101 research outputs found

    Exceptional Anti-Icing Performance of Self-Impregnating Slippery Surfaces

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    A heat exchange interface at subzero temperature in a water vapor environment, exhibits high probability of frost formation due to freezing condensation, a factor that markedly decreases the heat transfer efficacy due to the considerable thermal resistance of ice. Here we report a novel strategy to delay ice nucleation on these types of solid-water vapor interfaces. With a process-driven mechanism, a self-generated liquid intervening layer immiscible to water, is deposited on a textured superhydrophobic surface and acts as a barrier between the water vapor and the solid substrate. This liquid layer imparts remarkable slippery conditions resulting in high mobility of condensing water droplets. A large increase of the ensuing ice coverage time is shown compared to the cases of standard smooth hydrophilic or textured superhydrophobic surfaces. During deicing of these self-impregnating surfaces we show an impressive tendency of ice fragments to skate expediting defrosting. Robustness of such surfaces is also demonstrated by operating them under subcooling for at least 490hr without a marked degradation. This is attributed to the presence of the liquid intervening layer, which protects the substrate from hydrolyzation enhancing longevity and sustaining heat transfer efficiency.Comment: This document is the Accepted Manuscript version of a Published Work that appeared in final form in ACS Applied Materials & Interfaces, copyright (c) American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see pubs.acs.org/doi/abs/10.1021/acsami.7b0018

    Distinct patterns of temporal and directional connectivity among intrinsic networks in the human brain

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    To determine the spatiotemporal relationships among intrinsic networks of the human brain, we recruited seven neurosurgical patients (four males and three females) who were implanted with intracranial depth electrodes. We first identified canonical resting-state networks at the individual subject level using an iterative matching procedure on each subject's resting-state fMRI data. We then introduced single electrical pulses to fMRI pre-identified nodes of the default network (DN), frontoparietal network (FPN), and salience network (SN) while recording evoked responses in other recording sites within the same networks. We found bidirectional signal flow across the three networks, albeit with distinct patterns of evoked responses within different time windows. We used a data-driven clustering approach to show that stimulation of the FPN and SN evoked a rapid (&lt;70 ms) response that was predominantly higher within the SN sites, whereas stimulation of the DN led to sustained responses in later time windows (85–200 ms). Stimulations in the medial temporal lobe components of the DN evoked relatively late effects (&gt;130 ms) in other nodes of the DN, as well as FPN and SN. Our results provide temporal information about the patterns of signal flow between intrinsic networks that provide insights into the spatiotemporal dynamics that are likely to constrain the architecture of the brain networks supporting human cognition and behavior.SIGNIFICANCE STATEMENTDespite great progress in the functional neuroimaging of the human brain, we still do not know the precise set of rules that define the patterns of temporal organization between large-scale networks of the brain. In this study, we stimulated and then recorded electrical evoked potentials within and between three large-scale networks of the brain, the default network (DN), frontoparietal network (FPN), and salience network (SN), in seven subjects undergoing invasive neurosurgery. Using a data-driven clustering approach, we observed distinct temporal and directional patterns between the three networks, with FPN and SN activity predominant in early windows and DN stimulation affecting the network in later windows. These results provide important temporal information about the interactions between brain networks supporting human cognition and behavior.</jats:p

    Performing group-level functional image analyses based on homologous functional regions mapped in individuals

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    Functional MRI (fMRI) studies have traditionally relied on intersubject normalization based on global brain morphology, which cannot establish proper functional correspondence between subjects due to substantial intersubject variability in functional organization. Here, we reliably identified a set of discrete, homologous functional regions in individuals to improve intersubject alignment of fMRI data. These functional regions demonstrated marked intersubject variability in size, position, and connectivity. We found that previously reported intersubject variability in functional connectivity maps could be partially explained by variability in size and position of the functional regions. Importantly, individual differences in network topography are associated with individual differences in task-evoked activations, suggesting that these individually specified regions may serve as the localizer to improve the alignment of task-fMRI data. We demonstrated that aligning task-fMRI data using the regions derived from resting state fMRI may lead to increased statistical power of task-fMRI analyses. In addition, resting state functional connectivity among these homologous regions is able to capture the idiosyncrasies of subjects and better predict fluid intelligence (gF) than connectivity measures derived from group-level brain atlases. Critically, we showed that not only the connectivity but also the size and position of functional regions are related to human behavior. Collectively, these findings suggest that identifying homologous functional regions across individuals can benefit a wide range of studies in the investigation of connectivity, task activation, and brain-behavior associations. Author summary No two individuals are alike. The size, shape, position, and connectivity patterns of brain functional regions can vary drastically between individuals. While interindividual differences in functional organization are well recognized, to date, standard procedures for functional neuroimaging research still rely on aligning different subjects' data to a nominal average brain based on global brain morphology. We developed an approach to reliably identify homologous functional regions in each individual and demonstrated that aligning data based on these homologous functional regions can significantly improve the study of resting state functional connectivity, task-fMRI activations, and brain-behavior associations. Moreover, we showed that individual differences in size, position, and connectivity of brain functional regions are dissociable, and each can provide nonredundant information in explaining human behavior

    Extracellular Degradation Into Adenosine and the Activities of Adenosine Kinase and AMPK Mediate Extracellular NAD+-Produced Increases in the Adenylate Pool of BV2 Microglia Under Basal Conditions

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    Cumulating evidence has indicated NAD+ deficiency as a common central pathological factor of multiple diseases and aging. NAD+ supplement is highly protective in various disease and aging models, while two key questions have remained unanswered: (1) Does extracellular NAD+ also produce its effects through its degradation product adenosine? (2) Does extracellular NAD+ produce the protective effects by affecting cells under pathological insults only, or by affecting both normal cell and the cells under pathological insults? Since extracellular NAD+ can be degraded into adenosine, and endogenous adenosine levels are in the nanomolar range under physiological conditions, extracellular NAD+ may produce its effects through its degradation into adenosine. In this study we used BV2 microglia as a cellular model to test our hypothesis that NAD+ treatment can increase the intracellular adenylate pool under basal conditions through its extracellular degradation into adenosine. Our study has shown that extracellular NAD+ is degraded into adenosine extracellularly, which enters BV2 microglia through equilibrative nucleoside transporters under basal conditions. The intracellular adenosine is converted to AMP by adenosine kinase, which increases the intracellular ATP levels by both activating AMPK and increasing the intracellular adenylate pool. Collectively, our study has suggested a novel mechanism underlying the protective effects of NAD+ administration, which is mediated by extracellular NAD+ degradation into adenosine as well as the activities of adenosine kinase and AMPK. Our findings have also suggested that NAD+ administration in various disease and aging models may also produce its effects by affecting the microglia that are not under pathological insults

    Disseminated varicella-zoster virus infection in an aplastic anemia- paroxysmal nocturnal hemoglobinuria syndrome patient: A case report

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    BackgroundVaricella-zoster virus (VZV) is a common and widespread human-restricted pathogen. It is famous for its dermatological manifestations, such as varicella and herpes zoster. Patients with aplastic anemia-paroxysmal nocturnal hemoglobinuria (AA-PNH) syndrome complicated with fatal disseminated varicella zoster virus infection are very rare and in danger.Patient concernsA 26-year-old man with a history of AA-PNH syndrome was receiving cyclosporine and corticosteroid treatment in the hematology department. During his hospitalization in our hospital, he developed fever, abdominal pain, and lower back pain, and his face, penis, trunk, and limbs developed itchy rash. Subsequently, the patient had to undergo cardiopulmonary resuscitation because of sudden cardiac arrest, and be transferred to ICU for treatment. It was presumed that the cause is unknown severe sepsis. The patient’s condition quickly progressed to multiple organ failure, accompanied by liver, respiratory, and circulatory failure, and signs of disseminated intravascular coagulation. Unfortunately, the patient died after 8 h of active treatment. Finally, we collected all the evidence and concluded that the patient died of AA-PNH syndrome combined with poxzoster virus.ConclusionAA-PNH syndrome patients treated with steroids and immunosuppressants are prone to various infections, considering that herpes virus infection with chickenpox and rash as the initial manifestations is characterized by rapid progress and often accompanied by serious complications. It is more difficult to distinguish it from AA-PNH syndrome with skin bleeding points. If it is not identified in time, it may delay the treatment opportunity, make the condition worse, and cause serious adverse prognosis. Therefore, clinicians need to pay attention to it

    Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential

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    Ischemic stroke (IS) accounts for more than 80% of the total stroke, which represents the leading cause of mortality and disability worldwide. Cerebral ischemia/reperfusion injury (CI/RI) is a cascade of pathophysiological events following the restoration of blood flow and reoxygenation, which not only directly damages brain tissue, but also enhances a series of pathological signaling cascades, contributing to inflammation, further aggravate the damage of brain tissue. Paradoxically, there are still no effective methods to prevent CI/RI, since the detailed underlying mechanisms remain vague. Mitochondrial dysfunctions, which are characterized by mitochondrial oxidative stress, Ca2+ overload, iron dyshomeostasis, mitochondrial DNA (mtDNA) defects and mitochondrial quality control (MQC) disruption, are closely relevant to the pathological process of CI/RI. There is increasing evidence that mitochondrial dysfunctions play vital roles in the regulation of programmed cell deaths (PCDs) such as ferroptosis and PANoptosis, a newly proposed conception of cell deaths characterized by a unique form of innate immune inflammatory cell death that regulated by multifaceted PANoptosome complexes. In the present review, we highlight the mechanisms underlying mitochondrial dysfunctions and how this key event contributes to inflammatory response as well as cell death modes during CI/RI. Neuroprotective agents targeting mitochondrial dysfunctions may serve as a promising treatment strategy to alleviate serious secondary brain injuries. A comprehensive insight into mitochondrial dysfunctions-mediated PCDs can help provide more effective strategies to guide therapies of CI/RI in IS

    CRISPR-Cas13 in malaria parasite: Diagnosis and prospective gene function identification

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    Malaria caused by Plasmodium is still a serious public health problem. Genomic editing is essential to understand parasite biology, elucidate mechanical pathways, uncover gene functions, identify novel therapeutic targets, and develop clinical diagnostic tools. Recent advances have seen the development of genomic diagnostic technologies and the emergence of genetic manipulation toolbox comprising a host of several systems for editing the genome of Plasmodium at the DNA, RNA, and protein level. Genomic manipulation at the RNA level is critical as it allows for the functional characterization of several transcripts. Of notice, some developed artificial RNA genome editing tools hinge on the endogenous RNA interference system of Plasmodium. However, Plasmodium lacks a robust RNAi machinery, hampering the progress of these editing tools. CRISPR-Cas13, which belongs to the VI type of the CRISPR system, can specifically bind and cut RNA under the guidance of crRNA, with no or minimal permanent genetic scar on genes. This review summarizes CRISPR-Cas13 system from its discovery, classification, principle of action, and diagnostic platforms. Further, it discusses the application prospects of Cas13-based systems in Plasmodium and highlights its advantages and drawbacks

    Comparison of thoracoabdominal versus abdominal-transhiatal surgical approaches in Siewert type II adenocarcinoma at the esophagogastric junction: Protocol for a prospective multicenter randomized controlled trial

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    BackgroundSiewert type II adenocarcinoma of the esophagogastric junction (Siewert II AEG) can be resected by the right thoracoabdominal surgical approach (RTA) or abdominal-transhiatal surgical approach (TH) under minimally invasive conditions. Although both surgical methods achieve complete tumor resection, there is a debate as to whether the former method is superior to or at least noninferior to the latter in terms of surgical safety. Currently, a small number of retrospective studies have compared the two surgical approaches, with inconclusive results. As such, a prospective multicenter randomized controlled trial is necessary to validate the value of RTA (Ivor-Lewis) compared to TH.MethodsThe planned study is a prospective, multicenter, randomized clinical trial. Patients (n=212) with Siewert II AEG that could be resected by either of the above two surgical approaches will be included in this trial and randomized to the RTA group (n=106) or the TH group (n=106). The primary outcome will be 3-year disease-free survival (DFS). The secondary outcomes will include 5-year overall survival (OS), incidence of postoperative complications, postoperative mortality, local recurrence rate, number and location of removed lymph nodes, quality of life (QOL), surgical Apgar score, and duration of the operation. Follow-ups are scheduled every three months for the first 3 years after the surgery and every six months for the next 2 years.DiscussionAmong Siewert II AEG patients with resectable tumors, this is the first prospective, randomized clinical trial comparing the surgical safety of minimally invasive RTA and TH. RTA is hypothesized to provide better digestive tract reconstruction and dissection of mediastinal lymph nodes while maintaining a high quality of life and good postoperative outcome. Moreover, this trial will provide a high level of evidence for the choice of surgical procedures for Siewert II AEG.Clinical trial registrationChinese Ethics Committee of Registering Clinical Trials, identifier (ChiECRCT20210635); Clinical Trial.gov, identifier (NCT05356520)
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