Miracle-dz/UniFAR-FTUs huggingface dataset:
National Characteristics of Emergency Medical Services Responses in the United States

Abstract Objective. Despite its long history and current prominence in U.S. communities, only limited data describe the national characteristics of emergency medical services (EMS) care in the United States. We sought to characterize out-of-hospital EMS care in the United States. Methods. We conducted an analysis of the 2010 National Emergency Medical Services Information System (NEMSIS) research data set, encompassing EMS emergency response data from 29 states. From these data, we estimated the national number and incidence of EMS responses. We also characterized EMS responses and the patients receiving care. Results. There were 7,563,843 submitted EMS responses, corresponding to an estimated national incidence of 17.4 million EMS emergency responses per year (56 per 1,000 person-years). The EMS response incidence varied by U.S. Census region (South 137.4 per 1,000 population per year, Northeast 85.2, West 39.7, and Midwest 33.3). The use of lights and sirens varied across Census regions (Northeast 90.3%, South 76.7%, West 68.8%, and Midwest 67.5%). The percentage of responses resulting in patient contact varied across Census regions (range 78.4% to 95.7%). The EMS time intervals were similar between Census regions; response median 5 minutes (interquartile range [IQR] 3–9), scene 14 minutes (10–20), and transport 11 minutes (7–19). Underserved populations (the elderly, minorities, rural residents, and the uninsured) were large users of EMS resources. Conclusion. These data highlight the breadth and diversity of EMS demand and care in the United States.
Improved Brain Delivery of Benzylpenicillin with a Peptide-vector-mediated Strategy

Previous studies from our laboratory have demonstrated that the coupling of doxorubicin with SynB1 vector dramatically increases its brain uptake. In the present study, we have evaluated the broad application of this approach using another molecule: benzylpenicillin (B-Pc). We, therefore, have coupled the β -lactam antibiotic B-Pc with SynB1 and assessed its ability to cross the blood-brain barrier (BBB) using the in situ rat brain perfusion method. We first confirmed the very low brain uptake of free radiolabeled B-Pc. When B-Pc was coupled to SynB1, its uptake in brain was increased by a factor of 7, without compromising the BBB integrity. The vectorised B-Pc was distributed in all the gray areas assessed (frontal, parietal, and occipital cortex, thalamus, hippocampus, and striatum). Moreover, using a wash-out procedure and a capillary depletion method, we have shown that the radiolabeled B-Pc was associated mainly with brain parenchyma. In summary, this study demonstrates the successful application of the use of SynB1 vector for the transport of B-Pc across the BBB.
Methods Used to Improve Gamete Efficiency

Male factor infertility accounts for a significant percentage of problems in infertile couples. With clinical utilization of the technologies for selection of good-quality spermatozoa from the ejaculate, our ability to successfully treat the severely affected male factor couple has improved. However, it must be remembered that even with current technologies, fertilization success is reduced in these patients but remains above a 50% level. Other factors that can be used in the future to improve on these statistics are being investigated in regard to the in vitro environment for gametes, that is, the type of culture medium, the methods of coincubation of the sperm and egg, and other methods of enhancement of sperm fertilizing potential. However, methods of sperm preparation will achieve improvement in a percentage of these males treated, and can be used to improve fertilization and pregnancy success. It is important to understand the limitations of the zona-free hamster test, but it is also important to use that test as a screening method for sperm handling. By utilizing the SPA to select out the optimal method of sperm preparation, the fertilization and pregnancy outcome can be improved. Overall, the live-birth rate in male factor infertile couples is lower than non-male-factor couples treated by IVF and GIFT. Until more is known about basic spermatozoal function, and the ability to improve that function in affected males, the live-birth rate should not be expected to change substantially.
Hepatitis C virus inhibits interferon signaling through up-regulation of protein phosphatase 2A.

BACKGROUND AND AIMS To establish a chronic infection, hepatitis C virus (HCV) has to evade the host defense. Expression of HCV proteins in cultured cells and in hepatocytes of transgenic mice inhibits interferon-alpha-induced intracellular signaling through the Jak-STAT (signal transducer and activator of transcription) pathway. It is not known if interferon-alpha signaling is inhibited in patients with chronic hepatitis C as well, and the molecular mechanisms are not well defined. METHODS Interferon-alpha-induced signaling was investigated in liver biopsies from patients with chronic hepatitis C. The molecular mechanisms of HCV interference with Jak-STAT signaling were analyzed in cultured cells, HCV transgenic mice, and liver biopsies. RESULTS Interferon-alpha-induced DNA binding of STAT1 was significantly impaired in liver biopsies from patients with chronic hepatitis C compared with controls. Tyrosine and serine phosphorylation of STAT1 were intact, but methylation of STAT1 on arginine 31 was reduced. Hypomethylated STAT1 associated with PIAS1, an inhibitor of STAT DNA binding. Increased expression levels of Protein Phosphatase 2A were found in liver extracts from HCV transgenic mice and in liver biopsies of patients with chronic hepatitis C. Overexpression of PP2Ac in Huh7 cells resulted in hypomethylation of STAT1, increased binding to PIAS1, and reduced interferon-alpha-induced DNA binding of STAT1. CONCLUSIONS We conclude that HCV interferes with interferon-alpha signaling via up-regulation of PP2Ac, hypomethylation of STAT1, and increased STAT1-PIAS1 association, resulting in reduced transcriptional activation of interferon-alpha-stimulated genes.
Event extraction & image retrieval for story board generation using GLCM

Data mining is the process of extracting information or knowledge from a wide database. In addition, to provide a visually appealing storyboard, each event is mapped with a set of relevant images arranged along a timeline. In order to retrieve features of similar types of image shapes and texture, a feature called Weighted Euclidean distance is used. Image mining is the association of image data and extraction of hidden data. Image mining makes use of texture, color factors and size of an image. Traditional websites were driven by human-edited events which lead to huge web search traffic. This work suggests an automatic system to detect events from search log data and generate storyboards where the events are arranged along a timeline. Smooth Nonnegative Matrix Factorization framework (SNMF) based event discovery from log data is used. In addition, to provide a visually appealing storyboard, each event is mapped with a set of relevant images arranged along a timeline. Image texture is determined by a feature called Gray Level Co-occurrence Matrix (GLCM). In this case image retrieval feature will be sharp.
A Mechanism for the Rapid Development of Intracranial Aneurysms: A Case Study

BACKGROUND:Despite technical and diagnostic progress there are still open questions in the understanding of the pathophysiology of intracranial aneurysms. OBJECTIVE:Within 44 days we observed the de novo genesis and rupture of an aneurysm of the basilar artery in a patient. We performed computational fluid dynamics on 3-dimensional (3D) models of the inconspicuous vessel and the same vessel with aneurysm. Based on the simulations we propose a mechanism of genesis of fast-growing aneurysms. METHODS:Three-dimensional mesh models were built using computed tomography-angiography slices. Flow was modeled as a non-Newtonian blood model with shear-dependent dynamic viscosity. We investigated flow velocity, wall pressure, impingement point, wall shear stress (WSS), and asymmetric flows in 3D models of the vessel tree of the basilar artery. RESULTS:Impingement point and wall pressure had no clear relation to the origin of the aneurysm. The impingement point faded away during aneurysm growth. Instead we found an area of permanently low WSS in the original basilar artery. This location corresponded to the origin of the later developing aneurysm. Aneurysm growth was facilitated by an increasing overall expansion of the basilar tip and a constant decrease of WSS. CONCLUSION:Assuming a preexisting reduced resistibility of the vessel wall to pressure changes and an area of permanently low WSS, an increase in pressure induces geometrical changes. These cause changes of intravascular flow distribution, lowering the already low WSS in specific locations. This leads to endothelial damage in this area and to a decreasing stability of the vessel wall, causing aneurysm development, growth, and rupture.
p53 mediates mitochondria dysfunction-triggered autophagy activation and cell death in rat striatum

In vivo administration of the mitochondrial inhibitor 3-nitropropionic acid (3-NP) produces striatal pathology mimicking Huntington disease (HD). However, the mechanisms of cell death induced by metabolic impairment are not fully understood. The present study investigated contributions of p53 signaling pathway to autophagy activation and cell death induced by 3-NP. Rat striatum was intoxicated with 3-NP by stereotaxic injection. Morphological and biochemical analyses demonstrated activation of autophagy in striatal cells as evidenced by increased the formation of autophagosomes, the expression of active lysosomal cathepsin B and D, microtubule associate protein light chain 3 (LC3) and conversion of LC3-I to LC3-II. 3-NP upregulated the expression of tumor suppressor protein 53 (p53) and its target genes including Bax, p53-upregulated modulator of apoptosis (PUMA) and damage-regulated autophagy modulator (DRAM). 3-NP-induced elevations in pro-apoptotic proteins Bax and PUMA, autophagic proteins LC3-II and DRAM were significantly reduced by the p53 specific inhibitor pifithrin-α (PFT). PFT also significantly inhibited 3-NP-induced striatal damage. Similarly, 3-NP-induced DNA fragmentation and striatal cell death were robustly attenuated by the autophagy inhibitor 3-methyladenine (3-MA) and bafilomycin A1 (BFA). These results suggest that p53 plays roles in signaling both autophagy and apoptosis. Autophagy, at least partially, contributes to neurodegeneration induced by mitochondria dysfunction.
Serum‐free B27/neurobasal medium supports differentiated growth of neurons from the striatum, substantia nigra, septum, cerebral cortex, cerebellum, and dentate gyrus

Two fundamental questions about neuron cell culture were addressed. Can one serum‐free medium that was developed for optimum growth of hippocampal neurons support the growth of neurons from other regions of the brain? Is the region specific state of differentiation maintained in culture? To answer these questions, we isolated neurons from six other rat brain regions, placed them in culture in B27/NeurobasalTM defined medium, and analyzed their morphology and growth dependence on cell density after 4 days in culture. Neuronal identity was confirmed by immunostaining with antibodies to neurofilament 200. Neurons from each brain region maintained distinctive morphologies in culture in the virtual absence of glia. Cells isolated from embryonic day 18 cerebral cortex by digestion with papain showed the same high survival as hippocampal neurons, e.g., 70% survival for cells plated at 160/mm2. At this age and density, neurons from the septum showed slightly lower survival, 45%. Survival of dentate granule neurons from postnatal day four brains was 30‐40%, significantly lower, and relatively independent of plating density. This suggests an absence of dependence on trophic factors or contact for dentate granule neurons. Growth of cerebellar granule neurons isolated from postnatal day 7, 8, or 9 brains in B27/Neurobasal was compared to growth in BME/10% serum. Viability in serum‐free medium at 4 days was much better than that in serum, did not require KCI elevated to 25 mM, and occurred without substantial growth of glia. Cerebellar granule neurons plated at 1,280 cells/mm2 were maintained in culture for three weeks with 17 of the original cell density surviving. Survival of cells isolated from embryonic day 18 substantia nigra was 50% at 160 cells/mm2 after 4 days, similar to that of striatum, but slightly less than hippocampal neuron survival. The dopaminergic phenotype of the substantia nigral neurons was maintained over 2 weeks in culture as judged by immunoreactivity with antibodies to tyrosine hydroxylase. During this time, immunoreactivity was found in the processes as they grew out from the soma. Together, these studies suggest that B27/Neurobasal will be a useful medium for maintaining the differentiated growth of neurons from many brain regions. Potential applications of a common growth medium for different neurons are discussed. © 1995 Wiley‐Liss, Inc.
A nonconventional multilevel inverter for active power filtering using unified constant-frequency integration control

Nowadays, the increase in nonlinear loads has contributed to the generation of harmonics in the source current which in turn causes low power factor and disturbance in the power system. Active power filters (APFs) are known to provide one of the solutions to this harmonic related issue. Various types and configurations of APFs and control have been reported in literature. This paper proposes the integration of a single-phase nonconventional multilevel inverter known as the multistring Cross-Connected Source Multilevel Inverter (CCSMI) and a modified Unified Constant-Frequency Integration (UCI) controller as an active power filtering system. The results of the simulation work conducted on the proposed APF system have revealed its capability to effectively mitigate the source current harmonics with added advantages in terms of less parts counts and losses as well as reduced control complexity without the need for reference current generation.
Assessing Markov and time homogeneity assumptions in multi-state models: application in patients with gastric cancer undergoing surgery in the Iran cancer institute.

BACKGROUND Multi-state models are appropriate for cancer studies such as gastrectomy which have high mortality statistics. These models can be used to better describe the natural disease process. But reaching that goal requires making assumptions like Markov and homogeneity with time. The present study aims to investigate these hypotheses. MATERIALS AND METHODS Data from 330 patients with gastric cancer undergoing surgery at Iran Cancer Institute from 1995 to 1999 were analyzed. To assess Markov assumption and time homogeneity in modeling transition rates among states of multi-state model, Cox-Snell residuals, Akaikie information criteria and Schoenfeld residuals were used, respectively. RESULTS The assessment of Markov assumption based on Cox-Snell residuals and Akaikie information criterion showed that Markov assumption was not held just for transition rate of relapse (state 1-state 2) and for other transition rates - death hazard without relapse (state 1-state 3) and death hazard with relapse (state 2-state 3) - this assumption could also be made. Moreover, the assessment of time homogeneity assumption based on Schoenfeld residuals revealed that this assumption - regarding the general test and each of the variables in the model - was held just for relapse (state 1-state 2) and death hazard with a relapse (state 2-state 3). CONCLUSIONS Most researchers take account of assumptions such as Markov and time homogeneity in modeling transition rates. These assumptions can make the multi-state model simpler but if these assumptions are not made, they will lead to incorrect inferences and improper fitting.
Measurement of the top-quark mass using missing $E_T$+jets events with secondary vertex $b$-tagging at CDF II

We present a measurement of the top-quark mass in $p\bar p$ collisions at \hbox{$\sqrt{s}=1.96$} TeV which uses events with an inclusive signature of missing transverse energy and jets. % The event selection is sensitive to $t\bar t\to W^+bW^-\bar b\to l\nu b q q^\prime \bar b$ independent of the lepton flavor, and results in a large acceptance for $W\to\tau\nu$ decays. % All-hadronic $t\bar t$ decays and events with identified electrons or muons are vetoed to provide a statistically independent sample with respect to all previous measurements. % The top-quark mass is inferred from the distribution of the scalar sum of all jet transverse energies and the missing transverse energy. Using 311 pb$^{-1}$ of integrated luminosity recorded by the Collider Detector at Fermilab, we measure a top-quark mass $m_t = 172.3 ^{+10.8}_{-9.6}$(stat.)$\pm 10.8$(syst.) GeV/$c^2$. While the uncertainty on $m_t$ is larger than that of other measurements, the result is statistically uncorrelated with those of other methods, and thus can help to reduce the overall $m_t$ uncertainty when combined with other existing measurements.
Induction of Apoptosis by the c-Myc Helix-Loop-Helix/Leucine Zipper Domain in Mouse 3T3-L1 Fibroblasts *

The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The c-Myc protein is a transcriptional activator with a carboxyl-terminal basic region/helix-loop-helix (HLH)/leucine zipper (LZ) domain. It forms heterodimers with the HLH/LZ protein Max and transactivates gene expression after binding DNA E-box elements. We have studied the phenotype of dominant-negative mutants of c-Myc and Max in microinjection experiments. Max mutants with a deleted or mutated basic region inhibited DNA synthesis in serum-stimulated 3T3-L1 mouse fibroblasts. In contrast, mutants of c-Myc expressing only the basic region/HLH/LZ or HLH/LZ domains rapidly induced apoptosis at low and high serum levels. Co-expression of the HLH/LZ domains of c-Myc and Max failed to do so. We suggest that the c-Myc HLH/LZ domain induces apoptosis by specific interaction with cellular factors different to Max.
PCA3 and PSA gene activity correlates with the true tumor cell burden in prostate cancer lymph node metastases.

BACKGROUND Extent of pelvic lymph node (LN) dissemination is a critical prognostic feature for patients with prostate cancer (PCa) maintaining extended pelvic lymphadenectomy (LAD) as the gold standard for LN-staging. Unfortunately, conventional histopathological assessment may miss micrometastasis and recently presented immunocytochemical approach of the single cell analysis is still intricate. OBJECTIVE To comparatively assess the potential of Prostate cancer gene 3 (PCA3) and prostate specific antigene (PSA) to perform as markers for tumor cell load. METHODS Patients with high risk PCa for LN metastasis undergoing either a sentinel LN-guided staging LAD or retropubic radical prostatectomy with sentinel-guided pelvic LN dissection were included. LNs were investigated by routine histopathology. Tumor cell load was quantified by %immunocytochemistry. immunocytochemical single cell analysis. Gene activity was determined by qRT-PCR. RESULTS Twenty four out of 226 LNs were positive in routine histopathology and 51 in single cell analysis. PSA mRNA level correlated with tumor cell density in patients with a positive immunocytochemistry. Gene activity of PCA3 was upregulated in metastatic LNs and correlated with tumor cell density in patients with tumor-invaded LNs as detected by immunocytochemistry. CONCLUSIONS PCA3 gene expression discriminates LN metastasis and might outperform PSA gene activity in reflecting tumor cell burden in pelvic LNs of PCa patients.
XMU Neural Machine Translation Systems for WAT 2017

This paper describes the Neural Machine Translation systems of Xiamen University for the shared translation tasks of WAT 2017. Our systems are based on the Encoder-Decoder framework with attention. We participated in three subtasks. We experimented subword segmentation, synthetic training data and model ensembling. Experiments show that all these methods can give substantial improvements.
The P‐selectin, tissue factor, coagulation triad

Summary. The primary importance of tissue factor (TF) in blood coagulation and thrombus propagation has been recognized for many years. Nevertheless, our view about the origin of TF activity, necessary for normal hemostasis and found in pathologic conditions, needs to be revised in the light of recent observations. Pioneering work by Yale Nemerson's group showed that circulating TF on microparticles (MPs), could promote thrombus growth. The origin and characteristics of this ‘blood‐borne’ TF are targets of intense research as well as intense debate. Surprising observations now implicate the adhesion receptor P‐selectin (P‐sel), known for its role in inflammation, in these MPs’ generation. P‐sel, translocated from granules to the cell surfaces of activated platelets and endothelial cells, was recently found to play multiple roles in hemostasis. Expressed on endothelium, it can mediate platelet rolling. Signaling by P‐sel through its receptor on leukocytes, P‐selectin glycoprotein ligand 1 (PSGL‐1), induces the generation of TF‐positive, highly procoagulant MPs. In addition, P‐sel on activated platelets helps to recruit these MPs specifically to thrombi. In this review, we discuss the roles of P‐sel and TF‐positive MPs and highlight strategies to modulate hemostasis by modulating the P‐sel, TF, coagulation triad.
MET amplification identifies a small and aggressive subgroup of esophagogastric adenocarcinoma with evidence of responsiveness to crizotinib.

PURPOSE Amplification of the MET proto-oncogene in gastroesophageal cancer (GEC) may constitute a molecular marker for targeted therapy. We examined a GEC cohort with follow-up and reported the clinical response of four additional patients with MET-amplified tumors to the small molecule inhibitor crizotinib as part of an expanded phase I cohort study. PATIENTS AND METHODS From 2007 to 2009, patients with GEC were genetically screened as a consecutive series of 489 tumors (stages 0, I, and II, 39%; III, 25%; IV, 36%; n = 222 esophageal, including n = 21 squamous carcinomas). MET, EGFR, and HER2 amplification status was assessed by using fluorescence in situ hybridization. RESULTS Ten (2%) of 489 patients screened harbored MET amplification; 23 (4.7%) harbored EGFR amplification; 45 (8.9%) harbored HER2 amplification; and 411 (84%) were wild type for all three genes (ie, negative). MET-amplified tumors were typically high-grade adenocarcinomas that presented at advanced stages (5%; n = 4 of 80). EGFR-amplified tumors showed the highest fraction of squamous cell carcinoma (17%; n = 4 of 23). HER2, MET, and EGFR amplification were, with one exception (MET and EGFR positive), mutually exclusive events. Survival analysis in patients with stages III and IV disease showed substantially shorter median survival in MET/EGFR-amplified groups, with a rank order for all groups by median survival (from most to least aggressive): MET (7.1 months; P < .001) less than EGFR (11.2 months; P = .16) less than HER2 (16.9 months; P = .89) when compared with the negative group (16.2 months). Two of four patients with MET-amplified tumors treated with crizotinib experienced tumor shrinkage (-30% and -16%) and experienced progression after 3.7 and 3.5 months. CONCLUSION MET amplification defines a small and aggressive subset of GEC with indications of transient sensitivity to the targeted MET inhibitor crizotinib (PF-02341066).