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The integration of a thermal energy storage (TES) system is an effective way to improve the load cycling rate of coal-fired power plants (CFPPs). To evaluate the power increase potential and thermodynamic performance of CFPP supplied by heat release of the molten salt TES system, eight discharging modes for CFPP integrated with the TES system including steam injection, heater bypass, and additional turbine schemes were comparatively evaluated. The system simulation models of the integrated systems were developed and the thermodynamic performance of the proposed system were evaluated. Results show that the mode SI-HPT (high-pressure turbine steam injection) has the largest output power increase of 25.00 % under the benchmark condition of 75%THA, but the mode HB-LPH (low-pressure heater bypass) shows a very low output power increase of 2.08 %. Moreover, the power generation efficiency is changed by the external heat source through a change in the average heat absorption temperature of the Rankine cycle and the internal irreversibility of the steam/water cycle. Under the typical benchmark discharging condition of 75%THA, the power generation efficiency of the turbine in mode SI-LPT (low-pressure turbine steam injection) can be reduced from 47.41 % to 44.15 %, but it can be increased from 47.41 % to 48.86 % in mode SI-HPT. When the temperature ranges of the TES system are above 600 °C and below 450 °C, the modes SI-HPT and SI-LPT obtain the optimal comprehensive performance, respectively. This study can provide the scientific guidance for retrofit for CFPP to achieve efficient and flexible design. • Eight discharging modes of thermal energy storage system are comparatively studied. • The power increase potential and restrictions of thermal power plant are determined. • Thermodynamic performance of multiple heat sources Rankine cycle is analyzed. • The exergy destruction changes caused by external heat sources are calculated. • The optimized system for different thermal storage temperature ranges is obtained. [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial pneumonia, the available treatment option is limited because the etiology and pathological process are not well understood. Although gut-lung axis reported with an emerging area of host-associated microbiota exist in many chronic lung diseases, the connection between gut-lung microbiota composition with in-site inflammation in IPF development is not yet established. We aimed to address the microbiota and immunity connection, and make it clear how a listed drug, Xuanfei Baidu Decoction (XFBD) affect the lung-gut crosstalk for IPF amelioration, which was previously reported for restoring disrupted lung in IPF and protecting intestinal injury. Firstly, Micro-CT (μCT) and histopathology were used to check for pathological changes in the lungs and intestines of bleomycin (BLM)-induced IPF mice. Then, Reverse Transcription and Quantitative Real-time PCR (RT-qPCR) and Western blot (WB) assays were employed to detect the integrity of the barrier of lungs and intestines in IPF mice. Subsequently, flow cytometry and 16S rRNA sequencing were used to evaluate the immune and microbial microenvironment of the lungs and intestines. We analyzed the lung-gut microbiota crosstalk for further mechanism exploration. Firstly, we revealed that XFBD protected the integrity of the lung and intestinal barriers in the IPF mice, as evidenced by the up-regulation of ZO-1, Claudin-1, Occludin, and VE Cadherin protein expression. Then, we analyzed the changing microbiota and T cell in the gut-lung axis in IPF, and with XFBD, six highly relevant microenvironments were demonstrated that crossing damaged lung-gut barriers and XFBD could reverse these chaotic bacterial and immunity micro-environment, among them Akkermansia was an essential bacteria affecting the expression of systemic IFN-γ downstream STAT1/STAT3 axis was also studied. XFBD prominently up-regulated the production of IFN-γ and p-STAT1 and down-regulated p-STAT3, consequently exerting effects on the lung barrier and gut barrier. Taken together, XFBD ameliorated BLM-induced IPF mice by regulating IFNγ/STAT1/STAT3 axis. Altogether, our results revealed that XFBD improved the BLM-elicited IPF mice by regulating gut-lung crosstalk via IFN-γ/STAT1/STAT3 axis and provided a new insight of gut-lung crosstalk in IPF, especially the dynamic changes of microorganisms in the damaged lungs needed to pay more attention during IPF therapy. [Display omitted] [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2009.05.021 Byline: Sudan He (1)(2), Lai Wang (3), Lin Miao (2), Tao Wang (2), Fenghe Du (3), Liping Zhao (2), Xiaodong Wang (3) Keywords: HUMDISEASE; SIGNALING; MOLIMMUNO Abstract: Smac mimetics induce apoptosis synergistically with TNF-[alpha] by triggering the formation of a caspase-8-activating complex containing receptor interacting protein kinase-1 (RIPK1). Caspase inhibitors block this form of apoptosis in many types of cells. However, in several other cell lines, caspase inhibitors switch the apoptotic response to necrosis. A genome wide siRNA screen revealed another member of the RIP kinase family, RIP3, to be required for necrosis. The expression of RIP3 in different cell lines correlates with their responsiveness to necrosis induction. The kinase activity of RIP3 is essential for necrosis execution. Upon induction of necrosis, RIP3 is recruited to RIPK1 to form a necrosis-inducing complex. Embryonic fibroblasts from RIP3 knockout mice are resistant to necrosis and RIP3 knockout animals are devoid of inflammation inflicted tissue damage in an acute pancreatitis model. These data indicate RIP3 as the determinant for cellular necrosis in response to TNF-[alpha] family of death-inducing cytokines. Author Affiliation: (1) Graduate Program, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, China (2) National Institute of Biological Sciences, No. 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China (3) Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA Article History: Received 2 December 2008; Revised 16 February 2009; Accepted 11 May 2009 Article Note: (miscellaneous) Published: June 11, 2009

Evidence is scarce on the acute cardiovascular health effects of fine particulate matter (PM 2.5) and its respiratory tract depositions. We performed a panel study in Hefei, China to explore the relations of PM 2.5 and its depositions in 3 respiratory tract regions over different lag times with a range of cardiovascular biomarkers among 40 college students and the potential mediating effects of inflammation. We found significant effects of PM 2.5 exposure on the alterations of biomarkers at specific lag days, in a concentration-response manner, even at PM 2.5 level below Chinese Ambient Air Quality Standard (CAAQS) Grade I (35 μg/m3). For example, per 10 μg/m3 increase in PM 2.5 concentration was associated with −9.33% increase in ADAMTS13 on lag 0-1d. The corresponding increases in D-Dimer, GM-CSF, and MCP-1 for the same change in PM 2.5 concentration on lag 5-6d were 30.51%, 11.43%, and 20.05%. Besides, tracheobronchial region (TB) deposition presented more evident effects on these biomarkers than that in PM 2.5. Additionally, we observed greater associations of PM 2.5 -biomarkers among females, those with abnormal body mass index (BMI), and those with physical activity. The results indicated that short-term PM 2.5 exposure and its respiratory tract depositions were concentration-responsive associated with damaged cardiovascular health via inducing blood coagulation, oxidative stress and inflammation among healthy young adults even at concentration below CAAQS Grade I. Elevated serum levels of systemic inflammation may be partly responsible for the effects of PM 2.5 and its respiratory tract depositions on coagulation function. [Display omitted] • Evidence of association of PM 2.5 deposition with circulating biomarkers is limited. • PM 2.5 was concentration-responsive related to higher levels of circulating markers. • The adverse effects on biomarkers remained significant when PM 2.5 below CAAQS I. • Tracheobronchial and alveolar depositions showed stronger effects on biomarkers. • Gender, BMI and activity modified effects of PM 2.5 depositions on biomarkers. [ABSTRACT FROM AUTHOR]

Diagnosis of malignant biliary obstruction is complicated and lacks accuracy. Exosomes may be secreted by malignant tumors; intact miRNAs from exosomes might serve as potential biomarkers for the disease. To identify exosomal microRNAs in human bile among benign and malignant biliary obstructions. Bile samples were collected from patients undergoing therapeutic endoscopic retrograde cholangiopancreatography for biliary obstruction. Exosome microRNAs were determined by RNA-sequencing in the discovery cohort, which comprising benign (n = 5) cases and malignant biliary obstruction (n = 5) cases. Then, the diagnostic performance of the two up-regulated microRNAs (mir-483-5p and mir-126-3p) of bile exosomes was verified by analysis of 82 patients with a diagnosis of malignant (n=37) or nonmalignant (n=45) biliary obstruction. In both cohorts, the expressions of mir-483-5p and mir-126-3p were significantly higher in bile exosomes samples from patients with malignant biliary obstructions than controls. In the verification cohort, the two miRNAs can distinguished the benign and malignant groups with high diagnostic accuracy and specificity; the diagnostic values of the two microRNAs were better than serum carbohydrate antigen 19-9 (CA19-9), area under the curve (AUC) were 0.81 and 0.74. The expression of exosomal mir-483-5p and mir-126-3p in the bile samples discriminates between patients with malignant and nonmalignant biliary obstructions. NCT03102268 [ABSTRACT FROM AUTHOR]

Background Mounting epidemiologic studies have investigated the potential inverse association between Mediterranean diet (MD) adherence and colorectal cancer (CRC) incidence and mortality. Objectives This meta‐analysis aimed to investigate the association between MD adherence and CRC incidence and mortality. Methods PubMed, Embase, and Web of Science were searched to identify eligible studies through September 2019. A random-effects model was used to estimate summary RRs and 95% CIs. Results This meta-analysis included 13 prospective cohort studies, of which 9 reported CRC incidence and 5 reported CRC mortality. The summary RR of CRC incidence was 0.90 (95% CI: 0.84, 0.96) for highest compared with lowest MD adherence and 0.96 (95% CI: 0.94, 0.99) per 2-score increase in MD adherence. The summary RRs for highest compared with lowest MD adherence were 0.82 for rectal cancer (95% CI: 0.71, 0.95), 0.94 for proximal colon cancer (95% CI: 0.87, 1.02), and 0.91 for distal colon cancer (95% CI: 0.79, 1.04). Neither the summary HR of overall mortality for highest compared with lowest pre- and postdiagnosis MD adherence, nor the summary HR of CRC-specific mortality for highest compared with lowest prediagnosis MD adherence achieved a value with statistical significance. Conclusions Our meta-analysis supports the inverse association of MD adherence with CRC incidence, but not with overall mortality or CRC-specific mortality among those diagnosed with CRC. [ABSTRACT FROM AUTHOR]

Abstract Ethnopharmacological relevance Cynomorium songaricum Rupr. (CS) belongs to the genus of parasitic perennial flowering plants, mostly used in Chinese traditional medicine for benign prostatic hyperplasia (BPH) treatment. BPH is a chronic disease in men that both androgen and estrogen play a crucial role in promoting its development via their receptors. Previously we have showed that compounds from CS have the phytoestrogenic and/or phytoandrogenic activities that may have the potential suppressive effects on BPH, while the mechanism remains unclear. Aim of the study In this study, we aim to investigate the effect of CS and its derived compounds: luteolin (LUT), gallic acid (GA), protocatechuic acid (PA) and protocatechualdehyde (Pra) on inhibition of rat BPH and proliferation of BPH-1 cell line respectively, and further uncover whether it is related with the phytoestrogenic and / or phytoandrogenic activities. Materials and methods Estradiol/testosterone (1:100) was subcutaneous injected to induce BPH in a castrated rat model, and CS was orally administrated for 45 days. Then the weights of the body and prostate were recorded, the pathogenesis changes of prostate were analyzed by Hematoxylin and eosin (H&E) and immunohistochemical (IHC). The levels of 17β-estradiol (E 2), testosterone, and dihydrotestosterone (DHT) from rats' serum were measured by enzyme-linked immunosorbent assay (ELISA). In vitro , human benign prostatic epithelial cell BPH-1 was cultured and treated with or without different CS compounds and DHT or E 2. MTT and CCK-8 assays were performed to detect the regulatory effects on cell proliferation. The expressions of PCNA, AR, ERα, ERβ, and steroid 5-α-reductases (SRD5A1 and SRD5A2) were further analyzed by western blotting upon treatment. Results Treatment with CS significantly inhibited rat prostate enlargement, improved the pathological feature and reduced the thickness of smooth muscle layer. The up-regulated AR and ERα expressions and down-regulated ERβ in BPH rat prostate were significantly blocked after CS administration. Moreover, the enhanced values of E 2 /testosterone and the level of DHT in serum were also strongly inhibited in CS group compared with those in BPH groups. In cellular level, LUT, GA, PA, or Pra significantly inhibited DHT- or E 2 - induced BPH-1 cell proliferation and PCNA expressions. Consistently with the data in vivo, compounds from CS interfered the DHT or E 2 -regulated AR, ERα and ERβ expressions in BPH-1 cells as well. Importantly, the dramatic increased SRD5A1 and SRD5A2 expressions were observed in BPH rat prostates and DHT or E 2 -stimulated BPH-1 cells. However, treatment with CS in rat or with compounds isolated from CS in BPH-1 cells significantly blocked the induction of SRD5A1 and SRD5A2. Conclusions CS suppressed BPH development through interfering with prostatic AR, ERα/β, and SRD5A1/2 expressions, which provided evidence of CS for BPH treatment. Graphical abstract fx1 [ABSTRACT FROM AUTHOR]

Weichang'an pill (WCAP) is a traditional Chinese patent medicine, which is clinically used for the treatment of bowel syndrome and functional dyspepsia such as diarrhea, abdominal distension, and enteritis. So far, quality control studies of WCAP have mainly focused on the determination of chemical composition content, which has little relevance to biological activity and clinical effects. With the aim of identifying the multi-index ingredients with NF-κB inhibitory activities related to WCAP clinical effect, this present work described the chemical profile of WCAP by UHPLC-QE-MS, established the correlated relationship between chromatographic fingerprints and the NF-κB inhibitory activities based on multivariate statistical analysis, including hierarchical clustering analysis (HCA), Pearson correlation analysis, and Partial least squares regression analysis (PLSR). The spectrum-effect relationship analysis indicated 10 compounds, which were ferulic acid, naringin, narirutin, hesperidin, neohesperidin, aloe emodin, emodin, honokiol, magnolol, and physcion, might be the potential NF-κB inhibitory constituents in the pill. The NF-κB inhibitory effects of the ten compounds were verified by in vitro dual luciferase reporting detection system. Considering that the detection index should be representative of more medicinal materials, a rapid and efficient UPLC-DAD method was eventually developed to determine the content of the 13 components. Our findings will provide data support for WCAP quality control and advance the understanding of the quality assessment of traditional Chinese patent medicines. [ABSTRACT FROM AUTHOR]

Evidence on associations between outdoor air pollution and the risk of digestive diseases, especially seasonal disparity, is scarce. We aimed to compare the acute effects of air pollution on outpatient visits for gastritis between warm and cold seasons in China. We collected data on six criteria air pollutants [fine particulate matter (PM 2.5), inhalable particulate matter (PM 10), nitrogen dioxide (NO 2), sulfur dioxide (SO 2), carbon monoxide (CO), and ozone (O 3)], daily counts of gastritis outpatient visits, and meteorological variables during 2014–2020 (2536 days) in Hefei, China. A time-series analysis with generalized additive model was used, and potential effect modifiers were explored. Totally, 106,429 outpatient visits were recorded. The average concentrations of PM 2.5 , PM 10 , CO, NO 2 , SO 2 , and O 3 were 54.82, 81.95, 886.75, 39.51, 11.81, and 84.75 μg/m3, respectively, exceeding the updated WHO Air Quality Guidelines values. Short-term PM 2.5 , CO, and NO 2 exposures significantly increased the risk of gastritis outpatient visits and the lag response effects varied at different lag days. Each 10 μg/m3 increment of PM 2.5 , CO, and NO 2 at lag 0 day, the excess risks of gastritis outpatient visits increased by 0.50% (95% CI: 0.04%, 0.95%), 0.05% (0%, 0.10%), and 1.50% (0.54%, 2.47%), respectively. We found insignificant differences in age-, sex- or insurance-strata but significant differences in seasonal strata with stronger effects in cold seasons. Null association of exposure to O 3 , SO 2 , or PM 10 was observed. This study provided first-hand data that short-term exposure to PM 2.5 , CO, and NO 2 but not O 3 , SO 2 , or PM 10 was positively associated with gastritis outpatient visits, and such association was more evident in cold seasons, further suggesting the need for underscoring the continued efforts for public health intervention and air pollution control, especially in winter. [Display omitted] • This is the first larger-scale hospital-based study on examining air pollution and gastritis outpatient visits. • PM 2.5 , NO 2 and CO contributed more outpatient visits for gastritis. • For low exposures of O 3 , the risk significantly increased. • Cold seasons posed more outpatient visits for gastritis than warm seasons. • The associations occurred immediately at the current exposure day. [ABSTRACT FROM AUTHOR]

To accommodate high penetration of intermittent renewable power, including wind power and photovoltaic power, coal-fired power plants (CFPPs) are forced to enhance operational flexibility. The integration of a power-to-heat thermal energy storage (TES) system within a CFPP is a potential solution. In this study, the power-to-heat TES system was integrated within a CFPP, and the stored heat is released to heat live steam (scheme C1), reheat steam (scheme C), and high-pressure heater feedwater (scheme C3). The thermodynamic and economic performances of power-to-heat TES systems are evaluated and compared. Results show that the power-to-heat process can achieve zero output of CFPPs, but it has an exergy loss coefficient of more than 40%. When the boiler maintains a 75% rated thermal load, schemes C1, C2, and C3 can maximally increase output power by 150.0, 96.5, and 50.0 MW, accounting for 25.0%, 16.1%, and 8.3% of the rated load, respectively. Scheme C2 achieves the highest equivalent round-trip efficiency of 50.81%, which is slightly higher than that of scheme C1 (50.74%). Scheme C1 exhibits the lowest total cost of the equipment and storage materials at 63.68 million USD, and its net present value and payback period are 25.0 million USD and 13.5 years, respectively. • Coal-fired power plants integrated with P2H and thermal energy storage were proposed. • The operational flexibility of the integrated system is determined. • Exergy destructions and flows within the proposed systems are calculated. • The maximum equivalent round-trip efficiency of the proposed system is 50.81%. • The minimum payback period is 13.5 years. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM 2.5) has been associated with risk of oral and respiratory diseases. However, the biological mechanisms of adverse oral and respiratory health response to PM 2.5 fluctuation have not been well characterized. This study aims to explore the relationships of PM 2.5 with airway inflammation, salivary biomarkers and buccal mucosa microbiota. We performed a panel study among 40 college students involving 4 follow-ups from August to October 2021 in Hefei, Anhui Province, China. Health outcomes included fractional exhaled nitric oxide (FeNO), salivary biomarkers [C-reactive protein (CRP), cortisol, lysozyme and alpha-amylase] and buccal mucosa microbial diversity. Linear mixed-effect models were applied to explore the cumulative impacts of PM 2.5 on health indicators. PM 2.5 was positively correlated with FeNO, CRP, cortisol and alpha-amylase, while negatively with lysozyme. Per 10-μg/m3 increase in PM 2.5 was linked to maximum increments in FeNO of 10.71% (95%CI: 2.01%, 19.41%) at lag 0–24 h, in CRP of 7.10% (95%CI: 5.39%, 8.81%) at lag 0–24 h, in cortisol of 1.25% (95%CI: 0.44%, 2.07%) at lag 0–48 h, and in alpha-amylase of 2.12% (95%CI: 0.53%, 3.71%) at lag 0–24 h, while associated with maximum decrement in lysozyme of 0.53% (95%CI: 0.12%, 0.95%) at lag 0–72 h. Increased PM 2.5 was linked to reduction in the richness and evenness of buccal microbe and o_Bacillales and o_Bacteroidales were identified as differential microbes after PM 2.5 inhalation. Bio-information analysis indicated that immunity system pathway was the most important enriched abundant process altered by PM 2.5 exposure. In summary, short-term PM 2.5 exposure may impair oral and respiratory health by inducing inflammatory and stress responses, weakening immune function and altering buccal mucosa microbial diversity. [Display omitted] • We estimated the acute effects of PM 2.5 on adults' oral and respiratory health. • Short-term exposure to PM 2.5 may increase airway inflammation and stress levels. • Short-term exposure to PM 2.5 may weaken non-specific immune function. • Bio-information analysis revealed PM 2.5 most obviously influenced immunity system. • Short-term exposure to PM 2.5 may alter buccal mucosa microbial diversity. [ABSTRACT FROM AUTHOR]

Abstract: Postherpetic neuralgia is the most common complication of herpes zoster which is caused by a reactivation of latent varicella zoster virus. The pathogenesis of postherpetic neuralgia may involve peripheral and central mechanisms. Reported risk factors for postherpetic neuralgia include female gender, old age, diminished cell-mediated immunity and nutritional deficiencies. Based on our clinical observation which revealed that peptic ulcer disease (PUD) is one of the common comorbidities in patients with postherpetic neuralgia, we hypothesize that herpes zoster patients with PUD may be at a greater risk for the development of postherpetic neuralgia due to their impaired cellular immunity and depressed nutritional status. Major causes of PUD include Helicobacter pylori infection and usage of ulcerogenic medications. Patients with H. pylori infection may develop T cell dysfunctions and nutritional deficiencies including vitamin C, iron, cobalamin, carotenes and alpha-tocopherol. Ulcerogenic medications such as nonsteroidal anti-inflammatory drugs and steroids have been found not only to be ulcerogenic but also immunosuppressive to T cells. In addition, usage of steroids and nonsteroidal anti-inflammatory drugs may cause deficiencies of alpha-tocopherol, carotenes, cobalamin, iron, zinc and vitamin C. Vitamin C, carotenes and alpha-tocopherol are anti-inflammatory and the major oxidant scavengers in the aqua phase and biomembranes. Deficiencies of these nutrients may induce dysregulated inflammation and oxidative damage leading to neuropathic pain in patients with herpes zoster. Furthermore, nutrient deficiencies including zinc, iron, cobalamin and vitamin C are associated with dysregulation of Ca(v)3.2 T-channels and N-methyl-d-aspartate receptors, upregulation of nitric oxide synthase, the increase of nitric oxide formation and dysfunction of central norepinephrine inhibitory pain pathway. Prospective cohort studies are suggested to test the hypothesis. We further propose that a follow-up study that contains two groups of herpes zoster patients, i.e., with or without gastroendoscopy-proven PUD, be conducted to determine their incidence of postherpetic neuralgia. In addition, despite of the high proportion of zoster patients having been treated with antiviral therapies, prevention and treatment of postherpetic neuralgia remain challenging in clinical practice. The potential risk of postherpetic neuralgia in zoster patients with PUD could mean that physicians need to pay more attention to the comorbidity - PUD in patients with herpes zoster and treat PUD earlier in order to prevent the development of postherpetic neuralgia. [Copyright &y& Elsevier]

Abstract: Retinoic acid (RA) has been used as a chemopreventive agent for breast cancer. It has been shown that HOXA5 is a critical mediator of RA-induced cell growth inhibition. However, the molecular mechanisms underlying RA-induced HOXA5 expression remain largely unknown. Here we report that in addition to transcriptional regulation, post-transcriptional regulation also contributes to RA-induced HOXA5 expression. miR-130a, a c-Myc responsive miRNA, represses HOXA5 cellular levels under unstressed condition. Upon RA treatment, c-Myc is quickly degraded via the proteasome-dependent pathway. This in turn decreases miR-130a levels and de-represses the translation of HOXA5. We also show that the de-repression of HOXA5 translation is dependent on the RNA-binding protein Human antigen R (HuR), which binds to 3′UTR of HOXA5 mRNA and increases its stability in response to RA treatment. Collectively, these results demonstrate that HuR and miR-130a dynamically regulate HOXA5 gene expression via modulating HOXA5 mRNA turnover and translation, respectively, thereby contributing to RA-induced growth inhibition. [Copyright &y& Elsevier]

Abstract: Endothelial dysfunction such as hyperpermeability is one of the characteristics in an early stage of diabetic complications. Curcumin has been shown to inhibit the formation of advanced glycation end products (AGEs) and to trap methyglyoxal (MGO) in cell-free system and in human umbilical vein endothelial cells (HUVECs). Here, we investigated the effect of curcumin on dysfunctions of HUVECs induced by exogenous MGO (30μM), which significantly increased intracellular reactive oxygen species (ROS), endothelial permeability, and cytoskeleton rearrangement. In contrast, MGO decreased gap junctional intercellular communication and the expression of connexin 43 and zonula occludens. Pre-treatment of HUVECs with curcumin (0.25–2.5μM) significantly ameliorated MGO-induced endothelial dysfunction, whereas pre-treatment with vitamin E (10μM) only slightly ameliorated MGO-induced endothelial dysfunction, suggesting that ROS induced by MGO do not play a major role in endothelial dysfunction. These results suggest that curcumin is a potential protective agent against MGO-induced endothelial dysfunction. [Copyright &y& Elsevier]

Abstract: S100A8 and S100A9 are strongly expressed in epithelial cells of human prostate cancer. However, the regulation of their expression is unclear. Here we show that S100A8 and to a lesser extent S100A9 mRNA expression is induced by prostaglandin E2 in a dose and time-dependent manner in PC-3 prostate cancer cells as well as in BPH-1 benign prostatic epithelial cells. Prostanoid receptor EP2 antagonist AH6809 and EP4 antagonist AH23848, as well as protein kinase A inhibitor H89, inhibited prostaglandin E2 mediated increase in S100A8 mRNA expression as well as promoter activity. Sequence analysis detected a potential binding site of the transcription factor CCAAT/enhancer-binding-protein-beta within the proximal S100A8 promoter. CCAAT/enhancer-binding-protein-beta overexpression increased S100A8 mRNA and protein expression as well as its promoter activity. The latter was prevented by mutation of the potential CCAAT/enhancer-binding-protein-beta binding site within the S100A8 promoter. Chromatin immunoprecipitation revealed increased binding of CCAAT/enhancer-binding-protein-beta to the S100A8 promoter in prostaglandin E2 treated cells. Knockdown of CCAAT/enhancer-binding-protein-beta by siRNA blocked prostaglandin E2 mediated induction of S100A8 promoter activity and mRNA expression. Our results indicate that in prostate cancer cells, S100A8 expression is stimulated by prostaglandin E2 via EP2 and EP4 receptors through activation of the protein kinase A signaling pathway and subsequent stimulation of CCAAT/enhancer-binding-protein-beta binding to the S100A8 promoter. [Copyright &y& Elsevier]

Abstract: Epidemiologic studies suggest that lycopene may reduce the risk of certain cancers, but the underlying mechanisms are unclear. We hereby examined in vivo anticarcinogenic effects of supplemental lycopene on hepatic DNA damage (Comet formation and levels of 8-oxo-2′-deoxyguanosine, 8-oxo-dG) and human MutT homologue (hMTH1) mRNA expression in Mongolian gerbils injected i.p. with ferric nitrilotriacetate (Fe/NTA). Gerbils were pre-treated with two dose (10 and 20mg/kg BW) of lycopene on alternate morning for 10d. Six hours after the last lycopene supplementation, the gerbils received Fe/NTA (0.16mmol/10mL/kg BW) and were killed 3h later. We found that the livers of Fe/NTA-treated animals exhibited a 5-fold increase in Comet formation (expressed as tail moment), a 2.6-fold increase in 8-oxo-dG levels and a significant increase in hMTH1 mRNA expression. Supplemental lycopene completely inhibited Comet formation (P <0.001) and significantly suppressed 8-oxo-dG levels and hMTH1 expression in a dose-dependent manner. The expression levels of hMTH1 mRNA are highly correlated with hepatic levels of 8-oxo-dG and tail moment, suggesting that hMTH1 gene expression represents a molecular marker of oxidative DNA damage. These results demonstrate the potential of lycopene as a promising chemopreventive agent against hepatotumorigenesis. [Copyright &y& Elsevier]

Abstract: Preserved eggs are a special Asian food. Traditionally, the gelling of preserved eggs is tested intuitively by feeling the slight vibrations that occur when the preserved egg is tapped with a finger. However, the effects of extended tapping and individual subjectivity lead to inaccurate results. This study thus attempts to devise a scientific method for inspecting the gelling of preserved eggs. Regression analysis of the peaks of the time response starting at 50ms following the trigger yielded an exponential tendency line that indicates the decay rate of vibration theory. Distinct vibration analysis revealed that a decay below 80 represents complete gelling. Receiver operating characteristic curve analysis reveals an area under curve of 0.963, a cut-off point at 0.000 (x axis) and 0.882 (y axis), and a decay rate of 84.7995. The accuracy was 96.7%. This method provides a foundation for future development of an automatic preserved egg inspecting system. [ABSTRACT FROM AUTHOR]