Living with chronic heart failure: a review of qualitative studies of older people

Title. Living with chronic heart failure: a review of qualitative studies of older people Aim. This paper is a report of a systematic review of qualitative studies of how older people live with chronic heart failure. Background. Chronic heart failure is a global epidemic mainly affecting an ageing population. Understanding how older people live with this disease is important to help promote their adjustment to the distressing illness experience. Data sources. Eligible studies published in 1997–2007 were identified from several databases (Medline, CINAHL, PsycINFO and Sociological Abstracts). A manual search was conducted of bibliographies of the identified studies and relevant journals. Review methods. Two researchers independently reviewed the studies and extracted the data. Key concepts from the papers were compared for similarities and differences. The transactional model of stress was used to guide data synthesis. Findings. Fourteen qualitative studies were identified. Most described the illness experiences of older people with chronic heart failure and associated coping strategies. There was some emerging work exploring the adjustment process. The findings indicated that living with chronic heart failure was characterized by distressing symptoms, compromised physical functioning, feelings of powerlessness and hopelessness, and social and role dysfunction. There were gender differences in the way the disease was conceived. Adjustment required patients to make sense of the illness experience, accept the prognosis, and get on with living with the condition. Conclusion. Empowering older people to manage chronic heart failure, instilling hope and bolstering support system are means of promoting successful adjustment to the disease. Further research needs to explore the cultural differences in the adjustment process.     

Microdebrider vs electrocautery: a comparison of tonsillar wound healing histopathology in a canine model.

OBJECTIVE: To evaluate tonsillar wound healing histopathology in a canine model following microdebrider intracapsular and electrocautery tonsillectomy techniques. STUDY DESIGN: Randomized, controlled, single-blinded, paired comparison of histopathology. SUBJECTS AND METHODS: Twelve beagles underwent tonsillectomies by microdebrider on one side and electrocautery on the other. Punch biopsies were taken of the tonsillar fossae on postoperative days 3, 9, and 20. Specimens were graded with a novel mucosal wound healing scale (inter-rater reliability, r = 0.83) and appropriate statistical analysis performed. RESULTS: Combined mucosal wound healing scale scores showed significantly faster healing on the microdebrider side when compared to the electrocautery side on postoperative day 3 and day 9 (P < 0.05), which equalized by day 20. CONCLUSION: In a canine model of tonsillar wound healing, microdebrider intracapsular tonsillectomy produced significantly faster healing than electrocautery tonsillectomy in the early postoperative course. The "biologic dressing" theory of intracapsular tonsillectomy wound healing may account for observed differences in healing and suggests a mechanism for improved clinical outcomes.     

Effects of uremia and inflammation on growth hormone resistance in patients with chronic kidney diseases

Resistance to the anabolic action of growth hormone may contribute to the loss of strength and muscle mass in adult patients with chronic kidney disease. We tested this hypothesis by infusing growth hormone in patients to levels necessary to saturate hormone receptors. This led to a significant decrease of plasma potassium and amino acid levels in control and hyperkalemic patients with chronic kidney disease. These effects were completely or partially blunted in patients with elevated C-reactive protein levels. In forearm perfusion studies, growth hormone caused a further decrease in the negative potassium and protein balance of hemodialysis patients without inflammation but no effect was seen in patients with inflammation. Only IL-6 levels and age were found to be independent correlates in these growth hormone-induced variations in plasma potassium and blood amino acids. This shows that although a resistance to pharmacologic doses of growth hormone is not a general feature of patients with chronic kidney disease, there is a subgroup characterized by blunted growth hormone action. Our results support the hypothesis that uremia with inflammation, but not uremia per se, inhibits downstream growth hormone signaling contributing to muscle atrophy.     

Pharmacological modulation of wound healing in experimental burns

Factors involved in wound healing and their interdependence are not yet fully understood; nevertheless, new prospects for therapy to favor speedy and optimal healing are emerging. Reports about wound healing modulation by local application of simple and natural agents abound even in the recent literature, however, most are anecdotal and lack solid scientific evidence. We describe the effect of silver sulfadiazine and moist exposed burn ointment (MEBO), a recently described burn ointment of herbal origin, on mast cells and several wound healing cytokines (bFGF, IL-1, TGF-beta, and NGF) in the rabbit experimental burn model. The results demonstrate that various inflammatory cells, growth factors and cytokines present in the wound bed may be modulated by application of local agents with drastic effects on their expression dynamics with characteristic temporal and spatial regulation and changes in the expression pattern. Such data are likely to be important for the development of novel strategies for wound healing since they shed some light on the potential formulations of temporally and combinatory optimized therapeutic regimens.     

Protein kinase C-dependent mitochondrial translocation of proapoptotic protein Bax on activation of inducible nitric-oxide synthase in rostral ventrolateral medulla mediates cardiovascular depression during experimental endotoxemia

Sympathetic premotor neurons for the maintenance of vasomotor tone are located in rostral ventrolateral medulla (RVLM). We demonstrated previously that overproduction of nitric oxide (NO) by inducible NO synthase (iNOS) in RVLM, leading to caspase 3-dependent apoptotic cell death, plays a pivotal role in cardiovascular depression during endotoxemia induced by intravenous administration of Escherichia coli lipopolysaccharide. The interposing intracellular events remain unknown. We evaluated the hypothesis that these events encompass protein kinase C (PKC) activation, which triggers activation and translocation of Bax that opens mitochondrial permeability transition pore by interacting with adenine nucleotide translocase (ANT) or voltage-dependent anion protein (VDAC), followed by cytosolic release of cytochrome c. In Sprague-Dawley rats, coimmunoprecipitation and Western blot analyses revealed sequential manifestations during endotoxemia of membrane-bound translocation of PKC, dissociation of cytosolic PKC/Bax complex, mitochondrial translocation of activated Bax, augmented Bax/ANT or Bax/VDAC association, elevated cytosolic cytochrome c and caspase 3, and DNA fragmentation in ventrolateral medulla. Microinjection of iNOS inhibitor into bilateral RVLM significantly retarded PKC and Bax activation. The induced association of translocated Bax with ANT or VDAC and the triggered mitochondrial apoptotic signaling cascade were blunted by blockade in RVLM of PKC, mitochondrial translocation of Bax, Bax channels, ANT, or caspase 3, alongside significant amelioration of cardiovascular depression. We conclude that formation of mitochondrial Bax/ANT or Bax/VDAC complex that initiates caspase 3-dependent apoptosis in the RVLM as a result of PKC-dependent mitochondrial translocation of activated Bax activated by iNOS-derived NO plays a pivotal role in the manifestation of endotoxin-induced cardiovascular depression.