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Biomedical subjects

Y Tatemoto

Publications and source records attributed to Y Tatemoto.

At least 19 recordsLinked to original sources

Erythropoietin expressed in granular convoluted tubule cells of mice submandibular glands under hypoxia, anemia, and nephrectomy.

Immunohistochemically detectable erythropoietin-like substance(Epo) in granular convoluted tubule(GCT) cells of submandibular glands (SMG's) was examined in mice in which hemolytic anemia had been induced by phenylhydrazine (ph), and in mice subjected to hypoxia, nephrectomy, or testosterone (TP) injections. Staining for Epo was negative in GCT cells of SMG's in normal mice, while positive staining occurred in GCT cells of the anemic mice and mice subjected to hypoxia or nephrectomy. A positive Epo reaction was also revealed at the luminal borders of distal tubules, and in cells of proximal and distal tubules in the kidney, and in some hepatic and spleen cells, of mice that had received combination regimens producing anemia and hypoxia, or had been nephrectomized. Increased staining of Epo was found in GCT cells of SMG's, and in proximal and distal kidney tubules of mice given the combination treatment plus TP injections. The detection of Epo in GCT cells suggests these extrarenal cells to be sites of accumulation or biosynthesis of the protein under certain specific conditions such as hemolytic anemia and hypoxia.

Anemia, Hemolytic

Mucinous adenocarcinoma of the submandibular gland.

A rare tumor not easily classifiable among published histologic categories for salivary gland tumors is reported. The neoplasm developed within the submandibular gland of a 78-year-old woman with invasion of the mandible and metastasis to regional lymph nodes. Histopathologically, cuboidal cells possessing clear cytoplasm and displaced round nuclei proliferated and exhibited an adenomatous pattern. Many cystic spaces surrounded by tumor cell strands were seen, mucus substance filled in the cystic spaces, and the tumor cells seemed mucus-secreting, but neither epidermoid cells nor papillary appearance could be observed. Electromicroscopically, numerous mucous droplets of low electron density were prominent in the cytoplasm, and the tumor cells had sparse irregular microvilli on the luminal surface. Mucin histochemistry, including paradoxical concanavalin A staining, revealed that the tumor cells contained neutral and acid mucins, and these were identified as class II and III mucosubstances. No other neoplastic lesion, except recurrent metastatic neck nodes, has been detected 6 years after the first examination, and it seems that the tumor is a rare primary mucinous adenocarcinoma of the submandibular gland.

Adenocarcinoma, Mucinous

Immunohistochemical staining of infiltrates in oral lichen planus.

Immunohistochemical examination of lymphocyte and accessory cell infiltrates was performed in 24 cases of oral lichen planus using a double staining technique. The major population of the superficial stromal lymphocytes was T cells which were mostly composed of dominant CD 4+Leu8- (helper T cells) and lesser numbers of CD 8+11b- cells (cytotoxic T cells). Contrarily, many more CD 8+11b- cells than CD 4+Leu8- cells had infiltrated the epithelium. Some infiltrated T cells expressed interleukin-2 receptor and about half of cytotoxic T cells expressed class II antigen. HLA-DR-positive monocytes were also observed in both the superficial stroma and the epithelium. A number of HLA-DR-bearing CD 1+ cells (Langerhans/dendritic cells) and CD 11c+ cells (macrophages) were observed in the lower layers of the epithelium which were sometimes degenerative. Having significant correlation with the infiltration intensities of subepithelial macrophages and epithelial CD 8+ cells (cytotoxic/suppressor T cells), epithelial Langerhans cells variably infiltrated. Superficial stromal CD 8+ cells correlated with epidermal CD 8+ and CD 4+ cell (helper/inducer T cells) infiltrates. These findings are consistent with the notion that Langerhans cells and macrophages play an important role in antigen presentation, and suggest that cellular immunity, mediated by cytotoxic T cells with helper T cells, may be related to the pathogenesis of oral lichen planus.

Antigens, CD

Histochemical studies on irradiated and obstructive human submandibular glands. Protein distribution and lectin-binding in the degenerative glands.

Immunohistochemical protein distribution of alpha-amylase (Am), lysozyme (Ly), cytokeratinin (CK), S-100 protein (S-100) and secretory component (SC), and lectin-binding (SBA and UEA-I) profiles were studied in 10 obstructive and 20 irradiated human submandibular glands which were surgically extirpated. Degenerative intensity of the glands was graded as I, II and III based on the order of severity. All proteins generally existed in serous acinic cells of the intact glands. The proteins immunoreactivities became weak even in mildly inflamed glands (grade I), and nearly disappeared from the moderately damaged glands (grade II). Duct cells had clear CK and some cells reacted with the anti-SC antibody, but other proteins were not observed on the ducts. Mucous cells possessed none of the proteins, and their lectin-binding was only traceable in some glands. Compared with immunoreactivities in the proteins, lectin-binding profiles were different. SBA and UEA-I bound somewhat similarly to both acinic and duct cells, and the binding was hardly affected even by severe degeneration (grade III). Between obstructive and irradiated glands, no obvious difference was observed in either protein distribution or lectin-binding. From the above, it seems that some proteins are more affective to the degeneration and that lectin-binding sugar residues are non-affective against the degenerative changes of the tissues.

Histocytochemistry

Langerhans cells in odontogenic tumours and cysts as detected by S-100 protein immunohistochemistry.

Immunohistochemical demonstration of S-100 protein in Langerhans cells (LCs) was made in odontogenic epithelial tumours (71 cases), radicular cysts (40 cases), follicular cysts (28 cases), odontogenic keratocysts (11 cases), primordial cysts (7 cases) and fissual cysts (6 cases). With the use of polyclonal antiserum against S-100 protein, positive LCs, dendrical or irregular in shape were found in tumour or cystic epithelia, and sometimes in stromal connective tissue. Incidence of positive S-100 staining LCs was 11 cases out of 61 ameloblastomas, 22 cases out of 40 radicular cysts, 3 cases of 28 follicular cysts, and other lesions in both odontogenic tumours and cystic diseases lacked LCs. The cases with S-100 protein positive LCs were usually accompanied with a high degree of inflammatory infiltration in their lesions; on the contrary, the negative cases also generally lacked inflammatory responses.

Humans

Immunohistochemical distribution of epithelial membrane antigen in bladder carcinomas as detected with a monoclonal antibody.

Expression of epithelial membrane antigen (EMA) was investigated immunohistochemically in 27 cases of bladder carcinoma using a monoclonal antibody. Normal urothelial epithelium showed EMA staining restricted to the upper layer of the surface epithelium. G-I transitional cell carcinomas demonstrated positive EMA staining which could be divided into the following 3 types; type 1, in which highly stained cells occurred in the upper layer of the neoplastic epithelium; type 2, in which the whole tumour focus was slightly stained; and type 3, in which cells strongly positive for EMA were scattered throughout the tumour focus. G-III (undifferentiated) transitional cell lesions exhibited irregular expression of EMA whereas squamous cell demonstrated specific intense EMA staining within keratinized tumour cells.

Antibodies, Monoclonal

Involucrin expression in urinary bladder carcinoma.

Expression of involucrin was investigated immunohistochemically in 27 cases of urinary bladder carcinoma. Although no keratinization was observed in the transitional cell carcinomas examined all displayed involucrin staining to various degrees. Involucrin expression in foci of G-I transitional cell carcinomas was classified into 3 types: type 1, a mixture of intensely stained and slightly positive cells; type 2, highly positive cells intermingled with negative tumour cells; and type 3, all tumour cells slightly positive. Undifferentiated cell carcinomas demonstrated an irregular distribution of involucrin of varying staining intensity while deposition in squamous cell carcinomas was limited to keratinized areas.

Carcinoma, Squamous Cell

Immunostaining of involucrin in odontogenic epithelial tumors and cysts.

An immunoperoxidase method was used to detect involucrin in 47 odontogenic tumors and 35 radicular cysts. Of a total of 40 ameloblastomas, 9 cases were positive for involucrin expression and those positive cases exhibited acanthomatous or follicular patterns. Squamous odontogenic tumors were strongly positive for involucrin, whereas adenomatoid odontogenic tumors gave a negative staining reaction. Involucrin expression in odontogenic tumors was divided into three categories: single cell positive, focally positive, and squamous metaplastic cell positive. Radicular cysts showed a very irregular distribution of involucrin; nonstratified epithelium was generally negative or showed only trace staining for involucrin, whereas suprabasilar stratified squamous epithelial cells were strongly positive. Cells positive for involucrin in odontogenic tumors and in cystic epithelium are probably direct signs of epithelial differentiation; such cells were squamoid in appearance.

Cell Differentiation

Squamous odontogenic tumor: immunohistochemical identification of keratins.

Two cases of squamous odontogenic tumors are described in terms of histopathology and keratin immunohistochemistry. Histopathologically, the lesions were composed of squamous epithelial islands without peripheral columnar cells and well-differentiated stromal tissue. Immunohistochemical detection of keratin proteins was done with the use of polyclonal antikeratin antiserum (TK, detecting 41 to 65 kDa keratins) and monoclonal antibodies (KL1, 55 to 57 kDa; PKK1, 40, 45, and 52.5 kDa). Staining for PKK1-detectable keratin was absent in tumor epithelial cells and that with KL1 and TK immunoreagents was confined to squamous cells, being strong in the keratinized cells. In view of the results, the squamous odontogenic tumor appears to arise from the rests of Malassez in periodontal tissue rather than from oral squamous epithelium.

Adult

Immunohistochemical expression of keratin proteins in urinary bladder carcinoma.

Transitional carcinomas of the urinary bladder were examined immunohistochemically for keratin proteins with the use of polyclonal antiserum (TK, 41-65 kDa) and 3 monoclonal antibodies (KL 1, 55-57 kDa; PKK 1, nos. 19, 18, 8; and K 8.12, nos. 16, 13). Umbrella cells gave particularly strong staining for TK, KL 1 and PKK 1, whereas they were negative for K 8.12. Basal- and intermediate-layer cells in urothelial epithelium were moderately positive for all keratins. Brunn's nests cells showed comparatively slight or moderate keratin staining, and K 8.12 staining of Brunn's nests was higher than in urothelial epithelial cells. Transitional carcinoma (grades I and II) indicated uniform keratin distribution, and staining was strong with TK, while that of KL 1, PKK 1 and K 8.12 varied, and grade III tumors showed the lowest intensity of staining. K 8.12 staining in papillary transitional carcinomas was strongly positive in basal located tumor cells, as compared with apical tumor cells. Squamous cell carcinoma was varying positive to keratin reactions dependent on the degree of keratinization. Heterogenity of keratin distribution in papillary transitional carcinomas was given between basal tumor cells and well differentiated tumor cells including umbrella-like cells.

Antibodies, Monoclonal

Calcifying odontogenic cyst immunohistochemical detection of keratin and involucrin in cyst wall.

Calcifying odontogenic cysts (COC) were immunohistochemically described using different keratin proteins and involucrin as well as histopathology. The cystic lining epithelium was composed of calcifying, keratinizing, squamous, and columnar epithelial cells, and included calcified masses of irregular shape and various size as well as ghost cells. Calcifying epithelium gave negative or only trace staining for keratins detected with low molecular keratin (PKK1), but were regularly positive with high molecular keratin (KL1) and polyclonal antibody for keratin (TK). They were occasionally positive for involucrin. The cells located in the periphery of the calcified masses had a particular abundance of high molecular weight and total keratins (KL1 and TK). Calcified bodies and ghost cells were devoid of any immunoreactivity. Squamous epithelium was relatively similar to that of normal squamous cell epithelium in the oral mucosa. It were most commonly found in columnar cystic epithelial cells which displayed intense staining with all immunoreagents. It is postulated that such epithelial cells may have a strong potentiality to transform into ghost cells or to undergo metaplasia. They may develop altered synthesis of homogenous acellular materials and finally become transformed into calcifying epithelium containing dystrophic calcified masses.

Adolescent

Adenomatoid odontogenic tumour: co-expression of keratin and vimentin.

Immunohistochemical observations of intermediate sized proteins in five cases of adenomatoid odontogenic tumour (AOT) are described. The immunohistochemical detections of keratins were made with polyclonal antiserum (TK, 41-65 kDa) and three monoclonal keratin antibodies (KL1: 55-57 kDa; PKK1: 40, 45, and 52.5 kDa and nos. 19, 18, 8; K8.12: nos. 16, 13) and vimentin and desmin monoclonal antibodies. Histologically, the tumour epithelia could be divided into two types: type A cells were a spindle or columnar shape and formed solid, ductal, tubular or whorled structures. Type B cells were small and compact cells at the periphery of the A cell-containing focus. Immunohistochemically, the type A cells showed very slight reaction with all antibodies to keratins, whereas the type B cells indicated slight-to-moderate expression of keratin and vimentin, and showed coexpression. Both types of cell showed a negative reaction for desmin. Only one case was associated with cystic lesions, and the cyst-lining was composed of thin squamous epithelium. Keratin expression in this epithelium was strong. In the histogenesis of AOT it was postulated that the tumour cells may have originated from undifferentiated odontogenic epithelium or stratum intermedium cells.

Adolescent

Ameloblastic fibroma: growth potentiality of odontogenic epithelium and coexpression of intermediate filament proteins in fibromatous cells.

Four cases of ameloblastic fibroma are described immunohistochemically in terms of intermediate-sized proteins in both epithelial and mesodermal components. Keratin proteins were demonstrated by polyclonal anti-keratin antiserum (TK: detecting 41-65 kDa keratins) and 2 monoclonal antibodies to keratin (KL1: 55-57 kDa, PKK1: 44, 46, 52 and 54 kDa), and monoclonal antibodies to vimentin and desmin. Two types of odontogenic epithelial tumour cells were discriminated: undifferentiated odontogenic cells and common ameloblastoma cells. Keratin expression was found to be stronger in undifferentiated cells than in the ameloblastoma cells. Undifferentiated cells were PAS-positive, while ameloblastoma cells were negative. Fibroma cells were strongly positive for vimentin, and negative for desmin. Keratin proteins were also expressed slightly. Thus, coexpression of keratin and vimentin was seen in fibroma cells. Histogenesis is discussed from the standpoint of the distribution patterns of keratin and vimentin, as well as with respect to the histopathology.

Child

Immunohistochemical localization of intermediate filament proteins in calcifying epithelial odontogenic tumors.

Three calcifying epithelial odontogenic tumors (CEOT) were examined immunohistochemically. The localization of intermediate filaments was characterized through the use of polyclonal anti-keratin antiserum (TK which detects 41-65 kd keratins), 2 monoclonal keratin antibodies (PKK1 specific for the 44, 46, 52 & 53 kd keratins and KL1, specific for the 55-57 kd keratins) and monoclonal antibodies for vimentin and desmin. The tumor epithelial cells were slightly positive or negative for PKK1 detectable keratins, but slightly to strongly positive for KL1 and TK antibodies. Tumor epithelium was slightly positive for vimentin but negative for desmin. The tumor foci were composed of both dark-staining and pale-staining cells; the former had a more intense reaction with KL1 and TK antibodies than the latter. Homogeneous acellular material was either PAS-positive or negative, with or without calcification, and keratin-negative.

Adult

Immunohistochemical detection of human epidermal growth factor in submandibular glands and their tumors using a polyclonal antiserum and a monoclonal antibody.

We applied immunohistochemical procedures to detect hEGF in salivary glands and pleomorphic adenomas of salivary-gland origin using a polyclonal hEGF antiserum and a monoclonal antibody against hEGF synthesized by applying the synthetic gene technique using Escherichia coli. In normal salivary glands, hEGF was mainly localized in the ductal system (i.e., intercalated, striated, and excretory ducts). The staining intensity and intracellular localization exhibited some variation depending on the fixative used. When a polyclonal hEGF antiserum was used for immunostaining, slight background staining was observed in sections prepared using the fixatives tested. Therefore, precise localization of hEGF was obtainable only in formalin-fixed sections using the monoclonal antibody against hEGF. In pleomorphic adenomas, positive hEGF staining was seen on the luminal side of tumors and in cells of ductal origin; no reactivity was present on the outer side of tumors or in cells of myoepithelial origin. Occasionally, long, spindle-shaped tumor cells and chondroidally changed tumor cells also exhibited positive staining for hEGF.

Adenoma

Expression of keratins during experimentally induced carcinogenesis in hamster cheek pouch visualized polyclonal and monoclonal antibodies.

We obtained immunohistochemical profiles of several keratin proteins during experimentally induced carcinogenesis in hamster cheek-pouch mucosa using a polyclonal antibody (TK; detecting keratins with molecular masses of 41-65 kilodalton) and two monoclonal antibodies (KL1, 55- to 57-kilodalton keratins; PKK1; 40-, 45- and 52.5-kilodalton keratins). The squamous epithelium of normal pouch mucosa exhibited positive TK staining in all layers, KL1 staining in the spinous layer and PKK1 staining in the basal layer, thus indicating a regional or zonal distribution pattern. Epithelia undergoing basal hyperplasia showed irregular localization of PKK1 binding, while hyperkeratinized lesions exhibited the binding pattern found in normal epithelium. In case of epithelial dysplasia, there was reduced KL1 staining in spinous cells and decreased PKK1 staining in the basal and parabasal layers. Papillomas exhibited a rather zonal distribution of keratin staining. All squamous-cell carcinomas, irrespective of their degree of keratinization and infiltration pattern, showed slight or no PKK1 staining. Such lesions were only positive for KL1-detectable keratins in keratinizing tumour cells and exhibited an irregular distribution of TK binding. The expression of keratin proteins during carcinogenesis in hamster cheek-pouch mucosa may parallel that of keratins in human squamous-cell carcinomas originating in the oral mucosa.

Animals

Immunohistochemical observations of keratins, involucrin, and epithelial membrane antigen in urinary bladder carcinomas from patients infected with Schistosoma haematobium.

Squamous cell carcinomas of the urinary bladder and the epithelial lesions associated with infection by Schistosoma haematobium were histopathologically and immunohistochemically described for keratin proteins (TK, 41-65 kDa; KL1, 55-57 kDa; PKK1, 40, 45 and 52.5 kDa), involucrin, and epithelial membrane antigen (EMA). Normal urothelial epithelium was positive for all keratins, and showed absent or slight reactions for involucrin and EMA in superficial umbrella cells. The intestinal type of epithelium was composed of columnar cells and small basal cells; TK was positive in the basal cells, KL1 staining was positive in the columnar cells, whereas PKK1 was negative or slight in the columnar cells. Involucrin was confined to columnar cells. Squamous metaplastic epithelium showed a rather regional keratin distribution: TK was distributed in all layers, KL1 decorated upper spinous and granular layers, but PKK1 did not bind, and involucrin staining existed only in upper spinous and granular cells. Keratin expression in squamous cell carcinomas indicated heterogeneity and its stainability was dependent on the degree of keratinization: The G 1 type revealed strong reaction, the G 2 type showed a similar distribution pattern, but the staining intensity was less, and the G3 type showed irregular staining with decreased intensity. Involucrin staining was limited to keratinized cells of carcinoma as was that for EMA.

Adult

Immunohistochemical observations on binding of monoclonal antibody to epithelial membrane antigen in epithelial tumors of the oral cavity and skin.

A total of 211 cases of benign and malignant tumors of epithelial origin were studied by the immunoperoxidase method to determine the distribution profile of epithelial membrane antigen (EMA) with the use of monoclonal antibody. Normal epithelial cells in the oral mucosa and skin were usually negative for EMA staining, as were epithelial cells in hyperplastic lesions and papillomas. Paget cells and tumor cells of Bowen's disease (carcinoma in situ) demonstrated a high incidence of EMA positivity, whereas the frequency in basal cell carcinoma was unexpectedly low. Squamous cell carcinomas revealed positive EMA staining of cytoplasmic membranes, and the antigen was also present in keratinized areas. EMA expression in squamous cell carcinoma generally showed a high incidence (85%) and was higher in keratinized lesions than in unkeratinized or less well-differentiated neoplasms. EMA distribution could be classified into two forms: one in which the cytoplasmic membranes demonstrate positivity and in which a positive cytoplasmic pattern is found in parakeratinized cells in malignant foci.

Antibodies, Monoclonal