Part-time and fractional staff in the learning and skills sector

This Universities and College Union Launch Event presentation reported on the findings of Learning and Skills Research Network (LSRN) London and South East (LSE) Regional Research Project. The presentation reflected on research carried out during 2002-06 on the development and deployment of part-time staff in the Learning and Skills Sector. Although the lifelong learning sector is the largest UK education sector, little attention has as yet been paid to the role of LSC sector part-time staff. Worrying trends of an increasing casualisation of staffing have been reported. The role of part-timers as highly committed (philanthropic) but generally underpaid and exploited staff (ragged-trousered) emerged from the data collected by this investigation, which examined the role of part-timers in several colleges and adult education institutions in London and the South East. The metaphor of the 'ragged-trousered philanthropist' was consciously selected to investigate the interactivity between philantrophy, employment practices for PT staff, and education as social action, in addressing the need for good practice to achieve quality outcomes in learning and teaching. The results are to some extent transferable to other education and training sectors employing part-time staff, e.g. higher education institutions and work-based training organisations.

A NOVEL MODELING AND STATE OF CHARGE ESTIMATION SCHEME FOR LITHIUM-ION BATTERIES

Lithium Ion (Li-Ion) batteries have got attention in recent decades because of their undisputable advantages over other types of batteries. They are used in so many our devices which we need in our daily life such as cell phones, lap top computers, cameras, and so many electronic devices. They also are being used in smart grids technology, stand-alone wind and solar systems, Hybrid Electric Vehicles (HEV), and Plug in Hybrid Electric Vehicles (PHEV). Despite the rapid increase in the use of Lit-ion batteries, the existence of limited battery models also inadequate and very complex models developed by chemists is the lack of useful models a significant matter. A battery management system (BMS) aims to optimize the use of the battery, making the whole system more reliable, durable and cost effective. Perhaps the most important function of the BMS is to provide an estimate of the State of Charge (SOC). SOC is the ratio of available ampere-hour (Ah) in the battery to the total Ah of a fully charged battery. The Open Circuit Voltage (OCV) of a fully relaxed battery has an approximate one-to-one relationship with the SOC. Therefore, if this voltage is known, the SOC can be found. However, the relaxed OCV can only be measured when the battery is relaxed and the internal battery chemistry has reached equilibrium. This thesis focuses on Li-ion battery cell modelling and SOC estimation. In particular, the thesis, introduces a simple but comprehensive model for the battery and a novel on-line, accurate and fast SOC estimation algorithm for the primary purpose of use in electric and hybrid-electric vehicles, and microgrid systems. The thesis aims to (i) form a baseline characterization for dynamic modeling; (ii) provide a tool for use in state-of-charge estimation. The proposed modelling and SOC estimation schemes are validated through comprehensive simulation and experimental results.

Metaphors of Time and Installed Knowledge Organization Systems: Ouroboros, Architectonics, or Lachesis?

This paper describes three metaphors for time drawn from contemporary and historical literature on knowledge organization systems (KOS). It then links these metaphors to the evaluation of knowledge organization by describing the dominant paradigm in KOS evaluation to be judging whether a KOS is correct. We conclude by saying a foundational view of evaluating and theorizing about KOS must account for change and time in order for us to take a long view of improving knowledge organization and our understanding of KOS.

Subject Ontogeny: Subject Access through Time and the Dimensionality of Classification

Classification schemes undergo revision. However, in a networked environment revisions can be used to add dimensionality to classification. This dimensionality can be used to help explain conceptual warrant, explain the shift from disciplinary to multidisciplinary knowledge production, and as a component method of domain analysis. Further, subject ontogeny might be used in cooperative networked projects like digital preservation, online access tools, and interoperability frameworks.

Fixing, storage time and DNA extraction applied to dT-RFLP for ecological and molecular studies of marine nematodes assemblages

The application of molecular methods offers an alternative faster than traditional methods based on morphology It is nearly impossible to process all the samples in short period using traditional methods, and the deterioration of marine sediments rapidly occurs The dT-RFLP (directed Terminal-Restriction Fragment Length Polymorphism) allows a rapid assessment of biodiversity changes of nematodes assemblages The use of a not suitable fixing, storage time and DNA extraction could be a limitation in molecular analysis like dT-RFLP and real time PCR.Objetives: the best fixative •the level of DNA degradation over the time •the best DNA extraction method for marine nematodes and suitable for dT-RFLP analysis

The Palace of Quinta do Marquês do Alegrete: restitution strategies for space, time and memory

Palaces, as an architectural typology, can be found in recreation Quintas that surrounded the main cities in Portugal, which preserved its rural character since the 16th century until the middle of the 19th century. Consisting of cultivated land and farm buildings, the palace of the Quinta was the owner´s temporary residence, for summer holidays and festive events, with gardens, pavilions, fountains and lakes for recreational purposes and leisure. The focus on palaces, as a historic building and as in need of new uses, clearly shows how current the debate on contemporary interventions in this heritage typology is. Interventions in architectural heritage require multidisciplinary teams to identify conservation strategies which enable a qualified use of its spaces, such as for example the experience of security and well-being, which can contribute to a better quality of life and simultaneously to the quality of the urban environment. This paper presents the Palace of Quinta Alegre and its rehabilitation project for contemporary use and public esteem, both of which are considered fundamental prerequisites for its sustainable maintenance in space, in time and in memory. [versão Portuguesa] Sob a denominação de tipologia arquitectónica, o edifício Palácio pode ser encontrado nas Quintas de Recreio que rodeavam as principais cidades Portuguesas, tendo preservado o seu carácter rural, desde o século XVI até metade do século XIX. Consistindo as Quintas em terra cultivada e edifícios rurais, o Palácio da Quinta consistia na residência temporária do proprietário, para férias de verão e eventos comemorativos, dispondo de jardins, pavilhões, fontes e lagos para recreação e lazer. O tema dos Palácios, entendido como edifício histórico que procura novos usos, demonstra como é actual o debate sobre intervenções contemporâneas nesta tipologia de valor patrimonial. A intervenção em património arquitectónico requer a definição de estratégias de conservação por equipas multidisciplinares que permitam estabelecer um uso qualificado dos seus espaços, proporcionando experiências sensoriais de bem-estar e segurança, contribuindo para uma melhor qualidade de vida e, simultaneamente, para a qualidade do ambiente urbano em que se insere. Este artigo tem por objectivo apresentar o Palácio da Quinta Alegre e o projecto de reabilitação, devolvendo-o a um uso contemporâneo e à estima pública, factores fundamentais para a sua manutenção sustentável no espaço, no tempo e na memória.

Zinc deficiency induces apoptosis via mitochondrial p53- and caspase-dependent pathways in human neuronal precursor cells

Previous studies have shown that zinc deficiency leads to apoptosis of neuronal precursor cells in vivo and in vitro. In addition to the role of p53 as a nuclear transcription factor in zinc deficient cultured human neuronal precursors (NT-2), we have now identified the translocation of phosphorylated p53 to the mitochondria and p53-dependent increases in the pro-apoptotic mitochondrial protein BAX leading to a loss of mitochondrial membrane potential as demonstrated by a 25% decrease in JC-1 red:green fluorescence ratio. Disruption of mitochondrial membrane integrity was accompanied by efflux of the apoptosis inducing factor (AIF) from the mitochondria and translocation to the nucleus with a significant increase in reactive oxygen species (ROS) after 24 h of zinc deficiency. Measurement of caspase cleavage, mRNA, and treatment with caspase inhibitors revealed the involvement of caspases 2, 3, 6, and 7 in zinc deficiency-mediated apoptosis. Down-stream targets of caspase activation, including the nuclear structure protein lamin and polyADP ribose polymerase (PARP), which participates in DNA repair, were also cleaved. Transfection with a dominant-negative p53 construct and use of the p53 inhibitor, pifithrin- ␮, established that these alterations were largely dependent on p53. Together these data identify a cascade of events involving mitochondrial p53 as well as p53-dependent caspase-mediated mechanisms leading to apoptosis during zinc deficiency.

Sovereign wealth funds and state immunity

The study sheds light on the application of the rule of state immunity to sovereign wealth funds (SWFs). SWFs are Janus-faced investment vehicles established by their parent states to invest public resources in financial markets, with the aim of increasing long-term returns and pursuing macroeconomic goals. The ultimate purpose of the study is to assess if the hybrid nature of SWFs results in changes to the rule of state immunity when applied to them, and whether a generally accepted standard in this regard can be deduced from state practice. The research is conducted through a comparative analysis. It is based on the provisions of the UN Convention on Jurisdictional Immunities of States and Their Property (UNCSI), as well as on six domestic jurisdictions (US, UK, France, Germany, Italy and China) among those that have contributed most significantly to the international debate on state immunity and which host the largest amount of SWF investments.

Hypervalent organochalcogenanes as inhibitors of protein tyrosine phosphatases

A series of organochalcogenanes was synthesized and evaluated as protein tyrosine phosphatases (PTPs) inhibitors. The results indicate that organochalcogenanes inactivate the PTPs in a time- and concentration-dependent fashion, most likely through covalent modification of the active site sulfur-moiety by the chalcogen atom. Consequently, organochalcogenanes represent a new class of mechanism-based probes to modulate the PTP-mediated cellular processes.

Inactivation of human arylamine N-acetyltransferase 1 by the hydroxylamine of p-aminobenzoic acid

Human N-acetyltransferase 1 (NAT1) is a widely distributed enzyme that catalyses the acetylation of arylamine and hydrazine drugs as well as several known carcinogens, and so its levels in the body may have toxicological importance with regard to drug toxicity and cancer risk. Recently, we showed that p-aminobenzoic acid (PABA) was able to down-regulate human NAT1 in cultured cells, but the exact mechanism by which PABA acts remains unclear. In the present study, we investigated the possibility that PABA-induced down-regulation involves its metabolism to N-OH-PABA, since N-OH-AAF functions as an irreversible inhibitor of hamster and rat NAT1. We show here that N-OH-PABA irreversibly inactivates human NAT1 both in cultured cells and cell cytosols in a time- and concentration-dependent manner. Maximal inactivation in cultured cells occurred within 4 hr of treatment, with a concentration of 30 muM reducing activity by 60 +/- 7%. Dialysis studies showed that inactivation was irreversible, and cofactor (acetyl coenzyme A) but not substrate (PABA) completely protected against inactivation, indicating involvement of the cofactor-binding site. In agreement with these data, kinetic studies revealed a 4-fold increase in cofactor K-m, but no change in substrate K-m for N-OH-PABA-treated cytosols compared to control. We conclude that N-OH-PABA decreases NAT1 activity by a direct interaction with the enzyme and appears to be a result of covalent modification at the cofactor-binding site. This is in contrast to our findings for PABA, which appears to reduce NAT1 activity by down-regulating the enzyme, leading to a decrease in NAT1 protein content. BIOCHEM PHARMACOL 60;12: 1829-1836, 2000. (C) 2000 Elsevier Science Inc.

Effect of tamoxifen on the enzymatic activity of human cytochrome CYP2B6

Tamoxifen is primarily used in the treatment of breast cancer. It has been approved as a chemopreventive agent for individuals at high risk for this disease. Tamoxifen is metabolized to a number of different products by cytochrome P450 enzymes. The effect of tamoxifen on the enzymatic activity of bacterially expressed human cytochrome CYP2B6 in a reconstituted system has been investigated. The 7-ethoxy-4-(trifluoromethyl) coumarin O-deethylation activity of purified CYP2B6 was inactivated by tamoxifen in a time- and concentration-dependent manner. Enzymatic activity was lost only in samples that were incubated with both tamoxifen and NADPH. The inactivation was characterized by a K-l of 0.9 muM, a k(inact) of 0.02 min(-1), and a t(1/2) of 34 min. The loss in the 7-ethoxy-4-(trifluoromethyl) coumarin O-deethylation activity did not result in a similar percentage loss in the reduced carbon monoxide spectrum, suggesting that the heme moiety was not the major site of modification. The activity of CYP2B6 was not recovered after removal of free tamoxifen using spin column gel filtration. The loss in activity seemed to be due to a modification of the CYP2B6 and not reductase because adding fresh reductase back to the inactivated samples did not restore enzymatic activity. A reconstituted system containing purified CYP2B6, NADPH-reductase, and NADPH-generating system was found to catalyze tamoxifen metabolism to 4-OH-tamoxifen, 4'-OH-tamoxifen, and N-desmethyl-tamoxifen as analyzed by high-performance liquid chromatography analysis. Preliminary studies showed that tamoxifen had no effect on the activities of CYP1B1 and CYP3A4, whereas CYP2D6 and CYP2C9 exhibited a 25% loss in enzymatic activity.

Efficacy of euphorbia hirta latex as plant derived molluscicides against freshwater snails

The toxic effect of binary and tertiary combinations of Euphorbia hirta Linn latex powder with other plant molluscicidal compounds, were evaluated against the freshwater snails Lymnaea (Radix) acuminata and Indoplanorbis exustus in pond. These combinations showed significant time and dose dependent effect against both the snails. These compounds at higher doses were also lethal to freshwater fish Channa punctatus (Bloch) (Channidae {Ophicephalidae}), which shares the habitat with these snails, but the LC90 (24h) doses of snails have no apparent killing properties in fish populations when treated in mixed population of snails and fish.

Induction of calmodulin kinase IV by the thyroid hormone during the development of rat brain.

This communication reports the specific induction of calmodulin kinase IV by the thyroid hormone 3,3',5-triiodo-L-thyronine (T3) in a time- and concentration-dependent manner at a very early stage of brain differentiation using a fetal rat telencephalon primary cell culture system, which can grow and differentiate under chemically defined conditions. The induction of the enzyme that can be observed both on the mRNA and on the protein level is T3-specific, i.e. it cannot be induced by retinoic acid or reverse T3, and can be inhibited on both the transcriptional and the translational level by adding to the culture medium actinomycin D or cycloheximide, respectively. The earliest detection of calmodulin kinase IV in the fetal brain tissue of the rat is at days E16/E17, both on the mRNA as well as on the protein level. This is the first report in which a second messenger-dependent kinase involved in the control of cell regulatory processes is itself controlled by a primary messenger, the thyroid hormone.

Coating carbon nanotubes with a polystyrene-based polymer protects against pulmonary toxicity.

BACKGROUND: carbon nanotubes (CNT) can have adverse effects on health. Therefore, minimizing the risk associated with CNT exposure is of crucial importance. The aim of this work was to evaluate if coating multi-walled CNT (MWCNT) with polymers could modify their toxicity, thus representing a useful strategy to decrease adverse health effects of CNT. We used industrially-produced MWCNT uncoated (NT1) or coated (50/50 wt%) with acid-based (NT2) or polystyrene-based (NT3) polymer, and exposed murine macrophages (RAW 264.7 cell line) or Balb/c mice by intratracheal administration. Biological experiments were performed both in vitro and in vivo, examining time- and dose-dependent effects of CNT, in terms of cytotoxicity, expression of genes and proteins related to oxidative stress, inflammation and tissue remodeling, cell and lung tissue morphology (optical and transmission electron microscopy), and bronchoalveolar lavage fluid content analysis.RESULTS: extensive physico-chemical characterization of MWCNT was performed, and showed, although similar dimensions for the 3 MWCNT, a much smaller specific surface area for NT2 and NT3 as compared to NT1 (54.1, 34 and 227.54 m(2)/g respectively), along with different surface characteristics. MWCNT-induced cytotoxicity, oxidative stress, and inflammation were increased by acid-based and decreased by polystyrene-based polymer coating both in vitro in murine macrophages and in vivo in lung of mice monitored for 6 months.CONCLUSIONS: these results demonstrate that coating CNT with polymers, without affecting their intrinsic structure, may constitute a useful strategy for decreasing CNT toxicity, and may hold promise for improving occupational safety and that of general the user.

Up-regulation of placental leptin by human chorionic gonadotropin.

Leptin, the 16,000 molecular weight protein product of the obese gene, was originally considered as an adipocyte-derived signaling molecule for the central control of metabolism. However, leptin has been suggested to be involved in other functions during pregnancy, particularly in placenta, in which it was found to be expressed. In the present work, we have found that recombinant human chorionic gonadotropin (hCG) added to BeWo choriocarcinoma cell line showed a stimulatory effect on endogenous leptin expression, when analyzed by Western blot. This effect was time and dose dependent. Maximal effect was achieved at hCG 100 IU/ml. Moreover, hCG treatment enhanced leptin promoter activity up to 12.9 times, evaluated by transient transfection with a plasmid construction containing different promoter regions and the reporter gene luciferase. This effect was dose dependent and evidenced with all the promoter regions analyzed, regardless of length. Similar results were obtained with placental explants, thus indicating physiological relevance. Because hCG signal transduction usually involves cAMP signaling, this pathway was analyzed. Contrarily, we found that dibutyryl cAMP counteracted hCG effect on leptin expression. Furthermore, cotransfection with the catalytic subunit of PKA and/or the transcription factor cAMP response element binding protein repressed leptin expression. Thereafter we determined that hCG effect could be partially blocked by pharmacologic inhibition of MAPK pathway with 50 microM PD98059 but not by the inhibition of the phosphatidylinositol 3-kinase pathway with 0.1 microm wortmannin. Moreover, hCG treatment promoted MAPK kinase and ERK1/ERK2 phosphorylation in placental cells. Finally, cotransfection with a dominant-negative mutant of MAPK blocked the hCG-mediated activation of leptin expression. In conclusion, we provide some evidence suggesting that hCG induces leptin expression in trophoblastic cells probably involving the MAPK signal transduction pathway.