A case report of the laparoscopic repair of bilateral inguinal hernias performed under local anesthesia with intravenous sedation is presented. The combination of nitrous oxide for peritoneal insufflation and an ultrasonically activated scalpel for dissection made the procedure feasible. It is hoped that this technique can extend laparoscopic surgery to patients who are poor candidates for general anesthesia.

Much has been written about preoperative strategies in the treatment of pancreatic adenocarcinoma, yet there has been very little comment concerning other periampullary malignancies. This review discusses current issues relevant to the further development of preoperative adjuvant treatment of pancreatic adenocarcinoma. A small series of patients with ampullary adenocarcinomas treated with preoperative adjuvant chemoradiotherapy is also described.

Antiserum prepared against rat renal calcium-binding protein (CaBP) was used with the unlabeled antibody peroxidase-antiperoxidase (PAP) technique to localize the 28,000 molecular weight CaBP in the cerebellum of the bullfrog, Rana catesbeiana. Whole brains of premetamorphic tadpoles and adults were fixed in Bouin's solution for 2 or 24 h and embedded in paraffin. 8-µm parasagittal sections were prepared and treated by the PAP method. Purkinje cells of the cerebellum in tadpoles and adults were specifically stained for CaBP. In the premetamorphic corpus cerebelli, the stained Purkinje cells corresponded to the precociously developed Purkinje cells described previously. In the auricular lobe region of the cerebellum mature Purkinje cells were stained. In addition, smaller stained cells were seen. The latter were presumed to be immature Purkinje cells that would mature at the time of metamorphosis. Immunoblot procedure demonstrated cross-reactivity for the ranid brains in the 28,000 molecular weight region. This immunoreactive band comigrated with the immunoreactive band observed with purified rat renal CaBP. Although the exact functional significance of CaBP is unknown at this time, our immunocytochemical and immunological findings indicate that CaBP is an excellent marker for studies of Purkinje cell maturation.

Chimeric mouse/human B72.3 (cB72.3) antibodies having a human IgG1 (gamma 1) or IgG4 (gamma 4) constant region were compared to the native murine IgG1 B72.3 (nB72.3) monoclonal antibody (mAb) for their ability to participate with human effector cells in antibody-dependent cellular cytotoxicity (ADCC). Because the TAG-72 antigen recognized by B72.3 is poorly expressed on tissue-cultured tumor cell lines, the xenografted OVCAR-3 human ovarian carcinoma ascites was used as a cytotoxicity target. The lytic activity of the cB72.3(gamma 1) mAb with peripheral blood lymphocytes was 1.5- to 50-fold greater than that of the nB72.3 mAb and usually the cB72.3(gamma 4) mAb. However, lymphocytes from some donors had similar ADCC activity with either the cB72.3(gamma 1) or cB72.3(gamma 4) mAb. The cB72.3(gamma 1) and the murine anti-colon carcinoma CO17-1A mAb had comparable activity in mediating ADCC against the OVCAR-3 tumor. Exposure of lymphoid cells to interleukin-2 (IL-2) (100-500 U/ml) for 24 h to generate lymphokine-activated killer (LAK) cells augmented ADCC mediated by the cB72.3(gamma 1) mAb 2- to 22-fold. By contrast, LAK cells from most donors expressed weak non-specific cytotoxicity against OVCAR-3 ascites tumor cells. The cB72.3(gamma 1), and to a lesser extent, the cB72.3(gamma 4) chimera also participated with monocytes in mediating ADCC, but the antibody-dependent lytic potency of monocytic effectors was much weaker than that of IL-2-activated lymphoid cells. These studies show that the cB72.3(gamma 1) mAb has appreciable ADCC-mediating properties, suggesting a potential role for its incorporation into treatment strategies utilizing adoptive killer cell and/or lymphokine therapy.

The antibody-dependent cellular cytotoxicity (ADCC) properties of a murine monoclonal antibody (MAb), designated D612 (IgG2a), which reacts with human colon carcinomas, was studied using normal human peripheral blood lymphocytes (PBMNC). Although the level of ADCC of PBMNC with D612 varied among different donors, it was 20 to 30 times higher than the lytic activity of control cultures containing isotype-matched control MAb. Incubation of PBMNC with recombinant interleukin-2 (IL-2) resulted in a 2- to 5-fold augmentation in the cytotoxicity of effector cells exposed to MAb. This augmentation was apparent after subtracting nonspecific cellular cytotoxicity from the total cytotoxicity mediated by activated effector cells in the presence of D612. Optimal stimulation of specific ADCC with IL-2 appeared after 24 hr of culture in 500 U/ml of IL-2, resulting in a 3.8 +/- 1.7 fold increase in lytic units. However, stimulation of ADCC was also evident at 10 U/ml of IL-2. Furthermore, antibody dose titrations with untreated and IL-2 activated effectors showed that the threshold dose of MAb needed for efficient ADCC was reduced by 200-fold with IL-2. Depletion of FcR gamma III-positive lymphoid cells markedly reduced D612 ADCC, demonstrating the participation of NK/LAK cells in D612-mediated ADCC. Low levels of ADCC activity were found associated with adherent cells, either untreated or following their activation with gamma-interferon, while D612 was most active with non-adherent effectors. The specificity and ADCC properties of the D612 MAb suggest that it should be considered as a candidate for immunotherapy of colon cancer, particularly when used in combination with IL-2 plus LAK cell treatment.

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