• Tuberculosis and Respiratory Diseases
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• v.42 no.3
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• pp.375-380
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• 1995

The lymphangioleiomyomatosis(LAM) is a rare disorder, which afflicts mainly young woman of childbearing age, characterized by proliferation of immature smooth muscle cell in the lymphatics. We experienced a case of LAM in 26-years-old pregnant woman, confirmed pathologically by inguinal lymph node biopsy. She has suffered from exertonal dyspnea and dry coughing. The symptoms and chest X-ray were aggravated with pregnancy, but improved after delivery with two times of pregnancy. The chest X-ray showed diffuse reticulonodular infiltration and chest HRCT showed diffuse scattered tiny thin-walled cyst of lung parenchyma. We noted chylous ascites of which triglyceride level is 396 mg/dl. After delivery, the symptoms were getting better. We treated with medroxyprogesterone and planned close observation and follow-up.

• BMB Reports
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• v.47 no.6
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• pp.311-317
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• 2014

microRNAs (miRNAs) are a class of small, non-coding RNAs that play critical posttranscriptional regulatory roles typically through targeting of the 3'-untranslated region of messenger RNA (mRNA). Mature miRNAs are known to be involved in global cellular processes, such as differentiation, proliferation, apoptosis, and organogenesis, due to their capacity to target multiple mRNAs. Thus, imbalances in the expression and/or activity of miRNAs are involved in the pathogenesis of numerous diseases, including pulmonary arterial hypertension (PAH). PAH is a progressive disease characterized by vascular remodeling due to excessive proliferation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs). Recently, studies have evaluated the roles of miRNAs involved in the pathogenesis of PAH in these pulmonary vascular cells. This review provides an overview of recent discoveries on the role of miRNAs in the pathogenesis of PAH and discusses the potential for miRNAs as therapeutic targets and biomarkers of PAH.

• Journal of the Korean Society for Precision Engineering
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• v.32 no.8
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• pp.755-760
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• 2015

For proper wound healing, dermal contraction and remodeling are critical; during the natural healing process, differentiated fibroblasts called "myofibroblasts" typically undertake these functions. For severe wounds, however, a critical mass of dermal matrix and fibroblasts are lost, making self-regeneration impossible. To overcome this impairment, synthetic wound patches with embedded functional cells can be used to promote healing. In this study, we developed a polydioxanone (PDO)-based cell-embedded sheet on which dermal fibroblasts were cultured and induced for differentiation into myofibroblasts, whereby the following combinatorial physicochemical stimuli were also applied: aligned topology, electric field (EF), and growth factor. The results show that both the aligned topology and EF synergistically enhanced the expression of alpha smooth-muscle actin (${\alpha}$-SMA), a key myofibroblast marker. Our proof-of-concept (POC) experiments demonstrated the potential applicability of a myofibroblast-embedded PDO sheet as a wound patch.

• Journal of Chest Surgery
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• v.38 no.9 s.254
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• pp.640-643
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• 2005

Intravenous leiomyomatosis is a rare neoplasm characterized by intravenous growth of histologically benign smooth muscle cell tumor. We report a case of intravenous leiomyomatosis with right atrial extension in a 19-year-old we-man. Various surgical techniques and approaches have been previously reported. In this case, the tumor was re-moved with a single-stage approach via laparotomy without cardiopulmorary bypass.

• Interdisciplinary Bio Central
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• v.4 no.4
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• pp.13.1-13.6
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• 2012

The advanced glycation endproducts receptor (AGER) is a multiligand signal transduction receptor. One of its ligands, S100b molecules activates vascular smooth muscle cells and endothelial cells via its receptor, thus triggering activation of signaling cascades and generation of cytokines and proinflammatory molecules. Ubiquitin-conjugating enzyme Ubc9 is an E2 conjugating enzyme that transfers the activated small ubiquitin-related modifier to protein substrates, and thus it plays a critical role in SUR-Mylation-mediated cellular pathways. Previous studies have shown that both AGE-R and Ubc9 play roles in diverse cellular signaling pathways. However, until recently, little attention has been paid to interactions between AGE-R and Ubc9. In this study, sequence database searches allowed us to identify a potential interaction motif between AGE-R and Ubc9. The subsequent biochemical and molecular biological analysis suggested that there may be specificity in AGE-R and Ubc9 complex signaling in atherosclerosis and cancer cells in a cell-type specific manner. Although the determinant for specificity in AGE-R and Ubc9 complex signaling in cancer cells and atherosclerosis is yet to be determined, this study provides the basis to develop a specific therapeutic application of AGE-R, SURM (small ubiquitin-related modifier)-1, and Ubc9 complex activation pathways in atherosclerosis, diabetes, cancer and inflammatory diseases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.6
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• pp.809-817
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• 2013

The aim of this study was to evaluate the mechanism of vasodilation of Lespedezea cuneata(LC) in rabbit common carotid artery and cavernosal smooth muscle. LC relaxed arterial strips precontracted with norepinephrine and cavernosal strips precontracted with phenylephrine. The arterial relaxation effects of LC was endothelium-dependent. $N{\omega}$-nitro-L-arginine(L-NNA), NOS inhibitor, methylene blue(MB), cGMP inhibitor, indomethacin(IM), cyclo-oxygenase inhibitor and tetraethylammonium chloride(TEA), KCa-channel blocker attenuate the relaxation responses of LC in arterial strips. In $Ca^{2+}$-free krebs-ringer solution, pretreatment of LC extract significantly reduced the contraction induced by addition $Ca^{2+}$. L-NNA reduced LC extract-induced relaxation in cavernosal strips, but IM, TEA and MB didn't affect LC extract-induced relaxation. When LC extract was applicated on human umbilical vein endothelial cell, the nitric oxide concentration was increased. We conclude that in rabbit common carotid artery, LC may suppress influx of extra-cellular $Ca^{2+}$ through the release of endothelium derived relaxing factor including nitric oxide, prostacyclin, endothelium derived hyperpolarizing factor. And LC exerts a relaxing effect on corpus cavernosum through activating the NO.

• The Korean Journal of Cytopathology
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• v.17 no.2
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• pp.153-158
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• 2006

Low-grade fibromyxoid sarcoma (LGFMS) is a rare soft tissue tumor. There have been only a few prior fine-needle aspiration (FNA) cytological reports. Recognition of this tumor is important because of its potential for metastasis despite its indolent nature and its deceptively bland cytologic appearance. A 60-year-old male presented with a slowly growing mass in the left calf detected 10 years ago. The patient underwent surgical excision. FNA cytology was performed directly on the mass. The smears showed low cellularity composed of hypercellular tissue fragments, hypocellular loose aggregates, and stripped nuclei. The cytoplasm was seen as either collagenous material or very thin fibrillary collagen strands. Tumor cells had spindle, ovoid, or irregular nuclei, fine chromatin, and small nucleoli. Focally slight degree of nuclear pleomorphism is noted. There were no mitotic figures. Blood vessels were frequently seen. Immunocytochemically, tumor cells were negative for S-100 protein, desmin, smooth muscle actin, and CD34. The diagnosis of LGFMS is rarely possible by cytology alone; however, LGFMS should be included in the differential diagnosis of spindle-cell tumors consisting of hypercellular and hypocellular components with some capillary-sized vessels arising in the deep soft tissue of the lower extremities, particularly the thigh. The immunocytochemical findings are of help in the differential diagnosis.

• IMMUNE NETWORK
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• v.14 no.5
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• pp.237-240
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• 2014

Endoglin (also known as CD105 or TGF-${\beta}$ type III receptor) is a co-receptor involved in TGF-${\beta}$ signaling. In atherosclerosis, TGF-${\beta}$ signaling is crucial in regulating disease progression owing to its anti-inflammatory effects as well as its inhibitory effects on smooth muscle cell proliferation and migration. Endoglin is a regulator of TGF-${\beta}$ signaling, but its role in atherosclerosis has yet to be defined. This review focuses on the roles of the various forms of endoglin in atherosclerosis. The expression of the two isoforms of endoglin (long-form and short-form) is increased in atherosclerotic lesions, and the expression of the soluble forms of endoglin is upregulated in sera of patients with hypercholesterolemia and atherosclerosis. Interestingly, long-form endoglin shows an atheroprotective effect via the induction of eNOS expression, while short-form and soluble endoglin enhance atherogenesis by inhibiting eNOS expression and TGF-${\beta}$ signaling. This review summarizes evidence suggesting that the different forms of endoglin have distinct roles in atherosclerosis.

• Korean Journal of Veterinary Pathology
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• v.1 no.1
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• pp.72-76
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• 1997

Histological investigation of the number of follicles following gonadotropin treatments for superovulation was carried out in mature Sprague-Dwaley(SD) rats. Routinely serial sections of paraffin-embedded ovaries were stained with hematoxylin-eosin and evaluated with light microscope. During the study unusual cases of microscopic alterations were observed in the medulla of ovaries in two rats. Case one: An ovum and its follicular fluid outflowed in medulla of ovary. The follicular fluid was densly proteinuous. Corona raiata consisted of 2-6 layers thick cells in the periphery of the ovum. While the cortical side of the follicular wall was intact with normal granulosa cell layer the meullary side of it was ruptured. Case two: A large cyst was present in medulla of ovary hilus. The cyst occupied the entire medulla displacing the ovarian archetecture and enclosed by connective tissue and smooth muscle wall.

• Journal of Ginseng Research
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• v.32 no.2
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• pp.89-98
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• 2008

There are increasing evidences in the literatures on the potential role of ginsenosides in treating cardiovascular diseases. In this article, current information about ginsenosides-mediated vascular relaxation are reviewed. From the published studies using isolated organs, cell culture systems and animal models, ginsenosides are shown to relax blood vessels and improve blood flow through diverse mechanisms, including nitric oxide release by activating eNOS phosphorylation via PI3K/Akt and/or ERK1/2 pathways in endothelial cells, induction of inducible nitric oxide synthase through activation of NF-${\kappa}$B, reducing the intracelluar Ca$^{2+}$ levels by activating Ca$^{2+}$-activated K$^{+}$ channels in vascular smooth muscle cells and reducing platelet aggregation by decreasing thromboxane A$_2$ formation and intracelluar Ca$^{2+}$in platelets. In addition, the relevant clinical trials regarding the effects of ginsenosides on the cardiovascular disease are summarized, particulary focusing on managing hypertension and improving thrombotic disorders. Finally, antagonistic effects of ginsenosides on the prostaglandin H$_2$ receptor and scavenging effects on the generation of oxygen-derived free radicals in spontaneously hypertensive rats (SHR) are discussed.