scholarly journals Diffuse pleural thickening and thoracic contraction: An indistinguishable case from malignant pleural mesothelioma

2020 ◽  
Vol 8 ◽  
pp. 2050313X2094871
Author(s):  
Yuji Tada ◽  
Masatoshi Tagawa ◽  
Toshikazu Yusa ◽  
Mari Yatomi ◽  
Iwao Shimomura ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Glucose Transporter ◽  
Asbestos Exposure ◽  
Correct Diagnosis ◽  
Diagnostic Methods ◽  
High Concentration ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Pleural Thickening ◽  
Diffuse Pleural Thickening

The differential diagnosis of reactive mesothelial hyperplasia and mesothelioma is difficult. We present a rare case of diffuse pleural thickening with thoracic contraction that was indistinguishable from mesothelioma. A 66-year-old woman with no history of asbestos exposure visited our hospital with a complaint of dyspnea. The clinical findings included circumferential pleural thickening on chest computed tomography image and a high concentration of hyaluronic acid in the pleural fluid. Pleural biopsies obtained by thoracoscopy under local anesthesia were pathologically consistent with mesothelioma, but the patient refused to take any kind of mesothelioma treatments. Four months later, she consented to a surgical pleural biopsy under general anesthesia to obtain larger tissue samples, which included typical proliferating polygonal cells positive for CAM5.2, calretinin, WT-1, D2-40, CK5/6, epithelial membrane antigen, and glucose transporter-1 and negative for carcinoembryonic antigen, BerEP4, and MOC31. The analysis was consistent with diagnosis of epithelioid mesothelioma. Fluorescence in situ hybridization, however, showed the presence of p16 gene, and the expression of BRCA1-associated protein-1 was detected by immunohistochemistry. Our final diagnosis was diffuse pleural thickening unrelated to asbestos exposure. Differential diagnosis of diffuse pleural thickening and malignant mesothelioma is thus difficult and routine immunohistochemical examinations are often insufficient for accurate diagnosis. Multiple diagnostic methods are required for correct diagnosis in a clinically marginal case.

Differential glycolytic and glycogenogenic transduction pathways in male and female bovine embryos produced in vitro

2012 ◽  
Vol 24 (2) ◽  
pp. 344 ◽  
Author(s):  
M. Garcia-Herreros ◽  
I. M. Aparicio ◽  
D. Rath ◽  
T. Fair ◽  
P. Lonergan
Keyword(s):  
Glucose Metabolism ◽  
Protein Expression ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Glycogen Synthase ◽  
Bovine Embryos ◽  
High Concentration ◽  
Glucose Transporter 1 ◽  
Male And Female ◽  
Glut 1

Previous studies have shown that developmental kinetic rates following IVF are lower in female than in male blastocysts and that this may be related to differences in glucose metabolism. In addition, an inhibition of phosphatidylinositol 3-kinase (PI3-K) inhibits glucose uptake in murine blastocysts. Therefore, the aim of this study was to identify and compare the expression of proteins involved in glucose metabolism (hexokinase-I, HK-I; phosphofructokinase-1, PFK-1; pyruvate kinase1/2, PK1/2; glyceraldehyde-3-phosphate dehydrogenase, GAPDH; glucose transporter-1, GLUT-1; and glycogen synthase kinase-3, GSK-3) in male and female bovine blastocysts to determine whether PI3-K has a role in the regulation of the expression of these proteins. Hexokinase-I, PFK-1, PK1/2, GAPDH and GLUT-1 were present in bovine embryos. Protein expression of these proteins and GSK-3 was significantly higher in male compared with female blastocysts. Inhibition of PI3-K with LY294002 significantly decreased the expression of HK-I, PFK-1, GAPDH, GSK-3 A/B and GLUT-1. Results showed that the expression of glycolytic proteins HK-I, PFK-1, GAPDH and PK1/2, and the transporters GLUT-1 and GSK-3 is regulated by PI3-K in bovine blastocysts. Moreover, the differential protein expression observed between male and female blastocysts might explain the faster developmental kinetics seen in males, as the expression of main proteins involved in glycolysis and glycogenogenesis was significantly higher in male than female bovine embryos and also could explain the sensitivity of male embryos to a high concentration of glucose, as a positive correlation between GLUT-1 expression and glucose uptake in embryos has been demonstrated.

scholarly journals Yellow Nail Syndrome with Bilateral Pleural Plaques and Diffuse Pleural Thickening: A Mimic of Asbestos Related Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Adam Dallmann ◽  
Richard L. Attanoos
Keyword(s):  
Asbestos Exposure ◽  
Electron Microscopic ◽  
Yellow Nail Syndrome ◽  
Pleural Thickening ◽  
Pleural Plaques ◽  
Pulmonary Manifestations ◽  
Diffuse Pleural Thickening ◽  
Mineral Fibre ◽  
Asbestos Related Disease ◽  
Fibre Analysis

Yellow nail syndrome is a rare acquired condition of unknown aetiology associated with distinct nail discolouration/xanthonychia, pulmonary manifestations, and lymphoedema. Pleural plaques and diffuse pleural thickening are typically, although not exclusively, recognised as markers of prior commercial asbestos exposure. The presence of such biomarkers may assist an asbestos personal injury evaluation. A postmortem examination performed on a 72-year-old man with known long-standing yellow nail syndrome identified pleural plaques and diffuse pleural thickening. An evaluation of the occupational history identified no known asbestos exposure. Electron microscopic mineral fibre analysis detected no asbestos fibres. To the best of our knowledge, this is the only case of yellow nail syndrome in which these benign pleural changes are reported ex asbestos. Alternate causes for such pleural pathology were absent. There is merit in physicians and pathologists having an awareness of these new manifestations when considering claimed asbestos related changes during life and at postmortem.

scholarly journals High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

1999 ◽  
Vol 160 (3) ◽  
pp. 443-452 ◽  
Author(s):  
K Ogura ◽  
M Sakata ◽  
M Yamaguchi ◽  
H Kurachi ◽  
Y Murata
Keyword(s):  
Glucose Concentration ◽  
Glucose Transporter ◽  
Cytochalasin B ◽  
High Concentration ◽  
Glucose Transporter 1 ◽  
Protein Levels ◽  
Placental Cells ◽  
Glut1 Mrna

Facilitative glucose transporter-1 (GLUT1) is expressed abundantly and has an important role in glucose transfer in placentas. However, little is known about the regulation of GLUT1 expression in placental cells. We studied the changes in placental GLUT1 levels in relation to changes in glucose concentration in vitro and in vivo. In in vitro experiments, dispersed mouse placental cells were incubated under control (5.5 mM) and moderately high (22 mM) glucose concentrations, and 2-deoxyglucose uptake into cells was studied on days 1-5 of culture. After 4 days of incubation under both conditions, GLUT1 mRNA and proten levels were examined by Northern and immunoblot analyses. Treatment of cells with 22 mM glucose resulted in a significant decrease in 2-deoxyglucose uptake compared with control, from day 2 to day 5 of culture. Moreover, GLUT1 mRNA and protein levels on day 4 of culture were significantly reduced in cells incubated with 22 mM glucose compared with control. Next, we rendered mice diabetic by administering 200 micrograms/g body weight streptozotocin (STZ) on day 8 of pregnancy. Animals were killed on day 12 of pregnancy and placental tissues were obtained. [3H]Cytochalasin B binding study was carried out to assess total GLUTs, and GLUT1 mRNA and protein were measured as above. [3H]Cytochalasin B binding sites in placentas from STZ-treated mice were significantly less than those in control mice. Northern and immunoblot analyses revealed a significant decrease in GLUT1 mRNA and protein levels in diabetic mice compared with the controls. These findings suggest that the glucose concentration may regulate the expression of placental GLUT1.

scholarly journals Glucose transporter GLUT1 expression is an stage-independent predictor of clinical outcome in adrenocortical carcinoma

2009 ◽  
Vol 16 (3) ◽  
pp. 919-928 ◽  
Author(s):  
Wiebke Fenske ◽  
Hans-Ullrich Völker ◽  
Patrick Adam ◽  
Stefanie Hahner ◽  
Sarah Johanssen ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Adrenocortical Carcinoma ◽  
Glucose Transporter ◽  
Disease Free Survival ◽  
Immunohistochemical Analysis ◽  
Radical Resection ◽  
Tissue Microarrays ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Glut1 Expression

Owing to the rarity of adrenocortical carcinoma (ACC) no prognostic markers have been established beyond stage and resection status. Accelerated glycolysis is a characteristic feature of cancer cells and in a variety of tumour entities key factors in glucose metabolism like glucose transporter 1 and 3 (GLUT1 and -3), transketolase like-1 enzyme (TKTL1) and pyruvate kinase type M2 (M2-PK) are overexpressed and of prognostic value. Therefore, we investigated the role of these factors in ACC. Immunohistochemical analysis was performed on tissue microarrays of paraffin-embedded tissue samples from 167 ACCs, 15 adrenal adenomas and 4 normal adrenal glands. Expression was correlated with baseline parameters and clinical outcome. GLUT1 and -3 were expressed in 33 and 17% of ACC samples respectively, but in none of the benign tumours or normal adrenals glands. By contrast, TKTL1 and M2-PK were detectable in all benign tissues and the vast majority of ACCs. GLUT1 expression was strongly associated with prognosis in univariate and multivariate analysis (P<0.01), whereas GLUT3, TKTL1 and M2-PK did not correlate with clinical outcome. Patients with strong GLUT1 staining showed a considerably higher overall mortality (hazard ratio (HR) 6.34 (95% confidence interval 3.10–12.90) compared with patients with no GLUT1 staining. When analysing patients in their early stages and advanced disease separately, similar results were obtained. HR for survival was 5.31 (1.80–15.62) in patients with metatastic ACC and in patients after radical resection the HR for disease-free survival was 6.10 (2.16–16.94). In conclusion, GLUT1 is a highly promising stage-independent, prognostic marker in ACC.

scholarly journals MicroRNA-340 Inhibits Bladder Cancer Cell Growth by Downregulating Glucose Transporter-1

2020 ◽  
Author(s):  
Junlong Li ◽  
Gang Xu ◽  
Shouhua Pan
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Gene Networks ◽  
Glucose Transporter ◽  
Inverse Correlation ◽  
Western Blots ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Glut 1 ◽  
Bladder Cell

Abstract Background: MicroRNA (miRNA)-340 is emerging as a critical regulator for the development and progression of various cancers, such as oral squamous cell carcinoma and prostate cancer. However, little was known about the role of miR-340 in bladder cancer. Methods: Bladder cancer and adjacent non-tumor tissue samples were collected from thirty patients undergoing surgical resection at Shaoxing People's Hospital. The expression of miR-340 and Glut-1 were studied via real-time quantitative PCR (RT-qPCR) or western blots. Bladder cancer T24 cells were transfected with miR-340 mimics to explore cell proliferation and apoptosis via MTT assay, flow cytometer, RT-qPCR and western blots. Results: Compared with that of normal tissues, miR-340 expression was significantly lower, while both mRNA and protein expression of Glut-1 were higher in bladder cancer tissues. The miR-340 could negatively regulate Glut-1 expression in bladder cells. Moreover, bladder cell proliferation could be inhibited by miR-340 and the corresponding antitumor effect could partially reverse by the overexpression of Glut-1. In view of the complexity of gene networks, some other multiple pathways might also confer to miR-340 inducing bladder cell apoptosis, including downregulating PCNA, upregulating Bax and decreasing the phosphorylation levels of PI3K and AKT.Conclusion: This work suggested an inverse correlation between miR-340 and glucose transporter-1 (Glut-1) expression in bladder cancer. miR-340/Glut-1 axis might be a potential and novel therapeutic target for the treatment of bladder cancer. More investigations need to further explore the applications of miR-340 in bladder cancer.

scholarly journals Differential Diagnosis of Wide QRS Tachycardias

2020 ◽  
Vol 9 (3) ◽  
pp. 155-160
Author(s):  
Demosthenes G Katritsis ◽  
Josep Brugada
Keyword(s):  
Differential Diagnosis ◽  
Ventricular Tachycardia ◽  
Clinical Practice ◽  
Supraventricular Tachycardia ◽  
Correct Diagnosis ◽  
Diagnostic Methods ◽  
Qrs Duration

In this article, the authors discuss the differential diagnostic methods used in clinical practice to identify types of wide QRS tachycardias (QRS duration >120 ms). A correct diagnosis is critical to management, as misdiagnosis and the administration of drugs usually utilised for supraventricular tachycardia can be harmful for patients with ventricular tachycardia.

scholarly journals LAT-1 and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2968
Author(s):  
Miguel Sampedro-Núñez ◽  
Antonio Bouthelier ◽  
Ana Serrano-Somavilla ◽  
Rebeca Martínez-Hernández ◽  
Magdalena Adrados ◽  
...  
Keyword(s):  
Nutrient Uptake ◽  
Neuroendocrine Tumors ◽  
Glucose Transporter ◽  
Tumor Tissue ◽  
Hypoxia Inducible Factor ◽  
Gastroenteropancreatic Neuroendocrine Tumors ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Von Hippel Lindau ◽  
Glut 1

Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors.

Metabolic, enzymatic, and transporter responses in human muscle during three consecutive days of exercise and recovery

2008 ◽  
Vol 295 (4) ◽  
pp. R1238-R1250 ◽  
Author(s):  
Howard J. Green ◽  
Eric Bombardier ◽  
Todd A. Duhamel ◽  
Riley D. Stewart ◽  
A. Ross Tupling ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
Glucose Transporter ◽  
Vastus Lateralis ◽  
Sudden Onset ◽  
Adaptive Responses ◽  
Experimental Protocol ◽  
Tissue Samples ◽  
Glucose Transporter 1 ◽  
Metabolic Properties ◽  
Low Intensity Exercise

This study investigated the responses in substrate- and energy-based properties to repetitive days of prolonged submaximal exercise and recovery. Twelve untrained volunteers (V̇o2peak = 44.8 ± 2.0 ml·kg−1·min−1, mean ± SE) cycled (∼60 V̇o2peak) on three consecutive days followed by 3 days of recovery. Tissue samples were extracted from the vastus lateralis both pre- and postexercise on day 1 (E1), day 3 (E3), and during recovery (R1, R2, R3) and were analyzed for changes in metabolism, substrate, and enzymatic and transporter responses. For the metabolic properties (mmol/kg−1 dry wt), exercise on E1 resulted in reductions ( P < 0.05) in phosphocreatine (PCr; 80 ± 1.9 vs. 41.2 ± 3.0) and increases ( P < 0.05) in inosine monophosphate (IMP; 0.13 ± 0.01 vs. 0.61 ± 0.2) and lactate (3.1 ± 0.4 vs. 19.2 ± 4.3). At E3, both IMP and lactate were lower ( P < 0.05) during exercise. For the transporters, the experimental protocol resulted in a decrease ( P < 0.05) in glucose transporter-1 (GLUT1; 29% by R1), an increase in GLUT4 (29% by E3), and increases ( P < 0.05) for both monocarboxylate transporters (MCT) (for MCT1, 23% by R2 and for MCT4, 18% by R1). Of the mitochondrial and cytosolic enzyme activities examined, cytochrome c oxidase (COX), and hexokinase were both reduced ( P < 0.05) by exercise at E1 and in the case of hexokinase and phosphorylase by exercise on E3. With the exception at COX, which was lower ( P < 0.05) at R1, no differences in enzyme activities existed at rest between E, E3, and recovery days. Results suggest that the glucose and lactate transporters are among the earliest adaptive responses of substrate and metabolic properties studied to the sudden onset of regular low-intensity exercise.

Pleural Thickening and Calcification

Chest Imaging ◽  
2019 ◽  
pp. 175-179
Author(s):  
Christopher M. Walker
Keyword(s):  
Asbestos Exposure ◽  
Malignant Degeneration ◽  
Pleural Thickening ◽  
Pleural Plaque ◽  
Imaging Appearance ◽  
Pleural Plaques ◽  
Diffuse Pleural Thickening ◽  
Costophrenic Angle ◽  
Common Manifestation ◽  
Over Time

Pleural thickening and calcification discusses the radiographic and computed tomography (CT) manifestations of benign pleural thickening and pleural calcification. Benign pleural thickening must be differentiated from malignant pleural thickening and their differentiating characteristics will be discussed. Pleural plaque is the most common manifestation of asbestos exposure and carries no risk of malignant degeneration. The most common imaging appearance is bilateral sharply demarcated, multifocal areas of discontinuous pleural thickening that often calcifies over time. Pleural plaques spare the apical and costophrenic sulcus pleura and has a predilection for the diaphragmatic pleura. Diffuse pleural thickening is associated with hemothorax, empyema, connective tissue disorders, and asbestos exposure. It is generally unilateral, causes blunting of the costophrenic angle, spans multiple rib interspaces, and is irregular in shape. When diffuse pleural thickening calcifies and is associated with volume loss in the affected lung, it is termed fibrothorax.

scholarly journals Icaritin-Induced FAM99A Affects GLUT1-Mediated Glycolysis via Regulating the JAK2/STAT3 Pathway in Hepatocellular Carcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Xia Zheng ◽  
Yudong Gou ◽  
Ziyu Jiang ◽  
Aizhen Yang ◽  
Zhihui Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Glucose Transporter ◽  
Regulatory Mechanisms ◽  
Phase 2 ◽  
High Concentration ◽  
Glucose Transporter 1 ◽  
Stat3 Pathway ◽  
Promising Target ◽  
Stat3 Phosphorylation ◽  
Hcc Cells

Icaritin is a potential treatment option for hepatocellular carcinoma (HCC) based on the results of its phase 2 stage trial. Glucose transporter 1 (GLUT1), a critical gene in regulating glycolysis, has been recognized as a promising target in HCC treatment. Previous studies have reported that FAM99A, a new long noncoding (lncRNA), is associated with HCC metastasis. It has also been demonstrated that the JAK2/STAT3 pathway is related to HCC and is the target of icaritin treatment. However, whether FAM99A participates in icaritin treatment and regulates GLUT1-mediated glycolysis via the JAK2/STAT3 pathway in HCC cells remains to be explored. Our study aimed to clarify the mechanisms underlying glycolysis and understand the regulating effects of the FAM99A and JAK2/STAT3 pathway in HCC cells in icaritin treatment. Molecular mechanism studies were conducted to verify whether FAM99A could bind to the JAK2/STAT3 pathway and to identify the regulatory mechanisms in the HCC cells. It was revealed that icaritin inhibited proliferation, GLUT1 level, and the glycolysis of the HCC cells. FAM99A in HCC cells was upregulated after a high concentration treatment of icaritin. FAM99A inhibited GLUT1 by blocking the JAK2/STAT3 pathway. Mechanically, FAM99A interacted with EIF4B to inhibit gp130 and gp80 translation, which then interacted with miR-299-5p to upregulate SOCS3, causing the JAK2 pathway to inhibit STAT3 phosphorylation, so that JAK2/STAT3 was blocked in HCC cells. Overall, our study proved that icaritin-induced FAM99A can inhibit HCC cell viability and GLUT1-mediated glycolysis via blocking the JAK2/STAT3 pathway.

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