Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most chemotherapeutic agents can cause varying degrees of local tissue injuries when extravasated. The medical treatment of extravasation is based on proper maintenance of the intravenous (IV) line and application of cold or warm compresses, plus the use of antidotes when available. Antidotes for extravasation that have been shown to be useful are sodium thiosulfate for nitrogen mustard, dimethylsulfoxide for anthracyclines and mitomycin, and hyaluronidase for the vinca alkaloids. New treatments include dexrazoxane, sargramostim, and hyperbaric oxygen for doxorubicin extravasations. Tissue damage secondary to drug infiltration occurs as a result of one of two major mechanisms: (1) the drug is absorbed by local cells in the tissue and binds to critical structures (eg, DNA, microtubules), causing cell death; and (2) the drug does not bind to cellular DNA. Damage to immediately adjacent tissue is more readily neutralized than is damage to surrounding tissue.
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PMID:Extravasation of chemotherapeutic agents: prevention and treatment. 1647 51

Recognition of temperature is a critical element of sensory perception and allows mammals to evaluate both their external environment and internal status. The respiratory epithelium is constantly exposed to the external environment, and prolonged inhalation of cold air is detrimental to human airways. However, the mechanisms responsible for adverse effects elicited by cold air on the human airways are poorly understood. Transient receptor potential melastatin family member 8 (TRPM8) is a well-established cold- and menthol-sensing cation channel. We recently discovered a functional cold- and menthol-sensing variant of the TRPM8 ion channel in human lung epithelial cells. The present study explores the hypothesis that this TRPM8 variant mediates airway cell inflammatory responses elicited by cold air/temperatures. Here, we show that activation of the TRPM8 variant in human lung epithelial cells leads to increased expression of several cytokine and chemokine genes, including IL-1alpha, -1beta, -4, -6, -8, and -13, granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-alpha. Our results provide new insights into mechanisms that potentially control airway inflammation due to inhalation of cold air and suggest a possible role for the TRPM8 variant in the pathophysiology of asthma.
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PMID:Increased transcription of cytokine genes in human lung epithelial cells through activation of a TRPM8 variant by cold temperatures. 1844 Oct 98


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