具有三个CM公共值的亚纯函数的唯一性

本文指出仪洪勋和Brosch G在具有三个判别的CM公共值的亚纯函数的唯一性定理中,关于对数函数的导数是整函数的推导,可以用指数函数求导的方法来证明.改进了仪洪勋和Brosch G关于重值与唯一性定理.     

An elaborate pathway required for Ras-mediated epigenetic silencing

The conversion of a normal cell to a cancer cell occurs in several steps and typically involves the activation of oncogenes and the inactivation of tumour suppressor and pro-apoptotic genes. In many instances, inactivation of genes critical for cancer development occurs by epigenetic silencing, often involving hypermethylation of CpG-rich promoter regions. It remains to be determined whether silencing occurs by random acquisition of epigenetic marks that confer a selective growth advantage or through a specific pathway initiated by an oncogene. Here we perform a genome-wide RNA interference (RNAi) screen in K-ras-transformed NIH 3T3 cells and identify 28 genes required for Ras-mediated epigenetic silencing of the pro-apoptotic Fas gene. At least nine of these RESEs (Ras epigenetic silencing effectors), including the DNA methyltransferase DNMT1, are directly associated with specific regions of the Fas promoter in K-ras-transformed NIH 3T3 cells but not in untransformed NIH 3T3 cells. RNAi-mediated knockdown of any of the 28 RESEs results in failure to recruit DNMT1 to the Fas promoter, loss of Fas promoter hypermethylation, and derepression of Fas expression. Analysis of five other epigenetically repressed genes indicates that Ras directs the silencing of multiple unrelated genes through a largely common pathway. Last, we show that nine RESEs are required for anchorage-independent growth and tumorigenicity of K-ras-transformed NIH 3T3 cells; these nine genes have not previously been implicated in transformation by Ras. Our results show that Ras-mediated epigenetic silencing occurs through a specific, complex, pathway involving components that are required for maintenance of a fully transformed phenotype.     

Pain relief by xenograft of subarachnoid microencapsulated bovine chromaffin cells in cancer patients

The bovine chromaffin cells (BCC) implanted into the subarachnoid space can release analgesic substances such as opioid peptides and ealeeholamines. Clinical trials have provided the evidence that the implantation of polyvinylchloride ( PVC) hollow fiber encapsulated BCC by surgery can relief the pain in cancer patients. In the present study, BCC were encapsulated in alginate-polylysine-alginate (APA) mieroencapsules which protect the grafting of xenogeneic cells from host immune system anil allow BCC to function effectively without using immunosuppression agents. The microencapsulated BCCs (5 X 106~—8 X 106) were transplanted into the subarachnoid space I^._s of 17 patients who suffered from chronic cancer pain and had to have long-term administration of analgesics. The pain scores and morphine intake tesl showed that microencapsulated BCC graft totally stopped the chronic pain in three of the patients over a period of 200 days and in the other three over a period of 100 days. The resulls suggesl thai APA microencapsulated BCC xenotransplantation could be a novel alternative approach to managing pain of cancer patients.     

A novel nuclear export activity in HIV-1 matrix protein required for viral replication

An important aspect of the pathophysiology of human immunodeficiency virus type-1 (HIV-1) infection is the ability of the virus to replicate in non-dividing cells. HIV-1 matrix (MA), the amino-terminal domain of the Pr55 gag polyprotein (Pr55), bears a nuclear localization signal that promotes localization of the viral preintegration complex to the nucleus of non-dividing cells following virus entry. However, late during infection, MA, as part of Pr55, directs unspliced viral RNA to the plasma membrane, the site of virus assembly. How MA can mediate these two opposing targeting functions is not understood. Here we demonstrate that MA has a previously undescribed nuclear export activity. Although MA lacks the canonical leucine-rich nuclear export signal, nuclear export is mediated through the conserved Crm1p pathway and functions in both mammalian cells and yeast. A mutation that disrupts the MA nuclear export signal (MA-M4) mislocalizes Pr55 and genomic viral RNA to the nucleus, thereby severely impairing viral replication. Furthermore, we show that MA-M4 can act in a dominant-negative fashion to mislocalize genomic viral RNA even in the presence of wild-type MA. We conclude that the MA nuclear export signal is required to counteract the MA nuclear localization signal, thus ensuring the cytoplasmic availability of the components required for virion assembly.