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Biomedical subjects

F Rubio

Publications and source records attributed to F Rubio.

At least 55 records · Page 3Linked to original sources
PubMed1990

Giant basilar aneurysm in the course of subacute bacterial endocarditis.

We describe a man aged 42 years with mitral valve regurgitation who suffered from subacute bacterial endocarditis caused by Streptococcus morbillorum. The clinical picture began with a toxic syndrome. Five months later, the patient had an embolic episode and a right rostral pontine stroke, which was followed a few days later by an adversive focal seizure on the right. Despite antibiotic treatment, he suffered complete third nerve palsy. Arteriography, magnetic resonance imaging, and computed tomography of the brain showed a giant aneurysm in the rostral end of the basilar artery; the aneurysm was clipped. We discuss the clinical features, radiology, and characteristics of this aneurysm as a unique case of a giant bacterial aneurysm in the vertebrobasilar system.

Basilar Artery↗
PubMed1990

The effects of steroid therapy on pulmonary hypertension secondary to fibrosing mediastinitis.

Mediastinal fibrosis, a rare cause of pulmonary hypertension, may produce cough, dyspnea, and hemoptysis. Steroid therapy has been suggested for individuals with progressive symptoms, but data demonstrating the efficacy of such therapy are lacking. We present a case of pulmonary hypertension secondary to fibrosing mediastinitis. Hemodynamic and scintigraphic studies performed before and after a trial of corticosteroid therapy were unable to demonstrate any therapeutic benefit from the corticosteroids. In order to achieve better use of steroids for the treatment of this disease, we suggest that similar determinations be made on other patients with mediastinal fibrosis who receive such treatment.

Adult↗
PubMed1987

Determination of 6-(2'-chlorophenyl)-4-hydroxy-4H-imidazo[1,5-a] [1,4]benzodiazepine-3-carboxamide, a mixed agonist-antagonist anxiolytic agent, in human plasma and urine by gas chromatography-negative-ion chemical-ionization mass spectrometry.

A simple, sensitive and specific assay was developed for the determination in plasma and urine of 6-(2'-chlorophenyl)-4-hydroxy-4H-imidazo[1,5-alpha] [1,4]benzodiazepine- 3-carboxamide, compound I, a mixed agonist-antagonist anxiolytic agent. A hexadeuterated analogue of the compound was added to plasma or urine as the reference standard. The titled compound was extracted with benzene at pH 11. Following evaporation of the solvent, the residue was reacted with pentafluoropropionic anhydride in the presence of triethylamine. The derivatizing reagents were evaporated, and the carbonitrile derivative of the analyte was extracted into ethyl acetate at pH 11. The residue remaining after removal of the ethyl acetate was silylated with bis(trimethylsilyl)trifluoroacetamide, and a portion of this solution was analyzed by gas chromatography-negative-ion chemical-ionization mass spectrometry. The mass spectrometer was set to monitor, in the gas chromatographic effluent, the M-. ion of the titled compound and its hexadeuterated reference standard. The ratio of these two ions was calculated and converted to a concentration of analyte using a calibration curve that was generated from the analyses of control plasma fortified with various amounts of analyte and a fixed amount of the hexadeuterated reference standard. The limit of quantitation of the assay was 1 ng/ml for plasma and urine.

Anti-Anxiety Agents↗
PubMed1986

A multi-resistance plasmid isolated from commensal Neisseria species is closely related to the enterobacterial plasmid RSF1010.

pFM739, an R plasmid from Neisseria sicca that encodes penicillin, streptomycin and sulphonamide resistance, and the enterobacterial IncQ(P-4) plasmid RSF1010, which encodes streptomycin and sulphonamide resistance, were incompatible, and were mobilized by the same conjugative plasmids. Restriction mapping confirmed a high degree of similarity between both R plasmids; pFM739 carried DNA fragments corresponding to the known replication and resistance regions of RSF1010. pFM739 also carried an extra segment with the same restriction map as that described for the beta-lactamase-coding region of transposon Tn3. It is suggested that the R plasmids isolated from commensal Neisseria sp. could have resulted from transposition of a Tn3-like genetic element to an RSF1010-like plasmid, and that they contain deletion derivatives of transposon Tn3.

DNA Restriction Enzymes↗
PubMed1986

Urinary excretion of nitrosodimethylamine and nitrosoproline in humans: interindividual and intraindividual differences and the effect of administered ascorbic acid and alpha-tocopherol.

Gas chromatography-high resolution mass spectrometry methods were developed for quantifying nitrosodimethylamine (NDMA) and nitrosoproline (NPRO) in human urine. The limits of quantitation of these methods, which utilize stable isotope analogues of NDMA and NPRO as internal standards, were 5 pg per ml for NDMA and 0.14 ng per ml for NPRO. The assays were used to quantify NDMA and NPRO in urine samples collected 4 times a wk for 5 wk from 24 healthy volunteers. The mean urinary excretion of NDMA during this time was found to be 38.2 ng per day, and the mean urinary excretion of NPRO was found to be 3.26 micrograms per day. Treatment of the volunteers with 600 mg of ascorbic acid and 100 IU of alpha-tocopherol 4 times a day for the final 3 wk of the study did not influence the urinary excretion of NDMA or NPRO. Considerable person-to-person and day-to-day variations were observed for the urinary excretion of both nitrosamines, but the urinary excretion of NDMA was not correlated with the urinary excretion of NPRO. Person-to-person and day-to-day differences in the urinary excretion were greater for NPRO than for NDMA. The mean urinary excretion of NDMA by the 24 subjects was as much as 5-fold higher on some days than on other days, but this was not observed for NPRO. Day-to-day differences in the mean urinary excretion of NDMA were correlated with the concentrations of nitrogen dioxide in the air.

Adult↗
PubMed1985

Determination of acetyltrimoprostil and its metabolite trimoprostil in human or dog plasma by gas chromatography-negative-ion chemical ionization mass spectrometry.

A sensitive and specific procedure is described for the determination of the antisecretory prostaglandin acetyltrimoprostil and its metabolite trimoprostil in human or dog plasma using gas chromatography--negative-ion chemical ionization mass spectrometry (GC--NICI-MS). Trideuterated analogues of both compounds are added to plasma as the internal standards. The plasma is extracted at pH 7.3 with benzene--dichloromethane (9:1), and the residue of the organic extract is reacted at room temperature with pentafluorobenzyl bromide in the presence of 18-crown-6-ether and potassium acetate. The derivatives are reconstituted in heptane, and appropriate aliquots are analyzed by GC--NICI-MS with selected-ion monitoring of the intense (M--C6F5CH2)- fragment ions of acetyltrimoprostil (m/z 419), trimoprostil (m/z 377), and their respective trideuterated analogues (m/z 422 and m/z 380, respectively). Quantitation of an experimental plasma sample is based on a comparison of the m/z 419 versus m/z 422 and m/z 377 versus m/z 380 ion ratios in each sample to that obtained from the analysis of drug-free plasma fortified with various amounts of both protio compounds, and a fixed amount of each trideuterated internal standard. The limit of quantitation of the assay for human plasma is 0.2 ng ml-1 with mean relative standard deviations at this concentration of 15.5% and 9.7% for acetyltrimoprostil and trimoprostil, respectively.

Animals↗
PubMed1985

Neurocysticercosis: a new classification based on active and inactive forms. A study of 753 cases.

Cysticercosis of the central nervous system, because of the combination of inflammatory response, topography of lesions, degree of parasitic infestation, and sequelae of previous infestations produces a most variable clinical picture. The symptomatology may range from a discrete neurological disturbance to the most dramatic brain disorder. Severity of the disease, prognosis, and medical or surgical decision for treatment largely depend on the individual amalgam of the above-referred factors. An improved classification of neurocysticercosis (NCC) that delineates active from inactive forms of the disease will eventually be important in the research of immunodiagnosis and in therapeutic trials. In this report, a classification is presented that separates active from nonactive forms of NCC and is based on our experience with 735 patients studied. Characteristics of each form of NCC, frequency of principal signs and symptoms, and findings in cerebrospinal fluid analysis are discussed.

Adolescent↗
PubMed1982

Determination of (-)-threo-chlorocitric acid in human plasma by gas chromatography-positive chemical-ionization mass spectrometry.

A method is described for measuring (-)-threo-chlorocitric acid in human plasma. Plasma is acidified to pH 1 to minimize lactonization and a 13C analogue of (-)-threo-chlorocitric acid is added as internal standard. The acidified plasma is then extracted with ethyl acetate containing 10% methanol. The ethyl acetate-methanol extract is back-extracted with acetate buffer (pH 5). This extract, following adjustment to pH 1, is reextracted with ethyl acetate. The residue after removal of the ethyl acetate is treated with ethereal diazomethane. The wet residue is reconstituted in ethyl acetate and a portion of this solution is analyzed by gas chromatography-chemical ionization mass spectrometry. The mass spectrometer is set to monitor m/z 269 [MH+ of trimethylated (-)-threo-chlorocitric acid] and m/z 270 [MH+ of trimethylated (-)-threo-[13C]chlorocitric acid] in the gas chromatographic effluent. The m/z 269 to m/z 270 ion ratio in a sample containing an unknown amount of (-)-threo-chlorocitric acid is converted to an amount of compound using a calibration curve. The calibration curve is generated by analyzing control plasma spiked with various known amounts of (-)-threo-chlorocitric acid and a fixed amount of (-)-threo-[13C]chlorocitric acid. The limit of quantitation is 0.1-0.6 micrograms ml-1, depending on the characteristics of the calibration curve generated with each set of samples. The precision (relative standard deviation) at a concentration of 2 micrograms ml-1 is 3.3%.

Adult↗
PubMed1982

Determination of midazolam and two metabolites of midazolam in human plasma by gas chromatography--negative chemical-ionization mass spectrometry.

A method is described for measuring midazolam, a new anesthesia induction agent and hypnotic, and its hydroxymethyl and desmethyl metabolites in human plasma. Deuterated analogues of each compound are added to plasma as internal standards. The compounds are extracted from plasma with benzene containing 20% 1,2-dichloroethane and after removal of the extracting solvent are dissolved in a solution of bis-(trimethylsilyl)acetamide and acetonitrile. An aliquot of this solution is analyzed by gas chromatography--mass spectrometry with the mass spectrometer set to monitor in the gas chromatographic effluent the M.- ions of drug, metabolites and internal standards generated by methane electron-capture negative chemical ionization. For all three compounds, the limit of quantitation is 1 ng ml-1, and the precision (relative standard deviation) at a concentration of 5 ng ml-1 is less than 6%. Measurable amounts of the hydroxymethyl, but not the desmethyl, metabolite of midazolam could be found in the plasma of humans given either an intravenous or an oral dose of midazolam maleate.

Adult↗
PubMed1982

Determination of imidazobenzodiazepine-3-carboxamide, a new anxiolytic agent, in human plasma by gas chromatography--negative chemical-ionization mass spectrometry.

A method is described for measuring imidazobenzodiazepine-3-carboxamide, a new anxiolytic agent, in human plasma. A tetradeuterated analogue of the analyte is used as the internal standard. The drug and its internal standard are (1) extracted from plasma at pH 9 with benzene containing 20% 1,2-dichloroethane, (2) derivatized with pentafluoropropionic anhydride in the presence of triethylamine and (3) the nitrile derivative of the analyte and internal standard are analyzed by gas chromatography (GC)-negative chemical-ionization mass spectrometry (CIMS) using methane as both GC carrier gas and CI reagent gas. The mass spectrometer is set to monitor the intense (M-HCl)- ions of imidazobenzodiazepine-3-nitrile and its tetradeuterated analogue at m/z 316 and m/z 320, respectively. Quantitation of an experimental plasma sample is based on the comparison of the m/z 316 to m/z 320 ion ratio in each sample to that obtained from the analyses of control plasma spiked with various amounts of the drug and a fixed amount of internal standard. The limit of quantitation of the method is approximately 100 pg ml-1 of plasma and the precision (relative standard deviation) at a plasma concentration of 1 ng ml-1 is 4%.

Adult↗
PubMed1982

[Phenotyping Kell and Duffy antigens by a technic of coagglutination on the Groupamatic G 360].

By adapting the technique of coagglutination to the Groupamatic, we have developed an efficient rapid method of phenotyping donors for the Kell and Fya antigens. 340 specimens can be tested per hour; 800 tests can be performed with only 15 ml of antisera. Over 10,000 donor specimens were tested for Kell and 2,470 were simultaneously phenotyped for Fya. No false negatives were observed. The rate, of false positive results, due to autoagglutinins coating the donors' red cells, was the same as that seen with the continuous flow method. We conclude that this technique is suitable for routine use in screening donors for Kell and Fya antigens.

Autoanalysis↗
PubMed1981

High-performance liquid chromatographic determination of stereoselective disposition of carprofen in humans.

A high-performance liquid chromatographic (HPLC) assay was developed for the determination of the ratios of the (S)-(+) and (R)-(-) enantiomers of the anti-inflammatory drug carprofen in blood, urine, and feces. The procedure relies on: (a) extraction and purification of carprofen from biological fluids, (b) reaction of carprofen with (S)-(-)-alpha-methylbenzylamine to form the two diastereomeric (S)-(-)-alpha-methylbenzylamides via the 1,1'-carbonyldiimidazole intermediate, (c) purification of the reaction mixture by extraction of the diastereomeric derivatives into hexane at pH 11, and (d) analysis of the diastereomeric derivatives by HPLC with UV detection. The (S)-(+): (R)-(-) ratios in the blood of three subjects receiving single 100-mg oral doses of carprofen were greater than unity up to 16 hr after dosing. The mean +/- SD of the ratios in the early blood samples (0.5, 1, and 2 hr) was 1.21 +/- 0.09, while the mean of the ratios in the later blood samples (4,6,8,12, and 16 hr) was slightly higher (1.48 +/- 0.17). The blood level fall off curves for the (S)-(+) and (R)-(-) enantiomers were similar in each of the three subjects for the 4-16 hr period. The carprofen enantiomers were excreted stereoselectively by humans. An excess of the (S)-(+) enantiomer relative to the (R)-(-) enantiomer was excreted in the urine as the ester glucuronide, while unchanged (R)-(-) enantiomer predominated in the feces. The total urinary plus fecal excretion of the enantiomers (0-96 hr) revealed only a slight excess of the (S)-(+) enantiomer over the (R)-(-) enantiomer, which amounted to 2.1-49% of the dose. Since the amount of carprofen (free and glucuronide) excreted in 96 hr by the three subjects only accounted for 62-72% of the dose, no definitive statement could be made relative to the possible inversion of the carprofen chiral center.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1980

Metabolism of carprofen, a nonsteroid anti-inflammatory agent, in rats, dogs, and humans.

The metabolic disposition of 14C-labeled carprofen [(+/-)-6-chloro-alpha-methylcarbazole-2-acetic acid] was investigated in rats, dogs, and humans. Carprofen is eliminated predominantly by biotransformation in these three species. In dogs and rats, the direct conjugation of carprofen to form an ester glucuronide and oxidation to the C-7 and the C-8 phenols followed by their conjugation represent the major metabolic pathways. Small amounts of the alpha-hydroxy derivative also are formed by these species and are excreted free in the urine. In dogs, biliary secretion predominates, and 70% of an intravenous dose of carprofen is excreted in the feces while 8--15% of the dose is excreted in the urine. In rats, fecal excretion due to biliary secretion varies from 60 to 75%, and urinary excretion accounts for 20--30% of an intravenous dose. In humans direct conjugation of carprofen represents the only significant pathway of metabolism. Between 65 and 70% of the orally administered carprofen was found to be excreted as the ester glucuronide in the urine, and most of the remaining dose was estimated to be secreted as this metabolite in the bile. Due to enterohepatic circulation, only a fraction of the biliary metabolite was recovered in the feces in humans. Less than 5% of the dose was excreted in human urine as free, intact carprofen. In dogs and humans, plasma levels of carprofen and of total radioactivity exhibit a multiphasic decline. In the three human subjects studied, the terminal component declined with a 13--26 hr half-life; the terminal half-life was approximately 40 hr in dogs.

Adult↗
PubMed1980

Disposition of Dibekacin in patients undergoing haemodialysis.

The pharmacokinetics of Dibekacin were studied in 10 patients with terminal renal impairment (creatinine clearance < 5 ml/min) undergoing haemodialysis sessions lasting 4 h. The dialyzers were either the Gambro Lundia Major 13.5 or the Ultra Flo II 1.4., and the patients were divided into two groups according to the dialyzer used. Blood flow varied between 250 and 280 ml/min and dialyzate flow between 450 and 600 ml/min. All patients received a single i. v. dose of Dibekacin 1.5 mg/kg at the beginning of the dialysis session. The concentration of the antibiotic at the input and the output of the dialyzer were determine microbiologically by a plate diffusion method using B. subtilis as the test organism. The intravenously administered antibiotic followed an open two-compartment kinetic model. The type of dialyzer used did not influence the dialysis of Dibekacin. Haemodialysis significantly increased the elimination rate of the antibiotic with respect to the interdialysis periods. The plasma half-life in the slow disposition phase fell from 30 h in the interdialysis period to 4.0 h during dialysis sessions. From the calculated pharmacokinetic parameters, a dosage regimen for this kind of patient is proposed.

Adolescent↗