Bat species diversity and distribution in a disturbed regime at the Lake Bogoria National Reserve,Kenya

Human population growth drives intrusion and progressive conversion of natural habitats for agriculture. We evaluated human impacts on bat species diversity and distribution among four vegetation types in and around Lake Bogoria National Reserve between November 2012 and July 2013. Plants were surveyed using the Braun–Blanquet cover/abundance method, whereas bats were sampled using standard mist nets erected on poles at ground level. Floristic similarity analysis revealed three broad vegetation assemblages, namely riverine vegetation, farmland and Acacia woodland/Acacia–Commiphora woodland. Two hundred and 33 bats representing eleven species in eleven genera and seven families were recorded. These were Epomophorus minimus, Rhinolophus landeri, Hipposideros caffer, Cardioderma cor, Lavia frons, Nycteris hispida, Chaerephon pumilus, Mops condylurus, Neoromicia capensis, Scotoecus hirundo and Scotophilus dinganii. Species richness estimators indicated that sampling for bats at ground level was exhaustive. Bat species richness and diversity were highest in the more structurally complex Acacia woodland compared to more homogenous farmlands where we recorded only common and generalist species that often occur in open habitats. The higher bat species richness and diversity in the Acacia woodland as compared to farmland underscore the importance of remnant natural savannah woodlands in the conservation of bats and other elements of biodiversity .     

Structural and Functional Impact of SRP54 Mutations Causing Severe Congenital Neutropenia

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The spatial scaling of beta diversity

Beta diversity is an important concept used to describe turnover in species composition across a wide range of spatial and temporal scales, and it underpins much of conservation theory and practice. Although substantial progress has been made in the mathematical and terminological treatment of different measures of beta diversity, there has been little conceptual synthesis of potential scale dependence of beta diversity with increasing spatial grain and geographic extent of sampling. Here, we evaluate different conceptual approaches to the spatial scaling of beta diversity, interpreted from ‘fixed’ and ‘varying’ perspectives of spatial grain and extent. We argue that a ‘sliding window’ perspective, in which spatial grain and extent covary, is an informative way to conceptualize community differentiation across scales. This concept more realistically reflects the varying empirical approaches that researchers adopt in field sampling and the varying scales of landscape perception by different organisms. Scale dependence in beta diversity has broad implications for emerging fields in ecology and biogeography, such as the integration of fine‐resolution ecogenomic data with large‐scale macroecological studies, as well as for guiding appropriate management responses to threats to biodiversity operating at different spatial scales.     

Complexity and algorithms for copy-number evolution problems

Background

Cancer is an evolutionary process characterized by the accumulation of somatic mutations in a population of cells that form a tumor. One frequent type of mutations is copy number aberrations, which alter the number of copies of genomic regions. The number of copies of each position along a chromosome constitutes the chromosome’s copy-number profile. Understanding how such profiles evolve in cancer can assist in both diagnosis and prognosis.

Results

We model the evolution of a tumor by segmental deletions and amplifications, and gauge distance from profile \(\mathbf {a}\) to \(\mathbf {b}\) by the minimum number of events needed to transform \(\mathbf {a}\) into \(\mathbf {b}\). Given two profiles, our first problem aims to find a parental profile that minimizes the sum of distances to its children. Given k profiles, the second, more general problem, seeks a phylogenetic tree, whose k leaves are labeled by the k given profiles and whose internal vertices are labeled by ancestral profiles such that the sum of edge distances is minimum.

Conclusions

For the former problem we give a pseudo-polynomial dynamic programming algorithm that is linear in the profile length, and an integer linear program formulation. For the latter problem we show it is NP-hard and give an integer linear program formulation that scales to practical problem instance sizes. We assess the efficiency and quality of our algorithms on simulated instances.

Availability

https://github.com/raphael-group/CNT-ILP

     

Papillomavirus capsid mutation to escape dendritic cell-dependent innate immunity in cervical cancer

Infection with oncogenic human papillomaviruses (HPVs), typified by HPV type 16 (HPV16), is a necessary cause of cervical cancer. Prophylactic vaccination with HPV16 L1 virus-like particles (VLPs) provides immunity. HPV16 VLPs activate dendritic cells and a potent neutralizing immunoglobulin G (IgG) response, yet many cervical cancer patients fail to generate detectable VLP-specific IgG. Therefore, we examined the role of the innate recognition of HPV16 L1 in VLP-induced immune responses and its evasion during carcinogenesis. Nonconservative mutations within HPV16 L1 have been described in isolates from cervical cancer and its precursor, high-grade cervical intraepithelial neoplasia (CIN). We determined the effect of mutations in L1 upon in vitro self-assembly into VLPs and their influence upon the induction of innate and adaptive immune responses in mice. Several nonconservative mutations in HPV16 L1 isolated from high-grade CIN or cervical carcinoma prevent self-assembly of L1 VLPs. Intact VLPs, but not assembly-defective L1, activate dendritic cells to produce proinflammatory factors, such as alpha interferon, that play a critical role in inducing adaptive immunity. Indeed, effective induction of L1-specific IgG1 and IgG2a was dependent upon intact VLP structure. Dendritic cell activation and production of virus-specific neutralizing IgG by VLPs requires MyD88-dependent signaling, although the L1 structure that initiates MyD88-mediated signaling is distinct from the neutralizing epitopes. We conclude that innate recognition of the intact L1 VLP structure via MyD88 is critical in the induction of high-titer neutralizing IgG. Tumor progression is associated with genetic instability and L1 mutants. Selection for assembly-deficient L1 mutations suggests the evasion of MyD88-dependent immune control during cervical carcinogenesis.     

The anti-inflammatory effect of LMWF5A and N-acetyl kynurenine on macrophages: Involvement of aryl hydrocarbon receptor in mechanism of action

After a traumatic insult, macrophages can become activated leading to general inflammation at the site of injury. Activated macrophages are partially regulated by the aryl hydrocarbon receptor (AhR) which when activated suppresses inflammation by limiting the secretion of pro-inflammatory cytokines and promoting the over expression of immuno-modulatory mediators. This study aims to determine whether the low molecular weight fraction of 5% human serum albumin (LMWF5A) and N-acetyl kynurenine (NAK), an N-acetyl tryptophan (NAT) breakdown product in LMWF5A, can regulate inflammation by inhibiting macrophage activation through the AhR since kynurenine is a known AhR agonist. Using LCMS, we demonstrate that NAT is non-enzymatically degraded during accelerated aging of LMWF5A with high heat accelerating degradation. More importantly, NAK is a major degradation product found in LMWF5A. THP-1 monocytes were differentiated into macrophages using phorbol 12-myristate 13-acetate (PMA) and pre-treated with 2-fold dilutions of LMWF5A or synthetic NAK with or without an AhR antagonist (CH223191) prior to overnight stimulation with lipopolysaccharide (LPS). Treatment with LMWF5A caused a 50–70% decrease in IL-6 release throughout the dilution series. A dose-response inhibition of IL-6 release was observed for NAK with maximal inhibition (50%) seen at the highest NAK concentration. Finally, an AhR antagonist partially blocked the anti-inflammatory effect of LMWF5A while completely blocking the effect of NAK. A similar inhibitory effect was observed for CXCL-10, but the AhR antagonist was not effective suggesting additional mechanisms for CXCL-10 release. These preliminary findings suggest that LMWF5A and NAK partially promote the suppression of activated macrophages via the AhR receptor. Therefore, LMWF5A, which contains NAK, is potentially a useful therapeutic in medical conditions where inflammation is prevalent such as trauma, sepsis, and wound healing.