The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform
Stephen S Kroll - One of the best experts on this subject based on the ideXlab platform.
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fat Necrosis in free and pedicled tram flaps
Plastic and Reconstructive Surgery, 1998Co-Authors: Stephen S Kroll, Giulio Gherardini, John E Martin, Gregory R D Evans, Geoffrey L Robb, Gregory P Reece, Michael J Miller, Bao Guang WangAbstract:One purported advantage of the free transverse rectus abdominis musculocutaneous (TRAM) flap for breast reconstruction is that, compared with the conventional TRAM flap, it has a better blood supply and therefore a lower incidence of fat Necrosis. We tested this claim by reviewing the incidence of fat Necrosis, both clinically and mammographically, in a group of 110 patients with 116 TRAM flap breast reconstructions who had undergone mammography of their reconstructed breasts. Of the 49 breasts reconstructed with free TRAM flaps, 4 (8.2 percent) had clinically evident fat Necrosis, and 1 (2.0 percent) had fat Necrosis that was detectable by mammography. Of the 67 breasts reconstructed with conventional TRAM flaps, 18 (26.9 percent) had clinically detectable fat Necrosis, and 9 (13.4 percent) had fat Necrosis that was detectable mammographically. Both of these differences were statistically significant (p = 0.0113 for clinical fat Necrosis; p = 0.031 for mammographic fat Necrosis). Fat Necrosis was more common in patients who were obese or had a history of smoking, but neither association was statistically significant. We conclude that the use of the free TRAM flap reduces the incidence of fat Necrosis in the reconstructed breast. (Plast. Reconstr. Surg. 102: 1502, 1998.)
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Necrosis of abdominoplasty and other secondary flaps after tram flap breast reconstruction
Plastic and Reconstructive Surgery, 1994Co-Authors: Stephen S KrollAbstract:: The risks of abdominoplasty flap Necrosis, umbilical Necrosis, and mastectomy flap edge Necrosis were compared in a series of 227 patients who had undergone transverse rectus abdominis myocutaneous (TRAM) flap breast reconstructions. Abdominoplasty flap Necrosis was more common in patients who smoked or previously had smoked (27.5 percent) than in nonsmokers (5.9 percent). It also was more common in patients who had had conventional TRAM flaps (16.5 percent) than in those with free TRAM flaps (7.8 percent). Similarly, umbilical Necrosis was more common in smokers (27.5 percent) than in nonsmokers (11.8 percent). Current smokers had higher risks than ex-smokers, who in turn had higher risks than patients who had never smoked. Obesity appeared to have only a minor influence on abdominal flap and umbilical Necrosis. Mastectomy flap edge Necrosis, which had little or no impact on the final outcome, was more common after free TRAM flaps than after conventional TRAM flaps.
Kumudini Weerawarna - One of the best experts on this subject based on the ideXlab platform.
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protection against a lethal dose of endotoxin by an inhibitor of tumour Necrosis factor processing
Nature, 1994Co-Authors: Kendall M Mohler, Mark Alderson, Dauphine S Torranee, Carol Ottenevans, Teresa Greenstreet, Jeffrey N. Fitzner, Suresh S. Kerwar, P R Sleath, Douglas P. Cerretti, Kumudini WeerawarnaAbstract:TUMOUR Necrosis factor (tumour Necrosis factor-α/cachectin) plays a critical role in certain physiological defensive responses but causes severe damage to the host organism when produced in excess1. There are two forms of tumour Necrosis factor, a type II membrane protein of relative molecular mass 26,000 (26K) and a soluble, 17K form generated from the cell-bound protein by proteolytic cleavage2,3. The two forms of tumour Necrosis factor and lymphotoxin-α (tumour Necrosis factor-β/lymphotoxin), a related protein, have similar but apparently not identical biological activities4–6. A therapeutic agent which inhibited the release of tumour Necrosis factor, but did not reduce the cell-associated activity or the level of lymphotoxin-α, might preserve the benefits of these cytokines while preventing tumour Necrosis factor-induced damage. Here we describe a potent inhibitor of tumour Necrosis factor processing and report that it protects mice from a lethal dose of endotoxin.
David Lillicrap - One of the best experts on this subject based on the ideXlab platform.
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multicentric warfarin induced skin Necrosis complicating heparin induced thrombocytopenia
American Journal of Hematology, 1999Co-Authors: Theodore E Warkentin, William M Sikov, David LillicrapAbstract:Two patients developed catastrophic multicentric skin Necrosis while receiving warfarin to treat venous thromboembolism complicated by immune-mediated heparin-induced thrombocytopenia (HIT). Patient 1 developed skin Necrosis involving the breasts, thighs, and face, as well as venous limb gangrene and bilateral hemorrhagic Necrosis of the adrenal glands, resulting in death. The second patient developed bilateral mammary Necrosis necessitating mastectomies, as well as skin Necrosis involving the thigh. Neither patient had an identifiable hypercoagulable syndrome, other than HIT. HIT may represent a risk factor for the development of multicentric warfarin-induced skin Necrosis (WISN).
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Multicentric warfarin‐induced skin Necrosis complicating heparin‐induced thrombocytopenia
American Journal of Hematology, 1999Co-Authors: Theodore E Warkentin, William M Sikov, David LillicrapAbstract:Two patients developed catastrophic multicentric skin Necrosis while receiving warfarin to treat venous thromboembolism complicated by immune-mediated heparin-induced thrombocytopenia (HIT). Patient 1 developed skin Necrosis involving the breasts, thighs, and face, as well as venous limb gangrene and bilateral hemorrhagic Necrosis of the adrenal glands, resulting in death. The second patient developed bilateral mammary Necrosis necessitating mastectomies, as well as skin Necrosis involving the thigh. Neither patient had an identifiable hypercoagulable syndrome, other than HIT. HIT may represent a risk factor for the development of multicentric warfarin-induced skin Necrosis (WISN).
Daniel Closa - One of the best experts on this subject based on the ideXlab platform.
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Soluble receptors released during acute pancreatitis interfere with the detection of tumor Necrosis factor-alpha
Crit Care Med, 2001Co-Authors: Erik Folch, A Serrano, Ellen Gelpi, Joan Roselló-catafau, Lidia Sabater, Daniel ClosaAbstract:OBJECTIVE: To evaluate the interfering effect of tumor Necrosis factor-alpha soluble receptor when measuring circulating concentrations of tumor Necrosis factor-alpha in an experimental model of acute pancreatitis. DESIGN: Randomized, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: Acute pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Saline was administered in a control group. Serums were overloaded with known amounts of tumor Necrosis factor-alpha or macrophage inflammatory protein-2. MEASUREMENTS AND MAIN RESULTS: Three hours after induction, serum concentrations of free tumor Necrosis factor-alpha, total tumor Necrosis factor-alpha, and soluble receptor of tumor Necrosis factor-alpha were measured. No detectable concentrations of free tumor Necrosis factor-alpha were found in any experimental group. By contrast, significant increases in total tumor Necrosis factor-alpha and soluble receptor of tumor Necrosis factor-alpha were found after induction of pancreatitis. Overloading of serum with tumor Necrosis factor-alpha resulted in detection of 50% of the expected concentrations of free tumor Necrosis factor-alpha from control animals and only of 5% from the pancreatitis group. Overloading the serum with macrophage inflammatory protein-2 resulted in a detection of 100% of the expected concentrations in both control and treated animals. CONCLUSION: Circulating soluble receptor of tumor Necrosis factor-alpha could interfere with the detection of tumor Necrosis factor-alpha in some pathologies, such as pancreatitis, that are associated with increases in soluble receptor of tumor Necrosis factor-alpha.
Kendall M Mohler - One of the best experts on this subject based on the ideXlab platform.
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protection against a lethal dose of endotoxin by an inhibitor of tumour Necrosis factor processing
Nature, 1994Co-Authors: Kendall M Mohler, Mark Alderson, Dauphine S Torranee, Carol Ottenevans, Teresa Greenstreet, Jeffrey N. Fitzner, Suresh S. Kerwar, P R Sleath, Douglas P. Cerretti, Kumudini WeerawarnaAbstract:TUMOUR Necrosis factor (tumour Necrosis factor-α/cachectin) plays a critical role in certain physiological defensive responses but causes severe damage to the host organism when produced in excess1. There are two forms of tumour Necrosis factor, a type II membrane protein of relative molecular mass 26,000 (26K) and a soluble, 17K form generated from the cell-bound protein by proteolytic cleavage2,3. The two forms of tumour Necrosis factor and lymphotoxin-α (tumour Necrosis factor-β/lymphotoxin), a related protein, have similar but apparently not identical biological activities4–6. A therapeutic agent which inhibited the release of tumour Necrosis factor, but did not reduce the cell-associated activity or the level of lymphotoxin-α, might preserve the benefits of these cytokines while preventing tumour Necrosis factor-induced damage. Here we describe a potent inhibitor of tumour Necrosis factor processing and report that it protects mice from a lethal dose of endotoxin.
