Emergent structure and dynamics of tropical forest-grassland landscapes

It is thought that tropical forests can exist as an alternative stable state to savanna [1,2]. Therefore, perturbation by climate change or human impact may lead to crossing of a tipping point beyond which there is rapid large-scale forest dieback that is not easily reversed [3-5]. Empirical evidence for bistability due to fire-vegetation feedbacks relies on tree cover bimodality in satellite-observed data [1,2], but this may also be explained by spatial heterogeneity [6], or by biases in the data [7,8]. Theoretical evidence for bistability [9-11] does not consider the interaction of fire with the vegetation landscape. Focusing on landscapes consisting of tropical forest and grassland, we show that the microscopic rules of fire and vegetation spread (as proposed by [12]) lead to an emergent relation between macroscopic forest structure and dynamics. This relation defines a landscape-scale balance equation of forest area change in which the forest perimeter determines the nonlinearity in forest growth while the forest perimeter weighted by adjacent grassland area determines the nonlinearity in forest loss. We demonstrate that our equation enables analysis of resilience or abrupt shifts for a given landscape, using only the landscape state at a single point in time and measurable parameters of the underlying microscopic spatial processes, thereby avoiding the problems associated with reliance on bimodality

Amazonian forest-savanna bistability and human impact

AbstractA bimodal distribution of tropical tree cover at intermediate precipitation levels has been presented as evidence of fire-induced bistability. Here we subdivide satellite vegetation data into those from human-unaffected areas and those from regions close to human-cultivated zones. Bimodality is found to be almost absent in the unaffected regions, whereas it is significantly enhanced close to cultivated zones. Assuming higher logging rates closer to cultivated zones and spatial diffusion of fire, our spatiotemporal mathematical model reproduces these patterns. Given a gradient of climatic and edaphic factors, rather than bistability there is a predictable spatial boundary, a Maxwell point, that separates regions where forest and savanna states are naturally selected. While bimodality can hence be explained by anthropogenic edge effects and natural spatial heterogeneity, a narrow range of bimodality remaining in the human-unaffected data indicates that there is still bistability, although on smaller scales than claimed previously.</jats:p

Tropical Tree Cover in a Heterogeneous Environment: A Reaction-diffusion Model

Observed bimodal tree cover distributions at particular environmental conditions and theoretical models indicate that some areas in the tropics can be in either of the alternative stable vegetation states forest or savanna. However, when including spatial interaction in nonspatial differential equation models of a bistable quantity, only the state with the lowest potential energy remains stable. Our recent reaction-diffusion model of Amazonian tree cover confirmed this and was able to reproduce the observed spatial distribution of forest versus savanna satisfactorily when forced by heterogeneous environmental and anthropogenic variables, even though bistability was underestimated. These conclusions were solely based on simulation results. Here, we perform an analytical and numerical analysis of the model. We derive the Maxwell point (MP) of the homogeneous reaction-diffusion equation without savanna trees as a function of rainfall and human impact and show that the front between forest and nonforest settles at this point as long as savanna tree cover near the front remains sufficiently low. For parameters resulting in higher savanna tree cover near the front, we also find irregular forest-savanna cycles and woodland-savanna bistability, which can both explain the remaining observed bimodality.Comment: 28 pages, 6 figures, 2 tables, supplementary info include

Cochlear erosion due to a facial nerve schwannoma

Facial nerve schwannomas are rare benign neoplasms. We report a case of a 60-year-old woman who initially presented with vestibular complaints. Magnetic resonance imaging (MRI) revealed a facial nerve schwannoma centered on the right geniculate ganglion extending in the labyrinthine segment. The patient consulted again after 2 months because she developed a sudden and severe right-sided sensorineural hearing loss. MRI showed no progression or pathological enhancement in the membranous labyrinth. A cone beam computed tomography (CT) of the temporal bone was performed and revealed a large erosion at the region of the geniculate ganglion in open communication with the middle turn of the cochlea. This case report demonstrates the importance of CT in facial nerve schwannomas for evaluating the impact on the surrounding structures

Plasma cells are not restricted to the CD27+ phenotype:characterization of CD27-CD43+ antibody-secreting cells

Circulating antibody-secreting cells are present in the peripheral blood of healthy individuals reflecting the continued activity of the humoral immune system. Antibody-secreting cells typically express CD27. Here we describe and characterize a small population of antibody-secreting class switched CD19+CD43+ B cells that lack expression of CD27 in the peripheral blood of healthy subjects. In this study, we characterized CD27-CD43+ cells. We demonstrate that class-switched CD27-CD43+ B cells possess characteristics of conventional plasmablasts as they spontaneously secrete antibodies, are morphologically similar to antibody-secreting cells, show downregulation of B cell differentiation markers, and have a gene expression profile related to conventional plasmablasts. Despite these similarities, we observed differences in IgA and IgG subclass distribution, expression of homing markers, replication history, frequency of somatic hypermutation, immunoglobulin repertoire, gene expression related to Toll-like receptors, cytokines, and cytokine receptors, and antibody response to vaccination. Their frequency is altered in immune-mediated disorders. Conclusion: we characterized CD27-CD43+ cells as antibody-secreting cells with differences in function and homing potential as compared to conventional CD27+ antibody-secreting cells.</p

Heterozygous Loss-of-Function Mutations in DLL4 Cause Adams-Oliver Syndrome.

Adams-Oliver syndrome (AOS) is a rare developmental disorder characterized by the presence of aplasia cutis congenita (ACC) of the scalp vertex and terminal limb-reduction defects. Cardiovascular anomalies are also frequently observed. Mutations in five genes have been identified as a cause for AOS prior to this report. Mutations in EOGT and DOCK6 cause autosomal-recessive AOS, whereas mutations in ARHGAP31, RBPJ, and NOTCH1 lead to autosomal-dominant AOS. Because RBPJ, NOTCH1, and EOGT are involved in NOTCH signaling, we hypothesized that mutations in other genes involved in this pathway might also be implicated in AOS pathogenesis. Using a candidate-gene-based approach, we prioritized DLL4, a critical NOTCH ligand, due to its essential role in vascular development in the context of cardiovascular features in AOS-affected individuals. Targeted resequencing of the DLL4 gene with a custom enrichment panel in 89 independent families resulted in the identification of seven mutations. A defect in DLL4 was also detected in two families via whole-exome or genome sequencing. In total, nine heterozygous mutations in DLL4 were identified, including two nonsense and seven missense variants, the latter encompassing four mutations that replace or create cysteine residues, which are most likely critical for maintaining structural integrity of the protein. Affected individuals with DLL4 mutations present with variable clinical expression with no emerging genotype-phenotype correlations. Our findings demonstrate that DLL4 mutations are an additional cause of autosomal-dominant AOS or isolated ACC and provide further evidence for a key role of NOTCH signaling in the etiology of this disorder

Stabilized biocompatible and bioabsorbable trigyceride-based coatings for coronary stents

Cardiovascular diseases (e.g arthrosclerosis) are the primary cause of death in our Western Society. A possible treatment for arthrosclerosis is the implantation of a drug eluting stent (DES). Its advantage in comparison with bare stents is that the addition of drugs can prevent restenosis. The goal of this research project is to develop a coating that is biocompatible, bioabsorbable, plastically deformable and has a controllable drug release. The developed coatings are based on 3 or more triacylglycerols, which undergo an interesterification reaction to interexchange the acyl residues. The interesterification reaction is executed by weighing the triaglycerols, followed by drying them overnight in a vacuum oven at 100°C. Next, sodiummethoxide is added. The reaction completes within 1 hour under a nitrogen flow. To stop the reaction, 2 ml of a 20 wt% citric acid solution is added and the reaction compartment is cooled down. Afterwards the mixture is washed several times and dried at 100°C. The last step is to filter the mixture through a membrane filter in a vacuum oven at 100°C. To control the distribution of the randomized triacylglycerols, the coatings are analyzed with HPLC RI. The coatings are further characterized by their slip melting point (SMP) After interesterification, the coating material is checked for mechanical and drug release properties. Therefore, the coating is applied on stent samples with a home built spraying device. For each coating composition, the spraying parameters are optimized to obtain an equal coating distribution on the stent material. Mechanical properties are investigated by performing integrity tests and stent crimping and expansion tests. Coating integrity is checked with a simulated stenosis test at 37°C, in which the applied pressure can be changed. For a low pressure, the loss of coating material is about 5 %, while for a high pressure, the loss of coating rises up to 10 - 15%. Also, scratch tests with the Falex MUST tester are performed, which showed a good coating resistance against scratches. Stent crimping is performed manually. Before and after stent crimping and stent expansion, stents are visually checked with a light microscope for defects such as cracks or delaminations. In order to test the performance of the coatings, the in vitro release of paclitaxel and rapamycine from coated stents was tested. The in vitro drug release is performed at 37°C and is analyzed with HPLC UV-VIS. After an initial burst during the first 2 – 4 hours, the drug release is constant and mediated by diffusion. After 24 h, less then 10% is released, followed by a period of constant release for several weeks to months, depending on the coating composition. Triglyceride based coatings are promising to control drug release from stents during several weeks.status: accepte

sj-pdf-1-opp-10.1177_10781552231167824 - Supplemental material for Immunosuppressive therapy management in cancer patients with autoimmune diseases treated with immune checkpoint inhibitors: A case series and systematic literature review

Supplemental material, sj-pdf-1-opp-10.1177_10781552231167824 for Immunosuppressive therapy management in cancer patients with autoimmune diseases treated with immune checkpoint inhibitors: A case series and systematic literature review by Stephanie C.M. Wuyts, Charlotte A.H. Cappelle, Marthe Verhaert, Bert Bravenboer and Sandrine Aspeslagh in Journal of Oncology Pharmacy Practice</p

Anti-pneumococcal capsular polysaccharide antibody response and CD5 B lymphocyte subsets

The role of the CD19(+)CD5(+) and CD19(+)CD5(-) B-cell subpopulations in the antibody response to pneumococcal capsular polysaccharides (caps-PS) is controversial. In the present study we evaluated the role of the human CD19(+)CD5(+) and CD19(+)CD5(-) cell populations in the serotype-specific antibody response to caps-PS. After vaccination of 5 healthy human adults with Pneumovax® (PPV23), IgG anti-caps-PS serotype 4 antibody producing cells mainly resided in the CD19(+)CD5(-) B cell subset, as assessed by ELISpot analysis. Moreover, in a humanized SCID mice model, CD19(+)CD5(-) B cells were more effective than CD19(+)CD5(+) cells to produce IgG anti-cap-PS antibodies. Finally, an association was found between the level of IgG anti-caps-PS antibodies and the number of CD19(+)CD5(-) B cells in 33 humans vaccinated with PPV23. Taken together, our data suggest that CD5 defines a functionally distinct population of B cells in humans in the anti-caps-PS immune response.status: publishe