[A case of tuberculosis of the ascending colon associated with ileus and fistula formation].
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Aged↗
Biomedical subjects
N Maeda
Publications and source records attributed to N Maeda.
[Osteoclast-like giant cell tumor of the liver].
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Giant Cell Tumors↗
Hepatic clearance of chylomicron remnants in mice lacking apoprotein E.
Control and apoprotein E-deficient mice generated by gene targeting in embryonic stem cells were fed a fat load containing 3H-labeled retinol and the absorbed radioactivity present in the plasma, liver, and carcass measured 6 h later. The radioactivity in the plasma of the apoprotein E-deficient mice was several fold higher than in control animals, but it accounted for less than 1/5 of the absorbed radioactivity. In both groups of animals most of the absorbed radioactivity was recovered in the livers. These findings indicate that in apoprotein E-deficient mice chylomicron remnants can be taken up by the liver by a process that does not require the mediation of apoprotein E.
Animals↗
Multiple receptor-like protein tyrosine phosphatases in the form of chondroitin sulfate proteoglycan.
The possibility that some of the brain proteoglycans are receptor-like protein tyrosine phosphatases (PTPases) was investigated. Membrane-bound proteoglycan fractions were prepared from the postnuclear membrane fraction of 8-day-old rat brain by DEAE ion-exchange chromatography and CsCl density gradient centrifugation. The isolated proteoglycan fractions showed high PTPase specific activities together with the typical PTPase characteristics. Renaturation experiments indicated that chondroitin sulfate proteoglycans with 380- and 170-kDa core proteins carried the PTPase activity. The proteoglycan with 380-kDa core protein was identified as RPTP beta/zeta bearing HNK-1 carbohydrate.
Animals↗
Targeted disruption of the apolipoprotein C-III gene in mice results in hypotriglyceridemia and protection from postprandial hypertriglyceridemia.
Using gene targeting in embryonic stem cells, we have generated mice lacking apolipoprotein C-III (ApoC-III). Homozygous mutant animals show absence of ApoC-III protein and no expression of ApoC-III mRNA in the liver or in the intestine. Expression of the neighboring genes, coding for apolipoprotein A-I and apolipoprotein A-IV, are not altered in the liver but are reduced in the intestine. This suggests that these three genes share a tissue-specific element for intestinal expression and that insertion of an additional promoter for the neomycin-resistant gene into the locus affects interaction between the tissue-specific element and the promoter of the individual gene. Fasted plasma triglyceride levels in the homozygous mutants are reduced to about 70% of normal, while heterozygotes have values intermediate between those of the homozygous mutants and wild types. Plasma levels of total cholesterol and of high density lipoprotein cholesterol in homozygotes are consistently lower than those in normal mices but the reduction does not reach statistical significance. A fat meal test showed that postprandial hypertriglyceridemia is abolished in homozygotes lacking ApoC-III. The homozygous mutants also clear chylomicrons faster than wild type controls. These data indicate that ApoC-III modulates the catabolism of triglyceride-rich lipoproteins and plays a role in the postprandial management of triglycerides.
Animals↗
Simultaneous influence of erythrocyte deformability and macromolecules in the medium on erythrocyte aggregation: a kinetic study by a laser scattering technique.
The aggregation and sedimentation kinetics of human erythrocytes was studied by modifying the cellular properties and medium compositions simultaneously. Dextrans of average molecular weight 70400 and 494000 were used to provide suspending medium modifications, while diamide (diazene dicarboxylic acid bis(N,N-dimethylamide)) was used to alter the membrane structural properties. Laser scattering method was employed for this study, and it was compared with a kinetic method combined with a low-shear rheoscope and an image analyzer. From scattered light intensity profiles continuously obtained during aggregation of erythrocytes and sedimentation of the aggregates, characteristic kinetic parameters were computed. Kinetic parameters obtained from a phase of the one-dimensional aggregate formation and sedimentation corresponded well to the velocity of rouleaux formation obtained by the low-shear rheoscope technique. Dextrans accelerated the erythrocyte aggregation and the sedimentation, and diamide treatment suppressed the process by decreasing the erythrocyte deformability. The aggregating force by dextrans overcame the disaggregating force by the decreased deformability. However, the arrangement of erythrocytes as expressed in specific units for aggregates (i.e., rouleaux) became irregular by decreasing the erythrocyte deformability. In conclusion, the progression of erythrocyte aggregation and the structure of the aggregates were dependent on both erythrocyte properties and macromolecules in the medium.
Blood Sedimentation↗
Characterization of the synthesis and expression of the GTA-kinase from transformed and normal rodent cells.
The murine transformed cell line YC-8 and beta-adrenergic receptor agonist (isoproternol) treated rat and mouse parotid gland acinar cells ectopically express cell surface beta 1-4 galactosyltransferase during active proliferation. This activity is dependent upon the expression of the GTA-kinase (p58) in these cells. Using total RNA, cDNA clones for the protein coding region of the kinase were isolated by reverse transcriptase-PCR cloning. DNA sequence analysis failed to show sequence differences with the normal homolog from mouse cells although Southern blot analysis of YC-8, and a second cell line KI81, indicated changes in the restriction enzyme digestion profile relative to murine cell lines which do not express cell surface galactosyltransferase. The rat cDNA clone from isoproterenol-treated salivary glands showed a high degree of protein and nucleic acid sequence homology to the GTA-kinase from both murine and human sources. Northern blot analysis of YC-8 and a control cell line LSTRA revealed the synthesis of a major 3.0 kb mRNA from both cell lines plus the unique expression of a 4.5 kb mRNA in the YC-8 cells. Reverse transcriptase-PCR of LSTRA and YC-8 confirmed the increased steady state levels of the GTA-kinase mRNA in YC-8. In the mouse, induction of cell proliferation by isoproterenol resulted in a 50-fold increase in steady state mRNA levels for the kinase over the low level of expression in quiescent cells. Expression of the rat 3' untranslated region in rat parotid cells in vitro led to an increased rate of DNA synthesis, cell number an ectopic expression of cell surface galactosyltransferase in the sense orientation. Antisense expression or vector alone did not alter growth characteristics of acinar cells. A polyclonal antibody monospecific to a murine amino terminal peptide sequence revealed a uniform distribution of GTA-kinase over the cytoplasm of acinar and duct cells of control mouse parotid glands. However, upon growth stimulation, kinase was detected primarily in a perinuclear and nuclear immunostaining pattern. Western blot analysis confirmed a translocation from a cytoplasmic localization in both LSTRA and quiescent salivary cells to a membrane-associated localization in YC-8 and proliferating salivary cells.
Amino Acid Sequence↗
Possible involvement of the septo-hippocampal cholinergic and raphe-hippocampal serotonergic activations in the penile erection induced by fenfluramine in rats.
Fenfluramine (0.1-10 mg/kg, i.p.) induced penile erection in naive rats with a bell-shaped dose response curve. The response to fenfluramine (1 mg/kg) was antagonized by scopolamine (0.032-1 mg/kg) but not by methyl-scopolamine (0.032-1 mg/kg) pre-treatment. The septo-hippocampal cholinergic deafferentations by medial septum lesion or fimbria-fornix transection also attenuated the penile erection induced by fenfluramine, whereas dopaminergic blockade by sulpiride (3.2-100 mg/kg) had hardly any effect. Pindolol (0.1-3.2 mg/kg), a 5-HT1 antagonist, and ICS205-930, a 5-HT3 antagonist, but not ketanserin, a 5-HT2 antagonist, inhibited the penile erection induced by fenfluramine. Depletion of 5-HT not only by systemic injections of p-chlorophenylalanine (150 mg/kg i.p. at 72, 48 and 24 h before the test) but also by the injections of 5,7-dihydroxytryptamine (5,7-DHT), a serotonergic neurotoxin, into the median- and dorsal-raphe nuclei significantly attenuated the fenfluramine-induced penile erections. Neurochemical analyses revealed that the raphe-lesion significantly reduced the contents of serotonin (5-HT) and its major metabolite, 5-hydroxyindole acetic acid (5-HIAA) but not choline acetyltransferase (ChAT) activities in all the cortical and subcortical regions examined. The results suggest that fenfluramine facilitates the expression of penile erection in rats through an activation of the septo-hippocampal cholinergic pathway as a consequence of excitation of the raphe-hippocampal serotonergic pathway in which 5-HT1 and/or 5-HT3 receptors appear to play a regulatory role.
Adrenergic beta-Antagonists↗
Evolutional changes of cortical hypometabolism in West's syndrome.
The pathophysiological basis of the epileptic encephalopathy West's syndrome remains unknown. We have done serial positron emission tomography (PET) with fluorine-18-labelled 2-deoxy-3-fluoro-D-glucose (FDG) in twelve patients with newly diagnosed West's syndrome. Throughout follow-up, PET revealed diffuse or focal cortical hypometabolism in eleven patients, whereas magnetic resonance imaging (MRI) showed morphological abnormalities in only five. At disease onset, PET showed cortical hypometabolism in eight patients (diffuse in three, focal in five). The second PET showed normal metabolism in six of these patients but focal abnormalities in three of the four with normal results on first PET. In all seven patients with normal findings on the second PET, tonic spasms ceased after initial treatment and no epileptic seizure occurred thereafter. In the five patients with cortical hypometabolism on the second PET, tonic spasms persisted or recurred, or partial seizures appeared. However, in two patients PET abnormalities disappeared in accordance with the later resolution of epileptic seizures. All patients with normal MRI and second PET results had normal psychomotor development. Diffuse or focal cortical hypometabolism that cannot be detected by MRI or computed tomography is common in patients with West's syndrome. However, this anomaly is not permanent and changes with clinical symptoms. These functional abnormalities in the cerebral cortex may be associated with the development of West's syndrome.
Cerebral Cortex↗
The two-receptor model of lipoprotein clearance: tests of the hypothesis in "knockout" mice lacking the low density lipoprotein receptor, apolipoprotein E, or both proteins.
Apolipoprotein E (apoE) is hypothesized to mediate lipoprotein clearance by binding to two receptors: (i) the low density lipoprotein receptor (LDLR) and (ii) a chylomicron remnant receptor. To test this hypothesis, we have compared plasma lipoproteins in mice that are homozygous for targeted disruptions of the genes for apoE [apoE(-/-)], the LDLR [LDLR(-/-)], and both molecules [poE(-/-); LDLR(-/-)]. On a normal chow diet, apoE(-/-) mice had higher mean plasma cholesterol levels than LDLR(-/-) mice (579 vs. 268 mg/dl). Cholesterol levels in the apoE(-/-); LDLR(-/-) mice were not significantly different from those in the apoE(-/-) mice. LDLR(-/-) mice had a relatively isolated elevation in plasma LDL, whereas apoE(-/-) mice had a marked increase in larger lipoproteins corresponding to very low density lipoproteins and chylomicron remnants. The lipoprotein pattern in apoE(-/-); LDLR(-/-) mice resembled that of apoE(-/-) mice. The LDLR(-/-) mice had a marked elevation in apoB-100 and a modest increase in apoB-48. In contrast, the apoE(-/-) mice had a marked elevation in apoB-48 but not in apoB-100. The LDLR(-/-); apoE(-/-) double homozygotes had marked elevations of both apolipoproteins. The observation that apoB-48 increases more dramatically with apoE deficiency than with LDLR deficiency supports the notion that apoE binds to a second receptor in addition to the LDLR. This conclusion is also supported by the observation that superimposition of a LDLR deficiency onto an apoE deficiency [apoE(-/-); LDLR(-/-) double homozygotes] does not increase hypercholesterolemia beyond the level observed with apoE deficiency alone.
Animals↗
Possible involvement of brain somatostatin in the memory formation of rats and the cognitive enhancing action of FR121196 in passive avoidance task.
Using the passive avoidance learning task in rats, the role of brain somatostatin in cognitive function was investigated with special reference to that of the brain cholinergic system. In addition, the involvement of both the brain somatostatinergic and cholinergic systems in the anti-amnesic action of a newly introduced cognitive enhancer, FR121196 [N-(4-acetyl-1-piperazinyl)-4-fluorobenzenesulfonamide], was examined. Treatment with cysteamine (50, 100, 200 mg/kg, s.c.), a depletor of somatostatin, significantly and dose-dependently reduced the retention of single trial passive avoidance task. Similar memory impairments were found in rats which received central cholinergic blockade either by scopolamine (0.1-1 mg/kg) or by lesioning of the nucleus basalis magnocellularis (NBM). Intracerebroventricurally (i.c.v.) administered somatostatin (1-14) (10-1000 ng/rat) significantly ameliorated the memory impairments induced not only by cysteamine (200 mg/kg) but also by scopolamine (1 mg/kg) and NBM-lesioning. Although physostigmine (0.01-1 mg/kg) also ameliorated the memory impairments induced by cysteamine and scopolamine, it failed to affect the memory impairment seen in the NBM-lesioned rats. Administration of FR121196 (0.1-10 mg/kg) significantly ameliorated the memory deficits produced by scopolamine and NBM lesioning but not that induced by cysteamine.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
IP3-activated calcium-permeable channels in the inside-out patches of cultured cerebellar Purkinje cells.
Inositol-1,4,5-trisphosphate (IP3)-activated calcium-permeable channels were recorded from inside-out patches of cultured cerebellar Purkinje cells. When 2-5 microM of IP3 was applied to the internal surface of the inside-out patches, inward Ba2+ currents were activated within 10 sec following the application in 11 out of 24 patches. In the presence of heparin (100 micrograms/ml), activation of Ba2+ currents by IP3 was inhibited. Unitary currents with different amplitudes and kinetics were observed; small and large unitary currents, and rapid fluctuations with various amplitudes. The small unitary currents (single channel conductance; 5.6 pS) were most frequent. Addition of inositol 1,3,4-trisphosphate (2-5 microM) slightly activated Ba2+ currents in 2 out of 10 patches, but the amount of the increment was much smaller than that produced by IP3. These results suggest a possibility that IP3 directly activates Ca(2+)-permeable channels in the plasma membrane of cerebellar Purkinje cells.
Animals↗
A plasma lipoprotein containing only apolipoprotein E and with gamma mobility on electrophoresis releases cholesterol from cells.
Previous studies have identified lipid-poor high density lipoproteins with electrophoretic pre-beta mobility as the initial acceptors of cell-derived cholesterol in human plasma. These lipoproteins contain apolipoprotein A-I (apo A-I) as their sole apolipoprotein. In the present study, incubation of human plasma with [3H]cholesterol-laden skin fibroblasts has led to the identification of another lipoprotein that serves as a potent initial acceptor of cell-derived cholesterol. This lipoprotein, which we term gamma-LpE, exhibits gamma mobility on agarose gel electrophoresis. As determined by nondenaturing PAGE and by electron microscopy, the size of the spherical particle ranges between 12 and 16 nm. SDS/PAGE and subsequent immunoblotting identified apoE as its sole apolipoprotein. Plasma from normal and apoA-I-deficient mice, but not from apoE-deficient mice, released [3H]cholesterol from fibroblasts into a gamma-migrating lipoprotein. Cell culture media from hepatoma cells or mouse peritoneal macrophages, both of which contain apoE of cellular origin, also promoted efflux of [3H]cholesterol from fibroblasts into a gamma-migrating fraction. This was not observed with cell culture medium from fibroblasts alone. In conclusion, our results strongly indicate the presence in human plasma of a lipoprotein containing only apoE, gamma-LpE, which is secreted by peripheral cells and is a potent acceptor of cell-derived cholesterol.
Animals↗
Subcellular localization of the inositol 1,4,5-trisphosphate receptor, P400, in the vestibular complex and dorsal cochlear nucleus of the rat.
The subcellular localization of the inositol 1,4,5-trisphosphate receptor protein, P400, was studied in the vestibular complex, an area to which Purkinje cells project, as well as in neurons of the dorsal cochlear nucleus and in ectopic Purkinje cells of adult rat brain. The receptor was demonstrated by electron microscopical immunocytochemistry using the avidin-biotin peroxidase complex procedure, with the monoclonal antibody 4C11 raised against mouse cerebellar inositol 1,4,5-trisphosphate receptor protein. Immunoreactivity was found in preterminal fibres and terminal boutons in the nuclei of the vestibular complex, generally associated with the subsurface systems and stacks or fragments of smooth endoplasmic reticulum. Ectopic Purkinje cells and cartwheel cells of the dorsal cochlear nucleus also displayed immunoreactivity, but this was much less intense in the latter. The results of the present study suggest that this receptor protein, involved in the release of Ca2+, is located in sites that enable it to influence the synthesis, transport and release of neurotransmitters.
Animals↗
Immunoglobulin binding factor: a new tumor marker for prostatic tumors.
Human seminal plasma contains an immunoglobulin gamma binding factor (IgBF) with an estimated molecular weight of 16 kD under reducing condition. IgBF was detected only in the prostate, including benign prostatic hypertrophy (BPH) and neoplasm. The present study was performed to determine whether IgBF is a useful prostatic marker. Serum IgBF levels were measured in patients with prostatic tumors and in control patients without tumor by radioimmunoassay. Serum prostatic-specific antigen (PSA), the standard prostatic marker, was also determined. Serum IgBF levels in patients with prostate cancer were significantly higher than those in age-matched controls (P < 0.05). Also, patients with BPH tended to have elevated IgBF levels than the controls, although the values were not statistically significant. In control patients, serum IgBF levels increased with advancing age. There was no correlation between serum levels of IgBF and PSA in patients with prostate cancer. Using cut-off level at 28.5 ng/ml (2 S.D. above the mean IgBF level of age-matched control), the sensitivities were 41.2% (7/17) for prostate cancer, 23.1% (6/26) for BPH, and 5.6% (1/18) for control patients. In conclusion, serum IgBF is a useful marker in the diagnosis of patients with prostatic tumor, and in evaluating the course of treatment.
Adolescent↗
Parallel evolutionary events in the haptoglobin gene clusters of rhesus monkey and human.
Parallel occurrences of evolutionary events in the haptoglobin gene clusters of rhesus monkeys and humans were studied. We found six different haplotypes among 11 individuals from two rhesus monkey families. The six haplotypes include two types of haptoglobin gene clusters: one type with a single gene and the other with two genes. DNA sequence analysis indicates that the one-gene and the two-gene clusters were both formed by unequal homologous crossovers between two genes of an ancestral three-gene cluster, near exon 5, the longest exon of the gene. This exon is also the location where a separate unequal homologous crossover occurred in the human lineage, forming the human two-gene haptoglobin gene cluster from an ancestral three-gene cluster. The occurrence of independent homologous unequal crossovers in rhesus monkey and in human within the same region of DNA suggests that the evolutionary history of the haptoglobin gene cluster in primates is the consequence of frequent homologous pairings facilitated by the longest and most conserved exon of the gene.
Animals↗
Flow dynamics of erythrocytes in microvessels of isolated rabbit mesentery: cell-free layer and flow resistance.
A part of microvascular bed isolated from rabbit mesentery (composed of a few branches of superior mesenteric artery) was used for the study of the flow dynamics of erythrocytes in microvessels. The flow resistance in the microvascular bed was analyzed with respect to the thickness of a cell-free layer formed along the inner wall of vessels and the suspension viscosity of erythrocytes (in terms of hematocrit and erythrocyte deformability). The thickness of the cell-free layer increased with the increase in the inner diameter of microvessels. By lowering the hematocrit, the thickness increased and the flow resistance decreased. Meanwhile, by decreasing the erythrocyte deformability with diamide, the thickness decreased and the flow resistance increased. However, the thickness was not altered in microvessels less than 10 microns by the diamide treatment. The maximum inner diameter of microvessel required to induce parachute- and/or slipper-like deformation (at flow velocity of erythrocytes less than 2 mm s-1) was 13 microns for control cells and 6 microns for diamide-treated cells. The thickness of the cell-free layer could not be closely related to the flow resistance, while a good relationship applicable to both control and diamide-treated cells was obtained between the flow resistance and the suspension viscosity. The present results conclude that the flow resistance in the isolated microvascular bed is mainly provided by both hematocrit and erythrocyte deformability.
Animals↗
Developmentally regulated expression of a brain specific species of chondroitin sulfate proteoglycan, neurocan, identified with a monoclonal antibody IG2 in the rat cerebrum.
The mammalian brain contains many species of proteoglycan. To identify each proteoglycan species, we have raised monoclonal antibodies against soluble chondroitin sulfate proteoglycans purified from 10-day-old rat brains. One monoclonal antibody, named monoclonal antibody 1G2, recognized two proteoglycan species with 220,000 and 150,000 mol. wt core glycoproteins (chondroitin sulfate proteoglycan-220 and chondroitin sulfate proteoglycan-150). Partial amino acid sequences of N-termini of their core proteins coincided with those of neurocan, a brain-unique chondroitin sulfate proteoglycan species, whose complete coding sequence was recently reported [Rauch et al. (1992) J. biol. Chem. 269, 19,536-19,547]. Western blots revealed that chondroitin sulfate proteoglycan-220 became detectable in the rat cerebrum on embryonic day 14, and that it disappeared from the brain around postnatal day 30. In contrast, a fairly large amount of chondroitin sulfate proteoglycan-150 remained in the mature brain. Immunohistochemical studies revealed that 1G2 antigen was first localized in the preplate zone, then both in the marginal zone and in the subplate of the rat cerebrum on embryonic day 16, prior to arrival of the first thalamic afferents at the cortex. On embryonic day 20, immunolabeling with monoclonal antibody 1G2 began to spread from the subplate into the developing cortical plate. On postnatal day 10, the neuropil of the cerebrum, except for the barrel field, was diffusely stained with the antibody, intensely in the hippocampus and superficial layers (I-III) of the cerebral cortex and weakly elsewhere. The barrel hollows were stained very weakly compared with the barrel walls at this stage. The immunoreactivity in the hippocampus and superficial cortical layers was weakened in the mature brain, so that no particular staining pattern, but weak and diffuse staining was observed in the adult rat cerebrum. The 1G2 antigen was immunohistochemically associated largely with glial fibrillary acidic protein-positive cells in primary cultures of the neonatal rat cerebrum. Both chondroitin sulfate proteoglycan-220 and chondroitin sulfate proteoglycan-150 were detected in the conditioned media not only of highly enriched cultures of fetal rat cortical neurons but also of pure cultures of mature astrocytes; more (12- to 20-fold) in the astrocyte conditioned media. Astrocytes, in addition to neurons, may be a cellular source of neurocan in brain at least under certain physiological conditions. The spaciotemporal expression pattern of 1G2 epitope-bearing proteoglycan, or neurocan, suggests that this proteoglycan species plays some roles at least in forming the elongation pathway for early cortical afferent fibers as well as the functional barrel structure in the somatosensory cortex.
Amino Acid Sequence↗