Illuminating Massive Black Holes With White Dwarfs: Orbital Dynamics and High Energy Transients from Tidal Interactions

White dwarfs (WDs) can be tidally disrupted only by massive black holes (MBHs) with masses less than $\sim10^5 M_\odot$. These tidal interactions feed material to the MBH well above its Eddington limit, with the potential to launch a relativistic jet. The corresponding beamed emission is a promising signpost to an otherwise quiescent MBH of relatively low mass. We show that the mass transfer history, and thus the lightcurve, are quite different when the disruptive orbit is parabolic, eccentric, or circular. The mass lost each orbit exponentiates in the eccentric-orbit case leading to the destruction of the WD after several tens of orbits. We examine the stellar dynamics of clusters surrounding MBHs to show that single-passage WD disruptions are substantially more common than repeating encounters. The $10^{49}$ erg s$^{-1}$ peak luminosity of these events makes them visible to cosmological distances. They may be detectible at rates of as many as tens per year by instruments like Swift. In fact, WD-disruption transients significantly outshine their main-sequence star counterparts, and are the most likely tidal interaction to be detected arising from MBHs with masses less than $10^5 M_\odot$. The detection or non-detection of such WD-disruption transients by Swift is, therefore, a powerful tool to constrain lower end of the MBH mass function. The emerging class of ultra-long gamma ray bursts all have peak luminosities and durations reminiscent of WD disruptions, offering a hint that WD-disruption transients may already be present in existing datasets.Comment: Revised following response from refere

Miosite do músculo reto medial como forma atípica de apresentação de linfoma tipo MALT: relato de caso

Here we describe the rare case of a 55-year-old man with medial rectus muscle myositis as an atypical presentation of non-Hodgkin B-cell mucosa-associated lymphoma (MALT). Pathology and immunohistochemistry of the affected muscle confirmed the diagnosis of a neoplasm. The primary etiology of orbital myositis is Graves' ophthalmopathy, but several other diseases may cause this clinical presentation. Therefore, the neoplastic causes must be eliminated from the differential diagnoses. non-Hodgkin B-cell mucosa-associated lymphoma is the most common histological type of lymphoma in the orbit, with the conjunctiva and lacrimal glands being the most commonly affected sites. However, it may also present in atypical forms involving others sites and tissues.Descrevemos um raro caso de miosite do músculo reto medial como forma atípica de apresentação de linfoma não-Hodgkin de células B tipo MALT. A anatomia patológica e imuno-histoquímica do músculo afetado confirmaram o diagnóstico definitivo do caráter neoplásico da doença. As miosites orbitárias têm como principal etiologia a oftalmopatia de Graves, porém diversas outras causas podem apresentar-se dessa forma. Sendo assim, as causas neoplásicas devem ser descartadas. O linfoma não-Hodgkin de células B tipo MALT é o tipo histológico mais comum de linfoma orbitário, as regiões mais frequentemente acometidas são a conjuntiva e glândula lacrimal. No entanto, pode apresentar-se com formas clínicas atípicas, acometendo outras regiões e tecidos.Universidade Federal de São Paulo (UNIFESP) Department of OphthalmologyUNIFESP, Department of OphthalmologySciEL

Deficiency of the zinc finger protein ZFP106 causes motor and sensory neurodegeneration

Acknowledgements We are indebted to Jim Humphries, JennyCorrigan, LizDarley, Elizabeth Joynson, Natalie Walters, Sara Wells and the whole necropsy, histology, genotyping and MLC ward 6 teams at MRC Harwell for excellent technical assistance. We thank the staff of the WTSI Illumina Bespoke Team for the RNA-seq data, the Sanger Mouse Genetics Project for the initial mouse characterization and Dr David Adams for critical reading of the manuscript. We also thank KOMP for the mouse embryonic stem cells carrying the knockout first promoter-less allele (tm1a(KOMP)Wtsi) within Zfp016. Conflict of Interest statement. None declared. Funding This work was funded by the UK Medical Research Council (MRC) to A.A.-A. and a Motor Neurone Disease Association (MNDA) project grant to A.A.-A. and EMCF. D.L.H.B. is a Wellcome Trust Senior Clinical Scientist Fellow and P.F. is a MRC/MNDA Lady Edith Wolfson Clinician Scientist Fellow. Funding to pay the Open Access publication charges for this article was provided by the MRC grant number: MC_UP_A390_1106.Peer reviewedPublisher PD

Diagnostic effectiveness of high-sensitivity troponins

Background: Acute myocardial infarctions (AMI) are a leading cause of death in the United States. The key to increasing survivability is early recognition to expedite the proper treatment modalities. In conjunction with the clinical presentation and electrocardiograms, the use of cardiac biomarkers is exponentially important in not only recognizing a cardiac event but also determining the extent of injury. Advancement in laboratory technology has led to the development of high-sensitive troponin (hs-troponin) assays which can detect smaller cardiac troponin serum levels compared to conventional troponin assays. This implies that the use of hs-troponin assays is more effective in the early detection and extent of tissue ischemia, increasing the chances of AMI survival. Objective: The purpose of this review is to determine whether the use of hs-troponin assays have a superior diagnostic value compared to conventional troponin assays in earlier identification or ruling-out AMI in patients who present with chest pain or other AMI symptoms. Methods: A PubMed search was conducted using the following search terms and filters: high-sensitive troponin, cardiac biomarkers, hs-troponin vs. conventional troponin, articles in the last 10 years, English language, randomized control trials, meta-analysis reviews. Articles were excluded if direct comparison between hs-troponin and conventional was not observed, no full text of the article was available, and low participant numbers. Conclusion: While their use is not fully adopted in the United States, hs-troponin assays can detect lower concentrations of serum troponin levels at the time of presentation compared to conventional assays, which increases their sensitivity but comes with a reduction in specificity. This is promising in early recognition of tissue ischemia and can lead to earlier detection of an AMI and expedite proper treatment pathways but raises the concern of an increase in AMI over diagnosis that may be factitious. When collected as serial markers, the hs-sensitivity troponins were equal with conventional assays in their sensitivity/specificity, which leads to the determination that they are no more effective in cardiac monitoring compared to conventional testing

Lon adsorption behavior (in aqueous solutions) of lanthanum, cerium, and europium in organic adsorbents: review of kinetic, isothermal, and thermodynamic studies

Rare earth elements are present in a large number of raw materials for different applications in high technology, including lasers, magnets, fiber optics, X-ray machines, and lamps. Therefore, efforts have been made to find new alternatives that improve the recovery and recycling of these important elements, given that rare earth reserves worldwide are scarce and highly polluting. The aim is to counteract demand and help the environment by using alternative methods and making use of waste at the end of its useful life. Some of this waste is found in water sources from treatment plants and mining, which is significantly dangerous for nature and humans. As a viable alternative, the adsorption method has been chosen as it is an effective and low-cost process. This document aims to analyze different literature on the adsorption of lanthanum, cerium, and europium ions (in aqueous solutions) on organic adsorbents such as biomass and activated carbons, in order to verify whether the adsorption technique proves to be effective for the recovery of these elements, analyzing the kinetic, isothermal, and thermodynamic models. The results obtained confirm that the parameters that depend on adsorption are contact time, pH, and temperature, with a high capacity for removing metal ions. The isotherms most used by the different authors were Langmuir and Freundlich. For the kinetic study, a correlation was found with the activation energy taking place in chemisorption. Most of the literature studied showed that these were spontaneous and endothermic processes

Methods for Inactivating PEDV in Hog Trailers

Porcine epidemic diarrhea (PED) was first described in England in 1971 in growing pigs and the causative agent, porcine epidemic diarrhea virus (PEDV), was identified in 1978. The virus spread to the rest of Europe where it caused outbreaks of diarrhea and significant losses throughout the 1970s and 1980s. PEDV is considered endemic to Europe today, but does not cause widespread significant disease. In parts of Asia outbreaks were recognized first in 1982 and have continued to occur since. In May of 2013 PEDV was identified in swine for the first time in the United States. The virus has caused severe diarrhea in sows and piglets, with near 100% mortality in piglets across a wide geographical area of the United States. Genetic analysis of PEDV isolates from affected farms in the US found the virus to be 99% genetically similar to isolates from China, but efforts to determine the source of entry to the United States have been unsuccessful

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer.

Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance