Aims: To develop a microbially-assisted process for the removal of arsenic from contaminated groundwater. Methods and Results: A culture of Microbacterium lacticum oxidizing up to 50 mmol l -1 arsenic (III) was isolated from municipal sewage by an enrichment culture technique. Using culture immobilized on brick pieces and packed in a glass column, complete oxidation of As (III) from groundwater could be quickly achieved at neutral pH and ambient temperature with methanol as substrate. The oxidized As species were removed from groundwater using three different methods: zero valent iron, activated charcoal and ferric chloride. Conclusions: The oxidation of groundwater As (III) by a M. lacticum-immobilized column, followed by its removal using activated carbon, could be an efficient method for the treatment of As (III)-contaminated groundwater. Significance and Impact of the Study: The study will be useful in developing a combined microbiological-chemical process for treating arsenic-contaminated groundwater.

We measured the ability of the thrombin receptor activating peptide, SFLLR-NH2 (P5A) to stimulate 3H-thymidine incorporation in hamster CCL-39 fibroblasts either alone or in combination with the thrombin-derived polypeptides, YPPWNKNFTENDLL (TDP-1) and AGYKPDEGKRGDACEGDSGGPFV (TDP-2). In the presence (but not absence) of the amino peptidase inhibitor amastatin (10 microM), P5A alone (7.5 to 100 microM) caused a 1.5- to 2-fold stimulation of thymidine incorporation above basal, even though this inhibitor did not abrogate the degradation of P5A by other peptidases present in the assay medium. Neither TDP-1 nor TDP-2 alone had any effect on thymidine incorporation. However, TDP-1 (30 to 90 microM) considerably augmented P5A-mediated thymidine incorporation at low P5A concentrations (7.5 to 30 microM), shifting the P5A concentration-effect curve to the left. TDP-2 was inactive in this regard. The EC50 for this potentiating action of TDP-1 was approximately 40 microM. Further, thrombin, rendered proteolytically inactive by a low-molecular-weight bifunctional inhibitor, hirutonin-6, also acted synergistically with P5A to stimulate CCL-39 cell thymidine incorporation. We hypothesize that thrombin can cause its cellular effects, such as thymidine incorporation, not only via the proteolytic activation of its G-protein-coupled receptor, but also via the concurrent and synergistic interaction of its TDP-1 peptide domain with a separate cell surface docking site.

Walker tumor cell (1 x 10(6) cells/ml) were incubated at 37 degrees C in a stirred cuvette with rat peritoneal exudate cells (9 x 10(6) cells/ml) with or without the synthetic leukocyte chemo-attractant fMLP (2 x 10(6) M) or biologically active concentrations of the major endogenous chemo-attractant, C5a. Aggregation, induced by the chemo-attractants, was detected after 3 min by a platelet aggregometer and by studying cytocentrifuge preparations. The response was amplified in the presence of cytochalasin B (5 micrograms/ml). Tumor cells could be identified in the aggregates by their morphology or by autoradiography after labeling with 3H-thymidine. Although tumor cells were incorporated into the leukocyte aggregates, there was no appreciable change in the number of aggregates formed between tumor cells themselves. Levine III human breast tumor cells (1 x 10(6)/ml) in heparinized human blood were incorporated into leukocyte aggregates within 30 min of adding 50 U cobra venom factor to activate complement. Aggregation correlated with a decrease in complement hemolytic activity (CH50). The aggregation reaction was not cytotoxic to tumor cells when evaluated by Trypan blue exclusion or by 51Cr release. We conclude that local tumor cells can be incorporated into aggregates formed when leukocytes are stimulated by chemo-attractants. We postulate that intravascular activation of neutrophils might affect the localization of circulating tumor cells by incorporating them into microembolic cell aggregates and by causing damage to the pulmonary endothelium.

Anti-Ina antibodies have been observed in 30 of the 41 anti-Rh donors hyperimmunised with group O Ror In(a+) blood. They have also been found in four of 60 Rh immunised women. In three of these the husbands and previous children were In(a+). However, there was no evidence of haemolytic disease of the newborn due to anti-Ina antibodies alone. The Ina antigen is developed at birth though it is weaker than in adults. The strength of the Ina antigen decreases during pregnancy and returns to the previous level three months afer termination of pregnancy. The Ina antigen is affected by papain, trypsin, bromelin and neuraminidase. The antibodies in all the donors, even though their sera were preserved for more than 10 years at -20 degrees C, reacted in saline and albumin milieux and in the indirect antiglobulin procedure using anti-IgG reagents. These antibodies are complement binding as shown by the two-stage complement binding test. Treatment with 2-mercaptoethanol and DEAE-column chromatography suggested the anti-Ina antibodies were of the IgG class. Anti-Ina antibodies could possibly cause a transfusion reaction since In(a+) red cells when transfused into individuals possessing anti-Ina antibodies are eliminated from the circulation within 20 minutes.

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