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Biomedical subjects

S Huang

Publications and source records attributed to S Huang.

At least 595 records · Page 33Linked to original sources
PubMed1992

Mechanical properties of fibrin adhesives for blood vessel anastomosis.

Various methods have been used for anastomosing, or attaching, two ends of a severed blood vessel together. The most common method, suturing, is tedious, can be time-consuming, and requires special training in microvascular surgery. Other methods, such as mechanical devices and lasers, have some problems as well. The use of fibrin adhesives for blood vessel anastomosis might eliminate some of the current problems by allowing a quicker, simpler, and more reliable method of attachment. Although mechanical studies have been conducted to determine fibrin glue properties in shear, tensile, and burst tests; most of these studies have used skin or intestinal tissue. Therefore, to evaluate the feasibility of using fibrin glue as an adhesive for blood vessel anastomosis, the mechanical properties of blood vessels joined with fibrin glue were examined using tensile and burst tests. High and low fibrinogen concentrations were tested after 5- or 45-min time periods. In addition, three clinical methods of attachment were compared: end-to-end anastomosis, vessel overlapping, and suturing. In this study, because the adhesive strength was not found to increase significantly after 5 min, setting times for fibrin glue may be short enough to make it a clinical option when compared to suturing. In addition, the higher fibrinogen concentration did not result in a significantly higher adhesive strength, indicating that the lower concentration fibrin adhesives may be of comparable strength to the higher concentrations for clinical applications.

Anastomosis, Surgical↗
PubMed1992

Alpha-oxidation of 3-methyl-substituted fatty acids in rat liver.

3-Methyl-substituted fatty acids are first oxidatively decarboxylated (alpha-oxidation) before they are degraded further via beta-oxidation. We synthesized [1-14C]phytanic and 3-[1-14C]methylmargaric acids in order to study their alpha-oxidation in isolated rat hepatocytes, rat liver homogenates and subcellular fractions. alpha-Oxidation was measured as the production of radioactive CO2. In isolated hepatocytes, maximal rates of alpha-oxidation amounted to 7 and 10 nmol/min x 10(8) cells with phytanic acid and 3-methylmargaric acid, respectively. At equimolar substrate concentrations, alpha-oxidation of branched fatty acids was approximately 10- to 15-fold slower than the beta-oxidation of the straight chain palmitate. In whole liver homogenates, rates of alpha-oxidation that equaled 60 to 70% of those observed in the hepatocytes were obtained. Optimum rates required O2, NADPH, Fe3+, and ATP. Fe3+ could be replaced by Fe2+ and ATP could be replaced by a number of other phosphorylated nucleosides and even inorganic phosphate without loss of activity. NADH could substitute for NADPH but not always with full restoration of activity. A variety of other cofactors and metal ions was either inhibitory or without effect. Scavengers of reactive oxygen species, known to be formed during the NADPH-dependent microsomal reduction of ferric-phosphate complexes, were without effect on alpha-oxidation. No evidence was found for the accumulation of NADPH-dependent or Fe(3+)-dependent reaction intermediates. Subcellular fractionation of liver homogenates demonstrated that alpha-oxidation was located predominantly, if not exclusively, in the endoplasmic reticulum. alpha-Oxidation, measured in microsomal fractions, was not inhibited by CO, cytochrome c, or ferricyanide, indicating that NADPH cytochrome P450 reductase and cytochrome P450 are not involved in alpha-oxidation. Our results indicate that, contrary to current belief, alpha-oxidation is catalyzed by the endoplasmic reticulum. The cofactor requirements suggest that alpha-oxidation involves the reduction of Fe3+ by electrons from NADPH and that it is stimulated by phosphate ions and nucleotides.

Animals↗
PubMed1992

The retinoblastoma protein region required for interaction with the E2F transcription factor includes the T/E1A binding and carboxy-terminal sequences.

Recent experiments in understanding the mechanism of the retinoblastoma protein (RB) function have revealed the existence of several cellular proteins that are complexed with RB. One of these cellular proteins is the E2F transcription factor, which was originally identified due to its inducibility by E1A during an adenovirus infection. The E2F recognition sequence is found in the promoters of several cellular genes involved in growth control, including several oncogenes. In this report, we provide evidence that the interaction of E2F and RB is mediated through a region on RB where viral oncogenes such as SV40 T antigen and adenovirus E1A bind and where tumorigenic mutations also cluster. Additional carboxy-terminal sequences are also required for the interaction with E2F. These observations provide evidence for a direct connection between tumor suppressor function and the gene expression program leading to cellular growth regulation.

Adenovirus E1A Proteins↗
PubMed1992

Differences in snRNP localization between transformed and nontransformed cells.

We have examined the localization of snRNPs in a variety of mammalian cells and have observed differences in the organization of these factors in transformed cells, immortal cells, and cells of defined passage number. Cells of defined passage number exhibit a speckled staining pattern after immunolabeling with anti-Sm, anti-B'', or anti-m3G antibodies. Furthermore, 2-3% of the cells, in a given population, exhibit labeling of 1 or 2 round coiled bodies in addition to the speckled-labeling pattern. However, transformed cells exhibited 1-4 intensely stained coiled bodies, in 81-99% of the cells, in addition to the speckled-labeling pattern. Immortal cells exhibited 1-4 intensely stained smaller coiled bodies in 4-40% of the cells, in addition to the speckled-labeling pattern. When immortal cells (REF-52) that had been transformed by adenovirus (REF-52Ad5.4) were examined, these cells exhibited an increase in the percentage of cells containing 1 or 2 intensely stained coiled bodies, in addition to the speckled labeling, from 24 to 99%. On the basis of this study, we conclude that the organization of snRNPs within the mammalian cell nucleus is a reflection of the physiology of the cell that may change upon transformation or immortalization.

Animals↗
PubMed1992

Transcriptional regulation of left ventricular beta-adrenergic receptors during chronic hypoxia.

beta-Adrenergic receptor downregulation is the end result of cellular adaptation to prolonged agonist exposure. The factors mediating receptor downregulation include receptor phosphorylation, receptor movement from the plasma membrane to intracellular sites, and alterations in nascent receptor synthesis. We have previously demonstrated a downregulation of the left ventricular beta-receptor during chronic hypoxia in vivo. To determine the mechanism of this downregulation, we produced chronic hypoxia in seven newborn lambs by creating right ventricular outflow obstruction and an atrial septal defect. Oxygen saturation was reduced to 65-74% for 2 weeks. Six lambs served as normoxic controls. Sarcolemmal membrane and cytosolic fractions were prepared from left ventricular free wall samples. beta-Receptor density in each fraction was determined with the radioligand [125I]iodocyanopindolol. Steady-state levels of beta-receptor mRNA were determined by Northern blot analysis using a beta 1-adrenergic receptor cDNA probe. During chronic hypoxia, left ventricular membrane beta-adrenergic receptor density decreased by 55% (153 +/- 28 fmol/mg for hypoxic lambs versus 342 +/- 79 fmol/mg for control lambs, p < 0.05). There was no corresponding increase in beta-receptor density in the cytosolic fraction (23 +/- 3 fmol/mg for hypoxic lambs versus 33 +/- 9 fmol/mg for control lambs, p = NS), nor was there a significant change in the ratio of beta 1-receptor/beta 2-receptor subtypes as assessed by radioligand binding (beta 1 subtype, 84.1 +/- 10.1% for hypoxic lambs versus 93.2 +/- 8.8% for control lambs; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Efficacy and tolerability of enteric-coated naproxen in the treatment of osteoarthritis and rheumatoid arthritis: a double-blind comparison with standard naproxen followed by an open-label trial.

One hundred and twenty-three patients with osteoarthritis (n = 50) or rheumatoid arthritis (n = 73) were enrolled in a 6-week, double-blind, randomized, controlled, parallel trial comparing enteric-coated naproxen with standard naproxen. Ninety-eight patients subsequently entered a 20-week, open-label trial of enteric-coated naproxen. The study demonstrated that naproxen in both its standard formulation and its new enteric-coated formulation is a highly effective form of therapy for osteoarthritis and rheumatoid arthritis. The tolerability profiles of the two formulations were similar in terms of the types of complaints reported. It is concluded that enteric-coated naproxen is an efficacious and well-tolerated formulation for the treatment of osteoarthritis and rheumatoid arthritis.

Adult↗
PubMed1992

Open-label tolerability study of enteric-coated naproxen in the treatment of osteoarthritis and rheumatoid arthritis.

Two hundred and ninety-six patients were enrolled in a 6-month, open-label tolerability study of enteric-coated naproxen in patients with rheumatoid arthritis (n = 174) and osteoarthritis (n = 122). Thirty percent of the patients were greater than 65 years of age. Under standard clinical prescribing conditions, enteric-coated naproxen 500 mg twice daily and 375 mg twice daily demonstrated an acceptable tolerability profile that was not different from what one would expect with standard naproxen.

Adult↗
PubMed1992

Irreversible inhibition of thymidylate synthase by pyridoxine (B6) analogues.

Three vitamin B6 analogues have been synthesized and tested as inhibitors of thymidylate synthase. The compounds are: 4',5'-dichloro-, 4',5'-dibromo- and 4',5'-diiodo-pyridoxine. All three analogues inhibited the enzyme irreversibly. The kinetic data for the chloro- and bromo-analogues showed that a limiting rate of inhibition is approached as the inhibitor concentration is increased, which indicates that a reversible enzyme:inhibitor affinity complex is formed prior to the irreversible reaction. 4',5'-Dibromo-pyridoxine exhibited a greater binding affinity (lower Ki) for thymidylate synthase than 4',5'-dichloro-pyridoxine, and it also reacted faster to irreversibly inhibit the enzyme. The presence of the substrate dUMP (10 microM) completely protected thymidylate synthase from inhibition. These data suggest that the halogenated vitamin B6 analogues are active site-directed inhibitors of thymidylate synthase, which first bind reversibly to the catalytic site and then react irreversibly with the enzyme.

Kinetics↗
PubMed1992

10'-Desmethoxystreptonigrin, a novel analog of streptonigrin.

10'-Desmethoxystreptonigrin, a novel analog of streptonigrin produced by Streptomyces albus, was discovered in a screen for inhibitors of farnesylation of RAS p21 protein. The compound was isolated from the fermentation broth and its structure determined. It is markedly cytotoxic to several human tumor cell lines and also exhibits potent broad-spectrum antibacterial activity.

Animals↗
PubMed1992

The spectral VEP in normal subjects and dichromats.

The spectral VEP in 13 normal subjects (25 eyes), four cases (8 eyes) of protanopes and 8 cases (15 eyes) of deuteranopes were tested. In normal subjects, the shortest latencies of N1, P1, N2 were in 560 nm and the greatest amplitudes of N1-P1 and P1-N2 were 560-570 nm, around which the latencies were delayed and the amplitudes were decreased as the wavelengths of stimulative light increased or decreased gradually. The spectral VEP pattern of deuteranopes was similar to the normal subjects. In the protanopes, the shorter latencies of N1,P1,N2 and greater amplitudes of N1-P1, P1-N2 appeared in 520-530 nm and 570 nm, forming the two-thoughs and two-peaks shapes, with the shortest latencies and the greatest amplitudes in 520-530 nm. There were statistically significant differences of amplitudes and/or latencies in some wavelengths between the protanopes and normals and between the deuteranopes and normals.

Adolescent↗
PubMed1992

Detection of point mutations of the phenylalanine hydroxylase gene and prenatal diagnosis of phenylketonuria.

The known mutant alleles of the human phenylalanine hydroxylase (PAN) gene were analyzed in 25 phenylketonuria (PKU) families from North China by using polymerase chain reaction and allele-specific oligonucleotide dot blot hybridization techniques. The results showed that the six mutations analyzed accounted for 62% of all PKU genes. The three most frequent mutations were R243Q, R413P and Y204C. Seven prenatal gene diagnoses were carried out in 6 PKU families and were confirmed after birth or by examination of aborted materials.

Base Sequence↗
PubMed1992

Does lineage determine the dopamine phenotype in the tadpole hypothalamus?: A quantitative analysis.

The ancestry of dopaminergic (DA) neurons in the Xenopus laevis hypothalamus was investigated by combining intracellular lineage dye injections of 16- and 32-cell blastomeres with the immunofluorescent detection of tyrosine hydroxylase at tadpole stages. At these stages, DA neurons in the hypothalamus comprise a discrete nucleus that contains from 22 to 45 cells on each side [mean = 32.6 +/- 6.6 (SD)]. The DA nucleus descends from only four of the 16-cell blastomeres. The two dorsal midline blastomeres (D1.1) are the major progenitors, and in all embryos studied they contributed to the DA nucleus. The two dorsal lateral blastomeres (D1.2) contribute to the DA nucleus in only about half of the embryos. Thus, the DA nucleus descends only from a discrete group of progenitors, and the participation of some of the progenitors in the DA lineage is only probabilistic. The number of DA neurons generated by the same blastomere varied greatly in different animals. This variation in cell number correlated with the degree of coherence and the density of the clone in the hypothalamus, rather than with clonal ancestry. Bilateral deletion of the major 32-cell progenitor (D1.1.1) resulted in a nearly complete restitution of the DA nucleus in 74% of the embryos that successfully completed gastrulation and neurulation. In the rest, the hypothalamus was smaller than normal or missing, and the DA nucleus was significantly reduced in size or absent. These results show that the DA nucleus can be restored after its normal lineage is deleted, but complete regulation is not always accomplished. Several blastomere progenitors dramatically altered their contribution to the DA nucleus after D1.1.1 ablation, including two blastomeres that normally do not contribute to the DA lineage. Thus, the fate to produce DA neurons is not determined at cleavage stages.

Animals↗
PubMed1992

Expression of macrophage inflammatory protein-2 and KC mRNA in pulmonary inflammation.

This study sought to test the hypothesis that expression of mRNA for two cytokines, macrophage inflammatory protein-2 (MIP-2) and the KC gene product, is induced in rat lung cells during inflammatory responses in vitro and in vivo. Macrophage inflammatory protein-2 and KC are members of the platelet-factor 4 (PF-4) cytokine superfamily that cause marked neutrophil chemotaxis and activation in vitro. To investigate expression of the genes for MIP-2 and KC in rat models of lung injury, cDNA probes for these cytokines in the rat were made from polymerase chain reaction (PCR) products generated using mouse sequence-derived primers. Sequence analysis of these cDNAs showed marked homology to known murine sequences (89% and 92% MIP-2 and KC, respectively). These cDNAs were first used to study the expression of these two genes in rat alveolar macrophages (AMs) in vitro by Northern blot hybridization. Lipopolysaccharide (LPS) treatment of rat AMs in vitro caused marked increases in mRNA for both KC and MIP-2 within 30 minutes, which persisted through the 6 hours measured. To study expression during inflammation in vivo, rats were treated with LPS by intratracheal instillation. Bronchoalveolar lavage (BAL) cells and whole trachea homogenates were analyzed. There was a marked and rapid increase in MIP-2 and KC mRNA levels within both BAL cells and trachea homogenates after LPS instillation. The results support the hypothesis that MIP-2 and KC cytokines contribute to neutrophil chemotaxis and activation in this rat model of acute pulmonary inflammation.

Animals↗
PubMed1992

Effect of dietary protein on glomerular proteinase activities.

Recent studies suggest that proteolytic enzymes are involved in the degradation of extracellular matrix components of the renal glomerulus. In the present study, the effects of feeding 3 different protein diets on glomerular cysteine proteinase and metalloproteinase activities to healthy rats for 6 weeks were examined. The diets contained 5, 20, or 60% casein and were made isocaloric by starch. On sacrifice, the glomeruli were isolated by differential sieving. Proteolytic activities were measured using fluorogenic substrates and were expressed per glomerular DNA content. Body weight was virtually unchanged by the amount of protein ingested, whereas kidney weight was closely correlated with dietary protein content (5%: 1,625 +/- 324; 20%: 2,110 +/- 326; 60%: 2,705 +/- 910 mg). Activity of cathepsin B, the most abundant cysteine proteinase in the glomerulus, decreased with protein loading (5%: 1,498 +/- 110; 20%: 1,321 +/- 82; 60%: 914 +/- 84 pmol/min/micrograms DNA). The same pattern emerged with cathepsin L (5%: 869 +/- 71; 20%: 846 +/- 70; 60%: 517 +/- 83 pmol/min/micrograms DNA) and cathepsin H (5%: 498 +/- 45; 20%: 478 +/- 55; 60%: 330 +/- 39 pmol/min/micrograms DNA). The differences between the 20 and 60% groups were statistically significant for all 3 cathepsins measured. The intraglomerular activity of the metalloproteinase collagenase declined significantly with the amount of protein ingested (5%: 233 +/- 14; 20%: 189 +/- 13; 60%: 137 +/- 11 microU/micrograms DNA). Gelatinase activity also fell as protein intake increased (5%: 183 +/- 18; 20%: 115 +/- 10; 60%: 94 +/- 11 F/micrograms DNA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Role of glomerular proteinases in the evolution of glomerulosclerosis.

Recent studies suggest that proteolytic enzymes located within the glomerulus are involved in the degradation of extracellular matrix components. In the present investigation glomerular proteinase activities were followed in a variety of non-immune-mediated renal diseases as well as during different dietary manipulations. Azocaseinolysis was significantly reduced in the obese Zucker rat compared with lean littermates (pH 5.4:8.9 +/- 0.4 vs 11.4 +/- 0.7; pH 7.4:5.8 +/- 0.7 vs 9.3 +/- 0.6 arb. U/mg protein). When the glomerular proteolytic capacity was measured in old rats, again a significant decline in proteolysis was observed (pH 5.4:9.8 +/- 0.8 vs 17.7 +/- 0.8; pH 7.4:6.4 +/- 0.7 vs 11.7 +/- 0.5 arb. U/mg protein). In Goldblatt hypertensive rats the unclipped kidney, which is exposed to high blood pressure, revealed lower glomerular azocaseinolytic activity compared with the contralateral clipped kidney (pH 5.4:8.1 +/- 0.4 vs 12.9 +/- 0.5 arb. U/mg protein). In parallel, the cathepsin B content was also diminished in glomeruli from kidneys exposed to hypertension. When proteinases were followed in glomeruli from intact kidneys of rats fed protein-modified diets (fraction of casein 0.05, 0.20 or 0.60) a significant fall in the activities of cysteine proteinases, e.g. cathepsin B (casein 0.05:1,498 +/- 110 vs casein 0.60:914 +/- 84 microU/micrograms DNA), as well as metalloproteinases, e.g. collagenase (casein 0.05:233 +/- 14 vs casein 0.60:137 +/- 11 microU/micrograms DNA), occurred. These data indicate that in both early and late stages of glomerulosclerosis, proteolytic activities within the glomerulus tend to be reduced, which could allow extracellular matrix accumulation. Moreover, changes in dietary protein intake resulted in profound alterations of glomerular proteinases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

The NH2-terminal extension of rat liver arginyl-tRNA synthetase is responsible for its hydrophobic properties.

Rat liver arginyl-tRNA synthetase is found in extracts either as a component (Mr = 72,000) of the multienzyme aminoacyl-tRNA synthetase complex or as a low molecular weight (Mr = 60,000) free protein. The two forms are thought to be identical except for an extra peptide extension at the NH2-terminus of the larger form which is required for its association with the complex, but is unessential for catalytic activity. It has been suggested that interactions among synthetases in the multienzyme complex are mediated by hydrophobic domains on these peptide extensions of the individual proteins. To test this model we have purified to homogeneity the larger form of arginyl-tRNA synthetase and compared its hydrophobicity to that of its low molecular weight counterpart. We show that whereas the smaller protein displays no hydrophobic character, the larger protein demonstrates a high degree of hydrophobicity. No lipid modification was found on the high molecular weight protein indicating that the amino acid sequence itself is responsible for its hydrophobic properties. These findings support the proposed model for synthetase association within the multienzyme complex.

Amino Acid Sequence↗