Double scaffold networks regulate edible Pickering emulsion gel for designing thermally actuated 4D printing

3D and 4D printing of emulsion gels can be achieved by controlling the continuous phase and the interface. Edible high internal phase water-in-oil Pickering emulsion gels (PEGs) with a tunable double scaffold network structure are designed and prepared by food-grade phytosterol nanoparticles (PPs). In PEGs, PPs through hydrogen bonding enable binding of emulsion droplets to form the first scaffold network, giving PEGs high viscoelasticity for 3D printing. In the continuous oil phase, palm kernel stearin (PKST) can crystallize forming the second scaffold network of crystals to reinforce 3D printed objects of PEGs. The PEG can be used as a biocompatible template to engineer edible and rigid porous materials with adjustable strength and pore size depending on the degree of curing. 4D printing of PEGs is achieved by the thermal response of the PKST crystal network, leading to the unlimited potential of highly biocompatible PEGs in many applications

Carbapenem and cefoxitin resistance of Klebsiella pneumoniae strains associated with porin OmpK36 loss and DHA-1 β-lactamase production

Clinical isolates of carbapenem-resistant Klebsiella pneumoniae (K. pneumoniae) strains are being increased worldwide. Five pan-resistant K. pneumoniae strains have been isolated from respiratory and ICU wards in a Chinese hospital, and reveal strong resistance to all β-lactams, fluoroquinolones and aminoglycosides. Totally 27 β-lactamase genes and 2 membrane pore protein (porin) genes in 5 K. pneumoniae strains were screened by polymerase chain reaction (PCR). The results indicated that all of 5 K. pneumoniae strains carried blaTEM-1 and blaDHA-1 genes, as well as base deletion and mutation of OmpK35 or OmpK36 genes. Compared with carbapenem-sensitive isolates by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), the resistant isolates markedly lacked the protein band of 34-40 kDa, which might be the outer membrane proteins of OmpK36 according to the electrophoresis mobility. In addition, the conjugation test was confirmed that blaDHA-1 mediated by plasmids could be transferred between resistant and sensitive strains. When reserpine (30 µg/mL) and carbonyl cyanide m-chlorophenylhydrazone (CCCP) (50 µg/mL) were added in imipenem and meropenem, the MICs had no change against K. pneumoniae strains. These results suggest that both DHA-1 β-lactamase and loss or deficiency of porin OmpK36 may be the main reason for the cefoxitin and carbapenem resistance in K. pneumoniae strains in our hospital

Higher visceral adiposity index is associated with increased likelihood of abdominal aortic calcification

Background: The negative effects of visceral adiposity accumulation on cardiovascular health have drawn much attention. However, the association between the Visceral Adiposity Index (VAI) and Abdominal Aortic Calcification (AAC) has never been reported before. The authors aimed to investigate the association between the VAI and AAC in US adults. Methods: Cross-sectional data were derived from the 2013 to 2014 National Health and Nutrition Examination Survey (NHANES) of participants with complete data of VAI and AAC scores. Weighted multivariable regression and logistic regression analysis were conducted to explore the independent relationship between VAI and AAC. Subgroup analysis and interaction tests were also performed. Results: A total of 2958 participants were enrolled and participants in the higher VAI tertile tended to have a higher mean AAC score and prevalence of severe AAC. In the fully adjusted model, a positive association between VAI and AAC score and severe AAC was observed (β = 0.04, 95% CI 0.01‒0.08; OR = 1.04, 95% CI 1.01‒1.07). Participants in the highest VAI tertile had a 0.41-unit higher AAC score (β = 0.41, 95% CI 0.08‒0.73) and a significantly 68% higher risk of severe AAC than those in the lowest VAI tertile (OR = 1.68, 95% CI 1.04‒2.71). Subgroup analysis and interaction tests indicated that there was no dependence for the association of VAI and AAC. Conclusion: Visceral adiposity accumulation evaluated by the VAI was associated with a higher AAC score and an increased likelihood of severe AAC

Characterizing the heterogeneity of karst critical zone and its hydrological function:an integrated approach

Spatial heterogeneity in the subsurface of karst environments is high, as evidenced by the multi‐phase porosity of carbonate rocks and complex landform features that result in marked variability of hydrological processes in space and time. This includes complex exchange of various flows (e.g. fast conduit flows and slow fracture flows) in different locations. Here, we integrate various “state‐of‐the‐art” methods to understand the structure and function of this poorly‐constrained critical zone environment. Geophysical, hydrometric and tracer tools are used to characterize the hydrological functions of the cockpit karst critical zone in the small catchment of Chenqi, Guizhou province, China. Geophysical surveys, using electrical resistivity tomography (ERT), inferred the spatial heterogeneity of permeability in the epikarst and underlying aquifer. Water tables in depression wells in valley bottom areas, as well as discharge from springs on steeper hillslopes and at the catchment outlet, showed different hydrodynamic responses to storm event rainwater recharge and hillslope flows. Tracer studies using water temperatures and stable water isotopes (δD and δ18O) could be used alongside insights into aquifer permeability from ERT surveys to explain site‐ and depth‐dependent variability in the groundwater response in terms of the degree to which “new” water from storm rainfall recharges and mixes with “old” pre‐event water in karst aquifers. This integrated approach reveals spatial structure in the karst critical zone and provides a conceptual framework of hydrological functions across spatial and temporal scales

Effects of Expanded Hemodialysis with Medium Cut-Off Membranes on Maintenance Hemodialysis Patients: A Review

Kidney failure is associated with high morbidity and mortality. Hemodialysis, the most prevalent modality of renal replacement therapy, uses the principle of semipermeable membranes to remove solutes and water in the plasma of patients with kidney failure. With the evolution of hemodialysis technology over the last half century, the clearance of small water-soluble molecules in such patients is adequate. However, middle molecules uremic toxins are still retained in the plasma and cause cardiovascular events, anemia, and malnutrition, which significantly contribute to poor quality of life and high mortality in maintenance hemodialysis patients. A new class of membrane, defined as a medium cut-off (MCO) membrane, has emerged in recent years. Expanded hemodialysis with MCO membranes is now recognized as the artificial kidney model closest to natural kidney physiology. This review summarizes the unique morphological characteristics and internal filtration–backfiltration mechanism of MCO membranes, and describes their effects on removing uremic toxins, alleviating inflammation and cardiovascular risk, and improving quality of life in maintenance hemodialysis patients

S100A2 induces epithelial–mesenchymal transition and metastasis in pancreatic cancer by coordinating transforming growth factor β signaling in SMAD4-dependent manner

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive tumor and is associated with a poor prognosis. Treatment strategies for PDAC are largely ineffective primarily because of delay in its diagnosis and limited efficacy of systematic treatment. S100A2 is associated with the proliferation, migration, and differentiation of several tumors; however, its effects on PDAC and the associated molecular mechanisms remain to be explored. We studied the mechanisms underlying the effect of S100A2 on epithelial–mesenchymal transition (EMT) and metastasis in PDAC cells. We found that the level of S100A2 remarkably increased and was associated with poor PDAC prognosis. The overexpression of S100A2 in PANC-1 cells also induced EMT, in addition to increasing the invasion and migration of PDAC cells, whereas the knockdown of S100A2 markedly inhibited cell metastasis. Furthermore, S100A2 was found to enhance metastatic abilities in vivo. The overexpression of S100A2 increased SMAD4 expression, whereas the knockdown of S100A2 reduced SMAD4 expression. SMAD4 overexpression could effectively rescue the effects of S100A2 knockdown on EMT. S100A2 mechanistically activated the transforming growth factor (TGF)-β/Smad2/3 signaling pathway, upregulated SMAD4 expression, induced EMT, and increased PANC-1 cell metastasis. In conclusion, the S100A2/SMAD4 axis modulates EMT to accelerate PDAC development. Our results supplement and enrich the understanding of the pathogenesis underlying PDAC and provide a new theoretical basis and strategy targeting S100A2 for the diagnosis and treatment of PDAC