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J L Arnold

Publications and source records attributed to J L Arnold.

22 records · Page 2Linked to original sources

Natural cytotoxicity of human serum. A natural IgM 'antibody' sensitizes transformed murine cells to the lytic action of complement.

The natural cytotoxicity of human serum on murine L cells, EA and Sa 180 cells is expressed as a rapid cytolysis at 37 degrees C. This cytotoxic system is analyzed as to its active constituents and their functional relationships. Ultrastructural studies indicate that cell injury and death are initiated within 10 min by membrane disruption. A trypan blue assay for cell death was used to study serum toxicity in individual normal healthy adults, pregnant females and newborn infants. Pregnancy sera, particularly in the 2nd and 3rd trimesters, were consistently more toxic than male serum or nonpregnant females. Cord serum was typically nontoxic. Pools of normal fresh pregnancy serum were used for immunochemical analysis of the cytotoxic activity. By a variety of immunologic and immunochemical techniques it was shown that the cytotoxicity was, in part, due to the combined action of alternative and classical pathways of complement, the former being more prominent. The lytic action of complement was shown to be greatly amplified by the prior adsorption of IgM on the target cells' surface. This IgM is a critical determinant of the cytotoxic reaction. It probably contains a natural 'antibody' to cell surface antigen(s), whose combination activates both pathways of C.

Animals↗

Transformation of an arachidonic acid hydroperoxide into epoxyhydroxy and trihydroxy fatty acids by liver microsomal cytochrome P-450.

In the absence of NADPH, the addition of an arachidonic acid hydroperoxide, 15-hydroperoxyeicosa-5,8,11,13-tetraenoic acid, to liver microsomes, prepared from phenobarbital-treated rats, resulted in the formation of two major metabolites and several minor products, some of which have been purified by reverse-phase high-performance liquid chromatography. We propose the structures of the two major products to be 13-hydroxy-14,15-epoxyeicosa-5,8,11-trienoic acid and 11,14,15-trihydroxyeicosa-5,8,12-trienoic acid based on spectral characteristics and mass spectral analysis of derivatives of the compounds. A potential heterolytic cleavage product, 15-hydroxyeicosa-5,8,11,13-tetraenoic acid, was not a product of the reaction. Ferric cytochrome P-450 catalyzed the formation of these products as shown by the inability of boiled microsomes to support the reaction, the inhibition of epoxyhydroxy and trihydroxy fatty acid formation by imidazole derivatives which bind tightly to the ferric heme iron of cytochrome P-450, and the inability of carbon monoxide (which binds to ferrous P-450) and free iron chelators (EDTA and diethylenetriaminepentaacetic acid) to inhibit product formation. These results show that liver microsomal cytochrome P-450, in addition to its role in the NADPH-dependent metabolism of arachidonic acid, can utilize a hydroperoxide to produce an interesting series of potentially important arachidonic acid metabolites.

8,11,14-Eicosatrienoic Acid↗

A comparison of a new reflectance oximeter with the Hewlett-Packard ear oximeter.

The purpose of this study was to characterize the accuracy and dynamic response characteristics of traditional transmittance pulse oximeters and a new reflectance pulse oximeter with regard to the current standard in oximetry, the Hewlett-Packard ear oximeter. Studies were performed with 15 healthy male and female subjects. A rebreathing technique was employed to produce a steady fall in oxygen saturation and to maintain constant, eucapnic, end-tidal CO2 levels. The oximeters' analog outputs were recorded by a Western Graphtec Linearecorder and by an IBM-PC utilizing an analog-to-digital converter for data collection at 5 Hz. The agreement between two clinical methods of measurement was used as the statistical technique of comparing new technology (pulse oximetry) with the current standard (Hewlett-Packard ear oximetry). The mean of the difference between the Hewlett-Packard and the pulse oximeter with reflectance sensor was 0.28%, with a range of difference of +/- 3.49%. This value was similar to that of the transmittance oximeters (Criticare 501+: 0.92 +/- 2.11), (Physio-Control: 3.15 +/- 2.04), (Ohmeda 3700: 2.05 +/- 2.06). There was virtually no response-time difference between the reflectance oximeter with the sensor placed on the subject's forehead and the Hewlett-Packard ear oximeter. The authors conclude that the accuracy of the reflectance oximeter is within the limits of clinical acceptance for monitoring and trending of arterial oxygen saturation in healthy subjects.

Equipment Design↗