253 research outputs found
Great expectations? A qualitative study of health professionals' perspectives on breaking bad news about rehabilitation potential after traumatic brain injury or spinal injury
Background: Neurorehabilitation units play an important role in facilitating recovery for those with complex needs following a neurological event. National guidance highlights the importance of providing patients and their families with information and fostering realistic expectations. This may involve the breaking of bad news. The aim of this study is to explore health professionals’ perspectives on breaking bad news in the neurorehabilitation setting.
Method: 15 health professionals (physiotherapists, occupational therapists, nurses, speech therapists, psychologists and doctors) working at a 24 bedded neurorehabilitation unit in a National Health Service acute trust in England were recruited. A qualitative study was conducted using patient vignettes to facilitate discussions during semi-structured interviews and a focus group. The results were analysed using thematic analysis.
Results: Four major themes emerged: influencing factors, current approaches used, staff experiences, and strategies to improve breaking bad news. There was a need for better management of patients' and families' expectations. Breaking bad news was seen as emotionally demanding yet often unrecognised work.
Conclusions: Breaking bad news in the neurorehabilitation setting is complex and under-recognised work, involving multiple health professionals. There is a need for both experience and training to improve skills and confidence in breaking bad news
Aceite de oliva y la hemostasia
Olive oil is a key component of the traditional Mediterranean diet; a diet that may explain the low rate of cardiovascular disease (CVD) in Southern European. (Extra virgin) Olive oil is a good source of monounsaturated fatty acids (MUFA) and phenolic compounds, both of which have been investigated for their effects on plasma lipids and lipoproteins, measures of oxidation and factors related to thrombosis. This issue aims to summarise the current understanding of the effects of such dietary components on the haemostatic system and subsequent risk of CVD. To date, evidence suggests that diets rich in MUFA and thus in olive oil attenuate the thrombotic response via a reduction in platelet aggregation and in postprandial FVII levels. Thrombosis is a key event in causing heart attacks and strokes, which if modulated by diet could pose a cost-effective way of reducing CVD incidence in populations that adhere to MUFA/olive oil-rich diets long-term.El aceite de oliva es un componente esencial de la dieta Mediterránea que puede explicar el bajo Ãndice de enfermedad cardiovascular (CVD) en los paÃses del sur de Europa. El aceite de oliva (extra virgen) es una fuente de ácidos grasos monoinsaturados (MUFA) y de compuestos fenólicos, de gran interés por sus efectos, entre otros, sobre las lipoproteÃnas y los lÃpidos plasmáticos, su capacidad antioxidante y su papel en la expresión de factores relacionados con la trombosis. En este capÃtulo se presenta un resumen del conocimiento actual sobre la influencia derivada del consumo de aceite de oliva (extra virgen) en el sistema hemostático y el riesgo de CVD. Por ahora se sabe que dietas ricas en MUFA (aceite de oliva) pueden atenuar la respuesta trombótica mediante la reducción de la agregación plaquetaria y de las concentraciones postprandiales del factor VII de coagulación (FVII). La trombosis es un evento relevante en los ataques al corazón y el ictus, de manera que su modulación con la dieta puede constituir una forma rentable para la disminución de la incidencia de CVD en poblaciones que consumen dietas enriquecidas en MUFA/aceite de oliva durante largo tiempo
Clinical academic research internships for nurses, midwives and allied health professionals: a qualitative evaluation
Background: Nurses, midwives and allied health professionals are integral to research, yet rarely engage simultaneously in research and clinical practice. Clinical academic internships offer a route to access academic research training. This study aimed to elucidate facilitators and barriers to participation and engagement, and suggest improvements for future programmes. Method: The experiences of 10 health professional research interns were explored, using a method based on a synthesis between grounded theory and content analysis. Findings: Four categories emerged: 1) integrating clinical and research aspirations; 2) Support – or lack of it; 3) The hidden curriculum; 4) The legacy effect. Within these categories, respondents identified a variety of facilitators and barriers to engagement, including unforeseen challenges. Conclusion: Formal support is necessary but not sufficient to foster engagement and maximise benefits. Participation must be supported by colleagues and enabled by institutional structures. The potential impact of internships on engagement with research is considerable but requires collaboration between all stakeholders. Implications for Practice: Deeper institutional engagement is needed so that internship opportunities are fully supported by all colleagues and practically enabled by institutional structures. Future schemes should attempt to promote opportunities to collaborate via group projects to reduce researcher isolation
Direct and Indirect Effects of Guggulsterone on the Induction of Beiging in Mature 3T3-L1 Adipocytes
Phytochemicals have long demonstrated anti-obesity properties in adipocytes. Their ability, however, to induce browning in white adipose tissue is only beginning to emerge. We have recently established that the white adipocyte cell line, 3T3-L1, is capable of beiging under beta-adrenergic conditions. Using this information, we sought to investigate if the plant steroid guggulsterone (GS) can induce beiging in 3T3-L1s. 3T3-L1 preadipocytes were differentiated using established protocols supplemented with rosiglitazone and thyroid hormone. Direct effects of GS were measured by treating mature 3T3-L1s for 24 hours. Indirect effects were measured by treating mature 3T3-L1s with conditioned media from GS-treated RAW 264.7 macrophages. Direct treatment of 3T3-L1s with GS resulted in increased lipolysis, increased mitochondrial activity (11%), and increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) levels by 250% more than control. 3T3-L1s also demonstrated an increase in uncoupling protein 1 (UCP1) expression by 200% and beige marker, T-box protein 1 (TBX1) expression by 80% more than control. Furthermore, this was accompanied by increased levels of G protein-coupled bile acid receptor (TGR5) and its downstream target iodothyronine deiodinase 2 (DIO2). Treatment of RAW 264.7 macrophages with GS induced a 60% increase in catecholamine release into the media compared to control. Using this conditioned media from macrophages, 3T3-L1 adipocytes increased the expression of DIO2 and UCP1 following 24 hours of incubation. Results from this study demonstrate that GS can potentially induce beiging in white adipose tissue through two distinct mechanisms: (1) direct signaling through the TGR5-cAMP-DIO2 pathway and (2) indirectly through stimulating catecholamine release in macrophages. Thus, it is reasonable to conclude that GS may improve the metabolic capacity of adipose tissue thereby counteracting the effects of obesity
Phytochemicals as Novel Agents for the Induction of Browning in White Adipose Tissue
Obesity and its associated metabolic syndrome continue to be a health epidemic in westernized societies and is catching up in the developing world. Despite such increases, little headway has been made to reverse adverse weight gain in the global population. Few medical options exist for the treatment of obesity which points to the necessity for exploration of anti-obesity therapies including pharmaceutical and nutraceutical compounds. Defects in brown adipose tissue, a major energy dissipating organ, has been identified in the obese and is hypothesized to contribute to the overall metabolic deficit observed in obesity. Not surprisingly, considerable attention has been placed on the discovery of methods to activate brown adipose tissue. A variety of plant-derived, natural compounds have shown promise to regulate brown adipose tissue activity and enhance the lipolytic and catabolic potential of white adipose tissue. Through activation of the sympathetic nervous system, thyroid hormone signaling, and transcriptional regulation of metabolism, natural compounds such as capsaicin and resveratrol may provide a relatively safe and effective option to upregulate energy expenditure. Through utilizing the energy dissipating potential of such nutraceutical compounds, the possibility exists to provide a therapeutic solution to correct the energy imbalance that underlines obesity
Estradiol Reduces Inflammation in Rats Fed a High-fat Diet.
Previous research has shown that leptin and insulin resistance can occur after rats
are fed a high-fat (HF) diet for 72 hours. Because leptin and insulin resistance can be a
result of HF diet-induced inflammation, the purpose of this research was to determine if
inflammatory gene expression occurs after 72 hours of a HF diet. Additionally, since
estrogen (E2) is anti-inflammatory, the extent of which intact females and ovariectomized
(OVX) express inflammatory cytokines after 72 hours of a HF diet was also determined. Intact females in proestrus had reduced hypothalamic inflammatory gene
expression of TNFa, whereas males had increased hypothalamic expression of SOCS3
after 72 hours of a HF diet. Within the liver, females in proestrus had reduced expression
of all genes measured in addition to reduced XBP1 mRNA after a HF diet. However, no
such reductions were observed within males. To determine if these reductions in inflammatory gene expression was due to the
increased circulating E2 seen during proestrus, E2 was reintroduced in an OVX model.
After 24 hours of a HF diet, E2 treatment prevented increases in hypothalamic SOCS3
expression. However, this protection was attenuated at 72 hours and no other treatmentinduced
changes were observed
Guggulsterone Activates Adipocyte Beiging through Direct Effects on 3T3-L1 Adipocytes and Indirect Effects Mediated through RAW264.7 Macrophages.
Background: Plant-derived phytochemicals have been of emerging interest as anti-obesity compounds due to their apparent effects on promoting reduced lipid accumulation in adipocytes. Despite such promising evidence, little is known about the potential mechanisms behind their anti-obesity effects. The aim of this study is to establish potential anti-obesity effects of the phytochemical guggulsterone (GS). Methods: Mature 3T3-L1 adipocytes were treated with GS, derived from the guggul plant native in northern India, to investigate its effects on mitochondrial biogenesis and adipocyte beiging. Further, to explore the relationship between macrophages and adipocytes, 3T3-L1s were treated with conditioned media from GS-treated RAW264.7 macrophages. Markers of mitochondrial biogenesis and beiging were measured by western blot. Results: GS treatment in adipocytes resulted in increased mitochondrial density, biogenesis (PGC1α and PPARγ), and increased markers of a beige adipocyte phenotype (UCP1, TBX1, and β-3AR). This upregulation in mitochondrial expression was accompanied by increases oxygen consumption. In GS-treated macrophages, markers of M2 polarization were elevated (e.g., arginase and IL-10), along with increased catecholamine release into the media. Lastly, 3T3-L1 adipocytes treated with conditioned media from macrophages induced a 167.8% increase in UCP1 expression, suggestive of a role of macrophages in eliciting an anti-adipogenic response to GS. Conclusions: Results from this study provide the first mechanistic understanding of the anti-obesity effects of GS and suggests a role for both direct GS-signaling and indirect stimulation of M2 macrophage polarization in this model
Isoproterenol Increases Uncoupling, Glycolysis, and Markers of Beiging in Mature 3T3-L1 Adipocytes.
Beta-adrenergic activation stimulates uncoupling protein 1 (UCP1), enhancing metabolic rate. In vitro, most work has studied brown adipocytes, however, few have investigated more established adipocyte lines such as the murine 3T3-L1 line. To assess the effect of beta-adrenergic activation, mature 3T3-L1s were treated for 6 or 48 hours with or without isoproterenol (10 and 100 μM) following standard differentiation supplemented with thyroid hormone (T3; 1 nM). The highest dose of isoproterenol increased lipid content following 48 hours of treatment. This concentration enhanced UCP1 mRNA and protein expression. The increase in UCP1 following 48 hours of isoproterenol increased oxygen consumption rate. Further, coupling efficiency of the electron transport chain was disturbed and an enhancement of glycolytic rate was measured alongside this, indicating an attempt to meet the energy demands of the cell. Lastly, markers of beige adipocytes (protein content of CD137 and gene transcript of CITED1) were also found to be upregulated at 48 hours of isoproterenol treatment. This data indicates that mature 3T3-L1 adipocytes are responsive to isoproterenol and induce UCP1 expression and activity. Further, this finding provides a model for further pharmaceutical and nutraceutical investigation of UCP1 in 3T3-L1s
Isoproterenol Increases Uncoupling, Glycolysis, and Markers of Beiging in Mature 3T3-L1 Adipocytes.
Beta-adrenergic activation stimulates uncoupling protein 1 (UCP1), enhancing metabolic rate. In vitro, most work has studied brown adipocytes, however, few have investigated more established adipocyte lines such as the murine 3T3-L1 line. To assess the effect of beta-adrenergic activation, mature 3T3-L1s were treated for 6 or 48 hours with or without isoproterenol (10 and 100 μM) following standard differentiation supplemented with thyroid hormone (T3; 1 nM). The highest dose of isoproterenol increased lipid content following 48 hours of treatment. This concentration enhanced UCP1 mRNA and protein expression. The increase in UCP1 following 48 hours of isoproterenol increased oxygen consumption rate. Further, coupling efficiency of the electron transport chain was disturbed and an enhancement of glycolytic rate was measured alongside this, indicating an attempt to meet the energy demands of the cell. Lastly, markers of beige adipocytes (protein content of CD137 and gene transcript of CITED1) were also found to be upregulated at 48 hours of isoproterenol treatment. This data indicates that mature 3T3-L1 adipocytes are responsive to isoproterenol and induce UCP1 expression and activity. Further, this finding provides a model for further pharmaceutical and nutraceutical investigation of UCP1 in 3T3-L1s
Isoproterenol Increases Uncoupling, Glycolysis, and Markers of Beiging in Mature 3T3-L1 Adipocytes.
Beta-adrenergic activation stimulates uncoupling protein 1 (UCP1), enhancing metabolic rate. In vitro, most work has studied brown adipocytes, however, few have investigated more established adipocyte lines such as the murine 3T3-L1 line. To assess the effect of beta-adrenergic activation, mature 3T3-L1s were treated for 6 or 48 hours with or without isoproterenol (10 and 100 μM) following standard differentiation supplemented with thyroid hormone (T3; 1 nM). The highest dose of isoproterenol increased lipid content following 48 hours of treatment. This concentration enhanced UCP1 mRNA and protein expression. The increase in UCP1 following 48 hours of isoproterenol increased oxygen consumption rate. Further, coupling efficiency of the electron transport chain was disturbed and an enhancement of glycolytic rate was measured alongside this, indicating an attempt to meet the energy demands of the cell. Lastly, markers of beige adipocytes (protein content of CD137 and gene transcript of CITED1) were also found to be upregulated at 48 hours of isoproterenol treatment. This data indicates that mature 3T3-L1 adipocytes are responsive to isoproterenol and induce UCP1 expression and activity. Further, this finding provides a model for further pharmaceutical and nutraceutical investigation of UCP1 in 3T3-L1s
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