83 research outputs found
Prospective evaluation of a decision support system providing advice on ventilator settings of:Inspiratory oxygen, delivered pressure or volume and frequency
Analysis of arterial intimal hyperplasia: review and hypothesis
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign " intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl
Mechanism of cellular rejection in transplantation
The explosion of new discoveries in the field of immunology has provided new insights into mechanisms that promote an immune response directed against a transplanted organ. Central to the allograft response are T lymphocytes. This review summarizes the current literature on allorecognition, costimulation, memory T cells, T cell migration, and their role in both acute and chronic graft destruction. An in depth understanding of the cellular mechanisms that result in both acute and chronic allograft rejection will provide new strategies and targeted therapeutics capable of inducing long-lasting, allograft-specific tolerance
Muscle pain induced by hypertonic saline in the knee extensors decreases single-limb isometric time to task failure
Purpose: Increased nociceptive activity and the experience of exercise-induced pain (EIP) may contribute to fatigue during endurance exercise. To investigate this, a pain model that produces pain similar to EIP and decouples its’ relationship to exercise intensity is required. This study 1) compared the quality of pain caused by a hypertonic saline injection into the vastus lateralis in resting and exercise conditions, and 2) investigated whether this pain contributes to changes in time to task failure. Methods: On separate days, eighteen participants completed a time to task failure at 20% maximal voluntary torque (MVT), a resting hypertonic saline intramuscular injection, and in a further three visits a time to task failure at 10% MVT following injection of isotonic saline, hypertonic saline or a control (no injection). Results: In a subset of eligible participants (n = 12), the hypertonic saline combined with 10% MVT produced a qualitative experience of pain (assessed by the McGill Pain Questionnaire) that felt similar to EIP. 10% MVT with hypertonic saline significantly elevated pain intensity in the first 20% of the time to task failure and caused a significantly (P < 0.05) shorter time to task failure (448 ± 240 s) compared with the isotonic saline (605 ± 285 s) and control (514 ± 197 s) conditions. Conclusion: These findings demonstrate that hypertonic saline increases the intensity of pain during exercise, which results in a faster occurrence of exercise-induced fatigue. These results provide important evidence supporting pain as a limiting factor in endurance performance
Generation and characterization of xenospecific human suppressor T cells.
DESPITE continuous improvements in pharmacologic
strategies aimed to prevent transplant rejection, the
unwanted effect of nonspecific immunosuppression and the
irreversible nature of vascular rejection remain critical
problems. These problems are likely to be resolved only by
the development of new means for induction of donorspecific
tolerance in adult recipients.
Progress in this direction has been made recently through
the discovery of immunoregulatory T-suppressor cells that
inhibit the activation and proliferation of allospecific human
T-helper lymphocytes.1,2
Because xenotransplantation of pig organs into human
recipients is one of the most desirable solutions to the organ
shortage problem we have explored the possibility of generating
human suppressor T-cell lines (Ts), which can
inhibit T-helper-cell (Th) reactivity against pig MHC class
II antigens
Sharing of Class I MHC Molecules Between Donor and Host Promotes the Infiltration of Allografts by mHAg-Reactive CD8+ T cells
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