Biomedical subjects
Publications and source records attributed to T M Chang.
A novel approach is reported for the removal of ammonium formed from the conversion of urea by urease. By alkalinization, ammonium is converted into free ammonia. Free ammonia can then be very easily removed by a number of approaches: as gaseous ammonia by air bubbling, oxygenator, or air ventilation; by adsorbent for free ammonia; or other approaches.
The in-vitro removal of free phenols by means of perfusion over albumin coated cellulose nitrate microencapsulated activated charcoal (ACAC) was studied. The phenols tested were in the form of a standard solution comprised of phenol, p-cresol, and p-hydroxyphenylacetic acid in a ratio of 1:5:14. Four different activated charcoals were tested for their adsorption capacity. Further studies were conducted to determine; the effect of microencapsulation and albumin coating of the activated charcoal on the adsorption of phenols; the adsorption isotherm of phenols; the capacity; and the clearance values. The results obtained suggest that ACAC used in the management of patients with uremia or hepatic coma is extremely efficient in removing phenols in aqueous solution in the in-vitro situation.
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Plasma beta-endorphin was measured in 35 chronic schizophrenic patients (15.47 +/- 15.39 pmol/L) and 3 normal volunteers (19.55 +/- 11.23 pmol/L). There was no significant difference between the levels of the two groups.
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The present status of adsorbent hemoperfusion is introduced with emphasis on available systems and their roles in uremia, acute intoxication, fulminant hepatic failure and chronic schizophrenia.
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Microencapsulated activated charcoal has been used in this report to remove galactose from aqueous solution in-vitro and from blood of galactosemic rats. Coconut charcoal is not effective in removing galactose, whereas petroleum-based activated charcoal is very effective.
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In order to study the mechanism of entry of plant seed and bacterial toxins into mammalian cells, methods have been developed to synthesize artificial protein hybrid conjugates containing a moiety which binds to a cell membrane receptor and an active fragment of a toxin protein. Utilizing methyl-5-bromovalerimidate, a disulfide cross-linked conjugate of human placental lactogen (hPL) and diphtheria toxin fragment A (toxin A) was synthesized. The reagent was prepared from 5-bromovaleryl nitrile by Pinner synthesis and then used to amidinate hPL. The bromo group thus introduced was converted to S-sulfonate by nucleophilic displacement with 1 M aqueous sodium thiosulfate at room temperature overnight. The S-sulfonated hPL reacted readily with the-SH gorup of reduced toxin A to form a 1 mol/mol of disulfide conjugate in high yield. Thus when reduced toxin A was incubated with a 4-fold excess of the hPL S-sulfonate at 4 degrees and pH 6.5 for 120 h, a conjugate yield of 50% relative to the toxin A input was obtained. Homopolymer formation was negligible and the product was purified by gel filtration on Sephadex G-150. Purity of the conjugate estimated by quantitative analysis of sodium dodecyl sulfate gels was 90%. The toxin A-hPL conjugate retained the activities of both toxin A and hPL, as reported in the accompanying paper. This method of preparing protein hybrid conjugates appeared to have advantages over previous methods utilizing bifunctional reagents with respect to both yield and freedom from homopolymer formation.
The biochemical and biologic properties of a purified disulfide conjugate of diphtheria toxin fragment A and human placental lactogen (toxin A-hPL) have been studied by (a) assaying the ADP-ribosyltransferase activity of the intact conjugate, (b) assaying the binding of the intact conjugate to mammary gland plasma membrane lactogenic receptors, and (c) assaying the effect of the conjugate on the rate of protein synthesis in rabbit mammary gland explants maintained in organ culture. The toxin A-hPL conjugate retains one-third of the NAD+:EF-2 ADP-ribosyltransferase activity of toxin A, and 26% of the hPL-binding activity to lactogenic receptors. Binding activity was demonstrated by radioreceptor assay and by assaying toxin A activity bound to membranes which was competitively displaced by excess hPL. Since the toxin A-hPL conjugate retained activities of its separate subunits, it could be regarded as a structural analogue of nicked diphtheria toxin with replacement of the original membrane-binding chain by another binding chain that is specific for lactogenic receptor. However, the conjugate failed to inhibit protein synthesis in organ-cultured mammary gland explants, although these were sensitive to native diphtheria toxin and could bind hPL. It is concluded from these results that the toxin A-hPL conjugate does not act as a functional analogue of diphtheria toxin with altered receptor specificity, and that the hPL receptor cannot mediate the entry of toxin A or toxin A-hPL from membrane-bound conjugate into the cytosol site of action of toxin A.
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Control trials and statistical analysis were carried out to assess the effects of albumin-collodion microencapsulated activated charcoal (ACAC) hemoperfusion on fulminant hepatic coma. A rat model of galactosamine induced fulminant hepatic coma was used. Rats which did not recover died at 3.0+/-0.6 days after galactosamine injection. Those which survived this period recovered. Forty-eight hours after galactosamine injection, a test group of 21 rats were treated with 1 hour hemoperfusion and compared with an untreated group of 23 rats. 71.4% of the treated group survived as compared to 30.4% of the untreated rats. Statistical analysis (t test) shows a significant increase in recovery for the treated group (less than 0.01). Biochemical and histological results will be discussed.