ライフサイエンスコーパス: streptozocin

1 (-/-)) mice in which diabetes was induced by streptozocin.

2 iabetic via injection of the beta-cell toxin streptozocin.

3 Male rats were injected with two doses of streptozocin (40 mg/kg IP) on 2 consecutive days to indu

4 Diabetes was induced by injection of streptozocin (65 mg/kg, i.v.) and insulin was administer

5 gate efficacy from dose-limiting toxicity of streptozocin, a chemotherapeutic drug.

6 Rhesus macaques were rendered diabetic with streptozocin and given an intraportal infusion of approx

7 ologic management of bowel NETs; everolimus, streptozocin, and sunitinib are approved to treat pancre

8 7Bl/6 (H2b) mice were rendered diabetic with streptozocin, and they received BALB/c islet (H2d) trans

9 anging from 6% to 69% have been reported for streptozocin-based chemotherapy.

10 Autoimmune (BB-Ac) and streptozocin (BB-Sz) diabetic BB rats were recipients of

11 stine [BCNU], vincristine, flourouracil, and streptozocin [BOF-Strep]) after completion of the 125I-m

12 lets into subcutaneous tissue failed to cure streptozocin diabetes.

13 anging from 0.1 to 10 were transplanted into streptozocin diabetic male B6AF1 mice.

14 ese-enhanced MRI (MEMRI) data of control and streptozocin diabetic male Sprague-Dawley (SD) rats and

15 implanted into the epididymal fat pad(s) of streptozocin diabetic mice.

16 transport, and transporter translocation in streptozocin diabetic rats.

17 muscle glucose transport system to normal in streptozocin diabetic rats.

18 cid (PGA) polymers in subcutaneous tissue of streptozocin-diabetic mice either immediately (four in P

19 us and, in some cases, even cure diabetes in streptozocin-diabetic mice.

20 ed with 800 islets in subcutaneous tissue of streptozocin-diabetic mice.

21 devices were transplanted under the skin of Streptozocin-diabetic nude mice.

22 e levels of alpha-MPT and its metabolites in streptozocin-diabetic rats than in controls.

23 treated with fluorouracil, doxorubicin, and streptozocin (FAS) to determine the objective response r

24 Rats treated with streptozocin have reduced insulin and show hyperglycemia

25 I using the pancreatic islet beta-cell toxin streptozocin in C3H/HeN, C3H/HeJ, and C57BL/6 mouse back

26 ncapsulated or nonencapsulated) of rats with streptozocin-induced diabetes.

27 In the second experimental model, streptozocin-induced diabetic ACI rats were grafted with

28 e transplanted into the peritoneal cavity of streptozocin-induced diabetic B6AF1 mice (n = 32).

29 quate insulin replacement, we studied fasted streptozocin-induced diabetic Lewis rats either untreate

30 nsplanted under the left kidney capsule of a streptozocin-induced diabetic Lewis recipient.

31 cholangiocytes, whereas if into fat pads of streptozocin-induced diabetic mice, results in functiona

32 Retinal arterioles were isolated from streptozocin-induced diabetic pigs (2, 6, and 12 weeks o

33 s--the spontaneously diabetic BB rat and the streptozocin-induced diabetic rat--have been used to det

34 p38 activation and NCV were measured in streptozocin-induced diabetic rats treated with a p38 in

35 was significantly reduced in DRG of 12-week streptozocin-induced diabetic rats, confirming the previ

36 ar dorsal root ganglia (DRG) is deficient in streptozocin-induced diabetic rats, while expression of

37 These mice developed streptozocin-induced T1D, which was surprisingly not ass

38 significantly elevated in livers of db/db or streptozocin-induced type 1 diabetic mice.

39 greatly reduces allodynia in rats caused by streptozocin-induced type I diabetes.

40 In streptozocin-induced type I diabetic mice and geneticall

41 f glucose on growth in vivo was tested using streptozocin-induced, hyperglycaemic mice, which have si

42 Microglia activation was characterized in streptozocin-injected rats and in isolated microglial ce

43 antly higher response rate than those in the streptozocin-mitotane group (23.2% vs. 9.2%, P<0.001) an

44 the EDP-mitotane group and 2.2 months in the streptozocin-mitotane group.

45 ine EDP plus mitotane (17.1 month) than with streptozocin plus mitotane (4.7 months).

46 ntly better with EDP plus mitotane than with streptozocin plus mitotane as first-line therapy, with s

47 eter on days 3 and 4) (EDP) every 4 weeks or streptozocin (streptozotocin) (1 g on days 1 to 5 in cyc

48 mg/m2/d by continuous infusion for 4.5 days, streptozocin (STZ) 300 mg/m2 on days 1, 2, and 3 and cis

49 r 2.8 years of DBMT, diabetes was induced by streptozocin (STZ) and islets from bone marrow and kidne

50 e diabetes in AKR mice in which the low-dose streptozocin (STZ) model induces autoimmunity to the bet

51 es in peripheral somatic nerves in rats with streptozocin (STZ)-induced diabetes.

52 neic and xenogeneic islet graft rejection in streptozocin (STZ)-induced diabetic animals.

53 structure and function of the distal axon of streptozocin (STZ)-induced diabetic rats studied for 14

54 mitochondrial membrane in sensory neurons of streptozocin (STZ)-induced diabetic rats.

55 luate peripheral nerve regeneration (PNR) in streptozocin (STZ)-induced diabetic rats.

56 ize corneal functions and complications in a streptozocin (STZ)-induced rat model of type I diabetes

57 ified rat heart mitochondria from normal and streptozocin-treated diabetic rats show increased mitoch

58 Streptozocin was used to induce hyperglycemia in adult z

59 Intraperitoneal injections of streptozocin were used to initiate diabetes in healthy m

60 r weeks later, diabetes was established with streptozocin while controls were given saline.

61 er doxorubicin with fluorouracil (FU/DOX) or streptozocin with fluorouracil (FU/STZ).

62 emia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to