RESUMO
BACKGROUND: Ruptured finger distal interphalangeal (DIP) collateral ligament is a rare injury, with controversial treatment until the present. Our case series aimed to demonstrate feasible surgical intervention using a mini anchor. METHODS: The present study includes four patients with ruptured finger DIP collateral ligaments who received primary repair in a single institute. They have suffered from joint instability due to ligament loss caused by infection, motorcycle accidents, and work-related accidents. All patients were operated on similarly using a 1.0 mm mini anchor for ligament reattachment. RESULTS: The finger DIP joint range of motion (ROM) was documented in all patients during follow-up. Joint ROM recovered to almost normal degrees, and the pinch strength recovered to > 90% compared to the contralateral side in all patients. Additionally, collateral ligament re-rupture, DIP joint subluxation or re-dislocation, and infection were not noted during follow-up. CONCLUSIONS: Ruptured finger DIP joint ligament requiring surgery is usually based on a combination with other soft tissue injuries and defects. However, repair with a 1.0 mm mini anchor is a feasible surgical intervention to reattach the ligament with minimal complication.
RESUMO
The nucleolus is best known for its cellular role in regulating ribosome production and growth. More recently, an unanticipated role for the nucleolus in innate immunity has recently emerged whereby downregulation of fibrillarin and nucleolar contraction confers pathogen resistance across taxa. The mechanism of this downregulation, however, remains obscure. Here we report that rather than fibrillarin itself being the proximal factor in this pathway, the key player is a fibrillarin-stabilizing deubiquitinylase USP-33. This was discovered by a candidate-gene search of Caenorhabditis elegans in which CED-3 caspase was revealed to execute targeted cleavage of USP-33, thus destabilizing fibrillarin. We also showed that cep-1 and ced-3 mutant worms altered nucleolar size and decreased antimicrobial peptide gene, spp-1, expression rendering susceptibility to bacterial infection. These phenotypes were reversed by usp-33 knockdown, thus linking the CEP-1-CED-3-USP-33 pathway with nucleolar control and resistance to bacterial infection in worms. Parallel experiments with the human analogs of caspases and USP36 revealed similar roles in coordinating these two processes. In summary, our work outlined a conserved cascade that connects cell death signaling to nucleolar control and innate immune response.