Atividade nervosa simpática em pacientes com síndromes isquêmicas miocárdicas instáveis: estudo comparativo com marcadores inflamatórios

INTRODUÇÃO: Em pacientes com síndromes isquêmicas miocárdicas instáveis (SIMI), tanto a hiperatividade simpática quanto a resposta inflamatória exacerbada se associam a pior prognóstico. No entanto, ainda é desconhecido se existe alguma correlação entre esses dois marcadores de evolução desfavorável. OBJETIVOS: Correlacionar a atividade nervosa simpática muscular com marcadores inflamatórios nas fases precoce e tardia de pacientes portadores de SIMI. MÉTODOS: Pacientes hospitalizados com diagnóstico de SIMI e evolução favorável foram incluídos de forma prospectiva desde que apresentassem idade entre 18 e 65 anos e aterosclerose coronária comprovada por cinecoronariografia. Logo após a inclusão no estudo foram coletadas informações basais, e no quarto dia (± 1 dia) de internação os pacientes foram submetidos à avaliação da ANSM e coleta concomitante de amostra sanguínea para dosagem de proteína CReativa ultrassensível (PCR-us), interleucina-6 (IL6), e fosfolipase A2 associada à lipoproteína (Lp-PLA2). ANSM foi obtida pela técnica de microneurografia do nervo fibular. As medidas e respectivas análises de correlação foram repetidas em 1, 3 e 6 meses após a hospitalização. Correlações entre ANSM e marcadores inflamatórios foram analisadas por meio do teste de Pearson (variáveis de distribuição não-paramétrica foram transformadas logaritmicamente). Modelos de regressão linear múltipla foram criados para avaliar os efeitos independentes. RESULTADOS: Foram estudados 34 pacientes com idade média de 51,7±7,0 anos, sendo 79,4% do sexo masculino. A prevalência de hipertensão arterial foi de 64,7%, diabetes mellitus 8,8%, e doença arterial coronária prévia de 20,6%. A apresentação foi IAM com supradesnível de ST em 18 pacientes (52,9%), IAM sem supra de ST em 14 (41,2%) e angina instável em 02 pacientes (5,9%). Tanto ANSM quanto biomarcadores inflamatórios estavam elevados durante a fase aguda das SIMI e diminuíram ao longo do tempo. Na fase hospitalar, a mediana da PCR-us foi 17,75 (8,57; 40,15) mg/L, e IL-6 6,65 (4,45; 8,20) pg/ml, a Lp- PLA2 média foi 185,8 ± 52,2 nmol/min/ml, e ANSM média 64,2 ± 19,3 impulsos/100bpm. Após 6 meses, houve diminuição significativa de todas essas variáveis quando comparadas com a fase hospitalar. Entretanto, não houve correlação significativa entre a atividade simpática e qualquer dos marcadores inflamatórios analisados, em nenhuma das fases analisadas (p > 0,05), Por outro lado, ANSM se correlacionou independentemente com níveis de CKMB na fase aguda (p=0,027), e com fração de ejeção do VE na fase crônica (p=0,026). CONCLUSÃO: Apesar do aumento inicial dos níveis de marcadores inflamatórios e da atividade simpática em pacientes com SIMI, não houve correlação significativa entre esses parâmetros em nenhuma das fases analisadas, sugerindo que as alterações dessas variáveis estariam relacionadas a diferentes vias fisiopatológicas

Dominici Cotunnii ... De ischiade nervosa commentarius novis curis auctior.

Mode of access: Internet.

Rivista di patologia nervosa e mentale.

Mode of access: Internet.

Experimental investigations with trypan blue in connection with the intraspinal treatment of lues nervosa ...

"Stellingen" (2 leaves) laid in.

Dominici Cotunnii ... De ischiade nervosa commentarius

Mode of access: Internet.

The role of interpersonal functioning in the maintenance of eating psychopathology:a systematic review and testable model

This review aims to systematically evaluate the empirical literature relating to the interpersonal functioning of those with eating disorder psychopathology and presents a preliminary model to help the formulation of patients' problems. Following a thorough literature search, 35 papers were included in this systematic review. The vast majority of studies indicate a strong association between eating psychopathology and certain maladaptive personality traits. The origins of social anxiety and poor social support that have been described as maintaining eating disorders appear to differ according to diagnostic groups. Interpersonal difficulties in people with restrictive behaviors such as anorexia appear to be related to the avoidance of expressing feelings to others and to giving priority to other people's feeling over their own. While interpersonal difficulties in patients with bulimia nervosa appear to be more related to interpersonal distrust and negative interaction and conflict with others. These concepts are presented in a preliminary model of interpersonal functioning in the eating disorders. © 2012 Elsevier Ltd.

A, B, C… Anorexia, bulimia y comedor compulsivo. Manual para docentes

Los trastornos relacionados con la alimentación se han convertido, en los úl- timos años, en un grave problema de salud pública, tanto por la gravedad que estas patologías adquieren con el tiempo, como por la alarma social que se ha despertado frente a la, cada vez más frecuente, aparición de estos trastornos. A este respecto baste señalar que, según los últimos datos, de la población de jóvenes escolarizados en la Comunidad de Madrid, con edades comprendidas entre los quince y dieciocho años, un 3.4% padecen un TCA y un 7,6% presen- tan riesgo de padecerlo, lo que, unido a la prevalencia actual, supone que este problema de salud afecta a un 11% de los adolescentes escolarizados en Madrid. Junto a los jóvenes que padecen un trastorno relacionado con la alimentación hay una cantidad considerable de menores que presentan conductas de riesgo relacionadas con la aparición de estos trastornos. Así, según los últimos estudios con adolescentes, un 7,1% de los chicos y un 34,1% de las chicas han iniciado una dieta para adelgazar en el último año, mientras que un 1,1% de los chicos y un 9,1% de las chicas se han provocado el vómito con la intención de adelgazar. Un joven que está empezando a desarrollar una anorexia o una bulimia puede pasar desapercibido para su entorno, la diferencia entre la salud y la enfer- medad es, en sus orígenes, muy sutil. Así, es difícil diferenciar al adolescente que se pone a dieta porque es la moda y acaba dejando la dieta pasadas unas semanas, del joven que, con idéntico inicio, acaba desarrollando un trastorno. El INUTCAM, consciente de la compleja situación a la que se enfrentan los docentes en cuanto a los TCA, publica este manual con la intención de brindar una ayuda más de cara a la prevención, detección y atención a los jóvenes con estas patologías.

Alteraciones en la voz de las pacientes con anorexia nerviosa restrictiva: un estudio piloto

Se realiza un estudio sobre el tono (percepción acústica) de la voz en la anorexia nerviosa restrictiva (ANR). El objetivo es valorar la alteración en la voz de las pacientes con ANR cuando el trastorno se inicia en la pubertad. La muestra total son 148 sujetos distribuidos en dos grupos: grupo control (n = 102) y ANR (n = 46). Se determinó la frecuencia fundamental de la voz (F0) utilizando dos fonemas ("a" e "i") mediante un micrófono Plantronic 300 y grabador digital. Se analiza la voz con el programa Praat. Se presentan los primeros datos para la lengua española de los valores normales de la F0 de voz en población femenina sana de 9 a 17 años. Posteriormente se muestran los datos comparativos con el grupo de pacientes con ANR.

A propósito de un caso de malnutrición muy extrema en una paciente que presenta Anorexia Nerviosa Restrictiva de larga evolución y no recibía tratamiento

La anorexia nerviosa es un trastorno de la conducta alimentaria que con frecuencia ocasiona malnutrición y asocia riesgo de mortalidad. Requiere la colaboración de un equipo multidisciplinar con amplia experiencia clínica para obtener óptimos resultados, una exitosa educación nutricional y evitar el síndrome de realimentación. El caso que se presenta constituye la malnutrición más severa secundaria a anorexia nerviosa que hemos tratado en nuestra unidad: una paciente de 33 años con IMC de 8.8 kg/m² y elevación de enzimas hepáticas, que, a pesar de la situación de extrema gravedad en la que se encontraba, no presentó complicaciones durante el proceso de realimentación, que se detalla.

Interaction between disinhibition and restraint: Implications for body weight and eating disturbance

An increase in obesity is usually accompanied by an increase in eating disturbances. Susceptibility to these states may arise from different combinations of underlying traits: Three Factor Eating Questionnaire (TFEQ) Restraint and Disinhibition. Two studies were conducted to examine the interaction between these traits; one on-line study (n=351) and one laboratory-based study (n=120). Participants completed a battery of questionnaires and provided self-report measures of body weight and physical activity. A combination of high Disinhibition and high Restraint was associated with a problematic eating behaviour profile (EAT-26), and a higher rate of smoking and alcohol consumption. A combination of high Disinhibition and low Restraint was associated with a higher susceptibility to weight gain and a higher sedentary behaviour. These data show that different combinations of Disinhibition and Restraint are associated with distinct weight and behaviour outcomes.

The roles of the preproghrelin-derived peptides - ghrelin, desacyl ghrelin and obestatin - in prostate cancer

Prostate cancer is the second most common cause of cancer related deaths in Western men. Despite the significant improvements in current treatment techniques, there is no cure for advanced metastatic, castrate-resistant disease. Early detection and prevention of progression to a castrate-resistant state may provide new strategies to improve survival. A number of growth factors have been shown to act in an autocrine/paracrine manner to modulate prostate cancer tumour growth. Our laboratory has previously shown that ghrelin and its receptors (the functional GHS-R1a and the non-functional GHS-R1b) are expressed in prostate cancer specimens and cell lines. We have shown that ghrelin increases cell proliferation in the PC3 and LNCaP prostate cancer cell lines through activation of ERK1/2, suggesting that ghrelin could regulate prostate cancer cell growth and play a role in the progression of the disease. Ghrelin is a 28 amino-acid peptide hormone, identified to be the natural ligand of the growth hormone secretagogue receptor (GHS-R1a). It is well characterised as a growth hormone releasing and as an orexigenic peptide that stimulates appetite and feeding and regulates energy expenditure and bodyweight. In addition to its orexigenic properties, ghrelin has been shown to play a regulatory role in a number of systems, including the reproductive, immune and cardiovascular systems and may play a role in a number of pathological conditions such as chronic heart failure, anorexia, cachexia, obesity, diabetes and cancer. In cancer, ghrelin and its receptor are expressed in a range of tumours and cancer cell lines and ghrelin has been demonstrated to modulate cell proliferation, apoptosis, migration and invasion in some cell types. The ghrelin gene (GHRL) encodes preproghrelin peptide, which is processed to produce three currently known functional peptides - ghrelin, desacyl ghrelin and obestatin. Prohormone convertases (PCs) have been shown to cleave the preproghrelin peptide into two primary products - the 28 amino acid peptide, ghrelin, and the remaining 117 amino acid C-terminal peptide, C-ghrelin. C-ghrelin can then be further processed to produce the 23 amino acid peptide, obestatin. Ghrelin circulates in two different forms - an octanoylated form (known as ghrelin) and a non-octanoylated form, desacyl ghrelin. The unique post-translational addition of octanoic acid to the serine 3 residue of the propeptide chain to form acylated ghrelin is catalysed by ghrelin O-acyltransferase (GOAT). This modification is necessary for binding of ghrelin to its only known functional receptor, the GHS-R1a. As desacyl ghrelin cannot bind and activate the GHS-R1a, it was initially thought to be an inactive peptide, despite the fact that it circulates at much higher levels than ghrelin. Further research has demonstrated that desacyl ghrelin is biologically active and shares some of the actions of ghrelin, as well as having some opposing and distinct roles. Interestingly, both ghrelin and desacyl ghrelin have been shown to modulate apoptosis, cell differentiation and proliferation in some cell types, and to stimulate cell proliferation through activation of ERK1/2 and PI3K/Akt pathways. The third known peptide product of the ghrelin preprohormone, obestatin, was initially thought to oppose the actions of ghrelin in appetite regulation and food intake and to mediate its effects through the G protein-coupled receptor 39 (GPR39). Subsequent research failed to reproduce the initial findings, however, and the possible anorexigenic effects of obestatin, as well as the identity of its receptor, remain unclear. Obestatin plays some important physiological roles, including roles in improving memory, the inhibition of thirst and anxiety, increased secretion of pancreatic juice, and regulation of cell proliferation, survival, apoptosis and differentiation. Preliminary studies have also shown that obestatin stimulates cell proliferation in some cell types through activation of ERK1/2, Akt and PKC pathways. Overall, however, at the commencement of this PhD project, relatively little was known regarding the functions and mechanisms of action of the preproghrelin-derived functional peptides in modulating prostate cancer cell proliferation. The roles of obestatin, and desacyl ghrelin as potential growth factors had not previously been investigated, and the potential expression and regulation of the preproghrelin processing enzymes, GOAT and prohormone convertases was unknown in prostate cancer cell lines. Therefore, the overall objectives of this study were to: 1. investigate the effects of obestatin on cell proliferation and signaling in prostate cancer cell lines 2. compare the effects of desacyl ghrelin and ghrelin on cell proliferation and signaling in prostate cancer cell lines 3. investigate whether prostate cancer cell lines possess the necessary enzymatic machinery to produce ghrelin and desacyl ghrelin and if these peptides can regulate GOAT expression Our laboratory has previously shown that ghrelin stimulates cell proliferation in the PC3 and LNCaP prostate cancer cell line through activation of the ERK1/2 pathway. In this study it has been demonstrated that treatments with either ghrelin, desacyl ghrelin or obestatin over 72 hours significantly increased cell proliferation in the PC3 prostate cancer cell line but had no significant effect in the RWPE-1 transformed normal prostate cell line. Ghrelin (1000nM) stimulated cell proliferation in the PC3 prostate cancer cell line by 31.66 6.68% (p<0.01) with the WST-1 method, and 13.55 5.68% (p<0.05) with the CyQUANT assay. Desacyl ghrelin (1000nM) increased cell proliferation in PC3 cells by 21.73 2.62% (p<0.01) (WST-1), and 15.46 7.05% (p<0.05) (CyQUANT) above untreated control. Obestatin (1000nM) induced a 28.37 7.47% (p<0.01) (WST-1) and 12.14 7.47% (p<0.05) (CyQUANT) significant increase in cell proliferation in the PC3 prostate cancer cell line. Ghrelin and desacyl ghrelin treatments stimulated Akt and ERK phosphorylation across a range of concentrations (p<0.01). Obestatin treatment significantly stimulated Akt, ERK and PKC phosphorylation (p<0.05). Through the use of specific inhibitors, the MAPK inhibitor U0126 and the Akt1/2 kinase inhibitor, it was demonstrated that ghrelin- and obestatin-induced cell proliferation in the PC3 prostate cancer cell line is mediated through activation of ERK1/2 and Akt pathways. Although desacyl ghrelin significantly stimulated Akt and ERK phosphorylation, U0126 failed to prevent desacyl ghrelin-induced cell proliferation suggesting ghrelin and desacyl ghrelin might act through different mechanisms to increase cell proliferation. Ghrelin and desacyl ghrelin have shown a proliferative effect in osteoblasts, pancreatic -cells and cardiomyocytes through activation of ERK1/2 and PI3K/Akt pathways. Here it has been shown that ghrelin and its non-acylated form exert the same function and stimulate cell proliferation in the PC3 prostate cancer cell line through activation of the Akt pathway. Ghrelin-induced proliferation was also mediated through activation of the ERK1/2 pathway, however, desacyl ghrelin seems to stimulate cell proliferation in an ERK1/2-independent manner. As desacyl ghrelin does not bind and activate GHSR1a, the only known functional ghrelin receptor, the finding that both ghrelin and desacyl ghrelin stimulate cell proliferation in the PC3 cell line suggests that these peptides could be acting through the yet unidentified alternative ghrelin receptor in this cell type. Obestatin treatment also stimulated PKC phosphorylation, however, a direct role for this pathway in stimulating cell proliferation could not be proven using available PKC pathway inhibitors, as they caused significant cell death over the extended timeframe of the cell proliferation assays. Obestatin has been shown to stimulate cell proliferation through activation of PKC isoforms in human retinal epithelial cells and in the human gastric cancer cell line KATO-III. We have demonstrated that all of the prostate-derived cell lines examined (PC3, LNCaP, DU145, 22Rv1, RWPE-1 and RWPE-2) expressed GOAT and at least one of the prohormone convertases, which are known to cleave the proghrelin peptide, PC1/3, PC2 and furin, at the mRNA level. These cells, therefore, are likely to possess the necessary machinery to cleave the preproghrelin protein and to produce the mature ghrelin and desacyl ghrelin peptides. In addition to prohormone convertases, the presence of octanoic acid is essential for acylated ghrelin production. In this study octanoic acid supplementation significantly increased cell proliferation in the PC3 prostate cancer cell line by over 20% compared to untreated controls (p<0.01), but surprisingly, not in the DU145, LNCaP or 22Rv1 prostate cancer cell lines or in the RWPE-1 and RWPE-2 prostate-derived cell lines. In addition, we demonstrated that exogenous ghrelin induced a statistically significant two-fold decrease in GOAT mRNA expression in the PC3 cell line (p<0.05), suggesting that ghrelin could pontentially downregulate its own acylation and, therefore, regulate the balance between ghrelin and desacyl ghrelin. This was not observed, however, in the DU145 and LNCaP prostate cancer cell lines. The GOAT-ghrelin system represents a direct link between ingested nutrients and regulation of ghrelin production and the ghrelin/desacyl ghrelin ratio. Regulation of ghrelin acylation is a potentially attractive and desirable tool for the development of better therapies for a number of pathological conditions where ghrelin has been shown to play a key role. The finding that desacyl ghrelin stimulates cell proliferation in the PC3 prostate cancer cell line, and responds to ghrelin in the same way, suggests that this cell line expresses an alternative ghrelin receptor. Although all the cell lines examined expressed both GHS-R1a and GHS-R1b mRNA, it remains uncertain whether these cell lines express the unidentified alternative ghrelin receptor. It is possible that the varied responses seen could be due to the expression of different ghrelin receptors in different cell lines. In addition to GOAT, prohormone convertases and octanoic acid availability may regulate the production of different peptides from the ghrelin preprohormone. The studies presented in this thesis provide significant new information regarding the roles and mechanisms of action of the preproghrelin-derived peptides, ghrelin, desacyl ghrelin and obestatin, in modulating prostate cancer cell line proliferation. A number of key questions remain to be resolved, however, including the identification of the alternative ghrelin/desacyl ghrelin receptor, the identification of the obestatin receptor, a clarification of the signaling mechanisms which mediate cell proliferation in response to obestatin treatment and a better understanding of the regulation at both the gene and post-translational levels of functional peptide generation. Further studies investigating the role of the ghrelin axis using in vivo prostate cancer models may be warranted. Until these issues are determined, the potential for the ghrelin axis, to be recognised as a novel useful target for therapy for cancer or other pathologies will be uncertain.

Risk factors for malnutrition in community-dwelling people with Parkinson’s disease

In the elderly, the risks for protein-energy malnutrition from older age, dementia, depression and living alone have been well-documented. Other risk factors including anorexia, gastrointestinal dysfunction, loss of olfactory and taste senses and early satiety have also been suggested to contribute to poor nutritional status. In Parkinson’s disease (PD), it has been suggested that the disease symptoms may predispose people with PD to malnutrition. However, the risks for malnutrition in this population are not well-understood. The current study’s aim was to determine malnutrition risk factors in community-dwelling adults with PD. Nutritional status was assessed using the Patient-Generated Subjective Global Assessment (PG-SGA). Data about age, time since diagnosis, medications and living situation were collected. Levodopa equivalent doses (LDED) and LDED per kg body weight (mg/kg) were calculated. Depression and anxiety were measured using the Beck’s Depression Inventory (BDI) and Spielberger Trait Anxiety questionnaire, respectively. Cognitive function was assessed using the Addenbrooke’s Cognitive Examination (ACE-R). Non-motor symptoms were assessed using the Scales for Outcomes in Parkinson's disease-Autonomic (SCOPA-AUT) and Modified Constipation Assessment Scale (MCAS). A total of 125 community-dwelling people with PD were included, average age of 70.2±9.3(35-92) years and average time since diagnosis of 7.3±5.9(0–31) years. Average body mass index (BMI) was 26.0±5.5kg/m2. Of these, 15% (n=19) were malnourished (SGA-B). Multivariate logistic regression analysis revealed that older age (OR=1.16, CI=1.02-1.31), more depressive symptoms (OR=1.26, CI=1.07-1.48), lower levels of anxiety (OR=.90, CI=.82-.99), and higher LDED per kg body weight (OR=1.57, CI=1.14-2.15) significantly increased malnutrition risk. Cognitive function, living situation, number of prescription medications, LDED, years since diagnosis and the severity of non-motor symptoms did not significantly influence malnutrition risk. Malnutrition results in poorer health outcomes. Proactively addressing the risk factors can help prevent declines in nutritional status. In the current study, older people with PD with depression and greater amounts of levodopa per body weight were at increased malnutrition risk.

Encouraging, assisting, and time to eat : comparison of mealtime assistance interventions in elderly medical inpatients

BACKGROUND: The prevalence of protein-energy malnutrition in older adults is reported to be as high as 60% and is associated with poor health outcomes. Inadequate feeding assistance and mealtime interruptions may contribute to malnutrition and poor nutritional intake during hospitalisation. Despite being widely implemented in practice in the United Kingdom and increasingly in Australia, there have been few studies examining the impact of strategies such as Protected Mealtimes and dedicated feeding assistant roles on nutritional outcomes of elderly inpatients. AIMS: The aim of this research was to implement and compare three system-level interventions designed to specifically address mealtime barriers and improve energy intakes of medical inpatients aged ≥65 years. This research also aimed to evaluate the sustainability of any changes to mealtime routines six months post-intervention and to gain an understanding of staff perceptions of the post-intervention mealtime experience. METHODS: Three mealtime assistance interventions were implemented in three medical wards at Royal Brisbane and Women's Hospital: AIN-only: Additional assistant-in-nursing (AIN) with dedicated nutrition role. PM-only: Multidisciplinary approach to meals, including Protected Mealtimes. PM+AIN: Combined intervention: AIN + multidisciplinary approach to meals. An action research approach was used to carefully design and implement the three interventions in partnership with ward staff and managers. Significant time was spent in consultation with staff throughout the implementation period to facilitate ownership of the interventions and increase likelihood of successful implementation. A pre-post design was used to compare the implementation and nutritional outcomes of each intervention to a pre-intervention group. Using the same wards, eligible participants (medical inpatients aged ≥65 years) were recruited to the preintervention group between November 2007 and March 2008 and to the intervention groups between January and June 2009. The primary nutritional outcome was daily energy and protein intake, which was determined by visually estimating plate waste at each meal and mid-meal on Day 4 of admission. Energy and protein intakes were compared between the pre and post intervention groups. Data were collected on a range of covariates (demographics, nutritional status and known risk factors for poor food intake), which allowed for multivariate analysis of the impact of the interventions on nutritional intake. The provision of mealtime assistance to participants and activities of ward staff (including mealtime interruptions) were observed in the pre-intervention and intervention groups, with staff observations repeated six months post-intervention. Focus groups were conducted with nursing and allied health staff in June 2009 to explore their attitudes and behaviours in response to the three mealtime interventions. These focus group discussions were analysed using thematic analysis. RESULTS: A total of 254 participants were recruited to the study (pre-intervention: n=115, AIN-only: n=58, PM-only: n=39, PM+AIN: n=42). Participants had a mean age of 80 years (SD 8), and 40% (n=101) were malnourished on hospital admission, 50% (n=108) had anorexia and 38% (n=97) required some assistance at mealtimes. Occasions of mealtime assistance significantly increased in all interventions (p<0.01). However, no change was seen in mealtime interruptions. No significant difference was seen in mean total energy and protein intake between the preintervention and intervention groups. However, when total kilojoule intake was compared with estimated requirements at the individual level, participants in the intervention groups were more likely to achieve adequate energy intake (OR=3.4, p=0.01), with no difference noted between interventions (p=0.29). Despite small improvements in nutritional adequacy, the majority of participants in the intervention groups (76%, n=103) had inadequate energy intakes to meet their estimated energy requirements. Patients with cognitive impairment or feeding dependency appeared to gain substantial benefit from mealtime assistance interventions. The increase in occasions of mealtime assistance by nursing staff during the intervention period was maintained six-months post-intervention. Staff focus groups highlighted the importance of clearly designating and defining mealtime responsibilities in order to provide adequate mealtime care. While the purpose of the dedicated feeding assistant was to increase levels of mealtime assistance, staff indicated that responsibility for mealtime duties may have merely shifted from nursing staff to the assistant. Implementing the multidisciplinary interventions empowered nursing staff to "protect" the mealtime from external interruptions, but further work is required to empower nurses to prioritise mealtime activities within their own work schedules. Staff reported an increase in the profile of nutritional care on all wards, with additional non-nutritional benefits noted including improved mobility and functional independence, and better identification of swallowing difficulties. IMPLICATIONS: The PhD research provides clinicians with practical strategies to immediately introduce change to deliver better mealtime care in the hospital setting, and, as such, has initiated local and state-wide roll-out of mealtime assistance programs. Improved nutritional intakes of elderly inpatients was observed; however given the modest effect size and reducing lengths of hospital stays, better nutritional outcomes may be achieved by targeting the hospital-to-home transition period. Findings from this study suggest that mealtime assistance interventions for elderly inpatients with cognitive impairment and/or functional dependency show promise.