Occupational asthma in radiographers.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
A N Taylor
Publications and source records attributed to A N Taylor.
Expression of calbindin-D28k in developing and growing chick testes.
Calbindin, a 28-kDa vitamin D-dependent calcium-binding protein was localized immunohistochemically in developing and growing chick testes. The protein first appeared in the germinal epithelium of developing testes of the eight-day-old embryo and remained therein throughout development. Calbindin was not present in the germinal epithelium after hatching. Calbindin was next detected in the spermatogonia and spermatocytes of one-week-old and growing chick testes. Calbindin-positive spermatogonia and spermatocytes gradually increased in number and staining intensity as the seminiferous tubules further developed. A few interstitial Leydig cells were positive for calbindin from five-week-old and older chicks. Comparison of the time-course of appearance and increase in calbindin content in spermatogonia and spermatocytes with spermatogenesis in chickens suggests that calbindin may be involved in the mitotic process in spermatogonia and spermatocytes.
Animals↗
Prenatal exposure to alcohol enhances thymocyte mitogenic responses postnatally.
Previous studies have shown altered cell-mediated immune responses in animals prenatally exposed to ethanol. The present study was designed to determine the ontogeny of proliferative responses of thymocytes postnatally following prenatal exposure to ethanol. Thymocytes obtained from 44-day old Sprague-Dawley male rats exposed to 5% (w/v) ethanol during the last two weeks of gestation had a significantly greater response to mitogenic stimulation by concanavalin A (Con A, 5.0 micrograms/ml) than controls. A similar trend was observed in rats at postnatal days 30 and 72, but not at day 16. Con A-conditioned thymoblasts from day-44 fetal alcohol-exposed animals were less responsive to further activation by a crude Con A supernatant than controls, but this response normalized by day 72. These findings reveal that the effects of ethanol exposure in utero in male rats include alterations in the development of thymoproliferative responses to mitogen which persist through the peripubertal period and normalize in part by young adulthood.
Animals↗
Ethanol increases tumor progression in rats: possible involvement of natural killer cells.
The effects of acute and chronic ethanol administration on tumor progression and metastasis were studied in rat models of leukemia and breast cancer, respectively. Acute administration of 1.5-3.5 g of ethanol/kg body weight significantly reduced survival of rats injected with CRNK-16 leukemia cells in a dose-related manner. Acute administration of 2.5-3.5 g of ethanol/kg body weight, one hour before tumor inoculation, or chronic consumption of liquid diet containing ethanol for two weeks before and three weeks after tumor inoculation, significantly increased the number of lung metastases of MADB106 mammary adenocarcinoma. The ethanol-induced increase in the number of metastases was not correlated with plasma levels of corticosterone and was not altered by the opiate antagonist naltrexone. Incubation of spleen cells in vitro in the presence of ethanol, at concentrations comparable to those measured in the blood of ethanol-treated rats, significantly suppressed natural killer (NK) cell activity against MADB106 cells in a standard chromium-release assay and decreased the binding of effector to MADB106 tumor cells. However, neither acute nor chronic ethanol administration in vivo altered splenic NK activity against this tumor in the same in vitro assay, in which the ethanol would have been washed away. These results suggest that, in the presence of ethanol, tumor progression is facilitated. The possibility that this facilitation is related to ethanol-induced impairment of the normal tumoricidal interaction between NK and tumor cells is discussed.
Adenocarcinoma↗
Prenatal ethanol and the prepubertal sexually dimorphic nucleus of the preoptic area.
The volume of the sexually dimorphic nucleus of the preoptic area of the hypothalamus (SDN-POA) was determined in 14-31-day-old male and female rats whose mothers received a liquid diet containing 5% w/v ethanol from day 8 of gestation to parturition. Pair-fed dams received as a nutritional control an equal volume of an isocaloric liquid diet with maltose-dextrin in place of ethanol. Normal controls had laboratory rat chow and water available ad lib. The SDN-POA volume of ethanol-exposed males was significantly reduced compared to the pair-fed and normal males, and became indistinguishable from the SDN-POA volumes of the pair-fed and normal females. Ethanol-treated females also had a markedly reduced SDN-POA volume compared to the pair-fed and normal females. Our findings indicate that the SDN-POA of prepubertal rats of both sexes is sensitive to the effects of in utero ethanol exposure. While plasma testosterone, progesterone and estradiol titers, which we measured in fetuses on gestation day 22, were differentially affected by maternal ethanol consumption, the alterations by themselves cannot adequately explain the effects of prenatal ethanol exposure on the developing SDN-POA.
Animals↗
Fetal alcohol delays the developmental expression of myelin basic protein and transferrin in rat primary oligodendrocyte cultures.
This study has examined the development of immunoreactive myelin basic protein and transferrin in primary glial cell cultures. Cultures were initiated from control and experimental Sprague-Dawley rats 1-2 days postnatally. Experimental treatment involved exposure to 5% (w/v) ethanol in a liquid diet during the last two weeks of gestation. Prenatal alcohol administration delayed the expression of myelin basic protein and transferrin during the first three weeks postnatally. Other oligodendroglial and astroglial markers were little affected, if at all, by fetal alcohol exposure.
Animals↗
Stress increases metastatic spread of a mammary tumor in rats: evidence for mediation by the immune system.
Causal relationships among stress, immune suppression, and enhanced tumor development have often been suggested, but direct evidence is scant. We studied stress effects in Fischer 344 rats using a tumor model in which lung metastases of a syngeneic mammary tumor (MADB106) are controlled by natural killer (NK) cells. Animals exposed to acute stress showed a substantial decrease in NK cell cytotoxicity against this tumor in an in vitro assay and, when intravenously injected with this tumor, showed a twofold increase in surface lung metastases. The critical period during which stress increases metastases appears to be the same as that during which this tumor is known to be controlled by NK cells. These findings support the hypothesis that stress can facilitate the metastatic process via suppression of the immune system.
Adenocarcinoma↗
Changes with age in the proliferative response of splenic T cells from rats exposed to ethanol in utero.
The fetal alcohol syndrome is associated with altered immunity. Several laboratories have confirmed that rodents exposed to ethanol in utero demonstrate both diminished proliferative responses of T cells to mitogens and diminished proliferative responses of T-blast cells to human recombinant interleukin 2 (rIL2). We examined the developmental time course of these altered immune responses by testing the immune function of in utero ethanol-exposed rats at various ages. We found that while diminished splenic T cell proliferative responses could not be detected at 2 weeks, they were present at 6 weeks after birth and suppression was maximal at 6 weeks and 3 months. Thereafter, at 5 and 7 months, the altered immune responses gradually declined and normalized at 8 months of age. Thus, both altered T cell mitogenesis and the blunted IL2-induced proliferative response of T-blast cells could serve as biomarkers of fetal exposure to ethanol.
Age Factors↗
Asthma related to occupation of spouse.
Explore the source record for details and available documents.
Adult↗
Allergens and irritants.
The range of diseases caused by respiratory allergens and irritants is wide because they trigger different pathophysiological mechanisms. Surprisingly, though smoking promotes asthma it exerts the opposite effect on the development of extrinsic allergic alveolitis.
Air Pollutants↗
Genetic differences in opiate receptor concentration and sensitivity to ethanol's effects.
The hypothesis that genetic differences in opiate receptor concentration are involved in determining the sensitivity to some of the effects of alcohol was studied by comparing the hypothermic and analgesic effects of ethanol in four strains of mice that can be divided into three groups on the basis of their brain opiate receptor concentration: high (CXBH), low (CXBK) and intermediate (C57BL/6By and BALB/cBy). In the first experiment, animals within each strain were injected with either saline or 1.5 g/kg ethanol and their pain sensitivity was assessed 20 min later by the hot-plate test. The same procedure was repeated 10 days later with a higher dose of ethanol (2.5 g/kg). The lower dose produced analgesia only in CXBH mice, whereas the higher dose produced analgesia in CXBH, C57BL/6By and BALB/cBy mice, but had no effect in CXBK mice. In the second experiment, animals within each strain were injected with either saline or naloxone, followed 20 min later by an injection of 3.5 g/kg ethanol. CXBH mice were significantly more hypothermic and CXBK mice were significantly less hypothermic than all other strains. Naloxone attenuated ethanol's hypothermic effect in all strains except CXBK. These results suggest that the hypothermic and analgesic effects of ethanol are at least partly mediated by opiate receptors and are correlated with genetic differences in opiate receptor concentration.
Analgesia↗
Diminished proliferative response of con A-blast cells to interleukin 2 in adult rats exposed to ethanol in utero.
The fetal alcohol syndrome is associated with altered immunity. We attempted to delineate the mechanism of the decline in cell-mediated immunity observed by others by using rats which were exposed to alcohol in utero and tested for immune integrity 3 months after birth. We found that concanavalin A-stimulated T-lymphoblast (Con A T-blast) cells that were obtained from ethanol-exposed rats had significantly diminished proliferative responses to both crude and recombinant interleukin 2 compared to those obtained from normal and nutritional controls. The blunted response of Con A T-blast cells to interleukin 2 may be a biomarker of fetal exposure to alcohol.
Animals↗
Calbindin-D immunolocalization in developing chick thyroid: a light and electron microscopic study.
Antiserum to calbindin-D, a 28 KD vitamin D-dependent calcium binding protein, was used to localize the protein immunocytochemically in developing chick thyroid by both light and electron microscopy. The protein first appeared in future follicular cells of developing thyroid tissue from 8-day-old embryos. The number of calbindin-D-containing cells increased rapidly to a near-plateau level at day 10; this concentration was sustained until day 15, and then declined to an undetectable level just before hatching. The protein was distributed throughout organelle-free areas of the follicular cell cytoplasm and extended into the nucleus; it was not present in the follicular colloid. Comparison of the time course of changes in calbindin-D content with known differentiative changes taking place in follicular cells suggests that the protein may function in some yet to be determined mechanism related to normal development of the thyroid.
Animals↗
Maternal alcohol consumption and stress responsiveness in offspring.
Explore the source record for details and available documents.
Animals↗
Effects of ethanol on CRF release in vitro.
Acute ethanol exposure produces activation of the brain-pituitary-adrenal (BPA) axis, resulting in the release of ACTH, beta-endorphin, and glucocorticoids. While elevated levels of plasma glucocorticoids are also found after chronic ethanol administration, plasma ACTH and beta-endorphin are normal or reduced. It is also unclear whether chronic ethanol exposure results in tolerance to the stimulatory effect of ethanol on BPA activity. To determine the site and mechanism of ethanol action on the BPA axis we studied the CRF secretory profile in a superfused rat hypothalamic preparation after chronic ethanol administration in vivo and the CRF responses after acute ethanol exposure in vitro. Superfused hypothalami from normal and pair-fed control rats released CRF-like immunoreactive material (CRF-LI) in a pulsatile manner, with a mean (+/- SE) frequency of 5.1 +/- 0.7 pulses/h. In contrast, the pulse frequency of CRF-LI release from hypothalami of rats receiving chronic ethanol treatment (fed an alcohol-containing liquid diet for 2 weeks) increased dramatically; the basal mean CRF level, pulse amplitude, and pulse duration remained unchanged. Hypothalamic CRF content was decreased. This chronic ethanol exposure also altered the dose-response characteristics of CRF release when ethanol was introduced acutely, as a pulse, into the in vitro preparation. Acute exposure to 20 mg/100 ml ethanol produced greater release of CRF-LI from control hypothalami than from chronic ethanol-exposed hypothalami. A further elevation above basal levels was produced by 200 mg/100 ml ethanol in control, but not ethanol-exposed, hypothalami. Secretion of CRF from ethanol-exposed hypothalami in response to depolarizing concentrations of potassium chloride was suppressed. Chronic ethanol treatment had no effect on CRF-LI and CRF bioactivity responses to stimulation with acetylcholine. These findings suggest the presence of a high frequency pulse-generating mechanism for CRF release in the hypothalamus. This pulsatile secretory mechanism is altered by chronic ethanol exposure of the animals in vivo. Chronic intoxication resulted in tolerance to the stimulatory effect of ethanol on CRF release in vitro.
Acetylcholine↗
Vitamin D mediated intestinal calcium transport: ultrastructural distribution of calbindin-D28 K following calcitriol.
Explore the source record for details and available documents.
Animals↗
Localization of calbindin-D28K in calcitonin containing cells of chick ultimobranchial glands.
Specific antisera raised against calbindin-D28K (CaBP), the vitamin D-dependent calcium-binding protein from chick intestine, was used to localize the protein in chick ultimobranchial glands (UB glands) by the peroxidase-antiperoxidase technique. CaBP was localized in secretory cells in the cell cords and in a few cells of the epithelium lining the follicles. It was not found in the fibroblastlike cells in the cell cords nor in islands of parathyroid tissue present in the UB gland. The immunomarker for CaBP was distributed throughout the cytoplasm and nucleus of the secretory cells. The same cells demonstrated a positive reaction in their cytoplasm when reacted with an antiserum specific for salmon calcitonin (CT), thus confirming the presence of CaBP and CT in the same UB-gland secretory cells. In other tissues, the presence of CaBP is regarded as an end-organ marker for actions of the vitamin D endocrine system. This novel demonstration of CaBP in UB-gland cells responsible for secretion of calcitonin suggests a direct effect of the vitamin D endocrine system on those cells in addition to an indirect effect through the stimulation produced by elevated circulating calcium levels.
Animals↗
Calbindin-D in peripheral nerve cells is vitamin D and calcium dependent.
The vitamin D-induced calcium-binding protein calbindin-D (CaBP) was localized immunohistochemically in some but not all of the cell bodies and axons within the intestinalis nerve of the chicken. Unlike other nerve tissue thus far examined, the CaBP content of the intestinalis nerve was decreased in vitamin D deficiency and increased in chicken adapted to a calcium-deficient diet. These changes are qualitatively similar to the pattern of response of enterocytes. The inclusion of calcium-containing solutions within the duodenal lumen caused, directly or indirectly, a decrease in the amount of CaBP in this nerve in a dose-dependent manner. The exact role of CaBP in intestinalis nerve cells is unknown but may be in the regulation of intracellular ionic Ca2+ concentrations during excitation, although other functions of CaBP cannot be excluded.
Animals↗