1,252 research outputs found

    Calcutta Botanic Garden and the colonial re-ordering of the Indian environment

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    This article examines three hand-painted colour maps that accompanied the annual report of the Calcutta Botanic Garden for 1846 to illustrate how the Garden’s layout, uses and functions had changed over the previous 30 years. The evolution of the Calcutta Botanic Garden in the first half of the nineteenth-century reflects a wider shift in attitudes regarding the relationship between science, empire and the natural world. On a more human level the maps result from, and illustrate, the development of a vicious personal feud between the two eminent colonial botanists charged with superintending the garden in the 1840s

    The gammaretroviral p12 protein has multiple domains that function during the early stages of replication.

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    BACKGROUND: The Moloney murine leukaemia virus (Mo-MLV) gag gene encodes three main structural proteins, matrix, capsid and nucleocapsid and a protein called p12. In addition to its role during the late stages of infection, p12 has an essential, but undefined, function during early post-entry events. As these stages of retroviral infection remain poorly understood, we set out to investigate the function of p12. RESULTS: Examination of the infectivity of Mo-MLV virus-like particles containing a mixture of wild type and mutant p12 revealed that the N- and C-terminal regions of p12 are sequentially acting domains, both required for p12 function, and that the N-terminal activity precedes the C-terminal activity in the viral life cycle. By creating a panel of p12 mutants in other gammaretroviruses, we showed that these domains are conserved in this retroviral genus. We also undertook a detailed mutational analysis of each domain, identifying residues essential for function. These data show that different regions of the N-terminal domain are necessary for infectivity in different gammaretroviruses, in stark contrast to the C-terminal domain where the same region is essential for all viruses. Moreover, chimeras between the p12 proteins of Mo-MLV and gibbon ape leukaemia virus revealed that the C-terminal domains are interchangeable whereas the N-terminal domains are not. Finally, we identified potential functions for each domain. We observed that particles with defects in the N-terminus of p12 were unable to abrogate restriction factors, implying that their cores were impaired. We further showed that defects in the C-terminal domain of p12 could be overcome by introducing a chromatin binding motif into the protein. CONCLUSIONS: Based on these data, we propose a model for p12 function where the N-terminus of p12 interacts with, and stabilizes, the viral core, allowing the C-terminus of p12 to tether the preintegration complex to host chromatin during mitosis, facilitating integration

    The impact of the parenting for respectability programme on violent parenting and intimate partner relationships in Uganda: a pre-post study

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    Background There is a growing need for interventions that reduce both violence against children and intimate partner violence in low- and middle-income countries. However, few parenting interventions deliberately address this link. We tested the feasibility of a 16-session group-based parenting programme, Parenting for Respectability, in semi-rural Ugandan communities. Methods This was a pre-post study with parents and their children (N = 484 parents; 212 children). Results Pre-post comparisons found large effects for parent-reported reduced harsh parenting (Cohen’s f2 = 0.41 overall; f2 = 0.47 (among session attendees); with an overall reduction of 26% for harsh parenting. Session attendees reported higher reductions than non-attendees (p = 0.014), and male caregivers reported higher reductions than female caregivers (p<0.001). Children also reported reduced harsh parenting by attending fathers (f2 = 0.64 overall; f2 = 0.60) and attending mothers (f2 = 0.56 overall; f2 = 0.51); with reduction in harsh parenting ranging between 27% to 29% in the various categories. Overall, spousal violence reduced by 27% (f2 = 0.19 overall; f2 = 0.26 (among session attendees). Both parents and children reported reduced dysfunctional parent relationships; parents: f2 = 0.19 overall; f2 = 0.26 (among session attendees); and children: f2 = 0.35 overall; f2 = 0.32 (for attending parents); with reductions ranging between 22% to 28%. Parents who attended more than 50% of the program reported greater effects on reduced dysfunctional relationships than those who attended less than half of the program (B = -0.74, p = 0.013). All secondary outcomes were improved with f2 ranging between 0.08 and 0.39; and improvements ranging between 6% and 28%. Conclusion Results suggest the importance of more rigorous testing to determine program effectiveness

    Adipokines and adipocyte function in clock mutant mice that retain melatonin rhythmicity

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    Clockδ19+MEL mutant mice, which retain melatonin rhythmicity, but lack peripheral tissue rhythmicity have impaired glucose tolerance, but reduced plasma free fatty acids, increased plasma adiponectin, and improved insulin sensitivity. Here, we report their response to a high-fat diet and adipocyte rhythmicity and function. The diet increased epigonadal fat weight similarly (twofold) in both wild-type and Clockδ19+MEL mice. The Clockδ19 mutation abolished rhythmicity of Per2, Rev erbα and peroxisome proliferator-activated receptor-γ (Pparγ ) mRNA in epigonadal fat, but not Bmal1 mRNA, and reduced Rev erbα mRNA by 59 and 70% compared to the wild-type mice on the control and high-fat diets, respectively. The mutants had increased Adipoq mRNA expression in epigonadal fat (22%; P < 0.05) on a control diet, but showed no further change on a high-fat diet, and no change in Lep, Nampt or Retn mRNA on either diet. The Clockδ19 mutation abolished rhythmicity of genes in epigonadal fat that contribute to plasma free fatty acids for mice on both diets, and increased Lipe mRNA expression in those on the high-fat diet. The persistent melatonin rhythm and reduced plasma free fatty acids in Clockδ19+MEL mutants may contribute to their enhanced insulin sensitivity, ameliorate the extent of impaired glucose homeostasis, and protect against the adverse effects of a high-fat diet.David J. Kennaway, Julie A. Owens, Athena Voultsios and Nicole Wigh

    Parallel Writing on Zirconium Nitride Thin Films by Local Oxidation Nanolithography

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    Parallel pattern transfer of submicrometer-scale oxide features onto zirconium nitride thin films is reported. The oxidation reaction was verified by Auger microprobe analysis and secondary ion mass spectrometry. Oxide features of similar to70 nm in height can be formed and selectively etched in a dilute aqueous hydrogen fluoride solution. This provides an interesting route to potential new applications for high-melting point, biocompatible surfaces that possess small feature sizes with controlled geometries. (C) 2004 American Institute of Physics

    YY1 negatively regulates mouse myelin proteolipid protein (Plp1) gene expression in oligodendroglial cells

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    YY1 (Yin and Yang 1) is a multifunctional, ubiquitously expressed, zinc finger protein that can act as a transcriptional activator, repressor, or initiator element binding protein. Previous studies have shown that YY1 modulates the activity of reporter genes driven by the myelin PLP (proteolipid protein) (PLP1/Plp1) promoter. However, it is known that Plp1 intron 1 DNA contains regulatory elements that are required for the dramatic increase in gene activity, coincident with the active myelination period of CNS (central nervous system) development. The intron in mouse contains multiple prospective YY1 target sites including one within a positive regulatory module called the ASE (anti-silencer/enhancer) element. Results presented here demonstrate that YY1 has a negative effect on the activity of a Plp1-lacZ fusion gene [PLP(+)Z] in an immature oligodendroglial cell line (Oli-neu) that is mediated through sequences present in Plp1 intron 1 DNA. Yet YY1 does not bind to its alleged site in the ASE (even though the protein is capable of recognizing a target site in the promoter), indicating that the down-regulation of PLP(+)Z activity by YY1 in Oli-neu cells does not occur through a direct interaction of YY1 with the ASE sequence. Previous studies with Yy1 conditional knockout mice have demonstrated that YY1 is essential for the differentiation of oligodendrocyte progenitors. Nevertheless, the current study suggests that YY1 functions as a repressor (not an activator) of Plp1 gene expression in immature oligodendrocytes. Perhaps YY1 functions to keep the levels of PLP in check in immature cells before vast quantities of the protein are needed in mature myelinating oligodendrocytes

    Differential Effect of Saturated and Unsaturated Free Fatty Acids on the Generation of Monocyte Adhesion and Chemotactic Factors by Adipocytes: Dissociation of Adipocyte Hypertrophy From Inflammation

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    OBJECTIVE—Obesity is associated with monocyte-macroph-age accumulation in adipose tissue. Previously, we showed that glucose-stimulated production by adipocytes of serum amyloid A (SAA), monocyte chemoattractant protein (MCP)-1, and hyaluro-nan (HA) facilitated monocyte accumulation. The current objec-tive was to determine how the other major nutrient, free fatty acids (FFAs), affects these molecules and monocyte recruitment by adipocytes. RESEARCH DESIGN AND METHODS—Differentiated 3T3-L1, Simpson-Golabi-Behmel syndrome adipocytes, and mouse embryonic fibroblasts were exposed to various FFAs (250 mol/l) in either 5 or 25 mmol/l (high) glucose for evaluation of SAA, MCP-1, and HA regulation in vitro. RESULTS—Saturated fatty acids (SFAs) such as laurate, myris-tate, and palmitate increased cellular triglyceride accumulation, SAA, and MCP-1 expression; generated reactive oxygen species (ROS); and increased nuclear factor (NF) B translocation in both 5 and 25 mmol/l glucose. Conversely, polyunsaturated fatty acids (PUFAs) such as arachidonate, eicosapentaenate, and docosahexaenate (DHA) decreased these events. Gene expres-sion could be dissociated from triglyceride accumulation. Al-though excess glucose increased HA content, SFAs, oleate, and linoleate did not. Antioxidant treatment repressed glucose- and palmitate-stimulated ROS generation and NFB translocation and decreased SAA and MCP-1 expression and monocyte che-motaxis. Silencing toll-like receptor-4 (TLR4) markedly reduced SAA and MCP-1 expression in response to palmitate but not glucose. DHA suppressed NFB translocation stimulated by both excess glucose and palmitate via a peroxisome prolifterator– activated receptor (PPAR) –dependent pathway. CONCLUSIONS—Excess glucose and SFAs regulate chemotac-tic factor expression by a mechanism that involves ROS genera-tion, NFB, and PPAR, and which is repressed by PUFAs. Certain SFAs, but not excess glucose, trigger chemotactic factor expression via a TLR4-dependent pathway. Diabetes 59:386
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