PubMed Health⌕ Search

Biomedical subjects

S Morii

Publications and source records attributed to S Morii.

At least 37 records · Page 2Linked to original sources
PubMed1993

Mammary tumour induction by pituitary grafting in male mice: an animal model for male breast cancer.

Isologous anterior pituitary grafting, 4 each, to 3-4-month-old SHN and SLN male mice resulted in an appearance of mammary tumours from 8 months of age and the incidence at 12 months reached 53.8% in each strain. All tumours were diagnosed as type B adenocarcinomas. In association with the results, normal mammary gland growth and mouse mammary tumour virus (MMTV)-gp52 antigen levels in the submaxillary glands were stimulated by the treatment in these strains. The effect of pituitary grafting was much less in GR/A male mice in which no mammary tumours appeared.

Adenocarcinoma↗
PubMed1993

Growth of the mammary gland in rhino mouse.

The rhino mouse, so called because of its characteristic rhinocerous-like skin cannot raise its young. Although the animal has rudimentary mammary glands, these are thought to be defective due to their impossibility to raise their young. Morphological observations of the female mammary glands of rhino mice (hrrh/hrrh) were carried out and the results were compared with those of their normal litter mates (hrrh/+) at various ages from 1 month to 1 year. No morphological differences in mammary gland development was seen between the rhino mice and their normal litter mates, and normal secretory changes were observed in the rhino mice after delivery. Mouse mammary tumor virus (MMTV) expression and the occurrence of hyperplastic alveolar nodule (HAN) were analogous to these features in phenotypically normal hrrh/+ mice. Further, the sweat glands in the rhino mouse were normal. Thus, anomalies in the rhino mouse appeared to be limited to the skin and pilosebaceous apparatus.

Animals↗
PubMed1992

Keratin profiles in normal/hyperplastic prostates and prostate carcinoma.

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.

Adolescent↗
PubMed1992

Immunohistochemical staining patterns of tenascin in invasive breast carcinomas.

Eighty-two cases of primary invasive breast carcinoma and adjacent "normal" mammary glands were examined immunohistochemically for tenascin expression and distribution. Formalin-fixed tissues pretreated with actinase were processed by the avidin-biotin complex method using anti-human tenascin monoclonal antibody (RBC1). In normal mammary glands, tenascin was distributed around the ducts and ductules but not around the acini. In carcinomas, a high incidence of tenascin-positive cases (greater than 67%) was seen with various histological appearances, with the exception of lobular carcinoma where a low incidence was found (25%). Although intense staining was seen around cancerous foci when compared with normal mammary glands, tenascin was often expressed at cancer-mesenchymal junctions with dense fibrotic stroma, but not at junctions with active inflammatory change and a loose fibrotic stroma. Tenascin, expression is not an all-or-none marker for mammary malignancy and the staining pattern suggests either a role in stimulating cancer cells or a host defence mechanism accompanied by a desmoplastic response to them.

Adenocarcinoma, Mucinous↗
PubMed1992

Breast carcinoma in patients receiving neuroleptic therapy. Morphologic and clinicopathologic features of thirteen cases.

We report 13 cases of breast carcinoma in patients treated with neuroleptics (prolactin-releasing drugs). Twelve of the patients were female and one was male. Nine patients had unicentric carcinoma, one had multicentric tumors arising synchronously, and three had bilateral tumors (synchronous in one case and metachronous in two cases). Thirteen tumors in ten patients were invasive ductal carcinomas, two tumors in one patient were mucinous carcinomas, and the two other patients had lipid-secreting carcinomas. Immunohistochemical staining showed alpha-lactalbumin (alpha-LA) in the lipid-secreting carcinomas at sites exhibiting active lipid secretion. A precise cause-effect relationship is difficult to elucidate, since the patients ranged in age from 40 to 64 years (mean: 51 years) when cancer was first diagnosed. However, the relatively high incidence of multiple tumors and the production of lipid and alpha-LA by the cancer cells were unusual features suggesting an association with neuroleptic therapy.

Adult↗
PubMed1992

Immunohistochemical demonstration of breast-derived and/or carcinoma-associated glycoproteins in normal skin appendages and their tumors.

Sixty-six benign and malignant skin appendage tumors were studied for the expression and localization of the glycoproteins identified by the monoclonal antibodies (MoAbs) GCDFP-15, CU18, B72.3, and VU-1D9. Formalin-fixed, paraffin-embedded tissue was processed by the avidin-biotin complex method. In normal eccrine and apocrine sweat glands, GCDFP-15, CU18, B72.3, and VU-1D9 staining was localized differently (intracellular, membranous, or intraluminal), whereas eccrine glands showed no B72.3 staining. There were various patterns of positive staining of tumors arising from sweat glands, but no immunoreactivity for B72.3 was found in eccrine-derived tumors. CU18 and VU-1D9 labeled mature sebocytes in a vacuolar fashion and stained sebaceous carcinomas. VU-1D9 labeled membranes of the secondary germ cells in early anagen of a hair follicle bulb as well as the basaloid cells of trichoepitheliomas and basal cell carcinomas. These MoAbs appear to be valuable markers for the study of normal skin appendages and their tumors.

Antibodies, Monoclonal↗
PubMed1992

Lectin-binding profiles for normal skin appendages and their tumors.

A histochemical investigation of lectin-binding sites was carried out on formalin-fixed paraffin-embedded sections of 60 skin appendage tumors and adjacent normal skin appendages, using four different biotinylated lectins, peanut agglutinin (PNA), Dolichos biflorus agglutinin (DBA), soybean agglutinin (SBA), and Ulex europaeus agglutinin-1 (UEA-1), and avidin-biotin-horseradish peroxidase labeling. In the secretory segments of eccrine sweat glands, the superficial dark cells showed strong cytoplasmic staining with UEA-1, whereas DBA and SBA strongly stained the plasma membranes of basal clear cells. The acinar cells of apocrine sweat glands revealed sporadic apical membrane staining with all four lectins. In some cases, the luminal membranes of sweat gland ducts showed apical membranous staining with all four lectins. In the hair follicles, the inner root sheath was positive for all four lectins, and the outer root sheath was stained by PNA. The sebaceous ducts, as well as the outer root sheath at the level of sebaceous duct insertion, were also labeled by all four lectins. Sebaceous lobules showed cytoplasmic and membrane staining of mature sebocytes with PNA and SBA. Although sweat gland tumors revealed differences in lectin binding when compared to their corresponding normal tissues, the lectin-binding pattern of pilosebaceous tumors was analogous to the pilosebaceous apparatus.

Histocytochemistry↗
PubMed1992

Choroid plexus arteriovenous malformations.

Among 24 arteriovenous malformations (AVMs) involving the choroid plexus, 11 were plexal type AVMs predominantly located in the choroid plexus of the lateral ventricle, and 13 were parenchymal type AVMs mainly situated in the paraventricular cerebral parenchyma. 83% of all AVMs involved both the choroid plexus and the paraventricular cerebral parenchyma. Most cases presented with intracranial hemorrhage, particularly intraventricular hemorrhage. The most serious surgical problem was a small residual nidus unrecognized at the initial operation causing postoperative hemorrhage. Five parenchymal type AVMs presented residual niduses in the choroid plexus, causing death in two cases. Two plexal type AVMs resulted in residual AVMs supplied by the cisternal segment of the anterior choroidal artery, situated in the medial temporal lobe. To prevent postoperative hemorrhage from a small residual nidus, immediate postoperative angiography while the patient is still under general anesthesia should be performed to identify any residual nidus.

Adolescent↗
PubMed1992

A mixture of paraphenylenediamine and imidazole: its effect on the extraction of lipid droplets during electron microscopy staining.

To prevent extraction of lipids during a double staining procedure for electron microscopy, the tissue slices, double fixed with glutaraldehyde and osmium tetroxide to preserve microvesicular lipid droplets in the cytoplasm, were immersed for 2 hr in veronal buffer (pH 9.0) containing 0.5% p-phenylenediamine and 0.5% imidazole immediately after postfixation. The stained sections of the immersed tissue slice showed blackened, well circumscribed lipid droplets similar to those in corresponding unstained sections. Moreover, highly contrasting features of the cellular architecture could be visualized with the double stained, as well as routinely prepared sections.

Adrenal Cortex↗
PubMed1991

Immunohistochemical distribution of MAM-3 and MAM-6 antigens in developing salivary glands of the human fetus.

The immunohistochemical expression of MAM-3 and MAM-6 antigens was studied developing human fetal salivary gland removed at autopsy of 22 normal fetuses of varying maturity (10-40 weeks of gestation). The onset of functional maturation in the fetal gland was seen at 21 weeks of gestational maturity. The acini and ducts then underwent distinct alterations in antigen expression with growth and maturation until the late developmental stage (33-40 weeks of gestation) when they resemble the adult salivary gland. The role of maturing duct cells in histogenesis of salivary gland tumours is discussed.

Antibodies, Monoclonal↗
PubMed1991

Immunohistochemical demonstration of keratins 8 and 14 in benign tumours of the skin appendage.

The expression of keratins 8 and 14 was investigated immunohistochemically by the avidin-biotin-peroxidase (ABC) method using formalin-fixed paraffin-embedded specimens from 42 tumours of human skin appendages. Results were compared with the staining of 34 specimens from normal skin and skin appendages adjacent to the tumours. Keratin 14 was detected by the monoclonal antibody (mAb) 312C8-1, and was found in the basal cells of the epidermis, the outer root sheaths of hair follicles, and the peripheral cells of sebaceous glands. It was also detected in the inner and outer layers of cells in the ductal portion and the myoepithelial cells in the secretory portion of apocrine and eccrine sweat glands. Keratin 8 was detected by mAb 35BH11, and was present in the secretory cells of eccrine and apocrine sweat glands but not in myoepithelial or ductal cells. The pilosebaceous apparatus and the epidermis were uniformly negative. In benign skin appendage tumours, the staining patterns for both keratins generally resembled their distribution in the corresponding normal tissues. The demonstration of keratins 8 and 14 may be useful in the recognition, classification and diagnosis of skin appendage tumours.

Antibodies, Monoclonal↗
PubMed1991

Induction of tumors in the Japanese house musk shrew, Suncus murinus (Insectivora), by dimethylbenz[a]anthracene.

The carcinogenic effect of 7,12-dimethylbenz[a]anthracene (DMBA) was examined in the virgin female Japanese house musk shrew, Suncus murinus (family: Soricidae, order: Insectivora). Leukemia, musk gland tumors, pilosebaceous tumors and sarcomas were induced in the DMBA-treated shrews, whereas none of the controls developed any tumors up to 50 weeks of age. DMBA emulsion was administered i.p. at a dose of 1.25 or 2.5 mg once a week, with either four or eight doses being given from 8 weeks of age. Leukemia developed in 100% (9/9), 50% (5/10), 56% (5/9) and 0% (0/10) of the animals treated with a total dose of 20 mg (8 x 2.5 mg), 10 mg (8 x 1.25 mg), 10 mg (4 x 2.5 mg) and 5 mg (4 x 1.25 mg) of DMBA respectively. Leukemia was of the lymphatic and/or mast cell type, and the spleen was the organ invariably involved. A dose-dependent effect of DMBA was not observed for pilosebaceous and musk gland tumors. When 1 mg of DMBA powder was dusted into the subcutaneous tissue at 4 weeks of age, sarcomas developed at the dusted site (69%; 9/13).

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1991

Keratin expression in the normal breast and in breast carcinoma.

The immunohistochemical reactivities of 69 cases of breast carcinoma were examined on methacarn-fixed, paraffin-embedded sections using eight different monoclonal antibodies which recognize one or a few keratin polypeptides. In the normal breast, the monoclonal antibodies RPN1162, RPN1165 and AE1 stained almost all the luminal cells but not the basal (myoepithelial) cells. The monoclonal antibodies 35BH11, M20, CK5 and CK8.12 stained only a subset of the luminal cells. In contrast, 312C8-1 stained basal cells but not luminal cells. All the tumour specimens reacted with AE1, while over 80% of them also reacted with 35BH11 (57/69), CK5 (57/69) and RPN1165 (55/69); 30% reacted with CK8.12 (21/69) and 16% with RPN1162 (11/69). Basal cell-specific keratin, as defined by 312C8-1, was detected in only 1% of cases (1/69). Monoclonal antibodies to different keratin polypeptides may be of use in the characterization and subdivision of breast cancer.

Antibodies, Monoclonal↗
PubMed1991

An autopsy case of purulent mycobacterial meningitis in AIDS.

The patient was a 46-year-old male hemophiliac who died of acute mycobacterial meningitis associated with AIDS (acquired immune deficiency syndrome). Autopsy revealed severe basal meningitis which was characterized by an infiltration of numerous polymorphonuclear leukocytes. Severe mural inflammation of the subarachnoid arteries was noted, and innumerable acid-fast bacilli were demonstrated. Epithelioid cell granulomas were not found in the meningeal lesion. The lungs, liver, spleen, and bone marrow contained many epithelioid cell granulomas with caseous necrosis. Massive proliferation of swollen histiocytes could not be identified in any organ. The absence of epithelioid cell granulomas in the meningeal lesion indicate a severe impairment of cell-mediated immunity in the patient; this anergic type of lesion is one of the characteristics of tuberculosis occurring in association with terminal AIDS.

AIDS Dementia Complex↗
PubMed1991

Immunohistochemical localization of MAM-3 and MAM-6 antigens in adenoid cystic carcinoma.

MAM-3 and MAM-6 antigens were detected immunohistochemically in 34 cases of adenoid cystic carcinomas (ACC) of the salivary glands and these patterns were compared to these of epithelial membrane antigen (EMA) and laminin. ACC was histologically divided into three types; the cribriform pattern, the tubular and trabecular pattern, and the solid cluster pattern. Immunostaining of EMA and MAM-6 antigen had a similar distributions in the luminal borders of luminal tumor cells, whereas the MAM-3 antigen was slight or negative in luminal borders. Myoepithelial derived tumor cells of ACC accompanying hyaline stroma demonstrated positive staining for the MAM-6 antigen (whole cell positive type), and luminal tumor cells of microcysts showed strong staining for the MAM-3 antigen. Laminin staining was confined to the basement membrane and surface borders in pseudocyst cavities. In salivary gland ACC, laminin staining can be used as a marker of pseudocyst surfaces and immunostaining of EMA and the MAM-6 antigen as a marker of luminal borders of cyst. These two histochemical markers were useful for discriminating pseudocyst and cyst.

Antigens, Neoplasm↗
PubMed1991

Immunophenotypic difference of keratin expression in normal mammary glandular cells from five different species.

The immunohistochemical reactivity of human, monkey, shrew, rat and mouse normal mammary glands was examined using methacarn-fixed paraffin-embedded specimens and acetone-fixed frozen sections using the avidinbiotin-peroxidase method for cell phenotype comparison. Actin was visualized using anti-smooth muscle actin antibody and keratin expression was determined by employing 12 different monoclonal antibodies. All these antibodies cross-reacted specifically with the species examined. Basal (myoepithelial) cells from all species showed muscle-specific actin according to reactivity with HHF35 monoclonal antibody. Keratin expression showed significant phenotypic differences among species. In human and monkey, AEL-KS2, KL1, CK8.13, AE3 and 34BE12 stained luminal cells as well as basal cells. AE1, RPN1165, CK4.62, 35BE11, M20 and RPN1162 labeled only luminal cells whereas 312C8-1 preferentially bound to basal cells. In shrews, AEL-KS2, CK8.13 and AE3 reacted to both cell types, AE1 reacted only with luminal cells, and 35BE12 and 312C8-1 selectively stained basal cells. In rodents, AEL-KS2 reacted to both cell types, CK8.13, AE3, 34BE12 and 312C8-1 stained rat basal cells, and 34BE12 and 312C8-1 reacted to mouse basal cells. The data represents cytoskeletal differences among species.

Actins↗