Effects of taurine on microsomal enzyme activities involved in liver lipid metabolism of Wistar rats.
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Acyl Coenzyme A↗
Biomedical subjects
Y Sun
Publications and source records attributed to Y Sun.
Immunoscintigraphy with a new indium-111-labeled monoclonal antibody (MAb 1A3) in patients with colorectal cancer.
PURPOSE: This study was designed to evaluate a new anticolorectal carcinoma monoclonal antibody (1A3), conjugated with the bifunctional chelating agent N,N'-bis(2-hydroxybenzyl)1(4-bromoacetamidobenzyl)1,2-ethylenediam ine-N,N'- diacetic acid and labeled with indium-111, in a Phase I/II study involving 38 patients with localized or advanced colorectal cancer. METHODS: Patients were injected with indium-111-N,N'-bis(2-hydroxybenzyl) 1(4-bromoacetamidobenzyl)1,2-ethylenediamine-N,N'-diacetic acid-monoclonal antibody 1A3 (1-50 mg, 1-5 mCi) and imaged at two or three sessions one to five days later. Scintigraphic findings were compared with radiologic, pathologic, surgical, and other clinical findings to assess the accuracy of radioimmunoscintigraphy. RESULTS: At least one known tumor site was clearly defined by planar scintigraphy in 29 (76 percent) patients. Increased radioactivity was seen in 40 of 63 known tumor sites (37/43 abdominal-pelvic, 3/15 hepatic, and 0/5 pulmonary sites) without any apparent dose-related effects. Nineteen previously undetected sites were considered positive by imaging, and, of these, six were biopsy-proven tumor sites, four were probable tumor sites, three were definitely false positive sites, and six were probable false positive sites. Radioimmunoscintigraphy detected proven tumor in 15 of 16 patients with negative or equivocal computed tomography results. Of of the 28 patients with rectosigmoid cancer, 25 (89 percent) had positive studies with 34 of 47 tumor sites showing definite uptake on the scintigrams. This included 3 of 9 hepatic metastases. The only adverse reaction occurred in one patient who developed transient hives. Human anti-mouse antibody responses occurred in approximately one-half of the patients injected with doses of 10 or 50 mg. CONCLUSION: This study shows that radioimmunoscintigraphy with this indium-111-labeled monoclonal antibody is safe, it can detect most nonhepatic abdominal-pelvic tumors with a positive predictive value of 83 (44/53) percent, and it should prove to be useful, particularly in the diagnosis of recurrent rectal carcinoma.
Adenocarcinoma↗
Columbia respiratory-chamber indirect calorimeter: a new approach to air-flow modelling.
A new air-flow modelling approach for respiratory-chamber indirect calorimetry is introduced. Based on thermodynamic theory, differential equations describing the dynamics of the calorimeter are derived. These equations are then developed into a linear state space model that can be conceptualized as a modern control system. Furthermore, both the system/output noises and input/output delays are considered in the model in the context of real applications. Finally, system accuracy is analysed so that the parameters in the calorimeter can be selected to minimise the error in estimating energy expenditure in humans.
Basal Metabolism↗
Suitability of copper chloride as a reaction terminator for superoxide dismutase activity assay.
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Copper↗
DQA1*03 subtypes have different associations with DRB1 and DQB1 alleles.
Polymorphisms outside the hypervariable regions of HLA class II alleles that do not affect the peptide-binding site are probably not under selective pressure and could therefore be useful as markers of the evolutionary pathways of the HLA class II haplotypes. We have analyzed such a polymorphism in the variants of DQA1*03, which differ at residue 160 encoded in exon 3. Our study included homozygous BCLs of the 10th IHWS and samples of a multiracial panel of 723 unrelated subjects which were also typed for allelic variations in exon 2 by hybridization with SSOP. BCLs having DQA1*03 and 131 selected DQA1*03-positive samples were typed for the dimorphism in exon 3 that distinguishes DQA1*0301 and DQA1*0302. DQA1*0301 was found to be exclusively associated with DQB1*0302, while samples carrying DQB1*0201, 0301, 0303, and 0401 always had DQA1*0302. A few haplotypes carrying DQB1*0302 had DQA1*0302. The fact that DQA1*0301 is completely included in DQB1*0302, and not vice versa, suggests that DQA1*0301 may have arisen from a mutation in a haplotype containing DQA1*0302-DQB1*0302. DQB1*0302 was found to be associated with all DR4 subtypes, suggesting possibly that the current variants of DRB1-DR4 may be of more recent origin. DRB1*0405 was the only subtype of DR4 which was not associated with DQA1*0301 and had multiple associations with the DQB1 alleles, therefore, perhaps representing the oldest allele of this group.
Alleles↗
The endoscopic diagnosis and possible treatment of nerve root avulsions in the management of brachial plexus injuries.
The spinal cord, dorsal rootlets, and ventral rootlets at the cervical level were visualized by endoscopy in ten goats. It is currently possible to visualize and document avulsed rootlets. With refinement in techniques and instruments, it will be possible to perform repairs, transfers or implantation of avulsed rootlets in the brachial plexus.
Animals↗
Fibrosis and myocardial ACE: possible substrate and independence from circulating angiotensin II.
In order to determine the relation between myocardial fibrosis and (1) angiotensin converting enzyme (ACE) binding density, (2) receptor binding of ACE-related peptides, angiotensin II (AngII) and bradykinin (BK), and (3) the regulation of myocardial ACE by circulating Ang II, we used in vitro quantitative autoradiography to localize and assess ACE ([125I]351A), AngII receptor (125I[Sar1, IIe8]AngII), and BK receptor ([125I]Tyr8) binding densities in the rat myocardium. The experimental groups were (1) AngII (9 micrograms/h subcutaneously) or aldosterone (0.75 microgram/h subcutaneously in uninephrectomized rats on a high-sodium diet) administered by implanted minipump to chronically increase or decrease circulating AngII, respectively, (2) unoperated, untreated age- and sex-matched control rats, and (3) age- and sex-matched uninephrectomized control rats on a high-sodium diet. In the same heart studied at 2, 4, and 6 weeks of hormone treatment, serial sections were assessed for myocardial (hematoxylin and eosin) and fibrillar collagen (picrosirius red) morphology. The authors found that (1) marked ACE binding was coincident with sites of fibrous tissue that appeared in both ventricles as either a perivascular fibrosis of intramyocardial coronary arterioles or microscopic scarring in response to AngII or aldosterone infusion, (2) ACE binding was independent of circulating AngII, (3) BK, not AngII, receptor binding density was markedly increased at fibrous tissue sites, and (4) high-density ACE and BK receptor binding were anatomically coincident. Thus, in these experimental models, ACE is related to fibrous tissue formation where it may use BK, not angiotensin I, as a substrate, and its binding density is independent of circulating AngII.
Aldosterone↗
Effects of inoculation site and Matrigel on growth and metastasis of human breast cancer cells.
The co-injection of extracellular matrix components, such as Matrigel, with human tumour cells into nude mice has been reported to facilitate tumour formation and growth, but it is unknown whether such components exert similar effects on tumour progression and metastasis. Metastatic behaviour is known to be enhanced when tumour cells are implanted orthotopically, and it is inferred that full and efficient expression of this phenotype may involve some interactions with local connective tissue matrix. It was therefore decided to investigate whether manipulation of the mesenchymal environment by co-injection of extracellular matrix components, in the form of Matrigel, with human breast cancer cells into orthotopic or ectopic sites could augment their metastatic performance, as well as their growth at the site of inoculation. Standard aliquots of 10(6) cells of the polyclonal human breast carcinoma cell line MDA-MB-435, and of four clonal cell lines, two metastatic and two non-metastatic derived from it, were injected with and without Matrigel, orthotopically or subcutaneously into nude mice. The latent period of tumour formation at the inoculation site as well as final tumour size and metastatic performance at autopsy, 140 days after inoculation, were then assessed. The prevalence of metastasis of the parent, polyclonal, cell line and of its metastatic clones was increased if the cell inoculum was mixed with Matrigel. Non-metastatic clones were not induced to become metastatic by this treatment, but local tumour growth at the site of inoculation was enhanced in all experimental groups receiving Matrigel. Orthotopic inoculation acted synergistically with Matrigel to maximise both tumour growth and metastatic behaviour. The composition of the local extracellular matrix at the site of tumour growth influenced expression of the metastatic phenotype by cells which are constitutionally capable of this behaviour, but did not induce it in ones which are not. Previous reports that local tumour growth is facilitated by enrichment of the mesenchymal matrix are confirmed. The mechanisms by which such effects are exerted are worthy of study, to ascertain whether they might be subject to clinical manipulation designed to retard tumour growth and dissemination.
Animals↗
Angiotensin II receptor binding following myocardial infarction in the rat.
OBJECTIVE: The aim was to determine angiotensin II receptor binding and its relationship to angiotensin converting enzyme (ACE) binding and fibrous tissue formation in the rat heart. METHODS: A model of tissue repair (pericardiotomy and myocardial infarction with left coronary artery ligation) was used together with the following: quantitative in vitro autoradiography to determine angiotensin II receptor (125I[Sar1, Ile8]AngII) and ACE (125I-351A) binding densities. Angiotensin II receptor subtype was determined using an AT1 receptor antagonist (DuP753, losartan) and an AT2 receptor antagonist (PD123177). Five groups were studied: age and sex matched controls receiving this operative procedure without subsequent myocardial infarction (sham operated); rats with coronary artery ligation and myocardial infarction; rats with coronary artery ligation and lisinopril (20 mg.kg-1.d-1 in drinking water); sham operated rats receiving lisinopril; and unoperated rats which served as controls to pericardiotomy. Hearts were collected from each group on postoperative day 3 and weeks 1, 2, 4, and 8. RESULTS: There was (1) low angiotensin receptor binding in normal myocardium; (2) markedly increased angiotensin II receptor binding at the site of left ventricular myocardial infarction and endocardial fibrosis of the interventricular septum at day 3 and weeks 1, 2, 4, and 8; (3) high angiotensin II receptor binding in the pericardial fibrosis that followed pericardiotomy, and in the fibrosis that appeared in response to suture insertion around the left coronary artery, in both infarcted and sham operated rats; (4) total displacement of normal and connective tissue angiotensin II receptor binding by DuP753, but not by PD123177; (5) ACE inhibition by lisinopril, but no change in angiotensin II receptor binding, at all sites of fibrosis; and (6) significant attenuation by lisinopril of collagen formation in the visceral pericardium of sham operated controls. CONCLUSIONS: In this model of tissue repair, increased AT1 receptor binding density is associated with ACE binding and fibrillar collagen formation that appears within sites of fibrous tissue formation, including myocardial infarction, endocardial fibrosis, foreign body (silk suture), and pericardiotomy. AT1 receptors may play a role in mediating the fibrogenic response to tissue injury in the rat heart.
Angiotensin II↗
Angiotensin II associated cardiac myocyte necrosis: role of adrenal catecholamines.
OBJECTIVE: Cardiac myocyte necrosis is associated with an endogenous increase in angiotensin II or a subpressor dose of angiotensin II. In each case, raised plasma angiotensin II, together with aldosterone, results in cardiac myocyte necrosis followed by scarring. Arterial hypertension is non-contributory. The aim of this study was to determine whether myocyte necrosis is induced directly by angiotensin II, or indirectly by catecholamines or aldosterone released from adrenal glands in response to angiotensin II. METHODS: Right and left ventricular myocardium was examined over a two week period in rats receiving a subpressor yet cardiotoxic dose of angiotensin II (150 ng.min-1.kg-1 subcutaneously) alone or together with total adrenalectomy, bilateral medullectomy, or the aldosterone receptor antagonist spironolactone (150-200 mg.d-1.kg-1). Findings were compared to unoperated age/sex matched controls. Coronal sections obtained from the base, equator and apex of the heart were stained with antifibronectin antibody to detect myocyte injury, picrosirius red for fibrillar collagen, or haematoxylin and eosin. RESULTS: In both right and left ventricles (a) fibronectin labelling was distributed within injured cardiac myocytes and adjacent interstitium of both ventricles in rats receiving angiotensin II or angiotensin II plus spironolactone; (b) fibronectin labelling of myocytes was markedly diminished or absent in the ventricles of rats with total adrenalectomy or bilateral medullectomy; and (c) there was microscopic scarring of both ventricles after two weeks of either angiotensin II or angiotensin II plus spironolactone, but not in medullectomised or adrenalectomised animals. CONCLUSIONS: In the presence of increased circulating levels of angiotensin II, bilateral medullectomy and total adrenalectomy (in contrast to spironolactone) reduced myocyte injury and scarring of the right and left ventricular myocardium, suggesting that the cytotoxic effect of angiotensin II is largely indirect and related to circulating catecholamines released by the adrenal medulla.
Adrenal Medulla↗
Cardiac angiotensin converting enzyme and myocardial fibrosis in the rat.
OBJECTIVE: The aim was to test the hypothesis that cardiac angiotensin converting enzyme (ACE) is related to the accumulation of fibrous tissue in the heart. METHODS: A model of tissue repair (pericardiotomy with left coronary artery ligation) was used, together with the following: quantitative in vitro autoradiography (125I-351A) to determine ACE binding density; immunohistochemistry (monoclonal ACE antibody, 9B9) to identify cells expressing ACE; and in situ hybridisation to localise cells expressing type I collagen mRNA. Age and sex matched rats receiving this operative procedure without subsequent infarction (sham operated) served as controls to those with left ventricular myocardial infarction. Serial heart sections obtained from each group at 3 days and at 1, 2, 4, and 8 weeks following operation were examined for morphological evidence of injury and inflammatory cells (haematoxylin/eosin) and fibrillar collagen (picrosirius red). RESULTS: Following myocardial infarction: (a) on day 3, neutrophils and macrophages were present at the site of infarction, while fibrillar collagen and ACE binding were not increased compared with control; (b) at week 1, fibrillar collagen and ACE binding were present at the site of infarction and became progressively more advanced at 2, 4, and 8 weeks; (c) at week 2, there was increased ACE binding in the right ventricle and interventricular septum, when perivascular fibrosis of intramural coronary arteries and microscopic scars appeared, together with endomyocardial fibrosis of the septum; (d) there was marked ACE binding in the fibrosed visceral pericardium two weeks after operation in both myocardial infarction and sham operated groups; (e) there was type I collagen mRNA expression on postoperative week 1, localised within fibroblasts or fibroblast-like cells found at infarct and fibrous tissue sites in the right ventricle, septum, and pericardium; and (f) ACE-labelled cells included fibroblast-like cells, as well as macrophages and endothelial cells. CONCLUSIONS: Thus in this model of tissue repair, marked ACE binding density is associated with fibrillar collagen formation that appears within and remote to the site of myocardial infarction, including the pericardium. Cardiac ACE, originating from type I collagen producing cells, therefore represents an integral component of fibrous tissue formation in this rat model of tissue injury.
Animals↗
Identification and characterization of the protein product of gene 71 in equine herpesvirus 1.
Equine herpesvirus 1 (EHV-1) strain Ab4 gene 71 is predicted to encode a primary product with a M(r) of 80.1K. We have previously constructed a deletion/lacZ insertion mutant, ED71, and demonstrated that gene 71 is dispensable for growth of virus in cell culture. We have now constructed a gene 71 revertant, Re71. To identify and characterize the product of gene 71, we produced a specific antiserum, anti-71, against a beta-galactosidase fusion protein containing the carboxy terminus of the gene 71 polypeptide. Using the anti-71 serum, mutant ED71 and the revertant Re71, we have demonstrated that gene 71 encodes a 192K polypeptide. Experiments with glycosylation inhibitors revealed that the protein product of gene 71 is N-glycosylated and heavily O-glycosylated. When the 192K polypeptide is synthesized in the presence of monensin, the M(r) of the polypeptide is reduced to 80K, the predicted unmodified M(r) of the gene 71 polypeptide. The gene 71 product is found in virions and L particles in a fully processed form that runs as a diffuse band in electrophoresis, with a M(r) in excess of 200K. Immunofluorescence and virion surface labelling experiments showed that the polypeptide product of gene 71 is located on cellular membranes and the virion envelope. A time course of infection confirmed that gene 71 is regulated as a leaky late gene in infected cells. Finally, using wild-type EHV-1 Ab4, mutant ED71, revertant Re71 and two antibodies (P19 against EHV-1 glycoprotein gp300, and anti-71) we conclusively demonstrated that gene 71 encodes gp300. This contradicts published results with P19 alone, which indicated gp300 was the product of EHV-1 gene 28.
Amino Acid Sequence↗
Excited bands of 168Yb in an angular momentum projected theory.
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Journal Article↗
Varied signature splitting phenomena in odd proton nuclei.
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Journal Article↗
Nonlinear transforms of ECG signals for digital QRS detection: a quantitative analysis.
A class of algorithms has been developed which detects QRS complexes in the electrocardiogram (ECG). The algorithms employ nonlinear transforms derived from multiplication of backward differences (MOBD). The algorithms are evaluated with the American Heart Association ECG database, and comparisons are made with the algorithms reported by Okada and by Hamilton and Tompkins. The MOBD algorithms provide a good performance tradeoff between accuracy and response time, making this type of algorithm desirable for real-time microprocessor-based implementation.
Algorithms↗
Comparison of peptide enzyme-linked immunosorbent assay and radioimmunoprecipitation assay with in vitro-translated proteins for detection of serum antibodies to human papillomavirus type 16 E6 and E7 proteins.
Antibodies to human papilloma virus (HPV) type 16 (HPV-16) E6 and E7 proteins in serum are markers for HPV-associated invasive cervical carcinoma. We compared two assays, a radioimmunoprecipitation assay with in vitro-translated HPV-16 E6 and E7 proteins and an enzyme-linked immunosorbent assay (ELISA) with E6 and E7 synthetic peptides, for their abilities to discriminate serologically between patients with invasive cervical cancer and controls. Among the patients, antibody prevalences were higher by the E6 radioimmunoprecipitation assay (55.7%) than by the E6 peptide ELISA (15.5%), but among the controls, they were lower by the radioimmunoprecipitation assay (1.7%) than by the E6 peptide ELISA (5%). For E7, antibody prevalences among the patients were comparable by the radioimmunoprecipitation assay (43%) and the peptide ELISA (41%), but among the controls they were higher by the E7 peptide ELISA (17.4%) than by the radioimmunoprecipitation assay (4.1%). There was good agreement between the E7 radioimmunoprecipitation assay and the E7 peptide ELISA among patients but not among controls. In tests with representative sera, heat denaturation of the translated proteins resulted in a complete loss of reactivity to the E6 protein and a marked decrease in reactivity to the E7 protein. Our study showed that the radioimmunoprecipitation assay discriminates better than the peptide ELISA between patients with invasive cervical cancer and controls and that this is related to the ability of the radioimmunoprecipitation assay to detect conformational epitopes.
Antibodies, Viral↗
Cloning and characterization of the cDNA encoding a novel human pre-B-cell colony-enhancing factor.
A novel gene coding for the pre-B-cell colony-enhancing factor (PBEF) has been isolated from a human peripheral blood lymphocyte cDNA library. The expression of this gene is induced by pokeweed mitogen and superinduced by cycloheximide. It is also induced in the T-lymphoblastoid cell line HUT 78 after phorbol ester (phorbol myristate acetate) treatment. The predominant mRNA for PBEF is approximately 2.4 kb long and codes for a 52-kDa secreted protein. The 3' untranslated region of the mRNA has multiple TATT motifs, usually found in cytokine and oncogene messages. The PBEF gene is mainly transcribed in human bone marrow, liver tissue, and muscle. We have expressed PBEF in COS 7 and PA317 cells and have tested the biological activities of the conditioned medium as well as the antibody-purified protein in different in vitro assays. PBEF itself had no activity but synergized the pre-B-cell colony formation activity of stem cell factor and interleukin 7. In the presence of PBEF, the number of pre-B-cell colonies was increased by at least 70% above the amount stimulated by stem cell factor plus interleukin 7. No effect of PBEF was found with cells of myeloid or erythroid lineages. These data define PBEF as a novel cytokine which acts on early B-lineage precursor cells.
Amino Acid Sequence↗
Structural remodeling in hypertensive heart disease and the role of hormones.
In hypertension, the risk of adverse cardiovascular events, including heart failure, is increased in the presence of left ventricular hypertrophy. Morphological studies suggest that it is not the quantity but rather the quality, or structure, of myocardium that confers such risk. Iterations in tissue structure that appear in hypertensive heart disease include a remodeling of intramyocardial coronary arterioles, similar to that found in systemic organs, and a disproportionate accumulation of fibrillar collagen within their adventitia and neighboring interstitial space. Microscopic scars replacing necrotic cardiac myocytes are also evident. These expressions of fibrosis appear in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles and are linked to the renin-angiotensin-aldosterone system. Cardiac myocyte growth, the major determinant of myocardial mass, is related to ventricular loading. Mechanisms responsible for the reactive and reparative fibrosis with renin-angiotensin-aldosterone system activation are under investigation. In vitro quantitative autoradiography has identified angiotensin II, aldosterone, endothelin, and bradykinin receptors in the myocardium. A nonendothelial tissue angiotensin-converting enzyme, whose binding density is marked in the matrix of heart valves, adventitia, and sites of fibrosis, irrespective of its pathogenic basis, has also been found. This angiotensin-converting enzyme may be responsible for regulating local concentrations of angiotensin II and bradykinin that govern fibroblast collagen turnover. Based on a paradigm of discordant reciprocal regulation, in which a relative abundance of stimulators (eg, angiotensin II, aldosterone, and endothelins) of collagen synthesis exceeds inhibitors (eg, bradykinin, prostaglandins, and glucocorticoids), fibrous tissue appears.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗