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C Fiskerstrand

Publications and source records attributed to C Fiskerstrand.

6 recordsLinked to original sources
PubMed2001

The dopamine transporter gene (SLC6A3) variable number of tandem repeats domain enhances transcription in dopamine neurons.

The dopamine (DAT) and serotonin (SERT) transporter genes both contain variable number of tandem repeats (VNTR) in non-coding gene regions which have been correlated with a predisposition to a variety of CNS disorders. There is considerable homology between individual DAT and SERT repeat DNA sequences, which is reflected in their ability to compete with each other for specific protein binding as demonstrated by electrophoretic mobility shift assay. The SERT VNTR has recently been shown to act as a transcriptional enhancer. Because of the similarities between SERT and DAT VNTRs, the DAT VNTR may also enhance transcription. This study demonstrates by lipid transfection into an immortalized dopaminergic cell line and biolistic transfection into dopamine neurons in neonatal rat midbrain slices that the human nine-repeat DAT VNTR can enhance transcription. This enhancing activity suggests that the DAT VNTR may play a role in regulation of DAT gene expression.

Aldehyde Oxidoreductases↗
PubMed1996

The molecular biology of preprotachykinin-A gene expression.

The expression of neuropeptides is largely tissue-specific and under strictly regulated and complex control. In view of the diversity of neuronal phenotypes, with concomitant plasticity of gene expression within any phenotype, it is obvious that there is coordinated activation and repression of genes. One of the central observations from these studies is that neuropeptide gene expression is dependent upon the combinatorial interaction of multiple transcription factors with the regulatory elements which determine mRNA synthesis. These factors mediate both tissue specific and stimulus inducible gene expression. We will illustrate some of the mechanisms that regulate neuropeptide gene expression utilizing our own studies on the rat preprotachykinin-A gene (rPPT) and, where appropriate, expand on the generality of these findings to other neuropeptide genes.

Animals↗
PubMed1993

Expression and characterization of bioactive recombinant ovine TNF-alpha: some species specificity in cytotoxic response to TNF.

We have expressed and partially purified recombinant ovine tumour necrosis factor alpha (rovTNF-alpha) using a yeast Ty, virus like particle, expression system. RovTNF-alpha is at least as active as recombinant human TNF-alpha (rhTNF-alpha) in two different bio-assays performed on ovine material, whilst approximately 1000-fold more rovrTNF-alpha than rhTNF-alpha is required to induce the same level of cytotoxicity in TNF-sensitive murine cell lines L929 and WEHI 164 clone 13. When cytotoxic assays are performed on the porcine TNF sensitive cell line PK(15)-1512, rovTNF-alpha shows about 2 logs greater activity than on murine cells, whilst rhTNF-alpha is about 1 log more active. A monoclonal antibody, raised against rovTNF-alpha, has been used to demonstrate the presence of nanogram amounts of an appropriately sized glycoprotein to be native ovine TNF-alpha in supernants of LPS stimulated ovine alveolar macrophages. These samples show no detectable cytotoxicity to L929 cells, although they show activity attributable to TNF-alpha (through neutralization by a polyclonal antiserum raised to rovTNF-alpha) in an assay on ovine material. The relative lack of activity on murine cells helps to explain previous reports of inability to assay native ovine TNF-alpha using these cells, in spite of their routine use to assay TNF-alpha from several other species. The sequence features in ovine TNF-alpha which might reduce its affinity for the murine TNF type 1 receptor are discussed.

Amino Acid Sequence↗
PubMed1978

Serum factor affecting neutrophil function during acute viral hepatitis.

Sera from eight of 17 patients with acute viral hepatitis was deficient in its ability to support neutrophil bactericidal function in vitro. This defect appeared to be related to the viral infection itself. Sera from patients with drug hepatitis or mechanical obstructive jaundice did not show this effect.

Acute Disease↗
PubMed1977

Experimental liver necrosis: hepatic erythrocyte sequestration as a cause of acute anemia.

A prospective study was undertaken to determine the cause of the acute anemia previously observed in pigs manifesting acute liver necrosis after administration of acetaminophen in dosages in excess of the LD100. A highly significant correlation was found between the degree of anemia and increase in liver weight (P less than 0.001) and a similarly significant correlation was noted between the increase in liver weight and 51Cr activity in the liver after administration of autologous erythrocytes labeled with 51Cr. Marked hepatic erythrocyte sequestration was confirmed histologically, whereas there was minimal erythrocyte accumulation in extrahepatic tissue. Erythrocyte glutathione content was not altered by acetaminophen administration. It was concluded that hepatic sequestration of erythrocytes occurred to a sufficient extent to account for the precipitous fall in hematocrit observed.

Acetaminophen↗