Elvytyskoulutus Kiteen terveyskeskuksen vastaanoton ja päivystyksen henkilökunnalle

Opinnäytetyömme tarkoituksena oli järjestää hoitoelvytyskoulutus Kiteen terveyskeskuksen vastaanoton ja päivystyksen henkilökunnalle. Koulutuksen tavoitteena oli henkilökunnan elvytystaitojen ylläpito niin, että elvytyspotilaalle turvataan laadukas ammattilaisten toteuttama hoitoelvytys. Toiminnallinen opinnäytetyö toteutettiin Kiteen terveyskeskuksen vastaanottotiloissa marraskuussa 2012. Kohderyhmänä oli vastaanotolla/päivystyksessä työskentelevät sairaanhoitajat, lähi- ja perushoitajat sekä lääkintävahtimestari. Koulutukseen osallistui 16 henkilöä, 3 – 5 henkilön pienryhmissä. Koulutustilaisuus aloitettiin teoriaosuudella, jossa käytiin PowerPoint esityksen avulla läpi koulutuksen tarkoitus ja tavoitteet, käypä hoito -suosituksen muutokset elvytyksessä sekä elottomuuden toteaminen, elvytyksen kulku, defibrillointi, hengityksen turvaaminen, elvytyksessä käytettävät lääkkeet, johtaminen, rosc sekä elvytyksen jälkeinen hoito, elvytyksen lopettaminen ja siitä pidättäytyminen. Teoriaosuuden jälkeen järjestettiin käytännön harjoitus, jossa jokainen vuorollaan teki painantaelvytystä, hengityksen turvaamista, defibrillointia, suoniyhteyden avaamista ja lääkitsemistä sekä johtamista. Koulutuksen jälkeen keskusteltiin koulutuksesta ja koulutettavat saivat esittää kysymyksiä. Koulutukseen osallistuvat vastasivat myös palautekyselyyn elvytyskoulutuksen jälkeen. Elvytyskoulutukseen osallistuneet hoitajat olivat tyytyväisiä koulutuksen sisältöön ja kokivat koulutuksen hyödylliseksi ja toivoivat koulutusta järjestettävän 1 - 2 kertaa vuodessa.The purpose of our thesis was to organize advanced resuscitation training for the reception and emergency duty personnel of the Kitee health center. The objective of the training was to ensure quality advanced resuscitation for patients implemented by professionals. Functional study was conducted at the reception of the Kitee health center in November 2012. The target group was both registered and practical nurses as well as the orderly. The training was organised for 16 people, who were working in small groups consisting of 3 to 5 persons. The training session started with section on theory during which the purpose and objectives of the training as well as the changes in the national guideline for resuscitation were presented in a PowerPoint slideshow. The theory section also included the following; stating sb abiotic, the resuscitation process, defibrillation, ensuring respiration, medication used in the resuscitation, leading, ROSC, treatment after resuscitation as well as the termination and/or abstention from resuscitation. The section on theory was followed by a practical exercise. During the exercise, each participant practised CPR, ensuring respiration, defibrillation, opening the vein connection and medication. Finally, all partici-pants exercised leading the full resuscitation process. After the training, a discussion followed in which the trainees were able to ask questions. Each trainee also completed a feedback form. The feedback showed that all the nurses were satisfied with the content of the training and considered the training beneficial. The participants hoped that the advanced resuscitation training would be organised once or twice every year

Adipose tissue NAD(+)-homeostasis, sirtuins and poly(ADP-ribose) polymerases - important players in mitochondrial metabolism and metabolic health

Obesity, a chronic state of energy overload, is characterized by adipose tissue dysfunction that is considered to be the major driver for obesity associated metabolic complications. The reasons for adipose tissue dysfunction are incompletely understood, but one potential contributing factor is adipose tissue mitochondrial dysfunction. Derangements of adipose tissue mitochondrial biogenesis and pathways associate with obesity and metabolic diseases. Mitochondria are central organelles in energy metabolism through their role in energy derivation through catabolic oxidative reactions. The mitochondrial processes are dependent on the proper NAD(+)/NADH redox balance and NAD+ is essential for reactions catalyzed by the key regulators of mitochondrial metabolism, sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs). Notably, obesity is associated with disturbed adipose tissue NAD(+) homeostasis and the balance of SIRT and PARP activities. In this review we aim to summarize existing literature on the maintenance of intracellular NAD(+) pools and the function of SIRTs and PARPs in adipose tissue during normal and obese conditions, with the purpose of comprehending their potential role in mitochondrial derangements and obesity associated metabolic complications. Understanding the molecular mechanisms that are the root cause of the adipose tissue mitochondrial derangements is crucial for developing new effective strategies to reverse obesity associated metabolic complications.Peer reviewe

Preventing White Adipocyte Browning during Differentiation In Vitro : The Effect of Differentiation Protocols on Metabolic and Mitochondrial Phenotypes

Mitochondrial dysfunction in white adipose tissue is strongly associated with obesity and its metabolic complications, which are important health challenges worldwide. Human adipose-derived stromal/stem cells (hASCs) are a promising tool to investigate the underlying mechanisms of such mitochondrial dysfunction and to subsequently provide knowledge for the development of treatments for obesity-related pathologies. A substantial obstacle in using hASCs is that the key compounds for adipogenic differentiation in vitro increase mitochondrial uncoupling, biogenesis, and activity, which are the signature features of brown adipocytes, thus altering the white adipocyte phenotype towards brown-like cells. Additionally, commonly used protocols for hASC adipogenic differentiation exhibit high variation in their composition of media, and a systematic comparison of their effect on mitochondria is missing. Here, we compared the five widely used adipogenic differentiation protocols for their effect on metabolic and mitochondrial phenotypes to identify a protocol that enables in vitro differentiation of white adipocytes and can more faithfully recapitulate the white adipocyte phenotype observed in human adipose tissue. We developed a workflow that included functional assays and morphological analysis of mitochondria and lipid droplets. We observed that triiodothyronine- or indomethacin-containing media and commercially available adipogenic media induced browning during in vitro differentiation of white adipocytes. However, the differentiation protocol containing 1 mu M of the peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist rosiglitazone prevented the browning effect and would be proposed for adipogenic differentiation protocol for hASCs to induce a white adipocyte phenotype. Preserving the white adipocyte phenotype in vitro is a crucial step for the study of obesity and associated metabolic diseases, adipose tissue pathologies, such as lipodystrophies, possible therapeutic compounds, and basic adipose tissue physiology.Peer reviewe

Preventing White Adipocyte Browning during Differentiation In Vitro : The Effect of Differentiation Protocols on Metabolic and Mitochondrial Phenotypes

Mitochondrial dysfunction in white adipose tissue is strongly associated with obesity and its metabolic complications, which are important health challenges worldwide. Human adipose-derived stromal/stem cells (hASCs) are a promising tool to investigate the underlying mechanisms of such mitochondrial dysfunction and to subsequently provide knowledge for the development of treatments for obesity-related pathologies. A substantial obstacle in using hASCs is that the key compounds for adipogenic differentiation in vitro increase mitochondrial uncoupling, biogenesis, and activity, which are the signature features of brown adipocytes, thus altering the white adipocyte phenotype towards brown-like cells. Additionally, commonly used protocols for hASC adipogenic differentiation exhibit high variation in their composition of media, and a systematic comparison of their effect on mitochondria is missing. Here, we compared the five widely used adipogenic differentiation protocols for their effect on metabolic and mitochondrial phenotypes to identify a protocol that enables in vitro differentiation of white adipocytes and can more faithfully recapitulate the white adipocyte phenotype observed in human adipose tissue. We developed a workflow that included functional assays and morphological analysis of mitochondria and lipid droplets. We observed that triiodothyronine- or indomethacin-containing media and commercially available adipogenic media induced browning during in vitro differentiation of white adipocytes. However, the differentiation protocol containing 1 mu M of the peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist rosiglitazone prevented the browning effect and would be proposed for adipogenic differentiation protocol for hASCs to induce a white adipocyte phenotype. Preserving the white adipocyte phenotype in vitro is a crucial step for the study of obesity and associated metabolic diseases, adipose tissue pathologies, such as lipodystrophies, possible therapeutic compounds, and basic adipose tissue physiology.Peer reviewe

The role of paediatric nurses in medication safety prior to the implementation of electronic prescribing:a qualitative case study

Objectives: To explore paediatric nurses’ experiences and perspectives of their role in the medication process and how this role is enacted in everyday practice. Methods: A qualitative case study on a general surgical ward of a paediatric hospital in England, one year prior to the planned implementation of ePrescribing. Three focus groups and six individual semi-structured interviews were conducted, involving 24 nurses. Focus groups and interviews were audio-recorded, transcribed, anonymized and subjected to thematic analysis. Results: Two overarching analytical themes were identified: the centrality of risk management in nurses’ role in the medication process and the distributed nature of nurses’ medication risk management practices. Nurses’ contribution to medication safety was seen as an intrinsic feature of a role that extended beyond just preparing and administering medications as prescribed and placed nurses at the heart of a dynamic set of interactions, practices and situations through which medication risks were managed. These findings also illustrate the collective nature of patient safety. Conclusions: Both the recognized and the unrecognized contributions of nurses to the management of medications needs to be considered in the design and implementation of ePrescribing systems

Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia – the effects of blocking myostatin and activins

Objective Cancer cachexia and muscle loss are associated with increased morbidity and mortality. In preclinical animal models, blocking activin receptor (ACVR) ligands has improved survival and prevented muscle wasting in cancer cachexia without an effect on tumour growth. However, the underlying mechanisms are poorly understood. The present study aimed to identify cancer cachexia and soluble ACVR (sACVR) administration-evoked changes in muscle proteome. Methods Healthy and C26 tumour-bearing (TB) mice were treated with recombinant sACVR. The sACVR or PBS control were administered either prior to the tumour formation or by continued administration before and after tumour formation. Muscles were analysed by quantitative proteomics with further examination of mitochondria and nicotinamide adenine dinucleotide (NAD+) metabolism. To complement the first prophylactic experiment, sACVR (or PBS) was injected as a treatment following tumour cell inoculation. Results Muscle proteomics in TB cachectic mice revealed downregulated signatures for mitochondrial oxidative phosphorylation (OXPHOS) and increased acute phase response (APR). These were accompanied by muscle NAD+ deficiency, alterations in NAD+ biosynthesis including downregulation of nicotinamide riboside kinase 2 (Nrk2), and decreased muscle protein synthesis. The disturbances in NAD+ metabolism and protein synthesis were rescued upontreatment with sACVR. Across the whole proteome and APR in particular, Serpina3n represented the most upregulated protein and the strongest predictor of cachexia. However, the increase in Serpina3n expression associated with increased inflammation rather than decreased muscle mass and/or protein synthesis. Conclusions We present here an evidence implicating disturbed muscle mitochondrial OXPHOS proteome and NAD+ homeostasis in experimental cancer cachexia. Treatment of tumour-bearing mice with a blocker of activin receptor ligands restores depleted muscle NAD+ and Nrk2 as well as decreased muscle protein synthesis. These results point out putative new treatment therapies for cachexia. Our results also reveal that although acute phase protein Serpina3n may serve as a predictor of cachexia, it more likely reflects a condition of elevated inflammation.Peer reviewe

Muscle or liver-specific Sirt3 deficiency induces hyperacetylation of mitochondrial proteins without affecting global metabolic homeostasis

Sirt3 is a mitochondrial sirtuin, predominantly expressed in highly metabolic tissues. Germline ablation of Sirt3 has major metabolic consequences, including increased susceptibility to metabolic damage and oxidative stress after high fat feeding. In order to determine the contribution of liver and skeletal muscle to these phenotypes, we generated muscle-specific Sirt3 (Sirt3skm−/−) and liver-specific Sirt3 (Sirt3hep−/−) knock-out mice. Despite a marked global hyperacetylation of mitochondrial proteins, Sirt3skm−/− and Sirt3hep−/− mice did not manifest any overt metabolic phenotype under either chow or high fat diet conditions. Similarly, there was no evidence for increased oxidative stress in muscle or liver when Sirt3 was ablated in a tissue-specific manner. These observations suggest that the mitochondrial hyperacetylation induced by Sirt3-deletion in a tissue specific manner is not necessarily linked to mitochondrial dysfunction and does not recapitulate the metabolic abnormalities observed in the germline Sirt3 knock-out mice

Lack of cardiac and high-fat diet induced metabolic phenotypes in two independent strains of Vegf-b knockout mice

Peer reviewe

Niacin Cures Systemic NAD(+) Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy

NAD(+) is a redox-active metabolite, the depletion of which has been proposed to promote aging and degenerative diseases in rodents. However, whether NAD(+) depletion occurs in patients with degenerative disorders and whether NAD(+) repletion improves their symptoms has remained open. Here, we report systemic NAD(+) deficiency in adult-onset mitochondrial myopathy patients. We administered an increasing dose of NAD(+) booster niacin, a vitamin B3 form (to 750-1,000 mg/day; clinicaltrials.gov NCT03973203) for patients and their matched controls for 10 or 4 months, respectively. Blood NAD(+) increased in all subjects, up to 8-fold, and muscle-NAD(+) of patients reached the level of their controls. Some patients showed anemia tendency, while muscle strength and mitochondrial biogenesis increased in all subjects. In patients, muscle metabolome shifted toward controls and liver fat decreased even 50%. Our evidence indicates that blood analysis is useful in identifying NAD(+) deficiency and points niacin to be an efficient NAD(+) booster for treating mitochondrial myopathy.Peer reviewe