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Biomedical subjects

A Olazábal

Publications and source records attributed to A Olazábal.

16 recordsLinked to original sources

[Assessment of thoracic X-ray readings by emergency room physicians at a university hospital].

BACKGROUND: We aimed to find out whether systematic reading of chest radiography (CRx) by radiologists in the emergency unit might lead to a higher diagnostic efficiency and improve health care. MATERIAL AND METHOD: Descriptive study of consecutive admissions during 3 months in an internal medicine department. We registered the CRx interpretation by the emergency unit physician first, and a radiologist the next day. In cases with different interpretations, we assessed whether these differences would have modified the treatment. RESULTS: The overall disagreement between the emergency room physician and the radiologist was 13.7%. In 19 of 29 cases with different readings, the radiologist interpretation was in agreement with the final diagnosis. In 7 of these 19 cases, the radiologist reading of CRx would have led to a positive change of treatment. However, differences between both physicians were not statistically significant. CONCLUSIONS: There seems to be a higher diagnostic efficiency when the emergency room physician interpretation of CRx is complemented by a radiologist.

Adolescent↗

Chronic traumatic pseudoaneurysm of right subclavian artery.

A right subclavian artery pseudoaneurysm caused by blunt trauma is described. CT and digital subtraction angiography helped us to establish a correct diagnosis. Radiologic features of subclavian artery aneurysms and relevant literature are briefly discussed.

Adult↗

A randomized trial comparing preoperative chemotherapy plus surgery with surgery alone in patients with non-small-cell lung cancer.

BACKGROUND: The efficacy of surgery for patients with non-small-cell lung cancer is limited, although recent studies suggest that preoperative chemotherapy may improve survival. We conducted a randomized trial to examine the possible benefit of preoperative chemotherapy and surgery for the treatment of patients with non-small-cell lung cancer. METHODS: We studied 60 patients (59 men and 1 woman) with stage IIIA non-small-cell lung cancer. The patients were randomly assigned to receive either surgery alone or three courses of chemotherapy (6 mg of mitomycin per square meter of body-surface area, 3 g of ifosfamide per square meter, and 50 mg of cisplatin per square meter) given intravenously at three-week intervals and followed by surgery. All patients received mediastinal radiation after surgery. The resected tumors were evaluated by means of K-ras oncogene analysis and flow cytometry. RESULTS: The median period of survival was 26 months in the patients treated with chemotherapy plus surgery, as compared with 8 months in the patients treated with surgery alone (P < 0.001); the median period of disease-free survival was 20 months in the former group, as compared with 5 months in the latter (P < 0.001). The rate of recurrence was 56 percent in the group treated with chemotherapy plus surgery and 74 percent in the group treated with surgery alone. The prevalence of mutated K-ras oncogenes was 15 percent among the patients receiving preoperative chemotherapy and 42 percent among those treated with surgery alone (P = 0.05). Most of the patients treated with chemotherapy plus surgery had tumors that consisted of diploid cells, whereas the patients treated with surgery alone had tumors with aneuploid cells. CONCLUSIONS: Preoperative chemotherapy increases the median survival in patients with non-small-cell lung cancer.

Adult↗

Alterations in deoxyribonucleic acid and proteins in cerebral tissues from fetuses subject to alcohol in utero.

Critical period for intra-uterine growth retardation (IUGR), and biochemical parameters for tissue growth were studied in an animal model of Fetal Alcohol Syndrome (FAS) in rats. Our research used 40 animals, fed Lieber and DeCarli liquid diets, distributed into 4 groups: C, or control--non-alcoholic--, ad libitum; E, or alcoholic, fed ad libitum; F, or alcoholic, pair fed to E; and P, non-alcoholic, pair fed to E and F. Fetuses of group E were exposed to ethanol during the organogenic period, while those from group F exposed only during the last stage of pregnancy. Blood alcohol levels were determined both at the end of 42 days before pregnancy, and on days 3, 7, 14 and 19 of gestation. The brain content of total DNA and proteins was measured, along with the cell size of fetal tissues. Non-parametric statistics were applied, considering the litter as unit, and 5% as the significant level. Prenatal ethanol exposure was associated with a cell size, total DNA, and cerebral protein content all significantly lower (p less than or equal to 0.05) than in non-alcoholic groups. These facts strongly suggest that the critical period for growth retardation associated with FAS may be situated at the end of pregnancy, when metabolic disturbances of the brain could also arise, while major external malformations are likely to be produced during organogenesis.

Animals↗

Prostaglandin E2 and I2 treatment of acute experimental pancreatitis in rats.

Acute pancreatitis can be induced experimentally in rats by the retrograde pancreatic duct injection of deoxycholic acid. In order to evaluate if prostaglandins have a protective or therapeutic role, pancreatitis was induced with 0.03, 0.1, or 0.2 ml of 3% deoxycholic acid. Then, 16,16 dimethyl prostaglandin E2 or prostaglandin I2 were infused i.v. for 30 min before the deoxycholic acid injection or for 1 or 24 h beginning 30 min or 1 h after the injection. Deoxycholic acid, 0.1 and 0.2 ml, produced an 80-100% mortality at 24 h after the induction of pancreatitis, and prostaglandin administration had no appreciable effect. Induction of pancreatitis with 0.03 ml deoxycholic acid was associated with a 15% mortality at 24 h, and both prostaglandins significantly increased the mortality. In the experimental model of pancreatitis tested, the administration of exogenous PGI2 and 16,16 dimethyl PGE2 significantly worsened the outcome.

Acute Disease↗

Effect of prostaglandins E2 and I2 and of indomethacin on deoxycholic acid-induced damage to the rat bile-pancreatic duct.

Alterations in the permeability and histology of the pancreatic ductal mucosa have been demonstrated in the cat after an intraductal infusion of deoxycholic acid. In order to define the role of prostaglandins in the pathogenesis of the mucosal lesion, an isotonic electrolyte solution was perfused through a segment of the pancreatic duct of anesthetized rats for 1 h, before and after a 10-min perfusion with 10 mM deoxycholic acid. Prostaglandin E2 or I2 was infused (intraarterially, intravenously, or intraductally) for 30 min beginning 20 min before deoxycholic acid infusion. Indomethacin (5 mg/kg intravenously) was given 30 min before deoxycholic acid. Deoxycholic acid increased ductal permeability and produced severe epithelial necrosis. Neither prostaglandin nor indomethacin affected the alterations induced by deoxycholic acid. In the experimental model tested, neither inhibition of prostaglandin synthesis nor administration of exogenous prostaglandins altered the effects of deoxycholic acid.

Animals↗