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Biomedical subjects

T Christensen

Publications and source records attributed to T Christensen.

At least 73 records · Page 4Linked to original sources
PubMed1997

[A clinic for the study of dementia--110 consecutive patients].

Case reports of 110 patients referred to a neurological dementia clinic were reviewed to evaluate a standardized diagnostic program. The patients were evaluated by a neurologist, a gerontopsychiatrist, and a neuropsychologist. ICD-10 criteria were used. Fifty-two patients had dementia while 58 had not; of these, 27 suffered from other non-dementia diseases and 31 were without dementia or other psychiatric or neurological disease. Thirteen patients with Alzheimer's disease were treated with tacrine. Four patients underwent cobalamin substitution treatment and seven started antidepressant medication. Ten patients received acetylsalicylic acid (150 mg Q.D.) and two a levo-dopa-type drug. Twenty-six patients were followed by gerontopsychiatric district care. Because only 47% of the patients suspected of dementia actually fulfilled dementia criteria, the evaluation suggests that patients suspected of dementia benefit from a standardized diagnostic program in a specialist setting.

Aged↗
PubMed1997

Evidence for increased cellular uptake of glutamate and aspartate in the rat hippocampus during kainic acid seizures. A microdialysis study using the "indicator diffusion' method.

Using a newly developed technique, based on microdialysis, which allows cellular uptake of glutamate and aspartate to be studied in awake animals, we investigated uptake of glutamate and aspartate in the hippocampal formation of rats during limbic seizures induced by systemical administration of kainic acid (KA). With [14C]mannitol as an extracellular reference substance, the cellular extraction of the test substance [3H]D-aspartate was measured at different stages of seizure-activity. The results were compared to those obtained in a sham operated control group. During severe generalized clonic seizures, the extraction of [3H]D-aspartate was increased by 17%. The increase in uptake of [3H]D-aspartate was accompanied by a 24% increase in the extracellular level of aspartate, as obtained by conventional microdialysis. No significant changes were observed in the extracellular level of glutamate. The results indicate that during KA-induced seizures, uptake of glutamate and aspartate is increased, possibly aimed at maintaining the extracellular homeostasis of these two excitatory amino acids.

Animals↗
PubMed1997

Characterization of retroviruses from patients with multiple sclerosis.

These studies were performed to characterize retroviruses found in cell lines spontaneously developed from peripheral blood mononuclear cells (PBMNC) from 6 multiple sclerosis patients, a patient with progressive myelopathy and a healthy control. The cell lines are B-lymphoblastoid and produce Epstein-Barr virus (EBV) particles or express EBV proteins. The B-lymphoblastoid cell lines are also characterized by production of low, fluctuating amounts of retrovirus. The low productivity complicates purification and characterization, but implementation of product-enhanced reverse transcriptase (PERT) assays has provided a highly useful tool for monitoring retrovirus production. By electron microscopy, the retroviral particles appear type-C-like. Functional assays indicate the presence of Pol, Gag and Env. Indirect ELISA demonstrates a significant relation between disease activity and reactivity towards retroviral peptides. Molecular characterization is primarily based on RT-PCR, cloning, sequencing and Northern- or Southern analyses. Molecular characterization is continuing.

Autoantigens↗
PubMed1997

The implications of Epstein-Barr virus in multiple sclerosis--a review.

The objective of this article is to bring together knowledge about Epstein-Barr virus (EBV) in relation to multiple sclerosis (MS) in order to evaluate its implications in this disease. All MS patients are EBV seropositive, but EBV is not normally detected in the brain. EBV can explain many of the epidemiological dogmas known in MS. In addition, other studies point towards the involvement of EBV in MS. Despite this, other co-actors seem also to be involved. We still need to know whether EBV may be an initiating factor in MS or whether it is a factor in the pathogenesis. Possible ways of EBV involvement are discussed: direct involvement, an autoimmune inducing factor or a transactivating factor. A current treatment study of MS patients with a specific herpes antiviral drug may add further information to the etiology and pathogenesis of MS.

Autoimmune Diseases↗
PubMed1997

Cardiac function during iron chelation therapy in adult non-thalassaemic patients with transfusional iron overload.

It is well-documented that iron chelation by desferrioxamine protects/improves the cardiac function in blood transfusion-dependent children suffering from beta-thalassaemia. In patients who do not become dependent upon blood transfusion until adulthood (ANT-patients), iron chelation by desferrioxamine may affect the cardiac function in unknown ways, presumably because age-related changes in the heart may cause iron chelation to affect the cardiac function in different ways. We therefore followed the left ventricular ejection fraction (LVEF) by multigated radionuclide angiography in 16 iron-loaded ANT-patients during iron chelation alone and after increasing the efficacy of chelation by vitamin C supplementation. During 12 months of iron chelation the mean LVEF fell significantly from 63.3% to 58.0% (p=0.04). Individual changes in LVEF did not correlate significantly with age but with the pretreatment liver iron concentration. After initiation of vitamin C supplementation, the mean LVEF increased from 55.9% to 65.3% (p=0.01). Our data suggest that in ANT-patients prolonged desferrioxamine treatment without vitamin C supplementation may be associated with reduced LVEF, whereas vitamin C supplementation seems to benefit the cardiac function. Similar findings have not been described in beta-thalassaemia and may hence be specific for ANT-patients. However, our findings have to be confirmed by controlled studies.

Adolescent↗
PubMed1997

Large intravenous loads of bilirubin photoconversion products, in contrast to bilirubin, do not cause cholestasis in bile acid-depleted pigs.

BACKGROUND: Large intravenous bilirubin infusions in bile acid-depleted pigs (BADP) destroy hepatocyte canalicular membrane microvilli (CMV) and cause cholestasis. This study examines whether bilirubin photoconversion product infusions do the same. METHODS: The effects of systemic infusion of 135 mumol.kg-1 body weight bilirubin photoconversion products on CMV density and choleretic response to intraportal bile acid infusion were studied in BADP. Furthermore, the effects of 135 mumol.kg-1 b.w. bilirubin infusion, either through an arteriovenous bilirubin photoconversion shunt device (PCD) or intravenously, were measured in PCD-connected BADP. RESULTS: Intravenous bilirubin photoconversion product infusions affected neither the CMV density nor the choleretic response to cholic acid infusion, and neither did bilirubin infusion through the PCD. In contrast, intravenous bilirubin infusion caused canalicular injury and cholestasis in four of six PCD-connected BADP. CONCLUSION: Bilirubin photoconversion products do not destroy CMV or cause cholestasis in BADP. A bilirubin photoconversion shunt device can confer cholestasis protection to bilirubin-loaded BADP.

Animals↗
PubMed1996

Effects of phenylsuccinate on potassium-stimulated taurine release in cultured neurons and astrocytes and in rat hippocampus in vivo.

Swelling-induced release of taurine was investigated in vivo in hippocampus by microdialysis or in vitro in cultured neocortical neurons or astrocytes. Swelling was induced either by increasing the extracellular K+ concentration or by exposing the cells to hyposmotic conditions. It was found that the drug phenylsuccinate, which inhibits the mitochondrial dicarboxylate carrier as well as biosynthesis of neurotransmitter glutamate, inhibits swelling-induced taurine release both in vivo and in cultured cells. Thus, phenylsuccinate may be used to investigate the mechanism involved in taurine release associated with regulatory volume decrease in cells.

Amino Acids↗
PubMed1996

[MR-scanning in complex partial epilepsy].

In a prospective investigation concerning 50 consecutive patients suffering from complex partial epilepsy who all had a normal CT investigation pathological findings were recognized in 80% using MRI. The MRI examination included volume estimation of the hippocampus. The volume estimations were compared to a reference material. In 24% a focal pathology was recognized, that was suspected of being responsible for the epileptic condition. Only 20% of the examinations were evaluated as normal. Hippocampal atrophy was recognized in 50%. In the latter group a diagnosis of hippocampal sclerosis was established in 16%. It is concluded that MRI is the investigation of choice in complex partial epilepsy and that volume estimation of the hippocampus is important.

Epilepsies, Partial↗
PubMed1996

[Diagnosis of suspected thoracic aortic dissection. Focused on transesophageal echocardiography].

Over a five-year period (1990-1994), 72 consecutive patients were referred to transoesophageal echocardiography (TEE) on suspicion of thoracic aortic dissection. TEE was performed as the only or last investigation in 42 patients (58%). In 44 patients one or more other investigations were carried out before final clinical decision making: aortography (n = 30), X-ray computer tomography (CT, n = 18), and magnetic resonance imaging (MRI, n = 12). The final diagnosis was based on the combination of clinical information, the available examination results, and findings at surgery or autopsy; 31 of the patients were diagnosed as having aortic dissection. One patient with aortic dissection died during TEE while none of the other patients suffered major complications. The sensitivity (demonstration of dissection including correct classification in type A or B) was 81%, 80%, 45%, and 83% for TEE, aortography. CT, and MRI, respectively. The specificities were 88%, 93%, 71%, and 100%, respectively. Dissection of the thoracic aorta is a life-threatening condition demanding prompt and accurate diagnosis. None of the four techniques employed in the present study is ideal. Although TEE is adequate for immediate bedside examination our results show that more time-consuming and resource demanding investigations are sometimes required. Proper training and improved equipment may, however, increase the usefulness of TEE in patients with suspected aortic dissection.

Adolescent↗
PubMed1996

[Can magnetic resonance imaging differentiate between benign and malignant conditions in patients with skeletal or soft tissue tumors?].

The records of 437 patients referred preoperatively for magnetic resonance imaging (MRI) due to clinical or radiological suspicion of a bone or soft-tissue malignancy were examined retrospectively in order to evaluate how good MRI is at distinguishing malignant from benign lesions. The MR-examination tends to overestimate malignancy. In all cases, the preoperative MR-examination correctly identified all malignant tumours as malignant, but also estimated a number of benign lesions as malignant. Sensitivity, specificity and predictive value was 100%, 71.2% and 76.4% respectively. In case of bursa/ganglion and pseudotumour, MR was able to correctly identify these lesions as benign. MR could not differentiate between the different types of sarcomas.

Diagnosis, Differential↗
PubMed1996

Synthesis of stereoisomers and isoforms of a tryptic heptapeptide fragment of human growth hormone and analysis by reverse-phase HPLC and capillary electrophoresis.

The amino acid sequence Asn-Gly has at pH 7 a tendency to induce deamidation of asparagine to aspartic acid via the formation of a cyclic imide. This imide opens up to yield Asp-Gly or the isoaspartic acid (isoAsp) form, isoAsp-Gly. Both isomers may be found in their L-form or D-form. Like Asn-Gly, the sequence Asp-Gly has a tendency for isomerization and racemization via the formation of a cyclic imide intermediate. When human growth hormone is digested with trypsin, one of the fragments is a heptapeptide (amino acid residues 128-134) containing the amino acid sequence Asp-Gly (amino acid residues 130 and 131). This heptapeptide, as well as stereoisomers and isoforms where L-Asp was replaced by D-Asp, L-isoAsp, D-isoAsp or the L-cyclic imide, respectively, has been synthesized and used as a standard to achieve separation of the five forms by capillary electrophoresis and by reverse-phase HPLC. Capillary electrophoresis analysis was performed in uncoated capillaries by the use of aspartic acid/cyclodextrin buffers at low pH. The elution order of the aspartic-acid-containing heptapeptides was D-Asp, L-Asp, L-isoAsp, D-isoAsp and L-cyclic imide. Reverse-phase HPLC analysis was performed on a C18 column by the use of a shallow acetonitrile gradient in trifluoroacetic acid/water. The elution order was D-isoasp, L-isoASp, L-Asp, D-Asp and L-cyclic imide. Human growth hormone samples were degraded by incubation at high temperature and analyzed for their potential content of isomerization and racemization products. Only L-forms of aspartic acid and isoaspartic acid of the heptapeptide fragment were found.

Amino Acid Sequence↗
PubMed1996

Extended studies on the effect of glutamate antagonists on ischemic CA-1 damage.

Glutamate receptors are numerous on the ischemia vulnerable CA-1 pyramidal cells. Postischemic use of the AMPA antagonist NBQX has shown up to 80% protection against cell death. Three aspects of this were studied: In the first study, male Wistar rats were given NBQX (30 mg/kg x 3) either 20 hours or immediately (0 h) before 12 min of 4-vessel occlusion with hypotension. After six days of reperfusion comparison with an untreated group showed almost full protection in the 0 h group (4% cell loss, p < 0.001) but only slight protection in the 20 h group (62% cell loss, p < 0.05). After 12 min of ischemia in the present model, eosinophilic CA-1 cells are seen from day 2 on. Since there could be a late, deleterious calcium influx via NMDA receptors, one group of ischemic rats was given MK-801 (5 mg/kg i.p.) 24 hours after ischemia. However, quantitation 6 days later of remaining CA-1 cells showed no protection. In the third study referred here, two groups of ischemic rats were given NBQX (30 mg/kg x 3) immediately after ischemia. The groups survive for six and 21 days, respectively. Counting of CA-1 pyramidal cells showed an equal, significant protection in both groups (approx 20% cell loss).

Animals↗