Search Grantees

Abstract or Project Description

Abstract or Project Description

The Unquiet Professional is a organization committed to recognizing and honoring our nation’s Gold Star & Surviving Families, Veterans and military families by providing rewarding and purposeful opportunities to heal from the wounds of war.

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To research and prototype shared services for the field.

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A dance film based on an original poem aiming to uplift a love story out of violence, defying the common spectacularization of blackness and amplifying the devotion of two people to each other, survival and joy. Using stillness and minimalism, the piece invites witnesses to settle into a space of imagination, curiosity and receptivity.

Abstract or Project Description

TRiO Plus is creating an Affordable Housing Marketplace to support teachers of color in living where they work, aiming to enhance student performance by fostering diversity among educators and addressing housing barriers. By prioritizing recruitment and retention of Black, Latine and other teachers of color, TRiO Plus seeks to improve outcomes for Oakland’s diverse student population.

Abstract or Project Description

Ubuntu Theater Project creates transformative theatrical experiences that inspire compassion and reveal our shared humanity through collaborative productions. Partnering with local institutions like Oakland School for the Arts and Laney College, UTP provides affordable training and professional opportunities to bridge the opportunity gap for Oakland’s diverse artists, fostering a supportive community for aspiring and established professionals alike.

Abstract or Project Description

The Union City Police Department is the law enforcement agency responsible for ensuring public safety and enforcing laws within Union City, California. They work to protect and serve the community through crime prevention, investigation and community engagement initiatives.

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To administer The Rainin Arts Fellowship.

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To support basic and clinical scientists in developing novel cellular and immuno-therapies in multiple myeloma under the direction of Dr. Tom Martin and Dr. Jeff Wolf.

Abstract or Project Description

The microbes that flourish within our guts are central to many aspects of human health. Which microbes are present can dictate susceptibility to a number of acute and chronic diseases, including IBD. This proposal will use a mouse model with a defined and stable set of bacteria to probe how mice interact with specific members of their microbiota in health and during disease. First, each microbe will be tested for its ability to elicit an immune response in healthy mice. Once we have established the baseline response in normal healthy mice, we will use chemicals to disrupt the gut lining to elicit an inflammatory response, or we will disrupt genes known to limit intestinal inflammation. We will then investigate how immune recognition of the microbiota changes under these altered conditions. This system will enable us to track responses to the microbiota with unprecedented precision and will provide clues regarding which microbes drive immune activation during dysregulated responses to the microbiota. Such studies will pave the way for future work aimed at manipulating responses to key members of the microbiota responsible for inflammatory diseases of the gut.

Abstract or Project Description

In Inflammatory Bowel Disease (IBD), inflammation of the digestive tract lining results in the development of chronic ulcers appearing throughout the intestines, colon or rectum. Although symptoms of IBD can be managed through the use of corticosteroids, complete disease remission is rare, often leading to surgical intervention. High expression of the transcription factor HIF-1_ is a key feature of regeneration in the Murphy Roths Large mouse, an inbred laboratory strain displaying remarkable regenerative capabilities. Recently, our team demonstrated enhanced regeneration of acute and chronic tissue wounds in adult mice following transient therapeutic upregulation of HIF-1_ using the experimental drug DPCA. Previous studies of HIF-1_ in IBD have been limited to preventative therapy and have not explored fibrosis inhibition or regeneration. Therefore, we hypothesize that transient upregulation of HIF-1_ can inhibit fibrosis of IBD lesions. We propose to study the effects of DPCA on 1) fibrosis in a human intestinal organoid (HIO) model; and 2) lesion development in a murine TGFb-induced model of intestinal fibrosis. This project will contribute to the development of a new clinical treatment for IBD, as an alternative or adjunct to existing therapies that focus on resolving inflammation, but do not address fibrosis.

Abstract or Project Description

Various immune cells in the gut recognize and respond to microbes that live there, which are collectively known as the gut microbiota. This project focuses on a subset of immune cells termed B cells, which are important for functions such as antibody production. In particular, we are investigating how certain kinds of beneficial gut bacteria interact with B cells to improve gut health. Moreover, we are testing whether harmful bacteria found in the gut of patients with Inflammatory Bowel Disease do not interact with B cells, which may partly explain the altered immune responses observed during gut inflammation in these patients. Collectively, our work will have a significant impact on Inflammatory Bowel Disease by identifying and investigating new ways by which beneficial and harmful bacteria interact with B cells in the gut, which could have important implications for the future treatment of these diseases.

Abstract or Project Description

Ulcerative colitis (UC) is a chronic inflammatory disorder that affects the colon. There are multiple types of cells that drive inflammation and injury to the lining of the colon. Vedolizumab (VDZ) is a medication that blocks circulating immune cells from gaining access to the colon, but there are conflicting data about the primary cell types affected by this treatment. To identify the inflammatory cells that contribute to colitis and respond to VDZ, we performed a comprehensive single-cell transcriptomic and proteomic analysis of peripheral blood and colonic biopsies of patients with and without UC. We identified inflammatory cells called mononuclear phagocytes (MNPs) as a primary target of VDZ. We then used four new, complementary methods to look at where these cells are located in fixed tissue sections, and we discovered increased density and proximity of MNP and fibroblast subsets in UC biopsies when compared to HC, with inhibition by VDZ. We now want to confirm and extend these findings by looking in more detail at these cell types in tissue sections before and after therapy. We also want to culture epithelial cells from patients with MNPs and fibroblasts to see how these cells interact when grown in the lab.

Abstract or Project Description

The intestinal immune system must maintain a delicate balance between harmless bacteria in the gut and immunity against dangerous pathogens. Dysregulation of this balance can lead to Inflammatory Bowel Diseases (IBD) such as ulcerative colitis (UC) and Crohn’s disease. Many treatments for IBD focus on blocking inflammation and fail to repair damaged tissue and restore the integrity of the tissue. We have identified a long non-coding RNA that is only expressed in the colon. When this RNA is present the tissue is healthy and functional. In patients with ulcerative colitis however, the levels of this lncRNA decrease. To model this state, we generated mice lacking this lncRNA and like patients with UC, these mice develope colitis. The lncRNA localizes to the mitochondria in cells of the healthy colon. When the lncRNA is lost, the mitochondria in the cells in the colon are damaged, produce reactive oxygen species and damage colonic tissue. These findings provide new insights into how a lncRNA can help mitochondria work well to maintain homeostasis in the gut. These studies suggest new opportunities to restore tissue health by controlling the levels of this lncRNA.

Abstract or Project Description

Diet is thought to be a major environmental factor contributing to Inflammatory Bowel Disease (IBD) and represents a non-invasive path to improve this debilitating condition. To leverage diet to treat IBD the precise ways that dietary components influence development or healing of inflammation need to be determined. We discovered that different dietary protein sources have variable effects on intestinal inflammation and these effects are dependent on the community of microorganisms (microbiome) that inhabit the human colon. In particular, we discovered that soy protein promotes production of a beneficial metabolite called isobutyrate that reduces inflammation in a mouse model of IBD that we developed to mimic low fiber diet- and microbiome-driven inflammation. Isobutyrate is only produced by some bacteria and is derived from the dietary amino acid L-valine via at least two different metabolic pathways. Because soy protein specifically promotes isobutyrate, our model is that it is better at delivering L-valine-containing peptides to the colon after digestion, leading to bacterial isobutyrate production. The proposed experiments will uncover the specific component(s) of soy protein that promotes isobutyrate as well as the bacteria that produce this metabolite so that dietary protein can be optimized in the context of patients’ microbiomes to reduce inflammation.

Abstract or Project Description

Mental health profoundly impacts inflammatory diseases of the body. This is particularly apparent in Inflammatory Bowel Disease (IBD), where stressful events in a patient’s life often enhance the severity of subsequent disease flares. Psychological stress is also strongly linked to bowel motility problems in IBD patients. How the state of the brain influences inflammation in the gut is a fascinating question that remains poorly understood.

In this study, we will explore the mechanisms of brain-gut communication that link psychological stress to IBD severity. Using several different mouse models of IBD, we have recently discovered a pathway that links stress perception by the brain to the enteric nervous system (ENS), and in particular glia cells that reside in the gastrointestinal tract. We will explore how this neuronal brain-gut connection exacerbates the inflammatory state in the gut. We will also determine whether the same pathway is active in IBD patients in the context of stressful life events.

Collectively, this work will improve our understanding of how the brain and the gut communicate during psychological stress. We hope that an improved understanding of how stress influences intestinal inflammation will ultimately facilitate harnessing the power of brain-derived signals in the treatment of IBD.

Abstract or Project Description

Knowledge of the intestinal microbiota has transformed medical science, but not the treatment of Inflammatory Bowel Disease (IBD). The microbiota is difficult to use clinically because current analytical methods provide outputs that are too complex to provide useful data during an acute IBD flare. To solve these issues, we have developed a novel methodology, ‘MicFly’ that allows us to ‘count’ each type of bacteria present in the microbiota. Our method provides rapid, accurate, quantitative and simple measurements of the bacteria present in the microbiota and has the added benefit of being capable of identifying what genes are being expressed by each bacteria.

Clostridiodes difficile infection (Cdiff;CDI) is common in IBD patients because the pre-conditions for CDI, low microbiome diversity and immunosuppression, are common outcomes of treatment. Discriminating CDI from an IBD flare can be difficult because Cdiff is commonly found in IBD patients but is only dangerous when it expresses a toxin. As an example of the efficacy of MicFly, we propose to demonstrate that the technique can identify the number of Cdiff bacteria and their toxin expression. We will also measure whether a Fecal Microbiota Transplant for Cdiff has been successful in reducing Cdiff toxin levels and restoring microbiota diversity.