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Biomedical subjects

R Strange

Publications and source records attributed to R Strange.

50 records · Page 3Linked to original sources
PubMed1991

Mammary epithelial differentiation in vitro: minimum requirements for a functional response to hormonal stimulation.

Mammary epithelial differentiation is the culmination of responses to a complex sequence of hormonal stimuli. An in vitro model for this process should retain the basic features of in vivo epithelial differentiation. The IM-2 mouse mammary cell line responds to lactogenic hormone stimulation by synthesizing the milk protein beta-casein. Epithelial and fibroblastic clones derived from IM-2 lack this ability, but cocultures of these clones regain responsiveness to lactogenic hormone stimulation. Studies of the epithelial cell clone 31E under various culture conditions reveal that the role of fibroblastic cells in supporting synthesis and secretion of beta-casein can be supplanted by culture in filter chambers without addition of exogenous extracellular matrix components. Electron microscopic and immunofluorescence studies show that, under these conditions, 31E epithelial cells exhibit the morphology and intercellular organization characteristic of mammary epithelium. Transepithelial electrical resistance measurements indicate that the cells are well polarized. Analysis of glucose metabolism is consistent with this polarization; glucose is utilized from the basal chamber, and lactate is excreted into the basal chamber. Immunoblot analysis demonstrates the vectorial protein secretion expected of polarized mammary epithelium: laminin is secreted into the basal chamber, whereas beta-casein is secreted into the apical chamber in response to lactogenic hormone stimulation from the lower chamber. Thus, the maintenance of a polarized intercellular organization that permits access of the basolateral cell surface to nutrients is sufficient for a pure culture of an established mammary epithelial cell clone to retain differentiated epithelial function in vitro.

Animals↗
PubMed1991

Viral Ha-ras mediated mammary tumor progression.

An immortal mammary epithelial cell line, Comma 1D, and primary cultures of mammary epithelial cells were used to examine the effects of vHa-ras on mammary tumor development. In culture, Comma 1D and primary cells were morphologically indistinguishable. Infection with a replication defective vHa-ras retroviral vector (psi ras) did not alter their in vitro phenotype. Uninfected Comma 1D cells implanted into gland-cleared mammary fat pads gave rise to dysplastic outgrowths, while implants of primary cells gave rise to normal gland structures. After psi ras infection, implants of Comma 1D cells progressed to adenocarcinomas and those of primary cells resulted in initiated dysplastic outgrowths. High level infection of either cell type with replication competent HaMSV (psi ras plus helper virus) resulted in in vitro transformation and undifferentiated in vivo tumors. Thus, in vivo analysis was necessary to detect the observed correlation between tumorigenic stage and level of infection. In this system, expression of vHa-ras was vital but not sufficient for mammary tumor initiation and progression, which resulted from an accumulation of events that did not need to occur in a specific order.

Animals↗
PubMed1990

The alpha and pi isoenzymes of glutathione S-transferase in human fetal lung: in utero ontogeny compared with differentiation in lung organ culture.

Polyclonal antisera to the alpha and pi isoenzymes of glutathione S-transferase have been used in immunohistochemical studies of developing human lung. In utero expression of the pi set was down-regulated in distal airway cells and the first appearance of pi-negative cells coincided with phenotypic differentiation. In contrast, in the early phase of fetal lung organ culture pi isoenzyme was detected in all differentiated epithelial cells and only as culture progressed did focal negativity develop. The alpha set showed no developmental changes in utero or in organ culture.

Down-Regulation↗
PubMed1990

Glial and neuronal differentiation in the human fetal brain 9-23 weeks of gestation.

Nineteen human fetal brains ranging from 9-23 weeks of gestation were examined immunocytochemically for evidence of glial and neuronal differentiation. Radial glia were positive for vimentin and glial fibrillary acidic protein (GFAP) throughout the age range. S100-positive cells which were presumed to be astrocytes were present from 9 weeks; they were always more widespread in the cerebrum and the brainstem than GFAP-positive mature astrocytes, which could be detected with certainty only at 14 weeks. Carbonic anhydrase II (CA II)-positive oligodendrocytes were present in the brainstem in small numbers from 17 weeks. Neuronal fibre tracts in the cerebrum were positive for 160 kD phosphorylated neurofilament protein (BF10) from 9 weeks, but negative for 200 kD phosphorylated neurofilament protein (RT97) and for 70 and 200 kD non-phosphorylated neurofilament protein (NFP) whereas most tracts in the brainstem were positive for BF10 from 9 weeks and positive for the other neurofilament proteins from 14 weeks. Corticospinal tracts differed in remaining negative for neurofilament proteins other than BF10, which showed positive reaction throughout. Perikarya of differentiated neurons in all areas of the brain were neurofilament-negative but neuron specific enolase (NSE)-positive. Germinal eminence cells were focally vimentin-positive from 15 weeks, focally GFAP-positive from 17 weeks, and negative for all NFP and for NSE. The value of a short fixation time and pretreatment with trypsin in the immunocytochemical demonstration of GFAP is stressed.

Brain↗
PubMed1989

Differential expression of alpha and pi isoenzymes of glutathione S-transferase in developing human kidney.

Polyclonal antisera to the alpha and pi isoenzymes of glutathione S-transferase have been used in immunohistochemical studies to determine the developmental expression of these isoforms in human kidney. Before 35 weeks of gestation, both isoenzymes were expressed by the collecting tubules and developing nephrons. After this time, expression of the alpha set was restricted to the proximal tubule and that of the pi set to the distal and collecting tubules and the loop of Henle.

Adult↗
PubMed1989

Harvey-ras mediated neoplastic development in the mouse mammary gland.

The role of a Harvey-ras oncogene in mammary epithelial neoplasia was examined by infecting primary cultures of normal mouse mammary epithelial cells with either the Harvey murine sarcoma virus (psi 2HaMSV) alone or with HaMSV plus a helper virus. The biological effects of expression of the Ha-ras oncogene were determined by transplanting the infected cells into gland-cleared mammary fat pads of virgin Balb/c mice. Expression of the Ha-ras oncogene was correlated with the development of mammary epithelial neoplasms. Cells infected with replication-defective HaMSV alone formed dysplastic, non-invasive mammary outgrowths. Cells infected with HaMSV plus a helper virus developed poorly-differentiated, invasive mammary epithelial tumors. Uninfected cells and cells infected with only the helper virus formed normal mammary trees. Expression of the mutant viral Ha-ras p21 was detected in dysplastic outgrowths and tumors but not in normal mammary outgrowths. Use of this transgenic organ system to genetically alter epithelium of the mouse mammary gland has permitted correlation of expression of a Ha-ras oncogene with development of mouse mammary neoplasia.

Animals↗
PubMed1988

The use of antipyrine clearance to measure liver damage in psoriatic patients receiving methotrexate.

Salivary antipyrine clearance was measured in 15 patients with psoriasis receiving methotrexate and related to liver biopsy changes and routine liver function tests, to determine whether antipyrine clearance could be used as a non-invasive method for monitoring liver function. Comparison of the salivary antipyrine clearance in the methotrexate group (mean 0.51 ml/min/kg, range 0.26-0.81) with 15 matched psoriatic controls (mean 0.54 ml/min/kg, range 0.34-0.99) showed no significant difference. Liver biopsy changes were scored for fatty change, fibrosis, liver cell necrosis and portal tract infiltrate. Total liver biopsy scores correlated significantly with antipyrine clearance/kg body weight (r = -0.72, P less than 0.05). There was no significant correlation of total liver biopsy scores with the other liver function tests. Correlation of the individual liver biopsy changes and antipyrine clearance showed a significant correlation with fatty change (r = -0.75, P less than 0.01), but not with fibrosis (r = -0.53), liver cell necrosis (r = -0.54) or infiltrate (r = -0.41).

Adult↗
PubMed1987

Survey of int region DNA rearrangements in C3H and BALB/cfC3H mouse mammary tumor system.

Rearrangement of the int-1 and int-2 regions of mouse chromosomes was compared in the C3H and BALB/cfC3H hyperplastic alveolar nodule and its hyperplastic outgrowth (HPO) model systems by examining the DNA of the different stages of the neoplastic progression, with use of the Southern blot technique. Rearrangement of int region DNAs associated with proviral amplification occurred more frequently in spontaneous tumors (19 of 27) than in tumors from HPOs (7 of 37) and rarely occurred in HPOs (1 of 29). However, the int-1 rearrangement maintained in 1 BALB/cfC3H HPO line through 11 transplant generations suggests that the int-1 rearrangement is neither sufficient nor necessary for progression to mouse mammary carcinoma.

Animals↗
PubMed1985

Mammary tumors in feral mice lacking MuMTV DNA.

Two mammary tumors developed in feral mice treated with dimethylbenzanthracene. The tumors, livers, and spleens of these animals contained no MuMTV proviral DNA. Neither tumor had amplified or rearranged int-1 or int-2 loci. This demonstrates that mammary tumorigenesis can occur in mice in the absence of endogenous and exogenous MuMTV.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Who cares pays.

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Aged↗
PubMedDate not supplied

Apoptosis in the genesis and prevention of cancer.

A strong rationale exists for developing cancer control strategies designed to suppress or reverse the development of precancerous lesions in order to reduce the occurrence and recurrence of this disease. Whereas numerous agents have been identified that inhibit tumor development, little is known about how they work. Recently the hypothesis has been raised that misregulation of apoptosis results in a failure of tissue size regulation that contributes to the development of cancer. If validated, this concept has important implications for the prevention of carcinogenesis and could lead to the development of new cancer control approaches that have as their basis the restoration of competence to regulate tissue size. Thus, it is essential to consider the role of cell loss in the tumorigenic process. In this regard investigation of the role of specific types of cell death in tumorigenesis, particularly the role of apoptotic cell death in maintenance of tissue homeostasis, has been neglected. The fact that apoptosis is a highly conserved, specific, and selective means of controlling tissue mass and shape also suggests that it can be exploited for the prevention or control of cancer.

Apoptosis↗
PubMedDate not supplied

Pride in practice.

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Aged↗