Healing of articular cartilage is a major clinical challenge as it also lacks a direct vasculature and nerves, and carries a limited number of resident chondrocytes that do not proliferate easily. Damaged articular cartilages are usually replaced by fibrocartilages, which are mechanically and structurally weaker and less resilient. Regenerative medicine involving stem cells is considered to have a definitive potential to overcome the limitations associated with the currently available surgical methods of cartilage repair. Among various stem cell types, mesenchymal stem cells (MSCs) are preferred for clinical applications. These cells can be readily derived from various sources and have the ability to trans-differentiate into various tissue-specific cells, including those of the cartilage by the process of chondrogenesis. Compared to embryonic or induced pluripotent stem cells (iPSCs), no ethical or teratogenic issues are associated with MSCs. These stem cells are being extensively evaluated for the treatment of joint affections and the results appear promising. Unlike human medicine, in veterinary medicine, the literature on stem cell research for cartilage regeneration is limited. This review, therefore, aims to comprehensively discuss the available literature and pinpoint the achievements and limitations associated with the use of MSCs for articular cartilage repair in animal species.

Highlights Cryptorchid castration is technically demanding. Ultrasonography helped in assessing location, length and volume of retained testicles. Laparoscope-assisted retrieval of retained testicles safe in rams. First report of laparoscope assisted cryptorchid castration in sheep.

The hepatocyte nuclear factor-4α (HNF4α) and hepatocyte nuclear factor-1α (HNF1α) are transcription factors that influence the development and maintenance of homeostasis in a variety of tissues, including the liver. As such, disruptions in their transcriptional networks can herald a number of pathologies, such as tumorigenesis. Largely considered tumor suppressants in liver cancer, these transcription factors regulate key events of inflammation, epithelial–mesenchymal transition, metabolic reprogramming, and the differentiation status of the cell. High-throughput analysis of cancer cell genomes has identified a number of hotspot mutations in HNF1α and HNF4α in liver cancer. Such results also showcase HNF1α and HNF4α as important therapeutic targets helping us step into the era of personalized medicine. In this review, we update current findings on the roles of HNF1α and HNF4α in liver cancer development and progression. It covers the molecular mechanisms of HNF1α and HNF4α dysregulation and also highlights the potential of HNF4α as a therapeutic target in liver cancer.

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