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Biomedical subjects

R Birnbacher

Publications and source records attributed to R Birnbacher.

At least 19 recordsLinked to original sources

The clinical impact of magnetic resonance imaging in fetuses with central nervous system anomalies on ultrasound scan.

OBJECTIVES: Magnetic resonance imaging (MRI) was performed on fetuses with sonographically diagnosed central nervous system (CNS) anomalies to determine frequency and type of cases in which fetal MRI adds clinically relevant information. PATIENTS AND METHODS: Forty-three cases presenting with CNS anomalies by ultrasonography were investigated by MRI. The potential effect of MRI on parental counseling and pre- or postnatal management were the main endpoints. RESULTS: Fetal MRI confirmed the sonographic diagnosis in 28 of 43 cases, showed additional findings in 14 of 43 cases, and was inferior to sonography in 1 of 43 cases. The MRI diagnosis had therapeutic consequences in 11 of 43 patients, with the fetal MRI diagnosis influencing parental counseling in 8 of these 11 patients. Prenatal patient care was not influenced by the additional investigation with fetal MRI. CONCLUSION: MRI is well suited as additional imaging method in fetuses with CNS anomalies. Additional fetal MRI is particularly indicated if the findings might have a therapeutic consequence.

Adult↗

Brain abscesses after Serratia marcescens infection on a neonatal intensive care unit: differences on serial imaging.

Serratia are known to be a possible cause of severe cerebral infections in neonates. We describe imaging of three premature infants infected with Serratia marcescens. Born in the 31( st), 25( th) and 28( th) weeks of gestation, they presented with signs of septicaemia on postnatal days 9, 24 and 32. Initial sonography showed cysts in the first child, two areas with anechoic centre and echogenic rim in the second, and several echogenic areas in the third. Lesions were seen on CT, of low density in two cases and minimally increased density in the third. MRI in the first patient showed cysts with incomplete contrast enhancement of the lesions, while patient 2 showed five ring-enhancing fluid-containing lesions with thick walls. In the third patient two abscesses with contrast enhancement and several high-signal spots were seen. We discuss the pathophysiology of the lesions and the impact of the various imaging methods.

Brain Abscess↗

Preterm male infants need more initial respiratory support than female infants.

UNLABELLED: Female infants have a significantly greater chance of surviving than male infants at similar birthweights and gestational ages, and have an advantage over males for a better outcome with less morbidity. CONCLUSION: The exact mechanisms responsible for the gender differences, with a better chance of survival of female infants, remain to be determined. The paper by Elsmén et al. provides an important contribution to this most important area of clinical research.

Clinical Trials as Topic↗

Duodeno-jejunal atresia with volvulus, absent dorsal mesentery, and absent superior mesenteric artery: a hereditary compound structure in duodenal atresia?

Duodenal atresia predominantly represents an isolated entity, but could also be part of a complexly structured intestinal malformation. We report four children, including two from one family, with duodeno-jejunal atresia associated with malrotation, volvulus, and absent parietal attachment of the mesentery. Gross absence of the mesentery and absence of distal parts of the superior mesenteric artery were the most remarkable findings. The small intestine was supplied retrogradely from the right colic artery. Consideration of embryological theories of this malformation takes into account the important role of the duodeno-jejunal flexure during the process of entry of the small bowel loops into the abdomen. Familial occurrence suggests autosomal recessive inheritance. We propose differentiating the pathoanatomical findings in our patients from classical apple peel small bowel syndrome (APSB).

Abnormalities, Multiple↗

Sleep-wake cycles in preterm infants below 30 weeks of gestational age. Preliminary results of a prospective amplitude-integrated EEG study.

In the newborn, presence of sleep-wake cycles indicates integrity and maturity of the central nervous system. By spectral EEG analysis and polygraphic recordings subtle variations of EEG background activity and behavioural patterns corresponding to early sleep-wake cycles have been found in preterm infants as young as 27 weeks of gestation. The emergence of sleep-wake cycles at early gestational ages may have a positive predictive value for long-term neurological outcome. Sleep-wake cycles and their significance for later outcome have not been studied in very preterm infants so far. Accordingly, we prospectively investigated maturational changes of EEG activity and sleep-wake cycles in preterm infants below 30 weeks of gestational age using the Cerebral Function Monitor, an amplitude-integrated EEG. We present preliminary data on the emergence of sleep-wake cycles in preterm infants from this ongoing study. Of 100 infants enrolled during a 1-year period, 38 infants without neurological complications were included in the reference group. In this group (mean gestational age 27 weeks), we observed cyclical variations of EEG background activity resembling early sleep-wake cycles at a mean gestational age of 28 weeks and a median postnatal age of 6 days. It is hypothesised that these cyclical variations of EEG background activity may represent switches between thalamo-cortical and neo-cortical pattern generators and indicate integrity of central nervous system function. Amplitude-integrated EEG may thus serve as a useful noninvasive test for brain function in preterm infants.

Brain↗

Anti-inflammatory activity of nerve growth factor in experimental autoimmune encephalomyelitis: inhibition of monocyte transendothelial migration.

In order to analyze a putative immunomodulatory effect of NGF in experimental autoimmune encephalomyelitis (EAE) of the Lewis rat, we transduced myelin basic protein (MBP)-specific CD4(+) T cells with a recombinant retrovirus encoding NGF. These T(MBP)NGF cells secreted high levels of NGF, along with an unaltered Th1-like cytokine pattern. Transfer studies showed that T(MBP)NGF cells were unable to mediate clinical EAE, when transferred alone, and, more important, they efficiently suppressed induction of clinical EAE by non-transduced MBP-specific T cells (T(MBP )cells). In contrast, NGF transduced ovalbumin-specific T cells, which secreted high NGF levels, did not affect EAE induction. Suppression of clinical EAE by T(MBP)NGF cells was associated with a general reduction of inflammatory CNS infiltrates, with a most pronounced decrease of the monocyte/macrophage component. Using a culture model of the endothelial blood-brain barrier (BBB), we found that NGF directly acts on blood-derived monocytes via the p75 NGF receptor, thus interfering with monocyte migration through the activated BBB endothelium. Our data establish NGF as an anti-inflammatory mediator interfering with T cell mediated autoimmune disease in the CNS. They further point to monocyte migration through blood vascular endothelium as one possible mechanism of NGF action.

Animals↗

[Recent advances in neonatology--new tasks for the radiologist].

Modern neonatology comprises care for a growing number of infants with congenital abnormalities and an increasing number of premature born infants. The survival rates of premature infants have increased dramatically during the past decade. This increase in survival rates can be attributed to improved prenatal and obstetric management and to advances in neonatal intensive care medicine. RADIOLOGICAL SUPPORT: Neonatology has become a pediatric subspecialty of its own resulting in the demand for an equally specialised radiological support. Therefore the availability of a children's radiologist for radiological and sonographic examinations is mandatory (24 hours a day) for optimal patient care on a neonatal intensive care unit. A good cooperation between radiologist and neonatologist in neonatal intensive care medicine is therefore warranted.

Austria↗

Tracheal agenesis: evaluation by helical computed tomography.

We present a newborn infant with type II tracheal agenesis. Helical CT was performed and confirmed the diagnosis. Retrospective coronal and sagittal multiplanar reconstructions clearly demonstrated the complex anatomy of the malformation. The absence of a significant portion of healthy trachea did not present any possibility for surgical correction.

Fatal Outcome↗

Survival after intrauterine myocardial infarction: noninvasive assessment of myocardial perfusion with 99mTc-Sestamibi scintigraphy.

Survival after severe intrauterine myocardial infarction has not been reported previously. We describe the course of a neonate with a structurally normal heart, who presented with cardiogenic shock at birth due to intrauterine myocardial infarction with a huge ventricular aneurysm. Myocardial perfusion was assessed noninvasively by means of 99mTc-Sestamibi, a radiopharmaceutical agent recently introduced in nuclear cardiology to avoid repeated coronary angiography. The patient survived with improved cardiac function and normal neurodevelopmental outcome.

Adult↗

Echocardiographic evidence of aortopulmonary collaterals in premature infants after closure of ductus arteriosus.

Aortopulmonary collaterals occur in a variety of congenital heart diseases, in chronic pulmonary infection and abscesses, in association with lung tumors, and after multiple pulmonary emboli. In patients with congenital cyanotic heart disease aortopulmonary collaterals mainly occur in conditions with reduced pulmonary blood flow. We investigated 12 preterm low-birth-weight infants, gestational age 29.3+/-3.3 weeks, with respiratory failure who suffered from moderate to severe chronic lung disease after a period of mechanical ventilation. All patients developed aortopulmonary collaterals after closure of a patent ductus arteriosus. Aortopulmonary collaterals could be displayed clearly by color Doppler echocardiography and originated mainly from the descending aorta or the aortic arch. Hypoxic and hypercapnic episodes favored the development of aortopulmonary collaterals, which disappeared after pulmonary hemodynamics and respiratory function had improved. In only one patient coiling of a large col lateral vessel had to be performed. Systemic-to-pulmonary collateral vessels potentially aggravate chronic lung disease by increasing collateral pulmonary blood flow and reducing lung compliance. We conclude that aortopulmonary collaterals occur in bronchopulmonary dysplasia and can cause major problems in ventilated premature infants. Echocardiographic evaluation is important to prevent aggravation of chronic lung disease of infants at risk.

Aorta, Thoracic↗

Long-term treatment in children with hypopituitarism: pubertal development and final height.

Auxological data, pubertal development and final height were analyzed in 25 patients with growth hormone (GH) deficiency who were treated only with pituitary GH in 3 doses/week. 15 patients had a spontaneous onset of puberty and in 10 puberty was induced. The duration of therapy was 7.5 years, the dosage was about 11 U/m2/week and was not changed during puberty. 80% of the patients with induced puberty, but only 33% of the children with spontaneous puberty reached final heights within the 2 SD range. Final height was correlated with height at the start of treatment only in patients with spontaneous puberty, which shows the necessity of early treatment initiation in this group. The lack of this correlation in patients with induced puberty might be attributed to gonadotropin deficiency. Height at the onset of puberty was related to final height only in the group with gonadotropin deficiency. A prediction model for calculation of the first year height velocity which was derived from present treatment procedures showed a too favorable prediction for our patients. The reasons for the insufficient final results may be due to impure GH preparations, suboptimal dosage, low frequency of injections and late onset of therapy.

Adolescent↗

Hyperprolactinemia, a tool in treatment control of tetrahydrobiopterin deficiency: endocrine studies in an affected girl.

Severe tetrahydrobiopterin (BH4) deficiency is a naturally occurring model of cerebral catecholamine and serotonin shortage. Examination of the stimulated release and physiologic secretion pattern of several hormones in affected individuals permits certain conclusions concerning the involvement of these neurotransmitters in hormone regulation. Treatment, moreover, permits the ranking of the quality of the therapeutic regimens in use according to the degree of hormonal alteration. The 24-h secretion pattern of prolactin, GH, cortisol, and melatonin and the stimulated release of prolactin, GH, TSH, and gonadotropins were studied in an affected girl. Severe hyperprolactinemia with disruption of the pulsatile and circadian secretion pattern was the prevailing feature. The GH physiologic secretion pattern was not affected, but its stimulation was impaired. Melatonin displayed a normal circadian secretion pattern; the rhythm, however, was advanced by several hours. Conventional treatment of BH4 deficiency, i.e. BH4, 5-hydroxytryptophan, and L-DOPA/carbidopa (the last named given in three doses per day), suppresses prolactin levels merely for a few hours. L-DOPA/carbidopa given at shorter intervals or, even better, as a slow release preparation, is more effective in suppressing prolactin levels. Our data indicate immense hyperprolactinemia but few other hormonal disturbances in severe BH4 deficiency. Prolactin secretion may serve as an extremely sensitive marker for the hypothalamic dopamine content under different therapeutic regimens. Treatment with an L-DOPA/carbidopa slow release preparation produces virtually normal prolactin levels.

Adolescent↗

Cellular localization of insulin-like growth factor II mRNA in the human fetus and the placenta: detection with a digoxigenin-labeled cRNA probe and immunocytochemistry.

IGF-II plays a major role in the regulation of human fetal growth and development. However, more extensive information on the cellular sites of IGF-II synthesis in the fetus would provide more insight into its role in fetal organogenesis. Thus we have determined the sites of IGF-II synthesis in 18-26-wk gestation human fetal tissues using in situ hybridization with a digoxigenin-labeled cRNA probe to localize IGF-II mRNA in fetal liver, kidney, adrenal gland, cerebral cortex, costal cartilage, skeletal muscle, and lung, and in placental tissue. In human fetal tissues it has to date been impossible to clearly assign IGF-II mRNA to epithelial cells of entodermal origin. Besides their already known localization in cell matrix and a variety of mesodermal cell types, strong IGF-II mRNA-positive signals were detected in epithelial cells in the liver (hepatocytes), bronchial and bronchiolar epithelium, undifferentiated renal tubular epithelium, mature glomerular epithelium, pelvic urothelium, and adrenal epithelial cells of the zona persistens. To identify the cellular location of immunoreactive IGF-II, we also performed immunocytochemical studies in tissues of the same fetuses. Every tissue studied except the cerebral cortex contained immunoreactive cells; however, immunostaining was generally weaker than in situ hybridization signals. Our data show that the distribution of IGF-II in human fetal tissue is much more widespread than hitherto thought. A digoxigenin-labeled detection system for IGF-II is more capable of detecting the cellular expression pattern of IGF-II than radioactive probes and is suitable for analysis of routinely prepared paraffin-embedded material.

Abortion, Induced↗

Glycoxidation, and protein and DNA oxidation in patients with diabetes mellitus.

1. The role of oxidative stress in the pathogenesis of the diabetic state is being investigated extensively. Although oxidative stress has been reported in terms of glycoxidation, protein oxidation and DNA oxidation in diabetes mellitus, oxidation parameters have not been determined in parallel on the same study population.2. We studied 24 patients with diabetes mellitus (14 patients with Type I diabetes with a mean age of 62.3+/-6.3 years and 10 patients with Type II diabetes aged 67.3+/-5.9 years) and compared them with age-matched non-diabetic controls. Urinary o-tyrosine, 8-hydroxy-2'-deoxyguanosine and pentosidine measurements by HPLC were made on two occasions (t1 and t2).3.A clear statistical difference was found between diabetic patients and controls at t1 or t2 for 8-hydroxy-2'-deoxyguanosine and pentosidine, but not for o-tyrosine. No significant correlations were found between clinical and other laboratory parameters except high-density lipoprotein and uric acid. We revealed significantly increased glycoxidation and DNA oxidation in patients with Type I and Type II diabetes, but protein oxidation was not different from controls.4. The finding of increased glycoxidation reflects increased oxidation of the carbohydrate moiety, whereas the increased levels of oxidized DNA may also be interpreted as due to increased DNA repair. The increased 8-hydroxy-2'-deoxyguanosine does not indicate the generation of an individual active oxygen species, but DNA could have been oxidized simply by alkenals from lipid peroxidation, as e.g. malondialdehyde. As no difference in protein oxidation (i.e. o-tyrosine) between diabetics and controls could be revealed, the oxidation of DNA by hydroxyl radical attack is unlikely, as o-tyrosine was proposed as a marker for hydroxyl radical attack. Therefore, the message is that increased glycoxidation can be confirmed, protein oxidation does not appear to take place and increased DNA oxidation is still not proven, as increased 8-hydroxy-2'-deoxyguanosine may simply reflect repair.

8-Hydroxy-2'-Deoxyguanosine↗