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Biomedical subjects

N Maeda

Publications and source records attributed to N Maeda.

At least 397 records · Page 22Linked to original sources
PubMed1993

Rat parotid gland acinar cell proliferation: signal transduction at the plasma membrane.

Galactosyltransferase (Gal Tase) is involved in a "receptor-ligand-type" interaction at the cell surface that mediates signal transduction following isoproterenol (ISO) treatment leading to acinar cell proliferation. Evidence is presented herein for the identification of the cell-surface glycoprotein signaling component. Using intact cells or isolated plasma membranes, the EGF-receptor (EGF-R) was specifically radiolabeled with [14C]-Galactose following ISO treatment. Injection of a polyclonal antibody monospecific for rat EGF-R also inhibited proliferation in a dose-dependent manner. The immunoaffinity purified receptor demonstrated altered lectin binding and increased in vitro Gal Tase substrate capacity following beta-agonist treatment when compared with EGF-R isolated from control animals. When acinar cells were incubated in the presence of EGF, plasma membranes from control and ISO-treated animals showed autophosphorylation of EGF-R tyrosine moieties, transient increases in membrane associated phospholipase C gamma, and increased cellular levels of cAMP. These properties of the tyrosine phosphate signaling pathway could be duplicated by the exogenous addition of bovine Gal Tase to ISO-treated cells but not control cells. The results suggest that cell surface Gal Tase interacts with a form of the EGF-R, having altered carbohydrate moieties to promote intracellular signaling for acinar cell proliferation.

Animals↗
PubMed1993

Sympathetic nerve disturbance and fine structure of adrenergic nerve terminals in nasal mucosa after experimentally-induced nasal hypersensitivity.

Electron microscopic observations were used to study the relation between the adrenergic nerve terminal and the effector cell in the nasal mucosa of toluene diisocyanate-sensitized and non-sensitized guinea pigs. Adrenergic nerve terminals were abundantly distributed in the adventitia of arterioles, however, no synapse formation was observed in smooth muscle cells of the mesothelium, i.e., effector cells. Adrenergic nerve terminals were observed separated from smooth muscle cells of the mesothelium of the arteriole by distances of 1000 A-3000 A. Neurotransmission by the sympathetic nerve in the nasal mucosa is assumed to be by diffusion of norepinephrine (NE) or by diffusive synaptic conduction. The mechanism of sympathetic hypofunction in the nasal mucosa in nasal hypersensitivity is assumed to be as follows: Released histamine directly stimulates H-1 receptors at the sympathetic nerve terminal, leading to the release of NE. Once released, NE is not readily reabsorbed, and is gradually depleted in the sympathetic nerve terminal, leading to hypofunction of the sympathetic nerve.

Adrenergic Fibers↗
PubMed1993

[Cholesterin granuloma in a hemodialysis patient with polycystic kidney disease].

We report a case of cholesterin granuloma of the kidney masquerading as a renal tumor. A 59-year-old man with polycystic kidney disease had been on hemodialysis for 5 years when he developed asymptomatic gross hematuria. Ultrasonography and CT scanning showed a solid mass in the right kidney and nephrectomy was performed. The resected specimen was a 2.0 x 2.0 cm yellowish solid mass. Histological examination showed a granuloma containing numerous cholesterin crystals. A renal mass containing cholesterin crystals is very rare and only one case has been reported previously in Japan.

Cholesterol↗
PubMed1993

A base substitution in the promoter associated with the human haptoglobin 2-1 modified phenotype decreases transcriptional activity and responsiveness to interleukin-6 in human hepatoma cells.

An A-to-C base substitution at nucleotide position -61 in the promoter region of the human haptoglobin gene (Hp) has been shown to be strongly associated with the haptoglobin 2-1 modified (Hp2-1mod) phenotype. In order to investigate whether this base substitution is the cause of reduced expression of the Hp2 allele relative to the Hp1 allele in individuals with the Hp2-1mod phenotype, we used the chloramphenicol acetyl transferase (CAT) expression system to evaluate promoter function. In HepG2 cells, which normally express their endogenous haptoglobin genes, CAT plasmid constructs with the -61C base change in the promoter had about 10-fold-lower transcriptional activity after transfection than did the Hp control construct. The -61C substitution also rendered the construct unresponsive to treatment by interleukin-6 after transfection into Hep3B2 cells, which normally do not express haptoglobin but do so in response to stimulation by acute-phase reactants. In addition, two base substitutions, T to A and A to G, at positions -104 and -55G, respectively, in the promoter region of the Hp1 allele, are also associated with the Hp2-1mod phenotype. CAT constructs with both substitutions (-104A-55G) and with one substitution (-55G) showed activity similar to that in the Hp control when transfected into both HepG2 and Hep3B2 cells, although interleukin-6 induction was less than with the Hp control construct. These results further support the hypothesis that the Hp2-1mod phenotype results, in part, from the -61C mutation in the promoter region of the Hp2 gene.

Alleles↗
PubMed1993

[A study on ACTH dosage for treatment of West syndrome].

We conducted a retrospective study of 50 patients with West syndrome who had been treated with ACTH. The patients were classified into two groups; group I, receiving standard dose of ACTH (0.025 mg/kg/day); and group II, receiving low dose of ACTH (0.015 mg/kg/day). The short-term effect of treatment was evaluated. Each group was further divided into two subgroups; cryptogenic (I-C, II-C) and symptomatic (I-S, II-S). There was no significant difference in the control rate of clinical seizures, between the two dosage groups of cryptogenic etiology. In the symptomatic cases, a greater effectiveness was achieved in group II-S than I-S. None of the patients with cryptogenic etiology experienced any relapse of infantile spasms. Patients with symptomatic etiology had a higher incidence of relapse. The rate of clinical and EEG seizure control was lower, and the incidence of side effects was higher in group I-S patients. The poor short-term effect of treatment in group I-S patients may be due to a higher incidence of prenatal etiology.

Adolescent↗
PubMed1993

Nucleotide sequence encoding the carboxyl-terminal half of apolipoprotein B from spontaneously hypercholesterolemic pigs.

Previous studies from this laboratory characterized the hypercholesterolemia of pigs with a mutant allele of apolipoprotein B (apoB), designated Lpb5. This apoB allele is associated with low density lipoprotein (LDL) particles deficient in binding to the LDL receptor. To identify potential causative mutations in Lpb5 DNA, 10.6 kb of genomic DNA, encoding the carboxyl-terminal 58% of apoB were sequenced from the Lpb5 allele and from an allele encoding phenotypically normal apoB. Comparison of the two DNA sequences revealed 33 polymorphisms, 13 of which resulted in amino acid polymorphisms. To determine whether any of the amino acids at the polymorphic positions in Lpb5-encoded apoB were unique to that isoform, those positions were sequenced in four other pig apoB alleles encoding phenotypically normal apoB. None of the amino acids were by themselves uniquely encoded by the Lpb5 allele. However, a unique haplotype consisting of Asp3164 in conjunction with Ala3447 distinguished the Lpb5-encoded apoB from all other allelic isoforms sequenced in this region. To gain insight into changes in the tertiary structure of the mutant apoB, 13C-NMR analysis of LDL reductively methylated with [13C]-formaldehyde was performed. LDL has lysine residues that titrate at pH 10.5 and others that titrate at pH 8.9. The latter residues are thought to include those involved in the interaction of LDL with the LDL receptor. LDL from Lpb5 pigs possessed a smaller proportion of lysine residues titrating at pH 8.9 than did LDL from non-Lpb5 pigs, suggesting that the Lpb5-encoded apoB is altered in a manner affecting the microenvironment of particular lysine residues.

Alleles↗
PubMed1993

[Characteristics of day service center clients and their families based on their medical conditions].

Clients utilizing day service centers in Hokkaido, and their families were surveyed for the purpose of analyzing present conditions of health, ADL level, family structure, motivation, activities, and changes in physical and psychosocial status. The average age of subjects was 76 years old with women generally being older than men. Most were living with their families. As to disease, cerebrovascular diseases were most common followed by hypertension and spinal-articulation diseases. Women had more hypertension problems compared to men who had more cerebrovascular conditions. Effectiveness of these day service programs were seen in the improvement of psychological functions. Persons with cerebrovascular disease had greater participation in functional rehabilitation training programs, and their ADL skills were improved.

Activities of Daily Living↗
PubMed1993

[Atypical early infantile epileptic encephalopathy with suppression-burst].

We report an 8-month-old infant with tonic spasms that started at the age of 38 days and occurred in clusters. He had no myoclonic seizures, or erratic myoclonus. Repeated simultaneous video-EEG monitoring revealed abrupt flexion of the neck and extremities associated with high voltage slow waves preceded by multiple spikes and/or sharps, which resembled spasms seen in West syndrome. Interictal EEGs, before and after the onset of epilepsy, showed suppression-burst. The bursts consisted of irregular high voltage slow waves mixed with poorly developed spike before the onset of epilepsy. On the other hand, duration of suppression phase ranged from 1 to 27 seconds, and burst-burst interval from 2 to 30 seconds after the onset of epilepsy. He was considered as having an atypical early infantile epileptic encephalopathy with suppression burst.

Diagnosis, Differential↗
PubMed1992

Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.

Apolipoprotein E (apoE) is a ligand for receptors that clear remnants of chylomicrons and very low density lipoproteins. Lack of apoE is, therefore, expected to cause accumulation in plasma of cholesterol-rich remnants whose prolonged circulation should be atherogenic. ApoE-deficient mice generated by gene targeting were used to test this hypothesis and to make a mouse model for spontaneous atherosclerosis. The mutant mice had five times normal plasma cholesterol, and developed foam cell-rich depositions in their proximal aortas by age 3 months. These spontaneous lesions progressed and caused severe occlusion of the coronary artery ostium by 8 months. The severe yet viable phenotype of the mutants should make them valuable for investigating genetic and environmental factors that modify the atherogenic process.

Animals↗
PubMed1992

The structure and complete sequence of the gene encoding chicken ribosomal protein L5.

The nucleotide (nt) sequence of the gene encoding chicken ribosomal protein L5, which associates with 5S rRNA, was determined. The gene contains eight exons and seven introns which spread over 7252 bp. The transcription start point (tsp) is a C residue in a tract of 13 pyrimidines, and its 5'-flanking region lacks canonical TATA and CAAT boxes. The G+C content of the region around the tsp is calculated as high as 78%, and nine GC boxes exist within the 5'-flanking region and the first intron. The nt sequence at positions -36 to -22 is similar to an internal sequence at positions 56-70 of the gene encoding chicken 5S rRNA, which corresponds to the transcriptional internal control region of the 5S rRNA-encoding gene of Xenopus laevis. This region might contribute to the coordinate expression of the genes encoding protein L5 and 5S rRNA.

Amino Acid Sequence↗
PubMed1992

Marked reduction of high density lipoprotein cholesterol in mice genetically modified to lack apolipoprotein A-I.

Atherosclerosis is a major cause of morbidity and mortality in developed countries. In humans the risk of atherosclerosis is inversely correlated with plasma levels of high density lipoprotein (HDL). As a step in determining whether the experimental reduction of plasma HDL level will increase susceptibility to atherosclerosis, we have used gene targeting in embryonic stem cells to produce mice lacking apolipoprotein A-I, the major protein component of HDL particles. Mice homozygous for the disrupted gene have no plasma apolipoprotein A-I detectable by double immunodiffusion; their total plasma cholesterol and HDL-cholesterol levels after overnight fasting are reduced to about one-third and one-fifth of normal levels, and they are grossly deficient in alpha-migrating HDL particles.

Animals↗
PubMed1992

Trigeminal nerve endings of lingual mucosa and musculature of the rat.

Horseradish peroxidase conjugated with wheat germ agglutinin (HRP-WGA) was injected into the trigeminal ganglion of adult rats to label the peripheral sensory receptors of the tongue. The conjugate was transported anterogradely to all the ipsilateral fungiform papillae and filiform papillae. Some labeled fibers crossed over to the contralateral papillae. In the intrinsic tongue muscle undulating nerve fibers along or across muscle fibers were often observed, and formed simple spiral endings.

Animals↗
PubMed1992

Generation of mice carrying a mutant apolipoprotein E gene inactivated by gene targeting in embryonic stem cells.

We have inactivated the endogenous apolipoprotein E (apoE) gene by using gene targeting in mouse embryonic stem (ES) cells. Two targeting plasmids were used, pJPB63 and pNMC109, both containing a neomycin-resistance gene that replaces a part of the apoE gene and disrupts its structure. ES cell colonies targeted after electroporation with plasmid pJPB63 were identified by the polymerase chain reaction (PCR) followed by genomic Southern analysis. Of 648 G418-resistant colonies analyzed, 9 gave a positive signal after PCR amplification, and 5 of them were confirmed as targeted by Southern blot analysis. The second plasmid, pNMC109, contains the negatively selectable thymidine kinase gene in addition to the neomycin-resistance gene. After electroporation with this plasmid, 177 colonies resistant both to G418 and ganciclovir were analyzed; 39 contained a disrupted apoE gene as determined by Southern blotting. Chimeric mice were generated by blastocyst injection with 6 of the targeted lines. One of the lines gave strong chimeras, three of which transmitted the disrupted apoE gene to their progeny. Mice homozygous for the disrupted gene were produced from the heterozygotes; they appear healthy, even though they have no apolipoprotein E in their plasma.

Animals↗
PubMed1992

The inositol 1,4,5-trisphosphate receptor.

Inositol 1,4,5-trisphosphate (InsP3) is a second messenger that releases Ca2+ from its intracellular stores. The InsP3 receptor has been purified and its cDNA has been cloned. We have found that the InsP3 receptor is identical to P400 protein, first identified as a protein enriched in cerebellar Purkinje cells. We have generated an L-fibroblast cell transfectant that produces cDNA-derived InsP3 receptors. The protein displays high affinity and specificity for InsP3. InsP3 induces greater Ca2+ release from membrane vesicles from transfected cells than from those from control L-fibroblasts. After incorporation of the purified InsP3 receptor into lipid bilayers InsP3-induced Ca2+ currents were demonstrated. These results suggest that the InsP3 receptor is involved in physiological Ca2+ release. Immunogold labelling using monoclonal antibodies against the receptor showed that it is highly concentrated on the smooth-surfaced endoplasmic reticulum and slightly on the outer nuclear membrane and rough endoplasmic reticulum; no labelling of Golgi apparatus, mitochondria and plasmalemma was seen. Cross-linking experiments showed that the receptor forms a homotetramer. The approximately 650 N-terminal amino acids are highly conserved between mouse and Drosophila, and this region contains the critical sequences for InsP3 binding. We have investigated the heterogeneity of the InsP3 receptor using the polymerase chain reaction and have found novel subtypes of the mouse InsP3 receptor that are expressed in a tissue-specific and developmentally specific manner.

Amino Acid Sequence↗
PubMed1992

A biochemical analysis of parotid and submandibular salivary gland function with age after simultaneous stimulation with pilocarpine and isoproterenol in female NIA Fischer 344 rats.

This analysis of physiological, biochemical and molecular changes related to aging was made in 3-, 12- and 24-month-old rats. The salivary gland weight/body weight ratio and the structural membrane proteins did not change with age for either gland, but a significant age-related decline in DNA synthesis for both glands was detected, unrelated to the hormonal responsiveness at the level of the plasma membrane. There was a marked increase in the concentration of soluble proteins in adolescent parotid gland and, for the two older age groups, in submandibular gland. The saliva flow rate was different when expressed as volume per time, as volume per time and g glandular wet weight, and/or kg body weight. The concentration of secreted proteins was not affected by age in either gland. The total amount of proteins secreted over 30 min revealed no age-related perturbation for the parotid gland, but showed a significant age-related increase in submandibular saliva. Sodium dodecyl sulphate-polyacrylamide gel analysis revealed changes in the protein bands between 39 and 50 kDa in the Coomassie blue-stained gels from 12-month-old animals. Amylase showed an initial increase (12 months), followed by a marked decline in its activity in parotid saliva. The glandular supernatant had low residual cellular amylase activity after stimulation. Therefore, secretory impairment with age after pilocarpine-isoproterenol stimulation was excluded. Analysis of total RNA showed a pronounced decrease of amylase mRNA in the parotid gland between 12 and 24 months of age. No amylase mRNA was expressed in any of the submandibular samples. For epidermal growth factor, total saliva showed a decrease with age. It seemed that the submandibular gland followed the same picture with age as the parotid gland, with a specific decline in the biosynthesis of single secretory proteins.

Aging↗
PubMed1992

A chondroitin sulfate proteoglycan that is developmentally regulated in the cerebellar mossy fiber system.

It is known that the mammalian brain contains many kinds of proteoglycans, but almost all of them remain to be characterized. In this study, we prepared a monoclonal antibody against a phosphate-buffered saline-soluble brain proteoglycan (MAb 6B4). MAb 6B4 recognized a 600- to 1000-kDa chondroitin sulfate proteoglycan with a 250-kDa core protein (6B4 proteoglycan). The core protein of 6B4 proteoglycan carried the HNK-1 epitope. Immunohistochemical analysis of the adult rat brain indicated that this proteoglycan was expressed on the cell surfaces of a subset of neurons. In the hindbrain, 6B4 proteoglycan was highly expressed on the cerebellar Purkinje cells and Golgi cells, and at particular nuclei including the pontine nuclei and lateral reticular nucleus. Almost all of these nuclei were connected to the cerebellum through the mossy fiber system. A developmental study indicated that the expression of this proteoglycan changed dramatically during the formation of the cerebellar mossy fiber system. The mossy fibers from the pontine nuclei expressed 6B4 proteoglycan transiently from Embryonic Day 20 (E20) to Postnatal Day 30 (P30), during which time the axonal outgrowth and glomerular synapse formation occurred. The Purkinje cells, glomeruli, and Golgi cells began to be stained with MAb 6B4 from P10, P16, and P20, respectively. These expression stages correspond with the onset of their synapse formation. These results suggest that 6B4 proteoglycan is closely involved in the development of the cerebellar mossy fiber system.

Animals↗
PubMed1992

Usefulness of PET scan in a child with mesial frontal lobe epilepsy.

Positron emission tomography (PET) scan with 18F-fluorodeoxyglucose (18F-FDG) was performed in a 14-year-old boy who had seizures suspected to have originated in mesial frontal lobe. The seizures occurred in clusters and were characterised by a change in the facial expression at seizure onset and complex motor manifestations consisting of kicking, swaying and screaming. Ictal EEG showed rhythmic alpha-waves in the left frontal area association with the ictus. Cerebral CT, MRI and SPECT revealed nothing of significance, but the PET brain scans showed frontal and parietal hypometabolism, which was most prominent in the left mesial frontal lobe. The present case suggests that FDG-PET scanning may be useful for the diagnosis of the mesial frontal epilepsy, when other imaging studies fail to show abnormalities.

Adolescent↗