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Abstract Aging and lack of exercise are the most important etiological factors for muscle loss. We hypothesized that new factors that contribute to muscle loss could be identified from ones commonly altered in expression in aged and exercise-limited skeletal muscles. Mouse gastrocnemius muscles were subjected to mass spectrometry-based proteomic analysis. The muscle proteomes of hindlimb-unloaded and aged mice were compared to those of exercised and young mice, respectively. C1qbp expression was significantly upregulated in the muscles of both hindlimb-unloaded and aged mice. In vitro myogenic differentiation was not affected by altering intracellular C1qbp expression but was significantly suppressed upon recombinant C1qbp treatment. Additionally, recombinant C1qbp repressed the protein level but not the mRNA level of NFATc1. NFATc1 recruited the transcriptional coactivator p300, leading to the upregulation of acetylated histone H3 levels. Furthermore, NFATc1 silencing inhibited p300 recruitment, downregulated acetylated histone H3 levels, and consequently suppressed myogenic differentiation. The expression of C1qbp was inversely correlated with that of NFATc1 in the gastrocnemius muscles of exercised or hindlimb-unloaded, and young or aged mice. These findings demonstrate a novel role of extracellular C1qbp in suppressing myogenesis by inhibiting the NFATc1/p300 complex. Thus, C1qbp can serve as a novel therapeutic target for muscle loss.

Background and Purpose The accurate prediction of functional outcomes in patients with acute ischemic stroke (AIS) is crucial for informed clinical decision-making and optimal resource utilization. As such, this study aimed to construct an ensemble deep learning model that integrates multimodal imaging and clinical data to predict the 90-day functional outcomes after AIS. Methods We used data from the Korean Stroke Neuroimaging Initiative database, a prospective multicenter stroke registry to construct an ensemble model integrated individual 3D convolutional neural networks for diffusion-weighted imaging and fluid-attenuated inversion recovery (FLAIR), along with a deep neural network for clinical data, to predict 90-day functional independence after AIS using a modified Rankin Scale (mRS) of 3–6. To evaluate the performance of the ensemble model, we compared the area under the curve (AUC) of the proposed method with that of individual models trained on each modality to identify patients with AIS with an mRS score of 3–6. Results Of the 2,606 patients with AIS, 993 (38.1%) achieved an mRS score of 3–6 at 90 days post-stroke. Our model achieved AUC values of 0.830 (standard cross-validation [CV]) and 0.779 (time-based CV), which significantly outperformed the other models relying on single modalities: b-value of 1,000 s/mm2 (P

Abstract Background Sarcopenia is characterized by a progressive decrease in skeletal muscle mass and function with age. Given that sarcopenia is associated with various metabolic disorders, effective metabolic biomarkers for its early detection are required. We aimed to investigate the metabolic biomarkers related to sarcopenia in elderly men and perform experimental studies using metabolomics. Methods Plasma metabolites from 142 elderly men, comprising a sarcopenia group and an age‐matched control group, were measured using global metabolome profiling. Muscle and plasma samples from an aging mouse model of sarcopenia, as well as cell media and cell lysates during myoblast differentiation, were analysed based on targeted metabolome profiling. Based on these experimental results, fatty acid amides were quantified from human plasma as well as human muscle tissues. The association of fatty acid amide levels with sarcopenia parameters was evaluated. Results Global metabolome profiling showed that fatty acid amide levels were significantly different in the plasma of elderly men with sarcopenia (all Ps

Abstract Background Sarcopenia and osteoporosis frequently co‐occur in the elderly and have common pathophysiological determinants. Slit guidance ligand 3 (SLIT3) has been recently discovered as a novel therapeutic factor against osteoporosis, and a SLIT3 fragment containing the second leucine‐rich repeat domain (LRRD2) had a therapeutic efficacy against osteoporosis. However, a role of SLIT3 in the skeletal muscle is unknown. Methods Skeletal muscle mass, strength, and/or physical activity were evaluated in Slit3−/−, ovariectomized, and aged mice, based on the measurements of muscle weight and grip strength, Kondziella's inverted hanging test, and/or wheel‐running test. Skeletal muscles were also histologically evaluated by haematoxylin and eosin staining and/or immunofluorescence. The ovariectomized and aged mice were intravenously injected with recombinant SLIT3 LRRD2 for 4 weeks. C2C12 cells were used to know cellular effects of SLIT3, such as in vitro myogenesis, fusion, cell viability, and proliferation, and also used to evaluate its molecular mechanisms by immunocytochemistry, immunoprecipitation, western blotting, real‐time PCR, siRNA transfection, and receptor‐ligand binding ELISA. Results Slit3‐deficient mice exhibited decreased skeletal muscle mass, muscle strength, and physical activity. The relative masses of gastrocnemius and soleus were lower in the Slit3−/− mice (0.580 ± 0.039% and 0.033 ± 0.003%, respectively) than those in the WT littermates (0.622 ± 0.043% and 0.038 ± 0.003%, respectively) (all, P

Abstract Background This study investigated the clinical value of interleukin-6 (IL-6), pentraxin 3 (PTX3), and procalcitonin (PCT) in patients with sepsis and septic shock diagnosed according to the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Methods Serum levels of IL-6, PTX3, and PCT were measured in 142 enrolled subjects (51 with sepsis, 46 with septic shock, and 45 as controls). Follow-up IL-6 and PTX3 levels were measured in patients with initial septic shock within 24 h of hospital discharge. Optimal cut-off values were determined for sepsis and septic shock, and prognostic values were evaluated. Results Serum IL-6 levels could discriminate sepsis (area under the curve [AUC], 0.83–0.94, P

Time-series data provide important information in many fields, and their processing and analysis have been the focus of much research. However, detecting anomalies is very difficult due to data imbalance, temporal dependence, and noise. Therefore, methodologies for data augmentation and conversion of time series data into images for analysis have been studied. This paper proposes a fault detection model that uses time series data augmentation and transformation to address the problems of data imbalance, temporal dependence, and robustness to noise. The method of data augmentation is set as the addition of noise. It involves adding Gaussian noise, with the noise level set to 0.002, to maximize the generalization performance of the model. In addition, we use the Markov Transition Field (MTF) method to effectively visualize the dynamic transitions of the data while converting the time series data into images. It enables the identification of patterns in time series data and assists in capturing the sequential dependencies of the data. For anomaly detection, the PatchCore model is applied to show excellent performance, and the detected anomaly areas are represented as heat maps. It allows for the detection of anomalies, and by applying an anomaly map to the original image, it is possible to capture the areas where anomalies occur. The performance evaluation shows that both F1-score and Accuracy are high when time series data is converted to images. Additionally, when processed as images rather than as time series data, there was a significant reduction in both the size of the data and the training time. The proposed method can provide an important springboard for research in the field of anomaly detection using time series data. Besides, it helps solve problems such as analyzing complex patterns in data lightweight. [ABSTRACT FROM AUTHOR]

Introduction: Pentoxifylline (PTX) reduces the levels of pro-inflammatory cytokines; however, its effects on immune system is not well understood. The aim of this study was to investigate the effect of PTX on T cells under inflammatory conditions in co-culture with THP-1-derived macrophages. Methods: Toll-like receptor 4 (TLR4) and macrophage migration inhibitory factor (MIF) levels were measured after addition of PTX to lipopolysaccharide (LPS)-stimulated differentiated THP-1 cells. T cell viability and MIF levels were measured after PTX was added to prostaglandin E2 (PGE2)-stimulated Jurkat T-cell leukemia line. Co-culture was conducted to determine the effect of LPS-stimulated differentiated THP-1 cells that are affected by PTX on Jurkat cells. To prevent the direct effects of LPS and PTX on Jurkat cells, LPS and PTX were washed from THP-1 cells before co-culture. T cell viability and interleukin-2 (IL-2) levels were determined in Jurkat cells. Results: Increase in the MIF concentration and TLR4 expression level in differentiated THP-1 cells stimulated with LPS were reversed after PTX addition. However, PTX did not improve T cell viability in PGE2-stimulated Jurkat cells. Co-culturing Jurkat cell and LPS-stimulated differentiated THP-1 cells resulted in a decreased viability of T cells. The addition of PTX restored T cell viability to normal control levels and IL-2 expression level in Jurkat cells. Conclusion: LPS-stimulated THP-1-derived macrophages reduced the T cell viability under inflammation. However, PTX restored T cells viability and IL-2 back to normal levels. Therefore, the immunomodulatory action of PTX may be mediated by macrophage-T cell interactions. [ABSTRACT FROM AUTHOR]

While using the internet services, users tend to frequently experience the inconvenience in service due to buffering caused by overloads in the domain service server. If there are some margins for availabilities for the service server, the above issue does not occur, so it is possible to remove the inconvenience. In each time period of the domain that provides the service, the peak traffic data is collected to configure the data set, and the peak traffic data in each time period within the configured data set is summed up. After that, in this newly proposed model, the cumulative hourly peak traffic data is checked in terms of whether it exceeds the availability threshold set by an operator, and if it does, it is transferred to other pool group (pool N). The test results for the proposed model indicates that in the past, it normally took 2 hours to analyze the domain traffic data and 10 to 20 minutes to apply the analysis results, but in the newly proposed model, it takes only less than 5 minutes to analyze and apply results. System load frequency is reduced from 13 times a month to 1 time per month, and also the number of times to use the reserved server is reduced from 18 times to 2 times. The CPU margin rate is increased from 27% to 71%, which indicates that the usage rate is decreased. Overall, the operator's resource is reduced, and thus it is possible to achieve server stability as well. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Trauma & Emergency Surgery / Ulusal Travma ve Acil Cerrahi Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Stroke may occur during hospital admission (in-hospital stroke). Although patients with in-hospital stroke are potentially good candidates for reperfusion therapy, they often do not receive treatment as rapidly as expected. Aims: We investigated the effect of a code stroke program for in-hospital stroke, which included the use of computerized physician order entry, specific evaluation and treatment protocols for in-hospital stroke patients, and regular education of medical staffs. Methods: We implemented the program in the cardiology and cardiovascular surgery departments/wards (target-ward group) in November 2008. We compared time intervals from symptom onset to evaluation and reperfusion treatment before and after program implementation between the target-ward and other departments/wards (other-ward group). Results: Among 70 consecutive in-hospital stroke patients who received reperfusion therapy between July 2002 and February 2015, 28 and 42 were treated before and after program implementation, respectively. After program implementation, time intervals from symptom onset to neurology notification (50 min vs. 28 min; P=0.033), symptom onset to brain imaging (91 min vs. 41 min; P<0.001), and symptom recognition to notification (22 min vs. 9 min; P=0.011) were reduced in the target-ward group. Finally, times from symptom onset to intravenous tissue plasminogen activator administration and to arterial puncture were reduced by 55 min (120 min vs. 65 min; P<0.001) and 130 min (295 min vs. 165 min; P<0.001), respectively. However, time reductions in the other-ward group were not significant. Conclusions: The comprehensive program for in-hospital stroke that included the use of computerized physician order entry was effective in reducing time intervals to evaluation and reperfusion therapy. [ABSTRACT FROM AUTHOR]

Benzyl isothiocyanate (BITC) is a hydrolysis product of glucotropaeolin, a compound found in cruciferous vegetables, and has been shown to have anti-tumor properties. In the present study, we investigated whether BITC inhibits the development of prostate cancer in the transgenic adenocarcinoma mouse prostate (TRAMP) mice. Five-week old, male TRAMP mice and their nontransgenic littermates were gavage-fed with 0, 5, or 10 mg/kg of BITC every day for 19 weeks. The weight of the genitourinary tract increased markedly in TRAMP mice and this increase was suppressed significantly by BITC feeding. H and E staining of the dorsolateral lobes of the prostate demonstrated that well-differentiated carcinoma (WDC) was a predominant feature in the TRAMP mice. The number of lobes with WDC was reduced by BITC feeding while that of lobes with prostatic intraepithelial neoplasia was increased. BITC feeding reduced the number of cells expressing Ki67 (a proliferation marker), cyclin A, cyclin D1, and cyclin-dependent kinase (CDK)2 in the prostatic tissue. In vitro cell culture results revealed that BITC decreased DNA synthesis, as well as CDK2 and CDK4 activity in TRAMP-C2 mouse prostate cancer cells. These results indicate that inhibition of cell cycle progression contributes to the inhibition of prostate cancer development in TRAMP mice treated with BITC. [ABSTRACT FROM AUTHOR]

Purpose: In this study, we investigated the stroke mechanism and the factors associated with ischemic stroke in patients with nonvalvular atrial fibrillation (NVAF) who were on optimal oral anticoagulation with warfarin. Materials and Methods: This was a multicenter case-control study. The cases were consecutive patients with NVAF who developed cerebral infarction or transient ischemic attack (TIA) while on warfarin therapy with an international normalized ratio (INR) ≥2 between January 2007 and December 2011. The controls were patients with NVAF without ischemic stroke who were on warfarin therapy for more than 1 year with a mean INR ≥2 during the same time period. We also determined etiologic mechanisms of stroke in cases. Results: Among 3569 consecutive patients with cerebral infarction or TIA who had NVAF, 55 (1.5%) patients had INR ≥2 at admission. The most common stroke mechanism was cardioembolism (76.0%). Multivariate analysis demonstrated that smoking and history of previous ischemic stroke were independently associated with cases. High CHADS2 score (≥3) or CHA2DS2-VASc score (≥5), in particular, with previous ischemic stroke along with ≥1 point of other components of CHADS2 score or ≥3 points of other components of CHA2DS2-VASc score was a significant predictor for development of ischemic stroke. Conclusion: NVAF patients with high CHADS2/CHA2DS2-VASc scores and a previous ischemic stroke or smoking history are at high risk of stroke despite optimal warfarin treatment. Some other measures to reduce the risk of stroke would be necessary in those specific groups of patients. [ABSTRACT FROM AUTHOR]

Berteroin (5-methylthiopentyl isothiocyanate) is a sulforaphane analog present in cruciferous vegetables, including Chinese cabbage, rucola salad leaves, and mustard oil. We examined whether berteroin exerts anti-inflammatory activities using lipopolysaccharide (LPS)-stimulated Raw 264.7 macrophages and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse skin inflammation models. Berteroin decreased LPS-induced release of inflammatory mediators and pro-inflammatory cytokines in Raw 264.7 macrophages. Berteroin inhibited LPS-induced degradation of inhibitor of Ba (IBa) and nuclear factor-B p65 translocation to the nucleus and DNA binding activity. Furthermore, berteroin suppressed degradation of IL-1 receptor-associated kinase and phosphorylation of transforming growth factor ß activated kinase-1. Berteroin also inhibited LPS-induced phosphorylation of p38 MAPK, ERK1/2, and AKT. In the mouse ear, berteroin effectively suppressed TPA-induced edema formation and down-regulated iNOS and COX-2 expression as well as phosphorylation of AKT and ERK1/2. These results demonstrate that berteroin exhibits potent anti-inflammatory properties and suggest that berteroin can be developed as a skin anti-inflammatory agent. [ABSTRACT FROM AUTHOR]

Objective : The purpose of this study is to demonstrate the technical feasibility and clinical efficacy of emergent carotid angioplasty and stenting (CAS) for acute stroke due to athero-thrombotic occlusion of the cervical internal carotid artery (ICA). Methods : Review of medical records identified 17 patients who underwent emergent CAS for treatment of athero-thrombotic occlusion of the cervical ICA with acute stroke between 2009 and 2013. Eleven patients (64.7%) presented with concomitant intracranial artery occlusion, which was treated primarily by mechanical thrombectomy after CAS. Results : Successful revascularization of the cervical ICA with emergent CAS was achieved in all patients. After CAS, intracranial recanalization with Thrombolysis in Cerebral Infarction ≥2b flow was achieved in four of the 11 patients (36.4%). The overall recanalization rate (cervical ICA and intracranial artery) was 10 of 17 patients (58.8%). Symptomatic intracranial hemorrhage occurred in two patients (11.8%), resulting in death. Ten patients (58.8%) showed improvement (decrease in NIHSS score of ≥4 points) at seven days after recanalization. Nine patients (52.9%) showed a favorable outcome (mRS ≤2) at the last follow-up. A favorable outcome (mRS ≤2) was obtained in four of the six patients with isolated cervical ICA occlusion (4/6, 66.7%) and five of 11 patients with intracranial tandem occlusion (5/11, 45.5%). Conclusion : Emergent CAS for acute stroke due to athero-thrombotic occusion of the cervical ICA showed a good technical feasibility and favorable clinical outcome. [ABSTRACT FROM AUTHOR]

We previously noted that kaempferol, a flavonol present in vegetables and fruits, reduced cell cycle progression of HT-29 cells. To examine whether kaempferol induces apoptosis of HT-29 cells and to explore the underlying molecular mechanisms, cells were treated with various concentrations (0-60 µmol/L) of kaempferol and analyzed by Hoechst staining, Annexin V staining, JC-1 labeling of the mitochondria, immunoprecipitation, in vitro kinase assays, Western blot analyses, and caspase-8 assays. Kaempferol increased chromatin condensation, DNA fragmentation and the number of early apoptotic cells in HT-29 cells in a dose-dependent manner. In addition, kaempferol increased the levels of cleaved caspase-9, caspase-3 and caspase-7 as well as those of cleaved poly (ADP-ribose) polymerase. Moreover, it increased mitochondrial membrane permeability and cytosolic cytochrome c concentrations. Further, kaempferol decreased the levels of Bcl-xL proteins, but increased those of Bik. It also induced a reduction in Akt activation and Akt activity and an increase in mitochondrial Bad. Additionally, kaempferol increased the levels of membrane-bound FAS ligand, decreased those of uncleaved caspase-8 and intact Bid and increased caspase-8 activity. These results indicate that kaempferol induces the apoptosis of HT-29 cells via events associated with the activation of cell surface death receptors and the mitochondrial pathway. [ABSTRACT FROM AUTHOR]

Erucin, an isothiocyanate, is a hydrolysis product of glucoerucin found in arugula and has recently been reported to have anti-cancer properties in various cancer cells. In this study, we assessed the anti-inflammatory effects of erucin and the underlying mechanisms, using lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages and 12-O-tetradecanoylphorbol-13-acetate-treated mouse skin. In RAW 264.7 cells, erucin (2.5, 5 μmol/L) inhibited LPS-induced production of nitric oxide and prostaglandin E2. Erucin inhibited LPS-induced degradation of the inhibitor of κBα and translocation of p65 to the nucleus and, subsequently, reduced LPS-induced nuclear factor κB (NFκB) DNA binding activities, as well as the transcriptional activity of NFκB, leading to the decreased expression of NFκB-target genes, including tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, as well as transcriptional activity of iNOS and COX-2. In mice, erucin (100, 300 nmoles) treatment significantly inhibited phorbol ester-induced formation of ear edema and expression of iNOS and COX-2 proteins. These results indicate that erucin exerts a potent anti-inflammatory activity by inhibiting the pro-inflammatory enzymes and cytokines, which may be mediated, at least in part, via the inhibition of NFκB signaling. [ABSTRACT FROM AUTHOR]

In this study we found that licochalcone E (LicE), a recently isolated retrochalcone from Glycyrrhiza inflata, exhibits potent anti-inflammatory effects in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema and lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage models. Topical application of LicE (0.5-2 mg) effectively inhibited TPA-induced (1) ear edema formation; (2) phosphorylation of stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK), c-Jun, and extracellular signal regulated kinase 1/2; and (3) expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 proteins in mouse skin. The treatment of RAW 264.7 cells with LicE (2.5-7.5 µmol/L) induced a profound reduction in LPS-induced (1) release of NO and prostaglandin E2; (2) mRNA expression and secretion of interleukin (IL)-6, IL-1ß and tumor necrosis factor-a; (3) promoter activity of iNOS and COX-2 and expression of their corresponding mRNAs and proteins; (4) activation of AKT, p38 mitogen activated protein kinase (MAPK), SAPK/JNK and c-Jun; (5) phosphorylation of inhibitor of ?B (I?B) kinase-aß and I?Ba, degradation of I?Ba, translocation of p65 (RelA) to the nucleus and transcriptional activity of nuclear factor (NF)-?B; and (6) transcriptional activity of activator protein (AP)-1. These results indicate that the LicE inhibition of NF-?B and AP-1 transcriptional activity through the inhibition of AKT and MAPK activation contributes to decreases in the expression of pro-inflammatory cytokines and the inducible enzymes iNOS and COX-2. [ABSTRACT FROM AUTHOR]

Purpose: Continuous cardiac monitoring in a stroke unit (SU) may improve detection of atrial fibrillation (AF), and SU care may improve the rate of anticoagulation by better adherence to a standardized treatment protocol in patients with AF. We investigated the effects of the SU on the detection of AF and the rate of warfarin therapy in patients with AF. Materials and Methods: Acute stroke patients who had been admitted before or after the opening of the SU were included in our study. SU patients were monitored continuously with electrocardiography. Rates of AF and warfarin therapy were compared between patients admitted to the SU (SU group) and those admitted to the general ward (GW) prior to the opening of the SU (GW group). Results: Total 951 patients had been admitted to the GW prior to the opening of the SU (from January 2000 to November 2002), and 2349 patients to the SU (from January 2003 to December 2008). AF was found in 149 patients (15.7%) in the GW group and in 487 (20.7%) in the SU group. Most of AF detected during ad- mission was paroxysmal AF (84.8%). The frequency of newly detected AF was higher in the SU group than the GW group (2.5% vs. 0.7%, p=0.001). The rate of anticoagulation consideration was also higher in the SU group. Conclusion: SU care improved the detection of AF and the rate of anticoagulation consideration in acute stroke patients. Our findings support the benefits of continuous cardiac monitoring in the SU for stroke patients. [ABSTRACT FROM AUTHOR]

Working in a hazardous environment can decrease work efficiency and cause a variety of occupational diseases. To prevent occupational accidents and build a refreshing and pleasant work environment, therefore, it is necessary to develop an application system through which a worker's safety can be monitored on a realtime basis and provide related services. Recently, smartphones have become very popular across the nation, with over 10 million users. As a result, a variety of application services have been developed and provided in diverse sectors. This study proposes a system structure to develop application services which monitor work environment using smartphones and examines its applicability through the implementation of server and client interfaces. [ABSTRACT FROM AUTHOR]

The paper presents a new image template matching method for component inspection of electronic assembly systems. To recognize incorrectly assembled components, the input image of the components is matched with standard images, using a template matching algorithm. To produce a rapid inspection system, the processing time of the matching algorithm should be minimized. Since the standard images of all components located in a PCB are stored in the computer, it is desirable to minimize the memory size of the standard image. The discrete wavelet transformation is applied to minimize the image size as well as the processing time. Only 7% memory of the BMP image is used to discriminate between how well, or not, the components have been assembled. Comparative results are presented to verify the usefulness of the new proposed method. [ABSTRACT FROM AUTHOR]

BACKGROUND: In patients with a middle cerebral artery (MCA) occlusion, the involvement of the cortex may be affected by the presence of leptomeningeal anastomoses between the cerebral arteries. METHODS: The authors enrolled consecutive patients with acute infarctions in the MCA territory and MCA occlusion on angiographic studies. Infarct patterns were classified into three categories based on the extent of cortical surface involvement: total cortex (TC), partial cortex (PC) and no cortex (NC). The authors analysed the infarction patterns by stroke subtype, and investigated factors that resulted in cortex sparing. RESULTS: Out of 73 total patients, cortex-sparing infarctions were seen in 53 patients (72.6%, NC in 39 (53.5%) and PC in 14 (19.1%)). The extent of cortical involvement differed according to stroke subtype (p=0.036). TC was more frequent (42.9% vs 22.2%), and PC was less frequent (10.7% vs 27.9%, p=0.037) in cardioembolism than large-artery atherosclerosis. However, the proportion of patients with complete cortical sparing (NC) was similar between cardioembolism and large-artery atherosclerosis (46.4% vs 49.9%). In the upstream of leptomeningeal collateral arteries, the extent of cortical involvement was associated with significant stenosis of the ipsilateral anterior or posterior cerebral artery (p=0.011). CONCLUSION: This study suggests that pre-existing arteriolar connections, which may cover almost entire cortical surfaces of the MCA territory, exist in many patients. The findings also suggest that the extent of cortical involvement is different between stroke subtypes, and is critically affected by the status of upstream collateral arteries. [ABSTRACT FROM AUTHOR]

An improved diversity receiver having a new regulator for stable power supply in a 0.18 μm CMOS technology is presented. The regulator with soft-start is implemented to eliminate the battery damages at initial power-up. To reduce the external components, two switches for antenna diversity are integrated in front of LNA on the chip. A stacked inductor technique is adopted to reduce the chip area. The simulation and measurement results show that the soft-start time of the regulator can be controlled by a variable resistor from 200 μS to 6.2 mS. The front-end (LNA and mixer) can achieve a voltage gain of 33.5 dB, a noise figure (NF) of 3.8 dB, and 23 dB of the isolation between antennas when consuming 3.9 mW with a 1.8 V power supply. The NF includes the loss of a BALUN, BPF, and switches. © 2010 Wiley Periodicals, Inc. Microwave Opt Technol Lett 52: 611–615, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.25000 [ABSTRACT FROM AUTHOR]

Benzyl isothiocyanate (BITC) is detected in abundance in Brassica vegetables, and some previous studies have demonstrated that BITC may potentially function as a chemopreventive agent in humans. This study examined whether BITC inhibits lipopolysaccharide (LPS)-induced inflammatory responses in Raw 264.7 macrophages and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema formation. The treatment of macrophages with various concentrations of BITC resulted in a dose-dependent reduction in the LPS-induced secretion of interleukin (IL)-1β, TNF-α, and IL-6 and their corresponding mRNA levels, as well as in the production of nitric oxide and PGE2. Consistent with these findings, BITC inhibited the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 proteins and their corresponding mRNAs. BITC inhibited LPS-induced phosphorylation and the degradation of the inhibitor of κBα, translocation of p65 into the nucleus, and the DNA binding activity and transcriptional activity of NFκB. Moreover, the LPS-stimulated phosphorylation of extracellular signal regulated kinase (ERK)1/2 and Akt was suppressed by BITC. BITC also inhibited ear edema formation and the protein expression of iNOS and COX-2 in mouse skin treated with TPA. We demonstrate that BITC is a potent anti-inflammatory agent, and the anti-inflammatory properties of BITC may result from the downregulation of NFκB signaling. [ABSTRACT FROM AUTHOR]

AbstractConjugated linoleic acid (CLA), which is naturally present in a variety of foods such as milk fat and the meat of ruminant animals, has been demonstrated to exert chemoprotective effects in several tissues in experimental animals. CLA is a collective term, which denotes one or more positional and geometric isomers of octadecadienoic acid, with cis-9,trans-11 (c9t11) and trans-10,cis-12 CLA (t10c12) being the principal isomers in commercial preparations. We observed previously that physiological levels of CLA inhibited HT-29 cell growth, and the growth inhibitory effects of CLA were attributed to the effect of t10c12, but not c9t11. In the present study, we assessed the mechanisms by which physiological levels of CLA and t10c12 induce apoptosis in HT-29 cells. HT-29 cells were cultured for 3 days in serum-free medium in the presence of various concentrations of CLA (0–20 μmol/L) or t10c12 (0–4 μmol/L). Addition of CLA or t10c12 to culture medium resulted in a dose-dependent increase in the numbers of apoptotic cells. The results of western blot analysis of total cell lysates showed that CLA and t10c12 increased the levels of cleaved caspase-9, caspase-3, and poly(ADP-ribose) polymerase but did not alter the levels of Bcl-2 family member proteins. However, these fatty acids were shown to increase the translocation of Bad and Bax to the mitochondria, increase mitochondrial membrane permeability, and induce the release of cytochrome cand Smac/Diablo from the mitochondria. In addition, CLA and t10c12 diminished Akt content and Akt phosphorylation. These findings indicate that physiological levels of t10c12 induce apoptosis in HT-29 colon cancer cells, which is mediated via mitochondrion-mediated events associated with a decline in Akt activity, an increase in the translocation of the pro-apototic Bad and Bax to the mitochondria, and the subsequent disruption of normal mitochondrial membrane potential. [ABSTRACT FROM AUTHOR]

3,3′-Diindolylmethane (DIM), a major acid-condensation product of indole-3-carbinol, has been shown to have multiple anticancer effects in experimental models. Because recurrent or chronic inflammation has been implicated in the development of a variety of human cancers, this study examined the antiinflammatory effects of DIM and the underlying mechanisms using lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. DIM significantly decreased the release of nitric oxide (NO), prostaglandin (PG)E2, tumor necrosis factor α, interleukin (IL)-6, and IL-1β by RAW264.7 cells treated with LPS. DIM inhibited LPS-induced increases in protein levels of inducible NO synthase (iNOS), which were accompanied by decreased iNOS mRNA levels and transcriptional activity. The mRNA levels of phospholipase A2 decreased, whereas neither cyclooxygenases-2 protein nor transcript was altered by DIM. In addition, DIM suppressed LPS-induced nuclear factor-κB (NF-κB) transcriptional activity, NF-κB DNA-binding activity, translocation of p65 (RelA) to the nucleus, and degradation of inhibitor of κBα. Furthermore, DIM decreased LPS-induced transcriptional activity of activator protein (AP)-1, AP-1 DNA-binding activity, and phosphorylation of stress-activated protein kinase/Jun-N-terminal kinase and c-Jun. We demonstrate that DIM inhibits LPS-induced release of proinflammatory mediators in murine macrophages. Downregulation of NF-κB and AP-1 signaling may be one of the mechanisms by which DIM inhibits inflammatory responses. [ABSTRACT FROM AUTHOR]

Commercial preparations of conjugated linoleic acid (CLA) contain both positional and geometric isomers of octadecadienoic acid, with cis-9,trans-11 CLA (c9t11) and trans-10,cis-12 CLA (t10c12) as the principal isomers. We showed previously that CLA reduced the incidence of colon tumors in rats treated with 1,2-dimethylhydrazine. In addition, our previous in vitro studies showed that t10c12 inhibited the growth of HT-29 and Caco-2 human colon cancer cells, whereas c9t11 had no effect on cell growth. In the present study, to examine the effects of the CLA isomers on cell cycle and cell cycle regulatory proteins, we treated HT-29 cells with various concentrations (0–4 μmol/L) of the individual CLA isomers. A DNA flow cytometric analysis revealed that t10c12 induced a G1 arrest, whereas c9tq1 had no effect on the cell cycle. Western blot analysis of total cell lysates revealed no alteration in the protein expression of cyclin A, cyclin D, cyclin E, cyclin-dependent kinase (CDK) 2, or CDK4 due to t10c12 treatment. However, t10c12 substantially increased the protein expression and mRNA accumulation of the CDK inhibitor p21CIP1/WAF1 The t10c12 isomer increased the association of p21CIP1/WAF1 with CDK2 and proliferating cell nuclear antigen, but decreased the levels of phosphorylated retinoblastoma protein (Rb), with an increase in the levels of hypophosphorylated Rb protein. An in vitro kinase assay using histone Hi as a substrate showed that the activities of CDK2 were significantly decreased by t10c12. These results indicate that t10c12 exerts its growth inhibitory effects in colon cancer cells through the induction of G1 cell cycle arrest. The induction of p21CIP1/WAF1 may be one of the mechanisms by which t10c12 inhibits cell cycle progression in HT-29 cells. [ABSTRACT FROM AUTHOR]

Fisetin, a natural flavonol present in edible vegetables, fruits, and wine, was reported to exert anticarcinogenic effects. The objective of the current study was to examine the effect of fisetin on the cell cycle progression of the human colon cancer cell line HT-29. HT-29 cells were cultured in serum-free medium with 0, 20, 40, or 60 μmol/L fisetin. Fisetin dose dependently inhibited both cell growth and DNA synthesis (P < 0.05), with a 79 ± 1 % decrease in cell number observed 72 h after the addition of 60 μmol/L fisetin. Perturbed cell cycle progression from the G1 to S phase was observed at 8 h with 60 μmol/L fisetin treatment, whereas a G2/M phase arrest was observed after 24 h (P < 0.05). The phosphorylation state of the retinoblastoma proteins shifted from hyperphosphorylated to hypophosphorylated in cells treated with 40 μmol/L fisetin. (P < 0.05). Fisetin decreased the activities of cyclin-dependent kinases (CDK)2 and CDK4; these effects were likely attributable to decreases in the levels of cyclin E and D1 and an increase in p21CIP1/WAF1 levels (P < 0.05). However, fisetin also inhibited CDk4 activity in a cell-free system (P < 0.05), indicating that it may directly inhibit CDk4 activity. The protein levels of cell division cycles (CDC)2 and CDC25C and the activity of CDC2 were also decreased in fisetin-treated cells (P < 0.05). These results indicate that inhibition of cell cycle progression in HT-29 cells after treatment with fisetin can be explained, at least in part, by modification of CDK activities. [ABSTRACT FROM AUTHOR]

Examines whether the growth inhibitory effect of conjugated linoleic acid (CLA) is related to changes in the insulin-like growth factor (IGF) system in HT-29 cells, the human colon adenocarcinoma cell line. Incubation of HT-29 cells in serum-free medium in the presence of various concentrations of CLA; Decrease in protein levels of both mature and pro IGF-II and IGF-II transcripts by CLA.

The initial severity triage of patients in the emergency department (ED) is implemented differently worldwide, according to the characteristics of each country. However, better classification methods are being studied due to various problems with the current system. Therefore, the aim of this study was to determine the usefulness of patients' severity assessment in a new way that gives appropriate values to factors that can be obtained in the ED. We collected data from 158,246 patients who visited the ED from 01 January 2016 to 31 December 2020. Using the appropriate values of various factors obtained using the Rasch analysis method, the cut-off values for predicting hospitalization and discharge at the ED of patients were determined. Furthermore, using artificial intelligence, the patients who were hospitalized and discharged from the ED were classified and compared with the results of the Rasch analysis. The accuracy of the algorithms was analyzed as a combination of factors that could be obtained during the initial stage of the patient's visits. The area under the curve (AUC) value for the prediction of hospitalization and discharge by a combination of factors immediately obtained from the visit was 0.611. In addition, using the factors that could be obtained after a certain period, the AUC value of hospitalization and discharge prediction was 0.767. The results of analysis using artificial intelligence were similar to or slightly higher than the AUC value of the Rasch analysis. The prediction of hospitalization and discharge in the ED using clinical parameters with Rasch analysis can be used for medical assistance, which is expected to help in the efficient operation of the ED. [ABSTRACT FROM AUTHOR]

Although clinical scoring systems and biomarkers have been used to predict outcomes in sepsis, their prognostic value is limited. Therefore, machine learning (ML) models have been proposed to predict the outcomes of sepsis. This study aims to propose ML algorithms that create robust models for predicting mortality in patients with sepsis diagnosed using the Sepsis-3 definitions in the emergency department. This study was performed using a prospectively collected registry of adult patients with sepsis between January 2016 and February 2020. Among the 810 patients, 607 (75%) and 203 (25%) patients were assigned to the training and test sets, respectively. The primary outcome was 30-day mortality. Using the values of the area under the receiver operating characteristic curve (AUROC), the area under the precision-recall curve (AUPRC), balanced accuracy, and Brier score, we compared the performances of different ML algorithms with that of the logistic regression models and clinical scoring systems. The ML models' performance was superior to that of the clinical scoring systems. A light gradient boosting machine achieved the highest AUROC among the ML models in predicting 30-day mortality. Most of the ML models had significantly higher AUROC and balanced accuracy than the logistic regression models. All the ML models exhibited higher AUPRC and lower Brier scores compared to the scoring systems and logistic regression model. The ML models can be used as supportive tools for predicting mortality in sepsis patients. In future studies, the performance of the proposed models will be validated using more data from different hospitals or departments. [ABSTRACT FROM AUTHOR]

To evaluate the accuracy of presepsin levels in diagnosing sepsis and predicting mortality among organ failure patients with and without hypercreatinemia in the emergency department (ED). This retrospective study was conducted on patients with positive quick sequential organ failure assessment (qSOFA) score and increase in SOFA score of =2 points. Hypercreatinemia, indicated by a creatinine level of =1.2 mg/dL, was defined as points =1 on the renal component of the SOFA score. The patients were divided into group 1 (sepsis with hypercreatinemia), group 2 (sepsis without hypercreatinemia), group 3 (non-sepsis with hypercreatinemia), and group 4 (nonsepsis without hypercreatinemia), and their presepsin levels were compared. Receiver operating characteristic curve (ROC) analyses were performed to determine the accuracy of presepsin in diagnosing sepsis and predicting 30-day mortality. The optimal cutoff values were obtained to determine the presence of sepsis and predict the 30-day mortality. In all, 420 patients were eligible for this study. The presepsin levels in all pairwise comparisons between the groups were different (Group 1; 1311.5 (732.0-2179.5), Group 2; 566.5 (353.0-928.0), Group 3; 400.0 (291.0-579.0), Group 4; 231.0 (154.0-346.0)). Among patients with hypercreatinemia, the presepsin area under the ROC (AUROC) for diagnosing sepsis was 0.884 (optimal cutoff: 706 pg/mL). Among patients without hypercreatinemia, the presepsin AUROC for diagnosing sepsis was 0.854 (optimal cutoff: 352 pg/mL). The optimal cutoff values for predicting the patients' 30-day mortality with and without hypercreatinemia were 1077 pg/mL and 393 pg/mL, respectively. Different cutoff values of presepsin based on creatinine levels could effectively diagnose sepsis in ED patients with organ failure. Further, presepsin was found to be associated with 30-day mortality in ED patients with organ failure, regardless of hypercreatinemia. [ABSTRACT FROM AUTHOR]

Abstract Patients with acute ischemic stroke can benefit from reperfusion therapy. Nevertheless, there are gray areas where initiation of reperfusion therapy is neither supported nor contraindicated by the current practice guidelines. In these situations, a prediction model for mortality can be beneficial in decision-making. This study aimed to develop a mortality prediction model for acute ischemic stroke patients not receiving reperfusion therapies using a stacking ensemble learning model. The model used an artificial neural network as an ensemble classifier. Seven base classifiers were K-nearest neighbors, support vector machine, extreme gradient boosting, random forest, naive Bayes, artificial neural network, and logistic regression algorithms. From the clinical data in the International Stroke Trial database, we selected a concise set of variables assessable at the presentation. The primary study outcome was all-cause mortality at 6 months. Our stacking ensemble model predicted 6-month mortality with acceptable performance in ischemic stroke patients not receiving reperfusion therapy. The area under the curve of receiver-operating characteristics, accuracy, sensitivity, and specificity of the stacking ensemble classifier on a put-aside validation set were 0.783 (95% confidence interval 0.758–0.808), 71.6% (69.3–74.2), 72.3% (69.2–76.4%), and 70.9% (68.9–74.3%), respectively.

A vast of naturally occurring substances have been shown to protect against experimental carcinogenesis and an increasing amount of evidence suggests that flavonoids may been have cancer chemopreventative properties. We previously observed that kaempferol, one of the flavonoids, inhibit cell proliferation by inducing cell cycle arrest and stimulating apoptosis in HT-29 cells. To study the mechanisms by which kaempferol increases apoptosis, cells were treated with various concentrations (0, 20, 40, and 60 µmol/L) of kaempferol. Western blot analysis and in vitro kinase assay revealed that kaempferol decreased the phosphorylation of Akt levels and Akt kinase activity. Kaempferol did not alter bad protein levels but increased translocation of Bad to mitochondria. Also, kaempferol decreased Bcl-xL and increased Bik protein levels. Kaempferol increased permeability of the mitochondrial membrane, and induced release of cytochrome e from mitochondria to cytoplasm. In addition, kaempferol increased levels of cleaved caspase-9, -3, -7 and cleaved poly (ADP-ribose) polymerase. These results indicate that kaempferol induces apoptosis through the event associated with mitochondria, which may be mediated it ability to inactivate Akt. [ABSTRACT FROM AUTHOR]

Flavonoids have been reported to have ability to prevent cancer development. Fisetin, a naturally occurring flavonol, is commonly found in fruits, vegetables, and wine. We have previously observed that fisetin inhibits HT-29 human colon cancer cell growth. To examine the effect of fisetin on the NF-κB signaling that is known to play an important role in cell survival and apoptosis, HT-29 cells were treated with 0 or 60 µmol/L fisetin for 10 min, 30 min or 120 min. Western blot analysis revealed that fisetin increased p-IκBα protein levels at 10 and 30 min of culture, and decreased IκBα protein levels after 30 min treatment. Immunoprecipitation and in vitro kinase assay revealed that fisetin dose-dependently increased IκB kinase (IKK) activity. The subcellular fractionation and immunocytochemistry assay revealed that fisetin increased translocation of p65 (Re1A) to the nucleus. In addition, electrophoretic mobility shift assay indicated that fisetin increased NF-κB DNA binding activity in a concentration-dependent manner. These results raised the possibility that fisetin may inhibit HT-29 cell growth via its ability to upregulate NF-κB signaling. [ABSTRACT FROM AUTHOR]

ISL, 4,2′,4′-trihydroxychalcone, found in licorice, shallot, and bean sprouts, is a potent antioxidant with anti-carcinogenic effects. To elucidate the mechanisms underlying antitumorigenic activities of ISL, the effect of epidermal growth factor (EGF) and ISL on gene expression patterns in DU145 prostate cancer cells were examined. DU145 cells were treated with 10 ng/mL EGF and/or 20 µmol/L ISL for 12 h and total RNA was isolated, eDNA microarrays were performed using a Human 35K oligo chip after cDNAs were prepared by reverse transcription. We observed that EGF upregulated expression of genes involved in the regulation of cell adhesion but ISL suppressed the effect of EGF. ISL inhibited the basal and EGF-induced adhesion and invasion of DU145 cells. Western blot analysis revealed ISL decreased EGF-induced protein levels of integrin-α2, intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) in DU145 cells. Gelatin zymography and Western blot analysis revealed that ISL significantly suppressed the EGF-induced matrix metalloproteinase (MMP)-9 secretion. ISL decreased the protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 but increased TIMP-2 levels in concentration-dependent manners. The decrease in MMP-9, integrin-a2, ICAM, VCAM and increase in TIMP-2 expression .may be one of mechanisms by which ISL inhibits prostate cancer cell adhesion and invasion. [ABSTRACT FROM AUTHOR]

Background d‐Dimer level is a marker of hypercoagulability, which is associated with thrombus formation and resolution. We investigated the value of d‐dimer levels in predicting outcomes of acute ischemic stroke in patients who underwent endovascular treatment (EVT). Methods We analyzed data of patients who underwent only EVT from the SECRET (Selection Criteria in Endovascular Thrombectomy and Thrombolytic Therapy) registry. d‐Dimer levels were routinely measured in 10 of 15 participating hospitals. Patients were grouped into tertiles (tertile 1, tertile 2, and tertile 3) according to d‐dimer levels (lowest, moderate, and highest, respectively). We compared serial scores on the National Institutes of Health Stroke Scale at baseline, on day 1 of hospitalization, and at discharge; functional outcome 3 months after EVT; and rate of mortality within 6 months after EVT. Results In the 170 patients, the median d‐dimer level was 477 ng/mL (interquartile range, 249–988 ng/mL). In tertile 3, the National Institutes of Health Stroke Scale score was higher at discharge than on day 1 of hospitalization. Poor outcome 3 months after EVT (modified Rankin Scale score, ≥3) was more common with high d‐dimer levels (26.3% of tertile 1, 57.1% of tertile 2, and 76.4% of tertile 3; P

Background: Pulsatility index (PI) is a useful hemodynamic index that is generally thought to reflect arterial stiffness and distal microvascular resistance. We hypothesized that the PI in the basilar artery is associated with stroke severity in patients with acute unilateral pontine infarction. Methods: We retrospectively enrolled 129 patients with acute unilateral pontine infarction due to small vessel occlusion who presented within 48 hours of symptom onset between January 2015 and December 2020. Transcranial Doppler studies were performed within 5 days of symptom onset in all patients. We analyzed the relationship between the PI measured in the basilar artery and initial stroke severity using correlation and multivariable regression analyses. Results: The median age of the patients was 68.0 years (IQR, 59.5-74.0) and 87 (67.4%) were male. The PI was positively correlated with the National Institutes of Health Stroke Scale (NIHSS) score (r = 0.222, p = 0.011) and ischemic lesion volume (r = 0.187, p = 0.039). Multivariable analysis confirmed that a higher PI was an independent and significant predictor of a higher admission NIHSS score (B, 2.530; 95% confidence interval, 0.195 to 4.866; p = 0.034). In the mediation analysis, ischemic lesion volume had a complete mediating effect on the relationship between the PI and NIHSS score at admission (Z = 2.012, p = 0.043). Conclusions: Increased PI in the basilar artery was associated with severe stroke in patients with acute unilateral pontine infarction. [ABSTRACT FROM AUTHOR]

Abstract Background We investigated the diagnostic and prognostic value of presepsin among patients with organ failure, including sepsis, in accordance with the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Methods This prospective observational study included 420 patients divided into three groups: non-infectious organ failure (n = 142), sepsis (n = 141), and septic shock (n = 137). Optimal cut-off values of presepsin to discriminate between the three groups were evaluated using receiver operating characteristic curve analysis. We determined the optimal cut-off value of presepsin levels to predict mortality associated with sepsis and performed Kaplan–Meier survival curve analysis according to the cut-off value. Cox proportional hazards model was performed to determine the risk factors for 30-day mortality. Results Presepsin levels were significantly higher in sepsis than in non-infectious organ failure cases (p

Objective: Collateral flow is important for ischemic brain tissue after an acute occlusion of the cerebral artery. The purpose of this study was to evaluate baseline collateral flow, on CT angiography (CTA), as a predictor of functional outcome in patients who had endovascular recanalization, after acute pure first segment (M1) occlusion of the middle cerebral artery (MCA). Methods: Thirty patients with acute pure M1 occlusion treated by endovascular recanalization, who were ineligible for intravenous thrombolysis or resistant to intravenous thrombolysis, were reviewed. The relationship between baseline collateral flow, on CTA, and functional outcome, was analyzed. In addition, other factors affecting clinical outcome were assessed. Results: The mean NIHSS score on admission was 16.87 ± 4.86 (7-24). The mean time interval between onset of stroke symptoms and recanalization was 324.37 ± 68.38 (210-463) min. Successful recanalization (TICI 2b-3) was achieved in 18 patients (60%). Twenty-seven of 30 patients improved their NIHSS score (mean 8.4); NIHSS score 8.9 ± 5.4 (median 10, range 0-16) at seven days. Two patients had aggravated symptoms and one patient had no change on the NIHSS score. At 90 days after recanalization, a modified Rankin Scale (mRS) of <3 was achieved in 15 patients (50%) and a mRS of <2 was achieved in nine patients (30%). Symptomatic intra-cerebral hemorrhage occurred in two patients (6.7%). Multivariate regression analysis showed an initial NIHSS score (p = 0.004), grade of baseline collateral flow on CTA(p = 0.025), presence of diabetes mellitus (p = 0.037), and TICI scale (p = 0.049) were factors associated with an improved NIHSS. For the mRS at 90 days, only the grade of the baseline collateral flow on CTA was associated with a good functional outcome (p = 0.013). Conclusions: The results of this study suggest that the grade of baseline collateral flow, on CTA, is an independent predictor of functional outcome for endovascular recanalization of acute pure M1 occlusion of the middle cerebral artery. [ABSTRACT FROM AUTHOR]

Background: Cerebral embolism in patients with non-valvular atrial fibrillation (NVAF) is mainly caused by thrombus formation in the left atrial appendage. D-dimer is known to reflect the thrombogenic activity of the left atrium in NVAF patients. This study aimed to investigate the relationship between D-dimer levels and infarct pattern in ischemic stroke patients with NVAF. Methods: We enrolled 255 patients who developed cardioembolic stroke caused by NVAF and presented to the hospital within 7 days. We divided the infarct pattern into two groups: single lesions (SL) and multiple lesions (ML). The infarct pattern was also classified into two groups: ischemic lesions involving a single vascular territory (ST) and multiple vascular territories (MT). We analyzed the relationship between the infarct pattern and D-dimer levels. Results: Of the 255 patients, 79 (31.0%) and 176 (69.0%) were in the SL and ML groups, respectively. In addition, 207 (81.2%) and 48 (18.8%) patients were classified into the ST and MT groups, respectively. Compared with the SL group, a higher D-dimer level was observed in the ML group (p=0.006). Similarly, the MT group had higher D-dimer levels than the ST group (p=0.001). Logistic regression analysis showed that elevated D-dimer levels were significantly and independently associated with the presence of multiple ischemic lesions (p=0.021) and the involvement of multiple vascular territories (p=0.020). Conclusions: This study showed that elevated D-dimer levels were independently associated with multiple ischemic lesions involving multiple vascular territories in ischemic stroke patients with NVAF. [ABSTRACT FROM AUTHOR]

Background and Purpose We aimed to develop a model predicting early recanalization after intravenous tissue plasminogen activator (t-PA) treatment in large-vessel occlusion. Methods Using data from two different multicenter prospective cohorts, we determined the factors associated with early recanalization immediately after t-PA in stroke patients with large-vessel occlusion, and developed and validated a prediction model for early recanalization. Clot volume was semiautomatically measured on thin-section computed tomography using software, and the degree of collaterals was determined using the Tan score. Follow-up angiographic studies were performed immediately after t-PA treatment to assess early recanalization. Results Early recanalization, assessed 61.0±44.7 minutes after t-PA bolus, was achieved in 15.5% (15/97) in the derivation cohort and in 10.5% (8/76) in the validation cohort. Clot volume (odds ratio [OR], 0.979; 95% confidence interval [CI], 0.961 to 0.997; P=0.020) and good collaterals (OR, 6.129; 95% CI, 1.592 to 23.594; P=0.008) were significant factors associated with early recanalization. The area under the curve (AUC) of the model including clot volume was 0.819 (95% CI, 0.720 to 0.917) and 0.842 (95% CI, 0.746 to 0.938) in the derivation and validation cohorts, respectively. The AUC improved when good collaterals were added (derivation cohort: AUC, 0.876; 95% CI, 0.802 to 0.950; P=0.164; validation cohort: AUC, 0.949; 95% CI, 0.886 to 1.000; P=0.036). The integrated discrimination improvement also showed significantly improved prediction (0.097; 95% CI, 0.009 to 0.185; P=0.032). Conclusions The model using clot volume and collaterals predicted early recanalization after intravenous t-PA and had a high performance. This model may aid in determining the recanalization treatment strategy in stroke patients with large-vessel occlusion.

Abstract The eligibility of reperfusion therapy has been expanded to increase the number of patients. However, it remains unclear the reperfusion therapy will be beneficial in stroke patients with various comorbidities. We developed a reperfusion comorbidity index for predicting 6-month mortality in patients with acute stroke receiving reperfusion therapy. The 19 comorbidities included in the Charlson comorbidity index were adopted and modified. We developed a statistical model and it was validated using data from a prospective cohort. Among 1026 patients in the retrospective nationwide reperfusion therapy registry, 845 (82.3%) had at least one comorbidity. As the number of comorbidities increased, the likelihood of mortality within 6 months also increased (p