Search PubMed⌕ Search

Biomedical subjects

K W Chung

Publications and source records attributed to K W Chung.

69 records · Page 4Linked to original sources
PubMed1981

Effects of LH and oestrogen on the growth of feminising testicular tumours in mice.

Testicular tumours in mice with testicular feminisation (tfm/y) are made up of masses of large Leydig and lipid-laden cells, surrounded by darkly-stained smaller Leydig cells. The activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) is more apparent in the small cells of the peripheral than in the larger cells of the central part of the tumour. Oestrogen alone can stimulate the incorporation of thymidine into deoxyribonucleic acid (DNA) by cultured cells but not the activity of 3 beta-HSDH. On the other hand, luteinizing hormone (LH) promotes activity of the enzyme, but not the synthesis of DNA. Together, they have a greater effect on DNA synthesis and enzyme activity than if present separately. It seems that in tfm/y mice gonadotrophin is necessary for the proper action of oestrogen in control of testicular tumour growth.

3-Hydroxysteroid Dehydrogenases↗
PubMed1980

Immunocytochemical localization of nerve growth factor, submandibular glands of Tfm/Y mice.

The submandibular glands of mice with testicular feminization (Tfm/Y) and their normal adult male littermates (Ta/Y) were studied by immunocytochemical techniques for the demonstration of epidermal growth factor (EGF), nerve growth factor (NGF), renin and protease A. In the glands of both the affected and normal males, these polypeptides were restricted to cells of the granular convoluted tubules (GCT), with the exception of protease A, which was also found in small amounts in striated duct cells. Compared to those of Ta/Y males, GCTs were narrower in the glands of Tfm/Y mice and contained a markedly reduced number of cells immunoreactive for EGF, NGF and renin. However, the number of GCT cells that stained for protease A in the glands of Tfm/Y males was not as drastically decreased.

Androgen-Insensitivity Syndrome↗
PubMed1980

Spontaneous testicular neoplasm in mice with testicular feminization.

Testicular neoplasms occur spontaneously in androgen insensitive mice with testicular feminization (tfm/y); they are composed of Leydig cells, lipid-laden cells, fibroblastlike cells, and macrophages. The small Leydig cells in the periphery of the tumor are structurally similar to nontumorous tfm/y Leydig cells, whereas centrally located large Leydig cells contain numerous lipid droplets, mitochondria with tubular cristae, and abundant smooth endoplasmic reticulum. The lipid-laden cells exhibit a crescentic nucleus which is displaced toward the periphery of the cytoplasm by a large lipid vacuole. The fibroblastlike cells have a large amount of rough endoplasmic reticulum, lysosomes, free ribosomes, and lipid vacuoles. Macrophages are characterized by numerous layered and dense osmiophilic structures closely associated with crystalshaped bodies. An in vitro study shows that, in comparison with the normal testes, the tfm/y tumors produce significantly less testosterone but a larger quantity of androstenedione. Also, the tumors are capable of converting progesterone to estrone and estradiol-17 beta. The plasma level of testosterone is significantly lower in tumor-bearing animals than in normal littermates, but slightly higher than in the nontumorous tfm/y animals. Since the abnormal steroid enzyme activity is found in both tumor-bearing and nontumorous tfm/y mice, the basic cause of aberrations in sex steroid production appears to be genetic rather than the direct result of alterations in their Leydig cells.

Androgen-Insensitivity Syndrome↗
PubMed1980

Structural and functional factors related to testicular neoplasia in feminized rats.

Testicular tumors in King-Holtzman hybrid rats with testicular feminization (tfm) were seen as firm, rounded masses of tissue consisting of Leydig cells, myoid cells, and fibroblast-like cells. The cytoplasm of Leydig cells contained well-developed smooth endoplasmic reticulum, pleomorphic mitochondria with numerous cristae, and many lipid droplets. Mitochondria were numerous and varied in size and shape. Their cristae were in the form of tubules, and lipid-like inclusions were frequently seen in the mitochondrial matrix. Lysosomes, rough endoplasmic reticulum, and Golgi bodies were also scattered in the cytoplasm. An in vitro study showed that more testosterone was produced in the tumor than in the testes of rats with tfm; however, the amount in both was less than normal. Testicular tumor-bearing rats with tfm exhibited slightly higher levels of plasma testosterone than did non-tumor-bearing animals with tfm. Levels in both were significantly higher than normal. Testicular tumor cells growing in culture medium supplemented with luteinizing hormone (LH) contained more protein and synthesized more androgen and DNA than did those growing in culture medium without LH. Observed under the scanning and transmission electron microscopes, the LH-stimulated cells had well-developed cytoplasmic organelles and inclusions and surface specializations such as numerous microvilli, large blebs, and other microextensions. They adhered well to the glass surface. These results indicated that Leydig cells in testicular tumors of rats with tfm had morphologic characteristics of steroid-producing cells. In addition these cells were capable of producing steroids, and this capability was enhanced by the presence of LH.

Androgen-Insensitivity Syndrome↗
PubMed1980

Pericanalicular hepatocytic and bile ductular microfilaments in cholestasis in man.

The cytoplasmic microfilaments of hepatocytes in the pericanalicular area and of bile ductular cells in various types of human cholestasis were examined and compared with those seen in the noncholestatic human liver. An increase in the number of hepatocytic microfilaments with an increase in the apparent density of the filamentous network and in the thickness of bundles of filaments was evident in the vicinity of the bile canaliculi, in the pericanalicular ectoplasm, and in the surrounding cytoplasm in all types of cholestasis but more so in intrahepatic cholestasis. This increase in the number of microfilaments was also seen around undilated canaliculi. Microfilaments were also increased in number beneath the surface of the bile ductular cells facing the cytoplasm but not beneath the rest of the plasma membrane. More microfilaments also were found around ductular cell nuclei. No striking differences were noted between intrahepatic and extrahepatic cholestasis. These findings suggest that microfilaments play a role that is not established in human cholestasis.

Bile Ducts, Intrahepatic↗
PubMed1979

Ultrastructural and biochemical characteristics of Leydig cells from newborn androgen-insensitive rats.

Leydig cells of testis of newborn pseudohermaphrodite (tfm) rats have an ultrastructure similar to that of the normal, containing well developed organelles and inclusions. The cytoplasm is filled with smooth endoplasmic reticulum forming a network of interconnected tubules. Lipid droplets are surrounded by cisternae of smooth endoplasmic reticulum and are in close association with pleomorphic mitochondria. Many of the latter are cup-shaped and have tubular cristae and intramitochondrial dense bodies. Essentially, these are characteristics of normal Leydig cells. Accordingly, the production of testosterone by testes from newborn tfm rats is the same as that by testes from normal newborns and adults. However, it is significantly higher than that by testes of tfm adults. Also, the plasma testosterone levels of newborn tfm rats are the same as in the normal newborn, but lower than in normal adults and much lower than in adult tfm animals. Thus, since in the tfm rat the morphology of Leydig cells, androgen production, and maintenance of plasma levels of testosterone are normal in the newborn, but become abnormal with advancing age, it appears that defective androgen action rather than insufficient androgen production is the cause of male pseudohermaphroditism.

Androgens↗
PubMed1978

Effects of tropic hormones on ultrastructure and synthesis of androgens in adrenals of male pseudohermaphrodite rats.

Ultrastructural and biochemical study of the adrenals in the pseudohermaphrodite (tfm) rat reveals hypertrophic adrenocortical cells. The cytoplasm of the cells in the zonae fasciculata and reticularis contains an exceptionally well developed smooth endoplasmic reticulum closely applied to mitochondria and lipid droplets. Mitochondria are more numerous than in normals and have especially abundant tubular cristae. More lipid droplets (appearing as empty vacuoles) are surrounded by pleomorphic mitochondria. The incubation study indicates that the capacity of rat adrenal cortex of producing androgens is greater in tfm than in normal animals. Hypophysectomy and castration result in a significant decrease in androgen biosynthesis by tfm rat adrenals and cause a reduced concentration of plasma testosterone. Administration of tropic hormones to hypophysectomized-castrated rats appears to stimulate their adrenal androgenesis. It is suggested that in tfm rats the higher than normal luteinizing hormone (LH) together with adrenocorticotropic hormone (ACTH) stimulates the hypertrophy of cellular organelles in the adrenal cortex and causes an accompanying increase in androgenic steroids which may be responsible, at least in part, for the increased level of plasma androgens.

Adrenal Cortex↗
PubMed1975

Testicular lipids in mice with testicular feminization.

Morphological, histochemical and biochemical studies of the testis of mice with testicular feminization (tfm/y) reveal a large accumulation of lipids in Leydig cells and in Sertoli cells. In Leydig cells of tfm/y mice, lipid droplets do not exhibit the special relationship with smooth endoplasmic reticulum that exists in normal adult Leydig cells. Compared to the surgically-cryptorchid control, the tfm/y testis contains more lipid in Leydig cells but less in Sertoli cells. There are also quantitative differences in testicular lipids in tmf/y and normal testes but no significant differences were noted between tfm/y and surgically-cryptorchid testes. The testes of both the genetically defective and surgically-cryptochid animals contain increased amounts of total lipids and phospholipids, and of free and esterified cholesterols. Exogenous testosterone has no effect on lipids or other characteristics of these cells. The present results suggest that the increased lipids in tfm/y mice result from a genetic disorder that asserts itself (1) in Leydig cells where it is associated with, and is probably a result of, impaired lipid metabolism and steroidogenesis, and (2) in Sertoli cells where it is perhaps attributable to arrested spermatogenesis and impaired steroidogenesis.

Androgen-Insensitivity Syndrome↗
PubMedDate not supplied

Periovulatory and interleukin (IL)-1-dependent regulation of IL-6 in the immature rat ovary: a specific IL-1 receptor-mediated eicosanoid-dependent effect.

Interleukin (IL)-6, traditionally an IL-1-induced immune regulator, is nevertheless synthesized by a variety of tissues including the ovary. The purposes of this communication were to assess the ovarian expression of IL-6, examine its cyclic variation, and study its regulation by IL-1, a putative intermediary in the ovulatory process. Molecular probing revealed IL-6 transcripts to be most abundant in the thymus, liver, and ovary, which suggests that, in relative terms, untreated immature whole ovarian tissue is a significant site of IL-6 gene expression. Treatment of immature rats with pregnant mare serum gonadotropins resulted in a measurable, statistically significant (P <.05) increase in ovarian IL-6 mRNA compared with untreated controls. Isolated and indeed transient increments in the relative abundance of IL-6 transcripts were noted 4 hours after exposure to hCG, a point in time 8 hours from projected follicular rupture, a pattern highly reminiscent of that previously recognized for IL-1 beta transcripts. Treatment of whole ovarian dispersates from immature rats with IL-1 beta for 48 hours resulted in a significant (P <.05) increase (11-fold) over control in IL-6 transcripts. The IL-1 effect proved dose dependent; the first significant increase was noted at the 1-ng/mL dose level. Evaluation of the time requirements revealed IL-1 beta to significantly (P <.05) up-regulate (4.5-fold) IL-6 transcripts as early as 24 hours into the culture period. Cotreatment with the IL-1 receptor antagonist completely reversed the IL-1 effect, which suggests mediation through a specific IL-1 receptor. Treatment with indomethacin (10 microg/mL), an established inhibitor of prostaglandin biosynthesis, resulted in a significant (P <.05) decrease (79%) in the ability of IL-1 beta to up-regulate IL-6 transcripts. Importantly, the addition of prostaglandin E(2) (10 microg/mL) to untreated or indomethacin-treated cells significantly (P <.05) augmented the IL-1 beta effect. This suggests a role for eicosanoid signaling in IL-1 beta action. Treatment with aminoguanidine, an established inhibitor of nitric oxide synthase, significantly (P <.05) decreased (85%) the IL-1 beta effect. However, the addition of S-nitroso-n-acetyl-penicilamine, an established nitrite generator, failed to reverse the aminoguanidine effect, which suggests that the inhibitor effect of aminoguanidine may be nitrite independent. Treatment with cycloheximide produced dose-dependent inhibition of the ability of IL-1 to up-regulate IL-6 transcripts; the maximal inhibitory effect was 89%. Taken together, these findings (1) reaffirm the rat ovary as a site of IL-6 expression; (2) document an in vivo increase in IL-6 transcripts before ovulation; (3) disclose a marked dependence of IL-6 on IL-1 beta; and (4) reveal the IL-1 beta effect to be dose and time dependent, receptor mediated, contingent upon de novo protein biosynthesis, and eicosanoid dependent but nitric oxide independent. These findings suggest that IL-1 action in the ovary may require the intermediacy of IL-6 in a manner like that encountered in extraovarian sites.

Animals↗