A review of acoustic telemetry in Europe and the need for a regional aquatic telemetry network

Background Globally, there are a large and growing number of researchers using biotelemetry as a tool to study aquatic animals. In Europe, this community lacks a formal network structure. The aim of this study is to review the use of acoustic telemetry in Europe and document the contribution of cross-boundary studies and inter-research group collaborations. Based on this, we explore the potential benefits and challenges of a network approach to identify future priorities and best practices for aquatic biotelemetry research in Europe. Results Over the past decade, there was an approximately sevenfold increase in the number of acoustic telemetry studies published on marine and diadromous species in Europe compared to a sixfold increase globally. Over 90% of these studies were conducted on fishes and undertaken in coastal areas, estuaries, or rivers. 75% of these studies were conducted by researchers based in one of five nations (Norway, UK, France, Portugal, and Spain) and, even though 34% were based on collaborations between scientists from several countries, there was only one study with an acoustic receiver array that extended beyond the borders of a single country. In recent years, acoustic telemetry in European waters has evolved from studying behavioural aspects of animals (82.2%), into more holistic approaches addressing management-related issues (10%), tagging methods and effects (5%), and technology and data analysis development (2.8%). Conclusions Despite the increasing number of publications and species tracked, there is a prominent lack of planned and structured acoustic telemetry collaborations in Europe. A formal pan-European network structure would promote the development of (1) a research platform that could benefit the acoustic telemetry community through capacity building, (2) a centralized database, and (3) key deployment sites and studies on priority species requiring research in Europe. A network may increase efficiency, expand the scope of research that can be undertaken, promote European science integration, enhance the opportunities and success of acquiring research funding and, ultimately, foster regional and transatlantic collaborations. It may also help address research priorities such as the large-scale societal challenges arising from climate change impacts and assist the EU’s Marine Strategy Framework Directive via identification of good environmental status of endangered or commercially important species.info:eu-repo/semantics/publishedVersio

Increasing leadership capacity for HIV/AIDS programmes by strengthening public health epidemiology and management training in Zimbabwe

<p>Abstract</p> <p>Background</p> <p>Increased funding for global human immunodeficiency virus prevention and control in developing countries has created both a challenge and an opportunity for achieving long-term global health goals. This paper describes a programme in Zimbabwe aimed at responding more effectively to the HIV/AIDS epidemic by reinforcing a critical competence-based training institution and producing public health leaders.</p> <p>Methods</p> <p>The programme used new HIV/AIDS programme-specific funds to build on the assets of a local education institution to strengthen and expand the general public health leadership capacity in Zimbabwe, simultaneously ensuring that they were trained in HIV interventions.</p> <p>Results</p> <p>The programme increased both numbers of graduates and retention of faculty. The expanded HIV/AIDS curriculum was associated with a substantial increase in trainee projects related to HIV. The increased number of public health professionals has led to a number of practically trained persons working in public health leadership positions in the ministry, including in HIV/AIDS programmes.</p> <p>Conclusion</p> <p>Investment of a modest proportion of new HIV/AIDS resources in targeted public health leadership training programmes can assist in building capacity to lead and manage national HIV and other public health programmes.</p

Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

How cells regulate their lysosomal proteolytic capacity is only partly understood. Here, the authors show that lysosomal protease deficiency or substrate overload induces lysosomal stress leading to activation of a STAT3-dependent, TFEB-independent pathway of lysosomal hydrolase expression

Independent S-Locus Mutations Caused Self-Fertility in Arabidopsis thaliana

A common yet poorly understood evolutionary transition among flowering plants is a switch from outbreeding to an inbreeding mode of mating. The model plant Arabidopsis thaliana evolved to an inbreeding state through the loss of self-incompatibility, a pollen-rejection system in which pollen recognition by the stigma is determined by tightly linked and co-evolving alleles of the S-locus receptor kinase (SRK) and its S-locus cysteine-rich ligand (SCR). Transformation of A. thaliana, with a functional AlSRKb-SCRb gene pair from its outcrossing relative A. lyrata, demonstrated that A. thaliana accessions harbor different sets of cryptic self-fertility–promoting mutations, not only in S-locus genes, but also in other loci required for self-incompatibility. However, it is still not known how many times and in what manner the switch to self-fertility occurred in the A. thaliana lineage. Here, we report on our identification of four accessions that are reverted to full self-incompatibility by transformation with AlSRKb-SCRb, bringing to five the number of accessions in which self-fertility is due to, and was likely caused by, S-locus inactivation. Analysis of S-haplotype organization reveals that inter-haplotypic recombination events, rearrangements, and deletions have restructured the S locus and its genes in these accessions. We also perform a Quantitative Trait Loci (QTL) analysis to identify modifier loci associated with self-fertility in the Col-0 reference accession, which cannot be reverted to full self-incompatibility. Our results indicate that the transition to inbreeding occurred by at least two, and possibly more, independent S-locus mutations, and identify a novel unstable modifier locus that contributes to self-fertility in Col-0

Specific Humoral Immunity versus Polyclonal B Cell Activation in Trypanosoma cruzi Infection of Susceptible and Resistant Mice

Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 10–12 million people in Latin America. Patent parasitemia develops during acute disease. During this phase, polyclonal B cell activation has been reported to generate high levels of serum antibody with low parasite specificity, and delayed protective humoral immunity, which is necessary to prevent the host from succumbing to infection. In this manuscript, data show that relatively resistant mice have improved parasite-specific humoral immunity and decreased polyclonal B cell activation compared to susceptible mice. Parasite-specific humoral immunity was associated with differential expansion of B cell subsets and T cells in the spleen, as well as with increased Th1 and decreased Th2 cytokine production. These data suggest that host susceptibility/genetic biases impact the development of humoral responses to infection. Th2 cytokines are generally associated with improved antibody responses. In the context of T. cruzi infection of susceptible mice, Th2 cytokines were associated with increased total antibody production concomitant with delayed pathogen-specific humoral immunity. This study highlights the need to consider the effect of host biases when investigating humoral immunity to any pathogen that has reported polyclonal B cell activation during infection

Combination therapy with oral treprostinil for pulmonary arterial hypertension. A double-blind placebo-controlled clinical trial

Rationale: Oral treprostinil improves exercise capacity in patients with pulmonary arterial hypertension (PAH), but the effect on clinical outcomes was unknown. Objectives: To evaluate the effect of oral treprostinil compared with placebo on time to first adjudicated clinical worsening event in participants with PAH who recently began approved oral monotherapy. Methods: In this event-driven, double-blind study, we randomly allocated 690 participants (1:1 ratio) with PAH to receive placebo or oral treprostinil extended-release tablets three times daily. Eligible participants were using approved oral monotherapy for over 30 days before randomization and had a 6-minute-walk distance 150 m or greater. The primary endpoint was the time to first adjudicated clinical worsening event: death; hospitalization due to worsening PAH; initiation of inhaled or parenteral prostacyclin therapy; disease progression; or unsatisfactory long-term clinical response. Measurements and Main Results: Clinical worsening occurred in 26% of the oral treprostinil group compared with 36% of placebo participants (hazard ratio, 0.74; 95% confidence interval, 0.56–0.97; P = 0.028). Key measures of disease status, including functional class, Borg dyspnea score, and N-terminal pro–brain natriuretic peptide, all favored oral treprostinil treatment at Week 24 and beyond. A noninvasive risk stratification analysis demonstrated that oral treprostinil–assigned participants had a substantially higher mortality risk at baseline but achieved a lower risk profile from Study Weeks 12–60. The most common adverse events in the oral treprostinil group were headache, diarrhea, flushing, nausea, and vomiting. Conclusions: In participants with PAH, addition of oral treprostinil to approved oral monotherapy reduced the risk of clinical worsening. Clinical trial registered with www.clinicaltrials.gov (NCT01560624)

Gastrointestinal Hyperplasia with Altered Expression of DNA Polymerase β

Background: Altered expression of DNA polymerase β (Pol β) has been documented in a large percentage of human tumors. However, tumor prevalence or predisposition resulting from Pol β over-expression has not yet been evaluated in a mouse model. Methodology/Principal Findings: We have recently developed a novel transgenic mouse model that over-expresses Pol β. These mice present with an elevated incidence of spontaneous histologic lesions, including cataracts, hyperplasia of Brunner's gland and mucosal hyperplasia in the duodenum. In addition, osteogenic tumors in mice tails, such as osteoma and osteosarcoma were detected. This is the first report of elevated tumor incidence in a mouse model of Pol β over-expression. These findings prompted an evaluation of human gastrointestinal tumors with regard to Pol β expression. We observed elevated expression of Pol β in stomach adenomas and thyroid follicular carcinomas, but reduced Pol β expression in esophageal adenocarcinomas and squamous carcinomas. Conclusions/Significance: These data support the hypothesis that balanced and proficient base excision repair protein expression and base excision repair capacity is required for genome stability and protection from hyperplasia and tumor formation