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Biomedical subjects

P COHEN

Publications and source records attributed to P COHEN.

At least 19 recordsLinked to original sources
PubMed1965

FAT EMBOLISM.

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Diagnosis↗
PubMed1962

Intracellular oxidation-reduction states in vivo.

It now appears to be possible to continuously record changes in intracellular oxidation-reduction levels in terms of the fluorescence of reduced pyridine nucleotide in mitochondria of various tissues and organs in situ. Studies of kidney and brain cortex in the rat show that changes in fluorescence are not measurably affected by the presence of oxyhemoglobin. Nitrogen, sulfide, cyanide, and carbon monoxide cause increases in fluorescence to very nearly the same levels, and the increases are attributed to larger reduction of mitochondrial diphosphopyridine nucleotide. Amytal at a low blood concentration causes increased reduction in the kidney cortex, and at a high blood concentration, in the brain cortex. The qualitative response of the pyridine nucleotide to low oxygen concentrations shows the brain to be more sensitive than the kidney. The first measurable increase in pyridine nucleotide reduction observed on the brain occurs at a concentration of inspired oxygen of 8 percent. Breathing stops when the percentage increase of pyridine nucleotide reduction on the brain reaches about 90; at this point the percentage increase for the kidney is only about 30. This difference corresponds roughly to a tenfold difference in oxygen tension. Half-maximal increase in pyridine nucleotide reduction on the brain occurs at a concentration of inspired oxygen of about 4 percent and corresponds to an intracellular oxygen tension of about 0.2 mm (47).

Animals↗
PubMed1962

Cerebral palsy--the correlation of clinical and pathological observations.

Although the causes of cerebral palsy are well known, it is often difficult to assign a cause in specific cases. In some cases, the cause may have been determined on the basis of the history and findings, only to be found in error at autopsy. In four of the five cases of cerebral palsy reported herein, there was correlation between the clinical findings and the neuropathological findings. In the fifth case, before the patient died, the cause of brain damage was thought to be measles encephalitis; but neuropathological evaluation at autopsy indicated that the brain was microcephalic and inadequately developed as a result of genetic factors.

Autopsy↗