Kaposi's sarcoma and protection from HIV dementia.
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AIDS Dementia Complex↗
Biomedical subjects
J Maehlen
Publications and source records attributed to J Maehlen.
[1997 Nobel Prize in physiology or medicine].
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History, 20th Century↗
[Splenic atrophy and fatal pneumococcal infection in inflammatory bowel disease].
Fatal pneumococcal disease occurred in a young woman with ulcerative colitis that had been quiescent for ten years. Howell-Jolly bodies were present in the peripheral blood smear. Severe atrophy of the spleen (weight 7 g) was discovered at autopsy. The evidence that hyposplenism is associated with inflammatory bowel disease is reviewed and it is suggested that these patients should undergo ultrasound examination and examination of blood smear for detection of functional hyposplenism. We conclude that pneumococcal vaccination should be considered for all patients with inflammatory bowel disease.
Adult↗
The impact of primary central nervous system lymphoma in AIDS patients: a population-based autopsy study from Oslo.
This study comprises the 255 adult AIDS patients treated at Ullevål hospital 1983-1995. These patients, fulfilling the Centers of Disease Control (CDC) clinical criteria for AIDS, correspond to 91% of all adult AIDS cases in Oslo. By the end of the study period, 44 patients were alive and 211 had died. Full autopsy was performed on 153 (73%) of the deceased. Supplementary analyses were carried out on the 344 patients (225 deceased) fulfilling the U.S. definition of AIDS, which includes CD4 cell counts below 200 cells/mm3. In the autopsy group, histologically verified non-Hodgkin B-cell lymphoma was found in 29 cases (19%). Nineteen of these (12%) had primary central nervous system (PCNS) lymphoma. Survival curves indicate that PCNS lymphoma constitutes a small risk early in the AIDS stage, but it has a serious impact on long-term survival. For patients not contracting other fatal diseases, one fourth are estimated to die of PCNS lymphoma within about 3 years. Comparison of clinical diagnoses and autopsy results show that PCNS lymphoma has been difficult to separate from other CNS disorders, which probably has caused marked underestimation of the incidence in previous assessments. We conclude that PCNS lymphoma is a major threat to long-term survival in AIDS victims.
AIDS Dementia Complex↗
HIV dementia and apolipoprotein E.
The effect of apolipoprotein E genotypes on the occurrence of HIV dementia and HIV encephalitis was studied in a sample of 132 AIDS patients in whom clinical data on dementia was available and full autopsy had been performed. There was no statistically significant correlation between risk of HIV dementia or HIV encephalitis in relation to apolipoprotein E genotypes, even after correction for length of survival with AIDS and antiretroviral treatment.
AIDS Dementia Complex↗
High incidence and aggressive growth of non-AIDS-defining cancers among AIDS patients in Oslo.
The spectrum of cancers advanced by AIDS is disputed. To supplement the register-based investigations, we have studied the occurrence of non-AIDS-defining malignancies in a closely followed population of AIDS patients. The population comprises 255 patients fulfilling CDC's clinical AIDS definition, representing 91% of all adult AIDS patients from Oslo 1983-1995. Full autopsy was performed on 73% of the 211 fatal cases. Adding patients with CD4 cell counts below 200 cells/mm3 to match the US AIDS definition, the population increases to 344, including 225 deceased. The expected number of cancer cases was calculated from age- and sex-specific cancer incidence rates for Oslo 1988-1992. The number of non-AIDS-defining cancers was six (clinical CDC criteria) or eight (US AIDS definition), compared to expected numbers of 0.54 and 1.0, respectively. At autopsy, four of eight cases showed extensive tumor dissemination with involvement of the heart. These observations suggest that (at least some) non-AIDS-defining cancers occur at increased rates and show aggressive growth pattern in AIDS.
Acquired Immunodeficiency Syndrome↗
Retrograde axonal cytokine transport: a pathway for immunostimulation in the brain inducing hypoxia and sudden infant death?
The etiology and pathogenesis of sudden infant death syndrome (SIDS) remain unknown. A hypothesis for SIDS should explain three characteristic findings: (a) an age distribution peaking at 2-4 months; (b) frequent association with respiratory tract infections; and (c) occurrence during sleep. The diagnosis of SIDS is applied when death cannot be explained, and this syndrome therefore probably includes various underlying causes. Based on recent observations, however, we suggest a pathogenic pathway that might be common to most SIDS victims.
Astrocytes↗
Changing incidence of HIV-induced brain lesions in Oslo, 1983-1994: effects of zidovudine treatment.
OBJECTIVE: To investigate the relation between HIV-induced brain lesions, zidovudine (ZDV) treatment and survival length in a well-defined population of HIV-positive patients. METHODS AND PATIENTS: Ulleval Hospital has the responsibility for treating all AIDS patients from the city of Oslo except haemophiliac patients. The patient population in this autopsy study comprised all adult AIDS patients in Oslo who were treated at our hospital and died during 1983-1994 (n = 171). This represents 86% of all adult AIDS patients from Oslo who died during the same period. Full autopsy, including neuropathological examination of the brain and spinal cord, was performed on 128 (75%) of those who died. RESULTS: No significant differences were found between autopsy and non-autopsy cases with regard to sex, age, risk groups, survival length or ZDV treatment. In the autopsy material, multinucleated giant cells (MGC) in brain tissue were found in 29 cases and diffuse damage of white matter in 52 cases. Analysis shows that ZDV (600 mg per day) reduced the incidence of these brain lesions, but only if continued until death. A second finding was an increased incidence of HIV-induced brain lesions for those with long-term survival. Together these observations may explain a substantial part of the time-trend in the incidence of MGC in Oslo. MGC were frequent (40%) during the first years of the epidemic, although survival length was short in this period. The incidence fell markedly around the time ZDV was introduced and later remained low in those using ZDV until death. The incidence of MGC has, however, increased during the later years, the new cases mainly occurring in patients who had discontinued ZDV use. CONCLUSION: If continued until death, ZDV can reduce the incidence of HIV-induced brain lesions in AIDS patients. When ZDV treatment is terminated a rapid increase occurs in the incidence of HIV encephalitis.
Acquired Immunodeficiency Syndrome↗
Nerve-evoked electrical activity regulates molecules and cells with immunological function in rat muscle tissue.
Molecules coded by the major histocompatibility complex (MHC) are present on cell surfaces in most tissues, with the cells of the central nervous system and skeletal muscle as prominent exceptions. We show here that when rat skeletal muscles are rendered inactive by nerve impulse block, expression of MHC class I molecules occurs on the muscle fibres. In addition, the number of cells expressing MHC class II molecules in the muscle interstitium is increased by a factor of three after 2 weeks of impulse blockade. Similar effects obtained by denervation can be counteracted by direct electrical stimulation. Interferon-gamma-like immunoreactivity accumulates in inactive muscle fibres, and interferon-gamma or a related cytokine could be a link between inactivity and MHC up-regulation. These findings suggest that nerve-evoked muscle activity influences not only the phenotype of the muscle cells themselves, but also processes in the interstitium that may increase the immunoreactivity of inactive muscle tissue.
Animals↗
A model of selective synapse formation in sympathetic ganglia.
In the sympathetic system, neurons from several spinal segments are mapped onto targets in the periphery in a topographically ordered way by means of selective synaptic connections in the superior cervical ganglion. Experimental evidence points to a crucial role for chemoaffinity in establishing this topographic map. Furthermore, rearrangements of synapses after surgical manipulations indicate that this chemoaffinity is not based on rigid "key-and-lock" markers. Our model is used to study how such nonrigid markers may interact with other regulatory factors, including growth-regulating signals and the growth potential of individual neurons. In the model, these latter factors are limiting, so that an increasing number of synaptic contacts decreases the likelihood of further synapse formation. These factors are combined with chemoaffinity using a linear threshold model. The model is robust to parameter changes and reproduces experimental observations with reasonable detail. Simulation results are used to discuss characteristic experimental results, such as the substantial plasticity of the connections seen after partial denervation. A surprisingly small effect of transient hyperinnervation in the model may help explain why final connectivities are similar in two real situations with high and low degrees of transient hyperinnervation (development and adult reinnervation). It is shown that spatial restrictions on post-synaptic neurons (dendrites) may contribute significantly to the segmentally broad innervation of each ganglion cell. Finally, we discuss potential effects of presynaptic neuronal death in systems with a high degree of plasticity.
Animals↗
Affection of the hippocampal granule cells in pontosubicular neuron necrosis.
The dentate fascia of the hippocampus was studied in 25 infants with pontosubicular necrosis and in 21 control cases without hypoxic cerebral lesions. Of the control cases 19 were completely normal and 2 showed one single necrotic cell in the granule cell layer. In contrast 15 of the cases with pontosubicular necrosis showed varying degrees of neuronal karyorrhexis in the dentate fascia. The severity of these changes largely parallelled those in the subiculum but there were exceptions to this rule. It is concluded that the dentate fascia is frequently involved in pontosubicular necrosis.
Blood Glucose↗
[The carbohydrate deficient glycoprotein syndrome].
The carbohydrate-deficient glycoprotein syndrome is a newly described hereditary disorder which may be due to a defect in the glycoprotein metabolism. Predominant symptoms are mental retardation, epilepsy, cerebellar ataxia, polyneuropathy, squint, retinitis pigmentosa, retarded growth, hypothyroidism and liver steatosis. Increased serum glycoprotein-deficient transferrin is a marker of the disease and confirms the diagnosis. We describe four Norwegian children with this syndrome. Olivopontocerebellar degeneration was found upon examination of the brain in two patients who died.
Abnormalities, Multiple↗
Paramyxovirus infections alter certain functional properties in cultured sensory neurons.
Functional properties of cultured mouse dorsal root ganglion cells infected with paramyxoviruses have been studied using intracellular recording techniques. Mumps virus, which causes a persistent non-lytic infection, and Sendai virus, which causes an infection that leads to cell lysis after about a week were used. In the early phase of the infection (24-48 h) both viruses caused a reduction in the influx of calcium ions during the action potential, but did not alter resting membrane potential, action potential amplitude or input resistance. At later times functional properties became normal in mumps infected neurons. In contrast, Sendai virus infected neurons showed a reduction of action potential amplitude and input resistance at 48-72 h after infection, and finally there was also a reduction of membrane potential before the cells disintegrated. These results show that different paramyxovirus infections may cause different types of alterations in the functional properties of neurons. The reduced calcium influx resulting from mumps infection suggests that a non-lytic viral infection may have selective effects on important regulators of neuronal functions. Moreover, a lethal viral infection (Sendai) may influence specific membrane properties, such as calcium channel activation, several days prior to general structural and functional degeneration.
Action Potentials↗
[The pathogenesis of Alzheimer's disease--what do we know today?].
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Alzheimer Disease↗
Necrosis of granule cells of hippocampus in adrenocortical failure.
A case of untreated and rapidly progressive Addison's disease in a 23-year old woman showed selective necrosis with karyorhexis of the granule cells in the hippocampus. We suggest that this unique lesion was caused by a severe adrenocortical insufficiency. This explanation is in accordance with a recent report of selective loss of hippocampal granule cells after complete adrenalectomy in rats. No evidence of nerve cell loss was found in three cases of Addison's disease that had received cortisone treatment, which is consistent with the experimental observation that even very low levels of cortisone in adrenalectomized rats are sufficient to prevent granule cell loss.
Adrenal Cortex Diseases↗
Behavioural deficits and serotonin depletion in adult rats after transient infant nasal viral infection.
Dysfunction of subcortical serotoninergic neurons has been implicated in some behaviour disturbances. The serotoninergic neurons in the dorsal and median raphe project widely in the brain. They innervate the olfactory bulbs and can be targets for exogenous agents attacking the olfactory epithelium and bulbs. We report here an injury to the serotoninergic neurons after intranasal infection in 12-day-old rats with a temperature-sensitive mutant of vesicular stomatitis virus. The brain infection was focal and transient. Viral antigens could no longer be detected 13-15 days after infection. In spite of this the animals, as adults, had a severe serotonin depletion in the cerebral cortex and hippocampus, and showed abnormal locomotor and explorative behaviour as well as learning deficits. The neocortex was histologically intact and parameters related to other neurotransmitters such as dopamine, noradrenaline, GABA and acetylcholine showed no marked changes. A relatively selective damage to serotoninergic nuclei as a result of virus neuroinvasion through a natural portal of entry, may constitute a new pathogenetic mechanism for cortical dysfunction and behavioural deficits.
3,4-Dihydroxyphenylacetic Acid↗
Peripheral nerve injury causes transient expression of MHC class I antigens in rat motor neurons and skeletal muscles.
After a peripheral nerve lesion (rat facial and sciatic) an induction of major histocompatibility complex (MHC) antigens class I was detected immunohistochemically in skeletal muscle fibers and motor neurons. This MHC expression was transient after a nerve crush, when regeneration occurred, but persisted after a nerve cut, when regeneration was prevented. Since the time course of MHC class I expression correlates to that of regeneration a role for this cell surface molecule in regeneration may be considered.
Animals↗
Distribution of leukosialin (W3/13)-like immunoreactivity in the rat central nervous system.
The monoclonal antibody W3/13, which is directed against leukosialin (a molecule present on certain types of leukocytes), was found to react immunohistochemically with distinct regions and structures in the rat CNS. The leukosialin (W3/13)-like immunoreactivity occurred on neurite-like fibres and on bouton-like structures on nerve cell bodies and their dendrites. This labelling was most pronounced in certain subcortical areas and brain stem nuclei including different thalamic nuclei, olfactory tubercle, superior olive, cochlear and vestibular nuclei, motor and somatosensory nuclei. In the cerebellum, immunoreactive fibres were prominent in the molecular layer. In the spinal cord there was a dense labelling of fibres in the whole grey matter.
Animals↗