图书馆环境与读者健康

阐述了图书馆环境对读者生理及心理健康方面的影响,指出构建和谐的绿色图书馆是一项长期的工作任务,需要人们转变思想观念,同时争取社会各界的积极支持和广泛参与。     

A sparse algorithm for adaptive pruning least square support vector regression machine based on globalrepresentative point ranking

Least square support vector regression(LSSVR)is a method for function approximation,whose solutions are typically non-sparse,which limits its application especially in some occasions of fast prediction.In this paper,a sparse algorithm for adaptive pruning LSSVR algorithm based on global representative point ranking(GRPR-AP-LSSVR)is proposed.At first,the global representative point ranking(GRPR)algorithm is given,and relevant data analysis experiment is implemented which depicts the importance ranking of data points.Furthermore,the pruning strategy of removing two samples in the decremental learning procedure is designed to accelerate the training speed and ensure the sparsity.The removed data points are utilized to test the temporary learning model which ensures the regression accuracy.Finally,the proposed algorithm is verified on artificial datasets and UCI regression datasets,and experimental results indicate that,compared with several benchmark algorithms,the GRPR-AP-LSSVR algorithm has excellent sparsity and prediction speed without impairing the generalization performance.     

协同多点传输中迫零预编码和天线选择技术

MIMO无线传输技术极大地提高了系统的容量,在实际通信系统中,整个网络是一个干扰受限的系统,小区间干扰对MIMO系统传输的影响是显著的,每个相邻小区的基站天线都可以看成一个干扰源．由于基站端数据处理能力的提升和回程容量的增加,多个小区协同多点传输技术引起了人们的广泛关注．目前的大部分工作都是集中于研究系统的容量（吞吐量）,而在实际系统中,每个用户的接收等效信噪比（即公平性）对系统的性能如误帧率等有重要的影响．对于每个用户为单天线的情形,研究了总功率受限和每天线功率受限下采用迫零预编码的系统容量和公平性．对两种功率约束条件下的公平性进行了分析,得到了公平性算法的闭式表达式．当每个用户为多天线的情形,为了降低计算的复杂度,引入了信道范数最大的接收天线选择算法,把每个用户为多天线的情形转化成等效的每个用户单天线情形,推导的每用户为单天线的公平性算法仍然适用．仿真结果显示,采用迫零预编码的多小区协作可以使系统性能显著提升．在相同的迫零预编码下,不同的功率分配策略对系统的容量和公平性有显著的影响．和用户为单天线相比,采用天线选择算法可以提升系统的容量和公平性．考虑了用户公平性时的吞吐量和最大系统吞吐量之间的折中关系,并给出了仿真结果．     

Protein arginine deiminase 4: a target for an epigenetic cancer therapy

The recent approvals of anticancer therapeutic agents targeting the histone deacetylases and DNA methyltransferases have highlighted the important role that epigenetics plays in human diseases, and suggested that the factors controlling gene expression are novel drug targets. Protein arginine deiminase 4 (PAD4) is one such target because its effects on gene expression parallel those observed for the histone deacetylases. We demonstrated that F- and Cl-amidine, two potent PAD4 inhibitors, display micromolar cytotoxic effects towards several cancerous cell lines (HL-60, MCF7 and HT-29); no effect was observed in noncancerous lines (NIH 3T3 and HL-60 granulocytes). These compounds also induced the differentiation of HL-60 and HT29 cells. Finally, these compounds synergistically potentiated the cell killing effects of doxorubicin. Taken together, these findings suggest PAD4 inhibition as a novel epigenetic approach for the treatment of cancer, and suggest that F- and Cl-amidine are candidate therapeutic agents for this disease.     

Cdk5 targets active Src for ubiquitin-dependent degradation by phosphorylating Src(S75)

The non-receptor tyrosine kinase Src is a critical regulator of cytoskeletal contraction, cell adhesion, and migration. In normal cells, Src activity is stringently controlled by Csk-dependent phosphorylation of Src(Y530), and by Cullin-5-dependent ubiquitinylation, which affects active Src(pY419) exclusively, leading to its degradation by the proteosome. Previous work has shown that Src activity is also limited by Cdk5, a proline-directed kinase, which has been shown to phosphorylate Src(S75). Here we show that this phosphorylation promotes the ubiquitin-dependent degradation of Src, thus restricting the availability of active Src. We demonstrate that Src(S75) phosphorylation occurs in vivo in epithelial cells, and like ubiquitinylation, is associated only with active Src. Preventing Cdk5-dependent phosphorylation of Src(S75), by site-specific mutation of S75 or by Cdk5 inhibition or suppression, increases Src(Y419) phosphorylation and kinase activity, resulting in Src-dependent cytoskeletal changes. In transfected cells, ubiquitinylation of Src(S75A) is about 35% that of wild-type Src-V5, and its half-life is approximately 2.5-fold greater. Cdk5 suppression leads to a comparable decrease in the ubiquitinylation of endogenous Src and a similar increase in Src stability. Together, these findings demonstrate that Cdk5-dependent phosphorylation of Src(S75) is a physiologically significant mechanism of regulating intracellular Src activity.     

Identification of a bacterial inhibitor against g-type lysozyme

Lysozymes are antibacterial effectors of the innate immune system in animals that hydrolyze peptidoglycan. Bacteria have evolved protective mechanisms that contribute to lysozyme tolerance such as the production of lysozyme inhibitors, but only inhibitors of chicken (c-) and invertebrate (i-) type lysozyme have been identified. We here report the discovery of a novel Escherichia coli inhibitor specific for goose (g-) type lysozymes, which we designate PliG (periplasmic lysozyme inhibitor of g-type lysozyme). Although it does not inhibit c- or i-type lysozymes, PliG shares a structural sequence motif with the previously described PliI and MliC/PliC lysozyme inhibitor families, suggesting a common ancestry and mode of action. Deletion of pliG increased the sensitivity of E. coli to g-type lysozyme. The existence of inhibitors against all major types of animal lysozyme and their contribution to lysozyme tolerance suggest that lysozyme inhibitors may play a role in bacterial interactions with animal hosts.     

Protecting the boundary: the sentinel role of host defense peptides in the skin

The skin is our primary shield against microbial pathogens and has evolved innate and adaptive strategies to enhance immunity in response to injury or microbial insult. The study of antimicrobial peptide (AMP) production in mammalian skin has revealed several of the elegant strategies that AMPs use to prevent infection. AMPs are inducible by both infection and injury and protect the host by directly killing pathogens and/or acting as multifunctional effector molecules that trigger cellular responses to aid in the anti-infective and repair response. Depending on the specific AMP, these molecules can influence cytokine production, cell migration, cell proliferation, differentiation, angiogenesis and wound healing. Abnormal production of AMPs has been associated with the pathogenesis of several cutaneous diseases and plays a role in determining a patient’s susceptibility to pathogens. This review will discuss current research on the regulation and function of AMPs in the skin and in skin disorders.     

Histone deacetylase inhibitors augment doxorubicin-induced DNA damage in cardiomyocytes

Histone deacetylase inhibitors have emerged as a new class of anticancer therapeutics with suberoylanilide hydroxamic acid (Vorinostat) and depsipeptide (Romidepsin) already being approved for clinical use. Numerous studies have identified that histone deacetylase inhibitors will be most effective in the clinic when used in combination with conventional cancer therapies such as ionizing radiation and chemotherapeutic agents. One promising combination, particularly for hematologic malignancies, involves the use of histone deacetylase inhibitors with the anthracycline, doxorubicin. However, we previously identified that trichostatin A can potentiate doxorubicin-induced hypertrophy, the dose-limiting side-effect of the anthracycline, in cardiac myocytes. Here we have the extended the earlier studies and evaluated the effects of combinations of the histone deacetylase inhibitors, trichostatin A, valproic acid and sodium butyrate on doxorubicin-induced DNA double-strand breaks in cardiomyocytes. Using γH2AX as a molecular marker for the DNA lesions, we identified that all of the broad-spectrum histone deacetylase inhibitors tested augment doxorubicin-induced DNA damage. Furthermore, it is evident from the fluorescence photomicrographs of stained nuclei that the histone deacetylase inhibitors also augment doxorubicin-induced hypertrophy. These observations highlight the importance of investigating potential side-effects, in relevant model systems, which may be associated with emerging combination therapies for cancer.