A rare case of mesothelial/monocytic incidental cardiac excrescences (cardiac MICE) is described in the aspect of pathological interest. This cardiac lesion is pathologically characterized by exuberant proliferation of mixed mesothelia and monocytes and might be misdiagnosed as metastatic carcinoma, rhabdomyosarcoma, and histiocytoid hemangioma, if the disease is not in the minds of pathologists. The reactive nodular hyperplasia due to irritation to mesothelia by various causes is a most prevailing pathogenetic mechanism. About 20 cases have been reported in the worldwide literature. A 67-year-old female patient presented with cough and dyspnea for 2 months, without any history of previous cardiac operation. 2D echocardiography of the heart revealed moderate amount of pericardial effusion with posterior wall thickening. Under the impression of metastatic malignancy, pericardiostomy was performed. Grossly, the tissue was dark hemorrhagic and friable and the histologic sections revealed the solid tumor-like proliferation of round to polygonal histiocytic cells admixed with small cuboidal mesothelial cells which formed strips and tubular arrays. They were found within the fibrinous network and there were scattered empty vacuolar spaces. Immunohistochemical staining confirmed their biphasic nature with the CD68 positivity of the histiocytes and the cytokeratin positivity of the cuboidal cells. Factor VIII positivity was not detected in any cell components. The lesion was considered the monocytic and mesothelial proliferation of reactive nature, so-called cardiac MICE in the pericardial cavity. We report a typical case of so-called MICE first in the Korean literature.
Aged ; Animals ; Cellular Structures ; Cough ; Dyspnea ; Echocardiography ; Factor VIII ; Female ; Fibrin ; Heart ; Hemangioma ; Histiocytes ; Humans ; Hyperplasia ; Keratins ; Mice ; Monocytes ; Pericardial Effusion ; Pericardial Window Techniques ; Rhabdomyosarcoma

Medium-chain fatty acids (MCFAs) are mostly generated from dietary triglycerides and can penetrate the blood-brain barrier. Astrocytes in the brain use MCFAs as an alternative energy source. In addition, MCFAs have various regulatory and signaling functions in astrocytes. However, it is unclear how astrocytes sense and take up MCFAs. This study demonstrates that decanoic acid (DA; C10), a saturated MCFA and a ligand of G(αs) protein-coupled receptors (G(αs)-GPCRs), is a signaling molecule in energy metabolism in primary astrocytes. cAMP synthesis and lactate release were increased via a putative G(αs)-GPCR and transmembrane adenylyl cyclase upon short-term treatment with DA. By contrast, monoamine oxidase B-dependent gamma-aminobutyric acid (GABA) synthesis was increased in primary cortical and hypothalamic astrocytes upon long-term treatment with DA. Thus, astrocytes respond to DA by synthesizing cAMP and releasing lactate upon short-term treatment, and by synthesizing and releasing GABA upon long-term treatment, similar to reactive astrocytes. Our data suggest that astrocytes in the brain play crucial roles in lipid-sensing via GPCRs and modulate neuronal metabolism or activity by releasing lactate via astrocyte-neuron lactate shuttle or GABA to influence neighboring neurons.
Adenylyl Cyclases ; Animals ; Astrocytes* ; Blood-Brain Barrier ; Brain ; Energy Metabolism ; Fatty Acids ; gamma-Aminobutyric Acid* ; Lactic Acid* ; Metabolism ; Mice* ; Monoamine Oxidase ; Neurons ; Triglycerides

Purpose: Colorectal cancer (CRC) is the most frequent cancer with limited therapeutic achievements. Recently, adoptive cellular immunotherapy has been developed as an antitumor therapy. However, its efficacy has not been tested in CRC. This study investigated the ability of an immune cell cocktail of dendritic cells (DCs), T cells, and natural killer (NK) cells to overcome immunological hurdles and improve the therapeutic efficacy of cell therapy for CRC. Methods: CRC lysate-pulsed monocyte-derived DCs (Mo-DCs), CRC antigen-specifically expanded T cells (CTL), and in vitro-expanded NK cells were cultured from patient peripheral blood mononuclear cells (PBMC). The ability of the combined immune cells to kill autologous tumor cells was investigated by co-culturing the combined immune cells with patient-derived tumor cells. Results: The Mo-DCs produced expressed T cell co-stimulating molecules like CD80, CD86, human leukocyte antigen (HLA)-DR and HLA-ABC, at high levels and were capable of activating naive T cells. The expanded T cells were predominantly CD8 T cells with high levels of CD8 effector memory cells and low levels of regulatory T cells. The NK cells expressed high levels of activating receptors and were capable of killing other cancer cell lines (K562 and HT29). The immune cell cocktail demonstrated a higher ability to kill autologous tumor cells than single types. An in vivo preclinical study confirmed the safety of the combined immune cell adaptive therapy showing no therapy-related death or general toxicity symptoms. Conclusion The results suggested that combined immune cell adaptive therapy could overcome the limited efficacy of cell immunotherapy.