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Biomedical subjects

A Shirota

Publications and source records attributed to A Shirota.

At least 37 records · Page 2Linked to original sources
PubMed1981

Seedling leiomyoma of the esophagus and esophagogastric junction zone.

The esophagus was totally excised for histopathological examination in 276 autopsy cases and 66 surgical cases (total, 342 cases). Leiomyoma of the esophagus was observed in 27 of the 342 cases. The tumors were present in 22 of the 225 male cases and in 5 of the 117 female cases. There were 38 leiomyomas among the 27 cases. Most of the leiomyomas originated in the inner circular muscle. None of the tumors was more than 7 mm. in length. Twenty-five of the 38 leiomyomas were located in the esophagogastric junction zone. Thus, subserial histological examination revealed leiomyomas at a higher frequency than that in previous reports.

Adolescent↗
PubMed1981

Dysplasia and reserve cell hyperplasia-like change in human esophagus.

The esophagus was totally examined in 264 autopsied cases and 61 operated cases, for a total of 325 cases, to clarify the histogenesis of squamous cell carcinoma of the esophagus. Epithelial dysplasia of the mucosa was present in 27% and subclinical carcinoma was found in 2.4%. Hyperplasia of the duct of the esophageal gland proper was present in 34% and cysplasia of the ductal epithelium in 3%. Reserve cell hyperplasia-like change of the islet of the ectopic gastric mucosa was found in 4% and reserve cell hyperplasia-like change of the esophagogastric junction zone in 13%. Of the seven cases of microcarcinoma, two showed dysplasia and gradual transition and one presented dysplasia and abrupt transition. Another two were considered to have originated in the ductal epithelium. These findings suggested that they could all be the sites of origin of cancer development.

Adult↗
PubMed1980

Distribution of marker enzymes and mucin in intestinal metaplasia in human stomach and relation to complete and incomplete types of intestinal metaplasia to minute gastric carcinomas.

Intestinal metaplasia of the human stomach was classified into two types, complete and incomplete. The complete type was associated with the intestinal marker enzymes sucrose alpha-D-glucohydrolase, alpha, alpha-trehalase, aminopeptidase (microsomal) (APM), and alkaline phosphatase (ALP). Tissue of this type contained goblet cells and Paneth's cells but not high-iron diamine (HID)-positive mucin staining with HID-Alcian blue. The incomplete type of intestinal metaplasia was associated with sucrose alpha-D-glucohydrolase, APM, goblet cells, and HID-positive mucin but not with alpha, alpha-trehalase, ALP, or Paneth's cells. For the examination of the distribution of the complete and incomplete types in 84, 27, and 16 resected specimens of human stomach with gastric carcinoma, gastric ulcer, and duodenal ulcer, respectively, disaccharidases were located with Tes-Tape. Specimens with intestinal metaplasia were divided into three classes: complete type only (class I), incomplete type only (class II), and a mixture of areas of the complete and incomplete types (class III). Of the 84 specimens from patients with gastric carcinoma, intestinal metaplasia was found in 76 (01%), and the percentages of specimens of classes I, II, and III were 32, 22, and 46, respectively. In these specimens, the percent incidence of class I increased and that of class II decreased with age. Of the 27 specimens from patients with gastric ulcer, 16 (59%) shopwed intestinal metaplasia and 10 of the 16 (63%) specimens were of class II. Of the 16 specimens from patients with duodenal ulcer, only 3 (19%) specimens showed intestinal metaplasia and all of them were of class II. The relationships of the complete and incomplete types of intestinal metaplasia to gastric carcinoma wre studied in 26 foci of minute carcinoma of the stomach less than 5 mm in largest diameter. Nineteen of 20 (05%) foci of the intestinal type of minute carcinoma were surrounded by intestinal metaplasia and 16 foci (80%) were surrounded by the incomplete type of intestinal metaplasia.

Adult↗
PubMed1979

Effect of bradykinin to cyclic AMP levels and response of murine lymphocytes.

No information is available on the pharmacological effect of bradykinin to lymphocytes and immunological responses of them. In this study it was clarified that bradykinin as well as histamine elevated cyclic adenosine 3',5' monophosphate (cAMP) levels of murine splenic or lymph node lymphocytes and mature thymocytes (cortisone-resistant thymus), but did not increase cAMP levels of immature thymocytes as well as histamine. The increased cAMP ratios in T cell-enriched splenic lymphocytes by the impulse of bradykinin were higher than that in splenic and lymph node lymphoid cells by the stimulation of bradykinin. It was also demonstrated that bradykinin as well as histamine suppressed DNA synthesis by mitogenic (PHA-P, Con-A) stimulation of splenic lymphocytes, but not a effect to the response of lymphocytes by mitogenic (LPS) stimulation was observed. These facts suggest that bradykinin may play an important role in the regulation of immunologic lymphocyte responses.

Animals↗