Periodontitis-induced systemic inflammation exacerbates atherosclerosis partly via endothelial-mesenchymal transition in mice.

Growing evidence suggests close associations between periodontitis and atherosclerosis. To further understand the pathological relationships of these associations, we developed periodontitis with ligature placement around maxillary molars or ligature placement in conjunction with Porphyromonas gingivalis lipopolysaccharide injection at the ligature sites (ligature/P.g. LPS) in Apolipoprotein E knock out mice and studied the atherogenesis process in these animals. The mice were fed with high fat diet for 11 weeks and sacrificed for analyzing periodontitis, systemic inflammation, and atherosclerosis. Controls did not develop periodontitis or systemic inflammation and had minimal lipid deposition in the aortas, but mice receiving ligature or ligature/P.g. LPS showed severe periodontitis, systemic inflammation, and aortic plaque formation. The aortic plaque contained abundant macrophages and cells expressing both endothelial and mesenchymal cell markers. The severity of periodontitis was slightly higher in mice receiving ligature/P.g. LPS than ligature alone, and the magnitude of systemic inflammation and aortic plaque formation were also notably greater in the mice with ligature/P.g. LPS. These observations indicate that the development of atherosclerosis is due to systemic inflammation caused by severe periodontitis. In vitro, P.g. LPS enhanced the secretion of pro-inflammatory cytokines from macrophages and increased the adhesion of monocytes to endothelial cells by upregulating the expression of adhesion molecules from endothelial cells. Moreover, secretory proteins, such as TNF-α, from macrophages induced endothelial-mesenchymal transitions of the endothelial cells. Taken together, systemic inflammation induced by severe periodontitis might exacerbate atherosclerosis via, in part, causing aberrant functions of vascular endothelial cells and the activation of macrophages in mice

Graphene sensing meshes for densely distributed strain field monitoring

The objective of this study is to design and validate distributed strain field monitoring using a patterned nanocomposite “sensing mesh” that is coupled with an electrical impedance tomography (EIT) measurement strategy and algorithm. Although EIT has been used in other studies and in conjunction with a piezoresistive thin film for spatial damage detection, different strain components cannot be directly extracted from reconstructed EIT conductivity maps. Therefore, this study seeks to address this issue by patterning piezoresistive graphene-based thin films to form a mesh-like pattern. The high aspect ratio of each nanocomposite grid interconnect acts as a linear distributed strain sensor, capable of resolving strains along the entire length and direction of the element. This study first began with the design, fabrication, and characterization of the strain sensing response of a graphene-based thin film of high strain sensitivity. Second, the strain-sensitive film was spray-coated onto patterned polymer substrates to form the sensing meshes, which were then subjected to load tests. Upon validating distributed strain field monitoring through EIT, its applicability for field implementation and damage characterization was also demonstrated by instrumenting sensing meshes in the column of a seven-story reinforced-concrete building subjected to shaking table earthquake excitations. The large-scale shaking table test results successfully validated distributed damage detection

INVERSE SCATTERING TRANSFORM ANALYSIS OF STOKES-ANTI-STOKES STIMULATED RAMAN SCATTERING

Zakharov-Shabat--Ablowitz-Kaup-Newel-Segur representation for Stokes-anti-Stokes stimulated Raman scattering is proposed. Periodical waves, solitons and self-similarity solutions are derived. Transient and bright threshold solitons are discussed.Comment: 16 pages, LaTeX, no figure

Респираторная тактика во время искусственного кровообращения при кардиохирургических операциях

An important place in the structure of the causes of postoperative respiratory failure in cardiac surgery is occupied by atelectasis of the lung tissue, which is formed during cardiopulmonary bypass (CPB). The incidence of this complication makes 54–92%.The objective: to evaluate the effectiveness of various respiratory support techniques during CPB.Subjects and methods. 60 patients were randomly included in the study. CPAP Group (positive airway pressure +5 cm H2O) and VC Group (lung ventilation during CPB with parameters: tidal volume 3 ml/kg, respiratory rate 6/min, positive end-expiratory pressure +5 cm H2O).Results. The oxygenation index in VC Group was higher than in CPAP Group at the stages after the end of CPB (289.6 ± 100.0 in VC Group and 223.1 ± 152.0 in CPAP Group), at the end of surgery (in VC Group 318,7 ± 73.8 and in CPAP Group 275.2 ± 90.0) The frequency of intraoperative (VC 16% and CPAP 43%) and postoperative recruiting lung maneuvers (VC 7% and CPAP 26%) in VC Group was lower versus CPAP Group. The incidence of atelectasis in VC Group (10%) decreased compared to CPAP (36.6%).Conclusion: Low-volume ventilation during cardiopulmonary bypass has a more favorable effect on the oxygenating function compared to respiratory support in the CPAP mode.Большое место в структуре причин послеоперационной дыхательной недостаточности в кардиохирургии занимает ателектазирование легочной ткани, формирующееся во время искусственного кровообращения (ИК). Частота этого осложнения составляет 54‒92%.Цель: оценка эффективности различных методик респираторной поддержки во время ИК.Материалы и методы. В исследование рандомизировано 60 кардиохирургических пациентов. Группа CPAP (положительное давление в дыхательных путях +5 см H2O) и группа VC (вентиляция легких во время ИК с параметрами: дыхательный объем 3 мл/кг, частота дыхания 6/мин, положительное давление конца выдоха +5 см Н2О).Результаты. Индекс оксигенации в группе VC был выше, чем в группе СРАР, на этапах после окончания ИК (289,6 ± 100,0 в группе VC и 223,1 ± 152,0 в группе СРАР), на конец операции (в группе VC 318,7 ± 73,8 и в группе СРАР 275,2 ± 90,0). Частота интраоперационных (VC 16% и СРАР 43%) и послеоперационных рекрутирующих маневров легких (VC 7% и СРАР 26%) в группе VC по сравнению с группой СРАР была ниже. Частота развития ателектазов в группе VC (10%) снизилась по сравнению со СРАР (36,6%).Вывод. Проведение малообъемной вентиляции легких в период ИК оказывает более благоприятное влияние на оксигенирующую функцию легких по сравнению с респираторной поддержкой в режиме СРАР

Gender, ethnicity, health behaviour & self-rated health in Singapore

10.1186/1471-2458-7-184BMC Public Health718

Gold Nanoparticle-Based Surface-Enhanced Raman Scattering for Noninvasive Molecular Probing of Embryonic Stem Cell Differentiation

This study reports the use of gold nanoparticle-based surface-enhanced Raman scattering (SERS) for probing the differentiation of mouse embryonic stem (mES) cells, including undifferentiated single cells, embryoid bodies (EBs), and terminally differentiated cardiomyocytes. Gold nanoparticles (GNPs) were successfully delivered into all 3 mES cell differentiation stages without affecting cell viability or proliferation. Transmission electron microscopy (TEM) confirmed the localization of GNPs inside the following cell organelles: mitochondria, secondary lysosome, and endoplasmic reticulum. Using bright- and dark-field imaging, the bright scattering of GNPs and nanoaggregates in all 3 ES cell differentiation stages could be visualized. EB (an early differentiation stage) and terminally differentiated cardiomyocytes both showed SERS peaks specific to metabolic activity in the mitochondria and to protein translation (amide I, amide II, and amide III peaks). These peaks have been rarely identified in undifferentiated single ES cells. Spatiotemporal changes observed in the SERS spectra from terminally differentiated cardiomyocyte tissues revealed local and dynamic molecular interactions as well as transformations during ES cell differentiation

Trihydrophobin 1 Phosphorylation by c-Src Regulates MAPK/ERK Signaling and Cell Migration

c-Src activates Ras-MAPK/ERK signaling pathway and regulates cell migration, while trihydrophobin 1 (TH1) inhibits MAPK/ERK activation and cell migration through interaction with A-Raf and PAK1 and inhibiting their kinase activities. Here we show that c-Src interacts with TH1 by GST-pull down assay, coimmunoprecipitation and confocal microscopy assay. The interaction leads to phosphorylation of TH1 at Tyr-6 in vivo and in vitro. Phosphorylation of TH1 decreases its association with A-Raf and PAK1. Further study reveals that Tyr-6 phosphorylation of TH1 reduces its inhibition on MAPK/ERK signaling, enhances c-Src mediated cell migration. Moreover, induced tyrosine phosphorylation of TH1 has been found by EGF and estrogen treatments. Taken together, our findings demonstrate a novel mechanism for the comprehensive regulation of Ras/Raf/MEK/ERK signaling and cell migration involving tyrosine phosphorylation of TH1 by c-Src

Sexual dimorphism in cancer.

The incidence of many types of cancer arising in organs with non-reproductive functions is significantly higher in male populations than in female populations, with associated differences in survival. Occupational and/or behavioural factors are well-known underlying determinants. However, cellular and molecular differences between the two sexes are also likely to be important. In this Opinion article, we focus on the complex interplay that sex hormones and sex chromosomes can have in intrinsic control of cancer-initiating cell populations, the tumour microenvironment and systemic determinants of cancer development, such as the immune system and metabolism. A better appreciation of these differences between the two sexes could be of substantial value for cancer prevention as well as treatment