Social networks predict the life and death of honey bees

In complex societies, individuals' roles are reflected by interactions with other conspecifics. Honey bees (Apis mellifera) generally change tasks as they age, but developmental trajectories of individuals can vary drastically due to physiological and environmental factors. We introduce a succinct descriptor of an individual's social network that can be obtained without interfering with the colony. This 'network age' accurately predicts task allocation, survival, activity patterns, and future behavior. We analyze developmental trajectories of multiple cohorts of individuals in a natural setting and identify distinct developmental pathways and critical life changes. Our findings suggest a high stability in task allocation on an individual level. We show that our method is versatile and can extract different properties from social networks, opening up a broad range of future studies. Our approach highlights the relationship of social interactions and individual traits, and provides a scalable technique for understanding how complex social systems function. Honey bee workers take on different tasks for the colony as they age. Here, the authors develop a method to extract a descriptor of the individuals' social networks and show that interaction patterns predict task allocation and distinguish different developmental trajectories

Viral Immune signatures from cerebrospinal fluid extracellular vesicles and particles in HAM and other chronic neurological diseases

Background and objectivesExtracellular vesicles and particles (EVPs) are released from virtually all cell types, and may package many inflammatory factors and, in the case of infection, viral components. As such, EVPs can play not only a direct role in the development and progression of disease but can also be used as biomarkers. Here, we characterized immune signatures of EVPs from the cerebrospinal fluid (CSF) of individuals with HTLV-1-associated myelopathy (HAM), other chronic neurologic diseases, and healthy volunteers (HVs) to determine potential indicators of viral involvement and mechanisms of disease.MethodsWe analyzed the EVPs from the CSF of HVs, individuals with HAM, HTLV-1-infected asymptomatic carriers (ACs), and from patients with a variety of chronic neurologic diseases of both known viral and non-viral etiologies to investigate the surface repertoires of CSF EVPs during disease.ResultsSignificant increases in CD8+ and CD2+ EVPs were found in HAM patient CSF samples compared to other clinical groups (p = 0.0002 and p = 0.0003 compared to HVs, respectively, and p = 0.001 and p = 0.0228 compared to MS, respectively), consistent with the immunopathologically-mediated disease associated with CD8+ T-cells in the central nervous system (CNS) of HAM patients. Furthermore, CD8+ (p < 0.0001), CD2+ (p < 0.0001), CD44+ (p = 0.0176), and CD40+ (p = 0.0413) EVP signals were significantly increased in the CSF from individuals with viral infections compared to those without.DiscussionThese data suggest that CD8+ and CD2+ CSF EVPs may be important as: 1) potential biomarkers and indicators of disease pathways for viral-mediated neurological diseases, particularly HAM, and 2) as possible meditators of the disease process in infected individuals

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.Peer reviewe

Differentiation of group-valued outer measures

This thesis is divided into three parts. In Part I, we define and give properties of semigroup valued measures and of the indefinite integral ʃ₍ ₎f‧dµ , where f is a many-valued function (i.e. relation) with values In a group µ is an outer measure with values in another group, and "•" is an operation from the cartesian product of the two groups into a third. In particular, we present a Lebesgue decomposition for group-valued outer measures and show that the indefinite integral is an outer measure. In Part II, we construct the many-valued (outer) derivative D̅ of an outer measure Ʋ with respect to the outer measure µ based on the notion of the limit of "approximate ratios" Ʋ(A) to µ(A) as the set A shrinks to a point. D̅ depends upon the multiplication "•" , upon an auxiliary "remainder" function r , and upon the specification of convergence (formula omitted) of sets in the measure space. Conditions are given under which Ʋ =ʃ₍ ₎D̅‧dµ. We also provide a general Hahn decomposition theorem and discuss generalized types of Vitali differentiation systems. In Part III, we give some applications, including Radón-Nikodym theorems for outer measures Ʋ and µ: firstly, when µ has values in the non-negative reals and Ʋ has values in a locally convex space and secondly, when Ʋ and µ have values in a Banach space.Science, Faculty ofMathematics, Department ofGraduat

On character amenable Banach algebras

We obtain characterizations of left character amenable Banach algebras in terms of the existence of left phi-approximate diagonals and left phi-virtual diagonals. We introduce the left character amenability constant and find this constant for some Banach algebras. For all locally compact groups G, we show that the Fourier-Stieltjes algebra B(G) is C-character amenable with C \u3c 2 if and only if G is compact. We prove that if A is a character amenable, reflexive, commutative Banach algebra, then A congruent to C(n) for some n is an element of N. We show that the left character amenability of the double dual of a Banach algebra A implies the left character amenability of A, but the converse statement is not true in general. In fact, we give characterizations of character amenability of L(1)(G)** and A(G)**. We show that a natural uniform algebra on a compact space X is character amenable if and only if X is the Choquet boundary of the algebra. We also introduce and study character contractibility of Banach algebras