Prevention of arthrofibrosis after arthroscopic screw fixation of tibial spine fracture in children and adolescents.

Arthrofibrosis is a major complication of tibial spine fracture treatment in children, potentially resulting in knee pain, quadriceps weakness, altered gait, decreased function, inability to return to sports, and long-term osteoarthritis. Thus, prevention rather than treatment of arthrofibrosis is desirable. The purpose of this study was to evaluate an aggressive postoperative rehabilitation and early intervention approach to prevent permanent arthrofibrosis after tibial spine fracture treatment and to compare epiphyseal and transphyseal screws for fixation.

Absence of polo-like kinase 3 in mice stabilizes Cdc25A after DNA damage but is not sufficient to produce tumors.

The polo-like kinases (Plks1-5) are emerging as an important class of proteins involved in many facets of cell cycle regulation and response to DNA damage and stress. Here we show that Plk3 phosphorylates the key cell cycle protein phosphatase Cdc25A on two serine residues in its cyclinB/cdk1 docking domain and regulates its stability in response to DNA damage. We generated a Plk3 knock-out mouse and show that Cdc25A protein from Plk3-deficient cells is less susceptible to DNA damage-mediated degradation than cells with functional Plk3.

Role of 14-3-3σ in poor prognosis and in radiation and drug resistance of human pancreatic cancers.

Background: Pancreatic cancer is the fourth leading cause of death in the US. Unlike other solid tumors such as testicular cancer which are now curable, more than 90% of pancreatic cancer patients die due to lack of response to therapy. Recently, the level of 14-3-3σ mRNA was found to be increased in pancreatic cancers and this increased expression may contribute to the failure in treatment of pancreatic cancers.

The novel mouse Polo-like kinase 5 responds to DNA damage and localizes in the nucleolus.

Polo-like kinases (Plk1-4) are emerging as an important class of proteins involved in many aspects of cell cycle regulation and response to DNA damage. Here, we report the cloning of a fifth member of the polo-like kinase family named Plk5. DNA and protein sequence analyses show that Plk5 shares more similarities with Plk2 and Plk3 than with Plk1 and Plk4.

Magmatically triggered slow slip at Kilauea Volcano, Hawaii.

We demonstrate that a recent dike intrusion probably triggered a slow fault-slip event (SSE) on Kilauea volcano's mobile south flank. Our analysis combined models of Advanced Land Observing Satellite interferometric dike-intrusion displacement maps with continuous Global Positioning System (GPS) displacement vectors to show that deformation nearly identical to four previous SSEs at Kilauea occurred at far-field sites shortly after the intrusion. We model stress changes because of both secular deformation and the intrusion and find that both would increase the Coulomb failure stress on possible SSE slip surfaces by roughly the same amount.

Priming phosphorylation of Chk2 by polo-like kinase 3 (Plk3) mediates its full activation by ATM and a downstream checkpoint in response to DNA damage.

The tumor suppressor gene Chk2 encodes a serine/threonine kinase that signals DNA damage to cell cycle checkpoints. In response to ionizing radiation, Chk2 is phosphorylated on threonine 68 (T68) by ataxia-telangiectasia mutated (ATM) protein leading to its activation. We have previously shown that polo-like kinase 3 (Plk3), a protein involved in DNA damage checkpoint and M-phase functions, interacts with and phosphorylates Chk2.

Improved diagnostic effectiveness with a sequential diagnostic paradigm in idiopathic pediatric sensorineural hearing loss.

Objectives: To determine whether a stepwise diagnostic paradigm is more diagnostically efficient and cost-effective than a simultaneous testing approach in the evaluation of idiopathic pediatric sensorineural hearing loss (SNHL).

Design: Prospective prevalence study.

Setting: Tertiary referral children's hospital.

The Plk3-Cdc25 circuit.

Polo-like kinases (Plks) are key regulators of the cell cycle, especially in the G2 phase and mitosis. They are incorporated into signaling networks that regulate many aspects of the cell cycle, including but not limited to centrosome maturation and separation, mitotic entry, chromosome segregation, mitotic exit, and cytokinesis. The Plks have well conserved 30-amino-acid elements, designated polo boxes (PBs), located in their carboxyl-termini, which with their flanking regions constitute a functional Polo-box domain (PBD).

A diagnostic paradigm for childhood idiopathic sensorineural hearing loss.

Objective: Our objective was to determine the diagnostic yield of laboratory testing, radiological imaging, and GJB2 mutation screening in a large cohort of patients with differing severities of idiopathic sensorineural hearing loss (SNHL).

Design And Setting: We undertook a retrospective study of patients presenting with SNHL at our institution from 1993 to 2002.

Results: Laboratory testing had an extremely low yield.

Cdc25C phosphorylation on serine 191 by Plk3 promotes its nuclear translocation.

Mitosis in human cells is initiated at the end of G2 by activation of the Cdc2/cyclin B complex. Activation occurs by dephosphorylation of the inhibitory residues, threonine 14 (T14) and tyrosine 15 (Y15), on Cdc2 by the Cdc25C phosphatase. Entry into mitosis is regulated by the subcellular relocalization of Cdc2/cyclin B, which is rapidly imported into the nucleus at the end of G2.

Mammalian Polo-like kinase 3 (Plk3) is a multifunctional protein involved in stress response pathways.

The Polo-like kinases (Plks) are a conserved family of kinases that contribute to cell cycle regulation, particularly in G2 and mitosis. In mammals, there are at least three members of the Plk family. Here we show that Plk3 is a stress response protein that becomes phosphorylated following DNA damage or mitotic spindle disruption.