Alcohol-associated liver disease (ALD) is a major cause of liver-related morbidity and mortality and is characterized by dysregulated hepatic lipid metabolism. Experimental mouse models, including the National Institute on Alcohol Abuse and Alcoholism chronic-binge model, Lieber-DeCarli liquid diet model, and intragastric infusion model, are widely used to study ALD; however, their relative ability to recapitulate alterations in hepatic lipid metabolism, including cholesterol and fatty acid synthesis pathways, remains unclear. Comparative analysis of these models was performed to evaluate gene expression patterns associated with lipid synthesis and regulatory signaling pathways. Liver tissues were collected for RNA extraction, complementary DNA synthesis, and quantitative polymerase chain reaction analysis using the Livak method, followed by Student’s t-test. Expression of liver X receptor-regulated genes (Inmt, Srebf1) and de novo lipogenesis markers (Fasn, Acaca, Acly) was assessed, with 36b4 as a housekeeping control. Gene expression and physiological measurements, including liver-to-body weight ratios, were compared across models to assess consistency and translational relevance. These analyses identify model-dependent differences in hepatic lipid metabolism and support selection of an experimental model that most accurately reflects disease-associated metabolic alterations. These findings improve experimental standardization and provide a foundation for future functional studies and comparison with human datasets.

Aspiration Pneumonia (AP) is a respiratory tract infection that arises from the inhalation of bacteria-rich fluids, including gastric and oropharyngeal contents. AP is a significant yet under-recognized contributor to sepsis-related mortality globally, causing an estimated 58,576 deaths in the United States annually (1). Despite its impact, standardized prevention protocols are limited. This review evaluates the key factors in AP development–including dysphagia, oral health, and the gut microbiome–and their potential as targets for interventions to reduce sepsis risk. Approximately 40 peer-reviewed clinical studies analyzing interventions such as swallowing protocols, bedside risk assessments, oral hygiene-focused care, and microbiome modulation in hospitalized patients, were included. Although findings suggest that dysphagia, oral health, and the gut microbiome influence AP risk, the connection between aspiration pneumonia prevention and downstream reductions in sepsis mortality is not consistently addressed, highlighting a critical gap in both research and clinical practice. This review will inform an ongoing quality improvement initiative led by Dr. Russell Kerbel, who is developing a screening tool for AP prevention in the internal medicine departments of Ronald Reagan UCLA Medical Center. Overall, this literature review supports the need for a systematic prevention strategy that integrates dysphagia management, oral health optimization, and microbiome considerations to effectively reduce AP-related sepsis mortality.

ABCA4-associated retinopathies are inherited retinal degenerations characterized by progressive dysfunction of photoreceptors and the retinal pigment epithelium (RPE). Loss of ABCA4 leads to the accumulation of toxic bisretinoid lipofuscin within RPE cells. However, early cell-type–specific transcriptional changes remain incompletely defined. Here, we investigated molecular alterations in the RPE and neural retina of albino Abca4 knockout mice compared with wild-type controls. We performed single-nucleus RNA sequencing of RPE and single-cell RNA sequencing of retina from 3-month-old mice, a time point preceding overt structural degeneration. Single-nucleus profiling enabled robust characterization of RPE transcriptional states, while single-cell analysis captured diverse retinal cell populations. We identified transcriptional alterations within the RPE, including the presence of a de- differentiated RPE population characterized by reduced expression of the visual cycle genes and increased expression of stress-associated pathways related to lysosomal function, lipid metabolism, and oxidative stress. These findings indicate that early transcriptional remodeling is detectable in the RPE in ABCA4 deficiency before overt retinal degeneration. Ongoing longitudinal analyses at later time points will further define the temporal relationship between RPE alterations and retinal degeneration. Together, this study provides a cell-type–resolved framework for understanding early molecular changes in ABCA4-associated retinopathy.

Unhoused populations around the world experience heightened risk factors for multimorbidity, commonly defined as the co-occurrence of two or more chronic conditions. However, there is limited understanding of the multimorbidity burden in this underserved population globally. The purpose of this integrative review is to gain an understanding of the prevalence of multimorbidity among unhoused populations in the United States and abroad. A total of 8 studies were included in this integrative review using a combination of research designs (e.g., cross-sectional, retrospective, and mixed-method) located in North America (i.e., United States, Canada), Europe (i.e., England, Germany, Ireland), and Australia. In addition to the original purpose of identifying the prevalence of multimorbidity among unhoused populations, two additional themes emerged which included how multimorbidity is influenced by physical, mental health, and substance use and that multimorbidity is complex to manage for unhoused persons. These three themes highlight the importance of creating both tailored and accessible interventions for unhoused persons living with multimorbidity.

Air pollution is a leading environmental risk for cardiovascular disease, yet the mechanism by which inhaled particulate matter (PM) induces oxidative stress and inflammation remains unclear. The liver plays a key role in metabolic and inflammation regulation, making it a key target for systemic responses towards environmental stressors. Studies have shown that lipid metabolites contribute to oxidative stress. However, it remains unknown whether the absence of Heme oxygenase-1, an antioxidant and anti-inflammatory enzyme, in myeloid cells exacerbates oxidative and inflammatory processes. To answer this, we conducted a short-term exposure using floxed and HO-1 KO mice to either filtered air (FA) or 300µg/m^3 of ultrafine particles (UFP) for 5 consecutive days (6h/day). Plasma and liver samples were collected after euthanasia. Plasma oxidized lipids were quantified using liquid chromatography mass spectrometry, targeting polyunsaturated fatty acids and their metabolites. Liver inflammation was assessed via gene expression analysis of inflammasome-related markers and pro-inflammatory cytokines. Results show that UFP exposure significantly altered liver inflammatory genes and oxidized lipid species compared to FA controls. These findings demonstrate that short-term UFP exposure promotes both systemic lipid oxidation and liver inflammation, and demonstrate HO-1’s protective role.