Perihematomal Edema Expansion Rates And Patient Outcomes In Deep And Lobar Intracerebral Hemorrhage

Perihematomal edema (PHE) expansion rate may predict functional outcome following spontaneous intracerebral hemorrhage (ICH), but it has not been well characterized for the different anatomic subtypes of ICH. We hypothesized that the effect of PHE expansion rate on outcome is greater for deep versus lobar ICH. Subjects (n = 115) were retrospectively identified from a prospective ICH cohort enrolled from 2000 to 2013. Inclusion criteria were age \u3e 18 years, spontaneous supratentorial ICH, and known onset time. Exclusion criteria were primary intraventricular hemorrhage (IVH), trauma, subsequent surgery, or warfarin-related ICH. ICH and PHE volumes were measured from CT scans and used to calculate expansion rates. Logistic regression assessed the association between PHE expansion rates and 90-day mortality or poor functional outcome (modified Rankin Scale \u3e 2). Odds ratios are per 0.04 mL/h. PHE expansion rate from baseline to 24 hours (PHE24) was associated with mortality for deep (p = 0.03, OR 1.13[1.02-1.26]) and lobar ICH (p = 0.02, OR 1.03[1.00-1.06]) in unadjusted regression models and in models adjusted for age (deep: p = 0.02, OR 1.15[1.02-1.28]; lobar: p = 0.03, OR 1.03[1.00-1.06]), Glasgow Coma Scale (deep: p = 0.03, OR 1.13[1.01-1.27]; lobar: p = 0.02, OR 1.03[1.01-1.06]), time to baseline CT (deep: p = 0.046, OR 1.12[1.00-1.25]; lobar: p = 0.047, OR 1.03[1.00-1.06]), or ICH Score (deep: p = 0.03, OR 1.17[1.02-1.34]; lobar: p = 0.06, OR 1.03[1.0-1.06]). PHE expansion rate from baseline to 72 hours (PHE72) was associated with mRS \u3e 2 for deep ICH in models that were unadjusted (p = 0.02, OR 4.04[1.25-13.04]) or adjusted for ICH volume (p = 0.02, OR 4.3[1.25-14.98]), age (p = 0.03, OR 5.4[1.21-24.11]), GCS (p = 0.02, OR 4.19[1.2-14.55]), time to first CT (p = 0.03, OR 4.02[1.19-13.56]), ICH expansion (p = 0.02, OR 4.96[1.24-19.83]), or ICH Score (p = 0.04, OR 3.39[1.07-10.75]). In conclusion, PHE72 was associated with poor functional outcomes after deep ICH, whereas PHE24 was associated with mortality for deep and lobar ICH

grunwaldlab/metacoder_documentation: First documentation release

This manual was released with the v0.1.2 version of MetacodeR. This repository is used to created the online content available at https://grunwaldlab.github.io/metacoder_documentation/

grunwaldlab/metacoder: metacoder 0.1.3

metacoder 0.1.3 Mostly minor improvements and bug fixes. Larger changes are waiting on the taxa package to be done, which will be the new home of the taxmap class and the associated dplyr-like manipulating functions like filter_taxa. Improvements Provided helpful error message when the evaluation nested too deeply: infinite recursion / options(expressions=)? occurs due to too many labels being printed. heat_tree: improved how the predicted bondries of text is calcuated, so text with any rotation, justification, or newlines influences margins correctly (i.e. does not get cut off). heat_tree: Can now save multiple file outputs in different formats at once Minor changes heat_tree now gives a warning if infinite values are given to it extract_taxonomy: There is now a warning message if class regex does not match (issue #123) heat_tree: Increased lengend text size and reduced number of labels extract_taxonomy: added batch_size option to help deal with invalid IDs better Added CITATION file Breaking changes The heat_tree option margin_size funcion now takes four values instead of 2. Bug fixes heat_tree: Fixed bug when color is set explicitly (e.g. "grey") instead of raw numbers and the legend is not removed. Now a mixure of raw numbers and color names can be used. Fixed bugs caused by dplyr version update Fixed bug in heat_tree that made values not in the input taxmap object not associate with the right taxa. See this post. extract_taxonomy: Fixed an error that occured when not all inputs could be classified and sequences were supplied Fixed bug in primersearch that cased the wrong primer sequence to be returned when primers match in the reverse direction Fixed a bug in parse_mothur_summary where "unclassified" had got changed to "untaxmap" during a search and replace Fixed outdated example code for extract_taxonomy Fixed a bug in mutate_taxa and mutate_obs that made replacing columns result in new columns with duplicate names

poppr: poppr version 2.2.0

NEW FUNCTIONS incomp() will check your data to see if there are any incomparable samples. NEW FEATURES Threshold argument added to filter_stats() (see https://github.com/grunwaldlab/poppr/issues/94) The pipe operator (%>%) is now exported from magrittr to make chaining commands easier. mlg.filter() can now return multiple statistics. The user can now control the size of the labels in the index of association plots with the labsize and linesize arguments in the plot method. private_alleles() gains a drop argument. recode_polyploids() can now take haplodiploid data. BUG FIX An issue that caused errors in the imsn() code output was fixed (see https://github.com/grunwaldlab/poppr/issues/93) Caught bug where the mlg.filter() assignment method was using nei.dist() instead of diss.dist() when no distance was specified. A bug that resulted in significantly negative values from bitwise.ia() with large sample sizes was fixed. Spotted by @knausb (see https://github.com/grunwaldlab/poppr/issues/100) Fixed issue where plot_filter_stats() wasn't displaying the full range of MLGs Color vectors are now correctly parsed when passed to msn functions (see https://github.com/grunwaldlab/poppr/issues/55) for details. Long color vectors are now accepted, albiet with warning. An issue where mll.reset() did not reset non-MLG class objects in the mlg slot was fixed. MISC Documentation for mlg.filter() was clarified and updated with more examples. The vignette "Migration from poppr version 1" has been removed. Previously deprecated *hierarchy() functions have been removed

Proposal for Updated Nomenclature and Classification of Potential Causative Mechanism in Patent Foramen Ovale-Associated Stroke

Importance Recent epidemiologic and therapeutic advances have transformed understanding of the role of and therapeutic approach to patent foramen ovale (PFO) in ischemic stroke. Patent foramen ovale is likely responsible for approximately 5% of all ischemic strokes and 10% of those occurring in young and middle-aged adults. Observations Randomized clinical trials have demonstrated that, to prevent recurrent ischemic stroke in patients with PFO and an otherwise-cryptogenic index ischemic stroke, PFO closure is superior to antiplatelet medical therapy alone; these trials have provided some evidence that, among medical therapy options, anticoagulants may be more effective than antiplatelet agents. Conclusions and Relevance These new data indicate a need to update classification schemes of causative mechanisms in stroke, developed in an era in which an association between PFO and stroke was viewed as uncertain. We propose a revised general nomenclature and classification framework for PFO-associated stroke and detailed revisions for the 3 major stroke subtyping algorithms in wide use

Targeting VEGF in eye neovascularization: What's new?: A comprehensive review on current therapies and oligonucleotide-based interventions under development

Abstract Roughly ten years ago the FDA approved most of the presently used anti-VEGF drugs for the treatment of neovascular AMD and other eye pathologies characterized by ocular neoangiogenesis. However, the recent findings on the physiologic activities of VEGF isoforms impose to reconsider the inhibitory effects of pan-VEGF antagonists and the concept that to face pathological alterations at ocular level is possible only through the full block of all VEGF isoforms. In fact, although pan-VEGF agents rapidly and effectively contrast ocular neovascularization, vascular leakage, and other pathological changes, in the long-term the inhibition of all VEGF isoforms likely may result in the loss of the physiologic effects exerted by VEGF 121 and the anti-angiogenic VEGF 165 b. Notably, selective inhibitors of VEGF 165 a, such as pegaptanib, spare these targets. Moreover, preclinical and clinical evidence suggests that also systemic side effects, secondary to intraocular treatment with non-selective anti-VEGF drugs, may be reinterpreted in light of these recent findings, which may be useful to clinicians for the choice of the most appropriate anti-VEGF agent. Another aspect that should be considered is the involvement of VEGF-independent pathways in ocular neovascularization, therefore a combined therapy can represent a more effective pharmacological approach that might help also to counteract tachyphylaxis, an important issue in anti-VEGF treatment. This complex picture and the recent findings on current anti-VEGF drugs should be therefore taken into account to guide the development of novel agents targeting VEGF and/or other key factors involved in the pathogenesis of neovascular ocular diseases along the signaling pathways stimulated by the various isoforms. Accordingly, this review also reports on novel pharmacological molecules targeting VEGF at ocular level and currently under development, with a special attention to oligonucleotide-based interventions