Microring-Assisted Coupling Between Dissimilar Waveguides

The use of microring resonators to assist in the evanescent field coupling between dissimilar waveguides is proposed and analyzed. Theoretical analysis based on the coupled mode theory and nu-merical example show that complete cross power transfers can be obtained near the microring resonances. Applications of the device include power dividers, low-power thermo-optic or electro-optic switches, and modulators.     

污泥龄对活性污泥处理微量磺胺类药物的影响

为了研究污泥龄对活性污泥系统处理微量磺胺类药物（5 μg/L）的影响,共运行了4个试验室规模（3L）的序批式活性污泥反应器（SBR）,其污泥龄分别为2、8、14、20 d。批次摇瓶试验通过设置3个工况（正常运行,加入生物抑制剂,无微生物）来讨论在1个运行周期（8 h）中对浓度惟5 μg/L磺胺甲恶唑的吸附作用、生物降解作用和挥发损失。试验结果显示对磺胺甲恶唑的总去除量为2.14 ± 0.60 μg/g SS,吸附作用占总去除量的63%;磺胺嘧啶为1.14 ± 0.63 μg/g SS,83%;磺胺间二甲氧为2.33± 0.67 μg/g SS, 35%;磺胺甲基嘧啶为2.45 ± 0.85 μg/g SS,55%;磺胺类药物的去除效果与污泥的污泥龄有着非常显著的关系（p<0.02）。通过运行加入磺胺甲恶唑（进水5 μg/L)的反应器60 d,4个反应器对磺胺甲恶唑的平均去除率分别为10%、41%、51%、58%,处理效果随着污泥龄的增加而变好,同时单位污泥去除率随着污泥龄的增加而降低,SRT=2 d的反应器由于存在大量的丝状菌,使得单位污泥对磺胺甲恶唑去除率大大高于其他3个反应器。通过分子生物学分析,发现微生物群落结构的变化不大,从而说明了影响磺胺类药物处理效果的主要因素在于更强的吸附能力,更高的污泥浓度。     

Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells

A common feature of follicular lymphoma, the most prevalent haematological malignancy in humans, is a chromosome translocation (t(14;18] that has coupled the immunoglobulin heavy chain locus to a chromosome 18 gene denoted bcl-2. By analogy with the translocated c-myc oncogene in other B-lymphoid tumours bcl-2 is a candidate oncogene, but no biological effects of bcl-2 have yet been reported. To test whether bcl-2 influences the growth of haematopoietic cells, either alone or together with a deregulated c-myc gene, we have introduced a human bcl-2 complementary DNA using a retroviral vector into bone marrow cells from either normal or E mu-myc transgenic mice, in which B-lineage cells constitutively express the c-myc gene. Bcl-2 cooperated with c-myc to promote proliferation of B-cell precursors, some of which became tumorigenic. To determine how bcl-2 expression impinges on growth factor requirements, the gene was introduced into a lymphoid and a myeloid cell line that require interleukin 3 (IL-3). In the absence of IL-3, bcl-2 promoted the survival of the infected cells but they persisted in a G0 state, rather than proliferating. These results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.     

中东

Thomson Reuters 发布的全球系列研究报告表明,以阿拉伯、伊朗、土耳其为主的中东国家的科学研究与西文国家相比落后许多.当然,也有部分中东的科学家或研究机构从事着世界一流的研究工作.事实上,论文数量及引文指标都清晰地表明,近10年中东地区的研究工作有了很大的进步,表现出了鼓舞人心的发展趋势.     

Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling

Developing tissues and growing tumours produce vascular endothelial growth factors (VEGFs), leading to the activation of the corresponding receptors in endothelial cells. The resultant angiogenic expansion of the local vasculature can promote physiological and pathological growth processes. Previous work has uncovered that the VEGF and Notch pathways are tightly linked. Signalling triggered by VEGF-A (also known as VEGF) has been shown to induce expression of the Notch ligand DLL4 in angiogenic vessels and, most prominently, in the tip of endothelial sprouts. DLL4 activates Notch in adjacent cells, which suppresses the expression of VEGF receptors and thereby restrains endothelial sprouting and proliferation. Here we show, by using inducible loss-of-function genetics in combination with inhibitors in vivo, that DLL4 protein expression in retinal tip cells is only weakly modulated by VEGFR2 signalling. Surprisingly, Notch inhibition also had no significant impact on VEGFR2 expression and induced deregulated endothelial sprouting and proliferation even in the absence of VEGFR2, which is the most important VEGF-A receptor and is considered to be indispensable for these processes. By contrast, VEGFR3, the main receptor for VEGF-C, was strongly modulated by Notch. VEGFR3 kinase-activity inhibitors but not ligand-blocking antibodies suppressed the sprouting of endothelial cells that had low Notch signalling activity. Our results establish that VEGFR2 and VEGFR3 are regulated in a highly differential manner by Notch. We propose that successful anti-angiogenic targeting of these receptors and their ligands will strongly depend on the status of endothelial Notch signalling.     

The DNA sequence, annotation and analysis of human chromosome 3

After the completion of a draft human genome sequence, the International Human Genome Sequencing Consortium has proceeded to finish and annotate each of the 24 chromosomes comprising the human genome. Here we describe the sequencing and analysis of human chromosome 3, one of the largest human chromosomes. Chromosome 3 comprises just four contigs, one of which currently represents the longest unbroken stretch of finished DNA sequence known so far. The chromosome is remarkable in having the lowest rate of segmental duplication in the genome. It also includes a chemokine receptor gene cluster as well as numerous loci involved in multiple human cancers such as the gene encoding FHIT, which contains the most common constitutive fragile site in the genome, FRA3B. Using genomic sequence from chimpanzee and rhesus macaque, we were able to characterize the breakpoints defining a large pericentric inversion that occurred some time after the split of Homininae from Ponginae, and propose an evolutionary history of the inversion.     

Murine T lymphomas with retroviral inserts in the chromosomal 15 locus for plasmacytoma variant translocations

The frequent trisomy of murine chromosome 15 in T lymphomas suggests that it bears one or more genes conducive to T-cell neoplasia. One such gene seems to be c-myc, the oncogene frequently activated in B-lymphoid tumours either by retroviral insertion, as in the avian bursal lymphomas, or by a translocation to the immunoglobulin heavy-chain locus, as in the predominant t(12; 15) of murine plasmacytomas and the analogous t(14; 8) of human Burkitt lymphomas. The c-myc gene was strongly implicated in T-cell neoplasia when 15-25% of T lymphomas arising in AKR mice, a strain prone to leukaemia, were found to have retroviral inserts near c-myc. Proviruses near c-myc were also found in several T lymphomas induced by murine leukaemia viruses (MuLV) in both mice and rats, but many of the rat thymomas bear an insert instead at one of several other common sites, at least two of which have murine homologues on chromosome 15. We show here that some murine T lymphomas contain proviral inserts in the recently identified chromosome 15 locus for plasmacytoma variant (6; 15) translocations, which we have denoted pvt-1. Although 6; 15 breakpoints map cytogenetically to the same chromosome band as c-myc, the alterations of pvt-1 in tumours occur at least 72 kilobases (kb) from the c-myc promoters. The insertions in T lymphomas suggest that an altered pvt-1 locus is conducive to neoplasia in T cells as well as B cells, possibly via long-range effects on c-myc expression.     

Proxy evidence for an El Niño-like response to volcanic forcing

Past studies have suggested a statistical connection between explosive volcanic eruptions and subsequent El Ni?o climate events. This connection, however, has remained controversial. Here we present support for a response of the El Ni?o/Southern Oscillation (ENSO) phenomenon to forcing from explosive volcanism by using two different palaeoclimate reconstructions of El Ni?o activity and two independent, proxy-based chronologies of explosive volcanic activity from ad 1649 to the present. We demonstrate a significant, multi-year, El Ni?o-like response to explosive tropical volcanic forcing over the past several centuries. The results imply roughly a doubling of the probability of an El Ni?o event occurring in the winter following a volcanic eruption. Our empirical findings shed light on how the tropical Pacific ocean-atmosphere system may respond to exogenous (both natural and anthropogenic) radiative forcing.     

Comparative genomics of the neglected human malaria parasite Plasmodium vivax

The human malaria parasite Plasmodium vivax is responsible for 25-40% of the approximately 515 million annual cases of malaria worldwide. Although seldom fatal, the parasite elicits severe and incapacitating clinical symptoms and often causes relapses months after a primary infection has cleared. Despite its importance as a major human pathogen, P. vivax is little studied because it cannot be propagated continuously in the laboratory except in non-human primates. We sequenced the genome of P. vivax to shed light on its distinctive biological features, and as a means to drive development of new drugs and vaccines. Here we describe the synteny and isochore structure of P. vivax chromosomes, and show that the parasite resembles other malaria parasites in gene content and metabolic potential, but possesses novel gene families and potential alternative invasion pathways not recognized previously. Completion of the P. vivax genome provides the scientific community with a valuable resource that can be used to advance investigation into this neglected species.