Crisis Librarianship: An Examination of Online Librarianship Roles in the Wake of the COVID-19 Pandemic.

This study surveyed the members of a professional library organization for their perceptions of their online librarianship role. In particular, the survey sought to examine any change in online librarianship roles after March 2020 as a result of the COVID-19 pandemic lockdowns. Participants were administered a survey comprised of both quantitative and qualitative response options. Findings present a nuanced professional environment post-lockdown in which individual job duties largely remained the same; however participants reported increased demands stemming from workplace issues, including attrition and lack of resources.

Evaluation of a Falls and Fire Safety Program for Community-Dwelling Older Adults.

Remembering When™ (RW) is a falls and fire prevention program delivered by fire service personnel and homecare organizations to help older adults live safely at home for as long as possible. This study evaluated changes in falls prevention and fire safety behaviors and perceptions and social support associated with falls and residential fires among older adults following delivery of the RW program by fire service personnel. In a convenience sample of adults 65 + years residing in five Iowa communities, 70 received the RW program during a home visit and 75 received the RW program in a group presentation followed by a home visit. Baseline and follow-up telephone interviews were conducted to assess changes in falls and fire safety behaviors, perceptions and social support. Changes were assessed using McNemar's exact test and paired sample t-tests. To control for dependence of 26 households with two participants, one participant was randomly selected and included in the analysis (n = 119). The RW program improved falls and residential fire prevention behaviors among older adults. Perceived efficacy to prevent falls increased from baseline (p = 0.047). Perceived susceptibility (p = 0.021) and control of fires (p = 0.000) increased while perceived severity (p = 0.025) and fear of residential fires (p = 0.019) decreased when compared to baseline. The proportion of participants reporting discussing falls with friends and family increased (p < 0.001), and more participants reported discussing fire prevention with healthcare professionals (p = 0.039). Fire service personnel can be effective deliverers of falls prevention information to older adults.

E-cadherin can limit the transforming properties of activating ß-catenin mutations.

Wnt pathway deregulation is a common characteristic of many cancers. Only colorectal cancer predominantly harbours mutations in APC, whereas other cancer types (hepatocellular carcinoma, solid pseudopapillary tumours of the pancreas) have activating mutations in ß-catenin (CTNNB1). We have compared the dynamics and the potency of ß-catenin mutations in vivo. Within the murine small intestine (SI), an activating mutation of ß-catenin took much longer to achieve Wnt deregulation and acquire a crypt-progenitor cell (CPC) phenotype than Apc or Gsk3 loss. Within the colon, a single activating mutation of ß-catenin was unable to drive Wnt deregulation or induce the CPC phenotype. This ability of ß-catenin mutation to differentially transform the SI versus the colon correlated with higher expression of E-cadherin and a higher number of E-cadherin:ß-catenin complexes at the membrane. Reduction in E-cadherin synergised with an activating mutation of ß-catenin resulting in a rapid CPC phenotype within the SI and colon. Thus, there is a threshold of ß-catenin that is required to drive transformation, and E-cadherin can act as a buffer to sequester mutated ß-catenin.

Subtle Deregulation of the Wnt-Signaling Pathway Through Loss of Apc2 Reduces the Fitness of Intestinal Stem Cells.

The importance of the Wnt-signaling pathway on the regulation and maintenance of the intestinal stem cell (ISC) population is well recognized. However, our current knowledge base is founded on models using systems of gross deregulation of the Wnt-signaling pathway. Given the importance of this signaling pathway on intestinal homeostasis, there is a need to explore the role of more subtle alterations in Wnt-signaling levels within this tissue. Herein, we have used a model of Apc2 loss to meet this aim. Apc2 is a homolog of Apc which can also form a destruction complex capable of binding ß-catenin, albeit less efficiently than Apc. We show that systemic loss of Apc2 results in an increase in the number of cells displaying nuclear ß-catenin at the base of the intestinal crypt. This subsequently impacts the expression levels of several ISC markers and the fitness of ISCs as assessed by organoid formation efficiency. This work provides the first evidence that the function and fitness of ISCs can be altered by even minor misregulation of the Wnt-signaling pathway. Our data highlights the importance of correct maintenance of this crucial signaling pathway in the maintenance and function of the ISC population. Stem Cells 2018;36:114-122.

APC2 is critical for ovarian WNT signalling control, fertility and tumour suppression.

BACKGROUND: Canonical WNT signalling plays a critical role in the regulation of ovarian development; mis-regulation of this key pathway in the adult ovary is associated with subfertility and tumourigenesis. The roles of Adenomatous polyposis coli 2 (APC2), a little-studied WNT signalling pathway regulator, in ovarian homeostasis, fertility and tumourigenesis have not previously been explored. Here, we demonstrate essential roles of APC2 in regulating ovarian WNT signalling and ovarian homeostasis. METHODS: A detailed analysis of ovarian histology, gene expression, ovulation and hormone levels was carried out in 10 week old and in aged constitutive APC2-knockout (Apc2-/-) mice (mixed background). Statistical significance for qRT-PCR data was determined from 95% confidence intervals. Significance testing was performed using 2-tailed Student's t-test, when 2 experimental cohorts were compared. When more were compared, ANOVA test was used, followed by a post-hoc test (LSD or Games-Howell). P-values of < 0.05 were considered statistically significant. RESULTS: APC2-deficiency resulted in activation of ovarian WNT signalling and sub-fertility driven by intra-ovarian defects. Follicular growth was perturbed, resulting in a reduced rate of ovulation and corpora lutea formation, which could not be rescued by administration of gonadotrophins. Defects in steroidogenesis and follicular vascularity contributed to the subfertility phenotype. Tumour incidence was assessed in aged APC2-deficient mice, which also carried a hypomorphic Apc allele. APC2-deficiency in these mice resulted in predisposition to granulosa cell tumour (GCT) formation, accompanied by acute tumour-associated WNT-signalling activation and a histologic pattern and molecular signature seen in human adult GCTs. CONCLUSIONS: Our work adds APC2 to the growing list of WNT-signalling members that regulate ovarian homeostasis, fertility and suppress GCT formation. Importantly, given that the APC2-deficient mouse develops tumours that recapitulate the molecular signature and histological features of human adult GCTs, this mouse has excellent potential as a pre-clinical model to study ovarian subfertility and transitioning to GCT, tumour biology and for therapeutic testing.

Hunk/Mak-v is a negative regulator of intestinal cell proliferation.

BACKGROUND: Conditional deletion of the tumour suppressor gene Apc within the murine intestine results in acute Wnt signalling activation. The associated over-expression of a myriad of Wnt signalling target genes yields phenotypic alterations that encompass many of the hallmarks of neoplasia. Previous transcriptomic analysis aimed at identifying genes that potentially play an important role in this process, inferred the Hormonally upregulated Neu-associated kinase (HUNK/Mak-v/Bstk1) gene as a possible candidate. Hunk is a SNF1 (sucrose non fermenting 1)-related serine/threonine kinase with a proposed association with many different tumour types, including colorectal cancer. METHODS: Here we describe the generation of a novel Hunk kinase deficient mouse which has been used to investigate the involvement of Hunk-kinase activity in intestinal homeostasis and tumourigenesis. RESULTS: We show that in the morphologically normal intestine, Hunk-kinase negatively regulates epithelial cell proliferation. However, the increase in cell proliferation observed in the Hunk kinase deficient intestine is counteracted by increased cell migration, thereby maintaining intestinal homeostasis. Using qRT-PCR, we further demonstrate that Hunk is significantly over-expressed in Apc deficient / Wnt-signalling activated intestinal tissue. Using the classical intestinal tumourigenesis Apc (Min) mouse model we show that loss of Hunk-kinase activity significantly reduced tumour initiation rates in the small intestine. However, an accompanying increase in the size of the tumours counteracts the impact this has on overall tumour burden or subsequently survival. CONCLUSIONS: In the intestinal setting we demonstrate that Hunk has a role in normal intestinal proliferation and homeostasis and, although it does not alter overall survival rates, activity of this kinase does impact on tumour initiation rates during the early stages in tumourigenesis in the small intestine.

Conditional disruption of Axin1 leads to development of liver tumors in mice.

BACKGROUND & AIMS: Mutations in components of the Wnt signaling pathway, including ß-catenin and AXIN1, are found in more than 50% of human hepatocellular carcinomas (HCCs). Disruption of Axin1 causes embryonic lethality in mice. We generated mice with conditional disruption of Axin1 to study its function specifically in adult liver. METHODS: Mice with a LoxP-flanked allele of Axin1 were generated by homologous recombination. Mice homozygous for the Axin1fl/fl allele were crossed with AhCre mice; in offspring, Axin1 was disrupted in liver following injection of ß-naphthoflavone (Axin1fl/fl/Cre mice). Liver tissues were collected and analyzed by quantitative real-time polymerase chain reaction and immunoprecipitation, histology, and immunoblot assays. RESULTS: Deletion of Axin1 from livers of adult mice resulted in an acute and persistent increase in hepatocyte cell volume, proliferation, and transcription of genes that induce the G(2)/M transition in the cell cycle and cytokinesis. A subset of Wnt target genes was activated, including Axin2, c-Myc, and cyclin D1. However, loss of Axin1 did not increase nuclear levels of ß-catenin or cause changes in liver zonation that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activation of ß-catenin. After 1 year, 5 of 9 Axin1fl/fl/Cre mice developed liver tumors with histologic features of HCC. CONCLUSIONS: Hepatocytes from adult mice with conditional disruption of Axin1 in liver have a transcriptional profile that differs from that associated with loss of APC or constitutive activation of ß-catenin. It might be similar to a proliferation profile observed in a subset of human HCCs with mutations in AXIN1. Axin1fl/fl mice could be a useful model of AXIN1-associated tumorigenesis and HCC.

Proteomic profiling of a mouse model of acute intestinal Apc deletion leads to identification of potential novel biomarkers of human colorectal cancer (CRC).

Colorectal cancer (CRC) is the fourth most common cause of cancer-related death worldwide. Accurate non-invasive screening for CRC would greatly enhance a population's health. Adenomatous polyposis coli (Apc) gene mutations commonly occur in human colorectal adenomas and carcinomas, leading to Wnt signalling pathway activation. Acute conditional transgenic deletion of Apc in murine intestinal epithelium (AhCre(+)Apc(fl)(/)(fl)) causes phenotypic changes similar to those found during colorectal tumourigenesis. This study comprised a proteomic analysis of murine small intestinal epithelial cells following acute Apc deletion to identify proteins that show altered expression during human colorectal carcinogenesis, thus identifying proteins that may prove clinically useful as blood/serum biomarkers of colorectal neoplasia. Eighty-one proteins showed significantly increased expression following iTRAQ analysis, and validation of nine of these by Ingenuity Pathaway Analysis showed they could be detected in blood or serum. Expression was assessed in AhCre(+)Apc(fl)(/)(fl) small intestinal epithelium by immunohistochemistry, western blot and quantitative real-time PCR; increased nucelolin concentrations were also detected in the serum of AhCre(+)Apc(fl)(/)(fl) and Apc(Min)(/)(+) mice by ELISA. Six proteins; heat shock 60kDa protein 1, Nucleolin, Prohibitin, Cytokeratin 18, Ribosomal protein L6 and DEAD (Asp-Glu-Ala-Asp) box polypeptide 5,were selected for further investigation. Increased expression of 4 of these was confirmed in human CRC by qPCR. In conclusion, several novel candidate biomarkers have been identified from analysis of transgenic mice in which the Apc gene was deleted in the intestinal epithelium that also showed increased expression in human CRC. Some of these warrant further investigation as potential serum-based biomarkers of human CRC.

Myc deletion rescues Apc deficiency in the small intestine.

The APC gene encodes the adenomatous polyposis coli tumour suppressor protein, germline mutation of which characterizes familial adenomatous polyposis (FAP), an autosomal intestinal cancer syndrome. Inactivation of APC is also recognized as the key early event in the development of sporadic colorectal cancers, and its loss results in constitutive activity of the beta-catenin-Tcf4 transcription complex. The proto-oncogene c-MYC has been identified as a target of the Wnt pathway in colorectal cancer cells in vitro, in normal crypts in vivo and in intestinal epithelial cells acutely transformed on in vivo deletion of the APC gene; however, the significance of this is unclear. Therefore, to elucidate the role Myc has in the intestine after Apc loss, we have simultaneously deleted both Apc and Myc in the adult murine small intestine. Here we show that loss of Myc rescued the phenotypes of perturbed differentiation, migration, proliferation and apoptosis, which occur on deletion of Apc. Remarkably, this rescue occurred in the presence of high levels of nuclear beta-catenin. Array analysis revealed that Myc is required for the majority of Wnt target gene activation following Apc loss. These data establish Myc as the critical mediator of the early stages of neoplasia following Apc loss.

Mood and health-related quality of life among pediatric patients with heart failure.

Adult patients with heart failure (HF) commonly experience depression, with morbid and mortal consequences. However, mood disorders in pediatric patients with HF are poorly understood. This study examined mood and health-related quality of life (HRQOL) in children with HF and compared them cross-sectionally with those of healthy control subjects and heart transplant (Htx) recipients with good heart function. The 62 participants in this study were divided into three groups: HF subjects (n = 15), Htx subjects (n = 23), and healthy control subjects (n = 24). The HF subjects all had chronic HF with a left ventricular ejection fraction lower than 35 %. All the participants completed the Mini-Mental State Examination (MMSE), the Childhood Depression Inventory (CDI), and the Pediatric Quality-of-Life Inventory Cardiac Module (PedsQL CM). Overall, the MMSE scores and CDI subscale scores were similar for all the groups. The HF and Htx participants scored similarly on the PedsQL CM subscales for HRQOL, treatment anxiety, perceived physical appearance, cognitive function, and communication. However, the HF group had a significantly lower HRQOL related to heart problems and treatment than the Htx group. The prevalence of depression among children with HF is not as high as reported in the adult HF literature. However, certain aspects of HRQOL experienced by pediatric HF patients still suffer, especially those related to heart problems and treatment. Health-related QOL tended to be better for the Htx participants than for the HF participants. Exploring developmental and psychosocial outcomes is critical for patients with HF, especially because it has an impact on vital developmental, academic, and social outcomes.

Entopic overexpression of Ascl2 does not accelerate tumourigenesis in ApcMin mice.

OBJECTIVE: Expression of the Wnt target gene ASCL2 is elevated in 78% of intestinal neoplasia datasets (Oncomine), suggesting a role for deregulated ASCL2 in the aetiology of intestinal tumourigenesis. Furthermore, ectopic expression of Ascl2 has previously been shown to lead to hyperplasia in the mouse. However, elevated levels of ASCL2 does not have an impact on the overall survival or recurrence-free survival rates in colorectal cancer patients. Here the authors use a novel mouse model to analyse the role of Ascl2 in intestinal tumourigenesis and address the controversy surrounding the relevance of this gene to the aetiology of colorectal cancer. DESIGN: The authors have generated a mouse possessing a transgene carrying the Ascl2 gene together with its endogenous promoter and regulatory regions, thereby elevating Ascl2 expression in an authentic manner. The authors have further intercrossed these Ascl2 overexpressers to the classic Apc(Min) model, to study the consequence of elevated Ascl2 expression in intestinal tumourigenesis. RESULTS: Here the authors genetically demonstrate that elevated expression of Ascl2 in a Wnt signalling dependent manner specifically in the stem cell compartment of the intestine neither increases tumour formation nor diminishes survival in a well established intestinal tumour model, the Apc(min) mouse. CONCLUSION: The authors conclude that ectopic expression of Ascl2 is more important in the aetiology of neoplasia than overexpression of Ascl2.

Bags and blogs: creating an ostomy experience for nursing students.

BACKGROUND: There are well over three-quarters of a million people living in the United States with an ostomy. These individuals experience many physical and emotional challenges which nurses should address during the in-patient hospitalization experience. PURPOSE: The purpose of this educational activity was to provide undergraduate nursing students with a simulated laboratory experience which allowed the student to discuss and experience some of the challenges of living with an ostomy. METHOD: Small group work, an experiential learning activity, and blogging were used to foster the cognitive, psychomotor, and affective development of the nursing students. RESULTS: All 134 students participated in the small group work and blogging experience and over 100 students participated in the experiential learning activity of wearing an ostomy bag overnight with the bag containing a small amount of simulated fecal material. DISCUSSION: The impact of the simulated experience is evident in the depth of awareness and emotion expressed in the blogs. The students collectively acknowledged the value of the activity and the impact the gained awareness had on their careers as nurses. CONCLUSION: The use of social technology and the provision of learning activities, not available on the clinical unit, can have a significant impact on the cognitive, psychomotor, and affective development of nursing students.

Rectal epithelial cell mitosis and expression of macrophage migration inhibitory factor are increased 3 years after Roux-en-Y gastric bypass (RYGB) for morbid obesity: implications for long-term neoplastic risk following RYGB.

BACKGROUND: Rectal epithelial cell mitosis and crypt size, as well as expression of proinflammatory genes including macrophage migration inhibitory factor (MIF), are increased 6 months after Roux-en-Y gastric bypass (RYGB) in morbidly obese patients. Tests were carried out to determine whether these putative colorectal cancer risk biomarkers remained elevated long term after RYGB, and the mechanistic basis, as well as the functional consequences, of Mif upregulation in intestinal epithelial cells was investigated. METHODS: Rectal mucosa and blood were obtained a median of 3 years after RYGB from the original cohort of patients with RYGB (n = 19) for crypt microdissection, real-time PCR, immunohistochemistry for MIF and immunoassay of proinflammatory markers. Immunohistochemistry for Mif and bromodeoxyuridine labelling were performed on AhCre⁺ mouse and Apc(Min/⁺) mouse (with and without functional Mif alleles) intestine, respectively. RESULTS: Rectal epithelial cell mitosis and crypt size remained elevated 3 years after RYGB compared with preoperative values (1.7- and 1.5-fold, respectively; p < 0.05). There was a 40-fold (95% CI 13 to 125) increase in mucosal MIF transcript levels at 3 years associated with increased epithelial cell MIF protein levels. Conditional Apc loss in AhCre⁺ mice led to increased epithelial cell Mif content. Mif deficiency in Apc(Min/⁺) mice was associated with a combined defect in intestinal epithelial cell proliferation and migration, which was reflected by the longitudinal clinical data. CONCLUSIONS: Mucosal abnormalities persist 3 years after RYGB and include elevation of the protumorigenic cytokine MIF, which is upregulated following Apc loss and which contributes to intestinal epithelial cell homeostasis. These observations should prompt clinical studies of colorectal neoplastic risk after RYGB.

B-catenin deficiency, but not Myc deletion, suppresses the immediate phenotypes of APC loss in the liver.

Dysregulated Wnt signaling is seen in approximately 30% of hepatocellular carcinomas; thus, finding pathways downstream of the activation of Wnt signaling is key. Here, using cre-lox technology, we deleted the Apc gene in the adult mouse liver and observed a rapid increase in nuclear beta-catenin and c-Myc, which is associated with an induction of proliferation that led to hepatomegaly within 4 days of gene deletion. To investigate the downstream pathways responsible for these phenotypes, we analyzed the impact of inactivating APC in the context of deficiency of the potentially key effectors beta-catenin and c-Myc. beta-catenin loss rescues both the proliferation and hepatomegaly phenotypes after APC loss. However, c-Myc deletion, which rescues the phenotypes of APC loss in the intestine, had no effect on the phenotypes of APC loss in the liver. The consequences of the deregulation of the Wnt pathway within the liver are therefore strikingly different from those observed within the intestine, with the vast majority of Wnt targets being beta-catenin-dependent but c-Myc-independent in the liver.

Integrating service-learning into an MPH curriculum for future public health practitioners: strengthening community-campus partnerships.

Through a 3-year grant from the Community-Campus Partnerships for Health, the Virginia Commonwealth University MPH program adopted an incremental approach to implement service-learning focused on health disparities into its curriculum. We first incorporated service-learning into an elective course and then a required internship. We then worked with the Virginia Department of Health to develop a plan for first-year students to engage in additional experiential learning through a practicum. Students also were encouraged to organize community service events, such as health fairs. Service-learning was fully incorporated into the internship. The first-year student practicum, followed by the internship, has strengthened collaborations among faculty, students, and the Virginia Department of Health and expanded student service in the community. The number of student-supported community service events more than doubled. An incremental approach to incorporating service-learning led to successful implementation of the pedagogy. Service-learning benefits community partners, enriches student learning, and is well-suited for studies in public health.

Introduction of rehabilitation nursing concepts in Cambodia.

Cambodia is a poor country in Southeast Asia; 80% of its 14.1 million people are sustenance farmers (Central Intelligence Agency, 2006). Health Volunteers Overseas, based in Washington, DC, and Sihanouk Hospital of Hope in Phnom Penh, Cambodia, collaborate to recruit master's-prepared nurse educators to participate in volunteer teaching trips to enhance the knowledge and skill set of Cambodian staff nurses. A methodical series of steps were taken to develop a basic lecture series regarding the care of patients with brain and spinal cord injuries, taking into consideration Cambodian healthcare beliefs and health system resources. This article describes the processes used to develop the lectures and the realities of teaching on the other side of the world.

Embracing the Value of Confidence and Intention in Program Design.

Assessing participants' degree of confidence and intention related to use of knowledge and skill gained during continuing education programming provides insight into the effectiveness of methodologies used during program delivery. An analysis of participant confidence and intention levels from two programs demonstrates how using active learning strategies can positively influence the confidence and intention levels of learners. [J Contin Educ Nurs. 2021;52(1):5-7.].

Liver zonation occurs through a beta-catenin-dependent, c-Myc-independent mechanism.

BACKGROUND AND AIMS: The Wnt pathway has previously been shown to play a role in hepatic zonation. Herein, we have explored the role of 3 key components (Apc, beta-catenin, and c-Myc) of the Wnt pathway in the zonation of ammonia metabolizing enzymes. METHODS: Conditional deletion of Apc, beta-catenin, and c-Myc was induced in the livers of mice and the expression of periportal and perivenous hepatocyte markers was determined by polymerase chain reaction, Western blotting, and immunohistochemical techniques. RESULTS: Under normal circumstances, the urea cycle enzyme carbamoylphosphate synthetase I (CPS I) is present in the periportal, intermediate, and the first few layers of the perivenous zone. In contrast, glutamine synthetase (GS)--and nuclear beta-catenin--is expressed in a complementary fashion in the last 1-2 cell layers of the perivenous zone. Conditional loss of Apc resulted in the expression of nuclear beta-catenin and GS in most hepatocytes irrespective of zone. Induction of GS in hepatocytes outside the normal perivenous zone was accompanied by a reduction in the expression of CPS I. Deletion of beta-catenin induces a loss of GS and a complementary increase in expression of CPS I irrespective of whether Apc is present. Remarkably, deletion of c-Myc did not perturb the pattern of zonation. CONCLUSIONS: It has been shown that the Wnt pathway is key to imposing the pattern of zonation within the liver. Herein we have addressed the relevance of 3 major Wnt pathway components and show critically that the zonation is c-Myc independent but beta-catenin dependent.

Stasis predisposes ileal pouch inflammation in a rat model of ileal pouch-anal anastomosis.

BACKGROUND: While restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) has become the definitive surgical treatment for patients suffering from chronic ulcerative colitis (CUC), pouchitis still remains a major late complication. Fecal stasis has been implicated in the etiology of ileal inflammation; however, the mechanism(s) remain unclear, in part due to the lack of an animal model. Our goal was to surgically mimic the IPAA procedure in a rat to investigate the hypothesis that stasis leads to biochemical changes that predispose the ileal pouch to inflammation. MATERIALS AND METHODS: Thirty-two Sprague-Dawley rats underwent total colectomy with either straight ileorectal (IRA) or IPAA, and 11 nonoperated rats served as controls (Controls). Twenty-one d postoperatively, 48 h serial barium radiographs and 12 h charcoal transit follow-through studies were performed. Following sacrifice, ileal tissue was harvested for the measurement of myeloperoxidase activity (MPO) activity, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) mRNA levels, and histology. RESULTS: Serial barium radiographs showed stasis in the ileal pouch compared with IRA animals, and charcoal transit times that were two times longer (P ≤ 0.05) than that in the straight IRA rats. Ileal pouch MPO levels were significantly elevated in the IPAA rats compared with the straight IRA rats. ICAM-1 and VCAM-1 mRNA levels were not associated with neutrophil infiltration. CONCLUSIONS: These studies showed that ileal pouch stasis predisposes biochemical and histological evidence of ileal pouch mucosal inflammation. Studies such as this may provide the rationale for novel, adjunct therapies for the management of pouchitis in patients having undergone IPAA for CUC.

Changes in supervision needs following participation in a residential post-acute brain injury rehabilitation programme.

OBJECTIVE: Supervision needs typically increase following moderate-to-severe traumatic brain injury (TBI). Research assessing the impact of TBI residential rehabilitation programmes on supervision needs is limited. RESEARCH DESIGN: Prospective cross-sectional study. METHODS AND PROCEDURES: Ninety-four participants with moderate-to-severe TBI admitted to a post-acute brain injury rehabilitation programme (PABIR) were administered the supervision rating scale (SRS) at admission and at 1 month post-discharge. To account for spontaneous neurological recovery, patients were separated into those who were less than 1 year (L1Y, n = 55) or greater than 1 year (G1Y, n = 39) post-injury. EXPERIMENTAL INTERVENTION: None. MAIN OUTCOMES AND RESULTS: A mixed factorial design yielded a significant interaction (F(1, 92) = 18.2; p < 0.0001) with post-hoc results revealing that the L1Y group improved more dramatically in terms of supervision needs than the G1Y group. Using reliable change methodologies, 52.7% of the L1Y demonstrated decreasing scores on the SRS vs 20.5% of the G1Y group. CONCLUSIONS: Decreases in supervision needs following PABIR can be found, even after accounting for the impact of spontaneous neurological recovery both at the group and individual level.