Reflective Subcategories, Localizations and Factorization Systems: Corrigenda C. Cassidy, M. Hébert and G. M. Kelly, 1980 Mathematics subject classification (Amer. Math. Soc.): 18 A 20.

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Background: Observational studies have suggested that accelerated surgery is associated with improved outcomes in patients with a hip fracture. The HIP ATTACK trial assessed whether accelerated surgery could reduce mortality and major complications. Methods:We randomised 2970 patients from 69 hospitals in 17 countries. Patients with a hip fracture that required surgery and were ≥45 years of age were eligible. Patients were randomly assigned to accelerated surgery (goal of surgery within 6 hours of diagnosis; 1487 patients) or standard care (1483 patients). The co-primary outcomes were 1.) mortality, and 2.) a composite of major complications (i.e., mortality and non-fatal myocardial infarction, stroke, venous thromboembolism, sepsis, pneumonia, life-threatening bleeding, and major bleeding) at 90 days after randomisation. Outcome adjudicators were masked to treatment allocation, and patients were analysed according to the intention-to-treat principle; ClinicalTrials.gov, NCT02027896. Findings:The median time from hip fracture diagnosis to surgery was 6 hours (interquartile range [IQR] 4-9) in the accelerated-surgery group and 24 hours (IQR 10-42) in the standard-care group, p<0.0001. Death occurred in 140 patients (9%) assigned to accelerated surgery and 154 patients (10%) assigned to standard care; hazard ratio (HR) 0.91, 95% CI 0.72-1.14; absolute risk reduction (ARR) 1%, 95% CI -1-3%; p=0.40. The primary composite outcome occurred in 321 patients (22%) randomised to accelerated surgery and 331 patients (22%) randomised to standard care; HR 0.97, 95% CI 0.83-1.13; ARR 1%, 95% CI -2-3%; p=0.71.Interpretation: Among patients with a hip fracture, accelerated surgery did not significantly lower the risk of mortality or a composite of major complications compared to standard care.

This work is a detailed analysis of the relationship between reflective subcategories of a category and factorization systems supported by the category.

A high index of suspicion is necessary for the diagnosis of this specific pathogen and concordant infection. The willingness to surgically debride and amputate without hesitation at a very early point may be the only intervention capable of saving the lives of patients affected by Photobacterium (Vibrio) damsela.

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Rabbit retinas were incubated in vitro under conditions known to maintain their physiological function. The acetylcholine stores of the cholinergic amacrine cells were labelled by incubation in the presence of [ 3 H]choline. The tissue was then mounted in a fast-flow superfusion chamber, and the release of [ 3 H]acetylcholine under various conditions was measured by liquid cation exchange or high-voltage electrophoresis. When the retina was stimulated by flashing light, the rate of appearance of radioactive acetylcholine in the superfusate increased, with a latency shorter than the resolution of the system. The rate of release of acetylcholine remained elevated as long as the light was flashing, and returned rapidly to baseline when the light was extinguished. A one minute stimulation with steady light caused a burst of acetylcholine release following stimulus onset and a second, smaller, burst following stimulus cessation. In the presence of 2-amino-4-phosphonobutyrate (APB), an agent known to eliminate selectively the transmission of ON responses to the proximal retina, steady light caused acetylcholine release only at stimulus cessation. Other retinas were labelled with [ 3 H]choline, then incubated for 10-80 min in the presence of flashing light (to promote acetylcholine release) and either control medium or medium containing 100 μm APB (to prevent release from cells activated by stimulus onset). These retinas were quick-frozen, freeze-dried and radioautographed on dry emulsion. In retinas incubated under control conditions [ 3 H]acetylcholine was initially present within two bands within the inner plexiform layer. The two bands became fainter together as the tissue’s [ 3 H]acetylcholine was released. APB selectively retarded the depletion of [ 3 H]acetylcholine from the band nearest the ganglion cell layer. We conclude that the displaced cholinergic amacrine cells release acetylcholine at the transient when light appears, and the conventionally placed cholinergic amacrine cells release acetylcholine at the transient when light is extinguished. The retinal ganglion cells that receive a light-driven cholinergic input are distinguished from those that do not by a great sensitivity to slow stimulus motion. It is proposed that the dense plexus of cholinergic dendrites and the transient nature of acetylcholine release combine to create the local subunit that enables detection of motion within regions smaller than those ganglion cells’ receptive fields.

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