Aneurysm of vein of Galen and diffuse meningeal angiectasia. Occurrence in a neonate with cardiac failure.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Nelson.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Adenosine triphosphatase activated by divalent cations is apparently a component of the motile apparatus in flagella of Arbacia sperm, as judged by the activity of this enzyme in intact flagella, glycerol-extracted flagella, and soluble extracts prepared from flagella. However, the variation in the physical properties and in the amount of enzyme obtained after a variety of treatments suggests that additional components are involved in the motile mechanism. These features distinguish the soluble flagellar enzyme from adenosine triphosphatases of other motile cells.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
C57BL/6 mice with syngeneic B16-F10 melanomas were treated 7 days after tumor inoculation into the footpad with local hyperthermia (HT) of 43.5 degrees C for 90 min. A combination of local 30 Gy X-irradiation (XRT) given 2, 4 or 12 h after HT cured the primary tumor in 34/35 mice, with irreversible damage to normal foot tissues in most of the animals. When 7.5, 10 or 15 Gy XRT were delivered 4, 18 or 24 h after HT, there were only a small number of cures and also a much smaller incidence of irreversible normal tissue damage. HT alone resulted in a significant (P less than 0.001) increase in metastases to regional lymph nodes (RLN) and the lungs. The 'curative' doses of combined XRT and HT resulted in a significant (P less than 0.001) decrease in metastasis to RLN and to the lungs. Conversely, subcurative doses of combined therapy resulted in an increase in RLN and lung metastasis (P less than 0.001). Abdominal lymph node metastasis, not usually seen in control mice, is markedly increased after HT alone or in combination with subcurative XRT (P less than 0.001). The overall survival of mice treated with HT alone is decreased (P less than 0.0028). The survival of mice treated with HT followed 4, 18 or 24 h later with 10 Gy XRT is further decreased (P less than 0.0025). These data show that subcurative HT, or XRT plus HT, increases the incidence of spontaneous metastasis in this syngeneic mouse melanoma model. Curative doses prevent this effect on metastasis, but there is an unacceptable incidence of irreversible damage to the tumor-bearing foot. The cause(s) of this phenomenon are not known.
The effect of alloxan on anion transport in isolated mouse liver mitochondria was studied with the swelling technique. Mitochondria pre-incubated with alloxan exhibited partial inhibition of the transport of malate, citrate, pyruvate and glutamate. 2n-butylmalonate caused complete inhibition of malate transport, and the translocation of citrate was completely blocked by 1,2,3-benzenetricarboxylate, while N-ethylmaleimide inhibited glutamate transport partially. The observation that alloxan inhibits different mitochondrial anion transport mechanisms emphasizes that the drug profoundly affects mitochondrial function.
The swelling technique evidenced inhibition of Pi transport in isolated mouse liver mitochondria by 1 mM or higher concentration of alloxan inhibition was found under the following conditions: preincubation at 4 degrees C, or pretreatment with Pi, glucagon, succinate, malate or pyruvate. Complete protection was observed in isolated mitochondria from mice injected with glucagon. No protection was seen under the following conditions: preincubation at 37 degrees C, addition of microsomes, or pretreatment with insulin or glucagon in the presence of glucagon antibodies. So-called light and heavy mitochondria were as sensitive to alloxan as those obtained with the routine technique. Alloxanic acid had no effect, and addition of cysteine or glutathione abolished the inhibition by alloxan. Alloxan inhibited Pi transport also in isolated lung mitochondria. The findings suggest a direct action of alloxan on mitochondrial Pi transport which is affected by the energetic state. A relationship seems to exist between protection against alloxan toxicity in vivo and protection under the present experimental conditions.