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Introduction and Objectives: This study aimed to characterize a large cohort of Latinx patients with autoimmune hepatitis (AIH) and analyze clinical outcomes, including biochemical remission, duration of steroid treatment, fibrosis regression, and incidence of clinical endpoints (hepatic decompensation, need for liver transplant, and death)., Materials and Methods: This was a retrospective descriptive study of patients with biopsy proven AIH (2009-2019) at a single urban center. Demographics, medical comorbidities, histology, treatment course, biochemical markers, fibrosis using dynamic non-invasive testing (NIT), and clinical outcomes at three months and at one, two, and three years were analyzed., Results: 121 adult patients with biopsy-proven AIH were included: 43 Latinx (35.5%) and 78 non-Latinx (65.5%). Latinx patients were more likely to have metabolic dysfunction-associated steatotic liver disease (MASLD) (p = 0.004), and had higher Fibrosis-4 (FIB-4) (p = 0.0279) and AST-to-Platelet-Ratio-Index (APRI) (p = 0.005) at one year. Latinx patients took longer to reach biochemical remission than non-Hispanic Whites (p = 0.031) and longer to stop steroids than non-Hispanic Blacks (p = 0.016). There were no significant differences based on ethnicity in histological fibrosis stage at presentation or incidence of clinical endpoints., Conclusions: MASLD overlap is highly prevalent in Latinx AIH patients. Longer time to biochemical remission and worse NITs support that this population may have slower fibrosis regression with standard of care AIH treatment. This may indicate differing response rates due to genetic polymorphisms affecting drug metabolism and immune response among Latinx individuals and is less likely related to AIH/MASLD overlap based on the findings of this study., Competing Interests: Conflicts of interests Dr. Reau: consulting for Abbott, AbbVie, Gilead, Salix. Arbutus. Dr. Aloman has received research funding from NIAAA (R01 AA024762). Dr. Reau has received research funding from Eiger, AbbVie., (Copyright © 2024 Fundación Clínica Médica Sur, A.C. Published by Elsevier España, S.L.U. All rights reserved.)

Despite progress in treating rheumatoid arthritis, this autoimmune disorder confers an increased risk of developing cardiovascular disease (CVD). Widely used screening protocols and current clinical guidelines are inadequate for the early detection of CVD in persons with rheumatoid arthritis. Traditional CVD risk factors alone cannot be applied because they underestimate CVD risk in rheumatoid arthritis, missing the window of opportunity for prompt intervention to decrease morbidity and mortality. The lipid profile is insufficient to assess CVD risk. This review delves into the connection between systemic inflammation in rheumatoid arthritis and the premature onset of CVD. The shared inflammatory and immunologic pathways between the two diseases that result in subclinical atherosclerosis and disrupted cholesterol homeostasis are examined. The treatment armamentarium for rheumatoid arthritis is summarized, with a particular focus on each medication's cardiovascular effect, as well as the mechanism of action, risk-benefit profile, safety, and cost. A clinical approach to CVD screening and treatment for rheumatoid arthritis patients is proposed based on the available evidence. The mortality gap between rheumatoid arthritis and non-rheumatoid arthritis populations due to premature CVD represents an urgent research need in the fields of cardiology and rheumatology. Future research areas, including risk assessment tools and novel immunotherapeutic targets, are highlighted.

Objective: Using data from a longitudinal national sports injury surveillance program, this study aimed to calculate injury rates and describe injury patterns across high school swimmers and divers., Design: Descriptive Epidemiological Study. Athletic trainers (ATs) from participating high schools reported injuries from swimming and diving programs for the High School Reporting Information Online system., Setting: Convenience sample of high school boys and girls' swimming and diving injuries during the 2008 to 2019 school years., Patients or Other Participants: High school boy and girl swimmers and divers (aged ∼14-18 years)., Independent Variables: Exposure data on gender, location of injury (practice vs competition), mechanism of injury, and sport (swimming vs diving)., Main Outcome Measures: Injury rates, rate ratios (RRs) with 95% confidence intervals, and other descriptive statistics were performed., Results: 563 swimming and diving injuries occurred during 2 171 260 athlete exposures (0.26 per 1000 athlete exposures). Girls had higher injury rates than boys overall (RR 1.57, P < 0.05), in practice (RR 1.53, P < 0.05), and competition (RR 1.81, P < 0.05). In swimmers, most injuries were to the shoulder (48.6%), associated with the freestyle (67.3%), and classified as overuse/chronic (58.0%). Among divers, most injuries were to the head/face (36.6%) and from contact with the playing surface (68.3%)., Conclusions: Girls had statistically significantly higher injury rates than boys. The shoulder and head/face were the most injured body parts in swimmers and divers, respectively. Swimming injuries were most frequently of an overuse etiology, whereas diving injuries were more likely traumatic. Coaches and ATs should be aware of these findings to develop targeted strategies for injury prevention., Competing Interests: The authors report no conflicts of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Poster sessions are one of the most common platforms for presenting research at academic conferences, yet posters are often inefficient at transferring knowledge to their readers due to suboptimal design and content selection. Physician trainees may not receive education on constructing posters as a traditional part of their residency curriculum. The purpose of this work is to propose a curriculum that will provide residents foundational knowledge and skills needed for designing high-quality research posters. The curriculum uses the flipped classroom model, a pedagogical approach that reverses the traditional learning environment by delivering instructional content outside of the classroom and moves activities into the classroom. Preparatory work includes watching an educational video on 'how to create a better research poster in less time' and preparing a poster to be presented at an upcoming conference. An 1-hour workshop is conducted during protected resident didactic time. It incorporates a 10-min slide show presentation on poster design and 50 min of active learning. During the active learning component, learners are asked to 'think-pair-share' to construct a research poster rubric using the information they just learnt. The learners work as a group to evaluate sample research posters. The class is then broken down into small groups of 2-3 learners to spend time working on their own posters and provide peer feedback. Following the workshop, residents continue to develop their research posters for conference presentation. This curriculum has the potential to enhance the quality of resident research posters presented at academic conferences, advance research education and ultimately improve dissemination of research within academic communities. The lesson plan outlined in this work can be used as a guide for teaching poster design to physician trainees in a number of specialties and may encourage programmes to consider integrating poster design as a formal part of the residency curriculum., (© The Author(s) 2022. Published by Oxford University Press on behalf of Postgraduate Medical Journal. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Chronic lateral ankle instability often causes adults to require a surgical intervention with subsequent physical therapy to assist with returning to their prior level of function. This systematic review is hoping to provide an up to date understanding of surgical procedures performed to correct chronic lateral ankle instability and establish a protocol for others to follow when treating adults who are status-post chronic lateral ankle instability surgery. This review looked at level I to III research studies that included surgical interventions to correct chronic lateral ankle instability as well as a rehabilitation protocol. This study found implementation of a rehabilitation protocol after surgical intervention could improve balance and subjective functional outcomes. It also determined that early weight-bearing may allow for early strengthening as range of motion returns faster. Further research is required utilizing larger randomized studies to better evaluate the outcomes of specific rehabilitation protocols in this patient population., Competing Interests: Disclosure: The authors declare no conflict of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Tumor necrosis factor- (TNF-) α is a proinflammatory proatherogenic cytokine. Infliximab, an anti-TNF-α monoclonal antibody, is effective in treating rheumatoid arthritis. However, its impact on cardiovascular burden and lipid transport is unclear. The present study investigates the effect of TNF-α and infliximab on reverse cholesterol transport (RCT) proteins. Uptake of modified lipoproteins by macrophages in the vasculature leads to atherogenic foam cell formation. RCT is mediated by proteins including ATP binding cassette transporters A1 (ABCA1), G1 (ABCG1), liver X receptor- (LXR-) α, and 27-hydroxylase. RCT counteracts lipid overload by ridding cells of excess cholesterol. THP-1 human monocytes were incubated with either TNF-α alone or TNF-α with infliximab. Expression of proteins involved in cholesterol efflux was analyzed. TNF-α significantly reduced both ABCA1 and LXR-α mRNA (to 68.5 ± 1.59%, P < 0.05, and 41.2 ± 0.25%, P < 0.01, versus control set as 100%, resp.). Infliximab nullified the TNF-α effect. Results were confirmed by Western blot. Infliximab abolished the increase in foam cells induced by TNF-α. TNF-α treatment significantly reduces ABCA1 and LXR-α expression in monocytes, thus bringing about a proatherogenic state. The anti-TNF drug infliximab, commonly used in rheumatology, restored RCT proteins. This is the first report of an atheroprotective effect of infliximab on RCT in monocytes.

Immunologic derangements in rheumatoid arthritis (RA) patients likely contribute to premature atherosclerotic cardiovascular disease (CVD). Traditional CVD risk factors do not reliably identify at-risk RA patients, probably because disease-associated mechanisms are not taken into account. The purpose of this study was to determine whether plasma from subjects with RA exhibits atheroma-promoting properties leading to disruption of cholesterol homeostasis in human monocytes/macrophages. Twenty-one healthy controls (HC) and 22 RA patients were enrolled in an IRB approved study at Winthrop University Hospital. Naïve THP-1 macrophages were exposed to plasma from each HC and RA patient. Following incubation, RNA and protein were isolated. QRT-PCR and Western blotting techniques were then used to measure expression of proteins responsible for cholesterol efflux (ATP binding cassette transporter (ABC)A1, ABCG1, 27-hydroxylase) and cholesterol uptake (CD36, ScR-A1, lectin oxidized low density lipoprotein receptor (LOX)-1, CXCL16). To confirm the pro-atherogenic effects of RA plasma on macrophages, foam cell formation was quantified. Results showed that RA plasma downregulates cholesterol efflux proteins and upregulates scavenger receptors CD36, LOX1 and CXCL16. These pro-atherogenic changes in gene expression in the presence of RA plasma are associated with augmented lipid accumulation and foam cell formation by THP-1 macrophages. RA plasma induces macrophage cholesterol overload. Demonstration of disrupted cholesterol homeostasis mediated by RA plasma provides further evidence of the involvement of the immune system in atherogenesis. Our data suggest that chronic exposure to RA plasma adversely affects the capacity of monocytes/macrophages in the arterial wall to metabolize cholesterol and maintain lipid homeostasis, thereby contributing to the development of premature atherosclerosis.

Objective: The greater New York metropolitan area includes 8 medical schools. Their alumni association (AA) presidents formed a council 6 years ago, meeting 3 times a year to share ideas and identify best practices to solve mutual problems challenging students and alumni., Methods: A survey of the 8 medical AAs was conducted; all responded, and the results constitute the data in this report., Results: Mean AA membership was 2509 or 33% of mean alumni populations (7489). Two AAs conferred membership at graduation; hence, 100% of alumni were AA members. Omitting these 2 AAs reduced mean participation to 1722 or 23%. Alumni association support staff averaged 3.8 persons (range, 1-7 persons). The 2 most frequently cited AA challenges were membership and fund-raising. All AAs had annual or biennial reunions and considered the reunion to be a major commitment of resources. Despite this commitment, mean reunion attendance was only 242 alumni (range, 40-500 alumni) or 7.3% of alumni in anniversary years (5-year intervals). The mean number of alumni who contributed annually to their alma mater through its AA was 1936 alumni (range, 500-3500 alumni), or 26% (range, 5%-47%). Medical AAs reported mean assets of $2,755,000 (range, $6475-$11,000,000). The mean AA budget was $298,750, of which 65% (range, 13%-100%) was devoted to "medical student support". The most frequently cited student activities were "career night" (100%), "white coat ceremonies" (63%), medical equipment (stethoscopes, etc, 50%), and alumni host programs (38%). Eleven additional medical student activities received financial support from the 8 AAs in varying proportions., Conclusions: Each AA in the Greater Metropolitan Medical Alumni Council has derived significant benefit from the application of best practices to its individual problem set. In particular, a nascent AA developed significant momentum in its formation and development by its participation in the Greater Metropolitan Medical Alumni Council. Additionally, these data provide a foundation for the development of best practices within medical school AA for optimizing support of student programs and alumni participation. Stronger AAs will translate into enhanced support of educational programs for medical students. We urge formation of similar medical AA organizations in other metropolitan areas.

Objective: To investigate the occurrence, clinical correlates, and immunohistochemical phenotype of temporal small-vessel inflammation (TSVI) in temporal artery biopsies from patients presenting with clinical features of giant cell arteritis (GCA)., Methods: We retrospectively reviewed 41 temporal artery biopsy specimens for the presence of inflammatory infiltrates in small vessels external to the temporal artery adventitia (TSVI); 33 had sufficient clinical and pathological data for detailed analysis. Clinical and laboratory features at presentation and corticosteroid treatment patterns of patients with isolated TSVI were compared to those of patients with positive and negative biopsies. The cellular composition of the infiltrates was further characterized by immunohistochemistry., Results: Twenty-three (70%) specimens had evidence of TSVI including 10 with concurrent GCA and 13 (39%) with isolated TSVI. TSVI was found in all positive temporal artery biopsies. The proportion of macrophages and of lymphocyte subpopulations differed between infiltrates observed in TSVI and those of the main temporal artery wall. Initial erythrocyte sedimentation rate (ESR) was similar in the TSVI and positive biopsy groups and was significantly higher than in the negative biopsy group. Patients with isolated TSVI more often had symptoms of polymyalgia rheumatica compared to the positive biopsy group. Patients with TSVI received corticosteroid doses that were intermediate between patients with positive and those with negative biopsies., Conclusion: A significant number of patients with clinical features of GCA demonstrated isolated TSVI. Differences in the clinical presentation and cellular composition suggest that TSVI may represent a subset of GCA and should be considered in the interpretation of temporal artery biopsies and treatment decisions.

Atherosclerotic cardiovascular disease (ASCVD) contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Immunologic derangements may disrupt cholesterol balance in vessel wall monocytes/macrophages and endothelium. We determined whether lupus plasma impacts expression of cholesterol 27-hydroxylase, an anti-atherogenic cholesterol-degrading enzyme that promotes cellular cholesterol efflux, in THP-1 human monocytes and primary human aortic endothelial cells (HAEC). THP-1 monocytes and HAEC were incubated in medium containing SLE patient plasma or apparently healthy control human plasma (CHP). SLE plasma decreased 27-hydroxylase message in THP-1 monocytes by 47 +/- 8% (p < 0.008) and in HAEC by 51 +/- 5.5% (n = 5, p < 0.001). THP-1 macrophages were incubated in 25% lupus plasma or CHP and cholesterol-loaded (50 microg ml(-1) acetylated low density lipoprotein). Lupus plasma more than doubled macrophage foam cell transformation (74 +/- 3% vs. 35 +/- 3% for CHP, n = 3, p < 0.001). Impaired cholesterol homeostasis in SLE provides further evidence of immune involvement in atherogenesis. Strategies to inhibit or reverse arterial cholesterol accumulation may benefit SLE patients.

We present the first reported case of a patient with dermatomyositis found to have primary gastric melanoma. The possibility of primary gastric melanoma occurring before, concurrently or after the onset of dermatomyositis is the subject of this case report.

A 21-year-old woman with a history of systemic lupus erythematosus (SLE) presented to the emergency room with a chief complaint of substernal chest pain and palpitations. She had undergone a four-vessel coronary artery bypass graft operation with separate saphenous vein grafts to the left anterior descending (LAD), obtuse marginal (OM) 1 and 2, and distal right coronary arteries (RCA) 8 months prior to admission. The patient underwent angiography of the coronary vessels, which showed severe diffuse disease with a long, 90% narrowing of the vein graft to the LAD and closed vein grafts to OM1 and OM2. The RCA graft showed mild diffuse disease. An intervention was done in which the LAD was stented twice with subsequent TIMI 3 flow. Advances in medical therapy and a better understanding of the disease have contributed to a dramatic improvement in the long-term survival of patients with SLE. However, despite the overall long-term improvement, coronary artery disease remains a major cause of morbidity and mortality with an incidence of approximately nine-fold greater than would be expected for this population.

A 32-year-old woman presented with severe headache, photophobia, fever, nausea, vomiting, and worsening vision. She had also noted several months of amenorrhea. She was febrile to 38.9 degrees C. Laboratory evaluation revealed a markedly elevated erythrocyte sedimentation rate. Lumbar puncture revealed a cerebrospinal fluid lymphocytic pleocytosis and an elevated protein level. Endocrine studies revealed evidence of panhypopituitarism without diabetes insipidus. A magnetic resonance imaging study showed a 2-cm pituitary mass with optic chiasmal compression. The patient had a trans-sphenoidal resection of the mass. Pathology revealed multinucleated giant cells in necrotic debris, but no evidence of pituitary tumor. Studies looking for evidence of systemic granulomatous disease were negative. The patient was considered to have idiopathic giant-cell granulomatous hypophysitis. After surgery, the patient's vision improved and hormone replacement therapy was initiated. This case illustrates that idiopathic giant-cell granulomatous hypophysitis should be considered in the differential diagnosis of a patient presenting with a pituitary mass, hypopituitarism, and meningitis-like symptoms.

This article reviews common rheumatic diseases that most frequently occur in women including fibromyalgia, rheumatoid arthritis, Sjogren's syndrome, systemic lupus erythematosus and the antiphospholipid antibody syndrome. Many of these women are of child bearing potential and special considerations concerning pregnancy often arise. Rheumatic conditions that frequently affect older women such as osteoarthritis and polymyalgia rheumatica are discussed as well. Osteoporosis, which has emerged as a significant women's health issue, is also reviewed.

We describe dendritic cell progenitors within the CD34+ stem cell compartment in neonatal cord blood and identify growth factors contributing to their differentiation. Granulocyte-macrophage colony-stimulating factor (GM-CSF), although mainly promoting the growth and differentiation of monocyte-macrophages (mono-m psi s), also induced the differentiation of cells with the distinctive morphological features of dendritic cells (DCs). Tumor necrosis factor (TNF) in combination with GM-CSF promoted further growth of both cell types but most notably increased the DC content. In situ analysis revealed that the cells exhibiting DC morphology were positive for class II major histocompatibility complex antigens but were CD14 negative, did not exhibit nonspecific esterase activity, and were nonphagocytic. Moreover, the mixed leukocyte reaction stimulatory capacity of cultures with the higher DC content was greater. TNF, interleukin-1 (IL-1), IL-6, or platelet-derived growth factor (PDGF) was inactive in promoting stem cell proliferation or DC morphology. IL-1 or PDGF synergized with GM-CSF to increase mono-m psi-associated cell proliferation but did not increase the DC content. The development of a common DC-monocyte precursor was suggested by the presence of colony-forming unit-like clusters containing mono-m psi s and DCs and one sharp proliferative peak. The loss of DC morphology after 21 days, coupled with increases in mono-m psi-associated markers and a constant number of viable cells, further suggests that DC morphology may fluctuate in culture or is a transient feature acquired by certain cells of the mono-m psi lineage.