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Biomedical subjects

M J Adams

Publications and source records attributed to M J Adams.

At least 109 records · Page 6Linked to original sources
PubMed1989

The use of attributable fraction in the design and interpretation of epidemiologic studies.

Because of the etiologic heterogeneity present in many diseases and the interaction among causal factors in the development of disease, relative risks relating any one exposure to a disease may be low, especially in the presence of common exposures. Nevertheless, in the design of epidemiologic studies, arbitrary values of relative risks are often used to determine the sample size required to detect an association between a particular exposure and a disease outcome. Such an approach may not yield adequate statistical power to detect an association. In this commentary, the authors point out the value of using the attributable fraction to determine an appropriate value of relative risk to use for sample size calculations. The approach is particularly useful in cluster investigations where the magnitude of the expected attributable fraction can be readily estimated from the observed and expected rates of disease. Specification of an attributable fraction is also useful in the design of case-control studies of etiologically heterogeneous diseases, especially when common exposures are suspected. Finally, the relationship among attributable fraction, relative risk and exposure frequency is valuable in interpreting results of an epidemiologic study and gaining insight into the differences in relative risk estimates found in various studies.

Epidemiologic Methods↗
PubMed1989

On the measurement of susceptibility in epidemiologic studies.

Although relative effects of risk factors (relative risks) are commonly used in epidemiologic studies of disease, these measures do not provide estimates of the proportion of persons who are "susceptible" to the risk factor. Susceptibility may be defined under a simple sufficient cause model as the underlying factor (or set of factors) sufficient to make a person contract a disease following exposure. The authors derive simple estimates of the proportion of susceptibles in a population based on relative risk, and disease and exposure frequencies. The proportion of susceptibles increases with increasing disease frequency and relative risk but declines at high exposure frequency. For many chronic diseases with a lifetime risk in the range of 1-10 per cent, rare exposures suggest the presence of a large proportion of susceptibles, whereas common exposures suggest fewer susceptibles in the population. The estimation of the proportion of susceptibles is important in the search for genetic and environmental factors that interact with measured risk factors in etiologic studies of disease.

Abnormalities, Drug-Induced↗
PubMed1988

The epidemiology and public health significance of Rett syndrome.

Current data indicate that Rett syndrome is an important contributor to the total burden of idiopathic mental retardation. Studies from Sweden suggest that among girls the prevalence of Rett syndrome may be twice the prevalence of phenylketonuria. Successful epidemiologic studies of idiopathic mental retardation syndromes will require both large sample sizes and homogeneous populations. Because Rett syndrome is a relatively homogeneous and common syndrome of idiopathic mental retardation, epidemiologic methods may be more productive in the study of Rett syndrome than in other syndromes of mental retardation that are less clinically homogeneous. The approaches used in studying Rett syndrome epidemiologically may later be useful in the study of other syndromes of idiopathic mental retardation.

Ammonia↗
PubMed1988

An epidemiologic approach to ecogenetics.

Although "ecogenetics" seeks to examine genetically mediated differences in susceptibility to environmental agents, researchers often examine the relation between genetic markers and disease without regard to environmental determinants. By using epidemiologic definitions of genotype-environment interaction, it can be shown that the relative risk of disease for the genetic marker is a function of the frequency of exposure to the environmental agent, the strength of interaction between the genotype and the agent, and the specificity of the environmental effect vis-à-vis the genotype. Using examples from the literature, we illustrate under six patterns of genotype-environment interaction that the relative risk associated with the marker can fluctuate markedly. However, with infrequent exposures, the relative risk is close to unity (implying no genetic effect) even in the face of strong genotype-environment interaction. Alternatively, elevated relative risks imply a frequent environmental exposure or a strong pattern of interaction. We suggest that genetic marker-disease associations be evaluated within the context of an epidemiologic study design that considers specific environmental determinants of risk.

Disease Susceptibility↗
PubMed1987

Sequence identity between a lysine-containing peptide from Leuconostoc mesenteroides glucose-6-phosphate dehydrogenase and an active site peptide from human erythrocyte glucose-6-phosphate dehydrogenase.

Peptides recently isolated and sequenced from a bacterial (Leuconostoc mesenteroides) glucose-6-phosphate dehydrogenase are remarkably homologous to an active site region of the human erythrocyte enzyme, although the enzymes differ in their overall amino acid composition and kinetic properties. The computer program ALIGN, used to determine the best alignment between the two enzyme sequences, gives match-scores which are statistically highly significant.

Amino Acid Sequence↗
PubMed1987

Teaching generalization of purchasing skills across community settings to autistic youth using videotape modeling.

Three young autistic adults were trained to purchase items. Training was conducted in one setting with concurrent generalization probes taken in three community stores. Training in one setting failed to produce generalization to the three probe settings. Generalization training, which consisted of viewing videotapes of models who purchased items in the probe settings and answering questions about the models' responses, was then introduced. Training with the videotapes resulted in generalization to the three community stores. Results of the use of videotapes as a cost-effective means to program generalization in community training programs are discussed.

Activities of Daily Living↗
PubMed1984

Vietnam veterans' risks for fathering babies with birth defects.

Vietnam veterans' risks for fathering babies with major structural birth defects were assessed using a case-control study. Information regarding military service in Vietnam was obtained from interviews with mothers and fathers of babies in case and control groups and from review of military records. Vietnam veterans, in general, did not have an increased risk of fathering babies with defects (all types combined; relative risk estimate, 0.97). Vietnam veterans who had greater estimated opportunities for Agent Orange exposure did not seem to be at greater risk for fathering babies with all types of defects combined. However, for a few specific types of defects the estimated risks were higher for subgroups of Vietnam veterans that may have had a greater likelihood of exposure to Agent Orange. These seemingly higher risks could be chance events, the result of some experience in the Vietnam service of the father, or the result of some other unidentified risk factor.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1984

Trends in postneonatal mortality in the United States. 1962 through 1978.

Trends in postneonatal mortality (PNM) rates in the United States were analyzed for the period 1962 through 1978 using National Center for Health Statistics birth and death certificate data. The PNM rates declined from 5.5 to 3.6 per 1,000 live births for whites and from 15.6 to 7.6 per 1,000 live births for blacks. Most of the decline in PNM rates could be accounted for by a drop in mortality from infectious diseases. A dramatic increase occurred in the reported rates of unexplained sudden infant death (SID), which emerged as the leading reported cause of PNM. The second leading cause of PNM was birth defects among whites and infectious diseases among blacks. Gaps in PNM continued to exist between whites and blacks, and between metropolitan and nonmetropolitan areas. These gaps suggest that further improvement in PNM may be possible by improving access to health care. The massive increase in the rates of SID, although partially explained by coding or reporting phenomena, warrants active pursuit for a better pathophysiologic and etiologic delineation of the entity.

Black or African American↗
PubMed1984

Clinical interpretation of maternal serum alpha-fetoprotein concentrations.

Concentrations of maternal serum alpha-fetoprotein provide the basis for decisions to proceed to ultrasonography and amniocentesis in the multistaged screening/diagnostic process used for the prenatal detection of open neural tube defects, abdominal wall defects, and twins. The concentration of maternal serum alpha-fetoprotein at or above which women should be advised that amniocentesis is available (cutoff levels for amniocentesis) varies, depending upon a number of factors, such as maternal weight, race, residence, and gestational age. We briefly describe a methodology for computing the predicted risks of fetal conditions associated with a given concentration of maternal serum alpha-fetoprotein adjusted for important variables. This adjustment methodology provides a straightforward means for clinical laboratories to report results of assays of maternal serum alpha-fetoprotein in terms of predicted risks, to facilitate understanding by the physician and patient of the clinical meaning of the results of maternal serum alpha-fetoprotein testing.

Amniocentesis↗
PubMed1983

The three dimensional structure of sheep liver 6-phosphogluconate dehydrogenase at 2.6 A resolution.

The three-dimensional structure of sheep liver 6-phosphogluconate dehydrogenase has been determined at 2.6 A resolution by X-ray crystallographic studies. The amino acid sequence of the enzyme is now known and can be fitted to a modified electron density map. Use of 6 A electron density maps and the results of chemical modification experiments allows description of the active site and identification of residues which may be implicated in the binding of co-enzyme and substrate.

Animals↗
PubMed1983

Crystallisation and preliminary X-ray data of ribulose-1,5-bisphosphate carboxylase from spinach.

Crystals of a tertiary complex of spinach ribulose-1,5-bisphosphate carboxylase/oxygenase with the activators Mg and CO(2) have been grown. These crystals diffract strongly to 1.6 A resolution. The spacegroup is C222(1) with unit cell dimensions a = 158.6 A, b = 158.6 A, c = 203.4 A. Additional local symmetry is apparent in the pattern of absences and the intensity distribution of the X-ray precession photographs. The photographs have been interpreted in terms of a molecule (consisting of eight large and eight small subunits, L(8)S(8)) with 222 symmetry and a molecular centre shifted 2 A in the x direction from the origin of the unit cell. The asymmetric unit contains half the L(8)S(8) molecule. The intensity distribution suggests that the molecular symmetry does not deviate far from 422. These crystals are compared with other crystalline forms of the enzyme and the implications of these results are discussed.

Journal Article↗
PubMed1981

Localization of Fungal Components in the Pea-Fusarium Interaction Detected Immunochemically with Anti-chitosan and Anti-fungal Cell Wall Antisera.

Antisera specific for purified cell walls of Fusarium solani f. sp. pisi and phaseoli and of shrimp shell chitosan were utilized as immunochemical probes to determine the location of fungal components in the pea-Fusarium interaction.Within 15 minutes after inoculation, fungal cell wall components appear to enter the plant cell and to accumulate inside the plant cell wall as fungal growth on the plant tissue is inhibited. The accumulation patterns of chitosan and all components containing hexosamine polymers resembled those of the fungal wall components.Chitosan is present on, and is released from, the outer surface of the fungal spore. Within 15 minutes after applying [(3)H]chitosan to the surface of the plant tissue, the label is readily detectable within the plant cytoplasm and conspicuously detectable within the plant nucleus. It is proposed that the potential for transport of chitosan between the spores of Fusarium solani and pea cells, in addition to its potential to inhibit fungal growth and elicit disease resistance responses, suggests chitosan has a major regulatory role in this host-parasite interaction.

Journal Article↗
PubMed1979

Binding of coenzyme and substrate and coenzyme analogues to 6-phosphogluconate dehydrogenase from sheep liver. An X-ray study at 0.6 nm resolution.

The analogues of the coenzyme NADP+, nicotinamide--8-bromo-adenine dinucleotide phosphate (Nbr8ADP+) and 3-iodopyridine--adenine dinucleotide phosphate (io3PdADP+), were prepared. Nbr8ADP+ was found to be active in the hydrogen transfer adn io3PdADP+ is a coenzyme competitive inhibitor for 6-phosphogluconate dehydrogenase. The binding of NADP+, NADPH and NADPH together with 6-phosphogluconate as well as that of both analogues to crystals of the enzyme 6-phosphogluconate dehydrogenase has been investigated at 0.6-nm resolution using difference electron density maps. The molecules bind in a similar position in a cleft in the enzyme subunit distant from the dimer interface. The orientation of the coenzyme in the site has been determined from the io3PdADP+ -NADP+ difference density. The ternary complex difference density extends beyond that of the nicotinamide moiety of the coenzyme and tentatively indicates substrate binding. No clear identification of the bromine atom of Nbr8ADP+ can be made. However, the analogue is bound more deeply in the cleft than is NADP+. The NADPH density is the most clearly defined and has thus been used to fit a molecular model using an interactive graphics system, checking for preferred geometry. A possible conformation is presented which is significantly different from that of NAD+ in the lactate dehydrogenase ternary complex.

Animals↗