RESUMO
Congenital deformities of the foot significantly challenge the mobility and quality of life of affected individuals. While surgical interventions are common, rehabilitation protocols tailored to address the specific needs of adults with congenital foot deformities are less explored. This case series aims to evaluate the effectiveness of a specialized foot rehabilitation protocol in improving functional outcomes and quality of life in adults with congenital foot deformities. A series of cases involving adults diagnosed with congenital foot deformities were enrolled in a structured rehabilitation program. The protocol incorporated a combination of therapeutic exercises, manual therapy, gait training, and orthotic management tailored to individual needs. Outcome measures included functional assessments, gait analysis, pain levels, and patient-reported outcomes at baseline, midpoint, and endpoint of the rehabilitation program. Preliminary findings from the case series indicate significant improvements in various outcome measures following the foot rehabilitation protocol. Participants demonstrated enhanced gait parameters, reduced pain levels, increased range of motion, and improved functional capacity. Moreover, subjective assessments revealed enhanced satisfaction and perceived improvements in quality of life among participants. The findings suggest that a tailored foot rehabilitation protocol can be beneficial in improving functional outcomes and quality of life in adults with congenital foot deformities. This underscores the importance of integrating comprehensive rehabilitation strategies alongside surgical interventions to optimize long-term outcomes and enhance the overall well-being of individuals with congenital foot deformities. Further research with larger sample sizes and controlled study designs is warranted to validate these findings and establish evidence-based rehabilitation guidelines for this population.
RESUMO
Pes planus, commonly referred to as flatfoot, is a congenital foot deformity characterized by the descent of the medial longitudinal arch, resulting in reduced spring action and increased stress on the foot during ambulation. This condition, opposite to pes cavus, typically lacks symptomatic presentation despite its structural abnormality. This case report discusses a 20-year-old female presenting to the musculoskeletal department of physiotherapy with impaired gait attributed to developmental flatfeet and an underdeveloped heel on one foot since birth. Apart from these foot deformities, no other significant abnormalities were noted upon examination. Orthotic management and ongoing monitoring have been initiated to facilitate functional independence. The prognosis for the patient's gait impairment remains optimistic with continued rehabilitation efforts aimed at dispelling misconceptions and barriers surrounding the correction of flatfoot deformities. This report underscores the importance of comprehensive rehabilitation strategies in managing flatfoot conditions to optimize patient outcomes and quality of life.
RESUMO
The spindle position checkpoint (SPOC) is a mitotic surveillance mechanism in Saccharomyces cerevisiae that prevents cells from completing mitosis in response to spindle misalignment, thereby contributing to genomic integrity. The kinase Kin4, one of the most downstream SPOC components, is essential to stop the mitotic exit network (MEN), a signalling pathway that promotes the exit from mitosis and cell division. Previous work, however, suggested that a Kin4-independent pathway contributes to SPOC, yet the underlying mechanisms remain elusive. Here, we established the glycogen-synthase-kinase-3 (GSK-3) homologue Mck1, as a novel component that works independently of Kin4 to engage SPOC. Our data indicate that both Kin4 and Mck1 work in parallel to counteract MEN activation by the Cdc14 early anaphase release (FEAR) network. We show that Mck1's function in SPOC is mediated by the pre-replication complex protein and mitotic cyclin-dependent kinase (M-Cdk) inhibitor, Cdc6, which is degraded in a Mck1-dependent manner prior to mitosis. Moderate overproduction of Cdc6 phenocopies MCK1 deletion and causes SPOC deficiency via its N-terminal, M-Cdk inhibitory domain. Our data uncover an unprecedented role of GSK-3 kinases in coordinating spindle orientation with cell cycle progression.
Assuntos
Proteínas de Saccharomyces cerevisiae , Saccharomycetales , Humanos , Proteínas de Saccharomyces cerevisiae/genética , Quinase 3 da Glicogênio Sintase/genética , Quinase 3 da Glicogênio Sintase/metabolismo , Fuso Acromático/metabolismo , Saccharomycetales/metabolismo , Proteínas Serina-Treonina Quinases , Fosforilação , Saccharomyces cerevisiae/genética , Mitose , Proteínas de Ciclo Celular/metabolismo , Proteínas Tirosina Fosfatases/genética , Proteínas Tirosina Fosfatases/metabolismoRESUMO
Hook proteins are evolutionarily conserved dynein adaptors that promote assembly of highly processive dynein-dynactin motor complexes. Mammals express three Hook paralogs, namely Hook1, Hook2, and Hook3, that have distinct subcellular localizations and expectedly, distinct cellular functions. Here we demonstrate that Hook2 binds to and promotes dynein-dynactin assembly specifically during mitosis. During the late G2 phase, Hook2 mediates dynein-dynactin localization at the nuclear envelope (NE), which is required for centrosome anchoring to the NE. Independent of its binding to dynein, Hook2 regulates microtubule nucleation at the centrosome; accordingly, Hook2-depleted cells have reduced astral microtubules and spindle positioning defects. Besides the centrosome, Hook2 localizes to and recruits dynactin and dynein to the central spindle. Dynactin-dependent targeting of centralspindlin complex to the midzone is abrogated upon Hook2 depletion; accordingly, Hook2 depletion results in cytokinesis failure. We find that the zebrafish Hook2 homologue promotes dynein-dynactin association and was essential for zebrafish early development. Together, these results suggest that Hook2 mediates assembly of the dynein-dynactin complex and regulates mitotic progression and cytokinesis.