Aim: We test a new species distribution modelling (SDM) framework, while comparing results to more common distribution modelling techniques. This framework allows for the combination of presence-only ...(PO) and presence-absence (PA) data and accounts for imperfect detection and spatial bias in presence data. The new framework tested here is based on a Poisson point process model, which allows for predictions of population size. We compared these estimates to those provided by experts on the species. Species and Location: Presence data on Baird's tapir (Tapirus bairdii) throughout its range from southern Mexico to northern Colombia were used in this research, primarily from the years 2000 to 2016. Methods: Four SDM frameworks are compared as follows: (1) Maxent, (2) a presenceonly (PO) SDM based on a Poisson point process model (PPM), (3) a presence-absence (PA) SDM also based on a PPM and (4) an Integrated framework which combines the previous two models. Model averaging was used to produce a single set of coefficient estimates and predictive maps for each model framework. A hotspot analysis (Gi*) was used to identify habitat cores from the predicted intensity of the Integrated model framework. Results: Important variables to model the distribution of Baird's tapir included land cover, human pressure and topography. Accounting for spatial bias in the presence data affected which variables were important in the model. Maxent and the Integrated model produced predictive maps with similar patterns and were considered to be more in agreement with expert knowledge compared to the PO and PA models. Main conclusions: Total abundance as predicted by the model was higher than expert opinion on the species, but local density estimates from our model were similar to available independent assessments. We suggest that these results warrant further validation and testing through collection of independent test data, development of more precise predictor layers and improvements to the model framework.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NMLJ, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UILJ, UKNU, UL, UM, UPUK
Introducción: El déficit de alfa-1 Antitripsina (a1AT) es una de las enfermedades genéticas más prevalentes en el ser humano, lastimosamente como entidad clínica tiende a ser pobremente sospechada. ...Con más de 100 mutaciones conocidas, las que se encuentran asociadas a enfermedad hepática son los homocigotos Z en el alelo del gen a1AT que ocurre en 1 a 2000- 3500 nacimientos. A diferencia de la enfermedad pulmonar donde las secuelas ocurren primordialmente por el déficit propio de la a1AT con destrucción enzimática de la microestructura de la vía aérea, el compromiso hepático ocurre por acúmulo intracelular de la proteína Z mutante, que se desdobla de forma aberrante, en vez de ser secretada. Esta acumulación produce lesión celular, hepatitis, fibrosis, cirrosis y carcinoma hepatocelular (CHC) por desencadenar una serie de eventos que culminan con la apoptosis hepatocitaria, regeneración e injuria crónica. Materiales y métodos: Se presentan 9 casos de pacientes que se han encontrado bajo nuestro cuidado, con edades variadas desde infantes hasta adultos mayores. Resultados: Cada uno con una presentación clínica distinta que va desde la elevación de enzimas hepáticas y otros como cirrosis que se han trasplantado con diagnóstico confirmatorio postquirúrgico. Conclusión: Se comenta acerca del manejo de la hepatopatía y su progresión a lo largo del tiempo que se han mantenido en la clínica de hígado a nuestro cargo.
Alfa 1-antitrypsin deficiency is one of the most prevalent genetic diseases in the human being, sadly it is not a commonly suspected clinical entity. With more than 100 known mutations, those ...associated with hepatic disease are the Z homocygote allele mutations in the gene a1AT which occur in every 2000-3500 births. Opposing to the pulmonary disease, in which de sequelae are caused by the deficit of this protein which in turn fastens the enzymatic destruction of the airway microstructure, the hepatic compromise is secondary to the intracellular accumulation of the aberrant misfolded protein. This accumulation causes cellular damage, hepatitis, fibrosis, cirrhosis and hepatocellular carcinoma through activation of a series of mechanisms which culminate in hepatocitary apoptosis, regeneration and chronic cellular injury.
9 cases of confirmed a1AT deficiency are presented, from different ages ranging from adolescence through elderly patients.
Each of one of them with different clinical presentation going from asymptomatic liver enzyme elevations to transplanted cirrhosis in which the diagnosis was post procedural.
We comment about the management of the chronic liver disease and the evolution of these patients through time in the liver clinic.
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