ライフサイエンスコーパス: turpentine

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1 mation induced by intramuscular injection of turpentine.

2 t mice had a reduced acute phase response to turpentine.

3 on induced by the intramuscular injection of turpentine (50 microl/100 gm body weight) also produced

4 Oleoresin is a roughly equal mixture of turpentine (85% monoterpenes [C10] and 15% sesquiterpene

5 t of the systemic acute phase response after turpentine administration between wild-type and ICE -/-

6 In contrast to CCl(4)-induced liver damage, turpentine alone, whether administered as a single dose

7 etiologies including chemical inflammation (turpentine) and cancer (breast carcinoma).

8 ter bladder inflammation with intravesicular turpentine; and (3) after bilateral hypogastric neurecto

9 of mature IL-1 beta produced in response to turpentine did not differ between wild-type and ICE -/-

10 3 receptor KO mice subcutaneous injection of turpentine did not induce fever.

11 mpanies the acute phase response elicited by turpentine exposure or upon acute exposure to either non

12 The turpentine fraction of the oleoresin is a complex mixtur

13 The turpentine fraction of the oleoresin was shown to contai

14 acellular Zip14 epitope, showed both LPS and turpentine increased abundance of Zip14 at the plasma me

15 In mice, treatment with IL-6 or turpentine increased hepcidin expression and reduced ser

16 port we extended our studies and showed that turpentine induced, in a time-dependent manner, expressi

17 The uptake of scVEGF in turpentine-induced abscesses was specific and directly r

18 and ferrous sulphate (FeSO4) ameliorated the turpentine-induced AI in mice (indicated by increased ha

19 We have previously shown that although a turpentine-induced APR is not fibrogenic per se, it enha

20 screened for regulation in mouse liver after turpentine-induced inflammation and LPS administration.

21 and IL-6-induced HPA axis activation during turpentine-induced inflammation.

22 ssociated with lipopolysaccharide-induced or turpentine-induced inflammation.

23 Using the turpentine-induced model of unilateral orofacial inflamm

24 /- mice in two models of local inflammation, turpentine-induced tissue damage and zymosan-induced per

25 Our results demonstrate that in turpentine-induced tissue necrosis, precursor IL-1 beta

26 hypozincemia or the induction of Zip14 with turpentine inflammation.

27 eived a 20-microL intramuscular injection of turpentine into the right thigh.

28 uscular Staphylococcus aureus infections and turpentine oil-induced muscular inflammations, and (c) b

29 er thinner (OR = 3.5; 95% CI: 1.6, 7.8), and turpentine (OR = 10.4; 95% CI: 2.4, 44.8) were associate

30 aride, the locally acting inflammatory agent turpentine, or selected inflammatory cytokines.

31 P transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in

32 ammation model induced by local injection of turpentine to evaluate vascular leakage.

33 ek-old male mice were 48% larger (P<0.02) in turpentine-treated mice and 34% larger (P<0.05) in untre

34 Chronic turpentine treatment led to microcytic anemia, which was

35 Turpentine treatment per se did not affect the extent of

36 y due to single doses of LPS, poly(I:C), and turpentine, which is used to model chronic inflammatory

37 y due to single doses of LPS, poly(I:C), and turpentine, which is used to model chronic inflammatory

38 8 sesquiterpenes that represent 12.5% of the turpentine, with the monoterpenes comprising the remaind

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