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Biomedical subjects

T H Lin

Publications and source records attributed to T H Lin.

At least 127 records · Page 7Linked to original sources
PubMed1991

Prostaglandin E2 from macrophages of murine splenocyte cultures inhibits the generation of lymphokine-activated killer cell activity.

The present work investigated the association between prostaglandin E2 (PGE2) from macrophages and its inhibition of murine lymphokine-activated killer (LAK) cell generation. The coculture of indomethacin with interleukin-2 (IL-2) augmented LAK cell activity in an indomethacin dose-response manner, and diminished PGE2 content in the corresponding culture supernatant in a reverse dose-response manner. The correlation between the increase in LAK cell activity and the decrease in PGE2 content was highly significant. Identical results were obtained with diclofenac. A profound inhibition of LAK cell activity by exogenous PGE2 in a dose-response manner was detected. Polyclonal anti-PGE2 antiserum augmented in a dose-dependent manner the LAK cell activity, by neutralizing PGE2 in the medium. A reduction of PGE2 content in the culture supernatant was also detected when the macrophage subpopulations were cultured and was indomethacin dose-dependent. In comparison with that of normal mouse splenocytes, the incubation of whole splenocytes of tumor-bearing mice, which contained a greater subpopulation of macrophages (24% vs. 12%), produced a greater PGE2 content and a correspondingly depressed LAK cell activity. Additionally, PGE2 reduced protein kinase C (PKC) activity along with LAK cell activity generated from macrophage-depleted T cells and natural-killer-like cells. These results overall indicate that PGE2 from macrophages in murine splenocyte cultures inhibits the LAK cell generation, and PKC may be involved in the inhibition mechanism.

Adenocarcinoma↗
PubMed1991

Assessment of microleakage of cervical restorations.

Cervical lesions restored with composite resin seem to be more susceptible to marginal leakage, because the gingival margin is usually placed in cementum and/or dentin. The purpose of this study was to evaluate the effectiveness of five dentinal bonding agents, four composite resins and a glass ionomer cement in eliminating marginal gaps in an extraoral model. This study was accomplished using extracted human teeth and dye penetration method. The results indicated that none of the available dentinal bonding agents was able to eliminate marginal gaps completely. The cavities restored with the two component type dentinal adhesives leaked less than the negative control, glass ionomer cement.

Dental Cements↗
PubMed1991

Prognostic factors of stage Ib cervical carcinoma treated by radical abdominal hysterectomy.

From 1982 to 1984, 189 patients with stage Ib carcinoma of the uterine cervix underwent radical abdominal hysterectomies as primary treatment at Chang Gung Memorial Hospital. Of these patients, six were lost to follow-up. Nineteen of the 183 patients with regular follow-up recurred at intervals of from 9 to 55 months. An assessment of prognostic factors was made by reviewing the chart and pathological findings and correlating them with the patient's present status. Using univariate analysis, bulky tumor size was found to bear the greatest risk of tumor recurrence. Six of the 15 patients (40%) with a diameter of more than 4 cm recurred. The other risk factors included parametrial involvement, histologic type of adenosquamous or adenocarcinoma, lymph node metastasis, poor differentiation, deep cervical stromal invasion, and lymphatic or vascular space invasion. In conclusion, analysis of prognostic factors identified a group of patients at high risk of recurrence and decreased survival, for whom prospective trials of adjunctive treatment should be considered.

Adenocarcinoma↗
PubMed1990

Synthesis of specifically deoxygenated ligands related to (1----6)-beta-D-galacto-oligosaccharides, and studies on their binding to monoclonal antigalactan antibodies.

Synthetic deoxygenated derivatives of methyl beta-glycosides of (1----6)-beta-D-galacto-oligosaccharides were prepared, and their binding to antigalactan monoclonal antibodies X24 and J539 (Fab') was studied. The results suggest the involvement of an additional, critical hydrogen bond in the highest affinity subsite (A), which now appears to require two hydrogen bonds from the 2- and 3-hydroxyls of the galactosyl residue to the protein, and one from the protein to O-4 of that residue. The data obtained with a series of oligosaccharides deoxygenated at position 3(1), 3(2), 3(3), 4(1), 4(2), or 4(3) support the binding patterns and subsite-arrangement inferred previously from studies with large numbers of deoxyfluoro-substituted ligands and this family of antibodies.

Antibodies, Monoclonal↗
PubMed1990

Enhancement of murine lymphokine-activated killer cell activity by retinoic acid.

Since retinoids have been suggested to be capable of potentiating immunity, the present study was undertaken to determine the effect, if any, on lymphokine-activated killer (LAK) cell activity by retinoic acid, an active metabolite of vitamin A and a differentiation enhancer. Retinoic acid alone was shown to induce no cytotoxicity generated from nylon wool-treated nonadherent murine (BALB/c) splenocytes against natural killer-resistant, LAK-sensitive syngeneic target tumor cells. When combined with human recombinant interleukin-2 (IL-2), retinoic acid augmented LAK cell activity in both a dose- and time-dependent manner. The augmentation was detected at 10(-10) M retinoic acid and reached the maximum at 10(-7) M, a greater than 200% increase in lytic activity. Kinetic study revealed that retinoic acid augmented significantly LAK cell activity when incubated in IL-2-containing culture as short as for 6 h before cytotoxicity was measured. The removal of retinoic acid from culture resulted in the loss of the augmentation. Retinoic acid was found to augment LAK cell activity in a wide range of IL-2 concentrations (750-12,000 IU/ml), even at 6,000 IU/ml where the maximal induction of LAK cell activity had been reached. No phenotype or proliferation of LAK cells was altered by the addition of retinoic acid to IL-2-containing culture. However, cellular serine protease activity, measured as N-alpha-benzyloxycarbonyl-L-lysine thiobenzyl-esterase, in LAK cells was increased by retinoic acid also in a dose- and time-dependent manner. The increase in LAK cellular serine protease activity was significantly correlated with that of augmented LAK cell activity. Overall these results demonstrated that IL-2-induced LAK cell activity was enhanced by retinoic acid and that the augmentation may be mediated by means of enhanced expression of cellular serine protease activity. This study also suggests that, in addition to its use in chemoprevention of cancer, retinoic acid is of potential in adoptive immunotherapy.

Animals↗
PubMed1990

Interfacial strengths of various alloy surface treatments for resin-bonded fixed partial dentures.

A practical method for bonding or rebonding the resin-bonded retainer is eagerly being sought by general practitioners. This research introduces a new test apparatus for evaluating bond strength of base metal alloys after various alloy surface treatments. Five commercial base metal alloys and a resin luting cement for resin-bonded fixed partial dentures were examined. Sandblasting, oxidation, or etching treatment were determined to be effective in increasing the adhesive strength for the tested alloys. No statistical differences between various surface treatments were found for bonding of Unitbond metal. Inexpensive sandblasting, along with ultrasonic washing, provided superior bonding strengths for Biobond II and Litecast B materials. Electrochemical treatment was suitable for Wiron 77 and Lab metals.

Acid Etching, Dental↗
PubMed1990

Inappropriate adrenal androgen secretion with once-a-day corticosteroid therapy for congenital adrenal hyperplasia.

To determine whether cortisone acetate given as a single daily dose would be as effective as the same amount divided into three doses in suppressing adrenal androgen secretion in congenital adrenal hyperplasia, we studied three patients with the salt-losing variety, who were judged to have been adequately treated during the previous year. Each patient was receiving cortisone acetate, 20.6 to 22.6 mg/m2 body surface area per day, divided into three doses, and 9 alpha-fluorohydrocortisone, 0.05 to 0.1 mg/day. Their spontaneous and adrenocorticotropic hormone-stimulated blood concentrations of 17 alpha-hydroxyprogesterone, androstenedione, and testosterone were measured initially and were normal. Cortisone acetate was then given once a day in the same total daily dose. After 3 months, plasma adrenocorticotropic hormone concentration was increased in all three patients, and in two of them the plasma levels of 17 alpha-hydroxyprogesterone and androstenedione were also increased. In the third patient, after 7 months of once-daily therapy, plasma levels of 17 alpha-hydroxyprogesterone and androstenedione were increased. We conclude that a physiologic replacement dosage of cortisone acetate given once daily is not effective in controlling excessive adrenal androgen secretion in congenital adrenal hyperplasia.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Effects of protein binding and experimental disease states on brain uptake of benzodiazepines in rats.

The brain uptake of a number of benzodiazepines with different lipophilic and protein binding characteristics was investigated in male Sprague-Dawley rats using the rapid intracarotid artery injection technique. When the compounds were administered as a solution in Ringer's buffer, pH 7.4, the uptake was in the order of [14C]diazepam greater than [14C]L-663,581 (anxiolytic agent) greater than [3H]L-364,718 (morphine analgesia potentiator) greater than [14C]L-365,260 (anxiolytic agent) and their extraction ratio values were 71.0 +/- 6.8, 65.0 +/- 12.0, 42.0 +/- 5.0 and 6.0 +/- 2.0%, respectively. The respective permeability-surface product values were 0.755 +/- 0.152, 0.647 +/- 0.180, 0.329 +/- 0.05 and 0.035 +/- 0.011 ml/min/g. The rank order of brain extraction did not correlate well with the drugs' lipophilicity determined by octanol-buffer partition coefficient. For example, L-365,260 had the highest octanol/buffer partition coefficient, but the lowest brain extraction. Plasma protein binding significantly decreased the uptake by the brain but to a lesser extent than that predicted from the unbound drug fraction in vitro, suggesting that drug binding to plasma protein did not limit the transport of drug through the blood-brain barrier. For one compound, L-364,718, the extraction ratio and permeability-surface product values were increased markedly in CC1(4)-induced hepatic injury. Other disease states, uranyl nitrate-induced renal failure and streptozotocin-induced diabetes, had no apparent effect on the uptake of the compounds tested. The effect of disease state on the brain uptake of drug appeared to be dependent on the type of disease and the type of drug studied.

Animals↗
PubMed1989

Secondary structural analysis of retrovirus integrase: characterization by circular dichroism and empirical prediction methods.

The retrovirus integrase (IN) protein is essential for integration of viral DNA into host DNA. The secondary structure of the purified IN protein from avian myeloblastosis virus was investigated by both circular dichroism (CD) spectroscopy and five empirical prediction methods. The secondary structures determined from the resolving of CD spectra through a least-squares curve fitting procedure were compared with those predicted from four statistical methods, e.g., the Chou-Fasman, Garnier-Osguthorpe-Robson, Nishikawa-Ooi, and a JOINT scheme which combined all three of these methods, plus a pure a priori one, the Ptitsyn-Finkelstein method. Among all of the methods used, the Nishikawa-Ooi prediction gave the closest match in the composition of secondary structure to the CD result, although the other methods each correctly predicted one or more secondary structural group. Most of the alpha-helix and beta-sheet states predicted by the Ptitsyn-Finkelstein method were in accord with the Nishikawa-Ooi method. Secondary structural predictions by the Nishikawa-Ooi method were extended further to include IN proteins from four phylogenetic distinct retroviruses. The structural relationships between the four most conserved amino acid blocks of these IN proteins were compared using sequence homology and secondary structure predictions.

Amino Acid Sequence↗
PubMed1989

Growth hormone testing in short children and their response to growth hormone therapy.

Because current concepts of growth hormone (GH) testing and GH treatment have become controversial, we investigated the GH secretory patterns in children with normal and short stature. Twenty-four-hour serum GH levels were evaluated in three groups of children. Group 1 was composed of children with normal height (mean height = 0.02 SD, n = 33); group 2 was composed of short children (less than 5th percentile, n = 63) with normal results on provocative GH testing; and group 3 was composed of short children (less than 5th percentile, n = 7) with subnormal results on provocative GH testing. Mean +/- SD (range) GH levels during 24-hour studies of GH secretion were 1.6 +/- 1.1 (0.5 to 5.6), 1.8 +/- 1.2 (0.6 to 6.3), and 0.9 +/- 0.4 (0.5 to 1.7) ng/ml in groups 1, 2, and 3, respectively. No statistical difference existed in mean GH levels between groups 1 and 2 or between groups 1 and 3. The mean GH concentration from 24-hour studies in group 2 children did not correlate with chronologic age, height standard deviation, growth rates, or insulin-like growth factor 1 levels. The linear growth rate of 26 of 28 children in group 2 who received GH therapy for 6 months improved by 2 cm/yr or more; the mean +/- SD growth rate was 4.0 +/- 1.3 and 8.8 +/- 2.0 cm/yr during control and treatment periods, respectively, for these 28 children. Mean GH levels from testing did not predict response to GH during 6 months of therapy. Children with slower growth rates responded better to GH therapy (p less than 0.05). We conclude that (1) in 24-hour studies, GH levels in normal children overlapped with those of short children, including those with classic GH deficiency, (2) in 24-hour studies, GH levels did not predict responses of linear growth to short-term GH treatment, nor did they correlate with children's heights or growth velocities, and (3) the majority of short children in group 2 treated with GH for 6 months had an increase in linear growth velocity, the mean +/- SD change being 4.8 +/- 2.0 cm/yr.

Child↗
PubMed1988

Dialyzable serum cofactor(s) required for the protein-mediated transport of DL-propranolol into rat brain.

To elucidate the characteristics of promotion factor(s) in rat serum required for the protein-mediated transport of drugs into the brain, we examined the brain uptake of DL-propranolol as a model drug using the in vivo brain uptake index (BUI) method in rats. The protein-mediated transport was not observed in rats injected with the buffer solution containing either various concentrations of purified rat alpha 1-acid glycoprotein (alpha 1-AGP) or rat albumin. When the filtrate from rat serum was used as an injection vehicle to which a physiological concentration of purified rat serum protein(s) was added, the protein-mediated transport of DL-propranolol was observed in the rat brain. Moreover, the ability of protein-mediated transport of DL-propranolol was reduced in rats injected with the dialyzed serum compared with the undialyzed serum. These results suggest that the dialyzable promotion factor in serum is required for the protein-mediated transport of DL-propranolol into the brain.

Animals↗
PubMed1988

Autoradiographic localization of epidermal growth factor receptors to all major uterine cell types.

We have recently studied the structure and function of the uterine epidermal growth factor (EGF) receptor, its hormonal regulation, and its possible role in estrogen-induced uterine DNA synthesis. Since the uterus is composed of multiple cell types, we sought, in the work reported here, to localize EGF binding in this organ by autoradiography. Prior to the actual autoradiography, we performed a companion series of experiments to insure that EGF binding to uterine tissue in situ represented a true receptor interaction. Uteri from immature female rats were incubated in vitro with 125I-EGF at 25 degrees C. Tissue binding was maximal within 120 min and remained constant for at least an additional 120 min. This binding of labeled EGF was largely abolished by excess unlabeled EGF but not by other growth factors, indicating that binding was to specific receptors. The binding of 125I-EGF was saturable and reached a plateau at 4-8 nM; specific binding was half-maximal at 1-2 nM EGF. In situ cross-linking studies revealed that 125I-EGF was bound predominantly to a 170,000 MW EGF receptor similar to that seen in isolated uterine membranes. Incubation of uteri with 125I-EGF followed by autoradiography revealed binding to epithelial cells, stroma, and myometrium. These results provide evidence for the presence of specific EGF receptors in all major uterine cell types of the immature rat.

Animals↗
PubMed1988

Regulation of deoxyribonucleic acid polymerase activity in uterine luminal epithelium after multiple doses of estrogen.

Estradiol (E2) exerts both inhibitory and stimulatory effects on DNA synthesis in the rat uterine luminal epithelium (LE). This inhibitory effect is due to a shift in the time course of DNA synthesis, i.e. in animals receiving a single injection of E2, a peak of DNA synthesis occurs 24 h after treatment, but in animals receiving multiple injections of E2, DNA synthesis is suppressed until 10-12 h after hormone treatment ceases. In these previous studies LE DNA synthesis was assessed by measuring tritiated thymidine incorporation. In the present study, we sought to determine if the molecular basis for this decrease in DNA synthesis was due to a suppression of DNA polymerase activity in LE nuclei. Animals receiving a single injection of E2 exhibit a peak of nuclear DNA polymerase activity 20-24 h later. Animals receiving multiple injections of E2 (0, 12, 15, and 18 h) show more than a 50% decrease in DNA polymerase activity at 20-24 h, due to a shift in the maximum increase in enzyme activity to 32-36 h after the initial treatment. The observed differences between these groups are not due to different levels of DNase activity or different degrees of leakage of the nuclear enzyme. The observed enzyme activity is due to DNA polymerase-alpha, since it requires ATP as well as deoxyribonucleoside triphosphates, and is aphidicolin sensitive. These results indicate that the inhibitory effect of E2 on LE DNA synthesis is due at least in part to a suppression of nuclear DNA polymerase-alpha activity.

Animals↗
PubMed1988

Kinetic analysis of phenytoin disposition in rats with experimental renal and hepatic diseases.

The pharmacokinetics of phenytoin (DPH) was investigated in rats with uranyl nitrate induced renal failure, and with D-galactosamine induced hepatic failure. The serum disappearance of DPH after 10 mg/kg i.v. dose followed a two-exponential decline in normal and both types of intoxicated rats. The serum disappearance half-life (t1/2) and the volume of distribution (Vd) significantly increased in both types of intoxicated rats, while the total blood clearances (CLb) significantly decreased. The serum unbound fraction (fu) of DPH significantly increased in both types of intoxicated rats. The blood to plasma concentration ratio (RB) of DPH significantly increased in the uranyl nitrate-treated rats, while that of the D-galactosamine-treated rats did not show significant alteration. The tissue to serum concentration ratios (Kp) of most of tissues studied after i.v. bolus injection of DPH increased in both types of intoxicated rats. Except for the lung of the D-galactosamine-treated rats, the tissue to serum unbound concentration ratio (Kpu) of other tissues did not show a significant alteration. This suggested that the tissue uptake and/or binding of DPH is not affected by uranyl nitrate or D-galactosamine intoxication and that the increases in Vd and Kp are due mainly to the decrease in serum protein binding. The hepatic intrinsic clearance of unbound DPH (CLuint,H) also decreased in both types of intoxicated rats. Thus, the uranyl nitrate and D-galactosamine intoxication caused the increase in fu and the decrease in CLuint,H and these results may explain the significant decrease in CLb and increases in Vd and t1/2. The tissue concentration-time courses of DPH were predicted by a physiciologically based pharmacokinetic model and good agreement between the predicted and observed values in normal and in both types of intoxicated rats were obtained for serum, liver, kidney, brain and muscle.

Acute Kidney Injury↗
PubMed1988

Renal handling of drugs in renal failure. I: Differential effects of uranyl nitrate- and glycerol-induced acute renal failure on renal excretion of TEAB and PAH in rats.

Two etiologically different models of experimental acute renal failure were induced in rats by administration of either glycerol or uranyl nitrate. Both compounds caused a substantial decrease in the glomerular filtration rate (GFR) and the net tubular secretion of tetraethylammonium bromide (TEAB) and para-aminohippuric acid (PAH). The degree of renal impairment induced by uranyl nitrate and glycerol appeared to be dose related. Deprivation of drinking water 24 hr before the administration of glycerol potentiated the renal damage. In uranyl nitrate-induced renal failure, the decline of the net tubular secretion for TEAB and PAH was not proportional to the decrease in GFR; the secretion process deteriorated faster than the GFR. For example, when 0.5 mg/kg uranyl nitrate was administered, GFR fell to approximately 65% of normal, whereas the net tubular secretion was decreased to 30% of normal. These results suggest that the tubular transport was preferentially affected by uranyl nitrate. In contrast, in glycerol-induced renal failure, the decline of TEAB secretion fell in a parallel fashion with the GFR, suggesting that the glomeruli and the proximal tubules were equally damaged by glycerol. However, in this latter model, the decline of PAH secretion did not parallel the decrease in GFR, contradicting the proposal that glycerol affects equally the glomeruli and the proximal tubules. This discrepancy may be due to the selective competitive inhibition of PAH secretion by the accumulation of naturally occurring organic acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗