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Autophagy is activated in ischemic heart diseases, but its dynamics and functional roles remain unclear and controversial. In this study, we investigated the dynamics and role of autophagy and the mechanism(s), if any, during postinfarction cardiac remodeling. Acute myocardial infarction (AMI) was induced by ligating left anterior descending (LAD) coronary artery. Autophagy was found to be induced sharply 12-24 hours after surgery by testing LC3 modification and Electron microscopy. P62 degradation in the infarct border zone was increased from day 0.5 to day 3, and however, decreased from day 5 until day 21 after LAD ligation. These results indicated that autophagy was induced in the acute phase of AMI, and however, impaired in the latter phase of AMI. To investigate the significance of the impaired autophagy in the latter phase of AMI, we treated the mice with Rapamycin (an autophagy enhancer, 2.0 mg/kg/day) or 3-methyladenine (3MA, an autophagy inhibitor, 15 mg/kg/day) one day after LAD ligation until the end of experiment. The results showed that Rapamycin attenuated, while 3MA exacerbated, postinfarction cardiac remodeling and dysfunction respectively. In addition, Rapamycin protected the H9C2 cells against oxygen glucose deprivation in vitro. Specifically, we found that Rapamycin attenuated NFκB activation after LAD ligation. And the inflammatory response in the acute stage of AMI was significantly restrained with Rapamycin treatment. In vitro, inhibition of NFκB restored autophagy in a negative reflex. Sustained myocardial ischemia impairs cardiomyocyte autophagy, which is an essential mechanism that protects against adverse cardiac remodeling. Augmenting autophagy could be a therapeutic strategy for acute myocardial infarction.

Cotyledons play an important role in seedling establishment, although they may just exist for a short time and become senescent upon the emergence of euphylla. So far, the detailed function of cotyledons has not been well understood. Suaeda aralocaspica is an annual halophyte distributed in cold deserts; its cotyledons could exist for a longer time, even last until maturity, and they must exert a unique function in seedling development. Therefore, in this study, we conducted a series of experiments to investigate the morphological and physiological performances of cotyledons under salt stress at different developmental stages. The results showed that the cotyledons kept growing slowly to maintain the normal physiological activities of seedlings by balancing phytohormone levels, accumulating osmoprotectants and antioxidants, and scavenging reactive oxygen species (ROS). Salt stress activated the expression of osmoprotectant-related genes and enhanced the accumulation of related primary metabolites. Furthermore, differentially expressed transcriptional profiles of the cotyledons were also analyzed by cDNA-AFLP to gain an understanding of cotyledons in response to development and salt stress, and the results revealed a progressive increase in the expression level of development-related genes, which accounted for a majority of the total tested TDFs. Meanwhile, key photosynthetic and important salt stress-related genes also actively responded. All these performances suggest that “big cotyledons” are experiencing a delayed but active developmental process, by which S. aralocaspica may survive the harsh condition of the seedling stage.

•Prior infection and vaccination enhance post-vaccination influenza antibody responses.•Pre-vaccination antibody levels determine the effect of booster immunization.•Annual TIV vaccination for schoolchildren prevents influenza virus infection. The objective of this study was to evaluate the effects of prior-infection and repeated vaccination on post-vaccination antibody titers. A(H1N1)pdm09 strain was included in 2009 pandemic monovalent, 2010–2011, and 2011–2012 trivalent influenza vaccines (MIVpdm09, TIV10/11, TIV11/12) in Taiwan. During the 2011–2012 influenza season, we conducted a prospective sero-epidemiological cohort study among schoolchildren from grades 1 – 6 in the two elementary schools in Taipei with documented A(H1N1)pdm09 vaccination records since 2009. Serum samples were collected at pre-vaccination, 1-month, and 4-months post-vaccination (T1, T2, T3). Anti-A(H1N1)pdm09 hemagglutination inhibition titers (HI-Ab-titers) were examined. We also investigated the impact of four vaccination histories [(1) no previous vaccination (None), (2) vaccinated in 2009–2010 season (09v), (3) vaccinated in 2010–2011 season (10v), and (4) vaccinated consecutively in 2009–2010 and 2010–2011 seasons (09v + 10v)] and pre-vaccination HI-Ab levels on post-vaccination HI-Ab responses as well as adjusted vaccine effectiveness (aVE) against serologically-defined infection from T2 to T3. TIV11/12 had zero serious adverse events reported. A(H1N1)pdm09 strain in TIV11/12 elicited seroprotective Ab-titers in 98% of children and showed promising protection (aVE: 70.3% [95% confidence interval (CI): 51.0–82.1%]). Previously unvaccinated but infected children had a 3.96 times higher T2 geometric mean titer (T2-GMT) of HI-Ab than those naïve to A(H1N1)pdm09 (GMT [95% CI]: 1039.7[585.3–1845.9] vs. 262.5[65.9–1045], p = 0.046). Previously vaccinated children with seroprotective T1-Ab-titers had a higher T2-GMT and a greater aVE than those with non-seroprotective T1-Ab-titers. Repeatedly vaccinated children had lower T2-GMT than those receiving primary doses of TIV11/12. However, after controlling prior infection and T1-Ab-titers, differences in T2-GMT among the four vaccination histories became insignificant (p = 0.16). This study supports the implementation of annual mass-vaccination with A(H1N1)pdm09 in schoolchildren for three consecutive influenza seasons when vaccine and circulating strains were well matched, and found that prior infection and pre-vaccination HI-Ab levels positively impacted post-vaccination HI-Ab responses.

The HA1 domain of HA, the major antigenic protein of influenza A viruses, contains all of the antigenic sites of HA and is under continual immune-driven selection. To resolve controversies on whether only a few or many residue sites of HA1 have undergone positive selection, whether positive selection at HA1 is continual or punctuated, and whether antigenic change is punctuated, we introduce an approach to analyze 2,248 HA1 sequences collected from 1968 to 2005. We identify 95 substitutions at 63 sites from 1968 to 2005 and show that each substitution occurred very rapidly. The rapid substitution and the fact that 57 of the 63 sites are antigenic sites indicate that hitchhiking plays a minor role and that most of these sites, many more than previously found, have undergone positive selection. Strikingly, 88 of the 95 substitutions occurred in groups, and multiple mutations at antigenic sites sped up the fixation process. Our results suggest that positive selection has been ongoing most of the time, not sporadic, and that multiple mutations at antigenic sites cumulatively enhance antigenic drift, indicating that antigenic change is less punctuated than recently proposed.

After briefly summarizing the main concepts of conducting polymers, this book introduces micro/nanostructured conducting polymers, dealing with their synthesis, structure, formation, and physical and chemical properties. It then looks at their applications.

The R -linear convergence of the NQZ algorithm for computing the H -spectral radius of a class of weakly irreducible nonnegative tensors is established by utilizing the directed graphs of tensors. Meanwhile, an upper bound for the root convergence factor R is derived and a general condition ensuring the linear convergence of the NQZ algorithm is provided.

Background Esophageal squamous cell carcinoma (ESCC) is a common gastrointestinal malignant tumor, while the molecular mechanisms have not been fully elucidated. Multiple circular RNAs have been reported to involve in the onset and progression of malignant tumors through various molecular mechanisms. However, the clinical significance and functional mechanism of most circRNAs involved in the progression of ESCC remains obscure. Methods RNA-Seq was used to explore potential circRNAs in participated in 5 pairs of ESCC and their corresponding normal esophageal tissues. The up-regulated circCYP24A1 was selected. Fluorescence in situ hybridization was cunducted to verificated the expression and intracellular localization of circCYP24A1 by using the tissue microarray. The Kaplan–Meier method and Cox proportional hazards model was used to examine the potential prognostic value of circCYP24A1 on overall survival of ESCC patients. The biological function were confirmed by gain- and loss-of-function approaches in vivo. mRNA expression profile microarray was proformed to investigate the downstream signaling pathways involved in circCYP24A1. RNA pull-down assay and mass spectrometry were performed to identify the proteins associated with circCYP24A1. Rescue experiments were carried out to identified hypothetical regulatory role of circCYP24A1 on ESCC progression in vivo and in virto. Results In this study, we identified circCYP24A1 in ESCC tissues by RNA sequencing, which is up-regulated in 114 cases of ESCC tissues and acts as a novel prognosis-related factor. Moreover, circCYP24A1 promoted the ability of proliferation, migration, invasion and clone formation in vitro, as well as tumor growth in vivo. Mechanistically, chemokine (C-Cmotif) ligand 5 (CCL5) is functional downstream mediator for circCYP24A1, which is screened by mRNA microarray. Moreover, circCYP24A1 physically interacts with M2 isoform of pyruvate kinase (PKM2). Rescue experiments showed that PKM2 knockdown partly reverses the promotional effects of circCYP24A1. It was revealed that circCYP24A1 increases secretion of CCL5 through the mechanism mainly by interacting with PKM2, an activator of NF-κB pathway, and thereby accelerate malignant progression of ESCC. Conclusions Up-regulated circCYP24A1 could activate NF-κB pathway by binding PKM2, which promotes the secretion of CCL5 and accelerate malignant progression of ESCC. Our fndings recommended a novel function for circCYP24A1 as a potential effective biomarker for judging prognosis and a therapeutic target in ESCC.

Ionogels are compelling materials for technological devices due to their excellent ionic conductivity, thermal and electrochemical stability, and non-volatility. However, most existing ionogels suffer from low strength and toughness. Here, we report a simple one-step method to achieve ultra-tough and stretchable ionogels by randomly copolymerizing two common monomers with distinct solubility of the corresponding polymers in an ionic liquid. Copolymerization of acrylamide and acrylic acid in 1-ethyl-3-methylimidazolium ethyl sulfate results in a macroscopically homogeneous covalent network with in situ phase separation: a polymer-rich phase with hydrogen bonds that dissipate energy and toughen the ionogel; and an elastic solvent-rich phase that enables for large strain. These ionogels have high fracture strength (12.6 MPa), fracture energy (~24 kJ m −2 ) and Young’s modulus (46.5 MPa), while being highly stretchable (~600% strain) and having self-healing and shape-memory properties. This concept can be applied to other monomers and ionic liquids, offering a promising way to tune ionogel microstructure and properties in situ during one-step polymerization. Two monomers with distinct solubility of their corresponding polymers in an ionic liquid enable tuning of the microstructure of the copolymers during their polymerization. Thus, energy dissipative and elastic molecular domains are created, resulting in highly tough and stretchable ionogels.

High-precision land cover maps of remote sensing images based on an intelligent extraction method are an important research field for many scholars. In recent years, deep learning represented by convolutional neural networks has been introduced into the field of land cover remote sensing mapping. In view of the problem that a convolution operation is good at extracting local features but has limitations in modeling long-distance dependence relationships, a semantic segmentation network, DE-UNet, with a dual encoder is proposed in this paper. The Swin Transformer and convolutional neural network are used to design the hybrid architecture. The Swin Transformer pays attention to multi-scale global features and learns local features through the convolutional neural network. Integrated features take into account both global and local context information. In the experiment, remote sensing images from UAVs were used to test three deep learning models including DE-UNet. DE-UNet achieved the highest classification accuracy, and the average overall accuracy was 0.28% and 4.81% higher than UNet and UNet++, respectively. It shows that the introduction of a Transformer enhances the model fitting ability.

Valvular heart disease (VHD) is expected to cause an increase in public-health problems in the coming years, especially in elderly populations. We aim to estimate the incidence, mortality, and burden of VHD, by age, from 1990 to 2017 in 195 countries and territories. We estimated the incidence, mortality, and burden of VHD based on the Global Burden of Disease Study 2017. All metrics are presented with their 95% uncertainty intervals (UIs). The Socio-demographic Index was used to identify whether developmental status correlates with health outcomes. The global incidence of rheumatic heart disease (RHD) decreased by 8.67% between 1990 and 2017, while that of non-rheumatic VHD (NRVHD) increased by 45.10%. There was a 54.00% decrease in age-standardized death rate (ASDR) for RHD, but a small and non-significant decrease (-3.00%) in the ASDR for NRVHD. The global age-standardized disability-adjusted life years (DALY) rate of RHD decreased by 53.52%, while there was a 12.62% reduction in the age-standardized DALY rate of NRVHD. The burden from different VHDs demonstrated a diverse change at a global level between 1990 and 2017. Although RHD burden has an obvious means of mitigation, a substantially high incidence of NRVHD was observed over this time period, especially in the elderly, which may lead to high health care costs and signify the potential for even higher costs in the future.