Mindfulness-related meditation practices engage various cognitive skills including the ability to focus and sustain attention, which in itself requires several interacting attentional subfunctions. There is increasing behavioural and neuroscientific evidence that mindfulness meditation improves these functions and associated neural processes. More so than other cognitive training programmes, the effects of meditation appear to generalise to other cognitive tasks, thus demonstrating far transfer effects. As these attentional functions have been linked to age-related cognitive decline, there is growing interest in the question whether meditation can slowdown or even prevent such decline. The cognitive reserve hypothesis builds on evidence that various lifestyle factors can lead to better cognitive performance in older age than would be predicted by the existing degree of brain pathology. We argue that mindfulness meditation, as a combination of brain network and brain state training, may increase cognitive reserve capacity and may mitigate age-related declines in cognitive functions. We consider available direct and indirect evidence from the perspective of cognitive reserve theory. The limited available evidence suggests that MM may enhance cognitive reserve capacity directly through the repeated activation of attentional functions and of the multiple demand system and indirectly through the improvement of physiological mechanisms associated with stress and immune function. The article concludes with outlining research strategies for addressing underlying empirical questions in more substantial ways.

No abstract

No abstract

Multifrequency bioimpedance spectroscopy (BIS) is an established method for assessing fluid status in chronic kidney disease (CKD). However, the technique is lacking in predictive value and accuracy. BIS algorithms assume constant tissue resistivity, which may vary with changing tissue ionic sodium concentration (Na+). This may introduce significant inaccuracies to BIS outputs. To investigate this, we used 23 Na magnetic resonance imaging (MRI) to measure Na + in muscle and subcutaneous tissues of 10 healthy controls (HC) and 20 patients with CKD 5 (not on dialysis). The extracellular (Re) and intracellular (Ri) resistance, tissue capacitance, extracellular (ECW) and total body water (TBW) was measured using BIS. Tissue water content was assessed using proton density-weighted MRI with fat suppression. BIS-derived volume indices were comparable in the two groups (OH: HC-0.4±0.9L v CKD 0.5±1.9L, p=0.13). However, CKD patients had higher Na + (HC 21.2±3.0, CKD 25.3±7.4mmol/L; p=0.04) and significantly lower Re (HC 693±93.6, CKD 609±74.3Ohms; p=0.01); Ri and capacitance did not vary. Na + showed a significant inverse linear relationship to Re (rs=-0.598, p<0.01) but not Ri. This relationship of Re (y) and Na + (x) is described equation y=-7.39x+814. A 20% increase in tissue ionic Na + is likely to overestimate ECW by 1.2-2.4L. Tissue Na + concentration has a significant inverse linear relationship to Re. BIS algorithms to account for this effect could improve prediction accuracy of bioimpedance derived fluid status in CKD.

The significant increase of periodontitis, chronic kidney disease (CKD), Alzheimer's disease and cancer can be attributed to an ageing population. Each disease produces a range of biomarkers that can be indicative of disease onset and progression. Biomarkers are defined as cellular (intra/extracellular components and whole cells), biochemical (metabolites, ions and toxins) or molecular (nucleic acids, proteins and lipids) alterations which are measurable in biological media such as human tissues, cells or fluids. An interesting group of biomarkers that merit further investigation are the polyamines. The polyamines are a group of molecules consisting of cadaverine, putrescine, spermine and spermidine and these have been implicated in the development of a range of systemic disease, in part due to their production in periodontitis. Cadaverine and putrescine within the periodontal environment have demonstrated cell signalling interfering abilities, by way of leukocyte migration disruption.The polyamines spermine and spermidine in tumour cells have been shown to inhibit cellular apoptosis, effectively prolonging tumorigenesis and continuation of cancer within the host.Polyamine degradation products such as acrolein have been shown to exacerbate renal damage in CKD patients. Thus, the use of such molecules has merit to be utilised in the early indication of such diseases in patients.

Proteolysis of insulin-like growth factor-binding proteins (IGFBPs) may be an important mechanism to regulate IGF availability and IGF-independent functions of IGFBPs. We analyzed the secretion of IGFBP proteases in Madin-Darby canine kidney (MDCK) cells. The results showed that several specific proteases were secreted, cleaving IGFBP-2 to -6 at neutral pH. The proteolytic activity against IGFBP-6 differed at least from IGFBP-5 protease activity in its sensitivity both to IGF-II and to the hydroxamic acid-based disintegrin metalloprotease inhibitor, as well as serine protease inhibitors. During partial purification steps, the serine protease inhibitor-sensitive fraction with IGFBP-6 protease activity was separated from fractions characterized by the presence of a 30-kDa disintegrin immunoreactive band. Whereas the IGFBP-4 and -6 proteases are predominantly secreted across the basolateral membrane, the majority of IGFBPs are sorted to the apical medium from filter-grown cells. These studies indicate that the side-specific secretion of several distinct IGFBP proteases with partially overlapping IGFBP specificities may be another level in the regulation of IGF-dependent epithelial functions.

The reduction of bacteria and biofilm formation is important when designing surfaces for use in industry. Molybdenum disulphide surfaces (MoS2SUR) were produced using MoS2 particle (MoS2PAR) sizes of 90 nm 2 µm and 6 µm containing MoS2PAR concentrations of 5%, 10%, 15% and 20%. These were tested to determine the efficacy of the MoS2SUR to impede bacterial retention and biofilm formation of two different types of bacteria, Staphylococcus aureus and Pseudomonas aeruginosa. The MoS2SUR were characterised using Fourier Transform InfraRed Spectroscopy, Ion Coupled Plasma Atomic Emission Spectroscopy, Scanning Electron Microscopy, Optical Profilometry and Water Contact Angles. The MoS2SUR made with the smaller 90 nm MoS2PAR sizes demonstrated smaller topographical shaped features. As the size of the incorporated MoS2PAR increased, the MoS2SUR demonstrated wider surface features, and they were less wettable. The increase in MoS2PAR concentration within the MoS2SUR groups did not affect the surface topography but did increase wettability. However, the increase in MoS2PAR size increased both the surface topography and wettability. The MoS2SUR with the smaller topographical shaped features, influenced the retention of the S. aureus bacteria. Increased MoS2SUR topography and wettability resulted in the greatest reduction in bacterial retention and the bacteria became more heterogeneously dispersed and less clustered across the surfaces. The surfaces that exhibited decreased bacterial retention (largest particle sizes, largest features, greatest roughness, most wettable) resulted in decreased biofilm formation. Cytotoxicity testing of the surface using cell viability demonstrated that the MoS2SUR were not toxic against HK-2 cells at MoS2PAR sizes of 90 nm and 2 µm. This work demonstrated that individual surfaces variables (MoS2SUR topographic shape and roughness, MoS2PAR size and concentration) decreased bacterial loading on the surfaces, which then decreased biofilm formation. By optimising MoS2SUR properties, it was possible to impede bacterial retention and subsequent biofilm formation.

Chronic metabolic acidosis occurs commonly in chronic renal failure (CRF). The proximal renal tubular cell is the site in the kidney of high oxidative metabolic activity and in CRF is associated with adaptive hypertrophy and hypermetabolism. We hypothesised that chronic acidosis may lead to increased generation of reactive oxygen species due to increased oxidative activity. We developed a novel model of chronic acidosis in LLC-PK1 cells and measured markers of oxidative stress and metabolism. Acidosis led to a reduction in cellular total glutathione and protein thiol content and an increase in glutathione peroxidase activity and NH₃ generation. The expression of constitutively expressed heat stress protein (HSP) HSC70 and HSP60 increased at pH 7.0.