Bio-Inspired Preparation of Clay–Hexacyanoferrate Composite Hydrogels as Super Adsorbents for Cs+

A facile and low-cost fabrication route, inspired by the adhesive proteins secreted by mussels, has been developed to prepare a clay-based composite hydrogel (DHG(Cu)) containing hexacyanoferrate (HCF) nanoparticles for the selective removal of Cs+ from contaminated water. Initially, montmorillonite was exfoliated prior to coating with a thin layer of polydopamine (PDOPA) via the self-polymerization of dopamine. Mixing the composite (D-clay) with the HCF precursor, followed by the addition of copper ions, led to the self-assembly of the polymer-coated exfoliated clay nanosheets into a three-dimensional network and in situ growth of KCuHCF nanoparticles embedded within the gel structure. Analytical characterization verified the fabrication route and KCuHCF immobilization by a copper–ligand complexation. Rheology testing revealed the composite hydrogel to be elastic under low strain and exhibited reversible, self-healing behavior following high strain deformation, providing a good retention of KCuHCF nanoparticles in the membrane. The adsorbent DHG(Cu) showed a superior Cs+ adsorption capacity (∼173 mg/g), with the performance maintained over a wide pH range, and an excellent selectivity for Cs+ when dispersed in seawater at low concentrations of 0.2 ppm. On the basis of its excellent mechanico-chemical properties, the fabricated hydrogel was tested as a membrane in column filtration, showing excellent removal of Cs+ from Milli-Q water and seawater, with the performance only limited by the fluid residence time. For comparison, the study also considered other composite hydrogels, which were fabricated as intermediates of DHG(Cu) or fabricated with Fe3+ as the cross-linker and reactant for HCF nanoparticle synthesis

Functional features of an ssi signal of plasmid pGKV21 in Escherichia coli

A single-strand initiation (ssi) signal was detected on the Lactococcus lactis plasmid pGKV21 containing the replicon of pWV01 by its ability to complement the poor growth of an M13 phage derivative (M13??lac182) lacking the complementary-strand origin in Escherichia coli. This ssi signal was situated at the 229-nucleotide (nt) DdeI-DraI fragment and located within the 109 nt upstream of the nick site of the putative plus origin. SSI activity is orientation specific with respect to the direction of replication. We constructed an ssi signal-deleted plasmid and then examined the effects of the ssi signal on the conversion of the single-stranded replication intermediate to double-stranded plasmid DNA in E. coli. The plasmid lacking an ssi signal accumulated much more plasmid single-stranded DNA than the wild-type plasmid did. Moreover, deletion of this region caused a great reduction in plasmid copy number or plasmid maintenance. These results suggest that in E. coli, this ssi signal directs its lagging-strand synthesis as a minus origin of plasmid pGKV21. Primer RNA synthesis in vitro suggests that E. coli RNA polymerase directly recognizes the 229-nt ssi signal and synthesizes primer RNA dependent on the presence of E. coli single-stranded DNA binding (SSB) protein. This region contains two stem-loop structures, stem-loop I and stem-loop II. Deletion of stem-loop I portion results in loss of priming activity by E. coli RNA polymerase, suggesting that stem-loop I portion is essential for priming by E. coli RNA polymerase on the SSB-coated single-stranded DNA template.open5

The Cell Shape-determining Csd6 Protein from Helicobacter pylori Constitutes a New Family of L,D-Carboxypeptidase

Helicobacter pylori causes gastrointestinal diseases, including gastric cancer. Its high motility in the viscous gastric mucosa facilitates colonization of the human stomach and depends on the helical cell shape and the flagella. In H. pylori, Csd6 is one of the cell shape-determining proteins that play key roles in alteration of cross-linking or by trimming of peptidoglycan muropeptides. Csd6 is also involved in deglycosylation of the flagellar protein FlaA. To better understand its function, biochemical, biophysical, and structural characterizations were carried out. We show that Csd6 has a three-domain architecture and exists as a dimer in solution. The N-terminal domain plays a key role in dimerization. The middle catalytic domain resembles those of L,D-transpeptidases, but its pocket-shaped active site is uniquely defined by the four loops I to IV, among which loops I and III show the most distinct variations from the known L,D-transpeptidases. Mass analyses confirm that Csd6 functions only as an L,D-carboxypeptidase and not as an L,D-transpeptidase. The D-Ala-complexed structure suggests possible binding modes of both the substrate and product to the catalytic domain. The C-terminal nuclear transport factor 2-like domain possesses a deep pocket for possible binding of pseudaminic acid, and in silico docking supports its role in deglycosylation of flagellin. On the basis of these findings, it is proposed that H. pylori Csd6 and its homologs constitute a new family of L,D-carboxypeptidase. This work provides insights into the function of Csd6 in regulating the helical cell shape and motility of H. pylori.1165Ysciescopu

Seed-layer mediated orientation evolution in dielectric Bi-Zn-Ti-Nb-O thin films

Highly (hhh) -oriented pyrochlore Bi-Zn-Ti-Nb-O (BZTN) thin films were fabricated via metal-organic decomposition using orientation template layers. The preferred orientation was ascribed to the interfacial layer, the lattice parameter of which is similar to BZTN. High-resolution transmission electron microscopy supported that the interfacial layer consists of Bi and Pt. The (hhh) -oriented thin films exhibited a highly insulating nature enabling feasible applications in electronic devices, particularly voltage tunable application. The BZTN thin films did not show any apparent dielectric anisotropy and the slightly enhanced dielectric properties were discussed in connection to the internal stress and the grain boundary effect. © 2007 American Institute of Physics

Neural Tissue-Like, not Supraphysiological, Electrical Conductivity Stimulates Neuronal Lineage Specification through Calcium Signaling and Epigenetic Modification

Electrical conductivity is a pivotal biophysical factor for neural interfaces, though optimal values remain controversial due to challenges isolating this cue. To address this issue, conductive substrates made of carbon nanotubes and graphene oxide nanoribbons, exhibiting a spectrum of conductivities from 0.02 to 3.2 S m−1, while controlling other surface properties is designed. The focus is to ascertain whether varying conductivity in isolation has any discernable impact on neural lineage specification. Remarkably, neural-tissue-like low conductivity (0.02–0.1 S m−1) prompted neural stem/progenitor cells to exhibit a greater propensity toward neuronal lineage specification (neurons and oligodendrocytes, not astrocytes) compared to high supraphysiological conductivity (3.2 S m−1). High conductivity instigated the apoptotic process, characterized by increased apoptotic fraction and decreased neurogenic morphological features, primarily due to calcium overload. Conversely, cells exposed to physiological conductivity displayed epigenetic changes, specifically increased chromatin openness with H3acetylation (H3ac) and neurogenic-transcription-factor activation, along with a more balanced intracellular calcium response. The pharmacological inhibition of H3ac further supported the idea that such epigenetic changes might play a key role in driving neuronal specification in response to neural-tissue-like, not supraphysiological, conductive cues. These findings underscore the necessity of optimal conductivity when designing neural interfaces and scaffolds to stimulate neuronal differentiation and facilitate the repair process

Severity of Nonalcoholic Fatty Liver Disease is Associated with Development of Metabolic Syndrome: Results of a 5-Year Cohort Study

Aims: Nonalcoholic fatty liver disease (NAFLD) is considered to be a hepatic manifestation of metabolic syndrome (MS). However, a few studies have examined the effect of NAFLD on the development of MS. We evaluated the relationship between the development of MS and clinical severity of NAFLD according to alanine aminotransferase (ALT) levels. Methods: A retrospective cohort study was conducted. Participants who underwent abdominal ultrasonography and blood samplings for health check-ups both in 2005 and 2010 were recruited. NAFLD was diagnosed if a person showed fatty liver on ultrasonography without significant alcohol consumption. Subjects with MS at baseline were excluded. Results: A total of 2,728 subjects met the inclusion criteria. Fatty liver (FL) with normal ALT was found in 369 (13.5%) subjects and FL with elevated ALT in 328 (12.0%). During 5 years of follow up, 582 (21.3%) incident cases of MS developed between 2005 and 2010. The incidence of MS was higher in patients with NAFLD compared to control group (41.2% in FL with elevated ALT, 34.7% in FL with normal ALT and 15.7% in control, p<0.001). Multivariate analysis showed that odds ratio (OR) and 95% confidence interval (CI) for MS increased according to the severity of NAFLD [OR (95% CI), 1.29 (0.97−1.71) in FL with normal ALT and 1.54 (1.18−1.33) in FL with elevated ALT, p=0.01]. Conclusions: We have demonstrated that development of MS is significantly increased according to the clinical severity of NAFLD. These findings have implications in the clinical availability of NAFLD as a predictor of MS

Relationship between cloud condensation nuclei (CCN) concentration and aerosol optical depth in the Arctic region

To determine the direct and indirect effects of aerosols on climate, it is important to know the spatial and temporal variations in cloud condensation nuclei (CCN) concentrations. Although many types of CCN measurements are available, extensive CCN measurements are challenging because of the complexity and high operating cost, especially in remote areas. As aerosol optical depth (AOD) can be readily observed by remote sensing, many attempts have been made to estimate CCN concentrations from AOD. In this study, the CCN–AOD relationship is parameterized based on CCN ground measurements from the Zeppelin Observatory (78.91° N, 11.89° E, 474 m asl) in the Arctic region. The AOD measurements were obtained from the Ny-Ålesund site (78.923° N, 11.928° E) and Modern-Era Retrospective Analysis for Research and Applications, Version 2 reanalysis. Our results show a CCN–AOD correlation with a coefficient of determination R2 of 0.59. Three additional estimation models for CCN were presented based on the following data: (i) in situ aerosol chemical composition, (ii) in situ aerosol optical properties, and (iii) chemical composition of AOD obtained from reanalysis data. The results from the model using in situ aerosol optical properties reproduced the observed CCN concentration most efficiently, suggesting that the contribution of BC to CCN concentration should be considered along with that of sulfate

Response to imatinib rechallenge in a patient with a recurrent gastrointestinal stromal tumor after adjuvant therapy: a case report

<p>Abstract</p> <p>Introduction</p> <p>Adjuvant imatinib improves recurrence-free survival of patients following resection of primary KIT-positive gastrointestinal stromal tumors. However, it is unknown whether patients who previously received adjuvant imatinib therapy will respond to imatinib rechallenge as treatment for recurrent disease. Here we present the first report documenting the benefits of imatinib rechallenge in a patient previously exposed to imatinib during adjuvant treatment.</p> <p>Case presentation</p> <p>A 51-year-old Asian woman with a wedge-resected primary gastric gastrointestinal stromal tumor at high risk of relapse underwent two years of adjuvant treatment with imatinib. Only 10 months after the completion of adjuvant imatinib treatment, a computed tomography scan revealed gastrointestinal stromal tumor recurrence in this patient, with multiple peritoneal nodules in the upper abdomen being detected. Our patient was rechallenged with imatinib 400 mg/day and had a partial response after one month of treatment. Imatinib rechallenge was well tolerated by our patient; the only adverse events she experienced were grade 1 edema, anemia and fatigue. Our patient maintained a partial response two years and six months after the imatinib rechallenge. However, computed tomography scans three months later showed that our patient had disease progression.</p> <p>Conclusions</p> <p>This case report demonstrates that a patient with a gastrointestinal stromal tumor who had previously received adjuvant imatinib therapy responded to imatinib rechallenge as treatment for her recurrent disease. These results indicate that imatinib sensitivity can be maintained in a patient with previous exposure to adjuvant imatinib therapy.</p

Sphingosine 1-phosphate receptor 4 promotes nonalcoholic steatohepatitis by activating NLRP3 inflammasome

BACKGROUND & AIMS: Sphingosine 1-phosphate receptors (S1PRs) are a group of G-protein-coupled receptors that confer a broad range of functional effects in chronic inflammatory and metabolic diseases. S1PRs also may mediate the development of nonalcoholic steatohepatitis (NASH), but the specific subtypes involved and the mechanism of action are unclear. METHODS: We investigated which type of S1PR isoforms is activated in various murine models of NASH. The mechanism of action of S1PR4 was examined in hepatic macrophages isolated from high-fat, high-cholesterol diet (HFHCD)-fed mice. We developed a selective S1PR4 functional antagonist by screening the fingolimod (2-amino-2-[2-(4- n-octylphenyl)ethyl]-1,3-propanediol hydrochloride)-like sphingolipid-focused library. RESULTS: The livers of various mouse models of NASH as well as hepatic macrophages showed high expression of S1pr4. Moreover, in a cohort of NASH patients, expression of S1PR4 was 6-fold higher than those of healthy controls. S1pr4(++/-) mice were protected from HFHCD-induced NASH and hepatic fibrosis without changes in steatosis. S1pr4 depletion in hepatic macrophages inhibited lipopolysaccharide-mediated Ca++ release and deactivated the Nod-like receptor pyrin domaincontainning protein 3 (NLRP3) inflammasome. S1P increased the expression of S1pr4 in hepatic macrophages and activated NLRP3 inflammasome through inositol trisphosphate/inositol trisphosphate-receptor-dependent [Ca++] signaling. To further clarify the biological function of S1PR4, we developed SLB736, a novel selective functional antagonist of SIPR4. Similar to S1pr4(+/-) mice, administration of SLB736 to HFHCD-fed mice prevented the development of NASH and hepatic fibrosis, but not steatosis, by deactivating the NLRP3 inflammasome. CONCLUSIONS: S1PR4 may be a new therapeutic target for NASH that mediates the activation of NLRP3 inflammasome in hepatic macrophages