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Biomedical subjects

B Lundgren

Publications and source records attributed to B Lundgren.

At least 109 records · Page 6Linked to original sources
PubMed1989

Pulmonary disease in patients with human immunodeficiency virus infection.

Pulmonary disease is the most important cause of morbidity and mortality in patients infected with human immunodeficiency virus (HIV). All parts of the hospital system are expected to be involved in the diagnosis and treatment of HIV infected patients in the coming years. Many different processes cause pulmonary disease alone or in combination. Bilateral interstitial infiltrates are the most frequent chest x-ray abnormality and are most frequently caused by infection with Pneumocystis carinii. Cytomegalovirus, Mycobacterium tuberculosis, nonspecific interstitial pneumonitis and pulmonary Kaposi's sarcoma are the most important parts of the differential diagnosis. An aggressive approach to the diagnosis of pulmonary disease in this patient population is indicated in order to provide optimal care and assess new therapies.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Cardioselective beta-blockade with metoprolol in rest angina: a randomized, double-blind, placebo-controlled, cross-over trial.

The antiischemic effects of the beta-1 selective beta-blocker metoprolol were studied in 9 hospitalized patients with rest angina in a double-blind, placebo-controlled, cross-over study. After 3 days of placebo treatment, the patients were randomized to metoprolol 100 mg or placebo bid for 2 days, followed by 2 days on the alternative treatment. During the last 24 hours of each period, Holter monitoring was performed. The patients marked angina attacks and NTG consumption on diary cards. Metoprolol significantly reduced the mean number of ST-changes (run-in: 5.7 +/- 0.6; metoprolol: 2.2 +/- 0.9; p = 0.013), the mean maximal ST-change during the attacks (run-in: 3.0 +/- 1.2 mm; metoprolol: 1.5 +/- 0.4 mm; p = 0.015), the mean duration of the ST-changes (run-in: 7.0 +/- 0.6 min; metoprolol: 3.2 +/- 1.0 min; p = 0.015), and the total ischemic time/24 (run-in: 41.1 +/- 7.6; metoprolol: 13.1 +/- 7.2 min; p = 0.008). None of these parameters was modified by placebo. However, the difference between metoprolol and the randomized placebo did not reach statistical significance. Metoprolol also reduced the number of chest pain attacks (p = 0.008), the duration of the attacks (p = 0.051), the severity score of the attacks (p = 0.008), and NTG consumption (p = 0.018) with respect to the run-in period. Six of the patients showed marked improvement on metoprolol while 3 showed only slight improvement or no change. No patients experienced worsening of angina or ST-changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

The antianginal efficacy and tolerability of controlled-release metoprolol once daily: a comparison with conventional metoprolol tablets twice daily.

In a randomized, double-blind, cross-over study treatment with a new controlled-release (CR) preparation of metoprolol, given once daily, was compared with treatment with conventional metoprolol tablets, given twice daily, in 115 patients with stable effort angina pectoris. The patients were treated with 100 mg/day or 200 mg/day, depending on their previous beta-blocker dose. Antianginal efficacy was estimated by counting the number of anginal attacks, by noting the consumption of nitroglycerin tablets, and by exercise tolerance testing. Adverse effects were recorded by a standardized questionnaire. When all patients were analysed together there were no differences in antianginal efficacy between the two treatment regimens. However, when the group taking 200 mg daily was analysed separately better exercise tolerance was found during metoprolol CR therapy, as measured by onset of chest pain and ST-segment change, compared with conventional metoprolol therapy. The two formulations were well tolerated. When given once daily in a total daily dose of 100 mg, the CR preparation induced less adverse effects than the conventional tablets, 50 mg twice daily. It was concluded that the new metoprolol CR preparation, given once daily, possesses the same antianginal efficacy as conventional metoprolol tablets, given twice daily, and may be better tolerated in patients susceptible to side-effects. The antianginal effect of metoprolol CR, 200 mg/day, may be greater over 24 h than that produced by conventional metoprolol tablets, 100 mg twice daily.

Adult↗
PubMed1988

Induction of cytosolic and microsomal epoxide hydrolases in mouse liver by peroxisome proliferators, with special emphasis on structural analogues of 2-ethylhexanoic acid.

Using dietary administration, mice were exposed to eight substances known to cause peroxisome proliferation (i.e. clofibrate clofibric acid, 2,4-dichlorophenoxyacetic acid, 2,4,5-trichlorophenoxyacetic acid, nafenopin, ICI-55.897, S-8527 and Wy-14.643) or the related substance p-chlorophenoxyacetic acid (group A). Other animals received di(2-ethylhexyl)phthalate, mono(2-ethylhexyl)phthalate, 2-ethylhexanoic acid, or one of 12 other metabolically and/or structurally related compounds (group B). The effects of these treatments on liver cytosolic and microsomal epoxide hydrolases, microsomal cytochrome P-450, cytosolic glutathione transferase activity, the liver-somatic index and the protein contents of the microsomal and cytosolic fractions prepared from liver were subsequently monitored. In general, peroxisome proliferation was accompanied by increases in cytosolic epoxide hydrolase activity. Many peroxisome proliferators also caused increases in microsomal epoxide hydrolase activity, although the correlation was poorer in this case. Immunochemical quantitation by radial immunodiffusion demonstrated that the increases observed in both of these enzyme activities reflected equivalent increases in enzyme protein, i.e. that induction truly occurred. Induction of total microsomal cytochrome P-450 was obtained after dietary exposure to clofibrate, clofibric acid, 2,4-dichlorophenoxyacetic acid, 2,4,5-trichlorophenoxyacetic acid, nafenopin, Wy-14.643, di(2-ethylhexyl)phthalate and di(2-ethylhexyl)phosphate. The most pronounced effects on cytosolic glutathione transferase activity were the decreases obtained after treatment with clofibrate, clofibric acid and Wy-14.643. Our results, together with those reported by others, suggest that the processes of peroxisome proliferation and induction of cytosolic epoxide hydrolase are intimately related. One possible explanation for this is presented.

Animals↗
PubMed1988

Screening in breast cancer: a view from the front line.

Mammography screening presents the only real breakthrough in breast cancer in this century. Twenty-five percent of all cancer in women is breast cancer. About 50 percent of these women die from their disease. It has not been possible to reduce breast cancer mortality more than marginally by any mode of treatment. Single view mammography screening can do so, however, at the rate of 30 to 40 percent. Screening has many detractors, especially in the treatment camp. These detractors do not always act in the patients' best interests. Considering the vast resources used up until now in trying to improve on breast cancer treatment, and to little avail, it is time to divert some of these efforts to set up screening programmes wherever possible. Well handled, these are able to reduce suffering and health care costs and save lives.

Attitude↗
PubMed1987

Comparison of fibronectin receptors from rat hepatocytes and fibroblasts.

A cell-surface fibronectin receptor was isolated from primary rat hepatocytes by affinity chromatography on Sepharose conjugated with the cell-binding domain (105 kDa) of fibronectin. The receptor remained bound to the affinity column in the presence of 1 M NaCl but was eluted by 1.5 mM of glycl-arginyl-glycyl-aspartyl-seryl-cysteine peptide or by lowering the pH to 4. The eluted material migrated under nonreducing conditions in sodium dodecyl sulfate-polyacrylamide electrophoresis as two bands: the alpha- and beta-components had apparent Mrs of 155,000 and 115,000, respectively. After reduction the 155-kDa component gave rise to two peptides of Mrs 145,000 and 20,000, while the 115-kDa component shifted migration to an Mr of 130,000. Antibodies specifically recognizing the 155- and 115-kDa proteins from hepatocytes inhibited the attachment of these cells to fibronectin-coated dishes, whereas attachment to dishes coated with collagen or laminin was unaffected. A fibronectin receptor isolated from rat fibroblasts showed closely similar, but not identical, migration in sodium dodecyl sulfate-electrophoresis as the hepatocyte receptor. Furthermore, only the beta-subunit of the fibroblast receptor reacted with the antibodies. The results suggest that distinct alpha-subunits of the fibronectin receptors may be the basis for the different fibronectin-binding properties of these cells.

Animals↗
PubMed1987

Induction of cytosolic and microsomal epoxide hydrolases and proliferation of peroxisomes and mitochondria in mouse liver after dietary exposure to p-chlorophenoxyacetic acid, 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid.

The effects of dietary exposure to 0.125% (w/w) p-chlorophenoxyacetic acid, 2,4-dichlorophenoxyacetic acid or 2,4,5-trichlorophenoxyacetic acid on the content of peroxisomes and levels of certain xenobiotic-metabolizing enzymes in mouse liver have been investigated. In agreement with the literature on rat liver 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid were found to cause extensive proliferation of peroxisomes (as judged by the total levels of "mitochondrial" protein, carnitine acetyltransferase, cyanide-insensitive palmitoyl-CoA oxidation and catalase) in mouse liver. On the other hand, exposure to p-chlorophenoxyacetic acid did not significantly affect any of these parameters. As with certain other peroxisome proliferators, 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid increased total cytochrome oxidase activity as well. In addition, dietary exposure to 2,4-dichlorophenoxyacetic acid and to 2,4,5-trichlorophenoxyacetic acid resulted in increases in the activities of cytosolic and microsomal epoxide hydrolases in mouse liver and generally less pronounced increases in the total cytosolic glutathione transferase activity and microsomal content of cytochrome P-450. In the case of cytochrome P-450, this process can be said to be a true induction (i.e. the amount of enzyme protein is increased), because the assay procedure for cytochrome P-450 measures holoenzyme amount. Immunoquantitation demonstrated that this was also the case for the changes in cytosolic epoxide hydrolase. The dramatic differences in proliferation of peroxisomes and induction of xenobiotic-metabolizing enzymes seen here with compounds differing relatively little in structure may indicate that a receptor mechanism of some kind is involved.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1987

Examination of the structural requirements for proliferation of peroxisomes and mitochondria in mouse liver by hypolipidemic agents, with special emphasis on structural analogues of 2-ethylhexanoic acid.

We have found here that there are clear structural requirements for peroxisome proliferation (monitored as increases in carnitine acetyltransferase activity, cyanide-insensitive palmitoyl-CoA oxidation, catalase and increases in the protein designated PPA 80) in mouse liver. From the investigation of ten structural analogues of 2-ethylhexanoic acid, it could be concluded that the most effective proliferators all have an ethyl group as the substituent on carbon 2 of the main chain, which consists of six carbons. The further observation from this group of compounds that a charged group is required for effective proliferation leads us to speculate that such a group is involved in the molecular mechanism as well. Many, but not all, of the effective peroxisome proliferators in a second group of compounds contain a phenoxy group, often with a substituted alpha carbon. Interestingly, the 2,4-dichlorophenoxyacetic and 2,4,5-trichlorophenoxyacetic acids are both effective peroxisome proliferators, but the closely related p-chlorophenoxyacetic acid is inactive in this respect, indicating that the chlorine atom at position 2 must be essential to the process in these cases. The results presented here also indicate that the structural requirements for proliferation of mitochondria are similar to those for proliferation of peroxisomes. Certainly, the most effective peroxisome proliferators also cause large increases in 'mitochondrial' protein and cytochrome oxidase activity, i.e. there is an obvious qualitative correlation.

Animals↗
PubMed1987

Induction of xenobiotic-metabolizing enzymes and peroxisome proliferation in rat liver caused by dietary exposure to di(2-ethylhexyl)phosphate.

Exposure of rats to 1% or 3% (w/w) di(2-ethylhexyl)phosphate in the diet for five days results in two- to three-fold inductions of liver cytosolic epoxide hydrolase activity and microsomal cytochrome P-450 content. Cytochromes P-450b + e were induced 20- to 35-fold, but no increase was observed in cytochrome P-450c. Considerably smaller effects were obtained on NADPH-cytochrome c reductase, microsomal epoxide hydrolase and microsomal cytochrome b5 content, and there was no effect on cytosolic glutathione transferase activity, under the same conditions. A dramatic increase in cyanide-insensitive palmitoyl-CoA oxidation and total mitochondrial protein, together with smaller increases in total catalase and cytochrome oxidase activities, were observed after treatment with di(2-ethylhexyl)phosphate, indicating that this compound causes proliferation of both peroxisomes and mitochondria. It is suggested that the induction of cytosolic epoxide hydrolase and the proliferation of peroxisomes may be related processes.

Animals↗
PubMed1987

Alternatives for harvesting cells grown on microcarriers: effects on subsequent attachment and growth.

In order to facilitate the subpassaging of cells in microcarrier cultures for scaling up culture volumes, alternative procedures for harvesting cells from microcarriers were investigated. A variety of enzymes including trypsin and dextranase were tested separately and in combination to evaluate cell viability after detachment, recovery, and subsequent attachment and growth of cells following inoculation of the cells in the next microcarrier culture. Treatment of confluent microcarriers with dextranase detached cells efficiently and with high viability and in addition totally digested the dextran-based matrix of Cytodex, thus avoiding the possible need to separate the harvested cells from the microcarriers. Dextranase alone resulted in cells harvested as sheets, but if used in combination with trypsin, a single cell suspension of harvested cells was obtained.

Animals↗
PubMed1986

Increased beta I-adrenoceptor density after 6-hydroxydopamine pretreatment in rat colon and lung.

Estimation of beta-adrenoceptor-binding sites with 125I-(-)-pindolol in rat colon show a proportion of 30% beta I-adrenoceptors and 70% beta 2-adrenoceptors. Studies on the isolated colon strip have revealed a neuronal beta-adrenoceptor involved in the inhibitory response of colon motility to beta-adrenoceptor stimulation. In order to further characterize the beta-adrenoceptors in the colon, acute and chronic treatments with 6-hydroxydopamine were made. Both acute pretreatment of rats with 6-hydroxydopamine for 8 and 24 h (one intravenous injection) and chronic treatment for 3 days (implanted osmotic mini-pumps), reduced the noradrenaline tissue content by 90%, and successively increased the beta-adrenoceptor-binding sites from 14.2 to 21.7 fmol mg-I P-I in colon and from 158 to 240 fmol mg-I P-I in lung membranes. Displacement of the radiolabelled ligand by the selective beta-adrenoceptor antagonists, pafenolol and ICI 118.551 showed that the density of beta I-adrenoceptor binding sites was more than doubled, whereas the density of beta 2-adrenoceptor-binding sites was only marginally increased by chronic treatment with 6-hydroxydopamine. Thus sympathetic denervation by 6-hydroxydopamine treatment produced a selective increase in beta I-adrenoceptors in the rat colon. These results may indicate that stimulation of beta I-adrenoceptors in both colon and lung have a neuronal linkage.

Animals↗
PubMed1986

Efficacy of the acyclic guanosine analog buciclovir [(R)-9-(3,4-dihydroxybutyl)guanine] in experimental genital herpes.

The efficacy of the anti-herpesvirus drug buciclovir [(R)-9-(3,4-dihydroxybutyl)guanine] was investigated in guinea pigs and mice infected intravaginally with herpes simplex virus type 2. Topical treatment initiated early after infection was efficacious, in contrast to topical treatment delayed 24 h or more. Systemic treatment of infected mice could not prevent the spread of virus to the brain and mortality. Systemically administered buciclovir had an effect in guinea pigs, even after delayed onset of treatment, but this effect required high doses of the drug. Our results suggest that buciclovir has only a limited effect against herpesvirus infections once the virus is present in the nervous systems of infected animals.

Acyclovir↗