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Thor Willy Ruud Hansen

Publications and source records attributed to Thor Willy Ruud Hansen.

At least 19 recordsLinked to original sources
PubMed2006

Recovery after short-term bilirubin exposure in human NT2-N neurons.

We used human NT2-N neurons to investigate delayed effects of short-term exposure to unconjugated bilirubin (UCB). Cell viability was evaluated with MTT reduction assays and nuclear morphology. A 6-h exposure to 1, 5, or 25 microM UCB and serum deprivation (SED) significantly diminished MTT reduction. 96 h after rescue of neurons with removal of UCB and re-incubation in the original serum-containing medium, delayed effects were evident as recovery (1 microM UCB), intermediate cell death (5 microM UCB), or near complete cell death (25 microM UCB). The impact of 6 h of SED alone appeared to be modest in rescued neurons. In this model, co-treatment with the specific caspase-3 inhibitor, zDEVD.FMK (100 microM), or the pancaspase inhibitor zVAD.FMK (100 microM) did not improve viability in rescued neurons exposed to 5 microM UCB, while treatment with the NMDA receptor antagonist MK-801 (1 microM) enhanced the number of undamaged nuclei (86 +/- 14% versus 50 +/- 12%, P = 0.001). MK-801 had, however, no impact on MTT reduction. In a different model with a 102-h continuous exposure to UCB and SED, we found a significant additional toxic impact of serum deprivation. Separate experiments suggested that this was a result of late caspase-mediated toxicity. We conclude that UCB-mediated effects may be reversible in this model. Blockade of excitotoxic mechanisms, but not caspase activity may prevent delayed cell death.

Apoptosis↗
PubMed2006

A Quisling on neonatal jaundice.

BACKGROUND/METHODS: Nils Andreas Quisling was born in Telemark, Norway, in 1854 and became an obstetrician. In 1893 he published a monograph on neonatal jaundice. This monograph was studied and compared with other published sources from the same time period. RESULTS: Quisling discussed four theories on the cause of neonatal jaundice. "Suppression jaundice" held that jaundice was the result of suppressed liver function. "Haematogenous jaundice" claimed that bilirubin was formed from haemoglobin outside the liver, and had nothing to do with the liver. "Polycholia" held that neonatal jaundice was due to an increased secretion of all the constituents of bile. Quisling rejected these and supported the "hepatogenous" theory-jaundice was always a liver-related phenomenon. He described 50 cases of neonatal jaundice. The incidence of neonatal jaundice at the Kristiania Maternity Foundation was 26%. In Quisling's cases, gastrointestinal disturbances were common, and he felt this to be an under-reported complication of neonatal jaundice. He found that neonatal jaundice was often accompanied by fever. CONCLUSION: Gastrointestinal disturbances were causally involved in neonatal jaundice, resulting in impeded bile drainage. At the time of Quisling's study (1887), this "hepatogenous" theory of neonatal jaundice probably still had majority support in the European literature.

History, 19th Century↗
PubMed2005

[Quality evaluation of neonatal transports].

BACKGROUND: Neonatal transports carry risk of complications and technical mishaps which may cause deterioration of the patient's condition. MATERIAL AND METHODS: Prospective observational study on all transports from the subregional neonatal unit, Vestfold Hospital, Norway to other hospitals during the 23-year period 1982-2004. RESULTS: 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 ;p < 0.0001). 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. INTERPRETATION: 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.

Air Ambulances↗
PubMed2005

[Treatment of neonatal jaundice].

BACKGROUND: Examination for and treatment of jaundice is one of the most common occurrences in neonatal medicine. Neonatal jaundice has a foundation in normal physiology, but may be exacerbated by a number of factors. Therapy is given because pronounced jaundice carries a risk for brain damage (kernicterus). Intervention limits for therapy continue to be debated, as the scientific basis suffers from obvious weaknesses. MATERIAL AND METHODS: The American Academy of Pediatrics recently published new guidelines for the management of hyperbilirubinaemia in newborns. The new guidelines differ in important aspects from those published in 1994. Several new elements in the guidelines are of interest to Norwegian paediatricians. RESULTS: The goal of the new guidelines is to reduce the incidence of severe jaundice and kernicterus in neonates. As opposed to the 1994 guidelines, the new guidelines provide specific advice on the management of moderately premature infants, infants with haemolysis, and sick infants. The importance of early risk assessment is stressed, as well as the need for individualized follow up after discharge. INTERPRETATION: The new AAP guidelines introduce important elements compared to the previous ones and should contribute to safer management of jaundiced neonates. Norwegian paediatricians will find useful information in the new guidelines.

Bilirubin↗
PubMed2005

Changes in the utilization of diagnostic codes in neonatology following the introduction of activity-based financing.

Activity-based financing was introduced in public hospitals in Norway in 1997. Following this, hospitals have been financed in part by block grants, in part by grants based on productivity as measured through weighted diagnosis-related groups (DRGs). Insufficient national data were available to allow for proper calculation of DRG weights for neonatology. Thus, data from other countries were used to estimate weights. It seemed of interest to examine whether the use of diagnostic codes in neonatal medicine was changed following the introduction of activity-based financing and DRGs. Data from 1994, 1996, 1998, and 2000 were obtained from the proprietary database of the NICU at Rikshospitalet, University of Oslo, as well as from the hospital Patient Information Management System. Diagnoses were organized into 39 categories, counted for each of the 4 years, and analyzed by non-parametric ANOVA. There were significant changes in the use of diagnostic categories during the 1994-2000 time period. Some diagnoses which previously have been only rarely used, became more frequent. The use of other diagnoses varied in ways that could only be understood in terms of tactical usage. It is concluded that the use of DRGs as a basis for activity-based financing may result in changes in the use of certain diagnostic categories which are not related to biological changes in the patient population. This may complicate epidemiological research. On the other hand, activity-based financing may result in increased attention to the diagnostic process, leading to increased use of secondary diagnoses and thus more complete diagnostic coding.

Diagnosis-Related Groups↗
PubMed2005

Nils Rosén von Rosenstein and neonatal jaundice in the 18th century.

BACKGROUND: Nils Rosén von Rosenstein (1706-1773) was a Swedish nobleman and a professor at Uppsala University. His series of lectures on children's diseases and their treatment was published in 1764 under the title Underrättelser om Barn-Sjukdomar och Deras Bote-Medel. MATERIALS AND METHODS: Rosén von Rosenstein's book was translated into several languages. The present paper deals with the opinions and advice proffered on the jaundiced neonate in chapter 25 of the Danish edition from 1769. RESULTS: The distinction between jaundice in the neonate and jaundice in older children is not clear everywhere in the chapter, and much of Rosén von Rosenstein's advice on therapy appears to be intended for all age groups. Rosén von Rosenstein believed that neonatal jaundice was less common in Sweden than elsewhere, and ascribed this to the common practice of purging newborns with a manna sugar laxative. The principal cause of jaundice, according to Rosén von Rosenstein, was bile stasis. When milk curdled in the stomach, the curds could plug the common bile duct, and bile would be forced into the lymphatics and from there into the blood. Thus, the bile was carried around the body and caused the skin and the sclera, as well as other organs, to become yellow. Cure was usually easy-a laxative in the form of puréed manna with powdered rhubarb was what Rosén von Rosenstein recommended. CONCLUSION: Rosén von Rosenstein's opinions and advice concerning neonatal jaundice were not original, and did not differ from those found in other medical texts from the 18th and 19th centuries. The bile stasis explanation for all kinds of jaundice, including neonatal jaundice, was widely held in the 18th century, and continued to predominate in paediatric texts until the end of the 19th century. Similarly, laxatives and enemas as the cure-all for many ailments held sway until the late 1800s.

History, 18th Century↗
PubMed2004

Bilirubin induces apoptosis and necrosis in human NT2-N neurons.

Studies on primary cultures of newborn rodent neurons have suggested that neuronal death induced by unconjugated bilirubin (UCB) is mainly apoptotic in nature. We exposed a human teratocarcinoma-derived cell line, NT2-N neurons, to different concentrations of UCB and albumin at a 1.5 molar ratio and used multiple, independent measures of cell damage to evaluate neuronal injury after 6, 24, and 48 h. Low doses of UCB (0.66, 2, and 5 microM) induced a moderate loss of 3-4[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide (MTT) cleavage accompanied by delayed morphologic changes consistent with apoptosis (2 and 5 microM). Moderate concentrations of UCB (10 and 25 microM) resulted in early (6 h) necrosis in a subset of neurons, while remaining neurons underwent progressive impairment of MTT cleavage and increasing lactate dehydrogenase (LDH) release accompanied by predominantly delayed apoptosis. High concentrations of UCB (100 microM) induced severe impairment of MTT cleavage, extensive LDH release, and morphologic changes consistent with necrosis within 6 h. Used as a positive control for apoptosis, 2 microM STS induced progressive impairment of MTT cleavage and morphologic changes consistent with apoptosis over the entire observation period. DNA electrophoresis at 48 h was compatible with apoptosis both after treatment with STS and UCB concentrations <or=25, but not at 100 microM. Cleavage of poly (ADP-ribose) polymerase (PARP) was only seen in neurons treated with low UCB concentrations and STS. We conclude that UCB induces early necrosis at high and moderate concentrations and predominantly delayed apoptosis at low and moderate concentrations in cultured human NT2-N neurons.

Apoptosis↗
PubMed2004

Deaths in a neonatal intensive care unit: a 10-year perspective.

OBJECTIVE: To examine changes in the characteristics and management of infants dying in a regional neonatal intensive care unit in 1987-1988 vs. 1997-1998. SETTING: The level III Neonatal Intensive Care Unit (NICU) at Rikshospitalet, Oslo, Norway, handles both regional and national referrals. DESIGN/METHODS: The study was retrospective and observational. Patients who died in the neonatal intensive care unit were identified using our own and the hospital's data records. Charts were reviewed by the principal author. RESULTS: The mortality rate relative to admissions decreased significantly from 1987-1988 to 1997-1998 (6.9% vs. 3.4%, p <.0001). Infants who died in 1997-1998 were more mature and had higher birth weights than those who died in 1987-1988 (34.0 +/- 5.5 vs. 32 +/- 6.0 wks gestational age [mean +/- sd], p <.05; and 2,186 +/- 1,207 vs. 1,699 +/- 1,038 g, p <.05). There was a significantly higher proportion of infants with complex congenital malformations among those who died in 1997-1998 (54% vs. 28%, p <.005). Forgoing intensive care treatment was more commonly associated with the process of dying in 1997-1998 than 10 yrs earlier (63.5% vs. 22.8%, p <.0001). Parental involvement in the process leading to a decision to forgo life support was more frequently described in the charts from 1997-1998 (72.7% vs. 23.8%, p <.001). During the last time period, parents were also present at the time of death significantly more often. CONCLUSIONS: The mortality rate of sick infants decreased significantly between 1987-1988 and 1997-1998, showing the improvements in neonatal intensive care during that decade. In 1997-1998, congenital malformations had become the leading cause of death. Parental involvement in life-and-death questions seems to have become the rule, and almost two thirds of neonatal intensive care unit deaths followed a decision to forgo life support.

Cause of Death↗
PubMed2003

Recent advances in the pharmacotherapy for hyperbilirubinaemia in the neonate.

Jaundice is a common cause for diagnostic works-up and therapeutic intervention in neonates. This is motivated by the risk for severe neurological sequelae (kernicterus). The mainstays of treatment for the past decades have been exchange transfusion and phototherapy. Exchange transfusion is now becoming rare due to immune prophylaxis in Rhesus-negative women, and treatment of sensitised infants with intravenous immunoglobulin. Several different pharmacological approaches have been studied as far as the treatment of neonatal jaundice. Of these, the focus of attention in recent years has been on the haem oxygenase inhibitors (metal meso- and protoporphyrins). These are effective inhibitors of bilirubin production and have been shown to significantly reduce peak serum bilirubin levels in several clinical trials, both when used prophylactically and therapeutically. However, questions remain regarding long-term safety, as well as the advisability of whole-scale inhibition of bilirubin production. Nevertheless, in selected infants with a high risk of severe jaundice, the use of haem oxygenase inhibitors may be acceptable. Pharmacotherapy in jaundiced infants is fraught with risks, as many drugs may increase the entry of bilirubin into the brain and presumably, the risk for neurotoxicity. Both the displacement of bilirubin from its albumin binding and interference with the function of phosphoglycoprotein in the blood-brain barrier are documented mechanisms in this respect.

Animals↗
PubMed2002

[Screening for congenital hearing loss--a pilot project].

BACKGROUND: Until recently in Norway, congenital hearing loss has on average been diagnosed at 2.8 years of age. Delayed diagnosis is associated with loss of valuable opportunities for auditory habilitation and speech development. MATERIAL AND METHODS: Since September 1999 we have carried out universal screening for congenital hearing loss in both healthy and sick newborns. During the first screening period, all newborns were screened with automated auditory brainstem response audiometry. In the second period all healthy infants were screened primarily with otoacoustic emission audiometry, with automated auditory brainstem response audiometry as a second stage screening for those who failed the otoacoustic emission test. 3,996 infants were screened from start-up until December 2001. RESULTS: Hearing loss was confirmed in 25 patients (11 unilateral and 14 bilateral). A further two patients were referred but found to have normal hearing. The incidence of congenital hearing loss was 0.16% in presumed healthy infants and 2.2% in infants admitted to the intensive care nursery. INTERPRETATION: Screening for congenital hearing loss can be carried out with a very low rate of referrals and a low rate of false positive tests, particularly if there is access to otoacoustic emission as well as automated auditory brainstem response testing. In our opinion, Norway now needs to legislate for universal screening for congenital hearing loss in the neonatal period. Our departments of audiology should be given the opportunity and resources to upgrade their skills in relation to this new group of patients.

Audiometry↗
PubMed2002

[Fiberoptic phototherapy for neonatal icterus--comments to a Cochrane report].

Twenty-four studies filled the inclusion criteria for a Cochrane report on the use of fiberoptic phototherapy for neonatal jaundice. Fiberoptic phototherapy lowers serum bilirubin and may have a place in the treatment of neonatal jaundice. In term and near-term infants fiberoptic phototherapy is inferior to conventional phototherapy, whereas in premature infants the effects are comparable. A better effect is achieved when conventional and fiberoptic phototherapy are combined as compared to conventional phototherapy alone. Fiberoptic phototherapy has not been shown to interfere less with parent-infant bonding than conventional phototherapy. There is still a great need for more research on phototherapy for neonatal jaundice.

Evidence-Based Medicine↗
PubMed2002

Mechanisms of bilirubin toxicity: clinical implications.

The basic mechanism of kernicterus and bilirubin encephalopathy has not been unequivocally determined. Much knowledge has been gained about phenomena that contribute to bilirubin neurotoxicity, and this knowledge has implications for clinical practice. Conditions that impact on blood-brain barrier function, increase brain blood flow, or impact on bilirubin metabolism, including its transport in serum, should be avoided, if possible. Such conditions include drugs and drug stabilizers that compete with bilirubin binding to albumin, or that inhibit P-glycoprotein in the blood-brain barrier, prematurity/immaturity, and clinically significant illness in the infant that involves hemolysis, respiratory and metabolic acidosis, infection, asphyxia, hypoxia and (perhaps) hyperoxia, and hyperosmolality. If these conditions are not avoidable then there should be a more aggressive approach to the treatment of hyperbilirubinemia. The limits of tolerance for hyperbilirubinemia varies among neonates and there are no tools to determine with certainty when a particular infant is approaching the danger zone. Neurological symptoms in a jaundiced infant require extreme vigilance, and, in most cases, immediate intervention.

Bilirubin↗