Sexually differentiated actions of 3-PPP enantiomers on prolactin secretion

The ability of the enantiomers of the atypical dopamine receptor agonist 3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP) to counteract gamma-butyrolactone-induced hyperprolactinemia was compared in male and female rats. Following gamma-butyrolactone (GBL) pretreatment serum prolactin concentrations were higher in female than in male rats. In males (-)-3-PPP tended to be somewhat less effective than (+)-3-PPP in decreasing serum prolactin concentrations (levels after (+)-3-PPP and (-)-3-PPP: 21% and 33%, respectively, of levels in GBL-pretreated control(s). In females the (-)-form induced a much weaker response than did the (+)-form (levels after (+)-3-PPP and (-)-3-PPP: 8% and 74%, respectively, of levels in GBL pretreated controls). Parallel experiments replacing GBL by reserpine yielded similar results. Data are discussed in terms of sex differences in responsiveness of pituitary dopamine receptors.     

Osteocalcin 24-hour profiles during normal pregnancy.

The interpretation of previous data on osteocalcin during pregnancy has been complicated by the fact that serum levels, at least in nonpregnant women, display a significant circadian variation. In the present study, serum concentrations of osteocalcin were recorded for 24 h in 12 individual women. In 4 nonpregnant women, there were striking diurnal fluctuations during the sampling period, with values ranging from 0.5 to 4.0 ng/ml. One woman who was investigated in the 11th week of pregnancy showed similar fluctuations in osteocalcin concentrations whereas in the 15th and 17th week values were much lower with minor fluctuations. In 4 women investigated during late pregnancy (weeks 34-38), osteocalcin serum levels were extremely low (range 0.2-0.4 ng/ml), often below the detection limit of the assay, and there was no diurnal variation. Also, in 1 lactating woman, osteocalcin serum levels were low (0.3-0.8 ng/ml) and stable. Low osteocalcin values during pregnancy may indicate a reduced bone turnover possibly mediated via an altered estrogen and growth hormone secretion.     

Adhesion of human platelets to albumin is synergistically increased by lysophosphatidic acid and adrenaline in a donor-dependent fashion.

Lysophosphatidic acid (LPA) and adrenaline are weak platelet activators considered important for thrombus formation, and were previously shown to synergistically increase platelet aggregation. Here we investigate synergistic activation by LPA and adrenaline when measuring platelet adhesion. Platelet-rich plasma from healthy blood donors together with adrenaline and/or LPA were added to protein-coated microplates. Platelets were allowed to adhere and the amount of adhesion detected enzymatically. The LPA and adrenaline combination induced a synergistic increase of platelet adhesion to a normally non-adhesive albumin surface. The degree of synergy varied markedly between individuals; these variations could not be explained by age, gender, blood type or different amounts of platelets, oxidized low-density lipoprotein, insulin or glucose in plasma. There was a trend indicating increased synergistic effect for platelets sensitive to adrenaline stimulation. The synergistic effect was blocked by the alpha2-adrenoceptor antagonist yohimbine and inhibited by the ADP scavenger system creatine phosphate/creatine phosphokinase and antibodies against alphaIIbbeta3. Furthermore, platelets adhering to albumin after adrenaline and LPA treatment expressed P-selectin. In conclusion, LPA and adrenaline act synergistically to increase alphaIIbbeta3-mediated platelet adhesion to albumin, dependent on alpha2-adrenoceptor signalling and platelet secretion. We also confirm that synergistic platelet activation achieved with LPA and adrenaline is highly donor dependent.     

Prevalence of sleep apnea syndrome among Swedish men--an epidemiological study

The prevalence of the sleep apnea syndrome (SAS) among Swedish men 30-69 years old was estimated by a two-stage procedure. In the first stage, 4064 questionnaires were mailed to a random sample of a defined population in the municipality of Uppsala. The response rate was almost 80%; 15.6% of the responders were habitual snorers and 5.8% complained of daytime sleepiness. From these, a group of 166 men highly suspected of having SAS was selected. Eventually, 61 of these came for all-night polysomnographic studies, and 15 of these were found to have SAS. On this basis the lower limit of the prevalence of SAS was estimated to be as high as 1.3%. The majority of subjects with the syndrome were in the age group 50-59 years.     

Observations on two members of the Swedish family with congenital dyserythropoietic anaemia,type III

Abstract: Two affected individuals of the Swedish family with CDA, type III, in which the disease is transmitted as an autosomal dominant character, were studied. Both cases displayed features hitherto undescribed in this family but described in patients with CDA, type III, in whom the inheritance may have been as an autosomal recessive character. Such features were: (a) haemosiderinuria, (b) grossly disorganised erythroblast nuclei, (c) differences in the ultrastructural appearances of individual nuclei within the same multinucleate erythroblast and (d) intraerythroblastic inclusions resembling precipitated globin chains. In both cases the giant mononucleate erythroblasts and the multinucleate erythroblasts had total DNA contents up to 28c (1c = haploid DNA content) and 48c respectively, and some DNA synthesising bi- and multinucleate erythroblasts contained one or more nuclei which were unlabelled with ³H-thymidine. These findings are similar to those in patients with the autosomal recessive type of disease. Thus no major phenotypic differences are yet apparent between cases of CDA, type III, with different patterns of inheritance. Analysis of the surface erythrocyte proteins of the 2 Swedish CDA, type III, patients with monoclonal antibodies recognising Band 3, glycophorins A, B, C and D, Rh, CD44, CD47, CD55, CD58, CD59, Lutheran, Kell, LW and acetylcholinesterase did not reveal any gross abnormality of expression of these proteins. A slightly altered expression of blood group antigens A and H was revealed by the lectins Dolichos biflorus and Ulex europaeus and the Mr of Band 3 as judged by SDS polyacrylamide gel electrophoresis was also slightly reduced, suggesting that there may be minor alterations in the degree of N-glycosylation of some red cell membrane constituents.     

Magnetic resonance evaluation after temporomandibular joint diskectomy.

The aim of this study was to investigate the value of magnetic resonance imaging after diskectomy of the temporomandibular joint. Magnetic resonance images were obtained before and 12 months after unilateral diskectomy without disk replacement. Magnetic resonance findings at follow-up were correlated to residual pain. At the follow-up, 20 of 28 patients were free of pain in the joint that had been surgically treated, four patients had mild pain, and four patients had significant residual pain. The magnetic resonance images at follow-up showed that the joint space was filled with soft tissue after diskectomy. In patients without pain at follow-up, this soft tissue had a magnetic resonance signal that was equal or higher than that of the muscles. In the four patients with significant residual pain and in one patient with mild residual pain, the soft tissue in the joint space between the condyle and glenoid fossa had a magnetic resonance signal intensity that was lower than the muscle. On the basis of findings in a previous study, the areas of low signal intensity were interpreted as fibrous adhesions. The study suggests that areas of low signal intensity in the joint space appear to be associated with residual pain and that magnetic resonance imaging could be a valuable tool for assessment of the temporomandibular joint after diskectomy.     

Hydroxyurea-induced cell death in human T lymphoma cells as related to imbalance in DNA/protein cycle and deoxyribonucleotide pools and DNA strand breaks.

The aim of this study was to elucidate the mechanism(s) behind the cellular toxicity of therapeutic concentrations of hydroxyurea (HU). Treatment of human T lymphoma cells (CCRF-CEM) with 60-100 microM of HU for 24 h decreased the growth rate by 90% due to accumulation of cells in early S phase. It induced a marked imbalance in both the DNA/protein cycle (as measured by two-parameter flow cytometry) and the deoxyribonucleotide (dNTP) pools. HU treatment did not enhance the frequency of DNA single-strand breaks (SSBs), as measured by the alkaline unwinding technique. Cell viability was unaffected. However, removal of HU led to 10-15% cell loss during the following 12 h period in parallel with increasing SSBs, and a rapid progression of cells through S and G2 stages. The unbalanced DNA to protein content per cell and the dNTP pools were normalized 6-12 and 24 h after removal of HU, respectively. These results show that marked changes in the DNA to protein ratio and dNTP pools alone are not directly lethal, but when combined with a high replicative DNA synthesis rate, as found after removal of HU, apparently lead to elevated cell death.