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We compared the ability of head computed tomography (HCT) and MRI, respectively, obtained before or after target temperature management to predict neurologic outcomes in out-of-hospital cardiac arrest (OHCA) survivors.This retrospective study included adult comatose OHCA survivors who underwent neuroimaging scans within 6 h (first HCT) or 72-96 h (second HCT and MRI) after the return of spontaneous circulation (ROSC). We calculated the gray-white matter ratio (GWR), hypoxic-ischemic brain injury presence (loss of boundary at the basal ganglia level [LOB at BG], sulcal effacement at the centrum semiovale [SE at CS], and pseudo-SAH sign), and the overall score based on MRI findings (a total score of 21 brain regions individually scored according to the degree of signal abnormality).Overall, 78 patients were included in this analysis, of whom 45 (58%) showed poor outcomes. The second HCT scan showed greater prognostic performance than the first HCT scan for GWR (area under curve 0.92 vs. 0.70), LOB at BG (0.93 vs. 0.65), SE at CS (0.89 vs. 0.64), and pseudo-SAH sign (0.75 vs. 0.51). The overall score on MRI (0.99) showed the highest prognostic performance. However, on the second HCT scan, the combination of GWR and LOB at BG showed prognostic performance (0.96) comparable to the overall score on MRI (P = 0.12); the corresponding sensitivity and specificity values were 85.7% and 100%.Overall score on MRI and the combination of GWR and LOB at BG findings on second HCT scans may help predict poor outcomes in OHCA survivors.

Background Identifying biomarkers related to the diagnosis and treatment of gastric cancer (GC) has not made significant progress due to the heterogeneity of tumors. Genes involved in histological classification and genetic correlation studies are essential to develop an appropriate treatment for GC. Methods In vitro and in vivo lentiviral shRNA library screening was performed. The expression of Synaptotagmin (SYT11) in the tumor tissues of patients with GC was confirmed by performing Immunohistochemistry, and the correlation between the expression level and the patient’s survival rate was analyzed. Phospho-kinase array was performed to detect Jun N-terminal kinase (JNK) phosphorylation. SYT11, JNK, and MKK7 complex formation was confirmed by western blot and immunoprecipitation assays. We studied the effects of SYT11 on GC proliferation and metastasis, real-time cell image analysis, adhesion assay, invasion assay, spheroid formation, mouse xenograft assay, and liver metastasis. Results SYT11 is highly expressed in the stem-like molecular subtype of GC in transcriptome analysis of 527 patients with GC. Moreover, SYT11 is a potential prognostic biomarker for histologically classified diffuse-type GC. SYT11 functions as a scaffold protein, binding both MKK7 and JNK1 signaling molecules that play a role in JNK1 phosphorylation. In turn, JNK activation leads to a signaling cascade resulting in cJun activation and expression of downstream genes angiopoietin-like 2 (ANGPTL2), thrombospondin 4 (THBS4), Vimentin, and junctional adhesion molecule 3 (JAM3), which play a role in epithelial-mesenchymal transition (EMT). SNU484 cells infected with SYT11 shRNA (shSYT11) exhibited reduced spheroid formation, mouse tumor formation, and liver metastasis, suggesting a pro-oncogenic role of SYT11. Furthermore, SYT11-antisense oligonucleotide (ASO) displayed antitumor activity in our mouse xenograft model and was conferred an anti-proliferative effect in SNU484 and MKN1 cells. Conclusion SYT11 could be a potential therapeutic target as well as a prognostic biomarker in patients with diffuse-type GC, and SYT11-ASO could be used in therapeutic agent development for stem-like molecular subtype diffuse GC.

For patients with nonampullary duodenal epithelial tumors (NADETs), endoscopic forceps biopsy results that reflect the final histopathologic results of the entire lesion are indispensable for accurate diagnosis and appropriate treatment modality selection. This study aimed to investigate the histopathologic discrepancies between endoscopic forceps biopsy and endoscopic resection specimens in NADETs and to elucidate the factors contributing to such discrepancies. This retrospective observational study included 105 patients (105 lesions) who underwent endoscopic resection for NADETs at the Pusan National University Hospital between May 2006 and October 2019. NADETs were classified as low-grade intraepithelial neoplasms (LGINs), high-grade intraepithelial neoplasms (HGINs), or adenocarcinomas. Following slide reviews, the histopathologic concordance between endoscopic forceps biopsy and endoscopic resection specimens was assessed for each case. The histopathologic discrepancy rate between endoscopic forceps biopsy and endoscopic resection specimens was 19.0% (20/105 lesions). Among the 20 diagnostically discordant lesions, up- and downgrade of the histopathologic diagnosis occurred in 17 and 3 lesions, respectively. The predominant discrepancies involved upgrades from LGIN to HGIN (n = 14) and upgrades from LGIN to adenocarcinomas (n = 2). The 3 downgraded cases included 2 from LGIN to inflammation and 1 from HGIN to LGIN. In the multivariate analyses, the old age (>67 years) was the only factor significantly associated with histopathologic upgrade (odds ratio 4.553, 95% confidence interval 1.291–15.939; P = .018). Considerable histopathologic discrepancies were observed between endoscopic forceps biopsy and endoscopic resection specimens in NADETs. Older age was significantly associated with these discrepancies.

The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The identity of the molecular mechanisms that govern the R-point decision is one of the fundamental issues in cell biology. We found that early after mitogenic stimulation, RUNX3 binds to its target loci, where it opens chromatin structure by sequential recruitment of Trithorax group proteins and cell-cycle regulators to drive cells to the R-point. Soon after, RUNX3 closes these loci by recruiting Polycomb repressor complexes, causing the cell to pass through the R-point toward S phase. If the RAS signal is constitutively activated, RUNX3 inhibits cell cycle progression by maintaining R-point-associated genes in an open structure. Our results identify RUNX3 as a pioneer factor for the R-point and reveal the molecular mechanisms by which appropriate chromatin modifiers are selectively recruited to target loci for appropriate R-point decisions., The transcription factor RUNX3 plays a key role in the restriction point of cell cycle. Here the authors showed that RUNX3 binds and opens chromatin structure of restriction point associated genes, by sequential recruitment of chromatin remodeling complex, transcription complex and cell cycle regulators.

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a rare neurodegenerative disorder characterized by cerebral white matter abnormalities, myelin loss, and axonal swellings. ALSP is caused by mutations in colony stimulating factor 1 receptor gene. We report an ASLP patient with asymptomatic intracranial calcifications distributed in white matter found incidentally in a health screening. Keywords: Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, Calcification, Diffusion-weighted imaging

Rapid disease progression in neuroemergencies is associated with blood-brain barrier (BBB) disruption. We investigated a less invasive strategy for assessing BBB status by evaluating S100 calcium-binding protein B (S100B) and neuron-specific enolase (NSE) at early stages of the hypoxic-ischemic brain injury (HIBI) cascade.This retrospective study used prospectively collected data from patients with out-of-hospital cardiac arrest (August 2019-July 2021). Albumin specimens obtained from serum and cerebrospinal fluid via arterial catheter and lumbar puncture were used to measure the albumin quotient (Qa), which is widely accepted as the gold standard method for detecting BBB disruption. Serum S100B and NSE levels were measured simultaneously following the return of spontaneous circulation. We conducted linear regression to evaluate the relationship between S100B and Qa and the predictive performance of S100B for abnormal Qa. The primary study outcome was abnormal Qa (0.007).Forty-one patients were enrolled; 30 showed an abnormal Qa suggestive of BBB disruption. S100B levels were significantly higher than in those with a normal Qa (0.244 μg/L [interquartile range [IQR], 0.146-0.823 vs 0.754 μg/L [IQR, 0.317-2.228], P = .03). We report a positive correlation between serum S100B and Qa (R2 = 0.110; P = .04). The area under the receiver operating characteristics curve (AUROC) evaluating the predictive performance of S100B with respect to abnormal Qa was 0.718 (95% confidence interval, 0.556-0.847). The cutoff value for S100B (with respect to BBB disruption) in the total cohort was 0.283 μg/L (sensitivity, 80.0%; specificity, 72.7%). Subgroup analyses in patients with serum neuron-specific enolase (NSE) levels of40.8 ng/mL (excluding those with established neuronal cell injury) showed an improved correlation coefficient (R2 = 0.382; P.01) and predictive performance (AUROC, 0.836 [95% confidence interval, 0.629-0.954]) compared with the total cohort.Serum S100B obtained at an early stage of the HIBI cascade is associated with abnormal Qa, suggesting BBB disruption. The predictive performance of S100B and the correlation between serum S100B and Qa can be improved using a complementary strategy (i.e., evaluations of S100B and NSE levels) that combines considerations of cell damage in astrocytes and neurons.

For successful treatment of early gastric cancers (EGCs), it is crucial to define the horizontal border of the lesion with high accuracy. Acetic acid–indigo carmine (AI) chromoendoscopy has been used to determine the horizontal border in EGCs, but this technique is less potent in certain situations. Mucin phenotype in gastric cancers refers to biological differences in precursor lesions and differences in histopathologic findings, and it might affect AI chromoendoscopy findings. We aimed to investigate the association between mucin phenotype and AI chromoendoscopy findings in EGCs. We prospectively evaluated 126 lesions in 126 patients with endoscopically diagnosed EGCs. Conventional endoscopy and AI chromoendoscopy findings of these lesions before treatment were prospectively analyzed. The border distinction between the lesion and surrounding mucosa was classified as distinct or indistinct on conventional endoscopy and AI chromoendoscopy, respectively. Mucin phenotypes were classified as gastric, intestinal, gastrointestinal, or null type by immunohistochemistry. The lesion borders were distinct in 46.8% (59/126) of the lesions assessed using conventional endoscopy and in 73.0% (92/126) of those assessed with AI chromoendoscopy (p

Diabetes mellitus is a chronic disease and one of the fastest-growing health challenges of the last decades. Studies have shown that chronic low-grade inflammation and activation of the innate immune system are intimately involved in type 2 diabetes pathogenesis. Momordica charantia L. fruits are used in traditional medicine to manage diabetes. Herein, we report the purification of a new 23-O-β-d-allopyranosyl-5β,19-epoxycucurbitane-6,24-diene triterpene (charantoside XV, 6) along with 25ξ-isopropenylchole-5(6)-ene-3-O-β-d-glucopyranoside (1), karaviloside VI (2), karaviloside VIII (3), momordicoside L (4), momordicoside A (5) and kuguaglycoside C (7) from an Indian cultivar of Momordica charantia. At 50 µM compounds, 2-6 differentially affected the expression of pro-inflammatory markers IL-6, TNF-α, and iNOS, and mitochondrial marker COX-2. Compounds tested for the inhibition of α-amylase and α-glucosidase enzymes at 0.87 mM and 1.33 mM, respectively. Compounds showed similar α-amylase inhibitory activity than acarbose (0.13 mM) of control (68.0-76.6%). Karaviloside VIII (56.5%) was the most active compound in the α-glucosidase assay, followed by karaviloside VI (40.3%), while momordicoside L (23.7%), A (33.5%), and charantoside XV (23.9%) were the least active compounds. To better understand the mode of binding of cucurbitane-triterpenes to these enzymes, in silico docking of the isolated compounds was evaluated with α-amylase and α-glucosidase.

The implication of the heterogeneous spectrum of pro- and anti-inflammatory macrophages (Macs) has been an important area of investigation over the last decade. The polarization of Macs alters their functional phenotype in response to their surrounding microenvironment. Macs are the major immune cells implicated in the pathogenesis of atherosclerosis. A hallmark pathology of atherosclerosis is the accumulation of pro-inflammatory M1-like macrophages in coronary arteries induced by pro-atherogenic stimuli; these M1-like pro-inflammatory macrophages are incapable of digesting lipids, thus resulting in foam cell formation in the atherosclerotic plaques. Recent findings suggest that the progression and stability of atherosclerotic plaques are dependent on the quantity of infiltrated Macs, the polarization state of the Macs, and the ratios of different types of Mac populations. The polarization of Macs is defined by signature markers on the cell surface, as well as by factors in intracellular and intranuclear compartments. At the same time, pro- and anti-inflammatory polarized Macs also exhibit different gene expression patterns, with differential cellular characteristics in oxidative phosphorylation and glycolysis. Macs are reflective of different metabolic states and various types of diseases. In this review, we discuss the major differences between M1-like Macs and M2-like Macs, their associated metabolic pathways, and their roles in atherosclerosis.

We aimed to evaluate neurological outcomes associated with blood-brain barrier (BBB) disruption using contrast-enhanced magnetic resonance imaging (CE-MRI) in out-of-hospital cardiac arrest (OHCA) survivors. This retrospective observational study involved OHCA survivors who had undergone CE-MRI for prognostication. Qualitative and quantitative analyses were performed using the presence of BBB disruption (pBD) and the BBB disruption score (sBD) in CE-MRI scans, respectively. For the sBD, 1 point was assigned for each area of BBB disruption, and 6 points were assigned when an absence of intracranial blood flow due to severe brain oedema was confirmed. The primary outcome was poor neurological outcome at 3 months (defined as cerebral performance categories 3&ndash, 5). We analysed 46 CE-MRI brain scans (27 patients). Of these, 15 (55.6%) patients had poor neurological outcomes. Poor neurological outcome group patients showed a significantly higher proportion of pBD than those in the good neurological outcome group (22 (88%) vs. 6 (28.6%) patients, respectively, p &lt, 0.001) and a higher sBD (5.0 (4.0&ndash, 5.0) vs. 0.0 (0.0&ndash, 1.0) patients, p &lt, 0.001). Poor neurological outcome predictions showed that the sBD had a significantly better prognostic performance (area under the curve (AUC) 0.95, 95% confidence interval (CI) 0.84&ndash, 0.99) than the pBD (AUC 0.80, 95% CI 0.65&ndash, 0.90). The sBD cut-off value was &gt, 1 point (sensitivity, 96.0%, specificity, 81.0%). The sBD is a highly predictive and sensitive marker of 3-month poor neurological outcome in OHCA survivors. Multicentre prospective studies are required to determine the generalisability of these results.

We previously reported that vestigial-like 1 (VGLL1), a cofactor of transcriptional enhanced associate domain 4 (TEAD4), is transcriptionally regulated by PI3K and β-catenin signaling and is involved in gastric cancer malignancy. However, the precise mechanism underlying the regulation of VGLL1 activation remains unknown. Therefore, we aimed to investigate the molecular mechanism underlying the transforming growth factor-β (TGF-β)-mediated activation of VGLL1 and the VGLL1-TEAD4 interaction in gastric cancer cells. We showed that TGF-β enhanced VGLL1 phosphorylation and that this phosphorylated VGLL1 functioned as a transcription cofactor of TEAD4 in NUGC3 cells. TGF-β also increased the phosphorylation of ERK and ribosomal S6 kinase 2 (RSK2) in NUGC3 cells, thereby triggering the translocation of phosphorylated RSK2 to the nucleus. Site-directed mutagenesis and immunoprecipitation experiments revealed that RSK2 phosphorylated VGLL1 at S84 in the presence of TGF-β. Mutation of VGLL1 at S84 suppressed VGLL1-TEAD4 binding and the subsequent transcriptional activation of matrix metalloprotease 9 (MMP9). Moreover, VGLL1 peptide containing S84 suppressed the TGF-β-induced MMP9 expression and reduced the invasion and proliferation of gastric cancer cells, whereas VGLL1 peptide containing S84A did not. Furthermore, suppression of expression or activation of VGLL1 enhances the therapeutic effects of lapatinib. Collectively, these results indicate that VGLL1 phosphorylation via TGF-β/ERK/RSK2 signaling plays a crucial role in MMP9-mediated malignancy of gastric cancer. In addition, our study highlights the therapeutic potential of the peptide containing VGLL1 S84 for the treatment of gastric cancer.

We investigated whether a fibrinogen-thrombin collagen sponge patch reduces postoperative complications of parotid gland surgery. This single-blinded, randomized controlled study included 165 patients who underwent parotid surgery for benign tumors (2018–2019) at a tertiary center. Primary outcomes were postoperative drain amount, days until drain removal, and discharge. Patients were scheduled for follow-up at 1 and 4 weeks, and 3 months after surgery. Complications including surgical site infection, pain, seroma, sialocele, salivary fistula, facial nerve palsy, Frey’s syndrome with subjective symptoms, and facial asymmetry were analyzed. After identifying confounding variables, multivariate approaches were used. Histologic analysis was performed in a mouse model of salivary gland surgery. In total, 162 patients (77, fibrinogen-thrombin collagen patch group; 85, controls) were included, with no significant between-group differences other than resected tissue. Among postoperative total drain amount and days until drain removal and discharge, the only postoperative total drain was significantly lower in the patch group than in the control group in the adjusted model. Additionally, although validation through robust trials with longer follow-up is needed, we found the potential benefit of the fibrinogen patch on Frey’s syndrome and facial asymmetry. In conclusion, fibrinogen-thrombin-impregnated collagen patches in parotidectomy can reduce postoperative drainage and improve outcomes.

Bitter melon (Momordica charantia L.) has been used to manage diabetes and various inflammatory conditions. While studies have explored the use of bitter melon to manage these conditions, the bioactive components and molecular mechanisms mediating the anti-inflammatory effects remain elusive. In the current study, acetone and methanol extracts of bitter melon along with purified compounds (momordicoside A, momordicoside L, karaviloside VI, karaviloside VIII, and charantoside XV) from acetone extract were screened using RAW 264.7 macrophage cells. Acetone and methanol extracts decreased LPS-induced expression of genes related to the formation of the inflammasome complex (NF-κB, NLRP3, Pycard, Casp1). The purified triterpenoids had differential anti-inflammatory effects on the expression of the genes IL-1β, NF-κB, NLRP3, Pycard, Casp1, HMGB1, and HMOX-1. Additionally, molecular docking data suggest that these molecules may be a potent inhibitor of NF-κB. Taken together, the five bioactive compounds exerted anti-inflammatory effects in LPS-induced inflammation, likely via suppression of the NF-κB-NLRP3 pathway.

A novel heterogeneous rhodium-incorporated graphitic carbon nitride (Rh-g-C3N4) was investigated for a liquid-phase carbonylation of methanol to acetic acid (AA) to overcome disadvantages of the commercialized Rh-based homogeneous catalysts. The heterogeneous Rh-g-C3N4 catalyst showed a superior catalytic activity in a liquid-phase carbonylation with AA yield above 82% under the reaction conditions of 413 K and CO pressure of 4.0 MPa, where the initially formed MA intermediate can be easily hydrolyzed to form AA. A higher dispersion of the incorporated rhodium nanoparticles in the g-C3N4 matrix with a small crystallite size was responsible for a higher catalytic activity with a less leaching degree of active rhodium metals. The novel Rh-g-C3N4 with rhodium content of 1–3 wt% can be a candidate to substitute the commercial homogeneous Rh complex catalyst for AA production by methanol carbonylation.

Liver and adipose tissue are crucial for blood glucose and energy homeostasis, while impaired regulation of hepatic glucose production (HGP) and energy expenditure contribute to hyperglycemia and excessive fat storage in type 2 diabetes mellitus. Hepatokines are proteins secreted by hepatocytes, and several hepatokines have been shown to directly affect glucose and energy expenditure. In this study, we investigated the role of transforming growth factor beta 1 (TGF-β1) in hepatocytes in regulating glucose and energy homeostasis. We generated the liver-specific TGF-β1 knockout mice and found that the mice exhibited lower blood glucose, increased hepatic insulin sensitivity compared with wild type (WT) control mice. Using the mouse primary hepatocytes, we found that TGF-β1 deletion impaired HGP and TGF-β1 treatment promoted protein kinase A (PKA) signaling and stimulated the nuclear translocation of FoxO1. Under high fat diet (HFD) treatment, hepatic TGF-β1 deficiency protected mice from HFD-induced obesity and insulin resistance, decreased HGP and improved energy expenditure. Moreover, we used hepatic insulin receptor substrate-1, 2 (IRS1, 2) knockout (DKO) mice and deleted the TGF-β1 gene in the liver of DKO mice. We found that hepatic TGF-β1 ablation prevented hyperglycemia and hyperinsulinemia in DKO mice. Deletion of TGF-β1 or neutralization of TGF-β1 with antibody significantly decreased HGP of DKO hepatocytes. Additionally, hepatic TGF-β1 ablation enhanced thermogenesis and inguinal white adipose tissue (iWAT) browning in DKO mice. These findings underscore an important role of hepatic TGF-β1 in contribution to systemic glucose and energy homeostasis. Thus, hepatic TGF-β1 may serve as a therapeutic target for control of glucose and energy homeostasis in insulin resistance and type 2 diabetes mellitus. Disclosure Q. Pan: None. Y. Chen: None. D. Kim: None. Z. Shen: None. W. Yang: None. X. Li: None. Y. Sun: None. S. Guo: None. Funding American Diabetes Association (1-15-CD-09 to S.G.)

Chronic low-grade inflammation is a hallmark of obesity, which is directly linked to nonalcoholic Fatty Liver Disease (NAFLD) and systemic insulin resistance. Ghrelin receptor, a growth hormone secretagogue receptor (GHS-R), mediates the stimulatory effect of ghrelin on food intake and fat deposition. We previously reported that global ablation of GHS-R in mice decreases adipose inflammation, and GHS-R knockdown in macrophage cell line reduces the expression of pro-inflammatory cytokine genes. To determine the physiological role of GHS-R in macrophages, we generated myeloid-specific GHS-R knockout mice (LysM-Cre;Ghsrf/f). Under diet-induced obesity (DIO), LysM-Cre;Ghsrf/f mice showed reduced circulating inflammatory cytokine levels, attenuated insulin resistance, but no change in body weight. Moreover, DIO-induced NAFLD was ameliorated in LysM-Cre;Ghsrf/f mice, showing reduced inflammation and lipid accumulation in the liver. To understand the regulatory mechanism of macrophage GHS-R in NAFLD pathogenesis and systemic inflammation and insulin sensitivity, we conducted ex vivo studies using bone marrow-derived macrophages (BMDMs). GHS-R deficient BMDMs showed reduced macrophage pro-inflammatory polarization and decreased expression of pro-inflammatory cytokine genes; consistently, exhibiting elevated mitochondrial respiration and improved mitochondrial dynamics. Moreover, the primary hepatocytes treated with conditioned media from BMDMs of LysM-Cre;Ghsrf/f mice showed gene expression of reduced inflammatory cytokines and increased insulin signaling. Taken together, our findings reveal that GHS-R is an important immunometabolic regulator and governs macrophage polarization through regulating mitochondrial function and cellular metabolism of macrophages, moderating hepatic and systemic inflammation and insulin sensitivity. GHS-R antagonist may present a novel therapeutic strategy for the metabolic disorders such as NAFLD. Disclosure D. Kim: None. J. Lee: None. Q. Pan: None. J. Noh: None. H. Wang: None. H. Han: None. C. Wu: None. S. Guo: None. Y. Sun: None. Funding American Diabetes Association (1-15- BS-177 to Y.S.); National Institutes of Health

While active materials based on germanium (Ge) are considered as a promising alternative anodic electrode due to their relatively high reversible capacity and excellent lithium-ion diffusivity, the quite unstable structural/electrochemical stability and severe volume expansion or pulverization problems of Ge electrodes remain a considerable challenge in lithium ion batteries (LIBs). Here, we present the development of Ge embedded in one-dimensional carbon nanostructures (Ge/CNs) synthesized by the modified in situ electrospinning technique using a mixed electrospun solution consisting of a Ge precursor as an active material source and polyacrylonitrile (PAN) as a carbon source. The as-prepared Ge/CNs exhibit superior lithium ion behavior properties, i.e., highly reversible specific capacity, rate performance, Li ion diffusion coefficient, and superior cyclic stability (capacity retention: 85% at 200 mA g(-1)) during Li alloying/dealloying processes. These properties are due to the high electrical conductivity and unique structures containing well-embedded Ge nanoparticles (NPs) and a one-dimensional carbon nanostructure as a buffer medium, which is related to the volume expansion of Ge NPs. Thus, it is expected that the Ge/CNs can be utilized as a promising alternative anodic material in LIBs.

The purposes of this study are to confirm ways to reduce bacteria of minimally processed agricul- tural products, using antibacterial foods that are easily available in home and to improve bacterial hygienic condition of them. We chose garlic-allicin, ginger-gingerol, green tea-catechin, cinnamon-cinnamic aldehyde, wasabi-allyl isothiocyanate as antibacterial foods and their unique antibiotic materials. We confirmed the better washing effect when these antibiotic extracts were used, compared to washing effect by only distilled water. Their antibiosis was proved by statistical processing. PFGE (Pulsed Field Gel Electrophoresis) of Bacillus cereus shows continuous con- tamination probability of minimally processed vegetables by same product suppliers and the necessity of systematic measures against bacterial contamination.

Many efforts have been made to improve the electrochemical performance of Li-rich cathode materials such as metal ion doping, surface modification, and fabricating nanostructured materials. Here, we demonstrate Li2MnO3 (denoted as OLO) cathode materials coated with TiO2 (OLO@ TiO2) for high-performance LIBs. The ratio of layered Li2MnO3 to anatase TiO2 as well as the shell thickness in the OLO@TiO2 cathodes were controlled by increasing the addition of titanium butoxide. The structure and chemical states for TiO2 coated OLO electrodes were confirmed using field-emission scanning electron microscopy, field-emission transmission electron microscopy, X-ray diffraction, and X-ray photoelectron spectroscopy. To evaluate the performance of the electrodes for LIBs, charge/discharge curves, cycling performance, cyclic voltammograms, and Nyquist plots of the as-prepare cathode materials were obtained using lithium coin cells. In particular, since the TiO2 coating layer in OLO@TiO2 could stabilize the interface between the cathode and electrolyte, OLO@TiO2 exhibited high specific capacity, improved high rate cycling performance, and excellent cycle life due to the low interface resistance and high diffusion coefficient of lithium ion, compared with the uncoated OLO cathode.

Well-defined mesoporous nanostructure electrodes have been known to have improved lithium ion reaction properties such as the lithium ion reaction, cyclability, and high rate performance. We suggest mesoporous tungsten nitride nanoplates prepared via a template-free synthesis for lithium-ion batteries. The as-prepared tungsten nitride (m-WN) exhibited a face-centered cubic WN phase, well-defined mesoporous structure. Furthermore, to investigate a formation mechanism of the well-defined mesoporous WN structure formed from two-dimensional WO3 nanoplates. Finally, the m-WN showed improved electrochemical reaction properties of lithium ions such as high specific capacity and high rate cycling performance due to low transport resistance and high lithium ion diffusion coefficient.

Anode materials with excellent electrochemical properties as an alternative to carbon-based structures are suggested for advanced high-performance lithium-ion batteries. Here, composites containing MoS2 and carbon (MoS2/C) were in situ synthesized via heat treatment at 700 °C under a CH4 atmosphere with varying reaction times. XRD, Raman, XPS, and TEM data show that the MoS2/C composites consist of crystalline MoS2 and an amorphous carbon phase and show a homogeneous distribution of curved and bent MoS2 particles with a carbon matrix. In particular, the MoS2/C composite with an optimal content of the amorphous carbon phase exhibits relatively an excellent performance in lithium-ion batteries, facilitating the lithiation/delithiation process in MoS2 as an electroactive material.

Ge-based materials as anodes in lithium ion batteries (LIBs) having a large theoretical reversible capacity are needed to overcome the unstable structural and electrochemical properties and pulverization of the electrodes for high-performance LIBs. Here, we synthesized Ge/C composites as anodes for use in LIBs via heating a mixture of GeO2 powder and glucose as both a reductant and carbon source at 900 °C under a nitrogen atmosphere. The data from X-ray diffraction (XRD), Raman spectroscopy, and transmission electron microscopy (TEM) shows that the as-prepared samples consist of crystalline Ge particles and an amorphous carbon phase. Compared to pure Ge, the Ge/C samples exhibit discharge capacities of ∼627.1 mA h g−1, improved cyclability, and excellent rate properties at a current of 3200 mA g−1.

Sarcopenia is the aging-associated progressive loss of skeletal muscle; however, the pathogenic mechanism of sarcopenia is not clear. The orexigenic hormone ghrelin stimulates growth hormone secretion, increases food intake, and promotes adiposity. Here we showed that fasting-induced muscle loss was exacerbated in old ghrelin-null (Ghrl–/–) mice, exhibiting decreased expression of myogenic regulator MyoD and increased expression of protein degradation marker MuRF1, as well as altered mitochondrial function. Moreover, acylated ghrelin and unacylated ghrelin treatments significantly increased mitochondrial respiration capacity in muscle C2C12 cells. Consistently, acylated ghrelin and unacylated ghrelin treatments effectively increased myogenic genes and decreased degradation genes in the muscle in fasted old Ghrl–/– mice, possibly by stimulating insulin and adenosine monophosphate-activated protein kinase pathways. Furthermore, Ghrl–/– mice showed a profile of pro-inflammatory gut microbiota, exhibiting reduced butyrate-producing bacteria Roseburia and ClostridiumXIVb. Collectively, our results showed that ghrelin has a major role in the maintenance of aging muscle via both muscle-intrinsic and -extrinsic mechanisms. Acylated ghrelin and unacylated ghrelin enhanced muscle anabolism and exerted protective effects for muscle atrophy. Because unacylated ghrelin is devoid of the obesogenic side effect seen with acylated ghrelin, it represents an attractive therapeutic option for sarcopenia.

The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The identity of the molecular mechanisms that govern the R-point decision is one of the fundamental issues in cell biology. We found that early after mitogenic stimulation, RUNX3 bound to its target loci, where it opened chromatin structure by sequential recruitment of Trithorax group proteins and cell-cycle regulators to drive cells to the R-point. Soon after, RUNX3 closed these loci by recruiting Polycomb repressor complexes, causing the cell to pass through the R-point toward S phase. If the RAS signal was constitutively activated, RUNX3 inhibited cell cycle progression by maintaining R-point-associated genes in an open structure. Our results identify RUNX3 as a pioneer factor for the R-point and reveal the molecular mechanisms by which appropriate chromatin modifiers are selectively recruited to target loci for appropriate R-point decisions.

Spinel-type LiMn 2 O 4 has been studied as a promising cathode candidate capable of replacing LiCoO 2 in lithium-ion batteries. Here we demonstrate LiMn 2 O 4 powders prepared by a calcination process as a function of temperature and time. LiMn 2 O 4 structure electrode prepared at 700 °C for 10 h forms a truncated octahedral structure consisting of {111} and {100} surfaces. In particular, the truncated octahedral structure exhibits the crystal orientation toward dominant {111} surfaces of octahedral structure to minimize Mn dissolution and a particular portion of {100} surfaces of the truncated structure to stabilize the electrode. The truncated octahedral structure shows excellent discharge capacity (∼132.14 mAh g −1 at 1 C), high capacity retention (∼100%) and durable cycling performance (after 100 cycle) compared to the octahedral shaped electrodes. In particular, the truncated octahedral structure of LMO-700-10h exhibits the crystal orientation toward majority {111} surfaces of octahedral structure and minority {100} surfaces.

Well-defined nanocomposite electrodes based on active materials and graphene have been known to hold improved lithium ion reaction properties such as the lithium ion insertion/desertion reaction, cycle life, and high rate performance. Here, we report two-dimensional nanocomposites consisting of WO 3 nanoplates and graphene nanosheets (GNS) using a hydrothermal method and heating process for use in high-performance lithium ion batteries. A compilation of the data from XRD, SEM, and TEM suggests that the nanocomposites consist of high crystalline WO 3 nanoplates and GNS. The capacity and high rate cycling performance of the nanocomposites as an anode for lithium ion batteries are evaluated using coin cells. The nanocomposite electrode with an optimized amount of GNS exhibits high reversible capacity, good capacity retention, and excellent high rate cycling performance.

We demonstrate the well-defined tungsten suboxide nanoplates for pseudocapacitors via a low-temperature reduction reaction under hydrogen gas atmosphere. The as-prepared WO 3− x reduced at 500 °C using WO 3 nanoplates (500-WO 3− x ) shows a pure monoclinic structure and single crystalline nanoplates. The 500-WO 3− x exhibits much improved pseudocapacitive performance due to W 5+ and W 4+ oxidation states obtained by a reduction process and improved electrical conductivity.

In order to overcome the pulverization problem of Ge-based anode materials with high capacity, we use the co-sputtering deposition method to prepare thin film nanocomposites (Ge–TiN), containing amorphous Ge and TiN, as an anode for use in high-performance LIBs. Compilation of the data from XRD, Raman, and TEM suggests that the nanocomposites consist of amorphous Ge and TiN phases in the presence of phase separation. From the XPS and EDX data, the nanocomposites show homogeneous distribution of Ge and TiN both on the surface and in the bulk of the electrodes. In the active–inactive composite, Ge acts as a reactant during the lithiation process, forming LixGe, which is surrounded by an inactive TiN matrix. The Ge–TiN nanocomposites demonstrate relatively high reversible capacities, and show good capacity retention ratios and excellent high rate cycling performance even at a high current rate.

Well-defined nanostructured electrodes are known to have improved lithium ion reaction properties for lithium-ion batteries. Herein, we prepared shape-controlled Cu2O nanostructures as an anode material using ascorbic acid as a reducing agent with and without polyvinylpyrrolidone (PVP) as a surfactant. Using scanning electron microscopy, transmission electron microscopy, and X-ray diffraction methods, we observed that the sample prepared in the absence of PVP exhibited cubes with dominant {100} facets, whereas octahedral Cu2O nanostructures with dominant {111} facets were formed in the presence of PVP. During the charge–discharge process, an octahedron-shaped Cu2O nanostructured electrode having {111} facets favourable for lithium ion transport revealed an enhanced conversion reaction mechanism with high reversible capacity and high rate cycling performance, due to its low charge transfer resistance and high lithium ion diffusion coefficient.