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Biomedical subjects

M A Smith

Publications and source records attributed to M A Smith.

At least 235 records · Page 13Linked to original sources
PubMed1999

Greater stroke rate during hospitalization for acute heart disease among Mexican Americans than non-Hispanic whites.

BACKGROUND AND PURPOSE: This study compared the risk for stroke during acute myocardial infarction (AMI), percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG) between Mexican Americans (MAs) and non-Hispanic whites. METHODS: We examined the age-specific rate ratios (RR) of acute stroke during hospitalization for AMI, CABG and PTCA in a population-based study in Corpus Christi, Tex. by searching the cardiac surveillance data for ICD-9 codes for stroke (430-437). ICD-9 stroke codes were validated by comparing medical chart abstraction with ICD-9 discharge diagnoses. RESULTS: Stroke codes were found in 220 of the 5,697 admissions for AMI, CABG and PTCA. In the 45- to 59-year age-group MAs had a RR of 2.66 (95% CI 1.36-5.23) relative to non-Hispanic whites. In the 60- to 74-year age-group the RR was 1.52 (95% CI 1.11-2.08). There were no significant differences in the 25- to 44-year age-group. These ethnic relationships were found in nondiabetics but not in diabetics. Women in the 45- to 59-year age-group had a RR of 1.88 (95% CI 1.09-3.25) compared with men, but there were no significant sex differences in the 25- to 44- or 59- to 74-year age-groups. Stroke ICD-9 codes have a poor positive predictive value for acute stroke ranging from 10 to 76%. The stroke misclassifications were nondifferential with respect to ethnicity or sex. CONCLUSIONS: MAs have a higher stroke rate complicating acute heart disease in Corpus Christi. A rigorous stroke surveillance project is needed to study the burden of stroke in MAs, the United States' largest Hispanic population.

Adult↗
PubMed1999

Role of oxidative stress in frontotemporal dementia.

Recent reports have established oxidative stress and damage as playing a role in the pathogenesis of a number of neurodegenerative diseases including Alzheimer disease, Parkinson disease, corticobasal degeneration, Pick's disease and Alexander's disease. Here we present evidence that oxidative damage is also one of the earliest cytopathological markers of neuronal dysfunction in frontotemporal dementia.

Biomarkers↗
PubMed1999

Race/ethnicity and location of stroke mortality: implications for population-based studies.

BACKGROUND AND PURPOSE: Stroke community surveillance projects often focus on hospital data rates. We hypothesized that not including strokes which occurred in nursing homes or at home would differentially affect race/ethnic stroke rates. METHODS: Texas vital statistics data were studied to compare age-specific (45 to 59, 60 to 74, and >/=75 years) location of stroke death for African Americans (AAs), Hispanic Americans (HAs), and non-Hispanic whites (NHWs). Rate ratios are reported with 95% CIs; NHW is used as the referent group. RESULTS: During 1991 to 1996, there were 52 996 stroke deaths in Texas for individuals aged 45 years and older. HAs in the oldest age group (>/=75 years) were 33% more likely than NHWs to die in the hospital, and HAs aged 45 to 59 and 60 to 74 years were 4% and 10%, respectively, more likely to die in the hospital. AAs aged >/=75 years were 19% more likely to die in the hospital. HAs aged 60 to 74 years were 35% less likely to die in a nursing home, whereas HAs aged >/=75 years were 43% less likely than NHWs to die in a nursing home. AAs aged >/=75 were 33% less likely to die in a nursing home. Death at home was 19% more likely in HAs aged 60 to 74 years. Significant gender differences are also reported. CONCLUSIONS: Using hospital data alone would overestimate stroke mortality in the HA and AA groups. Stroke community surveillance projects should account for ethnic and gender differences in location of death to avoid bias in race/ethnic and gender comparisons.

Age Factors↗
PubMed1999

Quinone reductase (NQO1), a sensitive redox indicator, is increased in Alzheimer's disease.

NAD(P)H:quinone oxidoreductase 1 (NQO1), a redox-regulated flavoenzyme, plays a central role in monitoring cellular redox state. NQO1 acts to protect against oxidative stress induced by a variety of metabolic situations, including metabolism of quinones and other xenobiotics, by: (i) functioning as a two electron donor to provide a shunt that competes with the formation of reactive oxygen species; (ii) maintaining reduced coenzyme Q; and (iii) regulating the stress activated kinase pathway. In Alzheimer's disease, while there is abundant evidence for the involvement of oxidative stress, the cause or the consequences are largely unresolved. We suspected that increased NQO1 could signal a major shift in redox balance in Alzheimer's disease and, in this study, found that NQO1 is localized not only to neurofibrillary tangles but also the cytoplasm of hippocampal neurons. By marked contrast, there is very little NQO1 in the same neuronal populations in young and age-matched controls. This novel association of NQO1 further buttresses the nexus of oxidative stress, via free radicals, with selective neuronal vulnerability and also supports a fundamental abnormality in redox balance in Alzheimer's disease.

Aged↗
PubMed1999

Secondary leukemia or myelodysplastic syndrome after treatment with epipodophyllotoxins.

PURPOSE: The incidence of secondary leukemia after epipodophyllotoxin treatment and the relationship between epipodophyllotoxin cumulative dose and risk are not well characterized. The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan to obtain reliable estimates of the risk of secondary leukemia after epipodophyllotoxin treatment. METHODS: Twelve NCI-supported cooperative group clinical trials were identified that use epipodophyllotoxins at low (<1.5 g/m2 etoposide), moderate (1.5 to 2.99 g/m2 etoposide), or higher (> or =3.0 g/m2 etoposide) cumulative doses. Cases of secondary leukemia (including treatment-related myelodysplastic syndrome) occurring on these trials have been reported to CTEP, as has duration of follow-up for all patients, thereby allowing calculation of cumulative 6-year incidence rates of secondary leukemia for each etoposide dose group. RESULTS: The calculated cumulative 6-year risks for development of secondary leukemia for the low, moderate, and higher cumulative dose groups were 3.3%, (95% upper confidence bound of 5.9%), 0.7% (95% upper confidence bound of 1.6%), and 2.2%, (95% upper confidence bound of 4.6%), respectively. CONCLUSION: Within the context of the epipodophyllotoxin cumulative dose range and schedules of administration encompassed by the monitoring plan regimens, and within the context of multiagent chemotherapy regimens that include alkylating agents, doxorubicin, and other agents, factors other than epipodophyllotoxin cumulative dose seem to be of primary importance in determining the risk of secondary leukemia. Data obtained by the CTEP secondary leukemia monitoring plan support the relative safety of using epipodophyllotoxins according to the therapeutic plans outlined in the monitored protocols.

Adolescent↗
PubMed1999

[Is the lesion produced by oxidation a central part in the pathogenesis of Alzheimer's disease?].

The two most striking features of Alzheimer's disease are: a) the multitude of abnormalities affecting essentially every system, and b) the strict age dependence. Recent work suggests that both features are linked to increased oxidative stress that damages lipids, proteins and nucleic acids and results in redox-active metal accumulations, mitochondrial damage and formation of advanced glycation endproducts. Interestingly, beta-protein precursor, amyloid-beta, presenilins and apolipoprotein E have all been linked to reactive oxygen species production or with apoptosis, a process intimately associated with oxidative stress. In therapeutics, the commonality between a number of efficacious agents appears to be oxidative stress reduction. Therefore, we contend that oxidative stress is the element that links the multitude of changes in Alzheimer's disease and that a reduction of oxidative stress will have a dramatic effect on reducing the incidence or progression of Alzheimer's disease.

Alzheimer Disease↗
PubMed1999

Morphological features of regeneration of rabbit aortic endothelium after cryoinduced vascular damage.

Regeneration of endothelium after damage is an important factor, which limits the development of atherogenesis. This study examines the topographical characteristics of regenerating endothelial cells (EC) in rabbit aorta after de-endothelialization by cryodestruction. The effects of cloricromene on these processes were also studied. Vessels were harvested from 6-month-old NZW rabbits, 1 and 3 days after cryodestruction. The vessels were evaluated using scanning electron microscopy (SEM). One day after cryodestruction, there were defects in the endothelial monolayer in the zone of injury in saline treated animals. Large numbers of platelets and monocytes were observed in association with endothelium in the damaged zone. Three days after de-endothelialization the size of the area of the damage had decreased. On the surface of the new endothelial layer and below this defect, the number of adhering monocytes was increased, and many microdefects between endothelium could be seen. Administration of cloricromene for 1 or 3 days after damage reduced the number of endothelium-adherent platelets and monocytes, and microdefects in endothelium. The feature of endothelial repair in rabbits is a relatively large involvement of monocytes and platelets, which are visible below regenerated endothelium. Administration of cloricromene essentially restored re-endothelialization and significantly decreased the number of adherent monocytes and microdefects in the new endothelium.

Animals↗
PubMed1998

Mode switching characterizes the activity of large conductance potassium channels recorded from rat cortical fused nerve terminals.

1. Inside-out recordings from rat cortical fused nerve terminals indicate that the most common channel observed was a large conductance K+ (BK) channel with characteristics dissimilar to conventional cell body calcium-activated BK (BKCa) channels. 2. BK channels exhibit mode switching between low (mode 1) and high (mode 2) activity, an effect not influenced by membrane voltage. Increasing internal Ca2+ concentration increased time spent in mode 2 as did application of protein kinase A, an effect not mimicked by protein kinase C or protein kinase G. 3. Mode 1 activity was voltage independent although depolarization increased mode 2 channel activity. Global average channel activity was voltage and Ca2+ dependent. 4. Alkaline phosphatase treatment induced channel activity to reside permanently in mode 2, where activity was voltage and Ca2+ dependent but unaffected by protein kinases A, G or C. 5. Internal application of tetraethylammonium blocked BK channel activity in a manner identical to that reported for BKCa channels. 6. These results indicate that nerve terminal membranes have large conductance K+ channels with significant differences in gating kinetics and regulation of activity compared with BKCa channels of other neuronal preparations. The BK channel subtype may play a unique physiological role specific to the nerve terminal.

Alkaline Phosphatase↗
PubMed1998

Striation is the characteristic neuritic abnormality in Alzheimer disease.

In this study, we found that neuropil threads of Alzheimer disease, rather than being continuous filaments along cell processes, show multiple interruptions. They are segmental in nature and therefore appear as striations rather than continuous filaments along the length of the neurite. Neuritic striation is not an artifact of section thickness since the majority of abnormal filament accumulations are extremely short. The dominance of short striations demonstrates that argyrophilic grains, rather than being distinct structures, simply represent a short variant of striation and that longer striations are arbitrarily considered neuropil threads. Ultrastructural examination showed that the intervals between striations lack a cytoskeleton. We suggest that neuritic striations may interrupt the microtubule system functionally blocking fast neuritic transport as well as playing a role in loss of neuronal connectivity.

Aged↗
PubMed1998

Mortality attributed to respiratory problems among finisher pigs in the United States.

In the 1995 National Swine Study of the United States National Animal Health Monitoring System, producers identified respiratory problems as the leading cause of death in pigs during the grower/finisher phase of production. Over a six-month period, 61.7 +/- 4.1% (mean +/- SEM) of operations reported at least one death attributed to respiratory problems among finisher pigs (based on 388 operations representing operations with > or = 300 finisher pigs in 16 states). Mean mortality attributed to respiratory problems was 0.9 +/- 0.1% of finisher pigs per operation. Stepwise logistic regression (using SAS) was used to identify factors associated with operations attributing at least one death to respiratory problems, and to identify factors associated with reporting > or = 2% mortality attributed to respiratory problems. Final models were run with SUDAAN to account for the sampling strategy. Attributing at least one death to respiratory problems was associated with having > or = 3000 pigs enter the grower/finisher unit over a six-month period; diagnosis of Haemophilus (or Actinobacillus) in the past 12 months; and keeping pigs in the grower/finisher unit > 120 days (as compared to < 100 days). Not having a farrowing facility, mean weaning age < 28 days, and < 50% of finisher pigs on solid concrete only were associated with reporting > or = 2% mortality attributed to respiratory problems.

Animal Husbandry↗
PubMed1998

Ribosomal RNA in Alzheimer's disease and aging.

Ribosomal RNA genes are involved in cell transcription and translation processes and can modulate gene expression. In an earlier cytogenetic study, (Payão, S.L.M., Smith, M.de A.C., Kormann-Bortolotto, M.H., Toniolo, J., 1994 (Investigation of the nucleolar organizer regions in Alzheimer's disease. Gerontology 40, 13-17), reported a decreased activity of ribosomal genes in Alzheimer's disease (AD). We studied the ratio of mature rRNA 28S and 18S in peripheral blood samples derived from eight patients with AD, eight healthy elderly sisters of these patients (SA), eight healthy elderly (EC) and eight healthy young (YC) controls, all female. Our results showed a statistically significant decrease of mature rRNA 28S and 18S ratio in the elderly groups (AD, SA, EC) in relation to the young one, probably by fragmentation of 28S rRNA. The Alzheimer's patient group had the lowest 28S/18S ratio. Thus, we can suggest that there is a possible change in the transcriptional or maturation process, or a preferential degradation of the 28S subunit with ageing.

Adolescent↗
PubMed1998

Dimethylargininase, a nitric oxide regulatory protein, in Alzheimer disease.

In this study, we show that dimethylargininase, a zinc protein involved in the regulation of nitric oxide synthase, is specifically elevated in neurons displaying cytoskeletal abnormalities and oxidative stress in Alzheimer disease (AD) while none of this enzyme was found in neurons in age-matched control cases. Seen in the context of earlier studies showing widespread nitric oxide related damage in AD and the role of dimethylargininase to activate nitric oxide synthetase, through catalytic removal of its endogenous inhibitors, these findings indicate major alterations in nitric oxide regulation in AD. Further, that low levels of zinc specifically inhibit dimethylargininase may provide a link between the numerous studies showing specific abnormalities in zinc and oxidative stress. Finally, our results provide additional evidence that oxidative stress- and nitric oxide-mediated events play important roles in the pathogenesis of AD.

Aged↗
PubMed1998

CI-ATPase and Na+/K(+)-ATPase activities in Alzheimer's disease brains.

The enzyme activities and the protein levels of Cl(-)-ATPase and Na+/K(+)-ATPase were examined in Alzheimer's disease (AD) brains. Cl(-)-ATPase and Na+/K(+)-ATPase activities in AD brains (n = 13) were significantly lower than those in age-matched control brains (n = 12). In contrast, there was no significant difference in anion-insensitive Mg2(+)-ATPase activity between the two groups. Western blot analysis revealed that the protein levels of Cl(-)-ATPase, Na+/K(+)-ATPase and neuron specific Na+/K(+)-ATPase alpha3 isoform were also significantly reduced in AD brains, while the amount of protein disulfide isomerase, one of the house keeping membrane proteins, was not different between the two groups. The data first demonstrated that Cl(-)-ATPase and Na+/K(+)-ATPase are selectively impaired in AD brains, which may reduce the gradients of Na(+), K(+) and Cl(-) across the cell membranes to cause excitotoxic cellular response and the resulting neuronal death.

Adenosine Triphosphatases↗
PubMed1998

Trends in reported incidence of primary malignant brain tumors in children in the United States.

BACKGROUND: The reported incidence of primary malignant brain tumors among children in the United States increased by 35% during the period from 1973 through 1994. The purpose of our study was twofold: 1) to determine whether the reported incidence rates for this period are better represented by a linear increase over the entire period ("linear model") or, alternatively, by a step function, with a lower rate in the years preceding 1984-1985 and a constant higher rate afterward ("jump model"); and 2) to identify the specific brain regions and histologic subtypes that have increased in incidence. METHODS: Incidence data from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute for the period from 1973 through 1994 for primary malignant brain tumors in children were used to model the number of cases in a year as a random variable from a Poisson distribution by use of either a linear model or a jump model. RESULTS/CONCLUSIONS: The increase in reported incidence of childhood primary malignant brain tumors is best explained by the jump model, with a step increase in incidence occurring in the mid-1980s. The brain stem and the cerebrum are the primary sites for which an increase in tumor incidence has been reported. The increase in reported incidence of low-grade gliomas in the cerebrum and the brain stem (unaccompanied by an increase in mortality for these sites) supports the substantial contribution of low-grade gliomas to the overall increase in reported incidence for childhood brain tumors. IMPLICATIONS: The significantly better fit of the data to a jump model supports the hypothesis that the observed increase in incidence somehow resulted from changes in detection and/or reporting of childhood primary malignant brain tumors during the mid-1980s.

Adolescent↗