Development and Evaluation of Strategies to Support Rural Secondments for Junior Physiotherapists

AbstractPurposeRural workforce shortages are a national issue. One strategy is the use of secondments from larger healthcare sites to staff rural sites on a rotational basis. The purpose of this evaluation is to explore the impact of the development, implementation of an educational, training and supervision package for junior Physiotherapists undertaking rural secondments in Northern NSW.Design/methodology/approachPre post evaluation of a training, education and supervision package to support junior Physiotherapists undertaking rural secondments across Northern NSW.  A baseline survey of Physiotherapists who had undertaken a secondment in the previous 12 months defined current practice and limitations. From this a targeted education, training and supervision package was developed. Post implementation surveying for a period of 12 months was undertaken to evaluate the packages implementation.FindingsStatistically significant improvements in staff reporting they felt supported and were aware of escalation processes for patients under their care were reported. Additionally improvements were seen in staff reported access to and completing competencies relevant to their secondment.Research implicationsThese findings provide guidance in regards to junior Physiotherapists working on rural secondments and the importance of structured education, training and support mechanisms.Practical implicationsThe findings from this work support the development and implementation of structured education, training and supervision plans prior to undertaking rural secondments.Originality/valueThese findings provide evidence and support the need for structured and target training, education and supervision for staff undertaking rural secondments to ensure staff are confident to work in a rural setting.LimitationsLarger response rates for post implementation survey results may result in different outcomes being reported in comparison to pre implementation results

The cellular DNA helicase ChlR1 regulates chromatin and nuclear matrix attachment of the human papillomavirus type 16 E2 protein and high copy viral genome establishment

In papillomavirus infections, the viral genome is established as a double-stranded DNA episome. To segregate the episomes into daughter cells during mitosis, they are tethered to cellular chromatin by the viral E2 protein. We previously demonstrated that the E2 proteins of diverse papillomavirus types, including bovine papillomavirus (BPV) and human papillomavirus 16 (HPV16), associate with the cellular DNA helicase ChlR1. This virus-host interaction is important for the tethering of BPV E2 to mitotic chromatin and the stable maintenance of BPV episomes. The role of the association between E2 and ChlR1 in the HPV16 life cycle is unresolved. Here we show that an HPV16 E2 Y131A mutant (E2Y131A) had significantly reduced binding to ChlR1 but retained transcriptional activation and viral origin-dependent replication functions. Subcellular fractionation of keratinocytes expressing E2Y131A showed a marked change in the localization of the protein. Compared to that of wild-type E2 (E2WT), the chromatin-bound pool of E2Y131A was decreased, concomitant with an increase in nuclear matrix-associated protein. Cell cycle synchronization indicated that the shift in subcellular localization of E2Y131A occurred in mid-S phase. A similar alteration between the subcellular pools of the E2WT protein occurred upon ChlR1 silencing. Notably, in an HPV16 life cycle model in primary human keratinocytes, mutant E2Y131A genomes were established as episomes, but at a markedly lower copy number than that of wild-type HPV16 genomes, and they were not maintained upon cell passage. Our studies indicate that ChlR1 is an important regulator of the chromatin association of E2 and of the establishment and maintenance of HPV16 episomes

Identification of Morpholino Thiophenes as Novel Mycobacterium tuberculosis Inhibitors, Targeting QcrB

With the emergence of multidrug-resistant strains of <i>Mycobacterium tuberculosis</i> there is a pressing need for new oral drugs with novel mechanisms of action. Herein, we describe the identification of a novel morpholino–thiophenes (MOT) series following phenotypic screening of the Eli Lilly corporate library against <i>M. tuberculosis</i> strain H37Rv. The design, synthesis, and structure–activity relationships of a range of analogues around the confirmed actives are described. Optimized leads with potent whole cell activity against H37Rv, no cytotoxicity flags, and in vivo efficacy in an acute murine model of infection are described. Mode-of-action studies suggest that the novel scaffold targets QcrB, a subunit of the menaquinol cytochrome <i>c</i> oxidoreductase, part of the bc1-aa3-type cytochrome <i>c</i> oxidase complex that is responsible for driving oxygen-dependent respiration

The Vehicle, Spring 2013

Vol. 54, Issue 1 Table of Contents About Face!: A Confederacy of ClichesKaren Neuberg page 8 HopeJames Coxpage 9 IN or OUTTaryn DeVriespage 12 The Imagination of a ChildMaxwell Collinspage 16 How Free to be a TreeLeann Kirchnerpage 18 CrowsValentina Canopage 19 Old West PhotosFred Pollackpage 20 Lava LampFred Pollackpage 21 Mort MotGerry Mark Nortonpage 23 If ILaura Adrianpage 24 Finding my MonkeyDavid Lewitzkypage 25 Slow DragDavid Lewitzkypage 26 Political ScienceElizabeth Marlowpage 27 ...Were Punctuated By...Elizabeth Marlowpage 28 St. E Pt 1Elizabeth Marlowpage 29 The Steamboat CaptainElizabeth Marlowpage 30 Pretty EyesRyan Sheapage 31 The World is RoundRyan Sheapage 32 End SongsJason Graffpage 33 The Sensitive Youth Grows UpRichard King Perkins IIpage 41 Colors and LightKyle Owenspage 42 RE-TARDKarlyn Thayerpage 44 Where Is Waldo?Riley Parishpage 57 Beneath Shifting SoundsHolly Daypage 58 Talking Shop with Mike Kardospage 60 Winnie Davis Neely Award winner: Paper CutsGregory Robert Petersonpage 68 Paper-Mache PoetryGregory Robert Petersonpage 69 James K. Johnson Award winners: ValveChristopher Robinsonpage 72 Dear MotherEliot Thompsonpage 76 Why Are There Bars on the WindowsEliot Thompsonpage 77 To Be a ScholarEliot Thompsonpage 79 OccidentalEliot Thompsonpage 80 Falling is for the ClumsyEliot Thompsonpage 81 Scary MonstersC. David Banyaipage 83 I Called My Grandmother DollyRashelle Spearpage 90 Tender FleshH R Greenpage 92 Faking ItShelby Koehnepage 95 Contributor\u27s notespage 101https://thekeep.eiu.edu/vehicle/1095/thumbnail.jp

The Vehicle, Spring 2013

Vol. 54, Issue 1 Table of Contents About Face!: A Confederacy of ClichesKaren Neuberg page 8 HopeJames Coxpage 9 IN or OUTTaryn DeVriespage 12 The Imagination of a ChildMaxwell Collinspage 16 How Free to be a TreeLeann Kirchnerpage 18 CrowsValentina Canopage 19 Old West PhotosFred Pollackpage 20 Lava LampFred Pollackpage 21 Mort MotGerry Mark Nortonpage 23 If ILaura Adrianpage 24 Finding my MonkeyDavid Lewitzkypage 25 Slow DragDavid Lewitzkypage 26 Political ScienceElizabeth Marlowpage 27 ...Were Punctuated By...Elizabeth Marlowpage 28 St. E Pt 1Elizabeth Marlowpage 29 The Steamboat CaptainElizabeth Marlowpage 30 Pretty EyesRyan Sheapage 31 The World is RoundRyan Sheapage 32 End SongsJason Graffpage 33 The Sensitive Youth Grows UpRichard King Perkins IIpage 41 Colors and LightKyle Owenspage 42 RE-TARDKarlyn Thayerpage 44 Where Is Waldo?Riley Parishpage 57 Beneath Shifting SoundsHolly Daypage 58 Talking Shop with Mike Kardospage 60 Winnie Davis Neely Award winner: Paper CutsGregory Robert Petersonpage 68 Paper-Mache PoetryGregory Robert Petersonpage 69 James K. Johnson Award winners: ValveChristopher Robinsonpage 72 Dear MotherEliot Thompsonpage 76 Why Are There Bars on the WindowsEliot Thompsonpage 77 To Be a ScholarEliot Thompsonpage 79 OccidentalEliot Thompsonpage 80 Falling is for the ClumsyEliot Thompsonpage 81 Scary MonstersC. David Banyaipage 83 I Called My Grandmother DollyRashelle Spearpage 90 Tender FleshH R Greenpage 92 Faking ItShelby Koehnepage 95 Contributor\u27s notespage 101https://thekeep.eiu.edu/vehicle/1095/thumbnail.jp

Friend matters: sex differences in social language during autism diagnostic interviews

Background: Autistic individuals frequently experience social communication challenges. Girls are diagnosed with autism less often than boys even when their symptoms are equally severe, which may be due to insufficient understanding of the way autism manifests in girls. Differences in the behavioral presentation of autism, including how people talk about social topics, could contribute to these persistent problems with identification. Despite a growing body of research suggesting that autistic girls and boys present distinct symptom profiles in a variety of domains, including social attention, friendships, social motivation, and language, differences in the way that autistic boys and girls communicate verbally are not yet well understood. Closely analyzing boys’ and girls’ socially-focused language during semi-structured clinical assessments could shed light on potential sex differences in the behavioral presentation of autistic individuals that may prove useful for identifying and effectively supporting autistic girls. Here, we compare social word use in verbally fluent autistic girls and boys during the interview sections of the ADOS-2 Module 3 and measure associations with clinical phenotype. Methods: School-aged girls and boys with autism (N = 101, 25 females; aged 6–15) were matched on age, IQ, and parent/clinician ratings of autism symptom severity. Our primary analysis compared the number of social words produced by autistic boys and girls (normalized to account for differences in total word production). Social words are words that make reference to other people, including friends and family. Results: There was a significant main effect of sex on social word production, such that autistic girls used more social words than autistic boys. To identify the specific types of words driving this effect, additional subcategories of friend and family words were analyzed. There was a significant effect of sex on friend words, with girls using significantly more friend words than boys. However, there was no significant main effect of sex on family words, suggesting that sex differences in social word production may be driven by girls talking more about friends compared to boys, not family. To assess relationships between word use and clinical phenotype, we modeled ADOS-2 Social Affect (SA) scores as a function of social word production. In the overall sample, social word use correlated significantly with ADOS-2 SA scores, indicating that participants who used more social words were rated as less socially impaired by clinicians. However, when examined in each sex separately, this result only held for boys. Limitations: This study cannot speak to the ways in which social word use may differ for younger children, adults, or individuals who are not verbally fluent; in addition, there were more autistic boys than girls in our sample, making it difficult to detect small effects. Conclusions: Autistic girls used significantly more social words than boys during a diagnostic assessment—despite being matched on age, IQ, and both parent- and clinician-rated autism symptom severity. Sex differences in linguistic markers of social phenotype in autism are especially important in light of the late or missed diagnoses that disproportionately affect autistic girls. Specifically, heightened talk about social topics could complicate autism referral and diagnosis when non-clinician observers expect a male-typical pattern of reduced social focus, which autistic girls may not always exhibit

Denial of long-term issues with agriculture on tropical peatlands will have devastating consequences

Non peer reviewe

Genome-Wide Association Identifies Nine Common Variants Associated With Fasting Proinsulin Levels and Provides New Insights Into the Pathophysiology of Type 2 Diabetes

OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10−8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10−4), improved β-cell function (P = 1.1 × 10−5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10−6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

Common variants at 30 loci contribute to polygenic dyslipidemia

Blood low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglyceride levels are risk factors for cardiovascular disease. To dissect the polygenic basis of these traits, we conducted genome-wide association screens in 19,840 individuals and replication in up to 20,623 individuals. We identified 30 distinct loci associated with lipoprotein concentrations (each with P < 5 × 10-8), including 11 loci that reached genome-wide significance for the first time. The 11 newly defined loci include common variants associated with LDL cholesterol near ABCG8, MAFB, HNF1A and TIMD4; with HDL cholesterol near ANGPTL4, FADS1-FADS2-FADS3, HNF4A, LCAT, PLTP and TTC39B; and with triglycerides near AMAC1L2, FADS1-FADS2-FADS3 and PLTP. The proportion of individuals exceeding clinical cut points for high LDL cholesterol, low HDL cholesterol and high triglycerides varied according to an allelic dosage score (P < 10-15 for each trend). These results suggest that the cumulative effect of multiple common variants contributes to polygenic dyslipidemia