Miracle-dz/UniFAR-FTUs huggingface dataset:
Optimal Arterial Blood Oxygen Tension in the Early Postresuscitation Phase of Extracorporeal Cardiopulmonary Resuscitation: A 15-Year Retrospective Observational Study.

OBJECTIVES Hyperoxia could lead to a worse outcome after cardiac arrest. Few studies have investigated the impact of oxygenation status on patient outcomes following extracorporeal cardiopulmonary resuscitation. We sought to delineate the association between oxygenation status and neurologic outcomes in patients receiving extracorporeal cardiopulmonary resuscitation. DESIGN Retrospective analysis of a prospective extracorporeal cardiopulmonary resuscitation registry database. SETTING An academic tertiary care hospital. PATIENTS Patients receiving extracorporeal cardiopulmonary resuscitation between 2000 and 2014. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS A total of 291 patients were included, and 80.1% were male. Their mean age was 56.0 years. The arterial blood gas data employed in the primary analysis were recorded from the first sample over the first 24 hours in the ICUs after return of spontaneous circulation. The mean PaO2 after initiation of venoarterial extracorporeal membrane oxygenation was 178.0 mm Hg, and the mean PaO2/FIO2 ratio was 322.0. Only 88 patients (30.2%) demonstrated favorable neurologic status at hospital discharge. Multivariate logistic regression analysis indicated that PaO2 between 77 and 220 mm Hg (odds ratio, 2.29; 95% CI, 1.01-5.22; p = 0.05) and PaO2/FIO2 ratio between 314 and 788 (odds ratio, 5.09; 95% CI, 2.13-12.14; p < 0.001) were both positively associated with favorable neurologic outcomes. CONCLUSIONS Oxygenation status during extracorporeal membrane oxygenation affects neurologic outcomes in patients receiving extracorporeal cardiopulmonary resuscitation. The PaO2 range of 77 to 220 mm Hg, which is slightly narrower than previously defined, seems optimal. The PaO2/FIO2 ratio was also associated with outcomes in our analysis, indicating that both PaO2 and the PaO2/FIO2 ratio should be closely monitored during the early postcardiac arrest phase for postextracorporeal cardiopulmonary resuscitation patients.
Stimulation of the Posterior Cingulate Cortex Impairs Episodic Memory Encoding

Neuroimaging experiments implicate the posterior cingulate cortex (PCC) in episodic memory processing, making it a potential target for responsive neuromodulation strategies outside of the hippocampal network. However, causal evidence for the role that PCC plays in memory encoding is lacking. In human female and male participants (N = 17) undergoing seizure mapping, we investigated functional properties of the PCC using deep brain stimulation (DBS) and stereotactic electroencephalography. We used a verbal free recall paradigm in which the PCC was stimulated during presentation of half of the study lists, whereas no stimulation was applied during presentation of the remaining lists. We investigated whether stimulation affected memory and modulated hippocampal activity. Results revealed four main findings. First, stimulation during episodic memory encoding impaired subsequent free recall, predominantly for items presented early in the study lists. Second, PCC stimulation increased hippocampal gamma-band power. Third, stimulation-induced hippocampal gamma power predicted the magnitude of memory impairment. Fourth, functional connectivity between the hippocampus and PCC predicted the strength of the stimulation effect on memory. Our findings offer causal evidence implicating the PCC in episodic memory encoding. Importantly, the results indicate that stimulation targeted outside of the temporal lobe can modulate hippocampal activity and impact behavior. Furthermore, measures of connectivity between brain regions within a functional network can be informative in predicting behavioral effects of stimulation. Our findings have significant implications for developing therapies to treat memory disorders and cognitive impairment using DBS. SIGNIFICANCE STATEMENT Cognitive impairment and memory loss are critical public health challenges. Deep brain stimulation (DBS) is a promising tool for developing strategies to ameliorate memory disorders by targeting brain regions involved in mnemonic processing. Using DBS, our study sheds light on the lesser-known role of the posterior cingulate cortex (PCC) in memory encoding. Stimulating the PCC during encoding impairs subsequent recall memory. The degree of impairment is predicted by stimulation-induced hippocampal gamma oscillations and functional connectivity between PCC and hippocampus. Our findings provide the first causal evidence implicating PCC in memory encoding and highlight the PCC as a favorable target for neuromodulation strategies using a priori connectivity measures to predict stimulation effects. This has significant implications for developing therapies for memory diseases.
Design and Experimental Validation of a LoRaWAN Fog Computing Based Architecture for IoT Enabled Smart Campus Applications †

A smart campus is an intelligent infrastructure where smart sensors and actuators collaborate to collect information and interact with the machines, tools, and users of a university campus. As in a smart city, a smart campus represents a challenging scenario for Internet of Things (IoT) networks, especially in terms of cost, coverage, availability, latency, power consumption, and scalability. The technologies employed so far to cope with such a scenario are not yet able to manage simultaneously all the previously mentioned demanding requirements. Nevertheless, recent paradigms such as fog computing, which extends cloud computing to the edge of a network, make possible low-latency and location-aware IoT applications. Moreover, technologies such as Low-Power Wide-Area Networks (LPWANs) have emerged as a promising solution to provide low-cost and low-power consumption connectivity to nodes spread throughout a wide area. Specifically, the Long-Range Wide-Area Network (LoRaWAN) standard is one of the most recent developments, receiving attention both from industry and academia. In this article, the use of a LoRaWAN fog computing-based architecture is proposed for providing connectivity to IoT nodes deployed in a campus of the University of A Coruña (UDC), Spain. To validate the proposed system, the smart campus has been recreated realistically through an in-house developed 3D Ray-Launching radio-planning simulator that is able to take into consideration even small details, such as traffic lights, vehicles, people, buildings, urban furniture, or vegetation. The developed tool can provide accurate radio propagation estimations within the smart campus scenario in terms of coverage, capacity, and energy efficiency of the network. The results obtained with the planning simulator can then be compared with empirical measurements to assess the operating conditions and the system accuracy. Specifically, this article presents experiments that show the accurate results obtained by the planning simulator in the largest scenario ever built for it (a campus that covers an area of 26,000 m2), which are corroborated with empirical measurements. Then, how the tool can be used to design the deployment of LoRaWAN infrastructure for three smart campus outdoor applications is explained: a mobility pattern detection system, a smart irrigation solution, and a smart traffic-monitoring deployment. Consequently, the presented results provide guidelines to smart campus designers and developers, and for easing LoRaWAN network deployment and research in other smart campuses and large environments such as smart cities.
Dietary Chitooligosaccharide Inclusion as an Alternative to Antibiotics Improves Intestinal Morphology, Barrier Function, Antioxidant Capacity, and Immunity of Broilers at Early Age

Simple Summary At early an age, broilers are susceptible to exterior stressors and therefore have a higher disease incidence rate. Antibiotic growth promoters have been forbidden in animal production by the European Union and other countries since their usage has caused potentially adverse effects such as antibiotic residues in livestock, environmental pollution, and the generation of drug-resistant bacteria. The search for safe and environmentally friendly alternatives to antibiotics to prevent disease and promote growth has become necessary in poultry production. Chitooligosaccharide (COS), a natural alkaline polymer of glucosamine with a number of bioactive groups, is easily obtained by chemical and enzymatic hydrolysis of chitosan, which is the second most abundant carbohydrate polymer in nature. Our results indicated that dietary supplementation with chitooligosaccharide, at a dosage of 30 mg/kg, enhanced the feed conversion ratio, benefited the intestinal morphology and barrier function, and improved antioxidant capacity and immunity in broilers at 21 days of age. These effects were similar with those observed as a result of chlortetracycline inclusion. Therefore, dietary COS supplementation can be used as a potential alternative to antibiotics in broilers. Abstract This study aimed to investigate the effects of chitooligosaccharide (COS) inclusion as an alternative to antibiotics on growth performance, intestinal morphology, barrier function, antioxidant capacity, and immunity in broilers. In total, 144 one-day-old Arbor Acres broiler chicks were randomly assigned into 3 groups and fed a basal diet free from antibiotics (control group) or the same basal diet further supplemented with either chlortetracycline (antibiotic group) or COS, for 21 days. Compared with the control group, inclusion of COS reduced the feed to gain ratio, the jejunal crypt depth, the plasma diamine oxidase activity, and the endotoxin concentration, as well as jejunal and ileal malondialdehyde contents, whereas increased duodenal villus height, duodenal and jejunal ratio of villus height to crypt depth, intestinal immunoglobulin G, and jejunal immunoglobulin M (IgM) contents were observed, with the values of these parameters being similar or better to that of the antibiotic group. Additionally, supplementation with COS enhanced the superoxide dismutase activity and IgM content of the duodenum and up-regulated the mRNA level of claudin three in the jejunum and ileum, when compared with the control and antibiotic groups. In conclusion, dietary COS inclusion (30 mg/kg), as an alternative to antibiotics, exerts beneficial effects on growth performance, intestinal morphology, barrier function, antioxidant capacity, and immunity in broilers.
Integrating clinical, morphological, and molecular data to assess prognosis in patients with primary myelofibrosis at diagnosis: A practical approach

Currently available prognostic scoring systems in primary myelofibrosis (PMF) do not integrate clinical, histological, and molecular data, or they also required information on “other” mutations that are available in the clinical practice only in a very limited number of laboratories. In the present multicenter study, including 401 PMF patients, an integrated International Prognostic Scoring System (I‐IPSS) was developed by combining IPSS, grade of bone marrow fibrosis (GBMF), and driver mutations molecular status (MS) to define PMF prognosis at diagnosis. Four prognostic categories were identified: I‐IPSS–low risk (113 patients), I‐IPSS–intermediate‐1 risk (56 patients), I‐IPSS–intermediate‐2 risk (154 patients), and I‐IPSS–high risk (78 patients). Median overall survival was 26.7 years in I‐IPSS–intermediate‐1, 10.8 in I‐IPSS–intermediate‐2, and 6.4 in I‐IPSS‐high‐risk patients (log‐rank test <0.0001); instead, it was not reached in the I‐IPSS–low‐risk cohort because of the extremely low number of registered deaths. The addition of GBMF and MS to IPSS improved the efficacy for predicting the risk of death. Indeed, the sensitivity of I‐IPSS was significantly higher (P < .05) than that of IPSS, considering both total deaths and 5‐ and 10‐year mortality. This comprehensive approach allows clinicians to evaluate mutual interactions between IPSS, GBMF, and MS and identify high‐risk patients with poor prognosis who may benefit from aggressive treatments. More importantly, this integrated score can be easily applicable worldwide as it only required information that represent the good clinical practice in the management of PMF patients.
ZBP1/DAI Drives RIPK3-Mediated Cell Death Induced by IFNs in the Absence of RIPK1

Key Points IFNs induce RIPK3-dependent cell death in the absence of RIPK1. The IFN-stimulated gene product ZBP1 drives cell death in Ripk1−/− cells. ZBP1 and IFN signaling contribute to perinatal lethality of Ripk1−/− mice. Receptor-interacting protein kinase 1 (RIPK1) regulates cell fate and proinflammatory signaling downstream of multiple innate immune pathways, including those initiated by TNF-α, TLR ligands, and IFNs. Genetic ablation of Ripk1 results in perinatal lethality arising from both RIPK3-mediated necroptosis and FADD/caspase-8–driven apoptosis. IFNs are thought to contribute to the lethality of Ripk1-deficient mice by activating inopportune cell death during parturition, but how IFNs activate cell death in the absence of RIPK1 is not understood. In this study, we show that Z-form nucleic acid binding protein 1 (ZBP1; also known as DAI) drives IFN-stimulated cell death in settings of RIPK1 deficiency. IFN-activated Jak/STAT signaling induces robust expression of ZBP1, which complexes with RIPK3 in the absence of RIPK1 to trigger RIPK3-driven pathways of caspase-8–mediated apoptosis and MLKL-driven necroptosis. In vivo, deletion of either Zbp1 or core IFN signaling components prolong viability of Ripk1−/− mice for up to 3 mo beyond parturition. Together, these studies implicate ZBP1 as the dominant activator of IFN-driven RIPK3 activation and perinatal lethality in the absence of RIPK1.
Translating systems thinking into practice for community action on childhood obesity

We report on the first 18 months of two communities' efforts using methods inspired by community‐based participatory system dynamics for the development, implementation, and evaluation of whole of community efforts to improve the health of children. We apply Foster‐Fishman's theoretical framework for characterizing systems change to describe the initiatives. Bounding the system began with defining leaders more broadly than standard health interventions to be those who had the ability to change environments to improve health, including food retailers, government, and business, and using high‐quality childhood monitoring data to define the problem. Widespread access to junk food, barriers to physical activity, and efforts to promote health predominantly through programmatic approaches were identified as potential root causes. System interactions existed in the form of relationships between stakeholder groups and organizations. The approach described built new relationships and strengthened existing relationships. Willingness in taking risks, changing existing practice, and redesigning health promotion work to have a community development focus, were levers for change. This approach has resulted in hundreds of community‐led actions focused on changing norms and environments. Insights from this approach may be useful to support other communities in translating systems theory into systems practice. Further empirical research is recommended to explore the observations in this paper.
Loss of RNA Chaperone Hfq Unveils a Toxic Pathway in Pseudomonas aeruginosa

Here we show that the conserved RNA chaperone Hfq is important for the growth of the opportunistic pathogen Pseudomonas aeruginosa. We found that the growth defect of hfq mutant cells is dependent upon the expression of genes that are under the control of the transcription regulator MexT. These include a gene that we refer to as hilR, which we show is negatively regulated by Hfq and encodes a small protein that can be toxic when ectopically produced in wild-type cells. Thus, Hfq can influence the growth of P. aeruginosa by limiting the toxic effects of MexT-regulated genes, including one encoding a previously unrecognized small protein. We also show that MexT activity depends on an enzyme that synthesizes glutathione. ABSTRACT Hfq is an RNA chaperone that serves as a master regulator of bacterial physiology. Here we show that in the opportunistic pathogen Pseudomonas aeruginosa, the loss of Hfq can result in a dramatic reduction in growth in a manner that is dependent upon MexT, a transcription regulator that governs antibiotic resistance in this organism. Using a combination of chromatin immunoprecipitation with high-throughput sequencing and transposon insertion sequencing, we identify the MexT-activated genes responsible for mediating the growth defect of hfq mutant cells. These include a newly identified MexT-controlled gene that we call hilR. We demonstrate that hilR encodes a small protein that is acutely toxic to wild-type cells when produced ectopically. Furthermore, we show that hilR expression is negatively regulated by Hfq, offering a possible explanation for the growth defect of hfq mutant cells. Finally, we present evidence that the expression of MexT-activated genes is dependent upon GshA, an enzyme involved in the synthesis of glutathione. Our findings suggest that Hfq can influence the growth of P. aeruginosa by limiting the toxic effects of specific MexT-regulated genes. Moreover, our results identify glutathione to be a factor important for the in vivo activity of MexT. IMPORTANCE Here we show that the conserved RNA chaperone Hfq is important for the growth of the opportunistic pathogen Pseudomonas aeruginosa. We found that the growth defect of hfq mutant cells is dependent upon the expression of genes that are under the control of the transcription regulator MexT. These include a gene that we refer to as hilR, which we show is negatively regulated by Hfq and encodes a small protein that can be toxic when ectopically produced in wild-type cells. Thus, Hfq can influence the growth of P. aeruginosa by limiting the toxic effects of MexT-regulated genes, including one encoding a previously unrecognized small protein. We also show that MexT activity depends on an enzyme that synthesizes glutathione.
Management of Traumatic Injury and Osseointegration Failure in Children With Percutaneous Bone Conduction Implants.

OBJECTIVE This study examines the incidence and management of traumatic loss or osseointegration failure of percutaneous bone conduction implants in children. STUDY DESIGN Case series. SETTING Pediatric tertiary care institution. PATIENTS Children who underwent percutaneous osseointegrated implant placement from 1996 to 2016. INTERVENTIONS Clinical evaluation and revision surgery after implant loss. MAIN OUTCOME MEASURES This study compares the characteristics of children who experienced traumatic loss of implant to those who did not to calculate odds ratios (ORs) describing the risk of injury and investigate device utilization after implant failure. RESULTS One hundred forty-seven children received percutaneous bone conduction devices; 129 were followed for at least 1 year. Trauma occurred in 19 of 129 cases (15%). Among children with traumatic injury, mean age at initial surgery was 5 years (SD = ±3.3), and 42% had a developmental delay. Among children without traumatic injury, mean age at initial surgery was 6.5 years (SD = ±4.4), and 28% had a developmental delay. Multivariate logistic regression found no significant differences in age, sex, or developmental delay associated with implant loss. In five of 19 traumatic cases (26%), the implant remained in situ due to either skull fracture or abutment loss. In the remaining 14 of 19 cases (74%), there was osseointegration failure with extrusion of the implant. Seventeen children underwent revision surgery utilizing previously placed "sleeper," or backup, osseointegrated implant, and 14 (82%) of these continued to use their device. Two patients with extruded implants did not undergo revision surgery. CONCLUSION Traumatic injury or osseointegration failure leads to loss of percutaneous bone conduction implants in approximately 15% of children. Revision surgery is often successful.
Survival and complications: A 9- to 15-year retrospective follow-up of dental implant therapy.

BACKGROUND Long-term follow-up of oral implant therapy seldom report all biological and technical complications. OBJECTIVES The objective of this study was to evaluate the long-term (9-15 years) outcome after dental implant therapy, assess survival and complication rates. In addition, to identify the risk indicators of these complications at patient- and implant levels. METHODS Patients (n = 376) treated with dental implants (n = 1095) between 1999 and 2005 at a specialist clinic in Stockholm, Sweden, were included. Longitudinal data were collected retrospectively from digital dental records. A subset of the included patient underwent a clinical examination at the 9-15 years follow-up (n = 163). Chi-square tests, Kaplan-Meier analyses and the General Estimating Equations (GEE) procedure was adopted for multilevel analyses. RESULTS The cumulative implant survival rate up to 15 years was 82.6% (SE 4.1%). The prevalences of biological and technical complications at patient level were 52% and 32%, respectively. In total, 763 complications occurred, 65% of patients experienced at least one complications. Implant loss occurred significantly more frequently in subjects with a history of treated severe periodontitis Stage III-IV (p=0.008) and in cases when complications were registered during implant surgery (p=0.010). Smoking was a significant risk indicator for peri-implantitis (p=0.006). CONCLUSIONS The long-term implant survival- and complication rates at patient level were 83% and 79%, respectively. Implant loss was significantly more frequent for subjects with a history of treated severe periodontitis and if complication was registered during implant surgery. Smoking was a significant risk indicator for peri-implantitis.
Clinical Traits Characterizing an Exacerbation-Prone Phenotype in Chronic Rhinosinusitis

Objective Acute exacerbation of chronic rhinosinusitis (AECRS) is associated with significant quality-of-life decreases. We sought to determine characteristics associated with an exacerbation-prone phenotype in chronic rhinosinusitis (CRS). Study Design Cross-sectional. Setting Tertiary care rhinology clinic. Subjects Patients with CRS (N = 209). Methods Patient-reported number of sinus infections, CRS-related antibiotics, and CRS-related oral corticosteroids taken in the last 12 months were used as metrics for AECRS frequency. Sinonasal symptom burden was assessed with the 22-item Sinonasal Outcome Test (SNOT-22). Ninety patients reporting 0 for all AECRS metrics were considered to have had no AECRS in the prior 12 months. A total of 119 patients reported >3 on at least 1 AECRS metric and were considered as having an exacerbation-prone phenotype. Characteristics associated with patients with an exacerbation-prone phenotype were identified with exploratory regression analysis. Results An exacerbation-prone phenotype was positively associated with comorbid asthma (adjusted odds ratio [ORadj] = 3.68, 95% CI: 1.42-9.50, P = .007) and SNOT-22 (ORadj = 1.06, 95% CI: 1.04-1.09, P < .001). Polyps were negatively associated (ORadj = 0.27, 95% CI: 0.11-0.68, P = .005) with an exacerbation-prone phenotype. SNOT-22 score ≥24 identified patients with an exacerbation-prone phenotype with a sensitivity of 93.3% and a specificity of 57.8%. Having either a SNOT-22 score ≥24 with a nasal subdomain score ≥12 or a SNOT-22 score ≥24 with an ear/facial discomfort subdomain score ≥3 provided >80% sensitivity and specificity for detecting patients prone to exacerbation. Conclusions In total, these results point to a CRS exacerbation-prone phenotype characterized by high sinonasal disease burden with comorbid asthma but interestingly without polyps.