Sanctioned Social Workers: Report from Three Studies (Executive Summary)

This Executive Summary is an overview of the findings from three research projects, funded through a two year grant. The American Foundation for Research & Consumer Education in Social Work Regulation, the research arm of the Association of Social Work Boards awarded the two year grant to Kim Boland-Prom, Ph.D., Social Work Department, Governors State University. The research results are summarized in two different sections: section one discusses school social workers sanctioned by boards of education and licensing boards, and section two presents results on social workers who are sanctioned by their state licensing boards. For more detailed information about the research protocols including data collection and analysis, please refer to the papers cited below (see also notes field of this OPUS record): Boland-Prom, K.W. (under review) Ethical challenges: A descriptive study of sanctioned social workers, 2000-2009. Submitted to Social Work on 12/26/11. Boland-Prom, K.W., & Alvarez, M.E., (under review) Ethical challenges in school social work: A qualitative study. Submitted to School Social Work Journal on 12/16/11. Boland-Prom, K.W., & Alvarez, M. E., (under review) School social workers sanctioned by state departments of education and licensing boards. Submitted to Children & Schools on 10/19/11. Information from this study will be added to: Boland-Prom, K., & Vogt, A., (revising for resubmission) Examination of the behavior of sanctioned social workers. Submitted to Journal of Social Work Values and Ethics, 9/14/11. The data collected in this research is robust enough to support more articles about social workers sanctioned by regulatory boards. In 2017, the archived databases from these studies will be available for future researchers. Researchers can make requests directly to the American Foundation for Research & Consumer Education in Social Work Regulation

Transitional mucosa of the colon and tumor growth factors

Transitional mucosa of the colon is the tissue immediately adjacent to a cancer, which has histochemical and ultrastructural features similar to those seen in neoplasia. Therefore, it has been hypothesized in the past that this tissue represents the premalignant antecedent to colonic adenocarcinoma. Other investigators have disputed this explanation because similar changes are found adjacent to colonic lesions other than adenocarcinoma.The hypothesis offered here suggests that transitional mucosa may result from the paracrine influence of tumor growth factors released by the tumor. Candidate peptide hormones known to be produced by tumors are proposed, and a framework is outlined to explain the occurrence of transitional mucosa adjacent to non-neoplastic lesions. Transitional mucosa may be both a genuine reflection of the transformed phenotype and yet a "reactive" phenomenon secondary to the presence of the adjacent tumor.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26787/1/0000343.pd

Nuclear import of Avian Sarcoma Virus integrase is facilitated by host cell factors

<p>Abstract</p> <p>Background</p> <p>Integration of retroviral DNA into the host cell genome is an obligatory step in the virus life cycle. In previous reports we identified a sequence (amino acids 201–236) in the linker region between the catalytic core and C-terminal domains of the avian sarcoma virus (ASV) integrase protein that functions as a transferable nuclear localization signal (NLS) in mammalian cells. The sequence is distinct from all known NLSs but, like many, contains basic residues that are essential for activity.</p> <p>Results</p> <p>Our present studies with digitonin-permeabilized HeLa cells show that nuclear import mediated by the NLS of ASV integrase is an active, saturable, and ATP-dependent process. As expected for transport through nuclear pore complexes, import is blocked by treatment of cells with wheat germ agglutinin. We also show that import of ASV integrase requires soluble cellular factors but does not depend on binding the classical adapter Importin-α. Results from competition studies indicate that ASV integrase relies on one or more of the soluble components that mediate transport of the linker histone H1.</p> <p>Conclusion</p> <p>These results are consistent with a role for ASV integrase and cytoplasmic cellular factors in the nuclear import of its viral DNA substrate, and lay the foundation for identification of host cell components that mediate this reaction.</p

Analysis of cancer-associated colonic mucin by ion-exchange chromatography: evidence for a mucin species of lower molecular charge and weight in cancer

Cancer-associated mucins in the colon are antigenically distinct and glycosylated differently from their normal counterparts. Mucin-rich glycoconjugate preparations were made from nine non-neoplastic colons, seven colon cancers, and two different xenografts from mucin-producing human colon cancer cell lines, and radiolabeled with 3H. The preparation was applied to a DEAE-cellulose ion-exchange column, and eluted with a discontinuous ascending NaCl gradient resulting in seven discrete fractions or `species'. Over half of the 3H-labeled glycoconjugates from specimens of non-neoplastic colonic epithelium eluted in fraction V (eluted with 0.25 NaCl). Significantly less of the 3H-labeled glycoconjugates from specimens of colon cancer eluted in fraction V (34%, PPPPO-acetylation of the mucins. Mucin-type glycoconjugates from colon cancers are relatively less charged than those from the normal colon, and elute at lower ionic strengths. Of interest, cancer-associated mucins appear to be a lower molecular weight than their normal counterparts. Additional studies of oligosaccharide and apomucin structure will be required to explain the molecular basis of these differences in charge.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27933/1/0000358.pd

Chr21 protein–protein interactions: enrichment in proteins involved in intellectual disability, autism, and late-onset Alzheimer’s disease

Down syndrome (DS) is caused by human chromosome 21 (HSA21) trisomy. It is characterized by a poorly understood intellectual disability (ID). We studied two mouse models of DS, one with an extra copy of the Dyrk1A gene (189N3) and the other with an extra copy of the mouse Chr16 syntenic region (Dp(16)1Yey). RNA-seq analysis of the transcripts deregulated in the embryonic hippocampus revealed an enrichment in genes associated with chromatin for the 189N3 model, and synapses for the Dp(16)1Yey model. A large-scale yeast two-hybrid screen (82 different screens, including 72 HSA21 baits and 10 rebounds) of a human brain library containing at least 107 independent fragments identified 1,949 novel protein–protein interactions. The direct interactors of HSA21 baits and rebounds were significantly enriched in ID-related genes (P-value < 2.29 × 10−8). Proximity ligation assays showed that some of the proteins encoded by HSA21 were located at the dendritic spine postsynaptic density, in a protein network at the dendritic spine postsynapse. We located HSA21 DYRK1A and DSCAM, mutations of which increase the risk of autism spectrum disorder (ASD) 20-fold, in this postsynaptic network. We found that an intracellular domain of DSCAM bound either DLGs, which are multimeric scaffolds comprising receptors, ion channels and associated signaling proteins, or DYRK1A. The DYRK1A-DSCAM interaction domain is conserved in Drosophila and humans. The postsynaptic network was found to be enriched in proteins associated with ARC-related synaptic plasticity, ASD, and late-onset Alzheimer’s disease. These results highlight links between DS and brain diseases with a complex genetic basis

Clinical Significance of Microsatellite Instability in Sporadic Epithelial Ovarian Tumors

PURPOSE: We evaluated the expression of microsatellite instability (MSI) in sporadic ovarian tumors using 5 standard and 9 new MSI markers to determine the clinical significance of MSI in sporadic epithelial ovarian tumors. MATERIALS AND METHODS: MSI was examined in 21 borderline and 25 malignant ovarian tumors. Polymerase chain reaction (PCR) was performed using the 5 markers recommended by the National Cancer Institute (NCI) for colon cancer and 9 additional markers. MSI was determined using fractional analysis by mixing the PCR products and size markers. RESULTS: Using the 5 conventional MSI markers, MSI was found in 4 of 46 (8.6%) ovarian tumors, including 2 of 21 (9.5%) borderline ovarian tumors and 2 of 25 (8%) malignant ovarian tumors. Using the 9 additional MSI markers, MSI was observed in 7 of 46 (15.2%) ovarian tumors, including 3 of 21 (14.3%) borderline ovarian tumors and 4 of 25 (16%) malignant ovarian tumors. There was no statistically significant difference between MSI and clinicopathological factors, including histology and stage, although there was a trend toward an increased incidence of MSI in the serous type. CONCLUSION: MSI was infrequent in ovarian tumors, including both borderline and malignant tumors. MSI was found to be uncommon in sporadic ovarian tumors, even by using additional MSI markers. The clinical significance of MSI is not strong in patients with sporadic ovarian tumors.ope

Mutations in TGFbeta-RII and BAX mediate tumor progression in the later stages of colorectal cancer with microsatellite instability

Abstract Background Microsatellite instability (MSI) occurs in 15% of colorectal cancers (CRC). The genetic targets for mutation in the MSI phenotype include somatic mutations in the transforming growth factor beta receptor typeII (TGFbetaRII), BAX, hMSH3 and hMSH6. It is not clear how mutations of these genes mediate tumor progression in the MSI pathway, and the temporal sequence of these mutations remains uncertain. In this study, early stage CRCs were examined for frameshift mutations in these target genes, and compared with late stage tumors and CRC cell lines. Methods We investigated 6 CRC cell lines and 71 sporadic CRCs, including 61 early stage cancers and 10 late stage cancers. Mutations of repetitive mononucleotide tracts in the coding regions of TGFbetaRII, BAX, hMSH3, hMSH6, IGFIIR and Fas antigen were identified by direct sequencing. Results Thirteen (18.3%) of 71 CRC, including 9/61 (14.7%) early stage cancers and 4/10 (40%) late stage cancers, were identified as MSI and analyzed for frameshift mutations. No mutation in the target genes was observed in any of the 9 early stage MSI CRCs. In contrast, frameshift mutations of TGFbetaRII, BAX, hMSH3 and hMSH6 were present in 3/4 late stage MSI tumors. There is a statistical association (p = 0.014) between mutation in any one gene and tumor stage. Conclusions TGFbetaRII, BAX, hMSH3 and hMSH6 mutations are relatively late events in the genesis of MSI CRCs. The frameshift mutations in these target genes might mediate progression from early to late stage cancer, rather than mediating the adenoma to carcinoma transition.</p