Biomedical subjects

H Liang

Publications and source records attributed to H Liang.

At least 91 records · Page 5Linked to original sources

PubMed2000

[The study of p16 gene mutation and methylation in laryngeal squamous cell carcinoma].

OBJECTIVE: To investigate the development and mechanism of the p16 gene inactivation in laryngeal squamous cell carcinoma (LSCC). METHODS: With PCR-based methylation assay and PCR-SSCP, first and second exon mutation in p16 gene and methylation of endogenase in promoter in 32 cases of LSCC and paracancer tissue were studied. RESULTS: No mutation were found in first and second exon in the samples; methylation of Cfo I were detected in 6 cases in first exon, methylation of Sac II was found in 4 cases, and methylation of Hpa II in 4 cases. In second exon, methylation of Hpa II was detected in 5 cases and methylation of Cfo I in 6 cases. CONCLUSION: Methylation of promoter in p16 gene is one of the important mechanisms of the inactivation of the gene. The inactivation of p16 gene has a close relation with the development and progress of LSCC.

Carcinoma, Squamous Cell↗

PubMed2000

[Study on the interaction of Rhus vernicifera laccase with Hg2+ ion].

The influence of the mixed time of Hg2+ ion and Rhus vernicifera laccase on the oxidation of 5,6-dibromo-2,3-dicyanohydroquinone (DDBQH2) catalyzed by laccase has been studied at pH 4.4 and 30 +/- 0.2 degrees C. Hg2+ ion can activate the catalytic activity of laccase when the mixed time is short. With the extension of the mixed time, the activation is gradually converted into inhibition. The influence of Hg2+ ion on the absorption spectrum of laccase suggests that it may be the substitution that Hg2+ ion displaces Cu(II) from the type 1 site in laccase causing the inhibition of laccase activity.

English Abstract↗

PubMed2000

[The preparation of nanometer silver colloid by photochemical method and its resonance scattering spectroscopic study].

The maximum resonance scattering peak of the silver colloids prepared by ultraviolet-photochemical method is at 470 nm and the maximum absorption peak is at 412.2 nm. The intensity of resonance scattering light is linear to the silver concentration in the range of 0.456-9.12 micrograms.mL-1. It is the first time that the blue silver colloid was prepared photochemically. Its maximum resonance scattering peak is at 470 nm. It has two absorption peaks at 397.4 and 623.4 nm.

Colloids↗

PubMed1999

Endothelial nitric oxide synthase interactions with G-protein-coupled receptors.

The endothelial nitric oxide synthase (eNOS) is activated in response to stimulation of endothelial cells by a number of vasoactive substances including, bradykinin (BK), angiotensin II (Ang II), endothelin-1 (ET-1) and ATP. In the present study we have used in vitro activity assays of purified eNOS and in vitro binding assays with glutathione S-transferase fusion proteins to show that the capacity to bind and inhibit eNOS is a common feature of membrane-proximal regions of intracellular domain 4 of the BK B2, the Ang II AT1 and the ET-1 ETB receptors, but not of the ATP P2Y2 receptor. Phosphorylation of serine or tyrosine residues in the eNOS-interacting region of the B2 receptor results in a loss of eNOS inhibition due to a decrease in the binding affinity of the receptor domain for the eNOS enzyme. Furthermore, the B2 receptor is transiently phosphorylated on tyrosine residues in cultured endothelial cells in response to BK stimulation. Phosphorylation occurs during the time in which eNOS transiently dissociates from the receptor accompanied by a transient increase in nitric oxide production. Taken together, these data support the hypotheses that eNOS is regulated in endothelial cells by reversible and inhibitory interactions with G-protein-coupled receptors and that these interactions can be modulated by receptor phosphorylation.

Animals↗

PubMed1999

Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis.

The functions of many open reading frames (ORFs) identified in genome-sequencing projects are unknown. New, whole-genome approaches are required to systematically determine their function. A total of 6925 Saccharomyces cerevisiae strains were constructed, by a high-throughput strategy, each with a precise deletion of one of 2026 ORFs (more than one-third of the ORFs in the genome). Of the deleted ORFs, 17 percent were essential for viability in rich medium. The phenotypes of more than 500 deletion strains were assayed in parallel. Of the deletion strains, 40 percent showed quantitative growth defects in either rich or minimal medium.

Culture Media↗

PubMed1999

Regulation of angiotensin II-induced phosphorylation of STAT3 in vascular smooth muscle cells.

Ligand binding to the angiotensin II (Ang II) AT1 receptor on vascular smooth muscle cells (VSMCs) activates the Janus-activated kinase (JAK)/signal transducers and activators of transcription (STAT) pathway. We have shown previously that the JAK2 tyrosine kinase and the Src family p59 Fyn tyrosine kinase are required for Ang II-induced STAT1 tyrosine phosphorylation in VSMCs. The mitogen-activated protein kinase phosphatase, MKP-1, is required for STAT1 tyrosine dephosphorylation. In the present study, using specific enzyme inhibitors and antisense oligonucleotides, we show that Ang II-induced tyrosine phosphorylation and nuclear translocation of STAT3 in VSMCs is mediated by p60 c-Src, whereas tyrosine dephosphorylation is mediated by calcineurin. Calcineurin is activated in response to Ang II stimulation of VSMCs and is translocated to the nucleus. In addition, we show that Ang II-induced serine phosphorylation of STAT3 in VSMCs is mediated by mitogen-activated protein kinase and that dephosphorylation is mediated by protein phosphatase 2A (PP2A). PP2A translocates to the nucleus in response to Ang II stimulation of VSMCs and forms a complex with STAT3 in an Ang II-dependent manner.

Angiotensin II↗

PubMed1999

Hydrophobic interaction chromatography and capillary zone electrophoresis to explore the correlation between the isoenzymes of salivary alpha-amylase and dental caries.

High-performance hydrophobic interaction chromatography (HIC) and capillary zone electrophoresis (CZE) were utilized in an effort to find the correlation between the composition of some isoenzymes of human salivary alpha-amylase (HSA) and dental caries. The mixture of more than three isoenzymes of HSA, fractionated from human parotid saliva with HIC, was further separated by CZE at the optimum pH 6.50. The composition and relative quantity of these isoenzymes were compared between two groups of individuals with different caries-susceptibility. It is found that the present frequency of peak II on CZE in the caries-free group was higher than that in the caries-active group and the relative quantities of peak III and peak IV showed remarkable differences (p < 0.05) between the two groups. These results may indicate that the composition of HSA isoenzymes is related to the occurrence of dental caries. However, more work should be done to further affirm this correlation between the isoenzymes of salivary alpha-amylase and dental caries.

Chromatography, High Pressure Liquid↗

PubMed1999

An antisense transcript to SMAD5 expressed in fetal and tumor tissues.

SMAD5, a transducer of TGF-beta/BMP inhibitory signals and a tumor suppressor candidate, localizes to the region of invariant loss in human myeloid neoplasms, on chromosome 5q31.1. Recent evidence indicates a gene-dosage effect along the TGF-beta/BMP signaling pathways. We have identified a novel transcript designated DAMS, whose 3' exonic sequences contain in part an alternate 5' exon of SMAD5, in the antisense orientation. Expressed sequenced tags (ESTs) for DAMS are found in fetal tissues (heart, adrenal glands, and total fetus) and pancreatic tumor cDNA libraries. In contrast to SMAD5, DAMS expression is not readily detectable in adult and fetal tissues. Semiquantitative PCR suggests that the stoichiometry between SMAD5 and DAMS transcripts ranges between 15 and 120 in normal and malignant hematopoietic cells. The findings raise the possibility that DAMS may be a fail-safe mechanism for precise regulation of SMAD5 transcript levels that may be critical in maintaining normal homeostasis.

5' Untranslated Regions↗

PubMed1999

Bcl-xL regulates apoptosis by heterodimerization-dependent and -independent mechanisms.

A hydrophobic cleft formed by the BH1, BH2 and BH3 domains of Bcl-xL is responsible for interactions between Bcl-xL and BH3-containing death agonists. Mutants were constructed which did not bind to Bax but retained anti-apoptotic activity. Since Bcl-xL can form an ion channel in synthetic lipid membranes, the possibility that this property has a role in heterodimerization-independent cell survival was tested by replacing amino acids within the predicted channel-forming domain with the corresponding amino acids from Bax. The resulting chimera showed a reduced ability to adopt an open conductance state over a wide range of membrane potentials. Although this construct retained the ability to heterodimerize with Bax and to inhibit apoptosis, when a mutation was introduced that rendered the chimera incapable of heterodimerization, the resulting protein failed to prevent both apoptosis in mammalian cells and Bax-mediated growth defect in yeast. Similar to mammalian cells undergoing apoptosis, yeast cells expressing Bax exhibited changes in mitochondrial properties that were inhibited by Bcl-xL through heterodimerization-dependent and -independent mechanisms. These data suggest that Bcl-xL regulates cell survival by at least two distinct mechanisms; one is associated with heterodimerization and the other with the ability to form a sustained ion channel.

Amino Acid Sequence↗

PubMed1999

Understanding the cellular uptake of phosphopeptides.

Phosphopeptide-cellular uptake has been studied with a unique combination of tools designed to quantitate this phenomena and to understand properties that contribute to transmembrane penetration. High-affinity src-homology domain (SH2) hexapeptides for the phosphatidyl inositol 3-kinase system were used to judge cell penetration using red blood cells--a model system for the study of transmembrane cellular uptake. Hexapeptides without phosphate groups and devoid of charged residues poorly entered cells. N-terminal modification with bulky hydrophobic groups enhanced partitioning into octanol, an index of hydrophobicity, and allowed certain non-phosphorylated peptides to pass into red cells. However, tyrosine phosphorylation of hexapeptides markedly decreased octanol-water partitioning and completely eliminated cellular uptake. Inclusion of ion-pairing agents that masked the phosphate hydrophilic character enabled partitioning of phosphopeptides into octanol and achieved cellular uptake. This effect was demonstrated using fluorescent derivatives of phosphopeptides and CV1 cells in culture. The results validate the concept of facilitating cell entry by charge masking and open the way to future refinements of this principle. Various penetration techniques are compared and discussed in the context of maximizing cellular viability.

Acetic Anhydrides↗

PubMed1999

Complete biliary avulsion from blunt compression injury.

The liver is the solid organ most commonly injured as a result of blunt abdominal trauma. Complete avulsion of the common hepatic duct is a rare and devastating type of hepatobiliary trauma. Here the authors report the case of a 7-year-old child who had complete biliary disruption as a result of an abdominal crush injury that was not diagnosed correctly preoperatively. The intraoperative diagnosis and treatment of this injury is discussed.

Abdominal Injuries↗

PubMed1999

Parathyroid hormone stimulates cancellous bone formation at skeletal sites regardless of marrow composition in ovariectomized rats.

The purpose of the current report is to compare the skeletal effects of PTH treatment at red (hematopoietic) and yellow (fatty) marrow sites in ovariectomized (ovx) rats. In the first study, mature, slowly growing ovx rats that were 4 months of age and 4 weeks postovariectomy were treated with human parathyroid hormone [hPTH(1-34)] (80 microg/kg, 5 days/week) for 6 weeks. In the second study, aged ovx rats that were 15 months of age and 1 year postovariectomy were treated with PTH according to the same regimen for 10 weeks. The proximal tibial metaphysis (PTM) and first lumbar vertebra (LV), bone sites with red marrow, as well as the distal tibial metaphysis (DTM) and fifth caudal vertebra (CV), bone sites with yellow marrow, were processed undecalcified for quantitative bone histomorphometry. At the end of the first study in mature ovx rats, estrogen depletion induced a 73% loss of cancellous bone in the PTM and a 15% loss in the LV. In contrast, not even a trend for cancellous bone loss was observed in the DTM and CV of vehicle-treated ovx rats. PTH treatment of ovx rats increased cancellous bone volume by 191% in the PTM, 56% in the DTM, 47% in the LV, and 22% in the CV, compared with vehicle treatment of ovx rats. In addition, the hormone markedly increased cancellous bone formation by 177% in the PTM, 679% in the DTM, 309% in the LV, and 833% in the CV. Aged ovx rats (second study) exhibited moderate cancellous osteopenia in the LV but not the CV. PTH treatment increased cancellous bone volume by 67% and 37% and bone formation rate by 635% and 359% in the LV and CV, respectively, compared with vehicle treatment of ovx rats. Although the magnitude of the anabolic response to PTH may vary somewhat within the skeleton, the results indicate that PTH augments cancellous bone mass and markedly stimulates bone formation at skeletal sites, regardless of marrow composition.

Animals↗

PubMed1999

Effects of age, estrogen depletion, and parathyroid hormone treatment on vertebral cancellous wall width in female rats.

The main goal of this study was to determine whether vertebral cancellous wall width changes with age and parathyroid hormone (PTH) treatment in rats. Female Sprague-Dawley rats were subjected to sham surgery or ovariectomy at 3 months of age. One month after surgery, ovariectomized (ovx) rats were injected subcutaneously (s.c.) 5 days/week for 6 weeks with vehicle or human parathyroid hormone [hPTH (1-34)] at a dose of 80 microg/kg body weight. Sham-operated control rats were injected s.c. with vehicle alone. All rats from this first study were 5.5 months of age at the time of killing. In the second study, control and ovx rats were subjected to the same treatments for a 10-week period beginning at one year after surgery. These animals were 17.5 months of age at the end of the study. The first lumbar vertebra was collected from each rat and processed undecalcified for measurements of cancellous wall width. At 5.5 months of age, control and ovx rats had nearly identical mean values for vertebral cancellous wall width, but this remodeling variable was significantly increased in PTH-treated ovx rats. At 17.5 months of age, wall width in control and ovx rats decreased significantly compared with wall width in the younger rats. PTH treatment of aged ovx rats induced a significant increase in vertebral cancellous wall width when compared with vehicle treatment of aged ovx rats. These results, which are consistent with findings in humans, indicate that vertebral cancellous wall width decreases with age in intact female rats and in ovx rats, but increases in ovx rats in response to PTH treatment. Furthermore, the results add to the growing body of evidence that substantial cancellous bone remodeling occurs in the vertebral bodies of rats.

Aging↗

PubMed1999

Zinc ligand-disrupted recombinant human Endostatin: potent inhibition of tumor growth, safety and pharmacokinetic profile.

Endostatin, a potent endogenous inhibitor of angiogenesis, inhibits the growth of primary tumors without induction of acquired drug resistance in mice. We report that a soluble recombinant human (rh) Endostatin produced with characteristics of the native Endostatin, effectively inhibited the growth of primary tumors and pulmonary metastases in a dose-dependent manner. We also show that deletion of two of the four zinc ligands of rhEndostatin did not affect this potent tumor inhibiton. The growth of established Lewis lung primary tumors implanted into mice was inhibited (80-90%) upon systemic treatment with 50 mg/kg/12 h of rhEndostatin. Using the B16-BL6 murine experimental pulmonary metastases model, rhEndostatin administered at 1.5 mg/kg/day or 4.5 mg/kg/day beginning 3- or 11-days post tumor cell injection, respectively, resulted in an approximate 80% inhibition of tumor growth. At effective anti-tumor doses of 1.5 and 50 mg/kg, pharmacokinetic modeling in mice showed (a) the protein was 100% bioavailable, (b) the AUC ranged from 16 to 700 ng ml/h and (c) the Cmax ranged from 161 to 4582 ng/ml. At the highest dose tested (300 mg/kg), delivered as a single bolus, no drug-related toxicity was observed in a Cynomolgus monkey infused with rhEndostatin. No toxicity was observed even at AUC and Cmax values that were 1.3- to 56-fold higher than those observed in mice with tumors that were potently inhibited. Our production system yields a well characterized, soluble and potent rhEndostatin at quantities sufficient for human use. The preclinical studies described herein are an important first step toward the assessment of Endostatin in the clinic.

Journal Article↗

PubMed1999

Genomic profiling of drug sensitivities via induced haploinsufficiency.

Lowering the dosage of a single gene from two copies to one copy in diploid yeast results in a heterozygote that is sensitized to any drug that acts on the product of this gene. This haploinsufficient phenotype thereby identifies the gene product of the heterozygous locus as the likely drug target. We exploited this finding in a genomic approach to drug-target identification. Genome sequence information was used to generate molecularly tagged heterozygous yeast strains that were pooled, grown competitively in drug and analysed for drug sensitivity using high-density oligonucleotide arrays. Individual heterozygous strain analysis verified six known drug targets. Parallel analysis identified the known target and two hypersensitive loci in a mixed culture of 233 strains in the presence of the drug tunicamycin. Our discovery that both drug target and hypersensitive loci exhibit drug-induced haploinsufficiency may have important consequences in pharmacogenomics and variable drug toxicity observed in human populations.

Anti-Bacterial Agents↗

PubMed1999

Cross-sectional presurgical implant imaging using tuned aperture computed tomography (TACT).

OBJECTIVES: To investigate tuned aperture computed tomography (TACT) as an alternative to conventional tomography for cross-sectional imaging of potential implant sites. METHODS: Twenty potential implant sites in three dry human mandibles were selected. Sixteen TACT basis projections were recorded on film using a linear array of source positions. Films were scanned and 20 TACT and iterative TACT slices were reconstructed using TACT Workbench software. Maximum height and width were measured on one representative slice of each site. Results were compared with the ground truth using ANOVA and Wilcoxon signed rank tests. RESULTS: The means of relative difference in maximum height were 1.55 and 1.56% for TACT and iterative TACT respectively (P = 0.8643). The means of relative difference in width were 5.96 and 6.36% for TACT and iterative TACT respectively (P = 0.4845). More than 75% measurements were within +/- 1 mm of ground truth for both modalities. CONCLUSIONS: TACT may provide an alternative to conventional tomography for dental implant imaging. Further investigations should be performed to explore factors affecting image quality.

Anatomy, Cross-Sectional↗

PubMed1999

IgA production in MHC class II-deficient mice is primarily a function of B-1a cells.

Mice deficient in MHC class II expression (C2d mice) do not make antibody to protein antigens administered systemically, but their ability to produce IgA antibody to antigen administered at mucosal sites has not been described. We investigated IgA production by C2d mice and their IgA antibody response to antigen given orally. Young C2d mice had normal amounts of serum IgA, intestinal-secreted IgA and normal numbers of intestinal IgA plasma cells, compared to control C57BL/6 mice. IgA production by C2d mice increased with age. Following oral immunization with cholera toxin, C57BL/6 mice responded with IgA and IgG antibody, and had increased numbers of IgA plasma cells, but C2d mice gave no response. The Peyer's patch and mesenteric lymph node tissues of C2d mice contained very few CD4-expressing T cells. Thus, C2d mice have no typical mucosal CD4 Th cells and cannot respond to a strong oral immunogen, yet they still produced and secreted IgA. We hypothesized that B-1 lymphocytes could provide a source of IgA independent of antigen-specific T cell help. Young C2d mice had normal numbers of peritoneal B-1a cells and their frequency increased with age. To test the role of these B-1a cells, we bred C2d mice to obtain mice that had no MHC class II expression and expressed the Xid gene that confers deficiency in B-1a cells. These double-deficient mice had 10-fold less serum and secreted IgA than all other F2 littermates. We conclude that B-1a cells are essential for the majority of IgA production in C2d mice. Thus, the C2d mouse may provide a useful tool for analysis of the role of intestinal IgA provided by B-1a cells.

Animals↗

PubMed1999

A role for choroidal lymphatics during recovery from form deprivation myopia?

BACKGROUND: The choroid of the chick swells markedly during recovery from experimentally induced myopia. It has been demonstrated previously that the lymphatic sinusoids of the choroid contribute most to the expansion. This raises important questions about the particular ultrastructural changes occurring in choroidal lymphatics as a means of understanding the role these vessels might play in emmetropization. METHODS: Thirteen hatchling chicks were monocularly occluded for 2 weeks to induce myopia and then allowed normal visual experiences during recovery for periods of 0 to 72 h before sacrifice. RESULTS: Electron microscopic analysis detailed the temporal progression of vascular changes and provides qualitative evidence for edema in the extravascular space. Quantitative analysis showed that the frequency of open junctions between lymphatic endothelial cells (an indicator of passive fluid transfer) increased over the 3 days of recovery. Lymphatic fenestrations (an indicator of active fluid transfer) were rare in both nondeprived eyes and in form-deprived eyes at the time of occluder removal, but increased in density significantly over the first 24 h of recovery before returning to control levels by 72 h. The number of lymphatic endothelial caveolae did not change significantly during recovery, nor did the number of fenestrations along the walls of choriocapillaris vessels. CONCLUSIONS: The walls of the lymphatics of the chick choroid open to allow greater fluid transfer during re-emmetropization than normal; the lymphatics may play an important role in the maintenance of chorioretinal fluid balance and homeostasis.

Animals↗