[The evaluation of centric occlusion of a complete denture by mandibular kinesiography (MCK)].
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Biomedical subjects
Publications and source records attributed to C Y Yang.
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The complete amino acid sequence of proapolipoprotein (proapo) A-I of chicken high density lipoproteins was determined by sequencing overlapping peptides produced by trypsin, S. aureus V8 protease, and cyanogen bromide cleavage. There are 240 amino acid residues in mature chicken apoA-I. By direct sequence analysis of a cyanogen bromide peptide, we also determined the sequence of a 6-amino-acid prosegment which is present at approx. 10% the molar amount of the mature peptide in chicken plasma. Sequence comparison among apoA-I from chicken, human, rabbit, dog and rat, and secondary structure analysis indicate that while the degree of sequence homology is only moderate (less than 50% between chicken and man), there is good conservation of apoA-I secondary structure, especially in the N-terminal two-thirds of the protein in these widely separated species.
The primary structure of human apolipoprotein (apo) B-48 has been deduced and shown by a combination of DNA excess hybridization, sequencing of tryptic peptides, cloned complementary DNAs, and intestinal messenger RNAs (mRNAs) to be the product of an intestinal mRNA with an in-frame UAA stop codon resulting from a C to U change in the codon CAA encoding Gln2153 in apoB-100 mRNA. The carboxyl-terminal Ile2152 of apoB-48 purified from chylous ascites fluid has apparently been cleaved from the initial translation product, leaving Met2151 as the new carboxyl-terminus. These data indicate that approximately 85% of the intestinal mRNAs terminate within approximately 0.1 to 1.0 kilobase downstream from the stop codon. The other approximately 15% have lengths similar to hepatic apoB-100 mRNA even though they have the same in-frame stop codon. The organ-specific introduction of a stop codon to a mRNA appears unprecedented and might have implications for cryptic polyadenylation signal recognition and RNA processing.
Using an antibody against chicken apolipoprotein (apo) A-I, we identified multiple cDNA clones for the protein in two intestinal cDNA libraries in lambda gt11. The complete nucleotide sequence of chicken apoA-I cDNA was determined. The sequence predicts a mature protein of 240 amino acids, a 6-amino acid propeptide and an 18-amino acid signal peptide. Using a 32P-cDNA probe, we detected the presence of apoA-I mRNA in 21 day old chicken intestine, liver, kidney, spleen, breast muscle and brain. The primary sequence of apoA-I contains numerous tandem repeats of 11 and 22 residues in a manner similar to the mammalian proteins. Our analysis of apoA-I sequences from human, rabbit, dog, rat, and chicken indicates that the rate of amino acid substitution is considerably faster in the rat lineage than in other mammalian lineages.
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The amino acid sequence of human lecithin:cholesterol acyltransferase has been determined by degradation and alignment of peptides obtained from tryptic and staphylococcal digestions and the cleavage with cyanogen bromide and consisted of 416 amino acid residues. All of the tryptic peptides of lecithin:cholesterol acyltransferase were isolated and sequenced. Peptides resulting from digestion by staphylococcal protease, cyanogen bromide cleavage, or the combination of the two methods were employed to find overlapping segments. The N terminus of human lecithin:cholesterol acyltransferase was determined to be phenylalanine by sequencing the whole protein up to 40 residues while the C terminus was identified as glutamic acid through carboxypeptidase Y cleavage. Cys50 and Cys74 and Cys313 and Cys356 were identified as the two disulfide bridges while the free sulfhydryl groups were located at positions 31 and 184. The N-glycosylated sites of the protein were assigned to asparagines at positions 20, 84, 272, and 384. The active site of lecithin:cholesterol acyltransferase was identified as serine on position 181 according to its homology with other serine-type esterases which have a common structure of glycine-variable amino acid-active serine-variable amino acid-glycine (Gly-X-Ser-X-Gly) with the variable amino acids disrupting the homology. No long internal repeats or homologies with apolipoproteins were found. The secondary structure is consistent with the results of predictive algorithms. A simple model of the enzyme is proposed on the basis of available chemical data and predictive methods.
Ferritin is a complex of a hollow, spherical protein and a hydrous, ferric oxide core of less than or equal to 4500 iron atoms inside the apoprotein coat; the apoprotein has multiple (ca. 12) binding sites for monoatomic metal ions, e.g., Fe(II), V(IV), Tb(III), that may be important in the initiation of iron core formation. In an earlier study we observed that the oxidation of Fe(II) vacated some, but not all, of the metal-binding sites, suggesting migration of some Fe during oxidation, possibly to form nucleation clusters; some Fe(III) remained bound to the protein. Preliminary extended X-ray absorbance fine structure (EXAFS) analysis of the same Fe(III)-apoferritin complex showed an environment distinct from ferritin cores, but the data did not allow a test of the Fe cluster hypothesis. In this paper, with improved EXAFS data and with Mössbauer data on the same complex formed with 57Fe, we clearly show that the Fe(III) in the distinctive environment is polynuclear (Fe atoms with Fe-Fe = 3.5 A and TB = 7 K). Moreover, the arrangement of atoms is such that Fe(III) atoms appear to have both carboxylate-like ligands, presumably from apoferritin, and oxo bridges to the other iron atoms. Thus the protein provides sites not only for initiation but also for nucleation of the iron core. Sites commodious enough and with sufficient conserved carboxylate ligands to accommodate such a nucleus occur inside the protein coat at the subunit dimer interfaces. Such Fe(III)-apoferritin nucleation complexes can be used to study the properties of the several members of the apoferritin family.
Convergent beam electron diffraction (CBED) is a powerful technique for symmetry study of crystal. It has widespread application in physics and material sciences, as demonstrated in a recent superconducting oxide study. Using this technique, we have studied Ba-La-Cu-O superconductors with a transition temperature of about 40 degrees K and Ba-Y-Cu-O superconductors with a critical temperature (Tc) of about 90 degrees K. We have found that in Ba-La-Cu-O superconductors the superconducting phase La2-xBaxCuO4-y has a distorted K2NiF4-type structure and the space group Fmmm. The two other phases in Ba-La-Cu-O superconductors have also been studied. In our Ba-Y-Cu-O superconductors, the Ba2YCu3O7-x compound, which is responsible for 90 degrees K superconductivity, has two different space groups: An orthorhombic space group Pmmm and a tetragonal space group P4mm or P4/mmm.
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Survival data on colo-rectal cancer patients from eleven comprehensive cancer centers were analyzed to examine the effect of race, socioeconomic status and other factors on the probability of survival. Complete data on variables of interest were available for 3617 colon cancer patients (2545 Caucasians and 1072 Blacks) and 1528 rectal cancer patients (1179 Caucasians and 349 Blacks). No significant difference was observed between the races with respect to either the follow-up time or the censoring pattern. For each site, Caucasian patients had a lower risk of death at any time point compared to Black patients, and this difference was maintained within categories of disease stage, sex, age and SES. The race effect was statistically significant in all multivariate models. Moreover, only race was significant in models that considered both race and SES. For either cancer, the racial difference in survival was most prominent for localized disease.
This study proposed to determine whether the stimulation of insulin secretion observed in humans infused with fructose when glucose levels were elevated could be observed when fructose was consumed during postprandial hyperglycemia. At 2-wk intervals, healthy volunteers consumed drinks containing glucose, starch, glucose followed 20 min later by fructose, starch followed 20 min later by fructose, and water followed 20 min later by fructose. Fructose consumption following glucose or starch drinks produced significantly higher levels of plasma insulin, but not plasma glucose, as compared to corresponding drinks consumed without fructose. Ten subjects whose blood glucose response levels were above 155 mg% after a glucose-containing drink appeared to be particularly responsive to the effects of fructose with increases in insulin levels of 60-288%. Results indicate that oral fructose can be insulinogenic in humans when blood glucose levels are elevated.
This study describes the progressive effects on pancreatic enzyme activities from washings of the small intestine of rats fed diets containing either 62% starch (S) or fructose (F), with 0.6 mg copper/kg diet (-Cu) or 6.0 mg copper/kg diet (+Cu) from 21 to 61 d of age. Hepatic copper concentration of the copper-deficient groups was 50% of that of the copper-supplemented groups. Body and relative pancreatic weights were lower in the F-Cu dietary group than in any other group. Relative liver weight was significantly higher in the fructose dietary groups than in the starch dietary groups. There were significant carbohydrate (CHO) X week and Cu X week interactions for luminal amylase activities and the CHO X Cu X week interaction was significant for luminal lipase and trypsin activities. The lowest enzyme activities were observed in the F-Cu-fed rats. The CHO X week interaction was significant for chymotrypsin with the lowest enzyme activities in the fructose-fed rats. It appears that high dietary fructose and low dietary copper interact to produce greatly reduced pancreatic enzyme activities in small intestinal washings. We speculate that subsequent digestive and absorptive abnormalities during a period of rapid growth may account for the severe morbidity and mortality in copper-deficient, fructose-fed rats.
A controlled trial with synthetic protease inhibitor gabexelate mesilate (FOY) in the treatment of acute pancreatitis was conducted in a total of 42 patients. The age, sex, etiology of pancreatitis, initial serum amylase level, and amylase creatinine clearance ratio were comparable between FOY-treated and control groups. FOY did not alter the course of the disease, but there was a weak trend toward lower morbidity and mortality in the FOY-treated patients. These results may justify further, larger scale studies or evaluation of alternate dosage or route of administration.
The diagnostic and prognostic significance of IgM anti-HBc, studied by a solid phase u-antibody capture radioimmunoassay at a serum dilution of 1:4000, was prospectively evaluated in 73 adult patients with acute hepatitis seropositive for hepatitis B surface antigen (HBsAg). Of the 73 cases, 20 (27.4%) cleared their HBsAg within 6 months, while the remaining 53 (72.6%) did not. HBsAg seroconversion to its antibody occurred in 15 (93.8%) of the 16 patients positive for IgM anti-HBc with S/N ratios above 5.0, as did 5 (26.3%) of the 19 with S/N ratios between 2.1 to 5.0, and none (0%) of the 38 negative for IgM anti-HBc (S/N ratios less than 2.1). Therefore, a S/N ratio of IgM anti-HBc above 5.0 is diagnostic for acute type B hepatitis. However, low S/N ratios (2.1-5.0) of IgM anti-HBc were observed in the early stage of some patients with acute type B hepatitis, and would increase to a level greater than 5.0 when assayed again 1-2 weeks later. It was therefore suggested that repeated testing of anti-HBc IgM is mandatory for accurate diagnosis of acute type B hepatitis in patients whose initial serum specimens showed low S/N ratios of IgM anti-HBc. According to this criterion, only 22 (30.1%) of the 73 patients with acute hepatitis seropositive for HBsAg in Taiwan were true acute type B hepatitis, of whom 2 (9.1%) subsequently became chronic HBsAg carriers, while the remaining 51 (69.9%) were chronic HBsAg carriers with other superimposed forms of acute hepatic injury.
Synthetic human PTH N-terminal 1-34 peptide [hPTH-(1-34)] stimulates prostaglandin (PG) production by chick calvariae in culture. PGE2 was the predominant PG found by both RIA and HPLC. Stimulation of PGE2 synthesis was significant at 50 ng/ml (1.2 X 10(-8) M) hPTH-(1-34) and was dose dependent at concentrations up to 0.6 microgram/ml (1.4 X 10(-7) M). Continuous exposure of calvariae to hPTH-(1-34) showed that PGE2 production increased significantly by 1 h, reached a maximum at 24 h, and then persisted over 96 h. Indomethacin at concentrations above 5 X 10(-7) M inhibited PGE2 synthesis by both control and hPTH-(1-34)-treated bones. PTH-(1-34) stimulated bone cells to convert arachidonic acid to PGE2, but did not activate the bone to release stored arachidonate. In summary, our results show that hPTH-(1-34) stimulates PGE2 synthesis by chick calvariae. This endogenous PGE2 may be involved in bone remodeling.