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Biomedical subjects

M B Jones

Publications and source records attributed to M B Jones.

At least 109 records · Page 6Linked to original sources
PubMed1980

Sequential precession and diminishing returns in the acquisition of a motor skill.

As students progress to higher and higher levels in the acquisition of a skill their number gets smaller and smaller. This article concerns the average length of time it takes the members of these successively smaller groups to complete earlier stages of skill acquisition. In the data presented, which concern Red Cross swimming, the more advanced a group is the less time its members take on the average to complete a preceding stage (sequential precession). The discussion section brings out a second relation in the same data: Namely, the further the same students advance in skill acquisition the smaller the advantage they enjoy over other students at the same level (diminishing returns).

Journal Article↗
PubMed1980

Brothers, sisters and antisocial behaviour.

The brothers of 73 delinquent boys were found themselves to be more antisocial than the brothers of 73 matched control boys. Further, the average antisocial score of the probands' brothers increased with the number of brothers in the family, holding the number of sisters constant, and decreased with the number of sisters, holding the number of brothers constant. These results are interpreted in terms of male potentiation and female suppression of antisocial behaviour in boys. Results are also reported for 59 pairs of matched delinquent and control girls and their siblings.

Adolescent↗
PubMed1980

Physiologic and genetic alterations in human red cell DPGM.

Erythrocyte 2,3-diphosphoglycerate levels are determined principally by a single molecule which has both diphosphoglycerate mutase (DPGM) and diphosphoglycerate phosphatase activities. An antiserum containing precipitating antibodies against this molecule was used to measure its amount in red cells from normal controls, from subjects with hypothyroidism or hyperthyroidism, and from a Japanese proband who has hemolytic anemia attributed to heterozygosity for a genetic variant. The amount of DPGM in normal adult erythrocytes is 0.98 +/- 0.014 mg/gm Hb. Slightly increased amounts are found in normal cord blood and in subjects with hyperthyroidism. Hypothyroid subjects have a significantly decreased concentration of DPGM, 0.82 +/- 0.06 mg/gm Hb. Restoration of euthyroid status during treatment results in a return of DPGM amounts to normal. The red cells of the Japanese subject contained 0.67 mg/gm Hb of DPGM as measured by immunoprecipitation.

Adult↗
PubMed1979

Years of life lost through Down's syndrome.

A congenital genetic condition does not act either as a cause of death or at the time of death only. Hence, years of life lost through such a conditon cannot be calculated in the same way as for a conventional cause of death. The main difference is that a cause of death acting at age x cuts off as many years of life as the dead person might otherwise have expected to live (life expectancy at age x), whereas a congenital genetic condition exposes an affected person to a different schedule of life-threatening risks from birth onwards. In the latter case, years of life lost is calculated as the difference in life expectancy at birth for affected and non-affected persons. This reasoning is worked out in algebraic form and then applied to Down's syndrome. The data base is provided by two large and recent studies, one in Massachusetts and the other in Denmark, of mortality rates among all cases of Down's syndrome, whether in an institution or not, born during a given period of years or living at a given point in time in a fixed geographical area. So calculated, years of life lost through Down's syndrome relative to the United States general population in 1970 was 53.6 years per 1000 livebirths. Prenatal mortality is also discussed.

Actuarial Analysis↗
PubMed1979

Years of life lost due to Huntington disease.

Many genetic diseases shorten the lives of people who have them. Hence, it makes sense to speak of years of life lost due to cystic fibrosis or sickle-cell anemia or numerous other genetic disorders. In conventional practice, years of life lost is calculated for causes of death only, but a genetic disease is better understood as a risk-altering state or condition: it acts not at the time of death only but from birth onwards. Therefore, we must reformulate the concept of years of life lost before applying it to genetic conditions. This has already been done for congenital genetic diseases. This paper extends the reformulation to diseases with delayed onset. Huntington disease (HD) is used as an example.

Actuarial Analysis↗
PubMed1978

Fatal pulmonary hypertension and resolving immune-complex glomerulonephritis in mixed connective tissue disease. A case report and review of the literature.

Mixed connective tissue disease (MCTD) has been characterized as a benign rheumatic syndrome with a favorable response to immunosuppressive therapy. Serious renal and pulmonary involvement are reported to be rare in MCTD. We are describing a female adolescent with MCTD in whom fatal cor pulmonale developed due to recurrent thromboembolic primary pulmonary hypertension. Death occurred after two years of therapy with prednisone and azathioprine for an immune-complex glomerulonephritis. Paramesangial and intramembranous electron-dense deposits had been identified in several glomeruli at the start of treatment. Improved renal function and apparent histologic improvement were demonstrated four months after the institution of prednisone and azathioprine therapy, and stable renal function was maintained until death. The pulmonary hypertension was progressive and apparently not altered by either the prednisone or azathioprine. At necropsy, there was no evidence of a pulmonary arteritis or vascular immune-complex deposition to account for the recurrent thromboembolic lesions in the small pulmonary arteries and arterioles. This is a clinical course not previously described in patients with MCTD and may represent an extreme of the clinical spectrum of this syndrome.

Adolescent↗
PubMed1977

First-neighbor specificities of actinomycin-DNA bindings by circular dichroism.

The circular dichroism spectra of eleven double-stranded DNAs, five natural with known nearest neighbor frequencies and six synthetic polydimers and polytrimers, were measured from 210 to 310 nm in the absence and presence of increasing amounts of actinomycin up to saturation. Based on the fact that the circular dichroism of nucleic acids is a nearest-neighbor frequency-dependent property, matrix analysis of the problem revealed which neighbor sets were perturbed by actinomycin, presumably by intercalation of the planar moiety of the molecule. The intercalation sites can be separated into three families. The first-neighbor units GpC and CpG are very favorable binding sites for actinomycin. ApG, CpC, ApC, TpC, and TpG appear to be less attractive sites, while ApT, TpA, and ApA are unfavorable sites.

Binding Sites↗
PubMed1976

Carrier detection in classic hemophilia by combined measurement of immunologic (VIII AGN) and procoagulant (VIII AHF) activities.

Accurate carrier detection in classic hemophilia has been difficult because of (1) technical problems related to the performance of both immunologic (VIII AGN) and procoagulant (VIII AHF) determinations, and (2) statistical problems related to the analysis of these data. VIII AHF was determined by a one-stage assay based on the partial thromboplastin time (PTT). VIII AGN was measured by the method of quantitative immunoelectrophoresis. The discriminant function U. = 0.67 1n (AHF) -- 3.17 AGN X 10(-3) was calculated for a validation group of 20 normal persons and for seven obligate carriers, and tested for accuracy of prediction on a cross-validation group of seven additional normal women and ten additional obligate carriers. A U. score of greater than or equal to 2.54 correctly identified 25 of 27 normal persons. Sixteen of 17 obligate carriers had U. scores below 2.54. In addition, of seven possilbe carriers, four were identified as normal and three as carriers. Five normal women taking oral contraceptives had disproportionately high U. scores. It is concluded that detection of carriers of classic hemophilia should be possible in the clinical laboratory by calculation of a discriminant function from combined measurements of VIII AGN and VIII AHF.

Adolescent↗
PubMed1976

Visibility of the nailfold plexus and heredity.

The parents of 37 normal healthy teenagers selected on the basis of nailfold capillary patterns (16 low-plexus children and 21 high-plexus children) were examined by capillary microscopy and rated "blindly" for plexus visualization scores (PVS). The hypothesis that high PVS is a hereditary trait transmitted as a monogenic autosomal dominant is supported by these data. The additional hypothesis that the high PVS may be associated with a higher social class is also confirmed in this sample. The transmission of high PVS in schizophrenics, where it is frequently observed in association with more serious features of this disease, appears to follow the same mode of inheritance as in normal subjects. The importance of detecting a biological hereditary characteristic which appears to have a modifying effect on the schizophrenic process is emphasized.

Adolescent↗