PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8634684-0 1995 Participation of TNF-alpha and IL-1 in the pathogenesis of cyclophosphamide-induced hemorrhagic cystitis. Cyclophosphamide 59-75 interleukin 1 complex Mus musculus 31-35 9096241-4 1997 Supernatants collected from P388D1 cells treated with CA, VS, CS, MMC, HU or LPS demonstrated enhanced production of tumor necrosis factor (TNF) confirmed by bioassay on L929 tumor target cells and increased interleukin-1 (IL-1) production by standard thymocyte proliferation bioassay. Cyclophosphamide 62-64 interleukin 1 complex Mus musculus 208-227 8886850-1 1996 Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1. Cyclophosphamide 19-35 interleukin 1 complex Mus musculus 154-158 8886850-1 1996 Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1. Cyclophosphamide 37-39 interleukin 1 complex Mus musculus 154-158 12205906-4 1999 The results also showed that PLGC could restore the capacity of macrophage for secreting IL-1 that had been inhibited by cyclophosphamide and PLGC could enhance the release of IL-2 from spleen cell in the experiment group (P < 0.05-0.01). Cyclophosphamide 121-137 interleukin 1 complex Mus musculus 89-93 9673408-2 1998 Similarly, IL-1 is reported to accelerate recovery following myelosuppressive treatment with doxorubicin (AdR), cis-platinum (DDP) and cyclophosphamide (CTx). Cyclophosphamide 135-151 interleukin 1 complex Mus musculus 11-15 8176939-3 1994 This antitumor effect was abolished when administration of CPA preceded that of IL-1. Cyclophosphamide 59-62 interleukin 1 complex Mus musculus 80-84 1290956-7 1992 While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase. Cyclophosphamide 238-254 interleukin 1 complex Mus musculus 6-10 1290956-7 1992 While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase. Cyclophosphamide 238-254 interleukin 1 complex Mus musculus 141-145 2144844-2 1990 In normal mice and in mice pretreated with cyclophosphamide, hydrocortisone acetate, or sublethal total body irradiation, the outgrowth of Candida albicans in the kidney was significantly reduced by the administration of a single intraperitoneal dose of 80 ng of IL-1 (P less than 0.05). Cyclophosphamide 43-59 interleukin 1 complex Mus musculus 263-267 1761361-2 1991 Intact or cyclophosphamide-treated mice received human rIL-1 beta according to different regimens, and their sera were assayed for CSA at 4, 24 or 48 h. The results indicated that (1) cyclophosphamide alone significantly increased the level of circulating CSA, (2) administration of IL-1 to intact or neutropenic mice resulted in a biphasic pattern of CSA response, an early burst at 4 h being followed at 24-48 h by a significant decrease. Cyclophosphamide 10-26 interleukin 1 complex Mus musculus 56-60 2144844-3 1990 In mice treated with either cyclophosphamide or irradiation, IL-1 also significantly reduced the outgrowth of C. albicans in the spleen. Cyclophosphamide 28-44 interleukin 1 complex Mus musculus 61-65 2144844-4 1990 The protective effect of IL-1 was present when given 24 h before injection of C. albicans but also when IL-1 was given simultaneously with or 6 h after injection of C. albicans in cyclophosphamide-treated mice. Cyclophosphamide 180-196 interleukin 1 complex Mus musculus 25-29 2144844-4 1990 The protective effect of IL-1 was present when given 24 h before injection of C. albicans but also when IL-1 was given simultaneously with or 6 h after injection of C. albicans in cyclophosphamide-treated mice. Cyclophosphamide 180-196 interleukin 1 complex Mus musculus 104-108 2111738-7 1990 Assay of serum colony-stimulating activity (CSA) revealed that (a) cyclophosphamide treatment alone significantly increased the level of circulating CSA, (b) administration of a single dose of IL-1 to neutropenic mice induced an early, further increase in serum CSA, followed by depression, (c) a biphasic pattern of CSA response was also evident in mice repeatedly treated with IL-1. Cyclophosphamide 67-83 interleukin 1 complex Mus musculus 193-197 1966937-6 1990 Production of interleukin 1 (IL-1) was also stimulated in sera of CY-treated and untreated mice by administration of GLA-60. Cyclophosphamide 66-68 interleukin 1 complex Mus musculus 14-33 2111738-7 1990 Assay of serum colony-stimulating activity (CSA) revealed that (a) cyclophosphamide treatment alone significantly increased the level of circulating CSA, (b) administration of a single dose of IL-1 to neutropenic mice induced an early, further increase in serum CSA, followed by depression, (c) a biphasic pattern of CSA response was also evident in mice repeatedly treated with IL-1. Cyclophosphamide 67-83 interleukin 1 complex Mus musculus 379-383 2783314-6 1989 Both neutrophilia and augmented resistance to infection were eliminated by a second dose of cyclophosphamide administered during the IL-1 treatments. Cyclophosphamide 92-108 interleukin 1 complex Mus musculus 133-137 2643663-7 1989 IL-1 effects were observed in mice treated with a wide dose range (50 to 300 mg/kg) of cyclophosphamide, with optimal effects occurring at a dose of 200 mg/kg. Cyclophosphamide 87-103 interleukin 1 complex Mus musculus 0-4 2317799-9 1990 Enhanced antibacterial resistance by IL-1 and OK432 was also observed in cyclophosphamide- and aminomethylpyrimidinylmethylchloroethylnitrosourea hydrochloride-pretreated (day -5) normal hosts and in cyclophosphamide-treated tumor-bearing hosts. Cyclophosphamide 73-89 interleukin 1 complex Mus musculus 37-41 2317799-9 1990 Enhanced antibacterial resistance by IL-1 and OK432 was also observed in cyclophosphamide- and aminomethylpyrimidinylmethylchloroethylnitrosourea hydrochloride-pretreated (day -5) normal hosts and in cyclophosphamide-treated tumor-bearing hosts. Cyclophosphamide 200-216 interleukin 1 complex Mus musculus 37-41 2806435-1 1989 Previous reports have shown that interleukin 1 (IL-1) has radioprotective effects when given to mice 20 h before a lethal dose of irradiation and enhances granulocyte recovery in mice treated with cyclophosphamide. Cyclophosphamide 197-213 interleukin 1 complex Mus musculus 33-52 2784143-1 1989 Based on recently published data, IL-1 has been shown to provide radioprotective effects when given to mice 20 h before a lethal dose of irradiation and to enhance granulocyte recovery in mice treated with cyclophosphamide. Cyclophosphamide 206-222 interleukin 1 complex Mus musculus 34-38 19703244-3 2009 However, when the mice were pretreated with cyclophosphamide, bacteremia-induced mortality was significantly greater in the IL-1-deficient mice than in the WT mice (P < 0.01). Cyclophosphamide 44-60 interleukin 1 complex Mus musculus 124-128