Prolactin delays hair regrowth in mice

Mammalian hair growth is cyclic, with hair-producing follicles alternating between active (anagen) and quiescent (telogen) phases. The timing of hair cycles is advanced in prolactin receptor (PRLR) knockout mice, suggesting that prolactin has a role in regulating follicle cycling. In this study, the relationship between profiles of circulating prolactin and the first post-natal hair growth cycle was examined in female Balb/c mice. Prolactin was found to increase at 3 weeks of age, prior to the onset of anagen 1 week later. Expression of PRLR mRNA in skin increased fourfold during early anagen. This was followed by upregulation of prolactin mRNA, also expressed in the skin. Pharmacological suppression of pituitary prolactin advanced dorsal hair growth by 3.5 days. Normal hair cycling was restored by replacement with exogenous prolactin for 3 days. Increasing the duration of prolactin treatment further retarded entry into anagen. However, prolactin treatments, which began after follicles had entered anagen at 26 days of age, did not alter the subsequent progression of the hair cycle. Skin from PRLR-deficient mice grafted onto endocrine-normal hosts underwent more rapid hair cycling than comparable wild-type grafts, with reduced duration of the telogen phase. These experiments demonstrate that prolactin regulates the timing of hair growth cycles in mice via a direct effect on the skin, rather than solely via the modulation of other endocrine factors

Nernst effect of iron pnictide and cuprate superconductors: signatures of spin density wave and stripe order

The Nernst effect has recently proven a sensitive probe for detecting unusual normal state properties of unconventional superconductors. In particular, it may sensitively detect Fermi surface reconstructions which are connected to a charge or spin density wave (SDW) ordered state, and even fluctuating forms of such a state. Here we summarize recent results for the Nernst effect of the iron pnictide superconductor $\rm LaO_{1-x}F_xFeAs$, whose ground state evolves upon doping from an itinerant SDW to a superconducting state, and the cuprate superconductor $\rm La_{1.8-x}Eu_{0.2}Sr_xCuO_4$ which exhibits static stripe order as a ground state competing with the superconductivity. In $\rm LaO_{1-x}F_xFeAs$, the SDW order leads to a huge Nernst response, which allows to detect even fluctuating SDW precursors at superconducting doping levels where long range SDW order is suppressed. This is in contrast to the impact of stripe order on the normal state Nernst effect in $\rm La_{1.8-x}Eu_{0.2}Sr_xCuO_4$. Here, though signatures of the stripe order are detectable in the temperature dependence of the Nernst coefficient, its overall temperature dependence is very similar to that of $\rm La_{2-x}Sr_xCuO_4$, where stripe order is absent. The anomalies which are induced by the stripe order are very subtle and the enhancement of the Nernst response due to static stripe order in $\rm La_{1.8-x}Eu_{0.2}Sr_xCuO_4$ as compared to that of the pseudogap phase in $\rm La_{2-x}Sr_xCuO_4$, if any, is very small.Comment: To appear in: 'Properties and applications of thermoelectric materials - II', V. Zlatic and A. Hewson, editors, Proceedings of NATO Advanced Research Workshop, Hvar, Croatia, September 19 -25, 2011, NATO Science for Peace and Security Series B: Physics and Biophysics, (Springer Science+Business Media B.V. 2012

Manganites at Quarter Filling: Role of Jahn-Teller Interactions

We have analyzed different correlation functions in a realistic spin-orbital model for half-doped manganites. Using a finite-temperature diagonalization technique the CE phase was found in the charge-ordered phase in the case of small antiferromagnetic interactions between $t_{2g}$ electrons. It is shown that a key ingredient responsible for stabilization of the CE-type spin and orbital-ordered state is the cooperative Jahn-Teller (JT) interaction between next-nearest Mn$^{+3}$ neighbors mediated by the breathing mode distortion of Mn$^{+4}$ octahedra and displacements of Mn$^{+4}$ ions. The topological phase factor in the Mn-Mn hopping leading to gap formation in one-dimensional models for the CE phase as well as the nearest neighbor JT coupling are not able to produce the zigzag chains typical for the CE phase in our model.Comment: 16 pages with 16 figures, contains a more detailed parameter estimate based on the structural data by Radaelli et al. (accepted for publication in Phys. Rev. B

Plasma Metabolomics Implicate Modified Transfer RNAs and Altered Bioenergetics in the Outcome of Pulmonary Arterial Hypertension.

BACKGROUND: -Pulmonary arterial hypertension (PAH) is a heterogeneous disorder with high mortality. METHODS: -We conducted a comprehensive study of plasma metabolites using ultra-performance liquid chromatography mass-spectrometry to (1) identify patients at high risk of early death, (2) identify patients who respond well to treatment and (3) provide novel molecular insights into disease pathogenesis. RESULTS: -53 circulating metabolites distinguished well-phenotyped patients with idiopathic or heritable PAH (n=365) from healthy controls (n=121) following correction for multiple testing (p<7.3e-5) and confounding factors, including drug therapy, renal and hepatic impairment. A subset of 20/53 metabolites also discriminated PAH patients from disease controls (symptomatic patients without pulmonary hypertension, n=139). 62 metabolites were prognostic in PAH, with 36/62 independent of established prognostic markers. Increased levels of tRNA-specific modified nucleosides (N2,N2-dimethylguanosine, N1-methylinosine), TCA cycle intermediates (malate, fumarate), glutamate, fatty acid acylcarnitines, tryptophan and polyamine metabolites and decreased levels of steroids, sphingomyelins and phosphatidylcholines distinguished patients from controls. The largest differences correlated with increased risk of death and correction of several metabolites over time was associated with a better outcome. Patients who responded to calcium channel blocker therapy had metabolic profiles similar to healthy controls. CONCLUSIONS: -Metabolic profiles in PAH are strongly related to survival and should be considered part of the deep phenotypic characterisation of this disease. Our results support the investigation of targeted therapeutic strategies that seek to address the alterations in translational regulation and energy metabolism that characterize these patients

Galaxy And Mass Assembly (GAMA): the galaxy stellar mass function to z = 0.1 from the r-band selected equatorial regions

We derive the low-redshift galaxy stellar mass function (GSMF), inclusive of dust corrections, for the equatorial Galaxy And Mass Assembly (GAMA) data set covering 180 deg2. We construct the mass function using a density-corrected maximum volume method, using masses corrected for the impact of optically thick and thin dust. We explore the galactic bivariate brightness plane (M⋆–μ), demonstrating that surface brightness effects do not systematically bias our mass function measurement above 107.5 M⊙. The galaxy distribution in the M–μ plane appears well bounded, indicating that no substantial population of massive but diffuse or highly compact galaxies are systematically missed due to the GAMA selection criteria. The GSMF is fitted with a double Schechter function, with M⋆=1010.78±0.01±0.20M⊙ M⋆=1010.78±0.01±0.20M⊙ , ϕ⋆1=(2.93±0.40)×10−3h370 ϕ1⋆=(2.93±0.40)×10−3h703 Mpc−3, α1 = −0.62 ± 0.03 ± 0.15, ϕ⋆2=(0.63±0.10)×10−3h370 ϕ2⋆=(0.63±0.10)×10−3h703 Mpc−3 and α2 = −1.50 ± 0.01 ± 0.15. We find the equivalent faint end slope as previously estimated using the GAMA-I sample, although we find a higher value of M⋆ M⋆ . Using the full GAMA-II sample, we are able to fit the mass function to masses as low as 107.5  M⊙, and assess limits to 106.5  M⊙. Combining GAMA-II with data from G10-COSMOS, we are able to comment qualitatively on the shape of the GSMF down to masses as low as 106 M⊙. Beyond the well-known upturn seen in the GSMF at 109.5, the distribution appears to maintain a single power-law slope from 109 to 106.5. We calculate the stellar mass density parameter given our best-estimate GSMF, finding Ω⋆=1.66+0.24−0.23±0.97h−170×10−3 Ω⋆=1.66−0.23+0.24±0.97h70−1×10−3 , inclusive of random and systematic uncertainties

Scoping future research for air pollution recovery indicators (APRI). (Workshop report)

Atmospheric nitrogen (N) pollution is a major and ongoing cause of biodiversity loss across the UK, but in some locations N pollution pressures have been declining. In response to these dynamics, JNCC requested a workshop to help to scope Phase 2 of the Air Pollution Recovery Indicators (APRI) project. The damaging effects of excess N load and of gaseous ammonia on many ecosystems are clear. However, the processes and timescales of ecosystem recovery following a decrease in pollution pressure are less well understood. The APRI project aims to take practical steps to fill this knowledge gap by delivering new scientific research focused on indicators of ecosystem and species recovery from N pollution. In Phase 1, predominantly below-ground responses are being studied at a dry heathland site where experimental additions of N were made between 1998 and 2011, revealing lingering effects on soil chemistry, the soil fungi community and vegetation structure (Kowal et al. 2024). The effect on mycorrhizal fungi, and using these fungi as recovery indicators, is being examined in more detail with recently established assessment methods (Arrigoni et al. 2023). Phase 2 of APRI will consider recovery from N impacts more broadly, e.g. by studying other habitats or species. Further empirical research may be commissioned to better understand recovery pathways from air pollution. A workshop was held on 7–8 November 2023 to help develop an action plan for the remainder of the APRI project. This report summarises the workshop discussion and ensuing work. We note that the focus of the APRI project is on assessing recovery. It is therefore essential to contrast responses of ecosystems subject to decreased pollution pressure with indicators from ecosystems experiencing ongoing pollution. Properties that have been used previously to assess impacts can be used to understand recovery, and novel indicators of ecosystem change are also likely to be useful for assessing recovery. Whatever indicators are chosen to assess change, benchmarking data will be needed to assess the range of potential values and relationships with N deposition. Results from the workshop and subsequent discussions include: • Eleven criteria to help choose appropriate indicators in relation to declining N deposition: Speed of response, Sensitivity of response, Specificity of response, Generality to multiple habitats, Relatedness to recovery endpoints, Previous use, Breadth of pollution gradient, Added value to other policy areas, Resilience in face of anticipated change, Feasibility of collection, Measurement uncertainty. • The need to consider a basket of indicators to indicate recovery from N pollution. Such a basket could include examples from different categories e.g. indicators of pressure, biogeochemical response indicators, and biotic response indicators, with individual indicators likely responding over different timescales. The exact choice may depend on the habitat concerned and the availability of prior data, as well as the question being posed and/or policy goal. • Explicit recommendations on sites to target in APRI Phase 2 to gain information on recovery indicator trajectories, namely (i) well-designed field experiments where N addition has ceased, and (ii) point sources of emissions that have ceased to operate, preferably with a super-imposition of an experimental treatment or treatments. Given uncertainties associated with modelled historical, contemporary, and future N deposition and the potential for confounding variables, analysing survey data from across the UK will be unlikely to provide robust information within the timeframes of the APRI Phase 2. We recommend further assessments may help develop detailed plans for empirical work in Phase 2 of APRI. Potential next steps are to: • Finalise a list of potential and priority indicators of recovery from air pollution (which may differ by habitat type), specifically from high levels of N deposition and/or high atmospheric reactive N concentrations. This finalisation could be done through active participation of the air pollution community and the completion of ‘live’ spreadsheets that address potential indicator criteria. • Summarise relevant data on recovery indicators, across key semi-natural habitats. This summary should include data available from other countries with similar environmental contexts, to help disentangle drivers of change in the UK context. This evidence will help understand recovery pathways from air pollution. As above, this could be done through the active participation of the air pollution community and the completion of ‘live’ spreadsheets. Such an approach could also enable gap analyses, for example identifying where we are missing information by habitat and/or environmental conditions. • Identify areas where co-located monitoring of N with existing habitat/species monitoring could enhance the likelihood for establishing recovery indicators. This should enhance other similar activity such as through the Natural Capital and Ecosystem Assessment programme and the UK Air Pollution Impacts on Ecosystems Networks (APIENs). • Develop a list of priority habitats and sites where empirical research is needed to better understand recovery pathways, including a gap analysis of habitats, methods and/or indicators. • Encourage activities that enhance understanding of ammonia emission sources at local scale (e.g. 1 km or less), to help better identify areas where N pollution has decreased, and recovery might be detected. This could include intensive monitoring or collating and sharing information about permitted N sources. • Develop case studies, including potentially from APRI Phase 1, to demonstrate how existing evidence on localised recovery in semi-natural habitats of conservation importance can be used by policy- and decision-makers to help drive policy toward continued reductions in emissions of reactive N

Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension: A United Kingdom cohort study analysis

While traffic and air pollution exposure is associated with increased mortality in numerous diseases, its association with disease severity and outcomes in pulmonary arterial hypertension (PAH) remains unknown.Exposure to particulate matter ≤2.5 μm3 (PM2.5), nitrogen dioxide (NO2) and indirect measures of traffic-related air pollution (distance to main road and length of roads within buffer zones surrounding residential addresses) were estimated for 301 patients with idiopathic/heritable PAH recruited in the UK PAH national Cohort study. Associations with transplant-free survival and pulmonary hemodynamic severity at baseline were assessed, adjusting for confounding variables defined a priori.Higher estimated exposure to PM2.5 was associated with higher risk of death or lung transplant (Unadjusted hazard ratio (HR) 2.68; 95% CI 1.11-6.47 per 3 μg·m-3, p=0.028). This association remained similar when adjusted for potential confounding variables (HR 4.38; 95% CI 1.44-13.36 per 3 μg·m-3, p=0.009). No associations were found between NO2 exposure or other traffic pollution indicators and transplant-free survival Conversely, indirect measures of exposure to traffic-related air pollution within the 500-1000 m buffer zones correlated with the ERS/ESC risk categories as well as pulmonary hemodynamics at baseline. This association was strongest for pulmonary vascular resistance.In idiopathic/heritable PAH, indirect measures of exposure to traffic-related air pollution were associated with disease severity at baseline, whereas higher PM2.5 exposure may independently predict shorter transplant-free survival

Size Doesn't Matter: Towards a More Inclusive Philosophy of Biology

notes: As the primary author, O’Malley drafted the paper, and gathered and analysed data (scientific papers and talks). Conceptual analysis was conducted by both authors.publication-status: Publishedtypes: ArticlePhilosophers of biology, along with everyone else, generally perceive life to fall into two broad categories, the microbes and macrobes, and then pay most of their attention to the latter. ‘Macrobe’ is the word we propose for larger life forms, and we use it as part of an argument for microbial equality. We suggest that taking more notice of microbes – the dominant life form on the planet, both now and throughout evolutionary history – will transform some of the philosophy of biology’s standard ideas on ontology, evolution, taxonomy and biodiversity. We set out a number of recent developments in microbiology – including biofilm formation, chemotaxis, quorum sensing and gene transfer – that highlight microbial capacities for cooperation and communication and break down conventional thinking that microbes are solely or primarily single-celled organisms. These insights also bring new perspectives to the levels of selection debate, as well as to discussions of the evolution and nature of multicellularity, and to neo-Darwinian understandings of evolutionary mechanisms. We show how these revisions lead to further complications for microbial classification and the philosophies of systematics and biodiversity. Incorporating microbial insights into the philosophy of biology will challenge many of its assumptions, but also give greater scope and depth to its investigations