Search PubMed⌕ Search

Biomedical subjects

T Walker

Publications and source records attributed to T Walker.

At least 19 recordsLinked to original sources
PubMed2000

Trophic actions of neurotrophin-3 on postnatal rat myenteric neurons in vitro.

A number of neurotrophic factors have been implicated in the prenatal development of the enteric nervous system. Although several of these factors continue to be expressed in the gut during postnatal life, their actions on postnatal enteric neurons are not understood. One such factor is the neurotrophin, NT-3. Both NT-3 and its high affinity receptor, trk C, are expressed in the postnatal gut at a time when changes in the density of intestinal innervation are occurring. We have therefore examined the effects of NT-3 on postnatal myenteric neurons, using dissociated cell cultures of ganglia isolated from 6-8 day postnatal rat small intestine. Effects of NT-3 on neurite outgrowth and neuronal and glial cell numbers were measured after 2 days in vitro. The proportion of neurons was increased in NT-3 treated cultures, as was the proportion of neurons that extended processes. NT-3 treatment, at concentrations of between 0.1 ng and 10 ng/ml, also resulted in a significant increase in mean total neurite length. These results indicate that NT-3 may play a role in the postnatal development of the enteric nervous system.

Animals↗
PubMed1999

Decreased brain infarct following focal ischemia in mice lacking the transcription factor E2F1.

E2F1+/- mice subjected to 2 h middle cerebral artery occlusion developed an infarct of 77.0 +/- 3.2 mm3 (mean +/- s.e.m., n = 15) in the ischemic hemisphere after 24 h reperfusion. A significantly smaller infarct of 58.8 +/- 4.8 mm3 (n = 15; p < 0.01) was found in E2F1-/- animals. Both deficient and normal mice had similar cerebral angioarchitecture and intra-ischemic decreases in regional blood flow. Similar areas of hypoxia in both groups of ischemic animals were demonstrated directly by immunohistochemical detection of nitroimidazole adducts. It was concluded that all animals received the same ischemic insult, yet the subsequent damage was different in the mutant mice. This is the first indication that the E2F1 gene plays a role in ischemic death of post-mitotic neurons.

Animals↗
PubMed1999

Bone grafts.

Bone grafting provides a method of enhancing bone healing in veterinary orthopedic patients. Specifically, autogenous cancellous bone graft provides the cellular components and matrix proteins that can accelerate bone healing, dramatically. Allografts provide immediate mechanical support for fracture repair and patient function, but these grafts do not create the osteogenic environment seen with the use of autogenous cancellous bone graft. Xenograft bone implants may also hold a place for use in fracture management. With the advent of recombinant bone-derived tissue growth factor technology, bone grafting may some day become a practiced technique of the past. For now, however, bone grafting still holds a strong place in orthopedic surgery when dealing with bone defects in animals.

Animals↗
PubMed1999

Langerhans' cell histiocytosis--a rare cause of sudden onset unilateral sensorineural hearing loss.

Langerhans' cell histiocytosis is a rare disorder of unknown aetiology in which pathological Langerhans' cells accumulate and destroy local tissue. We report a 38-year-old female who presented with a sudden onset of left sensorineural hearing loss. Magnetic resonance imaging (MRI) revealed a contrast-enhancing lesion in the left mastoid and a second lesion in the hypothalamus. Following left mastoid exploration and biopsy a definitive diagnosis of Langerhans' cell histiocytosis was made and the patient was treated with external beam radiotherapy. Subsequent right femur and right mastoid involvement were successfully treated with steroids and cytotoxic chemotherapy. At one year follow-up the patient had residual left-sided sensorineural hearing loss with normal hearing in the right ear. To our knowledge, Langerhans' cell histiocytosis has not been previously reported as a cause of unilateral sudden onset sensorineural hearing loss. It should be considered in the differential diagnosis of this condition.

Adult↗
PubMed1999

Activation of DNA-dependent protein kinase may play a role in apoptosis of human neuroblastoma cells.

Treating SH-SY5Y human neuroblastoma cells with 1 microM staurosporine resulted in a three- to fourfold higher DNA-dependent protein kinase (DNA-PK) activity compared with untreated cells. Time course studies revealed a biphasic effect of staurosporine on DNA-PK activity: an initial increase that peaked by 4 h and a rapid decline that reached approximately 5-10% that of untreated cells by 24 h of treatment. Staurosporine induced apoptosis in these cells as determined by the appearance of internucleosomal DNA fragmentation and punctate nuclear morphology. The maximal stimulation of DNA-PK activity preceded significant morphological changes that occurred between 4 and 8 h (40% of total number of cells) and increased with time, reaching 70% by 48 h. Staurosporine had no effect on caspase-1 activity but stimulated caspase-3 activity by 10-15-fold in a time-dependent manner, similar to morphological changes. Similar time-dependent changes in DNA-PK activity, morphology, and DNA fragmentation occurred when the cells were exposed to either 100 microM ceramide or UV radiation. In all these cases the increase in DNA-PK activity preceded the appearance of apoptotic markers, whereas the loss in activity was coincident with cell death. A cell-permeable inhibitor of DNA-PK, OK-1035, significantly reduced staurosporine-induced punctate nuclear morphology and DNA fragmentation. Collectively, these results suggest an intriguing possibility that activation of DNA-PK may be involved with the induction of apoptotic cell death.

Apoptosis↗
PubMed1999

Y2K (year 2000)

Explore the source record for details and available documents.

Forecasting↗
PubMed1999

Use of telerehabilitation to manage pressure ulcers in persons with spinal cord injuries.

Pressure ulcers are a common and serious secondary complication of spinal cord injury. In addition to being costly and difficult to treat, pressure ulcers may interfere with many aspects of patient and family life, including the ability to meet educational, vocational, and social goals. Treatment of pressure ulcers includes weekly assessment by a clinician, a requirement that often is impossible for clients to meet. In an effort to improve outcomes in wound care treatment, a rehabilitation center undertook an exploratory project to determine whether wound care via telerehabilitation was a viable alternative to clinic visits. Telerehabilitation is the use of telecommunication technology to deliver rehabilitation services at a distance. Eight patients being followed in the outpatient clinic participated in the project. The Picasso Still-Image Videophone was used to capture and send images from the patients' homes to the clinic. Findings from the exploratory study demonstrated that pressure ulcers can be successfully managed via telerehabilitation.

Adult↗
PubMed1997

Inositol phospholipid 3-kinase is activated by cellular stress but is not required for the stress-induced activation of glucose transport in L6 rat skeletal muscle cells.

A characteristic response of cells subjected to a stress stimulus is a rapid activation of cellular glucose transport. The mechanisms governing this increase in glucose transport are poorly understood, but it has been suggested that the response may involve the intracellular-signaling components that also participate in the hormonal activation of glucose transport. In skeletal muscle and fat tissue, inositol phospholipid 3-kinase plays an integral role in the regulation of both basal and insulin-stimulated glucose transport. In this study, we have investigated whether inositol phospholipid 3-kinase is activated by chemical stress and, if so, whether it has a role to play in the stress-induced increase in glucose transport in L6 muscle cells. Furthermore, we have attempted to assess the basis by which inositol phospholipid 3-kinase may participate in the regulation of basal glucose transport. Acute exposure (30 min) of L6 muscle cells to 0.5 mM arsenite induced an 80% stimulation in glucose transport. This activation was due to a rise in the number of cell-surface glucose transporters, based on an increase in the Vmax of glucose transport and the observation that arsenite increases the plasma membrane content of GLUT1 and GLUT4 glucose transporters by 95% and 60%, respectively, from an intracellular compartment. Arsenite induced rapid activation (< 2 min) of inositol phospholipid 3-kinase with an approximately fourfold increase in phosphatidylinositol 3,4,5-trisphosphate (PtdIns3,4,5P3). In contrast, phosphatidylinositol 3-phosphate (PtdIns3P) levels were unaffected. Prior treatment of L6 cells with 100 nM wortmannin suppressed the arsenite-induced increase in PtdIns3,4,5P3 and reduced the cellular content of PtdIns3P by 50%. Under these conditions however, wortmannin failed to prevent the stress-induced activation of glucose transport, but suppressed basal glucose transport by 60% with an IC50 of about 10 nM. In the absence of arsenite, wortmannin caused a dose-dependent inhibition in the cellular levels of PtdIns3P and PtdIns3,4,5P3 with IC50 values of about 10 nM and 100 nM, respectively. In summary, the present results demonstrate that chemical stress activates inositol phospholipid 3-kinase and glucose transport in L6 muscle cells, but unlike the hormonal responses of these cells the activation of inositol phospholipid 3-kinase is not responsible for the stress-induced increase in glucose transport. This implies that stress-induced and hormonal stimulated increases in PtdIns3,4,5P3 levels are functionally distinct. By contrast, the maintenance of PtdIns3P levels, presumably involving a PtdIns-specific, wortmannin-sensitive inositol phospholipid 3-kinase may be required to support basal glucose transport.

Androstadienes↗
PubMed1997

Glutamate-treated rat cortical neuronal cultures die in a way different from the classical apoptosis induced by staurosporine.

The alkaloid protein kinase inhibitor staurosporine induced neuronal cell death with both the morphological and the biochemical characteristics of apoptosis. The punctate chromatin associated with apoptosis with retention of plasma membrane integrity was observed in neurons identified by colocalization of NeuN staining. Such cells had DNA fragmentation visualized by in situ end-labeling which was seen as a laddered pattern upon gel electrophoresis. In contrast cells treated with glutamate did not exhibit either of these morphological or biochemical hallmarks of apoptosis. Instead a much smaller and more compact pyknotic structure was observed associated with smeared DNA fragmentation patterns. A confocal time-lapse study of the appearance of the morphological changes in individual nuclei after staurosporine treatment showed collapse into punctate chromatin over a period of 10 min. In contrast, the collapse into small pyknotic nuclei after glutamate treatment was at least 10 times slower. It is concluded that excitotoxicity produced by glutamate did not induce cell death by an apoptotic mechanism in cultured cortical neurons.

Animals↗