The association between mental health nursing and hospital admissions for people with serious mental illness: a protocol for a systematic review

Background: Relapse in individuals with severe mental illness (SMI) is a frequent occurrence and can add considerably to the burden of disease. As such, relapse prevention is an essential therapeutic outcome for people with SMI. Mental health nurses (MHNs) are well placed to support individuals with SMI and to prevent relapse; notwithstanding, there has been no synthesis of the evidence to date to determine whether MHNs prevent relapse in this population. Methods: Electronic databases will be systemically searched for observational studies and clinical trials that report the association between mental health nursing and the hospitalisation of persons living with an SMI. The search will be supplemented by reference checking and a search of the grey literature. The primary outcome of interest will be hospital admission rate. Screening of articles, data extraction and critical appraisal will be undertaken by two reviewers, independently, with a third reviewer consulted should disagreement occur between reviewers. The quality of studies will be assessed using the Risk Of Bias In Non-randomised Studies - of Interventions (ROBINS-I) tool and the Cochrane Collaboration risk of bias tool. Depending on the number of studies and level of heterogeneity, the evidence may be synthesised using meta-analysis or narrative synthesis. Discussion: This review will explore for the first time the clinical potential of mental health nursing in preventing relapse in persons with SMI. The findings of this review will serve to inform future research and education in this area. The evidence may also help inform future policy, including decisions regarding future mental health workforce development and planning

Assessing and Strengthening African Universities' Capacity for Doctoral Programmes

Imelda Bates and colleagues developed and validated an evidence-based tool for evaluating doctoral programmes in African universities

Partial Resistance to Peroxisome Proliferator–Activated Receptor-α Agonists in ZDF Rats Is Associated With Defective Hepatic Mitochondrial Metabolism

OBJECTIVE—Fluxes through mitochondrial pathways are defective in insulin-resistant skeletal muscle, but it is unclear whether similar mitochondrial defects play a role in the liver during insulin resistance and/or diabetes. The purpose of this study is to determine whether abnormal mitochondrial metabolism plays a role in the dysregulation of both hepatic fat and glucose metabolism during diabetes

Adipose atrophy in cancer cachexia:morphologic and molecular analysis of adipose tissue in tumour-bearing mice

Extensive loss of adipose tissue is a hallmark of cancer cachexia but the cellular and molecular basis remains unclear. This study has examined morphologic and molecular characteristics of white adipose tissue in mice bearing a cachexia-inducing tumour, MAC16. Adipose tissue from tumour-bearing mice contained shrunken adipocytes that were heterogeneous in size. Increased fibrosis was evident by strong collagen-fibril staining in the tissue matrix. Ultrastructure of 'slimmed' adipocytes revealed severe delipidation and modifications in cell membrane conformation. There were major reductions in mRNA levels of adipogenic transcription factors including CCAAT/enhancer binding protein alpha (C/EBPα), CCAAT/enhancer binding protein beta, peroxisome proliferator-activated receptor gamma, and sterol regulatory element binding protein-1c (SREBP-1c) in adipose tissue, which was accompanied by reduced protein content of C/EBPα and SREBP-1. mRNA levels of SREBP-1c targets, fatty acid synthase, acetyl CoA carboxylase, stearoyl CoA desaturase 1 and glycerol-3-phosphate acyl transferase, also fell as did glucose transporter-4 and leptin. In contrast, mRNA levels of peroxisome proliferators-activated receptor gamma coactivator-1alpha and uncoupling protein-2 were increased in white fat of tumour-bearing mice. These results suggest that the tumour-induced impairment in the formation and lipid storing capacity of adipose tissue occurs in mice with cancer cachexia. © 2006 Cancer Research UK

Incomplete functional recovery after delirium in elderly people: a prospective cohort study

BACKGROUND: Delirium often has a poor outcome, but why some people have incomplete recovery is not well understood. Our objective was to identify factors associated with short-term (by discharge) and long-term (by 6 month) incomplete recovery of function following delirium. METHODS: In a prospective cohort study of elderly patients with delirium seen by geriatric medicine services, function was assessed at baseline, at hospital discharge and at six months. RESULTS: Of 77 patients, vital and functional status at 6 months was known for 71, of whom 21 (30%) had died. Incomplete functional recovery, defined as ≥10 point decline in the Barthel Index, compared to pre-morbid status, was present in 27 (54%) of the 50 survivors. Factors associated with death or loss of function at hospital discharge were frailty, absence of agitation (hypoactive delirium), a cardiac cause and poor recognition of delirium by the treating service. Frailty, causes other than medications, and poor recognition of delirium by the treating service were associated with death or poor functional recovery at 6 months. CONCLUSION: Pre-existing frailty, cardiac cause of delirium, and poor early recognition by treating physicians are associated with worse outcomes. Many physicians view the adverse outcomes of delirium as intractable. While in some measure this might be true, more skilled care is a potential remedy within their grasp

Glucose and Fatty Acids Synergize to Promote B-Cell Apoptosis through Activation of Glycogen Synthase Kinase 3β Independent of JNK Activation

The combination of elevated glucose and free-fatty acids (FFA), prevalent in diabetes, has been suggested to be a major contributor to pancreatic β-cell death. This study examines the synergistic effects of glucose and FFA on β-cell apoptosis and the molecular mechanisms involved. Mouse insulinoma cells and primary islets were treated with palmitate at increasing glucose and effects on apoptosis, endoplasmic reticulum (ER) stress and insulin receptor substrate (IRS) signaling were examined.Increasing glucose (5-25 mM) with palmitate (400 µM) had synergistic effects on apoptosis. Jun NH2-terminal kinase (JNK) activation peaked at the lowest glucose concentration, in contrast to a progressive reduction in IRS2 protein and impairment of insulin receptor substrate signaling. A synergistic effect was observed on activation of ER stress markers, along with recruitment of SREBP1 to the nucleus. These findings were confirmed in primary islets. The above effects associated with an increase in glycogen synthase kinase 3β (Gsk3β) activity and were reversed along with apoptosis by an adenovirus expressing a kinase dead Gsk3β.Glucose in the presence of FFA results in synergistic effects on ER stress, impaired insulin receptor substrate signaling and Gsk3β activation. The data support the importance of controlling both hyperglycemia and hyperlipidemia in the management of Type 2 diabetes, and identify pancreatic islet β-cell Gsk3β as a potential therapeutic target

Susceptibility of Pancreatic Beta Cells to Fatty Acids Is Regulated by LXR/PPARα-Dependent Stearoyl-Coenzyme A Desaturase

Chronically elevated levels of fatty acids-FA can cause beta cell death in vitro. Beta cells vary in their individual susceptibility to FA-toxicity. Rat beta cells were previously shown to better resist FA-toxicity in conditions that increased triglyceride formation or mitochondrial and peroxisomal FA-oxidation, possibly reducing cytoplasmic levels of toxic FA-moieties. We now show that stearoyl-CoA desaturase-SCD is involved in this cytoprotective mechanism through its ability to transfer saturated FA into monounsaturated FA that are incorporated in lipids. In purified beta cells, SCD expression was induced by LXR- and PPARα-agonists, which were found to protect rat, mouse and human beta cells against palmitate toxicity. When their SCD was inhibited or silenced, the agonist-induced protection was also suppressed. A correlation between beta cell-SCD expression and susceptibility to palmitate was also found in beta cell preparations isolated from different rodent models. In mice with LXR-deletion (LXRβ-/- and LXRαβ-/-), beta cells presented a reduced SCD-expression as well as an increased susceptibility to palmitate-toxicity, which could not be counteracted by LXR or PPARα agonists. In Zucker fatty rats and in rats treated with the LXR-agonist TO1317, beta cells show an increased SCD-expression and lower palmitate-toxicity. In the normal rat beta cell population, the subpopulation with lower metabolic responsiveness to glucose exhibits a lower SCD1 expression and a higher susceptibility to palmitate toxicity. These data demonstrate that the beta cell susceptibility to saturated fatty acids can be reduced by stearoyl-coA desaturase, which upon stimulation by LXR and PPARα agonists favors their desaturation and subsequent incorporation in neutral lipids

Leptin Administration Favors Muscle Mass Accretion by Decreasing FoxO3a and Increasing PGC-1α in ob/ob Mice

Absence of leptin has been associated with reduced skeletal muscle mass in leptin-deficient ob/ob mice. The aim of our study was to examine the effect of leptin on the catabolic and anabolic pathways regulating muscle mass. Gastrocnemius, extensor digitorum longus and soleus muscle mass as well as fiber size were significantly lower in ob/ob mice compared to wild type littermates, being significantly increased by leptin administration (P<0.001). This effect was associated with an inactivation of the muscle atrophy-related transcription factor forkhead box class O3 (FoxO3a) (P<0.05), and with a decrease in the protein expression levels of the E3 ubiquitin-ligases muscle atrophy F-box (MAFbx) (P<0.05) and muscle RING finger 1 (MuRF1) (P<0.05). Moreover, leptin increased (P<0.01) protein expression levels of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a regulator of muscle fiber type, and decreased (P<0.05) myostatin protein, a negative regulator of muscle growth. Leptin administration also activated (P<0.01) the regulators of cell cycle progression proliferating cell nuclear antigen (PCNA) and cyclin D1, and increased (P<0.01) myofibrillar protein troponin T. The present study provides evidence that leptin treatment may increase muscle mass of ob/ob mice by inhibiting myofibrillar protein degradation as well as enhancing muscle cell proliferation