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BACKGROUND The study was conducted to investigate the short-term complications and prognostic factors in patients with esophagogastric junction adenocarcinoma (EGJA). METHODS This retrospective study included 110 EGJA patients who underwent surgery from January 2010 to November 2012 at The First Affiliated Hospital of BengBu Medical College. The overall survival and short-term complications were analyzed according to the patients' clinical characteristics. RESULTS The incidence of postoperative cardiopulmonary complications was significantly higher in patients with preoperative cardiopulmonary disease or elderly patients (P < 0.05). Four cases of upper margin cancer residue were detected using the abdominal approach and three using the thoracic approach, which indicated that the cancer residue margin was related to surgical approach. The overall five-year survival rate was 34.3% and statistically differed according to pathological stage and en block resection (Pall < 0.05). Cox regression analysis showed that lymph node metastasis (P < 0.05) and the extent of tumor invasion (P < 0.05) were independent prognostic factors. CONCLUSION Elderly patients with preoperative cardiopulmonary disease had an increased risk of developing postoperative cardiopulmonary complications. Lymph node status and depth of tumor invasion were independent factors related to patient prognosis.

Triple negative breast cancer lacking estrogen receptor (ER), progesterone receptor and Her2 account for account for the majority of the breast cancer deaths, due to the lack of specific gene targeted therapy. Our current study aimed to investigate the role of miR-544 in triple negative breast cancer. Endogenous levels of miR-544 were significantly lower in breast cancer cell lines than in human breast non-tumorigenic and mammary epithelial cell lines. We found that miR-544 directly targeted the 3′-untranslated region (UTR) on both Bcl6 and Stat3 mRNAs, and overexpression of miR-544 in triple negative breast cancer cells significantly down-regulated expressions of Bcl6 and Stat3, which in turn severely inhibited cancer cell proliferation, migration and invasion in vitro. Employing a mouse xenograft model to examine the in vivo function of miR-544, we found that expression of miR-544 significantly repressed the growth of xenograft tumors. Our current study reported miR-544 as a tumor-suppressor microRNA particularly in triple negative breast cancer. Our data supported the role of miR-544 as a potential biomarker in developing gene targeted therapies in the clinical treatment of triple negative breast cancer.

The small (SK3) and intermediate (IK1) conductance calcium-activated potassium channels could have key roles in the endothelium-dependent hyperpolarization factor pathway, which is believed to contribute to normal penile erection function. We aimed to investigate the expression of SK3 and IK1 in diabetic rodents. The experimental diabetes model was induced in 8-week-old male Sprague–Dawley rats (250–300 g) by a single administration of streptozotocin. Both the diabetes mellitus group (DM group, n = 20) and the control group (NDM group, n = 10) were injected with a low dose of apomorphine to allow for the measurement and comparison of the corresponding penile erections. The mRNA and protein expression levels of SK3 and IK1 were measured by reverse transcription polymerase chain reaction and western blot, respectively. Erectile function was significantly decreased in the DM group compared with control group (P < 0.05). The mRNA and protein expression levels of SK3 and IK1 were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.05). Diabetes inhibits mRNA and protein expression of both SK3 and IK1 in the cavernous tissue of diabetic rats. This could play a key role in the development of erectile dysfunction in diabetic rats.

Our aim was to investigate the mechanisms of early protection by ischemic preconditioning (IPC) of transplanted rat kidneys.Thirty-six male donor and recipient Sprague-Dawley (SD) rats were randomly divided into 3 groups: sham-operated (A), transplantation (B), and IPC treatment (C) groups. Group A underwent exploratory laparotomy, group B received orthotopic transplantation, and group C, 15 minutes of ischemia followed by 10 minutes of reperfusion before transplantation. We measured the serum creatinine (SCr), blood urea nitrogen (BUN), and degree of kidney graft ischemic/reperfusion injury (IRI) by tumor necrosis factor-alpha (TNF-alpha) IkappaB kinase beta (IKK-beta) nuclear factor-kappa beta (NF-kappabeta) p65 subunit mRNA expressions.The SCr and BUN levels in groups C and B were higher than those in the sham-operated group (P.01), without a significant difference between groups C and B at 24 hours after transplantation (P.05). The degree of renal graft tubular injury in group C was significantly lower than that in group B (P.01). TNF-alpha transcription levels at 24 hours after transplantation were significantly lower compared with the non-IPC group (P.01). However, we failed to note a significant difference in IKK-beta or p65 mRNA expressions between groups C and B (P.05).One cycle of preconditioning (15 min/10 min) attenuated renal graft IRI in the early phase. The inhibiting effects on TNF-alpha and the positive feedback signaling of TNF-alpha/NF-KB pathways may play important roles in renal graft protection.