Kyuchang Kim

A 3‐year‐old neutered male Siamese cat with chronic anorexia showed anemia and elevated liver enzyme levels. Ultrasonography disclosed multiple diffusely heterogeneous hepatic lesions and peritoneal effusion, which was identified as hemoabdomen upon fluid analysis. Computed tomography showed finger‐like hypoattenuation extending from the left hepatic margin with focal margin loss in the delayed phase, suggesting hepatic rupture. Infiltrative hepatic diseases were considered, and amyloidosis was the top differential diagnosis given the patient's young age, breed predisposition, and suspected hepatic rupture. Blood oozing was confirmed via laparotomy, and Congo red staining established hepatic amyloidosis, though amyloid typing was not pursued.

Diaphragmatic tumors are uncommon in veterinary medicine. A 9‐year‐old neutered male Chihuahua was referred for evaluation of a suspected diaphragmatic hernia. Computed tomography revealed a soft tissue mass with a continuous border to the adjacent diaphragm, compressing the liver caudally. The tumor exhibited hypoattenuating lesions suspected of a mixture of fat and soft tissue. Histopathologic examination diagnosed a well‐differentiated liposarcoma. A mass exhibiting a continuous border with the diaphragm and displacement of the adjacent liver may indicate a diaphragmatic tumor. Attenuation indicating a mixture of fat and soft tissue may be a feature of well‐differentiated liposarcoma, but further studies on liposarcoma subtypes are needed.

Although radiotherapy plays a crucial in the management of pelvic tumors, its toxicity on surrounding healthy tissues such as the small intestine, colon, and rectum is one of the major limitations associated with its use. In particular, proctitis is a major clinical complication of pelvic radiotherapy. Recent evidence suggests that endothelial injury significantly affects the initiation of radiation-induced inflammation. The damaged endothelial cells accelerate immune cell recruitment by activating the expression of endothelial adhesive molecules, which participate in the development of tissue damage. Pravastatin, a cholesterol lowering drug, exerts persistent anti-inflammatory and anti-thrombotic effects on irradiated endothelial cells and inhibits the interaction of leukocytes and damaged endothelial cells. Here, we aimed to investigate the effects of pravastatin on radiation-induced endothelial damage in human umbilical vein endothelial cell and a murine proctitis model. Pravastatin attenuated epithelial damage and inflammatory response in irradiated colorectal lesions. In particular, pravastatin improved radiation-induced endothelial damage by regulating thrombomodulin (TM) expression. In addition, exogenous TM inhibited leukocyte adhesion to the irradiated endothelial cells. Thus, pravastatin can inhibit endothelial damage by inducing TM, thereby alleviating radiation proctitis. Therefore, we suggest that pharmacological modulation of endothelial TM may limit intestinal inflammation after irradiation.

Radiation-induced enteropathy remains a major complication after accidental or therapeutic exposure to ionizing radiation. Recent evidence suggests that intestinal microvascular damage significantly affects the development of radiation enteropathy. Mesenchymal stem cell (MSC) therapy is a promising tool to regenerate various tissues, including skin and intestine. Further, photobiomodulation (PBM), or low-level light therapy, can accelerate wound healing, especially by stimulating angiogenesis, and stem cells are particularly susceptible to PBM. Here, we explored the effect of PBM on the therapeutic potential of MSCs for the management of radiation enteropathy. In vitro, using human umbilical cord blood-derived MSCs, PBM increased proliferation and self-renewal. Intriguingly, the conditioned medium from MSCs treated with PBM attenuated irradiation-induced apoptosis and impaired tube formation in vascular endothelial cells, and these protective effects were associated with the upregulation of several angiogenic factors. In a mouse model of radiation-induced enteropathy, treatment with PBM-preconditioned MSCs alleviated mucosal destruction, improved crypt cell proliferation and epithelial barrier functions, and significantly attenuated the loss of microvascular endothelial cells in the irradiated intestinal mucosa. This treatment also significantly increased angiogenesis in the lamina propria. Together, we suggest that PBM enhances the angiogenic potential of MSCs, leading to improved therapeutic efficacy for the treatment of radiation-induced enteropathy.