ライフサイエンスコーパス: portal blood

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.

4 ts, intact labeled TC II was detected in the portal blood 4 and 8 h later.

5 to bile but could not reenter the liver from portal blood and accumulated in serum.

6 nstantly exposed to gut-derived antigens via portal blood and, as a consequence, they express a uniqu

7 Jejunal and ileal luminal BAs, portal blood BAs, and messenger RNA and protein for the

8 genital anomaly of the portal vein where the portal blood bypasses the liver.

9 bition, at the same time as increasing GLP-2 portal blood concentrations.

10 -6(+/+) mice with oral antibiotics decreased portal blood endotoxin levels, lowered the expression of

11 pitously in urine, breath, peripheral blood, portal blood, feces, and stomach contents.

12 rr (p<.01) and was inversely correlated with portal blood flow (r2 = .20; p<.05).

13 There was also a correlation between pHi and portal blood flow (r2 = .31; p<.01).

14 Portal blood flow and hepatic oxygenation were increased

15 treatment with MS-PPOH significantly reduced portal blood flow and portal pressure compared to vehicl

16 In portal-hypertensive humans, portal blood flow and pressure increase after a meal.

17 ially prominent role in liver by controlling portal blood flow and pressure within liver sinusoids.

18 regeneration process combined with increased portal blood flow and relative outflow limitation may ha

19 Portal blood flow and renal and splenic resistive indexe

20 here perfusion studies indicated that 56% of portal blood flow bypasses the liver sinusoids.

21 Portal blood flow increased similarly after meals contai

22 ly immunological events, and the rat's lower portal blood flow induces spasm of the intrahepatic port

23 ave muscular walls susceptible to spasm, and portal blood flow is four times greater in the guinea pi

24 fibrosis is minimal, increased resistance to portal blood flow may be mediated by ET-1.

25 ino acid concentration in portal vein blood, portal blood flow rate and glucagon concentration, with

26 Portal blood flow was determined using color-flow Dopple

27 Portal blood flow was monitored and maintained near base

28 For detection of a >50% reduction in portal blood flow, a Pco2 gap of 20 torr yielded a maxim

29 8-Br-cGMP increased portal blood flow, necessitating the two approaches to g

30 In this model of maintained portal blood flow, Pico2 - Paco2 remained essentially st

31 HVPG, arterial pressure, portal blood flow, serum flavonoids (catechin and epicat

32 els without producing significant changes in portal blood flow, suggesting a reduction in hepatic vas

33 both models of cirrhosis without changes in portal blood flow, suggesting a reduction in IHVR.

34 nificant decrease of mesenteric arterial and portal blood flow, without changing portal pressure and

35 In the three periods, portal blood fructose increased from <6 to 113 +/- 14, 2

36 ach sheep, time series from both hypophyseal portal blood (HPB) and peripheral blood were evaluated i

37 ow portal vein area index and intraoperative portal blood inflow may be negative prognostic factors f

38 Measured intraoperative portal blood inflow was the only significant clinical fa

39 portant role for GAT2 in taurine uptake from portal blood into liver.

40 Amounts of secondary BAs in portal blood, liver, and bile of Cftr-/- mice were much

41 t concentrations normally found in mammalian portal blood, may be capable of promoting enhanced hepat

42 detectable bacteremia or endotoxemia in the portal blood of trauma victims casts doubt on the role o

43 thesis was tested by examining the effect of portal blood plasma and mesenteric lymph on endothelial

44 e exposed to media, sham-shock, or postshock portal blood plasma or lymph, and permeability to rhodam

45 h bypass mesenteric lymph and directly enter portal blood, reduce intestinal antigen absorption into

46 Peripheral and portal blood samples from dogs were assayed for FFA, gly

47 er, small and large intestinal biopsies, and portal blood samples were collected.

48 Peripheral and portal blood samples were obtained from 50 patients with

49 anterior pituitary hormonal release into the portal blood stream.

50 with increasing arterialization and loss of portal blood supply; therefore, recognition of HCC requi

51 811, and 2002+/-370.9 IU/L for IPoC+CATR) in portal blood, the release of cytosolic cytochrome c, and

52 s by secreting the GnRH decapeptide into the portal blood vessels of the pituitary to stimulate the p

53 l tracer utilization and reappearance in the portal blood were used to calculate intestinal amino aci

54 ation increases gut-derived endotoxin in the portal blood, which activates Kupffer cells and causes l

55 ation increases gut-derived endotoxin in the portal blood, which activates Kupffer cells through nucl

56 s of complement and activated complexes from portal blood without obvious injury or impaired function