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Biomedical subjects

S F Chen

Publications and source records attributed to S F Chen.

At least 109 records · Page 6Linked to original sources
PubMed1990

Virological survey of rhesus monkeys in China.

A virological survey of rhesus monkeys captured in China for 13 viruses and/or antibodies was performed. Antigens used were SFV, SF40, HSV-1, Sa11, measles, vaccinia, epidemic or simian hemorrhagic fever, Langat, Kunming, poliomyelitis, HIV, SV41 and rubella. Monkeys were from Sichuan, Hunan, Guizhou, Yunnan and Guangxi provinces. Antibody was detected to all the listed viruses except HIV, SV41 and rubella. Both SFV and SV40 were recovered from monkeys, but H. simiae, LCM and coxsackieviruses were not.

Animals↗
PubMed1990

Reduced neurotoxicity in transgenic mice overexpressing human copper-zinc-superoxide dismutase.

The role of oxygen-derived free radicals, superoxide in particular, in the pathogenesis of neuronal cell death induced by glutamate was studied using cultured cortical neurons from transgenic mice overexpressing human copper-zinc-superoxide dismutase. Primary cortical neuron cultures were developed from 15-day-old fetuses of both transgenic mice and their normal littermates. Both human copper-zinc-superoxide dismutase and host mouse copper-zinc-superoxide dismutase activities in cultured neurons were identified by native gel electrophoresis followed by nitroblue tetrazolium staining. Cultured neurons grown for 10-12 days in vitro were exposed briefly to 0.5 mM glutamate for 5 minutes, followed by biochemical and morphological examinations at 2, 4, and 24 hours. Our data have demonstrated that glutamate neurotoxicity is significantly reduced in transgenic neurons at 2 and 4 hours following exposure to glutamate, as measured by the efflux of lactate dehydrogenase, the 3-O-methyl glucose space, and by phase-contrast and bright-field trypan blue staining. These data indicate that transgenic neurons containing twofold to threefold the normal amount of copper-zinc-superoxide dismutase activity as the result of expression of the human copper-zinc-superoxide dismutase transgene are protected against glutamate neurotoxicity in vitro. Our results suggest that oxidative stress, at least in part, plays an important role in the biochemical pathways amplifying N-methyl-D-aspartate receptor-mediated neurotoxicity.

Animals↗
PubMed1990

Study of morphology and deciduomal proteins of hamster endometrial cells during in vitro decidualization.

The objective of this study was first, to examine whether the morphological characteristics of deciduomal cells are correlate to differentiation or just to hyperplasia and hypertrophy, and second, to examine whether the deciduoma-associated proteins (DAPs) are expressed consistently during decidualization in vitro and in vivo. In vitro decidualization was implemented by dissociated cell culture of Day-4-pseudopregnant endometrium. The morphology of these cultures was compared with that of undifferentiated cultures of fetal hamster fibroblast. They appeared similar morphology in the stellate shape, the binucleation and the intracellular fibers. The DAPs were identified by comparing the electrophoretic maps of one-day cultures of decidualized and nondecidualized endometrium from unilaterally scratched Day-6-pseudopregnant animals. Analysis of cytosol fraction by SDS-PAGE demonstrated the presence of four DAPs. That only one of them was growth-associated, which was concluded from its increasing expression in fetal fibroblast, and that all of them were not endometrium-specific as evidenced by their presence in other tissues. By examining their expression during in vitro decidualization, we found that timing of the DAPs' expression in vitro was not consistent with it in vivo. These results indicate that some morphological characteristics which were accustomedly used to mark deciduomal cells may relate to hyperplasia and hypertrophy instead of differentiation, and that the in vitro and the in vivo decidualization are not identical.

Animals↗
PubMed1989

Teratogenic effects of combined use of anti-kidney serum and E-64 in the rat.

The teratogenic effects of rabbit anti-rat-kidney serum (AKS) combined with E-64 (a thiol protease inhibitor) were examined. Wistar rats were injected with 10 or 20 mg/kg of E-64 on days 9 and 10 of gestation, and with a subteratogenic dose (1 ml/kg) of AKS on day 9 or day 10. The most common malformations were hydronephrosis, hydrocephalus, ureteral dilatation, microphthalmia, anophthalmia, and heart defects. When AKS was given on day 9 or 10, the incidence of malformations was about 7% (10 mg/kg group) and 24% (20 mg/kg group). This indicated that the types of malformations are similar to those produced by AKS and E-64, and there is a synergistic effect between AKS and E-64.

Animals↗
PubMed1989

Enterotoxin effect on hepatocytes in experimental intestinal obstruction in the rat.

Thirty-two Wistar rats were studied for liver injury caused by enterotoxemia due to experimental intestinal obstruction. In the experimental group, enterotoxin titers were measured 1.83 +/- 0.38, 2.40 +/- 0.39, 10.80 +/- 2.97 (M +/- SE) in the group of the duration of intestional obstruction for 2-, 4-, and 7-day respectively. The distribution of E. coli endotoxin in the liver cell was started from Zone 3 and then extended into Zone 1 with prolonged obstruction. The experimental group which experienced the longest period of obstruction also exhibited elevated serum GPT and GOT levels. The severity of damage increased with time of obstruction. The disturbance of liver cells in enterotoxemia induced by intestional obstruction was clear and needed our attention in the management of intestional obstruction from this animal model.

Animals↗
PubMed1988

Distribution of the novel anticancer drug candidate Brequinar sodium (DuP 785, NSC 368390) into normal and tumor tissues of nude mice bearing human colon carcinoma xenografts.

The distribution of the novel anticancer drug candidate Brequinar Sodium (DuP 785, NSC 368390) was studied in control mice and mice implanted subcutaneously with human colon carcinoma xenografts. Mice were given radiolabeled 14C-Brequinar Sodium intravenously. Brequinar concentrations in blood and various tissues were determined at 1, 6, and 24 h after drug administration. Within 1 h Brequinar distributed to the tumor and all other tissues studied. The tumor-to-blood drug concentration ratios ranged from 0.19 to 0.41. Radioactivity in the liver and small intestine at 1 h accounted for 17% and 13%, respectively, of the dose given. Elimination rates of Brequinar from all tissues were approximately equal to that from blood. Comparison of blood concentrations determined by both radioactivity and HPLC methods suggests that the intact drug is probably the only form in the blood.

Adenocarcinoma↗
PubMed1988

Induction of intracellular superoxide radical formation by arachidonic acid and by polyunsaturated fatty acids in primary astrocytic cultures.

The effects of arachidonic acid and other polyunsaturated fatty acids (PUFAs) on both oxidative and metabolic perturbation were studied in primary cultures of rat cerebral cortical astrocytes. In the presence of 0.1 mM arachidonic acid, the rate of the reduction of nitroblue tetrazolium (NBT) to nitroblue formazan (NBF) was stimulated from 0.65 +/- 0.10 to 1.43 +/- 0.15 and from 0.092 +/- 0.006 to 0.162 +/- 0.009 nmol/min/mg protein in intact and broken cell preparations, respectively. The rate of superoxide radical formation, as measured by the superoxide dismutase (SOD)-inhibitable NBT reduction was 0.042 nmol/mg protein in broken cells and was negligible in intact cells. The latter is due to the impermeability of SOD into the intact cell preparation. NBF formation in intact astrocytes stimulated by arachidonic acid was both time- and dose-dependent. Other PUFAs, including linoleic acid, linolenic acid, and docosahexaenoic acid, were also effective in stimulating NBF formation in astrocytes, whereas saturated palmitic acid and monounsaturated oleic acid were ineffective. Similar effects of these PUFAs were observed in malondialdehyde formation in cells and lactic acid accumulation in incubation medium. These data indicate that both membrane integrity and cellular metabolism were perturbed by arachidonic acid and by other PUFAs. The sites of superoxide radical formation appeared to be intracellular and may be associated with membrane phospholipid domains, because liposome-entrapped SOD, which was taken up by intact astrocytes, reduced the level of superoxide radicals and lactic acid content, whereas free SOD was not effective.

Animals↗
PubMed1986

Mechanism of action of the novel anticancer agent 6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarbo xylic acid sodium salt (NSC 368390): inhibition of de novo pyrimidine nucleotide biosynthesis.

Exposure of cultured clone A human colon tumor cells to 25 to 75 microM of NSC 368390 [6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarbox yli c acid sodium salt, DuP 785] for 48 to 72 h resulted in a 99.9% cell kill as determined by clonogenic assay. Cells exposed to NSC 368390 became depleted in intracellular pools of uridine 5'-triphosphate and cytidine 5'-triphosphate. Both uridine 5'-triphosphate and cytidine 5'-triphosphate were decreased to 50% of levels in control cells at 3 h and were undetectable at 15 h after addition of 25 microM of NSC 368390 to the cultures. Similar effects were observed in L1210 leukemia cells. Addition of 0.1 mM of uridine or cytidine restored intracellular pools of uridine 5'-triphosphate and cytidine 5'-triphosphate to control levels and rescued clone A cells from NSC 368390 cytotoxicity. Addition of uridine circumvented NSC 368390 cytotoxicity in L1210 cells, but addition of cytidine did not. This result is consistent with the fact that L1210 cells lack cytidine deaminase and thus cannot form uridine or its anabolites from cytidine. These results indicated that NSC 368390 inhibits a step in the de novo biosynthetic pathway leading to uridine 5'-monophosphate. Therefore, the effects of NSC 368390 on the six enzymes that comprise the de novo pathway leading to the formation of uridine 5'-monophosphate were examined. The results showed that NSC 368390 was a potent inhibitor of dihydroorotate dehydrogenase, the fourth enzyme in the pathway; thus, this study demonstrates that NSC 368390 exerts its tumoricidal effect by inhibiting a step in de novo pyrimidine biosynthesis resulting in the depletion of critical precursors for RNA and DNA synthesis.

Antineoplastic Agents↗
PubMed1986

Changes in nucleoside transport of HL-60 human promyelocytic cells during N,N-dimethylformamide induced differentiation.

The rate of nucleoside transport decreased profoundly in human promyelocytic leukemia HL-60 cells after myeloid differentiation was induced by 5-6 days of exposure to 0.8% N,N-dimethylformamide (DMF). The facilitated diffusion of 100 microM radiolabeled adenosine and 2'-deoxyadenosine, measured by rapid transport assays, decreased 10- to 20-fold. The transport of 2 microM coformycin or 2'-deoxycoformycin, which is mediated by the same mechanism and was monitored by the adenosine deaminase titration assay, decreased 29-fold. The reduction in nucleoside transport capacity after DMF treatment was confirmed by a 19-fold decrease in the number of specific binding sites per cell (from 24-30 X 10(4) to 1.2-1.7 X 10(4)) for [3H]-6-p-nitrobenzylthioinosine, a nucleoside transport inhibitor. The binding affinity of 6-p-nitrobenzylthioinosine was not altered significantly and nucleoside transport remained sensitive to the transport inhibitors, 6-p-nitrobenzylthioinosine, dipyridamole, and dilazep after DMF-induced maturation. Time-dependence studies showed that the rate of 100 microM deoxyadenosine transport was unchanged for the first 24 h of exposure to DMF but fell to about 36% of control rates at 24-26 h and then gradually decreased further to about 4-5% of control rates after 5-6 days. In contrast, transport rates of the purine bases were reduced only 2- to 3-fold in HL-60 cells after 5 days of DMF treatment. The rates of adenosine and deoxyadenosine transport were unchanged or reduced by no more than 2-fold after 5-6 days of exposure to 0.8% DMF in the following human tumor cell lines that are not inducible with DMF: ARH-77 (multiple myeloma), KG-1 (acute myelogenous), and K-562 (chronic myelogenous). Thus, changes in nucleoside transport may serve as an early, membrane-associated marker of differentiation of the HL-60 cell line.

Adenosine↗
PubMed1985

[Germ cell tumor of the testis--clinicopathologic analysis of 114 cases].

The histologic features and clinical records of 114 cases of germ cell tumors of the testis proved by pathology in our hospital from 1951 to 1980 are reviewed. These cases were divided into six types: seminoma 49.1%, embryonal carcinoma 8.8%, yolk sac tumor 17.5%, choriocarcinoma 0.9%, teratoma 14.9% and mixed carcinoma 8.8%. The over-all incidence of metastasis observed on exploration was 41.2%, and in embryonal and mixed carcinoma it was the highest, each amounting to 80%. Site of metastasis was: inguinal and retroperitoneal lymph nodes 63.8%, mesenteric lymph nodes 6.4%, liver 12.8%, lung 8.5% and supraclavicular lymph nodes 8.5%. In the 24 followed cases, 13 were seminomas and 11 non-seminomatous germ cell tumors. 5 of the former and 9 of the latter died of the tumor. It is advised that, in addition to radical orchiectomy, supplementary radiotherapy to the original site in the testis and the retroperitoneal draining lymphatics be given to seminoma and retroperitoneal lymph node dissection be given to non-seminomatous germ cell tumors except the pure choriocarcinoma to improve the result.

Adolescent↗