The other Flexner report: how Abraham Flexner was diverted from medical schools to brothels.
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Biomedical subjects
Publications and source records attributed to H A Johnson.
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Urine and cerebrospinal fluid (CSF) were collected from 10 healthy male volunteers after ingestion of 120 g ethanol and under similar conditions without ethanol. Dopamine (DA), homovanillic acid (HVA), norepinephrine (NE), 4-hydroxy-3-methoxyphenylglycol (HMPG), 4-hydroxy-3-methoxymandelic acid (HMMA = VMA), 1-carboxysalsolinol (1-CSAL), salsolinol (SAL) and methylated salsolinol (M-SAL) were analyzed with gas chromatography-mass spectrometry. In CSF collected 6 h after ethanol intake the concentration of NE and its metabolite HMPG were significantly elevated (P less than 0.025 and P less than 0.005, respectively) compared to control conditions. The other compounds analyzed did not change significantly. In urine collected during 10 h after ethanol administration the excretion of HMMA was significantly reduced (P less than 0.01) and the HMPG/HMMA ratio was significantly elevated (P less than 0.005) reflecting a change in the peripheral red-ox state during ethanol oxidation. The excretion of DA and its major metabolite HVA did not change. However, the DA-derived condensation products 1-CSAL (from DA and pyruvate) increased (P less than 0.001), while SAL (from DA and acetaldehyde) decreased (P less than 0.005) after ethanol ingestion compared to the control situation. The increased excretion of 1-CSAL indicated that the ethanol metabolism interferes with the glucose metabolism, probably through an acetaldehyde-mediated inhibition of the pyruvate dehydrogenase complex.
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In this study the entire hippocampal formation, both grey and white matter, was analyzed as a unit and the number of neurons and glia per unit weight was determined. Tissues were obtained from the right cerebral hemispheres of 25 human brains. We found that the neuron population density increases slightly between 20 and 87 years of age. Previous studies using classical stereological techniques or electron-optical image analysis of histological sections have shown no increase of neuron density of the grey matter of the hippocampus with increasing age. However, our data, based upon a technique of cell dispersion and hemacytometer counting, are not strictly comparable. We attribute our findings of an apparent increase in neuron density with age to the fact that we analyzed the entire hippocampal formation, both with white and grey matter, which had undergone senescent shrinkage--particularly within the white matter. The findings of the present study are to be contrasted with an earlier study of the aging visual cortex using 20 of the same brains and employing the same techniques. Taken together, the two reports suggest that age-dependent neuron loss takes place at very different rates in different areas of the human brain and that the mean life span of neurons in the hippocampus is considerably longer than that of the neurons in the visual cortex.
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The rates of heat denaturation of a protein component of endoplasmic reticulum, NADPH cytochrome c reductase, measured in the temperature range of 37-47 degrees C, show that this protein is highly unstable in the range of temperatures used in clinical hyperthermia. The rate of enzyme inactivation increases some 20-fold as the temperature increases from 37 degrees C to 45 degrees C. The enzyme has an in vitro half-life of only 7 h due to thermal inactivation at 37 degrees C. This suggests a general scheme for the physiological degradation pathway of intracellular proteins in which the first step is rapid thermal denaturation of the molecule followed by a second and slower step of proteolytic degradation. The rapid physiological turnover of intracellular proteins may be an unavoidable cost of maintaining metabolic precision in the presence of thermal noise at normal body temperature.
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Measured by a cell dispersion technique, the neuron population densities of the macular projection areas of 23 individuals aged 20 to 87 years fell from about 46 million neurons per gram of tissue of age 20 to about 24 million neurons per gram at age 80. A corresponding increase in glial cells was found in the gray and subjacent white matter. Since the older brains showed a significant decrease in mass, the decrease in neuron population density could only reflect an absolute loss of neurons proportional to or greater than the nearly 50% loss indicated by these data. Neuron death in the macular projection area of the human visual cortex is evidently a major factor in the loss of visual acuity in old age.
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An excellent cleft lip repair demands and depends upon good postoperative care. The strain caused by crying can be minimized by eliminating restraints and by early hospital dismissal. Protein and vitamin C are important in healing. A nongreasy pressure dressing capable of absorbing serum is applied for the first night only, then the suture line is sponged with cold water after each feeding. Following suture removal, effective bridging is achieved by applying perforated Zonas adhesive directly to the wound. The care outlined has been used successfully for 93 cleft lip patients over 24 years. Both sides of bilateral clefts were closed at one operation. Two patients among 18 with bilateral clefts had one side break down; 1 patient had a partial breakdown on both sides. This same postoperative routine has been used successfully when operating under less than ideal circumstances in primitive areas. Good postoperative care consists of attention to many little details, none of which are important by themselves but which, when added together, give perfection.
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