PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7787867-8 1994 In contrast, patients with ATN and concomitance of acute rejection or CSA nephrotoxicity presented elevated beta 2M and creatinine serum levels. Cyclosporine 70-73 beta-2-microglobulin Homo sapiens 108-115 10064360-6 1996 Does any significant correlation between serum beta-2-M levels and blood cyclosporine A concentration exit? Cyclosporine 73-87 beta-2-microglobulin Homo sapiens 47-55 10064360-13 1996 Presence a significant positive correlation between serum beta-2-M level and blood cyclosporine A concentration suggest that beta-2-M level can be a good parametr to define cyclosporine A tubular toxicity. Cyclosporine 83-97 beta-2-microglobulin Homo sapiens 58-66 10064360-13 1996 Presence a significant positive correlation between serum beta-2-M level and blood cyclosporine A concentration suggest that beta-2-M level can be a good parametr to define cyclosporine A tubular toxicity. Cyclosporine 83-97 beta-2-microglobulin Homo sapiens 125-133 10064360-13 1996 Presence a significant positive correlation between serum beta-2-M level and blood cyclosporine A concentration suggest that beta-2-M level can be a good parametr to define cyclosporine A tubular toxicity. Cyclosporine 173-187 beta-2-microglobulin Homo sapiens 58-66 10064360-13 1996 Presence a significant positive correlation between serum beta-2-M level and blood cyclosporine A concentration suggest that beta-2-M level can be a good parametr to define cyclosporine A tubular toxicity. Cyclosporine 173-187 beta-2-microglobulin Homo sapiens 125-133 11704825-5 2001 Surprisingly, cyclosporin A (CsA), a known inhibitor of the mitochondrial permeability transition (MPT) pore, inhibited beta(2)m-induced apoptosis in HL-60/ADR cells but not in HL-60 and HL-60/VCR cells, suggesting that the pro-apoptotic effect of beta(2)m in these cells is not through MPT pore formation. Cyclosporine 14-27 beta-2-microglobulin Homo sapiens 120-128 11704825-5 2001 Surprisingly, cyclosporin A (CsA), a known inhibitor of the mitochondrial permeability transition (MPT) pore, inhibited beta(2)m-induced apoptosis in HL-60/ADR cells but not in HL-60 and HL-60/VCR cells, suggesting that the pro-apoptotic effect of beta(2)m in these cells is not through MPT pore formation. Cyclosporine 14-27 beta-2-microglobulin Homo sapiens 248-256 11704825-5 2001 Surprisingly, cyclosporin A (CsA), a known inhibitor of the mitochondrial permeability transition (MPT) pore, inhibited beta(2)m-induced apoptosis in HL-60/ADR cells but not in HL-60 and HL-60/VCR cells, suggesting that the pro-apoptotic effect of beta(2)m in these cells is not through MPT pore formation. Cyclosporine 29-32 beta-2-microglobulin Homo sapiens 120-128 11704825-5 2001 Surprisingly, cyclosporin A (CsA), a known inhibitor of the mitochondrial permeability transition (MPT) pore, inhibited beta(2)m-induced apoptosis in HL-60/ADR cells but not in HL-60 and HL-60/VCR cells, suggesting that the pro-apoptotic effect of beta(2)m in these cells is not through MPT pore formation. Cyclosporine 29-32 beta-2-microglobulin Homo sapiens 248-256 7696923-4 1994 In the patient treated with cyclosporin A alone, decreasing serum IL-6 and beta-2-microglobulin levels fell as the clinical response evolved. Cyclosporine 28-41 beta-2-microglobulin Homo sapiens 75-95 7787867-10 1994 However, serum beta 2M levels seemed to be useful in diagnosing acute rejection or CSA nephrotoxicity in patients with ATN. Cyclosporine 83-86 beta-2-microglobulin Homo sapiens 15-22 8518523-6 1993 Cyclosporin A induced a decrease in creatinine clearance with a decrease in fractional excretion of beta 2-microglobulin; sodium excretion was similar in the two treated groups and a transient decrease in fractional excretion of uric acid was seen only in patients receiving cyclosporin A. Cyclosporine 0-13 beta-2-microglobulin Homo sapiens 100-120 2662838-1 1989 In patients with heart transplant, the combined determination of serum beta 2-microglobulin and urinary neopterin, as rejection marker, prevented the interference by renal function and cyclosporin therapy. Cyclosporine 185-196 beta-2-microglobulin Homo sapiens 71-91 1720317-0 1991 Serum levels of alpha-1 microglobulin and beta-2 microglobulin in bone marrow transplant recipients treated with cyclosporin A. Cyclosporine 113-126 beta-2-microglobulin Homo sapiens 42-62 1720317-2 1991 In comparison to pre-transplant levels, the highest levels of alpha 1m and beta 2m were found during impairment of renal function, i.e., during cyclosporin-induced nephrotoxicity and during treatment with other nephrotoxic drugs (P less than 0.001). Cyclosporine 144-155 beta-2-microglobulin Homo sapiens 75-82 2645532-0 1989 Beta-2-microglobulin for differentiation between ciclosporin A nephrotoxicity and graft rejection in renal transplant recipients. Cyclosporine 49-62 beta-2-microglobulin Homo sapiens 0-20 2645532-7 1989 We conclude that parallel determination of beta 2-microglobulin in serum and urine allows to differentiate between ciclosporin A nephrotoxicity and rejection in 91% of the cases. Cyclosporine 115-128 beta-2-microglobulin Homo sapiens 43-63 3063418-0 1988 Enhanced beta 2-microglobulin levels in lymphocyte culture supernatants from patients with idiopathic nephrotic syndrome: inhibition of lymphocyte activation by cyclosporine. Cyclosporine 161-173 beta-2-microglobulin Homo sapiens 9-29 3063418-4 1988 In 13 patients treated with cyclosporine (Cs) (3-4.5 mg/kg/d) during 3 months, beta 2m levels were within the normal range. Cyclosporine 28-40 beta-2-microglobulin Homo sapiens 79-86 3063418-4 1988 In 13 patients treated with cyclosporine (Cs) (3-4.5 mg/kg/d) during 3 months, beta 2m levels were within the normal range. Cyclosporine 42-44 beta-2-microglobulin Homo sapiens 79-86 3063418-5 1988 Although the beta 2m of 7 Cs patients without proteinuria was lower than 5 Cs patients with residual proteinuria, the difference was not statistically significant. Cyclosporine 26-28 beta-2-microglobulin Homo sapiens 13-20 3063418-9 1988 In vitro addition of Cs (100 ng/ml) inhibited both beta 2m and VPF elevations observed in active INS. Cyclosporine 21-23 beta-2-microglobulin Homo sapiens 51-58 3063418-11 1988 High levels of beta 2m in LCS from INS are the consequence of an enhanced cellular synthesis and they are inhibited by Pr and Cs. Cyclosporine 126-128 beta-2-microglobulin Homo sapiens 15-22 3528611-12 1986 Urinary beta 2-microglobulin was still increased by 85% nine months after CyA treatment. Cyclosporine 74-77 beta-2-microglobulin Homo sapiens 8-28 3079033-0 1987 Serum beta 2 microglobulin levels are relatively depressed in cyclosporine A-treated patients who undergo kidney graft rejection. Cyclosporine 62-76 beta-2-microglobulin Homo sapiens 6-26 3020748-1 1986 In 83 renal transplant recipients, serum beta 2 microglobulin (beta 2m) levels were significantly elevated during pretransplant uremia, rejection, cyclosporine-induced nephrotoxicity, and infections. Cyclosporine 147-159 beta-2-microglobulin Homo sapiens 41-61 3020748-1 1986 In 83 renal transplant recipients, serum beta 2 microglobulin (beta 2m) levels were significantly elevated during pretransplant uremia, rejection, cyclosporine-induced nephrotoxicity, and infections. Cyclosporine 147-159 beta-2-microglobulin Homo sapiens 63-70 3020748-4 1986 Patients with stable renal allograft function receiving cyclosporine showed significantly higher serum beta 2m (P less than 0.001) and serum creatinine (P less than 0.01) levels than azathioprine treated patients. Cyclosporine 56-68 beta-2-microglobulin Homo sapiens 103-110 3890320-5 1985 Thus, beta 2-microglobulin might be a sensitive indicator of nephrotoxicity and of value for the evaluation of the long-term side effects of Cyclosporin A particularly in patients with extrarenal disease. Cyclosporine 141-154 beta-2-microglobulin Homo sapiens 6-26