Search

Your search keyword '"Rumbaut, Rolando"' showing total 316 results
Start Over Author "Rumbaut, Rolando"
316 results on '"Rumbaut, Rolando"'

22. Randomized Trial of Endobronchial Ultrasound-guided Transbronchial Needle Aspiration under General Anesthesia versus Moderate Sedation

Author

Casal, Roberto F., Lazarus, Donald R., Kuhl, Kristine, Nogueras-González, Graciela, Perusich, Sarah, Green, Linda K., Ost, David E., Sarkiss, Mona, Jimenez, Carlos A., Eapen, Georgie A., Morice, Rodolfo C., Cornwell, Lorraine, Austria, Sheila, Sharafkanneh, Amir, Rumbaut, Rolando E., Grosu, Horiana, and Kheradmand, Farrah

Published
2015
Full Text
View/download PDF

25. Platelet and Erythrocyte Extravasation across Inflamed Corneal Venules Depend on CD18, Neutrophils, and Mast Cell Degranulation

Author

De La Cruz, Angie, primary, Hargrave, Aubrey, additional, Magadi, Sri, additional, Courson, Justin A., additional, Landry, Paul T., additional, Zhang, Wanyu, additional, Lam, Fong W., additional, Bray, Monica A., additional, Smith, C. Wayne, additional, Burns, Alan R., additional, and Rumbaut, Rolando E., additional

Published
2021
Full Text
View/download PDF

27. Transendothelial flow inhibits neutrophil transmigration through a nitric oxide-dependent mechanism: potential role for cleft shear stress

Author

Burns, Alan R., Zheng, Zhilan, Soubra, Said H., Chen, Jie, and Rumbaut, Rolando E.

Subjects
Endothelium -- Properties, Neutrophils -- Properties, Cell migration -- Research, Nitric oxide -- Influence, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

Endothelial cells in vivo are well known to respond to parallel shear stress induced by luminal blood flow. In addition, fluid filtration across endothelium (transendothelial flow) may trigger nitric oxide (NO) production, presumably via shear stress within intercellular clefts. Since NO regulates neutrophil-endothelial interactions, we determined whether transendothelial flow regulates neutrophil transmigration. Interleukin-1[beta]-treated human umbilical vein endothelial cell (HUVEC) monolayers cultured on a polycarbonate filter were placed in a custom chamber with or without a modest hydrostatic pressure gradient ([DELTA]P, 10 cm[H.sub.2]O) to induce transendothelial flow. In other experiments, cells were studied in a parallel plate flow chamber at various transendothelial flows ([DELTA]P = 0, 5, and 10 cm[H.sub.2]O) and luminal flows (shear stress of 0, 1, and 2 dyn/[cm.sup.2]). In the absence of luminal flow, transendothelial flow reduced transmigration of freshly isolated human neutrophils from 57% to 14% (P < 0.05) and induced an increase in NO detected with a fluorescent assay (DAF-2DA). The NO synthase inhibitor L-NAME prevented the effects of transendothelial flow on neutrophil transmigration, while a NO donor (DETA/NO, 1 mM) inhibited neutrophil transmigration. Finally, in the presence of luminal flow (1 and 2 dyn/[cm.sup.2]), transendothelial flow also inhibited transmigration. On the basis of HUVEC morphometry and measured transendothelial volume flow, we estimated cleft shear stress to range from 49 to 198 dyn/[cm.sup.2]. These shear stress estimates, while substantial, are of similar magnitude to those reported by others with similar analyses. These data are consistent with the hypothesis that endothelial cleft shear stress inhibits neutrophil transmigration via a NO-dependent mechanism. endothelium; neutrophils; hydraulic conductivity; diapedesis; permeability

Published
2007

31. Endotoxin enhances microvascular thrombosis in mouse cremaster venules via a TLR4-dependent, neutrophil-independent mechanism

Author

Rumbaut, Rolando E., Bellera, Ricardo V., Randhawa, Jaspreet K., Shrimpton, Corie N., Dasgupta, Swapan K., Dong, Jing-Fei, and Burns, Alan R.

Subjects
Blood platelets -- Research, Blood platelets -- Analysis, Microcirculation -- Research, Microcirculation -- Analysis, Septic shock -- Research, Septic shock -- Complications and side effects, Vascular endothelium -- Research, Biological sciences
Abstract

Endotoxemia promotes adhesive interactions between platelets and microvascular endothelium in vivo. We sought to determine whether endotoxin (lipopolysaccharide, LPS) modified platelet thrombus formation in mouse cremaster venules and whether Toll-like receptor 4 (TLR4) and neutrophils were involved in the response. Intravital videomicroscopy was performed in the cremaster microcirculation of pentobarbital-anesthetized mice; venular platelet thrombi were induced with a light/dye endothelial injury model. C57BL/6 mice treated with Escherichia coli endotoxin had enhanced rates of venular platelet thrombus formation: the time to microvessel occlusion was reduced by ~50% (P < 0.005) compared with saline-treated animals. Enhanced microvascular thrombosis was evident as early as 2 h after LPS administration. LPS had no effect on thrombosis in either of two mouse strains with altered TLR4 signaling (C57BL/10ScNJ or C3H/HeJ), whereas it enhanced thrombosis in the control strains (C57BL/10J and C3H/HeN). LPS also enhanced platelet adhesion to endothelium in the absence of light/dye injury. Platelet adhesion, but not enhanced thrombosis, was inhibited by depletion of circulating neutrophils. LPS failed to enhance platelet aggregation ex vivo and did not influence platelet P-selectin expression, a marker of platelet activation. These findings support the notion that endotoxemia promotes platelet thrombus formation independent of neutrophils and without enhancement of platelet aggregation, via a TLR4-dependent mechanism. microcirculation; platelets; endothelium; endotoxemia

Published
2006

40. Leakage responses to L-NAME differ with the fluorescent dye used to label albumin

Author

Rumbaut, Rolando E., Harris, Norman R., Sial, Arshad J., Huxley, Virginia H., and Granger, D. Neil

Subjects
Albumin -- Physiological aspects, Optical brighteners -- Physiological aspects, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

The role of fluorescent dyes used in labeling albumin on the inhibition of nitric oxide synthase (NOS) on albumin leakage has been studied. Albumin leakage was observed in rat mesenteric venules during controlled conditions and after exposure to the NOS inhibitor N(super G)-nitro-L-arginine methyl ester (L-NAME). The fluorescent dyes used were FITC, sulforhodamine 101, dichlorotriazinyl aminofluorescein and Oregon Green 514. Results indicated that albumin leakage responses due to L-NAME varied among the four dyes. This finding suggests that caution should be used when comparing albumin leakage results from various dyes.

Published
1999

41. Obese mice show dyslipidemia and a changed meibum profile

Author

Osae, Eugene, Chintalapati, Madhavi, Bullock, Tiffany, Brodesser, Susanne, Steven, Philipp, Smith, C. Wayne, Rumbaut, Rolando, Burns, Alan Robert, Osae, Eugene, Chintalapati, Madhavi, Bullock, Tiffany, Brodesser, Susanne, Steven, Philipp, Smith, C. Wayne, Rumbaut, Rolando, and Burns, Alan Robert

Published
2020

42. Obese Mice with Dyslipidemia Exhibit Meibomian Gland Hypertrophy and Alterations in Meibum Composition and Aqueous Tear Production

Author

Osae, Eugene A., Bullock, Tiffany, Chintapalati, Madhavi, Brodesser, Susanne, Hanlon, Samuel, Redfern, Rachel, Steven, Philipp, Smith, C. Wayne, Rumbaut, Rolando E., Burns, Alan R., Osae, Eugene A., Bullock, Tiffany, Chintapalati, Madhavi, Brodesser, Susanne, Hanlon, Samuel, Redfern, Rachel, Steven, Philipp, Smith, C. Wayne, Rumbaut, Rolando E., and Burns, Alan R.

Abstract

Background: Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia. Methods: Male C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson's correlation and unpaired t-tests adjusted for multiple comparisons; significance set at p <= 0.05. Results: Compared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production. Conclusions: The majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD.

Published
2020

46. Munc18-2, not Munc18-1 or Munc18-3, regulates platelet exocytosis, hemostasis, and thrombosis

Author

Cardenas, Eduardo I, Gonzalez, Ricardo, Breaux, Keegan, Da, Qi, Gutierrez, Berenice A, Ramos, Marco A, Cardenas, Rodolfo A, Burns, Alan R, Rumbaut, Rolando E, Adachi, Roberto, Cardenas, Eduardo I, Gonzalez, Ricardo, Breaux, Keegan, Da, Qi, Gutierrez, Berenice A, Ramos, Marco A, Cardenas, Rodolfo A, Burns, Alan R, Rumbaut, Rolando E, and Adachi, Roberto

Abstract

Platelet degranulation, a form of regulated exocytosis, is crucial for hemostasis and thrombosis. Exocytosis in platelets is mediated by SNARE proteins, and in most mammalian cells this process is controlled by Munc18 (mammalian homolog of C. elegans uncoordinated gene 18) proteins. Platelets express all Munc18 paralogs (Munc18‑1, ‑2, and ‑3), but their roles in platelet secretion and function have not been fully characterized. Using Munc18‑1, ‑2, and ‑3 conditional knockout mice, here we deleted expression of these proteins in platelets and assessed granule exocytosis. We measured products secreted by each type of platelet granule and analyzed EM platelet profiles by design-based stereology. We observed that removal of Munc18‑2 ablates release of alpha, dense, and lysosomal granules from platelets, but we found no exocytic role for Munc18‑1 or ‑3 in platelets. In vitro, Munc18‑2-deficient platelets exhibited defective aggregation at low doses of collagen and impaired thrombus formation under shear stress. In vivo, megakaryocyte-specific Munc18‑2 conditional knockout mice had a severe hemostatic defect and prolonged arterial and venous bleeding times. They were also protected against arterial thrombosis in a chemically-induced model of arterial injury. Taken together, our results indicate that Munc18‑2, but not Munc18‑1 or Munc18‑3, is essential for regulated exocytosis in platelets and platelet participation in thrombosis and hemostasis.

Published
2019
Full Text
View/download PDF

47. Dyslipidemia and Meibomian Gland Dysfunction: Utility of Lipidomics and Experimental Prospects with a Diet-Induced Obesity Mouse Model

Author

Osae, Eugene A., Steven, Philipp, Redfern, Rachel, Hanlon, Samuel, Smith, C. Wayne, Rumbaut, Rolando E., Burns, Alan R., Osae, Eugene A., Steven, Philipp, Redfern, Rachel, Hanlon, Samuel, Smith, C. Wayne, Rumbaut, Rolando E., and Burns, Alan R.

Abstract

Meibomian gland dysfunction (MGD) is the leading cause of dry eye disease and loss of ocular surface homeostasis. Increasingly, several observational clinical studies suggest that dyslipidemia (elevated blood cholesterol, triglyceride or lipoprotein levels) can initiate the development of MGD. However, conclusive evidence is lacking, and an experimental approach using a suitable model is necessary to interrogate the relationship between dyslipidemia and MGD. This systematic review discusses current knowledge on the associations between dyslipidemia and MGD. We briefly introduce a diet-induced obesity model where mice develop dyslipidemia, which can serve as a potential tool for investigating the effects of dyslipidemia on the meibomian gland. Finally, the utility of lipidomics to examine the link between dyslipidemia and MGD is considered.

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results