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Biomedical subjects

C Palmer

Publications and source records attributed to C Palmer.

At least 37 records · Page 2Linked to original sources
PubMed2000

Conceptual and motor learning in music performance.

Are the mental plans for action abstract or specified in terms of the movements with which they are produced? We report motor independence for expert music performance but not for novice performance in a transfer-of-learning task. Skilled adult pianists practiced musical pieces and transferred to new pieces with the same or different motor (hand and finger) requirements and conceptual (melodic) relations. Greatest transfer in sequence duration was observed when the same conceptual relations were retained from training to transfer, regardless of motor movements. In a second experiment, novice child pianists performed the same task. More experienced child pianists showed transfer on both the motor and the conceptual dimensions; the least experienced child pianists demonstrated transfer only to sequences with identical motor and conceptual dimensions. These findings suggest that mental plans for action become independent of the required movements only at advanced skill levels.

Adult↗
PubMed2000

Regional body composition changes in women after 6 months of periodized physical training.

Data are lacking regarding regional morphological changes among women after prolonged physical training. This study employed dual-energy X-ray absorptiometry to assess changes in whole body and regional (i.e., trunk, legs, arms) fat mass, lean mass, and bone mineral content body composition adaptations in 31 healthy women pre-, mid-, and post-6 mo of periodized physical training. These results were compared with those of 1) a control group of women who had not undergone the training program and were assessed pre- and post-6 mo and 2) a group of 18 men that was tested only once. Additionally, magnetic resonance imaging was used to assess changes in muscle morphology of the thigh in a subset of 11 members of the training group. Physical training consisted of a combination of aerobic and resistance exercise in which the subjects engaged for 5 days/wk for 24 wk. Overall, the training group experienced a 2.2% decrease, a 10% decrease, and a 2.2% increase for body mass, fat mass, and soft tissue lean mass, respectively. No changes in bone mineral content were detected. The women had less of their soft tissue lean mass distributed in their arms than did the men, both before and after the women were trained. Novel to this study were the striking differences in the responses in the tissue composition of the arms (31% loss in fat mass but no change in lean mass) compared with the legs (5.5% gain in lean mass but no change in fat mass). There was a 12% fat loss in the trunk with no change in soft tissue lean mass. Dual-energy X-ray absorptiometry and magnetic resonance imaging fat mass measurements showed good agreement (r = 0. 72-0.92); their lean mass measurements were similar as well, showing approximately 5.5% increases in leg lean tissue. These findings show the importance of considering regional body composition changes, rather than whole body changes alone when assessing the effects of a periodized physical training program.

Absorptiometry, Photon↗
PubMed2000

Reduction of hypoxic-ischemic brain swelling in the neonatal rat with PAF antagonist WEB 2170: lack of long-term protection.

Platelet activating factor (PAF) is an inflammatory lipid mediator released by ischemic brain. Our objectives were to use an inhibitor of PAF that does not readily cross the blood-brain barrier, WEB 2170, to study the role of intravascular PAF on brain swelling and subsequent brain atrophy in a neonatal rat model of hypoxic-ischemic brain injury. We injured the right cerebral hemisphere of 7-d-old rats by ligating the right common carotid artery and exposing the rats to 8% oxygen for 2.25 h. Forty-two rats received saline or the PAF antagonist WEB 2170, 1 h before hypoxia. We found that WEB 2170 pretreatment reduced swelling by 64% (p = 0.003). In contrast, treatment immediately after hypoxic-ischemic injury did not reduce swelling. In two additional experiments involving 103 rats, we found that pretreatment or repeated doses of PAF antagonist before and after hypoxic-ischemic injury did not reduce atrophy. We also found that the brain-penetrating PAF antagonist, BN 52021, did not prevent atrophy in our Wistar rat model. In conclusion, we were unable to reduce long-term brain injury with either PAF antagonist. WEB 2170 pretreatment reduced brain swelling by 64% without reducing atrophy. This suggests that although brain swelling may accompany cerebral infarction, it does not contribute to the pathogenesis of infarction and subsequent atrophy in the neonatal rat. The ability to reduce early postischemic brain swelling without reducing atrophy may be particularly unique to the immature animal with a compliant skull.

Animals↗
PubMed1999

Preface

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Journal Article↗
PubMed1999

Changes in iron histochemistry after hypoxic-ischemic brain injury in the neonatal rat.

Iron can contribute to hypoxic-ischemic brain damage by catalyzing the formation of free radicals. The immature brain has high iron levels and limited antioxidant defenses. The objective of this study was to describe the early alterations in nonheme iron histochemistry following a hypoxic-ischemic (HI) insult to the brain of neonatal rats. We induced a HI insult to the right cerebral hemisphere in groups of 7-day-old rats. Rats were anesthetized, then their brains were perfused and fixed at 0, 1, 4, 8, 24 hr, and 1, 2, and 3 weeks of recovery. Forty-micron-thick frozen sections were stained for iron using the intensified Perls stain. Increased iron staining was first detected within the cytoplasm of cells with pyknotic nuclei at 4 hr of recovery. Staining increased rapidly over the first 24 hr in regions of ischemic injury. By 7 days recovery, reactive glia and cortical blood vessels also stained. Increased staining in gray matter persisted at 3 weeks of recovery, whereas white matter tracts had fewer iron-positive cells compared to normal. The early increase in iron staining could be caused by an accumulation of iron posthypoxicischemic injury or a change in iron from nonstainable heme iron to stainable nonheme iron. Regardless of the source, our results indicate that there is an increase in iron available to promote oxidant stress in the neonatal rat brain following hypoxia-ischemia.

Animals↗
PubMed1999

Rat model of perinatal hypoxic-ischemic brain damage.

To gain insights into the pathogenesis and management of perinatal hypoxic-ischemic brain damage, the authors have used an immature rat model which they developed many years ago. The model entails ligation of one common carotid artery followed thereafter by systemic hypoxia. The insult produces permanent hypoxic-ischemic brain damage limited to the cerebral hemisphere ipsilateral to the carotid artery occlusion. The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia. Future research will focus on molecular mechanisms of neuronal injury with a continuing focus on therapeutic strategies to prevent or minimize hypoxic-ischemic brain damage.

Animals↗
PubMed1999

Paradoxical labeling of radiosurgically treated quiescent tumors with Ki67, a marker of cellular proliferation.

Ki67 (also known as MIB) is a monoclonal antibody staining agent, which is routinely used as a marker of cellular proliferation. It is used to evaluate the proliferative potential of malignant tumors, since it is thought to stain only those cells undergoing active division. The paradoxical elevation of the Ki67 labeling index observed in radiosurgically treated benign and malignant tumors is reported. Ten patients, who had previously undergone either linac or Gamma Knife radiosurgery, underwent surgical resection for a radiographically quiescent tumor. One patient underwent autopsy after dying from complications of radiosurgery. All were thought to be suffering from adverse radiation effect (ARE) and were refractory to conservative management. None were thought to have a recurrent tumor. All of the resected tumors were subjected to analysis with Ki67 staining. Despite the radiographic stability of the tumors, all manifested significantly elevated populations of cells exhibiting positivity for Ki67 antigen. This staining pattern would suggest a significant proliferative potential, which did not match the observed clinical course. The literature is reviewed and possible mechanisms to explain the paradoxical findings are presented.

Adenocarcinoma↗
PubMed1999

Temporal lobe developmental malformations and hippocampal sclerosis: epilepsy surgical outcome.

BACKGROUND: Temporal lobe developmental malformations coexist with mesial temporal sclerosis in the form of dual pathology with a high frequency of bilateral amygdala or hippocampal abnormalities. OBJECTIVE: The aim of this study was to correlate and compare the MRI findings and the surgical outcome in patients with temporal lobe developmental malformations (n = 20) and isolated mesial temporal sclerosis (n = 36). METHODS: MRI-based normalized volumetry of the amygdala and hippocampal formation in patients with unilateral temporal lobe developmental malformations and isolated mesial temporal sclerosis who underwent temporal lobe resections was performed. Seizure outcome was compared between groups at follow-up. RESULTS: The frequency of bilateral hippocampal or amygdala atrophy (p < 0.04) and combined hippocampal-amygdala atrophy (p < 0.02) was higher in patients with temporal lobe developmental malformations. Although no significant difference in postsurgical seizure-free status was found between the temporal lobe developmental malformations and isolated mesial temporal sclerosis groups (70% versus 91%), patients with temporal lobe developmental malformations and bilateral amygdala or hippocampal-amygdala atrophy had a significantly worse outcome (p < 0.02). CONCLUSION: Bilateral hippocampal atrophy is frequent in patients with temporal lobe developmental malformations. However, it is the presence of bilateral amygdala or amygdalo-hippocampal atrophy that is associated with a higher risk of seizure recurrence.

Adolescent↗
PubMed1998

Cellular distribution of ferritin subunits in postnatal rat brain.

The normal development of the brain requires finely coordinated events, many of which require iron. Consequently, iron must be available to the brain in a timely manner and in a bioavailable form. However, the brain also requires stringent mechanisms to protect itself from iron-induced oxidative damage. The protein that is best suited to making iron available but also adequately protecting the cell is the intracellular iron storage protein ferritin. Typically, ferritin is composed of 24 subunits of H and L chains, which are functionally distinct. This study was undertaken to determine the expression of ferritin subunits during normal development of the postnatal rat brain. There is a shift in ferritin-containing cell types during development from predominantly microglia at postnatal day 5 (PND 5) to predominantly oligodendrocytes by PND 30. At PND 5, microglia are found throughout gray and white matter areas of the brain, but only amoeboid microglia in discrete foci in the subcortical white matter are ferritin positive. At PND 15, some oligodendrocytes in the subcortical white matter express ferritin, but the majority of ferritin-containing cells within white matter are still microglia. By PND 30, the predominant ferritin-containing cell type within white matter are oligodendrocytes. Generally, the cellular distribution of both ferritin subunits were identical with one major exception; H-ferritin, but not L-ferritin, was present in neuronal nuclei in the cortex. These data suggest that microglia play a role in brain iron homeostasis during normal postnatal development and may influence myelination by competing with oligodendrocytes for iron.

Animals↗
PubMed1998

Primary structure of ovine fibroblast growth factor-1 deduced by protein and cDNA analysis.

The amino acid sequence of full-length ovine fibroblast growth factor-1 (FGF-1) was determined by a combination of protein and cDNA sequencing. FGF-1 cDNA analysis indicated that ovine kidney cells express mRNAs encoding both full-length FGF-1 and a truncated FGF-1 variant. An overall comparison of the ovine FGF-1 primary sequence to the eight species studied to date revealed a high degree of conservation, with ovine FGF-1 sharing 90 and 95% sequence identity with human FGF-1 and bovine FGF-1, respectively. Additionally, the FGF-1 proteins from the various species have conserved cysteine residues at positions 30 and 97 and contain acetylated amino-terminal alanine residues. Mass spectrometry analysis confirmed that the blocking group of ovine FGF-1 is also consistent with that of an acetyl-moiety. In contrast to the other FGF-1 proteins, the 154 residue primary sequence of ovine FGF-1 contains three unique amino acid differences: Arg9, Arg44, and Ile123. Ovine FGF-1, unlike human FGF-1, is a potent mitogenic factor for NIH 3T3 fibroblasts in the absence of heparin. In the presence of exogenous heparin, the mitogenic activity of ovine FGF-1 is potentiated slightly.

3T3 Cells↗