Zobrazeno 1 - 10
of 33
pro vyhledávání: '"Li-Ke He"'
Autor:
Angela L. Gibson, Li-Ke He, Colette E. Johnston, Kelly F. Van Winkle, Sandy J. Schlosser, Andrea Szilagyi, John M. Centanni, B. Lynn Allen-Hoffmann, Ravi Shankar, Christina L. Thomas-Virnig
Publikováno v:
Wound Repair and Regeneration. 20:414-424
The innate immune system differentially regulates the expression of host defense peptides to combat infection during wound healing. We enhanced the expression of a host defense peptide, human beta defensin-3 (hBD-3), in keratinocytes to generate a th
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::530adf9520faefd0391ec8a6f913db09
https://doi.org/10.1111/j.1524-475x.2012.00786.x
https://doi.org/10.1111/j.1524-475x.2012.00786.x
Autor:
Yanxia Li, Ameet R. Kini, Ravi Shankar, Richard L. Gamelli, Li Ke He, Joseph A. Posluszny, Kuzhali Muthumalaiappan, Andrea Szilagyi
Publikováno v:
Journal of Trauma: Injury, Infection & Critical Care. 71:1288-1296
BACKGROUND: : Anemia in burn patients is due to surgical blood loss and anemia of critical illness. Because the commitment paradigm of common bone marrow progenitors dictates the production of erythroid, myeloid, and lymphoid cells, we hypothesized t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bf819357c47b022925973571871194eb
https://doi.org/10.1097/ta.0b013e31822e2803
https://doi.org/10.1097/ta.0b013e31822e2803
Autor:
Angela L. Gibson, Ruibing Chen, Li-Ke He, Colette E. Johnston, B. Lynn Allen-Hoffmann, Lingjun Li, Andrea Szilagyi, Kelly F. Van Winkle, John M. Centanni, Sandy J. Schlosser, Ravi Shankar, Christina L. Thomas-Virnig
Publikováno v:
Molecular Therapy. 17(3):562-569
When skin is compromised, a cascade of signals initiates the rapid repair of the epidermis to prevent fluid loss and provide defense against invading microbes. During this response, keratinocytes produce host defense peptides (HDPs) that have antimic
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e93255f9f26766f37fe6d5727d950ee5
Autor:
Ravi Shankar, Andrea Szilagyi, Marcin Filutowicz, Hideki Suzuki, Richard L. Gamelli, Kuzhali Muthu, Jennifer L. Wendt, Miguel Dominguez, Li-Ke He
Publikováno v:
Journal of Burn Care & Research. 28:6-12
Sepsis caused by multidrug-resistant bacterial infections in critically injured patients has become a major clinical problem. Recently, Acinetobacter baumannii (AB) wound infections, especially in our critically injured soldiers fighting in Iraq and
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4a05c91f865843a1e9a446c477924418
https://doi.org/10.1097/bcr.0b013e31802c8861
https://doi.org/10.1097/bcr.0b013e31802c8861
Autor:
Li Ke He, Kimberly A. Davis, John M. Santaniello, Richard L. Gamelli, Soman Sen, Stephen B. Jones, Kuzhali Muthu, Ravi Shankar
Publikováno v:
The Journal of Trauma: Injury, Infection, and Critical Care. 56:272-278
Despite improvements in the early resuscitation of the critically injured, mortality from multiple organ failure has remained stable, with the lung often the first organ to fail. Early intubation and mechanical ventilation predispose patients to the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::219c573ffb2f98acd426fc28f1533fe9
https://doi.org/10.1097/01.ta.0000108995.64133.90
https://doi.org/10.1097/01.ta.0000108995.64133.90
Publikováno v:
The Journal of Trauma: Injury, Infection, and Critical Care. 53:284-290
Background: The production of granulocyte colony-stimulating factor (G-CSF), the lineage specific essential regulator of neutrophil progenitor cell proliferation and differentiation, has been thought to be impaired in the setting of burn infection. T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::78cb0e379590a20144577f232afa4547
https://doi.org/10.1097/00005373-200208000-00016
https://doi.org/10.1097/00005373-200208000-00016
Publikováno v:
Journal of Burn Care & Rehabilitation. 21:64-69
The production and release of granulocytes and macrophages, crucial elements of the host defense system, are significantly impaired after burn injury and sepsis. Prostaglandin E2 (PGE2) is known to be myelosuppressive. We hypothesized that the macrop
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::643bb313af19c609433c0a22336b7ae9
https://doi.org/10.1097/00004630-200021010-00012
https://doi.org/10.1097/00004630-200021010-00012
Publikováno v:
The Journal of Trauma: Injury, Infection, and Critical Care. 45:215-221
Background: Cyclooxygenase-2 (COX-2) is a key enzyme in the production of prostaglandin E 2 (PGE 2 ) from activated macrophages. PGE 2 is increased during trauma and sepsis and has been implicated as a negative immunomodulator. The objective of this
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c90232b6e3e54f4e2a1372422c7a8c94
https://doi.org/10.1097/00005373-199808000-00003
https://doi.org/10.1097/00005373-199808000-00003
Publikováno v:
The Journal of Trauma: Injury, Infection, and Critical Care. 44:777-782
Prostaglandin E 2 (PGE 2 ) is significantly elevated in the plasma of septic or injured patients and is thought to be a component of the resultant immune suppression associated with augmented rates of infection and mortality. Many studies have examin
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::614e1806e370e2e446a6672295d992d9
https://doi.org/10.1097/00005373-199805000-00006
https://doi.org/10.1097/00005373-199805000-00006
Publikováno v:
The Journal of Trauma: Injury, Infection, and Critical Care. 44:469-474
Suppressed granulocyte and macrophage growth after burn infection or endotoxicosis appears to be mediated by macrophage-derived products. In this study, we found that after burn, burn plus infection, or endotoxicosis, peritoneal-elicited macrophages
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3effaf3f25b618d4a2b468741bb2398f
https://doi.org/10.1097/00005373-199803000-00008
https://doi.org/10.1097/00005373-199803000-00008