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R Porat

Publications and source records attributed to R Porat.

43 records · Page 3Linked to original sources
PubMed1987

Selective pressures and lipopolysaccharide subunits as determinants of resistance of clinical isolates of gram-negative bacilli to human serum.

Differences in molecular composition of lipopolysaccharides (LPS) between serum-sensitive (S) clinical isolates of Escherichia coli and serum-resistant (R) clones derived by serial passage in serum were demonstrated to determine sensitivity or resistance to killing by normal human serum (NHS). LPS from R clones had a greater proportion of higher-molecular-weight, more highly O-antigen-substituted subunits than LPS from their serum S parents. Utilization of a liposomal model with inserted LPS simulating bacterial cell walls established LPS as the site of serum bactericidal action. Liposomes containing S LPS were lysed, while liposomes containing R LPS were unaffected by NHS. R and S LPS were fractionated into higher (F1)- and lower (F2)-molecular-weight fractions. Liposomes containing R LPS or the F1 fraction of S and R LPS were not lysed by serum. Liposomes containing the F2 fraction of S or R LPS were lysed by serum analogous to that observed with liposomes containing intact S LPS. These findings establish LPS to be one site of serum bactericidal activity and demonstrate that the higher-molecular-weight, highly O-antigen-substituted LPS subunits mediate resistance to killing by NHS.

Bacteriolysis↗
PubMed1987

Tuberculosis in a general hospital: high incidence of extrapulmonary disease.

Twenty six patients with tuberculosis were admitted between 1979 and 1982 to the Tel Aviv Medical Center. Most were immigrants from Eastern Europe. In contrast to previous studies, patients were relatively young (mean age 57 years) and lacked predisposing medical illness. Eighteen (69%) had extrapulmonary infections, half of which involved the genitourinary tract. Two instances of miliary tuberculosis were diagnosed at autopsy.

Adult↗
PubMed1986

Ventricular septal thickness and cardiac function in neonates after in utero ritodrine exposure.

Cardiac septal hypertrophy occurs after in utero ritodrine exposure. To assess the effect of septal hypertrophy on cardiac function we obtained M-mode echocardiograms on day 1 of life in 41 infants exposed to ritodrine and 22 control infants matched for gestational age. Mean duration of ritodrine exposure was 16.2 +/- 13.2 days (range 1 to 49 days). Disproportionate septal hypertrophy (DSH) was defined as an interventricular septal thickness/posterior wall thickness ratio (ST/PW) of greater than 1.3. Infants exposed to ritodrine in utero had DSH and increased right systolic time intervals compared with control values (P less than 0.05). A subgroup, those infants exposed for 2 weeks or longer, had not only DSH but also an absolute increase in septal thickness compared with control infants and infants exposed to ritodrine for less than 2 weeks. ST/PW correlated well with the duration of ritodrine exposure (r = 0.96); the longer the exposure the thicker the septum. Although all echocardiographic changes lasted for less than 3 months, we have no information regarding the effect on the fetus of maternal ritodrine exposure for longer than 7 weeks. Until such information is available, cardiac evaluation is recommended in neonates exposed to ritodrine in utero for longer than 7 weeks.

Cardiomyopathy, Hypertrophic↗
PubMed1985

Relationship of prolonged pharmacologic serum levels of vitamin E to incidence of sepsis and necrotizing enterocolitis in infants with birth weight 1,500 grams or less.

The incidence of culture-proven neonatal sepsis and necrotizing enterocolitis (NEC) in preterm infants maintained at pharmacologic (mean 5.1 mg/dL +/- 1.45 SD) serum vitamin E levels for long periods was prospectively studied as part of a double-masked clinical trial of the effect of prophylactic vitamin E v placebo treatment on the development and course of retinopathy of prematurity (ROP). Within a few days of birth, 914 preterm infants were enrolled in the study; 545 (275 placebo-treated infants, 270 vitamin E-treated infants had birth weight of 1,500 g or less. A significant difference in incidence of neonatal sepsis (17 placebo-treated infants, 37 vitamin E-treated infants) and NEC (18 placebo-treated infants, 32 vitamin E-treated infants) was observed among infants who had been treated for eight or more days and who had developed neither sepsis nor NEC before that time. The association of vitamin E treatment with increased incidence of disease was much higher with sepsis than with NEC. The most likely reason for these observations is a pharmacologic serum vitamin E-related decrease in oxygen-dependent intracellular killing ability which results in a decreased resistance to infection in preterm infants. The data suggest that, if this occurs, it is clinically significant only in the more immature infants. In view of the known variability of absorption of oral vitamin E and the association between high serum vitamin E levels and increased incidence of sepsis and late-onset NEC reported here, it can be concluded that serum vitamin E levels must be monitored when supplemental vitamin E is administered to premature infants, especially those with birth weight 1,500 g or less. The risk-benefit ratio of long-term treatment using vitamin E at high serum levels should be clearly assessed.

Administration, Oral↗
PubMedDate not supplied

The effects of maternal magnesium sulfate treatment on newborns: a prospective controlled study.

OBJECTIVE: To evaluate the effects of maternal magnesium sulfate treatment on newborn outcome. METHODS: Subjects were newborn infants delivered at > or = 34 weeks of gestation whose mothers received a minimum of 12 hours of intravenous MgSO4 therapy before delivery. Control infants were the next born infants of similar gestational age. Outcome recorded at delivery included Apgar scores, whether resuscitation was required, and whether respiratory depression or decreased tone were noted by the physician in attendance. Pneumocardiograms on magnesium-exposed and control infants, obtained within 6 to 18 hours after delivery, were analyzed postdischarge by a single investigator who was blinded to group. The nursery course, feeding patterns, time to first stool, and time to first void were recorded. All patient care decisions, including admission to the neonatal intensive care unit (NICU) or term nursery, were independent of study protocol. RESULTS: A total of 26 magnesium-exposed and 26 control infants were enrolled. The mean total dose of MgSO4 before delivery was 51.2+/-24 gm; the mean duration of therapy was 23.1+/-10 hours. The mean maternal serum magnesium level before delivery was 5.8+/-1.1 mg/dl. The infants' mean cord or initial serum magnesium level was 5.2+/-1.0 mg/dl, which correlated with the maternal magnesium level before delivery (r=0.81, p < 0.001). MgSO4-exposed infants had a higher incidence of hypotonia and lower median Apgar scores than control infants (p < 0.001). However, there was no association between adverse outcomes and maternal serum magnesium concentrations at delivery, duration of treatment, or dose of MgSO4. No difference in dose or length of maternal MgSO4 treatment was noted between infants admitted to term nursery and those admitted to NICU. Pneumocardiogram data were similar between MgSO4-exposed and control infants (all p > or = 0.16). There were no significant differences in number of episodes of feeding intolerance or in time to first stool or void between MgSO4-exposed and control infants (all p > or = 0.31). CONCLUSION: Infants born to mothers treated with MgSO4 were more likely to be hypotonic and have lower Apgar scores at birth. Beyond the immediate postdelivery period, there were no additional complications in this cohort attributable to prenatal MgSO4 exposure. We suggest that pediatricians attend deliveries of magnesium-exposed infants.

Apgar Score↗