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Selection of papers presented at a conference 'Art, Patronage and Society in the Muslim Deccan from the Fourteenth Century to the Present Day' (4-6 July 2008) at St. Antony's College, Oxford, with support from the John Fell Fund, Barakat Trust and Alessandro Bruschettini.

A leading theory regarding the pathogenesis of biliary atresia (BA) is that bile duct injury is initiated by a virus infection, followed by an autoimmune response targeting bile ducts. In experimental models of autoimmune diseases, B cells have been shown to play an important role. The aim of this study was to determine the role of B cells in the development of biliary obstruction in the Rhesus rotavirus (RRV)-induced mouse model of BA. Wild-type (WT) and B cell-deficient (Ig-α(-/-)) mice received RRV shortly after birth. Ig-α(-/-) RRV-infected mice had significantly increased disease-free survival rate compared to WT RRV-infected BA mice (76.8% vs. 17.5%). In stark contrast to the RRV-infected BA mice, the RRV-infected Ig-α(-/-) mice did not have hyperbilirubinemia or bile duct obstruction. The RRV-infected Ig-α(-/-) mice had significantly less liver inflammation and Th1 cytokine production compared to RRV-infected WT mice. In addition, Ig-α(-/-) mice had significantly increased numbers of regulatory T cells (Tregs) at baseline and after RRV infection compared to WT mice. However, depletion of Tregs in Ig-α(-/-) mice did not induce biliary obstruction, indicating that the expanded Tregs in the Ig-α(-/-) mice were not the sole reason for protection from disease. Conclusion : B cell deficient Ig-α(-/-) mice are protected from biliary obstruction in the RRV-induced mouse model of BA, indicating a primary role of B cells in mediating disease pathology. The mechanism of protection may involve lack of B cell antigen presentation, which impairs T-cell activation and Th1 inflammation. Immune modulators that inhibit B cell function may be a new strategy for treatment of BA.

Seasonally inundated wetlands are threatened ecosystems worldwide and increasingly important targets for wetland restoration programs. However, restoring such ecosystems is difficult, as it requires mimicking the historical shifts between dry and flooded states. In this study, we evaluate the responses of agriculturally impacted seasonal wetlands to pasture-scale hydrological restoration. We selected 15 seasonal wetlands in central Florida (10 within restoration easements and five in unrestored pastures) and excluded cattle from five of the restored wetlands. We monitored each wetland from 2011 to 2016 to document potential changes in water levels, plant species richness, beta diversity, floristic quality, and cover of obligate wetland species. Vegetation responses to restoration were gradual and subtle, becoming detectable only five years following restoration. By 2016, restored wetlands had significantly lower cover of facultative upland species and higher cover of obligate wetland species. Species richness was higher in unrestored wetlands due to the presence of many facultative upland species. Beta diversity within wetlands and floristic quality based on coefficient of conservatism were not affected by restoration. We did not find strong effects of cattle exclusion on post-restoration diversity metrics, but we observed a large increase in the native grass, Panicum hemitomon Schult. This study showed mixed outcomes when measured against the goals of restoring wetland communities. It also highlighted the need for more active restoration approaches to regain historical communities or promote target species ( e.g. Coleataenia abscissa (Swallen) LeBlond). We emphasize the need for costly restoration activities to be coupled with long-term monitoring to assess success.

Despite advances in echocardiography and biomarkers, the pathophysiological complexities among heart failure categories remain incompletely understood. This study analyzed patients’ characteristics across heart failure with reduced ejection fraction, heart failure with midrange ejection fraction, and heart failure with preserved ejection fraction presenting at the emergency department. This is a retrospective analysis of 954 patients with acute heart failure (2016-2023) using electronic health records. Data were collected from patient triage and the emergency department and during hospitalization. Survival analysis was performed using Kaplan-Meier estimates, and an elastic net model was used to handle multicollinearity and high dimensionality in predictor variables. Patients (median age, 71 years) were categorized as heart failure with reduced ejection fraction (n = 363), heart failure with midrange ejection fraction (n = 131), and heart failure with preserved ejection fraction (n = 460). Patients with heart failure with preserved ejection fraction were older (80 vs 77 vs 74 years; P < .001). Heart failure with reduced ejection fraction showed higher prevalence of cardiomegaly, pleural effusion, and orthopnea (34% and 51%; P < .001), elevated diastolic blood pressure (P < .001), creatinine, N-terminal pro–B-type natriuretic peptide (P < .001), and hematocrit differences (P < .05) than heart failure with preserved ejection fraction. Echocardiographic measures differed significantly across subtypes. In-hospital prediction models achieved an area under the curve of 0.84 (91% sensitivity, 50% specificity); 30-day models had an area under the curve of 0.80 (98% sensitivity, 50% specificity). HF subtypes exhibit distinct clinical and biomarker profiles. Emergency nurses’ recognition of these differences during initial assessment may enhance risk stratification and tailored interventions (eg, prioritizing diuretics in heart failure with reduced ejection fraction, managing comorbidities in heart failure with preserved ejection fraction), improving outcomes. Integrating subtype-specific data into protocols could optimize emergency department care, particularly during prolonged boarding.

Seasonally inundated wetlands are threatened ecosystems worldwide and increasingly important targets for wetland restoration programs. However, restoring such ecosystems is difficult, as it requires mimicking the historical shifts between dry and flooded states. In this study, we evaluate the responses of agriculturally impacted seasonal wetlands to pasture-scale hydrological restoration. We selected 15 seasonal wetlands in central Florida (10 within restoration easements and five in unrestored pastures) and excluded cattle from five of the restored wetlands. We monitored each wetland from 2011 to 2016 to document potential changes in water levels, plant species richness, beta diversity, floristic quality, and cover of obligate wetland species. Vegetation responses to restoration were gradual and subtle, becoming detectable only five years following restoration. By 2016, restored wetlands had significantly lower cover of facultative upland species and higher cover of obligate wetland species. Species richness was higher in unrestored wetlands due to the presence of many facultative upland species. Beta diversity within wetlands and floristic quality based on coefficient of conservatism were not affected by restoration. We did not find strong effects of cattle exclusion on post-restoration diversity metrics, but we observed a large increase in the native grass, Panicum hemitomon Schult. This study showed mixed outcomes when measured against the goals of restoring wetland communities. It also highlighted the need for more active restoration approaches to regain historical communities or promote target species (e.g. Coleataenia abscissa (Swallen) LeBlond). We emphasize the need for costly restoration activities to be coupled with long-term monitoring to assess success.

Vascular disease progression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function. SMC contractile gene expression and, thus differentiation, is under direct transcriptional control by the transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC phenotype are not fully defined. Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype. PTEN interacts with the N-terminal domain of SRF and PTEN–SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes. Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation. Overall decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinical importance of these findings. The transcription factor, serum response factor, SRF regulates critical smooth muscle (SM) contractile gene expression but what else controls SM differentiation is unclear. Here, Horita et al . demonstrate that nuclear PTEN acts with SRF at the transcriptional level to maintain the differentiated SM phenotype.

Nonnative pasture grasses established for agriculture and livestock husbandry have replaced countless acres of natural habitat in the last century of Florida history. Many endemic species, such as cutthroat grass (Coleataenia abscissa), are now endangered and may not return to areas until the dominant pasture grass has been removed. To determine the best strategy for native revegetation, we examined the effects of two soil preparations (tilling and no tilling) in pasture plots dominated by bahiagrass (Paspalum notatum) on the Archbold Reserve in south-central Florida. In preparation for the experiment, the No-Till and Till plots were first herbicided with glyphosate and burned to remove bahiagrass cover and expose the seed bank, then the Till plots were disked to a depth of 5–10 cm. Reference plots were left undisturbed to provide a pre-restoration baseline. The pre-tilling herbicide application and burn reduced bahiagrass cover in experimental plots to an average of 24% compared to 80% in reference plots. In the first year following tilling, overall plant community composition differed between tillage treatments, with 52 and 38 plant taxa found in the No-Till and Till plots, respectively, compared to only 14 in the reference plots. Importantly, native species richness was significantly higher in the No-Till treatment, and tilling resulted in minimal reduction of cover of bahiagrass and other exotic grasses. Seedling species composition differed among experimental blocks, suggesting soil moisture or other local abiotic conditions may significantly influence seedling establishment and restoration outcomes regardless of mechanical soil preparations.

Published literature is sparse on topics associated with eared seal (otariid) dentistry. The objective of this study was to establish consensus on effective management of dental disease in otariids, using a Delphi approach. A total of 25 veterinarians with experience managing dental disease in seven species of otariids participated in the Delphi process. Oral lesions and their contributing risk factors were ranked according to perceived frequency. Consensus statements for best practices were agreed upon for a variety of topics within the categories of planning and preparation, procedural details, intervention strategies, and postoperative care. Panelist comments were collated into a Supplementary File to assist clinicians in forming their own conclusions on topics for which no consensus yet exists. Opportunities for future research include factors associated with oral lesions, ideal anesthetic management, identification of ideal candidates for endodontic therapies, ideal local and regional anesthesia, ideal suture and closure techniques, particularly with the goal of reducing dehiscence as a postoperative complication, and ideal postoperative care options.

OBJECTIVES/GOALS: Our lab previously identified a population of vascular smooth muscle (SMC)-derived progenitor cells (AdvSca1-SM) which expand robustly in response to disease and can differentiate into multiple cell types. We now aim to define the role of these AdvSca1-SM cells in atherosclerotic plaque progression. METHODS/STUDY POPULATION: Goal one uses SMC lineage tracing mice and a model of atherosclerosis to track reprogramming of SMCs to AdvSca1-SM cells in the setting of disease. Arteries are analyzed using flow cytometry and immunofluorescence to quantify changes in number of mature SMCs and AdvSca1-SM cells. Goal two uses AdvSca1-SM lineage tracing mice with high cholesterol-induced atherosclerosis and plaque neovascularization. Arteries are analyzed to quantify expansion of AdvSca1-SM cells, subsequent re-differentiation into mature SMC, endothelial cells, or macrophages, and contribution to plaque neovascularization. Mechanistic findings from both goals are being investigated in diseased human coronary arteries. RESULTS/ANTICIPATED RESULTS: Flow cytometry from SMC lineage tracing mice revealed a 7- to 13-fold expansion of AdvSca1-SM cells in carotid arteries (p<0.001) and aortas (p = 0.03) after 6 weeks of western diet; no differences in macrophage numbers were observed. Additional SMC and AdvSca1-SM cell lineage tracing mice are on atherogenic diets to assess early and advanced atherosclerosis. We predict that AdvSca1-SM cells will contribute to macrophage accumulation as well as plaque neovascularization in the setting of severe atherosclerosis. Translational relevance of mechanisms driving SMC reprogramming and AdvSca1-SM cell contribution to plaque progression are being applied to studies of diseased human coronary arteries. DISCUSSION/SIGNIFICANCE OF IMPACT: Our data suggest a role for AdvSca1-SM cells in atherosclerosis. Ongoing work will clarify the mechanisms driving plaque-associated AdvSca1-SM expansion and define the ultimate fates of these cells. In vivo modulation of this process could provide the basis for future anti-atherosclerotic therapies. CONFLICT OF INTEREST DESCRIPTION: AD - CCTSI TOTTS TL1TR002533; SL - 18POST34030397 from the American Heart Association; AJ – no conflicts; KS - 1F31HL147393 from the National Heart, Lung, and Blood Institute, NIH; MM – no conflicts; RT – no conflicts; KSM – no conflicts; RAN - R01CA236222 from the National Cancer Institute, NIH, and 2018-03 from the Lungevity Foundation; and MCMW-E - R01 HL121877 from the National Heart, Lung, and Blood Institute, NIH, and 25A8679 from the Chernowitz Foundation.