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C G Nilsson

Publications and source records attributed to C G Nilsson.

At least 37 records · Page 2Linked to original sources
PubMed1997

Comparison of a 10-mg controlled release oxybutynin tablet with a 5-mg oxybutynin tablet in urge incontinent patients.

Oxybutynin has long been used for the treatment of patients with detrusor overactivity and urinary urge incontinence. The short half-life of oxybutynin administered as a conventional tablet formulation or syrup requires 2-3 times daily dosage to be effective. A new controlled release (CR) tablet for once-daily administration has been developed. The efficacy and tolerability of this new controlled release tablet was compared to that of a 5-mg conventional oxybutynin tablet administered twice daily. Seventeen female incontinent patients were studied in a double-dummy crossover trial. Efficacy and tolerability were assessed by using a voiding diary, pad-weighing test, visual-analogue scale (VAS), and questionnaire. Adverse events were recorded spontaneously on a questionnaire by the patients themselves throughout the study. Serum concentrations of oxybutynin and its active metabolite N-desethyloxybutynin were studied after both a single dose and multiple dosage. There was no difference in efficacy between the two formulations. Depending on the parameters tested, the change from baseline values in a positive direction ranged from 15 to 53%. The incidence of adverse events was similar with both formulations. Oxybutynin or its metabolite showed no cumulation during the multiple dosage with a 10-mg CR tablet. The controlled release tablet formulation is as effective and as well-tolerated as the conventional one, but has the advantage of only once-a-day dosage, enhancing treatment compliance.

Adult↗
PubMed1996

Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis.

Memantine, a clinically employed drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as assessed by immunohistochemical evaluation of spinal cord tissue. Furthermore, numbers of interferon gamma (IFN gamma) mRNA expressing cells were not decreased, as assessed by in situ hybridization. Systemic immunity in terms of numbers of IFN gamma secreting cells in response to immunodominant myelin basic protein (MBP) peptides ex vivo was not reduced, and non-toxic doses of memantine did not affect lymphocyte proliferation or IFN gamma secretion in vitro. Considering these findings, we hypothesize that effector mechanisms responsible for reversible neurological deficits in EAE may involve NMDA receptors, and this highlights neurons as targets during autoimmune neuroinflammation.

Animals↗
PubMed1995

Cyclic guanosine 3',5'-monophosphate mediates 3-morpholinosydnonimine-induced inhibition of human natural killer cells.

Nitric oxide (NO) donors were used to investigate the effect of NO on and the role of cyclic GMP in the regulation of human natural killer (NK) cell function. NO-producing drugs, molsidomine and its metabolite 3-morpholinesydnonimine (SIN-1), inhibited NK cell-mediated cytotoxicity significantly at 0.04-5 mM. At 1 mM, SIN-1 completely inhibited NK cell activity while molsidomine decreased NK cell-mediated cytolysis by 35% of the control value. These data suggest that NO from exogenous NO-donors may down-regulate NK cell cytotoxic function. The stimulatory effect of interferon-gamma (IFN-gamma) on human NK cell-mediated killing could not overtake the NK cell inhibition induced by the NO releasing drugs, indicating different modes of action for IFN-gamma and SIN-1. The results in the present study also showed that SIN-1 (1 mM) stimulated cyclic GMP production 37-fold in NK cells. In the presence of 0.5 mM IBMX, a phosphodiesterase inhibitor, the increase in cyclic GMP was even more pronounced, demonstrating a relation between cyclic GMP stimulation and NK cell inhibition by SIN-1. Further evidence for mediation via cyclic GMP was provided by the finding that methylene blue (20 microM), an inhibitor of soluble guanylate cyclase, decreased both the inhibition of SIN-1-induced NK cell cytotoxicity as well as cyclic GMP formation. Moreover, membrane-penetrating cyclic GMP and its analogues inhibited NK cell-mediated cytolysis significantly. Molsidomine was without effect on cyclic GMP levels. Our data indicate that cyclic GMP may play a role in human NK cell regulation and suggest that the inhibitory effect of cGMP may be elicited by NO.

1-Methyl-3-isobutylxanthine↗
PubMed1995

ISIS-4.

Explore the source record for details and available documents.

Fibrinolysis↗
PubMed1994

[Environmental somatization syndrome. How to deal with the external milieu syndrome?].

Somatization is a tendency to experience and communicate psychogenic distress in the form of somatic symptoms and to seek medical help for them. Patients suffering from environmental somatization syndrome (ESS) consider their symptoms to be caused by exposure to chemical or physical components of the external environment or by ergonomic stress at work. ESS is distinguished by mental contagiousness and a tendency to cluster. Sometimes it explodes in wide-spread epidemics that may be escalated by mass-media campaigns. Extensive ESS epidemics have been connected to, i.a., arsenic, carbon monoxide ("generator gas poisoning"), mercury ("oral galvanism"), carbon-free copy papers, electromagnetic fields ("electric allergy") and repetitive movements ("repetition strain injury", RSI). The typical patient directs the interest on the external environment, refuses alternative explanations of his symptoms and abhors any suggestion of a psychogenic etiology. The community is often placed in difficult positions by lobby groups calling for drastic measures to eliminate alleged disease-inducing exposures. When hygienic evils occur simultaneously with an ESS epidemic, it is essential to strictly differ the hygienic problems from the ESS problems. If mismanaged, measures aimed at reducing hygienic inconveniences may aggravate the complex of ESS problems.

Arsenic Poisoning↗
PubMed1993

Effects and acceptability of a new 17 beta-oestradiol-releasing vaginal ring in the treatment of postmenopausal complaints.

The treatment of postmenopausal symptoms was studied in 26 healthy women using a new synthetic rubber (Kraton D 2109) vaginal ring containing 53 mg of 17 beta-oestradiol. All women were postmenopausal, at least 6 months after the last vaginal bleeding and suffering from daily hot flushes. The study was conducted in a double-blind placebo-controlled intrapatient cross-over fashion, and the study period was 6 months. The rings used give an initial in vitro release rate of 0.4 mg/E2 per day. The in vitro release rate decreases to about 0.2 mg/day after 20 days and levels off asymptotically to about 0.1 mg/day after 50 days. Serum E2 levels equivalent to the follicular phase of the normal menstrual cycle were measured after 1 month's use, and serum E2 level stayed above postmenopausal levels throughout the study period. FSH was suppressed during use of the E2-releasing vaginal ring, while LH showed no statistically significant suppression in continued use. Postmenopausal complaints were recorded by Visual Analogue Scales (VAS) as judged by both the patient and the examining doctor; all complaints had favourable outcomes during use of the E2-releasing vaginal ring without deterioration of symptoms during use of the placebo ring. No serious side-effects were encountered, and the possibility of managing all postmenopausal complaints with intravaginal oestrogen treatment is discussed.

Administration, Intravaginal↗
PubMed1993

[Biology of aging blood vessels].

The localisation of arteriosclerosis to foci of haemodynamic stress of sites of supporting collagen or elastic fibre deficiency illustrates the importance of mechanical factors in the fate of the smooth muscles. Excessive stress depletes stocks of ATP (adenosine triphosphate), resulting in osmotic lysis. Phosphate ions are released and precipitated in calcifications as apatite. The vascular lesion is followed by reparative and adaptive tissue inflammation. The haemodynamic stress is modified by a number of psychosocial factors, and is increased by traumatic and other injury to the ground substance. Some of the LDL (low-density lipoprotein) perfusing the intima is captured in the proteoglycan matrix, especially if the media is thickened. When cells and ground substance are lysed, fractions are incorporated in macrophages through metabolically uncontrolled receptors. Toxic oxidised LDL is then continuously ingested in the cells before they eventually die, leaving the amorphous lipid-rich mass of which an atheroma is formed. The macrophages produce free radicals which accelerate the damage and the inflammation. Thus, many factors working at different levels are involved in the aetiology of arteriosclerosis, with or without atheromatosis. The only theoretically feasible though insufficiently tested dietary recommendation for the general population would be to reduce the in vivo redox potential of food intake.

Adenosine Triphosphate↗
PubMed1990

Evidence of similar increases in bone turnover during nafarelin and danazol use in women with endometriosis.

Medical 'oophorectomy' by GnRH agonist or danazol is an effective treatment for endometriosis. Since increased bone loss is a potential risk of hypoestrogenism, we compared the effect of nafarelin and danazol treatment on bone metabolism. Twelve patients with laparoscopically confirmed endometriosis received nafarelin (400 micrograms day intranasally) and six patients danazol (600 mg day orally) for 6 months. Both treatments had already led to hypoestrogenism (E2 less than 21.6 pg/ml) after 3 months. They both were accompanied by an approximately 50% rise in 24-h urinary hydroxyproline output, suggesting accelerated bone resorption at 6 months; yet urinary calcium output did not change significantly. Serum osteocalcin rose by 80-120% and bone alkaline phosphatase activity by 34-40%, suggesting stimulated bone formation at the same time. No detectable changes ensued in cortical bone mineral content in the distal radius or in serum levels of calcium, calcitonin, parathyroid hormone, or aminoterminal propeptide of type III collagen. Three months after treatment, hydroxyproline output, serum osteocalcin and bone alkaline phosphatase were still elevated in women taking nafarelin, whereas only serum osteocalcin was elevated in women taking danazol. Our data thus suggest that bone turnover was increased during nafarelin and danazol therapy and that this effect was reversible.

Alkaline Phosphatase↗
PubMed1989

The biology of ageing arteries. An integrated view.

It is suggested that damaged arterial smooth muscle cells (SMC) and altered structural proteins are interpreted as foreign and degraded by the complement system and by macrophages. At the same time growth factors are liberated, stimulating hyperplasia of SMC. In atheromata this proliferation may be monoclonal. The long-lived proteins in the ground substance are glucosylated by Amadori reactions leading to virtually stable compounds and to polymerization. This process is enhanced by high blood sugar and possibly by vitamin B6 deficiency. The proteoglycans adsorb lipoproteins which are transported to macrophages during the reconstruction of the wall. The combined result of all these changes is a thickened and stiff intima with decreased nutritional flow to the cells and decreased transmissibility of macrophages and other cells. In addition to antihyperlipemic treatment, arteriosclerosis prevention should include antihypertensive treatment preferably with calcium blocking or beta blocking agents or both and antidiabetic treatment, but also nutritional measures including the supply of Mg, Vitamins E and B6 and possibly nitrites.

Aging↗