Quality control of home monitoring of blood glucose concentrations.
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Biomedical subjects
Publications and source records attributed to R Crane.
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Three patients had radionuclide lung perfusion images that we believe to be typical of tumor microembolism. Autopsy confirmation was available in two of these cases. A brief review of pulmonary tumor microembolism is included.
Beta,beta'-iminodipropionitrile (IDPN) produces a rearrangement of axoplasmic organelles with displacement of microtubules, smooth endoplasmic reticulum, and mitochondria toward the center and of neurofilaments toward the periphery of the axon, whereas the rate of the fast component of axonal transport is unchanged. Separation of microtubules and neurofilaments makes the IDPN axons an excellent model for study of the role of these two organelles in axonal transport. The cross-sectional distribution of [3H]-labeled proteins moving with the front of the fast transport was analyzed by quantitative electron microscopic autoradiography in sciatic nerves of IDPN-treated and control rats, 6 h after injection of a 1:1 mixture of [3H]-proline and [3H]-lysine into lumbar ventral horns. In IDPN axons most of the transported [3H] proteins were located in the central region with microtubules, smooth endoplasmic reticulum and mitochondria, whereas few or none were in the periphery with neurofilaments. In control axons the [3H]-labeled proteins were uniformly distributed within the axoplasm. It is concluded that in fast axonal transport: (a) neurofilaments play no primary role; (b) the normal architecture of the axonal cytoskeleton and the normal cross-sectional distribution of transported materials are not indispensable for the maintenance of a normal rate of transport. The present findings are consistent with the models of fast transport that envision microtubules as the key organelles in providing directionality and propulsive force to the fast component of axonal transport.
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Immediate bronchial artery reconstitution may be important in the prevention of bronchial anastomotic problems in lung transplantation. To facilitate this reconstitution in circumstances requiring allograft replacement of the right lung, we developed a method for transplanting the left lung together with its bronchial arterial supply into the right hemithorax. With this method, left lungs were allotransplanted into the right hemithorax of nine immunosuppressed dogs. Six recipients survived 1 to 4 weeks. Death resulted from pneumonia or rejection, and there were no bronchial anastomotic problems. Roentgenograms showed that the bronchial artery was patent and that the inverted transplanted left lungs could conform exactly to the thorax without space problems or radiographic abnormalities. Except for the unusual position of the large pulmonary arteries, angiographic patterns, function, and perfusion of the transplanted lungs were often normal and equivalent to those of the recipient's normal left lung. Thus it is possible to transplant a left lung into either hemithorax and immediately reconstitute its bronchial arterial circulation. Bronchial anastomotic problems may thereby be decreased.
A whole body plethysmograph (body box) equipped with a flow meter (see Figure 1) was used for objective quantification of the effects of single doses of clemastine fumarate 2.68 mg, chlorpheniramine 4 mg and placebo in a double-blind study of 48 patients with seasonal allergic rhinitis. This technique offers an objective means of assessing drug effects on nasal congestion and obstruction. Before the development of whole body plethysmography, only subjective assessments of antihistamines' effects on nasal blockage or congestion were available. These subjective reports usually noted that nasal blockage or congestion was refractory to antihistamines or minimally relieved by them. However, in this study, nasal and oral airway resistances, each measured by whole body plethysmography, were lowered by clemastine fumarate and chlorpheniramine. These results were corroborated by the patients' and physician's assessments of changes in symptom severity and the physician's evaluation of intranasal photographs taken for each patient. Oral airway resistance of patients treated with clemastine fumarate was improved to a significantly greater extent than in patients receiving placebo. At two hours post-drug, patients receiving clemastine fumarate usually showed a greater response in most assessments than those receiving chlorpheniramine, and the trend of most comparisons was clearly in favor of clemastine fumarate. Patients in all three treatment groups experienced drowsiness but both incidence and severity were lower with clemastine fumarate.
In double-blind trials clemastine fumarate 2.68 mg. chlorpheniramine 4 mg and placebo were randomly assigned to two groups of patients with seasonal allergic rhinitis. Thirty-nine desensitized patients were given one of the three test drugs in a parallel design; 67 nondesensitized patients each received two of the three drugs in a crossover design. Assessment of drug activity in each study was by whole body plethysmography and intranasal color photography as well as by subjective methods. Objective measurements showed clemastine fumarate was significantly superior to placebo and often better than chlorpheniramine in decreasing true nasal resistance and relieving nasal congestion. High placebo responses characterized the subjective evaluations, although the active drugs were clearly better. Responses varied somewhat between desensitized and nondesensitized patients. The number of reports of sedative effect, high in all groups, seemed to be more closely related to these antihistamine conditioned patients than to activity of the drugs themselves, based on previous reports of low sedation with clemastine fumarate. The techniques described proved very useful in distinguishing relative activity of antihistamines. Clemastine fumarate, the new antihistamine studied, appears to offer certain advantages over the older drug, chlorpheniramine.
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To evaluate a system for preserving and transporting lungs before transplantation, we removed the left lungs of 37 dogs, flushed them with a hypertonic solution having an electrolyte composition resembling intracellular fluid, and immersed them at 4 degrees C. for 7 to 24 hours. Some lungs were maintained at exactly 4 degrees C. during transport by means of a mixture of solid and liquid l-hexadecene. The lungs were allografted into immunosuppressed dogs whose right pulmonary artery was immediately ligated. Twelve recipients (32 per cent) survived 5 days or more solely on the function of the preserved lung. Four survived 10, 19, 40, and 40 days with lungs that had been preserved for 7 to 21 hours. Survival of recipients of preserved lungs (5 +/- 2 days) was equivalent to that of 75 comparably immunosuppressed recipients of nonpreserved allografts (6 +/- 1 days). One group of 10 dogs receiving lungs flushed against outflow resistance survived 12 +/- 5 days. In recipients of preserved allografts, arterial oxygen tensions remained in the normal range up to 5 weeks after transplantation, and radiographic infiltrates in the transplant were no greater than those present in recipients of nonpreserved transplants. Thus lungs transported and preserved up to 21 hours can provide total pulmonary function after transplantation and can function at least as well as nonpreserved transplants. The effectiveness and simplicity of this method are such that it might be considered for use in man.
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The uptake of 131I-fibrinogen in canine pulmonary allografts was compared to that in lung autografts or lungs with papain-induced unilateral hemorrhagic pneumonia. In addition to serial lung scans and the postmortem measurement of tissue radioactivity, all dogs had serial chest roentgenograms and histologic study of their lungs. All four animals in the allografted group had increased radioactive uptake on the side of the allograft lung at the same time as or slightly before radiographic abnormalities were evident. However, increases in lung radioactivity also occurred in animals with pneumonia or autografts at the time infiltrates were present. Thus the presence of increased lung scan activity, which occurs in rejecting lung allografts after the injection of 131I-fibrinogen, is not a specific index of pulmonary rejection.
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Lung allograft rejection can usually be diagnosed by the appearance of infiltrates on plain chest roentgenograms when these are interpreted in the light of other clinical and bacteriologic information. Large pulsed intravenous doses of methylprednisolone were usually effective in reversing lung allograft rejection that occurred in immunosuppressed dogs. In 10 of 15 animals the presence of moderate to severe rejection and its effective reversal with treatment were documented with roentgenograms and histologic sections. This ability to reverse the manifestations of lung allograft rejection, when they occur, has helped in the management of human lung allograft recipients.
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