Patient-Level Cancer Prediction Models From a Nationwide Patient Cohort: Model Development and Validation.

Background: Nationwide population-based cohorts provide a new opportunity to build automated risk prediction models at the patient level, and claim data are one of the more useful resources to this end. To avoid unnecessary diagnostic intervention after cancer screening tests, patient-level prediction models should be developed.

Objective: We aimed to develop cancer prediction models using nationwide claim databases with machine learning algorithms, which are explainable and easily applicable in real-world environments.

Cluster analysis of child homicide in South Korea.

Background: There has been an insufficient in-depth analysis of the nature and prevalence of the typologies of child homicide in Asia, particularly in South Korea.

Objective: In the current study, we sought to determine the prevalence and identify the heterogeneity of the child homicide phenomenon in South Korea.

Participant And Settings: All 341 original case files (i.

PTK6 inhibits down-regulation of EGF receptor through phosphorylation of ARAP1.

PTK6 (also known as Brk) is a non-receptor-tyrosine kinase containing SH3, SH2, and catalytic domains, that is expressed in more than 60% of breast carcinomas but not in normal mammary tissues. To analyze PTK6-interacting proteins, we have expressed Flag-tagged PTK6 in HEK293 cells and performed co-immunoprecipitation assays with Flag antibody-conjugated agarose. A 164-kDa protein in the precipitated fraction was identified as ARAP1 (also known as centaurin delta-2) by MALDI-TOF mass analysis.

Molecular dissection of the interaction between the SH3 domain and the SH2-Kinase Linker region in PTK6.

PTK6 (also known as Brk) is an intracellular tyrosine kinase that contains SH3, SH2, and tyrosine kinase catalytic (Kinase) domains. The SH3 domain of PTK6 interacts with the N-terminal half of the linker (Linker) region between the SH2 and Kinase domains. Site-directed mutagenesis and surface plasmon resonance studies showed that a tryptophan residue (Trp44) in the SH3 domain and proline residues in the Linker region, in the order of Pro177, Pro175, and Pro179, contribute to the interaction.