Grossmanarildsen0274

Sixteen internal medicine residents participated in the workshop and completed the pre/post survey. Our results showed immediate positive outcomes as a result of participating in the workshop.

Our results showed that participants increased their intent to incorporate CBT in their primary care practice and increased their comfort with the various components of CBT. Our future directions include examining how long-term behavior changes as a result of this training.

Our results showed that participants increased their intent to incorporate CBT in their primary care practice and increased their comfort with the various components of CBT. Our future directions include examining how long-term behavior changes as a result of this training.Medulloblastoma (MB) represents the most common malignant pediatric brain tumor and is defined by four molecular subgroups with WNT MB having the most favorable prognosis. Our work provides a rational therapeutic option in which the protective effects of WNT-driven MBs may be augmented in Group 3 and 4 MB.How ER exit sites disassemble during mitosis is not well understood. Transport ANd Golgi Organization 1 (TANGO1, also known as MIA3), a cargo receptor originally identified for collagens, acts as a hub for ER exit site disassembly under the control of Casein Kinase 1 (CK1)-mediated phosphorylation and Protein Phosphatase 1 (PP1)-mediated dephosphorylation. Impaired dephosphorylation during mitosis induces ER exit site disassembly.Widely metastatic cancers progress rapidly despite sharing genetic drivers with the primary tumor that seeds them. Our recent work indicates that metastatic pancreatic cancers evolve unique metabolic adaptations that are not genetically encoded. These adaptations harness niche-refined nutrients, such as hepatic glucose, to fuel malignant metaboloepigenetic programs that support widespread metastatic outgrowth.Oncogenic Wnt/β-catenin activation promotes cancer development and drug resistance to cancer treatments. We recently revealed an underlying mechanism linking linear ubiquitination with Wnt/β-catenin activation upon genotoxic treatments. SN-38 We showed that ABL1 (ABL proto-oncogene 1)-dependent phosphorylation of OTULIN (OTU deubiquitinase with linear linkage specificity) upon DNA damage drives β-catenin activation which promotes drug resistance in triple-negative breast cancer.Telomerase plays a key role in the immortalization of cancer cells by maintaining telomeres length. Using single-molecule imaging of telomerase RNA molecules in cancer cells, we recently reported novel insights into the role of Cajal bodies in telomerase biogenesis and the regulation of telomerase recruitment to telomeres.Limited therapeutic options impede the clinical outcome of triple-negative breast cancer (TNBC). Our recent study uncovered a novel signaling pathway implicating gamma-butyrobetaine hydroxylase 1 (BBOX1) in the control of cell growth in TNBC, via inositol 1, 4, 5-trisphosphate receptor type 3 (IP3R3) mediated calcium signaling which is essential for cellular energy metabolism.Biological roles of Pumilio1 (PUM1) in ubiquitous cells remain unclear. Here we identify 48 degrading target mRNAs by combined analysis of transcriptome-wide mRNA stabilities and the binding of mRNAs. Further analysis revealed that cells respond to DNA damage by inhibiting PUM1-mediated mRNA decay to activate translesion synthesis (46/50).Our work in rhabdomyosarcoma led us to the discovery of a novel oncogene, Advillin (AVIL) in glioblastoma. Multiple lines of evidence support that AVIL is an Achilles heel of glioblastoma, with its specific targeting potentially an effective treatment approach for the disease. A new signaling axis was also established.We recently identified E3 ligase RFWD3 as a modulator of stalled fork stability in BRCA2-deficient cells. We also show that BRCA1 might function upstream of BRCA2 during fork repair and that blocking fork degradation by depleting MRE11 does not guarantee fork repair. These findings provide new insights into the workings of BRCA1 and BRCA2 in the stalled fork repair pathway.Persistent socioeconomic disparity in mortality is a widely observed phenomenon despite improvements in the economic standard of living and the prevailing universal healthcare coverage policy. In this study, we selected Japan as a case in which public universal coverage has maintained horizontal equity in healthcare access while demographic and economic challenges have affected the life chances of vulnerable subpopulations over the past decade. We assessed the changing trends in the education-related disparity in mortality over a decade across demographic subpopulations for different causes of death, with the goal of generating social policy lessons to contribute to closing the mortality gap. Using a deterministic data merge between nationwide census and death records, we estimated age- and sex-specific mortality rates for 14 causes and their education-related gradients with absolute and relative indices of inequality in 2000 and 2010 via Poisson regression. Estimation parameters were standardized to the age structure of the sub-population of high school graduates in 2000 as the reference. The results demonstrated that the relative gaps in all-cause mortality persisted despite a decrease in the average mortality rate over the study period. The absolute gaps in mortality increased for preventable causes of death associated with lifestyle behavior choices. The average mortality worsened among socioeconomically vulnerable populations such as youth and women, who were left behind in the existing social/economic policy. External causes of death such as suicide and traffic accidents showed decreasing absolute gaps in a subpopulation targeted by universal social and labor policy measures. These change patterns indicate that, compared with a high-risk approach, a universal policy approach to dealing with societal and fundamental causes of health inequality seems more effective in reducing the education-related mortality gap in both absolute and relative terms.Increasing cigarette taxes has been the cornerstone of tobacco control policy. Recent work has argued that raising cigarette taxes alone may no longer be an effective strategy for lowering smoking rates. We largely confirm these findings but also find that increases in price continue to predict lower smoking participation in most model specifications. We argue that raising cigarette prices via taxation remains an effective public health policy. We discuss the advantages of homogeneous tax environments and minimum price laws for eliminating opportunities for consumers to offset tax increases by searching for lowest taxes.