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We began analyzing https://link.springer.com/article/10.1007/s10067-008-0910-4, but it redirected us to https://link.springer.com/article/10.1007/s10067-008-0910-4. The analysis below is for the second page.

Title[redir]:
BDNF in RA: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters | Clinical Rheumatology
Description:
The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFĪ±. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14 weeks after the initiation of anti-TNF therapy, i.e., 8 weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.

Matching Content Categories {šŸ“š}

  • Health & Fitness
  • Science
  • Education

Content Management System {šŸ“}

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Custom-built

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Traffic Estimate {šŸ“ˆ}

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šŸ™ļø Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,904,851 visitors per month in the current month.

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How Does Doi.org Make Money? {šŸ’ø}

We don't see any clear sign of profit-making.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {šŸ”}

article, google, scholar, pubmed, cas, bdnf, arthritis, factor, levels, nerve, synovial, cells, antitnf, neurotrophic, rheumatoid, patients, inflammatory, forsgren, treatment, umeƄ, plasma, brainderived, tissue, access, privacy, cookies, content, grimsholm, effects, inflammation, rheum, brain, neurotrophins, res, publish, search, clinical, rheumatology, ola, receptors, osteoarthritis, necrosis, immunoreactivity, sensory, therapy, role, chronic, growth, human, response,

Topics {āœ’ļø}

anti-tumour necrosis factor tumor necrosis factor-alpha brain-derived neurotrophic factor month download article/chapter anti-tnf treatment lead enzyme-linked immunosorbent assay computer-aided 3d reconstruction md solveig wƄllberg-jonsson anti-tnf treatment nucleus pulposus-induced damage anti-tnf therapy rheumatoid arthritis treated nerve-related cholinergic effects tnf-alpha blockers full article pdf nerve growth factor synovium showed immunoreactivity privacy choices/manage cookies shoulder joint region american rheumatism association rheumatoid arthritis chronic arthritis synovial tissue extracts brain natriuretic peptides solbritt rantapƤƤ-dahlqvist inflammatory brain lesions solbritt rantapaa-dahlqvist chronic inflammation herniated nucleus pulposus check access induced sympathetic neuron related subjects local injection therapy ms lena jonsson instant access anti-tnf article grimsholm acta radiol diagn european economic area trkb-receptor immunoreactions erythrocyte sedimentation rate including nerve structures therapeutic criteria committee histochemical findings favoring anterior cruciate ligament imply differential roles scapholunate interosseous ligament sympathetic nerve fibers increased norepinephrine release ms ulla hedlund

Questions {ā“}

  • Kerschensteiner M, Gallmeier E, Behrens L et al (1999) Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation?
  • Pezet S, Malcangio M, McMahon SB (2002) BDNF: a neuromodulator in nociceptive pathways?

Schema {šŸ—ŗļø}

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         headline:BDNF in RA: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters
         description:The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFĪ±. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14Ā weeks after the initiation of anti-TNF therapy, i.e., 8Ā weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.
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      headline:BDNF in RA: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters
      description:The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFĪ±. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14Ā weeks after the initiation of anti-TNF therapy, i.e., 8Ā weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.
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External Links {šŸ”—}(165)

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