West Los Angeles College

Abstract A large proportion of nutrient cycling and ecosystem services are supported by the activities of fungal and invertebrate communities. Though these communities have been comparatively understudied compared to more charismatic groups such as birds and mammals, there is a growing body of evidence that the structure of these communities is also impacted by urbanization. Here we analyzed species occurrences derived from environmental DNA (eDNA), taken from over 20,000 samples in California, to investigate patterns of diversity for a variety of fungal and invertebrate orders. We investigated their differences in both taxonomic richness and turnover by comparing communities sampled in urban and non-urban areas. We found taxonomic richness was significantly lower within fungal orders sampled in urban areas, and most invertebrate orders displayed a similar pattern. Both invertebrate and fungal communities were found to have undergone a significant level of biotic homogenization in urban areas. We demonstrated that the composition of fungal and invertebrate communities, classified using eDNA, is significantly affected by the process of urbanization.

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, disproportionately affecting underserved and safety-net populations. Los Angeles County Department of Health Services (LAC-DHS) Kidney Health Workgroup has developed pragmatic population health frameworks and Expected Practices for DKD co-management with primary-care providers: pragmatic definitions of low kidney function (LKF, <50% of normal) and very low kidney function (VLKF, <25%), and proteinuria severity classification as early (>150 mg/g), heavy (>1 g/g), and massive (>7 g/g) to guide referral urgency; biopsy-agnostic diagnosis of DKD when four out of five criteria are met, including diabetes history or A1c more than 6%, LKF, proteinuria, diabetic microangiopathy, and larger kidney length (>12 cm) or faster CKD progression (>25 ml/min/year); Kidney Disease Integrated Therapy (KDIT) combining four medication categories (RAAS blockade, SGLT2 inhibitors, GLP-1 agonists, nonsteroidal mineralocorticoid antagonist) and renal nutrition and lifestyle medicine (PLADO/PLAFOND diets), adequate hydration, and exercise; and eConsults to support timely detection, dialysis vascular access placement, shared decision-making, and ESRD care coordination. The DKD management model demonstrates that resource-limited systems can deliver innovative, high-quality kidney care and provide a scalable framework for equity-focused and pragmatic kidney care in municipal health systems.

As a central player in neuroinflammation, macrophages play multifaceted roles such as antigen presentation, phagocytosis, production of cytokines/chemokines, and growth/neurotrophic factors. Our previous work demonstrated that ocular infection with a recombinant herpes simplex virus type 1 (HSV-1) expressing interleukin-2 (HSV-IL-2) causes CNS pathology, independently of macrophages in different mouse strains. In contrast, wild type (WT) HSV-1 infection induces CNS demyelination in a macrophage-dependent manner. Therefore, in this study, we have two mouse models infected with either HSV-IL-2 or WT HSV-1 to examine the outcome of the absence of IL-17A, FoxP3, macrophages, or combined macrophage and FoxP3 depletion on CNS demyelination. Our data reveals several notable findings: deletion of FoxP3 alone in mice infected with either HSV-IL-2 or WT HSV-1 did not induce CNS demyelination. However, combined depletion of macrophages and FoxP3 in HSV-IL-2-infected mice triggered CNS demyelination, whereas the same combined depletion in WT HSV-1 infection prevented demyelination. Additionally, macrophage depletion alone in WT HSV-1-infected mice induced CNS demyelination, highlighting the non-redundant protective role of macrophages in this model. To further elucidate the role of macrophages in CNS demyelination, we investigated which macrophage subtype is responsible for modulating demyelination using M1 and M2 knockout mice. Our results indicate that M1 macrophages are key drivers of plaque formation, as infection with either HSV-IL-2 or WT HSV-1 failed to cause CNS demyelination in the absence of M1 macrophages. Conversely, M2-deficient mice exhibited demyelination, suggesting a protective role for M2 macrophages. Finally, depletion of macrophages in IL-17A-deficient mice infected with HSV-IL-2 did not restore CNS demyelination, indicating that, unlike the macrophage-FoxP3 double depletion in the HSV-IL-2 model, the IL-17A-macrophage absence is beneficial. Taken together, these findings highlight the distinct and non-redundant roles of FoxP3, IL-17A, and macrophage subsets in modulating CNS pathology during HSV-1 infection and suggest that targeting M1 macrophage activation may be a promising strategy for limiting demyelination.

Perspective taking is a basic social cognitive skill that has been shown to be impacted across the psychosis spectrum. Social cognitive abilities are important predictors of functional outcomes and may be related to symptom development in psychosis. However, no study has yet evaluated a model of how perspective-taking and other social cognitive domains relate to subclinical psychotic-like experiences among late adolescents and young adults. In this study, 137 non-help-seeking university students were assessed on their visual perspective-taking abilities using a computerized task as well as their attribution and hostility biases when completing a vignette-based questionnaire. Performance on the visual perspective-taking task was found to be predictive of distress related to positive and negative psychotic-like experiences. Visual perspective-taking was also associated with attributional biases under ambiguous circumstances, which were, in turn, associated with distressing psychotic experiences. The pattern of visual perspective-taking performance was also indicative of altercentric intrusion, or difficulty inhibiting irrelevant information related to another's perspective, rather than impairments in visualizing or simulating this perspective. These findings have implications for the understanding of basic social cognitive deficits in the psychosis spectrum and how they may relate or contribute to symptomatology.

To evaluate and compare characteristics and outcomes of dogs with gastrointestinal (GI) and non-gastrointestinal (non-GI) causes of septic peritonitis. Retrospective study from 2009 to 2022. A Midwest veterinary teaching hospital and a West Coast private practice in the United States. A total of 161 dogs diagnosed with septic peritonitis based on intracellular bacteria or a positive culture from peritoneal effusion. None. Of 161 dogs included in the study, 114 (70.8%) survived. Dogs that survived were younger (p=0.011) and, compared with nonsurvivors, had higher total plasma protein (TP) concentrations (p=0.039), higher serum albumin concentrations (p=0.0021), and higher systolic blood pressures (SBP) (p=0.0025) on presentation. Plasma lactate concentration on presentation was not associated with survival (p=0.097). There was no difference in survival between dogs diagnosed with a GI versus non-GI etiology of septic peritonitis. Dogs with GI etiologies weighed more than dogs with non-GI etiologies (p=0.0169). There were no differences in age, temperature, heart rate, SBP, PCV, TP, serum blood glucose concentration, plasma lactate concentration, serum albumin concentration, or Acute Patient Physiologic and Laboratory Evaluation-fast scores upon presentation in dogs with GI etiologies compared with dogs with non-GI etiologies. In a subgroup analysis, dogs with hepatobiliary etiologies were older (p=0.0004) and weighed less (p=0.003) compared with dogs with GI and other non-hepatobiliary etiologies, but there was no difference in survival (p=0.958). This study found no difference in survival to discharge in dogs with GI compared with non-GI etiologies of septic peritonitis. Regardless of the etiology of septic peritonitis, age, TP, serum albumin concentration, and SBP upon presentation were significantly associated with survival.

Intracranial atherosclerotic disease (ICAD) is a leading cause of ischemic stroke worldwide. However, research on the pathophysiology of ICAD is scarce due to the relative inaccessibility of histology samples and the lack of comprehensive experimental models. As a result, much of the current understanding of ICAD relies on research on extracranial atherosclerosis. This approach is problematic as intracranial and extracranial arteries are anatomically, structurally, physiologically, and metabolically distinct, indicating that intracranial and extracranial atherosclerosis likely develop through different biologic pathways. The current standard of care for ICAD treatment relies predominantly on therapeutics developed to treat extracranial atherosclerosis and is insufficient given the alarmingly high risk of stroke. To provide a definitive treatment for the disease, a deeper understanding of the pathophysiology underlying ICAD is specifically required. True mechanistic understanding of disease pathogenesis is only possible using robust experimental models. In this review, we aim to identify the advantages and limitations of the existing in vivo and in vitro models of ICAD and basic atherosclerotic processes, which may be used to inform better models of ICAD in the future and drive new therapeutic strategies to reduce stroke risk.