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Biomedical subjects

J J Li

Publications and source records attributed to J J Li.

At least 145 records · Page 8Linked to original sources
PubMed1991

Characterization of early kidney lesions in estrogen-induced tumors in the Syrian hamster.

Syrian hamsters were treated with diethylstilbestrol (DES), a potent estrogen and kidney carcinogen, or ethinyl estradiol (EE), a strong estrogen but weak carcinogen, for 1-9 months. At monthly intervals their kidneys were studied using light, immunoperoxidase, and electron microscopic techniques. At 5 months, DES-treated animals exhibited interstitial lesions composed of small round cells with a high nuclear:cytoplasmic ratio. Immunoperoxidase and ultrastructural studies showed these cells to be similar to cells in fully formed tumors at 9 months. Early lesions in EE-treated animals (seen as early as 1 month) were dissimilar, these lesions appeared in the deep cortex adjacent to the renal pelvis, where proximal tubules underwent hyperplastic changes, showing columnar cells with large nuclei, occasional mitoses, and sloughing of apical cytoplasm. Cells in early lesions of EE-treated animals did not resemble the fully developed tumor in either immunoperoxidase or ultrastructural features; although with longer treatment these tubular lesions progressed to dysplasia (3-5 months) and severe dysplasia/carcinoma in situ (7 months), they did not form grossly visible tumors during the 9-month study. Both early lesions identified were specific, inasmuch as they were not observed in control animals and animals treated with beta-dienestrol and 17 alpha-estradiol (noncarcinogenic weak estrogens). Animals given a combination of DES and EE showed tubular hyperplasia but not interstitial lesions; this finding was of particular interest because hamsters given this combination of estrogens do not develop gross renal tumors. These results strongly implicate the primitive interstitial cell in the hamster kidney as the cell of origin of the DES-induced neoplasm.

Animals↗
PubMed1991

Superoxide dismutase and catalase levels during estrogen-induced renal tumorigenesis, in renal tumors and their autonomous variants in the Syrian hamster.

Antioxidant enzyme levels were determined in kidneys during estrogen-induced cortical renal tumorigenesis in male Syrian hamsters. The activity of these enzymes in renal tumors were compared to those in the kidney cortex of untreated male castrated hamsters of different ages and in age-matched animals treated with diethylstilbestrol (DES) for varying periods. A transient increase in kidney Mn superoxide dismutase (MnSOD) and total SOD activity was seen after 1.5 and 3.1 months of DES treatment compared to untreated controls. However, after 4.4 months of DES exposure the activities of these antioxidant enzymes fell below untreated levels. The level of MnSOD and CuZnSOD was 3- to 10-fold lower compared to castrated male renal cortical values in DES-induced primary, serially transplanted and in autonomous renal tumour variants. Catalase activity declined steadily at 1.5 to 4.4 months of DES treatment. Low levels of catalase activity were found in all tumors examined. In general, Western blot analysis of immunoreactive proteins confirmed these findings, indicating that the low enzyme activities were due to low levels of enzyme proteins. Immunohistochemistry of the earliest tumor foci exhibited negligible antioxidant enzyme activity. The levels of these antioxidant enzymes were similar in all tumors surveyed, both primary and autonomous variants and in newborn kidneys, and they were about 10-fold lower than in normal kidney cortex or isolated proximal tubules.

Animals↗
PubMed1991

In vitro transfer of rabbit corneal epithelium from carriers to denuded corneas or cryolathed lenticules.

Rabbit corneal basal epithelial cells seeded onto fixed gelatin membranes or commercial collagen shields formed 3 to 5 cell layers after 1 to 3 weeks of culture at 35 degrees C in nutrient medium. The cells grew better, by comparison, in the collagen shields and eventually formed a multilayered tissue that resembled the stratified morphology of native epithelium. Transfer of multilayered cultures (prior to stratification) from these carriers in vitro to denuded corneal buttons or cryolathed lenticules resulted in complete adhesion of the grafted tissue to the underlying recipient buttons after 24- to 48-h incubations. After mechanically removing the carriers, most of the epithelial cells remained attached to the stromal surface. Our experimental findings indicated that both kinds of carriers may be suitable for epithelial transplantation, although the collagen shield is probably superior because of its better biocompatibility and physical characteristics.

Animals↗
PubMed1991

Detection of human papillomavirus DNA in squamous cell carcinoma of the nail bed and finger determined by polymerase chain reaction.

Increasing evidence supports the association of squamous cell carcinoma of the finger and nail bed with human papillomavirus infection. We treated 12 patients with squamous cell carcinoma of the finger and nail bed, none of whom was originally diagnosed as having a malignant lesion. Half of the patients were referred for carbon dioxide laser ablation of what was believed to be a recalcitrant verruca vulgaris. Our objective was to evaluate these lesions for the presence of human papillomavirus by in situ hybridization techniques and the polymerase chain reaction. This is the first report of use of the polymerase chain reaction to detect human papillomavirus in formalin-fixed, paraffin-embedded specimens of periungual squamous cell carcinoma. Seven of the 12 lesions were evaluated for the presence of human papillomavirus by both in situ hybridization and the polymerase chain reaction. Five of the seven periungual lesions were found to contain human papillomavirus type 16 but not type 18 DNA with use of the polymerase chain reaction technique. In situ hybridization failed to identify human papillomavirus in any of these patients' tumors. Our data confirm the association between human papillomavirus and squamous cell carcinoma of the periungual region and suggest that biopsies should be performed on chronic, isolated lesions of the finger in adults before therapy is initiated.

Adult↗
PubMed1991

Comparative morphologic and immunohistochemical studies of estrogen plus alpha-naphthoflavone-induced liver tumors in Syrian hamsters and rats.

Syrian hamsters were treated with ethinylestradiol and maintained on a diet containing alpha-naphthoflavone (alpha NF), a regimen that produces a high incidence of liver tumors. Morphologic analyses (light microscopy, immunoperoxidase studies, and electron microscopy) were performed on livers of these animals. After 4 months of hormone plus alpha NF treatment, marked hepatocyte cell changes were already present, as demonstrated by loss of eosinophilic staining of hepatocyte cytoplasm. Large multinucleated hepatocytes exhibiting frequent mitoses were observed around central veins. After 5 months of treatment, there was proliferation of bile ducts, and small cells with eosinophilic cytoplasm resembling hepatocytes appeared surrounding these bile ducts. At 7 to 8 months, the first tumor nodules (foci) were seen. Tumor foci in the portal area consisted of small clusters of large cells resembling hepatocytes with irregular nuclei. At the same time, dysplastic glands were identified among proliferating bile ducts. By 8 to 10 months, large tumors were present. These were trabecular hepatocellular carcinomas with widely varying individual cell morphology. Compared with adjacent liver, dysplastic glands in the portal areas, microcarcinomas, and large tumors all showed intense immunostaining for cytokeratin. Rats treated with the same regimen also developed hepatic tumors, but the light and electron microscopy results and immunohistochemical profiles were very different. Altered hepatic foci composed of small hepatocytes were typically prominent; however, malignant tumors did not arise from the portal area. Neither altered foci nor tumors stained significantly for cytokeratin. These data suggest that the biochemical events giving rise to these liver tumors differ between the species studied, despite the animals being exposed to the same treatment regimens.

Animals↗
PubMed1991

The rat lung organotypic culture: an in vitro model for studying surfactant metabolism abnormalities.

The amount of surfactant present in the intra-alveolar space is mainly regulated by the synthesis and recycling of surfactant by type II pneumocytes. Biochemical analyses have shown that the surfactant level is frequently diminished and that protein-rich exudate can further interfere with surfactant function in the lungs of adult respiratory distress syndrome (ARDS) patients. The microenvironmental changes that occur in the alveoli of burned patients, who are prone to developing ARDS, are unclear. Therefore, using an in vitro rat lung organotypic culture, we showed that the sera of rats with a 3-day old, third-degree thermal injury (25-30% total body surface area) inhibited surfactant synthesis in organotypically cultured rat lung cells. Surfactant precursor, 3H-choline, incorporation into the surfactant was 58% of control. Using liposomes made of dipalmitoyl phosphatidylcholine and phosphatidylglycerol (8:1, v/v) or surfactant we showed that surfactant endocytosis by purified type II alveolar cells is an active, temperature-dependent process, and correlates with the quantity of surfactant present in the milieu. We also found that plasma protein-rich fluid interfered with surfactant endocytosis by the purified type II pneumocytes. These two processes of inhibition of surfactant synthesis and its reutilization by these cells may contribute to the pathogenesis of ARDS.

Animals↗
PubMed1991

[A study of developmental order of secondary sexual characteristics in Beijing girls].

A six-year (1980-1986) study of the developmental status of the secondary sexual characteristics was made among 937 girls in Beijing. The mean age of the first appearance of the secondary sexual characteristics was breast 11.84 +/- 0.95 years, pubic hair 13.29 +/- 1.11 years, axillary hair 13.71 +/- 1.21 years; the average age of developmental maturation was breast 13.95 +/- 1.16 years, pubic hair 14.85 +/- 1.29 years, axillary hair 15.14 +/- 1.24 years. Their developmental order, as measured by the mean values of the groups, was breast, the first menarche (12.88 years), pubic hair, axillary hair. But when the individuals were examined only 22.85% was found to be in accord with the above order. The individual variation was very great. The course of development took about 3.5 years, but some needed one year to develop others six years. Some girls developed and finished at the same time, some finished earlier or later. Only a few girls have had no development of pubic hair and axillary hair until 18 years old.

Age Factors↗
PubMed1989

Identification of cellular proteins required for simian virus 40 DNA replication.

Study of the proteins involved in DNA replication of a model system such as SV40 is a first step in understanding eukaryotic chromosomal replication. Using a cell-free system that is capable of replicating plasmid DNA molecules containing the SV40 origin of replication, we conducted a series of systematic fractionation-reconstitution experiments for the purpose of identifying and characterizing the cellular proteins involved in SV40 DNA replication. In addition to the one viral-encoded replication protein, T antigen, we have identified and begun to characterize at least six cellular components from a HeLa cytoplasmic extract that are absolutely required for SV40 DNA replication in vitro. These include: (i) two partially purified fractions, CF IC and CF IIA, and (ii) four proteins that have been purified to near homogeneity, replication protein-A, proliferating cell nuclear antigen, DNA polymerase alpha-primase complex, and topoisomerase (I and II). Replication protein-A is a multi-subunit protein that has single-stranded DNA binding activity and is required for a T antigen-dependent, origin-dependent unwinding reaction which may be an important early step in initiation of replication. Fraction CF IC can stimulate this unwinding reaction, suggesting that it also may function during initiation. Proliferating cell nuclear antigen, DNA polymerase alpha-primase, and CF IIA all appear to be involved in elongation of nascent chains.

Antigens, Viral, Tumor↗
PubMed1989

Morphological and immunohistochemical studies of the estrogen-induced Syrian hamster renal tumor: probable cell of origin.

Chronic natural or synthetic estrogen treatment of Syrian golden hamsters leads to the development of malignant renal neoplasms. In the present study, morphological and immunohistochemical studies were performed to further characterize the estrogen-induced hamster renal tumors. The neoplasms were composed of two distinct cell populations: a large-cell component that appeared highly epithelial, and a poorly differentiated small-cell component. Importantly, both cell types had epithelial characteristics, since they contained desmosomes at their cell surfaces. However, the large-cell component possessed additional epithelial features such as microvilli, intracytoplasmic lumens, and cilia. Comparative studies of renal tumors and developing renal tissue from fetal and newborn hamsters revealed remarkable histological similarities. Morphologically, the large tumor cells resembled early metanephric tubules and the small tumor cells were very similar to the blastemal cells of the developing kidney. The earliest tumor foci were found after 4.5 months of treatment. They were consistently found in the kidney interstitium in proximity to large arteries. Immunohistochemical staining for intermediate filaments in developing fetal and newborn kidneys demonstrated cytokeratin in renal tubules, desmin in blastemal cells, and vimentin in stromal cells. Estrogen-induced renal tumor cells uniquely possessed reactivity for all three intermediate filaments, clearly demonstrating their epithelial and mesenchymal characteristics. Based on their morphological resemblance to developing embryonic kidney cells and the presence of both epithelial and mesenchymal intermediate filaments, our findings provide strong evidence that the cell of origin of this malignant tumor is a precursor cell that is committed to an epithelial differentiation pathway.

Animals↗
PubMed1989

Specific estrogen-induced cell proliferation of cultured Syrian hamster renal proximal tubular cells in serum-free chemically defined media.

It has long been recognized that the renal proximal tubular epithelium of the hamster is a bona fide estrogen target tissue. The effect of estrogens on the growth of proximal tubule cell explants and dissociated single cells derived from these explant outgrowths has been studied in culture. Renal tubular cells were grown on a PF-HR-9 basement membrane under serum-free chemically defined culture conditions. The cells of tissue explant outgrowths exhibited ultrastructural features typical of proximal tubules including junctional complexes, numerous mitochondria, peroxisomes, and microvilli. At 7-14 days in culture, cell number was enhanced 3-fold in the presence of either 17 beta-estradiol or diethylstilbestrol. Maximal proliferative response was observed at hormone concentrations of 0.6-1 nM. A similar 3-fold increase in cell number was also seen at 1 nM 17 beta-estradiol in subcultured dissociated single tubular cells derived from hamster renal tubular explant outgrowths at 21 days in culture. Neither progesterone, 5 alpha-dihydrotestosterone, nor the inactive diethylstilbestrol metabolite beta-dienestrol elicited this mitogenic effect. Concomitant exposure of tamoxifen at 3-fold molar excess in culture completely abolished the increase in cell number seen with 17 beta-estradiol. Tubular cells obtained from hamster medulla did not exhibit this proliferative response when exposed similarly to 17 beta-estradiol or diethylstilbestrol. The proliferative effect of estrogens on proximal tubular cell growth appears to be species specific since 17 beta-estradiol did not alter the growth of either rat or guinea pig proximal tubules in culture. In addition, at 7-10 days in culture in the presence of 17 beta-estradiol, [3H]thymidine labeling of hamster tubular cells was enhanced 3-fold. A similar increase in mitoses was also observed in cultures containing these potent estrogens during the same time interval of estrogen exposure. These results clearly indicate that estrogens can directly induce primary epithelial cell proliferation at physiologic concentrations and provide strong additional evidence for an important hormonal role in the neoplastic transformation of the hamster kidney.

Animals↗
PubMed1989

Variations in catechol O-methyltransferase activity in rodent tissues: possible role in estrogen carcinogenicity.

Catechol-O-methyltransferase (COMT) [EC 2.1.1.6] is a ubiquitous cytosolic enzyme which has a pertinent role in the inactivation of both natural and synthetic catechol estrogens in mammalian tissues. We have compared the COMT activity in mouse, hamster and rat kidney, liver and red blood cells and examined the kinetic characteristics of this enzyme in the latter two species using various catechol estrogens as substrates. Results presented here indicate that the ratios of COMT activity in the kidney versus the liver of the rat and mouse are nearly identical, 0.48-0.52, whereas there is a 29-fold ratio between the level of COMT activity in these two tissues in the hamster. In red blood cells, the level of COMT activity is 4- and 12-fold lower in the hamster compared to mouse and rat, respectively. When the kinetic characteristics of this enzyme were assessed in the hamster and rat kidney and liver, except for 2-hydroxymoxestrol which had an apparent Km value of 15-48 microM, the other catechol estrogen substrates exhibited Km values ranging from 1-10 microM. Generally, the Vmax values were markedly higher in the rat kidney and liver than those observed in corresponding hamster tissues. The significantly lower COMT activity in the hamster liver and red blood cells suggests that under chronic estrogen treatment at high doses, the concentration of catechol estrogens in these tissues may exceed the capacity of COMT to effectively catalyse their O-methylation into inactive metabolites. The resulting accumulation of catechol estrogens may contribute to the estrogen carcinogenicity observed in the hamster liver and kidney. Additionally, when 2-hydroxyestrone was used as a substrate, the estrogen-induced renal carcinoma exhibited only 8.6% of the COMT activity found in the normal kidney.

Animals↗
PubMed1989

Endotoxin suppresses surfactant synthesis in cultured rat lung cells.

Pulmonary complications secondary to postburn sepsis are a major cause of death in burned patients. Using an in vitro organotypic culture system, we examined the effect of E. coli endotoxin (LPS) on lung cell surfactant synthesis. Our results showed that E. coli endotoxin (1.0, 2.5, 10 micrograms LPS/ml) was capable of suppressing the incorporation of 3H-choline into de novo synthesized surfactant, lamellar bodies (LB), and common myelin figures (CMF) at 50%, 68%, and 64%, respectively. In a similar study, we were able to show that LPS also inhibited 3H-palmitate incorporation by cultured lung cells. LPS-induced suppression of surfactant synthesis was reversed by hydrocortisone. Our results suggest that LPS may play a significant role in reducing surfactant synthesis by rat lung cells, and thus contribute to the pathogenesis of sepsis-related respiratory distress syndrome (RDS) in burn injury.

Animals↗
PubMed1989

Impact of C-reactive protein (CRP) on surfactant function.

Plasma levels of the acute-phase reactant, C-reactive protein (CRP), increase up to one thousand-fold as a result of trauma or inflammation. CRP binds to phosphorylcholine (PC) in a calcium-ion dependent manner. The structural homology between PC and the major phospholipid component of surfactant, dipalmitoyl phosphatidylcholine (DPPC), led to the present study in which we examined if CRP levels might be increased in patients with adult respiratory distress syndrome (ARDS), and subsequently interfere with surfactant function. Our results showed that CRP levels in the bronchoalveolar fluid (BALF) was increased in patients with ARDS (97.8 +/- 84.2 micrograms/mg total protein vs. 4.04 +/- 2.2 micrograms/mg total protein in normals). Our results show that CRP binds to liposomes containing DPPC and phosphatidylglycerol (PG). As a result of this interaction, CRP inhibits the surface activity of a PG-DPPC mixture when tested with a Wilhelmy surfactometer or with the Enhorning pulsating bubble apparatus. Furthermore, the surface activity of a clinically used surfactant replacement, Surfactant TA (2 mg/ml), was also severely impaired by CRP in a dose-dependent manner (doses used ranging from 24.5 to 1,175 micrograms/ml). In contrast, human serum albumin (HSA) at 500 and 900 micrograms/ml had no inhibitory effect on Surfactant TA surface activity. These results suggest that CRP, although not an initiating insult in ARDS, may contribute to the subsequent abnormalities of surfactant function and thus the pathogenesis of the pulmonary dysfunction seen in ARDS.

1,2-Dipalmitoylphosphatidylcholine↗