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1.
Clin Case Rep ; 12(7): e9160, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-39011518

RESUMO

Key Clinical Message: Pericardial sarcoidosis is an uncommon cause of chest pain to consider, and it requires a heightened level of suspicion and thorough history gathering. If there is suspicion of inflammatory disease, pursuing advanced imaging and biopsies is crucial, as early immunosuppressive treatment can enhance outcomes. Abstract: Pericardial involvement in sarcoidosis is a rare condition with limited research. This case study discusses a 52-year-old African American woman who presented with subacute chest pain and was diagnosed with pericardial sarcoidosis. Diagnostic evaluation revealed extensive lymphadenopathy and pericardial effusion, and a pericardial biopsy confirmed non-caseating granulomatous inflammation. Treatment with steroids and methotrexate resulted in clinical improvement. Eight months follow-up showed near resolution of pericardial disease. This case emphasizes the importance of considering cardiac sarcoidosis in sarcoidosis patients, utilizing advanced imaging for accurate diagnosis, and tailoring treatment to the level of cardiac involvement.

2.
J Investig Med High Impact Case Rep ; 9: 23247096211044617, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34514900

RESUMO

Nodular regenerative hyperplasia (NRH) is a rare disease that is characterized by benign transformation of the hepatic parenchyma into small nodules with little to no fibrosis. Nodular regenerative hyperplasia is a cause of noncirrhotic portal hypertension. Symptoms can range from asymptomatic disease to more serious complications of portal hypertension such as esophageal varices and ascites. Nodular regenerative hyperplasia has been described in association with a variety of different rheumatologic, hematologic, and oncologic diseases, as well as in immune deficiency states and with exposures to certain toxins. Diagnosis is made by histology, and the treatment involves addressing the underlying disease. The first description of this rare disease was actually described in a patient with rheumatoid arthritis, neutropenia, and splenomegaly (Felty's Syndrome). We describe 2 cases of NRH associated with underlying rheumatic disorders, in one of which NRH was actually the presenting feature of the patient's underlying autoimmune condition. Subsequently, we provide a brief review of the literature of NRH in autoimmune disease with respect to epidemiology, cause, clinical manifestations, diagnosis, and treatment.


Assuntos
Hipertensão Portal , Doenças Reumáticas , Humanos , Hiperplasia , Regeneração Hepática , Doenças Reumáticas/complicações , Doenças Reumáticas/diagnóstico
3.
J Cell Commun Signal ; 15(2): 223-236, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33591483

RESUMO

Gap junctional intercellular communication (GJIC) is a homeostatic process mediated by membrane channels composed of a protein family known as connexins. Alterations to channel activity can modulate suppression or facilitation of cancer progression. These varying roles are influenced by the cancer cell genetic profile and the context-dependent mechanisms of a dynamic extracellular environment that encompasses fluctuations to nutrient availability. To better explore the effects of altered cellular metabolism on GJIC in breast cancer, we generated a derivative of the triple-negative breast cancer cell line MDA-MB-231 optimized for growth in low-glucose. Reduced availability of glucose is commonly encountered during tumor development and leads to metabolic reprogramming in cancer cells. MDA-MB-231 low-glucose adapted cells exhibited a larger size with improved cell-cell contact and upregulation of cadherin-11. Additionally, increased protein levels of connexin 43 and greater plasma membrane localization were observed with a corresponding improvement in GJIC activity compared to the parental cell line. Since GJIC has been shown to affect cellular invasion in multiple cancer cell types, we evaluated the invasive qualities of these cells using multiple three-dimensional Matrigel growth models. Results of these experiments demonstrated a significantly more invasive phenotype. Moreover, a decrease in invasion was noted when GJIC was inhibited. Our results indicate a potential response of triple-negative breast cancer cells to reduced glucose availability that results in changes to GJIC and invasiveness. Delineation of this relationship may help elucidate mechanisms by which altered cancer cell metabolism affects GJIC and how cancer cells respond to nutrient availability in this regard.

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