In Diamond Health

In contrast to the sparkling gemstone, diamond-like carbon (DLC) is a thin film coating that is dense, inert, low friction and hard wearing. Interdisciplinary research, involving materials scientists, physicists, mechanical engineers, biomedical specialists and clinicians, is continuously expanding the potential and applications of DLC and enhanced carbon-based materials in the medical sector

Foreground separation methods for satellite observations of the cosmic microwave background

A maximum entropy method (MEM) is presented for separating the emission due to different foreground components from simulated satellite observations of the cosmic microwave background radiation (CMBR). In particular, the method is applied to simulated observations by the proposed Planck Surveyor satellite. The simulations, performed by Bouchet and Gispert (1998), include emission from the CMBR, the kinetic and thermal Sunyaev-Zel'dovich (SZ) effects from galaxy clusters, as well as Galactic dust, free-free and synchrotron emission. We find that the MEM technique performs well and produces faithful reconstructions of the main input components. The method is also compared with traditional Wiener filtering and is shown to produce consistently better results, particularly in the recovery of the thermal SZ effect.Comment: 31 pages, 19 figures (bitmapped), accpeted for publication in MNRA

Weird weather in Bristol during the Grindelwald Fluctuation (1560–1630)

The Grindelwald Fluctuation (1560–1630) was a cooling phase during the ‘Little Ice Age’ (c.1300–1850). Poor weather during the Fluctuation contributed to harvest failures, mass starvation and political crises across the globe. This paper examines information taken from Bristol chronicles that discuss some of the extreme weather events of the period. The entries support the notion that the Grindelwald Fluctuation featured some extraordinarily poor weather, such as great frosts, floods, severe storms, unseasonal snowfalls and droughts

Postexercise hypotension and related hemodynamic responses to cycling under heat stress in untrained men with elevated blood pressure.

PURPOSE: To investigate the effect of heat stress on postexercise hypotension. METHODS: Seven untrained men, aged 21-33 years, performed two cycling bouts at 60% of oxygen uptake reserve expending 300 kcal in environmental temperatures of 21 °C (TEMP) and 35 °C (HOT) in a randomized, counter-balanced order. Physiological responses were monitored for 10-min before and 60-min after each exercise bout, and after a non-exercise control session (CON). Blood pressure (BP) also was measured during the subsequent 21-h recovery period. RESULTS: Compared to CON, systolic, and diastolic BPs were significantly reduced in HOT (Δ = - 8.3 ± 1.6 and - 9.7 ± 1.4 mmHg, P < 0.01) and TEMP (Δ = - 4.9 ± 2.1 and - 4.5 ± 0.9 mmHg, P < 0.05) during the first 60 min of postexercise recovery. Compared to TEMP, rectal temperature was 0.6 °C higher (P = 0.001), mean skin temperature was 1.8 °C higher (P = 0.013), and plasma volume (PV) was 2.6 percentage points lower (P = 0.005) in HOT. During the subsequent 21-h recovery period systolic BP was 4.2 mmHg lower in HOT compared to CON (P = 0.016) and 2.5 mmHg lower in HOT compared to TEMP (P = 0.039). CONCLUSION: Exercise in the heat increases the hypotensive effects of exercise for at least 22 h in untrained men with elevated blood pressure. Our findings indicate that augmented core and skin temperatures and decreased PV are the main hemodynamic mechanisms underlying a reduction in BP after exercise performed under heat stress

Dietary glycaemic index and glycaemic load among Australian adults – results from the 2011–2012 Australian Health Survey

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PGC-1 family coactivators and cell fate: roles in cancer, neurodegeneration, cardiovascular disease and retrograde mitochondria-nucleus signalling.

Over the past two decades, a complex nuclear transcriptional machinery controlling mitochondrial biogenesis and function has been described. Central to this network are the PGC-1 family coactivators, characterised as master regulators of mitochondrial biogenesis. Recent literature has identified a broader role for PGC-1 coactivators in both cell death and cellular adaptation under conditions of stress, here reviewed in the context of the pathology associated with cancer, neurodegeneration and cardiovascular disease. Moreover, we propose that these studies also imply a novel conceptual framework on the general role of mitochondrial dysfunction in disease. It is now well established that the complex nuclear transcriptional control of mitochondrial biogenesis allows for adaptation of mitochondrial mass and function to environmental conditions. On the other hand, it has also been suggested that mitochondria alter their function according to prevailing cellular energetic requirements and thus function as sensors that generate signals to adjust fundamental cellular processes through a retrograde mitochondria-nucleus signalling pathway. Therefore, altered mitochondrial function can affect cell fate not only directly by modifying cellular energy levels or redox state, but also indirectly, by altering nuclear transcriptional patterns. The current literature on such retrograde signalling in both yeast and mammalian cells is thus reviewed, with an outlook on its potential contribution to disease through the regulation of PGC-1 family coactivators. We propose that further investigation of these pathways will lead to the identification of novel pharmacological targets and treatment strategies to combat disease

Aquatic Macrophyte Change in the UK Upland Waters Monitoring Network

Established in 1988, the UK Upland Waters Monitoring Network (UKUWMN) was initiated by the UK Government to monitor the effects of emission control legislation on the water chemistry and biodiversity of 22 lakes and streams across the UK. Since monitoring commenced, the water chemistry of most sites has shown clear signs of recovery (e.g. rising pH and declining labile aluminium concentrations). Aquatic plants are a key component of freshwater biodiversity, but their response to changes in water acidity have received much less attention than other biological groups such as fish or macroinvertebrates. Project-specific standardised plant survey methodologies have been used throughout the time-series, and these have been augmented by Water Framework Directive Common Standards Monitoring Methodology survey techniques at lake sites since 2009, and at stream sites since 2019. The current study aims to determine the extent to which these stream and lake plant communities may have responded to regional reductions in aquatic acidity and to what degree any recovery may be confounded by other drivers such as climate-related changes in water temperature, hydrology, flow and storminess, hydromorphology and additionally the changing light climate/ice cover environment in lakes. A second aim is to examine the preservation and scientific potential of plant DNA in lakes for reconstructing past aquatic plant assemblages by comparing the current water sample eDNA, annual sediment trap sedDNA and sediment core sedDNA records with the known biomonitoring records

Phosphoproteome dynamics during mitotic exit in budding yeast

The cell division cycle culminates in mitosis when two daughter cells are born. As cyclin‐dependent kinase (Cdk) activity reaches its peak, the anaphase‐promoting complex/cyclosome (APC/C) is activated to trigger sister chromatid separation and mitotic spindle elongation, followed by spindle disassembly and cytokinesis. Degradation of mitotic cyclins and activation of Cdk‐counteracting phosphatases are thought to cause protein dephosphorylation to control these sequential events. Here, we use budding yeast to analyze phosphorylation dynamics of 3,456 phosphosites on 1,101 proteins with high temporal resolution as cells progress synchronously through mitosis. This reveals that successive inactivation of S and M phase Cdks and of the mitotic kinase Polo contributes to order these dephosphorylation events. Unexpectedly, we detect as many new phosphorylation events as there are dephosphorylation events. These correlate with late mitotic kinase activation and identify numerous candidate targets of these kinases. These findings revise our view of mitotic exit and portray it as a dynamic process in which a range of mitotic kinases contribute to order both protein dephosphorylation and phosphorylation