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J M Lin

Publications and source records attributed to J M Lin.

87 records · Page 5Linked to original sources
PubMed1988

Complexity of myosin species in the avian posterior latissimus dorsi muscle.

The myosin content of the avian posterior latissimus dorsi muscle, a small fast-twitch muscle similar in fibre type to the much-studied pectoralis major muscle (type IIB), has been explored using high resolution chromatography of the proteolytic fragment known as subfragment-1 and of the products of its limited tryptic digestion, followed by N-terminal sequencing of selected peptides. The complexity of species found greatly exceeds that anticipated from the fibre-type homogeneity of the muscle and from previous studies (Bandman et al., Cell 29 (1982) 645-50; Lowey et al., J. Musc. Res. Cell Motility 4 (1983) 695-716; Crow & Stockdale Dev. Biol. 118 (1986) 333-42). A minimum of four heavy chain species were identified. One form, approximately 40% of the heavy chain complement, appears to be identical to the well-characterized type IIB isoform of the pectoralis major muscle. The remaining species differ from the pectoralis major form in primary sequence. None is identical to the post-hatch isoform of the pectoralis major muscle.

Amino Acid Sequence↗
PubMed1987

[The effect of prolactin on the early embryogenesis of mice in vitro].

It is said the prolactin (PRL) is correlated with fetal lung maturation during late pregnancy. However, there are few reports about PRL during early pregnancy and the period of peri-implantation. Recently, transient hyperprolactinemia at the preovulatory phase or after follicle aspiration for in vitro fertilization has been reported. Nonetheless, the effect of high PRL on the folliculogenesis and the early embryogenesis is still controversial. Moreover, some researchers reported that human fetal umbilical cord sera was good for the development of ova fertilized in vitro. Therefore, we studied the effect of graded concentrations of PRL (10, 30, 100 ng/ml) on the development of embryos fertilized in vivo or in vitro using ddY mice. We concluded that higher PRL levels caused a smaller number of developed embryos, in statistical significance, into blastocysts and hatched blastocysts. In general, embryos fertilized in vivo developed better than those fertilized in vitro.

Animals↗
PubMed1987

Change in chromatogram patterns after volatilization of some aroclors, and the associated quantitation problems.

PCBs with the highest vapor pressures (fewest chlorines) in Aroclors 1016, 1242, 1254 and 1268 were enriched in the vapor phase relative to the original Aroclor during volatilization from a glass surface for up to 8 hr. PCBs with the lowest vapor pressures (most highly chlorinated) were enriched in the corresponding residue. Thus, visual matching of gas chromatograms with those of Aroclor standards may not be sufficient to identify a specific Aroclor since the past history of a sample is often unknown. The enrichment also was detected using isomeric classes, but not using total chlorine content. The perchlorination method and the Webb-McCall method using all chromatographic peaks agreed quantitatively; this was not always so for the NIOSH multiple peaks and the Webb-McCall methods.

Air↗
PubMed1987

Selective enhancement of pentamidine uptake in the lung by aerosolization and delivery in liposomes.

We examined the tissue distribution of pentamidine, both as free drug and encapsulated in liposomes, after intravenous (iv) and aerosol administration in healthy rodents. After iv injection, drug levels in the lung were increased as much as 34-fold by administration in liposomes. Concurrently, peak liver uptake was increased 4-fold and renal deposition reduced 3-fold. Liposome-mediated lung delivery was highly dependent on liposome size. Decreasing liposome mean diameter from 2.5 to 0.4 micron reduced lung uptake of pentamidine 90-fold while affecting extrapulmonary organ deposition to a much lesser degree. Aerosol delivery of pentamidine produced high, sustained lung levels, with no evidence of drug clearance from the lung between 1 and 48 h after administration. Extrapulmonary drug levels produced by aerosol delivery were negligible throughout this period. There were no significant differences in the organ distribution of aerosolized free versus liposome-encapsulated drug, apparently because of sequestration of pentamidine within the lung. Comparison of drug levels in material recovered by bronchoalveolar lavage suggests that aerosol delivery of pentamidine produces substantially higher deposition in the alveolar space than does iv drug injection. Light and electron microscopic (EM) examination of lung, kidney, and liver after iv or aerosol administration of liposomes revealed no tissue abnormalities, although isolated platelet clumps were noted in pulmonary capillaries by EM examination.

Aerosols↗
PubMedDate not supplied

Temperature effect on chiral recognition of some amino acids with molecularly imprinted polymer filled capillary electrochromatography.

L-Aromatic amino acid imprinted polymers were prepared using azobisnitriles as either photoinitiators or thermal initiators at temperature ranging from 4 to 60 degrees C. Methacrylic acid (MAA) was used as functional monomer and ethylene glycol dimethacrylate (EDMA) was used as cross-linker. The result polymers were ground and sieved to particles < or = 10 microns, filled into the capillary columns and used for enantiomeric separations in capillary electrochromatographic (CEC) mode. The polymer particles < or = 25 were packed into high performance liquid chromatographic (HPLC) columns and used for enantioseparations in the HPLC mode. The mobility and chiral separation of some amino acids were studied on CEC and HPLC columns at different temperature. The relationships of separation factor and column temperatures and demonstrated in linear between logarithm of the separation factor (in alpha) and the inverse of absolute temperature (1/T). Some thermodynamic parameters, such as the apparent change of enthalpy (delta H zero) and the apparent change of entropy (delta S zero), were obtained using van't Hoff plots. The information obtained from the thermodynamic study is discussed in developing strategies for chiral recognitions of amino acids by molecular imprinting technique.

Amino Acids↗
PubMedDate not supplied

Inhibition of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone pulmonary metabolism and tumorigenicity in mice by analogues of the investigational chemotherapeutic drug 4-ipomeanol.

4-Ipomeanol (IPO) is an investigational chemotherapeutic drug with specific toxicity toward the lung. It is metabolically activated to reactive intermediates by cytochrome P450 enzymes present in Clara cells. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a highly carcinogenic tobacco-specific nitrosamine with organo-specificity for the lung. Like IPO, which it resembles structurally, it is metabolically activated by cytochrome P450 enzymes of rat Clara cells. We synthesized nontoxic analogues of IPO and tested their activities as inhibitors of the metabolism and tumorigenicity of NNK. The IPO analogues synthesized were 4-hydroxy-1-phenyl-1-pentanone (HPP), 7-hydroxy-1-phenyl-1-octanone (HPO), 4-hydroxy-1-(2-thienyl)-1-pentanone (HTP), and 4-hydroxy-1-(3-pyridyl)-1-pentanone (HPYP). When added to A/J mouse lung microsomal incubations, all compounds significantly inhibited the oxidative pathways of NNK metabolism--alpha-hydroxylation and pyridine N-oxidation--to varying extents. Inhibition of carbonyl reduction of NNK was generally less effective. Inhibition of alpha-hydroxylation by IPO, HPP, and HTP was more pronounced in incubations with lung microsomes than with liver microsomes. None of the IPO analogues showed significant toxicity when given to A/J mice at a dose of 25 mumol; IPO itself was lethal at this dose. HPP and HPO, at doses of 25 mumol, significantly inhibited lung tumor multiplicity in mice treated with NNK; the other analogues and IPO itself were ineffective. The results of this study provide new leads for development of inhibitors of NNK metabolism and chemical probes for the active site of P450 enzymes in Clara cells.

Animals↗
PubMedDate not supplied

Distinct conformers of alkylchrysene diol epoxide-deoxyguanosine adducts detected by proton NMR.

Proton NMR spectra, obtained in MeOH-d4, of the major DNA adduct of 5,7-dimethylchrysene-1,2-diol 3,4-epoxide, identified as 1(R),2(S),3(S)-trihydroxy-4(S)-(N2-deoxyguanosyl)-1, 2,3,4-tetrahydro-5,7-dimethylchrysene, showed the presence of two distinct conformers. One conformer, similar to those observed previously in spectra of peracetates of related DNA adducts of anti-diol epoxides of polynuclear aromatic hydrocarbons, had a chair-like conformation of the tetrahydrobenzo ring. The other conformer, which has not been previously observed, had a boat-like conformation of the tetrahydrobenzo ring. This conformer was converted to the chair-like conformer upon addition of D2O or trifluoroacetic acid to the MeOH-d4 solutions of the adduct. The new conformers were also observed in proton NMR spectra of major DNA adducts of 5-methylchrysene- and 5,6-dimethylchrysene-1,2-diol 3,4-epoxides.

Carcinogens↗
PubMedDate not supplied

Synthesis of Fjord region diol epoxides as potential ultimate carcinogens of dibenzo[a,l]pyrene.

Dibenzo[a,l]pyrene (DB[a,l]P) is one of the strongest polynuclear aromatic hydrocarbon carcinogens known. This paper describes the synthesis of potential ultimate carcinogens of DB[a,l]P: anti- and syn-11,12-dihydroxy-13,14-epoxy-11,12,13,14- tetrahydroDB[a,l]P (DB-[a,l]P-11,12-diol-13,14-epoxides). The method employed is also useful for the preparation of key intermediates for the synthesis of 11,12-dihydroxy-13,14-epoxy-11,12,13,14-tetrahydrobenzo-[g]chrysene (BgC-11,12-diol-13,14-epoxide). Photochemical cyclization of the appropriately substituted phenanthrylphenylethylenes provided 9-carbomethoxy-11-methoxyBgC (4) and 11-methoxyBgC (3). The former was converted by reduction, oxidation, one-carbon chain extension, and cyclization to 11-methoxy DB[a,l]P (7). Compounds 3 and 7 were converted by hydrolysis and oxidation to BgC-11,12-dione (10) and DB[a,l]P-11,12-dione (11), respectively. The diones are the precursors for the synthesis of the corresponding diol epoxides. anti- and syn-DB-[a,l]P-11,12-diol-13,14-epoxides 13 and 14 were prepared in 38% and 55% yields, respectively, from 11. Both diol epoxides had predominantly pseudodiequatorial hydroxyl groups, as seen in other sterically hindered diol epoxides.

Benzopyrenes↗
PubMedDate not supplied

Direct synthesis and characterization of site-specific adenosyl adducts derived from the binding of a 3,4-dihydroxy-1,2-epoxybenzo[c]phenanthrene stereoisomer to an 11-mer oligodeoxyribonucleotide.

Site-specifically modified oligonucleotides were obtained in milligram quantities by reacting racemic 3t,4r-dihydroxy-1,2t-epoxy-1,2,3,4-tetrahydrobenzo[c]phenanthrene (B[c]PhDE-2, or anti-B[c]PhDE) with the single deoxyadenosine (dA) residue in the oligodeoxynucleotide d(CTCTCACTTCC). Enzyme digestion of the covalently modified oligonucleotides with the exonuclease spleen phosphodiesterase yielded covalently linked B[ca]PhDE-N6-deoxyadenosyl monophosphate (dAMP) adducts. Comparisons of the reverse phase HPLC retention times and CD spectra of these B[c]PhDE-3'-dAMP mononucleotide adducts, with those of standards derived from the reaction of the enantiomers (+)- and (-)-anti-B[c]PhDE with 3'-dAMP, show that two major oligonucleotide adducts (I and II) were obtained upon reacting racemic anti-B[c]PhDE with d(CTCTCACTTCC). In oligonucleotide adduct I, the lesion is a (+)-trans-anti-B[c]PhDE-N6-dA residue, and in oligonucleotide adduct II it is a (-)-trans-anti-B[c]PhDE-N6-dA residue. These assignments were further confirmed using a standard 32P postlabeling assay of B[c]PhDE-3'-dAMP mononucleotide adducts obtained from the digestion of oligonucleotides I and II by spleen phosphodiesterase. The melting points (Tm) of duplexes of modified oligonucleotides I and II and their natural complementary strands are not affected significantly by the presence of the covalently bound benzo[c]phenanthrenyl residues. Opposite stereoselective resistance to enzyme digestion by the exonucleases snake venom phosphodiesterase and spleen phosphodiesterase is exhibited by the stereoisomeric (+)-trans- and (-)-trans-anti-B[c]PhDE-modified oligonucleotide adducts I and II; these results are consistent with the intercalative insertion of the benzo[c]phenanthrenyl residues on the 5'-side of the modified dA residue in adduct I, and its insertion on the 3'-side of the dA residue in adduct II, as observed in the duplexes by high resolution NMR techniques [Cosman et al. (1993) Biochemistry 32, 12488-12497, and Cosman et all, Biochemistry, in press.

Adenosine↗
PubMedDate not supplied

Dimethylformamide-induced liver damage among synthetic leather workers.

Prevalence of liver injury associated with dimethylformamide (DMF) exposure was determined. Medical examinations, liver function tests, and creatine phosphokinase (CPK) determinations were performed on 183 of 204 (76%) employees of a synthetic leather factory. Air concentrations of solvents were measured with personal samplers and gas chromatography. The concentration of DMF in air to which each worker was exposed was categorized. High exposure concentrations of DMF (i.e., 25-60 ppm) were significantly associated with elevated alanine aminotransferase (ALT) levels (ALT greater than or equal to 35 IU/l), a result that did not change even after stratification by hepatitis B carrier status. Modeling by logistic regression demonstrated that exposure to high concentrations of DMF was associated with an elevated ALT (p = .01), whereas hepatitis B surface antigen (HBsAg) was slightly but independently associated with an elevated ALT (p = .07). In those workers who had normal ALT values, there occurred still significantly higher mean ALT and aspartate aminotransferase (AST) activities, especially among those who were not HBsAg carriers. A significant association existed between elevated CPK levels and exposure to DMF. However, an analysis of the CPK isoenzyme among 143 workers did not reveal any specific damage to muscles. This outbreak of liver injury among synthetic leather workers is ascribed to DMF. It is recommended that the occupational standard for DMF and its toxicity among HBsAg carriers be evaluated further.

Adult↗
PubMedDate not supplied

Left atrial appendage blood flow determined by transesophageal echocardiography in patients with complete atrioventricular block.

Function of the left atrial appendage (LAA) represented by LAA outflow is an important predictor for thrombus formation in patients with nonrheumatic atrial fibrillation, but the pattern of LAA flow in patients with complete atrioventricular (AV) block has rarely been studied. Twenty-one patients with complete AV block and an implanted VVI or VVIR pacemaker were studied with transesophageal echocardiography. The LAA outflow velocity obtained during the ventricular diastolic phase was significantly higher than that obtained during the ventricular systolic phase (41.5 +/- 6.0 vs. 34.9 +/- 9.7 cm/s; p < 0.001). The LAA inflow velocity obtained during the ventricular diastolic phase was also significantly higher that that obtained during the ventricular systolic phase (29.9 +/- 7.8 vs. 26.4 +/- 5.3 cm/s; p < 0.01). In addition, the LAA outflow and inflow velocity time integrals during the ventricular diastolic phase were significantly higher than those during the ventricular systolic phase (4.66 +/- 0.96 vs. 4.08 +/- 1.05 cm, p < 0.01, and 2.81 +/- 0.77 vs. 2.56 +/- 0.65 cm, p < 0.05, respectively). Thus, due to both diastolic augmentation of the LAA flow related to active atrial contraction and minor early diastolic LAA flow formation, left ventricle diastolic function might have some influence on LAA flow. Thus may have implications for the pathogenesis of LAA thrombi in left ventricular dysfunction.

Adult↗
PubMedDate not supplied

Relationship of pulmonary venous flow pattern to mean left atrial pressure and phasic pressure change.

To assess the correlation of pulmonary venous flow pattern with the magnitude of the dynamic change in left atrial pressure (i.e. x and y descents) and to elucidate the way how pulmonary venous flow pattern reflects left atrial pressure, we studied 35 patients with normal sinus rhythm undergoing transesophageal echocardiography and cardiac catheterization. The ratio of peak systolic/diastolic flow correlated well with the ratio of x/y descent (r = 0.88) and the ratio of systolic/diastolic velocity-time integral (r = 0.89). The correlation between the ratio of systolic/diastolic flow or velocity-time integral and mean atrial pressure was less strong (r = -0.49 and -0.70, respectively). We conclude that the ratio of peak systolic/diastolic flow velocity, or the ratio of systolic/diastolic velocity-time integral of pulmonary venous flow reflects the phasic change in left atrial pressure more appropriately than the mean left atrial pressure. Due to the good correlation between the phasic change in left atrial pressure and pulmonary venous flow pattern, the flow pattern of pulmonary veins could be used to identify diseases with specific patterns of left atrial pressure.

Adult↗
PubMedDate not supplied

Interference of mitral valve stenosis with left ventricular diastole and left atrial appendage flow.

Atrial fibrillation (AF) has been reported as an independent risk factor of systemic thromboembolism. Almost half of the left atrial thrombi are located in the left atrial appendage (LAA). LAA function, reflected by LAA flow, thus has an influence on the potential of distal embolic complications. To identify factors other than atrial contraction that influence LAA flow during AF, transthoracic and transesophageal echocardiographic studies were performed on 130 patients. Seventy patients with nonrheumatic AF were divided into two groups with higher peak LAA outflow velocity (group 1) and lower peak LAA outflow velocity (group 2) at the ventricular systolic phase. Sixty patients with rheumatic AF were classified as group 3. Group 1 had a higher peak LAA outflow velocity than group 2 at both the ventricular systolic and diastolic phases. Group 2 had a higher peak LAA outflow at the ventricular diastolic phase than group 3 (18.9 +/- 8.0 vs. 11.8 +/- 7.5 cm/s, p < 0.001), whereas there was no significant difference in the peak LAA outflow at the ventricular systolic phase between the two groups (9.6 +/- 4.0 vs. 10.8 +/- 6.8 cm/s, p = NS). Group 3 was subdivided according to mitral valve area. Patients with severe mitral stenosis (mitral valve area < 1 cm2) had a significantly lower diastolic augmentation of LAA outflow velocity (difference of LAA outflow velocity between ventricle systole and diastole) than patients with mild to moderate stenosis (0.5 +/- 3.2 vs. 2.6 +/- 4.9 cm/s, p < 0.05). In conclusion, patients with rheumatic AF, especially those with severe mitral stenosis, have a lower diastolic augmentation of LAA outflow velocity. The lower diastolic augmentation of the LAA outflow velocity at the ventricular diastolic phase might result from interference with the suction effect of the left ventricular diastole by the stenotic mitral valve.

Aged↗
PubMedDate not supplied

Influence of left ventricular diastole on left atrial appendage blood flow in patients with nonrheumatic atrial fibrillation.

The function of the left atrial appendage (LAA) reflected by the Doppler flow velocity at the outlet of the left atrial appendage has been reported to be correlated with spontaneous echo contrast and thrombus formation. To evaluate the influence of left ventricular diastole on LAA flow during atrial fibrillation (AF), 81 patients with chronic nonrheumatic AF were studied by transesophageal echocardiography. The peak outflow velocity of LAA during ventricular diastole was higher than that during ventricular systole (0.23 +/- 0.14 vs. 0.15 +/- 0.13 m/s, p < 0.001). The peak inflow velocity of LAA during ventricular diastole was also higher than that during ventricular systole (0.22 +/- 0.15 vs. 0.18 +/- 0.11 m/s, p < 0.01). Patients with a good left ventricular ejection fraction have a significantly higher peak LAA outflow velocity and a larger diastolic augmentation of LAA outflow (defined by the difference of LAA outflow between systolic and diastolic phases) than patients with an impaired left ventricular function. Thus, left ventricular diastole might have an influence on LAA flow during AF. In addition, the left ventricular function might be considered a predictor of subsequent thromboembolism from the viewpoint of its effect on LAA flow in patients with nonrheumatic AF.

Adult↗