TiB2和Al3Ti对近共晶Al?12.6Si合金组织、力学性能和断裂行为的影响

A near eutectic Al?12.6Si alloy was developed with 0.0wt%, 2.0wt%, 4.0wt%, and 6.0wt% Al?5Ti?1B master alloy. The microstructural morphology, hardness, tensile strength, elongation, and fracture behaviour of the alloys were studied. The unmodified Al?12.6Si alloy has an irregular needle and plate-like eutectic silicon (E_Si) and coarse polygonal primary silicon (P_Si) particles in the matrix-like α-Al phase. The P_Si, E_Si, and α-Al morphology and volume fraction were changed due to the addition of the Al?5Ti?1B master alloy. The hardness, UTS, and elongation improved due to the microstructural modification. Nano-sized in-situ Al₃Ti particles and ex-situ TiB₂ particles caused the microstructural modification. The fracture images of the developed alloys exhibit a ductile and brittle mode of fracture at the same time. The Al?5Ti?1B modified alloys have a more ductile mode of fracture and more dimples compared to the unmodified alloy.     

The northward extension of reptiles in the Palearctic,with the Jordan Valley (Israel) as a model: snakes outrace lizards (Reptilia: Squamata)

The geographical distribution of reptiles is known to be climate dependent. Our analysis of literature data from the Palearctic confirmed that snakes, as a group (186 species), tend to extend further to the north, into cooler climate, than lizards (460 species). This has also been reported for the Nearctic. On a smaller scale, as a model, we investigated the expansion of reptiles from the warm southern desert of Israel northwards along the Jordan valley into cooler climate, based on 587 locality records of 17 species. It transpired that the snakes significantly extend further to the north than the lizards, paralleling and exemplifying the global scale. The ability of snakes to inhabit relatively cooler climates appears to accord with three physiological traits of snakes: lower optimal body temperatures, absence of temperature-dependent sex determination, and ability to thrive on infrequent meals.     

Chemical investigation of the seeds ofAlbizzia procera benth

Zusammenfassung Aus dem Samen vonAlbizzia procera Benth wurden ausser Machaerinsäure 4 triterpenoide Sapogenine isoliert (Verbindung A und B, Proceragenin A und B). Es wurde bewiesen, dass die Verbindung A das 28 21-Lacton der Machaerinsäure mit einer Konformationsänderung am Ring D oder E ist, während die Verbindung B als Äthylmachaerinat identifiziert wurde. Bei Proceragenin A und B handelt es sich um Dihydroylactone.

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A part of the work was carried out at the Department of Chemistry, Bose Institute, Calcutta-9, India, and was supported in part by the Ministry of Education, Government of India. — The authors desire to express their sincere thanks to Dr.A. K. Barua, Reader in Chemistry, Bose Institute, Calcutta and to the Rev. Dr.H. Santapau, Director, Botanical Survey of India, Calcutta for their keen interest and encouragement.     

Modular epistasis in yeast metabolism

Epistatic interactions, manifested in the effects of mutations on the phenotypes caused by other mutations, may help uncover the functional organization of complex biological networks. Here, we studied system-level epistatic interactions by computing growth phenotypes of all single and double knockouts of 890 metabolic genes in Saccharomyces cerevisiae, using the framework of flux balance analysis. A new scale for epistasis identified a distinctive trimodal distribution of these epistatic effects, allowing gene pairs to be classified as buffering, aggravating or noninteracting. We found that the ensuing epistatic interaction network could be organized hierarchically into function-enriched modules that interact with each other 'monochromatically' (i.e., with purely aggravating or purely buffering epistatic links). This property extends the concept of epistasis from single genes to functional units and provides a new definition of biological modularity, which emphasizes interactions between, rather than within, functional modules. Our approach can be used to infer functional gene modules from purely phenotypic epistasis measurements.     

Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein

The distribution of fitness effects of protein mutations is still unknown. Of particular interest is whether accumulating deleterious mutations interact, and how the resulting epistatic effects shape the protein's fitness landscape. Here we apply a model system in which bacterial fitness correlates with the enzymatic activity of TEM-1 beta-lactamase (antibiotic degradation). Subjecting TEM-1 to random mutational drift and purifying selection (to purge deleterious mutations) produced changes in its fitness landscape indicative of negative epistasis; that is, the combined deleterious effects of mutations were, on average, larger than expected from the multiplication of their individual effects. As observed in computational systems, negative epistasis was tightly associated with higher tolerance to mutations (robustness). Thus, under a low selection pressure, a large fraction of mutations was initially tolerated (high robustness), but as mutations accumulated, their fitness toll increased, resulting in the observed negative epistasis. These findings, supported by FoldX stability computations of the mutational effects, prompt a new model in which the mutational robustness (or neutrality) observed in proteins, and other biological systems, is due primarily to a stability margin, or threshold, that buffers the deleterious physico-chemical effects of mutations on fitness. Threshold robustness is inherently epistatic-once the stability threshold is exhausted, the deleterious effects of mutations become fully pronounced, thereby making proteins far less robust than generally assumed.     

Metazoan evolution of the armadillo repeat superfamily

The superfamily of armadillo repeat proteins is a fascinating archetype of modular-binding proteins involved in various fundamental cellular processes, including cell–cell adhesion, cytoskeletal organization, nuclear import, and molecular signaling. Despite their diverse functions, they all share tandem armadillo (ARM) repeats, which stack together to form a conserved three-dimensional structure. This superhelical armadillo structure enables them to interact with distinct partners by wrapping around them. Despite the important functional roles of this superfamily, a comprehensive analysis of the composition, classification, and phylogeny of this protein superfamily has not been reported. Furthermore, relatively little is known about a subset of ARM proteins, and some of the current annotations of armadillo repeats are incomplete or incorrect, often due to high similarity with HEAT repeats. We identified the entire armadillo repeat superfamily repertoire in the human genome, annotated each armadillo repeat, and performed an extensive evolutionary analysis of the armadillo repeat proteins in both metazoan and premetazoan species. Phylogenetic analyses of the superfamily classified them into several discrete branches with members showing significant sequence homology, and often also related functions. Interestingly, the phylogenetic structure of the superfamily revealed that about 30 % of the members predate metazoans and represent an ancient subset, which is gradually evolving to acquire complex and highly diverse functions.     

T cell receptor bias for MHC: co-evolution or co-receptors?

In contrast to antibodies, which recognize antigens in native form, αβ T cell receptors (TCRs) only recognize antigens as peptide fragments bound to MHC molecules, a feature known as MHC restriction. The mechanism by which MHC restriction is imposed on the TCR repertoire is an unsolved problem that has generated considerable debate. Two principal models have been advanced to explain TCR bias for MHC. According to the germline model, MHC restriction is intrinsic to TCR structure because TCR and MHC molecules have co-evolved to conserve germline-encoded TCR sequences with the ability to bind MHC, while eliminating TCR sequences lacking MHC reactivity. According to the selection model, MHC restriction is not intrinsic to TCR structure, but is imposed by the CD4 and CD8 co-receptors that promote signaling by delivering the Src tyrosine kinase Lck to TCR–MHC complexes through co-receptor binding to MHC during positive selection. Here, we review the evidence for and against each model and conclude that both contribute to determining TCR specificity, although their relative contributions remain to be defined. Thus, TCR bias for MHC reflects not only germline-encoded TCR–MHC interactions but also the requirement to form a ternary complex with the CD4 or CD8 co-receptor that is geometrically competent to deliver a maturation signal to double-positive thymocytes during T cell selection.