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This study is to investigate changes of tolerance to ischemia-reperfusion (IR) injury and protection of ischemic preconditioning (IPC) of type 1 diabetes rat heart. Type 1 diabetes rat model was made by single injection of streptozotocin and divided into 4 wk (D-4w) group and 8wk (D-8w) group randomly. The two groups were further assigned to six teams: D-4w-con, D-4w-IR, D-4w-IPC, D-8w-con, D-8w-IR and D-8w-IPC team. Normal rats were correspondingly divided into N-4w-con, N-4w-IR, N-4w-IPC, N-8w-con, N-8w-IR and N-8w-IPC team. Heart function, myocardial infarct size, release of lactate dehydrogenase (LDH) and creatine kinase (CK) were detected. And injury increment rate, injury rate and protection rate were calculated. Ultrastructure of cardiomyocyte was observed by electron microscope. The myocardial injury increment rate, infarct sizes in D-con group were all significantly higher than those in N-con rat group, and the degree of injury in D-8w rat hearts was exacerbated compared to D-4w rat hearts. The myocardial injury rate and the injury of cardiomyocyte ultrastructure in D-4w-IR team were lower compared with N-4w-IR group. Compared with D-4w-IR team, IPC decreased infarct sizes in D-4w-IPC group, but its protection rate was lower than that in N-4w-IPC team. Infarct sizes in D-8w-IPC team had no significance with those in D-8w-IR team. The fundament cardiac function of type 1 diabetes rat heart was weakened. Diabetes self could induce heart injury, which could aggravate along with time. The tolerance of 4w type 1 diabetes rat to IR injury is stronger but the protection of IPC was weaker compared to normal rat. The protection of IPC disappears in D-8w group.

To investigate the effect of interferon regulatory factors (IRFs) on neointimal formation after vascular injury in the mouse, and its possible mechanism.Vascular injury was induced by polyethylene cuff placement around the left femoral artery of IRF-1-deficient mice and C57BL/6J mice. The mRNA expressions of IRF-1, IRF-2, angiotensin II type 2 (AT2) receptor, interleukin-1 beta converting enzyme (ICE), inducible nitric oxide synthase (iNOS) were detected by RT-PCR and immunohistochemical staining.Neointimal formation after vascular injury was significantly greater in IRF-1-deficient mice than that in C57BL/6J mice (P0.05). In contrast, TUNEL-positive nuclei to total nuclei in the neointima and media in vascular smooth muscle cell (VSMC) in the injured artery significantly attenuated in IRF-1-deficient mice compared to C57BL/6J mice (P0.05). The expressions of AT2 receptor as well as pro-apoptotic genes such as ICE and iNOS in C57BL/6J mice were up-regulated in response to vascular injury, but this upregulation was attenuated in IRF-1-deficient mice.Our results suggest that IRF-1 induces VSMC apoptosis and inhibits neointimal formation after vascular injury at least partly due to the upregulation of AT2 receptor, ICE and iNOS expressions. These results indicate that IRF-1 exerts an inhibitory effect on neointimal formation through the induction of apoptosis in VSMCs.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org/10.1016/j.biomag.2010.09.004. The duplicate article has therefore been withdrawn.

Prostate cancer ( PCa) is an important genitourinary malignancy with increasing morbidity and mortality. Glutathione S-transferase P1 ( GSTP1) , as a phrase- II enzyme, has an important role in the activation and detoxification of carcinogens. There is a close association between GSTP1 gene polymorphisms and the risk of Pca. GSTP1 CpG island hypermethylation can reliably distinguish Pca from benign prostatic hyperplasia( BPH) and promises to be an important molecular marker for the diagnosis of Pca. This paper summarizes the association of GSTP1 with the diagnosis and risk of Pca.