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Background: Microvessels in atheromatous plaques are well known to play a role in plaque vulnerability associated with intraplaque hemorrhage, but their architecture remains unclear. The morphometry of the microvasculature and hemorrhage of human carotid atheromatous plaques (CAPs) were evaluated, and 3-dimensional (3D) reconstruction of the microvessels was performed., Methods: CAPs were obtained by endarterectomy in 42 patients. The specimens were analyzed using light microscopy. Plaque hemorrhage was defined as an area-containing red blood cells (>1 mm2). To determine the histopathologic features of plaque hemorrhage, the plaque area was divided into 4 regions: cap, shoulder, lipid/necrotic core, and media. Then, the density of microvessels and macrophages in each region was quantified. Two representative lesions with either hemorrhagic or nonhemorrhagic plaque were cut into 90 serial sections. The sections were double stained with anti-CD34 and anti-α smooth muscle actin antibodies, scanned using a digital microscope, and reconstructed using TRI-SRF2 software., Results: The hemorrhagic plaques showed a higher density of microvessels than nonhemorrhagic plaques in the shoulder, cap, and lipid/necrotic core (P=.03, .009, and .001, respectively), and there was positive correlations between its density and macrophages in each regions (P<.001, .001, and .019, respectively). 3D imaging also revealed dense microvessels with a network structure in the cap and shoulder regions of hemorrhagic plaques, and some of the vessels were fenestrated to the arterial lumen., Conclusions: The microvasculature of plaques with intraplaque hemorrhage was dense, some of which fenestrated to the arterial lumen. The pathologic 3D imaging revealed precise architecture of microvasculature of plaques., (Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

So as to study the cell proliferation in a case with triple gastric cancers, we labeled an operated whole stomach with bromodeoxyuridine (BrdU) by the isolated organ perfusion system using artificial blood. Anti-BrdU immunohistochemical staining of sections from every part of the stomach was performed, and 3 separated cancerous lesions were all diagnosed as well differentiated adenocarcinomas. The labeling index (L.I.) of the cancerous lesions were found to differ from part to part. However, the L.I. tended to be higher in the superficial mucosal areas and in the cell-dense areas of the submucosa. In the almost normal fundic glands, the labeled zone was localized in the neck of the glands. The more metaplastic gastritis was advanced, the more the labeled zone shifted irregularly toward the bottom of the glands. Whenever the interstinal metaplasia was completed, the labeled zone was localized in the bottom of the glands. This method was found useful in studying the cell proliferation in the stomach without causing any harm to the human body.

We have experimentally studied whether or not repeated episodes of acute gastric mucosal lesions can induce chronic gastritic changes. Rats received pyloromyotomy and repeated per os administration of acetic acid-glycerin. Gastric mucosal lesions thus induced were studied histopathologically in cardiac glandular areas using morphometric analysis. It was found that pyloromyotomy induced fibrosis between the bottom of the gland and muscularis mucosa. On the other hand, the per os administration of acetic acid-glycerin induced hyperplastic change of mucous neck cells. They were increased in number and in size. Distribution of mucous neck cells were distended vertically to the mucosal surface and towards the bottom of the gland. Greater the amount of acetic acid-glycerin administration, stronger the changes of mucous neck cells, i.e., the distended zone of mucous neck cells spread more and more from the cardiac area. Parietal and chief cells were decreased in number in the course of the mucous neck cell hyperplasia. Branching of glands was occasionally seen in rats receiving greater amount of acetic acid-glycerin. It was concluded that there are basic structural similarity between the gastric mucosal changes induced by repeated episodes of acute gastric mucosal lesions and the change seen in human chronic gastritis. Thus acute gastric mucosal lesions can be one of the cause of chronic gastritis.

A 70-year-old woman was referred for an evaluation of evidence indicating occult bleeding found in the feces and epigastralgia. Radiologic and endoscopic examinations disclosed a duodenal polyp at the bulb. A pathological examination of a biopsied specimen revealed a well-differentiated adenocarcinoma. The patient underwent a gastrectomy and an extensive duodenectomy, and the surgical specimen examined indicated a pedunculated polyp (1.0*2.0) at the duodenal bulb which, histologically, consisted of two distinct parts: one, a tubular adenocarcinoma, and the other, non-tumorous tissue. Most of the lesion was the former, whereas the latter was found at the bottom and at the stalk of the polyp, and consisted of hyperplastic foveolar structures with gastric type cells and pyloric type glands. The histological findings of the mucosa, which was clearly duodenal around the root of the polyp, indicated that the carcinomatous portion was confined to the mucosal layer. These findings indicate that the adenocarcinoma in this case originated from a duodenal polyp composed of aberrant gastric mucosa. Also included in this study is a review of 57 cases of early duodenal cancer of the bulb, that have been reported in Japan.

Twenty cases of the entire course of the large intestine were obtained from autopsy materials within four hours after death and examined histologically. The autolytic changes were found to be minimal and the mucosal architecture was fairly well preserved in our studies. The morphometric analysis showed that the glandular lengths in the rectosigmoid colon were greater than those of the other parts of the large intestine. Cystic dilatations of the glands were most frequently observed in the distal colon, and tended to occur in the vicinity of neoplastic changes. These results indicate that the hyperplastic changes of the glands, occasionally with cystic dilatations, are important as the background for the development of neoplastic diseases in the large intestine.

Through X-ray and endoscopic examination of stomach, a 77 year-old man, who complained of epigastralgia, he was diagnosed to have Borrmann III type gastric carcinoma on the antrum. The gastric biopsy specimen obtained from the tumor revealed to be well differentiated adenocarcinoma. Since the patient refused receiving surgical treatment, a combined administration of futraful and uracil (UFT therapy) was performed. 4 weeks after receiving UFT therapy, the patient became less aware of subjective symptom and the gastrofiberscopic picture showed smaller mass lesion compared to that of prior to the treatment. 8 weeks later, the tumor was remarkable reducing its size. When compared 14 cases of gastric carcinoma receiving UFT therapy with 26 cases receiving Futraful therapy (FT therapy), the UFT group responded more effectively than the FT group. In the UFT therapy, complete (CR) and partial response (PR) were obtained in 4 of 13 cases of gastric carcinoma with an effective rate of 30.8% according to the response criteria proposed by the Koyama-Saitoh group and with a Karnofsky scale of IA or better in 6 (42.8%) of 14 cases. On the other hand, in the FT therapy CR and PR were obtained in 5 of 26 cases with that of 19.2%, while a Karnofsky scale of IA or better was achieved in 6 (23.1%). As for 3 cases of PR in the UFT therapy the microscopic view of the biopsy specimen from gastric carcinoma showed well differentiated adenocarcinoma, which responded to the UFT therapy remarkably 4-5 weeks after receiving UFT therapy.