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1 terocyte it is required for copper efflux to portal blood.
2 third of the protein intake appeared in the portal blood.
3 ted using the recipient IVC as the source of portal blood.
6 nstantly exposed to gut-derived antigens via portal blood and, as a consequence, they express a uniqu
10 -6(+/+) mice with oral antibiotics decreased portal blood endotoxin levels, lowered the expression of
11 centration of TCA cycle intermediates in the portal blood exceeds that in tail blood indicating that
16 treatment with MS-PPOH significantly reduced portal blood flow and portal pressure compared to vehicl
18 ially prominent role in liver by controlling portal blood flow and pressure within liver sinusoids.
19 regeneration process combined with increased portal blood flow and relative outflow limitation may ha
22 nown to be affected by elevated postprandial portal blood flow in patients with chronic liver disease
24 ly immunological events, and the rat's lower portal blood flow induces spasm of the intrahepatic port
25 ave muscular walls susceptible to spasm, and portal blood flow is four times greater in the guinea pi
27 ino acid concentration in portal vein blood, portal blood flow rate and glucagon concentration, with
35 els without producing significant changes in portal blood flow, suggesting a reduction in hepatic vas
37 nificant decrease of mesenteric arterial and portal blood flow, without changing portal pressure and
38 c IRI, and suggest a diagnostic screening of portal blood for reactivity to these PRRs might prove us
40 ach sheep, time series from both hypophyseal portal blood (HPB) and peripheral blood were evaluated i
42 ow portal vein area index and intraoperative portal blood inflow may be negative prognostic factors f
45 to complications related to the diversion of portal blood into the systemic circulation, which is cal
47 t concentrations normally found in mammalian portal blood, may be capable of promoting enhanced hepat
48 detectable bacteremia or endotoxemia in the portal blood of trauma victims casts doubt on the role o
49 thesis was tested by examining the effect of portal blood plasma and mesenteric lymph on endothelial
50 e exposed to media, sham-shock, or postshock portal blood plasma or lymph, and permeability to rhodam
51 h bypass mesenteric lymph and directly enter portal blood, reduce intestinal antigen absorption into
57 with increasing arterialization and loss of portal blood supply; therefore, recognition of HCC requi
58 811, and 2002+/-370.9 IU/L for IPoC+CATR) in portal blood, the release of cytosolic cytochrome c, and
59 s by secreting the GnRH decapeptide into the portal blood vessels of the pituitary to stimulate the p
60 l tracer utilization and reappearance in the portal blood were used to calculate intestinal amino aci
61 ation increases gut-derived endotoxin in the portal blood, which activates Kupffer cells and causes l
62 ation increases gut-derived endotoxin in the portal blood, which activates Kupffer cells through nucl
63 s of complement and activated complexes from portal blood without obvious injury or impaired function