Status

In progress

Funder

American Heart Association

Goals

To investigate the role of pulmonary endothelium-derived microvesicles, and their miRNA cargos, in the pathogenesis of pulmonary vascular remodeling and pulmonary hypertension.

Description

In the pulmonary vasculature, the pulmonary vascular endothelial cells (PVEC) and pulmonary artery smooth muscle cells (PASMC) are two key cell types that play a major role in the pathobiology of pulmonary hypertension (PH). As the “signal initiator” in the pulmonary vasculature, PVEC affect the function of PASMC by secreting bioactive agents, myoendothelial injunctions (MEJ) and/or releasing extracellular vesicles (EV) that contain various cargo components including proteins and RNAs etc., under both normal and pathological conditions. So far, our knowledge about the role of endothelial-derived EV and its cargo in the PASMC function and pathogenesis of PH is very limited. In this proposal, we will investigate the role of PVEC-derived microvesicles (MV), especially that of the miRNA cargo in these MV, in the pathogenesis of pulmonary vascular remodeling and PH. In preliminary studies we found that in hypoxia, MV released by mouse PVEC in culture (H-MV) induced mouse PASMC proliferation in vitro and pulmonary vascular remodeling and PH in mice in room air (vs MV released by mouse PVEC in normoxia, H-MV vs N-MV). Using miRNA deep sequencing, we identified 9 miRNAs that were significantly induced in H-MV (v.s. N-MV), including miR-210, a miRNA that is known to induce SMC proliferation and PH. Interestingly, all the other identified miRNAs either suppressed or did not alter SMC proliferation in vitro, including a novel miRNA, miR-212-5p, that had the strongest inhibitory effect on SMC proliferation. We also found that miR-212-5p played a protective role in the pathogenesis of hypoxia-induced PH in mice. Based on these findings, we hypothesize that the endothelium, via MV, promotes vascular remodeling during hypoxia but also provides a break against continued progression of the disease via releasing anti-proliferative miRNAs, such as miR-212, packaged in the MV.

Status

In progress

Funder

NIH: NHLBI

Description

This project aims to elucidate the molecular mechanisms underlying the microRNA-17~92/PDLIM5 signaling-mediated pulmonary artery smooth muscle cell phenotype change and its functional impact in the genesis of pulmonary hypertension. We are continuing to investigate the role of PDLIM5 in the metabolic shift and to carry out a PDLIM5-targeted drug development process for the treatment of pulmonary hypertension.

• Read more on NIH website

Status

In progress

Description

In this grant, the role of microRNAs and the endothelium derived extracellular vesicles in the pathogenesis of Pulmonary Hypertension is being studied. Another grant with this same title is developing a novel method of engineering the extracellular vesicles for treatment of pulmonary hypertension.

Status

In progress

Funder

NIH/NIGMS

Description

The counter balancing of pro- and anti-inflammatory gene transcription is crucial for normal homeostasis after septic tissue injury. Aberrant regulation of this transcriptional balance culminates in an unchecked systemic inflammation, leading to lung tissue damage and edema, respiratory failure and ultimately death. However, the exact mechanisms underlying pathological inflammation in sepsis are poorly understood, and thus the strategies to accelerate the resolution of sepsis are very limited. Studies in the proposal will test the novel hypothesis that pathogenic signaling caused by sepsis is the result of a macrophage-specific Fra-1/AP-1 restricted expression of anti- inflammatory A20, a crucial ubiquitin-editing enzyme that terminates uncontrolled activation of NF- κB and MAP kinase signaling. The proposed studies will offer novel insights and targets for therapies to accelerate lung injury repair in patients with pseudomonas pneumonia and sepsis.

Status

In progress

Funder

NIH: NHLBI

Status

In progress

Funder

NIH: NHLBI

Description

The higher number of mitochondria rich reticulocytes in circulating blood, could potentially promote the elevated levels of reactive oxygen species, changes in oxygen metabolism and the cell lysis seen in the SCD. The molecular mechanism of increased mitochondria in red blood cells associated with SCD is not clear. This study investigates to examine the link between the aberrant mitophagy and sickle cell pathology in order to develop new strategies for the treatment of SCD using mitophagy restoration drugs.

Status

In progress

Description

Sickle cell disease (SCD) is an inherited blood disorder that affects millions of people worldwide and results in health care costs of at least $2.4 billion per year in the United States alone.1 It is caused by a mutation in the β -globin gene which leads to the formation of hemoglobin S (HbS). HbS is able to polymerize and leads to RBC sickling, hemolysis, acute and chronic pain, chronic hemolytic anemia, multisystem organ damage, and a much-shortened life expectancy. Novel targeted therapeutic approaches are essential to overcome the cascade of the events that begin with HbS polymerization. Recently many investigators have demonstrated that SCD organ pathology is associated with oxidative stress. Oxidative stress occurs when there is an increase in oxidants without a similar increase in antioxidants. Excessive ROS accumulation triggers a cascade of oxidative reactions that damage lipids, proteins of red blood cells ultimately leading to hemolysis or early destruction. Although much progress has been made to ROS mediated complications in SCD patients, further studies are essential in an attempt to understand the source of ROS and factors involved in HbS polymerization and hemolytic process. We have demonstrated in our laboratory that SCD RBCs retain mitochondria. In addition, we have shown that these retained mitochondria create excessive intracellular ROS generation and are associated with hemolysis. Our preliminary data also show that these mitochondria cause an increased oxygen consumption in the red blood cells. We hypothesize that erythrocyte mitochondrial retention causes exacerbation of SCD pathogenesis by two non-mutually exclusive mechanisms 1) Mitochondria generate excessive ROS leading to hemolysis and 2) Mitochondria increased oxygen consumption leading to a hypoxic intracellular environment that causes Hb S polymerization. An understanding of mitochondrial oxygen consumption and consequential oxidative stress in the pathogenesis of SCD represents a novel opportunity for the development of targeted therapeutic agents. The possibility of mitochondria- derived ROS generation and oxygen consumption in RBCs are novel targets that have not been investigated before. Our long-term goal is to translate the novel finding of mitochondria-retaining SCD RBCs into new pharmaceutical therapies for sickle cell disease.

Status

In progress

Description

Elevated fetal hemoglobin levels lessen the severity of sickle cell disease (SCD) and increase the lifespan of patients. Effective treatment of the large numbers of SCD patients projected in the U.S. and worldwide in the coming years would be best accomplished with an affordable, easily-administered, orally-available drug therapy designed to increase Fetal Hemoglobin (HbF) levels to a target >30% distributed throughout a large percentage of erythrocytes. Hydroxyurea (HU), currently the sole FDA-approved drug for SCD, is only effective in approximately 50% of patients and the HbF remains heterogeneously distributed among erythrocytes resulting in a large fraction lacking the protective effects of HbF. A logical approach to increase HbF that has been successfully pursued by our laboratory is to intervene with the epigenetic mechanism executing the switch from HbF to HbA expression in adults using pharmacological inhibitors of enzymes that catalyze repressive epigenetic modifications associated with γ-globin gene silencing. Our laboratory has developed and utilized an in vivo baboon model for over thirty years to investigate globin gene regulation and the in vivo activity of HbF-inducing drugs. Simian primates such as the baboon are widely acknowledged as the best animal models for testing the ability of new drugs to increase γ-globin expression because the activity of HbF-inducing agents is predictive of effects in man due to conservation of the structure and developmental stage-specific regulation of the β-like globin genes in simian primates. Initial studies from our laboratory demonstrating that DNA methyltransferase (DNMT) inhibitors increased HbF in baboons were followed by a number of clinical trials that confirmed their effectiveness in SCD patients and validated use of the baboon model. Recently we have shown that the LSD1 inhibitor RN-1 increased γ-globin expression in the sickle cell disease mouse model and in baboons and that long term treatment of baboons was well tolerated. In this proposal we will 1) investigate a combinatorial drug regimen targeting both DNMT1 and LSD1 for effects on HbF induction and reduction of potentially adverse hematological side-effects, 2) continue to advance new highly specific “third generation” LSD1 inhibitors with reduced ability to cross the blood brain barrier with the goal of increasing HbF to therapeutic levels, maximizing F cell numbers, and raising the therapeutic index, and 3) investigate new compounds that expand the BFU-E subpopulation permissive for γ-globin expression, alone and in combination with inhibitors of epigenetic-modifying enzymes, for additional stimulation of HbF induction. We envision that the results of these studies will directly impinge in the design of new clinical trials to increase HbF for the therapy of sickle cell disease.

Status

In progress

Description

Although the cause of SCD, a mutation in the gene for hemoglobin, has been known for many years, there is little understanding of why the spectrum of symptoms varies so much among afflicted individuals. Our lab first linked hemolysis in sickle cell patients to abnormal mitochondrial ROS. In this study, we propose that the differences in disease severity that SCD patients experience is associated with selenium deficiency and reduced GPX1 activity, which is linked to mitochondrial RBC OCR and mitochondrial ROS generation. These proposed studies will address the gap in the research regarding the varying severity of anemia in SCD by examining the association between selenium levels and GPX1 activity and their impact on hemoglobin levels and increases the number of sickle cell associated events (SCE) in children and adults with SCD. Establishing an association between the expression and or activity of selenoproteins and mitochondrial RBC bioenergetics and mitochondrial ROS generation would likely lead to the development of a new intervention strategy for mitigating the burden of SCD, and decreasing the profound morbidity and early mortality. The potential of providing a safe dietary supplement to the SCD community could be a novel strategy that could be implemented in developed as well as developing nations and could profoundly alter people’s lives by effecting the course of the disease.

Status

Completed

Funder

Gilead

Goals

To investigate the role of miR-212 in pulmonary vascular smooth muscle and endothelial cells, and the transfer of miR-212 from endothelium to smooth muscle cells.

Description

Pulmonary hypertension (PH) is a devastating disease that results in a progressive increase in pulmonary vascular resistance, right ventricular failure, and ultimately death of patients. The endothelial and smooth muscle cells (EC and SMC) are two key cell types in the pulmonary vasculature. Crosstalk, like paracrine effects, between these two cell types plays an important role in maintaining the normal conditions of the vasculature and the pathogenesis of PH. However, the role of extracellular vesicle transfer between the two cell types and the exact mechanisms involved in the pathogenesis of PH are not well understood.

We found that under hypoxia, pulmonary artery EC (PAEC) release extracellular vesicles, specifically microvesicles (MV), that induce PASMC proliferation in vitro and PH in vivo, compared to that of normoxic PAEC. As we found that hypoxia exposure did not alter the number of PAECreleased MV, we reason that hypoxia exposure alters the cargo in PAEC-released MV and thereby their function to regulate PASMC proliferation and pathogenesis of PH. MicroRNAs (miRNAs, miRs) are small single-stranded non-coding RNAs and many of them have been identified to play important roles in disease development, including PH. Using miRNA deep sequencing analysis we found that, hypoxia exposure altered the miRNA cargo in PAEC-released MV: miR-210-3p level was increased, a miRNA that is known to stimulate SMC proliferation and induce PH. Meanwhile, hypoxia also induced a number of other miRNAs that inhibited SMC proliferation, principal among them being a novel miRNA, miR-212-5p, that had the highest inhibitory effect on SMC proliferation. Our data also showed that the endothelium and/or ECderived MV are critical for the induction of miR-212-5p in SMC in hypoxia as there was no induction of miRNA-212-5p in isolated SMC in hypoxia. Taking together, we hypothesize that EC-derived MV promote development of PH and vascular remodeling during hypoxia due to the presence of miRNA-210-3p but they may also provide a break against continued progression of the disease via anti-proliferative miRNAs, specifically miRNA-212-5p.

Status

Completed, archived 03/01/2019

Funder

American Lung Association

Status

Completed, archived on 01/03/2019

Funder

Acetylon Pharmaceuticals Inc

Status

Completed

Description

This project aims to elucidate the molecular mechanisms underlying the microRNA-17~92/PDLIM5 signaling-mediated pulmonary artery smooth muscle cell phenotype change and its functional impact in the genesis of pulmonary hypertension. We are continuing to investigate the role of PDLIM5 in the metabolic shift and to carry out a PDLIM5-targeted drug development process for the treatment of pulmonary hypertension.

• Read more on NIH website

Status

Completed

Funder

NIH: NHLBI

• Read more on the NIH website

Sponsor

Eli Lilly & Co

Title

A Randomized, Double-Blinded Study with an Open-Label Extension Comparing the Effect of Once-Weekly Dulaglutide with Placebo in Pediatric Patients with Type 2 Diabetes Mellitus (AWARD-PEDS) H9X-MC-GBG

Description

Clinical trial of a novel therapy for children with Diabetes Type2.

Sponsor

Lurie Children’s (Prime sponsor: NIH)

Title

Effectiveness of an e-health intervention

Description

UIC is a site for this trial, led by Lurie Children’s Hospital, which aims to determine effectiveness of the use of technology for care support in minority children with diabetes.

• Read more on the NIH website

Sponsor

North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS)

• Read more at NAPRTCS website

Title

Measurement of Negative Inspiratory Flow (NIF) in Children Aged 4-8 Years During an Acute Asthma Exacerbation to Predict Effectiveness of Dry Powder Inhaler – A Pilot Study

Description

There are several types of Dry Powder Inhaler (DPI) devices currently on the market used for delivering glucocorticoids, beta-agonists, or combination medication (i.e. diskus, twisthaler/turbuhaler, respiClick). Each type of DPI has a different intrinsic resistance to airflow that determines how much inspiratory flow needs to be created in the device to release the correct amount of drug. Children who cannot achieve the recommended/optimal negative inspiratory flow (NIF) through their prescribed DPI may not obtain the maximum benefit from their medication. In this study, we will evaluate the use of DPI use in children during an acute asthma exacerbation, when NIF is inherently reduced. We hypothesize that the use of DPIs in children aged 4<8 during an asthma exacerbation has limited benefit, as children are unable to generate the needed NIF.

Sponsor

London North West Healthcare NHS Trust (UK)

Title

Marie Sklodowska-Curie Actions – Research and Innovation Staff Exchange

Description

The role of Dr. Hsu and UIC Sickle Cell Center role will be specifically to “train the trainers” on sickle cell disease Community Health Workers and Implementation Science, including.

(1) In short courses and workshops, Dr. Lewis Hsu will train ARISE personnel in the principles of Community Health Workers (CHW) and Implementation Science, and practical application to sickle cell disease. The “train the trainer” approach will equip the ARISE personnel to identify local stakeholders in sickle cell, align the goals of these multiple stakeholder groups when introducing new programs, assess their readiness for change, and empower the stakeholders in continuous evaluation of program quality.

(2) ARISE exchange personnel may apply for courses at UIC, which has College of Medicine, College of Nursing, College of Pharmacy, College of Applied Health Sciences, School of Public Health, College of Business Administration, College of Education, College of Dentistry, College of Engineering, College of Urban Planning and Public Affairs, College of Social Work, College of Liberal Arts and Sciences.

(3) Regular check-in with the African and European faculty on program outcomes and sustainability. They will encourage publication of these Implementation Science experiences, which will facilitate further development of sickle cell programs in sub-Saharan Africa.

Funding

The University of Alabama at Birmingham (Prime sponsor: NIH)

Title

DISPLACE

Abstract

DISPLACE is a national, 28-site study, looking at what keeps some children from getting transcranial Doppler exams. Strokes are a common concern for people with sickle cell disease. Sickle cells are misshaped red blood cells that don’t flow easily in the body. They can clump up in brain arteries, damaging the walls of blood vessels and leading to strokes. A transcranial Doppler, or TCD, measures how quickly blood is flowing through vessels in the brain. If we do a TCD and it’s abnormal, you can start transfusion therapy and prevent stroke. Why doesn’t every child with sickle disease get transcranial Doppler screening as often as needed? That’s what the study will find out.

Sponsor

Lurie (Ann & Robert H) Children’s Hospital of Chicago (Prime Sponsor: NIH)

Title

The Pro-Inflammatory Effects of Acute Exercise in Children with Sickle Cell Anemia

Description

UIC is participating in a multi-site study hosted at Lurie Children’s Hospital of Chicago examining the pro-inflammatory effects of moderate to vigorous physical activity and exercise in children with sickle cell anemia (SCA). The ultimate goal of the study to develop evidence-based guidelines for exercise and physical activity as a transformative strategy to maintain physical functioning and health in children with SCA.

Funder

Children’s Hospital of Philadelphia (Prime sponsor: NIH)

Title

Chronic Kidney Disease in Children

Abstract

Chronic kidney disease (CKD) is a life-long condition that often results in substantial morbidity and premature death due to complications from a progressive decrease in kidney function. The early detection of, and initiation of therapy for, CKD is key to delaying or preventing progression to end-stage renal disease (ESRD). The CKiD (Chronic Kidney Disease in Children) study is a prospective cohort study of children with CKD that investigates risk factors and outcomes of the disease.

Funder

IL Dept of Public Health (IDPH)

Title

University of Illinois Administrative Perinatal Center

Funder

Gerber Foundation

Title

Optimizing Intravenous Protein Nutrition in Premature Infants Using Urine Metabolomics

Funder

Duke Clinical Research Institute (Prime Sponsor: NIH)

Title

Safety of Furosemide in Premature Infants at Risk of Bronchopulmonary Dysplasia

Funder

Children’s Oncology Group/Children’s Hospital of Philadelphia (Prime sponsor: NIH), St Baldrick’s Foundation, Circle of Service Foundation

Title

Many cancer studies

Title

A Retrospective Analysis of Acute Kidney Injury in VLBW Infants

Funder

Univ of WA (Primary sponsor: NIH NINDS)

Title

Preterm Epo Neuroprotection Trial (PENUT Trial) CCC

Description

The aim of this NINDS funded trial is to assess whether high dose Epo will improve survival without neurodevelopmental impairment (NDI) in infants born between 24 and 28 weeks of gestation (term is 40 weeks). 940 infants will be enrolled at 16 centers across the U.S. Subjects will be assessed at 2 years of age to see whether Epo treatment will improve neurodevelopmental outcomes.

• Learn more

Title

Wearable sensors and video recording for children (birth to 24 months) to monitor motor development

Title

Blood Pressure Trends in Very Low-Birth Weight Infants and Contributors of Neonatal Hypertension

Title

Infant Social-Emotional Development, Maternal Mental Well-being, Sense of Parenting Competency, and Parent-Infant Bonding in NICU Families During the COVID-19 Era

Title

Effect of Direct Parental Involvement on Achievement of Independent Oral Feeding in Late Preterm Infants

Title

Contributors of Renal Dysfunction and Neonatal Hypertension in Very Low-Birth Weight Infants

Title

Development, Validation and Implementation of Neonatal Pericardiocentesis and Thoracentesis Training Using a Surgical Simulation Assistant Platform

Funder

American Academy of Pediatrics (Merck)

Title

Adolescent Health Consortium project: Connecting Adolescents and Young Adults to Preventive Health Care Services

Description

This project aims to improve the quality of adolescent and young adult preventive services and promote the inclusion of private, confidential one-on-one interactions between clinicians and youth during routine primary care encounters. The project is in analysis and policy implementation work with national and global health organizations focused on adolescent and young adult health and professional education. There will be an opportunity to work on planning for the International Association for Adolescent Health November 2021 Global Congress in Lima, Peru.

Funder

American Academy of Pediatrics (Prime sponser: FAMRI)

Title

Preventing Children’s Exposure to Tobacco and Secondhand Smoke

Description

The American Academy of Pediatrics (AAP) Julius B Richmond Center is dedicated to the elimination of childrens’ exposure to tobacco and secondhand smoke by changing the clinical practice of pediatrics through the development and dissemination of practice tools; research; and improvement of community health. The Richmond Center is funded by the Flight Attendant Medical Research Institute and other public and private grants, and is based at the AAP with affiliated site and investigators at 7 academic medical centers. The Richmond Center works to create a healthy environment for children, adolescents, and families through public education and through the translation of research into practice and policy in clinical care and in communities in the US and globally. Current projects include surveys of the social climate of tobacco control, a rapid nanotechnology device for secondhand smoke measurement, a microbiome and respiratory illness project, dissemination of parent secondhand smoke interventions, and policy advocacy projects addressing youth and tobacco control. Dr. Klein serves as the Scientific Director of the Center.

Funder

M.R. Bauer Foundation

Title

Sickle Cell Transition Program

Description

Individuals with sickle cell disease suffer from chronic hemolytic anemia, vaso-occlusive pain crises, multisystem organ damage, and a shortened lifespan. The disease is caused by a mutation of the β-globin gene; this mutation allows for the polymerization of the sickle hemoglobin (HbS) when deoxygenated. Many patients are lost to healthcare follow-up during the transition from pediatric to adult care. The peer patient advocate is an individual with Sickle Cell Disease who serves as a community health worker. The peer patient advocate builds relationships and connections with patients, families, and the sickle cell community. The peer patient advocate will be closely connected to patients and families and will participate in the following areas of care: 1) group care sessions as facilitator 2) Sickle cell transition fair coordination 3) Visiting pediatric patients in hospital and clinic. The advocate will assist with the transition of the medical, social, and professional lives of adolescents living with Sickle Cell disease from pediatric to adult care.

Description

Health disparities research, built environment and behavioral interventions to promote healthy dietary behavior, dissemination and implementation science research to improve the translation of evidence-based interventions.

• Murphy, Shannon – Beginning: A University Partnership Program – Healthy Steps (PIHV-Prevention Initiative Home Visiting)
  Funder – Chicago (IL) City (Public Schools)
• Bernstein, Karen – Does Choice of Contraceptive Method influence frequency of STI screening and rates of STI’s among Adolescents and Young adults in an Urban Academic Setting
• Bernstein, Karen – Longitudinal Evaluation of the Required Level of Supervision for Pediatric Fellows
• Fitzgibbon, Marian – Mediterranean diet, weight loss, and cognition in obese older adults
  Funder: NIH
• Fitzgibbon, Marian – Cancer Education and Career Development Program
• Martin, Molly – The Asthma Action at Erie Trial
  Funder – NIH: NHLBI
• Martin, Molly – Coordinated Oral Health Promotion (CO-OP) Chicago
  Funder – NIH: NIDCR
• PI Martin, Molly – Value and Mechanisms of Home Visitation in Obesity Interventions for Low-Income Children
  Funder – Rush Univ Medical Ctr (Prime sponsor: NIH)
• Osta, Amanda – Addressing Social Key Questions for Helping Experienced Adversity in Life to Heal: the ASK Questions for HEALTH study
• Raghavan, Aarti – Neutral Head Positioning in Preventing Intraventricular Hemorrhage
• Shah, Reshma – Sit Down and Play Funder – SDBP. Integrating a preventive early childhood development intervention in clinics serving low-income communities
• Shah, Reshma – Leveraging healthcare settings to support early childhood development in LMICs
• Sierra-Fernandez, Hernan – Feasibility and acceptability of text messaging as a supplementary channel of communication between parents and NICU staff Funder – UIC Pediatric Seed Funding. This study will examine the feasibility and acceptability of a personalized, one-way, text messaging program to improve communication between parents and NICU staff.
• Sierra-Fernandez, Hernan – Impact of an NICU rounding report on resident’s time utilization and workload. The aim of this study is to determine time savings in residents workflow after the introduction of a NICU specific rounding report. Our main outcome is time spent preparing the NICU rounding flowsheet. Secondary outcomes are: time spent inside the NICU and time performing physical exam on patients.
• Solomon, Marla – Diabetes Care in Schools: An Educational Program for School Nurses and Delegated Care Aids
  Funder – Medtronic Inc
• Srivastava, Pavan – Validation of a Pediatric Clinical Judgment Exercise in Assessing Entrustability of Fourth Year Medical Students in Critical Clinical Decision-Making
• Van Voorhees, Benjamin – University of Illinois CHECK (Coordination of Healthcare for Complex Kids)
  Funder – US Dept of Health & Human Services (Centers for Medicare & Medicaid Services)
• Barnes, Michelle – Family-Physician Communication Study
• Glassgow, Anne – The Effect of Neighborhood Disorganization on Engagement in Health Care, Mental Health, and School Attendance of Children with Chronic Health Conditions (CHER)
  Funder – NIH/UIC Center for Health Equity Research – CHER
• Osta, Amanda – Universal Screening for Unmet Social Needs and ACE in Primary Care Medical Homes: Optimizing Identification of Social Needs and ACE Modifying the ASK Questionnaire
• Patel, Saurabh Kumar – National survey for Umbilical line insertion and maintenance practices
• Van Voorhees, Benjamin – Promoting Adolescent Health (PATH)
• Olorunyomi, Olalekan – Motivators and barriers of physical activity among adolescents with sickle cell disease
• Vander Roest, Daphne – Identifying electronic residency application service filters.
• Vander Roest, Daphne – Creation and implementation of a pediatric inpatient medicine curriculum: survey of pediatric resident physicians
• Vander Roest, Daphne – Assessing a Remote Curriculum for Supplementing Resident Education during a Pandemic
• Vander Roest, Daphne – Using resident virtual simulation to hone clinical skills

Funder

NIH

Title

Non-Covalent Nrf2 Activators for the Treatment of Chronic Wounds

Description

Chronic, non-healing wounds of the skin are serious medical complications that affect over 6.5 million Americans, especially older adults. These wounds include pressure sores, diabetic foot ulcers and venous ulcers. There are numerous surgical and dressing treatments for these wounds, but because there are over 70,000 lower-limb amputations each year arising from these wounds, it is clear that new treatments are needed. Strikingly, there are almost no pharmaceutical therapies to accelerate healing of chronic wounds. A major contributor to chronic wounds is a prolonged inflammatory state, and reducing inflammation may be a way to accelerate healing of chronic wounds. Unfortunately, many commonly used anti-inflammatory drugs hinder chronic wound healing; thus, new ways of reducing inflammation are needed. An essential factor in wound healing and an important regulator of inflammation is Nrf2, a transcription factor that induces many cytoprotective and antioxidant genes. As seen in other inflammatory disorders, activating Nrf2 could be a useful therapeutic strategy to treat chronic skin wounds. There are a number of covalent Nrf2 activators, but they are not selective for Nrf2, which is problematic because some of the off-target effects of these molecules are at proteins that hinder chronic wound healing. Thus, pharmacologic activation of Nrf2 with non-covalent small molecules will accelerate wound healing, which could lead to new therapeutics to treat chronic wounds. Our lab, in collaboration with Drs. DiPietro and Reddy labs at UIC, are using metabolism and pharmacokinetics studies, to develop high-affinity, metabolically stable, in vivo probes of Nrf2 activation for chronic wounds. These experiments are significant because they will develop novel in vivo probes of non-covalent Nrf2 activation, and they are innovative because they will open up new therapeutic strategies to treat chronic wounds.

• Baynard – The pro-inflammatory effects of acute exercise in children with sickle cell anemia
  Funder – Lurie (Primary sponsor: NIH)
• Donenberg, Geri – Peer Versus Adult-Led HIV Prevention for Juvenile Offenders: Effectiveness and Costs Funder – NIH/NIMHD. A randomized controlled trial comparing the effectiveness and cost of different types of intervention facilitators in order to identify the most effective and sustainable way to implement the PHAT Life program within juvenile justice settings. Karen Bernstein is a collaborating physician.
• Dudek, Steven – Cortactin in Regulation of Pulmonary Vascular Permeability
  Funder – NIH
• Gordeuk, Victor – Improving Sickle Cell Care in Adolescents and Adults in Chicago
  Funder – NIH
• Johnson, Jeremy – Rosemary as a Food Preservative: Implications for Gastrointestinal Health Funder – US Dept of Agriculture (Natl Inst of Food & Agriculture)(fmr CREES)
• Logan, Latania (Rush University Medical Center) – Colonization and Infection in Children with Multi-drug resistant Gram Negative Bacteria: A Comparative Study of Taxonomy, Risk Factors and outcomes. This is a study of  ESBL- positive,  gram negative organisms  in children in several Chicago hospitals, and their molecular characteristics. UIC is one of the local
• Mehta, Dolly – Mechanisms of endothelial regeneration and resolution of lung vascular injury Funder – NIH
• Powell, Lisa – SIP 14-022 Global and Territorial Health Research Collaborating Center: Illinois PRC
  Funder – US Dept of Health & Human Services (CDC)
• Raja, Sheela – Patient Perceptions about Sensitive Healthcare Questions
• Weiner, Saul – An Assessment of Open Access Audio of the Clinical Encounter on Veterans and their Care
• Weiner, Saul – Integrating an Audit & Feedback Program to Prevent Contextual Errors into the Ambulatory Setting Workflow
• Weiner, Saul – Integrating Contextual Factors into Clinical Decision Support to Reduce Contextual Error and Improve Outcomes in Ambulatory Care