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To investigate the regulation of ovine luteal receptors for prostaglandin F2 alpha (PGF2 alpha), reverse transcription-polymerase chain reaction was used to produce a 284-bp partial cDNA that was 98% identical to that reported for the bovine PGF2 alpha receptor (PGF2 alpha-R). In situ hybridization localized mRNA for PGF2 alpha-R specifically to large luteal cells. In experiment 1, pools of luteal tissue (n = 4/day) collected from ewes on Days 3, 6, 9, 12, and 15 of the estrous cycle were analyzed for mRNA encoding PGF2 alpha-R. There was no difference in mean steady-state concentrations of mRNA encoding PGF2 alpha-R among any of the days studied (range = 2.3 +/- 0.3 to 3.5 +/- 0.7 fmol PGF2 alpha-R mRNA/ microgram poly[A]+ RNA as assessed by slot-blot hybridization). In experiment 2, ewes on Day 11 or Day 12 of the estrous cycle were administered PGF2 alpha, and corpora lutea were collected 4, 12, or 24 h later (n = 4-5 per time point). Nontreated (n = 4) or saline-treated (n = 4) ewes served as controls. Luteal concentrations of mRNA encoding PGF2 alpha-R were decreased (p < 0.05) at 4, 12, and 24 h after injection of PGF2 alpha. In experiment 3, ewes (midluteal phase) were administered saline, PGF2 alpha, phorbol 12-myristate 13-acetate (PMA), or LH via ovarian arterial injection, and luteal tissue was collected 0, 4, 12, or 24 h later (n = 3-4 per treatment per time). Steady-state concentrations of mRNA encoding PGF2 alpha-R were decreased (p < 0.05) by PGF2 alpha and PMA treatment (4 and 12 h) but were increased (p < 0.05) at 24 h after LH treatment. In summary, 1) mRNA encoding PGF2 alpha-R was localized to large luteal cells; 2) concentrations of mRNA encoding PGF2 alpha-R did not vary during the estrous cycle; 3) treatment with PGF2 alpha or PMA to activate protein kinase C decreased concentrations of PGF2 alpha-R mRNA within 4 h of treatment; and 4) administration LH increased concentrations of mRNA encoding PGF2 alpha-R 24 h following injection.

Protein F1/GAP-43 is differentially expressed in brain with high levels present in regions associated with memory functions. However, in hippocampus the granule cells lack F1/GAP-43 expression. To determine if this lack of expression is due to inhibitory signals from the target cells, we selectively destroyed CA3 pyramidal cells unilaterally using microinjections of excitotoxins. Kainate lesions induced F1/GAP-43 mRNA expression bilaterally in granule cells at 24 h post-injection. Since the induction contralateral to the lesion was not due to loss of target cells, that induction may be ascribed to consequences of seizure activity. However, F1/GAP-43 mRNA hybridization decreased by 3 d post-lesion and was at background levels by 6 d, indicating that the lack of F1/GAP-43 expression in granule cells is restored despite a lack of target neurons. Unilateral lesions of CA3 cells using ibotenate, which are not as complete as kainate but do not cause seizures, did not induce F1/GAP-43 mRNA in granule cells on either the contralateral or, in 4 of 5 cases, the ipsilateral side. Taken together, these data suggest that the CA3 target is not essential for the absence of F1/GAP-43 expression in granule cells. To compare the extent of damage caused by the lesions, we investigated the location of astrocytes undergoing reactive gliosis, employing as a reporter glial fibrillary acidic protein (GFAP) gene expression. After both kainate and ibotenate injections GFAP hybridization increased in the lesioned area as well as in the contralateral hippocampus. These results indicate that injections of kainate, and possibly ibotenate to a lesser extent, may affect behavior not only by damaging cells at the injection site, but also by altering gene expression in cells at distant sites.

The phosphorylation of MARCKS, but not protein F1/GAP-43, is increased in the intermediate and medial portion of the hyperstriatum ventrale (IMHV) after chick imprinting. Here we investigated if MARCKS, but not F1/GAP-43, gene expression would also be altered after imprinting. We first investigated the constitutive mRNA distribution of MARCKS and F1/GAP-43 in chick brain. MARCKS mRNA was expressed in most cells and exhibited a relatively homogeneous distribution. In contrast, F1/GAP-43 mRNA levels were elevated in discrete brain regions, as we had observed in mammals. The highest F1/GAP-43 mRNA levels in the chick brain were in sensory and associational structures such as the hyperstriatal complex and neostriatum, and lower levels were in structures involved in motor control, such as paleostriatum. These results in chick are consistent with the previously drawn generalization that F1/GAP-43 mRNA is expressed in those brain regions which exhibit synaptic plasticity. After imprinting, MARCKS mRNA levels in IMHV were higher in good learners than poor learners. In contrast, analysis of F1/GAP-43 mRNA levels revealed no differences related to training in any brain region sampled. These selective results for MARCKS but not F1/GAP-43 parallel the prior findings on their phosphorylation, and are consistent with our hypothesis that the very same proteins that are post-translationally modified in association with learning and memory also undergo alterations in their gene expression.

In a population-based study cerebral palsy (CP) was diagnosed in 110 cases (2.4 per 1000) among children live born with birth weight > or = 500 g (n = 45,976) during the 20-year-period 1970-89 (CP cases with a postneonatal etiology excluded). The CP-incidence showed a linear trend of decline from 2.8 per 1,000 in the first 5-year-cohort born 1970-74, to 2.0 per 1,000 in children born 1985-89 (p = 0.17). Birth weight specific CP-incidence showed a trend of decline in very low birth weight infants (500-1,499 g) and in infants > or = 2,500 g from the first 10-year-cohort born 1970-79 to the second born 1980-89. The same trend occurred for the incidence of spastic diplegia in total and in children born preterm. These trends of decline did not achieve statistical significance (p > 0.05). The CP-incidence was 36.7 and 11.3 times higher among infants with birth weight 500-1,499 g and 1,500-2,499 g respectively compared to infants > or = 2,500 g (p < 0.01). 15.9% of the decline in CP-incidence from the first to the second 10-year-cohort could be explained by a decreased low birth weight rate (500-2,499 g) in the population, from 4.2% 1970-79 to 3.8% 1980-89 (p < 0.05). The origin of CP was considered prenatal in 22 (20%), perinatal in 47 (42.7%), and undifferentiated in 41 (37.3%) of the cases. More CP-children born in the 10-year-period 1980-89 were treated with mechanical ventilation in the neonatal period (13/46; 28.3%) than those born in the 10-year-period 1970-79 (4/64; 6.3%) (p < 0.01). The neonatal mortality rate declined significantly from 7.2 per 1,000 in the first to 3.9 per 1,000 in the last 10-year-cohort respectively (p < 0.01). Birth weight-specific neonatal mortality rates declined more than 50% in all weight groups (p < 0.01). The results are contradictive to other investigations showing increased CP-incidence following improved survival rates in low birth weight infants, and may reflect a different pattern for development of perinatal care (organization, intensive care). The overall effect of mechanical ventilation may be improved survival and prevention of brain damage, though the percentage of ventilated CP-children increased. Preventing low birth weight should be a main strategy for preventing CP.

In family care (FC) program for neonatal intensive care units (NICUs), parents are encouraged to reside together with their infant for 24 hours a day to actively be involved in the care. The aim of this study was to assess the impact of FC on maternal confidence and breast-feeding. Maternal confidence and rate of breast-feeding were assessed in 31 mothers offered FC that included special family rooms in the NICU, and in 30 mothers from a comparable NICU providing traditional care without such facilities. One week prior to hospital discharge, mothers in the FC group felt better informed regarding nursing issues and had more confidence in interpretation of the infants regarding feeding issues and in caregiving without staff attendance (P < .05). They also reported a higher level of empowerment (P < .05). Three months after discharge, the mothers in the FC group had a higher self-reported skill level for interpretation of the infant's signals and knowledge about breast-feeding (P < .05). Despite similar rate of breast-feeding at discharge, more infants in the FC group were breastfed 3 months after discharge (P < .05). An FC program in the NICU promoted better maternal confidence during the hospital stay and 3 months after discharge compared with traditional care.

In the adult rat hippocampus mRNA of F1/GAP-43, an axonal growth-associated protein, is highly expressed in pyramidal cells, but is absent in granule cells. To determine whether granule cells can be induced to express mRNA of F1/GAP-43, transcript levels were studied after limbic seizures, which can induce sprouting of granule cell mossy fibers. Seizure-inducing electrolytic lesions were made in the dentate gyrus hilus with stainless-steel electrodes and mRNA levels were measured in contralateral hippocampus by quantitative in situ hybridization. Induction of F1/GAP-43 mRNA expression was observed in granule cells at 24 h, but not at 6 or 12 h, after the hilar lesion. When equivalent sized hilar lesions were made with platinum electrodes, which do not induce seizures, no hybridization was apparent over the granule cells. Hybridization over granule cells had declined by 48 h post-lesion, but even at 10 days it was still slightly higher than in control rats. F1/GAP-43 mRNA expression was also increased 2-fold in CA1 pyramidal cells with peak expression at 48 h post-lesion. These are the first data to our knowledge that demonstrate that F1/GAP-43 gene expression can be altered in neurons located within the adult brain. Induction of F1/GAP-43 mRNA expression in the granule cells may be important for the sprouting of mossy fibers and could be triggered by the elevated levels of brain-derived neurotrophic factor in CA3 cells which precede the increased F1/GAP-3 gene expression in granule cells.

Catheterization of umbilical veins and arteries is a common intervention in newborns. Malpositioning of catheters is associated with complications. The objective of this study was to evaluate catheter positions after insertion.The study is based on retrospective evaluation of all relevant X-ray images of newborns admitted to the neonatal intensive care unit, Vestfold Hospital, Norway in the period 1.06.98 - 28.02.10. Accurate localization of the catheter tip was determined in all images. In term infants, acceptable positioning for venous catheters was defined asor= 10 mm above or below the level of diaphragma and in preterm infantsor= 5 mm. For arterial catheters, acceptable positioning of the catheter tip (irrespective of gestational age) was at the level of the 6th to 9th thoracic vertebral body (high position, preferred) or at the 3rd to 4th lumbar vertebral body (low position).278 umbilical vein and 99 umbilical artery catheters were inserted in 298 patients. 45/99 (45 %) of the arterial catheters and 77/278 (28 %) of the venous catheters were correctly positioned from the start. Significantly more arterial catheters were positioned too low (44/99; 44 %) than too high (10/99; 10 %) (p0.001). Correspondingly, more venous catheters were positioned too low (126/278; 45 %) than too high (75/278; 27 %) (p0.001). Coiling occurred in 14 (5 %) venous catheters and in 6 (6 %) arterial catheters.Umbilical vessel catheters are often malpositioned. This increases the risk of thromboses and circulation disturbances. X-ray images are important for evaluation and potential correction of the catheter position.

The guidelines for diagnosis and treatment of neonatal hyperbilirubinaemia were changed at Vestfold Hospital, Norway in 1994 and 2007. Universal screening for ABO-immunization was implemented in 2006. This article describes effects of these changes.Blood-type immunization, phototherapy and exchange transfusions were prospectively recorded in the 21-year period 1988-2008. Three cohorts comprised the basis for the analyses: infants born in the time-periods 1988-93, 1994-2006 or 2007-2008.6.2 % of the infants born 1988-93 and 6.7 % born 1994-2006 received phototherapy. Physiological hyperbilirubinaemia in term infants was the main reason for phototherapy in the first cohort, while it was hyperbilirubinemia in preterm infants in the second cohort. 4.8 % of the infants born 2007-8 received phototherapy. Exchange transfusion was performed in 0.02 % born 1994-2008 and 0.2 % born 1988-93. Such transfusions were undertaken more frequently in cases with RhD-immunization (7.8 %) than in those with ABO-immunization (2.0 %). Universal screening for ABO-immunization increased the percentage of diagnosed cases in the population from 2.1 % to 3.6 %. No case of kernicterus was diagnosed.Fewer term infants were treated with phototherapy for hyperbilirubinaemia after the changes of therapeutic guidelines in 1994, while more preterm infants were treated after this change. Far less exchange transfusions are performed nowadays than before 1994. ABO-immunization has been diagnosed more often after implementation of universal screening.

SAMMENDRAGNye indikasjoner for behandling av hyperbilirubinemi hos nyfødte (bilirubinskjema fra Hillingdon sykehus,England) ble innført ved Vestfold sentralsykehus primo 1994. Endringene i panoramaet av behandlingstiltak(lysbehandling, utskiftningstransfusjon) ble registrert i kohortene av levende fødte ved sykehuset i toårsperioden1994-95 og sammenlignet med foregående treårsperiode 1991-93. Total lysbehandlingsprevalens falt signifikantfra 6,9% av levende fødte i perioden 1991-93 til 5,5% i perioden 1994-95 (p < 0,005). Dette skyldtes helt etbetydelig fall i prevalensen av fullbårne barn som ble lysbehandlet for fysiologisk ikterus, fra 4,3% til 1,6% ihenholdsvis første og siste periode (p < 0,0005). Prevalensen av barn som ble behandlet for prematuritetshyperbilirubinemisteg signifikant fra 2,0% av levende fødte til 3,2% (p < 0,0005). Dette var delvis forårsaket av enøkning i prematuritetsinsidensen, som steg fra 4,5% i perioden 1991-93 til 5,9% i perioden 1994-95 (p < 0,0005).Andelen premature som ble lysbehandlet steg fra 45,2% i første til 53,1% i siste periode (p < 0,05). Prevalensenav blodgruppeimmuniserte barn som ble lysbehandlet var uforandret i de to periodene (henholdsvis 0,6% og0,7%) (p > 0,05). Det var en markert reduksjon i prevalensen av barn som gjennomgikk utskiftningstransfusjon(fra 0,2 til 0,06% henholdsvis i de to periodene) (p < 0,05). Mulighetene for uheldige psykologiske og biologiskeeffekter av lysbehandling til friske fullbårne barn med ikterus, reduseres relativt betydelig med de moderatejusteringer av indikasjonene som er foretatt. Rutineskiftet har også betydd ressurssparing. På landsbasis vil en slikrutineendring medføre at 1000-2000 fullbårne barn hvert år kan unngå lysbehandling. Indikasjonene for fototerapiog utskiftningstransfusjon for hyperbilirubinemi hos nyfødte i Norge må diskuteres på nytt i lys av ny forskningmed tanke på nasjonal konsensus. Kortere liggetider for nyfødte i sykehus etter fødselen gjør det nødvendig medgode rutiner for oppfølging av hyperbilirubinemi utenfor sykehus.Meberg A. Hyperbilirubinemia – a controversial topic. Experiences with new guidelines for phototherapyand exchange transfusion . Nor J Epidemiol 1997; 7 (1): 85-91.ENGLISH SUMMARYNew guidelines for treatment of hyperbilirubinemia in newborn infants (according to a bilirubin chart used atHillingdon Hospital, England) were introduced at Vestfold Central Hospital primo 1994. Changes in the panoramaof interventions (phototherapy, exchange transfusion) were recorded for the two-year period 1994-95 and comparedto the preceding three-year period 1991-93. Total prevalence of infants treated by phototherapy declinedfrom 6.9% among those born 1991-93 to 5.5% in those born 1994-95 (p < 0.005). This was entirely caused by adecline in the prevalence of term infants treated for physiological hyperbilirubinemia, from 4.3% in the cohortborn 1991-93 to 1.6% in the cohort born 1995-95 (p < 0.0001). The prevalence of preterm infants (gestational age< 37 weeks) treated by phototherapy increased from 2.0% to 3.2% respectively in the two periods (p < 0.0005).This was partly caused by an increase in the preterm incidence from 4.5% of live born 1991-93 to 5.9% amongthose born 1994-95 (p < 0.0005). The percentage of preterm infants treated by phototherapy increased from 45.2%to 53.1% respectively in the two periods (p < 0.05). No significant change in the incidence of infants treated byphototherapy for blood group immunization occurred (0.6% and 0.7% respectively for the two periods; p > 0.05).The prevalence of infants treated by exchange transfusion decreased from 0.2% 1991-93 to 0.06% 1994-95 (p <0.05). Psychological and biological side-effects from phototherapy in healthy term infants may have been reducedby the changes in guidelines undertaken. The change in therapeutic guidelines has also resulted in a save ofresources. Applying these routines on a national base will avoid phototherapy in 1000-2000 term infants annually.Successively shorter stay of newborns in hospital after birth necessitates good routines for follow-up ofhyperbilirubinemia after discharge. The guidelines for phototherapy and exchange transfusion for neonatalhyperbilirubinemia should be rediscussed to obtain a national consensus.

Congenital malformations of the kidneys and urinary tract may have changed over time.Data for diagnosis, treatment and results were retrospectively recorded in children born in one of three Norwegian counties 1987-2006; their age at time of recording was from 1 to 21 years.389 of 142 986 (2.7 per 1000) live born children had malformations of the kidneys and/or urinary tract. The prevalence was higher for children born in the period 1997-2006 (241/70 217; 3.4 per 1000) than in 1987-1996 (148/72 769; 2.0 per 1000), p0.0011. The percentage of children with anomalies diagnosed prenatally increased significantly from the first born 10-year cohort (35/148; 24 %) to the last (125/241; 52 %), p0.0011. Urosepsis occurred in 8 (1.1 per 1000) patients in the first 10-year cohort and in 9 (1.3 per 1000) patients in the last cohort (p = 0.75). 137 (35 %) patients had undergone surgery, of whom 68 (0.9 per 1000) were born 1987-96 and 69 (1 per 1000) were born 1997-2006. Chronic renal failure developed in 6 patients (0.1 per 1000) in each 10-year cohort; 4 (0.05 per 1000) and 11 (0.16 per 1000) patients died in the two cohorts (p = 0.07) respectively.More frequent use of prenatal ultrasound screening has caused a 69 % increase in the prevalence of malformations in kidneys and the urinary tract. The number of patients treated by surgery, deaths and the prevalence of urosepsis and chronic renal failure has remained unchanged. This may indicate increased detection of less severe malformations.

To study whether breech presentation is a risk factor for cerebral palsy (CP).Perinatal data from 177 272 children born in breech or vertex presentation in Norway during 1996 to 1998 were retrieved from the Medical Birth Registry of Norway. Data were collected between 1 January 2003 and 31 March 2006. Data on 245 children with CP were recorded in the Norwegian Cerebral Palsy Registry. Odds ratios (OR) with 95% confidence intervals (CI) for CP among children born in breech compared with vertex presentation were calculated. Confounding was addressed in logistic regression and stratified analyses.Among the 245 children with CP (46.5% females and 53.5% males), 31% had unilateral, 49% bilateral, 7% dyskinetic, and 5% the ataxic subtype, and 8% of cases were unclassified. Among children born in breech, the OR for CP was 3.6 (95% CI 2.4-5.3). The increased risk was reduced when adjusted for preterm birth, plurality, and smallness for gestational age. Among singletons born in breech by vaginal delivery at term, the OR for CP was 3.9 (95% CI 1.6-9.7). Severity or subtype of CP did not differ between breech and vertex presentation.Breech delivery is a significant risk factor for CP, in particular among singletons born by vaginal delivery at term.

Objective: To compare strategies with and without first-day of life pulse oximetry screening to detect critical congenital heart defects (CCHDs). Study design: Population based study including all live born infants in Norway in 2005 and 2006 (n = 116 057). Postductal (foot) arterial oxygen saturation (SpO2) was measured in apparently healthy newborns after transferral to the nursery, with SpO2 < 95% as cut-off point. Out of 57 959 live births in the hospitals performing pulse oximetry screening, 50 008 (86%) were screened. Results: A total of 136 CCHDs (1.2 per 1000) were diagnosed, 38 (28%) of these prenatally. Of the CCHDs detected after birth, 44/50 (88%) were detected before discharge in the population offered pulse oximetry screening (25 by pulse oximetry), compared to 37/48 (77%) in the non-screened population (p = 0.15). Median times for diagnosing CCHDs in-hospital before discharge were 6 and 16 h after birth respectively (p < 0.0001). In the screened population 6/50 (12%) CCHDs were missed and recognized after discharge because of symptoms. Two of the six missed cases failed the pulse oximetry screening, but were overlooked (echocardiography not performed before discharge). If these cases had been recognized, 4/50 (8%) would have been missed compared to 11/48 (23%) in the non-screened population (p = 0.05). Of the cases missed, 14/17 (82%) had left-sided obstructive lesions. Conclusion: First-day of life pulse oximetry screening provides early in-hospital detection of CCHDs and may reduce the number missed and diagnosed after discharge.

Masteroppgave i økonomi og administrasjon - Universitetet i Agder 2009 This study attempts to identify drivers for efficiency in Micro Finance Institutions (MFIs) and determine their effect on the overall cost-efficiency of MFIs. The study used cross sectional data of 377 MFIs from 74 countries. Multivariate regression analysis was applied in order to find the results. Operational expense to portfolio, operational expense to assets and cost per credit client were used as efficiency measurements, 13 hypotheses were proposed and 17 variables were studied. Our results revealed that all except for two variables had a significant effect on one or more of the efficiency measurements. Credit officer productivity, cost per employee, loan outstanding average and credit officer ratio had a strong significant effect on all measurements. Our findings suggest that MFIs should increase their credit officer productivity and decrease the personnel expenses per employee in order to increase the overall cost-efficiency. Moreover, the MFIs should put more of their staff into income generating activities. Our findings also indicate that the MFIs should focus on more costefficient operations to avoid increased average loan amount and mission drift. Performance pay had no significant effect on the MFIs overall efficiency, which indicates that the MFIs incentive schemes motivate other performance measures than cost-efficiency. Modified incentives schemes should be considered to improve the cost-efficiency of MFIs.

Protein F1/GAP-43 is a protein kinase C substrate associated with axonal growth and synaptic plasticity. We used in situ hybridization in rat brain to determine the cellular distribution of its gene expression. Throughout the septotemporal axis of the adult hippocampus, pyramidal cells express F1/GAP-43 mRNA, but granule cells do not. To determine if F1/GAP-43 expression in granule cells ever occurs, we studied its expression in development during mossy fiber outgrowth, when expression should be maximal. Quantitation of relative hybridization levels in the hippocampus revealed a modest increase in granule cell F1/GAP-43 mRNA coincident with mossy fiber outgrowth. But even the peak hybridization in granule cells on day 16 was 75% less than in pyramidal cells. The distribution of grains was over the entire granule cell layer at day 9, but was restricted by day 20 to the inner aspect of the layer, the site of the youngest cells which are still sending out axonal processes. Cell-selective expression of F1/GAP-43 within a particular brain structure was not restricted to the hippocampus. In cerebellum, F1/GAP-43 hybridization was detected in granule cells but not Purkinje cells; in olfactory bulb, mitral cells but not internal granule cells; in habenula, cells in the lateral but not medial nucleus; in substantia nigra, pars compacta cells but not cells in pars reticulata. Neurons containing biogenic amines exhibited intense F1/GAP-43 hybridization: substantia nigra pars compacta (dopamine), the locus coeruleus (norepinephrine), and dorsal raphe (serotonin). In contrast, cholinergic neurons exhibited little (basal forebrain) or no (medial habenula) hybridization. F1/GAP-43 expression is not restricted to a specific cell type and is not correlated with axon length. High F1/GAP-43 expression is apparent in many neurons having either neuromodulatory or memory storage functions. We propose that F1/GAP-43 is important for accelerating process outgrowth and synaptic remodeling, rather than directing growth itself.

UNLABELLED Infants with potentially life threatening congenital heart defects (CHDs) are discharged from hospital after birth with the condition unrecognized. Improved prenatal ultrasound imaging and universal pulse oximetry screening of babies in nurseries are strategies that probably most would contribute to avoid such defects to be missed. CONCLUSION In general combining first day of life pulse oximetry, clinical examination and echocardiography before discharge in suspect cases is a rational strategy for early postnatal detection of heart defects. Universal echocardiography screening of newborns may be too resource consuming to be cost-effective.

The present study was undertaken to separate the impacts of a declining incidence of low birth weight from the effects of an improved perinatal care on perinatal mortality and incidence of cerebral palsy (CP) in an unselected population of infants and children. In the total population of infants with birth weight 500 g or more born in a Norwegian county (Vestfold) 1970-84 (n = 34,756), the incidence of low birth weight (500-2499 g) declined significantly, from 5% during the 10-year period 1970-79, to 4.1% during the 5-year period 1980-84 (p less than 0.01). The decline was stronger for very low birth weight infants (500-1499 g) than for moderately low birth weight infants (1500-2499 g) (31% vs. 13%; p less than 0.01). Perinatal mortality decreased from 17 to 10.3% (p less than 0.01), and the incidence of CP from 2.6 to 2.1% (p = 0.4). Because low birth weight infants were at increased risk for perinatal death and CP, the declining incidence of low birth weight was attributable 41.4% of the decline in perinatal mortality, and 40% of the reduction of CP from the period 1970-79 to 1980-84. Strategies for prevention of low birth weight may be important for further reduction of perinatal mortality and handicaps related to low birth weight.

Background/aim To describe prevalence, subtypes and severity of cerebral palsy (CP) in Norway using criteria proposed by the Surveillance of Cerebral Palsy in Europe (SCPE) network. Material All children in Norway with CP born in January 1996–December 1998 were registered in the Cerebral Palsy Registry of Norway. The Medical Birth Registry of Norway provided the perinatal data. Results A total of 374 children with CP were identified with a prevalence of 2.1 per 1000 live births. Detailed information was obtained from 294 (79%) children. Median age at clinical assessment was 6.9 years (range: 1.9–10.2 years). Thirty-three percent of the children had spastic unilateral CP, 49% spastic bilateral, 6% dyskinetic, 5% ataxic CP and 7% were not classified. Severely impaired vision and hearing were present in 5% and 4% of the children, respectively. Active epilepsy was present in 28%, mental retardation in 31% and severely impaired or no speech in 28% children. The most severe impairments in gross motor function were observed in children with low Apgar scores, and the most severe impairments in fine motor function in children born at term, with normal birth weight and low Apgar scores. Conclusion Compared with other populations, the prevalence of CP as well as the proportions of subtypes and gross motor impairments were similar, whereas fine motor impairments and associated impairments were more common. The classification of children with mixed forms of CP is still a challenge. Children were more severely affected if Apgar scores were low, and if they were born at term.

To register mortality and causes of death in patients with congenital heart defects (CHDs).Prospective population-based observational study.553 infants with CHD (1.1% of live born) were observed for 1-22 y (median 10 7/12 y). Sixty-four died (11.6%), of whom 32 (50%) died during the first 4 wk, and 51 (79.7%) during the first year of life. Of the total neonatal deaths in the population (3 per 1000), CHDs occurred in 21.5%. Mortality for children with CHDs was not significantly different between the cohorts born in 1982-1991 and 1992-2002, for either neonatal deaths or deaths later on (p0.05). Out of 170 patients in whom therapeutic procedures (surgery, catheter interventions) were undertaken, 34 (20%) died. Nine cases (1.6%) died with unrecognized CHDs; seven of these on the first day of life with severe extracardiac malformations. In 50 (78.1%) cases, death was judged to be caused directly or indirectly from the CHD, and in 14 (21.9%) from extracardiac malformations or other conditions.CHDs occur in a substantial number of neonatal deaths. Most deaths are caused by cardiac insufficiency. The mortality rate remained unchanged.

Neonatal transports carry risk of complications and technical mishaps which may cause deterioration of the patient's condition.Prospective observational study on all transports from the subregional neonatal unit, Vestfold Hospital, Norway to other hospitals during the 23-year period 1982-2004.396 transports were undertaken with a total of 359 patients, 0.7% of live born infants (n = 49,250). Indications were prematurity/respiratory distress syndrome (RDS) in 84 (21%), congenital malformations in 188 (47%), and other conditions in 124 (31%). After the establishment a local respirator programme 1989, transports for prematurity/RDS declined significantly from the 7-year period 1982 - 88 to the 16-year period 1989-2004 (3.4 vs. 1.0 per 1000 live born infants ;p0.0001). Night-time transports declined by 55 %. Technical mishaps occurred in 4% of the transports. No deaths occurred during transport; however, 10 infants (2.8%) died within 24 hours on arrival.Neonatal transports were associated with risk of deterioration. High local competence and up-to-date technical equipment for neonatal intensive care improve the quality of transport, reduce the incidence of transports of premature infants with RDS, and of transports during night-time.

An 80m long retrievable "one-run" straddle assembly was successfully installed in order to shut off a gas breakthrough in the 130 degrees deviated reservoir section of a "U shape/Fish hook" sub sea oil producer in the Njord field. Coiled tubing with an internal electric line in combination with a tandem fluid driven tractor was used to convey the straddle assembly.

This study present a review of erythrocyte transfusions in a neonatal intensive care unit in a Norwegian county hospital.Prospective registration 1991-2002. A leucokyte-depleted erythrocyte solution, haematocrit 60%, was used.28 infants in circulatory collapse received 30 transfusions because of asphyxia (15), twin-twin transfusion (5), septicaemia (3), umbilical cord rupture (3) or other causes (4). Haemoglobin increased 1.8 +/- 1.4 g/dl per 10 ml/kg transfused, compared to 2.6 +/- 1.2 g/dl in 183 transfusions for anaemia in 122 infants (p0.05). All transfusions (n = 115) after the first week of life were given because of anaemia, 107 in preterm (37 weeks) infants, and at higher haemoglobin levels in preterm infants with anaemia symptoms than in those without (9.7 +/- 1.5 vs. 8.5 +/- .2 g/dl, p0.05).The rise in haemoglobin was higher for transfusions for anaemia than for circulatory collapse, probably because of dilution from other fluids given and mobilisation of extravascular fluid in the last group. A substantial percentage of the transfusions were given on indications deviating from the guidelines.

To register the prevalence of cerebral palsy (CP) and determine etiological factors for the condition.Population based study with registration of CP-cases in children born during the 30-year period 1970-99. Cases with postneonatal etiology were excluded.166 CP-cases were registered among 70 824 children, a prevalence of 2.3 per 1000 live born infants. The prevalence did not change significantly during the period. 66 (40%) were low birthweight infants (LBWIs;2500 g), and 100 (60%) normal birthweight infants (NBWIs;or = 2500 g). The origin was classified as prenatal in 37 (22%), perinatal/neonatal in 78 (47%) and unclassifiable in 51 (31 %). In LBWIs 39/66 (59%) had a perinatal/neonatal etiology, most frequently intra- or periventricular hemorrhages (IVH/PVH) and/or periventricular leukomalacia (PVL) or cerebral infarctions (CI) (17; 44%). In NBWIs 39/100 (39%) had a perinatal etiology, most frequently hypoxic-ischemic encephalopathy (HIE) (31; 79%).In a substantial percentage of CP-cases perinatal/neonatal brain injury was classified as the cause. Among these IVH/PVH/PVL/CI dominated in LBWIs, while HIE dominated in NBWIs. Our data may point to preventability of a larger part of CP than earlier suggested.

Primary cultures of rat and mouse hippocampus and cerebral cortex are widely used to study neuronal properties such as axonal extension, synaptic transmission, and excitotoxicity. Short-term culturing of these neurons can be very straightforward and is perhaps easier than culturing cells lines once dissections are made and cell stocks are frozen. Long-term cultures of relatively pure neuronal populations require slightly more effort, but protocols are described that are less complicated than most published protocols. These include simpler ways to clean and coat coverslips, as well as using glia-conditioned medium to eliminate the need to make individual cocultures of neurons and glia. These methods consistently yield hippocampal and cortical cultures expressing dendritic spines and synapses that survive over 3 weeks in culture. For investigators employing biochemical assays where a fairly large amount of protein is necessary, cortical neurons may be especially attractive to use as large amounts of tissue are obtained and available for culture.

Ischemic injury induces actin cytoskeleton disruption and aggregation, but mechanisms affecting these changes remain unclear. To determine the role of actin-depolymerizing factor (ADF)/ cofilin participation in ischemic-induced actin cytoskeletal breakdown, we utilized porcine kidney cultured cells, LLC-PKA4.8, and adenovirus containing wild-type (wt), constitutively active, and inactive Xenopus ADF/cofilin linked to green fluorescence protein [XAC(wt)-GFP] in an ATP depletion model. High adenoviral infectivity (70%) in LLC-PKA4.8cells resulted in linearly increasing XAC(wt)-GFP and phosphorylated (p)XAC(wt)-GFP (inactive) expression. ATP depletion rapidly induced dephosphorylation, and, therefore, activation, of endogenous pcofilin as well as pXAC(wt)-GFP in conjunction with the formation of fluorescent XAC(wt)-GFP/actin aggregates and rods. No significant actin cytoskeletal alterations occurred with short-term ATP depletion of LLC-PKA4.8cells expressing GFP or the constitutively inactive mutant XAC(S3E)-GFP, but cells expressing the constitutively active mutant demonstrated nearly instantaneous actin disruption with aggregate and rod formation. Confocal image three-dimensional volume reconstructions of normal and ATP-depleted LLC-PKA4.8cells demonstrated that 25 min of ATP depletion induced a rapid increase in XAC(wt)-GFP apical and basal signal in addition to XAC-GFP/actin aggregate formation. These data demonstrate XAC(wt)-GFP participates in ischemia-induced actin cytoskeletal alterations and determines the rate and extent of these ATP depletion-induced cellular alterations.

Primary cultures of rat and mouse hippocampus and cerebral cortex are widely used to study neuronal properties such as axonal extension, synaptic transmission, and excitotoxicity. Short-term culturing of these neurons can be very straightforward and is perhaps easier than culturing cells lines once dissections are made and cell stocks are frozen. Long-term cultures of relatively pure neuronal populations require slightly more effort, but protocols are described that are less complicated than most published protocols. These include simpler ways to clean and coat coverslips, as well as using glia-conditioned medium to eliminate the need to make individual cocultures of neurons and glia. These methods consistently yield hippocampal and cortical cultures expressing dendritic spines and synapses that survive over 3 weeks in culture. For investigators employing biochemical assays where a fairly large amount of protein is necessary, cortical neurons may be especially attractive to use as large amounts of tissue are obtained and available for culture.

In a population based study including 35,218 infants born alive during the 15-year period 1982-1996, 360 (1%) were diagnosed having a congenital heart defect (CHD). At a follow-up 3-18 years later (median 9.5 years) 154 patients (42.8%) were spontaneously cured, of whom 142 (92.2%) had ventricular septal defects (VSD). 42 patients (11.7%) had died, 22 of whom (52.4%) during the neonatal period (0-28 days after birth). A total of 119 patients (33.1%) underwent therapeutic procedures (surgery, catheter interventions), of whom 24 (20.2%) died. Of the 95 children surviving therapeutic procedures 54 (56.8%) had their defects completely repaired, while 41 (43.2%) had residual defects or cardiac sequelae, often of minor importance. Of 69 children (19.2%) with persistent untreated defects, 43 (62.3%) had VSD. A chromosomal disorder, various syndromes or extracardiac malformations occurred in 72 children (20%). The study underlines the fact that CHD presents itself in varying degrees of severity, including a high neonatal mortality rate as well as a high rate of spontaneous cure.

An investigation of the prevalence of cerebral palsy in relation to neonatal intensive care.Population based study in live-born children with birthweightor = 500 g in the Norwegian county of Vestfold over the 25-year period 1970-94 (n = 58,448). Retrospective and prospective control of cases (cases with a postneonatal origin of cerebral palsy excluded) with a minimum follow-up to four years of age.Cerebral palsy was diagnosed in 139 cases (2.4 per 1,000). The prevalence declined from 2.8 per 1,000 in the first five-year cohort born 1970-74, to 2.2 per 1,000 in children born in each of the three five-year cohorts born 1980-84, 1985-89, and 1990-94 (p = 0.24). The neonatal mortality rate declined significantly from 8.7 per 1,000 in the first to 2.8 per 1,000 in the last five-year cohort (p0.0001). The low birthweight (500-2,499 g) rate in live-born infants increased significantly in 1990-94 compared to 1985-89 (4.5% vs 3.9% respectively; p0.05). After a local ventilator treatment programme (operative from 1989) was established, transports of infants with severe respiratory distress syndrome to the regional hospital declined from 3 per 1,000 live-born infants to 1 per 1,000 (p0.0001).A decentralised neonatal intensive care programme can be developed, with substantial decline in neonatal mortality without a corresponding increase in cerebral palsy prevalence.

Previously, we constructed a set of mutants from which eight penicillin binding protein (PBP) genes were deleted in 192 combinations from Escherichia coli (S. A. Denome, P. K. Elf, T. A. Henderson, D. E. Nelson, and K. D. Young, J. Bacteriol. 181:3981-3993, 1999). Although these mutants were constructed correctly as determined by restriction mapping and the absence of relevant protein products, we recently discovered by PCR mapping that strains from which mrcA (PBP 1a) was deleted were also missing two neighboring genes of unknown function ( yrfE and yrfF ). We created a new deletion mutation in mrcA and reconstructed 63 strains lacking PBP 1a and other PBP mutant combinations. The new mrcA mutants do not exhibit mucoidy, phage resistance, temperature sensitivity, growth rate defects, or antibiotic resistance, suggesting that these phenotypes require the loss of either yrfE or yrfF alone or in combination with the absence of multiple PBPs.

It is becoming increasingly evident that proteins of the actin depolymerizing factor (ADF)/cofilin family are essential regulators of actin turnover required for many actin-based cellular processes, including motility. ADF can increase actin turnover by either increasing the rate of actin filament treadmilling or by severing actin filaments. In neurons ADF is highly expressed in neuronal growth cones and its activity is regulated by many signals that affect growth cone motility. In addition, increased activity of ADF causes an increase in neurite extension. ADF activity is inhibited upon phosphorylation by LIM kinases (LIMK), kinases activated by members of the Rho family of small GTPases. ADF become dephosphorylated downstream of signal pathways that activate PI-3 kinase or increase levels of intracellular calcium. The growth-regulating effects of ADF together with its ability to be regulated by a wide variety of guidance cues, suggest that ADF may regulate growth cone advance and navigation.

were born at term. In our opinion, the major problem with the paper is in the conclusion section where Andersen et al. state that the most noteworthy finding is a fourfold-increased risk for CP among singletons born at term and delivered vaginally. In the results section, however, they write that the risk for CP among singleton term infants is not significantly influenced by mode of delivery (odds ratio 1.7 for vaginal delivery compared with Caesarean section with confidence interval 0.5–6.4). Also, it should be pointed out that this comparison was based on 4 cases versus 5 cases only (Table II). Thus, the authors misinterpret their own data. After having established breech presentation as an independent risk factor for CP, it is misleading to compare infants born in breech presentation delivered vaginally with those born in vertex presentation. This misinterpretation is underlined in the last paragraph where the authors write, ‘It is possible that a few cases of CP could have been prevented had Caesarean section been performed in all cases of term breech delivery...’. This conclusion is not supported by the data presented in the paper. The appropriate conclusion from this study is that vaginal breech delivery of singleton infants at term in Norway is a safe procedure with good results, and the results do not provide any indications that routine Caesarean section in term breech presentation would prevent any cases of CP.

Growth cone motility and navigation in response to extracellular signals are regulated by actin dynamics. To better understand actin involvement in these processes we determined how and in what form actin reaches growth cones, and once there, how actin assembly is regulated. A continuous supply of actin is maintained at the axon tip by slow transport, the mobile component consisting of an unassembled form of actin. Actin is co-transported with actin-binding proteins, including ADF and cofilin, structurally related proteins essential for rapid turnover of actin filaments in vivo. ADF and cofilin activity is regulated through phosphorylation by LIM kinases, downstream effectors of the Rho family of GTPases, Cdc42, Rac and Rho. Attractive and repulsive extracellular guidance cues might locally alter actin dynamics by binding specific GTPase-linked receptors, activating LIM kinases, and subsequently modulating the activity of ADF/cofilin. ADF is enriched in growth cones and is required for neurite outgrowth. In addition, signals that influence growth cone behavior alter ADF/cofilin phosphorylation, and overexpression of ADF enhances neurite outgrowth. Growth promoting effects of laminin are mimicked by expression of constitutively active Cdc42 and blocked by expression of the dominant negative Cdc42. Repulsive effects of myelin and sema3D on growth cones are blocked by expression of constitutively active Rac1 and dominant negative Rac1, respectively. Thus a series of complex pathways must exist for regulating effectors of actin dynamics. The bifurcating nature of the ADF/cofilin phosphorylation pathway may provide the integration necessary for this complex regulation.

Growth cone motility is regulated by changes in actin dynamics. Actin depolymerizing factor (ADF) is an important regulator of actin dynamics, and extracellular signal-induced changes in ADF activity may influence growth cone motility and neurite extension. To determine this directly, we overexpressed ADF in primary neurons and analyzed neurite lengths. Recombinant adenoviruses were constructed that express wild-typeXenopusADF/cofilin [XAC(wt)], as well as two mutant forms of XAC, the active but nonphosphorylatable XAC(A3) and the less active, pseudophosphorylated XAC(E3). XAC expression was detectable on Western blots 24 hr after infection and peaked at 3 d in cultured rat cortical neurons. Peak expression was ∼75% that of endogenous ADF. XAC(wt) expression caused a slight increase in growth cone area and filopodia but decreased filopodia numbers on neurite shafts. At maximal XAC levels, neurite lengths increased >50% compared with controls infected with a green fluorescent protein-expressing adenovirus. Increased neurite extension was directly related to the expression of active XAC. Expression of the XAC(E3) mutant did not increase neurite extension, whereas expression of the XAC(A3) mutant increased neurite extension but to a lesser extent than XAC(wt), which was partially phosphorylated. XAC expression had minimal, if any, impact on F-actin levels and did not result in compensatory changes in the expression of endogenous ADF or actin. However, F-actin turnover appeared to increase based on F-actin loss after treatment with drugs that block actin polymerization. These results provide direct evidence that increased ADF activity promotes process extension and neurite outgrowth.

In a population-based study of 35,218 infants born alive during the 15 years from 1982 to 1996, 353(1%) were diagnosed as having a congenital heart defect, of whom 84 (24%) were diagnosed subsequent to discharge from hospital after birth (2.4/1000). Of these, 40 (48%) had a ventricular septal defect, 14 (17%) an atrial septal defect, 9 (11%) a patent arterial duct, 8 (10%) an aortic stenosis and 13 (15%) other defects. Compared with those in whom diagnosis was made before discharge, the group of patients with defects detected late had an increased prevalence of atrial septal defects, patent arterial duct and aortic stenosis, but less decreased prevalence of ventricular septal defects (p< 0.05). Median age at detection of the defects subsequent to discharge was 6 months (range 2 weeks–11 years). Seven patients (8%) presented with clinical symptoms of cardiac decompensation. The mortality rate was significantly lower in those in whom defects were detected late (1/84; 1%) as compared with those detected immediately after birth (37/269; 14%) (p< 0.05). The total rate for early detection was the same after using one clinical examination (8.2/1000) of newborns as our basic routine instead of two (7.1/1000) (p> 0.05). A substantial proportion of congenital cardiac malformations are detected after discharge from hospital after birth. Some patients with these lesions present with cardiac decompensation and are in need of medication and surgery. One clinical examination of newborns detects congenital malformations of the heart as efficient as two.

Dendritic arbor formation and the underlying mechanisms are crucial for the functional connectivity and plasticity of neurons. We used a focal electric field to locally raise calcium levels in individual dendritic shafts of isolated hippocampal pyramidal neurons, in order to develop an accessible system for studying dendritic branch formation, and to test the role of calcium as an intrinsic signal that may participate in arborization. Filopodia were induced in a manner temporally and spatially related to induced calcium rises. Certain filopodia also thickened and were transformed into dendritic branches. These results suggest that calcium-mediated signaling can induce branching in dendrites, and describe an accessible system for studying the intracellular machinery that drives dendritic arborization.

All medication administered to patients admitted to a neonatal intensive care unit was registered during a one-year period (1996). Only two (0.4%) of 469 infants admitted were not given any drug at all. A total of 12,019 single doses were administered, a mean of 33 per day. 7,042 (59%) were given orally, and 3,332 (28%) intravenously. 292 (63%) patients were given vitamin K as the only drug. 113 infants (24%) received systemic antibiotic treatment, 5% of all infants born alive at the hospital. Drugs accounted for 2.7% of the total expenses for running the unit. Surfactant (12 single doses) alone accounted for 47% of the costs of drugs. Drug monitoring by serum concentration measurements showed that 32% of the values were outside the therapeutic range. To a limited extent (44%) this was followed by correction of the dose. One single drug dose (1 per 10,000 doses) was administered to a patient for whom the drug was not prescribed. Quality assurance of medication is an important task in neonatal intensive care units.