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Isolated metanephrogenic mesenchyme can be induced for epithelial differentiation and tubule formation by an embryonic spinal cord that is cultivated in a transfilter position to the target cells. Under such conditions, determination of the cells starts at 12 hr and is completed around 24 hr. To correlate this event to DNA synthesis, thymidine incorporation was followed in such cultures from 2 to 96 hr after setting up the transfilter explants. Controls were cultured under conditions which did not result in induction. Incorporation into both induced and noninduced mesenchymes dropped rapidly during the first 12 hr when the tissues were transferred to the in vitro conditions. During the subsequent critical 12- to 24-hr period, mesenchymes continuously exposed to an inductor showed a marked increase in their incorporation of thymidine. If induction was interrupted during the first 10 hr there was no stimulation of incorporation when measured at 24 hr. Similarly, isolated mesenchymes and those exposed to a tissue devoid of inducing capacity did not show stimulation, and their incorporation remained at a low level when measured at 24 hr. Parallel DNA measurements were made by flow cytometry of individual nuclei from mesenchymes exposed to the inductor from 0 to 46 hr. No major changes in the distribution of the various phases of cell generation cycle were detected nor could any synchronization be shown. Hence the changes in the incorporation rate of thymidine seem to be due to variations in the total length of the cell cycle. We conclude that induction of differentiation of the metanephric mesenchyme is accompanied by a contact-mediated stimulation of DNA synthesis. The stimulation may represent a permissive effect on a predetermined cell population in the metanephrogenic mesenchyme.

We evaluated 58 patients who were still alive more than ten years after operative treatment of gastric cancer. We reexamined their histologic specimens and compared them with those of matched paired controls of the same sex and age who had died of gastric cancer. Forty-two patients consented to a follow-up study. The age of the patients did not affect survival. For patients with gastric cancer, those with distal cancer or an ulcer simulating cancer had had a better prognosis. Forty percent of the patients had had an early gastric cancer. Only two patients had had lymph node metastases in regional lymph nodes, and macroscopic tumor growth through the serosa had been recorded in only four cases. In 23 cases, a distal resection had proved successful. No significant correlation between intestinal or diffuse types of cancer and prognosis was observed. One recurrence after ten years was found; in one case, there was a new cancer in the gastric remnant. In addition, biopsy specimens from two patients showed grave dysplasia. We suggest that throughout their lives annual follow-up examinations be performed in patients who have undergone radical operations for gastric cancer.

The distribution of laminin, a basement membrane glycoprotein, was studied by an immunohistochemical technique in six samples of benign sclerosing lesions of extrahepatic bile ducts and in 11 sclerosing cholangiocarcinomas. The expression of laminin showed that benign glandular structures were surrounded by a mainly intact basement membrane. In sclerosing cholangiocarcinomas laminin was irregularly distributed, and in large areas totally absent. The findings suggest that deposition of basement membrane material is defective. Sclerosing cholangitis may be extremely difficult to distinguish from well differentiated sclerosing cholangiocarcinoma. This sample was small, but the diseases studied were relatively rare. Staining for laminin might be of additional use to surgical pathologists in the differential diagnosis of benign sclerosing lesions and sclerosing cholangiocarcinomas.

The distribution of laminin, a basement membrane glycoprotein, was studied by immunohistological techniques in 10 samples of normal pancreatic tissue, in 15 samples of chronic pancreatitis, and in 33 pancreatic neoplasms. Sections of formalin-fixed, paraffin-embedded specimens were pretreated with pepsin and immunostained for laminin. As judged by the expression of laminin, normal pancreatic glands were surrounded by a continuous, intact basement membrane. In chronic pancreatitis the basement membrane was also mainly continuous, but focally weaker and thinner than around normal glands. In pancreatic adenocarcinomas laminin was irregularly distributed and in large areas totally absent. In anaplastic carcinomas no extracellular laminin was seen, but two cases showed some intracellular laminin in a punctate pattern. The findings suggest that these cancers have defects in the deposition of a basement membrane or that it is degraded. Our data suggest that the integrity of the basement membrane correlates with the degree of malignancy in ductal adenocarcinomas, but this is not the case for mucinous cystic neoplasms or for islet cell tumors. In these neoplasms a nearly intact basement membrane was seen both in malignant tumors and in their benign counterparts.

On preparative cell electrophoresis mouse lymph node lymphocytes separate into fast-moving (T, thymus-dependent) and slow-moving (B, thymus-independent) fractions. After treatment with neuraminidase all lymphocytes move as one very slow fraction, indicating that the difference in the mobility of the two kinds of cells is due to differences in the density of exposed sialic acid on their surfaces.

Electrophoretically fractionated CBA/Ca spleen T cells alone respond to allogeneic cells in one-way MLC and to PHA. They do not respond to E. coli LPS. B cells alone do not respond to allogeneic cells nor to PHA, but do respond to LPS. When karyotypically distinguishable syngeneic mixtures of T and B lymphocytes are stimulated with allogeneic cells, at the most 5% of mitoses on 5-9th culture day are of B cell origin. This indicates that B cells are not substantially recruited to proliferate in the MLC.