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Biomedical subjects

J Kang

Publications and source records attributed to J Kang.

At least 127 records · Page 7Linked to original sources
PubMed1999

[Separation of p-aminobenzenearsonic acid and its oxide by ion-pair reversed-phase high performance liquid chromatography].

To study the separation of p-aminobenzenearsonic acid (PABAA) and its oxide, p-aminophenylarsine oxide (PAPAO), both the absorption spectra were scanned at the wavelengths from 200 nm to 380 nm. PABAA had absorption maximum at 254 nm and PAPAO 258 nm. The effects of salt concentration, column temperature, methanol and ion-pair agent concentrations on the capacity factor were investigated. Compounds of high polarity showed almost no retention on reversed-phase column; as the volume fraction of the methanol decreased from 90% to 10%, the retention time of PABAA gradually increased with broad peak, and partially eluted when methanol volume fraction being below 20%. With temperature rising, the retention time of PABAA was decreased. But PABAA capacity factor can be increased by selecting an appropriate salt concentration for the mobile phase. The cetyltrimethyl and tetrabutyl ammonium ions were separately added as ion-pair agents to the mobile phase containing methanol in phosphate buffer of 10 mmol/L, the changes of retention time were observed. The mechanism of retention based on reversed phase ion-pair model is proposed. Besides, the retention behaviour is also influenced by size exclusion in stationary phase as well as polar interactions with residual silanol group on the silica surface.

Arsanilic Acid↗
PubMed1999

[Preparation of the high-titer retroviral viruses for transducting PDGF-A gene].

OBJECTIVE: To prepare high-titer recombinant retrovirus for transducting platelet-derived growth factor A chain(PDGF-A) gene, which will pave the way for future research in vitro and in vivo on biological function of autocrine and paracrine of PDGF-A gene expression product. METHODS: The cDNA fragment of human PDGF-A was inserted into the polyclonal sites of retroviral vector GINa containing cytomegalovirus (CMV) promotor. The constructed recombinant plasmid was transformed into PA317 packaging cell line. The positive clones were obtained by selection in G418-medium and amplified. The supernatant virus was used to infect NIH3T3 cells and titrated. After drug resistance selection, NIH3T3 cell clones were amplified, and a histochemical analysis was performed. SDS-PAGE electrophoresis and Western blot as well as 3H-TdR incorporation methods were adopted to assay the presence and the mitogenic activity of the PDGF in the conditioned medium. RESULTS: The highest titer of the virus was 1.4 x 10(5) CFU/ml. The PDGF-A expression was verified with SDS-PAGE electrophoresis and Western blot and immunofluorescent staining. The cell mitogenic activitiy in the media was up to 51.2 U/(10(6).d). CONCLUSIONS: We had made high-titer recombinant retrovirus for transducting human PDGF-A gene. The gene was expressed with high efficiency. The expressed product has significant mitogenic effect on NIH3T3 cell line.

Cytomegalovirus↗
PubMed1999

[Supraglottic horizontal partial laryngectomy].

OBJECTIVE: To evaluate the supraglottic horizontal partial laryngectomy in the treatment of laryngeal cancers. METHODS: Some researches and modifications are performed on the standard supraglottic horzontal partial laryngectomy: the wounded area in the laryngeal cavity is covered with the lateral membrane of thyroid cartilage; the laryngeal cavity is closed as its anterior wall by folding and sewing up the sternohyoid muscles. From 1983 to 1993, 92 patients (80 men and 12 women) with quamous cell carcinoma of larynx were treated with supraglottic horizontal partial laryngectomy. The patients age ranged from 39 to 72 years; 72% aged from 50 to 59. There were 72 cases (78.3%) in the stages III and IV. RESULTS: The 3 and 5 year survival rates of the patients were 75% and 72% respectively. Most cases have acquired good speech and swallow function with 2-4 weeks; 84.8% (78 patients) were extubated. CONCLUSION: The authors believed that partial laryngectomy was safe and beneficial to some patients with laryngeal cancers.

Adult↗
PubMed1999

[Fluorescence spectra of lanthanide coordination compounds].

In this paper, the recent progress in fluorescence spectra of lanthanide coordination compounds including photophysics and photochemistry is briefly reviewed and the application of lanthanide complexes as fluorescent probes to structural analysis of coordination compounds and biomolecular systems is summed up.

English Abstract↗
PubMed1999

[Bonding behavior of 4f orbital].

In this paper, the bonding behavior of 4f orbital in lanthanide coordination compounds was discussed and corresponding theory and research methods were summed up with 36 references.

English Abstract↗
PubMed1998

Connexins regulate calcium signaling by controlling ATP release.

Forced expression of gap junction proteins, connexins, enables gap junction-deficient cell lines to propagate intercellular calcium waves. Here, we show that ATP secretion from the poorly coupled cell lines, C6 glioma, HeLa, and U373 glioblastoma, is potentiated 5- to 15-fold by connexin expression. ATP release required purinergic receptor-activated intracellular Ca2+ mobilization and was inhibited by Cl- channel blockers. Calcium wave propagation also was reduced by purinergic receptor antagonists and by Cl- channel blockers but insensitive to gap junction inhibitors. These observations suggest that cell-to-cell signaling associated with connexin expression results from enhanced ATP release and not, as previously believed, from an increase in intercellular coupling.

Adenosine Triphosphatases↗
PubMed1998

Transcriptional control of the glnD gene is not dependent on nitrogen availability in Escherichia coli.

Glutamine synthetase (GS) is one of the most important enzymes in the assimilation of nitrogenous compounds in Escherichia coli and related bacteria. For the control of its activity and biosynthesis, tricyclic cascades of uridylylation/deuridylylation of PII protein, adenylylation/deadenylylation of glutamine synthetase, and phosphorylation/dephosphorylation of Ntr1 are operating, where the regulation of uridylylation/deuridylylation by uridylyl transferase-uridylyl removing enzyme (UT-UR) (the product of the glnD gene) would play the ultimate nitrogen sensing role. However, the possible nitrogen-regulatable element in the upstream of the glnD gene has been debated. In the present experiment, we have cloned and sequenced the four minute regions of the Escherichia coli chromosome, where rpsB, map, glnD, and dapD genes have been identified in sequence. We could localize the transcriptional start site at seven nucleotides upstream of the translation initiation codon by primer extension analysis. The nitrogen dependency of the glnD gene has been analyzed by Northern blot, RNase protection, and promoter-luciferase activity assays. These data suggested a constitutive expression of the glnD gene independent of nitrogen availability. From these results, it could be concluded that the ultimate nitrogen sensing device for the bacteria should be the UT-UR itself, through modulation of its activity in response to the nitrogen status rather than its biosynthetic mechanism.

Amino Acid Sequence↗
PubMed1998

Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings.

1. The types of voltage-dependent calcium channels (VDCCs) present in the cholinergic terminals isolated from the electric organ of the ray, Narke japonica, were characterized on the basis of their pharmacological sensitivity to specific antagonists. Inhibition of these channel types by autoantibodies from patients with the Lambert-Eaton syndrome (LES) was then studied to determine the specificity of the pathogenic IgG. 2. In normal untreated synaptosomal preparations, maximal doses of N- and P and/or Q-type Ca2+ channel antagonists, omega-conotoxin GVIA and omega-agatoxin IVA, inhibited depolarization-evoked ACh release by 47 % and 43 %, respectively. Calciseptine, an L-type VDCC antagonist, caused a 20 % reduction in the release. This indicates that the exocytotic release process is predominantly mediated by N- and P/Q-type VDCCs. 3. LES IgG or sera caused an inhibition of ACh release by 39-45 % in comparison with the control antibody-treated preparations. The ionomycin-induced ACh release, however, was not altered by the antibodies. Additionally, the same LES antibodies inhibited whole-cell calcium currents (ICa) in bovine adrenal chromaffin cells. Thus, the pathogenic antibodies exert their action on VDCCs present in the synaptosomes. 4. The efficacy of three Ca2+ channel antagonists in blocking ACh release was determined in preparations pretreated with LES IgG. omega-Agatoxin IVA produced only an additional 3-5 % reduction in release beyond that obtained with LES antibodies. Despite the pretreatment with LES IgG, omega-conotoxin GVIA and calciseptine inhibited the release to nearly their control levels. 5. These results indicate that LES antibodies mainly downregulate P/Q-type Ca2+ channels which contribute to presynaptic transmitter release from the cholinergic nerve terminals of electric organ. 6. The present findings are consistent with the hypothesis that P/Q-type VDCCs at the neuromuscular junction are the target of LES antibodies and that their inhibition by the antibodies produces the characteristic neuromuscular defect in this disease.

Acetylcholine↗
PubMed1998

Astrocytic gap junctions remain open during ischemic conditions.

Gap junctions are highly conductive channels that allow the direct transfer of intracellular messengers such as Ca2+ and inositol triphosphate (IP3) between interconnected cells. In brain, astrocytes are coupled extensively by gap junctions. We found here that gap junctions among astrocytes in acutely prepared brain slices as well as in culture remained open during ischemic conditions. Uncoupling first occurred after the terminal loss of plasma membrane integrity. Gap junctions therefore may link ischemic astrocytes in an evolving infarct with the surroundings. The free exchange of intracellular messengers between dying and potentially viable astrocytes might contribute to secondary expansion of ischemic lesions.

Animals↗
PubMed1998

Identification of N-terminal residues on P-selectin glycoprotein ligand-1 required for binding to P-selectin.

The major high affinity ligand for P-selectin on human leukocytes is P-selectin glycoprotein ligand-1 (PSGL-1). To bind P-selectin, PSGL-1 must be modified with tyrosine sulfate and sialylated, fucosylated, core-2 O-glycan(s). The required sites for these modifications on full-length PSGL-1 have not been defined. The N-terminal region of mature PSGL-1, which begins at residue 42, includes tyrosines at residues 46, 48, and 51, plus potential sites for Thr-linked O-glycans at residues 44 and 57. We expressed full-length PSGL-1 constructs with substitutions of these residues in transfected Chinese hamster ovary cells. The cells were co-transfected with cDNAs for the glycosyltransferases required to construct sialylated and fucosylated, core-2 O-glycans on PSGL-1. The transfected cells were assayed for their abilities to bind fluid-phase P-selectin and to support rolling adhesion of pre-B cells expressing P-selectin under hydrodynamic flow. In both assays, substitution of Thr-57 with alanine eliminated binding of PSGL-1 to P-selectin without affecting sulfation of PSGL-1, whereas substitution with serine, to which an O-glycan might also be attached, did not affect binding. Binding was not altered by substituting alanines for the two amino acids on either side of Thr-57, or by substituting alanine for Thr-44. Substitution of all three tyrosines with phenylalanines markedly reduced sulfation and prevented binding to P-selectin. However, all constructs in which one or two tyrosines were replaced with phenylalanines bound P-selectin. These results suggest that full-length PSGL-1 requires an O-glycan attached to Thr-57 plus sulfation of any one of its three clustered tyrosines to bind P-selectin.

Alanine↗
PubMed1998

Regulating exercise intensity using ratings of perceived exertion during arm and leg ergometry.

The purpose of this investigation was to examine the validity of regulating exercise intensity using ratings of perceived exertion (RPEs) during arm crank and leg cycle exercise at 50 and 70% peak oxygen consumption (VO2peak). Ten men and seven women [26 (1) years old; mean (SE)] participated in this study. Each subject completed a maximal estimation trial and two submaximal exercise bouts (production trials) on both an arm and leg ergometer. During each maximal estimation trial, subjects were asked to give a RPE for each stage of the exercise. RPEs, heart rates (HR), and power outputs (PO) equivalent to 50 and 70% VO2peak for each exercise mode were then estimated from plots of RPE versus oxygen consumption (VO2), HR versus VO2, and PO versus VO2, respectively. During the submaximal trials, subjects were instructed to select workloads on an arm and leg ergometer that produced the previously estimated RPEs. Comparisons were made for VO2, HR, and PO between the estimation and production trials for each mode at each exercise intensity. HR did not differ between the trials at either 50 or 70% VO2peak during arm and leg ergometry. In addition, VO2 and PO did not differ between the trials at either 50 or 70% VO2peak during arm ergometry and at 50% VO2peak during leg ergometry. However, these two parameters were lower (P < 0.05) during the production trial [1.88 (0.15) l x min(-1) and 89.1 (10.1) W, respectively] as compared to the estimation trial [2.08(0.14) l x min(-1) and 102.4 (6.5)W, respectively] during leg ergometry at 70% VO2peak. In conclusion, using RPEs to regulate exercise intensity is physiologically valid during arm ergometry at both 50 and 70% VO2peak and during leg ergometry at 50% VO2peak. However, this prescriptive approach remains questionable during leg cycle exercise at 70% VO2peak.

Adult↗
PubMed1998

The developmental fate of T cells is critically influenced by TCRgammadelta expression.

Differentiation of gammadelta and alphabeta T cells from a common precursor cell depends on productive rearrangement and expression of TCRgammadelta or TCRbeta genes, but whether it is an instructive or a stochastic mechanism that is responsible for this process is unclear. We report that expression of the productively rearranged TCRgamma transgene competitively inhibits alphabeta thymocyte development under conditions where TCRbeta gene rearrangement is limiting. The status of TCRdelta gene rearrangements in the remaining alphabeta-lineage cells indicates that the effect is mediated by the intact gammadelta receptor. Paradoxically, in TCRbeta-/- mice, gammadelta receptor expression can also drive differentiation of some alphabeta-lineage cells. To resolve this paradox, we provide evidence for a minor population of gammadelta-dependent alphabeta-lineage cells in normal mice. The results indicate that the T cell lineage commitment process is either error-prone or stochastic.

Animals↗
PubMed1998

T cell receptor gamma gene regulatory sequences prevent the function of a novel TCRgamma/pTalpha pre-T cell receptor.

Expression of a TCRgamma transgene in RAG-1-/- mice resulted in the development of a limited number of CD4+CD8+ (DP) thymocytes. In vivo treatments with anti-TCRgamma antibody enhanced the number of DP thymocytes, demonstrating that TCRgamma chains were expressed on the cell surface in the absence of delta, alpha, or beta chains. Mutations in pTalpha or CD3epsilon genes abolished transgene-induced DP cell development, indicating that TCRgamma can associate with pTalpha and CD3 to form a novel pre-TCR. With a transgene containing additional regulatory sequences, TCRgamma expression was down-regulated in DP cells, and little DP cell development occurred. Thus, the function of the endogenous TCRgamma/pTalpha is limited by the transcriptional down-regulation of TCRgamma genes that normally accompanies DP cell development.

Animals↗
PubMed1998

Astrocyte-mediated potentiation of inhibitory synaptic transmission.

We investigated the role of astrocytes in activity-dependent modulation of inhibitory synaptic transmission in hippocampal slices. Repetitive firing of an interneuron decreased the probability of synaptic failures in spike-evoked inhibitory postsynaptic currents (unitary IPSCs) in CA1 pyramidal neurons. The GABAB-receptor antagonist CGP55845A abolished this effect. Direct stimulation of astrocytes, or application of the GABAB-receptor agonist baclofen, potentiated miniature inhibitory postsynaptic currents (mIPSCs) in pyramidal neurons. These effects were blocked by inhibition of astrocytic calcium signaling with the calcium chelator BAPTA or by antagonists of the ionotropic glutamate receptors. These observations suggest that interneuronal firing elicits a GABAB-receptor-mediated elevation of calcium in surrounding astrocytes, which in turn potentiates inhibitory transmission. Astrocytes may therefore be a necessary intermediary in activity-dependent modulation of inhibitory synapses in the hippocampus.

Animals↗
PubMed1998

Selective induction of apoptosis of NB4 cells from G2+M phase by sodium arsenite at lower doses.

Apoptosis of NB4 cells induced by sodium arsenite and arsenate was studied using flow cytometry and DNA gel electrophoresis in order to investigate their effects on cell cycle and determine the relationship between apoptosis and cell cycle. In this study, we found that: 1) at low doses, sodium arsenite selectively induced apoptosis of NB4 cells in G2+M phase of cell cycle after its being arrested in G2 phase. With increment of the cells blocked in G2 phase, dUTP-specifically labeling cells in G2+M phase increased without concomitant increment of dUTP-labeling cells in other two phases of cell cycle; 2) at high doses, extensive apoptosis was induced in NB4 cells from all phases of cell cycle without cell cycle preference and cell cycle blockade; 3) sodium arsenite-induced apoptosis of NB4 cells occurred in the presence of bcl-2 expression as the unapoptotic cells; 4) sodium arsenite with As3+ induced apoptosis of NB4 cells more strongly than sodium arsenate with As5+ did although both of them affected NB4 cells in the same pattern. These results not only suggested that both arsenite and arsenate induced apoptosis of NB4 cells through 2 different mechanisms--at low doses, arsenical might directly induce apoptosis through regulation of cell cycle checkpoint, while at high doses they might directly induce it, but also indicated that bcl-2 might not play an important role in arsenite or arsenate-induced apoptosis of NB4 cells, whereas chemical valence of As in a compound might be related to efficiency in arsenical induction of apoptosis.

Apoptosis↗
PubMed1998

Interaction of an adenovirus E3 14.7-kilodalton protein with a novel tumor necrosis factor alpha-inducible cellular protein containing leucine zipper domains.

Early region 3 (E3) of group C human adenoviruses (Ad) encodes several inhibitors of tumor necrosis factor alpha (TNF-alpha) cytolysis, including an E3 14.7-kDa protein (E3-14.7K) and a heterodimer containing two polypeptides of 10.4 and 14.5 kDa. To understand the mechanism by which the viral proteins inhibit TNF-alpha functions, the E3-14.7K protein was used to screen a HeLa cell cDNA library to search for interacting proteins in the yeast two-hybrid system. A novel protein containing multiple leucine zipper domains without any significant homology with any known protein was identified and has been named FIP-2 (for 14.7K-interacting protein). FIP-2 interacted with E3-14.7K both in vitro and in vivo. It colocalized with Ad E3-14.7K in the cytoplasm, especially near the nuclear membrane, and caused redistribution of the viral protein. FIP-2 by itself does not cause cell death; however, it can reverse the protective effect of E3-14.7K on cell killing induced by overexpression of the intracellular domain of the 55-kDa TNF receptor or by RIP, a death protein involved in the TNF-alpha and Fas apoptosis pathways. Deletion analysis indicates that the reversal effect of FIP-2 depends on its interaction with E3-14.7K. Three major mRNA forms of FIP-2 have been detected in multiple human tissues, and expression of the transcripts was induced by TNF-alpha treatment in a time-dependent manner in two different cell lines. FIP-2 has consensus sequences for several potential posttranslational modifications. These data suggest that FIP-2 is one of the cellular targets for Ad E3-14.7K and that its mechanism of affecting cell death involves the TNF receptor, RIP, or a downstream molecule affected by either of these two molecules.

Adenovirus E3 Proteins↗
PubMed1998

Effects of thiopental anesthesia on local rates of cerebral protein synthesis in rats.

We have examined the effects of a surgical level of thiopental anesthesia in adult male rats on local rates of cerebral protein synthesis with the quantitative autoradiographic L-[1-14C]leucine method. The relative contribution of leucine derived from protein breakdown to the intracellular precursor amino acid pool for protein synthesis was found to be statistically significantly decreased in the anesthetized rats compared with controls. In the brain as a whole and in 30 of the 35 brain regions examined, rates of protein synthesis were decreased (1-11%) in the anesthetized rats. Decreases were statistically significant (P < or = 0.05) in the brain as a whole and in six of the regions, and they approached statistical significance in an additional 13 regions, indicating a tendency for a generalized but small effect.

Amino Acids↗