amyloid/nekroz

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Tumor necrosis factor-alpha, interleukin-6, serum amyloid A, haptoglobin, and cortisol concentrations in sows following intramammary inoculation of Escherichia coli.

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OBJECTIVE To determine whether concentrations of proinflammatory cytokines, acute-phase proteins, and cortisol differ at parturition among 3 categories of sows (noninoculated, clinically affected and nonaffected following intramammary inoculation with Escherichia coll). METHODS 16 sows. METHODS Sows

Long-term follow-up of secondary amyloidosis patients treated with tumor necrosis factor inhibitor therapy: A STROBE-compliant observational study.

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There are no treatment modalities, which were proven to prevent the deposition of amyloid, proteinuria, and loss of renal function due to amyloidosis. Anti-tumor necrosis factor agents (anti-TNFs) were shown to decrease the production of serum amyloid A protein.We aimed to evaluate the long-term

Anti-tumor necrosis factor alpha therapy in fifteen patients with AA amyloidosis secondary to inflammatory arthritides: a followup report of tolerability and efficacy.

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OBJECTIVE Because anti-tumor necrosis factor alpha (anti-TNF) has emerged as a highly effective treatment for numerous inflammatory arthritides, which are a common cause of AA amyloidosis, we retrospectively evaluated the safety and efficacy of anti-TNF in a nationwide study. METHODS The

Genetic Deletion of Tumor Necrosis Factor-α Attenuates Amyloid-β Production and Decreases Amyloid Plaque Formation and Glial Response in the 5XFAD Model of Alzheimer's Disease.

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Increasing evidence suggests that neuroinflammation comprises a major characteristic of Alzheimer's disease (AD). Tumor necrosis factor-α (TNF-α) is a pleiotropic pro-inflammatory cytokine implicated in neurodegenerative diseases including AD, and has been proposed as a potent therapeutic target for

A rare case showing subacute thyroiditis-like symptoms with amyloid goiter after anti-tumor necrosis factor therapy.

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Anti-tumor necrosis factor (TNF)-α therapy is established as a new standard for the treatment of various autoimmune inflammatory diseases. We report the first case showing subacute thyroiditis-like symptoms with an amyloid goiter after anti-TNF-α therapy. A 56-year-old man with Crohn's disease

Acute-phase serum amyloid A regulates tumor necrosis factor α and matrix turnover and predicts disease progression in patients with inflammatory arthritis before and after biologic therapy.

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OBJECTIVE To investigate the relationship between acute-phase serum amyloid A (A-SAA) and joint destruction in inflammatory arthritis. METHODS Serum A-SAA and C-reactive protein (CRP) levels, the erythrocyte sedimentation rate (ESR), and levels of matrix metalloproteinase 1 (MMP-1), MMP-2, MMP-3,

Differential effects of tumor necrosis factor-alpha co-administered with amyloid beta-peptide (25-35) on memory function and hippocampal damage in rat.

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Effects of concurrent intracerebroventricular administration of amyloid-beta peptide 25-35 (Abeta(25-35)) and the proinflammatory cytokine tumor necrosis factor-alpha (TNFalpha) to rats were investigated. A battery of behavioral tests including radial arm maze, passive avoidance, elevated plus-maze

Effect of ascorbic acid and alpha-tocopherol supplementations on serum leptin, tumor necrosis factor alpha, and serum amyloid A levels in individuals with type 2 diabetes mellitus.

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OBJECTIVE Diabetes mellitus Type 2 is one of the most widespread chronic metabolic diseases. In most cases, this type of diabetes is associated with alterations in levels of some inflammatory cytokines and hormones. Considering anti-inflammatory properties of plant extracts rich in ascorbic acid

Two familial cases with tumor necrosis factor receptor-associated periodic syndrome caused by a non-cysteine mutation (T50M) in the TNFRSF1A gene associated with severe multiorganic amyloidosis.

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An adolescent boy had had recurrent episodes of fever, abdominal pain, and arthralgias since the age of 7 years. Progressive renal failure due to renal amyloidosis developed, leading to renal transplant at the age of 14.5 years. Five years later, he developed AA amyloidosis in the transplant as well

Alpha-MSH peptides inhibit production of nitric oxide and tumor necrosis factor-alpha by microglial cells activated with beta-amyloid and interferon gamma.

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Alpha-melanocyte stimulating hormone (alpha-MSH) is an ancient tridecapeptide with potent inhibitory activity in all major forms of inflammation. The anti-inflammatory message sequence of alpha-MSH resides in the COOH-terminal tripeptide alpha-MSH[11-13]. We tested the influence of alpha-MSH[1-13]

The secretases that cleave angiotensin converting enzyme and the amyloid precursor protein are distinct from tumour necrosis factor-alpha convertase.

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Angiotensin converting enzyme (ACE) and the Alzheimer's amyloid precursor protein are cleaved from the membrane by zinc metalloproteinases termed ACE secretase and alpha-secretase, respectively. Tumour necrosis factor-alpha (TNF-alpha) convertase (ADAM 17) is a recently identified member of the

Tumor necrosis factor-α gene polymorphisms in FMF and their association with amyloidosis.

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Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterized by periodic provocative attacks of fever with peritonitis, pleuritis, arthritis, or eriseplemya. Tumor necrosis factor-α (TNF-α) plays an important role in the regulation of the immune response as a part of the

Autosomal dominant periodic fever with AA amyloidosis: tumor necrosis factor receptor-associated periodic syndrome (TRAPS) in a Turkish family.

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We investigated the presence of tumor necrosis factor receptor-associated periodic syndrome (TRAPS) in a Turkish family with recurrent fever and systemic reactive (AA) amyloidosis. A missense mutation in exon 3 of the TNFRSF1A gene, resulting in an amino acid substitution Phe60Leu (F60L) was found

Amyloid precursor protein expression is induced by tumor necrosis factor alpha in 3T3-L1 adipocytes.

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Amyloid precursor protein (APP) has been characterized as an adipocyte-secreted protein that might contribute to obesity-related insulin resistance, inflammation, and dementia. In the current study, regulation of APP by the proinflammatory and insulin resistance-inducing cytokine tumor necrosis

Tumor necrosis factor alpha augments amyloid beta protein (25-35) induced apoptosis in human cells.

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No information is yet available on the effect of tumor necrosis factor alpha (TNFalpha) on amyloid beta protein (Abeta)-induced cytotoxicity in human cells. For this reason the induction of apoptosis by TNFalpha and Abeta (25-35) was studied in primary cultures of human thyroid and kidney cells as

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