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Biomedical subjects

K Andersson

Publications and source records attributed to K Andersson.

At least 235 records · Page 13Linked to original sources
PubMed1989

Fractionation of immunoglobulins by liquid-liquid partition chromatography in aqueous two-phase systems.

In this paper we show that although immunoglobulins are easily precipitated in solutions containing polyethylene glycol (PEG), especially at pH's where the conformation of the proteins should be close to native, human and rabbit IgG can be solubilized in aqueous dextran/PEG two-phase systems containing glycine and sodium chloride at pH 7.0 and that human IgA and IgM can be solubilized in such systems if the pH is increased to 9.0. Liquid-liquid partition chromatography (LLPC) on Li-ParGel was used to separate immunoglobulins into subfractions. Human IgG, IgM, and IgA all gave three peaks in the system used. These results indicate the possibility of separating different classes of immunoglobulins with this method. Specific IgG antibodies isolated from a rabbit antiserum against human serum proteins gave only two peaks in the LLPC system while the total IgG population gave three, as did human IgG. Thus, partitioning of immunoglobulins seems to be related to antibody activity.

Animals↗
PubMed1989

Neuroendocrine actions of nicotine and of exposure to cigarette smoke: medical implications.

Over many years a large number of studies have demonstrated that nicotine and exposure to cigarette smoke produce marked neuroendocrine changes in animals and in man. The initial effects of nicotine are characterized by a marked hypersecretion of ACTH, vasopressin, beta-endorphin, prolactin and LH. Many of these very acute stimulatory effects of nicotine rapidly disappear, probably due to a desensitization of the central nicotinic cholinergic receptors involved. Instead, upon acute intermittent treatment with nicotine or exposure to cigarette smoke, an inhibition of prolactin, LH and TSH secretion occurs, which is associated with maintained hypersecretion of corticosterone. These effects are probably mediated via activation of central cholinergic receptors of the ganglionic type. Evidence indicates that the inhibitory effects of nicotine on LH and prolactin secretion are produced via an activation by these nicotinic receptors of the tubero-infundibular dopamine neurons, releasing dopamine as a prolactin inhibitory factor. Dopamine inhibits LHRH release via an axonic interaction involving D1-like dopamine receptors in the median eminence. It therefore seems possible that the reduced fertility found in heavy smokers may be counteracted by D1 receptor antagonists. The symptoms associated with glucocorticoid hypersecretion induced by nicotine is discussed considering not only the peripheral side effects but also permanent deficits in hippocampal glucocorticoid receptors and loss of hippocampal neurons. In view of the important influence of hormones on immune functions, it seems likely that smoking will cause disturbances in immune responsiveness. Finally, the nicotine-induced alterations of neuroendocrine function, especially in the pituitary-adrenal axis and in vasopressin release, may also lead to behavioural consequences in smokers, especially in the withdrawal phase.

Animals↗
PubMed1989

Protective effects of chronic nicotine treatment on lesioned nigrostriatal dopamine neurons in the male rat.

The present results demonstrate that chronic nicotine treatment can in part protect against mechanically-induced and neurotoxin-induced degeneration of nigrostriatal DA neurons. These results indicate that in sufficient doses chronic treatment with nicotine may be considered in the pharmacological treatment of Parkinson's disease. It remains to be demonstrated whether these protective actions can be extended to include also other injured neurons such as the cholinergic neurons, known to be severely affected in Alzheimer's disease.

Animals↗
PubMed1989

Monitoring of parts-per-billion levels of formaldehyde using a diffusive sampler.

A diffusive sampler for formaldehyde originally designed for use in personal monitoring of worker exposure has been evaluated for static measurement of low formaldehyde levels in indoor air. The sampler consists of a 37-mm glass fiber filter impregnated with 2,4-dinitrophenylhydrazine and phosphoric acid and mounted in a polystyrene filter cassette. Formaldehyde is sampled by controlled diffusion and subsequent hydrazone formation on the filter. The hydrazone is eluted from the filter with acetonitrile and analyzed by liquid chromatography and a UV detector. The diffusive sampler was evaluated for static (area) sampling in several industries, offices, and homes with formaldehyde levels of 6-200 ppb. Results from diffusive samplers were compared with results from pumped samplers. Even at low wind velocities (less than 0.01 m.s-1) there was good agreement between pumped and diffusive samples. The sensitivity will be 1 ppb in a 24-h sample, making the sampler especially useful for indoor air monitoring of low formaldehyde levels.

Air Pollutants, Occupational↗
PubMed1989

Effect of physical exercise on the pharmacokinetics of digoxin during maintenance treatment.

Blood samples were taken repeatedly and urine was collected for digoxin assays on two occasions from 12 healthy male volunteers after an oral maintenance dose of digoxin. On one occasion the subjects exercised intermittently on a bicycle ergometer for 8 h after the dose. On the other occasion they rested in the supine position during the study period. Thirty and 45 min after the intake of digoxin, the serum digoxin concentration was significantly higher during exercise compared with rest, indicating increased absorption rate during exercise. Two and 4 h after the intake of digoxin, the serum digoxin concentration was significantly lower during exercise than during rest. Furthermore, the intermittent bicycle exercise decreased the renal excretion of digoxin during the study period. It also increased the steady state digoxin concentration measured after a terminating standardized period of rest. The most probable reason for these changes in the pharmacokinetics is a previously described increased binding of digoxin to exercising muscles. According to the results, there is reason to believe that the daily physical activity performed by digoxin-treated patients will determine to some extent the body content of digoxin. Changes in activity from day to day may therefore cause variations in the effect of the drug.

Adult↗
PubMed1989

Involvement of D1 dopamine receptors in the control of TSH secretion in the male rat.

The effects of SCH 23390 (D1 dopamine receptor antagonist), SK&F 38393 (D1 dopamine receptor agonist), raclopride and remoxipride (D2 dopamine receptor antagonists) and ketanserin (5-hydroxytryptamine 2 receptor antagonist) on TSH serum levels (radioimmunoassay) and on brain catecholamine levels (Falck-Hillarp methodology in combination with quantitative histofluorimetry) were studied. SCH 23390 produced a dose-dependent increase in serum TSH levels in the lower dose range (0.01-0.03 mg kg-1, i.p.) administered 30 min before decapitation and in the higher dose range (1.0-3.0 mg kg-1) when given 2 h before decapitation. Following 30 min of treatment with the high doses of SCH 23390, reductions in serum TSH levels were found. The changes observed following SCH 23390 treatment occurred without affecting catecholamine levels in the median eminence and the peri- and paraventricular hypothalamic regions. Raclopride (0.1-10 mg kg-1, i.p.), remoxipride (1.0 mg kg-1, i.p.) or ketanserin (0.3 mg kg-1, i.p.) changed neither serum TSH levels nor brain catecholamine levels, SK&F 38393 (1.0-10 mg kg-1, i.p.) produced an increase in serum TSH levels. The results suggest the existence of inhibitory and facilitatory mechanisms regulating TSH secretion mediated via D1 dopamine receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

WHO Collaborative Study on Alcohol Education and Young People: outcomes of a four-country pilot study.

In 1985 the Division of Mental Health, World Health Organization, Geneva, convened a group of investigators from centers in four countries--Australia, Chile, Norway, Swaziland--to participate in a pilot study on the efficacy of school-based alcohol education. The goal of the educational program was to delay onset and minimize involvement of alcohol use among 13- to 14-year-old adolescents. Twenty-five schools in the four countries, representing middle- and lower-class populations, were randomly assigned to peer-led education, teacher-led education, or a control condition. The educational program was derived from social-psychological theory and etiological research on adolescent alcohol use. The program focused on the social and environmental influences to drink alcohol and skills to resist those influences. It consisted of five lessons over 2 months. Baseline and posttest data measured alcohol use knowledge, attitudes, skills, and friends' drinking patterns. Data were collected immediately prior to and 2 months following the educational program. The data converge on the finding that peer-led education appears to be efficacious in reducing alcohol use across a variety of settings and cultures.

Adolescent↗
PubMed1989

Nucleotide sequence of the rat Bmyc gene.

We have cloned and sequenced the rat Bmyc gene. The rat Bmyc gene contains sequences related to the central part of c-myc, namely the first intron, the second exon, and the noncoding part of the third exon. The homology drops in the 3' part of the c-myc second exon, but continues in the noncoding part of the third exon. We have sequenced the total predicted coding region of the Bmyc. The longest open reading frame in Bmyc suggests a protein of 178 amino acids, which is only 41% of the c-myc protein size. To confirm the putative open reading frame, we have produced a trpE-Bmyc protein that is detected with a pan-myc antibody. We discuss these findings in the context of potential functional domains and the possibility of overlapping and distinct activities of myc-family proteins.

Amino Acid Sequence↗
PubMed1988

Chronic nicotine treatment counteracts the disappearance of tyrosine-hydroxylase-immunoreactive nerve cell bodies, dendrites and terminals in the mesostriatal dopamine system of the male rat after partial hemitransection.

Male Sprague-Dawley rats were partially hemitransected at the mesodiencephalic junction and treated with nicotine (nicotine hydrogen (+)-tartrate) using Alzet minipumps implanted subcutaneously. Nicotine was delivered for 2 weeks in a dose of 0.125 mg/kg/h resulting in a serum nicotine level of 50.0 +/- 5.1 ng/ml. Three other groups of rats were analyzed: hemitransected rats receiving saline treatment and sham-operated animals receiving nicotine and saline, respectively. The effects of hemitransection and nicotine rostrally as well as caudally to the lesion were evaluated with image analysis of tyrosine hydroxylase (TH)-immunoreactive (IR) nerve cell body and dendrite profiles in the rostral and caudal substantia nigra and of TH-IR nerve terminal profiles in the striatum. Adjacent sections were taken to Nissl staining. [3H]Nicotine binding in the midbrain and forebrain was studied by means of receptor autoradiography on partially hemitransected rats receiving no treatment. Catecholamine (CA) levels in the frontal cortex were measured using high-performance liquid chromatography (HPLC). Striatal dopamine (DA) function was analyzed studying apomorphine-induced (1.0 mg/kg) ipsilateral rotational behavior. The spontaneous behavior of the rats was evaluated with a hole board. Furthermore, body temperature and body weight were measured. The results demonstrated a lesion-induced disappearance of TH-IR cell body and dendrite profiles in the substantia nigra and of TH-IR nerve terminal profiles in the striatum. Similar findings were seen after Nissl staining. A significant counteraction of this disappearance was found in the nicotine-treated animals. On the lesioned animals a marked reduction of [3H]nicotine binding in the striatum and the substantia nigra was found. In the functional experiments an enhancement of the apomorphine-induced ipsilateral rotational behavior was demonstrated. The degree of rotation was positively correlated with the serum nicotine level. The study on spontaneous activity in the hole board showed a slower restoration of total activity in the hemitransected nicotine-treated rats. All these results are compatible with the hypothesis that the protective action of nicotine on the mesostriatal DA system may be due to a desensitization of excitatory nicotine cholinoceptors located on the nigral DA nerve cells, leading to a reduction of firing rate and reduced energy demands. Such an action of nicotine could be of importance for a possible anti-parkinsonian effect.

Animals↗
PubMed1988

Characterization of the binding epitope of a monoclonal antibody to sulphatide.

An IgG1 monoclonal antibody, Sulph I, reacting with sulphatide (3'-sulphogalactosylceramide), was produced by immunizing Balb/c mice with that glycolipid coated on Salmonella minnesota bacterial membrane. Radioimmunodetection of the binding of the monoclonal antibody to structurally related glycolipids adsorbed to microtitre plates or chromatographed on thin-layer plates was used to determine its binding epitope. The antibody showed similar binding avidity to three sulphated glycolipids: sulphatide, sulpholactosylceramide and seminolipid. Lysosulphatide did bind the antibody, but, compared with sulphatide, 30 times more antigen was needed for half-maximal binding. Bis(sulphogangliotriosyl)ceramide and bis-sulphogangliotetraosylceramide did not bind the antibody. These results suggest that terminal galactose-3-O-sulphate and part of the hydrophobic region of the glycolipid are recognized by the Sulph I antibody.

Antibodies, Monoclonal↗
PubMed1988

Effects of acute intermittent exposure to cigarette smoke on hypothalamic and preoptic catecholamine nerve terminal systems and on neuroendocrine function in the diestrous rat.

Diestrous female rats were exposed to the smoke from one to four cigarettes. Exposure to unfiltered cigarette smoke produced dose- and time-dependent reductions of catecholamine levels and dose- and time-dependent increase in catecholamine utilization in the various hypothalamic and preoptic dopamine and noradrenaline nerve terminal systems. These effects were counteracted by pretreatment with the ganglion blocking agent mecamylamine (1 mg/kg). Exposure to cigarette smoke was also found to produce a dose- and time-dependent inhibition of serum prolactin, LH and FSH levels which was counteracted by pretreatment with mecamylamine. Exposure to the smoke from one cigarette (but not from four cigarettes) increased serum TSH levels. In combination with tyrosine hydroxylase inhibition the exposure to cigarette smoke produced a dose- and time-dependent inhibition of plasma ACTH levels, an action which was counteracted by pretreatment with mecamylamine. The results demonstrated a sex difference (cf. Anderson et al. 1985c), in the nicotine-induced changes of TSH and ACTH secretion despite a general increase in hypothalamic and preoptic dopamine and noradrenaline utilization in both the male and the diestrous female rat. The differences in the neuroendocrine actions of acute intermittent exposure to cigarette smoke in the diestrous rat and the normal male rat are discussed.

Animals↗
PubMed1988

Distribution of nicotinic cholinergic receptors in the rat tel- and diencephalon: a quantitative receptor autoradiographical study using [3H]-acetylcholine, [alpha-125I]bungarotoxin and [3H]nicotine.

The topographical distribution of [alpha-125I]bungarotoxin [125I]BTX, [3H]nicotine ([3H]Nic), [3H]acetylcholine ([3H]ACh) (in the presence of atropine) binding in rat tel- and diencephalon was investigated using a quantitative receptor autoradiographical technique. With the [3H]ACh and [3H]Nic radioligands, a strong labelling was observed in various thalamic nuclei, including the medial habenula, a moderate labelling in different areas of the cortex cerebri, the nucleus caudatus putamen, the nucleus accumbens and tuberculum olfactorium and a uniform weak labelling in the hypothalamus. When the binding data for [3H]Nic were plotted against binding data for [3H]ACh in various brain nuclei, a significant correlation was obtained. Considering [125I]BTX, the strongest labelling was observed in the lateral mammillary nucleus and the hilus gyrus dentatus of the hippocampal formation. A weak labelling occurred in areas such as the nucleus causatus putamen, the thalamus and the cerebral cortex. No significant correlation was therefore obtained between the degree of [125I]BTX binding in various brain nuclei and the degree of binding observed with [3H]Nic or [3H]ACh. The present results underline the view that the high-affinity [3H]Nic and [3H]ACh binding sites label the same cholinergic nicotinic receptor binding site, while [125I]BTX labels another subpopulation of nicotinic cholinergic receptors, predominantly found in discrete areas of the hypothalamus and the limbic cortex.

Acetylcholine↗
PubMed1988

Smoking and inflammatory bowel disease. A case control study.

A population case controlled study of smoking habits at the time of diagnosis was done in 260 patients with ulcerative colitis and 144 with Crohn's disease. Smokers had a decreased risk of acquiring ulcerative colitis in comparison with never smokers (relative risk 0.7) which appeared to be dose dependent. In former smokers a rebound effect was seen, especially in former heavy smokers, where the risk was sharply increased (relative risk 4.4). No sex difference was recorded. Smoking doubled the risk of acquiring Crohn's disease without any dose dependent pattern. In former smokers a non-significantly increased risk was observed. This might be caused by a carry over effect after stopping smoking, however, which possibly is reduced by time. No sex difference was seen.

Adult↗
PubMed1988

Involvement of D1 dopamine receptors in the nicotine-induced neuro-endocrine effects and depletion of diencephalic catecholamine stores in the male rat.

Male rats were treated acutely with nicotine (4 x 2 mg/kg, 30-min time intervals, total treatment time 2 h) or exposed to cigarette smoke from 4 x 1 cigarette (30-min time intervals, total treatment time 2 h). Some rats were pretreated with the D1 dopamine (DA) receptor antagonist SCH 23390 (0.1-3.0 mg/kg, i.p.), or with the D2 DA receptor antagonists remoxipride and raclopride (1 mg/kg, i.p.), or with the 5-hydroxytryptamine 2 (5-HT2) receptor antagonist ketanserin (0.3 mg/kg, i.p.) 5 min before nicotine treatment or the acute intermittent exposure to cigarette smoke. Some rats were treated with the D1 DA receptor agonist SK&F 38393 (1-10 mg/kg, i.p.) 15 min, 30 min or 2 h before decapitation. Hypothalamic and pre-optic catecholamine (CA) levels were measured by quantitative histofluorimetry in discrete DA and noradrenaline (NA) nerve terminal systems. Serum thyroid-stimulating hormone (TSH), prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), vasopressin, corticosterone and testosterone levels were determined by radioimmunoassay procedures. Nicotine treatment and to a minor degree also acute intermittent exposure to cigarette smoke produced a reduction in serum prolactin, LH and TSH but not in serum FSH, vasopressin and testosterone levels. Nicotine treatment also increased serum corticosterone levels. Pretreatment with the D1 DA receptor antagonist SCH 23390 (1-3 mg/kg) counteracted the lowering of serum LH, but not of prolactin and TSH levels induced by nicotine or exposure to cigarette smoke. SCH 23390 alone (1-3 mg/kg) increased serum TSH levels. Remoxipride, raclopride or ketanserin did not counteract any of the neuro-endocrine actions induced by nicotine treatment. However, ketanserin alone lowered serum prolactin levels. SK&F 38393 increased serum TSH, prolactin and LH levels. It was found that nicotine treatment and exposure to cigarette smoke with few exceptions produced a depletion of CA stores in NA and DA nerve terminals of the hypothalamus, pre-optic area and median eminence which was counteracted by SCH 23390 (1 mg/kg) but not by remoxipride, raclopride (1 mg/kg) or ketanserin (0.3 mg/kg). The results indicate that D1 but not D2 DA or 5-HT2 receptors may modulate the NA and DA release in the median eminence, the hypothalamus and the pre-optic area induced by nicotinic cholinoceptor activation. Furthermore, D1 DA receptors in the median eminence may at least in part mediate the inhibitory effects of nicotine on LH but not on TSH and prolactin secretion, although there appears to exist a D1 DA receptor in the median eminence which inhibits TSH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Nutritional assessment of hospitalized patients with head and neck cancer.

Nutritional assessment is an important part of the oncologic management of the cancer patient. Although it may be easy to identify weight loss, the criteria for negative energy balance are difficult to display in an ordinary clinical setting. In the present study we assessed the nutritional status and calculated the energy balance in 10 randomly selected cancer patients who were hospitalized at our ENT department. Loss greater than 10% of habitual weight was apparent in 5 patients, while only 2 of these had subnormal serum albumin levels. Another 1 of these patients with weight loss demonstrated reduced arm muscle circumference. Weight index, total body potassium and other anthropometric data did not significantly correlate with weight loss. Although supplementary nutrition was administered to most patients during hospitalization, only 4 patients were in positive energy balance as calculated from food tables. Only 2 out of 5 patients with a history of weight loss were in a positive energy balance. A questionnaire disclosed that insufficient considerations for the patients' food availability were shown. We conclude that malnutrition is a common and often an occult phenomenon in hospitalized patients. This may have an unfavorable influence on oncologic treatment and clinical outcome.

Aged↗
PubMed1988

Indoor radon exposure and active and passive smoking in relation to the occurrence of lung cancer.

Exposure to indoor radon and radon daughters is currently attracting great interest as a possible cause of lung cancer. This concern is supported by several studies, most of them relatively small in numbers or weak in the assessment of exposure. This study encompasses 177 persons with lung cancer and 677 noncancer referents, all deceased and with 30 years or more of residency in the same house in an area with radon-leaking alum shale deposits in the central part of southern Sweden. Exposure categories based on building material, type of house, and ground conditions were created, but measurements of the indoor radon daughter concentration were also made for 142 cases and 264 referents. Active and passive smoking was ascertained through questionnaires sent to the next-of-kin. Overall, the lung cancer risk was approximately twofold with regard to the categories of assumed radon daughter exposure for the rural sector of the population but not for the same categories of the urban sector, possibly because of less precise exposure assessment and influence from other factors. Occasional and passive smokers, as well as passive smokers alone, had a particularly increased risk of lung cancer in association with the increased exposure categories.

Adult↗