Isolation and characterization of sea urchin P.lividus microbiota from coelomic fluid: bachelor's thesis : diploma 2016

The identification of the microbiota present in the coelomic fluid of Paracentrotus lividus has been highlighted in order to understand the role of bacteria in the physiology, ecology and aquaculture activities of this echinoderm

Period prevalence of SARS-CoV-2 infections and willingness to vaccinate in Swiss elite athletes.

Objectives (1) To assess the period prevalence of SARS-CoV-2 infections and willingness to vaccinate in Swiss elite athletes and (2) to evaluate whether sociodemographic and sport-related characteristics were associated with infection of SARS-CoV-2 in athletes. Methods A total of 1037 elite athletes (Mage=27.09) were surveyed in this cross-sectional study. They were asked whether they had been infected with SARS-CoV-2 and whether they would like to be vaccinated. Characteristics of a possible COVID-19 illness were also recorded. Results During the first year of the pandemic, 14.6% of all Swiss elite athletes were found to be infected with SARS-CoV-2, and 5.4% suspected that they had been infected. Male athletes, young athletes and team sports athletes had an increased likelihood of being infected with SARS-CoV-2. There was considerable heterogeneity in the duration and severity of a COVID-19 illness in athletes. Overall, 68% of respondents indicated a willingness to be vaccinated if they were offered an opportunity to do so. Conclusion In the first year of the pandemic, Swiss elite athletes were tested more often positive for SARS-CoV-2 than the general Swiss population. Because COVID-19 illness can impair health for a relatively long time, sports federations are advised to motivate athletes to be vaccinated

The Specificity and Polymorphism of the MHC Class I Prevents the Global Adaptation of HIV-1 to the Monomorphic Proteasome and TAP

The large diversity in MHC class I molecules in a population lowers the chance that a virus infects a host to which it is pre-adapted to escape the MHC binding of CTL epitopes. However, viruses can also lose CTL epitopes by escaping the monomorphic antigen processing components of the pathway (proteasome and TAP) that create the epitope precursors. If viruses were to accumulate escape mutations affecting these monomorphic components, they would become pre-adapted to all hosts regardless of the MHC polymorphism. To assess whether viruses exploit this apparent vulnerability, we study the evolution of HIV-1 with bioinformatic tools that allow us to predict CTL epitopes, and quantify the frequency and accumulation of antigen processing escapes. We found that within hosts, proteasome and TAP escape mutations occur frequently. However, on the population level these escapes do not accumulate: the total number of predicted epitopes and epitope precursors in HIV-1 clade B has remained relatively constant over the last 30 years. We argue that this lack of adaptation can be explained by the combined effect of the MHC polymorphism and the high specificity of individual MHC molecules. Because of these two properties, only a subset of the epitope precursors in a host are potential epitopes, and that subset differs between hosts. We estimate that upon transmission of a virus to a new host 39%–66% of the mutations that caused epitope precursor escapes are released from immune selection pressure

Plague risk in the western United States over seven decades of environmental change

After several pandemics over the last two millennia, the wildlife reservoirs of plague (Yersinia pestis) now persist around the world, including in the western United States. Routine surveillance in this region has generated comprehensive records of human cases and animal seroprevalence, creating a unique opportunity to test how plague reservoirs are responding to environmental change. Here, we test whether animal and human data suggest that plague reservoirs and spillover risk have shifted since 1950. To do so, we develop a new method for detecting the impact of climate change on infectious disease distributions, capable of disentangling long-term trends (signal) and interannual variation in both weather and sampling (noise). We find that plague foci are associated with high-elevation rodent communities, and soil biochemistry may play a key role in the geography of long-term persistence. In addition, we find that human cases are concentrated only in a small subset of endemic areas, and that spillover events are driven by higher rodent species richness (the amplification hypothesis) and climatic anomalies (the trophic cascade hypothesis). Using our detection model, we find that due to the changing climate, rodent communities at high elevations have become more conducive to the establishment of plague reservoirs—with suitability increasing up to 40% in some places—and that spillover risk to humans at mid-elevations has increased as well, although more gradually. These results highlight opportunities for deeper investigation of plague ecology, the value of integrative surveillance for infectious disease geography, and the need for further research into ongoing climate change impacts

Climate-driven introduction of the Black Death and successive plague reintroductions into Europe

The Black Death, originating in Asia, arrived in the Mediterranean harbors of Europe in 1347 CE, via the land and sea trade routes of the ancient Silk Road system. This epidemic marked the start of the second plague pandemic, which lasted in Europe until the early 19th century. This pandemic is generally understood as the consequence of a singular introduction of Yersinia pestis, after which the disease established itself in European rodents over four centuries. To locate these putative plague reservoirs, we studied the climate fluctuations that preceded regional plague epidemics, based on a dataset of 7,711 georeferenced historical plague outbreaks and 15 annually resolved tree-ring records from Europe and Asia. We provide evidence for repeated climate-driven reintroductions of the bacterium into European harbors from reservoirs in Asia, with a delay of 15 ± 1 y. Our analysis finds no support for the existence of permanent plague reservoirs in medieval Europe

Auxin-dependent cell cycle reactivation through transcriptional regulation of Arabidopsis E2Fa by lateral organ boundary proteins

Multicellular organisms depend on cell production, cell fate specification, and correct patterning to shape their adult body. In plants, auxin plays a prominent role in the timely coordination of these different cellular processes. A well-studied example is lateral root initiation, in which auxin triggers founder cell specification and cell cycle activation of xylem pole-positioned pericycle cells. Here, we report that the E2Fa transcription factor of Arabidopsis thaliana is an essential component that regulates the asymmetric cell division marking lateral root initiation. Moreover, we demonstrate that E2Fa expression is regulated by the LATERAL ORGAN BOUNDARY DOMAIN18/LATERAL ORGAN BOUNDARY DOMAIN33 (LBD18/LBD33) dimer that is, in turn, regulated by the auxin signaling pathway. LBD18/LBD33 mediates lateral root organogenesis through E2Fa transcriptional activation, whereas E2Fa expression under control of the LBD18 promoter eliminates the need for LBD18. Besides lateral root initiation, vascular patterning is disrupted in E2Fa knockout plants, similarly as it is affected in auxin signaling and lbd mutants, indicating that the transcriptional induction of E2Fa through LBDs represents a general mechanism for auxin-dependent cell cycle activation. Our data illustrate how a conserved mechanism driving cell cycle entry has been adapted evolutionarily to connect auxin signaling with control of processes determining plant architecture

The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes

BACKGROUND: HIV-1 viruses are highly capable of mutating their proteins to escape the presentation of CTL epitopes in their current host. Upon transmission to another host, some escape mutations revert, but other remain stable in the virus sequence for at least several years. Depending on the rate of accumulation and reversion of escape mutations, HIV-1 could reach a high level of adaptation to the human population. Yusim et. al. hypothesized that the apparent clustering of CTL epitopes in the conserved regions of HIV-1 proteins could be an evolutionary signature left by large-scale adaptation of HIV-1 to its human/simian host. RESULTS: In this paper we quantified the distribution of CTL epitopes in HIV-1 and found that that in 99% of the HIV-1 protein sequences, the epitope distribution was indistinguishable from random. Similar percentages were found for HCV, Influenza and for three eukaryote proteomes (Human, Drosophila, Yeast). CONCLUSION: We conclude that CTL epitopes in HIV-1 are randomly distributed, and that this distribution is similar to the distribution of CTL epitopes in proteins from other proteomes. Therefore, the visually apparent clustering of CTL epitopes in epitope maps should not be interpreted as a signature of a past large-scale adaptation of HIV-1 to the human cellular immune response

Long-Term Oncological Efficacy of Retroperitoneoscopic Radical Nephrectomy of Localized Renal Cell Cancer pT1-3 (≤12 cm)

Investigation of oncological efficacy in retroperitoneoscopic radical nephrectomy (RRN) of patients with localized renal cell carcinoma (RCC). Consecutive patients undergoing RRN for localized stage pT1-3 RCC in 2 tertiary care centers in Switzerland were evaluated. Excellent long-term oncological efficacy was found. Our long-term follow-up validates the survival outcome from comparable literature after conventional open or laparoscopic radical nephrectomy

Quasiparticle Lifetime in a Finite System: A Non--Perturbative Approach

The problem of electron--electron lifetime in a quantum dot is studied beyond perturbation theory by mapping it onto the problem of localization in the Fock space. We identify two regimes, localized and delocalized, corresponding to quasiparticle spectral peaks of zero and finite width, respectively. In the localized regime, quasiparticle states are very close to single particle excitations. In the delocalized state, each eigenstate is a superposition of states with very different quasiparticle content. A transition between the two regimes occurs at the energy $\simeq\Delta(g/\ln g)^{1/2}$, where $\Delta$ is the one particle level spacing, and $g$ is the dimensionless conductance. Near this energy there is a broad critical region in which the states are multifractal, and are not described by the Golden Rule.Comment: 13 pages, LaTeX, one figur