Electrochemical Analysis of Coffee

The objective of this study was to determine if there is a correlation between the chemical analysis of coffee and its variety of flavors. Different types of coffee have varying chemicals, with one of the components being the differing types and quantities of polyphenols. In order to study the correlation of coffee structure and flavor, electrochemical analysis of varying coffee samples was performed. The types of analyses utilized include Cyclic Voltammetry and UV Spectroscopy, along with pH. Cyclic Voltammetry was an excellent method since it is quick, easily performed, and cost effective. UV Spectroscopy was also used to compare the structures of the varying coffee types with the determined flavor profiles of each sample. The differing acidity and alkalinity between the coffee types may play a role in the taste of each sample, which was also analyzed in this study. Flavor profiles were determined by a panel of taste testers who were given specific parameters that were used to characterize the tastes of the coffees sampled. Although taste is usually subjective among individuals, the results of the electrochemical analyses were compared to the flavor profiles assigned to each sample

Biosensors Derived from Copolymers of Vinylferrocene with Various Para Substituted Phenylmaleimides

Smart Parking Lot is a product that allows the user to know how many parking spots are avail- able and where that parking is located. The Smart Parking Lot provides convenience and flexibility to the student efficient parking. People may spend a long time looking for parking that may or may not be available. This project allows drivers to avoid this annoyance by displaying how many parking spots are available at the lot entrance. There will be an application for a cell phone that provides the availability of parking before checking arrival

Novel Non-Halogenated Flame Retardant Compounds

Two different boron compounds, bis(tetramethylammonium) decaborate, TMAD, and bis (tetrabutylammonium) decaborate, TBAD were studied as potential replacements for halogenated flame retardants. Current commercially available, halogenated flame retardants are not environmentally friendly and release strong acids upon burning. TMAD and TBAD were combined with triphenylphosphine oxide and cast in polyurethane films at varying levels. These samples were then cut into strips and burned in a UL-94 flame chamber. These samples were also tested via TGA for degradation temperature. These varying levels were tested via several Design of Experiments constructed within Minitab software. Results thus far have shown the potential for these compound combinations to be used as flame retardants. Studies to determine the optimal ratio of additives for flame retardancy will be presente

Subjective well-being indicators for large-scale assessment of cultural ecosystem services

The substantial importance of cultural benefits as a source of human well-being is increasingly recognised in society-environment interactions. The integration of cultural ecosystem services (CES) into the ecosystem services framework remains a challenge due to the difficulties associated with defining, articulating and measuring CES. We operationalise a novel framework developed by the UK National Ecosystem Assessment that identifies CES as the interactions between environmental spaces (i.e. physical localities or landscapes), and the activities that occur there. We evaluate the benefits of the CES provided by 151 UK marine sites to recreational sea anglers and divers, using subjective well-being indicators. Factor analysis of an online questionnaire with 1220 participants revealed multiple CES benefits that contribute to human wellbeing e.g. including ‘engagement with nature’, ‘place identity’ and ‘therapeutic value’. In addition to regional differences, we also found that biophysical attributes of sites, such as the presence of charismatic species and species diversity, were positively associated with provision of CES benefits. The study provides evidence that could be used to inform designation of protected areas. The indicators used in the study may also be adapted for use across a range of marine and terrestrial spaces for improved integration of CES in environmental decisionmaking

What goes in does not always come out: The impact of the ruminant digestive system of sheep on plant material, and its importance for the interpretation of dung-derived archaeobotanical assemblages

On archaeological sites where livestock dung was a major fuel source, plant material that survives digestion intact may well be preserved in the remnants of dung-fuelled fires. Preserved plant remains which were derived from dung relate to the diet of animals, and thus provide a way of investigating the agro-pastoral economies of the past. In order to improve our understanding of the taphonomic processes to which plant material is exposed to during digestion, we applied archaeobotanical methods to the analysis of dung from sheep fed a known diet of cereal and wild plant material. Two clear patterns emerge from these investigations. First, cereal material (grain or chaff) survives digestion poorly and was rarely found in the dung analysed. Second, large proportions of seeds of various wild species survive digestion in an identifiable form, probably due to their small size and/or protective coating. These findings are crucial for reliable interpretation of dung-derived plant material in archaeological settings

Weak Responses to Auditory Feedback Perturbation during Articulation in Persons Who Stutter: Evidence for Abnormal Auditory-Motor Transformation

Previous empirical observations have led researchers to propose that auditory feedback (the auditory perception of self-produced sounds when speaking) functions abnormally in the speech motor systems of persons who stutter (PWS). Researchers have theorized that an important neural basis of stuttering is the aberrant integration of auditory information into incipient speech motor commands. Because of the circumstantial support for these hypotheses and the differences and contradictions between them, there is a need for carefully designed experiments that directly examine auditory-motor integration during speech production in PWS. In the current study, we used real-time manipulation of auditory feedback to directly investigate whether the speech motor system of PWS utilizes auditory feedback abnormally during articulation and to characterize potential deficits of this auditory-motor integration. Twenty-one PWS and 18 fluent control participants were recruited. Using a short-latency formant-perturbation system, we examined participants’ compensatory responses to unanticipated perturbation of auditory feedback of the first formant frequency during the production of the monophthong [ε]. The PWS showed compensatory responses that were qualitatively similar to the controls’ and had close-to-normal latencies (~150 ms), but the magnitudes of their responses were substantially and significantly smaller than those of the control participants (by 47% on average, p<0.05). Measurements of auditory acuity indicate that the weaker-than-normal compensatory responses in PWS were not attributable to a deficit in low-level auditory processing. These findings are consistent with the hypothesis that stuttering is associated with functional defects in the inverse models responsible for the transformation from the domain of auditory targets and auditory error information into the domain of speech motor commands

High-Content, High-Throughput Analysis of Cell Cycle Perturbations Induced by the HSP90 Inhibitor XL888

BACKGROUND: Many proteins that are dysregulated or mutated in cancer cells rely on the molecular chaperone HSP90 for their proper folding and activity, which has led to considerable interest in HSP90 as a cancer drug target. The diverse array of HSP90 client proteins encompasses oncogenic drivers, cell cycle components, and a variety of regulatory factors, so inhibition of HSP90 perturbs multiple cellular processes, including mitogenic signaling and cell cycle control. Although many reports have investigated HSP90 inhibition in the context of the cell cycle, no large-scale studies have examined potential correlations between cell genotype and the cell cycle phenotypes of HSP90 inhibition. METHODOLOGY/PRINCIPAL FINDINGS: To address this question, we developed a novel high-content, high-throughput cell cycle assay and profiled the effects of two distinct small molecule HSP90 inhibitors (XL888 and 17-AAG [17-allylamino-17-demethoxygeldanamycin]) in a large, genetically diverse panel of cancer cell lines. The cell cycle phenotypes of both inhibitors were strikingly similar and fell into three classes: accumulation in M-phase, G2-phase, or G1-phase. Accumulation in M-phase was the most prominent phenotype and notably, was also correlated with TP53 mutant status. We additionally observed unexpected complexity in the response of the cell cycle-associated client PLK1 to HSP90 inhibition, and we suggest that inhibitor-induced PLK1 depletion may contribute to the striking metaphase arrest phenotype seen in many of the M-arrested cell lines. CONCLUSIONS/SIGNIFICANCE: Our analysis of the cell cycle phenotypes induced by HSP90 inhibition in 25 cancer cell lines revealed that the phenotypic response was highly dependent on cellular genotype as well as on the concentration of HSP90 inhibitor and the time of treatment. M-phase arrest correlated with the presence of TP53 mutations, while G2 or G1 arrest was more commonly seen in cells bearing wt TP53. We draw upon previous literature to suggest an integrated model that accounts for these varying observations

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570