A US-based national surveillance study for the susceptibility and epidemiology of Clostridioides difficile isolates with special reference to ridinilazole: 2020-2021.

We have previously reported on the susceptibility and epidemiology of Clostridioides difficile isolates from six geographically dispersed medical centers in the United States. This current survey was conducted with isolates collected in 2020-2021 from six geographically dispersed medical centers in the United States, with specific attention to susceptibility to ridinilazole as well as nine comparators. C. difficile isolates or stools from patients with C. difficile antibiotic-associated diarrhea were collected and referred to a central laboratory. After species confirmation of 300 isolates at the central laboratory, antibiotic susceptibilities were determined by the agar dilution method [M11-A9, Clinical and Laboratory Standards Institute (CLSI)] against the 10 agents. Ribotyping was performed by PCR capillary gel electrophoresis on all isolates. Ridinilazole had a minimum inhibitory concentration (MIC) 90 of 0.25 mcg/mL, and no isolate had an MIC greater than 0.5 mcg/mL. In comparison, fidaxomicin had an MIC 90 of 0.5 mcg/mL. The vancomycin MIC 90 was 2 mcg/mL with a 0.7% resistance rate [both CLSI and European Committee on Antimicrobial Susceptibility Testing (EUCAST) criteria]. The metronidazole MIC 90 was 1 mcg/mL, with none resistant by CLSI criteria, and a 0.3% resistance rate by EUCAST criteria. Among the 50 different ribotypes isolated in the survey, the most common ribotype was 014-020 (14.0%) followed by 106 (10.3%), 027 (10%), 002 (8%), and 078-126 (4.3%). Ridinilazole maintained activity against all ribotypes and all strains resistant to any other agent tested. Ridinilazole showed excellent in vitro activity against C. difficile isolates collected between 2020 and 2021 in the United States, independent of ribotype.

Analysis of labeling and clearance of lung surfactant phospholipids in rabbit. Evidence of bidirectional surfactant flux between lamellar bodies and alveolar lavage.

Turnover and clearance of lung surfactant phospholipids were studied with particular reference to myoinositol-induced perturbation in the acidic phospholipids. Administration of myoinositol decreased [(3)H]palmitate and [(32)P]phosphate incorporation into phosphatidylglycerol by 80-90% in whole lung, and by 94-99% in lamellar bodies and in alveolar lavage. The increased incorporation of radioactive isotopes into phosphatidylinositol following myoinositol, was inverse to the decrease in phosphatidyl-glycerol incorporation. Myoinositol treatment affected neither content nor labeling of phosphatidylcholine or disaturated phosphatidylcholine as studied within 50 h of administration. Phosphatidylglycerol was pulse labeled by intravenous [(32)P]phosphate and [(3)H]palmitate, followed by myoinositol. The biological half-lives of phosphatidylglycerol in the microsomal fraction, lamellar bodies, and alveolar lavage were 1.6, 4.6, 5.4 h (with (3)H), and 2.8, 6.5, 7.0 h (with (32)P), respectively.(32)P-labeled lung surfactant tracer was applied to the airways in saline suspension and the clearance of phospholipid radioactivity was measured in alveolar lavage, alveolar macrophages, lamellar bodies and lung homogenates. The clearance rates of phosphatidylcholine, disaturated phosphatidylcholine, phosphatidylglycerol, and phosphatidylinositol as studied in whole lung over 6 h were 3.4-5.8% h. Only a small amount of phospholipid radioactivity was recovered in the alveolar macrophage fraction (including bis-[monoacylglycerol]phosphate). Phospholipid radioactivity in alveolar lavage fell to 40-70% of the maximum during the 1st h, and to 5-18% over the next 6 h. During 2 h after the application of phospholipids, the radioactivity in the lamellar body fraction increased, and the specific radioactivities approached those in alveolar lavage. The association of phosphatidylglycerol with lamellar bodies was unaffected by myoinositol. Phosphatidylinositol entered more slowly than did phosphatidylglycerol from microsomes to the alveolar lavage fraction, and from alveolar lavage to lamellar bodies. These differences may be of importance regarding the poor performance of phosphatidylinositol-containing surfactant at birth. Further investigations are needed to clarify the possible role for the postulated bidirectional surfactant flux between the lamellar body and alveolar lavage fractions in maintaining the activity of surfactant.

Evidence of lung surfactant abnormality in respiratory failure. Study of bronchoalveolar lavage phospholipids, surface activity, phospholipase activity, and plasma myoinositol.

Autopsy findings suggest that lung surfactant is damaged in the adult respiratory distress syndrome. In the present study 225 bronchoalveolar lavage specimens (78 from 36 patients, 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease, and 12 from healthy controls) were assayed for the lung profile [lecithin/sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol, and phosphatidylglycerol]. Bronchoalveolar lavage fluid was further analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2, and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity, and plasma was measured for myoinositol. There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. However, in respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the LO/S ratio, phosphatidylglycerol, and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure and tended to normalize during recovery. Low L/S ratio (less than 2), and low phosphatidylglycerol (1% or less of glycerophospholipids) in bronchoalveolar lavage was always associated with respiratory failure. Abnormal lavage phospholipids were not due to plasma contamination. The phospholipase studies revealed little evidence of increased catabolism of phospholipids. In respiratory failure, the lipid-protein complexes from lung lavage were not surface active, whereas that from healthy controls had surface properties similar to lung surfactant. Phospholipids from patients with respiratory failure were similar to those from respiratory distress syndrome in the newborn. However, the latter condition is characterized by fast recovery of surfactant deficiency and by high plasma myoinositol that suppresses the synthesis of surfactant phosphatidylglycerol and increases phosphatidylinositol (Pediatr. Res. 1981. 15: 720). On the other hand, in adult respiratory distress syndrome, the abnormality in surfactant phospholipids may last for weeks and in most cases is associated with low phosphatidylinositol, low phosphatidylglycerol, and low plasma myoinositol.

Elastase and alpha 1-proteinase inhibitor activity in tracheal aspirates during respiratory distress syndrome. Role of inflammation in the pathogenesis of bronchopulmonary dysplasia.

Pulmonary effluent samples were obtained from 26 preterm or term infants throughout the period of endotracheal intubation. Infants with respiratory distress syndrome, infants with this disorder developing bronchopulmonary dysplasia, and intubated infants without lung disease were compared daily in terms of lung effluent cellularity, albumin, elastase activity, alpha 1-proteinase content and activity, and elastase inhibitory capacity. The elastase activity was determined to be neutrophilic in origin. Polyacrylamide gel electrophoresis of pulmonary effluents from two infants with respiratory distress syndrome and exposed to FiO2 greater than or equal to 0.6 up to 6 d revealed cleavage of alpha 1-proteinase inhibitor to a 47,000-mol weight fragment suggestive of oxidation. Pulmonary effluent neutrophils, macrophages, and elastase activity were increased by day 3 of life in infants with respiratory distress syndrome eventually developing bronchopulmonary dysplasia. Elastase inhibitory capacity and alpha 1-proteinase inhibitor activity were reduced in infants developing chronic lung disease. Bronchopulmonary dysplasia developed in infants with enhanced inflammatory response, but with less or inhibited antiprotease activity.

Phosphatidylglycerol in lung surfactant. II. Subcellular distribution and mechanism of biosynthesis in vitro.

Lamellar inclusion bodies, apparent precursors for alveolar surfactant lining, have remarkably similar phospholipid composition to surfactant from alveolar lavage, but distinctly different from other fractions studied: mitochondria, microsomal fraction containing endoplasmic reticulum membranes, plasma membranes and nuclei. Surfactant contained (as % of total phospholipid phosphate): 75.5-77.0% lecithin, 11.0-11.2% phosphatidylglycerol, 4.2-4.6% phosphatidylethanolamine, 3.0-3.2% phosphatidylinositol, 1.5-1.7% bis-(monoacylglycerol) phosphate, 1.2-1.9% phosphatidylserine, and 0.7-1.5% sphingomyelin. Fatty acids of phosphatidylglycerol from lamellar bodies were similar to those from microsomes but different from those in mitochondria. Lung homogenate in continuous sucrose density gradient displayed two major activity peaks of phosphatidylglycerol synthesis: the heavier from mitochondria; the lighter from endoplasmic reticulum. Studies on mechanism of phosphatidylglycerol synthesis in vitro revealed (in these two fractions) CDP-diglyceride and sn-glycerol phosphate precursors to phosphatidylglycerol phosphate, that hydrolysed to phosphatidylglycerol. In microsomes disaturated CDP-diglycerides were 1.6-1.9 times more active substrates than in mitochondria, whereas CDP-diglycerides from egg lecithin were almost equally active. In contrast to lung mitochondria no cardiolipin synthesis was detected in microsomes. The highest specific activities for phosphatidate cytidyltransferase, CDP-diglyceride-inositol phosphatidyltransferase, choline phosphotransferase, and phosphatidylethanolamine methyltransferase were all found in microsomes. The present in vitro studies and additional evidence (M. Hallman and L. Gluck, (1975) Fed. Proc. 34, 274) support the hypothesis that de novo synthesis of surfactant lecithin phosphatidylinositol and phosphatidylglycerol takes place in the endoplasmic reticulum of alveolar cells.

Interferon alfa-2a in advanced renal cell carcinoma: treatment results and survival in 159 patients with long-term follow-up.

PURPOSE: Three trials were conducted to define the efficacy and toxicity of interferon alfa-2a in the treatment of metastatic renal cell cancer. Univariate and multivariate analyses were performed to identify prognostic factors for survival. PATIENTS AND METHODS: Prospectively, 159 patients were treated with interferon alfa-2a. In the first trial, 42 patients received 50 x 10(6) U/m2 intramuscularly three times per week. In the second trial, 64 patients received gradually escalating doses of interferon alfa-2a from 3 to 36 x 10(6) U subcutaneously administered daily. The third trial was randomized; 25 patients received daily interferon alfa-2a alone and 28 were treated with daily interferon alfa-2a and 0.15 mg/kg vinblastine every 3 weeks. RESULTS: The overall response proportion was 10% (two complete and 14 partial responses). The median response duration was 12.2 months. The median survival duration was 11.4 months, with 3% of patients alive at 5 or more years. A univariate statistical analysis showed that a Karnofsky performance status > or = 80, prior nephrectomy, and interval from diagnosis to treatment of longer than 365 days were significant prognostic factors for survival. In a multivariate analysis, only prior nephrectomy and Karnofsky performance status > or = 80 were shown to be independent predictors of survival. CONCLUSION: Interferon alfa-2a had minimal antitumor activity in patients with advanced renal cell carcinoma and long-term survival was achieved in a small proportion of patients. The need for continued investigation and the identification of more effective therapy for advanced renal cell carcinoma is evident from the poor overall survival rate observed in these 159 patients. The investigation of new agents and of interferon alfa-2a in combination with other agents remains a priority.

Diagnosis and follow-up of intraventricular and intracerebral hemorrhages by ultrasound studies of infant's brain through the fontanelles and sutures.

A technique to diagnose subependymal hemorrhage (SEH), intraventricular hemorrhage (IVH), intracerebral hemorrhage, and posthemorrhage hydrocephalus in tiny infants, using real time ultrasound studies of the brain ventricular system, is described. This is a bedside technique that visualizes the brain through the fontanelles and the sutures, in three planes: coronal, sagittal, and horizontal. Excellent visualization of the ventricular system, caudate nuclei, the thalamus, the choroid plexus, the corpus callosum, and the foramen of Monro is obtained. This method has good definition using high frequency transducers since there is no bone interference. The ultrasound diagnosis correlated well with computed tomography (CT) and with direct pathologic studies. This technique was more sensitive in diagnosing small IVH/SEH and organized clots than were CT studies. IVH/SEH were found in 90% of 113 infants less than or equal to 34 weeks of gestation; 49% of the hemorrhages were large and 41% were small. Most hemorrhages were found in the first scan, usually shortly after birth. Twenty-one premature infants who never had perinatal asphyxia or respiratory distress syndrome had IVH/SEH. The hemorrhages were followed until disappearance, usually in one to three months in cases of large hemorrhages.

Tc-99m HIDA scintigraphy in segmental biliary obstruction.

Segmental biliary obstruction as a result of primary or secondary hepatic malignancy has been reported with increasing frequency. For two representative patients, the clinical and Tc-99m HIDA scintigraphic findings in segmental biliary obstruction are described. The presence of photon-deficient dilated bile ducts in one segment of the biliary tree is highly suggestive of localized biliary obstruction and should be considered in the patient with suspected or proven hepatic malignancy despite the absence of jaundice.

Radiotoxicities of [3H]thymidine and of [3H]arginine compared in mouse embryos in vitro.

Tritium that is bound to organic molecules is of special risk for living systems, in particular when such molecules are components of the cell nucleus. Therefore, [3H]thymidine and [3H]arginine were studied for radiotoxicity in early mammalian embryo development. Starting with the two-cell stage, mouse embryos were incubated in vitro with [3H]thymidine or [3H]arginine at either 370 Bq/ml (10 nCi/ml) or 925 Bq/ml (25 nCi/ml). Development in vitro was followed up to the formation of the inner cell mass at 192 h postconception (p.c.). There was no difference in radiotoxicity of the two substances with respect to cell proliferation; however, formation of blastocysts, hatching of blastocysts, trophoblast outgrowth, and formation of inner cell mass were impaired more strongly by [3H]arginine than by [3H]thymidine when the external exposure concentrations were the same. Similarly, micronuclei were seen in blastocysts at 96 h p.c. at higher frequency after incubation with [3H]arginine. However, uptake of [3H]arginine by the embryos was considerably faster than that of [3H]thymidine, and this most probably accounts for the apparent difference in radiotoxicity.

Hypoxanthine: a marker for asphyxia.

It has been hypothesized that hypoxanthine concentrations in the blood of newborn infants are a marker of asphyxia. To test this hypothesis, we measured serum hypoxanthine levels in relationship to perinatal and neonatal asphyxia, and compared arterial hypoxanthine levels with arterial pH and base deficit. We also compared hypoxanthine levels of survivors with those of asphyxiated non-survivors. Forty-two newborns were classified as asphyxiated by either of two methods: 1) Infants from whom umbilical cord hypoxanthine levels were taken were classified as asphyxiated if they had an Apgar score of 6 or less at 1 or 5 minutes, fetal heart rate below 100 beats per minute, or meconium-stained amniotic fluid; and 2) infants from whom peripheral arterial hypoxanthine samples were taken were classified by clinical assessment, whereby one author, blinded to the infants' hypoxanthine levels, prospectively assessed each patient's condition for evidence of asphyxia. Hypoxanthine levels correlated with increased base deficit (P less than .001; r = 0.8) and with decreased pH (P less than .001; r = -0.5). By both of our asphyxia classification methods, hypoxanthine levels were significantly higher (P less than .002) in the asphyxiated groups. We also noted a higher hypoxanthine level in asphyxiated non-survivors as compared with all survivors (P less than .02). We propose that serum hypoxanthine levels may help define asphyxia. Because hypoxanthine, when metabolized by xanthine oxidase, generates oxygen radicals that are highly destructive to tissue, hypoxanthine levels may have important therapeutic implications for asphyxiated patients.

Premature labor. I. Prostaglandin precursors in human placental membranes.

Amnion and chorion from premature and term placentas after both spontaneous labor and elective cesarean section were assayed for phospholipids and fatty acid composition by 2-dimensional thin-layer chromatography and gas-liquid chromatography. In preterm placental phospholipids, phosphorus concentrations were higher in amnion than in chorion, whereas at term the membranes were similar owing to an increase in phospholipid concentration in the chorion late in gestation. PHosphatidylcholine (PC) accounted for 47% of the total phospholipid phosphorus, followed by sphingomyelin at 20%, phosphatidylethanolamine (PE) at 15%, phosphatidylserine (PS) at 12%, and phosphatidylinositol (PI) at 5%. These percentages were similar for amnion and chorion and they did not change during gestation. The percentage of arachidonic acid (AA) was higher in PS (40 to 65%) than in PE (30 to 53%) and PC (10 to 13%). The percentage of AA was significantly higher in PC, PE, and PS from the amnion in premature pregnancies than in those of the premature chorion. At term, these amnionic and chorionic phospholipids had similar concentrations of AA owing to a significant increase in AA in the chorion late in gestation. Amnionic PE from term and preterm elective cesarean section had a significantly higher percentage of AA than that from preterm and term labor. These data suggest that AA is consumed during labor and that amnionic phospholipids, particularly PE, may be its principal source. The amnion seems to be more important for the storage of AA than the chorion, particularly in preterm pregnancies in which the concentrations of phospholipids and the percentages of AA in PC, PE, and PS were significantly higher than in the chorion.

Premature labor. II. Bacterial sources of phospholipase.

Human term labor is thought to be initiated by amniotic and chorionic phospholipase A2, an enzyme that liberates arachidonic acid esters from the phospholipids of these membranes, leading to the synthesis of prostaglandins by the placental membranes. The striking association of premature labor with intrauterine infection or contamination, urinary tract infection, and early neonatal sepsis led us to study the microorganisms present in these infections for phospholipase A2 activity. Activity was found in Bacteroides fragilis, Peptostreptococcus, Fusobacterium necrophorum, Streptococcus viridans, Streptococcus fecalis, Streptococcus A and B, Escherichia coli, Klebsiella, Staphylococcus epidermidis, Pneumococcus, Lactobacillus, and Mycoplasma hominis. Bacteroides fragilis, Peptostreptococcus, Fusobacterium, and S viridans had the highest activities. The specific activities of phospholipase A2 from these organisms were several times higher than that of the membrane phospholipase A2 of the amnion and chorion. We postulate that premature labor may be initiated by microorganisms with phospholipase A2 activity from endocervical and/or intrauterine contamination or infection, producing deacylation of arachidonic acid from amniotic phospholipids with increased concentrations of free arachidonic acid and increased prostaglandin synthesis, which triggers labor.

Lung profile: sex differences in normal pregnancy.

The incidence of respiratory distress syndrome (RDS) is higher in male than in female infants. The lung profiles--lecithin/sphingomyelin (L/S) ratios, percent disaturated (acetone precipitated) lecithin, phosphatidylglycerol, and phosphatidylinositol--were obtained in amniotic fluid during 164 normal pregnancies of 30 or more weeks' gestation. The profiles were evaluated to determine any sex differences in fetal development of the surfactant components. According to regression analysis the L/S ratios for females reached 2:1 at 33.7 weeks, which is 1.4 weeks earlier than males. A similar trend was evident for disaturated lecithin. Phosphatidylglycerol first appeared at 34 weeks' gestation for females and 35 weeks for males. The rate of the increase in phosphatidylglycerol was higher in females than in males. Phosphatidylinositol began to decrease after 36 weeks for females and fell to levels below that of males after 37 weeks' gestation. All four indexes of the lung profile revealed a higher degree of lung maturity in female than in male fetuses during the last two months of normal pregnancy. This explains a higher incidence of RDS in male than in female infants.

Changes in the lecithin:sphingomyelin ratio during labor and the associated fetal heart rate patterns.

Serial samples of amniotic fluid were taken from 38 patients in spontaneous labor and the lecithin:sphingomyelin (L:S) ratios were estimated. The fetal heart rate (FHR) pattern for each patient was analyzed, and the baseline rate, long-term variability, and periodic changes wee determined. It was found that changes in the L:S ratios were significantly correlated with the duration of labor and FHR long-term variability. Very low L:S ratios were observed in some patients whose infants did not subsequently develop respiratory distress syndrome. This raises the possibility that during labor the amniotic fluid is no longer representative of lung fluid, perhaps because of reduced tracheal fluid efflux, a process which may operate when the fetus is under stress.

Real time ultrasound diagnosis of hemorrhagic pathological conditions in the posterior fossa of preterm infants.

Real time echoencephalography (RTE) was used to diagnose and serially follow intracranial pathological conditions in the posterior fossa of infants with a gestational age of less than 34 weeks. The posterior fossa was studied in four planes (coronal, modified coronal, sagittal, and parasagittal) with a sector scanner equipped with a high frequency transducer that was placed on the fontanelles and the sutures. Hemorrhagic complications were easily differentiated from normal anatomy. RTE diagnosis was confirmed with computed tomographic scans (5 patients) and postmortem examination of the brain (18 infants). RTE is a precise and noninvasive technique to visualize hemorrhagic and other forms of abnormalities in the infratentorial compartment.

Management of hydrocephalus secondary to intracranial hemorrhage in the high risk newborn.

The experience of the Special Care Nursery of the University of California Medical Center, San Diego, in the management of the high risk newborn with progressive ventricular enlargement is reviewed, and the physiopathological basis of progressive ventricular enlargement is analyzed.

Ventriculoperitoneal shunts in high risk newborns weighing under 2000 grams: a clinical report.

Fifty-three low birth weight high risk newborns who developed progressive hydrocephalus despite a trial period of intermittent lumbar punctures underwent cribside ventriculoperitoneal shunt placement. They all weighed less than 2000 g at the time of shunting (mean, 1308.6 g +/- 398.2 SD). The operative procedures were performed at a mean age of 31.5 days +/- 16.1 (SD). There were no deaths in this series. During the nursery stay, 14 patients required operative revisions for obstruction. The most common problem was infection, which occurred in 13 (24.5%) after the primary intervention and in another 5 of the 14 (35.7%) patients who required revision. The overall infection rate/patient was 26.9%. Shunt removal and intensive antibiotic therapy cured the infection in all but 1 patient. Premature, low birth weight newborns may undergo ventriculoperitoneal shunting, but close follow-up for complications such as infection and shunt obstruction is always required.

Reintroduction of continuous negative pressure ventilation in neonates: two-year experience.

Continuous negative pressure ventilation utilizes subatmospheric pressure around the thorax to improve oxygenation. It has not been routinely used since the mid-1970s. We treated 37 infants with the combination of continuous negative pressure (CNP) and intermittent mandatory ventilation (IMV), after failing to attain a PaO2 of greater than or equal to 50 torr on IMV alone. Lung diseases included pulmonary interstitial emphysema (PIE), respiratory distress syndrome (RDS), and pulmonary artery hypertension (PAH) due either to meconium aspiration syndrome (MAS) or other causes (non-MAS). All infants had evidence of severe parenchymal pulmonary disease, or pulmonary artery hypertension resulting in persistent hypoxemia and hypotension. In the PIE group, CNP was started later in the course of the disease, and both positive pressure and oxygen were maintained for a longer period. The group of infants with non-MAS PAH required CNP and positive pressure ventilation for the shortest period of time. The infants with PIE also had a greater incidence of bronchopulmonary dysplasia (BPD) and intraventricular hemorrhage (IVH). In addition, three patients with PIE died. In the non-MAS patients with PAH, no complications and no deaths occurred. The response to CNP was a rapid improvement in oxygenation in all groups with the greatest increase of PaO2 in the non-MAS PAH infants: from 30 torr prior to the initiation of CNP to 140 torr within 30 minutes. No significant changes in pH or PaCO2 occurred in any group. Significant decreases in ventilator rate, mean airway pressure (Paw) and FIO2 in peak inspiratory pressure were possible by 12 hours of CNP.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of myoinositol in regulation of surfactant phospholipids in the newborn.

According to animal studies myoinositol decreases surfactant phosphatidylglycerol and increases phosphatidylinositol. In the present study lung effluent phospholipids and serum myoinositol were analyzed in respiratory distress syndrome (RDS, 19 cases), in other lung disease (6 cases) and in 22 newborn with no lung disease. In addition, myoinositol was studied in amniotic fluid and in serum from umbilical vessels and from maternal vein (15 healthy newborn). There was a significant correlation between the fetal and amniotic fluid levels of myoinositol, but no detectable correlation between fetal and maternal myoinositol. Serum myoinositol was higher in preterm than in term newborns. In healthy newborns there was a negative correlation between lung effluent phosphatidylglycerol (expressed as percent of the phospholipids) and serum myoinositol (r = -0.968), and a positive linear correlation between myoinositol and lung effluent phosphatidylinositol (r = 0.849). In RDS at birth, undetectable phosphatidylglycerol corresponded with high serum myoinositol. During the first 5 neonatal days serum myoinositol either (1) decreased and phosphatidylglycerol appeared, (2) remained high and phosphatidylglycerol correspondingly low in some small preterm infants, or (3) decreased but phosphatidylglycerol did not expectedly increase and disaturated lecithin/sphingomyelin ratio remained low in other small preterm babies. We propose that a premature decrease in serum myoinositol among small preterm infants with RDS is not beneficial, since myoinositol may promote hormone-induced lung maturation and healing of lung damage.

Preventing obsolescence in the design of a perinatal unit.

Basic principles are offered to support the suggestion that use of special care space must be made with a mind toward prevention of obsolescence. Certain conventional design features should be examined critically and decisions made as to their applicability to the needs of a particular program.