Regarding Arcangeli et al. IJROBP 1998;42:1119-1126.
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Biomedical subjects
Publications and source records attributed to J D Dubois.
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We report a case of myeloma which presented as an acute abdomen with an associated pancreatic mass. This clinical picture has not been reported previously.
Fragments of ductal and lobular epithelium ('organoids') produced by collagenase digestion of reduction-mammoplasty specimens were injected into athymic 'nude' mice. These heterospecific tissues were accepted without rejection, and the presence of xenografts was confirmed by cytology, immunocytochemistry and chromatin staining. Lactation, as confirmed by immunocytochemical and ultrastructural criteria, was observed in the grafted human epithelium during murine pregnancy at both intra- and extra-mammary sites.
A case of biopsy-proven anal involvement in acute promyelocytic leukaemia is presented with management by local conservative measures and remission induction with chemotherapy. A brief review of the literature is given.
Epithelial components of the normal human breast and their response to hormonal manipulation have been studied in the nude mouse. Six to eight week-old female athymic nude mice were used as the recipients of enzymatically prepared breast organoids, composed of ductal and lobuloalveolar structures. After 12 weeks in situ in the mouse mammary fat pad the human breast tissue retains its normal morphology as demonstrated by the presence of myosin positive myoepithelial cells and keratin positive luminal cells. Monoclonal antibodies M8 and M18 raised to components of the human milk fat globule membrane give a similar staining pattern in the xenografted organoids to that seen in the donor tissue. On mating the recipient female nude mice, the human breast tissue responds with both an increased 3H-thymidine labelling index and alpha-lactalbumin production. This model in conjunction with in vitro studies is, therefore, suitable for the study of extrinsic and intrinsic factors controlling differentiation and morphogenesis in the human breast.
Nostoc sp. colonies from field collections were cultured and propagated on silica sand with aqueous N-free BG-11 medium. Laboratory experiments were conducted to characterize the in vivo freeze-recovery physiology of nitrogenase activity. Nitrogenase activity was monitored by the acetylene reduction technique. Frozen Nostoc sp. colonies were thawed and warmed to 10, 15, 20, 25, or 30 degrees C. At 25 and 30 degrees C, nitrogenase activity was detected within 6 h after thawing. At 20 degrees C or lower, nitrogenase activity was not detected until 12 h after thawing. Optimum thawing temperature with respect to the recovery of nitrogenase activity was 25 degrees C. In subsequent experiments, laboratory-grown Nostoc colonies were used along with the following conditions: prefreezing treatment of 3 days of exposure to light or darkness, freezing, and then thawing to 25 degrees C in light or darkness with or without metabolic inhibitors [3-(3,4-dichlorophenyl)-1, 1-dimethylurea (DCMU), monofluoroacetate, or chloramphenicol]. Approximately 30% of the energy in the initial recovery of nitrogenase activity (to 12 h after thawing) appeared to be supplied via the utilization of carbon compounds stored before freezing. Photosynthetic conditions (i.e., light and without DCMU) were necessary for maximum recovery of nitrogenase activity. In the presence of the protein synthesis inhibitor chloramphenicol, nitrogenase activity was still detected at 12 to 48 h after thawing. Although damage may occur to nitrogenase, some of the enzyme was capable of surviving the freeze-thaw period in vivo. However, complete recovery of nitrogenase activity (equal to prefreezing activity) may entail some de novo synthesis of nitrogenase.
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Sprague-Dawley rats were sacrificed by decapitation at 5, 7, 12, 14, 22, 26, 32, and 40 days of age. Adult animals (175 to 225 g) were also studied. Serum-free thyroxine (FT4) concentrations rose rapidly between 5 and 12 days to levels similar to adult concentrations, whereas the percentage of FT4 was relatively high between 5 and 12 days before declining to adult values by 14 days. Serum-free triiodothyronine (FT3) concentrations rose progressively to attain peak concentrations at 26 days and subsequently declined to adult levels by 40 days. The percentage FT3 rose in parallel with the FT3 concentrations to peak values at 22 to 26 days before declining to adult levels. FT4/thyroid-stimulating hormone (TSH) and FT3/THS ratios increased progressively through 22 days of age in parallel with the FT3/FT4 ratio. These data indicate that free thryoid hormone concentrations follow essentially the same developmental profile as do total thyroid hormone concentrations. Progressive maturation of the negative feedback control mechanism for the pituitary-thyroid axis, as assessed by the FT4/TSH and FT3/TSH ratios, occurs through 14 days. However, the continued rise in FT3 concentrations, FT3/TSH, and FT3/FT4 ratios through 26 days suggests a further resetting of the setpoint of the pituitary-thyroid axis possibly related to the stress of weaning.
Using highly specific double-antibody radioimmunoassay techniques, we have measured pituitary and serum prolactin (PRL) concentrations in neonatal rats from birth to 60 d. Pituitary PRL concentration was low at birth in both sexes and peak prepuberal values were attained at 25-28 d. Following this time, pituitary PRL concentrations in females were significantly higher than those observed in males (p less than 0.01). Serum PRL concentrations were low at birth in both sexes and remained low until 15 d, when they rose to peak values just before puberty. There were no significant sex differences with respect to serum PRL concentrations. These data indicate that hypothalamic control of PRL secretion developes during the neonatal period of the rat. The relationship of this developmental process in the neonatal rat as a possible model for the study of the midgestational hypothalamic maturation of the human fetus is discussed.
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To detect placental transfer of L-triiodothyronine (T3) in pregnant rats, we injected 1 muCi [125I]T3 on the 16th, 18th, and 20th day of gestation. Three hours after the injection, which corresponds to the equilibrium time determined by a method of constant infusion, the pregnant rats and their fetuses were killed. The [125I]T3 was extracted from the serum or the homogenate by butanol extractions and alkaline washes. The transfer rate was calculated from the quantity of [125I]T3 in the serum of the fetuses after 3 hr and from the maternal metabolic clearance rate (8.19 +/- 0.45 ml/hr/100 g body weight; mean +/- SEM). At the 16th day of gestation, the placental transfer of T3 was 0.82 +/- 0.11% of the total maternal clearance rate/litter weight; it was 1.05 +/- 0.25% at the 18th day of gestation and 0.58 +/- 0.10% at the 20th day of gestation. There were no significant differences between these results. The maternal T3 concentration was 68.27 +/- 20.6 ng/100 ml and its production rate was 5.57 +/- 0.31 ng/hr/100 g; with these data we calculated a maternal-fetal T3 transfer of 46 +/- 6 pg/hr. Furthermore, there was no T3 transfer observed when the mother received 1.9 mug unlabeled T3, which led to a significant rise in maternal T3 concentration (68.27 +/- 20.6 ng to 102.23 +/- 7.41 ng/100 ml; P less than 0.01); there was no detectable T3 in the fetal serum. From these results we conclude that there is minimal or no placental transfer of T3 in the rat and that the hypothalamic-pituitary-thyroid axis of the fetus develops autonomously.
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