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Biomedical subjects

B Andersson

Publications and source records attributed to B Andersson.

At least 451 records · Page 25Linked to original sources
PubMed1983

Obesity, serum steroid levels, and pulsatile gonadotropin secretion in polycystic ovarian disease.

Serum binding capacity of sex-hormone binding globulin (SHBG-BC), steroid concentrations, and secretion patterns of LH and FSH were compared between groups of seven nonobese and seven obese patients with polycystic ovarian disease (PCOD). Obese patients with PCOD differed from those with normal weight in having very low SHBG-BC and elevated serum levels of free and albumin bound testosterone. Compared to healthy women in the follicular phase, both nonobese and obese patients with PCOD showed equally elevated serum levels of androstenedione, estrone, and albumin-bound and free estradiol. Pattern of gonadotropin secretion was studied from blood samples taken at 15 min intervals for 6 h. In 6 patients of both groups low pulses of FSH were found coincidently with pulses of LH. Serum level of LH showed a clear pulsatile pattern in all patients with PCOD, varying from 4.5 to 7.5 pulses per 6 h. The mean pulse rate in the groups of nonobese and obese patients with PCOD was similar, 5.9 pulses per 6 h. In the obese patients the mean LH levels were, however, less elevated and the pulse amplitudes were smaller than those in the nonobese patients. We suggest that this difference is due to high levels of biologically active testosterone in obese patients with PCOD.

Adult↗
PubMed1983

Selective functional role of murine Tm and Tg cells in concanavalin-A-induced T-cell activation.

Murine splenic cells were separated on Ig-anti-Ig columns to yield cell populations depleted of IgM-FcR (Fc receptor)-expressing (TM) and IgG-FcR-expressing (TG) cells and also cells expressing neither of these two FcR (TO). The proliferative response to the lectin concanavalin A (Con A) was shown to be present mainly in cell populations depleted of TM cells (T cells lacking IgM FcR)--that is, TM and TO. The low Con A response in the other cell populations, namely TG and TTOT, was due to a selection against T-cell growth factor (TCGF)-reactive cells, since TCGF production within these subsets was not impaired and the low proliferative response was not reconstituted by preformed TCGF. TG-cells were able to inhibit the Con-A-induced proliferation of TO and TM cells dose-dependently. These data strongly suggest the presence of a step-one regulatory, suppressive mechanism comprised within the TM population.

Animals↗
PubMed1983

Drug careers in perspective.

This paper reports the results of a 10-year follow-up of a pioneer group of 36 opiate addicts treated at a detoxification unit at St Lars Hospital in Lund in the years 1971-72. Sixteen of them are now ex-addicts. Their way out of addiction is described. The results show that there exists a turning process during which some kind of therapeutic action could be of considerable value. The ex-addicts go through a period in which they show signs of an identity conflict. During this period women seem more inclined to relapse than men. This stresses the importance of long-term therapeutic strategies.

Adult↗
PubMed1983

Post mortem, ultrastructural cardiac muscle changes and anthracycline toxicity.

Anthracycline induced cardiomyopathy is commonly evaluated using the ultrastructural investigation of myocardial tissue. This is based to a large degree on subjectively evaluated, studies of post-mortem material which report various fin structural changes of cardiac tissue as being characteristic of this cardiomyopathy. We have studied the morphological variations of normal myocardial tissue in rats following perfusion fixation and immersion fixation of tissue obtained at death as well as at time points up to 6 hours after death, to examine the fine structural changes associated with immersion fixation and post mortal artefacts. Mitochondria profile area (reflecting mitochondrial swelling--a factor constantly reported as typical of anthracycline damage) increased significantly (p less than 0,01) if there was any delay between cell death and fixation. Many other fine structural changes were noted. We conclude that studies of this nature should ideally be carried out in experimental systems using perfusion fixation. Fixation procedures must always be defined in detail. If post mortem material must be used adequate information on the duration of the autolytic period must be given.

Animals↗
PubMed1983

Molecular mechanisms of adhesion of Streptococcus pneumoniae to human oropharyngeal epithelial cells.

Adherence of bacteria to mucosal surfaces is an early step in colonization and infection. Streptococcus pneumoniae colonizes the nasopharynx and causes localized and systemic disease. The higher adhesion capacity of strains isolated from patients with otitis as compared to strains from sepsis or meningitis patients indicates that binding to the nasopharyngeal mucosa is important in localized but not in invasive infections. The biochemical basis of the pneumococcal binding to epithelial cells has been investigated. Human nasopharyngeal epithelial cells were mixed with pneumococci, and adherence was determined microscopically. Inhibition of adherence with analogues of epithelial cell receptors was tested by preincubation of pneumococci before the addition of the epithelial cells. Competitive inhibition with glycoconjugates, representing receptor structures on the epithelial cell surface, showed receptor function of saccharides containing the disaccharide GlcNAcbeta1 leads to 3Galbeta-.

Disaccharides↗
PubMed1983

Progestin receptor levels in endometria with delayed or incomplete secretory changes.

In women with an infertility problem, cytosol progestin receptors were quantified in endometrial biopsies and correlated to histologic postovulatory dating. In 19 women (group A) the histologic dating corresponded to the cycle day; 14 women (group B) showed delayed or incomplete secretory changes. Group B showed significantly lower mean progestin receptor values (132 +/- 22 fmoles/mg protein [+/- SEM, P less than .01] ) than group A (236 +/- 29 fmoles/mg protein). The mean serum progesterone values did not differ significantly between groups A and B in the midluteal or the late luteal phase of the cycle. Inadequate maturation of the endometrium seems to correlate with insufficient development of progestin receptor binding sites rather than with decreased serum progesterone levels.

Cytosol↗
PubMed1982

Stimulation of the insulin secretory mechanism following barium accumulation in pancreatic beta-cells.

Electrothermal atomic absorption spectroscopy was employed for measuring barium in beta-cell-rich pancreatic islets microdissected from ob/ob-mice. Both the uptake and efflux of barium displayed two distinct phases. There was a 4-fold accumulation of barium into intracellular stores when its extracellular concentration was 0.26 mM. Unlike divalent cations with more extensive intracellular accumulation, the washout of Ba2+ was not inhibited by D-glucose. Ba2+ served as a substitute for Ca2+ both in maintaining the glucose metabolism after removal of extracellular Ca2+ and making it possible for glucose to stimulate insulin release. Furthermore, Ba2+ elicited insulin release in the absence of glucose and other secretagogues. The latter effect was reversible and was markedly potentiated under conditions known to increase the beta-cell content of cyclic AMP. It is likely that the observed actions of Ba2+ are mediated by Ca2+, since Ca2+ -dependent regulatory proteins, such as calmodulin, apparently cannot bind Ba2+ specifically.

Animals↗
PubMed1982

Prostaglandin synthetase catalyzed activation of paracetamol.

Prostaglandin synthetase has the ability to catalyze the metabolism of paracetamol to a reactive metabolite, which binds to protein and reduced glutathione (GSH). This was demonstrated with microsomes isolated from both sheep seminal vesicles (SSV) and rabbit kidney medulla. The activation of paracetamol occurred through cooxygenation during prostaglandin biosynthesis, the peroxidase activity of this enzyme being responsible for the reaction. In addition to being metabolized, paracetamol also stimulated the rate of prostaglandin biosynthesis probably by serving as a potent hydrogen donor. The metabolism of paracetamol to a reactive metabolite most likely involved the formation of a paracetamol radical species. This was indicated by an inhibitory effect of the antioxidant, butylated hydroxyanisole, as well as by a very rapid oxidation of GSH during the course of the prostaglandin synthetase catalyzed reaction. Whether this paracetamol radical is further oxidized to the quinone imine prior to reacting with GSH or protein, remains to be established. The ultimate reactive metabolite is evidently the same as that formed with liver microsomes and NADPH since the glutathione conjugates were apparently identical. The rate of paracetamol activation by SSV microsomes was, however, more than 100 times that by liver microsomes and furthermore the apparent Km was considerably lower. Finally, N-OH paracetamol was shown to be activated by prostaglandin synthetase in the presence of arachidonic acid to a metabolite apparently different from that formed from paracetamol.

Acetaminophen↗
PubMed1982

Transbilayer organization of the chlorophyll-proteins of spinach thylakoids.

To investigate the transverse bilayer organization of the chlorophyll-proteins of the three intrinsic chlorophyll-protein complexes, the effects of proteolytic enzymes, and an antibody against the light-harvesting complex were compared using right-side-out and inside-out thylakoid vesicles. The vesicles were isolated by aqueous polymer phase partitioning following the fragmentation of spinach thylakoids by passage through a Yeda press. Both vesicle types were agglutinated by an antiserum specific for the light-harvesting complex, although proteolytic degradation of the complex occurred only in right-side-out vesicles. In addition, there are different antigenic sites for the light-harvesting complex on the inner and outer thylakoid surfaces. Polypeptides of the chlorophyll-alpha-protein complex of photosystem II were degraded by proteases at both membrane surfaces. We concluded that both these chlorophyll-protein complexes are membrane spanning and transversely asymmetric, but that the light-harvesting complex polypeptides accessible at the inner thylakoid surface are more resistant to proteolytic attack. In contrast, the main chlorophyll-containing polypeptide (Mr = 64 500) of photosystem I complex was resistant to proteolytic attack at both the outer and inner thylakoid surfaces.

Chlorophyll↗
PubMed1982

Possible mechanisms of immunotherapy action in acute nonlymphocytic leukemia: macrophage production of colony-stimulating activity.

Earlier studies show that immunotherapy (IT) improves prognosis in acute nonlymphatic leukemia (ANLL), and that ANLL cells probably have tumor-associated antigens, for autologous lymphocytes can react to them. Also, IT seems to immunize against allogeneic ANLL cells, but there is no cross-immunity to autologous ones. Moreover, patients immunized against their ANLL cells have no better prognosis than patients not having lymphocytes reacting to their ANLL cells. It has also been suggested that IT causes nonspecific immunostimulation, but IT patient's lymphocytes actually react less than those of patients not given IT. The current hypothesis is macrophage activation: Lymphocyte suppression in IT could be explained by suppressor macrophages. Colony-stimulating activity, produced by bone marrow macrophages, decreases during remission in patients not given IT, but not in IT patients. Numerically, blood cells from patients given IT form more colonies than those from patients not given IT. Three of eight patients given IT had more colonies than the upper normal limit.

Acute Disease↗
PubMed1982

Prednimustine and vincristine compared with cytosine arabinoside and thioguanine for treatment of elderly patients with acute nonlymphoblastic leukemia.

Sixty-seven patients with acute nonlymphoblastic leukemia (ANLL) and above the age of 60 years were randomly allocated to treatment with either prednimustine + vincristine or cycles with cytosine arabinoside and thioguanine. Of the 67 patients, 13 (19%) entered a complete remission and four a partial remission. Of 33 patients randomized to prednimustine and vincristine (15 adequately treated), three entered a complete remission and one a partial remission. Four further patients went into complete remission after a switch to other treatment modalities. Of 34 patients randomized to cycles of ARA-C and thioguanine (22 adequately treated), four entered a complete remission and three a partial remission with the correct program. One patient entered a remission with intermittent cytosine arabinoside + thioguanine (wrong program) and one further patient entered a complete remission after a switch to prednimustine and vincristine. Prednimustine + vincristine did not appear to be superior to treatment with cytosine arabinoside thioguanine cycles for elderly patients with ANLL.

Acute Disease↗
PubMed1982

Stress hormones and placental steroids in physical exercise during pregnancy.

The hormonal responses to exercise during later pregnancy were studied in relation to an exercise test in ten healthy women. At the end of the 10-min exercise, maternal heart rate had risen from 93 +/- 3.2 (mean +/- SEM) to 157 +/- 6.3 beats/min, and systolic blood pressure from 120 +/- 3.4 to 148 +/- 5.4 mmHg, but diastolic blood pressure was unchanged. Plasma concentrations of noradrenaline and adrenaline rose rapidly during the exercise, from 2.9 +/- 0.3 to 6.9 +/- 1.2 nmol/l and from 0.31 +/- 0.04 to 0.47 +/- 0.08 nmol/l respectively. The serum concentration of prolactin did not change during the test, but 30 min after the exercise the value had risen from 146 +/- 17 to 212 +/- 22 mg/ml, thereafter slowly declining. The serum concentration of cortisol remained unchanged. The mean concentration of oestriol rose from 31.5 +/- 2.6 to 33.9 +/- 3.0 nmol/l at least 5 min after the exercise, thereafter declining to 29 +/- 2.6 nmol/l. After the test, levels of progesterone and oestradiol also fell slightly. Mild irregular uterine activity was found in four subjects. Cardiotocography revealed a transient fetal tachycardia in two subjects.

Adult↗
PubMed1982

Plasma levels of somatostatin following a test meal in dogs. Initial atropine resistant vagally mediated decrease of somatostatin levels and increase of gastrin and insulin levels.

Plasma levels of somatostatin like immunoreactivity (SLI), below referred to as somatostatin levels, were measured in peripheral plasma of conscious dogs. Basal somatostatin levels averaged 49 +/- 10 pM. Somatostatin as well as gastrin and insulin plasma levels were measured before and after feeding with and without prior atropinization. During the first 10 min after feeding somatostatin levels fell from 49 +/- 10 to 23 +/- 9 pM, whereas gastrin and insulin levels rose from 9 +/- 2 and 140 +/- 14 pM to 48 +/- 11 and 370 +/- 91 pM respectively. Atropine 0.01 or 0.1 mg/kg did not inhibit these responses. After the initial decrease, somatostatin level rose again and peaked at around 60 min after feeding (110 +/- 24 pM). This secondary rise was completely abolished by atropine in both doses tried. Gastrin and insulin levels remained elevated throughout the experiments with and without atropine. It is suggested that gastrin release and HCl secretion are inhibited by a tonic outflow of gastric somatostatin during basal conditions. The process of feeding induces an atropine resistant, vagally mediated decrease in somatostatin release from the gastrointestinal tract and this decreased output of somatostatin facilitates initiation of meal-related endocrine and exocrine gastric secretions.

Animals↗
PubMed1982

Potentiation of antidiuretic response to systemic angiotensin II by elevation of CSF NaCl concentration.

The antidiuretic effect of the simultaneous intracerebroventricular (ICV) infusion of 0.24 M NaCl (0.02 ml/min) and intravenous (i.v.) infusion of angiotensin II (12 ng/kg X min) was studied in hydrated goats, and was compared to the antidiuretic effects of the separate infusions. The combined infusions inhibited the water diuresis for 30 min, whereas the separate infusions only reduced the water diuresis by 25% (ICV NaCl) and by 50% (i.v. angiotensin). The combined infusions increased the urine osmolality on the average by 415%. Corresponding increases induced by ICV NaCl and by i.v. angiotensin were 100 and 160%. The results suggest that systemic angiotensin II and elevated CSF NaCl concentration interact and potentiate each other as stimuli for antidiuretic hormone secretion. It is postulated that this synergism may help to preserve body water in hypovolemic conditions associated with hyperactivity of the renal renin-angiotensin system.

Angiotensin II↗
PubMed1982

Vasopressin release in response to intracerebroventricular L-alanine and L-arginine, and its dependence upon CSF NaCl concentration.

Influences on renal water, electrolyte, and arginine vasopressin (AVP) excretions of 1 h infusions (20 microliters/min) of a neutral (L-alanine) and two basic (L-lysine and L-arginine) amino acids into the lateral cerebral ventricle were studied in hydrated goats, and were compared to effects of control infusions of hypertonic (0.25 M) NaCl. L-alanine (0.11 M) dissolved in hypotonic NaCl caused more pronounced inhibition of the water diuresis and greater increase in AVP excretion than did the control infusions, but, in comparison to the latter, the responses developed very slowly. The effects were further delayed and were much attenuated when L-alanine was administered in isotonic glucose, but became considerably accentuated when isotonic NaCl was used as the solvent. L-lysine (0.09 M) in hypotonic NaCl did not inhibit the water diuresis or cause any apparent AVP release, whereas the corresponding L-arginine infusions caused inhibition of the water diuresis and increase in AVP excretion of approximately the same magnitudes and time courses as the control infusions. Like for L-alanine, these effects became accentuated when L-arginine was dissolved in isotonic NaCl, and became delayed and much attenuated when isotonic glucose was used as the solvent. L-arginine induced a more pronounced increase in renal Na excretion than did L-alanine and 0.25 M NaCl. Since transport together with Na (increasing the Na influx) generally is much more important for cellular uptake of neutral than of basic amino acids, the possibility is discussed that L-alanine here might have caused AVP release by increasing transmembrane Na transport of juxtacerebroventricular Na sensors regulating the AVP secretion--a suggestion supported by the lack of response to the basic L-lysine. The antidiuretic effect of the other basic amino acid, L-arginine, can not be explained along this line. However, with regard to the characteristic differences observed between the responses to L-alanine and L-arginine, the possibility is discussed that the latter might not have acted at a sensory level, but on the final neuronal link in the release of neurohypophyseal hormones, the hypothalamic neurosecretory cells. In contrast to L-alanine and L-arginine, L-lysine appeared to stimulate the appetite of the goats.

Alanine↗