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nicotinamide/повръщане

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Metabolites of the radiosensitizer nicotinamide are unlikely to contribute to the degree of emesis observed with the parent drug.

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Nicotinamide is a potent radiosensitizer currently employed in the treatment of cancer of the bladder, head, and neck. Unfortunately, nicotinamide is also a potent emetic at the concentrations required for radiosensitization. Previously, we have demonstrated that nicotinamide-induced emesis is the

Pharmacology and toxicity of nicotinamide combined with domperidone during fractionated radiotherapy.

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OBJECTIVE Treatment of head and neck tumors by the ARCON regimen has yielded high local control rates. As a result of this treatment intensification there was some increase in mainly acute toxicity of radiotherapy, but nicotinamide by itself has specific side effects such as nausea and vomiting. Due

Tolerance of nicotinamide and carbogen with radiation therapy for glioblastoma.

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Nineteen patients with glioblastoma were treated with nicotinamide and carbogen and radiotherapy. Eight patients did not complete the protocol because of hepatic toxicity from phenytoin/nicotinamide drug interactions, persistent nausea or vomiting with nicotinamide, intolerance of the carbogen

Radiotherapy with carbogen breathing and nicotinamide in head and neck cancer: feasibility and toxicity.

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The feasibility and early toxicity of radiotherapy with carbogen breathing and nicotinamide was tested in 74 head and neck cancer patients. Forty patients with laryngeal and hypopharyngeal tumors were treated with an accelerated schedule combined with carbogen alone (16) or with carbogen and

Radiotherapy and chemotherapy with or without carbogen and nicotinamide in inoperable biopsy-proven glioblastoma multiforme.

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BACKGROUND Nicotinamide and carbogen have been shown to enhance the radiation effect in tumour models. OBJECTIVE Prospective evaluation of the toxicity and efficacy of carbogen and nicotinamide with external beam radiotherapy in the management of inoperable glioblastoma. METHODS From April 1995 to

Administration of nicotinamide during a five- to seven-week course of radiotherapy: pharmacokinetics, tolerance, and compliance.

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OBJECTIVE Nicotinamide was administered daily as a liquid formulation to head and neck cancer patients receiving a 5- to 7-week course of radiotherapy. The pharmacokinetics, compliance, and tolerance of this drug formulation were studied. METHODS Blood samples were drawn and nicotinamide levels

Carbogen and nicotinamide in locally advanced bladder cancer: early results of a phase-III randomized trial.

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OBJECTIVE Phase II studies in laryngeal and bladder carcinoma of accelerated radiotherapy with carbogen and nicotinamide (RT+CON) suggested a therapeutic advantage. Therefore, a randomized phase-III trial of RT+CON in locally advanced bladder carcinoma compared to radiotherapy (RT) alone was

ARCON: accelerated radiotherapy with carbogen and nicotinamide in non small cell lung cancer: a phase I/II study by the EORTC.

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BACKGROUND Non small cell lung cancers (NSCLC) are rapidly proliferating tumours, which are characterized by the presence of extensive hypoxic components, especially in patients with advanced loco-regional disease. Previous studies suggest a deleterious impact of acute (perfusion-limited) hypoxia on

Acute effects of accelerated radiotherapy in combination with carbogen breathing and nicotinamide (ARCON).

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Combining accelerated radiotherapy with carbogen and nicotinamide (NAM) has been proposed as a strategy to overcome the sparing effect of tumour clonogen repopulation and hypoxia. Six patients with squamous cell carcinomas of the head and neck were given accelerated radiotherapy, carbogen breathing
BACKGROUND Since there is increasing evidence that both acute (perfusion-limited) and chronic (diffusion-limited) hypoxia, and tumor repopulation may prejudice the outcome of radiotherapy, the combination of carbogen (95% oxygen-5% carbon dioxide) and nicotinamide with accelerated radiotherapy

Pharmacokinetics of nicotinamide in cancer patients treated with accelerated radiotherapy: the experience of the Co-operative Group of Radiotherapy of the European Organization for Research and Treatment of Cancer.

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BACKGROUND The EORTC has initiated studies to combine nicotinamide with carbogen in accelerated fractionation schedules (ARCON), since for some tumour types, acute and chronic hypoxia as well as treatment protraction may prejudice the outcome of radiotherapy. The tolerable dose of nicotinamide and

The effect of nicotinamide on spontaneous and induced activity in smooth and skeletal muscle.

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OBJECTIVE Nicotinamide (NA) is currently undergoing clinical trials as a tumour radiosensitizer. The dose that can be administered is currently 80 mg/kg per day, but this may be restricted to 60 mg/kg per day by the high incidence of nausea and vomiting. To investigate some of NA's underlying

Short communication: the addition of carbogen and nicotinamide to a palliative fractionation schedule for locally advanced breast cancer.

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Tumour cell hypoxia is a recognized cause of resistance to radiotherapy. Using clinically relevant dose-fractionation schedules in a mouse tumour model, the addition of carbogen and nicotinamide to overcome chronic and acute hypoxia results in a marked increase in radioresponsiveness with a lower

Accelerated radiotherapy, carbogen and nicotinamide (ARCON) in locally advanced head and neck cancer: a feasibility study.

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OBJECTIVE ARCON (Accelerated Radiotherapy, CarbOgen, Nicotinamide) achieves a large therapeutic gain in rodents. A phase I/II study was therefore undertaken to determine its feasibility in patients with locally advanced head and neck cancer. METHODS The accelerated regime CHART was used in 35

Interleukin 10 Restores Gastric Emptying, Electrical Activity, and Interstitial Cells of Cajal Networks in Diabetic Mice.

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OBJECTIVE Gastroparesis is a complication of diabetes characterized by delayed emptying of stomach contents and accompanied by early satiety, nausea, vomiting, and pain. No safe and reliable treatments are available. Interleukin 10 (IL10) activates the M2 cytoprotective phenotype of macrophages and
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