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Na 2 Ti 4 O 9 (NTO), an important chemical material, is used in chemical pigments, lithium ion batteries, catalyst carriers, and other fields. Nanoscale NTO crystal was firstly obtained by solvothermal process in this study, and the reactant conditions (time, temperature, solvent, and concentration of NaOH solution) for preparing NTO crystal were investigated. The result reveals that the as-prepared NTO crystal with one-dimensional (1D) rod-like morphology can be obtained in a solvent environment with H 2 O to C 2 H 5 OH via solvothermal process. And then investigating the formation mechanism of 1D NTO crystal based on the solvothermal soft chemical method. In addition, NTO crystal was utilized as the precursor for BaTiO 3 (BT) crystal at desired condition. The [010]-oriented BT polycrystals were directly obtained with NTO precursor via hydrothermal process in low concentration of Ba(OH) 2 solution. The transformation mechanism between BT polycrystals and NTO precursor was revealed, and the process of obtaining functional materials directly from NTO precursor was discussed. The study provides a novel way for the development of small-size barium titanate based functional materials. [ABSTRACT FROM AUTHOR]

Low-temperature co-fired ceramics (LTCC) with adjustable coefficients of thermal expansion (CTE) based on Li 2 O–BaO–Al 2 O 3 –B 2 O 3 –SiO 2 /quartz LTCC composites (glass/ceramics) have been employed in electronic packaging to address the interface thermal mismatch problem caused by different thermal expansion coefficients. In the present study, sintering behavior, phase structure, and CTE of LTCC composites is controlled by replacing quartz partly with α-Al 2 O 3 or ZrO 2. Accordingly, LTCC composites with the highest and lowest CTE values are achieved. The results show that the major phases of α-Al 2 O 3 substituted LTCC composites are hexacelsian, β-spodumene, and virgilite. Correspondingly, CTE values are in the range of 5.67–8.62 × 10−6/°C. Whereas, ZrO 2 substituted LTCC composites have exhibited increased CTE values to 12.27 to 13.2 × 10−6/°C with major phases of cristobalite, hexacelsian, and bazirite. Moreover, the negative effects of phase transformation of hexacelsian can be inhibited to a certain extent upon substitution of α-Al 2 O 3 up to 15 wt%. This work provides suitable methods for preparing LTCC composites with gradient CTE and resolving the thermal mismatch effects at different interfaces (e.g., chip/LTCC, metal electrode/LTCC) in electronic packaging structures. [ABSTRACT FROM AUTHOR]

A 3-year-old male Bichon Frise developed lethargy, anorexia and haematuria. B-scan ultrasonography examination revealed a small, irregular, soft-textured mass in the bladder. Histopathologically, there was an incomplete fibrous pseudocapsule around the tumour tissue and although there was clear demarcation from the surrounding tissue, there was invasion of the capsule. Tumour cells proliferated in nests or cords of variable size, separated by fibrovascular tissue. The neoplastic cells were immunopositive for chromogranin A, synaptophysin and neuron-specific enolase, and electron microscopy revealed that they contained cytoplasmic secretory granules. On the basis of these findings, the tumour was diagnosed as a primary paraganglioma of the urinary bladder. [ABSTRACT FROM AUTHOR]

In this work, by focusing on widespread problem of thermal mismatch caused by different coefficients of thermal expansion (CTE) in electronic packaging materials, low-temperature co-fired ceramic (LTCC) materials with tunable CTE values were designed. By substituting Ba2+ with Sr2+ and replacing quartz with alumina and zirconia, respectively, BaO–Al 2 O 3 –SiO 2 –B 2 O 3 /quartz LTCC composites with CTE of 7.05–9.52 × 10−6/°C were developed. Results show that major crystalline phases of LTCC composite materials are quartz and hexacelsian. By replacing quartz with alumina or zirconia, sintering behavior and subsequently thermal expansion and dielectric properties were modulated. On the other hand, substituting Ba2+ with Sr2+ can be beneficial to the densification of composite materials. The introduction of Sr2+ triggered mixed alkali effect and hindered the crystallization of hexacelsian phase, which can further improve mechanical properties. Finally, sandwich structure module of BaO–Al 2 O 3 –SiO 2 –B 2 O 3 /quartz with gradient CTE values was obtained, which showed potential for electronic packaging with sustained thermal compatibility under cyclic temperatures. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) continues to be a major healthcare problem and there is much to be explored regarding the secondary pathobiology to identify early predictive markers and new therapeutic targets. While documented changes in thrombosis and inflammation in major trauma have been well described, growing evidence suggests that isolated TBI also results in systemic alterations in these mechanisms. Here, we review recent experimental and clinical findings that demonstrate how blood-brain barrier dysfunction, systemic immune response, inflammation, platelet activation, and thrombosis contribute significantly to the pathogenesis of TBI. Despite advances in the links between thrombosis and inflammation, there is a lack of treatment options aimed at both processes and this could be crucial to treating vascular injury, local and systemic inflammation, and secondary ischemic events following TBI. With emerging evidence of newly-identified roles for platelets, leukocytes, the coagulation system and extracellular vesicles in processes of inflammation and thrombosis, there is a growing need to characterize these mechanisms within the context of TBI and whether these changes persist into the chronic phase of injury. Importantly, this review defines areas in need of further research to advance the field and presents a roadmap to identify new diagnostic and treatment options for TBI. • Traumatic brain injury (TBI) results in systemic alterations and complications. • Blood-brain barrier dysfunction after TBI drives thrombosis and inflammation. • Thromboinflammation is propagated by brain-derived extracellular vesicles. • Therapeutics are in development to target inflammation and coagulopathy. • Investigation of thromboinflammation after repetitive mild TBI is needed. [ABSTRACT FROM AUTHOR]

In order to demonstrate effectiveness of vibratory probe compaction at silt deposit, a self-developed vibratory probe with cross section and compaction equipment were adopted to treat silt deposit at Suqian-Xinyi Expressway liquefiable site in China. Field pilot tests were conducted to study spatial variation of compaction effect. It is shown that strength increase at vibration point is largest after ground improvement, while a small increase occured at 1m, but not 2m from vibration point. The radial influence range and effective reinforcement radius are 2m and 1m. The largest settlement is in a zone within a radius about twice the probe diameter. The major settlement occurred immediately after compaction, slightly increased with time. [ABSTRACT FROM AUTHOR]

A new polysaccharide (JSP-11) with a molecular weight of 1.25 × 10 6 Da was extracted and purified from jellyfish. Monosaccharide analysis showed that JSP-11 was composed of mannose, galactose and glucuronic acid with a molar ratio of 2.18:1.00:1.94. According to the analysis of fourier transform-infrared spectroscopy, methylation analysis, and NMR spectroscopy, JSP-11 was determined to contain a linear backbone which consisted of (1 → 3,6)-linked β - d -Man p and (1 → 6)-linked β - d -Gal p . The branch of (1→)-linked α- d -Glc p A was attached to the C-3 position of (1 → 3,6)-linked β - d -Man p in the backbone. The immunomodulatory assay exhibited that JSP-11 could significantly enhance the viability of RAW 264.7 macrophage cells, and promote the release of NO, TNF-α, and IL-1 β via activating NF- κ B, MAPKs and PI3K/Akt signal pathways. [ABSTRACT FROM AUTHOR]

Gold-silver bimetallic fluorescence quenching nanoprobe has been synthesized based on the gold triangular nanoplate with silver coating. In order to guarantee the specificity of the probe, surface modifications of the triangular nanoplates including carboxyl replacement, carboxyl activation and antibody connection have been carried out. The fluorescence spectral study indicates that the fluorescence intensity of carcinoembryonic antigen (CEA) could be effectively quenched by the silver coated-gold triangular nanoprobe. And the fluorescence quenching ability could be improved by optimizing the interaction time and amount of binding anti-CEA to modified nanoprobe, and the interaction time of binding CEA to anti-CEA. By using this sensing method, the CEA could be detected with an ultra low detection limit of 10 pg/mL, and the linear range spans a scope from 20 to 200 pg/mL. Interference experiment results show that the influence from the interfering proteins could be neglected in the detection procedure. And the CEA could be specifically detected by using this bimetallic triangular nanoplate probe. [ABSTRACT FROM AUTHOR]

In this work, a novel water-soluble homogeneous polysaccharide (LJP-31) with a molecular mass of 2.24 × 10 6 Da was isolated and purified from Laminaria japonica using DEAE-cellulose and Sephacryl S500 chromatography. Results showed that LJP-31 mainly consists of arabinose, mannose, glucose and galactose in a molar ratio of 1.0:7.8:6.6:0.8. LJP-31 exhibited significant stimulation on macrophages and enhanced the production of NO, TNF-α, IL-1β, IL-6 and IL-10 as well as the up-regulation of their gene expressions. Western blot analysis suggested that LJP-31 has the positive effects on the translocation of NF-κB p65 from cytoplasm to nucleus and the phosphorylation of IκBα, ERK1/2, JNK1/2 and P38 in macrophages. Flow cytometric and confocal laser-scanning microscopy analysis indicated that toll-like receptor 4 (TLR4) was at least one of the recognition receptors of LJP-31 on the plasma membrane of macrophages. Taken together, LJP-31 may exert its immunostimulating potency via TLR4 activation of MAPK and NF-κB signaling pathways. [ABSTRACT FROM AUTHOR]

Binding of platelet glycoprotein Ibα (GPIbα) to von Will-ebrand factor (VWF) initiates platelet adhesion to disrupted vascular surface under arterial blood flow. Flow exerts forces on the platelet that are transmitted to VWF-GPIbα bonds, which regulate their dissociation. Mutations in VWF and/or GPIbα may alter the mechanical regulation of platelet adhesion to cause hemostatic defects as found in patients with von Willebrand disease (VWD). Using a biomembrane force probe, we observed biphasic force-decelerated (catch) and force-accelerated (slip) dissociation of GPIbα from VWF. The VWF A1 domain that contains the N-terminal flanking sequence Gln1238-Glu1260 (1238-A1) formed triphasic slip-catch-slip bonds with GPIbα. By comparison, using a shortformof A1 that deletes this sequence (1261-A1) abolished the catch bond, destabilizing its binding to GPIbα at high forces. Importantly, shear-dependent platelet rolling velocities on these VWF ligands in a flow chamber system mirrored the force-dependent single-bond lifetimes. Adding the Gln1238-Glu1260 peptide, which interacted with GPIbα and 1261-A1 but not 1238-A1, to whole blood decreased platelet attachment under shear stress. Soluble Gln1238-Glu1260 reduced the lifetimes of GPIbα bonds with VWF and 1238-A1 but rescued the catch bond of GPIbα with 1261-A1. A type 2B VWD 1238-A1 mutation eliminated the catch bond by prolonging lifetimes at low forces, a type 2M VWD 1238-A1 mutation shifted the respective slip-catch and catch-slip transition points to higher forces, whereas a platelet type VWD GPIbα mutation enhanced the bond lifetime in the entire force regime. These data reveal the structural determinants of VWF activation by hemodynamic force of the circulation. [ABSTRACT FROM AUTHOR]

ABSTRACT: The renin–angiotensin–aldosterone system (RAAS) is known to be closely linked to the pathogenesis of insulin resistance. The angiotensin (Ang) II type 1 (AT1) receptor mediates the major effects of Ang II in adipose tissue, and blockade of the AT1 receptor improves insulin sensitivity, with enhanced adipocyte differentiation. In contrast, the role of angiotensin type 2 (AT2) receptor activation in insulin sensitivity is still controversial, although AT2 receptor functions are thought to be mutually antagonistic against those of the AT1 receptor in the cardiovascular system. Aldosterone exerts its biological roles via the mineralocorticoid receptor (MR), and inhibition of MR signaling in adipose tissue ameliorates inflammation, with upregulation of insulin-mediated glucose transport and adipocyte differentiation. Clinical studies indicate that blockade of RAAS prevents the new onset of type 2 diabetes and improves the metabolic syndrome in diabetic patients. We here review the recent concepts of the roles of RAAS in adipose tissue. [Copyright &y& Elsevier]

Abstract: Variability in patient drug responses is observed with increasing frequency, necessitating the establishment of causal associations between factors and drug response phenotypes. This individual variability can be caused by genetic factors and environmental factors (ENFs). Although pharmacogenetics has been instrumental in describing genetic variations, frameworks for understanding the association between ENFs (particularly chemical ENFs) and drug responses are lacking. In this study, we constructed a novel database, DEER, for interpretations of chemical ENF effects on drug responses. DEER includes computational predictions of the associations between chemical ENFs and drug responses. Putative regulatory intermediates such as transcription factors, cytochrome P450s (CYPs), drug targets, and transporters as well as chemical similarities are provided to support our predictions. DEER currently encompasses 579 drugs, 401 chemical ENFs, and 9247 predicted drug–ENF associations. The entire dataset can be easily queried through a search page. The results can be downloaded, and each drug–ENF association with intermediary factors can be displayed via a graphical viewer. DEER is available at http://bsb.kiz.ac.cn:90/DEER/. We expect this approach and resource to be valuable for personalized medicine and drug development. [Copyright &y& Elsevier]

Abstract: Additional beneficial effects of angiotensin II type 1 (AT1) receptor blockers beyond AT1 receptor blockade have been highlighted. Irbesartan is reported to act as an antagonist of the monocyte chemoattractant protein-1 (MCP-1) receptor, C-C chemokine receptor 2 (CCR2). We examined the possible synergistic effects of the combination of irbesartan with rosuvastatin on preventing vascular remodeling focusing on the MCP-1/CCR2 pathway. We observed that administration of irbesartan and CCR2 antagonist, propagermanium, at noneffective doses, decreased the neointima with a decrease in PCNA labeling index in the injured mouse femoral artery induced by cuff placement. We also observed that administration of a noneffective dose of rosuvastatin with propagermanium decreased the neointima area, suggesting that the inhibitory effect of rosuvastatin on neointima formation is at least partly attributable to blockade of the MCP-1/CCR2 pathway. Moreover, we demonstrated that the combination of irbesartan with rosuvastatin decreased neointima formation. MCP-1 mRNA level was significantly increased in injured femoral arteries, and administration of irbesartan with rosuvastatin decreased the mRNA levels of MCP-1, TNFα, and IL-1β, and increased PPARγ mRNA expression. These results suggest that the synergistic inhibitory effects of irbesartan with rosuvastatin on neointima formation may involve attenuation of MCP-1/CCR2 signaling. [Copyright &y& Elsevier]

Abstract: An adverse relationship between suboptimal fetal environments and the development of adult diseases, such as hypertension, type II diabetes, and cardiovascular disease, has been reported in numerous studies. The purpose of this study was to investigate the strain difference of offspring’s response to maternal malnutrition during pregnancy and the involvement of the renin-angiotensin system (RAS) in the development of adult hypertension using C57BL/6J (C57) mice and angiotensin II (Ang II) type 1 receptor-associated protein-transgenic (ATRAP-Tg) mice. Pregnant dams were fed an isocaloric diet containing either 20% (normal protein; NP) or 8% (low protein; LP) protein. Birth weight was significantly reduced in C57-LP offspring, but not in ATRAP-Tg-LP offspring. Arterial blood pressure was higher in C57-LP offspring than in the other groups. In contrast, ATRAP-Tg-LP offspring did not show an increase in blood pressure compared with NP offspring. Renal angiotensin II type 1 (AT1) receptor expression was not altered by maternal malnutrition, whereas angiotensin II type 2 receptor expression was significantly decreased in C57-LP offspring. In conclusion, these findings suggest that a suboptimal intrauterine environment induces adult hypertension because of an alteration of expression of RAS components, which was partly suppressed by sustained ATRAP overexpression via attenuation of the AT1 receptor-mediated pathological response. [Copyright &y& Elsevier]

Abstract: Angiotensin II type 2 (AT2) receptor-interacting protein (ATIP), which interacts with the C-terminal tail of the AT2 receptor, regulates the functions of the AT2 receptor. We have reported that AT2 receptor stimulation attenuated vascular senescence. Therefore, we examined the possible negative role of ATIP in regulating vascular senescence. We generated ATIP-transgenic (Tg) mice, and cultured vascular smooth muscle cells (VSMCs). Persistent angiotensin II stimulation induced increases in SA-β-gal–positive cells and the level of a DNA damage marker, 8-OHdG in VSMC, whereas these effects of angiotensin II were attenuated in VSMC prepared from ATIP-Tg mice. Angiotensin II treatment also upregulated the expression of methyl methanesulfonate-sensitive 2 (MMS2), a DNA repair factor, and Src homology 2 domain-containing protein-tyrosine phosphatase 1 (SHP-1) activity, whereas these effects of angiotensin II were further enhanced in ATIP-Tg VSMC. In vivo, x-ray irradiation to mice caused increases in SA-β-gal–positive area and 8-OHdG level in the thoracic aorta; however, these effects were reduced in ATIP-Tg mice, with a significant increase in MMS2 expression. These results suggest that ATIP could inhibit VSMC senescence, involving MMS2 expression and SHP-1 activity. ATIP might be a new therapeutic molecule to treat vascular aging and age-related vascular diseases. [Copyright &y& Elsevier]