Flexible null test for form measurement of highly astigmatic surfaces

We report the application of interferometry to the form measurement of a family of highly astigmatic optical surfaces. These measurements are based on a null test that employs a double-pass off-axis test arrangement with a tilted test surface and a reference sphere. This arrangement provides a perfect null test for an ellipsoid of revolution, or prolate spheroid. Its application is illustrated in detail in the presentation of results for the measurement of a specific family of eight differing surfaces that are incorporated into the K-Band Multi-Object Spectrometer Integral Field Unit. All surfaces measured here are sufficiently close to a prolate spheroid to justify its practical application. We discuss the application of the technique as a flexible low-cost approach for the generation of null interferograms in the measurement of a variety of complex surfaces.     

Adsorption of Chromium (VI) Using an Activated Carbon Derived from Petroleum Coke Feedstock

This study aims to determine the main adsorption mechanism by which chromium (VI) is adsorbed onto the surface of a petroleum-coke sourced activated carbon, a feedstock not prevalent in current literature. The study also aims to produce an activated carbon adsorbent that is both cost-effective and efficient for the removal of chromium (VI) in neutral waters. The efficacy of thermally-treated petroleum coke-activated carbon and nitrogenated petroleum coke-activated carbon using ammonium chloride is compared to the efficacy of commercially available activated carbon. X-ray photoelectron spectroscopy of the activated carbons was obtained both before and after exposure to chromium (VI) for characterization of the materials and confirmation of chromium adsorption. The thermally-treated and nitrogenated activated carbons showed significant enhancement of chromium (VI) removal compared to the non-treated petroleum coke-activated carbon (22.4 mg/g, 21.9 mg/g, and 17.0 mg/g, respectively). However, there was no significant difference observed between the thermally-treated and nitrogenated materials. This indicates that the nitrogenation of the surface does not improve the adsorption capacity of the activated carbon, but rather the thermal treatment itself. X-ray photoelectron spectroscopy showed a significant increase in the alcohol functional groups on the surface of the activated carbon material as a result of the heat-treatment process; from 16.02 atomic percent in the non-treated activated carbon to 26.3 atomic percent in the thermally-treated activated carbon. The alcohol functional groups present on the surface allow for chromium (VI) to undergo reduction to chromium (III) under a similar mechanism to the well-known Jones Oxidation Reaction where the reduced chromium (III) species are then physisorbed to the surface of the activated carbon. XPS results are consistent with this as the chromium species present on the surface of the adsorbent is primarily Cr(OH)₃ (85.6% in the standard AC and 82.5% in the thermally-treated AC). Pseudo-first-order and pseudo-second-order kinetic modeling of the adsorbents indicate that they follow a pseudo-second-order reaction where the rate-limiting step is the chemical sorption of the adsorbate itself.     

Prevention of surface defects in calendered poly(vinyl chloride) sheets using a succinate-capped poly(caprolactone) additive

Surface defects known as “gas checks” often mar the surfaces of poly(vinyl chloride) (PVC) calendered films. These defects are typically prevented through changes in the calender operating parameters, a costly exercise which also limits the sheet thickness and the production rate. Adding a low concentration of poly(caprolactone) (PCL)-based star-shaped compound can eliminate gas check defects in PVC calendering. The effects of a triheptylsuccinate-terminated PCL with a PCL triol core and number average molecular weight of 540 g/mol (i.e., PCL₅₄₀-[(succ)-C₇]₃) has been investigated on the material, thermal, and processing properties of PVC blends containing diisononyl phthalate (DINP) as a primary plasticizer and PCL₅₄₀-[(succ)-C₇]₃ in low quantities (i.e., 0, 5, or 10 parts per hundred rubber (phr)) as a secondary plasticizer and processing aid. The most significant differences between PVC blends containing PCL₅₄₀-[(succ)-C₇]₃ and those without are in the rheological properties of the PVC blends at higher temperatures and lower angular frequencies. Under these conditions, PVC blends containing 10 phr of PCL₅₄₀-[(succ)-C₇]₃ have a complex viscosity nearly three times higher than those containing only DINP. PVC/PCL₅₄₀-[(succ)-C₇]₃ blends had comparable tensile properties to those containing only DINP, with no significant change in maximum elongation and a small but significant increase of 28% in maximum stress. The addition of PCL₅₄₀-[(succ)-C₇]₃ made it possible to produce calendered films without gas checks that were twice as thick as those produced in its absence. In addition to reduced wastage of marred films, the increased calender operating range for PVC films containing PCL₅₄₀-[(succ)-C₇]₃ has the potential to significantly reduce energy costs for the calendering of thick PVC films.     

Genetic Variants Associated with Long-Terminal Repeats Can Diagnostically Classify Cannabis Varieties

Cannabis sativa (Cannabis) has recently been legalized in multiple countries globally for either its recreational or medicinal use. This, in turn, has led to a marked increase in the number of Cannabis varieties available for use in either market. However, little information currently exists on the genetic distinction between adopted varieties. Such fundamental knowledge is of considerable value and underpins the accelerated development of both a nascent pharmaceutical industry and the commercial recreational market. Therefore, in this study, we sought to assess genetic diversity across 10 Cannabis varieties by undertaking a reduced representation shotgun sequencing approach on 83 individual plants to identify variations which could be used to resolve the genetic structure of the assessed population. Such an approach also allowed for the identification of the genetic features putatively associated with the production of secondary metabolites in Cannabis. Initial analysis identified 3608 variants across the assessed population with phylogenetic analysis of this data subsequently enabling the confident grouping of each variety into distinct subpopulations. Within our dataset, the most diagnostically informative single nucleotide polymorphisms (SNPs) were determined to be associated with the long-terminal repeat (LTRs) class of retroelements, with 172 such SNPs used to fully resolve the genetic structure of the assessed population. These 172 SNPs could be used to design a targeted resequencing panel, which we propose could be used to rapidly screen different Cannabis plants to determine genetic relationships, as well as to provide a more robust, scientific classification of Cannabis varieties as the field moves into the pharmaceutical sphere.     

EPLIN,a Putative Tumour Suppressor in Colorectal Cancer,Implications in Drug Resistance

Colorectal cancer is a serious threat to human health. Poor prognosis and frequently reported drug resistance urges research into novel biomarkers and mechanisms to aid in the understanding of the development and progression of colorectal cancer and to optimise therapeutic strategies. In the current study, we investigated the roles of a putative tumour suppressor, EPLIN, in colorectal cancer. Our clinical colorectal cancer cohort and online databases revealed a downregulation of EPLIN in colorectal cancer tissues compared with normal tissues. The reduced expression of EPLIN was associated with poor clinical outcomes of patients. In vitro cellular function assays showed that EPLIN elicited an inhibitory effect on cellular growth, adhesion, migration and invasion. Utilising a protein microarray on protein samples from normal and tumour patient tissues suggested HSP60, Her2 and other signalling events were novel potential interacting partners of EPLIN. It was further revealed that EPLIN and HSP60 were negative regulators of Her2 in colorectal cancer cells. The clinical cohort also demonstrated that expression of HSP60 and Her2 affected clinical outcomes, but most interestingly the combination of EPLIN, HSP60 and Her2 was able to identify patients with the most unfavourable clinical outcome by independently predicting patient overall survival and disease free survival. Furthermore, EPLIN and HSP60 exhibited potential to regulate cellular response to chemotherapeutic and EGFR/Her2 targeted therapeutic agents. In conclusion, EPLIN is an important prognostic factor for patients with colon cancer and reduced EPLIN in CRC contributes to aggressive traits of CRC cells and their responses to chemotherapeutic drugs. Collectively, EPLIN is a pivotal factor for the development and progression of colorectal cancer and has important clinical and therapeutic values in this cancer type.     

eDNA,Amyloid Fibers and Membrane Vesicles Identified in Pseudomonas fluorescens SBW25 Biofilms

Pseudomonas fluorescens SBW25 is a model soil- and plant-associated bacterium capable of forming a variety of air–liquid interface biofilms in experimental microcosms and on plant surfaces. Previous investigations have shown that cellulose is the primary structural matrix component in the robust and well-attached Wrinkly Spreader biofilm, as well as in the fragile Viscous Mass biofilm. Here, we demonstrate that both biofilms include extracellular DNA (eDNA) which can be visualized using confocal laser scanning microscopy (CLSM), quantified by absorbance measurements, and degraded by DNase I treatment. This eDNA plays an important role in cell attachment and biofilm development. However, exogenous high-molecular-weight DNA appears to decrease the strength and attachment levels of mature Wrinkly Spreader biofilms, whereas low-molecular-weight DNA appears to have little effect. Further investigation with CLSM using an amyloid-specific fluorophore suggests that the Wrinkly Spreader biofilm might also include Fap fibers, which might be involved in attachment and contribute to biofilm strength. The robust nature of the Wrinkly Spreader biofilm also allowed us, using MALDI-TOF mass spectrometry, to identify matrix-associated proteins unable to diffuse out of the structure, as well as membrane vesicles which had a different protein profile compared to the matrix-associated proteins. CLSM and DNase I treatment suggest that some vesicles were also associated with eDNA. These findings add to our understanding of the matrix components in this model pseudomonad, and, as found in other biofilms, biofilm-specific products and material from lysed cells contribute to these structures through a range of complex interactions.     

Cerebral Folate Metabolism in Post-Mortem Alzheimer’s Disease Tissues: A Small Cohort Study

We investigated the cerebral folate system in post-mortem brains and matched cerebrospinal fluid (CSF) samples from subjects with definite Alzheimer’s disease (AD) (n = 21) and neuropathologically normal brains (n = 21) using immunohistochemistry, Western blot and dot blot. In AD the CSF showed a significant decrease in 10-formyl tetrahydrofolate dehydrogenase (FDH), a critical folate binding protein and enzyme in the CSF, as well as in the main folate transporter, folate receptor alpha (FRα) and folate. In tissue, we found a switch in the pathway of folate supply to the cerebral cortex in AD compared to neurologically normal brains. FRα switched from entry through FDH-positive astrocytes in normal, to entry through glial fibrillary acidic protein (GFAP)-positive astrocytes in the AD cortex. Moreover, this switch correlated with an apparent change in metabolic direction to hypermethylation of neurons in AD. Our data suggest that the reduction in FDH in CSF prohibits FRα-folate entry via FDH-positive astrocytes and promotes entry through the GFAP pathway directly to neurons for hypermethylation. This data may explain some of the cognitive decline not attributable to the loss of neurons alone and presents a target for potential treatment.     

The EcpD Tip Adhesin of the Escherichia coli Common Pilus Mediates Binding of Enteropathogenic E. coli to Extracellular Matrix Proteins

The attachment of enteropathogenic Escherichia coli (EPEC) to intestinal epithelial cells is facilitated by several adhesins; however, the individual host-cell receptors for pili-mediated adherence have not been fully characterized. In this study, we evaluated the hypothesis that the E. coli common pilus (ECP) tip adhesin protein EcpD mediates attachment of EPEC to several extracellular matrix (ECM) glycoproteins (fibronectin, laminin, collagens I and IV, and mucin). We found that the ΔecpA mutant, which lacks production of the EcpA filament but retains EcpD on the surface, adhered to these glycoproteins below the wild-type levels, while the ΔecpD mutant, which does not display EcpA or EcpD, bound significantly less to these host glycoproteins. In agreement, a purified recombinant EcpD subunit bound significantly more than EcpA to laminin, fibronectin, collagens I and IV, and mucin in a dose-dependent manner. These are compelling data that strongly suggest that ECP-producing EPEC may bind to host ECM glycoproteins and mucins through the tip adhesin protein EcpD. This study highlights the versatility of EPEC to bind to different host proteins and suggests that the interaction of ECP with the host’s ECM glycoproteins may facilitate colonization of the intestinal mucosal epithelium.     

Glial Cell-Mediated Neuroinflammation in Alzheimer’s Disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder; it is the most common cause of dementia and has no treatment. It is characterized by two pathological hallmarks, the extracellular deposits of amyloid beta (Aβ) and the intraneuronal deposits of Neurofibrillary tangles (NFTs). Yet, those two hallmarks do not explain the full pathology seen with AD, suggesting the involvement of other mechanisms. Neuroinflammation could offer another explanation for the progression of the disease. This review provides an overview of recent advances on the role of the immune cells’ microglia and astrocytes in neuroinflammation. In AD, microglia and astrocytes become reactive by several mechanisms leading to the release of proinflammatory cytokines that cause further neuronal damage. We then provide updates on neuroinflammation diagnostic markers and investigational therapeutics currently in clinical trials to target neuroinflammation.