CDMA系统及其降噪的实验方法：系统设计到硬件测试所通过的超大规模集成电路

本书介绍了意大利比萨大学一个团队的开发项目——CDMA移动终端接受器．以及从中获取的经验，为通信理论到VLSI实现建立了一座桥梁，呈现了从最初系统设计到最终硬件测试所需要的电信和电子相关知识，主要目的是为通信电路的设计提供理论和实践上的支持。书中介绍的知识和技术可以运用到更一般的无线调制解调器的构架设计和实现。     

Explaining Leibniz equivalence as difference of non-inertial appearances: Dis-solution of the Hole Argument and physical individuation of point-events

“The last remnant of physical objectivity of space–time” is disclosed in the case of a continuous family of spatially non-compact models of general relativity (GR). The physical individuation of point-events is furnished by the autonomous degrees of freedom of the gravitational field (viz., the Dirac observables) which represent—as it were—the ontic part of the metric field. The physical role of the epistemic part (viz. the gauge variables) is likewise clarified as embodying the unavoidable non-inertial aspects of GR. At the end the philosophical import of the Hole Argument is substantially weakened and in fact the Argument itself dissolved, while a specific four-dimensional holistic and structuralist view of space–time (called point-structuralism) emerges, including elements common to the tradition of both substantivalism and relationism. The observables of our models undergo real temporal change: this gives new evidence to the fact that statements like the frozen-time character of evolution, as other ontological claims about GR, are model dependent.     

Gain control by layer six in cortical circuits of vision

After entering the cerebral cortex, sensory information spreads through six different horizontal neuronal layers that are interconnected by vertical axonal projections. It is believed that through these projections layers can influence each other's response to sensory stimuli, but the specific role that each layer has in cortical processing is still poorly understood. Here we show that layer six in the primary visual cortex of the mouse has a crucial role in controlling the gain of visually evoked activity in neurons of the upper layers without changing their tuning to orientation. This gain modulation results from the coordinated action of layer six intracortical projections to superficial layers and deep projections to the thalamus, with a substantial role of the intracortical circuit. This study establishes layer six as a major mediator of cortical gain modulation and suggests that it could be a node through which convergent inputs from several brain areas can regulate the earliest steps of cortical visual processing.     

Description of the aberrant Leptopilina lasallei n. sp., with an updated phylogeny of Leptopilina Förster (Hymenoptera: Figitidae: Eucoilinae)

ABSTRACT

In the search for native Asian parasitoids of Drosophila suzukii, the notorious spotted-wing Drosophila (SWD), an odd new species of Eucoilinae was discovered. Leptopilina lasallei sp. nov. is herein described and diagnosed relative to other eucoilines associated with drosophilid hosts. Morphologically, L. lasallei is somewhat aberrant within Leptopilina; phylogenetically, L. lasallei is sister group to the core Leptopilina. In the process of investigating L. lasallei, a de novo molecular phylogeny of Leptopilina was generated and is included here. The integrated approach used for the characterisation of L. lasallei, and the resulting phylogeny of Leptopilina, produced data useful to select parasitoid species for SWD biological control.http://www.zoobank.org/urn:lsid:zoobank.org:act:402D504A-4616-4524-85D7-1C13A6276F06 http://www.zoobank.org/urn:lsid:zoobank.org:act:402D504A-4616-4524-85D7-1C13A6276F06     

Exome sequencing identifies ACAD9 mutations as a cause of complex I deficiency

An isolated defect of respiratory chain complex I activity is a frequent biochemical abnormality in mitochondrial disorders. Despite intensive investigation in recent years, in most instances, the molecular basis underpinning complex I defects remains unknown. We report whole-exome sequencing of a single individual with severe, isolated complex I deficiency. This analysis, followed by filtering with a prioritization of mitochondrial proteins, led us to identify compound heterozygous mutations in ACAD9, which encodes a poorly understood member of the mitochondrial acyl-CoA dehydrogenase protein family. We demonstrated the pathogenic role of the ACAD9 variants by the correction of the complex I defect on expression of the wildtype ACAD9 protein in fibroblasts derived from affected individuals. ACAD9 screening of 120 additional complex I-defective index cases led us to identify two additional unrelated cases and a total of five pathogenic ACAD9 alleles.     

Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumor

Mutations in the gene encoding the retinoblastoma tumor suppressor predispose humans and mice to tumor development. Here we have assessed the effect of Nras loss on tumor development in Rb1 heterozygous mice. Loss of one or two Nras alleles is shown to significantly reduce the severity of pituitary tumors arising in Rb1(+/-) animals by enhancing their differentiation. By contrast, C-cell thyroid adenomas occurring in Rb1(+/-) mice progress to metastatic medullary carcinomas after loss of Nras. In Rb1(+/-)Nras(+/-) animals, distant medullary thyroid carcinoma metastases are associated with loss of the remaining wild-type Nras allele. Loss of Nras in Rb1-deficient C cells results in elevated Ras homolog family A (RhoA) activity, and this is causally linked to the invasiveness and metastatic behavior of these cells. These findings suggest that the loss of the proto-oncogene Nras in certain cellular contexts can promote malignant tumor progression.     

Il Problema delle Tangenti nella „Géométrie“ di Descartes

Presentato da A. P. Youschkewitch