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Muscle strength and mass decline in sedentary individuals with aging. The present study investigated the effects of both age and 21 weeks of progressive hypertrophic resistance training (RT) on skeletal muscle size and strength, and on myostatin and myogenin mRNA expression in 21 previously untrained young men (26.0 ± 4.3 years) and 18 older men (61.2 ± 4.1 years) and age-matched controls. Vastus lateralis muscle biopsies were taken before and after RT. Type I and type II muscle fiber cross-sectional areas increased more in young men than in older men after RT ( P  < 0.05). Concentric leg extension increased ( P  < 0.05) more after 10.5 weeks in young men compared to older men, but after 21 weeks no statistical differences existed. The daily energy and protein intake were greater ( P  < 0.001) in young subjects. Both myostatin and myogenin mRNA expression increased in older when compared with young men after RT ( P  < 0.05). In conclusion, after RT, muscle fiber size increased less in older compared to young men. This was associated with lower protein and energy intake and increases in myostatin gene expression in older when compared to young men.

BackgroundRotator cuff disease (RCD) causes prolonged shoulder pain and disability in adults. RCD is a continuum ranging from tendinopathy to full-thickness tendon tear. Recent studies have shown that subacromial decompression and non-surgical treatments provide equivalent results in RCD without a full-thickness tendon lesion. However, the importance of surgery for full-thickness tendon tears remains unclear.MethodsIn a pragmatic, randomised, controlled trial, 417 patients with subacromial pain underwent 3-month initial rehabilitation and MRI arthrography (MRA) for the diagnosis of RCD. Of these, 190 shoulders remained symptomatic and were randomised to non-surgical or surgical treatments. The primary outcomes were the mean changes in the Visual Analogue Scale for pain and the Constant Murley Score for shoulder function at the 2-year follow-up.ResultsAt the 2-year follow-up, both non-surgical and surgical treatments for RCD reduced pain and improved shoulder function. The scores differed between groups by 4 (95% CI −3 to 10, p=0.25) for pain and 3.4 (95% CI −0.4 to 7.1, p=0.077) for function. Among patients with full-thickness ruptures, the reduction in pain (13, 95% CI 5 to 22, p=0.002) and improvement in function (7.0, 95% CI 1.8 to 12.2, p=0.008) favoured surgery.ConclusionsNon-surgical and surgical treatments for RCD provided equivalent improvements in pain and function. Therefore, we recommend non-surgical treatment as the primary choice for patients with RCD. However, surgery yielded superior improvement in pain and function for full-thickness rotator cuff rupture. Therefore, rotator cuff repair may be suggested after failed non-surgical treatment.Trial registration detailsClinicalTrials.gov, NCT00695981 and NCT00637013.

Although humor is generally associated with innocent amusement, in the case of crisis events it has various psychological, social and politically charged effects, both negative and positive. In times of crisis humor functions as a technique for neutralizing emotionally charged areas and by that means provides hope. On the other hand, in contemporary society there exist sensitive socially restricted and culturally dependent boundaries beyond which humor is not permitted to extend. This article discusses how humor becomes politicized when it functions as a part of crisis events, both as a trigger for crises and as a strategic tool to manage them. Specific attention is paid to the impact of spatiality by dissecting how the links between crisis and humor change when the scalar perspective shifts and how different spatial levels interact when humor becomes political. ‘Body’, ‘local’, ‘regional’, ‘national’ and ‘global’ are important spatial abstractions across which the sociopolitical meanings connecting humor and crisis events become produced.

The paper concerns the reading of humour, literary imaginativeness, social structures, local identities, as well as their emancipation, and their interconnected nature. Humour is approached here as a tool through which the writer as well as the reader can self-consciously rise above the social and cultural discourses within which the text itself is written. These themes are discussed by investigating how literary humour is used in the process of narrativizing the marginalized histories and identities of the Tornedalen (Torne Valley) region of Sweden. The specific focus is on the humour of novelist Mikael Niemi, a native of the region, and his novel Popularmusik Från Vittula. The paper examines how Niemi’s literary humour is embedded in the questions of spatiality and otherness, and how they are both constructed and contested through irony directed at the common regional stereotypes of Tornedalen, a ‘region with no identity’. The key argument here concerns how perceiving the world through humour, and humour through social criticism, are alternative manners of acknowledging, understanding and interpreting the processes on-going in space and society.

Studies of hereditary cancer syndromes have contributed greatly to our understanding of molecular events involved in tumorigenesis. Here we investigate the molecular background of the Peutz–Jeghers syndrome 1 , 2 (PJS), a rare hereditary disease in which there is predisposition to benign and malignant tumours of many organ systems. A locus for this condition was recently assigned to chromosome 19p ( ref. 3 ). We have identified truncating germline mutations in a gene residing on chromosome 19p in multiple individuals affected by PJS. This previously identified but unmapped gene, LKB1 ( ref. 4 ), has strong homology to a cytoplasmic Xenopus serine/threonine protein kinase XEEK1 ( ref. 5 ), and weaker similarity to many other protein kinases. Peutz–Jeghers syndrome is therefore the first cancer-susceptibility syndrome to be identified that is due to inactivating mutations in a protein kinase.

[...]there is still a group of cases described as kyphomelic dysplasia, which do not fit the profile of these or other disorders that manifest as dwarfism and kyphomelia. 16 The cases can be distinguished from campomelic dysplasia by the extraskeletal manifestations, mental retardation, ambiguous genitalia, severe tibial bowing, and hypoplastic scapulae in the latter, 17 and from femoral hypoplasia-unusual facies syndrome by the hypoplasia of the femur. 18 Several single case reports that show a related but still different phenotype have been described. 19- 21 Short-limbed dwarfism with normal intelligence does also occur in cartilage-hair hypoplasia (CHH; MIM 250250). CHH presenting in infancy can be difficult to diagnose. 23, 24 Mutations in the RMRP gene that codes for an RNA subunit of the mitochondrial RNA processing (MRP) RNAse complexes are the cause of CHH, with a common \"Finnish\" mutation +70A->G (A70G) in many of the known CHH patients. 25, 26 Here we report on a case with short-limb dwarfism diagnosed as having kyphomelic dysplasia in infancy, who developed severe aplastic anaemia, concurring with a combined immune deficiency of late onset.

Background: The Schmid type of metaphyseal chondrodysplasia (MCDS) is generally due to mutations in COL10A1 encoding for type X collagen of cartilage. Methods: We performed a study on the genes coding for the RNA components of RNase MRP (MRPR) and RNase P (H1RNA) among 20 patients with diagnosis of MCDS and no mutations in COL10A1. Results: Two patients were found to be homozygous for a base substitution G for A at nucleotide 70 of RMRP, which is the major mutation causing cartilage–hair hypoplasia. No pathogenic mutations were detected in H1RNA. Conclusion: Cartilage–hair hypoplasia diagnosis should be considered in patients with metaphyseal chondrodysplasia even in the absence of any extra-skeletal manifestations if no mutation in COL10A1 can be found and the family history is compatible with autosomal recessive inheritance. Correct diagnosis is important for genetic counselling and for proper follow up of the patients.

This paper reviews mutational activation of ras oncogenes and inactivation of the p53 tumor suppressor gene in human lung cancer. We discuss the frequency, type, and location of mutations in these genes in relation to known etiological factors for lung cancer. The most studied examples of these are exposure to tobacco smoke, and to radon and asbestos fibers at work. We summarize data from our laboratory on K-ras and p53 mutations in fresh tissue samples from patients with resected primary lung carcinoma whose smoking and occupational histories were known. Most of the tumors examined were histologically non-small cell carcinoma (NSCLC), mainly of the squamous cell carcinoma and adenocarcinoma types. We compare the prevalence and nature of mutations in the two histological types of NSCLC.

Pleiotropic, recessively inherited cartilage-hair hypoplasia (CHH) is due to mutations in the untranslated RMRP gene on chromosome 9p13-p12 encoding the RNA component of RNase MRP endoribonuclease. We describe 36 different mutations in this gene in 91 Finnish and 44 non-Finnish CHH families. Based on their nature and localisation, these mutations can be classified into three categories: mutations affecting the promoter region, small changes of conserved nucleotides in the transcript, and insertions and duplications in the 5′ end of the transcript. The only known functional region that seemed to avoid mutations was a nucleolar localisation signal region between nucleotides 23–62. The most common mutation in CHH patients was a base substitution G for A at nucleotide 70. This mutation contributed 92% of the mutations in the Finnish CHH patients. Our results using linkage disequilibrium based maximum likelihood estimates with close markers, genealogical studies, and haplotype data suggested that the mutation was introduced to Finland some 3900–4800 years ago, and before the expansion of the population. The same major mutation accounted for 48% of the mutations among CHH patients from other parts of Europe, North and South America, the Near East, and Australia. In the non-Finnish CHH families, the A70G mutation segregated with the same major haplotype, although shorter, as in most of the Finnish families. In 23 out of these 27 chromosomes, the common region extended over 60 kb, and, therefore, all the chromosomes most likely arose from a solitary event many thousands of years ago.