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Biomedical subjects

R Jimenez

Publications and source records attributed to R Jimenez.

At least 55 records · Page 3Linked to original sources

[Lactic acidosis in diabetic patients associated with buformin].

We report two diabetic patients who developed lactic acidosis following the use of Buformin. Treatment consisted of mechanical ventilation, massive bicarbonate administration, circulatory support with dopamine and peritoneal dialysis. Despite this, both patients died.

Acidosis, Lactic↗

Clinical and immunological findings in large B-cell chronic lymphocytic leukemia.

In order to define the characteristics of B-CLL cases in which the predominant cell population is composed of large lymphocytes, we studied 97 patients with B-CLL, comparing the cell morphological features with the clinical and biological findings and the immunological phenotype of the proliferating cells. Multivariant analysis showed that there were three significantly different morphological groups: Typical CLL, large lymphocyte CLL (LLL), and CLL with prolymphocytes (CLL/PL). The LLL group showed a greater incidence of lymphadenopathies (P less than 0.05) and higher percentages of both mu + delta + cells (P less than 0.01) and Fmc/7+ cells (P less than 0.001) than in typical CLL. The main differences between LLL and CLL/PL were the peripheral blood lymphocyte count and the percentage of Fmc/7+ cells (P less than 0.002)--both higher in the CLL/PL group--and the percentage of mouse rosette-forming cells (P less than 0.01)--lower in CLL/PL. Further studies including functional assays and survival analyses could contribute to elucidating whether these groups are different entities or a single disease with marked heterogeneity.

Antibodies, Monoclonal↗

Acetylsalicylate-induced cholestasis, unrelated to biliary bile acid excretion, in the rabbit.

Administration of lysine acetylsalicylate to anaesthetized rabbits induced a marked decrease in bile flow and biliary secretion rates of sodium, potassium, chloride and bicarbonate. Bile acid concentrations were increased but biliary bile acid outputs were similar to those observed in control animals after i.v. injection of saline or lysine. Our results confirm that different species have different susceptibilities to salicylates since in other species this group of drugs is choleretic. It is suggested that the cholestatic effect of acetylsalicylate in the rabbit is due to acetylsalicylate and that it is associated with a reduction in the bile acid-independent bile flow since bile acid outputs remained constant after administration of the drug.

Analgesics↗

Biliary bilirubin and biliverdin excretion in rabbits during fasting and feeding.

Biliary excretion rate of bilirubin and biliverdin from fasted and fed conscious rabbits has been investigated. The animals were cholecystectomized and fitted with a chronic surgical double recurrent choledoco-choledocal biliary fistula. The enterohepatic circulation of bile salts were maintained by bile administration. Mean bile flow, biliary concentrations and excretion rates of bilirubin and biliverdin remained constant during fasting conditions. After feeding bile flow and biliary output of biliverdin increased whereas that of bilirubin did not. The higher excretion rate of biliverdin after feeding could be explained by the low biliverdin reductase activity in this species and the stimulation of biliverdin formation by postprandial factors.

Animals↗

Iron deficiency anemia and iron therapy effects on infant developmental test performance.

The behavioral effects of iron deficiency and its treatment were evaluated in a double-blind randomized controlled community-based study of 191 Costa Rican infants, 12 to 23 months of age, with various degrees of iron deficiency. The Bayley Scales of Infant Development were administered before and both 1 week and 3 months after IM or oral administration of iron. Appropriate placebo-treated control infants were also tested. Infants with iron deficiency anemia showed significantly lower mental and motor test scores, even after considering factors relating to birth, nutrition, family background, parental IQ, and the home environment. After 1 week, neither IM nor oral iron treatments differed from placebo treatment in effects on scores. After 3 months, lower mental and motor test scores were no longer observed among iron-deficient anemic infants whose anemia and iron deficiency were both corrected (36%). However, significantly lower mental and motor test scores persisted among the majority of initially anemic infants (64%) who had more severe or chronic iron deficiency. Although no longer anemic, they still showed biochemical evidence of iron deficiency after 3 months of treatment. These persistent lower scores suggest either that iron therapy adequate for correcting anemia is insufficient to reverse behavioral and developmental disturbances in many infants or that certain ill effects are long-lasting, depending on the timing, severity, or chronicity of iron deficiency anemia in infancy.

Anemia, Hypochromic↗

Enhancement of biliary phospholipid secretion by diethyl maleate administration in the rabbit.

The effect of diethyl maleate administration on biliary phospholipid secretion was studied in male New Zealand rabbits. Bile flow was significantly enhanced during the first 40 min following i.p. injection of diethyl maleate at 3.2 mmol/kg body wt., after which it decreased progressively to values half those of the controls at 2 h of injection of the chemical. Bile acid secretion was not significantly modified during choleresis but was significantly reduced from 60 min of diethyl maleate administration onwards. A significant increase in biliary phospholipid secretion parallel to that occurring in bile flow was observed in diethyl maleate-treated rabbits. Our data confirm the uncoupling previously described for the rat between bile acid and phospholipid secretion into bile during diethyl maleate-induced choleresis.

Animals↗

Changes in biliary secretion and lactate metabolism induced by diethyl maleate in rabbits.

Diethyl maleate is a compound which binds with glutathione by means of a glutathione S-transferase and is excreted into bile leading to a rapid depletion of hepatic glutathione. In the rabbit, the activity of the enzyme is fairly low and we were thus prompted to study the possible effects of diethyl maleate on biliary secretion and metabolic status in this species. The administration of diethyl maleate induced a transient choleresis followed by cholestasis. The choleresis coursed with increases in the biliary output of sodium and unaccounted anions, whereas those of chloride, bicarbonate and bile acids were unaffected. Our data seem to confirm that choleresis is due to the osmotic activity of diethyl maleate compounds excreted into bile, as has been reported in rats and dogs. The cholestasis observed coursed with falls in the outputs of sodium, chloride and bicarbonate though that of bile acids remained constant. Following diethyl maleate administration, a metabolic acidosis appeared with progressive increases of blood lactate concentration. In bile the concentration of this anion closely followed that of plasma. The cholestasis is attributed to a lowered biliary secretion of bicarbonate probably secondary to the metabolic alteration. The hepatic values of cytoplasmatic and mitochondrial NADH/NAD ratios and of adenine nucleotide concentrations suggest that the increase in blood lactate results rather from a fall in its hepatic utilization that from an increase in its production.

Acid-Base Equilibrium↗

By-passing the sphincter of Oddi does not affect gallbladder emptying in the pig.

A study of the relationship between bile secretion and nutrition in the pig requires a complete and continuous collection of the bile and its reinfusion to the animal. In most of the studies performed in different species, bile has been directly reinfused into the duodenum, leading to the exclusion of the sphincter of Oddi from the biliary pathway. It has been postulated that such an exclusion could inhibit gallbladder emptying. The aim of the present work was to study postprandial gallbladder emptying in the pig, depending on the site of bile reinfusion, i.e. the duodenum or the lower bile duct. The gallbladder bile was coloured with indocyanine green (ICG) and marker secretion was recorded after a test-meal. The results showed that after meal intake, the gallbladder emptied over a similar period of time and according to similar kinetics, whatever the site of bile reinfusion.

Ampulla of Vater↗

Comparative in vitro activity of 1-oxa-beta-lactam (LY127935) and cefoperazone with other beta-lactam antibiotics against anaerobic bacteria.

The in vitro activity of 1-oxa-beta-lactam (LY127935), cefoperazone (T-1551), cefuroxime, cefsulodin, cefaclor, cefotaxime, and cefoxitin on 85 anaerobic clinical isolates (30 Bacteroides, 30 Clostridium, 25 Peptococcaceae) was simultaneously determined by the agar dilution test in two different media, Brucella Agar (Difco Laboratories) and Wilkins-Chalgren agar. In Wilkins-Chalgren agar, 90% of Bacteroides were inhibited by (micrograms per milliliter): LY127935, 0.5; T-1551, 64; cefoxitin or cefuroxime, 8; cefsulodin or cefotaxime, 32; and cefaclor, 128. All Clostridia were inhibited in Wilkins-Chalgren by (micrograms per milliliter): LY127935, 4; T-1551, 2; cefoxitin, 6; cefuroxime, 0.12; cefsulodin, 0.5; cefaclor, 1; and cefotaxime, 8. All Peptococccaceae were inhibited by T-1551, cefsulodin or cefotaxime at 4 microgram/ml and by cefoxitin or cefuroxime at 1 to 2 microgram/ml. With cefaclor at 8 microgram/ml, 92% of strains were inhibited, and LY127935 at 16 microgram/ml only inhibited 64% of strains. LY127935 was the most active of the antibiotics tested against Bacteroides, showing good activity against Clostridia and poor activity on Peptococcaceae, whereas T-1551 was more active against Peptococccaceae and had similar activity against Clostridia and poor activity on Bacteroides. There are no significant differences between minimal inhibitory concentrations obtained in Brucella Agar and those obtained in Wilkins-Chalgren.

Anaerobiosis↗