Comparison of short-term outcomes of 35-weeks' gestation infants cared for in a level II NICU vs mother-baby, a retrospective study.

BACKGROUND: Late preterm infants are at high risk for medical complications and represent a growing NICU population. While 34-weeks' gestation infants are generally admitted to the NICU and 36-weeks'gestation infants stay in mother-baby, there is wide practice variation for 35-weeks'gestation infants. The objective of this study was to compare short-term outcomes of 35-weeks' gestation infants born at two hospitals within the same health system (DUHS), where one (DRH) admits all 35-weeks' gestation infants to their level II NICU and the other (DUH) admits all 35-weeks' gestation infants to mother-baby, unless clinical concern. METHODS: We conducted a retrospective cohort analysis of 35-weeks' gestation infants born at DUHS from 2014-2019. Infant specific data were collected for birth, demographics, medications, medical therapies, LOS, ED visits and readmissions. 35-weeks' gestation infants at each hospital (DRH vs DUH) that met inclusion criteria were compared, regardless of unit(s) of care. RESULTS: 726 infants of 35-weeks' gestation were identified, 591 met our inclusion criteria (DUH -462, DRH -129). Infants discharged from DRH were more likely to receive medical therapies (caffeine, antibiotics, blood culture, phototherapy, NGT), had a 4 day longer LOS, but were more likely to feed exclusively MBM at discharge. There were no differences in ED visits; however, more infants from DUH were readmitted within 30 days of discharge. CONCLUSIONS: Our findings suggest admitting 35-weeks' gestation infants directly to the NICU increases medical interventions and LOS, but might reduce hospital readmissions.

Determination of tiamenidine in biological specimens by radioimmunoassay.

A simple and highly sensitive radioimmunoassay (RIA) procedure has been developed for the determination of the new antihypertensive drug 2-[(2-chloro-4-methyl-3-thienyl)amino]-2-imidazoline (tiamenidine) in serum, plasma and urine. Antisera to tiamenidine were produced in rabbits against its derivatives conjugated to bovine serum albumin. Studies with metabolites and imidazoline derivatives have shown that the antibodies thus produced are specific for tiamenidine. 3H-Labelled drug was used as tracer. The separation of free from antibody-bound tiamenidine was carried out by using polyethylene glycol. The radioimmunoassay (RIA) allows the determination of tiamenidine in 100 microliter biological specimens directly and without extraction down to a detection limit of 20 pg/ml. Reproducibility and accuracy of the assay are good. A sufficient correlation (r = 0.95) was obtained when serum samples were assayed by the RIA and the GC-MS method. The pharmacokinetic profile of the drug was determined in subjects after oral administration of 1 mg tiamenidine using the newly developed RIA. The course of serum levels up to 24 h after treatment may be well described by a Bateman function with an elimination half-life of about 3-5 h. These values correspond sufficiently well with the data obtained from the rate constant of the excretion via urine.

Metabolism of prostacyclin and 6-keto-prostaglandin F1 alpha in man.

Labeled and unlabeled prostacyclin and 6-keto-PGF1 alpha were infused into healthy volunteers; urine was chromatographed on different systems including high pressure liquid chromatography. The peaks obtained by the latter method were derivatized to the methoxime methyl ester trimethyl silyl ether and analyzed by gas-liquid chromatography-mass spectrometry. After infusion of prostacyclin the following metabolites could be identified: dinor-4-keto-7,9,13-trihydroxy-prosta-11,12-enoic acid (20.5%), dinor-4,13-diketo-7,9-dihydroxy-prostanoic acid (6.8%), dinor-4,13-diketo-7,9-dihydroxy-prostan-1,18-dioic acid (19.7%), and 6-keto-PGF1 alpha (14.2%), the in vitro hydrolysis product of prostacylin. 6-Keto-PGF1 alpha infusion resulted in the same metabolites with the relative amounts of 22.4, 5.4, 7.0, and 6.8%, respectively. Additionally, 6,15-diketo,13,14-dihydro-PGF1 alpha (5.7%) could be identified. These data show that the metabolic pathway of prostacyclin involves hydrolysis to 6-keto-prostaglandin F1 alpha, subsequent beta-oxidation, dehydrogenation at C-15, reduction of the double bond between C-13 and C14, and omega-oxidation to the dicarboxyl metabolite. We conclude that dinor-4-keto-7,9,13-trihydroxy-prosta-11,12-enoic acid and dinor-4,13-diketo-7,9-dihydroxy-prostan-1,18-dioic acid represent the major urinary metabolites of prostacyclin in man. 6-keto-PGF1 alpha is a minor urinary excretory product following the administration of prostacyclin or 6-keto-PGF1 alpha.

Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F1 alpha in man.

Human volunteers were infused with 3H- and 2H-labeled prostacyclin or 3H-labeled 6-ketoprostaglandin F1 alpha and, in separate experiments, with the unlabeled prostanoids. The urine was purified by different chromatographic steps and finally separated into several fractions by high-performance liquid chromatography. The major fractions contained 20.5 and 23.0% of the eluted readioactivity for the metabolites of prostacyclin and 6-ketoprostaglandin F1 alpha, respectively. The structure of both metabolites was identified by gas-liquid chromatography-mass spectrometry as dinor-6-ketoprostaglandin F1 alpha. It is concluded that the major metabolite of prostacyclin and 6-ketoprostaglandin F1 alpha in man is dinor-6-ketoprostaglandin F1 alpha.

Metabolism of prostacyclin and 6-keto-prostaglandin F1 alpha in man.

The major metabolites of prostacyclin and 6-keto-prostaglandin F1 alpha in man were investigated. Healthy male volunteers were infused with the labeled and unlabeled prostanoids. The urine was chromatographed on different systems including high-pressure liquid chromatography (HPLC). The material under the major peak was derivatized to the methyl ester methoxime trimethyl silyl ether and analyzed by gas chromatography-mass spectrometry (GC-MS). Open bed reversed-phase chromatography of the urine obtained from PGI2 infusion resulted in two peaks. On further separation by two different HPLC systems one major peak containing 20.5 % of the radioactivity was obtained and was shown by GC-MS to be identical with dinor-6-keto-prostaglandin F1 alpha. Urine obtained from 6-keto-prostaglandin F1 alpha infusion was chromatographed similarly. Its major peak on HPLC appeared with a retention volume and mass spectrum identical with the major metabolite of PGI2. It is concluded that the major metabolite of PGI2 and 6-keto-prostaglandin F1 alpha in human urine is dinor-6-keto-prostaglandin F1 alpha.

Determination of nomifensine by a sensitive radioimmunoassay.

1. A radioimmunoassay (RIA) has been developed for determination of both nomifensine and total nomifensine (nomifensine + conjugated nomifensine) in serum, plasma, and urine. 2. Antibodies were prepared in rabbits by immunization with N-(8-Nomifensine) succinamic acid-bovine serum albumin. 3H-labelled drug was used as tracer. Separation of free from antibody-bound nomifensine was carried out using dextran-coated charcoal. For determination of total nomifensine, the acid-labile conjugate was split by acidification. 3. The limit of detection for nomifensine is 300 pg/ml plasma and the cross-reactivity of the metabolites is less that 1%. The influence of conjugated nomifensine on the results of nomifensine can be corrected. 4. Pharmacokinetics of nomifensine were determined in healthy volunteers after oral administration of 100 mg 14C-labelled drug. Peak levels of 14C radioactivity (2,150 ng/ml), total nomifensine (1,252 ng/ml) and nomifensine (53 ng/ml) appeared within 1.5-2 h; the half-life of elimination from plasma was 1.5-2 hours. The advantages of this routine method are high sensitivity, the requirement of small amounts of plasma, and simple handling.