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Biomedical subjects

A Weber

Publications and source records attributed to A Weber.

At least 631 records · Page 35Linked to original sources
PubMed1976

Mechanism of inhibition of relaxation by N-ethylmaleimide treatment of myosin.

It has remained unexplained why N-ethylmalaeimide (NEM) treatment of myosin can inhibit relaxation in actomyosin systems from rabbit skeletal muscle which appear to be regulated solely through tropomyosin and troponin. Since rigor complexes between (nucleotide-free) myosin and actin affect the tropinin-tropomyosin system, the possibility was explored that, as a result of NEM treatment, some of the myosin maintains rigor complexes with actin in the presence of ATP which might be responsible for inhibition of relaxation. Evidence is presented indicating that such a mechanism might account for the effects of NEM treatment. First, after exhaustive NEM treatment of heavy meromysin (HMM), acto-HMM complexes were no longer dissociated by ATP. Second, admixture of such NEM-treated, enzymatically inactive HMM or myosin to native regulated actomyosin or acto-HMM inhibited relaxation.

Actins↗
PubMed1976

Aldolase B in the liver of senescent rats.

The process of enzymatic aging was studied in livers of adult and senescent rats for aldolase B. No "cross-reacting material" was found in livers of 27 to 30-month-old rats, estimated by the ratio aldolase activity-antigen amount. The activity towards the two substrates of aldolase, fructose 1,6-diphosphate and fructose 1-phosphate did not vary in senescent animals. Moreover, other physico-chemical properties of the enzyme such as thermal inactivation, immunological reactivity and Michaelis constant remain unchanged. These results provide arguments against the occurrence of errors in protein synthesis as a cause of aging.

Aging↗
PubMed1976

Irritating effects on man of air pollution due to cigarette smoke.

Sixty subjects were exposed to cigaretts smoke produced by a smoking machine in a climatic chamber. The irritating effects were recorded by questionnaire and related to concentrations of CO, formaldehyde, and acroleine. The eyes are most sensitive to these irritants, followed by the nose. Annoyance about air quality, and the desire to open the window or to leave the room proved to be other useful measures of sensitivity. With smoke produced by 10 cigarettes/30 m3 acroleine reaches 0.1 ppm, the threshold limit value for industries; simultaneously, CO and formaldehyde exceed the clean air standards for outdoor air. At this exposure level. 9 per cent of the subjects show a strong or very strong eye irritation, while 78 per cent "wish to leave the room." The most important of the measured irritants seems to be acroleine.

Acrolein↗
PubMed1976

[The infantile psychoorganic syndrome--a developmental psychological disorder?].

Many symptoms of infantile psychoorganic syndrome can be regarded as developmental variants or as the result of retarded development, particularly where they are not of marked degree. However, many symptoms are not assignable to either of these categories but, with respect to their pathology, must be classified otherwise. Thus it follows that infantile psychoorganic syndrome as a total entity--and only as a totality, of course, is it to any extent specific--cannot be viewed as a disorder of development.

Adolescent↗
PubMed1975

The dissociation constant of the actin-heavy meromyosin subfragment-1 complex.

We measured the binding of [14C]iodoacetamide labeled heavy meromyosin subfragment-1 (S-1) to F-actin by sedimenting the actin-S-1 complex and assaying the radioactivity remaining in the supernatant. The apparent dissociation constants (Kd) at 25 degrees, pH 7.0, were 0.01 to 0.04 muM at 0.027 and 0.08 ionic strengths and 0.07 to 0.14 muM at 0.14 ionic strength. Kd was not altered when the troponin-tropomyosin complex was bound on the actin, nor was it affected by free calcium concentration in the range 10(-4) to 10(-9) M. Measurements of the displacement of labeled S-1 from actin by native S-1 showed labeling had not altered Kd. In control experiments we found that at the low actin concentrations used (0.001-0.5 muM) not all of the actin sedimented and, furthermore, the data suggested that some of the S-1 in the supernatant was bound to supernatant actin. Our estimation of Kd, based on the assumption that all the supernatant S-1 was free, therefore resulted in an apparent Kd greater than the true Kd. We minimized the effect of the supernatant actin artefact by using only the data for high ratios of S-1 to actin, where no less than 75% of the actin sedimented; we estimate that the true Kd values could not be less than half the apparent Kd values.

Actins↗