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Biomedical subjects

L Yang

Publications and source records attributed to L Yang.

At least 19 recordsLinked to original sources

Importance of conserved and variable C-terminal residues for the activity and thermal stability of the beta subunit of tryptophan synthase.

To assess the functional roles of helix 13 and of the conserved and variable residues in the C-terminal region (residues 378-397) of the tryptophan synthase beta subunit, we have constructed four C-terminal truncations and 12 point mutations. The effects of these mutations on kinetic and spectroscopic properties and thermal stability are reported here. The mutant beta subunits all form stable alpha2beta2 complexes that have been purified to homogeneity. The mutant alpha2beta2 complexes are divided into two classes on the basis of activity in the reaction of L-serine with indole to form tryptophan. Class I enzymes, which have mutations at Arg-379 or Asp-381 or truncations (384-397 or 385-397), exhibit significant activity (1-38% of wild type). Class II enzymes, which have mutations at Lys-382 or Asp-383 or truncations (382-397 or 383-397), exhibit very low activity (<1% of wild type). Although Class II enzymes have drastically reduced activity in the reaction of L-serine with indole and an altered distribution of enzyme-substrate intermediates in the reaction of L-serine with beta-mercaptoethanol, they retain activity in the reaction of beta-chloro-L-alanine with indole. Correlation of the results with the three-dimensional structure of the alpha2beta2 complex suggests that Lys-382 and Asp-383 serve important roles in a proposed "open" to "closed" conformational change that occurs in the reactions of L-serine. Because mutant beta subunits having C-terminal truncations (383-397 or 384-397) undergo much more rapid thermal inactivation at 60 degrees C than the wild type beta subunit, the C-terminal helix 13 stabilizes the beta subunit.

Amino Acid Sequence

Identification of a novel, spliced variant of CREB that is preferentially expressed in the thymus.

A conserved decamer sequence, AGTGA(T/C)(G/A)TCA, related to the cAMP response element (CRE), is found in the promoter regions of most TCR V beta gene segments. It has been shown to be a critical element for T cell-specific transcriptional regulation of the TCR genes. However, none of the decamer or CRE-binding proteins identified thus far is restricted in its expression to cells of the T cell lineage. Therefore, to find T cell-restricted decamer-binding proteins, we screened thymus cDNA expression libraries using the decamer probe. One of the thymus cDNAs identified, clone pmLY2, a novel spliced variant of CREB, was shown to be preferentially expressed in thymus. Therefore, clone pmLY2 is the first T cell-enriched decamer-binding sequence identified. We hypothesize that this CREB variant may play a role in the developmental regulation of TCR and of other T cell specific genes.

Activating Transcription Factor 2

Regulation of CD28 costimulation in human CD8+ T cells.

Optimal stimulation and prevention of anergy in T cells requires signaling through the CD28 molecule. During HIV disease progression, CD28 expression is lost, particularly on CD8+ T cells. Because alterations in cytokine production patterns occur during HIV infection, we determined whether CD8+ T cell phenotype or function was affected by cytokine environment. Treatment of CD8+ T cells with IL-4 decreased levels of both CD28 surface expression and message and increased CD8 expression. Furthermore, CD8+ T cells that had down-regulated CD28 had reduced proliferative capacity. The inhibitory effects of CD28 reduction could be compensated either by increased anti-CD3 or by exogenous IL-2, suggesting that the strength of T cell signaling necessary for the production of IL-2 and subsequent proliferation is negatively regulated by IL-4. CD8+ subpopulations with differential CD28 expression produced different patterns of cytokines, particularly IL-2 and IFN-gamma. Furthermore, CD8+ T cells that had reduced CD28 levels but made their own IL-2 were able to proliferate in response to TCR stimulation. These results suggest that loss of CD28 expression and CD8 T cell function can be regulated by the cytokine environment, which may be altered during HIV disease progression. Whether the dysfunction of CD8+ T cells in HIV infection occurs by such a mechanism is the subject of future investigation.

Antibodies, Monoclonal

The effect of circulatory arrest and retrograde cerebral perfusion on microtubule-associated protein 2: an immunohistochemical study in pig hippocampus.

Microtubule-associated protein 2 (MAP2) immunohistochemical labeling in the hippocampus was studied to assess the protective effect of brain perfusion during surgery requiring hypothermic circulatory arrest in 24 pigs exposed to anesthesia alone (control), 120 min of complete circulatory arrest at 15 degrees C, min of retrograde cerebral perfusion at 15 degrees C, or 120 min of anterograde cerebral perfusion at 15 degrees C. Pigs were reperfused for 60 min and sacrificed. In the control anterograde perfusion groups, the intensity of MAP2 labeling was similar in all regions of the hippocampus. Circulatory arrest and retrograde perfusion resulted in significant reduction of MAP2 labeling (28% and 38% respectively of control, P < 0.001) of neurons in the CA1 region. MAP2 labeling may be useful for assessing early damage in the hippocampus in this model.

Animals

S-Methylthiocitrulline, a neuronal nitric oxide synthase inhibitor, protects against malonate and MPTP neurotoxicity.

Nitric oxide may be a key mediator of excitotoxic neuronal injury in the central nervous system. In the present experiments we found that S-methylthiocitrulline, a relatively selective neuronal nitric oxide synthase (NOS) inhibitor, produced significant neuroprotection against striatal lesions produced by malonate, and the protection was reversed by l-arginine but not by d-arginine. S-Methylthiocitrulline attenuated malonate-induced increases in 2,3- and 2,5-dihydroxybenzoic acid/salicylate and 3-nitrotyrosine/tyrosine, which may be a consequence of peroxynitrite generation. S-Methylthiocitrulline significantly protected against 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine-induced depletions of dopamine, 3, 4-dihydroxyphenylacetic acid, and homovanillic acid. These findings provide further evidence that relatively selective inhibitors of neuronal NOS are neuroprotective in vivo and that they might therefore be useful in the treatment of neurodegenerative diseases.

Animals

Effects of oren-gedoku-to and unsei-in, Chinese traditional medicines, on interleukin-8 and superoxide dismutase in rats.

This study was conducted to elucidate the mechanisms of action of two Chinese traditional drugs, Oren-gedoku-to and Unsei-in, which have been used for many years in the treatment of inflammatory disorders. In rats with acetic acid-induced inflammation, both drugs reduced interleukin-8 concentrations in the serum. Neither drug significantly affected superoxide dismutase activity in the serum, although Unsei-in increased superoxide dismutase activity in liver after 1 month of administration. Oren-gedoku-to showed no significant effect on liver superoxide dismutase activity. It was considered that these medicines exert their anti-inflammatory effects mainly on the early stages of inflammation, wherein increased capillary permeability and migration of leucocytes occur.

Animals

Differential response properties to amplitude modulated signals in the dorsal nucleus of the lateral lemniscus of the mustache bat and the roles of GABAergic inhibition.

We studied the phase-locking of 89 neurons in the dorsal nucleus of the lateral lemniscus (DNLL) of the mustache bat to sinusoidally amplitude modulated (SAM) signals and the influence that GABAergic inhibition had on their response properties. Response properties were determined with tone bursts at each neuron's best frequency and then with a series of SAM signals that had modulation frequencies ranging from 50-100 to 800 Hz in 100-Hz steps. DNLL neurons were divided into two principal types: sustained neurons (55%), which responded throughout the duration of the tone burst, and onset neurons (45%), which responded only at the beginning of the tone burst. Sustained and onset neurons responded differently to SAM signals. Sustained neurons responded with phase-locked discharges to modulation frequencies < or = 400-800 Hz. In contrast, 70% of the onset neurons phase-locked only to low modulation frequencies of 100-300 Hz, whereas 30% of the onset neurons did not phase-lock to any modulation frequency. Signal intensity differentially affected the phase-locking of sustained and onset neurons. Sustained neurons exhibited tight phase-locking only at low intensities, 10-30 dB above threshold. Onset neurons, in contrast, maintained strong phase-locking even at relatively high intensities. Blocking GABAergic inhibition with bicuculline had different effects on the phase-locking of sustained and onset neurons. In sustained neurons, there was an overall decline in phase-locking at all modulation frequencies. In contrast, 70% of the onset neurons phase-locked to much higher modulation frequencies than they did when inhibition was intact. The other 30% of onset neurons phase-locked to SAM signals, although they fired only with an onset response to the same signals before inhibition was blocked. In both cases, blocking GABAergic inhibition transformed their responses to SAM signals into patterns that were more like those of sustained neurons. We also propose mechanisms that could explain the differential effects of GABAergic inhibition on onset neurons that locked to low modulation frequencies and on onset neurons that did not lock to any SAM signals before inhibition was blocked. The key features of the proposed mechanisms are the absolute latencies and temporal synchrony of the excitatory and inhibitory inputs.

Acoustic Stimulation

An evaluation of the role of nuclear cytoplasmic ratios and nuclear volume densities as diagnostic indicators in metaplastic, dysplastic and neoplastic lesions of the human cheek.

The increase in nuclear cytoplasmic (N/C) ratio is one of the features of cellular atypia which is used in the histopathological assessment of premalignant lesions of the oral mucosa. Since this feature is readily quantifiable using morphometry, we have analysed both N/C and nuclear volume densities in basal and spinous cells from human cheek lesions with and without malignant potential in order to ascertain the validity of this parameter as a predictor. Using a strictly standardised sampling procedure, measurements of cellular and nuclear areas of basal and spinous cells from normal and pathological human cheek mucosa were made on haematoxylin and eosin-stained sections using a VIDAS image analyser. Cases examined comprised fibrous hyperplasia (FH), traumatic inflammation (IF), benign hyperkeratosis (HK), lichen planus (LI), leukoplakia with dysplasia (DYS), squamous cell papilloma (PP), dysplastic epithelium from the edges adjacent to invasive carcinoma (CE) and islands from invasive squamous cell carcinoma (CI). In basal cells, N/C ratios and nuclear volume densities were lower than values obtained for the normal controls. In spinous cells, these parameters were elevated in the potentially premalignant lesions (DYS, CE) as well as in CI but values were similarly elevated in FH, IF, HK and PP, lesions which appear to have no malignant potential. The N/C ratio is of no value as a predictor of malignant potential in basal or spinous cells from cheek lesions. The putative increase in N/C which has been previously described qualitatively is probably due to increased nuclear hyperchromatism, which may provide an illusory increase in relative nuclear size at the expense of the cytoplasm.

Carcinoma, Squamous Cell

CAND3: a ubiquitously expressed gene immediately adjacent and in opposite transcriptional orientation to the ATM gene at 11q23.1.

Using a magnetic beads-mediated cDNA selection procedure and a fetal brain expression library, we identified a transcriptional unit within a cosmid positive for the marker D11S384. Pursuit of its full-length cDNA led to the cloning of the third candidate gene (CAND3) we studied in our quest for the ataxia-telangiectasia (A-T) gene, ATM. CAND3 spans approximately 140 kb of genomic DNA and is located immediately centrimeric to ATM, with 544 bp of DNA separating the two genes. CAND3 encodes two ubiquitously expressed transcripts of approximately 5.8 kb and approximately 4.6 kb that are divergently transcribed from a promoter region common to ATM. Nucleotide sequence was determined for one of its alternately spliced transcripts. The predicted protein has 1175 amino acids and is novel in sequence, with only weak homologies to transcriptional factors, nucleoporin protein, and protein kinases, including members of the phosphatidylinositol 3-kinase (PI-3 kinase) family. Although neither homology to ATM nor any mutation of CAND3 in A-T patients has been found, the head-to-head arrangement of CAND3 and ATM, with expression of both housekeeping genes from a common stretch of 544 bp intergenic DNA, suggests a bi-directional promoter possibly for co-regulation of biologically related functions. YACs, BACs, cosmids, and STSs are defined to aid in further study of this gene.

Amino Acid Sequence

The anti-inflammatory effects of ketoprofen in animal experiments.

The authors investigated the anti-inflammatory actions of ketoprofen using a battery of tests: in the rat paw oedema test induced by five different inciters, in the capillary permeability test, and in measuring the interleukin-8 (IL-8) production and superoxide dismutase (SOD) activity. The findings in these studies show that ketoprofen inhibits rat paw oedema, suppresses capillary permeability, reduces IL-8 production and increases SOD activity in the acetic-acid-induced inflammatory state. These results would seem to provide a clear rationale for exploring the usefulness of ketoprofen in the treatment of acute and chronic inflammatory diseases.

Acetic Acid

Activation of protein-tyrosine kinase Syk in human platelets stimulated with lysophosphatidic acid or sphingosine 1-phosphate.

It has been reported that not only lysophosphatidic acid (LPA) but also its sphingolipid counterpart, sphingosine 1-phosphate (Sph-1-P), induce platelet functional responses. We report here Syk activation in human platelets stimulated with these lysophospholipids. LPA rapidly induced platelet protein-tyrosine phosphorylation, including that of Syk, and Syk activation, assessed by immunoprecipitation kinase assay. Sph-1-P, although rather weaker, mimicked LPA in inducing these tyrosine kinase-related events. Pretreatment of platelets with staurosporine, a potent protein kinase inhibitor, diminished LPA-induced Syk phosphorylation and activation, but not intracellular Ca2+ mobilization. These results demonstrate that, in platelets, the bioactive lysophospholipids induce Syk activation, which, however, may not be related to Ca2+ mobilization.

Blood Platelets

Capillary isoelectric focusing-electrospray ionization mass spectrometry for transferrin glycoforms analysis.

On-line capillary isoelectric focusing (CIEF)-electrospray ionization mass spectrometry (ESIMS) as a two-dimensional separation system is employed for high-resolution analysis of bovine serum apotransferrin glycoforms. On the basis of their differences in isoelectric point (pI), the di-, tri-, and tetrasialotransferrins are separated and resolved in CIEF. The focused protein zones of di-, tri-, and tetrasialotransferrins are eluted by combining gravity with cathodic mobilization. At the end of CIEF capillary, the mobilized transferrin zones are analyzed by mass spectrometry coupled on-line to an electrospray interface with a coaxial sheath flow configuration. Additional transferrin variants within each of di-, tri-, and tetrasialotransferrins, differing in their molecular weights, are easily distinguished by ESIMS. In combination with sialidase digestion, the distribution of pI and molecular weight of asialo-, mono-, di-, tri-, and tetrasialotransferrin variants was obtained from the CIEF-ESIMS measurements. In addition to the differences in the number of sialic acid, the microheterogeneity of bovine serum apotransferrin glycans might be complicated by the partial fucosylated structure and the alpha-Gal (1-3)-beta-Gal on the alpha-Man-(1-6) antenna.

Animals

Phospholipase C-gamma 1 binds to actin-cytoskeleton via its C-terminal SH2 domain in vitro.

Association of phospholipase C (PLC)-gamma 1 with the cytoskeleton has been postulated to be one of the crucial steps for PLC-gamma 1 activation and translocation to the plasma membrane. In this report, direct binding assays were carried out to study which fragment of PLC-gamma 1 Src homology region has been able to bind to the actin-cytoskeleton. Using GST fusion proteins containing various deletions of the PLC-gamma 1 Src homology region, it was found that PLC-gamma 1 binds to the actin-cytoskeleton directly via its C-terminal SH2 domain but not the SH3 domain in vitro. However, the binding of the C-terminal SH2 domain of PLC-gamma 1 to actin did not interfere with the SH2 domain's ability to associate with phosphotyrosine, which suggested that actin and phosphotyrosine residues may bind to different sequences in the C-terminal SH2 domain of PLC-gamma 1.

Actins

Formation of membrane domains during the activation of protein kinase C.

The lateral membrane organization of phosphatidylserine, diacylglycerol, substrate, and Ca(2+)-dependent protein kinase C in large unilamellar vesicles was investigated by using fluorescence digital imaging microscopy. The formation of phosphatidylserine domains could be induced by either Ca2+, the MARCKS peptide, or protein kinase C. However, only Ca2+ could induce diacylglycerol to partition into the phosphatidylserine domains. In the complete protein kinase C assay mixture, two separate triple-labeling experiments demonstrated the colocalization of phosphatidylserine, protein kinase C, diacylglycerol, and the MARCKS peptide in domains. The amounts of all the labeled components in whole vesicles and in domains were measured at various concentrations of either phosphatidylserine, Ca2+, diacylglycerol, or the MARCKS peptide or with the addition of polylysine. The role of each component in forming membrane domains and in mediating the enzyme activity was analyzed. The results indicated that the inclusion of the MARCKS peptide in the domains, not just the binding of the substrate to vesicles, was especially important for PKC activity. The formation of PKC domains required the presence of DAG and Ca2+ at physiological ionic strength. The PKC activity was proportional to the amounts of PKC and substrate in the domains. The results also showed that the MARCKS peptide left the domains after being phosphorylated. A model for the activation of protein kinase C involving sequestering of the reaction components into membrane domains is proposed. The efficiency of the reaction was greatly increased by concentrating the activators, the enzyme, and the substrate into domains.

Amino Acid Sequence

Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function.

Reactive oxygen species (ROS) generation may play a role in ototoxicity, however, the specific effects of ROS generation upon cochlear function are unstudied. Therefore, guinea pig cochleas were instilled with artificial perilymph (AP), H2O2, or confirmed generating systems for the superoxide anion (O2-) or the hydroxyl radical (OH.), or with an ROS system plus its respective scavenger -catalase (CAT), superoxide dismutase (SOD) or deferoxamine (DEF). O2- generating system instillation led to significantly greater mean high frequency compound action potential (CAP) threshold shifts at 10 and 120 min post infusion than seen in AP control or SOD/O2- groups. H2O2 group CAP threshold shifts were significantly greater than control and CAT/H2O2 group values at 10 (16-30 kHz), and 120 min (above 12 kHz). OH generating system instillation led to significantly greater CAP threshold shifts at 10 (12-30 kHz) and 120 min (above 6 kHz) than seen in control or DEF/OH groups. No significant CAP differences were found between controls and scavenger/ROS groups. Mean 1.0 microV cochlear microphonic isopotential curve shift values did not systematically differ among groups. The rapid degradation of high frequency CAP threshold sensitivity seen here may provide insight into the portion of cochlear dysfunction which is ROS-mediated following noise, radiation or chemical exposures.

Action Potentials

Asbestos induces apoptosis of human and rabbit pleural mesothelial cells via reactive oxygen species.

Mesothelial cells, the progenitor cell of the asbestos-induced tumor mesothelioma, are particularly sensitive to the toxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in mesothelial cells are not known. We asked whether asbestos induced apoptosis in mesothelial cells and whether reactive oxygen species were important. Pleural mesothelial cells (rabbit or human) were exposed to asbestos (crocidolite, amosite, or chrysotile) or control particles at moderate doses (1-10 microg/cm2) over 24 h and evaluated for oligonucleosomal DNA fragmentation, loss of membrane phospholipid asymmetry, and nuclear condensation. Asbestos fibers, not control particles, induced apoptosis in mesothelial cells by all assays and induction of apoptosis was dose dependent for all types of asbestos, with crocidolite (5 microg/cm2) inducing 15.0+/-1.1% (mean+/-SE; n = 12) apoptosis versus control particles < 4%. Apoptosis induced by asbestos, but not by actinomycin D, was inhibited by extracellular catalase, superoxide dismutase in the presence of catalase, hypoxia (8% oxygen), deferoxamine, 3-aminobenzamide [an inhibitor of poly(ADP-ribosyl) polymerase], and cytochalasin B. Only catalase and cytochalasin B decreased fiber uptake. We conclude that asbestos induces apoptosis in mesothelial cells via reactive oxygen species. Escape from this pathway could allow the abnormal survival of mesothelial cells with asbestos-induced mutations.

Animals

Membrane pores induced by magainin.

Magainin, found in the skin of Xenopus laevis, belongs to a broad class of antimicrobial peptides which kill bacteria by permeabilizing the cytoplasmic membrane but do not lyse eukaryotic cells. The 23-residue peptide has been shown to form an amphiphilic helix when associated with membranes. However, its molecular mechanism of action has been controversial. Oriented circular dichroism has detected helical magainin oriented perpendicular to the plane of the membrane at high peptide concentrations, but Raman, fluorescence, differential scanning calorimetry, and NMR all indicate that the peptide is associated with the head groups of the lipid bilayer. Here we show that neutron in-plane scattering detects pores formed by magainin 2 in membranes only when a substantial fraction of the peptide is oriented perpendicular to the membrane. The pores are almost twice as large as the alamethicin pores. On the basis of the in-plane scattering data, we propose a toroidal (or wormhole) model, which differs from the barrel-stave model of alamethicin in that the lipid bends back on itself like the inside of a torus. The bending requires a lateral expansion in the head group region of the bilayer. Magainin monomers play the role of fillers in the expansion region thereby stabilizing the pore. This molecular configuration is consistent with all published magainin data.

Alamethicin

Rate of cognitive decline in Alzheimer's disease is not affected by the alpha-1-antichymotrypsin A allele or the CYP2D6 B mutant.

Patients with Alzheimer's disease (AD) show considerable heterogeneity in the rate at which they decline cognitively. The biological basis for this heterogeneity is unknown. We genotyped 86 subjects with diagnoses of probable AD to determine if they carried the alpha-1-antichymotrypsin (ACT) A allele, which has been associated with AD, or the CYP2D6 B mutant, found at increased frequency in the Lewy body variant (LBV) of AD. We then examined longitudinally-collected cognitive data to determine if these genetic markers were associated with rate of cognitive decline. Our results indicate that neither the ACT A allele nor the CYP2D6 B allele have a significant association with rate of decline on the Folstein Mini Mental State examination. Further, subjects with both the ACT A allele and the apolipoprotein epsilon 4 allele showed no evidence of accelerated decline. These findings suggest that any increased risk of developing AD or LBV conferred by these markers is not necessarily accompanied by a more rapid rate of decline.

Aged