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1 sceptibility to glomerular damage induced by puromycin aminonucleoside.
2 d can be induced in rats by the injection of puromycin aminonucleoside.
3 romatic substitution with dimethylamine gave puromycin aminonucleoside [9-(3-amino-3-deoxy-beta-D-rib
4 ycin, cycloheximide, emetine, puromycin, and puromycin aminonucleoside, a negative analog, were evalu
5 Treatment of differentiated podocytes with puromycin aminonucleoside, an agent that causes foot pro
6 with proteinuria and hypoalbuminemia in the puromycin aminonucleoside and adriamycin rat models of n
7 cyte injury was induced in C57BL/6 mice with puromycin aminonucleoside, and the selective A(2A)R agon
8 to glomerular injury, because treatment with puromycin aminonucleoside enhanced proteinuria in TG mic
9 Sprague-Dawley rats by an i.v. injection of puromycin aminonucleoside in saline; seven control rats
10 us injection of OX-7 monoclonal antibody and puromycin aminonucleoside in which 10(7) SPIO- and DiI-l
11 docytes, before or after sublethal injury by puromycin aminonucleoside, in the presence or absence of
13 sion was underscored by the observation that puromycin aminonucleoside-induced cell migration was slo
14 ne significantly protected podocytes against puromycin aminonucleoside-induced injury (designed to mi
17 ing the peritoneum permeability of rats with puromycin aminonucleoside-induced nephrotic syndrome.
18 ation of alpha(3) integrin protected against puromycin aminonucleoside-induced podocyte detachment.
21 gnificantly increased GEN sprouting, whereas puromycin aminonucleoside-injured podocyte supernatant d
26 syndrome in humans, in animals treated with puromycin aminonucleoside, or in humans or animals with
27 docytes in the passive Heymann nephritis and puromycin aminonucleoside (PA) nephrosis rat models of p
29 accumulation and phosphorylation of hsp27 in puromycin aminonucleoside (PAN) -induced experimental NS
30 elevated in podocytes from rats treated with puromycin aminonucleoside (PAN) and from patients with f
31 proteinuria in a rat model of MCD induced by puromycin aminonucleoside (PAN) and in vitro cultured mo
34 ague-Dawley rats by intravenous injection of puromycin aminonucleoside (PAN), whereas control rats re
35 ) on renal function and structure in chronic puromycin aminonucleoside (PAN)-induced nephropathy in r
39 d this interaction is disrupted in GECs from puromycin aminonucleoside-, protamine sulfate-, or siali
40 me and GEC foot process effacement using the puromycin aminonucleoside rat model resulted in signific
42 Stimulation of receptor-operated channels in puromycin aminonucleoside-treated podocytes leads to inc
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