Proliferative activity of the anterior pituitary gland in 10 week-old male and female rats under normal conditions was investigated by counting mitotic figures and using single and double immunostaining of 5-bromo-2'-deoxyuridine (BrdU), proliferating cell nuclear antigen (PCNA), and six pituitary hormones. To determine which proliferative changes depend on the estrous cycle and circadian changes, respectively, six groups of female and two groups of male rats were studied at various times of day. Additionally, BrdU-incorporated cells were further classified by the six types of hormones they contained, or as immunonegative cells. Cell proliferative activity in the females fluctuated drastically with the highest activity in estrus and the lowest in diestrus. In the males, proliferative activity was at a relatively low level, and was similar to that in females in proestrus or early estrus, with the greater activity at night. Identified by their pituitary hormones, the distribution of the proliferating cells was almost the same in each sex, with prolactin (PRL) cells accounting for the highest proportion, followed by growth hormone (GH) cells, and adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH) cells. These percentages agreed well with previously reported levels of cell types among all pituitary cells of the rat. It is therefore suggested that the life span and cycle of rat pituitary cells does not differ among cell types. In another test, male and female rats were given BrdU continuously via an osmotic pump for 8 days to compare cell proliferative activity between sexes, exclusive of the influence of estrous cycle and circadian changes. In this way, we were able to demonstrate that the cumulative incorporation of BrdU in females was consistently twice as high as in males over a constant period of time, and to conclude that cell renewal occurs at a doubled rate in the pituitary of female rat.
There has recently been an increase in data indicating that autoimmune mechanisms are involved in the etiopathogenesis of idiopathic thrombocytopenic purpura (ITP) (1, 2). Although antibodies that react with platelets are found in most patients with ITP, the pathogenetic nature of the antibodies remains to be clarified . The discovery of an animal model for ITP has therefore been long-awaited. Here we have found that (NZW x BXSB)Fi (W/B Fi) mice, which develop lupus nephritis with myocardial infarction (3), show thrombocytopenia with age, and that this is due to the presence ofboth platelet-associated antibodies (PAA) and circulating antiplatelet antibodies.Recently, we have demonstrated that allogeneic bone marrow transplantation (ABMT) has curative effects on autoimmune diseases in (NZB x NZW)FI, BXSB, MRL/MP-lpr/lpr (MRL/lpr), and NOD mice (4-6) . These results prompted us to examine whether ABMT can be used to treat ITP. In the present study, we provide evidence that the transplantation of bone marrow from BALB/c mice to W/B F, mice does indeed have preventative and curative effects on ITP Materials and MethodsMice.Mice ofthe inbred strain BALB/c nu/nu, BALB/c, C57B/6, C3H/HeN, BXSB, NZW were raised under specific pathogen-free conditions in our animal facility. W/B F, males were obtained from the Nippon Shinyaku Research Laboratories, Kyoto, Japan.Staining Procedure andData Analysis.Platelet-rich plasma was obtained as described previously (7) . The platelets were suspended in 1% paraformaldehyde solution for 5 min. After
Immunoreactivities in 25 cases of prostatic adenocarcinoma and 10 normal/hyperplastic prostates were investigated in methacarn-fixed, paraffin-embedded serial sections using a panel of nine anti-keratin monoclonal antibodies (mAbs); 34 beta E12, CK8.12, 312C8-1, CK4.62, RPN1165, RPN1162, 35 beta H11, CK5, M20, and one of anti-actin mAb, HHF35. In normal/hyperplastic prostates, RPN1162, 35 beta H11, CK5 and M20 stained luminal cells without staining basal cells, and 34 beta E12, CK8.12 and 312C8-1 stained basal cells but not luminal cells. Other mAbs, CK4.62 and RPN1165, stained basal cells as well as luminal cells. All of the mAbs labelling luminal cells stained cancer cells with variable frequencies in a manner unrelated to the grade of tumour differentiation. Of the prostate cancer cases 92% were scored positive with M20, 84% with 35 beta H11, 80% with CK5, 68% with CK4.62, 60% with RPN1165 and 4% with RPN1162. However, basal cell-specific keratins labelled with 34 beta E12, CK8.12 and 312C8-1 were totally negative in the cancer cells. HHF35 showed no labelling in normal, hyperplastic or neoplastic epithelial cells of the prostate. Our findings indicate that the major part of the cells of prostatic adenocarcinomas have keratin phenotypes similar to luminal cells but not basal cells, and that no myoepithelial differentiation can be detected in epithelial cell of the prostate. Thus, mAbs for keratins facilitate the identification of epithelial cell phenotypes in normal, benign and malignant conditions of the prostate.
PATHOLOGY: HUGGINS, MOON, AND MORIH 379 days, the culture was green and thriving. This strain has been isolated and designated Chlorella pyrenoidosa C-37-2-G4. The modified strain grows well in the presence of progesterone. Cultures of the modified strain to which progesterone has been added deteriorate at a much slower rate than those cultures of the original strain to which androstenedione or dehydroisoandrosterone had been added. Furthermore, thin-layer silica-gel chromatography indicates that metabolic products from progesterone are formed by this modified strain. The incubation of dehydroisoandrosterone for 432 hr with Chlorella pyrenoidosa C-37-2 produced at least four different compounds. These were detected by means of thin-layer silica gel chromatography. From the position of the products on the chromatograms, it is probable that one of these was 5-androstene-3f3,17f3-diol while another was an hydroxylated 5-androstene-3#,17,3-diol. The structures of all the indicated conversion products and the possible transformation of steroids by other species and strains of algae are being investigated currently.
In the work now to be described, it was observed that a single dose of 7,12-dimethylbenz(a)anthracenO caused extraordinary changes in the rat consisting of adrenal apoplexy and massive necrosis in the two inner zones of the cortex while other regions of the adrenal glands were uninjured. In addition to the selectivity of the anatomic site of damage, there is high specificity of the molecular structure of the polynuclear aromatic hydrocarbon exerting this adrenocortieolyfic effect.Earlier it was found (1, 2) that a single dose of any of a number of polynuclear aromatic hydrocarbons, under special circumstances, selectively induced mammary cancer in every rat with very great rapidity. DMBA was the most effective of these compounds and tumors arose following a solitary feeding or an intravenous injection. At necropsy of rats with cancer of the breast induced by a solitary dose of DMBA which had been administered a few weeks previously, it was observed that the adrenal glands of most of the animals were calcified. The adrenals of rats bearing mammary cancer induced by hydrocarbons other than DMBA were not calcified. It was soon found that adrenal apoplexy and necrosis were produced invariably with DMBA soon after giving the hydrocarbon. This is a newly recognized property of DMBA.Several methods were employed in these experiments for detection and measurement of damage to the adrenal glands. These included: (a) direct inspection of the gland; (b) histological observation; (c) estimation of the amount of blood pigments; (d) determination of enzyme content of the adrenals; (e) roentgenologic detection of adrenal calcification.
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