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hydroxyproline/nekros

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Bone necrosis and urinary hydroxyproline excretion in rabbits.

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1. Aseptic necrosis of bone is a serious chronic complication of deep-sea diving and compressed-air work. 2. The changes to the bone which occur in this condition take time to develop to the stage where they cause the radiographic signs of bone necrosis, and consequently there is a delay of some
OBJECTIVE To evaluate the clinical significance of tumor necrosis factor-alpha (TNF-alpha) and hydroxyproline (HYP) in blood of patients with active pulmonary tuberculosis (APT). METHODS Contents of TNF-alpha and HYP in blood of 28 patients with APT and 17 normal subjects were determined with

Proceedings: The use of hydroxyproline excretion in the early detection of bone necrosis.

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Multiple oral doses of alpha-difluoromethyl-ornithine (alpha-DFMO), 18-24 g/day for up to 2 months, were administered to 2 patients with invasive and metastatic carcinoma of the bladder and to 3 patients with metastatic renal cancer in an open study. The moderate antigrowth effect of alpha-DFMO in
Tumor necrosis factor-alpha (TNF-alpha) is thought to be important in the development of pulmonary fibrosis. However, surfactant protein-C/TNF-alpha transgenic mice do not spontaneously develop pulmonary fibrosis but instead develop alveolar enlargement and loss of elastic recoil. We hypothesized
BACKGROUND The synergistic degradation of cartilage by oncostatin M (OSM) in combination with either interleukin 1 (IL1) or tumour necrosis factor alpha (TNFalpha) has been previously demonstrated using bovine nasal cartilage (BNC). OBJECTIVE (a) To investigate if human nasal cartilage (HNC)
Gelatin is an anti-inflammatory dietary component, and its predominant metabolites entering circulation are prolyl-hydroxyproline (Pro-Hyp) and glycine. We evaluated the protective effects of orally administered gelatin, glycine, and Pro-Hyp 10:3:0.8 (w/w/w) against dextran sodium sulfate

Tumor necrosis factor-alpha inhibits in vivo collagen synthesis.

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In this study we sought to determine the in vivo role of tumor necrosis factor-alpha (TNF-alpha) at the wound-healing site. In vivo abrogation of endogenous TNF-alpha activity in experimental wounds by administration of anti-murine TNF-alpha rabbit serum resulted in a significant 77.5% increase in

Deficiency of tumour necrosis factor-related apoptosis-inducing ligand exacerbates lung injury and fibrosis.

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BACKGROUND The death receptor ligand tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) shows considerable clinical promise as a therapeutic agent. TRAIL induces leukocyte apoptosis, reducing acute inflammatory responses in the lung. It is not known whether TRAIL modifies chronic lung
Cytokines, interleukin-1 (IL-1), tumor necrosis factor alpha, and the neurotransmitter, substance P, have been implicated in the pathogenesis of arthritis because they stimulate synovial cells to secrete prostaglandin E2 and collagenase in vitro. We investigated in vivo changes in intraarticular
Collagen analysis of articular cartilage and subchondral bone was performed on femoral heads obtained from patients of late stage of aseptic necrosis (ANF) (4 cases), and osteoarthritis (OA) (7 cases). In articular cartilage of both diseases, there was not observed any difference in the solubility

Tumor necrosis factor binding protein improves incisional wound healing in sepsis.

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BACKGROUND Sepsis is associated with poor wound healing; however, the exact role of tumor necrosis factor (TNF) as a mediator of sepsis-induced alterations in different types of tissue repair is unknown. This study examines the effects of a specific TNF antagonist (TNFbp) on the healing of

Tumor necrosis factor-alpha inhibits collagen synthesis in human and rat granulation tissue fibroblasts.

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The purpose of the study was to examine the effects of tumor necrosis factor-alpha (TNF-alpha) on collagen gene expression in rat and human granulation tissue fibroblast cultures. The cells were exposed to 0.1, 1, 10, or 100 ng/ml of TNF-alpha, and the rate of collagen synthesis was measured as

Rapid elevation of liver hydroxyproline content following a single administration of various chemical carcinogens to rats.

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The liver hydroxyproline content increased 14 days following a single administration of various chemical carcinogens, 2-N-fluorenylacetamide (FAA), 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), diethylnitrosamine (DEN), dimethylnitrosamine (DMN), and thioacetamide, to rats. The rapid elevation of
The contents of the various glycosaminoglycan (GAG) fractions, hydroxyproline and calcium in the thoracic aorta from the rat were studied. The effect on these contents of induced uraemia (3/4 kidney resection) combined with parathyroidectomy and/or 1-alpha-hydroxycholecalciferol (1-alpha-OH-D3)
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