A rare case of giant panda cancer:Pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma(PDAC)is a highly malignant cancer of the digestive system common among humans.However,it is rarely reported in wild animals.In 2018,a giant panda died in the Beijing Zoo.During subsequent histological observation of the pancreas,it was discovered that the glandular epithelial cells had lost the pancreatic acinar structure,tubular areas with obvious structure in the pancreas,and the ductal epithelium was substituted by high columnar mucus cells.Masson staining showed that there were several fibrous tissue proliferative reactions around the ductal adenocarcinoma and immunohistochemical staining revealed that CK7 and CK19 were positively expressed in the pancreatic tissue.Therefore,the pathological diagnosis indicated that the panda had PDAC.In this paper,the panda’s living conditions and pathological diagnosis results are examined,with the aim of providing a reference point for the future diagnosis of wild animal tumors.

PATHOLOGICAL AND MORPHOLOGICAL RESEARCH OF EXPERIMENTAL ACETABULAR DYSPLASIA

Objective To investigate the pathological mechanism of hip dysplasia. Methods The leftknee joints of eighteen rabbits were fixed in extending position with plaster cylinder for four weeks, but their hip joints were flexed. The right side served as control. Roentgenogram was made in all animals. The changes of the x-ray films and the pathological findings between left and right hips were compared. Results Appearance of hip dysplasia was obvious at four weeks after plaster fixation. There were pathological changes, including shallow ace-tabulum and flat femoral head, increased acetabular index and decreased acetabular head index on the x-ray films. Conclusion The hip dysplasia is the result of prolonged extending position of the knee joint. Abnormal knee posture seems to be one of the important factors of hip dysplasia. This kind of deformation may be worsened with time.

STUDY ON INFLAMMATORY CELLS IN BALF OF SMOKE-INDUCED CHRONIC BRONCHITIS RAT MODEL

Objective To establish a smoke-induced chronic bronchitis rat model and evaluate the patho-logical change semi-quantitatively, and study the characteristics of the inflammatory cells in the bronchoalveolar lav-age fluid (BALF) in various stages. Methods Chronic bronchitis sequential rat model was established by passively inhaling smoke mixture. Experiments were performed in 30 young male Sprague-Dawley rats, which comprised 5 groups in random, i.e.,4 chronic bronchitis model groups and 1 control group. After stained with hematoxylin and eosin, the specimens were studied by semi-quantitative method to evaluate the morphologic changes in various stages. Meanwhile, the inflammatory cells of the BALF and the activity of myeloperoxidase (MPO) of lung tissue were analysed. Results During the process of the chronic bronchitis, the pathologic score was increasing as time went on, and the typical morphologic changes of chronic bronchitis emerged in the group 7 weeks. The total number of inflammatory cells in BALF was increasing as time went on, correlated with the pathologic scores (P <0.01). And the percentage of lymphocyte increased as well as positively correlated with pathologic scores (P < 0. 05) , whereas that of macrophage decreased and negatively correlated with pathologic scores (P <0. 05). The MPO lever of lung tissue was correlated with the pathologic scores (P < 0. 01). But the percentage of the neutrophil in the BALF was just in a high level during the first week, then it maintained relatively lower. Conclusion Smoke-induced chronic bronchitis is a slowly progressive inflammation process. The model we established is convenient and simple for the longitudinal study on the inflammatory process of chronic bronchitis and the therapy in the early stage. The semi-quantitative evaluation for the pathological change is with much more value. During the inflammatory sequential process of early stage of chronic bronchitis, the cellular characteristics are similar to that of the common chronic inflammation.