Search PubMed⌕ Search

Biomedical subjects

C C Chang

Publications and source records attributed to C C Chang.

At least 523 records · Page 29Linked to original sources
PubMed1986

Expression and regulation of proopiomelanocortin-like gene in the ovary and placenta: comparison with the testis.

Proopiomelanocortin (POMC), a precursor protein for ACTH, beta-endorphin, and the MSHs, has been identified in the reproductive tracts of both male and female. With rat pituitary POMC complementary DNA (cDNA) as a hybridization probe, POMC-like messenger RNA (mRNA) was identified in the ovaries of rat, mouse, and monkey. The molecular size of POMC-like mRNA in the ovary was 150-200 bases smaller than in the pituitary and hypothalamus but identical to that in the testis and epididymis. The size heterogeneity of POMC mRNA observed in various tissues is not due to differences in the lengths of the poly(A) tail, as measured by RNase H digestion. S1 nuclease mapping analysis revealed that POMC mRNAs isolated from pituitary, testis, or ovary share the nucleotide sequences coding for ACTH, beta-lipotropin, and the 3'-untranslated region. The regulation of ovarian POMC-like mRNA was also investigated. Treatment of 25-day-old immature female rats with PMSG resulted in profound increases in the ovarian content of total RNA, poly(A) RNA, and POMC-like mRNA. The concentration of ovarian POMC-like mRNA during pregnancy increased increased to 3-4 times that in immature or normally cycling animals. POMC-derived peptides are present in the human placenta and are synthesized de novo in cultured placental cells. In this report we also demonstrate POMC-like mRNA in the placenta of rat, mouse, and human. The size of POMC-like mRNA in the placenta was similar to that observed in the testis, epididymis, and ovary and different from that found in the pituitary or hypothalamus. The concentration of placental POMC-like mRNA did not change throughout pregnancy. In conclusion, we have demonstrated that 1) POMC-like mRNA is present in the ovary and placenta of rodents and primates; 2) the size of POMC-like mRNA in the ovary and placenta, like that in the testis and epididymis, is smaller than that in the pituitary and hypothalamus, probably owing to a shortening of the 5'-ends; and 3) the expression of this gene is regulated by gonadotropins in the ovary but probably not in the placenta.

Animals↗
PubMed1986

Evidence for the existence of stereoselective presynaptic beta 1-adrenoceptors on noradrenergic and dopaminergic neurons in the rat hypothalamus.

Using high performance liquid chromatography with an electrochemical detector, we examined antagonistic effects of l- and d-acebutolol and atenolol against isoproterenol-induced facilitation of impulse-evoked release of endogenous norepinephrine and dopamine in rat hypothalamic slices. Isoproterenol (10 nM) increased the release of the both catecholamines, and this facilitation was similarly antagonized by 100 nM l-acebutolol and 100 nM atenolol, but was not antagonized by 100 nM d-acebutolol. In conclusion, there exist stereoselective presynaptic beta 1-adrenoceptors on noradrenergic and dopaminergic neurons in the rat hypothalamus.

Animals↗
PubMed1986

Diagnosis of Alzheimer's disease and multiple infarct dementia by tomographic imaging of iodine-123 IMP.

Tomographic imaging of the brain was performed using a rotating slant hole collimator and [123I]N-isopropyl p-iodoamphetamine (IMP) in normal subjects (n = 6) and patients with either Alzheimer's disease (n = 5) or multiple infarct dementia (n = 3). Four blinded observers were asked to make a diagnosis from the images. Normal subjects and patients with multiple infarct dementia were correctly identified. Alzheimer's disease was diagnosed in three of the five patients with this disease. One patient with early Alzheimer's disease was classified as normal by two of the four observers. Another patient with Alzheimer's disease had an asymmetric distribution of IMP and was incorrectly diagnosed as multiple infarct dementia by all four observers. Limited angle tomography of the cerebral distribution of 123I appears to be a useful technique for the evaluation of demented patients.

Alzheimer Disease↗
PubMed1986

The lipofuscin in neuroglial cells of the optic nerve of Formosan rock-monkey (Macaca cyclopis).

The ultrastructure of lipofuscin granules in neuroglial cells of the optic nerve of the Formosan Rock-Monkey was investigated by electron microscopy. In the cytoplasm of astroglial cells, numerous irregular lipofuscin granules were characterized by the presence of large lipid droplets, small electron-dense pigment granules, and some lamellar structures. The lipofuscin granules of the oligodendroglial cells were composed largely of dense, coarse pigment granules, multilinear structures, and a few small lipid droplets. The lipofuscin granules in microglial cells were characterized by numerous lipid droplets in various sizes, small electron-dense pigment granules, and prominent lamellar structures. It was reported that the lipofuscin granules are wear-and-tear materials and products from the cells in lower functional activity. However, our observations suggest that the presence of lipofuscin granules in the neuroglial cells of the optic nerve is likely a characteristic product of active phagocytosis.

Animals↗
PubMed1986

Growth-promoting effect of 12-O-tetradecanoylphorbol-13-acetate on cultured normal human fetal kidney epithelial cells.

Normal human epithelial cells have been reported to be sensitive to growth inhibition by 12-O-tetradecanoylphorbol-13-acetate in contrast to neoplastic counterparts. Our studies with normal human fetal kidney epithelial cells, however, show that 12-O-tetradecanoylphorbol-13-acetate may increase cell density and promote the growth of these cells at early passages. The result, together with three previous reports showing similar effects in normal human melanocytes, prostatic epithelial cells, and an unidentified cell type in human epidermal cell culture, indicates that human cells may exhibit divergent responses to 12-O-tetradecanoyl-phorbol-13-acetate for induction of cellular differentiation or proliferation.

Cell Communication↗
PubMed1986

Characterization of a human teratocarcinoma cell assay for inhibitors of metabolic cooperation.

Although a Chinese hamster V79 cell-based assay for inhibitors of metabolic cooperation is currently available, the development of a human cell-based assay is desirable in order to avoid inappropriate extrapolation from animal cells to human cells. Cells derived from a human teratocarcinoma cell line (designated PA-1), which has a stable pseudodiploid karyotype and excellent in vitro growth properties, were used in a metabolic cooperation assay. The assay was based on the metabolic isolation of hypoxanthine-guanine phosphoribosyltransferase (HGPRT)-deficient variants in the presence of HGPRT-proficient cells and 6-thioguanine. Chemicals which inhibit the transfer of the lethal metabolite of 6-thioguanine from HGPRT-proficient to HGPRT-deficient cells will allow for recovery of the 6-thioguanine-resistant (HGPRT-deficient) cells. Chemicals tested included 12-O-tetradecanoylphorbol-13-acetate and related analogues phorbol-12,13-didecanoate, mezerein, and 4-phorbol-12,13-didecanoate. Concurring with results previously obtained in V79 cells, 12-O-tetradecanoylphorbol-13-acetate and phorbol-12,13-didecanoate strongly inhibited metabolic cooperation, whereas mezerein was moderately inhibitory and 4 alpha-phorbol-12,13-didecanoate was inactive. These cells thus hold promise as a human cell-based assay for inhibitors of metabolic cooperation.

Biological Assay↗
PubMed1985

Failure to induce mutations in Chinese hamster V79 cells and WB rat liver cells by the polybrominated biphenyls, Firemaster BP-6, 2,2',4,4',5,5'-hexabromobiphenyl, 3,3',4,4',5,5'-hexabromobiphenyl, and 3,3',4,4'-tetrabromobiphenyl.

Firemaster BP-6 (FM), a mixture of polybrominated biphenyls (PBB), and the congeners 2,2',4,4',5,5'-hexabromobiphenyl (2,4,5-HBB), 3,3',4,4',5,5'-hexabromobiphenyl (3,4,5-HBB), and 3,3',4,4'-tetrabromobiphenyl (3,4-TBB) were tested for their ability to induce mutations in mammalian cells in culture. A rat liver microsome-mediated (S 15) Chinese hamster V79 cell mutation assay was used to test the mutagenicity of PBB and 3,4-TBB. V79 cells and WB rat liver cells were used to detect the mutagenicity of 2,4,5-HBB and 3,4,5-HBB. No mutagenic effects were detected at the dose levels tested. The possibility that these compounds promote liver neoplasms via a nongenotoxic mechanism is discussed.

Animals↗
PubMed1985

Cell proliferation and cell cycle dependent changes in the methylthioadenosine phosphorylase activity in mammalian cells.

The objective of this study is to investigate the activity of methylthioadenosine phosphorylase (MTA-Pase) in mammalian cells stimulated by serum to proliferate and during their cell cycle. A direct correlation between growth rate and MTA-Pase activity in chinese hamster ovary (CHO) cells was observed. High MTA-Pase activity was observed during the exponential growth phase followed by a low enzyme activity during plateau phase of growth. To understand whether the fluctuations in the enzyme activity was cell cycle dependent, initially the activity of MTA-Pase was studied in plateau phase (G0) CHO cells as they synchronously go into S phase upon plating in fresh medium. The MTA-Pase activity in G0 cells before initiation of growth was 10.3 n.mol/mg protein/30'. A peak activity of 16.0 n.mol/mg/30 min was found at 12 hr after stimulation of proliferation by serum. These results indicate a peak MTA-Pase activity between 10-12 hr after stimulation of proliferation coinciding with the initiation of DNA synthesis. The activity of the enzyme slowly decreased as the cells completed their DNA synthesis. To understand whether these fluctuations are cell cycle specific, HeLa cells were synchronized in different phases and MTA-Pase activity was studied. The specific activities of the enzyme were 2.76, 2.99, 3.97, 3.28 and 3.65 n.moles/mg/30 min. in mitosis, early G1, late G1, S and G2 phases of the cell cycle respectively. These results indicate that MTA-Pase activity peaks in late G1 phase before the initiation of DNA synthesis, similar to the polyamine biosynthetic enzymes and might play a role in the initiation of DNA synthesis by salvage of adenine into nucleotide pools.

Animals↗
PubMed1985

Inhibition of metabolic cooperation by the anticonvulsants, diphenylhydantoin and phenobarbital.

High densities of 6-thioguanine-sensitive Chinese hamster V79 cells reduce the recovery of co-cultured 6-thioguanine-resistant cells through a form of intercellular communication (metabolic cooperation). Diphenylhydantoin and phenobarbital, suspected human and animal teratogens and tumor promoters, were able to inhibit intercellular communication at noncytotoxic doses. A potentiation was observed when a mixture of the two chemicals was used.

Animals↗
PubMed1985

Role of tumor promotion in affecting the multi-hit nature of carcinogenesis.

The assessment of risk from low-level exposure to radiation and chemicals is hindered by the basic lack of scientific understanding of the complex nature of the multiple levels of protective or synergistic interactions. Radiation and chemicals have the potential of inducing mutations, cell death and altered gene expression. The biological consequences of each of these effects is again complex, since many factors can enhance or mask the effect of a single mutation, cytotoxic or gene modulatory change. Carcinogenesis, representing but one chronic disease state, is a multi-step process, involving the clonal expansion of a single altered cell (that is, the initiation event). Radiation and chemicals appear to contribute to the initiation process by their ability to induce viable mutations. Insufficient theoretical and empirical knowledge precludes a determination of whether mutagenesis and, hence, initiation exhibit a threshold phenomenon. Because of a variety of redundancy mechanisms on the genetic and cellular levels, the physiological impact of a single dysfunctional cell is felt only after it is amplified to a large number (the promotion phase of carcinogenesis). Radiation and chemical-induced cytotoxicity, as well as noncytotoxic chemical induction of mitogenesis, can induce surviving single dysfunctional stem cells to multiply. If during this multiplication of dysfunctional cells, the initiated cells are further exposed chronically to low levels of mutagens, there is an enhanced probability of additional genetic changes. The accumulation of foci of dysfunctional cells can occur in any stem cell population of any tissue. As with mutagens, the existence of threshold levels for promoting conditions and chemicals is still not yet scientifically validated. However, specific examples of the actions of a few promoters does seem to be consistent with that idea. The concepts of initiation and promotion imply the existence of anti-initiation and antipromotion conditions. Together with genetic factors, the complex and unpredictable interactions of radiation and chemicals as initiators, anti-initiators, promoters and antipromoters, defy prospects of an easy means to predict the consequences of exposure to chronic low levels of radiation and chemicals.

Animals↗