Critical random forests

Let $F(N,m)$ denote a random forest on a set of $N$ vertices, chosen uniformly from all forests with $m$ edges. Let $F(N,p)$ denote the forest obtained by conditioning the Erdos-Renyi graph $G(N,p)$ to be acyclic. We describe scaling limits for the largest components of $F(N,p)$ and $F(N,m)$, in the critical window $p=N^{-1}+O(N^{-4/3})$ or $m=N/2+O(N^{2/3})$. Aldous described a scaling limit for the largest components of $G(N,p)$ within the critical window in terms of the excursion lengths of a reflected Brownian motion with time-dependent drift. Our scaling limit for critical random forests is of a similar nature, but now based on a reflected diffusion whose drift depends on space as well as on time

Cyber HIV/AIDS Intervention in Singapore: Collective Promises and Pitfalls

This article examines the opportunities and challenges of using the Internet both to promote collective action and identity in the Singapore gay community and as a medium for health intervention. It presents a case study of a community-empowerment project by civil society group Action for AIDS. Framed within a societal context which is hostile toward gay people, and in a place where mixed-media campaigns targeting men who have sex with other men (MSM) are prohibited, this article explores the viability of the Internet as an alternative channel to mass media in reaching out to MSM in Singapore. Through a series of semi-structured interviews and virtual ethnographic content analyses, this article weighs the democratizing and collaborative affordances of the Internet against the uninhibited nature of online discussions in the formation of a counterpublic of sexuality where gay individuals collectively elaborate on meanings about erotic practices, identity, and relations between each other and with the state

Age evolution in the mean field forest fire model via multitype branching processes

We study the distribution of ages in the mean field forest fire model introduced by Ráth and Tóth. This model is an evolving random graph whose dynamics combine Erdos–Rényi edge-addition with a Poisson rain of lightning strikes. All edges in a connected component are deleted when any of its vertices is struck by lightning. We consider the asymptotic regime of lightning rates for which the model displays self-organized criticality. The age of a vertex increases at unit rate, but it is reset to zero at each burning time. We show that the empirical age distribution converges as a process to a deterministic solution of an autonomous measure-valued differential equation. The main technique is to observe that, conditioned on the vertex ages, the graph is an inhomogeneous random graph in the sense of Bollobás, Janson and Riordan. We then study the evolution of the ages via the multitype Galton–Watson trees that arise as the limit in law of the component of an identified vertex at any fixed time. These trees are critical from the gelation time onwards

Histologic and phenotypic factors and MC1R status associated with BRAF(V600E), BRAF(V600K), and NRAS mutations in a community-based sample of 414 cutaneous melanomas

Cutaneous melanomas arise through causal pathways involving interplay between exposure to UV radiation and host factors, resulting in characteristic patterns of driver mutations in BRAF, NRAS, and other genes. To gain clearer insights into the factors contributing to somatic mutation genotypes in melanoma, we collected clinical and epidemiologic data, performed skin examinations, and collected saliva and tumor samples from a community-based series of 414 patients aged 18 to 79, newly diagnosed with cutaneous melanoma. We assessed constitutional DNA for nine common polymorphisms in melanocortin-1 receptor gene (MC1R). Tumor DNA was assessed for somatic mutations in 25 different genes. We observed mutually exclusive mutations in BRAF (26%), BRAF (8%), BRAF (5%), and NRAS (9%). Compared to patients with BRAF wild-type melanomas, those with BRAF mutants were significantly younger, had more nevi but fewer actinic keratoses, were more likely to report a family history of melanoma, and had tumors that were more likely to harbor neval remnants. BRAF mutations were also associated with high nevus counts. Both BRAF and NRAS mutants were associated with older age but not with high sun exposure. We also found no association between MC1R status and any somatic mutations in this community sample of cutaneous melanomas, contrary to earlier reports

Leucine-enriched protein feeding does not impair exercise-induced free fatty acid availability and lipid oxidation: beneficial implications for training in carbohydrate-restricted states

Given that the enhanced oxidative adaptations observed when training in carbohydrate (CHO) restricted states are potentially regulated through free fatty acid (FFA) mediated signalling and that leucine rich protein elevates muscle protein synthesis, the present study aimed to test the hypothesis that leucine enriched protein feeding enhances circulating leucine concentration but does not impair FFA availability nor whole body lipid oxidation 56 during exercise. Nine males cycled for 2 h at 70% VO2peak when fasted (PLACEBO) or having consumed a whey protein solution (WHEY) or a leucine enriched whey protein gel (GEL), administered as 22 g 1 hour pre-exercise, 11 g/h during and 22 g thirty minutes post-exercise. Total leucine administration was 14.4 g and 6.3 in GEL and WHEY, respectively. Mean plasma leucine concentrations were elevated in GEL (P= 0.001) compared 60 with WHEY and PLACEBO (375 ± 100, 272 ± 51, 146 ± 14 μmol.L-1 respectively). No differences (P= 0.153) in plasma FFA (WHEY 0.53 ± 0.30, GEL 0.45 ± 0.25, PLACEBO 0.65 ± 0.30, mmol.L-1) or whole body lipid oxidation during exercise (WHEY 0.37 ± 0.26, GEL 0.36 ± 0.24, PLACEBO 0.34 ± 0.24 g/min) were apparent between trials, despite elevated (P= 0.001) insulin in WHEY and GEL compared with PLACEBO (38 ± 16, 35 ± 16, 22 ± 11 pmol.L-1 respectively). We conclude that leucine enriched protein feeding does not impair FFA availability nor whole body lipid oxidation during exercise, thus having practical applications for athletes who deliberately train in CHO restricted states to promote skeletal muscle adaptations

Improving quality of life through the routine use of the Patient Concerns Inventory for head and neck cancer patients: a cluster preference randomized controlled trial

This trial is funded by the RfPB on behalf of the NIHR (PB-PG-0215-36047).Background: The consequences of treatment for Head and Neck cancer (HNC) patients has profound detrimental impacts such as impaired QOL, emotional distress, delayed recovery and frequent use of healthcare. The aim of this trial is to determine if the routine use of the Patients Concerns Inventory (PCI) package in review clinics during the first year following treatment can improve overall quality of life, reduce the social-emotional impact of cancer and reduce levels of distress. Furthermore, we aim to describe the economic costs and benefits of using the PCI. Methods: This will be a cluster preference randomised control trial with consultants either ‘using’ or ‘not using’ the PCI package at clinic. It will involve two centres Leeds and Liverpool. 416 eligible patients from at least 10 consultant clusters are required to show a clinically meaningful difference in the primary outcome. The primary outcome is the percentage of participants with less than good overall quality of life at the final one-year clinic as measured by the University of Washington QOL questionnaire version 4 (UWQOLv4). Secondary outcomes at one-year are the mean social-emotional subscale (UWQOLv4) score, Distress Thermometer (DT) score ≥ 4, and key health economic measures (QALY-EQ-5D-5 L; CSRI). Discussion: This trial will provide knowledge on the effectiveness of a consultation intervention package based around the PCI used at routine follow-up clinics following treatment of head and neck cancer with curative intent. If this intervention is (cost) effective for patients, the next step will be to promote wider use of this approach as standard care in clinical practice. Trial registration: 32,382. Clinical Trials Identifier, NCT03086629. Protocol: Version 3.0, 1st July 2017.Publisher PDFPeer reviewe

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function.

Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease