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A 21-year-old man developed the adult respiratory distress syndrome (ARDS) within five hours of receiving antilymphocyte globulin. No other identifiable cause of ARDS was present. The mechanism for development of acute lung injury is unknown, but may be related either to direct lung cytotoxicity or to complement-mediated leukocyte and platelet destruction with secondary lung injury from inflammatory mediators. 相似文献
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J K Stoller H P Wiedemann J Loke P Snyder J Virgulto R A Matthay 《British journal of diseases of the chest》1988,82(3):242-250
We conducted a double-blind, randomized crossover trial to evaluate whether oral terbutaline (2.5 mg orally three times daily for a week) increased the force of diaphragmatic contraction in normocapnic patients with chronic obstructive pulmonary disease. Ten patients with moderate to severe airway obstruction completed the trail. Compared with placebo, terbutaline produced a mean increase of 5.8 cmH2O in peak inspiratory mouth pressure and a mean increase of 5.0 cmH2O in transdiaphragmatic pressure during a maximal inspiratory manoeuvre. These small changes with terbutaline failed to achieve statistical significance. Also, terbutaline failed to alter flow rates (FEV1, Vmax50) or patients' dyspnoea ratings using two separate clinical scales (Pneumoconiosis Research Unit Score and the Modified Dyspnoea Index). Because all observed changes in respiratory muscle strength were small and because the trial had power to detect small changes in inspiratory mouth pressures, we suggest that oral terbutaline at the dose administered in this study has little noteworthy effect on respiratory muscle strength in normocapnic patients with chronic obstructive pulmonary disease. 相似文献
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This paper describes the tragic case of a young woman who died of cancer of
the colon after successfully donating eggs to her younger sister. Although
there is no direct link between her operation and the subsequent
development of bowel carcinoma, this case imparts a feeling of unease when
seen in conjunction with other cases reported during the last few years. It
is a reminder that little is known of the long-term consequences of some
aspects of assisted conception. Women undergoing ovarian stimulation for
themselves or a matched recipient have the right to be advised, in an
agreed format, that there is some concern about unproven potential risks
from the stimulatory drugs. The safety of egg donors must assume priority
over all other considerations, including lack of donors or any moral
position. The recent decision by the Human Fertilisation and Embryology
Authority (HFEA) to withdraw any form of payment or recompense to egg
donors does not seem to us to be based on a balance of scientific advances,
patient needs and the ethics of gamete supply. They state that the
intention to withdraw payments was implicit in the 1990 Human Fertilisation
and Embryology (HFE) Act. However the Act was based on the Warnock report
made 6 years earlier. Even in 1990 ovum donation was uncommon and fertility
drugs had not yet caused any unease. The Act provided the HFEA with
discretionary powers to issue directions so that the future policies would
be consistent with any emerging new medical evidence. It is imperative that
the HFEA provide convincing evidence on how the current policy of payment
to donors harms society, donors or recipients, and how in the UK the new
policy will improve medical practice in assisted conception. Successful
pilot studies must precede the implementation of any new policy. Failure to
do this could cause irreversible harm to the practice of assisted
conception using donor gametes, which will ultimately be against the basic
aims of the 1990 HFE Act.
相似文献
9.
W. D. Ratnoff M. A. Matthay M. Y. S. Wong Y. Ito K. H. Vu J. Wiener-Kronish E. J. Goetzl 《Journal of clinical immunology》1988,8(4):250-258
The human pulmonary edema fluid concentrations of LTC4 and of LTD4 and LTE4, derived peptidolytically from LTC4, were assessed by radioimmunoassays of the mediators resolved by reverse-phase high-performance liquid chromatography. The mean pulmonary edema fluid concentration (± SD) of LTD4 of 19.2±25.6 nM for 12 patients with the adult respiratory distress syndrome and of LTE4 of 192±309 nM for 10 of the patients were significantly higher (P<0.005 andP<0.05) than those of 2.2±2.4 and 11.0±18.2 nM, respectively, for 10 patients with cardiogenic pulmonary edema, whereas the lower mean concentrations of LTC4 were not significantly different for the two groups. Pulmonary edema fluid from five patients with adult respiratory distress syndrome, one with cardiogenic pulmonary edema, and one with an indeterminate syndrome contained similar concentrations of peptidoleukotriene peptidases. The LTC4 and LTD4 peptidolytic activities in ARDS fluids were 81 and 142 kD, respectively, by gel filtration. The extents of peptidolysis of [3]LTC4 and [3]LTD4 by 100 µl of pulmonary edema fluid attained respective mean maximum levels of 74.5±2.9% (N=5) and 37.7±10.2% (N=4) after 30 min at 37°C and were inhibited by serine-borate and by cysteine, respectively. The predominance of LTD4 and LTE4 over LTC4 in states of altered pulmonary vascular pressure and permeability thus is attributable to two distinct peptidases. 相似文献
10.
Mutations in the Ca(2+)-sensing receptor gene cause autosomal dominant and sporadic hypoparathyroidism 总被引:3,自引:0,他引:3
Baron J; Winer KK; Yanovski JA; Cunningham AW; Laue L; Zimmerman D; Cutler GB Jr 《Human molecular genetics》1996,5(5):601-606
Parathyroid hormone secretion is negatively regulated by a 7- transmembrane
domain, G-protein coupled Ca(2+)-sensing receptor. We hypothesized that
activating mutations in this receptor might cause autosomal dominant
hypoparathyroidism (ADHP). Consistent with this hypothesis, we identified,
in two families with ADHP, heterozygous missense mutations in the
Ca(2+)-sensing receptor gene that cosegregated with the disorder. None of
50 normal controls had either mutation. We also identified a de novo,
missense Ca(2+)-sensing receptor mutation in a child with severe sporadic
hypoparathyroidism. The amino acid substitution in one ADHP family affected
the N-terminal, extracellular domain of the receptor. The other mutations
involved the transmembrane region. Unlike patients with acquired
hypoparathyroidism, patients with these mutations had hypercalciuria even
at low serum calcium concentrations. Their greater hypercalciuria
presumably reflected activation of Ca(2+)-sensing receptors in kidney
cells, where the receptor negatively regulates calcium reabsorption. This
augmented hypercalciuria increases the risk of renal complications and thus
has implications for the choice of therapy.
相似文献