Dietary fat: sources of information used by men.
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Adult↗
Biomedical subjects
R D Terry
Publications and source records attributed to R D Terry.
Adherence to the cardiac diet: attitudes of patients after myocardial infarction.
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Aged↗
Increased immunoreactivity of brain spectrin in Alzheimer disease: a marker for synapse loss?
Alzheimer disease (AD) is characterized, among other pathological alterations, by an extensive synapse loss. Brain spectrin is a membrane skeleton protein found in synapses, and its immunoreactivity has been shown to increase in the rat model of denervation. In order to test the hypothesis that there is an increase in brain spectrin immunoreactivity in relation to the synapse pathology in AD, we studied brain sections and homogenates from AD and control cases and found increased anti-brain spectrin immunostaining of neurons, fibers, and plaques, with a relative decrease in the granular pattern of neuropil immunoreactivity. Western blot analysis showed a 25% increase in the 150 kDa bands (degradation products) in the cytosolic fraction and a decrease in the 240 kDa band (intact brain spectrin) in the particulate fraction. Altered immunostaining of brain sections and Western blot was not observed with an antibody against red blood cell spectrin demonstrating the specific change of brain spectrin. These results support the contention that increased brain spectrin immunoreactivity is a marker of synapse or neuronal loss and further supports the concept of synapse pathology in AD.
Alzheimer Disease↗
Aberrant casein kinase II in Alzheimer's disease.
Abnormal protein phosphorylation has been identified in Alzheimer's disease (AD) for several proteins including a Mr 60,000 protein, a Mr 86,000 protein and a microtubule-associated protein tau. The Mr 86,000 protein is phosphorylated by protein kinase C, whereas protein kinases responsible for other aberrant phosphorylation reactions are not known. In addition to protein kinase C, another kinase, casein kinase II (CK-II), has now been shown to be aberrant in AD. The spermine-dependent CK-II activity is reduced by 84% in AD and the amount of CK-II as determined by its immunoreactivity on a Western blot is reduced by 63%. Furthermore, the distribution of CK-II in AD is altered. Although the neuronal cell body reacts well with CK-II antisera in the normal cortex, the non-tangle-bearing neurons in the AD cortex showed a 15-30% decrease in anti-CK-II immunoreactivity. The neurofibrillary tangles, on the other hand, stain very strongly with rabbit anti-CK-II and indicates that CK-II may be involved in the pathology of AD. The study of CK-II immunoreactivity for dementing diseases other than AD revealed a similar reduction, suggesting the CK-II involvement in the common process of neurodegeneration.
Aged↗
Variability in the developmental toxicity of bropirimine with the day of administration.
The aim of this study was to determine the mechanism by which bropirimine exerts its developmental toxicity. This drug is an immunomodulator and interferon inducer with antiviral and antitumor activities in experimental models. Timed-pregnant Upj:TUC(SD)spf (Sprague-Dawley) rats were given a single oral (gastric intubation) dose of bropirimine at 200 or 400 mg/kg (doses as high as 100 mg/kg/day have been employed in human cancer trials) on days 5, 6, 7, 8, 9, 10, 11, or 12 of gestation and in a second experiment on day 12, 13, 14, 15, 16, 17, 18, or 19 of gestation. The dams were killed 24 hours after dosing and their uterine contents examined. In a third experiment, bropirimine (400 mg/kg) was administered on day 4 of gestation and the uteri of different groups were examined on day 8, 9, 10, 11, or 12 of gestation. Serum progesterone levels were measured at sacrifice. In the first two experiments a battery of hematologic/clinical chemistry assays also were performed. In all three experiments, bropirimine-related maternal toxicity was observed; such toxicity was characterized by significant decreases in weight gain, relative to the concurrent vehicle controls, as well as significant differences in several blood parameters including platelets, white blood cells, alanine aminotransferase, and aspartate transaminase. In the first experiment, bropirimine treatment on day 11, but not day 12, resulted in significant decreases in the mean number of live embryos per litter. In the second experiment, significant decreases in the number of live fetuses per litter occurred 24 hours after dosing on day 18 (200 and 400 mg/kg groups) or day 19 (400 mg/kg group). Decreases in serum progesterone appeared to correlate well with the embryolethal effects seen after treatment between days 6 and 11 of gestation, but not with the fetal lethality seen when treatment was given on day 17 or 18. The decreases in serum progesterone levels found most likely were the result of a luteolytic effect, although it is unknown if bropirimine has a direct or indirect effect on the corpora lutea. In the third experiment, bropirimine treatment on day 4 of gestation resulted in only slight preimplantational losses, but significant decreases were found in mean number of live embryos per litter after day 9. Uterine decidual necrosis has been observed in the first experiment where bropirimine was given on day 11; however, treatment on day 4 resulted in an apparent decrease in decidual development but not necrosis.
Animals↗
Changes in signal transduction in Alzheimer's disease.
We studied the signal transduction system including the receptor and protein kinase C (PKC) in Alzheimer's disease (AD) brains. We used 3H-TCP as a ligand for the NMDA receptor-ion channel complex. The total concentrations of 3H-TCP binding sites were significantly reduced in AD frontal cortex. 3H-TCP binding sites spared in AD brains retained the affinity for the ligand and the reactivity to NMDA, L-glutamate, and glycine. We utilized antibodies to assess the degree of involvement of different PKC isoforms in AD. The concentration of PKC (beta II) was lower in AD particulate fractions and higher in AD cytosol fractions. Immunocytochemical studies revealed reduced numbers of anti-PKC (beta II)-immunopositive neurons. Anti-PKC (alpha) faintly stained entire plaques and surrounding glial cells. Anti-PKC (beta I) stained dystrophic plaque neurites. Anti-PKC (beta II) stained the amyloid-containing portions of plaques. These results suggest an involvement of second messenger cascades in the pathogenesis of AD in addition to neurotransmitters and their receptors.
Aged↗
Nucleus basalis lesions fail to induce senile plaques in the rat.
Fourteen months after receiving bilateral ibotenic acid lesions of the nucleus basalis magnocellaris (NBM), male rats demonstrated impairment in spatial learning in a water maze task, increased incidence of high voltage spindles, and significant depletion of cortical choline acetyltransferase (ChAT) activity. Histological evaluation revealed decreased acetylcholinesterase (AChE) staining but no plaque-like structures in the cortex.
Acetylcholinesterase↗
Quantitative immunohistochemistry of synaptophysin in human neocortex: an alternative method to estimate density of presynaptic terminals in paraffin sections.
Currently available specific synaptic markers have made it possible to estimate the synaptic density by immunochemical techniques. In the present study we labeled the neocortical presynaptic terminals in histological sections of human autopsy tissue with a monoclonal antibody against synaptophysin. The characteristic granular neuropil reaction was quantified by measuring the average optical density (OD) in the different layers of the parietal cortex with the aid of image analysis equipment. The raw neuropil OD was corrected by subtracting the OD of the white matter in the same section. Our study showed that consistent microdensitometric results can be obtained on 5-microns paraffin sections from specimens with less than 8 hr of post-mortem time before fixation, incubated with 5 micrograms/ml of anti-synaptophysin. The corrected OD measurements were slightly larger in neocortical layers II, III, and V than in layers I, IV, and VI, but the differences were not statistically significant. In area 17, layer IV was denser than the others. We conclude that with certain precautions this method can be used to measure relative amounts of synaptophysin-like immunoreactivity and to infer the density of presynaptic boutons in human situations and in animal models.
Aged↗
Diffuse plaques do not accentuate synapse loss in Alzheimer's disease.
Applying the relatively new technique of laser confocal imaging, vibratome sections which were double immunolabeled for amyloid beta protein and the presynaptic terminal marker synaptophysin were examined. It was found that while synaptic density was generally diminished in Alzheimer's disease (AD) cortical neuropil as compared to controls, the reduction was no greater within the diffuse plaques than outside them. Synapse loss was accentuated, however, within immature and mature plaques. These findings suggest that the pathogenetic process in AD might commence with synapse loss and neurodegeneration rather than with deposition of amyloid beta protein.
Aged↗
Health characteristics of rural elderly Malay females in selected villages in Negeri Sembilan.
Health indices of 317 healthy elderly Malay females 55 years and older from two rural subdistricts in Negeri Sembilan were collected through personal interviews. About 33% of the respondents perceived their health condition as good to excellent, 63.4% rated their health status compared to a year earlier as about the same, 48.3% had no worry about their health, and 49.2% perceived themselves as physically active as their peers. Arthritis was the major ailment which affected the daily activities of about 64% of the respondents. The classical age-related problems of poor hearing, poor sight and difficulty in chewing were also prevalent among these elderly.
Aged↗
Normal aging and Alzheimer's disease: growing problems.
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Aging↗
Differential involvement of protein kinase C isozymes in Alzheimer's disease.
Decreased levels of protein kinase C (PKC) and a reduction in the in vitro phosphorylation of a Mr 86,000 protein (P86), the major PKC substrate, are biochemical characteristics of brain tissue from patients with Alzheimer's disease (AD) (Cole et al., 1988). In the current study, we utilized antibodies against individual isozymes of PKC to assess the degree of involvement of different PKC isoforms in AD. The concentration of PKC(beta II) was lower in particulate fractions prepared from AD hippocampal and cortical tissue than in controls and higher in AD cytosol fractions from the cortex than in controls. Immunohistochemical studies in AD neocortex revealed reduced numbers of anti-PKC(beta II)-immunopositive neurons and diminished staining intensity. In contrast, AD hippocampal neurons in CA3-CA4 were more intensely stained with anti-PKC(beta II) antiserum than were controls. The concentration of PKC(beta I) was lower in particulate fractions prepared from AD hippocampus than in controls and was higher in soluble fractions prepared from AD cortex than in controls. The concentration of PKC(alpha) was lower in AD particulate fractions than in controls in the hippocampus. Immunohistochemistry with PKC(alpha) antiserum revealed moderately intense neuron staining and an intense staining of glial cells in AD neocortex. The concentrations and histochemical distributions of PKC(gamma) were not altered in the disease. PKC immunoreactivity was also found in neuritic plaques. The staining patterns of neuritic plaques with different isoform antibodies varied considerably. Anti-PKC(alpha) faintly stained entire plaques and surrounding glial cells; anti-PKC(beta I) stained dystrophic plaque neurites; and anti-PKC(beta II) stained the amyloid-containing portions of plaques.
Aged↗
Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer disease.
Alzheimer disease (AD) as well as other dementing disorders are characterized by a continuous loss of neurons in cortical and subcortical areas and probably by an extensive synaptic loss. In order to substantiate and localize the loss of synapses in AD, we quantified by microdensitometry the neuropil immunoreactivity to an antibody that labels the protein synaptophysin (p38), which is localized in the presynaptic terminals. We found in the AD cases an average 50% decrease in the density of the granular neuropil immunoreaction in parietal, temporal and midfrontal cortex. In contrast, Pick disease cases presented close to normal values in parietal cortex, but major losses in temporal and frontal cortex. Our data strongly suggest an important role of synapse loss in dementia.
Aged↗
An antiserum against amyloid beta-protein precursor detects a unique peptide in Alzheimer brain.
An antiserum was raised against an amino acid sequence predicted from the DNA sequence of amyloid beta-protein precursor (ABPP), and it was then affinity-purified. This affinity-purified antibody (anti-GID) intensely stained neurons and dystrophic neurites in plaques of Alzheimer's disease (AD) patients, but marginally stained neurons of age-matched normal individuals. Anti-GID antibody detected a series of protein bands with a molecular weight centered at 100,000 and a second band at 55,000 on a blot of the human brain particulate fraction. It also stained a set of bands with a molecular weight around 95,000 and a doublet of Mr 16,000 in the soluble fraction. A band at Mr 35,000 was detected in the soluble fraction prepared from brain tissue of AD patients but not from control brain tissue. A strong immunostaining of AD sections with anti-GID and the presence of a Mr 35,000 band unique to AD might reflect an altered processing of ABPP in AD brains.
Alzheimer Disease↗
A neuropathological subset of Alzheimer's disease with concomitant Lewy body disease and spongiform change.
The neuropathological heterogeneity of Alzheimer's disease (AD) is increasingly recognized. Diffuse Lewy body disease, for example, most frequently occurs in cases fulfilling histopathological criteria for AD, and these patients usually present with dementia rather than parkinsonism. We report five cases of concomitant AD and diffuse Lewy body disease with still another coexistent neuropathological feature: localized and stereotyped spongiform change in the neuropil. This spongiform change was most striking in the superior and inferior temporal, entorhinal, and insular cortex and the amygdala and was virtually indistinguishable from that seen in Creutzfeldt-Jakob disease. Electron microscopic study on one case revealed membrane-containing vacuoles in close association with neuritic plaques and plaired helical filament-filled processes. Immunocytochemistry using antibodies to prion proteins (PrPsc or PrP27-30) failed to label plaque or vascular amyloid in the five cases. Four primates inoculated with brain tissue from one case have not evidenced neurological disease in the 3 years since the transmission experiment. We conclude that these cases represent a neuropathological subset of AD with relatively widespread Lewy bodies and a localized spongiform change, predominantly involving the medial temporal region. Despite the light and electron microscopic commonality with Creutzfeldt-Jakob disease, there is no clear evidence that these cases represent a form of transmissible spongiform encephalopathy.
Aged↗
Substance P and somatostatin coexist within neuritic plaques: implications for the pathogenesis of Alzheimer's disease.
In recent years the present authors and others have sought to determine the neurochemical composition of the dilated neuronal processes found within neuritic plaques of patients with Alzheimer's disease. To date a number of neurotransmitter and neuropeptide systems have been observed within different plaques, yet at present it is unclear whether individual human plaques contain more than one transmitter substance. In the present study a highly sensitive dual-immunolabeling procedure was employed and it was demonstrated that substance P and somatostatin-immunoreactive profiles coexist within single senile plaques of patients with Alzheimer's disease. Coexistence of somatostatin and substance P immunoreactivity within plaques was observed in the hippocampus and amygdala but not in the neocortex, although the latter region contained plaques within which somatostatin and substance P existed alone. The frequency with which we observed one or more neuropeptide within plaques was relatively low and in fact most plaques contained neither substance P nor somatostatin immunoreactivity. In addition, a large number of swollen peptidergic processes were observed outside of plaques. The significance of these observations with respect to the pathogenesis of Alzheimer's disease is discussed.
Aged↗
Tissue plasminogen activator-mediated thrombolysis of cerebral emboli and its effect on hemorrhagic infarction in rabbits.
Tissue plasminogen activator (tPA) dissolves intravascular thrombus and restores blood flow after thromboembolic vascular occlusion. The utility of this agent for treatment of stroke in humans may be limited by post-reperfusion hemorrhagic complications. We studied tPA-mediated thrombolysis in an animal model of cerebrovascular occlusion in order to determine what factors, if any, predispose tPA-treated animals to suffer hemorrhage. Small blood clot emboli were injected into the internal carotid arteries of rabbits. Angiograms confirmed occlusion of the middle cerebral artery or internal carotid artery in 100% of subjects. tPA or saline was administered as a 30-minute infusion at various times after embolization. Hemorrhage rates were similar in all groups regardless of treatment. tPA increased the prothrombin time and the thrombin time but not the partial thromboplastin time. There was no correlation between these changes in blood coagulation and the finding of cerebral hemorrhage. We observed a significant association between stroke severity and cerebral hemorrhage. We conclude that tPA treatment successfully causes thrombolysis of cerebral emboli without causing an increase in the incidence of cerebral hemorrhage in rabbits.
Animals↗
Developing a strategy for understanding adolescent nutrition concerns.
Disseminating nutrition information that adolescents will incorporate into their lives has been a difficult challenge for nutrition educators. The communication of such information has often been a "one-way street"; adolescents are given information that educators feel they need to have. Researchers contend that a more effective way to communicate is for adolescents to describe what they need to know in order to relate nutrition messages to their own worlds. A research model based on Brenda Dervin's work with the "sense-making" theory of communication was used to better determine adolescents' perceived nutrition concerns. Adolescents aged 14 to 16 across six states were interviewed to record personal situations they experienced concerning food, nutrition, and/or eating. Situation "movement states" were identified to determine the qualitative ways in which the adolescents perceived themselves as dealing with the situations they described. Data indicate that this theoretical base may be used by nutrition educators to identify adolescents' nutrition needs and to design appropriate education materials.
Adolescent↗