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Y Huang

Publications and source records attributed to Y Huang.

At least 937 records · Page 52Linked to original sources
PubMed1995

Fundamental mechanical limitations on the visualization of elasticity contrast in elastography.

Elastography is a new ultrasonic imaging technique that produces images (elastograms) of the elastic properties of complaint tissue. To determine the Young's modulus it is necessary to measure or estimate any five of seven relevant variables. In elastography, the measured quantity is the normal strain component in the direction of the applied load, and the three normal components of stress may be estimated using the modified Love's analytical models while assuming a value close to 0.5 (incompressible) for Poisson's ratio. The distribution of Young's moduli can thus be computed and displayed in the form of two-dimensional images called elastrograms. The analytical models used for the estimation of the three normal components of stress assume that the target is semi-infinite and homogeneous in composition. The objective of this article is to determine some of the errors associated with the assumption of homogeneity of the target. Experiments using computer simulations were performed to study the efficiency with which elastograms display the contrast in the Young's modulus of a lesion or target, with respect to its background under certain conditions. It was observed (using the definition of contrast-transfer efficiency of elastography as the ratio of the elasticity contrast as measured from an elastogram, to the true contrast) that elastograms were consistently efficient in quantitatively depicting the elasticity contrast of hard lesions; however, they showed suboptimal contrast-transfer efficiency in cases of soft lesions in a hard background. In general, elastograms are efficient in displaying the elasticity contrast of hard or soft lesions which have a low contrast level with respect to the surroundings, irrespective of their size and location.

Algorithms↗
PubMed1995

Electrostatic interactions of S4 voltage sensor in Shaker K+ channel.

The S4 segment comprises part of the voltage sensor in Shaker K+ channels. We have used a strategy similar to intragenic suppression, but without a genetic selection, to identify electrostatic interactions of the S4 segment that may be important in the mechanism of voltage-dependent activation. The S4 neutralization mutations K374Q and R377Q block maturation of the protein, suggesting that they prevent proper folding. K374Q is specifically and efficiently rescued by the second site mutations E293Q and D316N, located in putative transmembrane segments S2 and S3, respectively. These results suggest that K374, E293, and D316 form a network of strong, local, electrostatic interactions that stabilize the structure of the channel. Some other double mutant combinations result in inefficient suppression, identifying weak, presumably long-range electrostatic interactions. A simple structural hypothesis is proposed to account for the effects of the rescued double mutant combinations on the relative stabilities of open and closed channel conformations.

Animals↗
PubMed1995

Regulation of serpin gene-1 in Manduca sexta.

Hemolymph of Manduca sexta contains proteins from the serpin superfamily, which are inhibitors of serine proteinases. We have used probes specific for M. sexta serpin gene-1 mRNA and protein to study the expression and hormonal regulation of this gene. Serpin gene-1 is expressed at a high level in larval fat body and at a lower abundance in hemocytes, where serpin protein is localized in the granules of granular cells. Serpin gene-1 mRNA is abundant in the fat body of feeding fourth and fifth instar larvae, but disappears abruptly at molts and at the wandering stage. The concentration of serpin proteins in hemolymph during development is correlated with the abundance of serpin mRNA in fat body. Results of in vivo and in vitro experiments indicate that 20-hydroxyecdysone has a role in negative regulation of serpin gene-1.

Animals↗
PubMed1995

Electrorotational studies of the cytoplasmic dielectric properties of Friend murine erythroleukaemia cells.

Electrorotation (ROT) spectra of Friend murine erythroleukaemia DS19 cells were measured in the frequency range 10 kHz-100 MHz as a function of suspension osmolality and cell differentiation treatment with hexamethylene bisacetamide (HMBA). A minimization program was employed to curve-fit the measured spectra using a single-shell dielectric model, allowing the derivation of cellular interior conductivity and permittivity (valid for the frequency range 10-100 MHz) and the cytoplasmic membrane capacitance (its dependence on the cell differentiation state and suspension osmolality having been reported earlier). Following HMBA treatment, DS19 cells exhibited a slight increment in average interior permittivity and a decrement in interior conductivity, although the changes were not statistically significant. For both untreated and HMBA treated samples, the average interior conductivity increased and permittivity decreased with increasing suspension osmolality. Of significance was that the average permittivity of cell interiors was larger than that of pure water. The electrorotation spectra of freshly prepared cell nuclei were measured, and the derived nuclear dielectric parameters were employed in numerical simulations to investigate the effects of nuclei on the ROT spectra of intact cells. Other cellular internal structures such as mitochondria were also analysed using theoretical simulations. It was concluded that the derived large permittivity values did not result from cell nuclei or mitochondria, and, instead, we suggest that they may arise from the combined effects of several cytoplasmic organelles.

Animals↗
PubMed1995

Type 1 interferon as an antiinflammatory agent: inhibition of lipopolysaccharide-induced interleukin-1 beta and induction of interleukin-1 receptor antagonist.

The effect of two type 1 interferons (r-metIFN-con1 and IFN-alpha 2b) on the induction of specific cytokines and IL-1Ra in whole blood was examined. IFN-gamma was induced at low levels following treatment of diluted whole blood in some but not all subjects. IL-1Ra was induced by both r-metIFN-con1 and IFN-alpha 2b, but with 10- to 100-fold higher induction per ng IFN with r-metIFN-con1 than with IFN-alpha 2b. There was no detectable induction of TNF-alpha, IL-4, or IL-6 by either IFN. The effect of both IFN preparations was measured on LPS-induced inflammatory cytokines. Both IFN preparations inhibited the production of IL-1 beta when added to the diluted blood samples before LPS addition. However, neither IFN had any effect on IL-1 beta synthesis when added at the same time or after LPS induction. When added to total blood cells in the absence of LPS at low concentration (up to 100 pg/ml), IFN slightly stimulated IL-1 beta production, but at 1000 pg/ml or greater there was significant inhibition of IL-1 beta production. These results suggest that type I IFNs play a role in regulating the inflammatory response.

Anti-Inflammatory Agents↗
PubMed1995

Carcinoma of the ampulla of Vater and mesenteric fibromatosis (desmoid tumor) associated with Gardner's syndrome: problems in management.

To date, 29 patients with Gardner's syndrome have been identified who developed carcinoma of the ampulla of Vater, and many others have been identified with mesenteric fibromatosis (desmoid tumor), but there have been only four cases of Gardner's syndrome with both ampullary carcinoma and mesenteric fibromatosis reported in the world literature. This article focuses on the complications and major problems in management resulting from the simultaneous occurrence of these two known features of Gardner's syndrome: carcinoma of the ampulla of Vater and fibromatosis (desmoid tumor) of the intestinal mesentery.

Adolescent↗
PubMed1995

BaCl2- and 4-aminopyridine-evoked phasic contractions in the rat vas deferens.

1. The actions of BaCl2 and 4-aminopyridine, blockers of K+ channels, on the mechanical activity of the epididymal half of the rat vas deferens were investigated. 2. Both BaCl2 and 4-aminopyridine dose-dependently evoked phasic contractions. High extracellular potassium (35-40 mM) caused a tonic contraction but abolished the BaCl2- and 4-aminopyridine-induced phasic activity and reduced the BaCl2-induced sustained component of contraction, but increased the 4-aminopyridine-induced tonic contraction. 3. Omission of calcium from the extracellular medium totally abolished the 4-aminopyridine-induced response but only reduced the mean amplitude of phasic contractions induced by BaCl. 4. Procaine (10 mM), an inhibitor of internal calcium release, completely abolished the phasic activity and reduced the sustained contraction induced by BaCl2. The remaining tone was abolished by nifedipine (1 microM). 5. Tetraethylammonium (1 mM) suppressed the amplitude of the BaCl2-induced phasic contractions, and induced a biphasic increase in tonic tension. 6. The BaCl2-induced responses were resistant to prazosin (1 microM), yohimbine (3 microM), propranolol (3 microM) or atropine (3 microM); in contrast, the 4-aminopyridine-induced activity was effectively inhibited by prazosin (1 microM) attenuated by yohimbine (1 microM) and atropine (1 microM) but not by propranolol (3 microM). The 4-aminopyridine-induced response was abolished by pretreatment of the vas deferens with 6-hydroxydopamine (0.5 mM). 7. The results indicate that the BaCl2-evoked activity in the vas deferens was mainly due to blockade of Ba(2+)-sensitive K+ channels on the smooth muscle plasma membrane. Subsequent calcium entry through the depolarized plasma membrane was needed to trigger generation of phasic contractions. 4-Aminopyridine-induced action, however, was largely mediated by neurotransmitters released from the depolarized nerve terminals as a result of blockade of K+ channels.

4-Aminopyridine↗
PubMed1995

Neuropharmacology of progressive myoclonus epilepsy: response to 5-hydroxy-L-tryptophan.

Low concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF) of patients with progressive myoclonus epilepsy (PME) suggest hypofunctional serotonergic neurotransmission. To study this hypothesis, we enrolled 6 patients with PME [Unverricht-Lündborg disease (U-L), mitochondrial encephalomyopathy, or Lafora disease] in a controlled, double-blinded, dose-ranging, cross-over add-on pilot clinical trial of 5-hydroxy-L-tryptophan (L-5-HTP) plus carbidopa after 2 other patients had received open-label L-5-HTP for compassionate use. Prestudy CSF 5-HIAA concentrations were low (< 20 ng/ml) in 6 patients regardless of the etiology of PME. One patient with U-L disease showed clinical improvement and a fivefold increase in CSF 5-HIAA, and 1 with Lafora disease showed a twofold increase in CSF 5-HIAA without improvement. A patient with Lafora disease reported enough improvement in myoclonus-evoked convulsions to continue chronic use of the drug. One patient with mitochondrial encephalomyopathy developed status epilepticus during treatment with L-5-HTP. As a group, patients had no statistically significant changes in myoclonus evaluation scale scores, subjective and objective measures of ataxia, seizure frequency, antiepileptic drug (AED) levels, or routine blood tests. These data suggest a serotonergic abnormality regardless of the underlying etiology of PME, but one that seldom responds to acute treatment with L-5-HTP.

5-Hydroxytryptophan↗
PubMed1995

Stability of cytomegalovirus antibodies in plasma during prolonged storage of blood components.

Cytomegalovirus (CMV) antibody testing is currently limited by manufacturers' guidelines to specimens stored for 7 days or less. We examined the stability of CMV antibodies in plasma from platelets and whole-blood units during storage using a rapid, automated, recombinant protein-based immunoassay which qualitatively detects total antibody to human CMV. Testing of single-donor apheresis platelets was performed on baseline serum and platelet-free plasma and on platelet-free plasma 8 days later. Indeterminate, positive, and negative CMV antibody results were maintained over time for 97% (75 of 77) of the platelet specimens. For whole-blood units, initial testing of donor serum and plasma obtained from erythrocyte segments took place within 7 days of phlebotomy. Indeterminate, positive, and negative CMV antibody results were maintained on subsequent analyses performed on erythrocyte segments at 2, 4, 6, and 8 weeks for 100% of whole-blood specimens. An important potential benefit of CMV antibody testing of stored platelets and blood is the elimination of a costly, dedicated, CMV-negative inventory. The study suggests that CMV antibody testing can be conveniently and reliably performed on blood components over the entire storage period.

Antibodies, Viral↗
PubMed1995

Glucosyl diglyceride lipid structures in Deinococcus radiodurans.

The structures of two lipids from the radiation-resistant bacterium Deinococcus radiodurans are reported here: 1,2-diacyl-3-alpha-glucopyranosyl-glycerol and 3-O-[6'-O-(1",2"-diacyl- 3"-phosphoglycerol)-alpha-glucopyranosyl]-1,2-diacylglycerol. These lipids are strikingly different from previously characterized polar lipids from this organism, in that they are not unique to the genus Deinococcus and indeed have counterparts in both gram-negative and gram-positive bacteria. Moreover, as examples of glucose-containing lipids, they further illustrate the diversity of carbohydrate-containing lipids in D. radiodurans, from which lipids containing galactose and N-acetylglucosamine have already been structurally characterized.

Carbon Isotopes↗
PubMed1995

Characterization of nef sequences in long-term survivors of human immunodeficiency virus type 1 infection.

Studies with the simian immunodeficiency virus have shown that nef deletion results in a low level of viremia and a lack of disease progression in monkeys. Given the similarity of this clinical profile to that observed in long-term survivors of human immunodeficiency virus type 1 (HIV-1) infection, we sought to examine the nef gene in 10 patients who are clinically healthy and immunologically normal despite 12 to 15 years of infection. PCR and DNA sequencing were used to determine nef sequences in peripheral blood mononuclear cells obtained from long-term survivors. We found that there is no gross deletion within nef in the cases studied; most nef sequences (91.1%) obtained from 10 subjects contained a full-length and intact open reading frame. In addition, at the protein level, there were no discernible differences between the Nef consensus sequences derived from long-term survivors and those from patients with AIDS. We therefore conclude that deletion of or gross sequence abnormality within nef is not likely to be a common explanation for the well-being of long-term survivors of HIV-1 infection. Moreover, phylogenetic analysis of nef sequences suggests that HIV-1 strains found in our study subjects do not have a common origin.

Amino Acid Sequence↗
PubMed1995

Biological characterization of nef in long-term survivors of human immunodeficiency virus type 1 infection.

We have previously shown that there were no gross deletions or obvious sequence abnormalities within nef of human immunodeficiency virus type 1 (HIV-1) in the 10 long-term survivors studied (Y. Huang, L. Zhang, and D. D. Ho, J. Virol. 69:93-100, 1995). Here we extend our study to examine these nef alleles in a functional context. Using a new technique, termed site-directed gene replacement, we have precisely replaced the nef of an infectious molecular clone, HIV-1HXB2, with nef alleles derived from 10 long-term survivors as well as from a patient with AIDS. The replication properties of these chimeric viruses demonstrated that the nef alleles derived from long-term survivors neither significantly increased nor decreased viral replication, compared with the nef allele of Nef+ HIV-1HXB2 and that derived from a patient with AIDS. However, Nef+ viruses always replicated faster than virus lacking nef. Moreover, single-cell infection analysis by the MAGI assay showed that these chimeric viruses, as well as Nef+ HIV-1HXB2, were more infectious than Nef- HIV-1HXB2 was. Therefore, we conclude that the genotypic and phenotypic features of nef are not likely to account for the nonprogression of HIV-1 infection in the 10 cases studied, unless the function of the nef gene in vivo is not accurately reflected by the in vitro assays we used.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Specific inhibition of granzyme B by parainfluenza virus type 3.

T-cell-mediated cytotoxicity is an important means of defense against viral pathogens; however, several viruses possess mechanisms to disrupt cytotoxicity, thereby allowing them to avoid immune clearance. These viruses have been shown to inhibit cytotoxicity by interfering with the capacity of T lymphocytes to specifically recognize infected cells. An alternative mechanism for virally induced cytotoxic dysfunction is identified in this report. We show that parainfluenza virus type 3, a negative-stranded RNA virus, can inhibit cytotoxicity by causing a defect in the cytotoxic effector apparatus. This defect is identified as a selective inhibition of granzyme B mRNA.

Adult↗
PubMed1995

Aromatic hydrocarbon receptor in cultured fetal cells from C57BL/6J and DBA/2J mice: similarity in molecular mass to receptors in adult livers.

In liver of adult responsive C57BL/6J (B6) mice the aromatic hydrocarbon receptor (AHR) has high affinity for specific halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), as well as nonhalogenated aromatic hydrocarbons (PAHs), such as benz[a]anthracene (BA) or 3-methylcholanthrene (MC). In livers of adult nonresponsive DBA/2J (D2) mice TCDD binds to a low-affinity variant form of AHR. Both TCDD and MC induce aryl hydrocarbon hydroxylase (AHH) in adult B6 mice, whereas adult D2 mouse liver is nonresponsive to MC. In fetal cell cultures derived from D2 mice AHH is induced by PAHs such as MC or BA, and these PAHs bind to cytosolic AHR (P.A. Harper, C.L. Golas, and A.B. Okey. Mol. Pharmacol. 40: 818-826, 1991). We compared AHR from fetal cell cultures with AHR from adult livers to determine whether there was some structural differences in receptors expressed in fetal cell culture that might permit cells from "nonresponsive" mice to respond to PAHs. The apparent molecular mass of AHR from cells cultured from 18-day fetuses is identical with that from adult liver within each strain of inbred mice tested (M(r) approximately 95 kDa in B6 and approximately 105 kDa in D2 mice). The AHR in D2 fetal cells was able to activate a transfected chloramphenicol acetyltransferase linked to a dioxin-responsive element nucleotide sequence (DRE-CAT) when the cells were treated with TCDD or MC. The potency of CAT expression in D2 fetal cells was similar to that in B6 fetal cells. Our data suggest that the responsiveness of fetal cells from "nonresponsive" mice is likely mediated by AHR in these cells but is not due to expression of a different allelic form of AHR ligand-binding subunit in fetal cells versus adult liver.

Affinity Labels↗
PubMed1995

Generation of pre-beta 1-HDL and conversion into alpha-HDL. Evidence for disturbed HDL conversion in Tangier disease.

HDL encompasses several apoA-I-containing particles that differ by size and show pre-beta- or alpha-mobility on agarose gel electrophoresis: pre-beta 1-LpA-I, pre-beta 2-LpA-I, pre-beta 3-LpA-I, alpha-LpA-I2, and alpha-LpA-I3. The quantitatively minor subclass pre-beta 1-LpA-I serves as an initial acceptor of cell-derived cholesterol. In this study, we generated a pre-beta 1-LpA-I-like particle in vitro by the incubation of biotinylated apoA-I with cholesterol-loaded macrophages. Both native pre-beta 1-LpA-I and in vitro-generated pre-beta 1-LpA-I were indistinguishable from lipid-free apoA-I by two-dimensional nondenaturing polyacrylamide gradient gel electrophoresis but exhibited a different size upon gel filtration. In vitro-generated biotin-pre-beta 1-LpA-I took up twofold to threefold more [3H]cholesterol from labeled fibroblasts during a 1-minute pulse incubation than lipid-free apoA-I. The in vitro conversion of biotin-pre-beta 1- LpA-I was investigated in the presence of plasmas of healthy probands and patients with Tangier disease, with apoA-I deficiency, and with lecithin-cholesterol acyltransferase (LCAT) deficiency. Incubation of biotin-pre-beta 1-LpA-I with plasmas either from normoalphalipoproteinemic probands or from a patient with apoA-I deficiency generated a biotinylated particle with the size and electrophoretic mobility of alpha-LpA-I2. This conversion was sensitive to heating at 56 degrees C but not to the removal of calcium. Inhibition of LCAT by dithiobisnitrobenzoic acid led to the formation of alpha-LpA-I3 instead of alpha-LpA-I2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Lipoproteins containing apolipoprotein A-IV but not apolipoprotein A-I take up and esterify cell-derived cholesterol in plasma.

Two-dimensional nondenaturing polyacrylamide gradient gel electrophoresis (2D-PAGGE) identifies distinct apoA-I-or apoE-containing subclasses of high-density lipoproteins (HDLs), each of which plays a different role in reverse cholesterol transport. In this study we used 2D-PAGGE to investigate the role of apoA-IV-containing lipoproteins in reverse cholesterol transport in native plasma. Incubation of 2D electrophoretograms with anti-apoA-IV antibodies identified up to three subclasses of particles. The smaller particle subclasses, LpA-IV-1 and LpA-IV-2, were found in every plasma sample. The largest particle subclass, LpA-IV-3, was observed in fewer than 10% of the plasmas analyzed. 2D-PAGGE of apoA-I-deficient plasma and apoA-I-depleted plasma and anti-apoA-I immunosubtracting 2D-PAGGE of normal plasma revealed that LpA-IV-1 and LpA-IV-2 do not contain apoA-I. The importance of LpA-IV-1 and LpA-IV-2 for uptake and esterification of cell-derived cholesterol was investigated using pulse-chase incubations of plasma with [3H]cholesterol-labeled fibroblasts followed by anti-apoA-I immunosubtracting 2D-PAGGE. During 1-minute pulse incubation with cells, [3H]cholesterol was taken up by gamma-LpE > LpA-IV-1 > pre-beta 1-LpA-I > LpA-IV-2 (">" denotes "more than"). During subsequent chase incubation without cells, proportionately less radioactivity disappeared from LpA-IV-1 and LpA-IV-2 than from pre-beta 1-LpA-I and gamma-LpE. During 5-minute pulse incubations, radioactive cholesteryl esters were formed in pre-beta 3-LpA-I > alpha-LpA-I > LpA-IV-1 > LpA-IV-2. The fractional estertification rate was highest in pre-beta 2-LpA-I and lowest in alpha-LpA-I.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗
PubMed1995

Reverse cholesterol transport in plasma of patients with different forms of familial HDL deficiency.

HDLs encompass structurally heterogenous lipoproteins that fulfill specific functions in reverse cholesterol transport. Two-dimensional nondenaturing gradient gel electrophoresis (2D-PAGGE) of normoalphalipoproteinemic plasma and subsequent immunoblotting with anti-apoA-I-antibodies differentiates pre-beta 1-LpA-I, pre-beta 2-LpA-I, pre-beta 3-LpA-I, alpha-LpA-I2, and alpha-LpA-I3. Immunodetection with anti-apoE antibodies differentiates gamma-LpE and alpha-LpE. Pulse-chase incubations of plasma with [3H]unesterified cholesterol ([3H]UC)-labeled fibroblasts and subsequent 2D-PAGGE revealed that cell-derived [3H]UC is taken up by pre-beta 1-LpA-I and gamma-LpE. From these initial acceptors, [3H]UC is transferred to LDL via pre-beta 2-LpA-I-->pre-beta 3-LpA-I-->alpha-LpA-I. Some UC is esterified in pre-beta 3-LpA-I, and some is esterified in alpha-LpA-I after its retransfer from LDL. In this study we investigated the effect of various forms of familial HDL deficiency on reverse cholesterol transport. Plasma samples of patients with various forms of HDL deficiency are characterized by the lack of specific HDL subclasses. ApoE-containing HDLs, including gamma-LpE, are present in all kinds of HDL deficiency. However, all forms of LpA-I are absent in apoA-I-deficient plasma, pre-beta 3-LpA-I and alpha-LpA-I from the plasma of patients with Tangier disease (TD), and pre-beta 3-LpA-I and large alpha-LpA-I from the plasma of patients with lecithin:cholesterol acyltransferase (LCAT) deficiency and fish-eye disease (FED). After a 1-minute pulse with labeled fibroblasts, efflux of [3H]UC into HDL-deficient plasmas decreased, compared with normal plasma, by 49% (apoA-I deficiency), 36% (TD), 21% (LCAT deficiency), and 28% (FED). In apoA-I deficiency, only gamma-LpE takes up cell-derived [3H]UC. In the three other HDL-deficiency states, cell-derived [3H]UC is initially taken up by both pre-beta 1-LpA-I and gamma-LpE. The four HDL deficiencies are also characterized by differences in the esterification of cell-derived [3H]UC. No esterification occurs in LCAT-deficient plasma. In FED plasma, [3H]UC is esterified in LDL. In apoA-I deficiency and TD, however, [3H]UC is esterified in lipoproteins free of apoA-I and apoB. In the two latter cases, the transfer of [3H]cholesteryl ester to LDL is enhanced compared with normal plasma. The lack of specific HDL subclasses and the consequent changes in reverse cholesterol transport pathways differently affect net mass efflux of cholesterol from fibroblasts into HDL-deficient plasma.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗