[Suggestions and recommendations for standardization of the systematic routine controls during the production of pharmaceutical dosage forms and their manufacturing].
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Biomedical subjects
Publications and source records attributed to A Colombo.
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This article reviews many of the applications of intravascular ultrasonic imaging for coronary and peripheral arterial disease. In vitro studies demonstrate an excellent correlation between ultrasound measurements of lumen and plaque cross-sectional area compared with histologic sections. In vivo clinical studies reveal the enhanced diagnostic capabilities of this technology compared with angiography. Ultrasonic imaging also permits visualization of the atherosclerotic plaque itself for the first time in vivo. In addition to accurately describing the plaque morphology, ultrasonography can identify some of the tissue characteristics of the plaque. During interventional procedures, ultrasonic imaging has been shown to be beneficial for enhanced diagnosis as well as improvement of our understanding of the mechanism of newer interventional devices such as directed atherectomy, rotational or TEC atherectomy, or excimer laser. Initial studies suggest that ultrasound guidance of intravascular stent deployment may be critical for optimizing stent placement. Randomized studies are currently in progress to determine whether the guidance provided by intravascular ultrasonic imaging will alter the results of interventional procedures so that the restenosis rate can be improved.
Examination for lung asbestos bodies and pleural plaques was made in 996 consecutive unselected autopsies in Torino. The prevalence of asbestos bodies was 12.4% and that of pleural plaques 19.1%. Both findings were found with significantly greater frequency in men, and in the age group above 50 years. In addition, their occurrence increased with age up to 70 years, then decreased thereafter. A significant association between the severity of plaque lesions and the presence of asbestos bodies was found, whereas the number of asbestos bodies was not related to the presence of pleural plaques. It is suggested that pleural plaques are more reliable markers of asbestos exposure started many years earlier, and that lung asbestos bodies are more reliable indicators of more recent exposure.
Seven girls with precocious puberty, idiopathic in 6 and associated with the McCune Albright syndrome in 1, were treated with 70 mg/M2/die of cyproterone acetate (CPA) for 11 to 36 months. Before and during treatment clinical parameters (weight, height, bone age, height velocity, prediction of adult height and pubertal development) were evaluated and plasma hormone assays in basal conditions (LH, FSH, 17 beta-estradiol, progesterone, testosterone, PRL, ACTH and cortisol) and after stimulation (LH, FSH, cortisol, GH) were carried out to assess the efficacy and eventual side effects of CPA. The regression observed in the clinical signs of puberty was considered satisfactory and the increase observed in the developmental quotient indicated an improved prognosis for adult height. No symptoms of adrenal insufficiency were observed but an adrenal suppressive effect of CPA was evident from the response to insulin hypoglycemia observed in 4 patients.
The use of intravascular ultrasound catheters to produce images of lumen and plaque cross-sectional areas has had a profound effect on the practice of interventional cardiology. This imaging modality provides, for the first time, a low-power microscopic view of vascular anatomy within a living patient. This article will review some of the advantages of intravascular ultrasound imaging compared with angiography when used for diagnostic or interventional therapeutic procedures.
Congenital misalignment of pulmonary vessels (MPV) with alveolar capillary dysplasia is a rare condition consisting of anomalous veins in bronchovascular bundles, a decreased number of alveolar capillaries, and increased muscularization of pulmonary arterioles. In the literature, infants reported as having such a malformation developed respiratory distress with persistent pulmonary hypertension and ultimately died. We report the case of an infant with MPV and alveolar capillary dysplasia who was unresponsive to maximal cardiorespiratory support, including high-frequency oscillatory ventilation and inhaled nitric oxide; the infant died of pulmonary hemorrhage after 19 days, during venoarterial extracorporeal membrane oxygenation bypass. We conclude that the diagnosis of MPV and alveolar capillary dysplasia should be considered during autopsy of infants who have died of irreversible persistent pulmonary hypertension. If a lung biopsy in infants with prolonged refractory hypoxemia confirms such diagnosis before death, expensive and invasive treatments such as extracorporeal membrane oxygenation could be avoided.
A screening procedure to select, in autopsy populations, subjects having a major likelihood of previous occupational exposure to asbestos is described. To test our necropsy population we searched for pleural plaques (PPs); the optical count of both lung asbestos bodies (ABs) and uncoated mineral fibers (UMFs) at least 10 microns in length was recorded. In the adult autopsy population studied in the Turin area, the predictive value given by a positive test for large-size PPs (mostly bilateral) was about 55%. This level of probability did not rise in relation to the AB counts, whereas an increase to over 75% was observed if more than 10,000 UMFs/g dry lung were present. In subjects without PPs or with small-size plaque lesions (mostly unilateral), predictive values of positive tests were 20 to 30% when ABs and UMFs were found to be below 100 and 10,000/g, respectively, and increased to approximately 40% if the AB count exceeded 500/g and to almost 70% for an UMF count above 100,000/g. In subjects without PPs or with small-size plaque lesions, the probability of being nonexposed was greater than 90% if neither ABs nor UMFs were found. This autopsy screening may be a reliable tool in selecting cases most probably related to occupational exposure.
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BACKGROUND: Radioactive (32)P beta-emitting stents have been shown to reduce intrastent neointimal hyperplasia in a substantial dose-related manner in the animal model. The aim of this dose-response study was to evaluate, in the clinical setting, the safety and efficacy at 6-month follow-up of this approach to reducing restenosis. METHODS AND RESULTS: A total of 122 (32)P radioactive beta-emitting stents (initially the Palmaz-Schatz and later the BX Isostent) with an activity level of 0.75 to 3.0 microCi (group 1), 3.0 to 6.0 microCi (group 2), and 6.0 to 12.0 microCi (group 3) were implanted in 91 lesions in 82 patients. There were no procedural events. At 6-month follow-up, no deaths had occurred, and only 1 patient had stent thrombosis. Pure intrastent binary restenosis was 16% in group 1, 3% in group 2, and 0% in group 3. However, intralesion restenosis was 52% in group 1, 41% in group 2, and 50% in group 3. CONCLUSIONS: The use of (32)P radioactive beta-emitting stents in patients with CAD is feasible. At 6-month follow-up, intrastent neointimal hyperplasia was reduced in a dose-related manner. However, in the 3 groups, intralesion restenosis was high because of a high late lumen loss in the reference segments at the stent edges, possibly as a result of a low activity level of radiation at the edges of the stent combined with an aggressive approach to stenting. We called this "edge effect" the "candy wrapper."
The effectiveness of cerebral antiedema agents in stroke has been questioned. Animal and clinical work is inconclusive about steroids and osmotic drugs. A retrospective study of a continuous series of 227 stroke patients treated in the acute stage (some with dexamethasone alone, some with dexamethasone plus hyperosmotic mannitol infusions, and some without antiedema therapy) showed no significant difference in the ten-day survival rate. On this criterion, there is no ground for the systematic use of such agents against this type of brain swelling.
In patients with trauma or sepsis, carnitine is known to be produced to a greater extent; deficient production could impair the energy management that is required in such patients. To clarify the requirements of carnitine after injury, we studied carnitine elimination (in 10 critically ill injured patients) both during fasting and early parenteral nutrition. Increased carnitine (mainly, free) output after injury (9.36 +/- 1.63 mumol/kg p less than 0.02 vs reference) was negatively related to nitrogen balance (p less than 0.05) and positively to 3-methyl-histidine output (p less than 0.01), acting as a market of body mass catabolism. The output of both total and free carnitine progressively decreased (p less than 0.01) throughout the course of total parenteral nutrition. In conclusion, our data definitively suggest that carnitine loss after injury reflects body cell mass wastage and does not necessarily mean an increased need.