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.

[Placebo response: in studies on pain and under other clinical conditions]. / Placeboresponse: In Studien zum Schmerz und anderen klinischen Bedingungen.

This contribution compares unexplained essential questions regarding the placebo response with current empirical evidence: (1) Are the placebo response rates equivalent in the groups treated with medication or placebo? Very little evidence has been gathered to support this generally accepted additivity while some findings negate its validity. (2) Is the placebo response a function of the probability of receiving medication or placebo? There are indications that the number of study groups included in a trial determines the level of placebo and medication response. (3) How great is the placebo response in trials that directly compare a (new) medication with one that for example is already on the market? There are indications that such comparative studies produce higher placebo response rates. (4) How high is the placebo response rate in everyday clinical practice--or does the response to a medication in trials substantiate the effect of the medication in everyday clinical practice?

Postnatally acquired CMV meningitis diagnosed via BioFire FilmArray: A case report.

Postnatally acquired cytomegalovirus (CMV) is commonly acquired via breast milk, with premature infants more frequently developing symptoms of CMV infection in comparison to term infants. Meningitis is a rare clinical manifestation of CMV infection. The diagnosis of meningitis is difficult to make in infants, particularly those who are preterm. Consequentially, broad-spectrum empiric antimicrobial coverage is often administered for several days while waiting for current gold standard CSF testing to result. The BioFire FilmArray (BFA) simultaneously tests for 14 different pathogens, including CMV, allowing for quicker diagnosis and shorter time to definitive treatment. Here, we report a very low birth weight infant with postnatally acquired CMV meningitis, the first to our knowledge to be diagnosed using the BioFire FilmArray.

Stress reactivity in childhood functional abdominal pain or irritable bowel syndrome.

BACKGROUND: Frequent abdominal pain (AP) in childhood has been shown to be associated with elevated experience of stress and with deficits in stress coping, but psychophysiological stress reactivity has been studied rarely. METHODS: We examined whether children with frequent AP show altered reactions of the parasympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis during and following an afternoon laboratory social stress task in comparison to healthy children and children with anxiety disorders. Twenty-four children with frequent AP (18 with functional AP and six with irritable bowel syndrome; M = 9.9 years), and 24 healthy controls underwent stressful free speech and arithmetic tasks. Twelve children with anxiety disorders served as second comparison sample. Groups were compared regarding parasympathetic reaction and saliva cortisol concentration. RESULTS: We found no differences in parasympathetic withdrawal between the groups. Concerning the HPA axis, we detected an attenuated cortisol reactivity in children with AP compared to both other groups. CONCLUSIONS: This study provides preliminary evidence that childhood AP is not associated with altered parasympathetic withdrawal during stress. It seems to be related to a down-regulated reactivity of the HPA axis. This pattern was ascertained in comparison to healthy children and also in comparison to children with anxiety disorders. SIGNIFICANCE: Childhood abdominal pain could be related to down-regulated HPA axis reactivity to stress but not to altered parasympathetic reaction. Children with abdominal pain and children with anxiety disorders exhibit a divergent stress-related HPA axis reaction.

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.

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.

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.

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.

Coronary heart disease risk factors in women with polycystic ovary syndrome.

The goal of the study was to compare cardiovascular heart disease risk factors in women with polycystic ovary syndrome (PCOS) and matched control subjects. Women with PCOS have risk factors, including anovulation, hyperandrogenism, and insulin resistance, that suggest a male coronary heart disease risk-factor profile. A total of 206 women with PCOS were recruited by using records from a large reproductive endocrinology practice. A clinical diagnosis of PCOS was made if there was a history of chronic anovulation in association with either clinical evidence of androgen excess (hirsutism) or if total testosterone level was > 2 nm/L or the luteinizing hormone/follicle-stimulating hormone ratio was greater than 2. The overall response rate for cases was 76%. A control population was obtained by using a combination of area voters' registration tapes and directories of households. A control subject was matched to each case subject by age +/- 5 years, race, and neighborhood. The response rate for recruitment of the first or second eligible control subject was 83.6%. The average age at initial interview was 35.9 +/- 7.4 years for case and 37.2 +/- 7.8 years for control subjects. Women with PCOS had significantly increased cardiovascular disease risk factors compared with control women. These included increases in body mass index, insulin, and triglyceride levels (P < .001), decreased total HDL and HDL2 levels (P < .01), and increased total cholesterol and fasting LDL levels, waist/hip ratio, and systolic blood pressure (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

A radioimmunoassay for determination of glibenclamide and other sulfonylureas.

An antiserum was prepared for the determination of glibenclamide and for the estimation of other commercially available sulfonylureas. Rabbits were immunized with a glibenclamide-BSA conjugate. Tritiated glibenclamide was used as the tracer. The assay was performed in the presence of 8-anilinonaphthalenesulfonic acid to displace glibenclamide bound to serum protein, and free and antibody bound tracer were separated by dextran-coated charcoal. For glibenclamide determination in serum and plasma the limit of detection was 3 ng/ml. Sensitivity calculated for the whole determination range was 102 cpm for a 10 % concentration difference. Specificity studies showed a cross-reaction of less than 0.1 % for glibenclamide metabolite M1 and 9 % for metabolite M2. Other sulfonylurea drugs display cross-reactivities from 0.1% (chlorpropamide) to 190% (gliquidone). Both intra-assay and inter-assay imprecision were below 10 %. Accuracy was established by comparison of the present method with HPLC. The assay was applied to the specific determination of glibenclamide in clinical trials and for diagnosing factitious hypoglycemia caused by sulfonylureas.

Immunogenicity of human hepatitis B virus P-gene derived proteins.

The frequency and specificity of antibodies to P-gene encoded proteins of human hepatitis B virus was tested in sera of acute and chronically infected patients with and without hepatocellular carcinoma (HCC). For antibody detection an immunoprecipitation gel assay was performed with radioactively labeled polypeptides produced by in vitro translation of RNA of different P-gene regions. Thus, five antigenic regions were identified. All anti-P antibody positive sera reacted with carboxy-terminal P-poly-peptides, a subset with polypeptides of the amino-terminal and middle region, and none reacted with P-protein derived from the most sequence variable region. Anti-P antibodies were detected at very high frequency in sera of acute (73%) and chronically infected patients without HCC (87%), but less often in HCC patients (27%). These data indirectly demonstrate the expression of most hepatitis B virus P-gene sequences and the immunogenicity of P-proteins in vivo. Moreover, they establish hepatitis B virus anti-P-antibodies as a frequent serologic marker of infection and identify the carboxy-terminal region of the P-protein(s) as immunodominant.

Construction of a GT polymorphism map of human 9q.

To construct a framework map of human chromosome 9 consisting of highly informative markers, we identified 36 cosmid clones from chromosome 9 that contained long GT repeat sequences. The cosmids were found to cluster on the long arm of the chromosome, particularly in the q32-34 region. Thirteen highly informative polymorphisms from 9q were identified, with median observed heterozygosity 0.75 and median calculated heterozygosity based upon allele frequencies of 0.75. These new GT repeat polymorphisms (D9S56, D9S58-67), as well as anchor GT polymorphisms for D9S15 (MCT112, 9q13), and ABL and ASS (both 9q34.1) were utilized to construct a linkage map of human 9q by the typing of the Venezuelan Reference Pedigree. Care was taken to avoid errors, including analysis of the data with CHROMLOOK and verification of all double crossover events detected within a 30 cM interval by repetition of the marker analysis. The map was generated using the MAPMAKER program. All positions in the resulting map are favored by odds of greater than 10(4):1. The map has a sex-averaged length of 90 cM (Kosambi function) with a single maximum intermarker recombination fraction of 26%. All other intermarker recombination fractions are less than 15%. As D9S15 is known to be closely linked to markers on proximal 9p, and ASS/ABL are in band 34.1, this set of GT polymorphisms spans the length of 9q and provides a useful panel for linkage analysis of disease genes to this region. The marker order was confirmed by in situ hybridization of the cosmid clones to metaphase spreads of normal human chromosomes, which indicated an excess of recombination in the telomeric region in comparison to centromeric 9q, in agreement with previous chiasmata distribution observations. Two spontaneous new mutations for these GT repeat markers were identified, giving an overall observed spontaneous mutation rate of 0.00045 per locus per gamete. Direct observation of new mutations has not been previously reported for dinucleotide polymorphisms, but the observed rate is consistent with frequencies observed for other VNTR polymorphisms.

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.