scholarly journals STUDIES ON ENDOTHELIAL REACTIONS

1920 ◽  
Vol 32 (5) ◽  
pp. 533-546 ◽  
Author(s):  
Nathan Chandler Foot
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Colloidal Suspension ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Normal Lung ◽  
Capillary Endothelium ◽  
Alveolar Wall ◽  
Living Animal ◽  
Capillary Walls

1. The injection of a colloidal suspension, or sol, of carbon into the veins of a living animal, as recommended by McJunkin, furnishes an apparently reliable means of tracing the so called epithelioid cell of the pulmonary tubercle from its origin in the vascular endothelium to the lesion. 2. Experimental tubercles are formed in the lung, as in the liver, primarily by cells originating in the capillary endothelium. These cells are probably present in small numbers in the normal lung, lying free both in the alveolar wall and the air vesicles. In response to infection they proliferate in the capillary walls in the vicinity of the invading organisms, migrate in steadily increasing numbers, and, arriving at the site of the infection, further multiply and to some extent fuse to form the syncytia known as giant cells. 3. The epithelial cell takes no active part in the process; its proliferation tends to repair denuded surfaces and is regenerative rather than combative or phagocytic in nature. This cell is free from carbon and stains only diffusely with carmine, in contradistinction to the endothelial cell which readily takes up both pigments in granular form. 4. The cells of endothelial origin not only phagocytose tubercle bacilli, but carry them into the tissues, for example into lymph nodes, by way of the lymphatics, or into other lung lobules by way of the air passages, in which they are readily demonstrable.

Selective expression of stromal-derived factor-1 in the capillary vascular endothelium plays a role in Kaposi sarcoma pathogenesis

Blood ◽  
2003 ◽  
Vol 102 (12) ◽  
pp. 3900-3905 ◽  
Author(s):  
Lei Yao ◽  
Ombretta Salvucci ◽  
Adela R. Cardones ◽  
Sam T. Hwang ◽  
Yoshiyasu Aoki ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Kaposi Sarcoma ◽  
Skin Lesions ◽  
Capillary Endothelium ◽  
Flow Conditions ◽  
Endothelial Cell Surface ◽  
Spindle Cells ◽  
Selective Expression ◽  
Infected Cells

Abstract Kaposi sarcoma (KS), the most common neoplasm in patients with AIDS, typically presents with multiple skin lesions characterized by “spindle cells,” the vast majority of which are infected with KSHV (Kaposi sarcoma herpes virus, also named HHV-8). In patients with AIDS, the presence of cell-associated KSHV DNA in blood is predictive of subsequent KS development, but the mechanisms by which circulating KSHV-infected cells contribute to AIDS-KS pathogenesis are unclear. Here, we show that the chemokine stromal-derived factor-1 (SDF-1), which is constitutively expressed by skin capillary endothelium and displayed on the endothelial cell surface in association with heparan sulfate, can trigger specific arrest of KSHV-infected cells under physiologic shear flow conditions. Moreover, in the presence of soluble SDF-1 gradients, SDF-1 expressed on the endothelial barrier can promote transendothelial migration of KSHV-infected cells. By triggering specific adhesion of circulating KSHV-infected cells and favoring their entry into the extravascular cutaneous space, endothelial cell–associated SDF-1 in cutaneous capillaries may dictate the preferential occurrence of KS in the skin.

scholarly journals Leukoplakia or LPR: The Misdiagnosis of Laryngeal Tuberculosis

2019 ◽  
pp. 014556131989126
Author(s):  
Zheng cai Lou ◽  
Xiuguo Li
Keyword(s):  
Pulmonary Tuberculosis ◽  
Histopathological Examination ◽  
Laryngopharyngeal Reflux ◽  
Case Series ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Normal Lung ◽  
Acute Epiglottitis ◽  
Type Giant ◽  
Laryngeal Tuberculosis

Objective:The objective is to reduce the rates of misdiagnosis and inappropriate treatment of laryngeal tuberculosis (LTB).Study Design:Retrospective case series.Materials and Methods:Medical records of 3 histopathology-confirmed cases at a tertiary medical center from 2000 to 2018.Results:Seventeen patients with LTB included in this study. Of the 17 patients, 16 patients were male and 1 was female; 11 patients had a history of smoking. Odynophagia was the chief complaint in 6 cases, and 11 patients complained of hoarseness. The appearance of the affected larynx was ranged from diffuse swelling (n = 7, 41.2%), mucosa white lesion (n = 5,29.4%), and granulomatous tumors (n = 2, 11.76%), and these features presented together (n = 2, 11.76%). Seventeen patients with LTB were misdiagnosed as acute epiglottitis in 4 (23.5%) patients, acute laryngitis in 1 (5.9%) patient, leukoplakia in 5 (29.4%) patients, laryngopharyngeal reflux (LPR) in 6 (35.3%) patients, and laryngocarcinoma in 1 (5.9%) patient. Chest computed tomography reported old pulmonary tuberculosis in 2 (11.7%) patients, active pulmonary tuberculosis in 7 (41.2%) patients, and normal lung status in 8 (47.1%) patients. Histopathological examination reported Mycobacterium tuberculosis infection by revealing epithelioid cell granulomas with Langhans-type giant cells in 14 (82.4%) patients and epithelioid cell granulomas with caseous necrosis and Langhans-type giant cells in 3 (17.6%) patients.Conclusions:Laryngeal tuberculosis was easily misdiagnosed as acute epiglottitis or leukoplakia because of diffuse swelling of the epiglottis or white lesions over the true vocal cord, especially patients with increasing LTB were misdiagnosed as LPR with the enhancement of LPR awareness among otolaryngologist. Clinicians should be aware of the possibility of LTB for chronic intractable laryngitis with failure treatment of proton pump inhibitor and recurrent acute epiglottitis with foreign body injury.

scholarly journals Hepatocellular carcinoma with regional lymphadenopathy caused by sarcoid-like reaction: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Tomoko Mizota ◽  
Masato Suzuoki ◽  
Saya Kaku ◽  
Kenichi Mizunuma ◽  
Kazuto Ohtaka ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Lymph Node ◽  
Lymph Nodes ◽  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Imaging Modalities ◽  
Hepatoduodenal Ligament ◽  
Regional Lymph Nodes ◽  
Multiple Imaging

Abstract Background Sarcoid-like reaction (SLR) is a histological pattern of granulomatous inflammation that is clinically differentiated from sarcoidosis. Since SLR is known to occur in several neoplasias and occasionally causes lymphadenopathy and mimics metastatic malignancy, it needs to be considered whether lymphadenopathy is due to metastasis or SLR for the choice of cancer treatment. Few cases of hepatocellular carcinoma (HCC) with SLR have been reported. Here, a case of HCC with lymphadenopathy diagnosed as SLR without metastasis is presented. Case presentation A 69-year-old woman was admitted to our hospital because of upper abdominal pain. She tested positive for hepatitis C virus ribonucleic acid. Imaging modalities showed an 81 × 65-mm-sized tumor with multiple nodules in segment 3 and a 17 × 12-mm-sized tumor in segment 5 with a common HCC enhancement pattern. In addition, a lymph node in the hepatoduodenal ligament was enlarged at 13 mm in size, suggesting the metastasis of HCC. Hepatectomy of the lateral segment and segment 5 and lymph node dissection in the hepatoduodenal ligament were performed. Both tumors in segments 3 and 5 were pathologically diagnosed as HCC without vessel invasion. The tumors contained necrotic cells and epithelioid cell granulomas with multinucleated giant cells, which is typically observed in sarcoidosis. The dissected lymph nodes also contained epithelioid cell granulomas, as well as giant cells with asteroid bodies. There was no malignancy in the lymph nodes. The pathological findings suggested the coexistence of malignancy and sarcoidosis. However, since the patient did not show any typical findings of pulmonary or cardiac sarcoidosis, the case was diagnosed as HCC with SLR in the primary lesion and regional lymph nodes. Conclusions SLR needs to be considered in the differential diagnosis when a cancer patient develops lymphadenopathy. However, lymphadenopathy due to SLR is indistinguishable from that due to metastasis even when using multiple imaging modalities. Pathological examinations may be helpful for the diagnosis.

scholarly journals Disseminated Bacillus Calmette–Guérin (BCG) infection and acute exacerbation of interstitial pneumonitis: an autopsy case report and literature review

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Gen Shimizu ◽  
Ryota Amano ◽  
Itaru Nakamura ◽  
Akane Wada ◽  
Masanobu Kitagawa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bladder Cancer ◽  
Acute Exacerbation ◽  
Interstitial Pneumonitis ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Bacillus Calmette Guerin ◽  
Antituberculosis Drugs ◽  
First Case ◽  
Intravesical Bcg

Abstract Background Intravesical administration of Bacillus Calmette–Guérin (BCG) has proven useful for treatment and prevention of recurrence of superficial bladder cancer and in situ carcinoma. However, fatal side effects such as disseminated infections may occur. Early diagnosis and accurate therapy for interstitial pneumonitis (IP) are important because exacerbation of IP triggered by infections is the major cause of death. Although some fatality reports have suggested newly appeared IP after intravesical BCG treatment, to our knowledge, there are no reports which have demonstrated acute exacerbation of existing IP. Moreover, autopsy is lacking in previous reports. We report the case of a patient with fatal IP exacerbation after BCG instillation and the pathological findings of the autopsy. Case presentation A 77-year-old man with a medical history of IP was referred to our hospital because of fever and malaise. He had received an intravesical injection of BCG 1 day before the admission. His fever reduced after the use of antituberculosis drugs, so he was discharged home. He was referred to our hospital again because of a high fever 7 days after discharge. On hospitalisation, he showed high fever and systemic exanthema. Hepatosplenomegaly and myelosuppression were also observed. Biopsies revealed multiple epithelioid cell granulomas with Langhans giant cells of the liver and bone marrow. Biopsy DNA analyses of Mycobacterium bovis in the bone marrow, sputum, and blood were negative. His oxygen demand worsened drastically, and the ground-glass shadow expanded on the computed tomography scan. He was diagnosed with acute exacerbation of existing IP. We recommenced the antituberculosis drugs with steroid pulse therapy, but he died on day 35 because of respiratory failure. The autopsy revealed a diffuse appearance of multiple epithelioid cell granulomas with Langhans giant cells in multiple organs, although BCG was not evident. Conclusions We report the first case of acute exacerbation of chronic IP by BCG infection. This is also the first case of autopsy of a patient with acute exacerbation of existing IP induced by intravesical BCG treatment. Whether the trigger of acute IP exacerbation is infection or hypersensitivity to BCG is still controversial, because pathological evidence confirming BCG infection is lacking. Physicians who administer BCG against bladder cancer should be vigilant for acute exacerbation of IP.

Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier

1995 ◽  
Vol 82 (6) ◽  
pp. 1053-1058 ◽  
Author(s):  
Paul A. Grabb ◽  
Mark R. Gilbert
Keyword(s):  
Endothelial Cell ◽  
Rat Brain ◽  
Phospholipase A ◽  
Cell Permeability ◽  
Capillary Endothelium ◽  
Brain Capillary ◽  
Content Type ◽  
Endothelial Cell Permeability ◽  
Fine Print

✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

scholarly journals Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Takamasa Kinoshita ◽  
Hiroyuki Tomita ◽  
Hideshi Okada ◽  
Ayumi Niwa ◽  
Fuminori Hyodo ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Heparan Sulfate ◽  
Vascular Endothelium ◽  
Wild Type ◽  
Brain Capillaries ◽  
Gene Encoding ◽  
Glioma Growth ◽  
Underlying Mechanisms ◽  
The Brain

Abstract Purpose Heparan sulfate (HS) is one of the factors that has been suggested to be associated with angiogenesis and invasion of glioblastoma (GBM), an aggressive and fast-growing brain tumor. However, it remains unclear how HS of endothelial cells is involved in angiogenesis in glioblastoma and its prognosis. Thus, we investigated the effect of endothelial cell HS on GBM development. Methods We generated endothelial cell-specific knockout of Ext1, a gene encoding a glycosyltransferase and essential for HS synthesis, and murine GL261 glioblastoma cells were orthotopically transplanted. Two weeks after transplantation, we examined the tumor progression and underlying mechanisms. Results The endothelial cell-specific Ext1 knockout (Ext1CKO) mice exhibited reduced HS expression specifically in the vascular endothelium of the brain capillaries compared with the control wild-type (WT) mice. GBM growth was significantly suppressed in Ext1CKO mice compared with that in WT mice. After GBM transplantation, the survival rate was significantly higher in Ext1CKO mice than in WT mice. We investigated how the effect of fibroblast growth factor 2 (FGF2), which is known as an angiogenesis-promoting factor, differs between Ext1CKO and WT mice by using an in vivo Matrigel assay and demonstrated that endothelial cell-specific HS reduction attenuated the effect of FGF2 on angiogenesis. Conclusions HS reduction in the vascular endothelium of the brain suppressed GBM growth and neovascularization in mice.

Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin

1997 ◽  
Vol 82 (2) ◽  
pp. 382-388 ◽  
Author(s):  
L. Ermert ◽  
H.-R. Duncker ◽  
H. Brückner ◽  
F. Grimminger ◽  
T. Hansen ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Structural Integrity ◽  
Ultrastructural Changes ◽  
Capillary Endothelium ◽  
High Dose ◽  
Edema Formation ◽  
Endothelial Layer ◽  
Total Weight Gain ◽  
Microfilament System

Ermert, L., H.-R. Duncker, H. Brückner, F. Grimminger, T. Hansen, R. Rössig, K. Aktories, and W. Seeger.Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin. J. Appl. Physiol. 82(2): 382–388, 1997.—The role of the endothelial cytoskeleton for the structural integrity of the pulmonary gas exchange area was probed with the use of Clostridium botulinumC2toxin. This agent causes selective loss of nonmuscle F-actin. In buffer-perfused rabbit lungs, vascular pressures were kept within physiological ranges. In different groups, low-dose [0.3 (C2,I)/0.6 (C2,II) ng/ml] and high-dose [10 (C2,I)/20 (C2,II) ng/ml] toxin were applicated into the buffer fluid; experiments were terminated after a total weight gain of either 1 or 7.5 g. Electron microscopy revealed extensive attenuations, undulations, and protrusions of the endothelial layer, suggestive of “remodeling” and “flowing” of the cell membrane in low C2toxin-treated lungs accompanied by few disruptions of the endothelial layer and edema formation. In addition, endothelial cells displayed vesiculation and bleb formation. Lungs that were exposed to high-toxin doses displayed marked attenuations of the endothelial layer in addition to large endothelial cell disruptions, which did not include interendothelial junctions. Interestingly, type II epithelial cells displayed fusion of lamellar bodies. Collectively, these data suggest that the actin microfilament system is instrumental in supporting endothelial cell membrane configuration and integrity and maintains the intimal barrier function of the lung microvasculature.

scholarly journals Distribution of sialoglycoconjugates on the luminal surface of the endothelial cell in the fenestrated capillaries of the pancreas.

1985 ◽  
Vol 33 (5) ◽  
pp. 474-476 ◽  
Author(s):  
V Muresan ◽  
M C Constantinescu
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Binding Sites ◽  
Sodium Periodate ◽  
Luminal Surface ◽  
Nonspecific Binding ◽  
Coated Pits ◽  
Neuraminidase Treatment ◽  
Plasmalemmal Vesicles ◽  
Endothelial Surface

Sialic acid-bearing molecules on the luminal surface of the vascular endothelium in mouse and rat pancreatic capillaries were detected electron microscopically by using a procedure with ferritin hydrazide (FH), after preferential oxidation of sialyl residues with sodium periodate. The distribution of FH on the endothelial surface demonstrated the existence of microdomains with various densities of sialoglycoconjugates oxidizable by sodium periodate and accessible to the tracer. On the plasmalemma proper, FH binding sites were heterogeneously distributed. Their concentration on various microdomains decreased as follows: plasmalemma proper greater than coated pits greater than stomal diaphragms of plasmalemmal vesicles and transendothelial channels, and fenestral diaphragms. The membrane of plasmalemmal vesicles and transendothelial channels was not labeled by FH. Nonspecific binding of FH to the nonoxidized endothelial surface or that oxidized after neuraminidase treatment was relatively low.

The endothelial cell

2017 ◽  
Author(s):  
Ingrid Fleming ◽  
Brenda R. Kwak ◽  
Merlijn J. Meens
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Endothelium ◽  
Structural Heterogeneity ◽  
Physical Barrier ◽  
Physiological Functions

The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.

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