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Biomedical subjects

I Johansson

Publications and source records attributed to I Johansson.

At least 163 records · Page 9Linked to original sources
PubMed1990

Evaluation of different hybridization procedures for the detection of mycoplasma contamination in cell cultures.

Cell culture samples were analysed for mycoplasma contaminations with two different DNA probes which have been described earlier. One probe (the H900 probe), derived from the 23S rRNA gene of Mycoplasma hyorhinis, cross-hybridized with virtually all mycoplasmas (including the acholeplasmas). The other probe (the T2 probe), derived from a protein gene of Acholeplasma laidlawii, cross-hybridized with most acholeplasmas. The two probes were compared in three different direct filter hybridization procedures without previous isolation of DNA or RNA. One of the procedures, developed in the present study, gave the highest sensitivity in DNA-RNA hybridization but also worked satisfactorily in DNA-DNA hybridization. The sensitivity of the H900 probe in filter hybridization experiments was compared with the sensitivity of a commercial probe for detection of mycoplasma contaminations in cell cultures. The H900 probe was found to be at least 25 times more sensitive for all cell culture mycoplasmas except for A. laidlawii, for which they were equally sensitive.

Animals↗
PubMed1990

Substrate-, hormone-, and cAMP-regulated cytochrome P450 degradation.

The hepatic cytochrome P450 system, with numerous different P450 enzymes, is characterized by its inducibility by a variety of endogenous and exogenous compounds. Specific forms of P450, exhibiting distinct but partially overlapping substrate specificities, are increased in response to a given chemical. Consequently, the rate of elimination of the inducing compound is often enhanced and the system is in this respect adaptive to changes in the environment. Transcriptional activation mechanisms for the endo- or xenobiotically controlled P450 synthesis are well documented. Here we describe a mechanism for posttranslational ligand-dependent stabilization of ethanol-inducible P450IIE1 in hepatocyte cultures. Glucagon or 8-bromoadenosine 3',5'-cyclic monophosphate causes an enhanced rate of P450IIE1 degradation in the hepatocytes as well as phosphorylation on Ser-129, a reaction which denatures the protein under in vitro conditions. Substrates for the enzyme, such as ethanol and imidazole, protect the enzyme from phosphorylation and degradation in hepatocytes but do not influence phosphorylation or degradation of phenobarbital-inducible P450IIB1. Our proposed mechanism, which remains to be shown under in vivo conditions, describes the P450 molecules as receptors for the compounds in question and might provide a way by which endo- and xenobiotics regulate their own rate of metabolism.

1-Propanol↗
PubMed1990

Prognosis in patients with transient ischaemic attacks and minor stroke associated with a normal angiogram.

61 patients with a transient ischaemic attack (TIA) or minor stroke and a normal angiogram and with no other explanation for the ischaemic event were followed up for a mean period of 6.3 years. Of 19 patients with a TIA 5 suffered further TIAs, and 1 of the 5 also an ischaemic stroke. 3 of 42 patients with a minor stroke had a new ischaemic stroke, in 1 case preceded by a TIA. In 2 stroke patients the lesion affected a new arterial region. 3 patients died of cerebral haematoma, in 1 preceded by an ischaemic stroke. 4 patients suffered myocardial infarction, and 1 of these died. The overall incidence of recurrent cerebral and cardiovascular symptoms was 23% (14 of 61 patients). The mean age was significantly higher (p less than 0.01) in patients with recurrent cerebral and cardiovascular lesions. No correlation emerged between risk factors. Patients with a TIA or minor stroke and a normal angiogram and with no other known source of embolism have a better prognosis than patients with a known source of embolism. However, elderly patients in particular run an increased risk of cardiac and cerebral vascular incidents.

Adolescent↗
PubMed1989

Central post-stroke pain--neurological symptoms and pain characteristics.

The intention of the present study was to characterize patients with central post-stroke pain (CPSP) with regard to type and location of the cerebrovascular lesion (CVL), the characteristics of the pain and the neurological symptoms and signs in addition to the pain. Twenty men and 7 women with a mean age of 67 years and a mean pain duration of 44 months were examined 9-188 (mean 53) months after their stroke. The clinical symptoms and signs and the CT scans indicated that the CVL were located in the lower brain-stem in 8 patients, involved the thalamus in 9 patients and were located lateral and superior to the thalamus in 6 patients. In the remaining 4 patients the location of the CVL could not be determined with certainty. The 3 identified hematomata were all located in the thalamus. The onset of the pain was immediate in 4 patients, within the first post-stroke months in 10 patients and delayed by 1-34 months in the rest. The pain was on the left side in 18 patients. Twenty patients had hemipain. Most patients experienced more than one type of pain. The most common qualities were burning, aching, pricking and lacerating, with some differences in the frequencies according to the location of the CVL. Burning pain was most common, except among the patients with thalamic CVL, in whom lacerating pain was more common. Aching and pricking pain were also frequent. All patients considered the pain to be a great burden and most rated the pain intensity as high on a visual analogue scale. The intensity was increased by external stimuli, the most common being joint movements, cold and light touch. Five patients reported aggravation by emotional stimuli. Besides pain, the only neurological symptom common to all patients was decreased temperature sensibility, as shown by quantitative methods. It is possible that pain sensibility was also abnormal in all. Hypersensitivities to cutaneous stimuli, including evoked dysesthesias were found in 88% of the patients, while the detection thresholds for touch and vibration were abnormal in only 52% and 41%, respectively. Similarly, low figures were found for paresis and ataxia, which were present in 48% and 62%, respectively. It is concluded that only a minority of patients with central pain after stroke have thalamic lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1989

Central post-stroke pain--a study of the mechanisms through analyses of the sensory abnormalities.

The somatosensory abnormalities in 20 men and 7 women (mean age 67 years, range 53-81) with central post-stroke pain (CPSP) have been analysed in detail with traditional neurological tests and quantitative methods. The cerebrovascular lesions were located in the lower brain-stem in 8 patients, involved the thalamus in 9 and in 6 were suprathalamic. In 4 patients the location of the CVL could not be determined. All patients had abnormal temperature and pain sensibility, with a severe deficit in most cases. All except 2 had raised thresholds to thermal pain and all except 1 had abnormal sensibility to pin-prick. Eighty-eight percent exhibited hyperpathia with combined loss and suprathreshold exaggeration of somatic sensibility. In 85% somatic stimuli evoked dysaesthesia and about half of these patients also experienced spontaneous dysaesthesia. Paraesthesias were reported by 41%, radiation of stimuli by 50%, after-sensations by 45% and allodynia by 23%. Vibration sensibility was abnormal in 41%; raised thresholds to the perception of touch were found in 52%, to 2-PD in 35%, to dermolexia in 45% and to joint movements in 37%. The results indicate that all patients with CPSP have lesions that affect the major pathways for temperature and pain sensibility, i.e., the spino-thalamo-cortical pathways. Furthermore it appears that neither the level of the lesion along the neuraxis nor concomitant injury to the medial lemniscal pathways is crucial for the development of CPSP. The results confirm the notion that CPSP is a deafferentation syndrome, but they also provide evidence against the hypothesis that CPSP is a release phenomenon caused by a lesion that removes inhibitory influences of the lemniscal pathways on neurones that evoke pain.

Aged↗
PubMed1989

Effects of chronic stimulation of salivary gland beta-adrenoceptors on saliva composition and caries development in the rat.

The effects of long-term beta-adrenoceptor stimulation or inhibition on parotid and submandibular glands, saliva secretion, and caries development were studied. Groups of rats were treated daily with: 0.5 or 5 mg/kg body weight of isoproterenol (IPR), 0.5 or 5 mg/kg bw propranolol (PRO), or saline. After 42 days, saliva was collected and analyzed for secretion rate, total protein, amylase, sialic acid and electrolytes. Total protein and amylase in saliva decreased and potassium increased in the high IPR group. Phosphate increased in both IPR groups and decreased in the high PRO group. The average weight of parotid glands increased 3.7 times in the high IPR group and 1.8 times in the low IPR group. Amylase and total protein in parotid gland extracts decreased in both IPR groups. The submandibular gland weight increased 1.5 times in the high IPR group. Total protein decreased in the high IPR group. There was no difference in caries development.

Amylases↗
PubMed1989

Effect of moderate protein-deficiency on ultrastructure in parotid and submandibular acinar cells in the adult rat.

Powdered diets, of three different levels of protein, were given to groups of adult male rats for 21 days. Two diets with reduced protein content, 5% or 10% casein, were given to experimental rats. A diet with an adequate protein content, 20% casein, was given to controls. A reference group of rats was fed a standard pellet diet for the same period. At the end of the experimental period, the parotid and the submandibular glands were removed and subjected to electron microscopy. The zymogen granules of acinar cells in the parotid glands from the rats receiving the 5% protein diet had lost their normal opaqueness and turned electron lucid whereas parotid glands from the rats fed the 20%, the 10%, and the standard pellet diet exhibited normal acinar cells. The ultrastructure of submandibular acinar cells was not affected in any dietary group.

Animals↗
PubMed1989

Effect of a moderate vitamin A deficiency on saliva secretion rate and some salivary glycoproteins in adult rat.

The study presents the effect of a low vitamin A intake on saliva secretion rate and some salivary glycoproteins in the adult rat. Sixteen rats in the experimental group were fed a vitamin A deficient diet (0.11 micrograms retinol/g diet) and 14 rats in the control group a diet with adequate content of vitamin A (4.74 micrograms/g diet). At the end of the experimental period of 10 wk, whole saliva, blood, and liver samples were collected. No difference in the serum content of retinol was seen between the two groups. The liver values were significantly lower for the rats in the experimental group compared to the values in the control group. No difference was seen between the two groups in saliva secretion rate, salivary peroxidase activity, or the concentrations of total protein and markers for total glycoprotein secretion. However, the activity of a bacteria agglutinating glycoprotein, BAGP, was significantly reduced in the rats fed the vitamin A deficient diet.

Animals↗
PubMed1989

Effects of a 900-kcal liquid or solid diet on saliva flow rate and composition in female subjects.

Eleven healthy females of normal weight participated in a study on the effects of two 900-kcal (5,548 kJ) diets, one solid and one liquid, given for 8-day periods. Unstimulated and stimulated whole saliva was collected before, during, between, and after the two different experimental periods. The dietary intake was recorded and evaluated for its content of energy and nutrients during normal and experimental periods. The 900-kcal liquid diet caused a reduction in saliva secretion rate, sialic acid, and phosphate concentrations and an increase in the sodium concentration as well as in the ratio of total protein to sialic acid. Chewing a 900-kcal solid diet restored saliva secretion and composition. The rate of dental plaque formation was increased by both 900-kcal diets, but more during the liquid period.

Adult↗
PubMed1988

Centrilobular expression of ethanol-inducible cytochrome P-450 (IIE1) in rat liver.

Western blot analysis of digitonin eluates as well as immunohistochemical analysis revealed a 30-fold higher concentration of cytochrome P-450IIE1 in the centrilobular than in the periportal regions of the rat liver. Ethanol treatment caused a selective centrilobular induction of P-450IIE1, whereas phenobarbital induced P-450IIB1/2 in both liver lobule regions. The heterogeneous distribution pattern of P-450IIE1 was also observed in cells isolated from either region and correlated to the relative content of P-450IIE1 mRNA in the two cell types. The regiospecific expression and induction of P-450IIE1 may explain why several hepatotoxins, known to be metabolized by this isozyme, primarily damage the centrilobular region in the liver.

Alanine Transaminase↗
PubMed1988

Benzene metabolism by ethanol-, acetone-, and benzene-inducible cytochrome P-450 (IIE1) in rat and rabbit liver microsomes.

Ethanol is known to exert a synergistic effect on the toxicity of benzene. In the present investigation it was found that benzene was metabolized at a rate 20-65-fold higher in liver microsomes from ethanol- or acetone-treated rats than in microsomes from control animals. One high affinity site [Km = 19 +/- 5 (SD) microM] and one low affinity site [Km = 0.3 +/- 0.1 mM] for benzene metabolism were present in microsomes of acetone-treated rats, and similar sites were seen in microsomes from control or ethanol-treated rats. Treatment of the animals with either ethanol or acetone mainly influenced the Vmax values for benzene metabolism. Also benzene treatment of rats caused an increased rate of microsomal benzene metabolism. The hepatic microsomal NADPH-dependent metabolism of benzene was inhibited by compounds known to interact with the ethanol-inducible form of P-450 such as imidazole, ethanol, aniline, and acetone but was unaffected by addition of metyrapone. Anti-IgG against ethanol-inducible cytochrome P-450 from rat (P-450j) or rabbit liver (P-450 LMeb) inhibited the microsomal benzene metabolism effectively in rat or rabbit liver microsomes, respectively, whereas preimmune IgG was without effect. The level of rat ethanol-inducible P-450 (P-450j) was induced to an extent similar to that for the microsomal benzene metabolism, by either benzene, acetone, or ethanol. The data indicate that benzene is metabolized mainly by the ethanol-inducible P-450 form in liver microsomes and that the induction of this isozyme by ethanol can provide an explanation for the synergistic action of ethanol on benzene toxicity.

Acetone↗
PubMed1988

Ethanol-, fasting-, and acetone-inducible cytochromes P-450 in rat liver: regulation and characteristics of enzymes belonging to the IIB and IIE gene subfamilies.

Two major forms of hepatic microsomal cytochrome P-450 were purified from starved and acetone-treated rats. On the basis of amino acid sequence analysis, they were identified as P-450j and P-450b. Ethanol or acetone treatment of rats caused a 9-fold increase in the amount of P-450j in liver microsomes accompanied by similar increases in the rate of NADPH-dependent metabolism of carbon tetrachloride, acetone, and benzene. Immunological experiments indicated that P-450j constitutes the major catalyst of the microsomal metabolism of the latter agents and contributes by about 50% to microsomal P-450-dependent ethanol oxidation under the conditions used. The P-450j-dependent catalytic activities had a high rate of turnover. In contrast, this was not the case for the immunodetectable P-450j, indicating the occurrence of inactive forms of this protein in microsomes. Starvation or ethanol or acetone treatment caused 10-30-fold increases in the amount of both mRNA and apoprotein of P-450b,e compared to control. Run-on experiments and the concomitant increases of the P-450b,e gene products at the mRNA and protein levels indicated the appearance of mainly a transcriptional activation by acetone, ethanol, or starvation. Fasting exerted, in addition, a pronounced synergistic effect on acetone-dependent induction of P-450b,e mRNA (3-fold), apo-P-450b,e (4.3-fold), P-450j mRNA (2-fold), and apo-P-450j (2-fold). No increase of mRNA coding for P-450j, compared to control, was seen after acetone or ethanol treatment alone. The results indicate that effects of ethanol, acetone, and/or starvation on drug and xenobiotic metabolism are caused by the induction of P-450 forms belonging to at least two gene subfamilies.

Acetone↗
PubMed1988

Ligand-dependent maintenance of ethanol-inducible cytochrome P-450 in primary rat hepatocyte cell cultures.

Administration of ethanol, dimethylsulphoxide, 2-propanol or imidazole to rats caused 2-7-fold increases in the level of hepatic ethanol-inducible cytochrome P-450 (P-450j), without any concomitant enhancement of corresponding mRNA. All the compounds were able to stabilize P-450j in hepatocyte cultures for at least three days, whereas P-450j mRNA rapidly disappeared from the cultures. A correlation was reached between the concentration of Me2SO, ethanol and 2-propanol necessary to maintain P-450j in the cell cultures and their binding affinities to the enzyme. It is suggested that the ligand-bound form of P-450j in the hepatocytes is protected from degradation.

1-Propanol↗
PubMed1988

Selenium and vitamin E treatment of Duchenne muscular dystrophy: no effect on muscle function.

16 boys with Duchenne muscular dystrophy (DMD) were treated with sodium selenite and vitamin E for one year. One group of patients (10 boys) was examined using a battery of tests to assess muscular strength and function and cardiopulmonary function, and by CT scanning of 2 muscle groups over the 4 years prior to treatment. Six boys with DMD entered the study when the treatment was begun. Tests of muscular force and function, cardiopulmonary tests and CT-scanning were performed at the onset of treatment, and after 6 and 12 months. No beneficial effect on either muscular force or function was found during the treatment period. It is concluded that selenium and vitamin E in high doses do not improve muscle function in DMD.

Adolescent↗
PubMed1988

Effect of long-term isoproterenol treatment on caries development in the rat using a low-cariogenic model.

Forty-eight Sprague-Dawley rats were divided into four groups. Two groups were injected daily with saline (groups 1 and 2) and two groups with isoproterenol (0.5 mg/kg body weight, groups 3 and 4) beginning at the age of 21 days. Groups 1 and 3 were each day fed nine subsequent sucrose-containing meals followed by eight starch-containing meals. Groups 2 and 4 were fed alternating sugar- or starch-containing meals, totally 17 meals per day. The animals were sacrificed after 14 weeks. At the end of the experiment, the animals in the isoproterenol groups had higher body weights. Caries development increased significantly after isoproterenol treatment. The diet regimen with alternating sugar- or starch-containing meals increased caries development, particularly in combination with isoproterenol treatment. Using low cariogenic conditions, we found that an unspecific beta-agonist (isoproterenol), given posteruptively at a low dose, enhances caries development.

Animals↗