Utilizing Counseling Skills in the Classroom to Promote Student Well-Being and Success

The success of institutions of higher education is dependent upon student academic success. Current research with students in higher education links academic success with student well-being. Members of the faculty are in critical positions to ensure student success and thus, the institution, but may be unsure how to promote well-being in the classroom setting. This article examines challenges professors face and shares a professional performance review process. Strategies and skills used by professional counselors that university faculty can implement to foster a sense of student well-being and establish supportive relationships through an integration of Miller’s Relational Cultural Theory and Social Cognitive Theory from Bandura are provided. Some of these counseling skills include rapport building, validation, empathy, grounding techniques, and mindfulness

Accelerated phosphatidylcholine turnover in macrophages promotes adipose tissue inflammation in obesity.

White adipose tissue (WAT) inflammation contributes to the development of insulin resistance in obesity. While the role of adipose tissue macrophage (ATM) pro-inflammatory signalling in the development of insulin resistance has been established, it is less clear how WAT inflammation is initiated. Here, we show that ATMs isolated from obese mice and humans exhibit markers of increased rate of de novo phosphatidylcholine (PC) biosynthesis. Macrophage-specific knockout of phosphocholine cytidylyltransferase A (CCTα), the rate-limiting enzyme of de novo PC biosynthesis pathway, alleviated obesity-induced WAT inflammation and insulin resistance. Mechanistically, CCTα-deficient macrophages showed reduced ER stress and inflammation in response to palmitate. Surprisingly, this was not due to lower exogenous palmitate incorporation into cellular PCs. Instead, CCTα-null macrophages had lower membrane PC turnover, leading to elevated membrane polyunsaturated fatty acid levels that negated the pro-inflammatory effects of palmitate. Our results reveal a causal link between obesity-associated increase in de novo PC synthesis, accelerated PC turnover and pro-inflammatory activation of ATMs

Impact of baryons on the cluster mass function and cosmological parameter determination

Recent results by the Planck collaboration have shown that cosmological parameters derived from the cosmic microwave background anisotropies and cluster number counts are in tension, with the latter preferring lower values of the matter density parameter, $\Omega_\mathrm{m}$, and power spectrum amplitude, $\sigma_8$. Motivated by this, we investigate the extent to which the tension may be ameliorated once the effect of baryonic depletion on the cluster mass function is taken into account. We use the large-volume Millennium Gas simulations in our study, including one where the gas is pre-heated at high redshift and one where the gas is heated by stars and active galactic nuclei (in the latter, the self-gravity of the baryons and radiative cooling are omitted). In both cases, the cluster baryon fractions are in reasonably good agreement with the data at low redshift, showing significant depletion of baryons with respect to the cosmic mean. As a result, it is found that the cluster abundance in these simulations is around 15 per cent lower than the commonly-adopted fit to dark matter simulations by Tinker et al (2008) for the mass range $10^{14}-10^{14.5}h^{-1} \mathrm{M}_\odot$. Ignoring this effect produces a significant artificial shift in cosmological parameters which can be expressed as $\Delta[\sigma_8(\Omega_\mathrm{m}/0.27)^{0.38}]\simeq -0.03$ at $z=0.17$ (the median redshift of the $\mathit{Planck}$ cluster sample) for the feedback model. While this shift is not sufficient to fully explain the $\mathit{Planck}$ discrepancy, it is clear that such an effect cannot be ignored in future precision measurements of cosmological parameters with clusters. Finally, we outline a simple, model-independent procedure that attempts to correct for the effect of baryonic depletion and show that it works if the baryon-dark matter back-reaction is negligible.Comment: 10 pages, 5 figures, Accepted by MNRA

Proximity proteomics reveals UCH-L1 as an essential regulator of NLRP3-mediated IL-1β production in human macrophages and microglia

Activation of the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome complex is an essential innate immune signaling mechanism. To reveal how human NLRP3 inflammasome assembly and activation are controlled, in particular by components of the ubiquitin system, proximity labeling, affinity purification, and RNAi screening approaches were performed. Our study provides an intricate time-resolved molecular map of different phases of NLRP3 inflammasome activation. Also, we show that ubiquitin C-terminal hydrolase 1 (UCH-L1) interacts with the NACHT domain of NLRP3. Downregulation of UCH-L1 decreases pro-interleukin-1β (IL-1β) levels. UCH-L1 chemical inhibition with small molecules interfered with NLRP3 puncta formation and ASC oligomerization, leading to altered IL-1β cleavage and secretion, particularly in microglia cells, which exhibited elevated UCH-L1 expression as compared to monocytes/macrophages. Altogether, we profiled NLRP3 inflammasome activation dynamics and highlight UCH-L1 as an important modulator of NLRP3-mediated IL-1β production, suggesting that a pharmacological inhibitor of UCH-L1 may decrease inflammation-associated pathologies

Cardiovascular examination using hand-held cardiac ultrasound

Echocardiography is the first-line imaging modality for assessing cardiac function and morphology. The miniaturisation of ultrasound technology has led to the development of hand-held cardiac ultrasound (HCU) devices. The increasing sophistication of available HCU devices enables clinicians to more comprehensively examine patients at the bedside. HCU can augment clinical exam findings by offering a rapid screening assessment of cardiac dysfunction in both the Emergency Department and in cardiology clinics. Possible implications of implementing HCU into clinical practice are discussed in this review paper

TESS Duotransit Candidates from the Southern Ecliptic Hemisphere

Discovering transiting exoplanets with long orbital periods allows us to study warm and cool planetary systems with temperatures similar to the planets in our own Solar system. The TESS mission has photometrically surveyed the entire Southern Ecliptic Hemisphere in Cycle 1 (August 2018 - July 2019), Cycle 3 (July 2020 - June 2021) and Cycle 5 (September 2022 - September 2023). We use the observations from Cycle 1 and Cycle 3 to search for exoplanet systems that show a single transit event in each year - which we call duotransits. The periods of these planet candidates are typically in excess of 20 days, with the lower limit determined by the duration of individual TESS observations. We find 85 duotransit candidates, which span a range of host star brightnesses between 8 < $T_{mag}$ < 14, transit depths between 0.1 per cent and 1.8 per cent, and transit durations between 2 and 10 hours with the upper limit determined by our normalisation function. Of these candidates, 25 are already known, and 60 are new. We present these candidates along with the status of photometric and spectroscopic follow-up.Comment: 25 pages, 16 figures, submitted to Monthly Notices of the Royal Astronomical Societ

Acceleration of dormant storage effects to address the reliability of silicon surface micromachined Micro-Electro-Mechanical Systems (MEMS).

Qualification of microsystems for weapon applications is critically dependent on our ability to build confidence in their performance, by predicting the evolution of their behavior over time in the stockpile. The objective of this work was to accelerate aging mechanisms operative in surface micromachined silicon microelectromechanical systems (MEMS) with contacting surfaces that are stored for many years prior to use, to determine the effects of aging on reliability, and relate those effects to changes in the behavior of interfaces. Hence the main focus was on 'dormant' storage effects on the reliability of devices having mechanical contacts, the first time they must move. A large number ({approx}1000) of modules containing prototype devices and diagnostic structures were packaged using the best available processes for simple electromechanical devices. The packaging processes evolved during the project to better protect surfaces from exposure to contaminants and water vapor. Packages were subjected to accelerated aging and stress tests to explore dormancy and operational environment effects on reliability and performance. Functional tests and quantitative measurements of adhesion and friction demonstrated that the main failure mechanism during dormant storage is change in adhesion and friction, precipitated by loss of the fluorinated monolayer applied after fabrication. The data indicate that damage to the monolayer can occur at water vapor concentrations as low as 500 ppm inside the package. The most common type of failure was attributed to surfaces that were in direct contact during aging. The application of quantitative methods for monolayer lubricant analysis showed that even though the coverage of vapor-deposited monolayers is generally very uniform, even on hidden surfaces, locations of intimate contact can be significantly depleted in initial concentration of lubricating molecules. These areas represent defects in the film prone to adsorption of water or contaminants that can cause movable structures to adhere. These analysis methods also indicated significant variability in the coverage of lubricating molecules from one coating process to another, even for identical processing conditions. The variability was due to residual molecules left in the deposition chamber after incomplete cleaning. The coating process was modified to result in improved uniformity and total coverage. Still, a direct correlation was found between the resulting static friction behavior of MEMS interfaces, and the absolute monolayer coverage. While experimental results indicated that many devices would fail to start after aging, the modeling approach used here predicted that all the devices should start. Adhesion modeling based upon values of adhesion energy from cantilever beams is therefore inadequate. Material deposition that bridged gaps was observed in some devices, and potentially inhibits start-up more than the adhesion model indicates. Advances were made in our ability to model MEMS devices, but additional combined experimental-modeling studies will be needed to advance the work to a point of providing predictive capability. The methodology developed here should prove useful in future assessments of device aging, however. Namely, it consisted of measuring interface properties, determining how they change with time, developing a model of device behavior incorporating interface behavior, and then using the age-aware interface behavior model to predict device function

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

BCL11A is a triple-negative breast cancer gene with critical functions in stem and progenitor cells.

Triple-negative breast cancer (TNBC) has poor prognostic outcome compared with other types of breast cancer. The molecular and cellular mechanisms underlying TNBC pathology are not fully understood. Here, we report that the transcription factor BCL11A is overexpressed in TNBC including basal-like breast cancer (BLBC) and that its genomic locus is amplified in up to 38% of BLBC tumours. Exogenous BCL11A overexpression promotes tumour formation, whereas its knockdown in TNBC cell lines suppresses their tumourigenic potential in xenograft models. In the DMBA-induced tumour model, Bcl11a deletion substantially decreases tumour formation, even in p53-null cells and inactivation of Bcl11a in established tumours causes their regression. At the cellular level, Bcl11a deletion causes a reduction in the number of mammary epithelial stem and progenitor cells. Thus, BCL11A has an important role in TNBC and normal mammary epithelial cells. This study highlights the importance of further investigation of BCL11A in TNBC-targeted therapies