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Biomedical subjects

L Feder

Publications and source records attributed to L Feder.

5 recordsLinked to original sources
PubMed1998

Mutation screening of the dopamine D1 receptor gene in Tourette's syndrome and alcohol dependent patients.

We report a single stranded conformational polymorphism (SSCP) analysis of the coding region of the dopamine D1 receptor (DRD1) in Tourette's syndrome (n = 50) and control (n = 50) subjects. Tourette's syndrome populations with comorbidity for attention deficit-hyperactivity disorder (AD-HD) (n = 35) and obsessive compulsive disorder (OCD) (n = 30) were also screened. As a related study, we also screened patients diagnosed with alcohol dependence (n = 72). The present study discovered no DRD1 coding region mutations in any of the Tourette's syndrome or alcohol dependent patients. One silent mutation, a C for a T at Ile49, was discovered in one control subject. The non-polymorphic structure of the DRD1 gene among the Tourette's syndrome, Tourette's syndrome comorbid with AD-HD and OCD and the alcohol dependent populations screened by SSCP suggests that coding region mutations of the DRD1 gene are unlikely to contribute to the inheritance of these disorders.

Alcoholism↗
PubMed1995

Heparin fails to potentiate the effects of IL-1 beta-mediated bone resorption of fetal rat long bones in vitro.

Heparin has been identified as a potent modulator of bone resorption. Heparin induces osteoporosis during long-term administration and has been shown in vitro to enhance the effects of other bone resorbing factors, including parathyroid hormone. In this study, we examined the effects of heparin on the bone-resorbing activity of the inflammatory cytokine IL-1 beta. Resorption was determined by measuring release of previously incorporated 45Ca from fetal rat long bones cultured in medium supplemented with either 0.1% bovine serum albumin or 10% heat-inactivated fetal calf serum. Heparin, in the absence of serum, decreased basal resorption at 4 and 10 units/ml, and slightly increased resorption at 30 units/ml. Heparin had no effect on IL-1 beta-stimulated resorption. In the presence of serum, heparin induced a two-fold increase in resorption alone, however, when cocultured with IL-1 beta, heparin failed to further enhance IL-1 beta-stimulated resorption.

Animals↗
PubMed1994

Effects of plasminogen and interleukin-1 beta on bone resorption in vitro.

Inflammatory bone resorption, a characteristic feature of periodontal disease and rheumatoid arthritis, appears to be mediated by interleukin-1 beta (IL-1 beta). IL-1 beta has been shown to stimulate a wide range of proteolytic enzymes, including collagenases and plasminogen activators, in particular chondrocytes, synovial cells, and isolated osteoblasts. In this study, we have examined the hypothesis that IL-1 beta may stimulate bone loss by inducing the activity of plasminogen activators (PAs) in bone cultures. The latter would convert plasminogen to plasmin, which in turn can activate precursor procollagenase to collagenase. Active collagenase would then break down the bone collagen matrix. In the present study, release of 45Ca from fetal rat long bones in culture was studied in the presence of plasminogen and IL-1 beta. Plasminogen and IL-1 beta separately enhance resorption of fetal rat long bones in vitro. When plasminogen and IL-1 beta are added together at suboptimal levels, mainly additive effects are observed. The presence of heat-inactivated serum does not alter these results. These data tend to indicate that IL-1 beta is stimulating bone resorption through both PA-dependent and PA-independent pathways.

Animals↗