Size and location of radish 1 chromosome regions carrying the fertility restorer Rfk1 gene in spring turnip rape

In spring turnip rape (Brassica rapa L. spp. oleifera) the most promising F1 hybrid system would be the Ogu-INRA CMS/Rf system. A Kosena fertility restorer gene Rfk1, homologue of the Ogura restorer gene Rfo, was successfully transferred from oilseed rape into turnip rape and that restored the fertility in female lines carrying Ogura cms. The trait was, however, unstable in subsequent generations. The physical localization of the radish chromosomal region carrying the Rfk1 gene was investigated using 8 GISH (genomic in situ hybridization) and BAC-FISH (bacterial artificial chromosome fluorescence in situ hybridization) methods. The metaphase chromosomes were hybridized using radish DNA as the genomic probe and BAC64 probe, which is linked with Rfo gene. Both probes showed a signal in the chromosome spreads of the restorer line 4021-2 Rfk of turnip rape but not in the negative control line 4021B. The GISH analyses clearly showed that the turnip rape restorer plants were either monosomic (2n=2x=20+1R) or disomic (2n=2x=20+2R) addition lines with one or two copies of a single alien chromosome region originating from radish. In the BAC-FISH analysis, double dot signals were detected in sub-terminal parts of the radish chromosome arms showing that the fertility restorer gene Rfk1 was located in this additional radish chromosome. Detected disomic addition lines were found to be unstable for turnip rape hybrid production. Using the BAC-FISH analysis, weak signals were sometimes visible in two chromosomes of turnip rape and a homologous region of Rfk1 in chromosome 9 of the B. rapa A genome was verified with BLAST analysis. In the future this homologous area in A genome could be substituted with radish chromosome area carrying the Rfk1 gene.Comment: "The final publication is available at http://www.springerlink.com". http://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0 non-commercial pre-print servers like arXiv.org can ... be updated with the author's accepted version. ... Acknowledgement ... accompanied by the text "The final publication is available at http://www.springerlink.com

Changes in thiamine concentrations, fatty acid composition, and some other lipid-related biochemical indices in Baltic Sea Atlantic salmon (Salmo salar) during the spawning run and pre-spawning fasting

Salmonines in the Baltic Sea and North American lakes suffer from thiamine (vitamin B1) deficiency, which is connected to an abundant lipid-rich diet containing substantial amounts of polyunsaturated fatty acids (PUFAs). In the Baltic region, this is known as the M74 syndrome. It affects both adult salmon (Salmo salar) and especially their offspring, impairing recruitment. However, very little is known about the thiamine and lipid metabolism of salmon during feeding and spawning migrations in the Baltic Sea. In this study, salmon females were sampled along the spawning run from the southern Baltic Proper in four locations at sea and finally at spawning in a river at the Bothnian Bay in a year with insignificant M74 mortality. Changes in concentrations of thiamine and its components in muscle, ovaries, and the liver and other biochemical indices potentially relating to lipid and fatty acid metabolism were investigated. The results provide further evidence of the role of peroxidation of PUFAs in eliciting thiamine deficiency in salmon: During the entire spawning run, the muscle total lipid content decreased by 50%, palmitic acid (16:0) by 62%, and docosahexaenoic acid (DHA, 22:6n-3) by 45%. The concentration of total thiamine decreased significantly until the spawning in the liver and ovaries, 66 and 70% respectively. In the muscle, the proportion of thiamine pyrophosphate of total thiamine increased with the use of muscular lipid stores. There was no trend in the concentration of total carotenoids during the spawning run. The doubling of the concentration of hepatic malondialdehyde indicated peroxidation of PUFAs, and the mobilisation of body lipids suppressed the activity of glucose-6-phosphate dehydrogenase, as consumed dietary lipids would also have done.Peer reviewe

Model for estimating thiamine deficiency-related mortality of Atlantic salmon (Salmo salar) offspring and variation in the Baltic salmon M74 syndrome

Thiamine (vitamin B1) deficiency of salmonines, caused by an abundant lipid-rich fish diet and consequently, the abundance of polyunsaturated fatty acids, is called the M74 syndrome in the Baltic Sea. Because of its deleterious effects on wild Atlantic salmon (Salmo salar) stocks and progeny production in fish cultivation, a model was developed to derive the annual female-specific mortality percentages of yolk-sac fry (YSFM) from the free thiamine concentrations of unfertilized eggs. In years with a high M74 incidence, thiamine-deficient females were larger, with a larger condition factor (CF) than non-M74 females. Otherwise, M74 females were generally smaller. The mean CF of M74 females was in most years higher than that of non-M74 females. The model compiled enables the cost-effective estimation of YSFM of individual female salmon, without the incubation of eggs and hatched yolk-sac fry for several months, thus benefitting the management of salmon stocks and their efficient utilization.Peer reviewe

Milk protein-derived peptide inhibitors of angiotensin-I-converting enzyme

peer-reviewedNumerous casein and whey protein-derived angiotensin-I-converting enzyme (ACE) inhibitory peptides/hydrolysates have been identified. Clinical trials in hypertensive animals and humans show that these peptides/hydrolysates can bring about a significant reduction in hypertension. These peptides/hydrolysates may be classified as functional food ingredients and nutraceuticals due to their ability to provide health benefits i.e. as functional food ingredients in reducing the risk of developing a disease and as nutraceuticals in the prevention/treatment of disease

High Lipid Content of Prey Fish and n−3 PUFA Peroxidation Impair the Thiamine Status of Feeding-Migrating Atlantic Salmon (Salmo salar) and Is Reflected in Hepatic Biochemical Indices

Signs of impaired thiamine (vitamin B1) status in feeding-migrating Atlantic salmon (Salmo salar) were studied in three Baltic Sea areas, which differ in the proportion and nutritional composition of prey fish sprat (Sprattus sprattus) and herring (Clupea harengus). The concentration of n−3 polyunsaturated fatty acids (n−3 PUFAs) increased in salmon with dietary lipids and n−3 PUFAs, and the hepatic peroxidation product malondialdehyde (MDA) concentration increased exponentially with increasing n−3 PUFA and docosahexaenoic acid (DHA, 22:6n−3) concentration, whereas hepatic total thiamine concentration, a sensitive indicator of thiamine status, decreased with the increase in both body lipid and n−3 PUFA or DHA concentration. The hepatic glucose 6-phosphate dehydrogenase activity was suppressed by high dietary lipids. In salmon muscle and in prey fish, the proportion of thiamine pyrophosphate increased, and that of free thiamine decreased, with increasing body lipid content or PUFAs, or merely DHA. The thiamine status of salmon was impaired mainly due to the peroxidation of n−3 PUFAs, whereas lipids as a source of metabolic energy had less effect. Organochlorines or general oxidative stress did not affect the thiamine status. The amount of lipids, and, specifically, their long-chain n−3 PUFAs, are thus responsible for generating thiamine deficiency, and not a prey fish species per se

Opioid peptides encrypted in intact milk protein sequences

peer-reviewedOpioid agonistic and antagonistic peptides which are inactive within the sequence of the precursor milk proteins can be released and thus activated by enzymatic proteolysis, for example during gastrointestinal digestion or during food processing. Activated opioid peptides are potential modulators of various regulatory processes in the body. Opioid peptides can interact with subepithelial opioid receptors or specific luminal binding sites in the intestinal tract. Furthermore, they may be absorbed and then reach endogenous opioid receptors

Peroxisomal membrane channel Pxmp2 in the mammary fat pad is essential for stromal lipid homeostasis and for development of mammary gland epithelium in mice

AbstractTo understand the functional role of the peroxisomal membrane channel Pxmp2, mice with a targeted disruption of the Pxmp2 gene were generated. These mice were viable, grew and bred normally. However, Pxmp2−/− female mice were unable to nurse their pups. Lactating mammary gland epithelium displayed secretory lipid droplets and milk proteins, but the size of the ductal system was greatly reduced. Examination of mammary gland development revealed that retarded mammary ductal outgrowth was due to reduced proliferation of epithelial cells during puberty. Transplantation experiments established the Pxmp2−/− mammary stroma as a tissue responsible for suppression of epithelial growth. Morphological and biochemical examination confirmed the presence of peroxisomes in the mammary fat pad adipocytes, and functional Pxmp2 was detected in the stroma of wild-type mammary glands. Deletion of Pxmp2 led to an elevation in the expression of peroxisomal proteins in the mammary fat pad but not in liver or kidney of transgenic mice. Lipidomics of Pxmp2−/−mammary fat pad showed a decrease in the content of myristic acid (C14), a principal substrate for protein myristoylation and a potential peroxisomal β-oxidation product. Analysis of complex lipids revealed a reduced concentration of a variety of diacylglycerols and phospholipids containing mostly polyunsaturated fatty acids that may be caused by activation of lipid peroxidation. However, an antioxidant-containing diet did not stimulate mammary epithelial proliferation in Pxmp2−/− mice.The results point to disturbances of lipid metabolism in the mammary fat pad that in turn may result in abnormal epithelial growth. The work reveals impaired mammary gland development as a new category of peroxisomal disorders

Mood Changes Following Social Dance Sessions in People with Parkinson’s Disease

This document is the accepted manuscript version of the following article: Carine Lewis, Lucy E Annett, Sally Davenport, Amelia A Hall and Peter Lovatt, ‘Mood changes following social dance sessions in people with Parkinson’s disease’. The final, definitive version of this paper has been published in Journal of Health Psychology, Vol 21(4): 483-492, April 2014, published by SAGE Publishing. All rights reserved. The final, definitive version is available online at doi: http://dx.doi.org/10.1177/1359105314529681Dance interventions have physical benefits for the elderly, especially those with Parkinson’s disease. This study assessed the psychological benefits of dance. Thirty-seven participants with Parkinson’s (n=22) or age-matched controls (n=15) completed mood questionnaires before and after a ten-week dance intervention. An overall reduction in mood and a specific reduction in anger were observed. In addition, less fatigue was found for those initially scoring higher in depression. This suggests dance can provide psychological benefits for both people with Parkinson’s and the elderly with findings suggesting that this is an avenue to be explored further.Peer reviewedFinal Accepted Versio

Brain TSPO-PET predicts later disease progression independent of relapses in multiple sclerosis

Overactivation of microglia is associated with most neurodegenerative diseases. In this study we examined whether PET-measurable innate immune cell activation predicts multiple sclerosis disease progression. Activation of microglia/macrophages was measured using the 18-kDa translocator protein (TSPO)-binding radioligand 11C-PK11195 and PET imaging in 69 patients with multiple sclerosis and 18 age- and sex-matched healthy controls. Radioligand binding was evaluated as the distribution volume ratio from dynamic PET images. Conventional MRI and disability measurements using the Expanded Disability Status Scale were performed for patients at baseline and 4.1 ± 1.9 (mean ± standard deviation) years later. Fifty-one (74%) of the patients were free of relapses during the follow-up period. Patients had increased activation of innate immune cells in the normal-appearing white matter and in the thalamus compared to the healthy control group (P = 0.033 and P = 0.003, respectively, Wilcoxon). Forward-type stepwise logistic regression was used to assess the best variables predicting disease progression. Baseline innate immune cell activation in the normal-appearing white matter was a significant predictor of later progression when the entire multiple sclerosis cohort was assessed [odds ratio (OR) = 4.26; P = 0.048]. In the patient subgroup free of relapses there was an association between macrophage/microglia activation in the perilesional normal-appearing white matter and disease progression (OR = 4.57; P = 0.013). None of the conventional MRI parameters measured at baseline associated with later progression. Our results strongly suggest that innate immune cell activation contributes to the diffuse neural damage leading to multiple sclerosis disease progression independent of relapses