ライフサイエンスコーパス: AKR mice

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1 insulin and are more insulin sensitive than AKR mice.

2 SWR mice but not in the gallstone-resistant AKR mice.

3 ted in either C57BL/6 or DBA/2 (and possibly AKR) mice.

4 development in B6 Fog2-/+ or Gata4(ki)/+ XY(AKR) mice.

5 Compared with adipose tissue of AKR mice, adipose tissue of B6 mice contained about thre

6 Lymph node cells from susceptible C3H and AKR mice also had increased ability to lyse YAC-1 target

7 ior horn neurons of immunosuppressed C58 and AKR mice and cause paralytic disease (age-dependent poli

8 errin saturation, with the highest values in AKR mice and the lowest values in C3H mice.

9 Furthermore, DBA/2J (D2) Fog2-/+ XY(AKR) mice and (B6 x D2)F1 hybrid Gata4(ki)/+ XY(AKR) mic

10 e B6 mice are more glucose intolerant, obese AKR mice are more insulin resistant.

11 SAMP mice showed greater ABL compared with AKR mice by 12 weeks of age, with maximal differences ob

12 s development was restored in B6 T(Orl)/+ XY(AKR) mice carrying a Mus musculus Sry transgene.

13 everely impaired in these mice compared with AKR mice (controls).

14 mice develop ovaries, and B6 Gata4(ki)/+ XY(AKR) mice develop ovaries and ovotestes (gonads containi

15 the AKR Y chromosome (Y(AKR)), B6 Fog2-/+ XY(AKR) mice develop ovaries, and B6 Gata4(ki)/+ XY(AKR) mi

16 ) mice and (B6 x D2)F1 hybrid Gata4(ki)/+ XY(AKR) mice develop testes.

17 C57BL/6 and AKR mice developed a chronic disease course resulting in

18 AKR mice developed obesity and a prestage of metabolic s

19 reputial gland homogenates demonstrated that AKR mice had an ACAT protein with a lower molecular mass

20 on the prevention of autoimmune diabetes in AKR mice in which the low-dose streptozocin (STZ) model

21 When injected into neonatal AKR mice, MCF ProEn was more pathogenic than the parenta

22 Upon inoculation into AKR mice, mink cell focus-forming murine leukemia virus

23 n of leptin to peripherally leptin-resistant AKR mice on 45% fat diet resulted in a robust response t

24 erage video intensity, in SAMP vs uninflamed AKR mice (P < .001) or SAMP given nonspecific MB (P < .0

25 In AKR mice, peripheral leptin significantly decreased food

26 sk whether adrenocortical lipid depletion in AKR mice results from an Acact mutation.

27 normal testis development in B6 T(Orl)/+ XY(AKR) mice results from a biologically insufficient level

28 Analysis of Acact cDNA from AKR mice revealed a deletion of the first coding exon an

29 sis of mice from crosses between C57BL/6 and AKR mice should allow the mapping and subsequent identif

30 re more PGS clusters in uninfected C57BL and AKR mice than in uninfected SAMP8 and SAMR1 mice.

31 e gene led to hepatic iron levels in Hfe -/- AKR mice that were 2.5 or 3.6 times higher than those of

32 We bred SAMP1/Fc to disease-resistant AKR mice to identify additional susceptibility genes tha

33 t on alloengraftment, sublethally irradiated AKR mice underwent transplantation with TCD B6 BM plus l

34 Obesity-susceptible AKR mice were fed with high-fat diet (HFD) or normal low

35 AKR mice were sensitized with conalbumin followed by two

36 inal nematode Trichuris muris in susceptible AKR mice, which mount a Th1 response, is associated with

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