Awareness Of Racial Disparities Among Breast Cancer Providers

Background: Cancer patients who self-identify as Black and Hispanic are more likely to receive delays in care as compared to their Non-Hispanic White counterparts. Current research suggests that while providers are aware of racial-ethnic disparities in access to treatment at a nationallevel, they either fail to recognize hospital-level or practice-level disparities (occurring within the provider’s own clinical care) or attribute it to patient-level factors. However, this phenomenon of decreased awareness among providers regarding factors specific to them or their hospital/practice is not well understood and has yet to be studied in the oncology space. Methods: We conducted a non-randomized pre-post educational intervention pilot study with 18 breast cancer providers at the Smilow Cancer Center in February 2023. Prior to the educational intervention providers completed an online cross-sectional survey that assessed baseline understanding of disparities at three levels (national-level, within Smilow, and within the provider’s own practice also referred to as individual-level). The providers then watched a live data presentation focusing on racial-disparity metrics and completed a post-intervention crosssectional survey. Differences between pre- and post-intervention survey responses were evaluated with Fisher’s exact tests. Results: Among 18 breast cancer providers, awareness of race as a factor in influencing differences in oncological care increased significantly (from 33.3% to 77.8%, p = 0.02) pre-topost intervention at the Smilow-level, but did not change at the national- or individual-level. Providers identified social determinants of health—non-medical factors that have an impact on health, such as housing insecurity, poor employment conditions, and food insecurity—as the main cause of disparities both nationally and within Smilow. At the individual-level, most providers believed that patient-level factors rather than provider-level factors were driving differences in oncological care metrics and reported that larger systems, such as healthcare or government, were responsible for reducing disparities. Conclusion: In this small pilot study among providers with relatively high awareness of racial/ethnic disparities regarding cancer care at baseline, a brief educational intervention did not increase awareness of national- and individual-level factors, but did increase awareness of Smilow-level factors. As the oncology field is starting to address inequities in care, it is crucial for providers to not only acknowledge existence of these disparities in access to care, but also to establish clinically actionable guidelines to reduce these disparities within their own practice. Future studies should focus on how systemic factors influence oncology care and identify strategies to address these inequities

Effects of Spaceflight on the Modulation of Shock Wave Transmission to the Head During Locomotion

The ability to maintain gaze stability during locomotion requires the normal function and integration of the vestibulo-ocular reflex, vestibulo and cervico-colic reflexes with effective coordination between the trunk and lower limb segments. One hypothesized constraint on the coordination between segments during locomotion is the regulation of energy flow or shock wave transmissions through the body at high impact phases with the support surface. Allowing these excessive transmissions of energy to the head may result in compromised gaze stability during locomotion. The aim of this study was to determine the effects of microgravity adaptation on the transmissibility of shock wave to the head during locomotion. Before and after spaceflight (3-6 months) six subjects walked (6.4 km/h) on a motorized treadmill while fixating their gaze on a centrally located earth-fixed target. Triaxial accelerometers mounted on the shank and the head measured the shock wave transmission through the body during locomotion. During postflight locomotion the peak shock at the shank and the head were significantly reduced, however, the ratio of peak head to shank shock was significantly increased. These results indicate that exposure to spaceflight causes adaptive modifications in the short-latency vestibulospinal head stabilization responses required to compensate for the rapid shocks transmitted to the head during locomotion. This study was supported by NASA

Reduction of ocular counter-rolling by adaptation to space

We studied the three-dimensional vestibulo-ocular reflex (VOR) of rhesus monkeys before and after the COSMOS Biosatellite 2229 Mission of 1992-1993. This included tests of ocular counter-rolling (OCR), the gain of the vestibulo-ocular reflex (VOR), and spatial orientation of velocity storage. A four-axis vestibular and oculomotor stimulator was transported to the Institute of Biomedical Problems in Moscow for the pre- and postflight ground-based testing. Twelve normal juvenile male rhesus monkey were implanted surgically with eye coils and tested 60-90 days before spaceflight. Two monkey (7906 and 6151), selected from the twelve as flight animals, flew from 12/29/92 to 1/10/93. Upon recovery, they were tested for 11 days postflight along with three control animals. Compensatory ocular torsion was produced in two ways: (1) Lateral head tilts evoked OCR through otolith-ocular reflexes. OCR was also measured dynamically during off-vertical axis rotation (OVAR). (2) Rotation about a naso-occipital axis that was either vertical of horizontal elicited torsional nystagmus through semicircular canal-ocular reflexes (roll VOR). OCR from the otoliths was substantially reduced (70 percent) for 11 days after reentry on both modes of testing. The gain of the roll VOR was also decreased, but less than OCR. These data demonstrate that there was a long-lasting depression of torsional or roll eye movements after adaptation to microgravity in these monkeys, especially those movements produced by the otolith organs

Surface temperature trends in Russia over the past five centuries reconstructed from borehole temperatures

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94976/1/jgrb13614.pd

Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19.

Dysregulated immune responses against the SARS-CoV-2 virus are instrumental in severe COVID-19. However, the immune signatures associated with immunopathology are poorly understood. Here we use multi-omics single-cell analysis to probe the dynamic immune responses in hospitalized patients with stable or progressive course of COVID-19, explore V(D)J repertoires, and assess the cellular effects of tocilizumab. Coordinated profiling of gene expression and cell lineage protein markers shows that S100

Aβ42 Mutants with Different Aggregation Profiles Induce Distinct Pathologies in Drosophila

Aggregation of the amyloid-β-42 (Aβ42) peptide in the brain parenchyma is a pathological hallmark of Alzheimer's disease (AD), and the prevention of Aβ aggregation has been proposed as a therapeutic intervention in AD. However, recent reports indicate that Aβ can form several different prefibrillar and fibrillar aggregates and that each aggregate may confer different pathogenic effects, suggesting that manipulation of Aβ42 aggregation may not only quantitatively but also qualitatively modify brain pathology. Here, we compare the pathogenicity of human Aβ42 mutants with differing tendencies to aggregate. We examined the aggregation-prone, EOFAD-related Arctic mutation (Aβ42Arc) and an artificial mutation (Aβ42art) that is known to suppress aggregation and toxicity of Aβ42 in vitro. In the Drosophila brain, Aβ42Arc formed more oligomers and deposits than did wild type Aβ42, while Aβ42art formed fewer oligomers and deposits. The severity of locomotor dysfunction and premature death positively correlated with the aggregation tendencies of Aβ peptides. Surprisingly, however, Aβ42art caused earlier onset of memory defects than Aβ42. More remarkably, each Aβ induced qualitatively different pathologies. Aβ42Arc caused greater neuron loss than did Aβ42, while Aβ42art flies showed the strongest neurite degeneration. This pattern of degeneration coincides with the distribution of Thioflavin S-stained Aβ aggregates: Aβ42Arc formed large deposits in the cell body, Aβ42art accumulated preferentially in the neurites, while Aβ42 accumulated in both locations. Our results demonstrate that manipulation of the aggregation propensity of Aβ42 does not simply change the level of toxicity, but can also result in qualitative shifts in the pathology induced in vivo