JMJD5 belongs to the protein family of JMJD and is closely related to tumorigenesis. JMJD5 plays a carcinogenic role in some tumors, such as oral cancer, prostate cancer, breast cancer, colon cancer and atypical meningiomas, JMJD5 promotes the proliferation, migration and invasion of cancer cells. However, JMJD5 not only plays a carcinogenic role in some tumors, but also plays an anticancer role. For example, in bladder cancer, JMJD5 inhibits the metastasis of bladder cancer; in liver cancer, on the one hand JMJD5 promotes the replication of hepatitis B virus (HBV), and on the other hand it inhibits the growth of cancer cells; in lung cancer, on the one hand JNJD5 promotes the proliferation of cancer cells, and on the other hand it inhibits the metastasis of cancer cells by promoting the stabilization of microtubules. This article will focus on the mechanisms of JMJD5 in tumors, in order to provide a new target for tumor prevention and treatment.

Objective To investigate the roles of sphingosine kinasel (SPK1) in apoptosis,invasiveness and multidrug resistance of human hepatocellular carcinoma cell line BEL-FU.Methods BEL-FU cells were infected with adenovirus carrying SPK1wT gene and SPK1siRNA (Ad-H1-SPK1) gene.Their effects on biological characteristics of BEL-FU cells were evaluated by MTT,cellular SPK enzyme activity assay,Transwell Migration Technology and Western-blot,respectively.Results AdSPK1wT significantly increased SPK activity but SPK1siRNA(Ad-H1-SPK1) decreased SPK activity.Over expression of SPK1 suppressed the apoptosis induced by DMS(Dimethyl sphingosine,DMS) and enhanced migration of BEL-FU cells.The cells infected with SPK1 siRNA( Ad-H1-SPK1)significantly increased the apoptosis induced by DMS and inhibited the migration of human hepatocellular carcinoma cells.The expression of multidrug resistance-related protein (MRP1) of cells infected with SPK1siRNA (Ad-H1-SPK1) was suppressed significantly compared with the control group,while the expression of MRP1 infected with Ad- SPK1wT was enhanced.Conclusion SPK1 activity is closely associated with apoptosis、migration and multidrug resistance of human hepatocellular carcinoma cells,therefore,it may serve as a new target for HCC treatment.

Objective To investigate the effect of somatostatin on the electrophysiological changes of early diabetic rats,and to clarify its therapeutic effects on retinopathy in early diabetic rats.Methods 20 Wistar male rats, which were induced into diabetic rat models by intraperitoneal injection of streptozotocin (STZ),were randomly divided into somatostatin therapy group and model control group, 10 in each group.The rats in somatostatin therapy group were injected with somatostatin 10μg·kg-1 ·d-1,for 8 weeks;the rats in model control group received the same volume of saline.Another 10 male Wistar rats were used as normal control group.The changes of blood glucose and electroretinogram were measured, and the indicators were used for statistical analysis. Results Compared with model control group,the blood glucose was declined in somatostatin therapy group at the 8th week (P<0.05).Compared with normal control group,the latent periods of a-wave,b-wave of rod-response and max-response were significantly extended in somatostatin therapy group and model control group at the 1 st, 2nd,4th,6th,and 8th week (P<0.05).The latent periods of a-wave,b-wave of rod-response and max-response in somatostatin therapy group were shorter than those in model control group at the 8th week (P<0.05 ). Compared with model control group, the amplitude had no changes at each observation time point in somatostatin therapy group (P>0.05).Conclusion Somatostatin has a therapeutic effect on early diabetic retinopathy in rats.

Objective To evaluate the etiology and clinical features of jejunoileum bleeding.Methods Seventy-two patients admitted in 7 hospitals of Shangdong province for jejunoileum bleeding from January 1998 to December 2008 were enrolled in the study. There were 46 males and 26 females with mean age of 47 years (ranged 13-85 years). The jejunoileum bleeding was confirmed by means of endoscopy, images or surgery. The causes, diagnostic methods and major clinical manifestations were retrospectively analyzed. Results The most frequent cause of jejunoileum bleeding was tumor (42/72,58.3 %), followed by enteritis (9/72, 12.5 %), diverticulum ( 7/72, 9. 7%), angiopathy (7/72,9.7%), Crohn's disease (3/72,4.2%). Differences were significant in constituent ratio of cause of jejunoileum hemorrhage between male and female and between jejunum and ileum (P＜0.05).Hematochezia or hematochezia with abdominal pain was the first presentation. The jejunoileum bleeding in 54. 2% patients was diagnosed by laparotomy, 23. 6% by capsule endoscopy, 9.7% by selective angiography, 6.9% by small bowel series and enteroclysis, 2.8% by colonoscopy and 2.8% by push enteroscopy. The complications of jejunoileum bleeding were anemia, intestinal obstruction,peritoneal metastasis, shock, ankylenteron and intestinal perforation. Conclusions Intestinal tumor is the most common cause in jejunoileum bleeding, especially in jejunum. Whereas the enteritis,diverticulum and angiopathy were often found in ileum. The capsule endoscopy and push enteroscopy are recommended in diagnosis of jejunoileum bleeding.

The seat of human intelligence is the human cerebral cortex, which is responsible for our exceptional cognitive abilities. Identifying principles that lead to the development of the large-sized human cerebral cortex will shed light on what makes the human brain and species so special. The remarkable increase in the number of human cortical pyramidal neurons and the size of the human cerebral cortex is mainly because human cortical radial glial cells, primary neural stem cells in the cortex, generate cortical pyramidal neurons for more than 130 days, whereas the same process takes only about 7 days in mice. The molecular mechanisms underlying this difference are largely unknown. Here, we found that bone morphogenic protein 7 (BMP7) is expressed by increasing the number of cortical radial glial cells during mammalian evolution (mouse, ferret, monkey, and human). BMP7 expression in cortical radial glial cells promotes neurogenesis, inhibits gliogenesis, and thereby increases the length of the neurogenic period, whereas Sonic Hedgehog (SHH) signaling promotes cortical gliogenesis. We demonstrate that BMP7 signaling and SHH signaling mutually inhibit each other through regulation of GLI3 repressor formation. We propose that BMP7 drives the evolutionary expansion of the mammalian cortex by increasing the length of the neurogenic period.
Animals ; Mice ; Humans ; Ependymoglial Cells/metabolism* ; Hedgehog Proteins/metabolism* ; Ferrets/metabolism* ; Cerebral Cortex ; Neurogenesis ; Mammals/metabolism* ; Neuroglia/metabolism* ; Bone Morphogenetic Protein 7/metabolism*