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.     

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.     

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.     

创建新事业失败有4大陷阱

大部分企业在进入新事业时都遭遇了失败。除了受机遇短缺和固有风险等不可抗拒因素影响外;还有一些悲剧原本可以规避,因为它们缘自管理者思考工作的方式     

The Role of the Choroid in Stargardt Disease

Stargardt disease is the commonest juvenile macular dystrophy. It is caused by genetic mutations in the ABCA4 gene. Diagnosis is not always straightforward, and various phenocopies exist. Late-onset disease can be misdiagnosed with age-related macular disease. A correct diagnosis is particularly critical because of emergent gene therapies. Stargardt disease is known to affect retinal pigment epithelium and photoreceptors. Many studies have also highlighted the importance of the choroid in the diagnosis, pathophysiology, and progression of the disease. The choroid is in an integral relationship with the retinal pigment epithelium and photoreceptors, and its possible involvement during the disease should be considered. The purpose of this review is to analyze the current diagnostic tools for choroidal evaluation and the extrapolation of useful data for ophthalmologists and researchers studying the disease.     

Creation and control of high-dimensional multi-partite classically entangled light

Vector beams, non-separable in spatial mode and polarisation, have emerged as enabling tools in many diverse applications, from communication to imaging. This a...