A fresh look at an old concept: home-range estimation in a tidy world.
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ABSTRACT:
SUBMITTER: Signer J
PROVIDER: S-EPMC8048401 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundFamily Rhinolophidae (horseshoe bats), Hipposideridae (leaf-nosed bats) and Rhinonycteridae (trident bats) are exclusively distributed in the Old-World, and their biogeography reflects the complex historic geological events throughout the Cenozoic. Here we investigated the origin of these families and unravel the conflicting family origin theories using a high resolution tree covering taxa from each zoogeographic realm from Africa to Australia. Ancestral range estimations were performed using a probabilistic approach implemented in BioGeoBEARS with subset analysis per biogeographic range [Old-World as whole, Australia-Oriental-Oceania (AOO) and Afrotropical-Madagascar-Palearctic (AMP)].ResultOur result supports an Oriental origin for Rhinolophidae, whereas Hipposideridae originated from the Oriental and African regions in concordance with fossil evidence of both families. The fossil evidence indicates that Hipposideridae has diversified across Eurasia and the Afro-Arabian region since the Middle Eocene. Meanwhile, Rhinonycteridae (the sister family of Hipposideridae) appears to have originated from the Africa region splitting from the common ancestor with Hipposideridae in Africa. Indomalaya is the center of origin of Rhinolophidae AOO lineages, and Indomalayan + Philippines appears to be center of origin of Hipposideridae AOO lineage indicating allopatric speciation and may have involved jump-dispersal (founder-event) speciation within AOO lineage. Wallacea and the Philippines may have been used as stepping stones for dispersal towards Oceania and Australia from the Oriental region. Multiple colonization events via different routes may have occurred in the Philippines (i.e., Palawan and Wallacea) since the Late Miocene. The colonization of Rhinolophidae towards Africa from Asia coincided with the estimated time of Tethys Ocean closure around the Oligocene to Miocene (around 27 Ma), allowing species to disperse via the Arabian Peninsula. Additionally, the number of potential cryptic species in Rhinolophidae in Southeast Asia may have increased since Plio-Pleistocene and late Miocene.ConclusionOverall, we conclude an Oriental origin for Rhinolophidae, and Oriental + African for Hipposideridae. The result demonstrates that complex historical events, in addition to species specific ecomorphology and specialization of ecological niches may shape current distributions.
| S-EPMC9528145 | biostudies-literature
Project description:Mechanical stress from haemodynamic perturbations or interventional manipulation of epicardial coronary atherosclerotic plaques with inflammatory destabilization can release particulate debris, thrombotic material and soluble substances into the coronary circulation. The physical material obstructs the coronary microcirculation, whereas the soluble substances induce endothelial dysfunction and facilitate vasoconstriction. Coronary microvascular obstruction and dysfunction result in patchy microinfarcts accompanied by an inflammatory reaction, both of which contribute to progressive myocardial contractile dysfunction. In clinical studies, the benefit of protection devices to retrieve atherothrombotic debris during percutaneous coronary interventions has been modest, and the treatment of microembolization has mostly relied on antiplatelet and vasodilator agents. The past 25 years have witnessed a relative proportional increase in non-ST-segment elevation myocardial infarction in the presentation of acute coronary syndromes. An associated increase in the incidence of plaque erosion rather than rupture has also been recognized as a key mechanism in the past decade. We propose that coronary microembolization is a decisive link between plaque erosion at the culprit lesion and the manifestation of non-ST-segment elevation myocardial infarction. In this Review, we characterize the features and mechanisms of coronary microembolization and discuss the clinical trials of drugs and devices for prevention and treatment. In this Review, Kleinbongard and Heusch characterize the features and mechanisms of coronary microembolization and discuss the clinical trials of drugs and devices for the prevention and treatment of this phenomenon. Key points Coronary microembolization results from spontaneous or interventional erosion or rupture of an epicardial coronary atherosclerotic plaque. Atherothrombotic plaque debris causes physical obstruction of coronary microvessels and results in microinfarcts with an inflammatory response. The surviving myocardium around the patchy microinfarcts has reduced contractile function as a result of inflammatory signal transduction leading to myofibrillar oxidation. Atherosclerotic plaque erosion or rupture releases soluble substances that induce coronary microvascular endothelial dysfunction, vasoconstriction, platelet aggregation and coagulation. Routine use of interventional protection devices does not improve patient outcomes but these devices are indicated in cases of high atherothrombotic plaque burden. Plaque stabilization with statins and canakinumab prevents coronary microembolization, whereas platelet inhibitors, vasodilators and interleukin antagonists attenuate coronary microvascular impairment.
| S-EPMC8593642 | biostudies-literature
Project description:BackgroundThe number of Phase III trials that include a biomarker in design and analysis has increased due to interest in personalised medicine. For genetic mutations and other predictive biomarkers, the trial sample comprises two subgroups, one of which, say B+ is known or suspected to achieve a larger treatment effect than the other B-. Despite treatment effect heterogeneity, trials often draw patients from both subgroups, since the lower responding B- subgroup may also gain benefit from the intervention. In this case, regulators/commissioners must decide what constitutes sufficient evidence to approve the drug in the B- population.Methods and resultsAssuming trial analysis can be completed using generalised linear models, we define and evaluate three frequentist decision rules for approval. For rule one, the significance of the average treatment effect in B- should exceed a pre-defined minimum value, say ZB->L. For rule two, the data from the low-responding group B- should increase statistical significance. For rule three, the subgroup-treatment interaction should be non-significant, using type I error chosen to ensure that estimated difference between the two subgroup effects is acceptable. Rules are evaluated based on conditional power, given that there is an overall significant treatment effect. We show how different rules perform according to the distribution of patients across the two subgroups and when analyses include additional (stratification) covariates in the analysis, thereby conferring correlation between subgroup effects.ConclusionsWhen additional conditions are required for approval of a new treatment in a lower response subgroup, easily applied rules based on minimum effect sizes and relaxed interaction tests are available. Choice of rule is influenced by the proportion of patients sampled from the two subgroups but less so by the correlation between subgroup effects.
| S-EPMC8411475 | biostudies-literature
Project description:Elevated serum lactate dehydrogenase (sLDH) is associated with poor clinical outcomes in patients with stage IV metastatic melanoma (MM). It is currently unknown if sLDH elevation correlates with distinct molecular, metabolic, or immune features of melanoma metastases. The identification of such features may identify rational therapeutic strategies for patients with elevated sLDH. Thus, we obtained sLDH levels for melanoma patients with metastases who had undergone molecular and/or immune profiling. Our analysis of multi-omics data from independent cohorts of melanoma metastases showed that elevated sLDH was not significantly associated with differences in immune cell infiltrate, point mutations, DNA copy number variations, promoter methylation, RNA expression, or protein expression in melanoma metastases. The only significant association observed for elevated sLDH was with the number of metastatic sites of disease. Our data support that sLDH correlates with disease burden, but not specific molecular or immunological phenotypes, in metastatic melanoma.
| S-EPMC7666738 | biostudies-literature
Project description:To determine whether nucleolar channel systems (NCSs) in the midluteal endometrium are associated with overall fertility status and/or with unexplained infertility.Retrospective and prospective clinical studies.Repository of stored specimens from prior multicenter study and private infertility center.Retrospective study that included 97 women (49 fertile couples, 48 infertile couples) who had been randomized for endometrial biopsy during the midluteal or late luteal phase. The prospective study included 78 women with a variety of infertility diagnoses.Endometrial biopsies were obtained and assessed for the presence of NCSs by indirect immunofluorescence.The presence of NCS was graded semiquantitatively and dichotomized as normal versus low or absent.Normal presence of NCS was significantly associated with the midluteal phase compared with the late luteal phase (80% vs. 29%). However, there was no association between presence of NCS and fertility status or between presence of NCS and unexplained infertility.Midluteal phase endometrium consistently forms NCSs regardless of fertility status, including unexplained infertility. This indicates a possible role for the NCS in initiating the window of endometrial receptivity. However, the consistent presence of NCSs across several different types of infertility challenges the likelihood that inadequate secretory transformation is a cause of infertility.
| S-EPMC3347775 | biostudies-other
Project description:Primate Ribosomal DNA (rDNA) containing BAC clones sequencing
| PRJNA309608 | ENA
Project description:The Institute for Research in Biomedicine (IRB) Barcelona meeting on Cancer Metabolism took place in November 2010. It was organized with the support of the Banco Bilbao Vizcaya Argentaria Foundation and offered an outstanding line-up of acclaimed speakers within an intimate setting that allowed plenty of opportunity for informal interactions.
| S-EPMC3077258 | biostudies-other
Project description: Not available
| S-EPMC2631055 | biostudies-literature
Project description:Attempts to explain abducens vulnerability have centered around the petroclival segment of its pathway in the skull base, in particular, its relations to the Dorello's canal and the petrosphenoidal ligament of Grüber. This study aims to contribute to the definition of the Dorello's canal and to the understanding of abducens vulnerability from an evolutionary perspective. The petroclival region and the Dorello's canal in particular were examined in a sample of 86 primate skulls. The sample contains 20 Pan troglodytes (common chimpanzee), 35 Gorilla gorilla, 20 Pongo pygmaeus (orangoutan), and 11 Hylobates moloch (gibbon) skulls. Distance between the petrous apex and tip of the posterior clinoid process was measured using a 10-mm scale that was inserted into the endocranium. Complete absence of the Grüber ligament and an uninterrupted osseous circumference of the Dorello's canal (foramen) was demonstrated in all nonhuman primate species. Whatever the reason for the morphological difference between the human and ape Dorello's canal, it is without a doubt suggestive of the source of vulnerability of the abducens nerve, as the ligament of Grüber, unique to the human configuration, renders the contents of the Dorello's canal susceptible to compression against the cranial base.
| S-EPMC3312418 | biostudies-other
Project description:A considerable volume of research over the last decade has focused on understanding the fundamental mechanisms for the progression of atherosclerosis-the underlying cause for the vast majority of all cardiovascular (CVD)-related complications. Aging is the dominant risk factor for clinically significant atherosclerotic lesion formation, yet the heightened impact of aging on the disease is not accounted for by changes in traditional risk factors, such as lack of physical activity, smoking, hypertension, hyperlipidemia, or diabetes mellitus. This review will examine the pathological and biochemical processes of atherosclerotic plaque formation and growth, with particular focus on the aging risk vis-a-vis arterial homeostasis. Particular focus will be placed on the impact of a number of important contributors to arterial homeostasis including bone marrow (BM)-derived vascular progenitor cells, differential monocyte subpopulations, and the role of cellular senescence. Finally, this review will explore many critical observations in the way the disease process has been reassessed both by clinicians and researchers, and will highlight recent advances in this field that have provided a greater understanding of this aging-driven disease.
| S-EPMC5735066 | biostudies-literature