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Träfflista för sökning "WFRF:(Theodorsson Elvar) ;pers:(Hildebrand Claes)"

Sökning: WFRF:(Theodorsson Elvar) > Hildebrand Claes

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1.
  • Hoe-Hansen, Carsten, et al. (författare)
  • Acute local inflammation elicits sprouting of sensory axons in the rat supraspinatus tendon
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Inflammation activates nociceptive nerve endings and can elicit local sprouting of axons. We hypothesized that axon sprouting might be one factor behind the emergence of painful inflammatory conditions in the shoulder. Here we examine the distribution of sensory and sympathetic axons in the rat subacromial space under normal conditions and after local induction of inflammation with carrageenan. Furthermore, we measured the neuropeptide content in the supraspinatus tendon. In normal rats protein gene product 9.5- (POP 9.5-), substance P- (SP-), calcitonin gene related peptide- (CGRP-), neuropeptide Y- (NPY-) and tyrosine hydroxylase- (TH-) like immunoreactive (LI) axon profiles occurred in the subacromial space and around the glenohumeral joint. In the supraspinatus tendon axon profiles were limited to the tendon-muscle junction. After carrageenan injection inflammatory cells invaded the tendon and the subacromial bursa with a maximum at 2-3 weeks. Moreover, the tendon and the bursa showed signs of sprouting of PGP-9.5-, SP- and CGRP-LI axons, but not NPY- and TH-LI axons. The tendon was also invaded by blood vessels. The occurrence of axon profiles had a maximum at 2 weeks after injection and then subsided. Also, these axons were GAP-43-LI indicating collateral sprouting of nociceptive nerve fibres. There was no significant increase in the concentration of the neuropeptides SP and CGRP in the supraspinatus tendon. No inflammatory reaction or sprouting of nerve fibres was seen in saline-injected controls. We conclude that an acute inflammation in the subacromial space of the rat shoulder region can elicit a transient local sprouting of sensory axons in the tendon stroma and associated aberrant blood vessels.
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2.
  • Hoe-Hansen, Carsten, et al. (författare)
  • Increased Occurrence of Nerve Fibres and some Neuropeptides in Subacromial Tissue Biopsies from Patients with Impingement Syndrome of the Shoulder
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Background: The pathophysiology of subacromial inflammation is not fully understood. In the present study we evaluate the presence of sensory and sympathetic nerve fibres and some neuropeptides in biopsies from the supraspinatus tendon and the subacromial bursa of patients with chronic subacromial inflammation as well as of control cases.Methods: The occurrence of nerve fibres was subjectively assessed by immunohistochemistry. The concentration of substance P (SP), calcitonin generelated peptide (CGRP) and neuropeptide Y (NPY) was measured by radioimmunoassay (RIA).Results: In tendon biopsies from patients with an intact or partially ruptured tendon protein gene product 9.5-like immunoreactive (LI), SP-LI and CGRP-LI nerve fibres were abnormally abundant. In patients with a total tendon rupture nerve fibre occurrence was normal. All biopsies from the bursa exhibited an abnormally high occurrence of SP- and CGRP-LI nerve fibres. In all biopsies the tendon and the bursa contained more blood vessels than normal. The vessels were surrounded by NPY- and tyrosine hydroxylase-LI nerve fibres in a subjectively normal pattern. RIA analysis revealed that the concentration of all three neuropeptides was abnormally high in tendon biopsies from patients with an intact or partially ruptured tendon. Tendon biopsies from patients with total tendon rupture showed statistically normal levels. Biopsies from the bursa showed abnormally high levels of SP and CGRP but normal levels of NPY in all patients.Conclusion: We conclude, that the supraspinatus tendon and the subacromial bursa exhibit an increased occurrence of nerve fibres and some neuropeptides in patients with chronic subacromial inflammation.Clinical relevance: Patients with chronic subacromial inflammation have a disabling pain problem. The increased local occurrence of sensory andsympathetic axons in the inflamed tissues as well as the elevated tissue concentration of certain neuropeptides may represent important factors behind that problem.
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3.
  • Mohseni, Simin, 1959-, et al. (författare)
  • Hypoglycaemic neuropathy : Occurrence of axon terminals in plantar skin and plantar muscle of diabetic BB/Wor rats treated with insulin implants
  • 2000
  • Ingår i: Acta Neuropathologica. - 0001-6322 .- 1432-0533. ; 99:3, s. 257-262
  • Tidskriftsartikel (refereegranskat)abstract
    • It is generally believed that diabetic neuropathy is due to chronic hyperglycaemia. However, experience from insulinoma patients and experimental studies show that hypoglycaemia may also cause neuropathy. Accordingly, the plantar nerves of diabetic eu-/hypoglycaemic BB/Wor rats treated with insulin implants exhibit a distinct neuropathy. To what extent hypoglycaemic neuropathy affects axon terminals in skin and muscle is unknown. In the present study we examine the occurrence of epidermal axon profiles and the neuropeptide calcitonin gene-related peptide (CGRP) in plantar skin, and of end plate axon terminals in a plantar muscle of diabetic BB/Wor rats subjected to long periods of hypoglycaemia. The number of protein gene product-immunoreactive axon profiles was found to be normal in heel skin biopsy specimens from eu-/hypoglycaemic rats, but many profiles were short and thin. The content of CGRP in the skin biopsy samples was significantly below normal. After staining with antibodies against the vesicular acetylcholine transporter protein, the occurrence of end plate axon terminals was significantly reduced in sections from the flexor hallucis brevis muscle of eu-/hypoglycaemic rats. Moreover, the end plate axon terminals tended to be abnormally small in these rats. We conclude that the hypoglycaemic neuropathy seen in plantar nerve trunks of diabetic BB/Wor rats treated with insulin implants is accompanied by mild alterations in the epidermal innervation of plantar skin and a more obviously abnormal nerve terminal pattern in plantar muscle.
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