Bacteria living within guts of animals can provide protection against infection by pathogens. Some pathogens have been shown to use a molecular weapon known as a T6SS to kill beneficial bacteria during invasion of the mouse gut.

A Cu2+ complex for bimodal imaging of cellular hypoxia using 19F magnetic resonance and fluorescence.

The animal microbiota (including the human microbiota) plays an important role in keeping the physiological status of the host healthy. Research seeks greater insight into whether changes in the composition and function of the microbiota are associated with disease. We analyzed published 16S rRNA and shotgun metagenomic sequencing (SMS) data pertaining to the gut microbiotas of 99 subjects monitored over time. Temporal fluctuations in the microbial composition revealed significant differences due to factors such as dietary changes, antibiotic intake, age, and disease. This article shows that a fluctuation scaling law can describe the temporal changes in the gut microbiota. This law estimates the temporal variability of the microbial population and quantitatively characterizes the path toward disease via a noise-induced phase transition. Estimation of the systemic parameters may be of clinical utility in follow-up studies and have more general applications in fields where it is important to know whether a given community is stable or not. IMPORTANCEThe human microbiota correlates closely with the health status of its host. This article analyzes the microbial composition of several subjects under different conditions over time spans that ranged from days to months. Using the Langevin equation as the basis of our mathematical framework to evaluate microbial temporal stability, we proved that stable microbiotas can be distinguished from unstable microbiotas. This initial step will help us to determine how temporal microbiota stability is related to a subject's health status and to develop a more comprehensive framework that will provide greater insight into this complex system.

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Preliminary human studies show that reduced skin temperature minimises the risk of mechanically-induced skin damage. However, the mechanisms by which cooling enhances skin tolerance to pressure and shear remain poorly understood. We hypothesized that skin cooling below thermo-neutral conditions will decrease friction at the skin-material interface. To test our hypothesis, we measured the friction coefficient of a thermally pre-conditioned index finger sliding at a normal load (5N) across a plate maintained at three different temperatures (38, 24, and 16°C). To quantify the temperature distribution of the skin tissue, we used 3D surface scanning and Optical Coherence Tomography to develop an anatomically-representative thermal model of the finger. Our data indicated that the sliding finger with thermally affected tissues (up to 8mm depth) experienced significantly (p<0.01) lower frictional forces at 16°C-plate temperature than at the 24°C [-23% (19% SD)] and 38°C plate interactions [-35% (11% SD)], respectively. This phenomenon occurred without changes in skin hydration during sliding. Accordingly, our experiments demonstrate thermal modulation of skin friction in the absence of skin-moisture effects. Our complementary experimental and theoretical results provide new insight into thermal modulation of skin friction that can be employed for developing thermal technologies to maintain skin integrity under mechanical loading.