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C H Anderson

Publications and source records attributed to C H Anderson.

16 recordsLinked to original sources
PubMed1992

Cellular kinetics of rat mammary gland terminal end bud epithelium exposed to N-methyl-N-nitrosourea in vivo.

Administration of the direct acting carcinogen N-methyl-N-nitrosourea (NMU) to 50-55-day-old virgin female rats on different days of the estrous cycle yields differential breast tumor biology (T. A. Ratko and C. W. Beattie, Cancer Res., 45: 3042-3047). One basis for these estrous cycle-dependent differences may be the duration of cell cycle stages of susceptible structures such as mammary terminal end buds or the quantity and duration of repair effected following adduct formation within these structures. The terminal end bud (TEB) epithelial cell cycle was characterized using pulse injections of [3H]thymidine (0.5 mCi/g body weight). On estrus, TEB epithelial cell cycle was significantly shorter (15.5 h) than on proestrus (19.9 h) and diestrus (18.8 h). The shorter duration in TEB cell cycle on estrus was likely due to a shorter TG1 (3-4 h) (P less than 0.05) since TS and TG2 did not differ between estrous cycle days. When NMU was injected 1 h after [3H]thymidine, the labeled mitotic wave within TEB of diestrus rats recovered approximately 2-3 h sooner than those given injections during proestrus (P less than 0.01), suggesting less initial damage or a slightly faster rate of DNA adduct repair. When [3H]thymidine was injected 1-5 days after the NMU, the percentage of labeled mitoses of rats given injections during diestrus and proestrus recovered to near normal 48 h after NMU, although the proportion of all cells labeled was still low compared to non-NMU-treated rats. The percentage of labeled mitoses and labeling of cells were normal 3 and 5 days after NMU. Rats receiving a carcinogenic but sublethal dose of NMU (5 mg/100 g body weight), followed by [3H]thymidine injection within 1 min, had one-half the intensity of thymidine incorporation into the terminal end bud DNA of non-NMU-treated rats. Unscheduled DNA synthesis was not demonstrable within the first 48 h following injection of NMU. The results support and extend the finding that rat mammary epithelial cell carcinogenicity of NMU is estrous cycle dependent and appears to be correlated with a differential response in the cell cycle of TEB (shorter at estrus) or delayed recovery in response to NMU (proestrus versus diestrus).

Animals↗
PubMed1992

Information processing in the primate visual system: an integrated systems perspective.

The primate visual system contains dozens of distinct areas in the cerebral cortex and several major subcortical structures. These subdivisions are extensively interconnected in a distributed hierarchical network that contains several intertwined processing streams. A number of strategies are used for efficient information processing within this hierarchy. These include linear and nonlinear filtering, passage through information bottlenecks, and coordinated use of multiple types of information. In addition, dynamic regulation of information flow within and between visual areas may provide the computational flexibility needed for the visual system to perform a broad spectrum of tasks accurately and at high resolution.

Animals↗
PubMed1992

Carboxypeptidase M in brain and peripheral nerves.

Carboxypeptidase M (CPM), a plasma membrane-bound enzyme, cleaves C-terminal basic amino acids with a neutral pH optimum. We studied its distribution in human, baboon, and dog brain and in dog peripheral nerves. Areas were dissected, homogenized, centrifuged, and assayed for activity with dansyl-Ala-Arg. The corpus callosum and the pyramidal and optic tract were especially rich in CPM, whereas basal ganglia and cortex had low activity. The identity of the basic carboxypeptidase activity with CPM was shown by similarities in subcellular localization, membrane attachment, substrate hydrolysis, inhibition by a specific basic carboxypeptidase inhibitor, and cross-reaction with anti-human CPM antiserum. This antiserum immunoprecipitated an average of 85% of the activity in human and baboon brain and approximately 66% in dog brain. CPM co-purified with myelin extracted from the brain. Consistent with results obtained in placenta and cultured kidney cells, CPM in the brain appears to be membrane-bound via a phosphatidylinositol glycan anchor. In the peripheral nerves, the specific activity in dog sciatic nerve and in vagus was high (98 and 149 nmol/h/mg of protein, respectively). In immunohistochemical studies, glia in the brain, which appear to be oligodendrocytes or astrocytes, and the outer aspects of myelin sheaths and Schwann cells in sciatic and vagus nerves were stained. We conclude that in some areas of the CNS and the PNS, CPM is closely associated with myelin and myelin-forming cells. Northern blot analysis revealed the presence of mRNA coding for CPM in the brain, showing that the enzyme is indeed synthesized there.

3-Mercaptopropionic Acid↗
PubMed1991

Estrous cycle dependence of nitrosomethylurea (NMU)-induced preneoplastic lesions in rat mammary gland.

Virgin 50-55-day-old rats exhibiting regular estrous cycles were injected i.v. with the direct acting carcinogen 1-nitroso-1-methylurea (NMU) on the morning of proestrus, estrus, or diestrus. Rats were killed at weekly intervals following NMU administration to identify source and number of microscopically identifiable dysplasias. Terminal end bud (TEB) abnormalities appeared within 1 week following NMU administration, with a significantly greater number of abnormal TEBs in mammary glands of rats injected on proestrus (PE) and estrus (E) than on diestrus (DE). Ductal (DH) and ductal alveolar hyperplasias (DAH) and hyperplastic alveolar nodules (HAN) appeared during week 3, with significantly more of each type of lesion appearing by 6 weeks after NMU injection. HAN were most numerous in glands from rats injected on estrus. Adenocarcinomas arose from both the proximal and distal ductal network; at 10 and 12 weeks post NMU, significantly more tumors were found in rats injected on proestrus than diestrus and estrus. These results support the theory that the hormonal environment at the time of NMU administration significantly alters early development of mammary tumors in the rat.

Analysis of Variance↗
PubMed1990

Blur into focus.

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Humans↗
PubMed1989

Estrous cycle status alters N-methyl-N-nitrosourea (NMU)-induced rat mammary tumor growth and regression.

The relationship between mammary carcinoma growth, ovariectomy-induced regression and estrogen receptor status were determined in Sprague-Dawley rats with 5-day estrous cycles after injection of N-methyl-N-nitrosourea (NMU) on metestrus (ME), diestrus-1 (DE-1), proestrus (PE) or estrus (E). Rats exposed to NMU on PE had a shorter tumor latency than those injected on ME and E, as well as more carcinomas per rat than those exposed on ME and DE-1. Mammary carcinomas grew faster in rats injected on ME (doubling time, 6.4 days) and DE-1 (6.9 days) compared with PE (15.2 days) and E (16.3 days). Tumor regression was also significantly faster in rats injected on ME (time to 50% vol., 5.5 days) and DE-1 (5.3 days) compared with PE (8.2 days) and E (8.5 days) following bilateral-ovariectomy during log phase growth. Significantly, total nuclear estrogen receptor (ERN) content was increased in carcinomas from rats injected on PE compared with DE-1 (70.8 +/- 11.3 vs. 32.9 +/- 7.3 fm/mg DNA) (P less than 0.05) and DE-1 and ME combined (P less than 0.01). These observations generalize the concept that estrous cycle stage at the time of NMU injection alters subsequent mammary carcinoma biology, and represents the first experimental evidence that slower growing and responding estrogen receptor positive rat mammary carcinomas may be associated with an increase in circulating estrogen prior to carcinogen exposure.

Animals↗
PubMed1987

Shifter circuits: a computational strategy for dynamic aspects of visual processing.

We propose a general strategy for dynamic control of information flow between arrays of neurons at different levels of the visual pathway, starting in the lateral geniculate nucleus and the geniculorecipient layers of cortical area V1. This strategy can be used for resolving computational problems arising in the domains of stereopsis, directed visual attention, and the perception of moving images. In each of these situations, some means of dynamically controlling how retinal outputs map onto higher-level targets is desirable--in order to achieve binocular fusion, to allow shifts of the focus of attention, and to prevent blurring of moving images. The proposed solution involves what we term "shifter circuits," which allow for dynamic shifts in the relative alignment of input and output arrays without loss of local spatial relationships. The shifts are produced in increments along a succession of relay stages that are linked by diverging excitatory inputs. The direction of shift is controlled at each stage by inhibitory neurons that selectively suppress appropriate sets of ascending inputs. The shifter hypothesis is consistent with available anatomical and physiological evidence on the organization of the primate visual pathway, and it offers a sensible explanation for a variety of otherwise puzzling facts, such as the plethora of cells in the geniculorecipient layers of V1.

Animals↗
PubMed1986

Comparison of the effects of muscarine and vasopressin on inositol phospholipid metabolism in the superior cervical ganglion of the rat.

Both muscarine and vasopressin have been shown previously to increase the accumulation [3H]inositol phosphates in superior cervical ganglia in which the phospholipids were labeled with [3H] inositol. In this study, we have compared the effects of muscarine and of vasopressin on phospholipid metabolism in the ganglion. The effects of these agents on [3H]inositol phosphate accumulation are additive. The response to muscarine levels off after approximately 10 min, whereas the response to vasopressin increases for at least 30 min. The incorporation of [3H]inositol into phospholipids is enhanced in decentralized ganglia and in ganglia maintained in organ culture compared to freshly isolated ganglia. These treatments appear to potentiate the effect of muscarine on [3H]inositol phosphate accumulation, but do not affect the response of the ganglia to vasopressin. Muscarine and vasopressin also increase the incorporation of [3H]inositol into phospholipids in the ganglion. Autoradiographic techniques were used to localize the inositol-containing phospholipids in the ganglion. Muscarine increases phospholipid labeling primarily in the cell bodies of the principal ganglionic neurons, whereas vasopressin increases phospholipid labeling primarily in the neuropil. These data are consistent with the hypothesis that muscarine and vasopressin stimulate the hydrolysis of different pools of ganglionic phospholipids.

Animals↗
PubMed1976

Effect of hypophysectomy on estrogen conjugation and on plasma and tissue concentrations of tritium after administration of 3H-estradiol-17beta.

Estradiol-17beta-6,7-3H was injected into ovariectomized (control) and ovariectomized, hypophysectomized (hypox) rats in order to study the binding of estradiol in the brain. Hypophysectomy resulted in a significant increase in the concentration of tritium in the hypothalamus, and preoptic area, as well as cortex, muscle, plasma and liver. However, since the liver was lighter in hypox rats, the total tritium content in the liver was unchanged from controls. Part of the weight reduction in the liver was due to a loss of stainable glycogen, which took place within 24 hours of hypox. The increase in circulating tritiated estradiol after hypox led us to investigate hepatic metabolism of estradiol. In vitro studies on liver slices from control and hypox rats demonstrated a significant reduction in the formation of conjugates of estrogen. Specifically, estradiol glucuronide and estrone sulfate formation were reduced in hypox rats and conversely the unmetabolized estradiol concentration was higher. Hypophysectomy for 24 hours results in a significant decrease in hepatic metabolism of estradiol-17beta.

Animals↗
PubMed1976

Effects of early treatment with antiserum to ovine follicle-stimulating hormone and luteinizing hormone on gonadal development in the rat.

Neonatal rats secrete considerable amounts of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) between 5 and 15 days of age. Antisera to LH and FSH were injected during this 11-day period in an attempt to study the importance of gonadotropins for functional development of the gonads. Autopsies at 15 days of age revealed normal ovarian follicular histology after either antiserum treatment, but antiserum to LH significantly retarded differentiation of interstitial tissue. Uterine weights were increased, and some of the serum samples showed elevated FSH levels following the antiserum treatments. The testes of antiserum-treated rats were heavier at 15 days of age, while accessory sex organ weights were unchanged. Vaginal opening after antiserum treatment was more variable than in controls, but tended to be earlier. The first appearance of penile serum was not significantly changed. Both males and females were fertile as adults. Important limitations to the use of chronic antiserum injections were found in immature rats. The antisera were present for at least 34 days after injection. The ways in which this pool of antiserum might have influenced the results are discussed.

Animals↗
PubMed1975

Localization of cells retaining 3H-estradiol in the forebrain of rabbits.

Ovariectomized rabbits received 3H-estradiol via an ear vein and were killed one hour later. Autoradiograms were prepared and exposed up to six months. Labeled cells, as indicated by many silver grains over the nucleus of a neuron, were found in many nuclei of the brain. Thus, the bed nucleus of the stria terminalis had labeled cell bodies. The stria terminalis leads into the medial preoptic area where great numbers of cells concentrated the estrogen. Farther into the hypothalamus the labeled cells were numerous in the ventromedial and arcurate nuclei. Other locations with labeled cells were the lateral septal nucleus and nucleus accumbens septi, the periventricular preoptic nucleus, anterior hypothalamic nucleus, nucleus supraopticus diffusus, posterior hypothalamic nucleus, and premammillary nucleus. The labeled cells could be followed into the central gray surrounding the aqueduct of Sylvius. The amygdaloid nuclei, and in particular the medial amygdaloid nucleus, had labeled cells as did the most ventral posterior part of the hippocampal cortex. The results are discussed in comparison with those in the rat, and with reference to physiologic data.

Amygdala↗