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Recently a $f$-deformed Fock space which is spanned by $|n>_{\lambda}$ has been introduced. These bases are indeed the eigen-states of a deformed non-Hermitian Hamiltonian. In this contribution, we will use a rather new non-orthogonal basis vectors for the construction of coherent and squeezed states, which in special case lead to the earlier known states. For this purpose, we first generalize the previously introduced Fock space spanned by $|n>_{\lambda}$ bases, to a new one, spanned by an extended two-parameters bases $|n>_{\lambda_{1},\lambda_{2}}$. These bases are now the eigen-states of a non-Hermitian Hamiltonian $H_{\lambda_{1},\lambda_{2}}=a^{\dagger}_{\lambda_{1},\lambda_{2}}a+1/2$, where $a^{\dagger}_{\lambda_{1},\lambda_{2}}=a^{\dagger}+\lambda_{1}a + \lambda_{2}$ and $a$ are respectively, the deformed creation and ordinary bosonic annihilation operators. The bases $|n>_{\lambda_{1},\lambda_{2}}$ are non-orthogonal (squeezed states), but normalizable. Then, we deduce the new representations of coherent and squeezed states, in our two-parameters Fock space. Finally, we discuss the quantum statistical properties, as well as the non-classical properties of the obtained states, numerically., Comment: 14 pages, accepted in Chinees Physics C

The typical small biological laboratory is cmposed of electronic scientific equipment and wet laboratory equipment where staff record reesults into paper workbooks. There is oftern a lack of expert staff to guide new users, and hard won experience is locked away with individual staff and their workbooks. The Proteomics Laboratory System and Digital Mentor aims to: facilitate the capture, analysis and sharing of results; facilitate the creation and documentation of standardised work flows and experimental procedures; and mentore inexperienced users in best practice when engaged in particular procedures in the laboratory. In this paper we discuss the design of the system and report on the initial production release. This is nased on a relational database and web-server framework. A novel aspect of the system is the exploitation of custom extensions to a wiki-style interface that add functionality for non-expert end-users.

In this paper we present part of an ongoing study to telemetry data of Phaethontis, aregion in the western hemisphere of Mars' Southern Highlands. in particular, we focus on an approximately 57,000 km2 area in Gorgonum Chaos. We selected THEMIS visual, MOC narrow angle and MOLA data abvailable from the Arizona State University and Malin Space Sceince Systems web-sites. We carried out multi-level processing of THEMIS and MOC data using the ISIS software and prcessed MOLA gridded data by the GMT software. After processing we input the images into ArcGIS software, We observed, identified and described, both 2- and 3-dimentionally, impact craters, chaotic and polygonal terrains, grabens and gullies. These landforms suggest a complex geological history involving sedimentary and tectonic processes such as meteoritic impact, the presence of underground water and ice, desiccation or freezing of wet sediemnts at least two episodes of extension, and recent aeolian activity.

Two cDNA clones for human liver alcohol dehydrogenase (ADH) were identified, together covering 1450 nucleotides that contain the cDNA sequence of the ADH1 locus and include a coding region of 1122 nucleotides for the alpha subunit of the enzyme. In parallel, direct peptide analyses of the carboxymethylated protein also established most of the amino acid sequence. Nucleotide and peptide data were in complete agreement and show exchanges at 24 positions in the alpha relative to the beta subunit. One of the cDNA clones had a 139-nucleotide internal deletion at a position of possible interest in relation to mRNA processing, ancestral connections, or DNA replication. The structure of the alpha subunit is homologous to that of the beta and gamma subunits but has many exchanges, also of functionally important residues, explaining the different enzymatic properties. In total, 35 of 374 amino acid residues differ between the class I isozymes, and the substitutions add an extra SH group in the alpha subunit. Only in the beta-pleated sheet region of the coenzyme-binding domain is almost complete lack of substitutions noted, illustrating the importance of this region. In contrast, the active site region is far less conserved. However, similar exchanges of functional significance have also been found in distantly related alcohol and polyol dehydrogenases.

The cross-fertilisation between biological and cultural evolution has led to an extensive borrowing of key concepts, theories, and statistical methods for studying temporal variation in the frequency of cultural variants. Archaeologists have been among the front-runners of those engaging with this endeavour, and the last 2 decades have seen a number of case studies where modes of social learning were inferred from the changing frequencies of artefacts. Here, we employ a simulation model to review and examine under-discussed assumptions shared by many of these applications on the nature of what constitutes the ‘population’ under study. We specifically ask (1) whether cultural transmission via ‘objects’ (i.e. public manifestations of cultural traits) generates distinct patterns from those expected from direct transmission between individuals and (2) whether basing inference on the frequency of objects rather than on the frequency of mental representations underlying the production of those objects may lead to biased interpretations. Our results show that the rate at which ideational cultural traits are embedded in objects, and shared as such, has a measurable impact on how we infer cultural transmission processes when analysing frequency-based archaeological data. At the same time, when cultural transmission is entirely mediated by the material representation of ideas, we argue that copying error should be interpreted as a two-step process which may occur in either one or both of embedding information in objects and retrieving it from them.

Tuberculosis treatment requires months-long combination chemotherapy with multiple drugs, with shorter treatments leading to relapses. A major impediment to shortening treatment is that Mycobacterium tuberculosis becomes tolerant to the administered drugs, starting early after infection and within days of infecting macrophages. Multiple lines of evidence suggest that macrophage-induced drug tolerance is mediated by mycobacterial drug efflux pumps. Here, using assays to directly measure drug efflux, we find that M. tuberculosis transports the first-line antitubercular drug rifampicin through a proton gradient-dependent mechanism. We show that verapamil, a known efflux pump inhibitor, which inhibits macrophage-induced rifampicin tolerance, also inhibits M.tuberculosis rifampicin efflux. As with macrophage-induced tolerance, the calcium channel-inhibiting property of verapamil is not required for its inhibition of rifampicin efflux. By testing verapamil analogs, we show that verapamil directly inhibits M. tuberculosis drug efflux pumps through its human P-glycoprotein (PGP)-like inhibitory activity. Screening commonly used drugs with incidental PGP inhibitory activity, we find many inhibit rifampicin efflux, including the proton pump inhibitors (PPIs) such as omeprazole. Like verapamil, the PPIs inhibit macrophage-induced rifampicin tolerance as well as intramacrophage growth, which has also been linked to mycobacterial efflux pump activity. Our assays provide a facile screening platform for M. tuberculosis efflux pump inhibitors that inhibit in vivo drug tolerance and growth.

It is often observed that there is a high individual variability in the response to exercise-induced muscle damage (EIMD), even when tested in a homogeneous cohort accounting for age, sex, ethnicity and physical activity. The response to EIMD is very complex as several tissues, including skeletal muscle fibres, the extra-cellular matrix (ECM), and tendon, play a potential role in the damage response. Therefore, the overall aim of this PhD thesis was to investigate the physiological and genetic factors underpinning the response to muscle damaging exercise. For that, the following objectives were (i) to comprehensively assess the physiological mechanisms and recovery pattern of neuromuscular fatigue of the hamstring muscle group following an intermittent sprint (IS) intervention; (ii) to investigate inter-individual differences in skeletal muscle repair/recovery after an artificial wounding (scratch) assay using of primary human skeletal muscle cells in vitro; (iii) to ascertain whether multiple genetic variations, which are linked to varying tissues, forming a polygenic profile could distinguish between high and low responders following muscle damage in vivo and in vitro; and (iv) to assess whether a genetic profile is linked with the response to both EIMD and chronic resistance exercise. The methodological and analytical approaches utilised in this thesis identified a number of important, novel and impactful findings. Following IS, the impaired hamstring muscle function and delayed recovery is probably caused primarily by damage to the contractile tissue, and participants with a greater force generating capacity (larger physiological cross-sectional area) of the biceps femoris long head were less susceptible to hamstring strength loss immediately after IS, providing evidence that the structure of the muscle protects it against peripheral fatigue/damage. The in vitro study showed that skeletal muscles with an increased number of stem cells of the connective tissue (fibroblasts) might have a better capacity to reorganise the complex ECM, which results in a faster muscle strength recovery after muscle damaging exercise. However, a larger number of active muscle stem cells (myoblasts) seems to be important for the latter stage of muscle regeneration. Individuals possessing a non-preferential genetic profile demonstrated increased rate of muscle damage biomarkers than individuals with a preferential genetic profile. Lastly, we calculated a second polygenic profile which was linked with both the EIMD and the chronic resistance exercise response. These polygenic profiles may be used to anticipate an individual’s response/adaptation to EIMD and to chronic resistance exercise, thus enabling resistance exercise to be prescribed on a personalised level to improve muscle health and function.