoforms with keratan sulphate in the developing chick brain.

Protein tyrosine phosphatase zeta (PTPzeta/RPTPbeta) is a proteoglycan-type receptor-like protein tyrosine phosphatase specifically expressed in the brain. In addition to the transmembrane form (PTPzeta-A), the extracellular splice variant (PTPzeta-S) occurs as a major soluble chondroitin sulphate proteoglycan in the brain. We prepared antibodies which specifically recognize PTPzeta-A and -S, and analysed the carbohydrate structures on the two PTPzeta isoforms in the developing chick brain. Immunoprecipitation experiments using these antibodies revealed that almost all of the keratan sulphate recognized by a monoclonal antibody (5D4) was exclusively bound to PTPzeta-A and PTPzeta-S. Addition of keratan sulphate to these proteoglycans markedly increased from embryonic day (E) 11, in contrast to the addition of Le(x) and HNK-1 carbohydrates, which gradually increased during development in accordance with expression of the core proteins, suggesting that keratan sulphate modification plays some specific roles. Moreover, at the early embryonic stage keratan sulphate was observed only in several restricted regions, especially at boundary regions such as the roof plate of the tectum, the zona limitans intrathalamica in the diencephalon, and the mesencephalon-metencephalon boundary. At the mesencephalon-metencephalon boundary, keratan sulphate modification of PTPzeta isoforms was specifically observed from E3 to E6 on a ring of cells encircling the neural tube and their radially oriented processes, which were identified as radial glial fibres. This expression pattern of keratan sulphate spatiotemporally corresponded well to the formation of the fovea isthmi, a groove separating the mesencephalon from the metencephalon. These results suggest that carbohydrates including keratan sulphate on PTPzeta isoforms play important roles in brain development by modulating the cell-cell and/or cell-substrate interactions mediated by these molecules.

Animals↗
PubMed1997

NG-methyl-L-arginine, an inhibitor of nitric oxide synthase, affects the central nervous system to produce peripheral hyperglycemia in conscious rats.

To determine whether the nitric oxide (NO) system in the central nervous system (CNS) is involved in the peripheral metabolism of carbohydrate we injected NG-methyl-L-arginine (L-NMA), an inhibitor of NO synthase, into the third cerebral ventricle of unanesthetized, unrestrained rats and determined the plasma level of glucose. This intracerebroventricular (i.c.v.) injection of the drug increased the plasma level of glucose dose-dependently, whereas an intravenous (i.v.) injection had no effect. The hyperglycemia thus induced was suppressed by concomitant i.c.v. or prior i.v. administration of L-arginine. Concomitant administration of D-arginine did not affect hyperglycemia by L-NMA. The i.c.v. injection of 5 x 10(-6) mol L-NMA increased plasma levels of glucose, epinephrine and norepinephrine, and serum levels of glucagon. However, plasma levels of insulin were unchanged, despite the presence of hyperglycemia. The hyperglycemia produced by L-NMA was completely inhibited by bilateral adrenalectomy. It was also inhibited by prior intraperitoneal injection of phentolamine, but not of propranolol or naloxone. Results suggest that L-NMA acts on the CNS to stimulate adrenal secretion of epinephrine and, subsequently, to elevate glucose levels in the peripheral blood. The NO system thus seems to be involved in the neural regulation of the adrenal by the GNS, which in turn regulates peripheral blood glucose levels.

Adrenalectomy↗
PubMed1997

Effects of genotype and diet on cholesterol efflux into plasma and lipoproteins of normal, apolipoprotein A-I-, and apolipoprotein E-deficient mice.

We investigated the contribution of apoE to cholesterol efflux into plasmas of normal, apoA-I-, and apoE-deficient mice, which were fed with chow- and cholesterol-rich diets. Plasmas of normal and apoA-I-deficient mice contain apoE in pre-beta-migrating VLDL as well as in HDL-like lipoproteins, which have either electrophoretic alpha- or gamma-mobilities. The latter particle resembled gamma-LpE in human plasma also by its mobility on nondenaturing two-dimensional electrophoresis. No apoE-containing lipoproteins were found in plasmas of apoE-deficient mice. When apoA-I- and apoE-deficient mice received both chow- and fat-rich diets, their plasmas released significantly less 3H-cholesterol from radiolabeled fibroblasts than did plasma of normal mice. Removal of apoE from plasmas of normal and apoA-I-deficient mice by anti-apoE immunoaffinity chromatography decreased their cholesterol efflux capacities (per 1 minute/per 1 hour) by 26%/40% (P = 0.0092/0.0007) and 30%/26% (P = 0.0092/0.0003), respectively. Net cholesterol efflux from fibroblasts into apoA-I-deficient plasma was 45% lower compared with plasma of normal mice. Incubation of fibroblasts with apoE-deficient plasma caused net influx of cholesterol. Prior addition of human apoE to or removal of apoB-containing lipoproteins from apoE-deficient plasma restored its ability to cause net cholesterol efflux to 50% of normal plasma. Some of the differences between cholesterol efflux into normal and apoE-deficient plasmas were attributable to the failure of apoE-deficient plasmas to take up cell-derived 3H-cholesterol into gamma-LpE. Compared with normal plasma, both apoA-I-deficient and apoE-deficient plasmas were significantly decreased in their activity to esterify cell-derived 3H-cholesterol. Anti-apoE chromatography decreased significantly cholesterol esterification in normal plasma and apoA-I-deficient plasma but not in apoE-deficient plasma. Taken together, the data provide evidence that apoE is an important contributor to reverse cholesterol transport, partially because of initial uptake of cell-derived cholesterol by gamma-LpE and partially because of the contribution of apoE-containing lipoproteins to esterification of cholesterol in plasma.

Animals↗
PubMed1997

The pressor response induced by repeated injections of neostigmine into the central nervous system is desensitized in adrenalectomized, but not in intact rats.

To investigate whether or not pressor responses to repeated stimulation of central cholinoceptive neurons are desensitized, mean arterial blood pressure (MAP) and heart rate (HR) were measured following repeated injections of neostigmine, an acetylcholinesterase inhibitor, into the third cerebral ventricle in conscious, unrestrained intact or adrenalectomized (ADX) rats. Neostigmine (5 x 10(-9) or 5 x 10(-8) mol) in 1 milliliter saline increased MAP dose-dependently and increased HR in intact rats. The peak values in MAP and HR after three repeated injections at 4 hour intervals did not wane. Neostigmine (5 x 10(-8) mol) also increased MAP in ADX rats, and the peak values after the first injection were higher in the ADX rats than in the intact rats. The pressor responses to the second and third injection, however, were less than to the first injection in the ADX rats. HR responses to the repeated injections in the ADX rats were identical to those in the intact rats. These findings suggest that the adrenal gland plays a role in antagonizing the development of desensitization in the neostigmine-induced pressor response.

Adrenalectomy↗
PubMed1997

Restoration of disturbed tooth eruption in osteopetrotic (op/op) mice by injection of macrophage colony-stimulating factor.

Osteopetrotic (op/op) mice show severe osteosclerosis caused by an inherited deficiency of osteoclast and resultant failure of tooth eruption, which can be cured by the injection of macrophage colony-stimulating factor (M-CSF). The present study revealed that consecutive injections of M-CSF in these mutant mice brought about a recovery of bone resorption resulting in the resumption of growth of tooth root and periodontal ligament. Bone resorption at the inner surface of bony crypts was noted on the 5th day after the start of M-CSF injections. This activity was reduced with the progress of root and periodontal ligament formation, being confined to the basal and crestal portion of bony crypts by the 15th day of the experiment. Second molars emerged into the oral cavity on the 15th day, but no eruption of first molars was observed until the 20th day. Throughout the experiment, first molars exhibited appreciable root deformity, which was less severe in second molars. Delayed eruption of first molars was thought to be related to the severity of the disturbance of root formation.

Age Factors↗
PubMed1997

Imaging of oxygen saturation and distribution of erythrocytes in microvessels.

OBJECTIVE: To construct images of oxygen saturation and the distribution of erythrocytes in a network of microvessels. METHODS: The image of a small group of microvessels under an inverted microscope was incorporated into an image processor through a video camera and was digitized. Based on the information obtained through six visible interference filters of different wavelengths, oxygen saturation and the amount of erythrocytes in microvessels were calculated with a computer. The system was applied to a microvascular bed of isolated rabbit mesentery perfused with a suspension of human erythrocytes. RESULTS: In a steady flow, with lowering of tissue oxygen tension by superfusion with nitrogen-bubbled isotonic saline containing 20 mmol/L sodium dithionite, the decrease of oxygen saturation of erythrocytes from arterioles to venules was imaged. Simultaneously, the distribution of erythrocytes in the microvessels was imaged and the marginal cell-free layer was profiled under high magnification. No significant alteration of the erythrocyte distribution on the deoxygenation of erythrocytes was observed. The exposure of erythrocytes to acidic pH and the decrease of the flow velocity of erythrocytes increased the release of oxygen from the erythrocytes in microvessels. CONCLUSIONS: The present method will be useful for the comprehensive analysis of oxygen transfer in the microvascular network, on the basis of both changes of the oxygen saturation and the flow behavior of erythrocytes.

Animals↗
PubMed1997

[Primary localized amyloidosis of the urinary bladder: a case report].

A case of primary localized amyloidosis of the urinary bladder is reported. A 57-year-old male who complained of macrohematuria visited our hospital. Cystoscopic examination revealed a broad basic tumor from the anterior wall to the right wall. Suspecting a bladder tumor we performed a transurethral resection. However, the histopathological examination of the specimen revealed amyloid deposition and no malignant changes. Serum electrophoresis pattern was normal and urinary Bence-Jones protein was negative. Neither rectal nor gastric biopsy revealed amyloids. From these findings, we made a diagnosis of the primary localized amyloidosis of the urinary bladder. We collected 42 cases from the Japanese literature and discuss the clinical features of this disease.

Amyloidosis↗
PubMed1997

Glucocorticoid- and mineralocorticoid receptors in microglial cells: the two receptors mediate differential effects of corticosteroids.

Effects of steroid hormones on the regulation of function and morphology of microglial cells were investigated using the cultured cells isolated from forebrain of newborn rats. Cortisol, corticosterone, and aldosterone at 100 nM caused a strong shrinkage of microglial cells cultured in a serum-supplemented medium. However, cholesterol, pregnenolone, testosterone, estradiol, and dehydroepiandrosterone did not exhibit any significant effects. The corticosteroids also inhibited the GM-CSF-mediated ramification of microglia in a serum-free medium. An anti-glucocorticoid agent RU38486 abolished the effects of corticosteroids on the microglial morphology, suggesting the presence of functional glucocorticoid receptor (GR) in microglial cells. The presence of GR was confirmed by immunoblotting with an antibody to the receptor. Cytokines GM-CSF and interleukin-3 altered the level of GR expression. Binding experiments with [3H]-corticosterone demonstrated the presence of not only GR but also mineralocorticoid receptor (MR): the dissociation constants (Kd) and the number of binding sites (Bmax) were 0.8 nM and 15 fmol/mg protein for MR and 5.0 nM and 73 fmol/mg protein for GR, respectively. The pure glucocorticoid RU28362 and dexamethasone at 20 nM (but not aldosterone and corticosterone at the same concentration) inhibited proliferation of microglial cells, as revealed by PCNA immunocytochemistry. RU28362 inhibited the activities of inducible nitric oxide synthase and acid phosphatase at concentrations higher than 1 nM. Aldosterone and corticosterone exhibited the similar inhibitory effect at 100 nM, and this inhibition was completely overcome by RU38486. On the other hand, corticosterone and aldosterone at concentrations lower than 1 nM enhanced the activities of both enzymes. The antimineralocorticoid agent spironolactone eliminated the stimulatory effects of corticosterone on the enzyme activities. In accordance with these biochemical results, electron microscopic observations revealed that glucocorticoids enhanced the formation of lysosomal vacuolation in microglial cells and aldosterone increased the number and size of lysosomes. In conclusion, it is suggested that GR and MR mediated the opposite effects of corticosterone on the functions of microglial cells; the hormone acted as an inhibitor through GR and as an stimulator through MR.

Adrenal Cortex Hormones↗
PubMed1997

Inhibition of syncytium formation by antisense oligonucleotide phosphorothioates complementary to tax mRNA of human T-cell leukemia virus type 1 (HTLV-1).

HTLV-1 infection is known as the factor to cause adult T-cell leukemia (ATL). Antisense oligonucleotide phosphorothioates against tax gene and control oligonucleotide phosphorothioates were synthesized. Antisense oligonucleotide was complementary to the region of initiation codon of tax gene. Two control oligonucleotides were tax sense and random. HTLV-1-positive human T-cell line, C91/PL and HTLV-1 non-infected human glioma cell line, U251-MG were co-cultured in the presence of antisense or control oligonucleotides for 24 hours. Oligonucleotides used in this study were not toxic at 10 microM concentration. Antisense oligonucleotide against tax gene inhibited 59% the syncytium formation assay at 10 microM concentration.

Adult↗