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48 results on '"Raghu P."'

2. Topical captopril: a promising treatment for secondary lymphedema

Author

Stav Brown, Gabriela D.G. Nores, Ananta Sarker, Catherine Ly, Catherine C. Li, Jason Gardenier, Geoffrey E. Hespe, Tal Brown, Hyeung Ju Park, Adana Campbell, Jinyeon Shin, Raghu P. Kataru, Omer Aras, Joseph H. Dayan, and Babak J. Mehrara

Subjects
Physiology (medical), Biochemistry (medical), Public Health, Environmental and Occupational Health, General Medicine
Published
2023
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3. Topical captopril: a promising treatment for secondary lymphedema

Author

Brown, Stav, primary, Nores, Gabriela D.G., additional, Sarker, Ananta, additional, Ly, Catherine, additional, Li, Catherine C., additional, Park, Hyeung Ju, additional, Hespe, Geoffrey E., additional, Campbell, Adana, additional, Kataru, Raghu P., additional, Aras, Omer, additional, and Mehrara, Babak J., additional

Published
2023
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4. Lymphatics act as a signaling hub to regulate intestinal stem cell activity

Author

Niec, Rachel E., primary, Chu, Tinyi, additional, Schernthanner, Marina, additional, Gur-Cohen, Shiri, additional, Hidalgo, Lynette, additional, Pasolli, Hilda Amalia, additional, Luckett, Kathleen A., additional, Wang, Zhong, additional, Bhalla, Sohni R., additional, Cambuli, Francesco, additional, Kataru, Raghu P., additional, Ganesh, Karuna, additional, Mehrara, Babak J., additional, Pe’er, Dana, additional, and Fuchs, Elaine, additional

Published
2022
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5. SARS-CoV-2 seroprevalence in the city of Hyderabad, India in early 2021

Author

Laxmaiah, Avula, primary, Rao, Nalam Madhusudhan, additional, Arlappa, N., additional, Babu, Jagjeevan, additional, Kumar, P. Uday, additional, Singh, Priya, additional, Sharma, Deepak, additional, Anumalla, V. Mahesh, additional, Kumar, T. Santhosh, additional, Sabarinathan, R., additional, Kumar, M. Santhos, additional, Ananthan, R., additional, Basha, D. Anwar, additional, Blessy, P.P.S., additional, Kumar, D. Chandra, additional, Devaraj, P., additional, Devendra, S., additional, Kumar, M. Mahesh, additional, Meshram, Indrapal I., additional, Kumar, B. Naveen, additional, Sharma, Paras, additional, Raghavendra, P., additional, Raghu, P., additional, Rao, K. Rajender, additional, Ravindranadh, P., additional, Kumar, B. Santosh, additional, Sarika, G., additional, Rao, J. Srinivasa, additional, Surekha, M.V., additional, Sylvia, F., additional, Kumar, Deepak, additional, Rao, G. Subba, additional, Tallapaka, Karthik Bharadwaj, additional, Sowpati, Divya Tej, additional, Srivastava, Surabhi, additional, Murhekar, V. Manoj, additional, Hemalatha, Rajkumar, additional, and Mishra, Rakesh K., additional

Published
2022
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8. Maternal opioid use disorder: Placental transcriptome analysis for neonatal opioid withdrawal syndrome

Author

Radhakrishna, Uppala, primary, Nath, Swapan K., additional, Vishweswaraiah, Sangeetha, additional, Uppala, Lavanya V., additional, Forray, Ariadna, additional, Muvvala, Srinivas B., additional, Mishra, Nitish K., additional, Southekal, Siddesh, additional, Guda, Chittibabu, additional, Govindamangalam, Hiranjith, additional, Vargas, Derek, additional, Gardella, William G., additional, Crist, Richard C., additional, Berrettini, Wade H., additional, Metpally, Raghu P., additional, and Bahado-Singh, Ray O., additional

Published
2021
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9. Placental DNA methylation profiles in opioid-exposed pregnancies and associations with the neonatal opioid withdrawal syndrome

Author

Radhakrishna, Uppala, primary, Vishweswaraiah, Sangeetha, additional, Uppala, Lavanya V., additional, Szymanska, Marta, additional, Macknis, Jacqueline, additional, Kumar, Sandeep, additional, Saleem-Rasheed, Fozia, additional, Aydas, Buket, additional, Forray, Ariadna, additional, Muvvala, Srinivas B., additional, Mishra, Nitish K., additional, Guda, Chittibabu, additional, Carey, David J., additional, Metpally, Raghu P., additional, Crist, Richard C., additional, Berrettini, Wade H., additional, and Bahado-Singh, Ray O., additional

Published
2021
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13. Regulatory T Cells Mediate Local Immunosuppression in Lymphedema

Author

Catherine L. Ly, Raghu P. Kataru, Geoffrey E. Hespe, Ira L. Savetsky, Babak J. Mehrara, Stanley G. Rockson, Gabriela D. García Nores, and Swapna Ghanta

Subjects
0301 basic medicine, Regulatory T cell, Biopsy, chemical and pharmacologic phenomena, Mice, Transgenic, Dermatology, Lymphocyte Activation, T-Lymphocytes, Regulatory, Biochemistry, Article, Immune tolerance, Mice, 03 medical and health sciences, Immune system, Antigen, Immune Tolerance, medicine, Animals, Humans, Lymphedema, Molecular Biology, Cell Proliferation, Lymphatic Vessels, Antigen Presentation, business.industry, Forkhead Transcription Factors, Cell Biology, Dendritic cell, medicine.disease, Acquired immune system, Immunity, Innate, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Lymphatic system, medicine.anatomical_structure, Immunology, Lymph Node Excision, Female, Lymph Nodes, business
Abstract

Patients who suffer from lymphedema have impaired immunity and, as a result, are at an increased risk for infections. Furthermore, previous studies have shown that lymphadenectomy impairs acquisition of adaptive immune responses and antibody production in response to foreign antigens. Although it is clear that antigen presentation in lymph nodes plays a key role in adaptive immunity, the cellular mechanisms that regulate impaired immune responses in patients with lymphedema or following lymphatic injury remain unknown. We have previously found that axillary lymph node dissection (ALND), both clinically and in a mouse model, results in a marked increase in the number of T-regulatory cells (Tregs) in the ipsilateral limb. In this study, we focus on the role of Tregs in immunosuppression and show that Treg proliferation in tissues distal to site of lymphatic injury contributes to impaired innate and adaptive immune responses. More importantly, using Foxp3-diptheria toxin receptor (Foxp3-DTR) transgenic mice, we show that depletion of Tregs in the setting of lymphatic injury restores these critical immune-mediated responses. These findings provide additional evidence that immune responses following lymphatic injury play a key role in mediating the pathology of lymphedema.

Published
2018
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17. Lymphatic Function Regulates Contact Hypersensitivity Dermatitis in Obesity

Author

J. Brandon Dixon, Raghu P. Kataru, Babak J. Mehrara, Gabriela D. García Nores, Jeremy S. Torrisi, Tyler S. Nelson, Nicholas J. Albano, Geoffrey E. Hespe, Jason C. Gardenier, Daniel A. Cuzzone, Matthew D. Nitti, and Ira L. Savetsky

Subjects
Male, Vascular Endothelial Growth Factor A, Chemokine, Injections, Subcutaneous, Fluorescent Antibody Technique, Enzyme-Linked Immunosorbent Assay, Inflammation, Dermatology, Diet, High-Fat, Biochemistry, Article, Lymphatic System, Mice, Random Allocation, Reference Values, Psoriasis, medicine, Animals, Obesity, Molecular Biology, dermatitis, biology, business.industry, Biopsy, Needle, Cell Biology, Atopic dermatitis, Flow Cytometry, medicine.disease, Immunohistochemistry, 3. Good health, Lymphangiogenesis, Mice, Inbred C57BL, Endothelial stem cell, Disease Models, Animal, Vascular endothelial growth factor A, Treatment Outcome, Lymphatic system, inflammation, Dermatitis, Allergic Contact, Immunology, biology.protein, lymphatics, medicine.symptom, business, Follow-Up Studies
Abstract

Obesity is a major risk factor for inflammatory dermatologic diseases, including atopic dermatitis and psoriasis. In addition, recent studies have shown that obesity impairs lymphatic function. As the lymphatic system is a critical regulator of inflammatory reactions, we tested the hypothesis that obesity-induced lymphatic dysfunction is a key regulator of cutaneous hypersensitivity reactions in obese mice. We found that obese mice have impaired lymphatic function, characterized by leaky capillary lymphatics and decreased collecting vessel pumping capacity. In addition, obese mice displayed heightened dermatitis responses to inflammatory skin stimuli, resulting in both higher peak inflammation and a delayed clearance of inflammatory responses. Injection of recombinant vascular endothelial growth factor-C remarkably increased lymphangiogenesis, lymphatic function, and lymphatic endothelial cell expression of chemokine (C-C motif) ligand 21, while decreasing inflammation and expression of inducible nitrous oxide synthase. These changes resulted in considerably decreased dermatitis responses in both lean and obese mice. Taken together, our findings suggest that obesity-induced changes in the lymphatic system result in an amplified and a prolonged inflammatory response.

Published
2015
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20. Regulation and implications of inflammatory lymphangiogenesis

Author

Gou Young Koh, Raghu P. Kataru, and Honsoul Kim

Subjects
Inflammation, Immunology, Adaptive Immunity, Biology, Acquired immune system, Lymphangiogenesis, Vascular endothelial growth factor, chemistry.chemical_compound, Immune system, Lymphatic system, Vascular endothelial growth factor C, chemistry, Cell Movement, medicine, Animals, Humans, Immunology and Allergy, medicine.symptom, Dendritic cell migration, Lymphatic Vessels
Abstract

Lymphatic vessels (LVs) are highly dynamic structures that intimately interact with their surrounding microenvironment. They have a profound influence on the immune system and therefore can manipulate inflammatory processes. Inflammation is a major cause of adulthood lymphangiogenesis and LV remodeling. In turn, LVs can reciprocally manipulate inflammatory processes. For instance, LV growth and/or activation regulate antigen presentation and inflammatory cell recruitment to lymph nodes (LNs), and therefore critically affect adaptive immunity. The vascular endothelial growth factor (VEGF)-C-VEGF receptor-3 and VEGF-A-VEGF receptor-2 signaling pathways are particularly important in inflammatory lymphangiogenesis. LVs contribute to the pathophysiology of various inflammatory conditions. Knowledge of lymphatic biology can be applied to manipulate inflammatory disorders and divert immune responses. This review summarizes basic concepts of inflammation-relevant lymphatic biology, and describes recent progress and practical implications.

Published
2012
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21. T Lymphocytes Negatively Regulate Lymph Node Lymphatic Vessel Formation

Author

Sudheer Gollamudi, Honsoul Kim, Dong-kyu Choi, Minah Kim, Bong-Ihn Koh, Seung-Hyo Lee, Gou Young Koh, Yun-Keun Kim, Cholsoon Jang, and Raghu P. Kataru

Subjects
Endothelium, T-Lymphocytes, government.form_of_government, Antigen presentation, Immunology, Mice, Nude, Biology, Lymphocyte Depletion, Article, Interferon-gamma, Mice, Cell Movement, Paracrine Communication, Lymphatic vessel, medicine, Lymph node stromal cell, Animals, Immunology and Allergy, Lymphangiogenesis, Lymph node, Lymphatic Vessels, Feedback, Physiological, Mice, Knockout, Antigen Presentation, Mice, Inbred BALB C, Dendritic Cells, Cell biology, Mice, Inbred C57BL, Lymphatic Endothelium, medicine.anatomical_structure, Lymphatic system, Infectious Diseases, cardiovascular system, government, Lymph Nodes, Lymph, Endothelium, Lymphatic
Abstract

SummaryLymph node lymphatic vessels (LNLVs) serve as a conduit to drain antigens from peripheral tissues to within the lymph nodes. LNLV density is known to be positively regulated by vascular endothelial growth factors secreted by B cells, macrophages, and dendritic cells (DCs). Here, we show that LNLV formation was negatively regulated by T cells. In both steady and inflammatory states, the density of LNLVs was increased in the absence of T cells but decreased when T cells were restored. Interferon-γ secretion by T cells suppressed lymphatic-specific genes in lymphatic endothelial cells and consequently caused marked reduction in LNLV formation. When T cells were depleted, recruitment of antigen-carrying DCs to LNs was augmented, reflecting a compensatory mechanism for antigen presentation to T cells through increased LNLVs. Thus, T cells maintain the homeostatic balance of LNLV density through a negative paracrine action of interferon-γ.

Published
2011
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22. Role of CD11b+ Macrophages in Intraperitoneal Lipopolysaccharide-Induced Aberrant Lymphangiogenesis and Lymphatic Function in the Diaphragm

Author

Jin-Man Kim, Cholsoon Jang, Kyung-Eun Kim, Jinah Han, Bong-Hyun Jeon, Young Jun Koh, Reto A. Schwendener, Raghu P. Kataru, and Gou Young Koh

Subjects
Lipopolysaccharides, Pathology, medicine.medical_specialty, government.form_of_government, Diaphragm, Inflammation, Peritonitis, Ligands, Pathology and Forensic Medicine, Mice, Peritoneal cavity, Fibrosis, Cell Adhesion, medicine, Animals, Lymphangiogenesis, Cell Proliferation, Lymphatic Vessels, CD11b Antigen, biology, business.industry, Macrophages, Peritoneal fluid, Endothelial Cells, Organ Size, Vascular Endothelial Growth Factor Receptor-3, medicine.disease, Lymphatic Endothelium, medicine.anatomical_structure, Lymphatic system, Integrin alpha M, Liposomes, Immunology, government, biology.protein, Blood Vessels, Lymph Nodes, Clodronic Acid, medicine.symptom, business, Injections, Intraperitoneal, Regular Articles
Abstract

Lymphatic vessels in the diaphragm are essential for draining peritoneal fluid, but little is known about their pathological changes during inflammation. Here we characterized diaphragmatic lymphatic vessels in a peritonitis model generated by daily i.p. administration of lipopolysaccharide (LPS) in mice. Intraperitoneal LPS increased lymphatic density, branching, sprouts, connections, and network formation in the diaphragm in time- and dose-dependent manners. These changes were reversible on discontinuation of LPS administration. The LPS-induced lymphatic density and remodeling occur mainly through proliferation of lymphatic endothelial cells. CD11b+ macrophages were massively accumulated and closely associated with the lymphatic vessels changed by i.p. LPS. Both RT-PCR assays and experiments with vascular endothelial growth factor-C/D blockade and macrophage-depletion indicated that the CD11b+ macrophage-derived lymphangiogenic factors vascular endothelial growth factor-C/D could be major mediators of LPS-induced lymphangiogenesis and lymphatic remodeling through paracrine activity. Functional assays with India ink and fluorescein isothiocyanate-microspheres indicated that impaired peritoneal fluid drainage in diaphragm of LPS-induced peritonitis mice was due to inflammatory fibrosis and massive attachment of CD11b+ macrophages on the peritoneal side of the diaphragmatic lymphatic vessels. These findings reveal that CD11b+ macrophages play an important role in i.p. LPS-induced aberrant lymphangiogenesis and lymphatic dysfunction in the diaphragm.

Published
2009
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29. Rational bitmap scaling

Author

Raghu P. Menon, Raj S. Acharya, Eric Andres, and Claudio H. Sibata

Subjects
Discrete mathematics, ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISION, Scaling algorithm, computer.file_format, Transformation (function), Artificial Intelligence, Simple (abstract algebra), Signal Processing, Bitmap, Computer Vision and Pattern Recognition, Algorithm, computer, Scaling, Software, Interpolation, Mathematics
Abstract

A simple mathematical approach is presented for scaling a bitmap image by a rational factor without interpolation. The transformation is reversible. As application of these results, we present a step-by-step scaling algorithm.

Published
1996
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30. Lymphatic Function Regulates Contact Hypersensitivity Dermatitis in Obesity

Author

Savetsky, Ira L., primary, Albano, Nicholas J., additional, Cuzzone, Daniel A., additional, Gardenier, Jason C., additional, Torrisi, Jeremy S., additional, García Nores, Gabriela D., additional, Nitti, Matthew D., additional, Hespe, Geoffrey E., additional, Nelson, Tyler S., additional, Kataru, Raghu P., additional, Dixon, J. Brandon, additional, and Mehrara, Babak J., additional

Published
2015
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47. Preeclampsia

Author

Lee, Soo Bong, Wong, Amy P., Kanasaki, Keizo, Xu, Yong, Shenoy, Vivek K., McElrath, Thomas, Whitesides, George, and Kalluri, Raghu

Abstract

Inadequate invasion of the uterus by cytotrophoblasts is speculated to result in pregnancy-induced disorders such as preeclampsia. However, the molecular mechanisms that govern appropriate invasion of cytotrophoblasts are unknown. Here, we demonstrate that under low-oxygen conditions (2.5% oxygen), 2-methoxyestradiol (2-ME), which is a metabolite of estradiol and is generated by catechol-o-methyltransferase (COMT), induces invasion of cytotrophoblasts into a naturally-derived, extracellular matrix. Neither low-oxygen conditions nor 2-ME alone induces the invasion of cytotrophoblasts in this system; however, low-oxygen conditions combined with 2-ME result in the appropriate invasion of cytotrophoblasts into the extracellular matrix. Cytotrophoblast invasion under these conditions is also associated with a decrease in the expression of hypoxia-inducible factor-1α (HIF-1α), transforming growth factor-β3 (TGF-β3), and tissue inhibitor of metalloproteinases-2 (TIMP-2). Pregnant COMT-deficient mice with hypoxic placentas and preeclampsia-like features demonstrate an up-regulation of HIF-1α, TGF-β3, and TIMP-2 when compared with wild-type mice; normal levels are restored on administration of 2-ME, which also results in the resolution of preeclampsia-like features in these mice. Indeed, placentas from patients with preeclampsia reveal lower levels of COMT and higher levels of HIF-1α, TGF-β3, and TIMP-2 when compared with those from normal pregnant women. We demonstrate that low-oxygen conditions of the placenta are a critical co-stimulator along with 2-ME for the proper invasion of cytotrophoblasts to facilitate appropriate vascular development and oxygenation during pregnancy., Chemistry and Chemical Biology, Version of Record

Published
2010
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