Cerebral blood flow in neurolept-analgesia.
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Biomedical subjects
Publications and source records attributed to E Nilsson.
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A predominantly type-specific mu-capture radioimmunoassay (RIA) of IgM antibodies to Coxsackie B1-B5 (CB1-CB5) viruses was previously described (Frisk et al., 1984). The present study is concerned with the specificity of this assay, using as antigen different strains of one serotype (CB5) and procapsids of two serotypes (CB3 and CB5). Eight strains of CB5 virions were tested against acute and/or convalescent sera from 10 patients from whom CB5 had been isolated. Seven patients' sera were tested against their own strain. The frequency of IgM-positive patients varied from 9 of 10 (90%) to 5 of 10 (50%). In three cases the highest titres were obtained with the patients' own strain. When sera from patients with other enterovirus infections were tested against the CB5 strains, heterotypic titres were obtained to a certain extent (0-15.6%). The strains giving a high frequency of homotypic titres varied concerning heterotypic reactions. It is concluded that the choice of strain is important if a high frequency of homotypic titres with no or only a few heterotypic reactions is to be obtained. When procapsids were used as antigen, both homotypic and heterotypic titres were seen to a large extent. All patients with homotypic IgM against CB3 or CB5 virions showed IgM against the CB3 or the CB5 procapsids, respectively. When sera from patients with other enterovirus infections were tested, IgM was found in 54 of 93 patients (58%) with use of the CB3 procapsid and in 52 of 87 patients (60%) with the CB5 procapsid. It was often not the same patients who showed IgM against the two different procapsids. When both procapsids were used, IgM positivity was found in 62 of 81 patients (77%) with other enterovirus infections. It is concluded that the use of two or more procapsids in combination is of value for the diagnosis of a recent or current enterovirus infection.
The Ca2(+)-dependent neutral proteases calpain I and II as well as their specific inhibitor, calpastatin, were isolated from normal and Alzheimer-degenerated frozen human brain tissue. In the Alzheimer group calpain I activity was higher in cortex than in mesencephalon. The calpastatin activity was lower in cortex in both groups. This may implicate a higher Ca2(+)-dependent proteolysis in cortex compared to mesencephalon. In the Alzheimer group the cortical calpain II level decreased with an increasing degree of neuropathological changes. In the control group, the level of calpastatin decreased as the number of plaques and tangles increased. Evidence was obtained for a correlation of net calpain activity and the extent of neuropathological changes in cortex.
Specific factors that mediate local cell--cell interactions in the ovary related to the initiation and progression of follicle development will be discussed. Recently, several factors produced locally by the primordial follicle have been shown to induce primordial follicle development from a quiescent state to promote follicle development. Kit ligand/stem cell factor (KL/SCF) produced by the immature granulosa cells appears to promote theca cell organization. Basic fibroblast growth factor produced predominately by the oocyte, but by all cells at reduced levels, also was found to induce primordial follicle development similar to KL. It is likely that numerous locally produced factors will mediate cellular interactions and interact between each other to control the induction of primordial follicle development and influence processes such as the onset of puberty and menopause. After follicle development has been induced, theca cells and granulosa cells interact through classical mesenchymal-epithelial type interactions to influence the progression of follicle development. Mesenchymally derived theca cells have been shown to produce transforming growth factor alpha (TGF-alpha), keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), and transforming growth factor beta to regulate granulosa cell growth and function. The epithelial granulosa cells have been show to produce KL/SCF that can feed back on the theca cells to regulate theca cell growth and stimulate the production of the theca cell factors (TGF-alpha, KGF, and HGF). Therefore, a positive feedback loop between the theca cells and granulosa cells appears to exist to promote the dramatic cell growth required during folliculogenesis. Interestingly, hormones such as estrogen and gonadotropins stimulate the expression of these paracrine growth factors. Therefore, the actions of hormones to stimulate follicle development and growth are mediated in part through altering these local cell--cell interactions. In summary, the locally produced paracrine factors that mediate cell-cell interactions involved in primordial follicle development and the progression of follicle development during folliculogenesis are starting to be elucidated.
The prevailing opinion on lysosomal endurance is that, as long as the cells are still alive, these organelles are generally quite stable and, thus, do not induce cell damage by leaking their numerous powerful hydrolytic enzymes to the cytosol. We suggest that this opinion is basically wrong and consider that many lysosomes are quite vulnerable, especially to oxidative stress. Moreover, we suggest that cellular degeneration, including apoptosis as well as necrosis, follows upon lysosomal disruption. We have found differing stability of lysosomal membranes to oxidative stress, not only among different cell types, but also between cells of the same type and between lysosomes of individual cells. We suggest that cellular resistance to oxidative stress is mainly a function of three parameters: (i) the capacity to degrade hydrogen peroxide before it reaches, and may diffuse into, the acidic vacuolar compartment; (ii) the resistance to reactive oxygen species of lysosomal membranes; and (iii) the intralysosomal amounts of redox-active, low molecular weight iron. Iron-catalysed intralysosomal reactions, if pronounced enough, result in peroxidation and destabilization of the lysosomal membrane. Owing to differences in the cellular synthesis of hydrogen peroxide-degrading enzymes, degree of autophagocytotic degradation of iron-containing metalloproteins, lysosomal localization within the cytoplasm and intralysosomal iron chelation, the above three parameters may vary between both different and similar cells and between lysosomes of individual cells as well, explaining their observed variability with respect to resistance against oxidative stress.
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335 ears from 210 childred in which tympanometry initially indicated middle ear pressure less than or equal to -100 mm H2O or a flat tympanogram have been reinvestigated 3 years later. When the inital investigation was performed all children were 7 years old. The present study reveals that 25% of these ears still have middle ear pressure less than or equal to -100 mm H2O and 16% middle ear pressure less than or equal to -150 mm H2O. In normal material of the same age group 9% have middle ear pressure less than or equal to -100 mm H2O and 4% middle ear pressure less than or equal to -150 mm H2O. The study also reveals effusion in 10% of ears with normal screening audiograms. In ears with normal screening audiograms and middle ear pressure greater than or equal to -145 mm H2O effusion was found in 5% and in ears with abnormal screening audiograms and middle ear pressure less than or equal to -150 mm H2O effusion was found in 81%. As tympanometric criterion for otologist referral, middle ear pressure less than or equal to -150 mm H2O or a flat tympanogram is suggested. The inclusion of tympanometry in routine screening for middle ear pathology in children is recommended.
PURPOSE: This article analyzes the influence of different pretreatments on the bond strength between inlays and the resin cement of three different composite inlay systems: Z-100, Targis, and Art Glass. MATERIALS AND METHODS: Four separate treatments of the composite-bonding agent interface were investigated: (1) untreated surface, (2) grinding, (3) sandblasting, and (4) sandblasting followed by silane treatment. Surface topography, roughness, and shear bond strength were evaluated using digital scanning electron microscopy, confocal laser scanning profilometry, and a Lloyd LRX equipped for shear bond testing, respectively. RESULTS: The bond strength is presented both with respect to composite surface pretreatment and with respect to different composite inlay systems. Independent of the composite inlay system, the sandblasted and silane-treated surface was found to give the highest bond strength values, followed by the sandblasted and ground surfaces. The untreated surface showed the lowest bond strength. For pretreated surfaces, Targis showed the highest (P < 0.05) bond strength values, followed by Art Glass and Z-100. This distribution, however, was reversed for the untreated interface, where Z-100 showed the highest bonding strength (P < 0.05). CONCLUSION: Surface pretreatment and roughness as well as the inlay material have an impact on the bond strength and the retention of composite inlays.
Using radioimmunoassays (RIA) we measured the concentrations of prolactin, cortisol, dehydroepiandrosterone sulphate (DHEAS), pregnenolone sulphate (5-PS) and testosterone sulphate (TS) in peripheral blood and synovial fluid (SF) from 50 patients with arthritis of the knee associated with different diagnoses. These included RA (25 cases); and psoriasis, ankylosing spondylitis, reactive arthritis, post-traumatic arthritis, unspecified polyarthritis, polyarthritis and sacroilitis, and regional enteritis (25 cases). Fifty-six healthy subjects (age 19 to 60 years) were used as controls. No significant difference was found between the blood prolactin levels in patients and controls. The mean levels of cortisol, 5-PS, DHEAS and TS were significantly reduced in the patients with RA (mean 133 vs 286 nmol/l cortisol, 26 vs 80 nmol/l 5-PS, 930 vs 3290 nmol/l DHEAS and 25 vs 40 nmol/l TS; p less than 0.001 for cortisol, 5-PS and DHEAS, and p less than 0.05 for TS). The reduction was more marked in the DHEAS levels in patients with positive rheumatoid factor (RF) reactivity. Patients with diagnoses other than RA had normal levels of the various steroids except patients on steroid treatment, who also exhibited reduced levels. The 5 hormones measured in the SF were found in relatively high concentrations, parallelling those in the blood. The ratios (SF/blood) varied from 0.66 for 5-PS to 1.1 for cortisol, and the correlation coefficients between 0.66 for 5-PS and 0.94 for DHEAS (p less than 0.001). Low blood and SF levels of sulpho-conjugated steroids, particularly DHEAS, are a permanent disorder in patients with RA and positive RF reactivity.(ABSTRACT TRUNCATED AT 250 WORDS)
In a clinical study the blood levels of dehydroepiandrosterone sulphate (DHEAS), pregnenolone sulphate (5-PS), testosterone sulphate (TS) and their respective unconjugated steroids were measured in: 20 patients with systemic lupus erythematosus (SLE) who were receiving either no treatment (11 patients) or else treatment with chloroquine (9 patients), in some cases combined with non-steroidal anti-inflammatory drugs (NSAIDs); in 26 patients receiving corticosteroid (Prednisolone) treatment; and in healthy men and women. The patients not on corticosteroid exhibited substantially reduced DHEAS, 5-PS and TS levels (geom. mean: 2300 vs. normal 4300 nmol/l DHEAS; 200 vs. 320 nmol/l 5-PS; and 120 vs. 360 nmol/l TS; p less than 0.001), irrespective of the difference in sex, age or chloroquine treatment. The patients on corticosteroid treatment displayed a similar pattern of levels, but the reduction was much more marked than in the patients not on the steroid (geom. mean: 610 nmol/l DHEAS, 55 nmol/l 5-PS; and 35 nmol/l TS; p less than 0.001). No consistent changes were observed in the unconjugated steroid levels, although they were also reduced by the treatment with prednisolone. The data indicate that a deficiency in sulpho-conjugated steroids is a permanent feature of patients with SLE and that this is accentuated by the administration of corticosteroid derivatives. Further studies are needed to establish the pathophysiological significance of these findings.
The fatigue of the stapedius reflex was studied in 100 normal ears. Stimulus frequencies 500 and 1000 Hz were used,and the decrement of the stapedius reflex at 5, 10, and 15 dB above the reflex threshold was estimated. No decrement at all (less than 10% decay 10 sec after the onset of a stimulus 10 dB above the reflex threshold) was present in a majority of the ears. Between 27 and 58% of the ears showed reflex decay depending on variations of different factors such as stimulus frequency, intensity of the stimulus, and the method to register the reflex. Reflex decay was more often seen at 1000 Hz than at 500 Hz stimulus frequency. Reflex decay was also more often seen 5 dB above the reflex threshold than at higher intensity levels. The reflex decay thus observed in normal ears was generally small and did only very occasionally reach values which can be regarded as pathological.
T lymphocyte subpopulations were determined by monoclonal antibodies Leu 2 (suppressor/cytotoxic subset) and Leu 3 (helper/inducer subset) in synovial fluid (SF) and blood of 9 patients with acute non-septic synovitis (duration less than 1 month), 28 patients with chronic synovitis (16 with rheumatoid arthritis (RA), 7 with ankylosing spondylitis, 4 with psoriatic arthritis and one with juvenile rheumatoid arthritis) and 37 age- and sex-matched healthy controls. The patients with acute synovitis had a significantly higher percentage of Leu 3+ cells and a significantly lower percentage of Leu 2+ cells in SF than had patients with RA or other forms of chronic synovitis. In patients with acute synovitis the ratio of Leu 3+ to Leu 2+ cells was significantly higher in SF (4.0) than in blood (1.9) whereas in patients with RA the ratio was significantly lower in SF (1.1) than in blood (2.7). Patients with other forms of chronic synovitis also had a lower Leu 3/Leu 2 ratio in SF (1.1) than in blood (1.9). Two patients with acute synovitis who were retested after 10 days and 10 months respectively (the latter patient having developed definite RA) showed a decrease of the synovial Leu 3/Leu 2 ratio. Thus it appears that the distribution of T lymphocyte subsets in SF was related to the duration of the synovitis.
Blood levels of dehydroepiandrosterone sulphate (DHEAS) were measured by radioimmunoassay (RIA) in patients with: a) polymyalgia rheumatica/giant cell arteritis (PMR:TA; N = 25), with and without cortisone derivative treatment (N = 10 and N = 15, respectively); and b) primary fibromyalgia (PF; N = 15). The mean DHEAS levels were found to be significantly reduced in PMR:TA, compared to those in PF (Geom. mean 820 vs. 2300 nmol/l, respectively; p < 0.001), and the reduction was more marked in patients on cortisone derivative treatment. The DHEAS levels found in PF were found to be normal and consistent with those previously reported in non-immune mediated rheumatological diseases such as osteoarthritis, and in healthy subjects, using the same method of analysis. The low levels found in patients with PM:TA are in accordance with those previously reported in immune-mediated diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis, suggesting that diminution of DHEAS is a constant endocrinologic feature in these categories of patients. The pathophysiological significance of these low DHEAS levels needs to be investigated.
To assess the relationship between blood and tissue steroid levels, cortisol and dehydroepiandrosterone sulphate (DHEAS) were measured by radioimmunoassay (RIA) in blood and joint tissues from a group of patients with RA (N = 29) ranging in age from 26 to 80 years (mean 63, SD: 13) and another group with secondary osteoarthritis (OA; N = 23), ranging in age from 47 to 86 years (mean 66, SD: 9), all of whom were scheduled for surgical correction of joint dysfunction. Seventeen of the RA patients were on steroid treatment at the time of the study. Assessing all the patients together, it was found that the tissue concentrations of DHEAS very closely paralleled the blood levels (r = 0.875; p < 0.001). The mean blood and tissue concentrations of DHEAS were found to be significantly reduced in RA, compared to those in OA (geometric means 540 vs. 2100 nmol/l blood, respectively, and 160 vs. 420 nmol/kg tissue, p < 0.001). Individual data indicated, however, that: (a) 3/29 patients with RA exhibited normal levels; (b) the reduction was more accentuated in those patients on steroid treatment; and (c) 5/23 patients with OA, who were treated for cardiovascular disorders, also had reduced DHEAS levels. Significant differences were not found between the mean cortisol levels in RA and those in OA, nor was there a correlation between the blood and tissue levels of this steroid. The possible influence of reduced DHEAS levels on immune-mediated diseases and/or pathophysiology is unknown, and needs to be investigated.