A clinicopathological analysis of the risk factors for lymph node metastasis was performed in 177 patients with submucosal invasive colorectal carcinoma (CRC). The submucosal deepest invasive portion was histologically subclassified as well (W), moderately (M), or poorly (Por) differentiated. M type was further subdivided into moderately-well (Mw) and moderately-poorly (Mp) differentiated. The pattern of tumor growth was classified as polypoid growth (PG) and non-polypoid growth (NPG). Lymph node metastasis was detected in 21 (12%) of the 177 patients. Macroscopically, type IIc and IIa + IIc lesions showed a significantly higher incidence of lymph node metastasis (44% and 30%) than type IIa and I (4% and 8%). Regarding the histologic subclassification, Por and Mp lesions showed a significantly higher incidence of lymph node metastasis (67% and 37%) than W and Mw lesions (4% and 14%). NPG tumors showed a significantly higher incidence of lymph node metastasis (29%) than PG tumors (7%). The depth of submucosal invasion and lymphatic invasion (ly) were also significantly correlated with the incidence of lymph node metastasis (submucosal scanty (sm-s) invasion 4%, massive invasion 20%; ly(+) 23%, ly(-) 5%). None of the lesions with both sm-s invasion and of W or Mw type showed lymph node metastasis. These results indicate that submucosal invasive CRC with both sm-s invasion and of W or Mw type, which shows no ly, is the appropriate indication for endoscopic curative treatment.
Abstract. Twenty-five 22-to 46-day-old broilers with Newcastle disease (ND) were investigated pathologically and immunohistochemically in order to evaluate the mechanism of ND outbreak in vaccinated broilers. The broilers were vaccinated with ND live vaccine via drinking water. Clinical signs were neurologic and respiratory in nature. Macroscopically, bursal atrophy, white spots on the pancreas, and discoloration and enlargement of kidneys and spleen were observed in the broilers. Histologically, perivascular cuffing, neuronal degeneration and necrosis, and glial proliferation were present in the cerebrum, cerebellum, and medulla oblongata. There was extensive rarefaction and malacia in the parenchyma of severely affected brains. There were extensive degeneration, necrosis, and depletion of acinar cells in the pancreas. There was proliferation of macrophages in the lungs with congestion, tubulointerstitial nephritis, hepatocytic necrosis with thrombi in the sinusoids, and lymphocytic depletion in the cloacal bursa. Immunohistochemically, ND virus antigens were detected in the lesions. ND virus isolated from the present cases did not cause encephalitis or pancreatitis in specific-pathogenfree chickens, but it induced mortality with hepatocytic sinusoidal thrombi, splenic necrosis, lymphoid necrosis and depletion, and conjunctival hemorrhage. Severe nonpurulent encephalitis with extensive rarefaction and malacia, and necrotizing pancreatitis in the present case may suggest a close possibly causal relation with vaccination.
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