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Biomedical subjects

R S Mitchell

Publications and source records attributed to R S Mitchell.

8 recordsLinked to original sources

Health effects of urban air pollution. Special consideration of areas at 1,500 m and above.

Urban air pollution, when sufficiently severe, can cause death in humans; these deaths occur preponderantly among those with increased susceptibility. Pollution--carbon monoxide and oxidants in particular--is capable of aggravating preexisting chronic heart and lung diseases. Pollution and tobacco (especially cigarette) smoke act synergistically in a causative role in chronic bronchitis and in an aggravating role in emphysema. Susceptibility to the effects of urban air pollution varies widely, with the most susceptible being fetuses, the newborn, the elderly, the infirm, those with chronic heart and lung diseases, and those who smoke. The carbon monoxide standards for sea level are probably too lenient for an altitude of 1,500 m and above. Using a broad definition of health, which takes into account concepts such as quality of life and social and mental well-being, few metropolitan residents would deny that their health is compromised by air that is malodorous, that irritates mucous membranes, and that obscures beautiful scenery.

Adult

Proliferation of Rous sarcoma virus-infected, but not of normal, chicken fibroblasts in a medium of reduced calcium and magnesium concentration.

Both normal and Rous sarcoma virus-infected chicken fibroblasts proliferate actively in a culture medium containing physiological concentrations of calcium (1.2 mM) and magnesium (0.7 mM). In the presence of a physiological concentration of magnesium, reduction of the calcium concentration to 0.125 mM resulted in a significant decrease in the proliferation of the normal, but not of the neoplastic, fibroblasts. Reduction of the magnesium concentration to 0.05 mM in the presence of a physiological concentration of calcium had a similar effect. In a culture medium containing reduced concentrations of both calcium (0.20 mM) and magnesium (0.05 mM), the normal fibroblasts were maintained without proliferation, whereas the Rous sarcoma virus-infected fibroblasts continued to proliferate actively. The cytosol concentrations of ionized calcium and magnesium are known to be regulated by a balance between net passive influx and active extrusion and sequestration. On the basis of this consideration and the findings described above it can be hypothesized that: (i) Fibroblast replication is initiated when cytosolic concentrations of calcium, magnesium, or both rise above a critical level. (ii) Autonomous initiation of replication of neoplastic fibroblasts is a result of failure of cytoplasmic divalent cation homeostasis; alternatively, sarcoma virus infection may endow cells with a divalent cation-independent mechanism that bypasses an initiation mechanism that is, normally, divalent cation-dependent. (iii) Proliferation of normal fibroblasts is controlled by extracellular matrix components that interact with cell surfaces in a manner that limits the permeability of plasma membranes to divalent cations or otherwise functions to lower cytosol divalent cation concentrations.

Avian Sarcoma Viruses

Thymidine and hypoxanthine requirements for the proliferation of normal and Rous sarcoma virus-infected chicken fibroblasts in the presence of methotrexate.

Cultured normal and Rous sarcoma virus-infected chicken fibroblasts do not differ in the concentrations of thymidine or of hypoxanthine that they require to proliferate in the presence of a methotrexate block. For maximal proliferation, thymidine is required at 10(-6) M, while hypoxanthine is required at 10(-5) M. The normal and Rous-infected fibroblasts show very similar, if not identical, decreases in proliferation rates at suboptimal concentrations of thymidine or hypoxanthine. These results suggest that conversion of fibroblasts to the neoplastic state does not alter their capacity to salvage thymidine or purines from the extracellular fluid or to metabolize these compounds.

Animals

5-Methyltetrahydrofolic acid, 5-formyltetrahydrofolic acid (folinic acid), and folic acid requirements of normal and Rous sarcoma virus-infected chicken fibroblasts.

Normal and Rous sarcoma virus-infected chicken fibroblasts proliferate maximally in a culture medium containing a physiological (10 ng/ml) concentration of 5-methyltetrahydrofolic acid or folinic acid (5-formyltetrahydrofolic acid), while their maximal proliferation requires a hyperphysiological (1000 ng/ml) concentration of folic acid. The normal and Rous-infected fibroblasts do not differ in their requirements for 5-methyltetrahydrofolate, folinic acid, or folic acid.

Animals

Proliferation of Rous sarcoma virus-infected, but not of normal, chicken fibroblasts in oxygen-enriched environment: preliminary report.

Both normal and Rous sarcoma virus-infected chicken fibroblasts proliferate in an incubator containing 95% air, 5% CO2. In an incubator atmosphere enriched with oxygen, however, the normal fibroblasts are maintained without proliferation, while the Rous sarcoma virus-infected fibroblasts continue to proliferate. This suggests that a respiratory function may be involved in the regulation of proliferation of normal cells, and that neoplastic cells may proliferate autonomously because of a deficiency in this regulatory function.

Atmosphere

The right ventricle in chronic airway obstruction: a clinicopathologic study.

In men 40 or more years of age at death, the upper limits of normal (means plus 2 SD) cardiac ventricular weights were 69 g for the right ventricle and 203 g for the left ventricle plus septum. Right ventricular thickness, as usually determined at autopsy, was a relatively poor index of hypertrophy. When one ventricle hypertrophies as a result of stress, the other tends to enlarge simultaneously, even if no stress on it has been evident. Right ventricular weight correlated positively, although not strongly, with severity of emphysema and with the severity of clinical chronic airway obstruction. Correlations between right ventricular weight and pathologic changes in the airways were weak or absent, except that subjects with abnormal large airways, but normal small airways, showed improved correlation between severity of emphysema and right ventricular hypertrophy, compared with the entire series. There was no correlation between left ventricular weight and severity of emphysema. The electrocardiogram was very reliable in the diagnosis of right ventricular hypertrophy (corpulmonale) due to chronic airway obstruction; the chest roentgenogram was somewhat less sensitive in this regard.

Cardiomegaly