Expression of urokinase type plasminogen activator receptor (uPAR) in the bovine oviduct: Relationship with uPA effect on oviductal epithelial cells.

Urokinase type plasminogen activator (uPA) is an oviductal fluid component whose activity is regulated by binding to urokinase type plasminogen activator receptor (uPAR). In this study uPAR and uPA gene expression in bovine oviduct were evaluated and similar expression patterns for both uPAR and uPA mRNAs were observed during the estrous cycle. Immunolocalization of uPAR at the apical zone of epithelial cells suggests that uPA action would be focalized in the oviductal lumen, triggering intracellular signaling pathways. As uPAR expression was also observed in in vitro cultures of oviductal epithelial cells, the effect of uPA was explored using this culture model. Real-time RT-PCR demonstrated that c-fos expression in oviductal cell cultures increases under uPA stimulation. These results suggest that uPA/uPAR binding would be involved in signaling pathways that activate transcription factors and would regulate the synthesis of molecules concerned with the arrangement of a particular oviductal microenvironment.

The use of plasmid profile analysis and ribotyping for typing Acinetobacter baumannii isolates.

Plasmid profiles were used to analyse 39 Acinetobacter baumannii isolates from 36 patients at three hospitals. The isolates were prevously classified by biotyping and rDNA fingerprinting. Ribotyping was useful to establish the lineage of isolates and to confirm genospecies identification. Thirty-seven isolates (94.9%) contained plasmids. The variable number of plasmids with different molecular weights in each isolate enabled the identification of 13 profiles without the need for endonuclease digestion. Fifteen A. baumannii biotype 2 isolates of similar ribotype and antibiotype contained identical plasmids over a two-month outbreak at one hospital. Plasmid typing discriminated these isolates from sporadic A. baumannii isolates of close ribotype obtained from different hospitals. A few isolates of different lineage, however, showed similar plasmid profile. Our results suggest that plasmid typing is a practical method to assist infection control of nosocomial A baumannii. A combination of plasmid typing and ribotyping is suggested to confirm genospecies classification and to identify strains against reference band profiles.

The emergence of resistance to amikacin in Serratia marcescens isolates from patients with nosocomial infection.

Administration of either amikacin (1985) or gentamicin (1984, 1986-1991) as first-choice aminoglycoside did not decrease the high incidence of amikacin-resistant Serratia marcescens (ARSm) isolates responsible for nosocomial infections at the J.A. Fernández Hospital of Buenos Aires (42% in 1984, 31% in 1985 and 41% in 1987, differences not significant). In addition, a significant peak (P = 0.003) was detected in 1986, with an ARSm incidence of 70%. The incidence of ARSm decreased by 1988-1991 for reasons not related to aminoglycoside use. In the period 1984-1987 all S. marcescens isolates carried the 6'-aminoglycoside-acetyltransferase-Ic [aac(6')-Ic] gene, while in addition 20% of the isolates contained the plasmid-encoded 3'-aminoglycoside-phosphotransferase-VIa[aph(3')-VIa] and 2% the 6'-aminoglycoside-acetyltransferase-Ib [aac(6')-Ib] genes. From 1988 to 1992 resistance to amikacin was associated with only 4 ARSm isolates and correlated with the appearance of Tn1331-related sequences in these isolates. This transposon or related sequences, however, was not widely spread in the S. marcescens population under investigation. Combined use of restriction fragment length polymorphism (RFLP), ribotyping and plasmid profile analysis revealed that S. marcescens strains of the same genotype, including isolates either expressing or not the aac(6')-Ic gene, were involved in outbreaks occurring in May 1984, May 1985 and May 1986. Furthermore, these epidemiological tools permitted discrimination of different S. marcescens clones, each bearing a particular amikacin-resistance marker.

Adenosine infusion improves oxygenation in term infants with respiratory failure.

OBJECTIVES: Adenosine infusion causes selective pulmonary vasodilation in fetal and neonatal lambs with pulmonary hypertension. We investigated the effects of a continuous infusion of adenosine on oxygenation in term infants with persistent pulmonary hypertension of newborn (PPHN). DESIGN: A randomized, placebo-controlled, masked trial comparing the efficacy of intravenous infusion of adenosine to normal saline infusion over a 24-hour period. SETTING: Inborn and outborn level III neonatal intensive care units at a university medical center. PARTICIPANTS: Eighteen term infants with PPHN and arterial postductal PO2 of 60 to 100 Torr on inspired O2 concentration of 100% and optimal hyperventilation (PaCO2 <30 Torr) were enrolled into the study. Study infants were randomly assigned to receive a placebo infusion of normal saline, or adenosine infusion in doses of 25 to 50 microg/kg/min over a 24-hour period. PARTICIPANTS: Eighteen term infants with PPHN and arterial postductal PO2 of 60 to 100 Torr on inspired O2 concentration of 100% and optimal hyperventilation (PaCO2 <30 Torr) were enrolled into the study. Study infants were randomly assigned to receive a placebo infusion of normal saline, or adenosine infusion in doses of 25 to 50 microg/kg/min over a 24-hour period. RESULTS: Nine infants each received adenosine or placebo. The two groups did not differ in birth weight, gestational age, or blood gases and ventilaator requirements at the time of entry into the study. Four of nine infants in the adenosine group and none of the placebo group had a significant improvement in oxygenation, defined as an increase in postductal PaO2 of > or =20 Torr from preinfusion baseline. The mean PaO2 in the adenosine group increased from 69 +/- 19 at baseline to 94 +/- 15 during 50 microg/kg/min infusion rate of adenossine and did not change significantly in the placebo group. Arterial blood pressure and heart rate did not change during the study in either group. The need for extracorporeal membrane oxygenation, incidence of bronchopulmonary dysplasia, and mortality were not different in the two groups. CONCLUSION: Data from this pilot study indicate that adenosine infusion at a dose of 50 microg/kg/min improves PaO2 in infants with PPHN without causing hypotension or tachycardia. Larger trials are needed to determine its effects on mortality and/or need for extracorporeal membrane oxygenation in infants with PPHN.

Sequences related to Tn1331 associated with multiple antimicrobial resistance in different Salmonella serovars.

Serovars of Salmonella resistant to ampicillin, third-generation cephalosporins and aminoglycosides but sensitive to chloramphenicol, cefoxitin and ceftibuten emerged in one pediatric hospital of Buenos Aires. All isolates expressed AAC(6')-I and AAC(3)-V enzyme activities, making them resistant to all aminoglycosides marketed in Argentina by the time this investigation was performed. The cefotaxime resistance marker, the AAC(3)-V enzyme activity and Tn1331-related sequences were associated with plasmid DNAs from different Salmonella serovars.

An 8-year study of resistance to amikacin in gram-negative bacilli isolates from patients with nosocomial infection at one hospital in Argentina.

Administration of either gentamicin or amikacin induced an increase in the number of amikacin-resistant (AR) isolates of certain Enterobacteriaceae and Acinetobacter species in a hospital in Buenos Aires. A total of 127 AR isolates was selected to study the molecular mechanisms of resistance involved. The aac(6')-Ic gene was found by dot-blot hybridisation in every Serratia marcescens isolate. A gene different from aac(6')-Ia, aac(6')-Ib and aac(6')-Ic encoding the AAC(6')-I activity was found in a 15.5-kb plasmid in Acinetobacter spp. Plasmids from 27 Enterobacteriaceae contained and aac(6')-Ib gene and 26 of these carried sequences related to the Tn1331 transposon, whereas one Escherichia coli plasmid showed homology in another fragment of the Tn1331 transposase. Because plasmids bearing the aac(6')-Ib gene were heterogeneous, dissemination of the aac(6')-Ib gene may have been due to transposition of Tn1331 rather than the spread of an epidemic plasmid. The rate of AR isolates varied within each species in spite of the presence of Tn1331, and it is likely, therefore, that this transposon may not be the sole factor responsible for the observed variation. The aph(3')-VIa gene (originally described in Acinetobacter spp.) was found with high frequency (80%) in this Acinetobacter population. Furthermore, this gene was found also in plasmids from 20% of other gram-negative organisms commonly involved in nosocomial infections in this hospital.

Use of mammography in Jamaica: the Jamaica Cancer Society experience

This is a study of the number of patients seen at the Jamaica Cancer Society during the year 1993. It was shown that less than one per cent of Jamaican women over the age of 20 years use this service. A lack of knowledge as well as difficulty in accessing the service, e.g. distance, appears to be the main contributing factor for this deficiency.

Use of mammography in Jamaica: the Jamaica Cancer Society experience

This is a study of the number of patients seen at the Jamaica Cancer Society during the year 1993. It was shown that less than one per cent of Jamaican women over the age of 20 years use this service. A lack of knowledge as well as difficulty in accessing the service, e.g. distance, appears to be the main contributing factor for this deficiency. (AU)

An outbreak of multiply resistant Pseudomonas aeruginosa in a neonatal unit: plasmid pattern analysis.

An outbreak of infection due to multiply resistant Pseudomonas aeruginosa occurred from March to April 1986 in a neonatal unit. Affected neonates were receiving ventilation support and the mortality rate was high. Plasmid analysis and antibiograms indicated that the outbreak was due to a single strain. A survey of bacteria isolated from respirators, potable water and hands of personnel working in the unit failed to recover the outbreak strain. Lack of sterilization of respirators and overcrowding were considered to be the causes of the outbreak and reinforcement of the importance of aseptic techniques helped in its termination.