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Biomedical subjects

K Kidd

Publications and source records attributed to K Kidd.

11 recordsLinked to original sources
PubMed1999

Neurotrophic factors BDNF and GDNF protect embryonic chick spinal cord motoneurons from ethanol neurotoxicity in vivo.

Maternal consumption of ethanol is widely recognized as a leading cause of mental and physical deficits. Many populations of the central nervous system are affected by the teratogenic effects of ethanol. Neurotrophic factors (NTFs) have been shown to protect against ethanol neurotoxicity in culture, although there have been no demonstrations of such protection in vivo, in specific neuronal populations. Previous studies have demonstrated that ethanol is toxic to developing chick embryo motoneurons when administered from embryonic day 10 (E10) to E15. NTFs such as brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) have been shown to support developing spinal cord motoneurons, and when exogenously applied, decrease naturally occurring cell death, and protect against axotomy. The concurrent delivery of BDNF or GDNF with ethanol to the embryonic chick from E10 to E15 was designed to examine the capacity of these NTFs to provide in vivo neuroprotection for this ethanol-sensitive motoneuron population. Analysis of motoneuron numbers indicated that both BDNF and GDNF provided protection to developing spinal cord motoneurons from ethanol toxicity, restoring motoneuron numbers to control levels. This study represents the first demonstration of in vivo neuroprotection from ethanol toxicity with respect to specific neuronal populations.

Animals↗
PubMed1996

DNA workbench: a database package to manage regional physical mapping.

DNA Workbench (DW) is a client-server database to manage physical mapping data that will form the basis for sequencing and efforts in biologically interesting regions of a chromosome. DW draws maps at different levels of resolution in either of two modes: proportional, when the sizes of objects and the physical distances between them are known accurately or approximately, and nonproportional, when most physical distance information in a region is not available, but order information is. DW interacts with the user primarily through the map graphic. Selection of individual objects on the graphic lets the user inspect and modify the underlying data. DW also manages dependency tracking between map objects and has a rudimentary form of version control. It is currently used to manage information on the DRD2 region on chromosome 11, and on the HOX region of chromosome 17.

Chromosome Mapping↗
PubMed1995

The CEPH consortium linkage map of human chromosome 16.

A Centre d'Etude du Polymorphisme Humain (CEPH) consortium map of human chromosome 16 has been constructed. The map contains 158 loci defined by 191 different probe/restriction enzyme combinations or primer pairs. The marker genotypes, contributed by 9 collaborating laboratories, originated from the CEPH families DNA. A total of 60 loci, with an average heterozygosity of 68%, have been placed on the framework genetic map. The genetic map contains 7 genes. The length of the sex-averaged map is 165 cM, with a mean genetic distance between loci of 2.8 cM; the median distance between markers is 2.0 cM. The male map length is 136 cM, and the female map length is 197 cM. The map covers virtually the entire chromosome, from D16S85, within 170 to 430 kb of the 16p telomere, to D16S303 at 16qter. The markers included in the linkage map have been physically mapped on a partial human chromosome 16 somatic cell hybrid panel, thus anchoring the genetic map to the cytogenetic-based physical map.

Animals↗
PubMed1993

Glutathione depletion increases the cytotoxicity of melphalan to PC-3, an androgen-insensitive prostate cancer cell line.

Prostate cancer that is androgen-insensitive is unresponsive to a wide spectrum of cytotoxic agents, including all of the alkylating agents. Since a major pathway for the detoxification of the alkylating agents is conjugation with glutathione (GSH), GSH depletion has proved to be effective as a technique to restore melphalan sensitivity in melphalan-resistant cancer cell lines. However, the effect of GSH depletion has not been widely studied in tumor cell lines that have not developed resistance due to previous exposure to alkylating agents. Thus, we decided to investigate GSH depletion as a technique to increase melphalan cytotoxicity to PC-3 cells, an androgen-insensitive prostate cancer line. After 2 and 6 h incubation with 0.25-5 microM melphalan, virtually no effect was observed on either clonogenic lethality or MTT viability until 5 microM exposures. A 24-h incubation of the cells with 100 microM buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, reduced the GSH content by 70%-75%. Following GSH depletion, an increase in clonogenic lethality and a decrease in MTT viability occurred after exposure to concentrations as low as 0.25 microM. The dose modification factor ranged from 2.9 after 2 h incubation to 4.5 at 6 h. These results provide support for additional studies in prostate cancer for further investigation of GSH depletion as a technique to induce sensitivity to alkylating agents in this chemotherapy-resistant tumor.

Buthionine Sulfoximine↗
PubMed1993

Interfaces between host and uncemented femoral hip prostheses.

The authors analyzed 200 uncemented hip prostheses that were retrieved. They determined the type and extent of host-implant interfaces, but found little correlation between subjective pain relief and the histology of the interfaces. Wear debris, bone resorption and looseness were related to pain, although even with these the relationship was not statistically significant.

Alloys↗
PubMed1990

Strong linkage disequilibrium between the XY274 polymorphism and the pseudoautosomal boundary.

The pseudoautosomal boundary is defined by an Alu repeat element on the Y chromosome. The Alu element is found on all Y chromosomes and on no X chromosomes, establishing it as part of Y-specific sequences. Distal to the Alu element, sequences from the X and Y are strictly homologous, suggesting that the boundary is formed by an abrupt break in sequence homology. Further investigation of the function of the boundary has been undertaken by examining the population structure of an MspI restriction-site polymorphism (XY274), which is located 274 bp distal to the Alu insertion site. Southern blot and polymerase chain reaction analysis demonstrate fixation of the high allele (noncutting or AT base pair) of XY274 on the Y chromosome in most populations, while a full range of high allele frequencies is found on the X chromosomes of different populations. Two exceptions to fixation on the Y chromosome were found in African populations. The level of linkage disequilibrium suggests that the first few hundred base pairs of the pseudoautosomal region on the Y chromosome share a single common origin more recent than the origin of the species.

Base Sequence↗
PubMed1989

Outbreak of multiply resistant Staphylococcus aureus in a pediatric intensive care unit after consolidation with a surgical intensive care unit.

Patients in a pediatric intensive care unit were placed with patients in an adult surgical intensive care unit (SICU) in a large, 12-bed room previously occupied exclusively by the adult patients. The occurrence of multiply resistant Staphylococcus aureus (MRSA) in pediatric patients increased from zero cases during the preceding 12 months to seven cases (p less than 0.001) for the 95 days that the units were combined. The rate of acquisition of MRSA by the patients in the SICU remained unchanged. Pediatric patients who acquired MRSA had longer lengths of stay (p less than 0.001) and underwent more surgical (p less than 0.01) and invasive procedures than did pediatric patients who did not acquire MRSA. Removal of the pediatric patients to their own unit returned their rate of MRSA acquisition to the previous low level.

Adult↗
PubMedDate not supplied

Apparent monomorphism of ALDH2 in seven American Indian populations.

Deficiency of mitochondrial aldehyde dehydrogenase (ALDH2) has been previously reported in South American Indians. We therefore assayed five individuals from each of five South American Indian populations (Quechua, Karitiana, Ticuna, Surui, Guahiba), and two North American populations (Maya and Moskoke) for the presence of the Oriental ALDH2(2) variant. These samples were also surveyed for other alleles altering ALDH2 function. Allele-specific amplification assay (ASA) did not detect the ALDH2(2) allele in any of the New World populations studied. The entire coding sequence of the ALDH2 cDNA was enzymatically amplified in partially overlapping fragments. Each fragment was digested using restriction endonucleases and subfragments 148-285 b.p. in length were analyzed by the single-stranded conformation polymorphism (SSCP) technique. No variants were detected within the coding region of the ALDH2 gene in any of the seven American Indian populations. Three potentially correct explanations for these results are suggested. First, an ALDH2 polymorphism is present but undetectable by SSCP; second, none of the studied individuals were ALDH2 negative; third, the polymorphism occurs beyond the coding region of ALDH2 gene.

Aldehyde Dehydrogenase↗