PubMed Health⌕ Search

Biomedical subjects

S Boros

Publications and source records attributed to S Boros.

At least 37 records · Page 2Linked to original sources

Predictors of survival in children with acquired immunodeficiency syndrome in Italy, 1983 to 1995.

To evaluate length and predictors of survival among children with AIDS, 529 pediatric cases diagnosed in Italy from 1983 to August 1995 were reviewed. Data were analyzed using Kaplan-Meier curves and the Cox proportional hazards regression model. Various survival patterns were subsequently analyzed. All survival analyses were truncated on March 1, 1996. Cases were examined by gender, age at diagnosis, HIV transmission category, type and number of the first AIDS-defining diseases, level of immunosuppression at AIDS diagnosis, HIV transmission category of the mother, and period of diagnosis. The overall median survival time was approximately 24 months. There wer no significant differences in survival by gender, HIV transmission category, mother's risk factor, or period of diagnosis. The Kaplan-Meier analysis showed the greatest differences in survival time between children less than 6 months of age at diagnosis (median survival 6.4 months) and all others (median 28.7 months). Children with recurrent bacterial infections or lymphoid interstitial pneumonia (LIP) had a survival time at least four times longer than those with Pneumocystis carinii pneumonia (PCP), mycobacteriosis, cytomegalovirus, tumors, or progressive multifocal leukoencephalopathy. At the multivariate analysis, the risk of death was lower among children with LIP (Relative Hazard [RH] 0.72) compared with other opportunistic diseases, whereas age less than 6 months, diagnosis of PCP or of two or more diseases, and severe immunosuppression at diagnosis increased the risk of death. Both demographic factors (age) and clinical factors (type and number of initial diseases, level of immunosuppression) were found to be independent predictors of a poor prognosis in children with AIDS. This information may be of use in improving prognosis and planning healthcare and treatment.

Acquired Immunodeficiency Syndrome↗

Synthesis of 4-cyanophenyl 1,5-dithio-beta-D-glucopyranoside and its 6-deoxy, as well as 6-deoxy-5-ene derivatives as oral antithrombotic agents.

Condensation of 5-thio-D-glucopyranose pentaacetate with 4-cyanobenzenethiol, in the presence of trimethylsilyl triflate, gave 4-cyanophenyl 2,3,4,6-tetra-O-acetyl-1,5-dithio-alpha-D-glucopyranoside 7 and 3,4,6-tri-O-acetyl-2,5-anhydro-5-thio-D-mannose bis(4-cyanophenyl) dithioacetal 9 in a 2:3 ratio. The latter is probably formed from the 4-cyanophenyl 2,3,4,6-tetra-O-acetyl-1,5-dithio-beta-D-glucopyranoside 6 via a transannular participation of the ring sulfur atom. When 2,3,4,6-tetra-O-acetyl-5-thio-alpha-D-glucopyranosyl bromide was used as donor and the reaction was carried out in the presence of potassium carbonate, 6, 7, 4-cyano-2-(2,3,4,6-tetra-O-acetyl-5-thio-alpha-D-glucopyranosyl)phenyl and 4-cyano-2-(2,3,4,6-tetra-O-acetyl-5-thio-beta-D-glucopyranosyl)phenyl 1,5-dithio-beta-D-glucopyranoside (14 and 16) were formed in a 23:4:2:1 ratio. The mechanism of formation of 14 and 16 is discussed. Condensation of 2,3,4,-tri-O-acetyl-6-deoxy-5-thio-alpha-D-glucopyranosyl bromide with 4-cyanobenzenethiol in the presence of potassium carbonate gave 4-cyanophenyl 2,3,4-tri-acetyl-6-deoxy-1,5-dithio-alpha- and beta-D-glucopyranoside (29 and 30) as well as 4-cyano-2-(2,3,4-tri-O-acetyl-6-deoxy-5-thio-alpha-D-glucopyranosyl)phen yl 2,3,4-tri-O-acetyl-6-deoxy-1,5-dithio-beta-D-glucopyranoside in a ratio of approximately 1:8:1. Compound 30 could be obtained in a higher overall yield using 2 as starting material and converting it via its 4-cyanophenyl 2,3,4-tri-O-acetyl-6-O-methanesulfonyl-1,5-dithio-beta-D-glucopyranoside derivative into the 4-cyanophenyl 2,3,4-tri-O-acetyl-6-deoxy-6-iodo-1,5-dithio-beta-D-glucopyranoside 33 which gave 30 on reduction with sodium borohydride-nickel(II) chloride. Treatment of 33 with silver acetate gave 4-cyanophenyl 2,3,4-tri-O-acetyl-6-deoxy-1,5-dithio-beta-D-xylo-hex-5-enopyranoside 35. The compounds obtained on deacetylation of 6, 9, 14, 30 and 35 showed a stronger oral antithrombotic effect in rats as compared to beciparcil, used as reference.

Administration, Oral↗

Synthesis of 4-cyanophenyl 4-azido-4-deoxy-1,5-dithio-beta-D-xylopyranoside.

L-Arabinose diethyl dithioacetal was converted, via its 4-azido-5-S-benzoyl-4-deoxy-2,3-O-isopropylidene-5-thio-D-xylose diethyl dithioacetal, into 4-azido-4-deoxy-5-thio-alpha-D-xylo-pyranose triacetate 29. Glycosidation of 29 with 4-cyanothiophenol in the presence of trimethylsilyl triflate gave the 4-cyanophenyl 2,3-di-O-acetyl-4-azido-4-deoxy-1,2-dithio-alpha- and -beta-D-xylopyranosides 31 and 33 as well as 3-O-acetyl-2,5-anhydro-4-azido-4-deoxy-5-thio-D-lyxose bis (4-cyanophenyl) dithioacetal 34 in a 8:2:1 respective ratio. Treatment of 29 with hydrogen bromide in acetic acid yielded a 1:4 mixture of 2,3-di-O-acetyl-4-azido-4-de-oxy-5-thio-D-xylopyranosyl bromide 38 and 2,3-di-O-acetyl-5-bromo-5-deoxy-4-thio-L-arabinofuranosyl bromide 40. Reaction of the mixture of bromides 38 and 40 with 4-cyanothiophenol in the presence of potassium carbonate afforded the expected 31 and 33 only in traces, while 2-(1R,2S,-1,2-di-O-acetyl-1,2-dihydroxy-but-3-en-1-yl)-5-cyano-1, 3-benzo-dithiole and 4-cyanophenyl 2,3-di-O-acetyl-5-S-(4-cyanophenyl)-1,4,5-trithio-alpha-L-ar abinofuranoside (42) were isolated in 18% and 20% yield, respectively. The formation of these two derivatives is tentatively explained by involvement of a radical reaction mechanism. When O-(2,3-di-O-acetyl-4-azido-4-deoxy-5-thio-alpha-D-xylopyranosyl) trichloroacetimidate was used as donor and boron trifluoride ethyl etherate as promoter, 31 and 33 were formed in excellent yield (96%) in a 2:1 ratio. The glycosides, obtained on deacetylation of 33, 34 and 42 showed a significant antithrombotic activity on rats.

Animals↗

Microbial conversion of mevinolin.

About 3000 microorganisms (bacteria, Actinomyces, Zygomyces, Deuteromyces) were screened for their capacity to convert mevinolin. Absidia coerulea IDR 705 was found to produce two hydroxylated derivatives of mevinolin, 2 and 3. Compound 2 is a new transformation product while compound 3 was described as a chemical modification product of mevinolin. By combination of spectroscopic techniques, the structures of 2 and 3 were identified with beta,delta-dihydroxy-7-(1,2-dihydro-2-hydroxymethyl-6-methyl-naphthal en-1-yl)-heptanoic acid delta-lactone and beta,delta-dihydroxy-7-[1,2,3,5,6,7,8,8a-octahydro-3,5-dihydroxy-2, 6-dimethyl-8-(2-methyl-butyryloxy)-naphthalen-1-yl]-hepta noi c acid delta-lactone, respectively. The inhibitory effects of the two derivatives on the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase were similar to that of mevinolin.

Animals↗

Synthesis of 6-deoxy-5-thio-D-glucose.

Three routes were investigated for the conversion of D-glucose into the title compound. In the first approach, reduction of the 5,6-thiirane ring of 5,6-dideoxy-5, 6-epithio-1,2-O-isopropylidene-alpha-D-glucofuranose (17) as well as that of its 3-O-allyl derivative (13) with lithium aluminium hydride was investigated; 17 afforded the corresponding 6-deoxy derivative besides di-, tri-, and poly-mers, whereas only polymers were formed from 13. In the second approach, the oxirane ring of 3-O-allyl-5,6-anhydro-1,2-O-isopropylidene-beta-L-idofuranose was reduced by sodium borohydride and the resulting 6-deoxy derivative was converted into the 5-thiobenzoate; the corresponding hex-4-enofuranose was formed as a byproduct. In the third approach partial mesylation of methyl 5-thio-alpha-D-glucopyranoside was attempted, but the 6-mesylate 27 could be isolated only in modest yield (28%) together with rearranged 2,5-thioanhydromannofuranoside derivatives. The mechanism of this rearrangement is discussed in detail. The 6-mesylate 27 was converted via the 6-iodo derivative into the title compound.

Aluminum Compounds↗

One-year follow-up evaluation of 260 premature infants with respiratory distress syndrome and birth weights of 700 to 1350 grams randomized to two rescue doses of synthetic surfactant or air placebo. American Exosurf Neonatal Study Group I.

A multicenter, randomized, double-blind, placebo-controlled trial of synthetic surfactant therapy for premature infants with respiratory distress syndrome (RDS) and birth weights of 700 to 1350 gm demonstrated a reduction in severity of RDS, morbidity, and neonatal and 1-year mortality. Of the 419 infants who were entered in the study, 80% of the surviving infants in both the air placebo group (122) and the synthetic surfactant group (138) returned for the follow-up evaluation at 1-year adjusted age. The only significant difference observed at follow-up was a reduction in the incidence of mild cerebral palsy in the synthetic surfactant group (air placebo group, 8 of 122 (7%); synthetic surfactant group, 3 of 138 (2%); relative risk 0.306; 95% confidence interval 0.094, 0.999). No differences were observed between the air placebo and synthetic surfactant treatment groups with respect to health status of the infants, including the incidence of retinopathy of prematurity and neurodevelopmental delays. The difference in the overall incidence of impairment among the 1-year survivors in the air placebo group (43 of 122 (35%)) and in the synthetic surfactant group (40 of 138 (29%)) was not statistically significant. The results of this 1-year follow-up study show that rescue treatment with synthetic surfactant in infants weighing 700 to 1300 gm is not associated with adverse developmental consequences despite the improvement in survival.

Air↗

Retrospective search for bleeding diathesis among premature newborn infants with pulmonary hemorrhage after synthetic surfactant treatment. The American Exosurf Neonatal Study Group I, and the Canadian Exosurf Neonatal Study Group.

In an across study analysis of five multicenter, placebo-controlled trials of the synthetic surfactant, Exosurf Neonatal, involving infants with birth weights 700 gm or greater the incidence of clinical pulmonary hemorrhage was 1.9% in treated infants and 1.0% in control infants. To determine whether this apparent increase in pulmonary hemorrhage was the result of a bleeding diathesis, we retrospectively reviewed charts for 39 of 41 infants with clinical pulmonary hemorrhage. The incidence of nonpulmonary bleeding was the same in control- and surfactant-treated infants. Platelet counts, hematocrit values, and the number of transfusions with platelets or red blood cells did not differ between the two groups. There was no evidence that surfactant treatment was specifically associated with a generalized bleeding diathesis.

Double-Blind Method↗

Prediction of digoxin treatment failure in infants with supraventricular tachycardia: role of transesophageal pacing.

Transesophageal atrial pacing was used to initiate and terminate tachycardia in 24 infants (seven female and 17 male, aged 1 to 34 days) with ECG documentation of supraventricular tachycardia. Six infants received no chronic treatment, and chronic oral digoxin prophylaxis was administered to 18 infants in an effort to prevent recurrences of tachycardia. In these 18 infants, the effectiveness of digoxin therapy in preventing the initiation of tachycardia by transesophageal pacing was compared with its ability to prevent spontaneous recurrences of supraventricular tachycardia. While receiving chronic oral digoxin therapy, tachycardia could be reinitiated in 15/18 (83%) infants. In these infants, the cycle length of tachycardia and the atrioventricular interval were the same before and during chronic digoxin treatment. Three infants in whom tachycardia could not be initiated during chronic digoxin therapy had no spontaneous recurrences during 6 months of follow-up, whereas 10/15 (67%) infants in whom tachycardia could be reinitiated had clinically significant recurrences in spite of chronic digoxin therapy. Six infants who received no chronic drug treatment had no documented recurrences during 6 months of follow-up. This study demonstrates that digoxin was effective in preventing significant spontaneous recurrences of supraventricular tachycardia in only 8/18 (44%) infants treated with digoxin. The ability to initiate supraventricular tachycardia with transesophageal pacing may be useful in determining which digoxin-treated infants are at risk for recurrence. Finally, not all infants with supraventricular tachycardia require chronic prophylaxis; six of the untreated infants had no documented recurrences.

Atrioventricular Node↗

CO2 responses in infants: on-line display and analysis using a microcomputer and waveform analyzer.

This report describes a new system for measuring and recording ventilatory responses to inspired CO2 in infants, which consists of a nasal pneumotach, microcomputer, and a waveform analyzer. The waveform analyzer measures ventilatory responses on-line and displays them in real-time, breath-by-breath. Thirty-two ventilation studies were performed in 24 normal, full-term infants (3-300 days of age). The mean ratio of delta VE/ delta PACO2 was 44.3 +/- 22.9 (SD) ml/kg X min X mm Hg BTPS (range 15.0-121.2). We believe this new system is a significant improvement over previous methods for measuring and recording ventilatory responses of infants.

Carbon Dioxide↗

Neonatal high-frequency jet ventilation.

Ten neonates with intractable respiratory failure were treated with high-frequency jet ventilation (HFJV). Nine had progressive pulmonary air leaks with either bronchopleural fistulas or pulmonary interstitial emphysema as the primary cause of their respiratory failure. Following HFJV, x-ray film evidence of pulmonary air leaks decreased in seven of the nine neonates. PaO2/FIO2 increased in eight of the ten patients (P less than .05), and PaCO2 values decreased in nine of the ten patients (P less than .01). Five patients survived. Three of the six patients exposed to HFJV for more than 20 hours developed significant tracheal obstruction. From this experience, it may be concluded that HFJV can successfully ventilate certain neonates with intractable respiratory failure secondary to progressive pulmonary air leaks. In its present form, long-term neonatal HFJV carries a risk of airway obstruction and/or damage.

Airway Obstruction↗