Rolandic spikes and cognitive function.
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Biomedical subjects
Publications and source records attributed to A Hurst.
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Electromagnetically generated extracorporeal shock waves (without waterbath) were applied after intravenous premedication with 10-15 mg diazepam and 100 mg tramadol in the treatment of 33 patients (aged 32 to 91 years) with multiple intrahepatic stones (n = 4) or huge common bile duct stones (n = 29, 18-30 mm in diameter), which could not be removed by conventional endoscopy. Stone disintegration was achieved in 70% of common bile duct stones and in all intrahepatic concrements after 800-7500 discharges, which were applied during one (n = 21), two (n = 6) or three sessions (n = 6). Apart from mild fleabite-like petechiae at the side of shock wave transmission no other side effects were observed for a total of 51 procedures. We believe electromagnetically generated shock waves are safe, easy to apply, and relatively effective in the therapy of common bile duct and intrahepatic stones.
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We reviewed all closed obstetric claims in the records of a major physician-sponsored malpractice insurer that has written policies from 1982 to the present. Of the 54 files closed during the 6.5-year period covered by this study, 21 (39%) involved physician reports of bad outcomes that did not lead to a formal claim. Of the 33 formal claims, 14 (42%) were dismissed, either by the plaintiff's attorney or by the courts. Eighteen of the remaining 19 claims were settled before trial, with an average payment to the plaintiff of $185,000. The one suit that went to trial resulted in a defense verdict. A review of the case histories demonstrated that in the majority of cases when a payment was made, probable medical negligence had taken place. Non-meritorious claims were not compensated. For those cases in which a payment was made, the size of the settlement was commensurate with the seriousness of the injury, which almost always involved damage to the infant. Poor physician judgment was the most common source of error.
Cells of Staphylococcus aureus heated at 52 degrees C in magnesium-chelating buffers [pH 7.2, 50 mM potassium phosphate or 50 mM tris(hydroxymethyl)-aminomethane containing 1 mM ethylenediaminetetraacetic acid] leaked 260-nm absorbing material, shown to be RNA, and suffered destruction of their ribosomes. These cells did not regain their salt tolerance when repair was carried out in the presence of actinomycin D (5 microgram/ml). Cells similarly heated in magnesium-conserving buffers [pH 7.2, 50 mM tris(hydroxymethyl)aminomethane containing 10 mM MgCl2 or piperazine buffer] did not leak RNA, suffered no ribosomal damage when heated for 15 min, and recovered, at least partially, in the presence of actinomycin D. Ribosomal damage, is therefore, a consequence of Mg2+ loss and is not an effect of heat per se. Cells suspended in either Mg2+-chelating or Mg2+-conserving buffers lost salt tolerance to about the same extent during heating at 52 degrees C. Therefore, sublethal heat injury can not be attributed to ribosomal damage.
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The effect of 45 substances to restore the salt tolerance of sublethally heat-injured Staphylococcus aureus was tested. Sodium pyruvate, yeast extract, L-histine, casitone (Difco), adenosine triphosphate, and acetylphosphate were effective. For enumeration a repair medium was first used, containing sodium pyruvate and penicillin in 1% skim milk. This step was followed by counting on Baird-Parker agar with penicillinase. This method was selective; fewer than 100 staphylococci/g food could be enumerated and it gave counts about 8 times higher than the method of Giolitti and Cantoni used as a five-tube most probable number technique. Heat injury sensitized S. aureus to polymyxin.
Heating in potassium phosphate buffer causes Staphylococcus aureus to lose its salt tolerance and 30-40% of its cellular Mg2+. Repair from injury (regain of salt tolerance) occurred when injured cells were incubated under optimal conditions in synthetic media containing penicillin to prevent growth. Cells died when phosphates or amin acids were omitted from the medium. Omission of vitamins, glucose, Na+, and K+ had no effect. Omission of Mg2+ diminished repair. In a minimal repair medium (MRM) which contained only 3 X 10(-6) M Mg (as an impurity), injured cells rapidly regained their original Mg content. About 20-50% of the cells also regained their salt tolerance provided that less than 10(9) cells/ml were used. With 10(10) cells/ml there was no repair and cellular Mg content was half that of the control. Addition of 10(-3) M ethylenediamine-tetraacetic acid (EDTA) to MRM also prevented repair. Addition of 10(-2) M Mg to MRM EDTA permitted complete repair.
Staphylococcus aureus S6 sublethally heated at 52 degrees C for 15 min to 0-1 M-potassium phosphate buffer pH 7-2, lost neither the ribitol teichoic acid of the wall nor the glycerol teichoic acid of the membrane. Hurst et al. (1974) showed that this heating caused 40% loss of the cellular Mg, and we now report the loss of 65% of the ester-bound D-alanine of teichoic acid. Repair from sublethal heat injury, measured by the return of salt tolerance, occurs in a simple no-growth medium provided that the cell concentration is less than 5 x 10(8)/ml. During repair, D-alanine is rapidly synthesized. Fully-repaired cells contain four times more D-alanine than do freshly-injured cells. Magnesium is present in the medium at only 3 x 10(-6) M, yet the cellular Mg concentration returns to normal within 1 h of incubation, even in the presence of EDTA. The results suggest that repair occurs in two stages. Soon after injury, in the absence of the competitive effect of D-alanine, Mg is strongly bound to teichoic acid. In repaired or uninjured cells Mg is less strongly bound. The implications of these findings are discussed in relation to the cation-binding function of teichoic acid.
Staphylococcus aureus was grown in a complex (HK) medium either by a batch technique or by a modified batch technique after growth in a chemostat. These cultures were heat-treated at 52 degrees C, and counted on trypticase soy agar (TSA) or trypticase soy agar containing 7.5% NaCl (TSAS). When linear heat-survivor curves were obtained decimal reduction times (D52 degrees C) could be calculated from the TSA counts and pseudodecimal reduction times (D' 52 degrees C) from the TSAS counts. The D or D' values of batch-grown cells varied from 22 to 133 min and from 3 to 12 min, respectively. With cells grown by the modified technique the values were less variable (D was 22-51 min and D' was 3-7 min). D and D' values could be calculated from the same heat treatment in two of the six estimations with cells grown by the modified technique.
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Thin sections of stationary-phase Streptococcus lactis cells showed that the wall and membrane are 20 and 7 nm thick, respectively. Whole cells were examined by negative staining with ammonium molybdate and by shadowing. On air-drying of whole cells, the membrane pulled away from the wall revealing adhesions between these organelles. Adhesions could not be seen after subculture of the stationary-phase cells into complex media or into solutions containing glucose, KCl, and CaCl(2) in tris(hydroxymethyl)aminomethane buffer. The adhesions were also observed in stationary-phase cells of other gram-positive bacteria. Fractured freeze-etched cells of S. lactis had a smooth outside surface, but the inside of the wall (or outside of the membrane) had a regular structure, repeating at 10 nm, which could correspond to the adhesions observed in the negatively stained air-dried cells. Freeze-etching also revealed holes in the outside wall which had the shape of inverted truncated cones. The outside diameter of the cone was 60 nm, and the diameter on the inside surface of the wall was 20 nm. The membrane had upstanding plugs, 20 nm in diameter, which could fill the holes in the wall.