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Abstract or Project Description

Abstract or Project Description

This one-time capacity building grant supports Tandem, Partners in Early Learning, in implementing a broader organizational-wide sabbatical program.

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A new play and modular community performance by poet and activist Yosimar Reyes created through a participatory storytelling process with Teatro Visión’s community in East San José. The piece blends local history and music to elevate community voices and inspire neighborhood civic engagement.

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Support for research into climate change and arts organizations, as well as the development of an impact evaluation report.

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Provides administrative support to OUSD’s Structured Literacy Initiative.

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Funding supports Plain Talk Flights and Administrative Fees to manage the Plain Talk Reimbursement Fund.

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Provides general support.

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Provides anti-racist and healing programming for educators and leaders.

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The Rest and Care Award is a one-time, invite-only program for current and past Education and Arts nonprofit grantees, offering six-week sabbaticals with pro-rated salary, benefits, leave expenses and organizational support, recognizing the dedication and resilience of leaders in our grantee community. The Teaching Well supports educator retention by consulting with school leaders on human-centered policies and providing educators with trauma healing and wellness programming. Their executive director for three years is Lindsey Fuller.

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To support responsive communications and operations needs.

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To support the distribution of funds to diverse Bay Area micro dance and theater organizations and individual artists.

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To support Oakland’s primary nonprofit organization focused on expanding affordable housing for early elementary teachers who are responsible for teaching early literacy.

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A three-day theatrical production that explores self-love and self-acceptance through monologues, poems and dance collaborations by Black Trans emerging artists.

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

T cells are major drivers of Inflammatory Bowel Disease (IBD) but the full set of factors promoting inflammatory intestinal T cell accumulation in affected individuals is not understood. We have found that deficiency in a signaling molecule (G-protein) in mouse hematopoietic cells leads to a reduction in inflammatory intestinal T cells. Here we will define the cell types requiring this signaling pathway for induction of inflammatory T cells in the intestine, and the upstream receptors involved. We will characterize how the pathway controls cell behavior to promote inflammatory T cell accumulation and determine the importance of the pathway in a mouse colitis model. These studies will provide a foundation for defining the contribution of the signaling pathway to human IBD and may lead to the identification of new avenues for therapeutic intervention to treat this condition.

Abstract or Project Description

Our skin and gut house multitudes of bacteria that influence our health via interactions with key immune sentinel cells that engulf these microbes and respond dynamically to their signals. Previously we have had to rely heavily on animal models to try to decode this language between our immune sentials and the bacteria they sense, because we have lacked to tools to meaningfully capture the relevant information from human tissues. To overcome this hurdle we have recently developed a novel single-cell genomic method for simulatenously capturing and sequencing DNA from both these immune sentinel cells and the bacteria they contain, therby providing us with an unprecendented view into the nature of these bacteria-immune cell interactions. By applying this novel approach to samples of healthy human skin and gut, we hope to shed new light on how helpful and harmful bacteria are sensed at these barrier tissues, how the immune system decides when (and what) to attack, and the molecular and cellular cues that guide these decisions. These studies will transform our understanding of bacterial influences on our health and set the stage for future work to interrogate their role in specific human diseases such as Inflammatory Bowel Disease.

Abstract or Project Description

Clinical decision making in ulcerative colitis relies on practice guidelines and physician experience, but both have limitations. Guidelines offer broad advice that may not apply to individual patients while physician experience is subjective and error prone. Dr. Rudrapatna will address these limitations using reinforcement learning, a type of artificial intelligence that learns to make optimal decisions over time. Reinforcement learning has successfully been used in autonomous driving and it will now be adapted and applied to ulcerative colitis.

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

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.