Studies on novel 3-isoxazolylvinyl-cephalosporins: I. Synthesis and biological activity of 7-[2-(2-aminothiazol-4-yl)-2-(alkoxy)-iminoacetamido] derivatives.
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Animals↗
Biomedical subjects
J H Cha
Publications and source records attributed to J H Cha.
Studies on novel 3-isoxazolylvinyl-cephalosporins: II. Synthesis and biological activity of 7-[2-(2-aminothiazol-4-yl)-2-hydroxy-iminoacetamido] derivatives.
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Animals↗
Huntingtin immunoreactivity in the rat neostriatum: differential accumulation in projection and interneurons.
Huntington's disease is caused by a mutation of the gene encoding the protein huntingtin. Features of the human disease, characterized by selective loss of neurons from the neostriatum, can be replicated in rodents by administration of excitotoxins. In both affected individuals and the rodent model, there is massive loss of striatal projection neurons with selective sparing of interneurons. Furthermore, in the human disease the earliest evidence of striatal injury is found in striosomal regions of the striatum. The mRNA encoding huntingtin is known to be expressed by neurons throughout the brain, a distribution which does not account for the selective patterns of neuronal death which are observed. Using fluorescence immunocytochemistry and confocal microscopy with an antibody to huntingtin, we have observed that in rats a subset of striatal projection neurons contains dense accumulations of huntingtin immunoreactivity (HT-ir), while most neurons in the striatum contain much smaller amounts. The intensely stained neurons are concentrated within the striatal striosomes, as defined by calbindin-D28K staining. In the matrix regions, relatively few neurons contain dense accumulations of HT-ir, and these cells always lack perikaryal staining for calbindin-D28K. Striatal interneurons, identified by the presence of immunoreactivity for choline acetyltransferase, parvalbumin, calretinin, or neuronal nitric oxide synthase, exhibit little or no HT-ir. The paucity of HT-ir in striatal interneurons, as well as the prominence of staining in a subset of striosomal neurons, mirrors the selective vulnerability of these different types of cells in early stages of human Huntington's disease and in rodent excitotoxic models of the disorder. Our observations suggest that mechanisms which modulate the accumulation of huntingtin may play a central role in the neuronal degeneration of Huntington's disease.
Animals↗
The divIVA minicell locus of Bacillus subtilis.
The Bacillus subtilis divIVA1 mutation causes misplacement of the septum during cell division, resulting in the formation of small, circular, anucleate minicells. This study reports the cloning and sequence analysis of 2.4 kb of the B. subtilis chromosome including the divIVA locus. Three open reading frames were identified: orf, whose function is unknown; divIVA; and isoleucyl tRNA synthetase (ileS). We identified the point mutation in the divIVA1 mutant allele. Inactivation of divIVA produces a minicell phenotype, whereas overproduction of DivIVA results in a filamentation phenotype. Mutants with mutations at both of the minicell loci of B. subtilis, divIVA and divIVB, possess a minicell phenotype identical to that of the DivIVB- mutant. The DivIVA-mutants, but not the DivIVB- mutants, show a decrease in sporulation efficiency and a delay in the kinetics of endospore formation. The data support a model in which divIVA encodes the topological specificity subunit of the minCD system. The model suggests that DivIVA acts as a pilot protein, directing minCD to the polar septation sites. DivIVA also appears to be the interface between a sporulation component and MinCD, freeing up the polar septation sites for use during the asymmetric septation event of the sporulation process.
Alleles↗
Ultrastructural localization of osteopontin in the kidney: induction by lipopolysaccharide.
Osteopontin is a secreted phosphoprotein that is expressed in the normal kidney and induced during various pathologic conditions associated with tubulointerstitial injury. However, the exact cellular location of osteopontin in the kidney has been a matter of controversy, and little is known about the role of osteopontin in the kidney. The purpose of this study was to establish the cellular and intracellular distribution of osteopontin in the rat kidney under normal conditions and after injection of a bacterial endotoxin lipopolysaccharide (LPS). Animals received injections of LPS or vehicle at different time intervals from 4 to 20 h before sacrifice. Kidneys were preserved by in vivo perfusion with paraformaldehyde-lysine-periodate (PLP) and processed for light and electron microscope immunocytochemistry using monoclonal antibodies to rat osteopontin. By light microscopy, immunostaining was observed in the descending thin limb and the papillary surface epithelium of both control and LPS-treated animals. After injection of LPS, osteopontin immunostaining was observed throughout the distal nephron and was also present in segments of the proximal tubule, where it was distributed in a punctate pattern. Staining was already present 4 h after injection of LPS and was maximal 6 h after injection. Electron microscopy revealed that osteopontin immunoreactivity in the descending thin limb and distal tubule cells was located in the Golgi apparatus and in small cytoplasmic vesicles, whereas in the proximal tubule labeling was observed in the vacuolar-lysosomal system. Western blot analysis demonstrated a band at approximately 70 kD and confirmed the increase in osteopontin expression after administration of LPS. These results demonstrate that osteopontin is constitutively expressed in cells of the descending thin limb and papillary surface epithelium and is induced throughout the distal tubule after administration of LPS.
Animals↗
Adult T-cell leukemia/lymphoma with features of CD30-positive anaplastic large cell lymphoma--a case report.
We experienced a 58-year-old Korean man with adult T-cell leukemia/lymphoma with features of histologically anaplastic large cell lymphoma involving the skin and testis. The patient had cutaneous nodules in both extremities and a palpable right testicular mass. Right orchiectomy was performed and specimens of removed testicle and skin nodules showed immunohistologically anaplastic large cell lymphoma with T-cell phenotype, and CD30 antigen was positive. A human T-cell lymphotropic virus type 1 (HTLV-1) antibody titer was over 1 : 256 and integration of HTLV-1 proviral DNA pX gene was identified in the peripheral blood mononuclear cells and lymphoma tissue by polymerase chain reaction. Peripheral blood and bone marrow did not show any evidence of characteristic neoplastic T-cells.
Diagnosis, Differential↗
Studies on new catechol containing cephalosporins. III. Synthesis and structure-activity relationships of cephalosporins having a pyridone moiety at the C-7 position.
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Bacteria↗
Platelet-activating factor contributes to immune cell and oxidant-mediated intestinal secretion.
The sensitivity of the Ussing-chambered rat colon to stimulation of Cl- secretion (as measured by the change in short-circuit current) by exogenous platelet-activating factor (PAF) was increased significantly by washing the colon in vitro with Ringer's solution containing fatty acid-free albumin. When the wash solution was extracted with chloroform/methanol and the lipid extract was added back to Ussing-chambered colons, inhibition of PAF-stimulated short-circuit current was observed, whereas short-circuit current responses to bradykinin or vasoactive intestinal peptide were not affected. Hypoxia appears to be an important trigger for the down-regulation of the PAF response. These data suggest that hypoxia releases PAF or an endogenous lipid PAF inhibitor that desensitizes PAF receptors on colonic epithelial or mucosal cells. The short-circuit current response of rabbit colon to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine was not inhibited by any PAF antagonist devoid of cyclooxygenase inhibitory activity but was strongly inhibited by indomethacin. In contrast, anti-IgE- or H2O2-stimulated short-circuit current in rat colon was inhibited by specific PAF antagonists, and this inhibition was additive with indomethacin. Both anti-IgE and H2O2 significantly increased PAF production by rat colon. These data suggest that PAF plays an important role in oxidant (H2O2)- and anti-IgE-mediated colonic Cl- secretion but not in Cl- secretion mediated by formyl-methionyl-leucyl-phenylalanine-stimulated phagocytes.
Animals↗
Role of apoptotic and nonapoptotic cell death in removal of intercalated cells from developing rat kidney.
In the developing rat kidney, both type A and type B intercalated cells are present throughout the medullary collecting duct (MCD), as well as the papillary surface epithelium. After birth, intercalated cells gradually disappear from the papillary surface epithelium and the terminal MCD, and type B cells disappear from the entire MCD. The purpose of this study was to establish the mechanism(s) by which intercalated cells are deleted from the MCD during development. Kidneys from 14-, 16-, 18-, and 20-day-old fetuses and 1-, 3-, 7-, and 14-day-old pups were preserved for light microscopic immunohistochemistry and electron microscopy. Intercalated cells were identified by immunostaining for H(+)-adenosinetriphosphatase (H(+)-ATPase) and band 3 protein. Apoptosis was identified by nick end labeling of DNA fragments, staining with the vital dye toluidine blue, and transmission electron microscopy. Two distinct mechanisms of elimination of intercalated cells were detected. Cells with apical labeling for H(+)-ATPase and basolateral labeling for band 3 protein protruded into the lumen of the MCD as if they were being extruded from the epithelium, and many had lost contact with the basement membrane. Extrusion of the cells with basolateral H(+)-ATPase or with no labeling for H(+)-ATPase was never observed. Apoptosis was observed in the MCD from shortly before birth to 7 days after birth, gradually progressing from the papillary tip toward the outer medulla. Staining for apoptosis was present in H(+)-ATPase-positive apoptotic bodies, located in cells that were negative for H(+)-ATPase. Staining was also occasionally observed in apoptotic cells with basolateral H(+)-ATPase but never in cells with apical H(+)-ATPase. Electron microscopy confirmed the presence of apoptotic intercalated cells in the MCD and demonstrated that apoptotic bodies were located in inner medullary collecting duct (IMCD) cells and principal cells. These results demonstrate that intercalated cells are deleted from the MCD by two distinct mechanisms, one involving apoptosis and subsequent phagocytosis by neighboring principal cells or IMCD cells. Elimination by extrusion affects only type A intercalated cells, whereas deletion by apoptosis appears to occur only in type B intercalated cells.
Aging↗
Trimethoprim and sulfonamide-associated meningoencephalitis with MRI correlates.
Early recognition of trimethoprim and sulfonamide-induced aseptic meningitis is important because drug cessation leads to rapid clinical improvement. We present clinical and laboratory findings in two typical cases. In both cases, MRI revealed previously undescribed diffuse white matter abnormalities that resolved within a few months. These MRI findings are important because they may aid in early diagnosis of this condition in the appropriate clinical setting. In addition, the white matter abnormalities suggest an encephalitic component in addition to the meningitis.
Adult↗
Studies on new catechol containing cephalosporins. I. Synthesis and structure-activity relationships of cephalosporins having a catechol moiety at the C-3 position.
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Catechols↗
Studies on new catechol containing cephalosporins. II. Synthesis and structure-activity relationships of cephalosporins having a catechol moiety at the C-7 position.
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Catechols↗
Trinucleotide repeats in neurologic diseases: an hypothesis concerning the pathogenesis of Huntington's disease, Kennedy's disease, and spinocerebellar ataxia type I.
Three neurodegenerative diseases, Huntington's disease (HD), Kennedy's disease (hereditary spinobulbar muscular atrophy, SBMA), and type 1 spinocerebellar ataxia (SCA-1) have been found to share a common genetic defect: an unstable region of repeated CAG trinucleotides which are thought to be translated into a polyglutamine moiety. The unstable repeat regions occur near the N-termini of the predicted proteins for HD and SBMA, but the location of the CAG repeat region is not known for SCA-1. Each disease is notable for a relatively circumscribed region of central nervous system pathology, and the lack of predicted similarity of the abnormal proteins makes a common mechanism related to the function of each protein unlikely. In order to reconcile the similar genetic abnormalities with the disparities in phenotypes, we suggest a common thread with regard to the pathogenesis of neuronal death. We hypothesize that the mechanism of neurotoxicity in these diseases occurs not through the production of abnormal proteins, but by the generation of abnormal posttranslational cleavage products. These products, in part consisting of abnormally large polyglutamine moieties, act to disturb the cellular and mitochondrial milieu such that energy metabolism is impaired, rendering specific regions of the nervous system vulnerable, and resulting in the clinical phenotypes of HD, SBMA, and SCA-1. We offer this interpretation of recent genetic findings from a neurobiologic perspective, in addition to suggesting testable hypotheses concerning potential disease mechanisms.
Base Sequence↗
RNA editing of a human glutamate receptor subunit.
AMPA receptors are comprised of individual subunits, and the divalent cation permeability of assembled AMPA receptors is determined by a single amino acid residue in the second transmembrane region of the GluR-B subunit. At this site, GluR-B subunits contain an arginine while other AMPA receptor subunits contain glutamine. Interestingly, the murine gene for GluR-B actually specifies a glutamine at the divalent cation permeability site. The appearance of arginine and not glutamine in the mature GluR-B protein is thought to be a result of RNA editing of the GluR-B messenger RNA. In that AMPA receptors are thought to mediate the bulk of fast excitatory signalling within the mammalian central nervous system, this process of RNA editing may play a pivotal role in normal neural function by mediating divalent cation permeability of AMPA receptors. Disruptions of RNA editing could lead to phenotypically altered AMPA receptors, with implications for pathogenic brain processes. We report that the human GluR-B gene sequence is also edited such that there is a difference between the human GluR-B gene and the complementary DNA (cDNA), as demonstrated both with allele-specific polymerase chain reaction (PCR) and restriction enzyme digestion of PCR products. Thus, as in the rodent brain, RNA editing of an AMPA receptor subunit appears to be an important process in the human brain. Disruptions of RNA editing may have neuropathological consequences.
Base Sequence↗
Rapid nonisotopic analysis of glutamate receptor gene expression using reverse transcription-polymerase chain reaction.
We describe a simple nonisotopic method for analyzing receptor gene expression using reverse transcription-polymerase chain reaction (RT-PCR) and laser densitometry of agarose gels. Densitometry of known amounts of double stranded DNA molecular weight standards was used to estimate yield of glutamate receptor RT-PCR product (in ng DNA) obtained from rat brain. While unable to provide absolute quantitation of gene expression, this method using standard techniques allows for rapid analysis of relative levels of receptor gene expression without using radioactivity.
Animals↗
Catalytic properties of the cloned amylase from Bacillus licheniformis.
A gene encoding a new amylolytic enzyme of Bacillus licheniformis (BLMA) has been cloned, and we characterized the enzyme expressed in Escherichia coli. The genomic DNA of B. licheniformis was double-digested with EcoRI and BamHI and ligated the pBR322. The transformed E. coli was selected by its amylolytic activity, which carries the recombinant plasmid pIJ322 containing a 3.5-kilobase fragment of B. licheniformis DNA. The purified enzyme encoded by pIJ322 was capable of hydrolyzing pullulan and cyclodextrin as well as starch. It was active over a pH range of 6-8 and its optimum temperature was 50 degrees C. The molecular weight of the enzyme was 64,000, and the isoelectric point was 5.4. It degraded soluble starch by cleaving maltose units preferentially but did not attack alpha-1,6-linkage. The enzyme also hydrolyzed pullulan to panose units exclusively. In the presence of glucose, however, it transferred the panosyl moiety to glucose with the formation of alpha-1,6-linkage. The specificity of transferring activity is evident from the result of the maltosyl-transferring reaction which produces isopanose from maltotriose and glucose. The molecular structure of the enzyme deduced from the nucleotide sequence of the clone maintains limited similarity in the conserved regions to the other amylolytic enzymes.
Amino Acid Sequence↗
Glutamic acid-insensitive [3H]kainic acid binding in goldfish brain.
Kainic acid is supposed to be a specific agonist for a subclass of excitatory glutamate receptors in the vertebrate CNS. An investigation of (2 nM) [3H]kainic acid binding sites in goldfish brain, using quantitative autoradiography, has revealed evidence for two types of kainic acid receptors which differ in sensitivity to glutamic acid. L-Glutamic acid (0.1-1 mM) displaced over 95% of specific [3H]kainic acid binding elsewhere in the brain but only 10-50% in the cerebellum and cerebellar crest. These structures apparently contain [3H]kainic acid binding sites that are extremely insensitive to glutamic acid. The glutamic acid-insensitive [3H]kainic acid binding was not displaced by quisqualic acid, kynurenic acid, alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA), or N-methyl-D-aspartatic acid, but was completely displaced by the kainic acid analogue domoic acid. The data indicate that two types of high affinity binding sites for [3H]kainic acid exist in the goldfish brain: glutamic acid-sensitive and glutamic acid-insensitive. High affinity [3H]kainic acid binding may therefore not always represent binding to subsets of glutamic acid receptors.
Animals↗
[The current status of psychology in Korea].
This paper read as the special lecture at the Annual Convention of The Japanese Psychological Association, held at Tokyo Metropolitan University in 1990, and reported on the recent trends of psychology in the Republic of Korea. This report dealt essentially with four topics; 1) the history of Korean psychology which was divided into four periods of creation, reconstruction, development, and current status, after the liberation at the end of the World War II in 1945, 2) the distribution and academic status of 26 universities, with formal department of psychology, 3) general situation of job opportunities for the graduates in psychology of these universities, 4) the composition of Korean Psychological Association (KPA), consisting of nine divisions (social, industrial and organizational, clinical, consultations and psychotherapy, experimental and cognitive, developmental, biological and physiological psychology) with the total of about 400 members. Last, some directions of Korean psychology to the future was suggested.
Adult↗