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"Tilney, Nicholas L"
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Invasion of the Body
A pioneering organ transplant surgeon narrates in gripping detail the revolutions that have transformed modern surgery, and the turmoil in medical education and health care reform as new capacities to prolong life and restore health run headlong into unsustainable costs. Tilney’s stage is the famous Boston teaching hospital, Brigham and Women's.
eBook
Risk factors and outcomes of pancreatitis after open heart surgery
We sought to analyze the risk factors and natural history associated with post-cardiac surgery acute pancreatitis.
Retrospective analysis of all patients having undergone cardiac surgery at our hospital between January 1, 1992, and October 1, 2001.
A total of 10,249 cardiac operations were performed. Thirty-nine (0.4%) patients developed postoperative pancreatitis. There was a higher incidence during the period spanning 1992 through 1996 than 1997 through 2001 (0.6% versus 0.2%,
P < .05). Patients with pancreatitis had longer postoperative length of stay (51 ± 5 days versus 10 ± 1 days,
P < .05) and a greater in-hospital mortality rate (28% versus 4%,
P < .05) than patients who did not develop pancreatitis. A history of alcohol abuse, cardiac surgery performed during 1992 to 1996, increased cardiopulmonary bypass time, and increased cross-clamp time were independent risk factors for the development of pancreatitis. Multiple-organ failure was an independent predictor for death among patients with pancreatitis.
Although the frequency of post-cardiac surgery pancreatitis is diminishing, it is still associated with significant mortality.
Journal Article
Sequential Cytokine Dynamics in Chronic Rejection of Rat Renal Allografts: Roles for Cytokines RANTES and MCP-1
Chronic rejection, the most important cause of long-term graft failure, is thought to result from both alloantigen-dependent and -independent factors. To examine these influences, cytokine dynamics were assessed by semiquantitative competitive reverse transcriptase-PCR and by immunohistology in an established rat model of chronic rejection of renal allografts. Isograft controls develop morphologic and immunohistologic changes that are similar to renal allograft changes, although quantitatively less intense and at a delayed speed; these are thought to occur secondary to antigen-independent events. Sequential cytokine expression was determined throughout the process. During an early reversible allograft rejection episode, both T-cell associated [interleukin (IL) 2, IL-2 receptor, IL-4, and interferon γ] and macrophage (IL-1α, tumor necrosis factor α, and IL-6) products were up-regulated despite transient immunosuppression. RANTES (regulated upon activation, normal T-cell expressed and secreted) peaked at 2 weeks; intercellular adhesion molecule (ICAM-1) was maximally expressed at 6 weeks. Macrophage products such as monocyte chemoattractant protein (MCP-1) increased dramatically (to 10 times), presaging intense peak macrophage infiltration at 16 weeks. In contrast, in isografts, ICAM-1 peaked at 24 weeks. MCP-1 was maximally expressed at 52 weeks, commensurate with a progressive increase in infiltrating macrophages. Cytokine expression in the spleen of allograft and isograft recipients was insignificant. We conclude that chronic rejection of kidney allografts in rats is predominantly a local macrophage-dependent event with intense up-regulation of macrophage products such as MCP-1, IL-6, and inducible nitric oxide synthase. The cytokine expression in isografts emphasizes the contribution of antigen-independent events. The dynamics of RANTES expression between early and late phases of chronic rejection suggest a key role in mediating the events of the chronic process.
Journal Article
Renal allograft protection with losartan in Fisher→Lewis rats: Hemodynamics, macrophages, and cytokines
Renal allograft protection with losartan in Fisher→Lewis rats: Hemodynamics, macrophages and cytokines.
We sought to assess the effects of angiotensin receptor blockade on glomerular hypertension, macrophage recruitment, and cytokine expression, all of which contribute to the development of chronic graft injury in this model.
The effects of treatment with the specific angiotensin II type 1 (AT1) receptor antagonist, losartan, were assessed over 24 weeks in F344→LEW rats (LOS, N = 9) versus vehicle-treated F344→LEW controls (CON, N = 9).
UprotV rose progressively in CON (from 7.0 ± 2.9 to 41 ± 17 mg/day at 24 wk) but remained at baseline in LOS (4.2 ± 0.6 to 9.4 ± 1.3 mg/day, P < 0.05 vs. CON). Glomerular capillary pressure (PGC) was increased in CON (71 ± 1 mm Hg at week 20), but remained within the normal range in LOS rats (54 ± 2 mm Hg, P < 0.05). Glomerulosclerosis averaged 0.3 ± 0.2% in LOS versus 4 ± 2% in CON rats (P < 0.05). Tubulointerstitial injury was minimal in both LOS and CON rats (+). The overexpression of renal cortical cytokine mRNA levels for the monocyte chemoattractants, monocyte chemoattractant protein-1 (MCP-1) and RANTES, as well as interleukin-1, inducible nitric oxide synthase, and transforming growth factor-β, assessed by competitive reverse transcription-polymerase chain reaction, was suppressed in LOS versus CON rats at 20 weeks. Macrophage and T-cell numbers were decreased, and MCP-1, RANTES, and intercellular adhesion molecule-1 staining in the graft, identified by immunohistochemistry, were attenuated in LOS versus CON rats.
The renoprotective effects of losartan in F344→LEW rats were associated with lowered PGC, inhibition of macrophage chemoattractants and recruitment, and suppression of macrophage-associated cytokines at 20 weeks. These findings suggest that chronic allograft injury in F344→LEW rats is, to a large extent, mediated by angiotensin II-dependent mechanisms and that these involve glomerular hemodynamics, macrophages, and macrophage-associated cytokines.
Journal Article
Operations on the Heart
Late one winter night in 1971 the nurse in the emergency room of the Peter Bent Brigham Hospital received a call that a man had been shot in the chest. The ambulance had picked him up and was on its way. She immediately paged me from the ward where the intern and I were examining a patient. I was the senior surgical resident in the hospital at the time, in my fifth year of training. We rushed down to the emergency room while she called the cardiac surgeon at home. He said he would be there in half an hour.
Book Chapter
Shifting Foundations
I recently attended the goodbye ceremony for the graduating senior surgical residents, a yearly event well in keeping with the enduring rituals of academic medicine and its educational precepts. It was held in the hospital amphitheater, the same large, portrait-filled hall I first entered fifty years before and where I had sat through untold numbers of rounds and lectures during my career. Faculty and trainees filled many of the seats in front; spouses and a scattering of parents beamed from the upper rows. An occasional baby made itself heard. The programs were printed on crisp paper. The colored shields of
Book Chapter
Making a Surgeon, Then and Now
Young doctors entering a surgical career soon learn that they have become part of an evolving system in which much of the care they will deliver and many of the operations they will master were developed during their lifetimes, were in their infancy for their parents, and were nonexistent for their grandparents. Indeed, their grandchildren may one day express incredulity about the primitive nature of the strategies and approaches now regarded as state of the art. Less likely to change are both surgeons’ and patients’ expectations that any given procedure will enhance or prolong life. They expect excellent results, minimal
Book Chapter
The Mechanical Heart
John Gibbon Jr., a surgical resident at the MGH in 1931, was typical of those training in prestigious programs at that time. A fourth-generation physician from Philadelphia, he had been educated at Princeton University and Jefferson Medical College. Patrician, tall, spare, and handsome, he was quietly dedicated to his career. One evening the nurses called him urgently to the bedside of a postoperative patient who had suddenly lost consciousness. Her skin, lips, and fingernails were blue, her breathing was labored, her pulse was weakening. She was dying before his eyes from a pulmonary embolus. Despite hours of support with intravenous
Book Chapter
The Promise of Surgical Research
I had always planned a career as a clinical surgeon, and so my early involvement with the emerging area of kidney transplantation was serendipitous. It was unknown territory. While some organ recipients did relatively well, larger numbers developed problems with which we were completely unfamiliar or which hadn’t even been described. Question after question arose that ranged from the meaning of obscure, obvious, or frightening physical abnormalities to the possible application of emerging data from research laboratories. We had few answers, and many of the patients died. Because scientists in Great Britain were providing much of the basic information on
Book Chapter