No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

No description available.

Bakgrund: Fibromyalgi är ett syndrom som kännetecknas av utbredd smärta, överkänslighet vid beröring men även att övriga delar av kroppen påverkas. Metod: En litteraturstudie har genomförts där 10 stycken vetenskapliga artiklar har analyserats och utgjort resultatet. Syfte: Huvudsyftet är att undersöka möjliga riskfaktorer som kan påverka utvecklandet av fibromyalgi. Resultat: Studiens resultat har tagit upp fyra teman med tänkabara riskfaktorer. Traumatiska barndomshändelser, där både fysisk och verbal misshandel och sexuellt utnyttjande var riskfaktorer. Att bli utsatt för trauma som vuxen, där fysisk misshandel, operation och arbetsrelaterad skada ingick, var också en riskfaktor. Stress och ett högt BMI-värde var också riskfaktorer relaterade till utvecklandet av fibromyalgi. Diskussion: Studiens resultat visade på att det är flera riskfaktorer som påverkar utvecklandet av detta syndrom. Alla som utsätts för en av dessa riskfaktorer utvecklar dock inte fibromyalgi, utan med största sannolikhet så är det en kombination av flera riskfaktorer som gör att man utvecklar fibromyalgi. Slutsats: Det behövs mer forskning för att studera sambandet mellan fysiska, psykiska och sociala riskfaktorer. / Background: Fibromyalgia is a syndrome characterized by widespread pain, hypersensitivity to the touch but other body areas are also affected. Method: A literature study was conducted in which 10 scientific articles were analyzed and discussed. Purpose: The main purpose was to investigate possible risk factors that may affect the development of fibromyalgia. Results: The results of this study raised four themes describing risk factors. Traumatic childhood events, including both physical and verbal abuse and sexual abuse, were risk factors. Becoming a victim of trauma as an adult, where physical abuse, operation and work related injuries were included, was a risk factor as was stress and a high BMI. Discussion: Study results showed that there are many risk factors that affect the development if this syndrome. All persons exposed to one of these risk factors however does not develop fibromyalgia, so most likely it is a combination of several risk factors that makes the development of fibromyalgia possible. Conclusion: More research is needed to study the connection between physical, psychological and social risk factors.

Few weeks after birth, a switch in peptide elongation factor 1As from EF-1alpha/EF1A-1 to S1/EF1A-2 occurs in brain neurons, heart and skeletal muscles of mammalians. In order to elucidate the reason behind this switch, I studied the expression of both homologous proteins during muscle differentiation and apoptosis and, documented the relation between peptide elongation factors and caspase-3 activation. I found that during in vitro muscle differentiation of L6 myoblasts, a switch in peptide elongation factors 1A occurs as physiologically observed in skeletal muscles. While EF-1alpha/EF1A-1 is expressed in replicating myoblasts, S1/EF1A-2 is solely found in differentiated myotubes where it replaces EF-1alpha/EFIA-1 as the major elongation factor. Similarly, upon serum deprivation-induced apoptosis, a reversion in peptide elongation factors 1A is observed: EF-1alpha/EF1A-1 replaces S1/EF1A-2 and becomes the major form of elongation factor 1A present in dying myotubes. This switch correlates in myotubes with the activation of caspase-3 protein, a cysteine protease involved in apoptosis. When L6 myotubes constitutively express S1/EF1A-2 as caused by adenoviral gene transfer, they become resistant to serum deprivation-induced apoptosis. In contrast, when L6 myotubes are transfected with EF-1alpha/EF1A-1 gene, they die more rapidly from serum deprivation-induced apoptosis than control cells. Transfection using anti-sense EF-1alpha/EF1A-1 gene protects myotubes from apoptotic cell death. Thus, both elongation factor 1As exert opposing effect on muscle survival: while EF-1alpha/EF1A-1 accelerates apoptotic cell death, S1/EF1A-2 protects muscles against apoptosis. / I found that skeletal muscles are the only tissues where, despite the constitutive expression of caspase-3 mRNA, the protein can be absent. Furthermore, I found that while immediately after birth, caspase-3 protein is present in skeletal muscles, a few weeks afterwards, the protein cannot be detected by Western blotting. In skeletal muscle, this change correlates with the observed switch in peptide elongation factors from EF-1alpha/EF1A-1 to S1/EF1A-2 and suggests that caspase-3 is translationally regulated in skeletal muscles. The laboratory previously reported that while EF-1alpha/EF1A-1 protein reappears; S1/EF1A-2 protein becomes absent from regenerating muscles. However, once tissue regeneration is completed, the situation returns to normal as EF-1alpha/EF1A-1 disappears and S1/EF1A-2 reappears to become the only type 1A elongation factor expressed in muscle. / In conclusion, I found that the developmental switch observed in peptide elongation factors from EF-1alpha/EF1A-1 to S1/EF1A-2 partly serves to protect muscle cells from apoptosis. Thus, I am the first to identify a noncanonical function for S1/EF1A-2. (Abstract shortened by UMI.)

This cross-sectional study examines data from the 2008-2009 Youth Smoking Survey among never, current and former smoking grade 9-12 students using logistic regression. Path analysis examining correlates of former from current smoking was conducted for females and males. Former smokers represent a distinct, often intermediary, group of students between current and never smokers. Former smokers have similarities with current smokers on individual factors but more closely resemble never smokers on social and environmental factors. Among females, social factors were most influential; whereas environmental and individual factors played more of a role in male smoking cessation. These results further describe youth who quit smoking. The strong effects from social factors suggest the importance of family and peer support for quitting. These findings inform the development of youth cessation programming by providing a target profile and highlighting areas for intervention focus.