PubMed Health⌕ Search

Biomedical subjects

E M Løberg

Publications and source records attributed to E M Løberg.

At least 19 recordsLinked to original sources
PubMed2003

Oats induced villous atrophy in coeliac disease.

The current trend is to allow coeliac disease (CD) patients to introduce oats to their gluten free diet. We sought further data from the clinical setting with regards to oats consumption by coeliac patients. Several oat products were tested for wheat contamination using a commercial enzyme linked immunoassay (ELISA) kit, and six samples were examined by an ELISA using a cocktail of monoclonal antibodies, mass spectrometry, and western blot analysis. Nineteen adult CD patients on a gluten free diet were challenged with 50 g of oats per day for 12 weeks. Serological testing and gastroduodenoscopy was performed before and after the challenge. Biopsies were scored histologically and levels of mRNA specific for interferon gamma were determined by reverse transcription-polymerase chain reaction analysis. Oats were well tolerated by most patients but several reported initial abdominal discomfort and bloating. One of the patients developed partial villous atrophy and a rash during the first oats challenge. She subsequently improved on an oats free diet but developed subtotal villous atrophy and dramatic dermatitis during a second challenge. Five of the patients showed positive levels of interferon gamma mRNA after challenge. Some concerns therefore remain with respect to the safety of oats for coeliacs.

Adult↗
PubMed2003

Effect of global hypoxia-ischaemia followed by 24 h of mild hypothermia on organ pathology and biochemistry in a newborn pig survival model.

BACKGROUND: Perinatal asphyxia may lead to multiorgan damage as well as brain injury. Posthypoxic hypothermia (HT) may protect other organs in addition to the brain. The aim of this study was to assess the systemic effects of our global hypoxic-ischaemic (HI) insult and compare the effect of mild 24-hour HT with normothermia (NT) during unsedated recovery. METHOD: Thirty-eight newborn pigs were subjected to 45 min of global HI by ventilating them with approximately 6% O2. On reoxygenation, pigs were randomised to NT or HT. The 18 NT piglets were maintained at rectal temperature 39.0 degrees C for 72 h. Twenty-three HT pigs (20 experimental HT and 3 sham controls) were cooled to rectal temperature 35 degrees C for 24 h before NT was resumed and the animals then survived a further 48 h. RESULTS: All lesions were small with no apparent clinical effect. The incidence of any damage to the heart (6 HT vs. 9 NT), liver (9 HT vs. 7 NT), kidney (6 HT vs. 9 NT) or intestinal injury (8 HT vs. 2 NT, p = 0.07) was not different in the two groups. More HT piglets developed lung injury, 10 HT and 3 NT. Plasma [Na], [K], [Ca] and [Mg] increased significantly after the HI insult as compared to baseline values. For the 24-hour period plasma [K] and [Ca] were significantly higher in the HT group, the mean area under the curve (AUC) being for [K] AUC(HT) 4.4 mmol/l vs. AUC(NT) 3.9 mmol/l, p = 0.04 and for [Ca] AUC(HT) 2.7 mmol/l vs. AUC(NT) 2.5 mmol/l, p = 0.01, respectively. Aspartate aminotransferase peaked at 48 h in the HT group and at 24 h in the NT group. Creatinine peaked at >72 h in the HT pigs and at 48 h in the NT pigs. White blood cells (WBC) peaked at 12 h for the HT pigs and at 6 h for the NT animals. AUC of the WBC during the cooling was significantly lower in the HT pig (AUC(HT) 11.1 vs. AUC(NT) 15.3 10(3)/mm3, p = 0.04). The HT pigs needed more glucose to maintain normal glucose during the last 12 h of HT. Also HT animals needed more oxygen during cooling to maintain PaO2. CONCLUSION: Twenty-four hours of mild HT did not reduce damage in any organ. There was a slight increase in lung damage in the HT group. None of the biochemical or pathological changes were of clinical significance. We conclude that mild HT for 24 h does not affect the organ systems adversely when compared to NT. Additional glucose and oxygen is needed during cooling to maintain normal values.

Adrenal Glands↗
PubMed2001

Qualitative and quantitative relationship between dysplastic aberrant crypt foci and tumorigenesis in the Min/+ mouse colon.

The multiple intestinal neoplasia (Min)/+ mouse, which harbors only one functional allele of the Apc gene, is susceptible to environmental factors that disrupt this gene and subsequently trigger Apc-driven tumorigenesis in the colon. Aberrant crypt foci (ACF) are assumed to be preneoplastic lesions in colon carcinogenesis. Recently, we reported the absence of "classical" ACF in the colon of untreated Min/+ mice. Instead we identified flat dysplastic lesions, which we denoted ACF(Min) (J. E. Paulsen et al., Scand. J. Gastroenterol., 35: 534-539, 2000). In contrast to the classical type, ACF(Min) are not elevated above the surrounding mucosa, and their detection is totally dependent on methylene blue staining and transillumination. In the present study, we treated Min/+ mice with 5 mg/kg body weight azoxymethane (AOM) at weeks 1 and 2 and demonstrated induction of both types of lesions. However, only ACF(Min) appeared to be associated with the development of adenomas. Monocryptal ACF(Min), large ACF(Min), and adenomas showed a uniform histopathological picture of dysplasia and cytoplasmic overexpression of beta-catenin, indicating a qualitative relationship between these lesions. Also a quantitative relationship was suggested because the dramatic decrease in ACF(Min) number from week 7 to 11 was paralleled by a reciprocal increase in tumor number, indicating fast-crypt multiplication of ACF(Min). In AOM-treated +/+ (wild-type) littermates, a low number of ACF(Min) and tumors with the same characteristics as in Min/+ mice was seen. In contrast to ACF(Min), histopathological and immunohistochemical examination of classical ACF showed normal or hyperplastic crypts with normal levels of beta-catenin expression. In AOM-treated Min/+ mice, the number of classical ACF was virtually constant from week 7 to 11, and only a modest increase of crypt multiplicity was observed. The number of AOM-induced classical ACF at week 11 was not different in Min/+ mice and +/+ mice. In conclusion, we identified two distinct populations of altered crypts in the colon of Min/+ mice after AOM treatment. The ACF(Min), which resemble the dysplastic ACF described previously, clearly showed a continuous development from the monocryptal stage to adenoma, and they were characterized by fast-growing crypts with altered control of beta-catenin. In contrast, the classical ACF, which resemble the hyperplastic ACF described previously, were characterized by slow-growing crypts with normal beta-catenin expression, and they were probably not related to tumorigenesis.

Adenoma↗
PubMed2001

Mucinous ductal ectasia of the biliary tree secondary to mucous metaplasia. A case report.

Mucinous ductal ectasia is an uncommon disorder, characterized by ductal dilatation and filling with thick, viscid mucus, described in the pancreas. We report a case of mucinous ductal ectasia of the biliary tree. The cause of the mucus production was mucous metaplasia in the biliary epithelium. The patient was followed for 16 years, treated with serial saline flushings of the biliary tree whenever he became symptomatic.

Aged↗
PubMed2001

Evidence for intraaxonal spread of Listeria monocytogenes from the periphery to the central nervous system.

Rhombencephalitis due to Listeria monocytogenes is characterized by progressive cranial nerve palsies and subacute inflammation in the brain stem. In this paper, we report observations made on mice infected with L. monocytogenes. Unilateral inoculation of bacteria into facial muscle, or peripheral parts of a cranial nerve, induced clinical and histological signs of mainly ipsilateral rhombencephalitis. Similarly, unilateral inoculation of bacteria into lower leg muscle or peripheral parts of sciatic nerve was followed by lumbar myelitis. In these animals, intraaxonal bacteria were seen in the sciatic nerve and its corresponding nerve roots ipsilateral to the bacterial application site. Development of myelitis was prevented by transsection of the sciatic nerve proximally to the hindleg inoculation site. Altogether, our results support the hypothesis that Listeria rhombencephalitis is caused by intraaxonal bacterial spread from peripheral sites to the central nervous system.

Animals↗
PubMed2001

Twenty-four hours of mild hypothermia in unsedated newborn pigs starting after a severe global hypoxic-ischemic insult is not neuroprotective.

Three to 12 h of mild hypothermia (HT) starting after hypoxia-ischemia is neuroprotective in piglets that are anesthetized during HT. Newborn infants suffering from neonatal encephalopathy often ventilate spontaneously and are not necessarily sedated. We aimed to test whether mild posthypoxic HT lasting 24 h was neuroprotective if the animals were not sedated. Thirty-nine piglets (median weight 1.6 kg, range 0.8-2.2 kg; median age 24 h, range 7-48 h) were anesthetized and ventilated and subjected to a 45-min hypoxic (FiO(2) approximately 6%) global insult (n = 36) or sham hypoxia (n = 3). On reoxygenation, 18 were maintained normothermic (NT, 39.0 degrees C) for 72 h, and 21 were cooled from 39 (NT) to 35 degrees C (HT) for the first 24 h before NT was resumed (18 experimental, three sham hypoxia). Cardiovascular parameters and intermittent EEG were documented throughout. The brain was perfusion fixed for neuropathology and five main areas examined using light microscopy. The insult severity (duration in minutes of EEG amplitude < 7 microV) was similar in the NT and HT groups, mean +/- SD (28 +/- 7.2 versus 27 +/- 8.6 min), as was the mean FiO(2) (5.9 +/- 0.7 versus 5.8 +/- 0.8%) during the insult. Six NT and seven HT piglets developed posthypoxic seizures that lasted 29 and 30% of the time, respectively. The distribution and degree of injury (0.0-4.0, normal-maximal damage) within the brain (hippocampus, cortex/white matter, cerebellum, basal ganglia, thalamus) were similar in the NT and HT groups (overall score, mean +/- SD, 2.3 +/- 1.5 versus 2.4 +/- 1.3) as was the EEG background amplitude at 3 h (13 +/- 3.5 versus 10 +/- 3.3 microV). The HT animals shivered and were more active. The sham control group (n = 3) shivered but had normal physiology and neuropathology. Plasma cortisol was significantly higher in the HT group during the HT period, 766 +/- 277 versus 244 +/- 144 microM at 24 h. Mild postinsult HT for 24 h was not neuroprotective in unsedated piglets and did not reduce the number of animals that developed posthypoxic seizures. Cortisol reached 3 times the NT value at the end of HT. We speculate that the stress of shivering and feeling cold interfered with the previously shown neuroprotective effect of HT. Research on the appropriateness of sedation during clinical HT is urgent.

Adult↗
PubMed2000

[Will the revolutionary knowledge of apoptosis play an important role in medicine?].

Apoptosis is a phenomenon of fundamental importance in embryonal development and the homeostatic regulation of mature tissue. We review the present knowledge on apoptosis and the evidence that apoptosis may play a role in the pathogenesis of human disease. As examples we discuss its role in cancer, ischemic diseases, heart failure and neurodegenerative diseases.

Apoptosis↗
PubMed1999

[Brain stem infection caused by Listeria monocytogenes].

Rhombencephalitis due to Listeria monocytogenes is a serious form of brainstem inflammation. It is difficult to diagnose on the basis of clinical and laboratory findings alone. We describe a fatal case of Listeria monocytogenes rhombencephalitis in a previously healthy female teenager. Clinical and pathogenetic aspects of this condition are discussed.

Adolescent↗
PubMed1999

[Listeria monocytogenes--the perfect parasite?].

The pathogen Listeria monocytogenes has an extraordinary intracellular life cycle, based on adaption to and exploitation of normal cellular mechanisms. Extracellular organisms induce their own phagocytosis, followed by destruction of the phagosomal membrane. Cytoplasmatic bacteria organize the intracellular protein actin into "comet tails", and thus gain motility. In contact with the plasma membrane, motile bacteria induce a pseudopodium, corresponding to an invagination of the plasma membrane of the neighbouring cell. Eventually, the pseudopodium is engulfed by the neighbouring cell, creating a double membrane vacuole. L. monocytogenes destroys the double membrane, and escapes into the cytoplasm. This article reviews the molecular biology of Listeria infection, and how research in this field has yielded increased insight into normal cellular processes. Finally, we propose that the neuroinvasive properties of L. monocytogenes is caused by actin-dependent transport within axons from the periphery to the central nervous system.

Actins↗
PubMed1999

Hemispheric asymmetry in schizophrenia: a "dual deficits" model.

BACKGROUND: The aim was 1) to investigate left hemisphere functional integrity for auditory language processing in schizophrenic patients; and 2) to investigate the interaction between brain laterality and attentional processing by having subjects shift attention to the left or right ear. METHODS: The subjects were 33 schizophrenic inpatients, and 33 healthy comparison subjects with the same age, handedness, and gender distribution as the patient subjects. All subjects were tested with dichotic listening (DL) to consonant-vowel syllables, which is a measure of lateralized temporal lobe language processing. The subjects were tested under three different attentional conditions: a non-forced attention condition, attention focused to the right ear stimulus, and attention focused to the left ear stimulus. RESULTS: The main findings were 1) an absence of the expected right ear advantage in the schizophrenic group during the non-forced attention condition; and 2) a failure to modify DL performance through shifting of attention to either the right or left ear. The comparison group showed a right ear advantage during the non-forced and forced-right attention conditions (increased right ear advantage during the forced-right condition), and a left ear advantage during the forced-left attention condition. There were no significant effects of handedness. CONCLUSIONS: This pattern of results may indicate a "dual deficit" involving both automatic and controlled processing deficits in schizophrenia.

Adult↗
PubMed1999

Granulocyte marker protein is increased in stools from rats with azoxymethane-induced colon cancer.

BACKGROUND: We wanted to investigate the relationship between the fecal levels of granulocyte marker protein (GMP) and the presence of aberrant crypt foci (ACF) and colorectal cancer in rats given injections of azoxymethane (AOM) and fed either of two different diets, a basal diet plus 20% corn oil or 20% beef suet, respectively. METHODS: The rats received intraperitoneal injections of AOM, 15 mg/kg, once weekly for 6 weeks and were killed after 22 weeks. RESULTS: In the group fed beef suet 17 of 19 rats developed colon cancer, whereas in the group fed corn oil 4 of 14 rats developed cancer. None of the 20 control rats fed either the beef suet or corn oil diets developed cancer or aberrant crypts, and GMP remained unchanged. Surprisingly, the numbers of ACF were significantly higher (467 versus 295; P = 0.004) in the group fed corn oil than in the group fed beef suet. On the other hand, the size (crypts/focus) of the ACF was significantly higher (P = 0.03) in the beef suet group. Furthermore, fecal GMP was significantly higher in the beef suet group than in the corn oil group after 18 weeks, and this difference increased further toward the end of the study. GMP was greatly increased in all rats with colorectal cancer. CONCLUSIONS: Fecal GMP may have provided us with a valuable tool for further studies of the induction and progression of neoplasia in rats and, possibly, in mice, since the anti-GMP antibody cross-reacts with feces extracts from mice.

Animals↗
PubMed1998

[Cytomegalovirus as the cause of toxic dilatation of the colon].

Toxic dilatation of the colon is sometimes a complication which occurs during exacerbations of inflammatory bowel disease. It often requires immediate surgical intervention. We describe here a male patient with known ulcerative colitis who was investigated for fever of unknown cause, diarrhoea, and general illness. Upon admission he had only modest symptoms of colitis and received no immunosuppressive treatment. The condition worsened considerably, and subsequent colonoscopy demonstrated widespread lesions compatible with viral disease, but not with ulcerative colitis. Antiviral treatment for cytomegalovirus was started immediately, but progression of the condition with toxic dilatation called for a rapid colectomy. Histological examination showed widespread lesions compatible with cytomegalovirus infection. This clinical picture is rarely seen in immunocompetent patients.

Colectomy↗
PubMed1998

Protective effects of moderate hypothermia after neonatal hypoxia-ischemia: short- and long-term outcome.

We have previously shown that mild hypothermia applied after hypoxia-ischemia in newborn piglets and rats reduces brain injury evaluated 3-7 d after the insult. The aim of the present study was to assess the neuroprotective efficacy of hypothermia with respect to short- (neuropathology) and long-term (neuropathology and sensorimotor function) outcome after hypoxia-ischemia in 7-d-old rats. One hundred fourteen animals from 13 litters survived either 1 or 6 wk after a hypoxic-ischemic insult. The animals were randomized to either 1) normothermic recovery for the whole 1- or 6-wk period or 2) cooling to a rectal temperature of 32.0 degrees C for the first 6 h followed by normothermic recovery with the dam. Hypothermia offered a uniform protection of 27, 35, 28, and 25% in cerebral cortex, hippocampus, basal ganglia, and thalamus, respectively, in the 1-wk survivors (n = 32). The corresponding values for the 6-wk survivors (n = 61) were 22, 28, 37, and 35%. There was a significant correlation between sensorimotor performance and infarct volume (r = 0.66; p < 0.001). However, the sensorimotor function was not significantly improved by hypothermia if all animals were included, but in female pups the total functional score was higher in the hypothermia group (150 +/- 35 versus 100 +/- 34, p < 0.0007) which corresponded to a marked (51%) reduction of the neuropathology score in this subgroup. This is the first neonatal study to show a long-term histopathologic protection of the brain after posthypoxic hypothermia.

Animals↗
PubMed1998

Lactate and pyruvate changes in the cerebral gray and white matter during posthypoxic seizures in newborn pigs.

Cerebral lactate rises after chemically induced seizures, but it is not known if this occurs with posthypoxic seizures. We examined changes in lactate and pyruvate in gray and white matter in the newborn pig brain after a hypoxic insult known to produce seizures and permanent brain damage. Fourteen halothane-anesthetized piglets aged 24-49 h, were instrumented with a two-channel scalp EEG and microdialysis probes positioned in white and gray matter. Forty-five minutes of hypoxia were induced by reducing the fraction of inspired O2 to the maximum concentration at which EEG amplitude was < 7 microV. Postinsult EEG was classified as electroconvulsive activity (ECA) (n = 4) or burst suppression (n = 2), persistently low amplitude (n = 2), or intermittent spikes on normal background activity (n = 6). Six hours after the insult the brains were perfusion fixed for histologic probe localization. Plasma lactate and brain lactate had different time courses with brain having a persistently elevated lactate/pyruvate (L/P) ratio. The highest L/P ratios in gray and white matter were in the two pigs with persistently low amplitude EEG. There was no association between onset of electroconvulsive activity and an increase in lactate or L/P ratio. Posthypoxic energy metabolism is disturbed in both gray and white matter probably because of mitochondrial dysfunction. Seizure activity does not increase cerebral lactate or L/P ratio above the already raised levels found in posthypoxic encephalopathy. These findings cast further doubt on the hypothesis that such seizures are, in themselves, damaging.

Animals↗
PubMed1997

Post-hypoxic hypothermia reduces cerebrocortical release of NO and excitotoxins.

Hypothermia applied after hypoxia offers neuroprotection in neonatal animals, but the mechanisms involved remain unknown. Hypoxia was induced in newborn piglets and changes in excitatory amino acids (EAAs) and the citrulline:arginine ratio (CAR) were followed by microdialysis for 5 h. After the 45 min hypoxic insult, the animals were randomized to receive normothermia (39 degrees C; n=7) or hypothermia (35 degrees C; n = 7). After reoxygenation, extracellular glutamate, aspartate and the excitotoxic index were significantly lower in the cerebral cortex of hypothermic animals than in normothermic animals. A progressive rise of the CAR occurred during reoxygenation in the normothermic group whereas the ratio tended to decrease in the hypothermic group. In conclusion, post-hypoxic hypothermia attenuated NO production and overflow of EAAs.

Animals↗
PubMed1997

Posthypoxic hypothermia in newborn piglets.

The purpose of this study was to determine whether mild hypothermia after a moderate hypoxic-ischemic insult reduces the extent of brain damage. Hypoxia was achieved in newborn piglets (n = 24; age, 14-72 h) by abrupt reduction of the inspired oxygen concentration (FiO2) to the maximum concentration (approximately 6%) giving low amplitude (< 7.0 microV) EEG. FiO2 was temporarily increased if heart rate, blood pressure, or end expiratory partial pressure of alveolar CO2 (PAco2) were markedly reduced. This intermittently resulted in EEG amplitude greater than 7 microV, the EEG traces were therefore later examined to determine the duration of low amplitude EEG. After 45 min of hypoxia, the animals were randomized to normothermia (39 degrees C) or hypothermia (35 degrees C) for 3 h. Hypothermia was achieved by applying packs containing ice water. Neurologic assessments and EEG recordings were performed regularly until 3 d when the brains were perfusion fixed. Histologic damage in cortex/white matter, cerebellum, hippocampus, basal ganglia, and thalamus was graded by a pathologist blind to treatment allocation. We found that the severity of brain damage (by histopathologic and neurologic evaluation) was not significantly different when the piglets were normothermic after hypoxia compared with the group made hypothermic. Increased duration of low amplitude EEG and seizure activity were associated with increased damage. When controlling for duration of hypoxia and excluding seizures, piglets undergoing hypothermia had approximately 50% less severe histopathologic damage in cortex/white matter, cerebellum, and hippocampus than those kept normothermic. Thalamus and basal ganglia had no or minor damage. It was concluded that there was no general beneficial effect of postinsult hypothermia. However, when controlling for the duration of the insult and occurrence of seizures, hypothermia reduced the severity of brain damage. This indicates a significant neuroprotective effect of 3 h of mild hypothermia on moderate, but not severe, hypoxic-ischemic insults.

Animals↗
PubMed1996

[Ischemic colitis in young patients].

Ischaemic colitis is an established clinical entity in the elderly, characterized by acute onset of abdominal pain, diarrhoea and rectal bleeding. Six women 20-49 years old have been admitted to our hospital with ischaemic colitis during the last seven years. One of the cases in described, followed by a discussion of associated factors and clinical aspects. We emphasize that ischaemic colitis is an important differential diagnosis of colitis even in younger patients.

Adult↗