6 research outputs found

    Use of Cis-[18F]Fluoro-Proline for Assessment of Exercise-Related Collagen Synthesis in Musculoskeletal Connective Tissue

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    Protein turnover in collagen rich tissue is influenced by exercise, but can only with difficulty be studied in vivo due to use of invasive procedure. The present study was done to investigate the possibility of applying the PET-tracer, cis-[18F]fluoro-proline (cis-Fpro), for non-invasive assessment of collagen synthesis in rat musculoskeletal tissues at rest and following short-term (3 days) treadmill running. Musculoskeletal collagen synthesis was studied in rats at rest and 24 h post-exercise. At each session, rats were PET scanned at two time points following injection of cis-FPro: (60 and 240 min p.i). SUV were calculated for Achilles tendon, calf muscle and tibial bone. The PET-derived results were compared to mRNA expression of collagen type I and III. Tibial bone had the highest SUV that increased significantly (p<0.001) from the early (60 min) to the late (240 min) PET scan, while SUV in tendon and muscle decreased (p<0.001). Exercise had no influence on SUV, which was contradicted by an increased gene expression of collagen type I and III in muscle and tendon. The clearly, visible uptake of cis-Fpro in the collagen-rich musculoskeletal tissues is promising for multi-tissue studies in vivo. The tissue-specific differences with the highest basal uptake in bone are in accordance with earlier studies relying on tissue incorporation of isotopic-labelled proline. A possible explanation of the failure to demonstrate enhanced collagen synthesis following exercise, despite augmented collagen type I and III transcription, is that SUV calculations are not sensitive enough to detect minor changes in collagen synthesis. Further studies including kinetic compartment modeling must be performed to establish whether cis-Fpro can be used for non-invasive in-vivo assessment of exercise-induced changes in musculoskeletal collagen synthesis

    Co-infection with coxsackievirus A5 and norovirus GII.4 could have been the trigger the first episode of a severe encephalopathy in a six-year-old child with the intermittent form of maple syrup urine disease (MSUD)

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    In this case study, a coxsackievirus A5 (Picornaviridae) and a norovirus GII.4 (Caliciviridae) co-infection were detected using RT-PCR from a faecal sample of a 6-year-old girl with symptoms of severe acute encephalopathy subsequently diagnosed as intermittent form of maple syrup urine disease (MSUD). The two co-infecting viruses were hiding and triggering the underlying metabolic disorder. The genotyping of the viruses as well as the chronological course, wide spectra of laboratory tests and clinical presentations of this case which includes recurrent vomiting without diarrhoea, metabolic acidosis, unconsciousness, seizure and circulatory collapse, but with positive final outcome is also presented

    Inborn errors of metabolism and expanded newborn screening: review and update

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