An Investigation of Premature Discharges from Residential Addiction Treatment Centers in the United States in 2019

The purpose of this study was to identify predictors associated with the length of stay in patients prematurely discharged from residential addiction treatment facilities in the United States.  This study sought to provide a more in-depth understanding regarding which patients may be at a greater risk for a shortened length of stay and to help fill the gap in the literature pertaining to the length of stay and related variables in prematurely discharged patients.  The research methodology for this study was a quantitative, non-experimental design using pre-existing, secondary data from the Substance Abuse and Mental Health Administrations Treatment Episode Data Set-Discharge (TEDS-D) from the year 2019.  The Treatment Episode Data Set-Discharge is a collection of data reported on a national level regarding discharges from substance abuse treatment facilities. Data analysis included an examination of the relationship between the predictor variables, the number of times a patient has been admitted to treatment, admission wait time, gender, and age, with the criterion variable, length of stay for an N = 49080.  The data was ex post facto; therefore, this was a non-experimental design that utilized secondary analyses of pre-existing data to answer the research questions.  A significant relationship was discovered to exist between the criterion/dependent variable, length of stay, predictor/independent variables days waiting for admission, the number of prior treatment episodes, and gender.  When controlling for days waiting to include only those waiting one or more days for treatment admission, a subsequent significant relationship was found.  This study examined variables that serve as predictive of length of stay in patients who were prematurely discharged from residential addiction treatment facilities under the premise of having been administratively discharged or in the event that the patient left treatment against professional advice. &nbsp

Promotion of functional heterotrimeric type I collagen via transfection in osteogenesis imperfecta fibroblasts

Abstract only availableOsteogenesis imperfecta (OI) is a heritable disorder due to mutations in type I collagen. Normal type I collagen forms a heterotrimeric protein comprised of two pro1(I) chains and one pro2(I) chain [1(I)22(I)]. The osteogenesis imperfecta murine (oim) model mouse contains a single nucleotide deletion in the pro2(I) gene (COL1A2) resulting in non-functional pro2(I) chains and production of homotrimeric type I collagen containing three pro1(I) collagen chains, [1(I)3], resulting in small body size, increased bone fragility and altered bone mineralization. The overall goal of this study is to correct the oim defect by introducing normal COL1A2 genes into oim cells. Oim dermal fibroblasts were transfected with a series of COL1A2 gene constructs containing the full-length murine pro2(I) collagen cDNA driven by various lengths of the murine COL1A2 promoter (1.5kb, 3.0kb, and 6.0kb) along with a COL1A2 enhancer. These DNA constructs were cotransfected with pcDNA3 containing a neomycin resistance gene, which allows for selection of stably transfected cell lines. Various assays have been developed to monitor proa2(I) collagen expression at the DNA, RNA and protein levels. A PCR assay was used to confirm genomic incorporation of transgenic COL1A2 gene constructs and an RT-PCR assay used to confirm expression of normal pro2(I) collagen mRNA. Denaturing urea-SDS polyacrylamide gel electrophoresis along with Western blotting analyses using anti-murine 1(I) and 2(I) collagen antibodies were used to confirm normal pro2(I) collagen expression at the protein level as well as its incorporation into normal heterotrimeric type I collagen. All the necessary tools have been established for evaluating the efficacy of transfection. Currently, the first series of stably transfected oim cell lines are being expanded for analyses as described above. Although this study is aimed at 'fixing' the oim mutation via gene therapy, valuable data will also be collected regarding the effectiveness of the variable length promoter regions in enhancing the expression of the normal COL1A2 gene.Life Sciences Undergraduate Research Opportunity Progra

Bringing the feelings back : returning emotions to criminal justice practice

This article argues that probation policy needs to take much greater account of the important role of emotion in probation and other criminal justice practice. Drawing on the findings of three separate pieces of research, we argue that emotions play a critical role in practice despite their absence from policy in recent years. Emotions, we argue, are important in terms of developing effective practice. Moreover, there are several consequences of using emotion in practice and relevant organisations need to recognise this and provide sufficient support for staff in dealing with such consequences. This, we argue, would allow for practitioners to be both emotionally literate whilst also enabling practice which encourages offenders to take responsibility for their actions. In sum, it will lead to an intuitively intelligent system of justic

Comparison of the progression of glomerulosclerosis between Oim-C57BL/6 and Oim-B6C3Fe a/a [abstract]

Abstract only availableOsteogenesis Imperfecta (OI), a heritable connective tissue disorder, resulting from mutations in the type I procollagen genes is characterized by bone deformity and fragility. The OI mouse model (oim) is homozygous for a null mutation in the COL1A2 gene of type I collagen, displaying a bone phenotype mimicking type III OI in humans. These mice also have glomerulosclerosis characterized by α1(I) homotrimeric type I collagen deposition within their glomeruli. Previous studies in our laboratory demonstrate that oim-B6C3Fe a/a mice exhibit accumulation of glomerular fibrillar collagen beginning post-natally by one week of age, showing increasing severity with continued development. Heterozygous (het) mice have an intermediate glomerular phenotype between homozygous (oim) and wildtype (wt) mice. Although the oim mutation on the C57BL/6 mouse background shows a more severe bone phenotype than its B6C3Fe a/a counterpart, the impact on the glomerular progression and severity is unknown. Preliminary morphometry mapping and lesion scoring data suggest the oim mutation on C57BL/6 and B6C3Fe a/a backgrounds exhibit similar glomerulosclerotic lesion progression between one and four months of age. Het mice of both backgrounds exhibited mild lesions, and little progression of the glomerulopathy beyond one month (0.3075 ± 0.23 and 0.712 ± 0.29 for C57BL/6 and B6C3Fe a/a, respectively). Within oim mice, glomerulosclerosis varies in severity as reflected by a large standard deviation. However, both oim-C57BL/6 and oim-B6C3Fe a/a mouse strains exhibit similar patterns of glomerulosclerotic development with age. One month oim-C57BL/6 mice have less affected glomeruli (1.65 ± 0.55) as compared to oim-B6C3Fe a/a mice (2.1 ± 1.0) suggesting slower progression of disease in oim-C57BL/6, although they reach the same severity by four months of age (3.04 ± 0.4 and 3.29 ± 0.49, respectively). This suggests that regardless of strain, glomerulosclerotic lesions progress similarly, and C57BL/6 mice are appropriate for further studies.CAFNR On Campus Research Internshi

Social and Emotional Barriers in Online Graduate Counseling Programs: Recommendations for Effective Practice for Working with Hispanic Adult Learners

Hispanic learners in higher education face unique challenges and barriers to success. An understanding of Adult Learning Theory through the lens of Hispanic culture is imperative, particularly in relation to both social and emotional barriers that are likely to disrupt the graduate learning process.  The responsibility to effectively lead and educate such learners falls into the hands of counselor educators in higher education. When considering ethnic diversity among adult learners, it is imperative to explore effective practice methodologies for students from specific cultures/ethnic origins. The purpose of this semi-systematic review was to explore the case of Jen, a Hispanic/Latina graduate student enrolled in an online masters in clinical mental health counseling program, and to synthesize implications for effective practice in educating and working with Hispanic students

The use of primary dermal fibroblast cultures to evaluate type I collagen expression in the oim model mouse

Abstract only availableOsteogenesis imperfecta type III is a heritable disorder leading to impaired connective tissue function in type I collagen containing tissues including bone fragility, blue-grey sclera, short stature, and hearing loss. Normal type I collagen is a heterotrimeric molecule containing two pro1(I) collagen chains and a similar but genetically distinct pro2(I) collagen chain. The osteogenesis imperfecta murine (oim) model mouse produces only homotrimeric type I collagen due to a single nucleotide deletion in the COL1A2 gene resulting in a non-functional pro2(I) collagen chain. The result is expression of an abnormal type I collagen molecule which leads to the above phenotype. This study is aimed at developing a methodology whereby dermal fibroblast cultures can be utilized for a variety of assays, including type I collagen RNA and protein quantification. For genotype identification, primers flanking the site of the single nucleotide deletion allow for differentiation of wild type, heterozygous and homozygous animals at the genomic level. Upon confirmation, skin was removed from both oim and wildtype mice and the dermal layer harvested. Fibroblasts originating from the dermal layer of each genotype were then cultured and grown to confluence as separate cultures and the RNA and/or protein harvested from both cell types. Total RNA was harvested using the Qiagen RNeasy kit and used to make cDNA, which was then used in conjunction with specific PCR primers to differentiate between wildtype and oim transcripts. For protein studies, the cells were treated with ascorbic acid to maximize the production of collagen prior to harvesting. Type I collagen expression was then confirmed via a western blot using a type I collagen-specific antibody. Initial results indicate the presence of both pro1(I) and pro2(I) collagen chains from harvested wildtype dermal fibroblasts, while media harvested from oim dermal fibroblasts indicated the presence of only the pro1(I) collagen chains. These results confirm the in vivo protein expression profile seen in skin of both oim and wildtype mice is exhibited in vitro in the respective dermal fibroblast cultures. These results will allow us to quantitate pro1(I) and pro2(I) collagen mRNA and protein expression levels. Future experiments will include the quantitation of type I collagen mRNA levels using RT-PCR, as well as the use of densitometry to quantitate type I collagen protein levels by western blot analysis. This in turn promises to provide insight into the mechanism of formation of abnormal type I collagen in the oim model mouse.Life Sciences Undergraduate Research Opportunity Progra

An Evaluation of a Humanities-Oriented, Cognitive Stimulation Model to Improve Descriptive Writing Development of Underprepared College Freshmen.

The primary purpose of this investigation was to test the efficacy of a humanities-oriented, cognitive stimulation unit, incorporating visual and verbal stimuli, observation practice, inferencing skills, and prewriting, on underprepared college students\u27 ability to write descriptive compositio

Sodium-dependent multivitamin transporter: a potential novel cause of cardiomyopathy

PhD ThesisCardiomyopathy is a heterogeneous disorder affecting adults and children and is a leading cause of death globally. Paediatric cardiomyopathies affect ~1:100,000 children, with around one third requiring a heart transplant or risk death within two years of diagnosis. A homozygous missense mutation in the human Sodium Multivitamin Transporter (SMVT) gene, SLC5A6, was identified in sisters with paediatric cardiomyopathy. The transporter is a plasma membrane protein that transports biotin, pantothenic acid and lipoic acid throughout several tissues including the brain, intestine and heart. These substrates play an essential role in energy metabolism and homeostasis, suggesting reduced functionality of Slc5a6 within the heart could result in cardiomyopathy. Mouse models were employed to conditionally delete Slc5a6 within cardiomyocytes resulting in the development of cardiomyopathy markers throughout early adulthood leading to sudden death at five months of age. Cardiac functionality was assessed using electrocardiography (ECG) which showed atrioventricular block, and histological analysis demonstrated myocardial fibrosis and cardiomyocyte hypertrophy. Cardiac magnetic resonance imaging (CMR) revealed a reduction in ejection fraction, cardiac output and stroke volume, hallmarks of left ventricular dysfunction. Together, these changes confirm the presence of cardiomyopathy within the cardiomyocyte specific Slc5a6 knockout model. Gross abnormalities in mitochondrial structure and organisation were observed using electron microscopy, and quadruple immunofluorescence staining revealed a reduction in complex I of the mitochondrial electron transport chain. This suggests that loss of Slc5a6 has a negative impact on energy metabolism through deficiency of complex I, causing excess stress upon the heart ultimately resulting in cardiomyopathy. Preliminary data from vitamin supplementation to pregnant females and their Slc5a6 knockout offspring shows a delay in the onset of cardiomyopathy markers including myocardial fibrosis and cardiomyocyte hypertrophy, as shown by ECG and histology. Collectively this data suggests that Slc5a6 is important for normal cardiac structure and function, with potential for therapeutic intervention in patients with variants in SLC5A6

An improved method for surface immobilisation of RNA: application to small Non-Coding RNA - mRNA pairing

Characterisation of RNA and its intermolecular interactions is increasing in importance as the inventory of known RNA functions continues to expand. RNA-RNA interactions are central to post-transcriptional gene regulation mechanisms in bacteria, and the interactions of bacterial small non-coding RNAs (sRNAs) with their mRNA targets are the subject of much current research. The technology of surface plasmon resonance (SPR) is an attractive approach to studying these interactions since it is highly sensitive, and allows interaction measurements to be recorded in real-time. Whilst a number of approaches exist to label RNAs for surface-immobilisation, the method documented here is simple, quick, efficient, and utilises the high-affinity streptavidin-biotin interaction. Specifically, we ligate a biotinylated nucleotide to the 3' end of RNA using T4 RNA ligase. Although this is a previously recognised approach, we have optimised the method by our discovery that the incorporation of four or more adenine nucleotides at the 3' end of the RNA (a poly-A-tail) is required in order to achieve high ligation efficiencies. We use this method within the context of investigating small non-coding RNA (sRNA)-mRNA interactions through the application of surface technologies, including quantitative SPR assays. We first focus on validating the method using the recently characterised Escherichia coli sRNA-mRNA pair, MicA-ompA, specifically demonstrating that the addition of the poly-A-tail to either RNA does not affect its subsequent binding interactions with partner molecules. We then apply this method to investigate the novel interactions of a Vibrio cholerae Qrr sRNA with partner mRNAs, hapR and vca0939; RNA-RNA pairings that are important in mediating pathogenic virulence. The calculated binding parameters allow insights to be drawn regarding sRNA-mRNA interaction mechanisms

Hfq binding changes the structure of Escherichia coli small noncoding RNAs OxyS and RprA, which are involved in the riboregulation of rpoS

OxyS and RprA are two small noncoding RNAs (sRNAs) that modulate the expression of rpoS, encoding an alternative sigma factor that activates transcription of multiple Escherichia coli stress-response genes. While RprA activates rpoS for translation, OxyS down-regulates the transcript. Crucially, the RNA binding protein Hfq is required for both sRNAs to function, although the specific role played by Hfq remains unclear. We have investigated RprA and OxyS interactions with Hfq using biochemical and biophysical approaches. In particular, we have obtained the molecular envelopes of the Hfq–sRNA complexes using small-angle scattering methods, which reveal key molecular details. These data indicate that Hfq does not substantially change shape upon complex formation, whereas the sRNAs do. We link the impact of Hfq binding, and the sRNA structural changes induced, to transcript stability with respect to RNase E degradation. In light of these findings, we discuss the role of Hfq in the opposing regulatory functions played by RprA and OxyS in rpoS regulation