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Few studies have investigated parent's experiences with racism in the neonatal intensive care unit (NICU). Our objective was to explore how parents perceive their interactions with NICU staff and if/how racism in the NICU was experienced. Parents of infants receiving care in an urban NICU completed fixed choice surveys regarding their experiences and demographics, with 6 open-ended questions to elaborate on their fixed-choice responses. Using a constant comparative method informed by Constructivist Grounded Theory, we identified 3 main themes from the comments provided by 97 respondents: Care and harm coexisting, racism often manifesting as neglectful care, and the power differential is most impactful during times of parent advocacy. Parents spoke positively regarding their experiences and also reported disparate treatment attributed to their racial/ethnic identity. Racism was experienced by inappropriate comments and apathy toward parent requests, occurring during intimate interactions between staff and parents. Descriptions of parental advocacy efforts highlighted the lack of power they held in relation to the NICU staff. We recommend strengthening the focus on equity and mitigating power imbalances in the NICU. [ABSTRACT FROM AUTHOR]

Research has illustrated that school counselors "do not" provide Latina/o students with sufficient information about higher education (Immerwahr, 2003; Zalaquett, 2005), high expectations (Martinez, 2003), and individual counseling and guidance (Vela Gude et al., in press). Because school counselors are supposed to play an important role in helping Latina/o students pursue higher education (Villalba, Akos, Keeter, & Ames, 2007), the current article identifies seven myths concerning a growing Latina/o population: (1) parents do not value education, (2) students do not value education, (3) low expectations do not exist, (4) students are receiving sufficient guidance, (5) perceived ability level is the most important factor in eventual academic achievement, (6) personal barriers are more detrimental than systemic barriers, and (7) students do not have the ability to adopt a futuristic orientation. Hopefully, this article will encourage school counselors to help Latina/o students by providing quality attention and advisement, high expectations, and information about higher education.

Rationale: Acute lung injury (ALI) carries a high risk of mortality but has no established pharmacologic therapy. We previously found that experimental ALI occurs through natural killer (NK) cell NKG2D receptor activation and that the cognate human ligand, MICB, was associated with ALI after transplantation. Objectives: To investigate the association of a common missense variant, MICBG406A, with ALI. Methods: We assessed MICBG406A genotypes within two multicenter observational study cohorts at risk for ALI: primary graft dysfunction (N= 619) and acute respiratory distress syndrome (N= 1,376). Variant protein functional effects were determined in cultured and ex vivo human samples. Measurements and Main Results: Recipients of MICBG406Ahomozygous allografts had an 11.1% absolute risk reduction (95% confidence interval [CI], 3.2-19.4%) for severe primary graft dysfunction after lung transplantation and reduced risk for allograft failure (hazard ratio, 0.36; 95% CI, 0.13-0.98). In participants with sepsis, we observed 39% reduced odds of moderately or severely impaired oxygenation among MICBG406A-homozygous individuals (95% CI, 0.43-0.86). BAL NK cells were less frequent and lessmature in participants with MICBG406A. Expression of missense variant proteinMICBD136N in cultured cells resulted in reduced surface MICB and reduced NKG2D ligation relative to wild-type MICB. Coculture of variantMICBD136N cells with NK cells resulted in less NKG2D activation and less susceptibility to NK cell killing relative to the wild-type cells. Conclusions: These data support a role for MICB signaling through the NKG2D receptor in mediating ALI, suggesting a novel therapeutic approach. [ABSTRACT FROM AUTHOR]

Natural killer (NK) cells are innate lymphocytes capable of mediating immune responses without prior sensitization. NK cells express Fc-gamma receptors (FcγRs) that engage the Fc region of IgG. Studies investigating the role of FcγRs on mouse NK cells have been limited due to lack specific reagents. In this study, we characterize the expression and biological consequences of activating mouse NK cells through their FcγRs. We demonstrate that most NK cells express the activating CD16 receptor, and a subset of NK cells also expresses the inhibitory CD32b receptor. Critically, these FcγRs are functional on mouse NK cells and can modulate antibody-mediated responses. We also characterized mice with conditional knockout alleles of Fcgr3 (CD16) or Fcgr2b (CD32b) in the NK and innate lymphoid cell (ILC) lineage. NK cells in these mice did not reveal any developmental defects and were responsive to cross-linking activating NK receptors, cytokine stimulation, and killing of YAC-1 targets. Importantly, CD16-deficient NK cells failed to induce antibody-directed cellular cytotoxicity of antibody-coated B-cell lymphomas in in vitro assays. In addition, we demonstrate the important role of CD16 on NK cells using an in vivo model of cancer immunotherapy using anti-CD20 antibody treatment of B-cell lymphomas. [ABSTRACT FROM AUTHOR]

Methylmercury (MeHg) is a developmental neurotoxicant, and one potential mechanism of MeHg toxicity is epigenetic dysregulation. In a recent metaanalysis of epigenome-wide association studies (EWAS), associations between prenatal MeHg exposure and DNA methylation at several genomic sites were identified in blood from newborns and children. While EWASs reveal humanrelevant associations, experimental studies are required to validate the relationship between exposure and DNA methylation changes, and to assess if such changes have implications for gene expression. Herein, we studied DNA methylation and gene expression of five of the top genes identified in the EWAS meta-analysis, MED31, MRPL19, GGH, GRK1, and LYSMD3, upon MeHg exposure in human SH-SY5Y cells exposed to 8 or 40 nM of MeHg during differentiation, using bisulfite-pyrosequencing and qPCR, respectively. The concentrations were selected to cover the range of MeHg concentrations in cord blood (2-8.5 µg/L) observed in the cohorts included in the EWAS. Exposure to MeHg increased DNA methylation at MED31, a transcriptional regulator essential for fetal development. The results were in concordance with the epidemiological findings where more MED31 methylation was associated with higher concentrations of MeHg. Additionally, we found a non-significant decrease in DNA methylation at GGH, which corresponds to the direction of change observed in the EWAS, and a significant correlation of GGH methylation with its expression. In conclusion, this study corroborates some of the EWAS findings and puts forward candidate genes involved in MeHg's effects on the developing brain, thus highlighting the value of experimental validation of epidemiological association studies. [ABSTRACT FROM AUTHOR]

Brain development is highly dependent on hormonal regulation. Exposure to chemicals disrupting endocrine signaling has been associated with neurodevelopmental impairment. This raises concern about exposure to the suspected thousands of endocrine disruptors, and has resulted in efforts to improve regulation of these chemicals. Yet, the causal links between endocrine disruption and developmental neurotoxicity, which would be required for regulatory action, are still largely missing. In this review, we illustrate the importance of two endocrine systems, thyroid hormone and retinoic acid pathways, for neurodevelopment. We place special emphasis on TH and RA synthesis, metabolism, and how endocrine disrupting chemicals known or suspected to affect these systems are associated with developmental neurotoxicity. While it is clear that neurodevelopment is dependent on proper hormonal functioning, and evidence is increasing for developmental neurotoxicity induced by endocrine disrupting chemicals, this is not grasped by current chemical testing. Thus, there is an urgent need to develop test methods detecting endocrine disruption in the context of neurodevelopment. Key to this development is further mechanistic insights on the involvement of endocrine signaling in neurodevelopment as well as increased support to develop and validate new test methods for the regulatory context. [ABSTRACT FROM AUTHOR]

Resistance comes from older managers. Acceptance comes from younger viewers. As CNN's urban affairs correspondent and the host of National Public Radio's 'Latino USA,' veteran journalist Maria Hinojosa reports on [...]

The article discusses pediatric melatonin ingestions reported to Texas Poison Centers. Melatonin is a hormone that affects various bodily functions and is commonly used as a sleep aid. The prevalence of melatonin supplement use has increased over the years, and children are at an increased risk of ingestion. The article provides data on the number of melatonin ingestions reported to Texas poison centers from 2000 to 2023, with the majority of cases involving young children and most ingestions occurring at home. The majority of ingestions involved only melatonin and did not result in serious outcomes. The article concludes by providing contact information for the poison center in case of melatonin ingestion concerns. [Extracted from the article]

The article offers information on the increase in pediatric ocular hand sanitizer exposures during 2020, influenced by the widespread handwashing recommendations in response to the COVID-19 pandemic. It discusses the rise in such exposures among children aged 0-19; changes in exposure patterns at different locations (e.g., home, school); and variations in management outcomes, highlighting potential implications of the pandemic on these trends.

The article provides information on the video recording of the talk given by Mexican American broadcast journalist Maria Hinojosa during the Scholar & Feminist Conference XXXII, entitled Fashioning Citizenship: Gender and Immigration held at Barnard College in New York City on March 24, 2007.

The article discusses the cases of foreign body ingestions by children during the Covid-19 pandemic as reported to the Texas Poison Centers. Also cited are the foreign bodies that could cause serious injuries like magnets and batteries, and the ingestion data on metrics like patient demographics, exposure circumstances, management site, and medical outcomes.

Although interactions between inhibitory Ly49 receptors and their self-MHC class I ligands in C57BL/6 mice are known to limit NK cell proliferation during mouse CMV (MCMV) infection, we created a 36-marker mass cytometry (CyTOF) panel to investigate how these inhibitory receptors impact the NK cell response to MCMV in other phenotypically measurable ways. More than two thirds of licensed NK cells (i.e., those expressing Ly49C, Ly49I, or both) in uninfected mice had already differentiated into NK cells with phenotypes indicative of Ag encounter (KLRG1 + Ly6C - ) or memory-like status (KLRG1 + Ly6C + ). These pre-existing KLRG1 + Ly6C + NK cells resembled known Ag-specific memory NK cell populations in being less responsive to IL-18 and IFN-α stimulation in vitro and by selecting for NK cell clones with elevated expression of a Ly49 receptor. During MCMV infection, the significant differences between licensed and unlicensed (Ly49C - Ly49I - ) NK cells disappeared within both CMV-specific (Ly49H + ) and nonspecific (Ly49H - ) responses. This lack of heterogeneity carried into the memory phase, with only a difference in CD16 expression manifesting between licensed and unlicensed MCMV-specific memory NK cell populations. Our results suggest that restricting proliferation is the predominant effect licensing has on the NK cell population during MCMV infection, but the inhibitory Ly49-MHC interactions that take place ahead of infection contribute to their limited expansion by shrinking the pool of licensed NK cells capable of robustly responding to new challenges., (Copyright © 2022 by The American Association of Immunologists, Inc.)