The Oriental stork (Ciconia boyciana), an endangered species, faces significant threats despite extensive conservation efforts aimed at their reintroduction and long-term survival in South Korea. Understanding the primary causes of mortality and identifying predominant pathological lesions are crucial for enhancing these efforts. This study aimed to investigate the causes of unexplained mortality in Oriental storks between 2019 and 2023 through comprehensive postmortem examinations. Twelve storks, including both wild and captive birds, classified as “unknown“ deaths, were examined. The results revealed that parasitic infections, particularly in wild storks, were frequently observed (41.7%). Additionally, gastrointestinal obstruction due to the ingestion of foreign materials was identified in a wild stork, highlighting the impact of environmental pollution. Despite the prevalence of inflammatory lesions in liver (58.3%), no cases of hepatitis were confirmed, except for one case of liver rupture in a wild stork. Notably, three nestling death cases from a single litter of captive storks suggested potential parental infanticide or lack of parental care. The overall results highlight the importance of addressing parasitic infections and environmental risks to improve the survival of wild Oriental storks, and emphasize the need for effective management in breeding facilities. Continuous monitoring and pathological evaluations for mortality cases are essential for understanding disease trends and developing adaptive conservation strategies to ensure the long-term preservation of this endangered species.

BACKGROUND: This study was undertaken to explore the effects of aging on the kidneys in mouse models of diabetes and chronic kidney disease (CKD), and to compare the expression of two isoforms of matrix metalloproteinase-2 (MMP-2)–secretory full-length MMP-2 and intracellular N-terminal truncated MMP-2 (NTT-MMP-2)–in these models. METHODS: Two experimental ICR mouse models were used: a streptozotocin (STZ)-induced type 1 diabetes mellitus model and a 5/6 nephrectomized (5/6Nx) CKD model. The abundance of each isoform of MMP-2 was determined by quantitative polymerase chain reaction (qPCR), and functional analyses were conducted. Moreover, the protein levels of the two MMP-2 isoforms were determined semi-quantitatively by immunohistochemical staining, and their association with tissue damage was assessed. RESULTS: Both isoforms of MMP-2 were upregulated in the kidney tissues of STZ-induced diabetic mice and 5/6Nx mice, irrespective of age. Characteristically, NTT-MMP-2 protein expression was elevated in old control mice, in line with the qPCR results. NTT-MMP-2 expression was limited to the renal cortex, and to the tubulointerstitial area rather than the glomerular area. In terms of tissue damage, tubulointerstitial fibrosis was more severe in old 5/6Nx mice than in their young counterparts, whereas glomerulosclerosis was comparable in old and young 5/6Nx mice. CONCLUSION: The intracellular isoform of MMP-2 was induced by ageing, irrespective of the presence of diabetes or CKD, and its induction may be related to tubulointerstitial fibrosis in chronic kidney disease.
Aging ; Animals ; Diabetes Mellitus* ; Diabetes Mellitus, Type 1 ; Fibrosis ; Kidney ; Matrix Metalloproteinase 2* ; Mice* ; Mice, Inbred ICR ; Polymerase Chain Reaction ; Protein Isoforms* ; Renal Insufficiency, Chronic* ; Streptozocin