A proposed system whereby a (colcemid-induced) S2 phase is responsible for the tetraploidy found in cultured human amniotic fluid cells

The results of this study, using cultured amniotic fluid cells (AFC) and colcemid, together with results of several other investigators who worked with colcemid and DNA synthesis, have led to the proposal of a hypothesis suggesting a mechanism by which tetraploidy may be induced. Data from this study of 24,455 mitotic spreads indicate increased concentrations of colcemid, as well as extended exposure times, results in a higher incidence of tetraploidy in cultured AFC, with no concomitant increase in the unexposed control cells.     

Spinal cord energy metabolism following compression trauma to the feline spinal cord

The purpose of this study was to determine the spinal cord metabolic state for 24 hours after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190-gm weight on the spinal cord for 5 minutes. Biochemical analysis of the injured segment revealed a significant depletion in the levels of adenosine triphosphate (ATP), phosphocreatine (P-creatine), and total adenylates for the entire 24-hour recovery period. Glucose levels initially declined, but by 1 hour had normalized, and at 8 and 24 hours were significantly supranormal. The lactate/pyruvate ratio and tissue lactate concentrations increased four and five and half times, respectively, for the first 4 hours after injury. Between 8 and 24 hours, lactate levels remained elevated, whereas the lactate/pyruvate ratio declined to contol levels as the result of a significant rise in the tissue pyruvate concentration. This sequence of metabolic changes suggested that metabolism was probably not homogeneous throughout the injured segment, and that tissue metabolic rate was depressed for the initial 4 hours after trauma then increased in metabolically active tissue for the remainder of the 24-hour recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes results from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.     

Partial development of the corpus callosum

PURPOSE: To determine whether the MR findings of callosal dysgenesis suggest that the partially formed corpus callosum in humans is the result of arrested growth or delayed continued development. METHODS: The MR scans of 25 patients with callosal dysgenesis were reviewed to determine whether the observed corpus callosum corresponded to the form and position of a portion of a normal corpus callosum, as suggested by a theory of arrested growth. RESULTS: In 10 of the 25 cases, the partially formed corpus callosum corresponded to a portion of a normal corpus callosum. In the remaining 15 cases, the partially formed corpus callosum was located posterior to the expected location of a normal genu and inferior to the expected location of a normal body. CONCLUSIONS: Corpus callosum dysgenesis in humans may be caused by arrested growth in some cases; in other cases it is most likely caused by delayed continued development that attempts to compensate for earlier abnormalities in the evolution of midline structures.     

Development of a model angiography informed consent form based on a multiinstitutional survey of current forms

PURPOSE: To develop an informative consent form for angiography that can be read and understood by a patient with an eighth-grade level of education. MATERIALS AND METHODS: Consent forms from 125 medical centers were evaluated with RightWriter 4.0 software. The readability index, a measure of educational grade level needed to understand a document, was determined for each form. Features of forms and discussion of complications were evaluated. A model consent form was developed. RESULTS: Analysis of 27 consent forms revealed a mean readability index of 14.2; to adequately understand the documents, an average of 2.2 years of college were required. Alternatives to the procedure were listed in 14 forms (52%). All consent forms listed potential complications, but only 15 (56%) identified specific numeric risks, and attempts to classify complications according to severity were made in only five (18%). CONCLUSION: An angiography consent form has been developed that can be understood with an eight-grade level of education. It should allow patients to more easily understand the procedure and its risks, benefits, and alternatives. It remains the obligation of the physician to tailor the discussion for each procedure to meet the needs of each patient.     

Antibody selection for immunohistochemical survey of equine tissue

A membrane-bound protease induced by sulfur mustard in cultured normal human epidermal keratinocytes (NHEK) was purified and partially characterized. Maximum enzyme stimulation occurred at 16 hr after normal human epidermal keratinocytes were exposed to 300 microM sulfur mustard. Purification to homogeneity of the protease was accomplished by Triton X-100 solubilization, ultracentrifugation, and dialysis, followed by ion-exchange chromatography through DEAE-cellulose and finally hydrophobic column chromatography through phenyl Sepharose. Analysis of the purified enzyme by SDS-PAGE revealed a single polypeptide at the 80 kDa region. Further investigation of biochemical properties showed that a synthetic serine-specific Chromozym TRY peptide and the physiological protein laminin were good substrates for this enzyme. Moreover, this enzyme was inhibited mostly by the serine-protease inhibitors leupeptin and di-isopropyl fluorophosphate and not by the cysteine protease inhibitor E-64 or the metalloprotease inhibitor 1,10-phenanthroline (Component H, CH), indicating the serine protease nature of this enzyme. This enzyme had a pH optimum in the range of 7.0 to 8.0. Amino acid sequencing of the purified enzyme revealed that this enzyme belongs to the endopeptidase family (serine protease), and is homologous with a mammalian-type bacterial serine endopeptidase that can preferentially cleave K-X, including K-P. These results suggest that serine-protease stimulation may be one of the mechanisms of mustard-induced skin blister formation, and that some specific serine-protease inhibitors may be useful for the treatment of this sulfur mustard toxicity.