Bjørnar Hassel

• Dahlberg, Daniel; Holm, Sverre; Sagen, Ellen Lund; Michelsen, Annika Elisabet; Stensland, Maria & De Souza, Gustavo Antonio [Vis alle 10 forfattere av denne artikkelen] (2023). Bacterial Brain Abscesses Expand Despite Effective Antibiotic Treatment: A Process Powered by Osmosis Due to Neutrophil Cell Death. Neurosurgery. ISSN 0148-396X. doi: 10.1227/neu.0000000000002792. Fulltekst i vitenarkiv
• Bull, Emilie Meyer; Nærland, Terje; Lahlum, Silje; Szabo, Attila; Andreassen, Ole & Quintana, Daniel (2023). Development and Validation of the Non-Verbal Patient-Caregiver Understanding Questionnaire (NPUQ): Assessing Communication Challenges and Their Impacts. OSF Preprints. doi: 10.31234/osf.io/89ktd.
• Bull, Emilie Meyer; Audunsdottir, Kristin; Jacobsen, Henrik Børsting; Kang, Heemin; Sartorius, Alina Marie & Glaser, Bernt Damian [Vis alle 13 forfattere av denne artikkelen] (2023). Heart Rate Variability and Pain: A Protocol for a Systematic Review and Meta-Analysis. OSF Preprints. doi: 10.31219/osf.io/arfm6.
• Øderud, Tone; Boysen, Elin Sundby; Strisland, Frode; Dahl, Inger-Lise; Bull, Emilie Meyer & Hassel, Bjørnar (2023). Identifying pain and distress in non-verbal persons with intellectual disability: Professional caregivers' and parents' attitudes towards using wearable sensors. Technology and Disability. ISSN 1055-4181. 35(3), s. 207–216. doi: 10.3233/TAD-220390. Fulltekst i vitenarkiv
• Jamali, Ahmed; Kristensen, Erle; Tangeraas, Trine; Arntsen, Vibeke; Sikric, Alma & Kupliauskiene, Guste [Vis alle 12 forfattere av denne artikkelen] (2023). The spectrum of pyridoxine dependent epilepsy across the age span: A nationwide retrospective observational study. Epilepsy Research. ISSN 0920-1211. 190. doi: 10.1016/j.eplepsyres.2023.107099. Fulltekst i vitenarkiv Vis sammendrag

  Background Pyridoxine-dependent epilepsy (PDE) is a rare seizure disorder usually presenting with neonatal seizures. Most cases are caused by biallelic pathogenic ALDH7A1variants. While anti-seizure medications are ineffective, pyridoxine provides seizure control, and dietary interventions may be of benefit. As the natural history beyond adolescence is insufficiently explored, our study aimed to assess the spectrum of PDE at various ages in Norway. Methods Patients were ascertained by contacting all Norwegian paediatric, neurological, and neurohabilitation departments and relevant professional societies. Medical records were collected and reviewed. Results We identified 15 patients treated for PDE; 13 had ALDH7A1 variants (PDE-ALDH7A1), one had PNPO deficiency, and in one, aetiology remained obscure. Of those with PDE-ALDH7A1, 12 were alive at time of study; five were > 18 years old and six were 1 h) or uncertain effect. Median delay from first seizure to continuous treatment was 11 days (range 0–42). Nine experienced breakthrough seizures with intercurrent disease or due to pyridoxine discontinuation. Cognitive outcomes ranged from normal to severe intellectual disability. The condition appeared to remain stable in adult life. Significance We found a much higher prevalence of PDE-ALDH7A1 in children relative to adults, suggesting previous underdiagnosis and early mortality. Perinatal complications are common and can delay diagnosis and initiation of pyridoxine treatment. Lifelong and continuous treatment with pyridoxine is imperative. Due to better diagnostics and survival, the number of adult patients is expected to rise.

• Watne, Leiv Otto; Pollmann, Christian Thomas; Neerland, Bjørn Erik; Paulsen, Else Quist; Halaas, Nathalie Bodd & Idland, Ane-Victoria [Vis alle 19 forfattere av denne artikkelen] (2022). Cerebrospinal fluid quinolinic acid is strongly associated with delirium and mortality in hip-fracture patients. Journal of Clinical Investigation. ISSN 0021-9738. 133(2). doi: 10.1172/JCI163472. Fulltekst i vitenarkiv Vis sammendrag

  Background: The kynurenine pathway (KP) has been identified as a potential mediator linking acute illness to cognitive dysfunction by generating neuroactive metabolites in response to inflammation. Delirium (acute confusion) is a common complication of acute illness and is associated with increased risk of dementia and mortality. However, the molecular mechanism underlying delirium, particularly in relation to the KP, remain elusive. Methods: We undertook a multi-center observational study with 586 hospitalized patients (248 with delirium) and investigated associations between delirium and KP metabolites measured in cerebrospinal fluid (CSF) and serum by targeted metabolomics. We also explored associations between KP metabolites and markers of neuronal damage and one-year mortality. Results: In delirium, we found concentrations of the neurotoxic metabolite quinolinic acid in CSF (CSF-QA, OR 2.26 [1.78, 2.87], p

• Rogne, Ane Gretesdatter & Hassel, Bjørnar (2022). Improvement of attention deficit/hyperactivity disorder (ADHD) in three adult men during testosterone treatment: a case series. Journal of Medical Case Reports. ISSN 1752-1947. 16(1), s. 1–7. doi: 10.1186/s13256-022-03651-w. Fulltekst i vitenarkiv
• Svae, Gøril Brevik; Hassel, Bjørnar & Søndenaa, Erik (2022). People with intellectual disabilities and harmful sexual behaviour: Professionals' views on the barriers to prevent harm. JARID: Journal of applied research in intellectual disabilities. ISSN 1360-2322. 36(1), s. 176–185. doi: 10.1111/jar.13048. Fulltekst i vitenarkiv Vis sammendrag

  Background People with intellectual disabilities can be exposed to sexual abuse and they can display harmful sexual behaviour. This study aimed to identify barriers to preventing harmful sexual behaviour in people with intellectual disabilities within the support sector and the justice system. Method We conducted focus group interviews with 20 participants from hospital-based habilitation centres, community residences, schools and the criminal justice system. Results The interviews identified a lack of education and guidelines for stakeholders or carers on regulating the sexual behaviour of people with intellectual disabilities. The criminal justice system faces challenges related to prioritising, understanding and communicating. People with intellectual disabilities may lack an understanding of the concepts of sexual consent and acceptable sexual behaviour. Conclusion There is a need to improve knowledge about intellectual disability and how to prevent harmful sexual behaviour for professional caregivers in the support sector and the criminal justice system.

• Kildal, Emilie Smith-Meyer; Hassel, Bjørnar & Bjørnebekk, Astrid (2022). ADHD symptoms and use of anabolic androgenic steroids among male weightlifters. Scientific Reports. ISSN 2045-2322. 12(1), s. 1–8. doi: 10.1038/s41598-022-12977-w. Fulltekst i vitenarkiv
• Hassel, Bjørnar; Niehusmann, Pitt; Halvorsen, Bente & Dahlberg, Daniel (2022). Pro-inflammatory cytokines in cystic glioblastoma: A quantitative study with a comparison with bacterial brain abscesses. With an MRI investigation of displacement and destruction of the brain tissue surrounding a glioblastoma. Frontiers in Oncology. ISSN 2234-943X. 12. doi: 10.3389/fonc.2022.846674. Fulltekst i vitenarkiv
• Dahlberg, Daniel; Rummel, Jutta; Distante, Sonia; De Souza, Gustavo Antonio; Stensland, Maria & Mariussen, Espen [Vis alle 7 forfattere av denne artikkelen] (2022). Glioblastoma microenvironment contains multiple hormonal and non-hormonal growth-stimulating factors. Fluids and Barriers of the CNS. ISSN 2045-8118. 19. doi: 10.1186/s12987-022-00333-z. Fulltekst i vitenarkiv Vis sammendrag

  Background The growth of malignant tumors is influenced by their microenvironment. Glioblastoma, an aggressive primary brain tumor, may have cysts containing fluid that represents the tumor microenvironment. The aim of this study was to investigate whether the cyst fluid of cystic glioblastomas contains growth-stimulating factors. Identification of such growth factors may pave the way for the development of targeted anti-glioblastoma therapies. Methods We performed hormone analysis of cyst fluid from 25 cystic glioblastomas and proteomics analysis of cyst fluid from another 12 cystic glioblastomas. Results Glioblastoma cyst fluid contained hormones within wide concentration ranges: Insulin-like growth factor 1 (0–13.7 nmol/L), insulin (1.4–133 pmol/L), erythropoietin (4.7–402 IU/L), growth hormone (0–0.93 µg/L), testosterone (0.2–10.1 nmol/L), estradiol (0–1.0 nmol/L), triiodothyronine (1.0–11.5). Tumor volume correlated with cyst fluid concentrations of growth hormone and testosterone. Survival correlated inversely with cyst fluid concentration of erythropoietin. Several hormones were present at concentrations that have been shown to stimulate glioblastoma growth in vitro. Concentrations of erythropoietin and estradiol (in men) were higher in cyst fluid than in serum, suggesting formation by tumor or brain tissue. Quantitatively, glioblastoma cyst fluid was dominated by serum proteins, illustrating blood–brain barrier leakage. Proteomics identified several proteins that stimulate tumor cell proliferation and invasiveness, others that inhibit apoptosis or mediate adaption to hypoxia and some that induce neovascularization or blood–brain barrier leakage. Conclusion The microenvironment of glioblastomas is rich in growth-stimulating factors that may originate from the circulation, the tumor, or the brain. The wide variation in cyst fluid hormone concentrations may differentially influence tumor growth.

• Henjum, Kristi; Godang, Kristin; Quist-Paulsen, Else; Idland, Ane-Victoria; Neerland, Bjørn Erik & Sandvig, Heidi Vihovde [Vis alle 12 forfattere av denne artikkelen] (2021). Cerebrospinal fluid catecholamines in delirium and dementia. Brain Communications. ISSN 2632-1297. 3(3), s. 1–11. doi: 10.1093/braincomms/fcab121. Fulltekst i vitenarkiv Vis sammendrag

  Dopamine and noradrenaline are functionally connected to delirium and have been targets for pharmacological interventions but the biochemical evidence to support this notion is limited. To study the CSF levels of dopamine, noradrenaline and the third catecholamine adrenaline in delirium and dementia, these were quantified in three patient cohorts: (i) cognitively normal elderly patients (n¼122); (ii) hip fracture patients with or without delirium and dementia (n¼118); and (iii) patients with delirium precipitated by another medical condition (medical delirium, n¼26). Delirium was assessed by the Confusion Assessment Method. The hip fracture cohort had higher CSF levels of noradrenaline and adrenaline than the two other cohorts (both P<0.001). Within the hip fracture cohort those with delirium (n¼65) had lower CSF adrenaline and dopamine levels than those without delirium (n¼52, P¼0.03, P¼0.002). Similarly, the medical delirium patients had lower CSF dopamine levels than the cognitively normal elderly (P<0.001). Age did not correlate with the CSF catecholamine levels. These findings with lower CSF dopamine levels in hip fracture- and medical delirium patients challenge the theory of dopamine excess in delirium and question use of antipsychotics in delirium. The use of alpha-2 agonists with the potential to reduce noradrenaline release needs further examination.

• Eide, Per Kristian; Mariussen, Espen; Uggerud, Hilde Thelle; Pripp, Are Hugo; Lashkarivand, Aslan & Hassel, Bjørnar [Vis alle 8 forfattere av denne artikkelen] (2021). Clinical application of intrathecal gadobutrol for assessment of cerebrospinal fluid tracer clearance to blood. JCI Insight. ISSN 2379-3708. 6(9), s. 1–13. doi: 10.1172/jci.insight.147063. Fulltekst i vitenarkiv
• Kildal, Emilie; Stadskleiv, Kristine; Boysen, Elin Sundby; Øderud, Tone; Dahl, Inger-Lise & Seeberg, Trine Margrethe [Vis alle 9 forfattere av denne artikkelen] (2021). Increased heart rate functions as a signal of acute distress in non-communicating persons with intellectual disability. Scientific Reports. ISSN 2045-2322. 11(1). doi: 10.1038/s41598-021-86023-6.
• Sumathipala, Dulika Sanjeewani; Strømme, Petter; Gilissen, Christian; Einarsen, Ingunn Holm; Bjørndalen, Hilde & Server, Andrés [Vis alle 10 forfattere av denne artikkelen] (2020). Sudden death in epilepsy and ectopic neurohypophysis in Joubert syndrome 23 diagnosed using SNVs/indels and structural variants pipelines on WGS data: a case report. BMC Medical Genetics. ISSN 1471-2350. 21:96, s. 1–6. doi: 10.1186/s12881-020-01024-y. Fulltekst i vitenarkiv
• Rogne, Ane Gretesdatter; Müller, Ebba Gløersen; Udnæs, Eirin; Sigurdardottir, Solrun; Raudeberg, Rune & Connelly, James Pattrick [Vis alle 8 forfattere av denne artikkelen] (2020). β-Amyloid may accumulate in the human brain after focal bacterial infection: An 18F-flutemetamol positron emission tomography study. European Journal of Neurology. ISSN 1351-5101. 28(3), s. 877–883. doi: 10.1111/ene.14622. Fulltekst i vitenarkiv
• Zhou, Yun; Eid, Tore; Hassel, Bjørnar & Danbolt, Niels Christian (2020). Novel aspects of glutamine synthetase in ammonia homeostasis: Glutamine synthetase and ammonia. Neurochemistry International. ISSN 0197-0186. 140, s. 1–18. doi: 10.1016/j.neuint.2020.104809. Fulltekst i vitenarkiv
• Raheel, Tayyaba Qureshi; Bjørkmo, Mona; Nordengen, Kaja; Gundersen, Vidar; Utheim, Tor Paaske & Watne, Leiv Otto [Vis alle 8 forfattere av denne artikkelen] (2020). Slc38a1 Conveys Astroglia-Derived Glutamine into GABAergic Interneurons for Neurotransmitter GABA Synthesis . Cells. ISSN 2073-4409. 9(7), s. 1–12. doi: 10.3390/cells9071686. Fulltekst i vitenarkiv
• Raheel, Tayyaba Qureshi; Sørensen, Christina; Berghuis, Paul; Jensen, Vidar; Dobszay, Marton B. & Farkas, Tamás [Vis alle 14 forfattere av denne artikkelen] (2019). The glutamine transporter Slc38a1 regulates GABAergic neurotransmission and synaptic plasticity. Cerebral Cortex. ISSN 1047-3211. 29(12), s. 5166–5179. doi: 10.1093/cercor/bhz055. Fulltekst i vitenarkiv
• Hassel, Bjørnar; Rogne, Ane Gretesdatter & Hope, Sigrun (2019). Intellectual disability associated with pyridoxine-responsive epilepsies: The need to protect cognitive development. Frontiers in Psychiatry. ISSN 1664-0640. 10:116, s. 1–8. doi: 10.3389/fpsyt.2019.00116. Fulltekst i vitenarkiv
• Holmøy, Anne Katrin; Johannessen, Cecilie Haggag; Hope, Sigrun; Van Walsem, Marleen Regina; Aanonsen, Nils Olav & Hassel, Bjørnar (2019). Uncovering health and social care needs among myotonic dystrophy patients: Utility of the Needs and Provisions Complexity Scale. Acta Neurologica Scandinavica. ISSN 0001-6314. 139(6), s. 526–532. doi: 10.1111/ane.13086.
• Vohra, Rupali; Dalgaard, Line Marie; Vibæk, Jeppe; Langbøl, Mia Aggergaard; Bergersen, Linda Hildegard & Olsen, Niels Vidiendal [Vis alle 8 forfattere av denne artikkelen] (2019). Potential metabolic markers in glaucoma and their regulation in response to hypoxia. Acta Ophthalmologica. ISSN 1755-375X. s. 1–10. doi: 10.1111/aos.14021.
• Hassel, Bjørnar; Mariussen, Espen; Idland, Ane-Victoria; Dahl, Gry Torsæter; Ræder, Johan & Frihagen, Frede Jon [Vis alle 9 forfattere av denne artikkelen] (2018). CSF sodium at toxic levels precedes delirium in hip fracture patients. Neurotoxicology. ISSN 0161-813X. 69(December), s. 11–16. doi: 10.1016/j.neuro.2018.08.010.
• Zhou, Yun; Dhaher, Roni; Parent, Maxime; Hu, Qiu Xiang; Hassel, Bjørnar & Yee, Siu-Pok [Vis alle 9 forfattere av denne artikkelen] (2018). Selective deletion of glutamine synthetase in the mouse cerebral cortex induces glial dysfunction and vascular impairment that precede epilepsy and neurodegeneration. Neurochemistry International. ISSN 0197-0186. s. 1–12. doi: 10.1016/j.neuint.2018.07.009. Fulltekst i vitenarkiv
• Zhou, Yun; Hassel, Bjørnar; Eid, Tore & Danbolt, Niels Christian (2018). Axon-terminals expressing EAAT2 (GLT-1; Slc1a2) are common in the forebrain and not limited to the hippocampus. Neurochemistry International. ISSN 0197-0186. 123, s. 101–113. doi: 10.1016/j.neuint.2018.03.006. Fulltekst i vitenarkiv
• Morland, Cecilie; Frøland, Anne-Sofie; Nguyen, Mi Mong Tran; Storm-Mathisen, Jon; Gundersen, Vidar & Rise, Frode (2018). Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia. Biochemical Journal. ISSN 0264-6021. 475(4), s. 749–758. doi: 10.1042/BCJ20170814.
• Hu, Qiu Xiang; Hansen, Sigrid Ottestad; Holmseth, Silvia; Hassel, Bjørnar; Danbolt, Niels Christian & Zhou, Yun (2018). Expression of glutamate transporters in mouse liver, kidney, and intestine. Journal of Histochemistry and Cytochemistry. ISSN 0022-1554. 66(3), s. 189–202. doi: 10.1369/0022155417749828. Fulltekst i vitenarkiv Vis sammendrag

  Glutamate transport activities have been identified not only in the brain, but also in the liver, kidney, and intestine. Although glutamate transporter distributions in the central nervous system are fairly well known, there are still uncertainties with respect to the distribution of these transporters in peripheral organs. Quantitative information is mostly lacking, and few of the studies have included genetically modified animals as specificity controls. The present study provides validated qualitative and semi-quantitative data on the excitatory amino acid transporter (EAAT)1-3 subtypes in the mouse liver, kidney, and intestine. In agreement with the current view, we found high EAAT3 protein levels in the brush borders of both the distal small intestine and the renal proximal tubules. Neither EAAT1 nor EAAT2 was detected at significant levels in murine kidney or intestine. In contrast, the liver only expressed EAAT2 (but 2 C-terminal splice variants). EAAT2 was detected in the plasma membranes of perivenous hepatocytes. These cells also expressed glutamine synthetase. Conditional deletion of hepatic EAAT2 did neither lead to overt neurological disturbances nor development of fatty liver.

• Dahlberg, Daniel; Struys, Eduard A.; Janssen, EE; Mørkrid, Lars; Midttun, Øivind & Hassel, Bjørnar (2017). Cyst Fluid From Cystic, Malignant Brain Tumors: A Reservoir of Nutrients, Including Growth Factor-Like Nutrients, for Tumor Cells. Neurosurgery. ISSN 0148-396X. 80(6), s. 917–924. doi: 10.1093/neuros/nyw101. Vis sammendrag

  BACKGROUND: Brain tumors may have cysts, whose content of nutrients could influence tumor cell microenvironment and growth. OBJECTIVE: To measure nutrients in cyst fluid from glioblastoma multiforme (GBM) and metastatic brain tumors. METHODS: Quantification of nutrients in cyst fluid from 12 to 18 GBMs and 4 to 10 metastatic brain tumors. RESULTS: GBM cysts contained glucose at 2.2 mmol/L (median value; range <0.8-3.5) and glutamine at 1.04 mmol/L (0.17-4.2). Lactate was 7.1 mmol/L (2.4-12.5) and correlated inversely with glucose level (r = -0.77; P < .001). Amino acids, including glutamate, varied greatly, but median values were similar to previously published serum values. Ammonia was 75 μmol/L (11-241). B vitamins were present at previously published serum values, and riboflavin, nicotinamide, pyridoxal 5΄-phosphate, and cobalamin were higher in cyst fluid than in cerebrospinal fluid. Inorganic phosphate was 1.25 mmol/L (0.34-3.44), which was >3 times higher than in ventricular cerebrospinal fluid: 0.35 mmol/L (0.22-0.66; P < .001). Tricarboxylic acid cycle intermediates were in the low micromolar range, except for citrate, which was 240 μmol/L (140-590). In cystic metastatic malignant melanomas and lung tumors values were similar to those in GBMs. CONCLUSION: Tumor cysts may be a nutrient reservoir for brain tumors, securing tumor energy metabolism and synthesis of cell constituents. Serum is one likely source of cyst fluid nutrients. Nutrient levels in tumor cyst fluid are highly variable, which could differentially stimulate tumor growth. Cyst fluid glutamate, lactate, and phosphate may act as tumor growth factors; these compounds have previously been shown to stimulate tumor growth at concentrations found in tumor cyst fluid.

• Hassel, Bjørnar; De Souza, Gustavo Antonio; Stensland, Maria; Ivanovic, Jugoslav; Voie, Øyvind Albert & Dahlberg, Daniel (2017). The proteome of pus from human brain abscesses: Host-derived neurotoxic proteins and the cell-type diversity of CNS pus. Journal of Neurosurgery. ISSN 0022-3085. 129(3), s. 829–837. doi: 10.3171/2017.4.JNS17284. Vis sammendrag

  OBJECTIVE What determines the extent of tissue destruction during brain abscess formation is not known. Pyogenic brain infections cause destruction of brain tissue that greatly exceeds the area occupied by microbes, as seen in experimental studies, pointing to cytotoxic factors other than microbes in pus. This study examined whether brain abscess pus contains cytotoxic proteins that might explain the extent of tissue destruction. METHODS Pus proteins from 20 human brain abscesses and, for comparison, 7 subdural empyemas were analyzed by proteomics mass spectrometry. Tissue destruction was determined from brain abscess volumes as measured by MRI. RESULTS Brain abscess volume correlated with extracellular pus levels of antibacterial proteins from neutrophils and macrophages: myeloperoxidase (r = 0.64), azurocidin (r = 0.61), lactotransferrin (r = 0.57), and cathelicidin (r = 0.52) (p values 0.002-0.018), suggesting an association between leukocytic activity and tissue damage. In contrast, perfringolysin O, a cytotoxic protein from Streptococcus intermedius that was detected in 16 patients, did not correlate with abscess volume (r = 0.12, p = 0.66). The median number of proteins identified in each pus sample was 870 (range 643-1094). Antibiotic or steroid treatment prior to pus evacuation did not reduce the number or levels of pus proteins. Some of the identified proteins have well-known neurotoxic effects, e.g., eosinophil cationic protein and nonsecretory ribonuclease (also known as eosinophil-derived neurotoxin). The cellular response to brain infection was highly complex, as reflected by the presence of proteins that were specific for neutrophils, eosinophils, macrophages, platelets, fibroblasts, or mast cells in addition to plasma and erythrocytic proteins. Other proteins (neurofilaments, myelin basic protein, and glial fibrillary acidic protein) were specific for brain cells and reflected damage to neurons, oligodendrocytes, and astrocytes, respectively. Pus from subdural empyemas had significantly higher levels of plasma proteins and lower levels of leukocytic proteins than pus from intracerebral abscesses, suggesting greater turnover of the extracellular fluid of empyemas and washout of pus constituents. CONCLUSIONS Brain abscess pus contains leukocytic proteins that are neurotoxic and likely participate actively in the excessive tissue destruction inherent in brain abscess formation. These findings underscore the importance of rapid evacuation of brain abscess pus.

• Idland, Ane-Victoria; Wyller, Torgeir Bruun; Støen, Randi; Dahl, Gry Torsæter; Frihagen, Frede Jon & Brækhus, Anne [Vis alle 7 forfattere av denne artikkelen] (2017). Cerebrospinal Fluid Phosphate in Delirium after Hip Fracture. Dementia and Geriatric Cognitive Disorders Extra. ISSN 1664-5464. 7(3), s. 309–317. doi: 10.1159/000478723. Fulltekst i vitenarkiv
• Hassel, Bjørnar & Dingledine, Raymond (2016). A New Approach for Epilepsy. Cerebrum. ISSN 1524-6205. s. 7–16.
• Moen, Marivi Nabong; Fjær, Roar; Hamdani, El Hassan; Lærdahl, Jon Kristen; Menchini, Robin Johansen & Vigeland, Magnus Dehli [Vis alle 12 forfattere av denne artikkelen] (2016). Pathogenic variants in KCTD7 perturb neuronal K+ fluxes and glutamine transport. Brain. ISSN 0006-8950. 139, s. 3109–3120. doi: 10.1093/brain/aww244.
• Watne, Leiv Otto; Idland, Ane-Victoria; Fekkes, Durk; Ræder, Johan; Frihagen, Frede Jon & Ranhoff, Anette Hylen [Vis alle 9 forfattere av denne artikkelen] (2016). Increased CSF levels of aromatic amino acids in hip fracture patients with delirium suggests higher monoaminergic activity. BMC Geriatrics. ISSN 1471-2318. 16(149). doi: 10.1186/s12877-016-0324-0. Fulltekst i vitenarkiv
• Morland, Cecilie; Pettersen, Mi Nguyen & Hassel, Bjørnar (2016). Hyperosmolar sodium chloride is toxic to cultured neurons and causes reduction of glucose metabolism and ATP levels, an increase in glutamate uptake, and a reduction in cytosolic calcium. Neurotoxicology. ISSN 0161-813X. 54, s. 34–43. doi: 10.1016/j.neuro.2016.03.005.
• Dahlberg, Daniel; Ivanovic, Jugoslav & Hassel, Bjørnar (2016). Toxic levels of ammonia in human brain abscess. Journal of Neurosurgery. ISSN 0022-3085. 124(3), s. 854–860. doi: 10.3171/2015.1.JNS142582.
• Solyga, Volker; Western, Elin; Solheim, Hanne; Hassel, Bjørnar & Kerty, Emilia (2015). Posterior kortikal atrofi. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 135(10), s. 949–952. doi: 10.4045/tidsskr.14.1127.
• Dahlberg, Daniel; Mariussen, Espen; Goverud, Ingeborg Løstegaard; Tonjum, Tone; Mæhlen, Jan & Antal, Ellen-Ann (2015). Staphylococcal α-hemolysin is neurotoxic and causes lysis of brain cells in vivo and in vitro. Neurotoxicology. ISSN 0161-813X. 48, s. 61–67. doi: 10.1016/j.neuro.2015.03.001.
• Dahlberg, Daniel; Ivanovic, Jugoslav; Mariussen, Espen & Hassel, Bjørnar (2015). High extracellular levels of potassium and trace metals in human brain abscess. Neurochemistry International. ISSN 0197-0186. 82, s. 28–32. doi: 10.1016/j.neuint.2015.02.003.
• Hassel, Bjørnar; Elsais, Ahmed; Frøland, Anne-Sofie; Taubøll, Erik; Gjerstad, Leif & Quan, Yi [Vis alle 7 forfattere av denne artikkelen] (2015). Uptake and metabolism of fructose by rat neocortical cells in vivo and by isolated nerve terminals in vitro. Journal of Neurochemistry. ISSN 0022-3042. 133(4), s. 572–581. doi: 10.1111/jnc.13079.
• Dahlberg, Daniel; Ivanovic, Jugoslav & Hassel, Bjørnar (2014). High extracellular concentration of excitatory amino acids glutamate and aspartate in human brain abscess. Neurochemistry International. ISSN 0197-0186. 69(1), s. 41–47. doi: 10.1016/j.neuint.2014.03.001.
• Hassel, Bjørnar; Dahlberg, Daniel; Mariussen, Espen; Goverud, Ingeborg Løstegaard; Antal, Ellen-Ann & Tonjum, Tone (2014). Brain infection with Staphylococcus aureus leads to high extracellular levels of glutamate, aspartate, γ-aminobutyric acid, and zinc. Journal of Neuroscience Research. ISSN 0360-4012. 92(12), s. 1792–1800. doi: 10.1002/jnr.23444. Vis sammendrag

  Staphylococcal brain infections may cause mental deterioration and epileptic seizures, suggesting interference with normal neurotransmission in the brain. We injected Staphylococcus aureus into rat striatum and found an initial 76% reduction in the extracellular level of glutamate as detected by microdialysis at 2 hr after staphylococcal infection. At 8 hr after staphylococcal infection, however, the extracellular level of glutamate had increased 12-fold, and at 20 hr it had increased >30-fold. The extracellular level of aspartate and γ-aminobutyric acid (GABA) also increased greatly. Extracellular Zn2+ , which was estimated at ∼2.6 µmol/liter in the control situation, was increased by 330% 1-2.5 hr after staphylococcal infection and by 100% at 8 and 20 hr. The increase in extracellular glutamate, aspartate, and GABA appeared to reflect the degree of tissue damage. The area of tissue damage greatly exceeded the area of staphylococcal infiltration, pointing to soluble factors being responsible for cell death. However, the N-methyl-D-aspartate receptor antagonist MK-801 ameliorated neither tissue damage nor the increase in extracellular neuroactive amino acids, suggesting the presence of neurotoxic factors other than glutamate and aspartate. In vitro staphylococci incubated with glutamine and glucose formed glutamate, so bacteria could be an additional source of infection-related glutamate. We conclude that the dramatic increase in the extracellular concentration of neuroactive amino acids and zinc could interfere with neurotransmission in the surrounding brain tissue, contributing to mental deterioration and a predisposition to epileptic seizures, which are often seen in brain abscess patients.

• Madslien, Elisabeth Henie; Rønning, Helene; Lindback, Toril; Hassel, Bjørnar; Andersson, M.A. & Granum, Per Einar (2013). Lichenysin is produced by most Bacillus licheniformis strains. Journal of Applied Microbiology. ISSN 1364-5072. 115(4), s. 1068–1080. doi: 10.1111/jam.12299.
• (2013). Tetanus: Pathophysiology, Treatment, and the Possibility of Using Botulinum Toxin against Tetanus-Induced Rigidity and Spasms. Toxins. ISSN 2072-6651. 5(1), s. 73–83. doi: 10.3390/toxins5010073.
• Zhou, Yun; Holmseth, Silvia; Guo, C; Hassel, Bjørnar; Höfner, G & Huitfeldt, Henrik [Vis alle 7 forfattere av denne artikkelen] (2012). Deletion of the γ-aminobutyric acid transporter 2 (GAT2 and SLC6A13) gene in mice leads to changes in liver and brain taurine contents. Journal of Biological Chemistry. ISSN 0021-9258. 287(42), s. 35733–35746. doi: 10.1074/jbc.M112.368175.
• (2012). Hans (Hansemann) Tønnesen, en diagnostisk gåte fra Amalie Skram [A description of early hydrocephalus with macrocephaly, cerebral palsy, epilepsy, intellectual disability, and growth retardation by Norwegian novelist Amalie Skram (1846-1905)]. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 132, s. 2632–2635. doi: 10.4045/tidsskr.12.0912.
• (2012). 13C Magnetic Resonance Spectroscopy in Neurobiology - Its Use in Monitoring Brain Energy Metabolism and in Identifying Novel Metabolic Substrates and Metabolic Pathways. InTech. ISSN 0192-303X. http://cdn.intechopen.com/pdfs-wm/30447.pdf. doi: 10.5772/33095.
• Hassel, Bjørnar; Taubøll, Erik; Shaw, Renee; Gjerstad, Leif & Dingledine, Ray (2010). Region-specific changes in gene expression in rat brain after chronic treatment with levetiracetam or phenytoin. Epilepsia. ISSN 0013-9580. 51(9), s. 1714–1720. doi: 10.1111/j.1528-1167.2010.02545.x.
• Hassel, Bjørnar; Tessler, S.; Faull, R. L. M. & Emson, P. C. (2008). Glutamate uptake is reduced in prefrontal cortex in Huntington's disease. Neurochemical Research. ISSN 0364-3190. 33, s. 232–237.
• Herrman, Helle; Brækhus, Anne; Aaserud, Olaf; Aukrust, Pål; Stubhaug, Audun & Hassel, Bjørnar (2008). Early treatment of tetanus-induced trismus with botulinum toxin A. Anesthesia and Analgesia. ISSN 0003-2999. 106, s. 1591–1591. doi: 10.1213/ANE.0b013e31816a30f0.
• Hassel, Bjørnar; Solyga, Volker & Lossius, Andreas (2008). High-affinity choline uptake and acetylcholine-metabolizing enzymes in CNS white matter. A quantitative study. Neurochemistry International. ISSN 0197-0186. 53, s. 193–198. doi: 10.1016/j.neuint.2008.06.008.
• Bough, Kristopher J.; Paquet, Maryse; Pare, Jean-Francois; Hassel, Bjørnar; Smith, Youland & Hall, Randy A. (2007). Evidence against enhanced glutamate transport in the anticonvulsant mechanism of the ketogenic diet. Epilepsy Research. ISSN 0920-1211. 74(2-3), s. 232–236. doi: 10.1016/j.eplepsyres.2007.03.002. Vis sammendrag

  Excessive glutamatergic neurotransmission is considered an underlying factor of epilepsy. Energy-dependent glutamate transporters clear extracellular glutamate to limit neuronal excitability. Evidence suggests that reduced expression and/or activity of glutamate transporters contribute to hyperexcitability and progressive seizure activity in rats. By comparison, treatment with the anticonvulsant ketogenic diet (KD) results in increased mRNA expression of the neuronal glutamate transporter EAAC1, elevated energy reserves, and an increased resistance to seizures in rats. The goal of the current study was to determine whether the expression and/or re-uptake activity of glutamate transporters were elevated in hippocampal tissue of rats after KD treatment. Rats were fed either a ketogenic- or control diet for 4-5 weeks. Western blot analysis showed that protein levels of EAAC1, GLT-1 and GLAST glutamate transporters were not changed in hippocampus, cerebral cortex, or cerebellum after KID. Electron microscopic evidence indicated that the KD did not affect hippocampal EAAC1 distribution. In addition, the re-uptake activity of H-3-glutamate into hippocampal proteoliposomes was similar in both KID and control tissue extracts. These multiple studies suggest that the anticonvulsant nature of the KID does not stem from enhanced glutamate re-uptake. (C) 2007 Elsevier B.V. All rights reserved.

• Henjum, Solveig & Hassel, Bjørnar (2007). High-affinity glycine and glutamate transport in pig forebrain white and gray matter: A quantitative study. Neurochemistry International. ISSN 0197-0186. 50(5), s. 696–702. doi: 10.1016/j.neuint.2007.01.002. Vis sammendrag

  High-affinity uptake of glycine and glutamate modulates glutamatergic neurotransmission in gray matter. N-Methyl-D-aspartate (NMDA) receptors were recently described on white matter oligodendrocytes, therefore uptake of glutamate and glycine in white matter may also modulate NMDA receptor function. We found that glycine uptake in white structures of pig forebrain (corpus callosum, fimbria, subcortical pyramidal tracts, and occipital subcortical white matter) was similar to that in gray structures (frontal and temporal cortices and hippocampus), and that it was sensitive to sarcosine, a GLYT1 inhibitor (IC50 15 mu M). Glutamate uptake in white matter was similar to 10% of that in gray; it was sensitive to dihydrokainate, an EAAT2 inhibitor. The levels of glycine and its precursor serine were similar in white and gray matter: approximately 2 and 1 nmol/mg tissue, respectively. The white matter level of glutamate was similar to 7.6 nmol/mg tissue, or similar to 74% of gray matter levels. The activity of serine hydroxymethyl transferase, which converts serine into glycine, was similar in white and gray matter (11-18 pmol/(mg tissue) min), whereas the white matter activity of phosphate-activated glutaminase, which converts glutamine into glutamate, was similar to 100 pmol/(mg tissue) min, or similar to 34% of gray matter activity. The white matter activity of glutamine synthetase, the glial enzyme that converts glutamate into glutamine, was 20-40 nmol/ (mg tissue) min in neocortex and 5-6 nmol/(mg tissue) min in white matter. The data show that forebrain white matter is equipped to regulate extracellular levels of glycine and glutamate, functions that may modulate white matter NMDA receptor function. (c) 2007 Elsevier Ltd. All rights reserved.

• Henjum, Solveig & Hassel, Bjørnar (2007). High-affinity GABA uptake and GABA-metabolizing enzymes in pig forebrain white matter: A quantitative study. Neurochemistry International. ISSN 0197-0186. 50(2), s. 365–370. doi: 10.1016/j.neuint.2006.09.004. Vis sammendrag

  GABA receptor activation in central nervous white matter may be protective during white matter hypoxia in the adult, and it may modify axonal conduction, especially in the developing brain. GABA uptake is important for the shaping of the GABA signal, but quantitative data are lacking for GABA uptake and GABA-metabolizing enzymes in central nervous white matter. We report that high-affinity uptake of GABA in adult pig corpus callosum, fimbria, subcortical pyramidal tracts, and occipital white matter is similar to 20% of that in temporal cortex gray matter. Tiagabine (0.1 mu M), an antiepileptic drug that specifically inhibits the GAT-I GABA transporter inhibited GABA uptake 50% in temporal cortex and 60-68% in white structures. This finding indicates that GAT-1 is an important GABA transporter in white matter and suggests that white matter GABA uptake is inhibited during tiagabine therapy. GABA transaminase activity in white structures was similar to 20% of neocortical values. Glutamate decarboxylase (GAD) activity in white structures was only 4% of that in neocortex (7-12 pmol/mg tissue x min(-1) versus similar to 200 pmol/mg tissue x min-1). Since white matter activity of citrate synthase of the tricarboxylic acid cycle was similar to 25% of neocortical values (similar to 0.4 nmol/mg tissue x min(-1) versus similar to 1.5 nmol/mg tissue x min(-1)), the low GAD activity suggests a slower metabolic turnover of GABA in white than in gray matter. (c) 2006 Elsevier Ltd. All rights reserved.

• Morland, Cecilie; Henjum, Solveig; Iversen, Evy Grini; Skrede, Knut Kristian & Hassel, Bjørnar (2007). Evidence for a higher glycolytic than oxidative metabolic activity in white matter of rat brain. Neurochemistry International. ISSN 0197-0186. 50(5), s. 703–709.
• Morland, Cecilie; Henjum, Solveig; Iversen, Evy Grini; Skrede, Knut Kristian & Hassel, Bjørnar (2007). Evidence for a higher glycolytic than oxidative metabolic activity in white matter of rat brain. Neurochemistry International. ISSN 0197-0186. doi: 10.1016/j.neuint.2007.01.003..
• Nguyen, Nga H. T.; Morland, Cecilie; Villa Gonzalez, Susana; Rise, Frode; Storm-Mathisen, Jon & Gundersen, Vidar (2007). Propionate increases neuronal histone acetylation, but is metabolized oxidatively by glia. Relevance for propionic acidemia. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1111/j.1471-4159.2006.04397.x..
• Nguyen, Nga H. T.; Villa Gonzalez, Susana & Hassel, Bjørnar (2007). Formation of glycerol from glucose in rat brain and cultured brain cells. Augmentation with kainate or ischemia. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1111/j.1471-4159.2006.04433.x..
• Nguyen, Nga H. T.; Villa Gonzalez, Susana; Rise, Frode & Hassel, Bjørnar (2007). Cerebral metabolism of glucose and pyruvate in soman poisoning. A 13C nuclear magnetic resonance spectroscopic study. Neurotoxicology. ISSN 0161-813X. doi: 10.1016/j.neuro.2006.09.007..
• Nguyen, Nga H. T.; Gonzalez, Susan Villa & Hassel, Bjørnar (2007). Formation of glycerol from glucose in rat brain and cultured brain cells. Augmentation with kainate or ischemia. Journal of Neurochemistry. ISSN 0022-3042. 101, s. 1694–1700.
• Bough, Kristopher J.; Wetherington, Jonathon; Hassel, Bjørnar; Pare, Jean-Francois; Gawryluk, Jeremy W & Greene, James G [Vis alle 9 forfattere av denne artikkelen] (2006). Mitochondrial biogenesis in the anticonvulsant mechanism of the ketogenic diet. Annals of Neurology. ISSN 0364-5134. doi: 10.1002/ana.20899..
• (2006). Nicotinic mechanisms contribute to soman-induced symptoms and lethality. Neurotoxicology. ISSN 0161-813X. doi: 10.1016/j.neuro.2006.01.007..
• Villa Gonzalez, Susana; Nguyen, Nga Huynh Tran; Rise, Frode & Hassel, Bjørnar (2005). Brain metabolism of exogenous pyruvate. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1111/j.1471-4159.2005.03365.x..
• Morland, Cecilie; Boldingh, Karen A; Iversen, Evy Grini & Hassel, Bjørnar (2004). Valproate is neuroprotective against malonate toxicity in rat striatum: an association with augmentation of high-affinity glutamate uptake. Journal of Cerebral Blood Flow and Metabolism. ISSN 0271-678X. 24(11), s. 1226–1234.
• Hassel, Bjørnar; Boldingh, Karen Astrid; Morland, Cecilie; Iversen, Evy Grini & Skrede, Knut Kristian (2003). Glutamate transport, glutamine synthetase and phosphate-activated glutaminase in rat CNS white matter. A quantitative study. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.2003.01984.x..
• Nguyen Pettersen, Nga Huynh Tran; Bråthe, Anders & Hassel, Bjørnar (2003). Neuronal uptake and metabolism of glycerol and the neuronal expression of mitochondrial glycerol-3-phosphate dehydrogenase. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.2003.01762.x..
• Hassel, Bjørnar; Bråthe, Anders & Petersen, Dirk (2002). Cerebral dicarboxylate transport and metabolism studied with isotopically labelled fumarate, malate and malonate. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.2002.00986.x..
• Hassel, Bjørnar & Sonnewald, Ursula (2002). Effects of potassium and glutamine on metabolism of glucose in astrocytes. Neurochemical Research. ISSN 0364-3190. doi: 10.1023/a:1014827327690..
• (2002). Carboxylation and anaplerosis in neurons and glia. Molecular Neurobiology. ISSN 0893-7648. doi: 10.1385/MN:22:1-3:021..
• (2001). Pyruvate carboxylation in neurons. Journal of Neuroscience Research. ISSN 0360-4012. doi: 10.1002/jnr.10044..
• Landmark, Cecilie Johannessen; Petersen, Dirk; Fonnum, Frode & Hassel, Bjørnar (2001). The acute effect of valproate on cerebral energy metabolism in mice. Epilepsy Research. ISSN 0920-1211. doi: 10.1016/s0920-1211(01)00308-4..
• Landmark, Cecilie Johannessen; Qu, H; Sonnewald, Ursula; Hassel, Bjørnar & Fonnum, Frode (2001). Estimation of aspartate synthesis in GABAergic neurons in mice by 13 C NMR spectroscopy. NeuroReport. ISSN 0959-4965. doi: 10.1097/00001756-200112040-00025..
• Hassel, Bjørnar; Iversen, Evy Grini; Gjerstad, Leif & Taubøll, Erik (2001). Up-regulation of hippocampal glutamate transport during chronic treatment with sodium valproate. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.2001.00349.x..
• Hassel, Bjørnar; Taubøll, Erik & Gjerstad, Leif (2001). Chronic lamotrigine treatment increases rat hippocampal GABA shunt activity and elevates cerebral taurine levels. Epilepsy Research. ISSN 0920-1211. doi: 10.1016/s0920-1211(00)00196-0..
• Hassel, Bjørnar & Bråthe, Anders (2000). Cerebral metabolism of lactate in vivo: evidence for neuronal pyruvate carboxylation. Japanese Journal of Cerebral Blood Flow and Metabolism. ISSN 0915-9401. doi: 10.1097/00004647-200002000-00014..
• Hassel, Bjørnar & Bråthe, Anders (2000). Neuronal pyruvate carboxylation supports formation of transmitter glutamate. Journal of Neuroscience. ISSN 0270-6474. doi: 10.1523/JNEUROSCI.20-04-01342.2000..
• Olsen, Christel Moræus; Rustad, Anne; Paulsen, Ragnhild Elisabeth Heimtun & Hassel, Bjørnar (1999). 3-Nitropropionic acid: an astrocyte-sparing neurotoxin in vitro. Brain Research. ISSN 0006-8993. doi: 10.1016/s0006-8993(99)02115-0..
• Hassel, Bjørnar; Ilebekk, Arnfinn & Tønnessen, Theis (1998). Cardiac accumulation of citrate during brief myocardial ischaemia and reperfusion in the pig in vivo. Acta Physiologica Scandinavica. ISSN 0001-6772. doi: 10.1046/j.1365-201X.1998.0400e.x..
• Hassel, Bjørnar; Landmark, Cecilie Johannessen; Sonnewald, Ursula & Fonnum, Frode (1998). Quantification of the GABA shunt and the importance of the GABA shunt versus the 2-oxoglutarate dehydrogenase pathway in GABAergic neurons. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.1998.71041511.x..
• Hassel, Bjørnar & Sawcer, Stephen (1998). Neuralgic amyotrophy. Tidsskrift for Den norske legeforening. ISSN 0029-2001.
• Hassel, Bjørnar; Bachelard, Herman; Jones, Paula; Fonnum, Frode & Sonnewald, Ursula (1997). Trafficking of amino acids between neurons and glia in vivo. Effects of inhibition of glial metabolism by fluoroacetate. Journal of Cerebral Blood Flow and Metabolism. ISSN 0271-678X. doi: 10.1097/00004647-199711000-00012..
• Fonnum, Frode; Johnsen, Arnt Magne & Hassel, Bjørnar (1997). Use of fluorocitrate and fluoroacetate in the study of brain metabolism. Glia. ISSN 0894-1491.
• Hassel, Bjørnar & Sonnewald, Ursula (1995). Glial formation of pyruvate and lactate from TCA cycle intermediates: implications for the inactivation of transmitter amino acids? Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.1995.65052227.x..
• Hassel, Bjørnar & Sonnewald, Ursula (1995). Selective inhibition of the tricarboxylic acid cycle of GABAergic neurons with 3-nitropropionic acid in vivo. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.1995.65031184.x..
• Hassel, Bjørnar & Sonnewald, Ursula (1995). Glial-neuronal interactions as studied by cerebral metabolism of [2-13C]acetate and [1-13C]glucose: an ex vivo 13C NMR spectroscopic study. Journal of Neurochemistry. ISSN 0022-3042. doi: 10.1046/j.1471-4159.1995.64062773.x..
• Hassel, Bjørnar; Westergaard, Niels; Schousboe, Arne & Fonnum, Frode (1995). Metabolic differences between primary cultures of astrocytes and neurons from cerebellum and cerebral cortex. Effects of fluorocitrate. Neurochemical Research. ISSN 0364-3190. doi: 10.1007/BF00973096..
• Løberg, Else Marit; Hassel, Bjørnar; Fonnum, Frode & Torvik, Ansgar (1994). Early entry of plasma proteins into damaged neurons in brain infarcts. An immunohistochemical study on experimental animals. APMIS - Journal of Pathologiy, Microbiology and Immunology. ISSN 0903-4641. doi: 10.1111/j.1699-0463.1994.tb05233.x..

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• Rogne, Ane Gretesdatter; Sigurdardottir, Solrun; Raudeberg, Rune; Hassel, Bjørnar & Dahlberg, Daniel (2024). Cognitive and everyday functioning after bacterial brain abscess: a prospective study of functional recovery from 8 weeks to 1 year post-treatment. Brain Injury. ISSN 0269-9052. doi: 10.1080/02699052.2024.2347565. Vis sammendrag

  Objective A bacterial brain abscess may damage surrounding brain tissue by mass effect, inflammatory processes, and bacterial toxins. The aim of this study was to examine cognitive and functional outcomes at 8 weeks and 1 year following acute treatment. Methods Prospective study of 20 patients with bacterial brain abscess (aged 17–73 years; 45% females) with neuropsychological assessment at 8 weeks and 1 year post-treatment. Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A) and Patient Competence Rating Scale (PCRS) were used to assess everyday functioning and administered to patients and informants. Results Cognitive impairment was found in 30% of patients at 8 weeks and 22% at 1 year. Significant improvements were seen on tests of perceptual reasoning, attention, verbal fluency, and motor abilities (p 

• Kildal, Emilie Smith-Meyer; Quintana, Daniel; Szabo, Attila; Tronstad, Christian; Andreassen, Ole & Nærland, Terje (2023). Heart rate monitoring to detect acute pain in non-verbal patients: a study protocol for a randomized controlled clinical trial. BMC Psychiatry. ISSN 1471-244X. 23(1). doi: 10.1186/s12888-023-04757-1. Fulltekst i vitenarkiv
• Jamali, Ahmed; Kristensen, Erle; Tangeraas, Trine; Arntsen, Vibeke; SIKIRIC, ALMA & Kupliauskiene, Guste [Vis alle 12 forfattere av denne artikkelen] (2023). Corrigendum to “The spectrum of pyridoxine dependent epilepsy across the age span: A nationwide retrospective observational study” [Epilepsy Res. 190 (2023) 107099] (Epilepsy Research (2023) 190, (S0920121123000244), (10.1016/j.eplepsyres.2023.107099)). Epilepsy Research. ISSN 0920-1211. doi: 10.1016/j.eplepsyres.2023.107113.
• Rogne, Ane G.; Dahlberg, Daniel; Udnæs, Eirin; Raudeberg, Rune; Sigurdardottir, Solrun & Hassel, Bjørnar (2019). Cognitive dysfunction in brain abscess patients is not attributable to beta-amyloid deposition.
• Hassel, Bjørnar & Strisland, Frode (2019). Forstå hvordan jeg har det. Sensorteknologi for personer med sterkt begrensende kommunikasjonsevner. Vis sammendrag

  Mennesker med alvorlig grad av utviklingshemming eller andre omfattende funksjonsnedsettelser kan ha sterkt reduserte eller manglende evner til å uttrykke seg verbalt eller på andre måter. De kan derfor ha problemer med å uttrykke smerte eller andre ubehag, og de kan reagere med selvskadende eller aggressiv atferd uten at bakenforliggende årsak blir kjent. Kan enkle fysiologiske målinger, slik som pulsmåling, brukes som en ekstra indikator for å hjelpe tjenestene tolke hva som foregår?

• Aarønæs, Lars; Hassel, Bjørnar; Rogne, Ane & Dahlberg, Daniel (2018). Puss kan gi hjerneskade. [Internett]. Forskning.no.
• (2018). Michelangelos David - et syndrome for fremtiden? I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 107–113.
• (2018). Religiøs anatomi i hofteregionen. I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 95–97.
• (2018). Jakobs delirium og overbevisningens nevrobiologi. I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 87–94.
• Zhou, Yun; Hassel, Bjørnar; Eid, Tore & Danbolt, Niels Christian (2018). Axon-terminals expressing EAAT2 (GLT-1; slc1a2) are common in the forebrain and not limited to the hippocampus.
• (1998). Improvement of muscle function in Charcot-Marie-Tooth disease by transcutaneous electric nerve stimulation. Muscle Nerve. doi: 10.1002/(sici)1097-4598(199802)21:2%3C267::aid-mus27%3E3.0.co;2-y..
• (1997). Pickwickian syndrome, a misnomer. Human Pathology. ISSN 0046-8177. doi: 10.1016/s0046-8177(97)90216-1..
• (1997). Resolution of primary vaginismus and introital hyperesthesia by topical anesthesia. Anesthesia and Analgesia. ISSN 0003-2999. doi: 10.1097/00000539-199712000-00055..
• Cordero, Patricia Reyes; Rise, Frode & Hassel, Bjørnar (2020). NMR and spectrophotometric investigations of D-glyceraldehyde metabolism via methylglyoxal. Universitetet i Oslo. Vis sammendrag

  Aldehydes are toxic carbonylcompoundsthatcanreact with proteins and modify theirfunction, stability and shape, e.g by inducing AGEs production. This class of compounds can be formed intracellularly and can betransported to the extracellular environment. D-glyceraldehyde, a hydroxyaldehyde, can cross thecellmembrane,but the transport mechanism has notyetbeenfullyelucidated.Transport of D-GA across a cell membrane has been studied in isolated nerve terminals from the formation of D-lactate, which is recovered in the extracellular fluid, and the specificity of the aldehyde transport mechanism has been studied by the inhibitory effect of other aldehydes on D-lactate formation from D-GA. However, it is not known whether other aldehydes inhibit the D-GA transport mechanism or if they inhibit the enzymatic reactionsleading from D-GA to D-lactate.The objective of this investigation was to study the enzymatic pathway from D-GA to D-lactate and the effect of differentaldehydes on the enzyme activities in this pathway.By identifying aldehydes that do not inhibit these enzymes, one can more safely assume that they are pure inhibitors of the aldehyde transport mechanism in the cell membrane.The competing aldehydes were acetaldehyde, acrolein, butanal, crotonaldehyde, formaldehyde, L-glyceraldehyde,methylglyoxal and propanal. Another objective was to evaluate the fibrillation of the protein glucagon by various aldehydes. Nuclear magnetic resonance (NMR)spectroscopyand UV spectrophotometry were used to study enzymatic reactions involved in D-GA metabolism. Liquid-state 1H NMR was used to investigate if aldehydes induced fibrillation of glucagon, a protein that readily undergoes fibrillation.The aldehydes that inhibited the phosphorylation of D-glyceraldehyde or the glyoxalase system werebutanal, formaldehyde, methylglyoxaland L-glyceraldehyde. Aldehydes that did not inhibit these enzymes wereacetaldehyde, acrolein, crotonaldehyde and propanal.The latter aldehydes are probably inhibitors of the aldehyde transport mechanism in the cell membrane. None of the aldehydes seemed to initiate the fibrillogenesisof glucagon.

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