Uterine Leiomyoma or Sarcoma?

2021 ◽  
pp. 289-304
Author(s):  
Theodoros Theodoridis ◽  
Dimitra Aivazi ◽  
Leonidas Zepiridis ◽  
Nikolaos Vlachos
Keyword(s):  
Differential Diagnosis ◽  
Smooth Muscle ◽  
Connective Tissue ◽  
Muscle Cells ◽  
Uterine Sarcoma ◽  
Current Evidence ◽  
Optimal Management ◽  
Benign Neoplasms ◽  
Uterine Sarcomas ◽  
Epithelial Neoplasms

Uterine leiomyomas are benign neoplasms derived from the smooth muscle cells of the myometrium. In contrast, uterine sarcomas are rare tumors, with a prevalence of 3-7 per 100,000 women, originating from myometrial cells or endometrial connective tissue. Uterine sarcomas and especially leiomyosarcomas are more aggressive than uterine epithelial neoplasms. The differential diagnosis between leiomyoma and uterine sarcoma preoperatively remains challenging for the clinical practitioner in order to determine optimal treatment. The chapter aims to summarize current evidence regarding differential diagnosis and optimal management of these two challenging clinical entities.

scholarly journals Immunocytochemical characteristics of submucosal uterine myomas

2010 ◽  
Vol 67 (12) ◽  
pp. 977-982 ◽  
Author(s):  
Aleksandra Mladenovic-Mihailovic ◽  
Zorica Mladenovic-Bogdanovic ◽  
Predrag Mitrovic ◽  
Irena Tanaskovic ◽  
Slavica Usaj-Knezevic ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Synthetic Activity ◽  
Benign Tumors ◽  
Paraffin Sections ◽  
Weak Reaction ◽  
Synthetic Phenotype

Background/Aim. Myomas of the uterus, the most common benign tumors, have been studied for decades from the aspects of different basic and clinical disciplines. Despite this fact, their pathogenesis is still poorly understood. The aim of this study was to determine immunocytochemical characteristics of smooth muscle cells and connective tissue components of submucosal myomas of the uterus. Method. During the course of this study, 25 samples of submucosal myomas of the uterus were analyzed, all of them obtained during the surgery, after abdominal histerctomy by Aldridge. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 ?m thickness were stained immunocytochemically using the DAKO LSAB+/HRP technique to identify ?- smooth muscle actin (?-SMA), vimentin, desmin, CD34, CD45, CD68 and PCNA (DAKO specification). Results. Our results suggest that submucosal myomas of the uterus are build-up of smooth muscle cells which are immunoreactive to ?-SMA and desmin, but also to a certain number of smooth muscle cells which are immunoreactive to ?-SMA and vimentin. Some of vimentin-immunoreactive cells also show an immunoreactivity of PCNA. In the build-up of connective stroma CD34-immunoreactive fibroblasts and neovascular formations are also present. By examining the distribution of CD45 antigen, at all the analyzed samples we observed a weak reaction. Conclusion. Submucosal myomas of the uterus are made-up of smooth muscle cells of the highly differentiated contractile phenotype (?-SMA- and desminimmunoreactivity), as well as smooth muscle cell of the synthetic phenotype which proliferate (?-SMA-, vimentin- and PCNA-immunoreactivity). In submucosal myoma of the uterus there is a significant presence of connective tissue as a result of synthetic activity of fibroblasts, which clearly differ in their immunocytochemical characteristics from smooth muscle cells of the synthetic phenotype.

The Role of Endothelial Cell Injury and Platelet Response in Atherogenesis

1977 ◽  
Author(s):  
L. A. Harker ◽  
R. Ross ◽  
J. Glomset
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Lipid Accumulation ◽  
Blood Platelets ◽  
Muscle Cells ◽  
Endothelial Injury ◽  
Intimal Proliferation ◽  
Flowing Blood

Endothelium forms a resistant barrier between flowing blood and vessel wall structures. Endothelial thromboresistance is maintained in part by the synthesis of prostacyclin, a potent prostaglandin inhibitor of platelet function. Loss of endothelial cells, mediated by physical, chemical, infectious or immune mechanisms, exposes the sub endothelium to flowing blood. Platelets react to the subendothelial connective tissue structures, undergoing adhesion and release of intracellular constituents, including a factor that is mitogenic to smooth muscle cells. This growth factor is a heat stable, basic protein (IP 7.4–9.4) of 20,000 Daltons and appears to be responsible for the intimal proliferation of smooth muscle cells that follows endothelial cell desquamation. After a single injury event the intimal lesion regresses over several months. Repeated or continuous endothelial cell loss results in progressive intimal proliferation of smooth muscle cells, their secretion of connective tissue matrix components (collagen, elastin and proteoglycans) and accumulation of lipid when animals are on a hypercholesterolemic diet to form early atherosclerotic intimal lesions. Discontinuance of endothelial injury and restoration of the endothelium appear to be followed by lesion regression except when lipid accumulation is extensive. Possible approaches to atherosclerosis prevention include: 1) protection of the endothelium by interruption or avoidance of endothelial injury factors, and perhaps by pharmacologic protection; 2) inhibition of platelet reactivity; 3) modification of SMC proliferation, secretion or lipid accumulation.

Mast cell enzymes alter the connective tissue phenotype of bladder wall fibroblasts and smooth muscle cells

Urology ◽  
2001 ◽  
Vol 57 (6) ◽  
pp. 112-113 ◽  
Author(s):  
P.S Howard ◽  
D Renfrow ◽  
S Ford ◽  
U Kucich ◽  
N Schechter
Keyword(s):  
Mast Cell ◽  
Smooth Muscle ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Bladder Wall ◽  
Muscle Cells

scholarly journals Seminal Vesicles and Bulbourethral Glands of Mammals: Morphology, Physiology, Ecology, Action of Extreme Destabilizing Factors

2021 ◽  
Vol 10 (3) ◽  
pp. 98-107
Author(s):  
N. N. Shevlyuk ◽  
M. F. Ryskulov
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Connective Tissue ◽  
Smooth Muscle Cells ◽  
Seasonal Pattern ◽  
Prostate Gland ◽  
Muscle Cells ◽  
Seminal Vesicles ◽  
Natural Ecosystems ◽  
Secretory Cycle

In mammals, the adnexal sex glands are represented by seminal vesicles, the prostate gland, urethral and bulbourethral glands, as well as glands that coagulate sperm and ampullary glands. The secret of the accessory genital glands increases the volume of the ejaculate (the share of secretions of these glands accounts for about 95% of the volume of ejaculate) promotes sperm, causes increased contraction of smooth muscle cells in the walls of the female genital tract.The purpose of this review is to analyze the morphofunctional organization of seminal vesicles and bulbourethral glands of mammalian animals and humans.The presence or absence of seminal vesicles is a species-specific feature. Among mammals, seminal vesicles are well developed in some rodents, insectivores, a number of domestic animals (cattle, pigs), and primates. These glands are absent in cloacae, marsupials, some carnivores, a number of insectivores, artiodactyls. Bulbourethral glands are well developed in rodents, bats, primates, and some ungulates.In the wall of the seminal vesicles, the mucous, muscular and outer membranes are isolated. The epithelium of the secretory parts is pseudomultitial, the interstitium is represented by loose fibrous connective tissue and a significant number of smooth muscle cells. In the wall of the bulbourethral glands, the mucosa and adventitial membrane are isolated. The secretory end sections of the bulbourethral glands are lined with a single-layer single-row epithelium, glandular cells produce a mucosal or mixed secret. The seminal vesicles and bulbourethral glands are androgen-dependent glands. In species with a seasonal pattern of reproduction, their morphofunctional characteristics undergo significant changes during the circannual rhythm of reproduction.The epithelium of seminal vesicles and bulbourethral glands is very sensitive to the action of various adverse factors (heavy metal compounds, organic xenobiotics, electromagnetic radiation, ultrasound, etc.). When exposed to various negative factors in the adnexal glands, a complex of changes occurs (edema of connective tissue and epithelium, decreased secretory activity of epithelial cells, desynchronization of the secretory cycle, desquamation of glandular epithelial cells, proliferation of interstitial connective tissue).There is a lack of information on many aspects of the characteristics of the adnexal glands of the male reproductive system, primarily on the morphology and physiology of the adnexal glands of animals in natural ecosystems, on the ultrastructural and immunohistochemical characteristics of these glands, as well as on the mechanisms of regulation of morphofunctional rearrangements of the adnexal glands during seasonal reproduction rhythms, in the conditions of adaptation to various negative influences.

Calcium and potassium currents in canine gastric smooth muscle cells

1992 ◽  
Vol 262 (5) ◽  
pp. G859-G867 ◽  
Author(s):  
S. M. Sims
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Outward Current ◽  
Muscle Cells ◽  
Current Evidence ◽  
Equilibrium Potential ◽  
Inward Current ◽  
K Current ◽  
Gastric Corpus ◽  
Ca2 Channels

Membrane ionic currents were recorded in single smooth muscle cells dissociated from circular muscle of dog stomach (corpus region). When studied under voltage clamp with K+ in the patch electrode, depolarization to potentials more positive than -40 mV, from a holding potential of -70 or -80 mV, evoked transient inward current followed by outward current. Evidence that the outward current was due to K+ came from analysis of deactivation tail currents, which reversed direction close to the K+ equilibrium potential. In addition, the outward current was reduced by tetraethylammonium (TEA, 1-5 mM) applied to the external surface of cells. The Ca(2+)-channel blocker Cd2+ blocked the inward current and also reduced outward current, suggesting Ca(2+)-activated K+ current contributed to the outward current. The voltage-activated inward current was studied in isolation with Cs+ and TEA in the recording electrode to block K+ current. In standard bathing solution containing 2.5 mM Ca2+, the inward current activated between -50 and -40 mV, with peak inward current at +10 mV. The depolarization-activated inward current was blocked by nifedipine and enhanced by BAY K 8644, providing evidence that it was Ca2+ current. The Ca2+ current showed transient and sustained components, both of which showed similar voltage activation and inactivation ranges. The half-inactivation potential was approximately -37 mV. These results provide evidence that smooth muscle cells from the canine gastric corpus possess K+ and Ca2+ channels. Based on the voltage dependence of activation and inactivation and sensitivity to dihydropyridines, L-type Ca2+ channels predominate in canine gastric corpus smooth muscle.

scholarly journals Magnolol, A Novel Antagonist of Thrombin and PAR-1, Inhibits Thrombin-Induced Connective Tissue Growth Factor (CTGF) Expression in Vascular Smooth Muscle Cells and Ameliorate Pathogenesis of Restenosis in Rats

2020 ◽  
Vol 10 (23) ◽  
pp. 8729
Author(s):  
Wen-Chin Ko ◽  
Chia-Ti Tsai ◽  
Kai-Cheng Hsu ◽  
Yu-Che Cheng ◽  
Tony Eight Lin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Connective Tissue Growth Factor ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tissue Growth ◽  
Functional Assay

Restenosis and destructive vascular remodeling are the main reasons for treatment failure in patients undergoing percutaneous coronary intervention (PCI). In this study, we explored the efficacy of magnolol (a traditional Chinese medicine) in the treatment of restenosis. The results of this study showed that the activities of thrombin and PAR-1 (protease-activated receptor 1) were significantly decreased by the treatment of magnolol. Based on protein docking analysis, magnolol exhibits its potential to bind to the PAR-1 active site. In addition, thrombin-induced connective tissue growth factor (CTGF) expression and the upstream of CTGF such as JNK-1 (but not JNK-2), c-Jun, and AP-1 were distinctly inhibited by magnolol (50 μM) in vascular smooth muscle cells (VSMC). For the functional assay, magnolol (50 μM) significantly inhibited the migration of VSMC, and rats treated with magnolol (13 mg/kg/day) after balloon angioplasty has observed a significant reduction in the formation of common arterial neointima. In conclusion, we identified a novel mechanism by which magnolol acts as the thrombin activity inhibitor and may be the PAR-1 antagonist. In accordance with these functions, magnolol could decrease thrombin-induced CTGF expression in VSMCs via PAR-1/JNK-1/AP-1 signaling.

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