Characterization of Red Mangrove Proproot Epibiont Communities of St. Johns USVI

In May 1989, Hurricane Hugo impacted St. Johns USVI destroying the Red Mangrove (Rhizophora mangle) Forest of Great Lameshur Bay. The impact restricted the tidal flow and caused massive destruction in the mangroves. Hurricane Marilyn (1995) hit St. John causing the storm wall formed by Hugo to be washed out. It returned limited tidal flow to the dead forest. It was not until a subsequent hurricane in 2010 broke down the sediment wall and natural flow returned. Up to that point, water quality restricted any fouling organisms’ survival on the prop roots. By using photo identification, three different bays of St. John were assessed to identify the local fouling community diversity; comparing the new fouling communities of Great Lameshur to that of Hurricane Holes community. The second objective of this study was to use remote sensing data to map the growth rate of the forest. The subsequent Great Lameshur study years showed an increase in similarity to Hurricane Hole as the years progressed. Which is in line with the remote sensing data showing the forest slowly recovering. Given enough time, Great Lameshur Bay’s fouling community is expected to increase in diversity and become similar to undisturbed sites

Conception de réseau iBGP

L’Internet est constitué de plus de 25,000 AS (Autonomous System) échangeant des informations de routage grâce à BGP (Border Gateway Protocol). Dans un AS de taille importante,il n’est pas possible d’établir une session BGP entre chaque paire de routeur pour des raisons de scalabilité. On a alors recours à la réflexion de route. Cependant, cette technique induit une opacité en terme de diffusion des routes, et peut provoquer l’apparition de routages sous-optimaux (en terme de coût IGP), des déflexions de routes, voire des boucles de routage. Dans ce travail nous proposons une solution pour construire une topologie de réflexion de route permettant d’avoir un routage identique à celui d’un full mesh iBGP, y compris en cas de panne simple d’équipement, et en installant un minimum de sessions iBGP. Nous avons appliqué cette méthode sur le réseau d’un opérateur tier-1 et calculé une topologie iBGP robuste à tout cas de panne simple. La topologie obtenue reste de taille comparable à celle actuellement déployée

Designing Optimal iBGP Route-Reflection Topologies

The Border Gateway Protocol (BGP) is used today by all Autonomous Systems (AS) in the Internet. Inside each AS, iBGP sessions distribute the external routes among the routers. In large ASs, relying on a full-mesh of iBGP sessions between routers is not scalable, so route-reflection is commonly used. The scalability of route-reflection compared to an iBGP full-mesh comes at the cost of opacity in the choice of best routes by the routers inside the AS. This opacity induces problems like suboptimal route choices in terms of IGP cost, deflection and forwarding loops. In this work we propose a solution to design iBGP route-reflection topologies which lead to the same routing as with an iBGP full-mesh and having a minimal number of iBGP sessions. Moreover we compute a robust topology even if a single node or link failure occurs. We apply our methodology on the network of a tier-1 ISP. Twice as many iBGP sessions are required to ensure robustness to single IGP failure. The number of required iBGP sessions in our robust topology is however not much larger than in the current iBGP topology used in the tier-1 ISP network

Consecutive Eyeball Pressure Tests Reflect Clinically Relevant Vagal Dysfunction and Recovery in a Patient With Guillain-Barré-Syndrome With Tenacious Cardiac Dysautonomia

Cardiac dysautonomia is a potentially life-threatening complication of Guillain-Barré syndrome (GBS). Proper and prompt recognition of patients at risk and subsequent intensive care unit (ICU) monitoring are mandatory to prevent fatal outcome. Eyeball pressure testing (EP) has been suggested as an easy applicable bedside test for vagal overreactivity in GBS and thus identifying patients at risk. Yet, there is only sparse follow-up data concerning the course of EP findings in GBS. We report a 25 years-old male patient with GBS who underwent consecutive EP (n = 11) during his ICU stay over a period of 11 weeks. The series of tests performed in this patient (and corresponding clinical events) show that EP data might represent an approximation of vagal dysfunction and vagal recovery in GBS. Interestingly, we observed a much longer duration of pathological EP compared to a previous report. The tenacious cardiac dysautonomia in this patient necessitated long-term application of a transvenous temporary pacemaker

A retrospective multi‐center study of treatment, outcome, and prognostic factors in 34 dogs with disseminated aspergillosis in Australia

Background Disseminated aspergillosis (DA) in dogs has a guarded prognosis and there is a lack of a gold standard treatment protocol. Objective To retrospectively assess survival times and factors influencing survival times. Animals Dogs diagnosed with DA from January 2007 to June 2017. Methods Disseminated aspergillosis case data were retrieved from 13 Australian veterinary referral centers, with a diagnosis confirmed with culture or PCR. Factors influencing survival time after diagnosis were quantified using a Cox proportional hazards regression model. Results Thirty-four dogs met the study inclusion criteria. Twenty-two dogs were treated with antifungal treatment and 12 dogs received no antifungal treatment. Accounting for censoring of dogs that were either still alive on the date of data collection or were loss to follow-up, dogs treated with itraconazole alone (n = 8) had a median survival time (MST) of 63 (95% CI: 20−272) days compared to 830 (95% CI: 267-1259) days for the n = 14 dogs that received multimodal antifungal therapy

Clinical and cellular features in patients with primary autosomal recessive microcephaly and a novel CDK5RAP2 mutation

Background Primary autosomal recessive microcephaly (MCPH) is a rare neurodevelopmental disorder that results in severe microcephaly at birth with pronounced reduction in brain volume, particularly of the neocortex, simplified cortical gyration and intellectual disability. Homozygous mutations in the Cyclin-dependent kinase 5 regulatory subunit-associated protein 2 gene CDK5RAP2 are the cause of MCPH3. Despite considerable interest in MCPH as a model disorder for brain development, the underlying pathomechanism has not been definitively established and only four pedigrees with three CDK5RAP2 mutations have been reported. Specifically for MCPH3, no detailed radiological or histological descriptions exist. Methods/Results We sought to characterize the clinical and radiological features and pathological cellular processes that contribute to the human MCPH3 phenotype. Haplotype analysis using microsatellite markers around the MCPH1-7 and PNKP loci in an Italian family with two sons with primary microcephaly, revealed possible linkage to the MCPH3 locus. Sequencing of the coding exons and exon/intron splice junctions of the CDK5RAP2 gene identified homozygosity for the novel nonsense mutation, c.4441C > T (p.Arg1481*), in both affected sons. cMRI showed microcephaly, simplified gyral pattern and hypogenesis of the corpus callosum. The cellular phenotype was assessed in EBV-transformed lymphocyte cell lines established from the two affected sons and compared with healthy male controls. CDK5RAP2 protein levels were below detection level in immortalized lymphocytes from the patients. Moreover, mitotic spindle defects and disrupted γ-tubulin localization to the centrosome were apparent. Conclusion These results suggest that spindle defects and a disruption of centrosome integrity play an important role in the development of microcephaly in MCPH3

Delphi:A Democratic and Cost-Effective Method of Consensus Generation in Transplantation

The Thrombotic Microangiopathy Banff Working Group (TMA-BWG) was formed in 2015 to survey current practices and develop minimum diagnostic criteria (MDC) for renal transplant TMA (Tx-TMA). To generate consensus among pathologists and nephrologists, the TMA BWG designed a 3-Phase study. Phase I of the study is presented here. Using the Delphi methodology, 23 panelists with &gt;3 years of diagnostic experience with Tx-TMA pathology listed their MDC suggesting light, immunofluorescence, and electron microscopy lesions, clinical and laboratory information, and differential diagnoses. Nine rounds (R) of consensus resulted in MDC validated during two Rs using online evaluation of whole slide digital images of 37 biopsies (28 TMA, 9 non-TMA). Starting with 338 criteria the process resulted in 24 criteria and 8 differential diagnoses including 18 pathologic, 2 clinical, and 4 laboratory criteria. Results show that 3/4 of the panelists agreed on the diagnosis of 3/4 of cases. The process also allowed definition refinement for 4 light and 4 electron microscopy lesions. For the first time in Banff classification, the Delphi methodology was used to generate consensus. The study shows that Delphi is a democratic and cost-effective method allowing rapid consensus generation among numerous physicians dealing with large number of criteria in transplantation.</p

Thrombotic Microangiopathy in the Renal Allograft:Results of the TMA Banff Working Group Consensus on Pathologic Diagnostic Criteria

The Banff community summoned the TMA Banff Working Group to develop minimum diagnostic criteria (MDC) and recommendations for renal transplant TMA (Tx-TMA) diagnosis, which currently lacks standardized criteria. Using the Delphi method for consensus generation, 23 nephropathologists (panelists) with &gt;3 years of diagnostic experience with Tx-TMA were asked to list light, immunofluorescence, and electron microscopic, clinical and laboratory criteria and differential diagnoses for Tx-TMA. Delphi was modified to include 2 validations rounds with histological evaluation of whole slide images of 37 transplant biopsies (28 TMA and 9 non-TMA). Starting with 338 criteria in R1, MDC were narrowed down to 24 in R8 generating 18 pathological, 2 clinical, 4 laboratory criteria, and 8 differential diagnoses. The panelists reached a good level of agreement (70%) on 76% of the validated cases. For the first time in Banff classification, Delphi was used to reach consensus on MDC for Tx-TMA. Phase I of the study (pathology phase) will be used as a model for Phase II (nephrology phase) for consensus regarding clinical and laboratory criteria. Eventually in Phase III (consensus of the consensus groups) and the final MDC for Tx-TMA will be reported to the transplantation community.</p

Multi-Level Interactions between the Nuclear Receptor TRα1 and the WNT Effectors β-Catenin/Tcf4 in the Intestinal Epithelium

Intestinal homeostasis results from complex cross-regulation of signaling pathways; their alteration induces intestinal tumorigenesis. Previously, we found that the thyroid hormone nuclear receptor TRα1 activates and synergizes with the WNT pathway, inducing crypt cell proliferation and promoting tumorigenesis. Here, we investigated the mechanisms and implications of the cross-regulation between these two pathways in gut tumorigenesis in vivo and in vitro. We analyzed TRα1 and WNT target gene expression in healthy mucosae and tumors from mice overexpressing TRα1 in the intestinal epithelium in a WNT-activated genetic background (vil-TRα1/Apc mice). Interestingly, increased levels of β-catenin/Tcf4 complex in tumors from vil-TRα1/Apc mice blocked TRα1 transcriptional activity. This observation was confirmed in Caco2 cells, in which TRα1 functionality on a luciferase reporter-assay was reduced by the overexpression of β-catenin/Tcf4. Moreover, TRα1 physically interacted with β-catenin/Tcf4 in the nuclei of these cells. Using molecular approaches, we demonstrated that the binding of TRα1 to its DNA target sequences within the tumors was impaired, while it was newly recruited to WNT target genes. In conclusion, our observations strongly suggest that increased β-catenin/Tcf4 levels i) correlated with reduced TRα1 transcriptional activity on its target genes and, ii) were likely responsible for the shift of TRα1 binding on WNT targets. Together, these data suggest a novel mechanism for the tumor-promoting activity of the TRα1 nuclear receptor