To determine if a tiny enhancing dot is characteristic of small hemangiomas with low attenuation during the hepatic arterial phase (HAP) and portal venous phase (PVP) of two-phase spiral computed ...tomography (CT).
Among 249 consecutive patients with 377 hemangiomas who underwent two-phase spiral CT (performed 30 and 65 seconds after the start of injection), 34 hemangiomas in 20 patients were less than 2 cm in diameter, had low attenuation during the HAP and PVP, and showed characteristic findings on dynamic contrast material-enhanced magnetic resonance (MR) images. The CT scans were retrospectively reviewed for tiny enhancing dots and correlated with the MR images.
Tiny enhancing dots were found in 26 of 34 hemangiomas (76%). The dots were seen during the HAP and PVP in 15 lesions (58%) and during the PVP alone in 11 lesions (42%). The lesions showed a tendency toward slow fill-in at MR imaging (only four lesions completely filled with contrast material within 5 minutes). The dots seen at CT corresponded to the initial enhancing area at MR imaging.
Small hemangiomas with persistent low attenuation at two-phase spiral CT can be diagnosed with the "bright dot" sign.
Background: Apolipoprotein A5 plays an important role in modulating triacylglycerol metabolism in experimental animal models. Objective: The objective was to determine associations of the common ...apolipoprotein A5 gene (APOA5) -1131TC polymorphism with postprandial lipemic response and other cardiovascular disease risk factors in humans. Design: Healthy, nonobese subjects n = 158; mean (+/-SEM) age: 33.8 +/- 1.2 y; body mass index (in kg/m2): 23.3 +/- 0.3 were subdivided into 3 genotype groups: TT (n = 85), TC (n = 56), and CC (n = 17). We measured fasting and postprandial lipid concentrations, lipid peroxidation, C-reactive protein concentrations, and DNA damage. Results: Fasting triacylglycerol concentrations in carriers of the C allele were higher (P < 0.05) than in carriers of the TT genotype. No other significant genotype-related differences were observed for any of the other baseline measures. After consumption of a mixed meal, carriers of the C allele had significantly greater increases in total chylomicron and VLDL triacylglycerol than did subjects with the TT genotype. Moreover, carriers of the C allele had higher dense LDL, serum C-reactive protein, and urinary 8-epi-prostaglandin F2α concentrations and more lymphocyte DNA damage. Conversely, we did not find significant genotype-related differences in postprandial glucose, insulin, or free fatty acid measures. Conclusions: Our data confirm the genetic modulation of serum fasting triacylglycerol concentrations by the APOA5 gene polymorphism and extend this observation to postprandial triacylglycerol concentrations and to markers of oxidation and inflammation. The presence of the C allele in the APOA5 promoter region at position 1131 could be a significant factor contributing to higher cardiovascular disease risk in Koreans independently of common environmental factors.
Abstract We present the first measurement of the branching fraction of the singly Cabibbo-suppressed (SCS) decay Λ c + $$ {\Lambda}_c^{+} $$ → pη′ with η′ → ηπ + π − , using a data sample ...corresponding to an integrated luminosity of 981 fb −1, collected by the Belle detector at the KEKB e + e − asymmetric-energy collider. A significant Λ c + $$ {\Lambda}_c^{+} $$ → pη′ signal is observed for the first time with a signal significance of 5.4σ. The relative branching fraction with respect to the normalization mode Λ c + $$ {\Lambda}_c^{+} $$ → pK − π + is measured to be B Λ c + → pη ′ B Λ c + → pK − π + = 7.54 ± 1.32 ± 0.73 × 10 − 3 , $$ \frac{\mathcal{B}\left({\Lambda}_c^{+}\to p\eta^{\prime}\right)}{\mathcal{B}\left({\Lambda}_c^{+}\to {pK}^{-}{\pi}^{+}\right)}=\left(7.54\pm 1.32\pm 0.73\right)\times {10}^{-3}, $$ where the uncertainties are statistical and systematic, respectively. Using the world-average value of B Λ c + → pK − π + $$ \mathcal{B}\left({\Lambda}_c^{+}\to {pK}^{-}{\pi}^{+}\right) $$ = (6.28 ± 0.32) × 10 −2, we obtain B Λ c + → pη ′ = 4.73 ± 0.82 ± 0.46 ± 0.24 × 10 − 4 , $$ \mathcal{B}\left({\Lambda}_c^{+}\to p\eta^{\prime}\right)=\left(4.73\pm 0.82\pm 0.46\pm 0.24\right)\times {10}^{-4}, $$ where the uncertainties are statistical, systematic, and from B Λ c + → pK − π + $$ \mathcal{B}\left({\Lambda}_c^{+}\to {pK}^{-}{\pi}^{+}\right) $$ , respectively.
Aim
We isolated Lactobacillus brevis G‐101 from kimchi lactic acid bacteria (LAB) strains, which induced IL‐10 expression in lipopolysaccharide (LPS)‐stimulated peritoneal macrophages. To evaluate ...the inflammatory effect of G‐101, we examined its inhibitory effect in 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced colitic mice.
Materials and Results
The colitic mice were prepared by intrarectal injection of TNBS. We measured intestinal mucosal cytokines by enzyme‐linked immunosorbent assay; activation of transcription factors, by immunoblotting; and macrophage polarization markers, by real‐time polymerase chain reaction. Of 200 LAB strains tested, Lact. brevis G‐101 showed most potent activity for induction of IL‐10 expression in LPS‐stimulated peritoneal macrophages. However, it significantly inhibited the expression of TNF‐α, IL‐1β and IL‐6 and the phosphorylation of IRAK1 and AKT, and activated NF‐κB and MAPKs. Treatment with TNBS caused colon shortening; increased myeloperoxidase activity; and increased IL‐1β, IL‐6 and TNF‐α expression in mice. Oral administration of Lact. brevis G‐101 significantly inhibited these activities. Lactobacillus brevis G‐101 inhibited TNBS‐induced IRAK‐1 phosphorylation and NF‐κB activation, as well as the expression of COX‐2 and iNOS. Lactobacillus brevis G‐101 inhibited the expression of M1 macrophage markers, but increased the expression of M2 macrophages in the colons of TNBS‐treated mice.
Conclusions
Lactobacillus brevis G‐101 may improve colitis by inhibiting the IRAK1/NF‐κB, MAPK and AKT pathways and by polarizing M1 macrophages to M2‐like macrophages.
Significance and Impact of the Study
These results suggest that IL‐10 expression‐inducing LAB can ameliorate colitis by inhibiting NF‐κB activation and macrophage polarization.
A new cassane diterpene, dipteryxic acid (1), and a new isoflavonolignan, 5-methoxyxanthocercin A (2), as well as four known active compounds, isoliquiritigenin (3), 6,4'-dihydroxy-3'-methoxyaurone ...(4), sulfuretin (5), and (+/-)-balanophonin (6), and five known inactive compounds, butin, eriodictyol, 7-hydroxychromone, 7,3'-dihydroxy-8,4'-dimethoxyisoflavone, and (-)-lariciresinol, were isolated from an ethyl acetate-soluble extract of the seeds of Dipteryx odorata, using a bioassay based on the induction of quinone reductase (QR) in cultured Hepa 1c1c7 mouse hepatoma cells to monitor chromatographic fractionation. The structures of compounds 1 and 2 were elucidated by spectroscopic data interpretation. Single-crystal X-ray diffraction analysis was used to confirm the relative stereochemistry of compound 1. Selected compounds (3-5) were evaluated in a mouse mammary organ culture assay, with isoliquiritigenin (3) found to exhibit 76% inhibition at a dose of 10 microg/mL.
Hrp1 of Schizosaccharomyces pombe is a member of the CHD protein family, characterized by a chromodomain, a Myb-like telobox-related DNA-binding domain and a SNF2-related helicase/ATPase domain. CHD ...proteins are thought to be required for modification of the chromatin structure in transcription, but the exact roles of CHD proteins are not known. Here we examine the sub-cellular localization and biochemical activity of Hrp1 and the phenotypes of hrp1 Delta and Hrp1-overexpressing strains. Fluorescence microscopy revealed that Hrp1 protein is targeted to the nucleus. We found that Hrp1 exhibited DNA-dependent ATPase activity, stimulated by both single- and double-stranded DNA. Overexpression of Hrp1 caused slow cell growth accompanied by defective chromosome condensation in anaphase resulting in a 'cut' (celluntimelytorn) phenotype and chromosome loss. The hrp1 Delta mutation also caused abnormal anaphase and mini-chromosome loss phenotypes. Electron micrographs demonstrated that aberrantly shaped nucleoli appeared in Hrp1-overexpressing cells. Therefore, these results suggest that Hrp1 may play a role in mitotic chromosome segregation and maintenance of chromatin structure by utilizing the energy from ATP hydrolysis.
Cu-Cu direct bonding facilitates fine-pitch interconnection with low electrical resistivity and high electromigration (EM) resistance. However, reliable Cu-Cu bonds result only from high temperature, ...high pressure and long process time mainly because of its tendency to generate a native oxide that negatively impacts device reliability. Presently, high process temperature is one of the major bottlenecks of Cu-Cu thermo-compression bonding. We developed the optically-aligned, low-temperature Cu-Cu thermo-compression bonding process with sub-micron alignment accuracy. The quantitative analyses of the interfacial adhesion energies and seam voids of Cu-Cu bonds, performed with varying process parameters, showed that bonding temperature and post-bond annealing have the most significant influence on bond properties. By optimizing experimental parameters, we could achieve, even with a short bonding time, the sufficient interfacial adhesion energy (≥ 5 J/m 2 for subsequent processes) with no interfacial seam voids. Postbond annealing performed at ≥ 250°C drastically improves the interfacial adhesion energy. SmartView™ alignment, enabling the face-to-face Cu-Cu bonding of non-IR transparent wafers, allows less than 0.2 μm (3σ) and 1.0 μm (3σ) of the pre-bond and post-bond alignment accuracies, respectively.
The study on bacteremia helps empirically select the proper antibiotics before the results of culture test about causative pathogen. The purpose of this study is to investigate causative pathogen in ...bloodstream infection, changing aspects based on elapsed time after burn, relationship with other sites and resistance of important causative pathogen against antibiotics through analysis on bacteria isolated from blood culture of patients hospitalized in burn intensive care unit (BICU).
A retrospective study was conducted targeting patients hospitalized in BICU from January 2007 to June 2011. Changes of causative pathogen in bloodstream infection based on elapsed time after injury were analyzed. We would like to examine the relationship between bloodstream infection and infection on other body parts by comparing results of cultures in burn wound site, sputum, urine and catheter tip. Antibiotics resistance patterns of Pseudomonas aeruginosa, Acinetobacter baumannii, Staphylococcus aureus, Enterococcus species, and Klebsiella pneumoniae were studied.
A total of 2,337 burn patients were hospitalized in BICU for 54 months. Causative pathogen was cultured in blood cultures from 397 patients (17.0%). P. aeruginosa (169, 30.1%) was the most cultured and A. baumannii (107, 19.0%) and S. aureus (81, 14.4%) were followed. It was confirmed that the relative frequency of A. baumannii tended to get lower as the period got longer after injury, but the relative frequency of K. pneumoniae got higher as the period got longer after injury. With comparison without bacteremia, P. aeruginosa bacteremia showed high probability in which the same bacteria were cultured in wound site, sputum and cathether tip, and A. baumannii bacteremia and candida bacteremia had high probability in sputum, and urine and catheter tip, respectively. 95.9% of P. aeruginosa and 95.3% of A. baumannii showed the resistance against carbapenem. 96.3% of S. aureus was methicillin resistant and 36.2% of Enterococcus species were vancomycin resistant. 75.0% of K. pneumonia were extended-spectrum beta-lactamase (ESBL)-producing bacteria.
Since the highly antibiotic resistant microorganisms were isolated from the patients hospitalized in BICU during early phase, the empirical selection of antibiotics targeting these pathogens should be considered before the results of microbiologic culture test. In addition, use of empirical antifungal agent after 1 week of injury can be considered for patients who have risk factor of fungal infection.
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