Some thoughts on the monitoring and preservation of waterlogged archaeological sites in eastern England

This study reviews five hydrological monitoring projects used on archeological sites in the waterlogged landscapes of fenland East Anglia and east Yorkshire in England. The project design, recorded variables, and implications of each are discussed. In particular, the importance of understanding the landscape context is paramount, and retrieving an appropriate dataset over a sufficiently lengthy period of time to obtain reliable results and predictability. Some of the lessons learnt and outstanding problems are explored. As former wetlands are fast disappearing around the world through dewatering and a host of wider development threats such as urbanization and gravel extraction, the low intrusion suite of methods described here for measuring the degree and certainty of organic preservation is doubly important for establishing the viability of preservation in situ schemes for waterlogged archeological sites. This is crucial to get right, as wetland archeological records are an irreplaceable resource which offer extraordinarily full and diverse datasets of human lifeways which are all too often either poorly preserved or erroneously interpreted because of the skewed datasets recovered from dryland sites.English Heritage, Huntings Technical Services (for Over), ARC (Central) Ltd. (for Etton), Hanson Building Products and SLR Consulting Ltd. (for Must Farm), the Society of Antiquaries and Fenland Archaeological Trust (for Etton), Cambridge Archaeological Unit (for Over and Must Farm), the McBurney Laboratory and the McDonald Institute for Archaeological Research, University of Cambridge (for Over and Must Farm), the Department of Archaeology, University of York and the European Research Council (for Star Carr), and the Meteorological Office (for Etton and Over

Linoleic Acid-Induced Ultra-Weak Photon Emission from Chlamydomonas reinhardtii as a Tool for Monitoring of Lipid Peroxidation in the Cell Membranes

Reactive oxygen species formed as a response to various abiotic and biotic stresses cause an oxidative damage of cellular component such are lipids, proteins and nucleic acids. Lipid peroxidation is considered as one of the major processes responsible for the oxidative damage of the polyunsaturated fatty acid in the cell membranes. Various methods such as a loss of polyunsaturated fatty acids, amount of the primary and the secondary products are used to monitor the level of lipid peroxidation. To investigate the use of ultra-weak photon emission as a non-invasive tool for monitoring of lipid peroxidation, the involvement of lipid peroxidation in ultra-weak photon emission was studied in the unicellular green alga Chlamydomonas reinhardtii. Lipid peroxidation initiated by addition of exogenous linoleic acid to the cells was monitored by ultra-weak photon emission measured with the employment of highly sensitive charged couple device camera and photomultiplier tube. It was found that the addition of linoleic acid to the cells significantly increased the ultra-weak photon emission that correlates with the accumulation of lipid peroxidation product as measured using thiobarbituric acid assay. Scavenging of hydroxyl radical by mannitol, inhibition of intrinsic lipoxygenase by catechol and removal of molecular oxygen considerably suppressed ultra-weak photon emission measured after the addition of linoleic acid. The photon emission dominated at the red region of the spectrum with emission maximum at 680 nm. These observations reveal that the oxidation of linoleic acid by hydroxyl radical and intrinsic lipoxygenase results in the ultra-weak photon emission. Electronically excited species such as excited triplet carbonyls are the likely candidates for the primary excited species formed during the lipid peroxidation, whereas chlorophylls are the final emitters of photons. We propose here that the ultra-weak photon emission can be used as a non-invasive tool for the detection of lipid peroxidation in the cell membranes

Efeito da técnica de oscilação oral de alta freqüência aplicada em diferentes pressões expiratórias sobre a função autonômica do coração e os parâmetros cardiorrespiratórios

O objetivo deste estudo foi avaliar o efeito da técnica de oscilação oral de alta freqüência (com o aparelho Shaker), aplicada em diferentes pressões expiratórias (PE), sobre a função autonômica e parâmetros cardiorrespiratórios. Foram coletados dados de 20 voluntários jovens saudáveis (21,6±1,3 anos), que permaneceram em repouso inicial por 10 minutos e, em seguida, fizeram três séries de dez expirações no aparelho (com intervalo de descanso de 2 minutos entre as séries) em três diferentes PE - pressão livre (PL), de 10 (P10) e de 20 (P20) cmH2O - permanecendo por mais 10 minutos em repouso final. Os dados foram analisados estatisticamente, com nível de significância de 5%. Após a aplicação da técnica, constatou-se diferença significante nos índices de variabilidade da freqüência cardíaca em PL e um aumento significante na pressão arterial sistólica em P20. Na pressão arterial diastólica, freqüência respiratória e saturação periférica de oxigênio não foram encontradas diferenças antes, durante e após a técnica, nas diferentes PE. A percepção do esforço aumentou significantemente ao longo das séries em PL e P20 e entre P10 e P20 em cada série. A freqüência cardíaca (FC) aumentou e diminuiu em sincronia com os movimentos de inspiração e expiração, respectivamente. Foram observadas modificações na modulação autonômica do coração em PL. A aplicação da técnica nessa população, nas diferentes PE analisadas, promoveu modificações no comportamento da FC, no esforço percebido e, em PL, na modulação autonômica do coração.The aim of this study was to analyse the effect of oral high-frequency oscillation technique (with the Shaker device), applied at different expiratory pressures (EP), onto autonomic heart function and cardiorespiratory parameters. Data were collected from 20 young healthy volunteers (aged 21,6±1,3 years old) who remained at initial rest for 10 minutes and then performed three series of ten expirations each with the Shaker device (with rest intervals of 2 minutes between series) in three EP: free pressure (FP) and pressures of 10 (P10) and of 20 cmH2O (P20), then remained at rest for additional 10 minutes. Data were statistically analysed, with significance level set at 5%. After the breathing technique, a statistically significant difference was noticed at heart rate variability indices at FP and a significant increase in systolic blood pressure at P20. Measures of diastolic blood pressure, respiratory frequency and peripheral oxygen saturation showed no difference before, during and after the technique at any EP. Perceived exertion increased significantly along the series at FP and P20, as well as between P10 and P20 in all series. Heart rate increased and decreased in synchronization with inspiration and expiration, respectively. The application of the technique in this population at different expiratory pressures promoted changes in hear rate behaviour, in perceived exertion and, at FP, in heart autonomic modulation

Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells

<p>Abstract</p> <p>Background</p> <p>Although lung cancer is among the few malignancies for which we know the primary etiological agent (i.e., cigarette smoke), a precise understanding of the temporal sequence of events that drive tumor progression remains elusive. In addition to finding that cigarette smoke (CS) impacts the functioning of key pathways with significant roles in redox homeostasis, xenobiotic detoxification, cell cycle control, and endoplasmic reticulum (ER) functioning, our data highlighted a defensive role for the unfolded protein response (UPR) program. The UPR promotes cell survival by reducing the accumulation of aberrantly folded proteins through translation arrest, production of chaperone proteins, and increased degradation. Importance of the UPR in maintaining tissue health is evidenced by the fact that a chronic increase in defective protein structures plays a pathogenic role in diabetes, cardiovascular disease, Alzheimer's and Parkinson's syndromes, and cancer.</p> <p>Methods</p> <p>Gene and protein expression changes in CS exposed human cell cultures were monitored by high-density microarrays and Western blot analysis. Tissue arrays containing samples from 110 lung cancers were probed with antibodies to proteins of interest using immunohistochemistry.</p> <p>Results</p> <p>We show that: 1) CS induces ER stress and activates components of the UPR; 2) reactive species in CS that promote oxidative stress are primarily responsible for UPR activation; 3) CS exposure results in increased expression of several genes with significant roles in attenuating oxidative stress; and 4) several major UPR regulators are increased either in expression (i.e., BiP and eIF2α) or phosphorylation (i.e., phospho-eIF2α) in a majority of human lung cancers.</p> <p>Conclusion</p> <p>These data indicate that chronic ER stress and recruitment of one or more UPR effector arms upon exposure to CS may play a pivotal role in the etiology or progression of lung cancers, and that phospho-eIF2α and BiP may have diagnostic and/or therapeutic potential. Furthermore, we speculate that upregulation of UPR regulators (in particular BiP) may provide a pro-survival advantage by increasing resistance to cytotoxic stresses such as hypoxia and chemotherapeutic drugs, and that UPR induction is a potential mechanism that could be attenuated or reversed resulting in a more efficacious treatment strategy for lung cancer.</p