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Biomedical subjects

K Andersson

Publications and source records attributed to K Andersson.

At least 217 records · Page 12Linked to original sources

Risk of developing atopic disease after early feeding with cows' milk based formula.

A follow up of a cohort of 736 healthy full term children with exposure to cows' milk based formula and breast milk from donors on the maternity ward was performed. The children were divided into three exposure groups according to the feeding patterns on the maternity ward. Group 1 received only mother's milk, group 2 mother's milk and human donors' milk, and group 3 received mother's milk, donors' milk and cows' milk based formula. The children were investigated at 7 years of age, by examining their medical files, and at 11 and 14 years, by questionnaires regarding symptoms of atopic disease. No significant differences between the three groups at follow up were found in the cumulative incidences of atopic diseases. The amount of formula given did not affect the risk of developing atopic disease. Children with a family history of such diseases ran the same risk of subsequent atopic disease whether they were fed formula or breast milk alone. Cows' milk based formula given on the maternity ward does not seem to increase the risk of developing atopic disease.

Animals↗

Diagnosis of psychogenic dysphonia.

Background factors, symptoms and signs were analysed in 40 consecutive patients with psychogenic dysphonia. Their voice profile was compared with that of 40 patients with infectious laryngitis. The majority of the patients were young females, non-smokers, who were not professional voice users. Criteria for acute infectious laryngitis prior the voice disorder were met in no more than 10% of the patients. Nevertheless as many as 40% of the patients had been treated with various antibiotics. The prevalence of reported asthma/allergy-like symptoms was high, 37.5%. Perceptual analysis of voice profiles demonstrated similarity of aberrancies in psychogenic dysphonia and in acute laryngitis. Since it may be difficult to distinguish psychogenic dysphonia from acute laryngitis, careful analysis of anamnestic data may be helpful for a correct diagnosis.

Acute Disease↗

Interaction of phospholipids with rhodamine 6G in toluene.

Upon interaction of various glycerophospholipids with Rhodamine 6G in toluene, a typical difference spectrum with an absorption maximum at approximately 515 nm is obtained . This spectrum is obtained with phosphatidylcholine only after treatment with NaCl, which presumably weakens intra- and/or inter-molecular electrostatic binding between the negatively charged phosphate moiety and the protonated nitrogen in this molecule. Absorption at 515 nm was linear for all of the phospholipids investigated from a concentration of approximately 1.2 microM up to at least 50 microM. The highest extinction coefficient was obtained for diphosphatidylglycerol (251 mM-1 cm-1) and all of the compounds tested, with the exception of phosphatidylethanolamine, demonstrated extinction coefficients higher than that of palmitic acid. Thus, the absorption spectrum which results from the interaction of purified glycerophospholipids with Rhodamine 6G in organic solvent is a sensitive measure of the amount of phospholipid present.

Coloring Agents↗

A randomized study of long-term out-patient treatment in alcoholics. Psychiatric treatment versus multimodal behavioural therapy, during 1 versus 2 years of treatment.

Seventy-two alcoholic patients (60 men and 12 women) were randomized into four groups who received psychiatric treatment (PT) or multimodal behavioural therapy (MBT), for either 1 or 2 years. PT was based on psychodynamic principles, and MBT is a cognitive-behavioural treatment. The patients accepting treatment had a mean age of 37 +/- 9 years, and they were socially stable. There was no difference in attrition rate (35%) in relation to therapy and length of treatment. The rate of favourable drinking outcome during the third year was similar in all four alternatives, at 40-44%. A favourable drinking outcome was predicted by a better initial psychic status and few psychiatric symptoms at intake. In PT patients a favourable outcome was more strongly related to a better psychic status than in MBT patients (P = 0.58). The mean number of sessions, 23, did not differ in relation to outcome. The main conclusion from this study is that there were only small and inconclusive differences between the therapies of different types and different duration.

Alcoholism↗

Intrauterine release of levonorgestrel--a new way of adding progestogen in hormone replacement therapy.

Forty perimenopausal women with climacteric complaints were randomly allocated to one of two estrogen-progestogen regimens. One group was treated cyclically for 3-week periods with 2 mg of estradiol (E2) valerate; during the last 10 days 250 micrograms of levonorgestrel was added. Another group was given 2 mg of E2 valerate a day and had a 20-micrograms/24-hour levonorgestrel-releasing intrauterine device (IUD) inserted. The study period was 1 year. Climacteric symptoms, bleeding patterns, and endometrial histopathology were recorded during the study. Subjective symptoms were equally diminished in both groups. In the IUD group, bleeding disturbances were gradually reduced, and 15 of 18 women became amenorrheic after 12 months, compared with the group given cyclic treatment in which all women bled regularly. No endometrial proliferation was found in any woman after 12 months. Thus, intrauterine release of 20 micrograms of levonorgestrel per day, in combination with orally administered E2, prevented endometrial proliferation and reduced uterine bleeding. This new approach to continuous combined hormone replacement therapy may be a well-tolerated treatment alternative in perimenopausal women.

Biopsy↗

Studies on the intracellular distributions of soluble epoxide hydrolase and of catalase by digitonin-permeabilization of hepatocytes isolated from control and clofibrate-treated mice.

Digitonin permeabilization of hepatocytes from control and clofibrate-treated (0.5% by mass, 10 days) male C57bl/6 mice was used to study the intracellular distributions of soluble ('cytosolic') epoxide hydrolase and of catalase. The following conclusions were drawn. (1) About 60% of the total soluble epoxide hydrolase activity in control mouse hepatocytes is situated in the cytosol. (2) The rest is not mitochondrial, but probably peroxisomal. (3) Of the total catalase activity in control mouse hepatocytes, 5-10% is found in the cytosol. (4) Treatment of mice with clofibrate increases the total hepatocyte activity of soluble epoxide hydrolase 4-fold, but does not influence the relative distribution of this enzyme between cytosol and peroxisomes. (5) The total catalase activity is increased 3.5-fold by clofibrate treatment and 15-35% of this activity is shifted from the peroxisomes to the cytosol.

Animals↗

Asphyctic lesion: proliferation of tyrosine hydroxylase-immunoreactive nerve cell bodies in the rat substantia nigra and functional changes in dopamine neurotransmission.

Asphyxia was induced in male rat pups by performing a delayed cesarean section on pregnant Sprague-Dawley rats. Oxygen saturation and heart rate were recorded during induction of asphyxia. Animals were sacrificed at 3 weeks of age. Brain sections were stained for tyrosine-hydroxylase (TH), dopamine-and-cyclic-AMP-regulated-phosphoprotein-32 (DARPP-32) immunoreactivity (IR) and thionein. Increasing time of asphyxia caused a reduction in the number of nerve cell bodies in the CA1 and CA3 regions of the hippocampus reflecting neuronal death. Furthermore, asphyxia resulted in an increased number of TH-IR nerve cell bodies indicative of a proliferation of dopaminergic neurons in the zona compacta of the substantia nigra. Finally, a significant decrease in rearing was observed in asphyctic animals during the habituation phase, as well as following apomorphine-induced (1 mg/kg s.c.) postsynaptic dopamine receptor stimulation. On the other hand, the apomorphine-induced increase in locomotion was enhanced in asphyctic animals. The implications of these findings for hyperkinesia and attention deficits in disorders resulting from asphyxia are discussed.

Animals↗

A comparison of flurbiprofen, tranexamic acid, and a levonorgestrel-releasing intrauterine contraceptive device in the treatment of idiopathic menorrhagia.

Treatment with flurbiprofen (100 mg twice a day for 5 days), tranexamic acid (1.5 gm three times a day for 3 days and 1 gm twice a day for another 2 days), and an intrauterine contraceptive device releasing 20 micrograms levonorgestrel per day was compared in women with idiopathic menorrhagia. The menstrual blood loss during two control periods in 15 women subsequently treated with flurbiprofen and tranexamic acid was 295 +/- 52 ml and 203 +/- 25.2 ml in the 16 women later fitted with a levonorgestrel-releasing intrauterine contraceptive device. Menstrual blood loss was reduced by all three forms of treatment. The reduction in menstrual blood loss expressed as a percentage of the mean of two control cycles for each form of treatment was as follows: flurbiprofen, 20.7% +/- 9.9%; tranexamic acid, 44.4% +/- 8.3%; levonorgestrel-releasing intrauterine contraceptive device after 3 months, 81.6% +/- 4.5%; levonorgestrel-releasing intrauterine contraceptive device after 6 months, 88.0% +/- 3.1%; levonorgestrel-releasing intrauterine contraceptive device after 12 months, 95.8% +/- 1.2%. The reduction in menstrual blood loss achieved by the levonorgestrel-releasing intrauterine contraceptive device was greater than that recorded with flurbiprofen (p less than 0.001) and tranexamic acid (p less than 0.01), and was greater for tranexamic acid when compared with flurbiprofen (p less than 0.05). The levonorgestrel-releasing intrauterine contraceptive device was the only form of treatment to reduce mean menstrual blood loss below 80 ml per menstruation, the upper limit of normal menstrual blood loss.

Adult↗

[Cerebrospinal fluid cytology--a valuable diagnostic method in various neurologic problems].

Cytological examination of cerebrospinal fluid can provide vital diagnostic information, particularly in inflammatory and neoplastic disorders of the nervous system. Not only can the cause of a pleocytosis be established but cytological abnormalities can also be detected in cases where the cell count is normal. Monoclonal antibodies can be used for the characterisation of leukaemic cells.

Antibodies, Monoclonal↗

Regulation of endocrine function by the nicotinic cholinergic receptor.

One important neuroendocrine action of nicotine in the male rat is an increase in the secretion of corticosterone which is seen upon acute and acute intermittent exposure to nicotine. Tolerance develops to this action of nicotine upon chronic exposure, and in the withdrawal phase serum corticosterone levels are substantially reduced. In contrast, no significant increases of serum corticosterone levels were observed upon acute intermittent treatment with nicotine in the dioestrous rat. Available evidence indicates that corticosterone can modulate dopamine transmission in the basal ganglia via glucocorticoid receptors within the nucleus accumbens and neostriatum, and via glucocorticoid receptor immunoreactivity in nigrostriatal and mesolimbic dopamine pathways. Through concerted pre- and postsynaptic actions glucocorticoids may decrease dopamine transmission, especially that mediated by D2 receptors in these regions. In view of the hypothesis that the mesolimbic dopamine pathways mediate the euphoric effects of nicotine, the secretion of corticosterone induced by nicotine in the smoking male may substantially influence the mood elevating activity of nicotine. Thus, individual smoking habits may depend on the ability of nicotine to induce corticosterone secretion, which obviously would also vary with the degree of stress. The glucocorticoids may in a similar way influence the arousal action of nicotine because of the high number of glucocorticoid receptors present both in noradrenaline cell bodies of the locus ceruleus and within the entire cerebral cortex.

Animals↗

Chronic nicotine treatment increases dopamine levels and reduces dopamine utilization in substantia nigra and in surviving forebrain dopamine nerve terminal systems after a partial di-mesencephalic hemitransection.

In order to further study the previously demonstrated protective action of chronic nicotine treatment on lesioned meso-striatal dopamine (DA) pathways, the following study was carried out on DA utilization in these lesioned neurons. Male Sprague-Dawley rats were partially hemitransected at the meso-diencephalic junction and treated with nicotine (0.125 mg.kg-1.h-1) by means of Alzet minipumps implanted subcutaneously for 2 weeks. The overall serum nicotine level obtained was 64.6 +/- 2.7 ng.ml-1. The results demonstrated that partial di-mesencephalic hemitransections produced a marked reduction of DA fluorescence (quantitative histofluorimetry) on the lesioned side in the nucleus caudatus putamen, anterior nucleus accumbens and posterior lateral tuberculum olfactorium. No significant effects were observed on the intact side. Furthermore, studies on changes in DA utilization as evaluated 2 h after tyrosine hydroxylase inhibition showed an augmentation in the alpha-methyl-(+/-)-p-tyrosine methyl ester (alpha-MT)-induced depletion of the DA stores on the hemitransected side in comparison with the operated side of the sham-operated animals. On the hemitransected side chronic nicotine treatment increased DA stores in the DA nerve terminals of the nucleus caudatus putamen and the posterior lateral tuberculum olfactorium. No significant effects were observed on the intact side. Following chronic nicotine treatment a marked and preferential attenuation of the alpha-MT-induced depletion of DA stores was seen in the various DA nerve terminal systems of the forebrain on the hemitransected side. In the substantia nigra reduced DA levels (HPLC) were demonstrated on the hemitransected side, while no effects on the non-operated side were observed. Also an increase of the alpha-MT-induced depletion of the DA stores was seen on the hemitransected side in comparison with the operated side of the sham-operated animals. In contrast, on the non-operated side an attenuation of the alpha-MT-induced depletion of the DA stores was found. Following chronic nicotine treatment the lesion induced reduction of the nigral DA stores on the hemitransected side was counteracted, as was the lesion induced increase in the alpha-MT-induced depletion of DA stores, which was replaced by a reduction of the alpha-MT-induced depletion of the nigral DA stores. However, on the non-operated side an increased DA depletion was observed after alpha-MT treatment in rats treated chronically with nicotine. Chronic nicotine treatment under the present conditions did not significantly alter serum levels of corticosterone and reduced prolactin serum levels in sham-operated rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Effect of clomipramine on premenstrual syndrome.

Clomipramine (25-50 mg) was administered daily for 5 consecutive menstrual cycles to 5 nondepressed women with severe premenstrual irritability and sadness. All subjects reported a dramatic reduction in premenstrual complaints.

Adult↗

Effect of 20 weeks' ranitidine treatment on plasma gastrin levels and gastric enterochromaffin-like cell density in the rat.

In this study, the effect of ranitidine treatment on the activation and proliferation of rat gastric enterochromaffin-like (ECL) cells was investigated. The drug was given in a high dose in the food (1.7-1.8 g/kg/day) for 20 weeks. This dose corresponds to the high dose given in the ranitidine oncogenicity study performed by Glaxo. With this dose regimen ranitidine induced hypergastrinaemia for 10 h of the day. The duration and the extent of the hypergastrinaemia closely followed the occurrence of ranitidine in plasma, strongly suggesting that the hypergastrinaemia was secondary to inhibition of acid secretion. Following 20 weeks treatment with ranitidine, both the relative weight of the stomach and that of the oxyntic mucosa were increased. The oxyntic histamine concentration and ECL-cell density were also increased significantly. These results show that when ranitidine is given in the diet the resulting hypergastrinaemia, which had a duration of 10 h each day, leads to a general increase in the oxyntic mucosal weight and a proliferation and activation of the ECL cells, indicating that sustained hypergastrinaemia is not a necessary requirement for development of ECL-cell hyperplasia.

Animals↗

The role of gastric mucosal histamine in acid secretion and experimentally induced lesions in the rat.

The role played by histamine from enterochromaffin-like (ECL) cells and mast cells in gastric acid secretion and in the development of ethanol-induced gastric lesions was studied in the rat. This was done by examining the effects of inhibition of the histamine-producing enzyme histidine decarboxylase (HDC) with alpha-fluoromethylhistidine (alpha-FMH) and the effects of degranulation of the mucosal mast cells with dexamethasone. A single dose of alpha-FMH (50 mg/kg p.o.) inhibited the HDC activity by 94% but did not affect histamine levels in the gastric mucosa 2 h after dose. Repeated treatment resulted in an almost complete inhibition of HDC activity and in a reduction of histamine levels by 75%. Pentagastrin failed to stimulate acid secretion after 4 days treatment with alpha-FMH, whereas the acid response to histamine was unaffected in chronic gastric fistula rats. Ethanol failed to induce gastric lesions in rats pretreated for 4 days with dexamethasone whereas 4 days pretreatment with alpha-FMH did not influence ethanol-induced lesion formation. The present results show that histamine synthesis is required for pentagastrin-stimulated gastric acid secretion and that mucosal mast-cell histamine plays a role in the development of ethanol-induced gastric lesions.

Animals↗

Tritiated thymidine incorporation into DNA in rat gastric mucosal cells.

The parietal cell acid pump inhibitor, omeprazole, has undergone numerous genotoxicity studies, the conclusions of which have all been negative. A recent report by Burlinson described a method which is claimed to measure unscheduled DNA synthesis (UDS) in gastric mucosa, based on the incorporation of tritiated thymidine (3H-TdR) into DNA. In a subsequent letter it was concluded that omeprazole induces a significant increase in UDS, and it was suggested that 'for omeprazole, a genotoxic action cannot be discounted'. The Burlinson method of measuring UDS relies upon selective separation of non-dividing oxyntic mucosal surface cells from the stem cells located in the proliferative zone. These stem cells undergo normal cell division, subsequently migrate to the top and bottom of the gland, differentiating into the various specialized cells of the gland such as surface, parietal and chief cells. In the oxyntic mucosa the majority of stem cells are located at a level corresponding to one fifth of the mucosal thickness from the surface. The purpose of this study was to evaluate the Burlinson method, which depends upon the selective isolation of non-dividing surface cells by pronase digestion. The fraction used for measurement was investigated in terms of 3H-TdR uptake, the cellular distribution of 3H-TdR by autoradiography, the number of parietal cells and the sensitivity of 3H-TdR uptake for hydroxyurea (an inhibitor of normal, scheduled DNA synthesis). The results show that pronase digestion did not selectively isolate surface epithelial cells and that the digest contained both parietal cells (15 +/- 1.5%) and glandular fragments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Evidence for the existence of a population of arcuate neurons costoring choline acetyltransferase and tyrosine hydroxylase immunoreactivities in the male rat.

By combined immunoperoxidase and immunofluorescence histochemistry we have analyzed the distribution of choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) immunoreactive (IR) perikarya within the same sections of the mediobasal hypothalamus of the male rat. Evidence was obtained for the existence of perikarya costoring TH and ChAT immunoreactivities in both the dorsomedial and ventrolateral part of the arcuate nucleus and in the adjacent periarcuate nucleus at all rostrocaudal levels. The results strongly implicate interactions between dopamine and acetylcholine as well as acetylcholine and growth hormone releasing factor in dorsomedially and ventrolaterally located TH/ChAT costoring tuberoinfundibular neurons, respectively.

Animals↗

Effects of withdrawal from chronic exposure to cigarette smoke on hypothalamic and preoptic catecholamine nerve terminal systems and on the secretion of pituitary hormones in the male rat.

A 48 h but not a 72 h or 7 day withdrawal from chronic exposure to cigarette smoke was associated with increased noradrenaline levels (quantitative histofluorimetry) in the subependymal layer (SEL) of the median eminence, the anterior periventricular hypothalamic region (PV I) and the parvocellular part of the hypothalamic nucleus (PA FP) and an increased noradrenaline utilization (tyrosine hydroxylase inhibition by alpha MT) in the SEL and the PV I. Following a 48 h or 72 h but not a 7 day withdrawal from chronic exposure to cigarette smoke an increased catecholamine utilization was found in the medial palisade zone (MPZ) of the median eminence. Reduced serum prolactin, FSH and corticosterone levels were found following a 48 h withdrawal from chronic exposure to cigarette smoke. Following a 72 h withdrawal from chronic exposure to cigarette smoke a reduced concentration of serum prolactin was noted. Chronic exposure to cigarette smoke reduced serum TSH levels and lead to a tolerance development with regard to noradrenaline levels and utilization within the preoptic region with the exception of the periventricular preoptic region. The finding of special interest in the present study is the demonstration of a highly significant lowering of corticosterone serum levels despite maintained blood levels of ACTH as seen 48 h following withdrawal. It is suggested that this type of endocrine change may lead to changes in fear-motivated behaviour and contribute to behavioural withdrawal reactions. The maintained reductions of serum prolactin levels found after 48 h and 72 h of withdrawal from cigarette smoke exposure (cf. Andersson et al. 1985a) is discussed in terms of an increased catecholamine utilization in the medial palisade zone of the median eminance. This activation is suggested to be caused by the development of a prolactin receptor supersensitivity within the medium eminence. The present evidence indicates withdrawal effects mainly in the noradrenaline nerve terminals of the subependymal layer of the median eminence, the anterior periventricular hypothalamic region and the parvocellular part of the paraventricular hypothalamic nucleus which inter alia are involved in regulation of ACTH secretion (cf. Andersson et al. 1985a).

Animals↗