Validating self-reported Toxic Release Inventory data using Benford's Law: investigating toxic chemical release hazards in floodplains.

Introduction: Acute and long-term health impacts from flooding related toxic chemical releases are a significant local health concern and can disproportionately impact communities with vulnerable populations; reliable release data are needed to quantify this hazard.

Methods: In this paper, we analyze US Federal Emergency Management Agency designated floodplain data and US Environmental Protection Agency Toxic Release Inventory (TRI) data to determine if geographically manipulated databases adhere to Benford's Law.

Results: We investigated multiple variants and discovered pollution releases adhere to Benford's Law and tests which thereby validates the self-reported toxic release dataset.

"Ripping Off the Band-Aid": uncovering future health care Professionals' "Fractured Knowledge" about sexual and reproductive health.

Background: Research has shown the role of identity on future health professionals' confidence and competence in addressing the sexual and reproductive health (SRH) needs of their patients. While there has been some work in increasing the sexual health literacy of future providers via various curricular approaches and comprehensive clinical-based training, there are research gaps on how social differences around identity impact future healthcare professionals' knowledge and practices around SRH.

Objectives: This article presents research findings on the experiences of US undergraduate students attending a campus that provides training in the health sciences and health professions.

From pandemic to endemic: Divergence of COVID-19 positive-tests and hospitalization numbers from SARS-CoV-2 RNA levels in wastewater of Rochester, Minnesota.

Traditionally, public health surveillance relied on individual-level data but recently wastewater-based epidemiology (WBE) for the detection of infectious diseases including COVID-19 became a valuable tool in the public health arsenal. Here, we use WBE to follow the course of the COVID-19 pandemic in Rochester, Minnesota (population 121,395 at the 2020 census), from February 2021 to December 2022. We monitored the impact of SARS-CoV-2 infections on public health by comparing three sets of data: quantitative measurements of viral RNA in wastewater as an unbiased reporter of virus level in the community, positive results of viral RNA or antigen tests from nasal swabs reflecting community reporting, and hospitalization data.

Just in case: undergraduate students identifying and mitigating barriers to their sexual and reproductive health needs.

Background: Many U.S. colleges and universities offer access to a healthcare center that provides sexual and reproductive health (SRH) resources, services, and products.

Using Artificial Intelligence to Identify Sources and Pathways of Lead Exposure in Children.

Context: Sources and pathways of lead exposure in young children have not been analyzed using new artificial intelligence methods.

Objective: To collect environmental, behavioral, and other data on sources and pathways in 17 rural homes to predict at-risk households and to compare urban and rural indicators of exposure.

Design: Cross-sectional pilot study.

Creating an Integrated Undergraduate Public Health Curricula: Inspiring the Next Generation to Solve Complex Public Health Issues.

This article takes a novel approach of highlighting the creation and development of an integrated undergraduate public health curricula geared to students in the health sciences. In our practice, undergraduate and public health pedagogy supports innovative and proven approaches of experiential learning in our classrooms. We show how public health faculty take a team approach to teaching which has allowed them to collaborate in and outside of the classroom resulting in inherent knowledge of course materials, student engagement, and outcomes.

A Data Driven Approach for Prioritizing COVID-19 Vaccinations in the Midwestern United States.

Considering the potential for widespread adoption of social vulnerability indices (SVI) to prioritize COVID-19 vaccinations, there is a need to carefully assess them, particularly for correspondence with outcomes (such as loss of life) in the context of the COVID-19 pandemic. The University of Illinois at Chicago School of Public Health Public Health GIS team developed a methodology for assessing and deriving vulnerability indices based on the premise that these indices are, in the final analysis, classifiers. Application of this methodology to several Midwestern states with a commonly used SVI indicates that by using only the SVI rankings there is a risk of assigning a high priority to locations with the lowest mortality rates and low priority to locations with the highest mortality rates.

A second wave of COVID-19 in Cook County: What lessons can be applied?

During the ongoing public health crisis, many agencies are reporting COVID-19 health outcome information based on the overall population. This practice can lead to misleading results and underestimation of high risk areas. To gain a better understanding of spatial and temporal distribution of COVID-19 deaths; the long term care facility (LTCF) and household population (HP) deaths must be used.

Does neighborhood social and environmental context impact race/ethnic disparities in childhood asthma?

Utilizing over 140,000 geocoded medical records for a diverse sample of children ages 2-12 living in Houston, Texas, we examine whether a comprehensive set of neighborhood social and environmental characteristics explain racial and ethnic disparities in childhood asthma. Adjusting for all individual risk factors, as well as neighborhood concentrated disadvantage, particulate matter, ozone concentration, and race/ethnic composition, reduced but did not fully attenuate the higher odds of asthma diagnosis among black (OR=2.59, 95% CI=2.

Comprehensive Neighborhood Portraits and Child Asthma Disparities.

Objectives Previous research has established links between child, family, and neighborhood disadvantages and child asthma. We add to this literature by first characterizing neighborhoods in Houston, TX by demographic, economic, and air quality characteristics to establish differences in pediatric asthma diagnoses across neighborhoods. Second, we identify the relative risk of social, economic, and environmental risk factors for child asthma diagnoses.

Utilizing Exploratory Spatial Data Analysis to Examine Health and Environmental Disparities in Disadvantaged Neighborhoods.

Health disparities research has focused primarily on racial and socioeconomic differences in health outcomes. Although neighborhood characteristics and the concept of built environment have been shown to affect individual health, measuring the effects of environmental risks on health has been a less developed area of disparities research. To examine spatial associations and the distribution of geographic patterns of sociodemographic characteristics, environmental cancer risk, and cancer rates, we utilized existing data from multiple sources.

Highly active antiretroviral therapy potently suppresses HIV infection in humanized Rag2-/-gammac-/- mice.

Humanized Rag2(-/-)gamma(c)(-/-) mice (Hu-DKO mice) become populated with functional human T cells, B cells, and dendritic cells following transplantation with human hematopoietic stem cells (HSC) and represent an improved model for studying HIV infection in vivo. In the current study we demonstrated that intrasplenic inoculation of hu-DKO mice with HIV-1 initiated a higher level of HIV infection than intravenous or intraperitoneal inoculation, associated with a reciprocal decrease in peripheral CD4(+) T cells and increase in peripheral CD8(+) T cells. HIV infection by intrasplenic injection increased serum levels of human IgG and IgM including human IgM and IgG specific for HIV-1 gp120.

CD4-specific transgenic expression of human cyclin T1 markedly increases human immunodeficiency virus type 1 (HIV-1) production by CD4+ T lymphocytes and myeloid cells in mice transgenic for a provirus encoding a monocyte-tropic HIV-1 isolate.

Human immunodeficiency virus type 1 (HIV-1)-encoded Tat provides transcriptional activation critical for efficient HIV-1 replication by interacting with cyclin T1 and recruiting P-TEFb to efficiently elongate the nascent HIV transcript. Tat-mediated transcriptional activation in mice is precluded by species-specific structural differences that prevent Tat interaction with mouse cyclin T1 and severely compromise HIV-1 replication in mouse cells. We investigated whether transgenic mice expressing human cyclin T1 under the control of a murine CD4 promoter/enhancer cassette that directs gene expression to CD4(+) T lymphocytes and monocytes/macrophages (hu-cycT1 mice) would display Tat responsiveness in their CD4-expressing mouse cells and selectively increase HIV-1 production in this cellular population, which is infected primarily in HIV-1-positive individuals.

CCL2/monocyte chemoattractant protein-1 mediates enhanced transmigration of human immunodeficiency virus (HIV)-infected leukocytes across the blood-brain barrier: a potential mechanism of HIV-CNS invasion and NeuroAIDS.

Encephalitis and dementia associated with acquired immunodeficiency syndrome (AIDS) are characterized by leukocyte infiltration into the CNS, microglia activation, aberrant chemokine expression, blood-brain barrier (BBB) disruption, and eventual loss of neurons. Little is known about whether human immunodeficiency virus 1 (HIV-1) infection of leukocytes affects their ability to transmigrate in response to chemokines and to alter BBB integrity. We now demonstrate that HIV infection of human leukocytes results in their increased transmigration across our tissue culture model of the human BBB in response to the chemokine CCL2, as well as in disruption of the BBB, as evidenced by enhanced permeability, reduction of tight junction proteins, and expression of matrix metalloproteinases (MMP)-2 and MMP-9.

Identification of granulocyte-macrophage colony-stimulating factor and lipopolysaccharide-induced signal transduction pathways that synergize to stimulate HIV type 1 production by monocytes from HIV type 1 transgenic mice.

HIV-1-infected monocyte/macrophages located in lymph nodes and tissues are highly productive sources of HIV-1 and may function as a persistent reservoir contributing to the rebound viremia observed after highly active antiretroviral therapy is stopped. Mechanisms activating latently infected, primary monocyte/macrophages to produce HIV-1 were investigated using monocytes isolated from a transgenic mouse line carrying a full-length proviral clone of a monocyte-tropic HIV-1 isolate, HIV-1(JR-CSF), regulated by the endogenous long terminal repeat (LTR) (JR-CSF mice). Granulocyte-macrophage colony-stimulating factor (GM-CSF) combined with lipopolysaccharide (LPS) induced infectious HIV-1 production by JR-CSF mouse monocytes over 10-fold and 100-fold higher than that stimulated by GM-CSF or LPS alone, respectively.

Microglia from mice transgenic for a provirus encoding a monocyte-tropic HIV type 1 isolate produce infectious virus and display in vitro and in vivo upregulation of lipopolysaccharide-induced chemokine gene expression.

A large body of evidence has indicated that microglia are the predominant cellular location for HIV-1 in the brains of HIV-1-infected individuals and play a direct role in the development of HIV-1-associated dementia (HAD). Therefore, investigation of the mechanism by which HIV-1-infected microglia contribute to the development of HIV-associated dementia should be facilitated by the creation of a mouse model wherein microglia carry replication-competent HIV-1. To circumvent the inability of HIV-1 to infect mouse cells, we developed a mouse line that is transgenic for a full-length proviral clone of a monocyte-tropic HIV-1 isolate, HIV-1(JR-CSF) (JR-CSF mice), whose T cells and monocytes produce infectious HIV-1.

Development of a novel transgenic mouse/SCID-hu mouse system to characterize the in vivo behavior of reservoirs of human immunodeficiency virus type 1-infected cells.

To develop a system in which transgenic and knockout technologies are used to study the in vivo behavior of human immunodeficiency virus type 1 (HIV-1) reservoirs, 2 different mouse models were combined: transgenic mice carrying full-length provirus encoding the monocyte-tropic HIV-1(JR-CSF) isolate (JR-CSF mice) and severe combined immunodeficient mice implanted with human fetal thymus and liver tissues (thy/liv-SCID-hu mice). Extensive HIV-1 infection of human thymic implants occurred after injection of JR-CSF mouse leukocytes into thy/liv-SCID-hu mice, indicating that these cells provide an in vivo source of replication-competent HIV-1. In vivo persistence of transferred JR-CSF mouse leukocytes carrying replication-competent HIV-1 in thy/liv-SCID-hu mice was indicated by the emergence of HIV-1 infection in mice that had no detectable HIV-1 infection until after highly active antiretroviral therapy.

Human acid beta-glucosidase: isolation and amino acid sequence of a peptide containing the catalytic site.

Human acid beta-glucosidase (D-glucosyl-N-acylsphingosine glucohydrolase, EC 3.2.1.

Gaucher disease types 1, 2, and 3: differential mutations of the acid beta-glucosidase active site identified with conduritol B epoxide derivatives and sphingosine.

To elucidate the genetic heterogeneity in Gaucher disease, the residual beta-glucosidase in cultured fibroblasts from affected patients with each of the major phenotypes was investigated in vitro and/or in viable cells by inhibitor studies using the covalent catalytic site inhibitors, conduritol B epoxide or its bromo derivative, and the reversible cationic inhibitor, sphingosine. These studies delineated three distinct groups (designated A, B, and C) of residual activities with characteristic responses to these inhibitors. Group A residual enzymes had normal I50 values (i.

Use of activators and inhibitors to define the properties of the active site of normal and Gaucher disease lysosomal beta-glucosidase.

Lysosomal beta-glucosidase ('glucocerebrosidase') in peripheral blood lymphocyte and spleen extracts from normal individuals and Ashkenazi-Jewish Gaucher disease type-1 patients were investigated using several modifiers of glucosyl ceramide hydrolysis. The negatively charged lipids, phosphatidylserine and taurocholate, had differential effects on the hydrolytic rates of the normal and Gaucher disease enzymes from either source. With the normal enzyme, either negatively charged lipid (up to 1 mmol/l) increased the reaction rates, while decreasing hydrolytic rates were obtained at greater concentrations.