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B Carlander

Publications and source records attributed to B Carlander.

At least 37 records · Page 2Linked to original sources
PubMed1994

Family studies in narcolepsy.

Out of a population of 188 unrelated narcoleptic probands, we identified 14 probands (7.44%) with a family history of narcolepsy, 23 (12.23%) with a family history of isolated repeated episodes of naps and/or lapses into sleep and 151 (80.31%) without a family history of either condition. Clinical, polysomnographic or zygotic differences could not be evidenced in the three groups. Empirical risk for narcolepsy was 40.7 times greater among first-degree relatives of narcoleptics than in the general population. Narcolepsy and the condition characterized by isolated repeated episodes of naps and/or lapses into sleep have a common genetic component. This finding has important implications. Indeed, when the latter condition is included in the spectrum of narcolepsy, the empirical risk figure is relatively close to that expected in cases of simple mode of inheritance. A trend in favor of a more frequent transmission through mothers than fathers is emphasized.

Age of Onset↗
PubMed1994

[Somatosensory evoked potentials in amyotrophic lateral sclerosis and primary lateral sclerosis].

Somatosensory evoked potentials (SEPs) were studied in 21 cases of amyotrophic lateral sclerosis (ALS) and 7 cases of primary lateral sclerosis (PLS). Despite the lack of clinical sensory abnormalities, SEPs showed abnormalities in both diseases: lack or delay of some components. In ALS these abnormalities indicate widespread sensory disturbance. In PLS only, the Brodmann area 4 seems to be affected.

Adult↗
PubMed1993

Autoimmune hypothesis in narcolepsy.

Since the discovery of an almost 100% association of HLA-DR2 with narcolepsy-cataplexy, many efforts have been made to demonstrate the intervention of immune factors in the pathogeny of the disease. Some epidemiological features could support this hypothesis: age of onset around 25, triggering factors, association with multiple sclerosis. Molecular studies at the DNA level have, up to now, failed to uncover an abnormal gene in the HLA system, which would imply that the DR2 antigen acts through its role in the immune response. However, results have been largely inconclusive as far as classical features of autoimmunity in blood and CSF are concerned. In canine narcolepsy, a linkage with a human immunoglobulin-related gene has recently been shown, and may constitute a counterpart of the HLA association in man. Thus, the hypothesis of a transient and discrete autoimmune aggression may be ruled out.

Animals↗
PubMed1993

Sleep polygraphic studies using cystomanometry in twenty patients with enuresis.

Polygraphic exploration during sleep using cystomanometry was performed in 20 patients aged 7-17 years with primary (17) or secondary (3) enuresis. In this group of patients, 9 presented with isolated nocturnal enuresis while 11 patients had associated diurnal micturition troubles. During this study we documented 24 episodes of enuresis. There was no disturbance in sleep architecture or correlation between the uncontrolled micturition and any particular state or stage of sleep. Most episodes of enuresis occurred in a unique pattern in which a sudden or progressive intravesical increased pressure was associated with an awakening reaction. From a physiopathologic point of view, our findings are in favor of immaturity of the central system of inhibition of micturition reflex during sleep.

Adolescent↗
PubMed1993

Hallervorden-Spatz syndrome and MRI: the "tiger's eye". One case.

The MRI exploration of a woman suspected, on clinical grounds, of having Hallervorden-Spatz disease (or rather syndrome) revealed, on T2-weighted sequences, the "tiger's eye" or "target" image of the pallidum described by previous authors: i.e. a high-intensity signal in the centre of a distinct low-intensity signal; it also showed an abnormal low-intensity signal of the substantia nigra. These changes are related to the iron deposits and neuro-axonal lesions which characterize the disease. The MRI semeiology of Hallervorden-Spatz disease has been analyzed in the literature. The images we obtained in this patient with the echo-gradient technique using T1-weighted sequences were unusual, showing a low-intensity signal of the globi pallidi surrounded by central and peripheral low-intensity signal areas, whereas the images obtained with spin-echo T1-weighted sequences were normal.

Adult↗
PubMed1992

Sleep in human narcolepsy revisited with special reference to prior wakefulness duration.

Sleep of 11 narcoleptic subjects was recorded on baseline and after 16 and 24 hours of prior wakefulness (16 and 24 hours sleep deprivation). Eleven sex- and age-matched control subjects were recorded for comparisons. All recordings in narcoleptic subjects were characterized by frequent sleep onset rapid eye movement (REM) episodes, increased amounts of wake time after sleep onset and low sleep efficiencies. Mean total sleep time (TST) was significantly decreased in narcoleptic subjects after sleep deprivation (SD). Recovery sleep after 24 hours SD showed reduced nonREM (NREM) sleep stage 2 percentage, whereas percentages of stage 4 and slow-wave sleep (SWS = stages 3 + 4) were significantly increased. The values of REM sleep percentage of TST were remarkably constant throughout and did not differ significantly as a function of experimental conditions, indicating a normal REM sleep pressure in narcolepsy. Sleep stage analysis per sleep cycles revealed significant differences between the two groups. Percentages of stage 4 and SWS were increased during the first cycle of recovery sleep in narcoleptic subjects. Stage 2 was decreased during the third cycle, and SWS decreased rapidly from cycle 1 to cycle 2 and slightly increased thereafter. These results indicate that sleep need is increased in narcolepsy, whereas its decrease over the first NREM-REM cycle is accelerated. We hypothesize that this could reflect an alteration of the homeostatic process of sleep regulation in narcolepsy.

Adolescent↗
PubMed1992

Surgical alternatives to uvulopalatopharyngoplasty in sleep apnea syndrome.

Uvulopalatopharyngoplasty (UPPP) is the surgery most often performed for sleep apnea syndrome (SAS). However, good results with UPPP, demonstrated by polysomnography, have been reported in only 50% of cases. Failure of UPPP may be caused by: 1) bad management of the SAS, which is better treated in some patients with nasal CPAP than with surgery; and 2) an airway obstruction located not only at the palatopharynx (PP) level. Other surgical procedures to enlarge other sites of obstruction are described. Retro-tongue-base-pharynx (RTBP) surgery is emphasized, including mandibular advancement, hyoid bone suspension, and tongue base reduction. Maxillomandibular advancement is the most efficient technique but also the most complicated.

Airway Obstruction↗
PubMed1992

Sleep onset rapid-eye-movement episodes in narcolepsy: REM sleep pressure or nonREM-REM sleep dysregulation?

Thirty-two narcoleptic subjects with excessive daytime sleepiness and cataplexy were recorded for 33 continuous hours. The continuous polysomnographic recording (CPSG) was followed by a standard MSLT at 2-h intervals. There were 64 sleep onset REM episodes (SOREMs) vs 64 sleep onset nonREM episodes (SONREMs) during the CPSG, and 102 SOREMs vs 50 SONREMS during the MSLT. Both sleep onset types peaked at 13-15 h during the CPSG while sleep onsets were evenly distributed during the MSLT. In the latter procedure, the mean sleep latency was significantly shorter with SOREMs occurrence than with SONREMs occurrence. Two factors were extracted in each procedure by means of a Varimax Rotated Factor Analysis. During the CPSG, SOREMs were related to the preceding nocturnal sleep parameters in the first factor, and to the daytime total sleep time and the total number of sleep onsets in the second factor. During the MSLT, SOREMs were related only to the mean sleep latency and the total number of sleep onsets. It was concluded that the occurrence of SOREMs is primarily due to the residual somnolence in narcoleptic subjects. However, their occurrence during the MSLT is largely independent of the prior history of sleep and waking. Thus, we propose a nonREM-REM sleep dysregulation hypothesis to account for the appearance of SOREMs in narcolepsy.

Journal Article↗
PubMed1990

CSF immune variables in patients with narcolepsy.

Cerebrospinal fluid (CSF) and serum from 15 patients with narcolepsy were examined regarding presence of oligoclonal bands on isoelectric focusing, IgG index elevation as indicator of intrathecal IgG production and CSF/serum albumin ratios. Two of 15 patients (13%) showed oligoclonal IgG bands in CSF, one of whom had increased IgG index. Slight disturbance of blood-brain-barrier function as reflected by elevated CSF/serum albumin ratios was present in 4 other patients. The frequency of oligoclonal IgG bands in CSF from patients with narcolepsy is within the range of what is found in other neurological, non-inflammatory diseases. These findings do not support the hypothesis of an immune-mediated pathogenesis of narcolepsy.

Adolescent↗
PubMed1989

Uptake of retinyl ester in HL-60 cells via the low-density-lipoprotein-receptor pathway.

Newly absorbed retinol is transported in association with chylomicrons and their remnants. In addition, after intake of high doses of retinol, significant amounts are also found in low-density lipoprotein (LDL). As both chylomicron remnants and LDL may be taken up by cells via the LDL receptor, and retinoids inhibit proliferation of some leukaemic cells, we have studied the uptake of retinol in leukaemic cells via the LDL-receptor pathway. HL-60 cells contain saturable binding sites for LDL. The binding of LDL to its receptor has a dissociation constant of about 3.2 x 10(-9) M, and the number of receptors per cell was calculated to be about 2700. Uptake of 125I-LDL by HL-60 cells was increased 2-fold by preincubating the cells with mevinolin. The presence of specific receptors for LDL on HL-60 cells was further confirmed by the finding that exogenous LDL cholesterol was able to up-regulate the ACAT (acyl-CoA: cholesterol acyltransferase) activity of HL-60 cells. We then tested the uptake of retinyl ester in leukaemic cells via the LDL-receptor pathway. HL-60 cells were incubated with LDL or chylomicron remnants labelled with [3H]retinyl palmitate. Uptake of retinyl ester associated with both LDL and chylomicron remnants was observed. Furthermore, the presence of excess LDL decreased the uptake by 75-100%, supporting the hypothesis that the uptake of retinyl ester occurred via the LDL receptor in HL-60 cells.

Cell Line↗
PubMed1983

Metabolism of asialoglycoproteins in cultured rat hepatocytes: evidence for receptor mediated uptake and degradation which is not feed-back regulated.

1. Cultured rat hepatocytes took up and degraded asialofetuin by a saturable mechanism. 2. The uptake was specific for desialylated fetuin; native fetuin and was taken up to a much lesser extent. 3. Degradation was inhibited by lysosomotropic agents; both uptake and degradation were, however, unaffected by cycloheximide. 4. The uptake was also unaffected by incubating the cells for 24 hr in the presence of large extracellular concentrations of unlabelled asialofetuin. 5. The data suggest that the asialoglycoprotein receptor is recycled and not subject to down-regulation.

Ammonium Chloride↗
PubMed1982

Injury to human cells in culture induced by low density lipoprotein: an effect independent of receptor binding and endocytotic uptake of low density lipoprotein.

Cultured human endothelial cells isolated from umbilical cord veins and erythrocytes obtained from healthy donors were injured when exposed to low density lipoprotein (LDL). A close relationship between the amount of 125I-LDL associated with the cell surface and the degree of cell injury was demonstrated. This association occurred before any morphological signs of cell injury were observed and before any substantial release of 51Cr into the medium could be measured. Subsequent endocytotic uptake and lysosomal degradation of LDL did not seem to be a prerequisite for the LDL-induced cell injury to occur. Human serum albumin had an inhibitory effect on the association of 125I-LDL with the cell surface and in parallel a lowering effect on the 51Cr release.

Arteriosclerosis↗
PubMed1979

The effect of serum lipoproteins on cholesterol content and sterol exchange in cultured human endothelial cells.

Cultured human endothelial cells preincubated with the infranatant of human serum increased their content of cholesterol when subsequently exposed to low density lipoproteins (LDL) as compared to control cultures further incubated in the presence of infranatant only. Replacing LDL with high density lipoproteins (HDL) resulted in no change in the cellular cholesterol content compared to the control. The addition of HDL did not influence the increase in cellular cholesterol content mediated by LDL. HDL stimulated the efflux of endogenously synthesized 14C-labelled sterols compared to the infranatant fraction, whereas LDL had only a slight effect. Cells preincubated with whole serum did not change their cholesterol content when subsequently exposed to LDL, compared to cultures further incubated in presence of whole serum. Replacing whole serum (during the final incubation) with infranatant, resulted in a decrease of the cellular cholesterol content, which was not influenced by further addition of HDL.

Cells, Cultured↗
PubMed1979

Injury to human endothelial cells in culture induced by low density lipoproteins.

Low density lipoproteins (LDL) have been shown to injure culture endothelial cells derived from the human umbilical cord. During a 48 h incubation period LDL significantly increased 51Cr release from prelabelled cells and induced marked cellular injury if the ratio between the LDL cholesterol and the infranatant proteins was kept above 0.1-0.12 mmol/g protein. Actually, an injurious effect of a fixed concentration of LDL could be completely prevented by increasing the concentration of infranatant proteins. High density lipoproteins within physiological concentration ranges had no effect when tested in the presence of infranatant proteins. The effects of LDL were not cell specific because normal as well as LDL receptor negative human skin fibroblasts were injured by LDL.

Arteriosclerosis↗
PubMed1979

Injury to cultured endothelial cells induced by low density lipoproteins: protection by high density lipoproteins.

Cultured human endothelial cells derived from umbilical cord veins were injured when exposed to low density lipoproteins (LDL). Addition of high density lipoproteins (HDL), together with LDL, inhibited the cellular injury induced by LDL as demonstrated by lowered 51Cr release and prevention of morphological changes. Serum albumin had a similar, but far weaker effect. Preincubation of the cells with HDL did not reduce injury inflicted during a subsequent incubation with LDL, while preincubation with LDL aggravated later damage. The protective effect of HDL could be overcome by increasing the DLD concentration.

Arteriosclerosis↗