Grants

NIAID - National Institute of Allergy and Infectious Diseases

Project summary Herpes simplex virus (HSV) establishes latency in ganglionic neurons of the peripheral nervous system. Latent HSV can later reactivate, causing recurrent disease and possible transmission to new hosts. Current anti-HSV therapy is inadequate, in that it does not eliminate latent HSV, and thus is only suppressive rather than curative. We developed a therapeutic approach based on gene editing using HSV-specific meganucleases. We showed that intravenous (IV) administration of adeno-associated virus (AAV) encoding anti-HSV-1 meganucleases can eliminate up to 97% of latent HSV DNA from dorsal root ganglia in mouse models of latent HSV-1 genital infection. We also demonstrated that this reduction in ganglionic viral load led to a corresponding reduction of viral shedding from treated vs. control mice. This approach offers the potential for a durable means of controlling latent HSV infection and subsequent reactivations, or even achieving a functional cure. In the R21 phase, we propose to extend our work to target HSV-2, and to determine whether IV or localized intrathecal (IT) administration is the optimal route. In the specific aims of the R33 phase we plan to address simultaneously several outstanding issues regarding both HSV biology and the safety and efficacy of in vivo gene therapy that are critical for clinical translation of our work. R21 Phase: Specific Aim 1. Evaluate IT vs. IV delivery of AAV/meganuclease therapy as a means to reduce AAV dose, minimize systemic exposure, and avoid pre-existing/induced anti-AAV immunity. We will evaluate the AAV biodistribution, antiviral efficacy, and dose response after IT vs. IV administration, and the doses at which toxicity occurs. We will also evaluate the ability of IT-delivered AAV to avoid neutralizing antibody present in serum, and whether IT administration will allow re-dosing of AAV. R33 Phase: Specific Aim 2. Compare the natural history of ganglionic HSV load and peripheral viral shedding in latently infected mice after IT or IV meganuclease therapy vs. untreated control animals. We will perform long-term studies of the ganglionic viral load and the frequency and quantity of peripheral shedding in control vs. AAV-meganuclease treated animals. These studies will shed light on the stability of reservoirs, the relationship of ganglionic viral load reductions with the frequency and quantity of viral shedding, and provide new insights into possible HSV re-seeding of ganglionic reservoirs after viral reactivations. R33 Phase: Specific Aim 3. Determine the host genomic consequences of AAV/meganuclease therapy, and compare to the effects after CRISPR/Cas9 exposure. We will perform an unbiased evaluation of genomic disruptions after our meganuclease therapy, and directly compare with CRISPR/Cas9 approaches, using the state-of-the-art techniques for the detection of off-target events, including GUIDE-seq, improved DISCOVER-Seq+, and analyses for the insertion of AAV vector (ITR-Seq) and HSV DNA (hybridization capture coupled with next generation sequencing) into the host genome.

Up to $233K

2028-03-31

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AAV-mediated PERM1 Overexpression as a New Therapy for Heart Failure with Reduced Ejection Fraction

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Heart failure is a leading cause of death in developed countries, affecting 6 million people in the United States and approximately 64.3 million people worldwide. Mortality rates remain high, with 50% of patients dying within five years of diagnosis. About half of these patients have heart failure with reduced left ventricular ejection fraction (HFrEF), which is characterized by an ejection fraction of 40% or less and adverse cardiac remodeling. HFrEF is associated with reduced cardiac contractility and mitochondrial impairment. Currently, no therapies specifically target both muscle contractility and mitochondrial function. PERM1, a striated muscle-specific regulator of energy metabolism, is predominantly expressed in the heart and skeletal muscle. We have demonstrated that PERM1 is downregulated in both human and mouse failing hearts and that its loss in mice leads to reduced cardiac contractility and energy reserves. Our preliminary data show that gene delivery of PERM1 to the mouse heart via adeno-associated virus (AAV) fully prevents the onset of HFrEF during pressure overload in mice, preserving systolic function and promoting mitochondrial biogenesis. This study will address the hypothesis that AAV-medicated PERM1 overexpression can serve as a novel therapeutic approach to prevent and reverse contractile dysfunction under pathological stress. This translational study will initiate testing of this promising gene therapy in a well-established mouse model of HFrEF and a preclinical swine model of HFrEF induced by myocardial infarction. Additionally, it will further elucidate the novel mechanisms by which PERM1 simultaneously regulates muscle contractility and energy metabolism in the heart.

Up to $819K

2030-01-31

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Abatement Project

City of Kansas City

Sustainability & Environment

Up to $496K

environment

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Abberior MIRAVA STED Microscope

OD - NIH Office of the Director

Project Summary/Abstract Nine NIH-funded investigators with similar but independent super-resolution microscopy needs are requesting funding to acquire an Abberior Mirava 3D STED microscope to enable imaging of molecular topographies in fixed or live tissues and cells at unprecedented resolution at the scale of tens of nanometers with fluorescent probes. This platform will be maintained in the Washington University Center for Cellular Imaging (WUCCI), an institution-wide shared technology resource. There is no instrument like this at WUCCI or anywhere else on campus. One huge advantage of this system is that it works just like a confocal microscope in terms of the field of view, imaging depth, and data acquisition interface. As such, many investigators will be ready to utilize it immediately. Sample preparation is nearly identical to conventional confocal microscopy, except for the use of specific fluorescent probes, and care taken to use mounting or immersion media and cover slips with matching refractive indexes to enable maximum resolution. STED technology breaks the traditional barrier of optical microscopy set by the diffraction-limited point spread function (PSF) by PSF engineering, achieving 40 nm resolution, exceeding the resolution of the already heavily subscribed Nikon NSPARC and Zeiss Airyscan. The major user group comprises nine investigators from 6 departments who will utilize this microscope to enable a wide range of basic and translational research studies. Scientific goals include understanding primary cilia, the role of actin cytoskeleton dynamics in intracellular networks, energy and lipid storage and lipid droplet or to resupply membranes with lipids, mechanobiological mechanisms underlying kidney glomerular filtration, glutamate receptor geography at cochlear synapses, receptor dynamics in pancreatic islet hormone secretion and neuroinflammation biomarkers for biological imaging and chemotherapeutics. Given its location in a busy core facility, we expect this microscope to be impactful to many research programs beyond the initial major user groups. The expertise and institutional support for this instrument are excellent. Dr. Mark Rutherford, Associate Professor of Otolaryngology, used STED microscopy extensively during the historical development of this technology. Dr. Rosa-Molinar and the WUCCI staff have a long-standing track record of training NIH- funded researchers to optimize their use of state-of-the-art microscopy methods. In support of this S10 grant application, the Washington University School of Medicine will commit $176,647 of matching funds for the acquisition of the instrumentation plus an additional $125,000 operational support ($25,000 per year for five years) to ensure the long-term success of this equipment.

Up to $750K

2027-05-14

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AbbVie Foundation — Health Access Grants

health accesscommunity healthchronic disease

AbbVie Foundation

Funds community health programs expanding access to care for underserved.

$25K – $250K

Annual

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Abdul Latif Jameel Foundation Programs

Abdul Latif Jameel Foundation

Supports poverty alleviation, job creation, health, education, and climate change mitigation.

$50K – $1M

poverty alleviationemploymentHealth+2

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Abernathy Steelhead Weir Project

Fish and Wildlife Service

Support a study to determine the reproductive success of hatchery versus wild steelhead.

$100 – $70K

rolling

Education

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Aberrant m6A methylation correlating with hippocampal pathology in multiple sclerosis

NINDS - National Institute of Neurological Disorders and Stroke

ABSTRACT Multiple sclerosis (MS) is an immune-mediated disease of the human central nervous system (CNS) affecting more than two million people worldwide. Among the spectrum of cognitive disability, memory dysfunction ranks primary among MS patients. Several studies have linked memory loss with hippocampal changes in MS patients. Investigating hippocampal pathology in MS patients, we reported demyelination of the hippocampus in greater than 60% of MS brains. Our previous studies found decreased axonal transport and loss of synapses following demyelination in both human and mouse hippocampus. It is however not clear how demyelination affects neuronal and synaptic changes. The field of epigenetics have been instrumental in changing our view about how factors, like DNA methylation, could change the expression and/or function of genes in several neurological diseases. N6-methyladenosine (m6A) is the most abundant and conserved co-transcriptional modification in eukaryotic RNAs controlled by m6A methyltransferases (m6A writers), recognized by m6A-binding proteins (m6A readers) and removed by the demethylases (m6A erasers). Balance between these three processes controls effective transcription and function of individual genes. Our preliminary results show a selective decrease in `m6A erasers' with concomitant increases in both `m6A writers' and `m6A readers' in MS hippocampal neurons. These abnormalities in the m6A pathway were supported by identification of several m6A methylated regions in genes belonging to synaptic structures. These results formed the basis of our hypothesis that “demyelination alters m6A methylation patterns in gene transcripts associated with synaptic plasticity and neuronal function in MS hippocampus”. This exploratory proposal will build on preliminary findings and use both human and mouse tissue to a) examine the levels and cellular identify of key m6A pathway members following hippocampal demyelination; and b) identify conserved m6A methylated residues and gene transcripts following hippocampal demyelination/remyelination. Our results will provide necessary data towards linking m6A modification, demyelination and neuronal function. Several drugs targeting the m6A pathway are of great interest in several diseases. We feel this study will pave the way for development of alternative interventions from the avenue of epigenetics to address neuronal dysfunction in MS.

Up to $432K

2028-04-30

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AbilityOne DOW Contract Management Services

DEPT OF DEFENSE.WASHINGTON HEADQUARTERS SERVICES (WHS).WASHINGTON HEADQUARTERS SERVICES

AbilityOne DOW Contract Management Services

general

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Abiotic Constraints to Survival of Lake Sturgeon Eggs and Age-0 with Implications for Restoration

Environmentalsustainability

Fish and Wildlife Service

The Coastal Program is a voluntary habitat conservation program that provides technical and financial assistance to partners for restoration projects that benefit Federal trust species. The service will provide $70,568 to Michigan Technological University to determine the physical characteristics needed for young lake sturgeon to survive in native habitat located in Michigan and Wisconsin. This will guide restoration actions in degraded rivers for the benefit of lake sturgeon, as well as conserve and protect other plants and animals native to the area.

Up to $71K

rolling

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ABL kinase signaling networks regulate Transcription-Replication Collisions in Small Cell Lung Cancer

NCI - National Cancer Institute

Maintenance of genomic stability requires coordinated spatial and temporal regulation of the replication and transcription machineries on DNA. Deregulated transcription in cancer cells can promote transcription-replication conflicts (TRCs) through increased collisions with the replication machinery, thereby generating breaks on the DNA. Unexpectedly, we discovered that inhibition of the ABL tyrosine kinase enhances accumulation of TRCs in small cell lung cancer (SCLC), thereby revealing a novel role for ABL in the regulation of collisions between the transcription and DNA replication machineries. Notably, we found that ABL inactivation markedly impairs outgrowth of SCLC tumors in mouse models, resulting in prolonged animal survival. Further, ABL inactivation impairs the expression and function of proteins implicated in transcription-coupled homologous recombination (TC-HR). SCLC is a highly aggressive neuroendocrine lung cancer with an overall 5-year survival rate of only ~7%, which has remained unchanged for over 30 years. SCLC tumors exhibit a high degree of genomic instability with upregulation of proteins in the TC-HR pathway. TC-HR promotes repair of DNA double strand breaks (DSBs) at sites of active transcription and is associated with formation of R-loops comprised of DNA-RNA hybrids and displaced single-stranded DNA. Abnormal accumulation of R-loops increases TRCs, leading to enhanced DNA damage and cell death. Because ABL inactivation markedly increased TRCs and DNA damage, we evaluated whether blocking the activity DNA damage-repair pathways by targeting ATR in the presence of ABL inhibitors might synergize to promote SCLC cell death. We found that co-inactivation of ABL and ATR kinases induces profound synergistic inhibition of SCLC cell survival and impairs SCLC dissemination and outgrowth in mouse models. Here we will evaluate the hypothesis that ABL inactivation enhances SCLC vulnerabilities by increasing TRCs, resulting in enhanced DNA damage, and rendering SCLC cells hypersensitive to inactivation of components of DNA damage-repair pathways. The specific aims are: 1) Define the mechanisms by which ABL inactivation increases TRCs and DNA damage in SCLC subtypes. 2) Identify novel combination therapies to treat SCLC revealed by unbiased ABL inhibitor-mediated sensitization screens with SCLC cell lines, clinicalbiopsy- derived micro-organospheres, and SCLC metastases from mouse models treated with single and combination therapies. 3) Define the transcriptional landscapes of patient-derived SCLC subtypes, and metastatic SCLC in situ in mouse models treated with single and combination therapies. Justification for use of animal models: The use of mouse models is required for lung cancer metastasis studies to assess the contribution of multiple cell types, including immune cells, implicated in the metastatic cascade. There are no in vitro co-culture systems that faithfully mimic the complex interactions of SCLC metastases and cell types in the tumor microenvironment required for the multi-step process of metastasis observed in vivo. Completion of the proposed research will reveal novel mechanistic insights into pathways that promote SCLC metastasis, uncover the mechanisms whereby ABL signaling networks regulate TRCs, and reveal the effectiveness of co-inactivation of ABL kinase and DNA damage-repair pathways to impair dissemination and outgrowth of deadly SCLC tumors.

Up to $646K

2031-06-30

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ABMR Annual Meeting 2026 & 2027

NIA - National Institute on Aging

Project Summary/Abstract The Academy of Behavioral Medicine Research (ABMR) is guided by its mission to advance the field of behavioral medicine by creating and disseminating knowledge, cultivating discourse, and inspiring change that culminates in better health for all. ABMR Fellows are distinguished mid-level and senior scientists, including MDs and PhDs, elected by their peers for contributions to behavioral medicine research. Our mission primarily is accomplished through the annual scientific meeting that brings together our diverse membership and invited thought leaders to share the latest scientific advances, exchange cutting-edge ideas, and provide stimulating and engaging discussions in an informal but rigorously scientific atmosphere. ABMR Fellows lead extensive NIH-supported programs of research that integrate biomedical, behavioral, and social sciences to support healthy gaining and reduce chronic disease burden across the lifespan. Our Fellows focus on revealing biolobehavioral mechanisms of aging that underlie leading causes of death and disability (e.g., heart disease, cancer, Alzheimer's, diabetes) and developing and implementing effective interventions to maintain health and reduce the burden of age-related chronic conditions. In 2021, we added an early-stage investigators (ESI) program to the ABMR annual meeting, specifically to foster career development and leadership skills of promising behavioral medicine scholars with their first K- or R-level award from NIH. This R13 conference grant will support the planned 2026 and 2027 Annual Scientific Meetings, including participation of invited Keynote Speakers each year and our 10 ESI Program Fellows per year. The 2026 meeting will be held June 24-27, 2026, at The Stonewall Resort in Roanoke, WV; the 2027 meeting will be held June 25-28, 2025 in SeaTac, WA. Our R13 has 3 Aims. Aim 1 is to disseminate recommendations for implementing the behavioral medicine evidence base to promote healthy aging and reduce chronic disease burden. The meetings will specifically focus on: 1) the clinical trials enterprise; 2) AI; and 3) evidence-based prevention and patient care delivery models, each as concerns the behavioral factors associated with healthy aging, digital/mHealth, precision behavioral medicine interventions, and methods to ‘kick start’ health promotion as a life-long practice. With support through the R13, both meetings will feature Keynote Speakers who are thought leaders on these issues but from adjacent fields. For Aims 2 and 3, we will support 10 up-and-coming ESIs each year through the ABMR ESI Fellowship Award, providing a leadership workshop, mentorship and career development training focused on strategies for sustaining and strengthening independence and leadership. This R13 enables ABMR to nurture the success of the next generation of behavioral medicine researchers and leaders, which aligns with NIH’s Next Generation Researchers Initiative, and enables ABMR to advance the field of behavioral medicine as it has since its inception almost 50 years ago.

Up to $50K

2028-02-29

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Abramson Cancer Center Lead Academic Participating Sites (LAPS)

NCI - National Cancer Institute

PROJECT SUMMARY/ABSTRACT The University of Pennsylvania Abramson Cancer Center (ACC) has been highly engaged in the National Cancer Institute (NCI) National Clinical Trials Network (NCTN) for many years and has demonstrated an extraordinary commitment to the mission of the NCTN. The ACC has fostered an extensive cooperative group membership with many investigators serving in group or NCI committee leadership roles (44 group committee chair positions, 34 NCI committee roles, 16 study chairs, 14 study co-chairs, and nine study champions), robust accrual to NCTN clinical trials, leadership of large national trials, delivery of innovative ideas to the NCTN, and mentorship and career development of young investigators. The ACC has made a significant investment in the NCTN through the development of a centralized clinical research infrastructure focused exclusively on the conduct of NCTN trials—the NCTN@ACC. The leader of this enterprise and the PI of this LAPS grant is Dr. Jennifer Eads, Professor of Medicine in medical oncology. She has extensive experience in clinical trials, including through NCTN, for which she was named ECOG-ACRIN Investigator of the Year (2022). As Director of NCTN@ACC, Dr. Eads oversees the centralized NCTN administrative, operational, regulatory, auditing, monitoring activity, and financial aspects of the program. The NCTN@ACC is supported by five NCTN@ACC staff and three NCTN committees, all of which provide critical roles in the visionary and operational aspects of the program. Ensuring access to and representation of the communities in our catchment area in NCTN trials is a major effort across departments and the University of Pennsylvania Health System network of hospitals, led by Dr. Eads. The NCTN@ACC collaborates extensively with multiple research centers, scientific research programs, core facilities and the ACC Cancer Service Line to bring innovative ideas from these groups into the NCTN for further development of clinical trials. The NCTN@ACC is strongly committed to career development of young investigators through multiple mentoring mechanisms, including exposure to the NCTN where scientific and leadership contributions are encouraged. Specifically, NCTN@ACC aims to (1) lead an expansive NCTN clinical research program at the ACC through an efficient, centralized enterprise that enables rapid enrollment across the Penn network and the conduct of high-quality clinical research with a focus on outreach to the community; (2) drive exceptional leadership and innovation of NCTN clinical research at the national and institutional level; and (3) expand the ACC commitment to mentorship and career development of faculty and staff, as well as enrollment of populations across our catchment area including patients with rare cancers.

Up to $369K

2032-02-29

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Academic

NYS Department of Corrections and Community Supervision

The major goal of the education program is to ensure that every incarcerated individual who leaves the system possesses a High School Equivalency diploma (HSE). To this end, the Department mandates participation in the education program for all incarcerated individuals who do not have a verified High School diploma or High School Equivalency diploma at reception. Because a High School diploma or High School Equivalency diploma is required for the higher paying inmate jobs, there is an added incentive to obtain it.

Up to $27.9M

Educationworkforce

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Academic Career Excellence (ACE) Award (K32 Independent Clinical Trial Not Allowed)

National Institutes of Health

The purpose of the Academic Career Excellence (ACE) Award (K32) is to support rigorous, mentored scientific research and career development for up to three years for early-stage postdoctoral scholars. Candidates must submit their application up to one year prior to beginning their postdoctoral position or no more than two years after their postdoctoral training begins (resubmissions included). The ACE K32 will foster early, goal-directed planning and encourage innovative applications with the potential for a significant impact on scientific research and career development. Inclusion of preliminary data are not required as the ACE K32 emphasizes innovative research ideas and thoughtful plans for training and mentorship that will facilitate the development of the postdoctoral scholars who have the potential to become productive, independent investigators in research fields relevant to the missions of the participating NIH Institutes and Centers.

2029-07-12

Healthhealthcare

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Academic Career Excellence (ACE) Award (K32 Independent Clinical Trial Not Allowed)

National Institutes of Health

Academic Career Excellence (ACE) Award (K32 Independent Clinical Trial Not Allowed)

2029-07-12

general

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Academic Career Excellence (ACE) Award (K32 Independent Clinical Trial Not Allowed)

National Institutes of Health

2029-07-12

Health

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Academic Leadership Career Award

NIA - National Institute on Aging

The burden of ADRD remains high in the US and it is expected to increase with devastating impact on patients, families, and a large impact on health care related costs. Whereas there are promising developments in treatments, the effects are still limited. Thus, there is a critical need to understand the modifiable ADRD risk factors to develop preventive interventions. The Lancet commission reports that half of ADRD cases could be prevented with the elimination or control of 14 modifiable risk factors Research has also indicated that brain changes occur around 20 years before onset of disease, which highlights the opportunity for early intervention. Life-course approaches are therefore key but underutilized methods to understand best windows for risk factor modification. To address this gap, the central goal of this application is to create a program in life-course epidemiology of ADRD and aging, which will establish Albert Einstein College of Medicine as a leading institution in this area. Einstein has well-established ADRD research programs, but a life-course approach with emphasis in prevention is missing. This is of particular urgency given that the Bronx, where Einstein is located, is in the top 3 counties with the highest prevalence of ADRD in the US. The long-term plan of this award is to build a national resource in life-course epidemiology and train the next generation of ADRD researchers, with the ultimate goal of reducing the burden of ADRDs in the Bronx and elsewhere.

Up to $134K

2031-04-30

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Not Allowed)

National Institutes of Health

The purpose of this Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutionsis to support small scale research grants at institutions that do not receive substantial funding from the NIH, with an emphasis on providing biomedical research experiences primarily for undergraduate students, and enhancing the research environment at applicant institutions. Eligible institutions must award baccalaureate science degrees and have received no more than $6 million dollars per year of NIH support (in both direct and F and A/indirect costs) in 4 of the last 7 fiscal years. For institutions composed of multiple schools and colleges, the $6 million funding limit is based on the amount of NIH funding received by all the non-health professional schools and colleges within the institution as a whole. See Part II. Section 3.1 Eligible Organizations for more information.

Healthincome_security_and_social_servicesfood_and_nutrition+2

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Not Allowed)

National Institutes of Health

Education

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Not Allowed)

National Institutes of Health

Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Not Allowed)

research

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Required)

National Institutes of Health

Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Required)

research

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Required)

National Institutes of Health

<p>The purpose of this Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions is to support small scale research grants at institutions that do not receive substantial funding from the NIH, with an emphasis on providing biomedical research experiences primarily for undergraduate students and enhancing the research environment at applicant institutions.Eligible institutions must award baccalaureate science degrees and have received no more than $6 million dollars per year of NIH support (in both direct and F and A/indirect costs) in 4 of the last 7 fiscal years. For institutions composed of multiple schools and colleges, the $6 million funding limit is based on the amount of NIH funding received by all the non-health professional schools and colleges within the institution as a whole.This Notice of Funding Opportunity (NOFO) supports investigator-initiated mechanistic and/or minimal risk clinical trials addressing the mission and research interests of the participating NIH institutes. For the purpose of this NOFO, minimal risk clinical trials are defined as those that do not require FDA oversight, do not intend to formally establish efficacy, and have low risks to potentially cause physical or psychological harm.</p>

EducationHealthincome_security_and_social_services

2027-01-07

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Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions (R15 Clinical Trial Required)

National Institutes of Health

The purpose of this Academic Research Enhancement Award (AREA) for Undergraduate-Focused Institutions is to support small scale research grants at institutions that do not receive substantial funding from the NIH, with an emphasis on providing biomedical research experiences primarily for undergraduate students and enhancing the research environment at applicant institutions.Eligible institutions must award baccalaureate science degrees and have received no more than $6 million dollars per year of NIH support (in both direct and F and A/indirect costs) in 4 of the last 7 fiscal years. For institutions composed of multiple schools and colleges, the $6 million funding limit is based on the amount of NIH funding received by all the non-health professional schools and colleges within the institution as a whole.This Notice of Funding Opportunity (NOFO) supports investigator-initiated mechanistic and/or minimal risk clinical trials addressing the mission and research interests of the participating NIH institutes. For the purpose of this NOFO, minimal risk clinical trials are defined as those that do not require FDA oversight, do not intend to formally establish efficacy, and have low risks to potentially cause physical or psychological harm.