Stimulation of proliferation in human colon cancer cells by human monoclonal antibodies against the TF antigen (galactose β1-3 N-acetyl-galactosamine)

In many tissues, the TF (Thomsen-Friedenreich) blood group antigen (Galβ1-3GalNAcα-) behaves as an onco-foetal carbohydrate antigen, showing increased expression in malignancy and hyperplasia. Dietary lectins which bind the TF antigen have marked effects on proliferation of epithelial cells without cytotoxicity. This led us to speculate that anti-TF antibodies, including those that naturally occur in humans, might have similar effects. Five anti-TF antibodies, TF2 (human), TF5 (human), 5A8 (mouse), 8D8 (mouse) and BM22 (mouse), but not TF1 (human) or 49H.9 (mouse), showed marked dose-dependent stimulation (95–192%) of [³H]thymidine incorporation by HT29 human colon cancer cells. Similar stimulation of proliferation of HT29 cells by these monoclonal antibodies (MAbs) was found when cell count assessment was used. Antibody-stimulated proliferation was inhibited by co-incubation with glycoproteins expressing Galβ1-3GalNAcα- (asialo glycophorin or [Galβ1-3GalNAcα-O-p-aminophenyl]_n-human serum albumin). A proliferative effect of these antibodies was also demonstrated on human colon cancer cell lines LS174T and HT29-MTX but not on Caco-2 cells. Although immunoblotting showed similar binding patterns of all the antibodies on HT29 cell membrane extracts, there was little correlation between cell surface binding assessed by immunofluorescence and proliferative response, and internalization of the biotinylated antibody TF5 was demonstrated by confocal microscopy. Our results provide further evidence that cell surface glycoproteins which express TF antigen may play an important role in the regulation of cell proliferation and also suggest that human anti-TF antibodies may have proliferative effects on cells which express TF antigen. Int. J. Cancer 73:424–431, 1997. © 1997 Wiley-Liss, Inc.     

The combined rehabilitation of patients with congenital clefts of the hard and soft palate

Effective speech rehabilitation of patients with complete clefts of the hard and soft palate can be achieved by multiple-modality treatment including logopedic training, surgical intervention, electrostimulation of the palatal and perioral muscles and nerves. Use of such treatment in 50 patients has cut down the periods of treatment from 6-7 to 2.5-4 months.     

Neuromodulation of Motor Functions Using Noninvasive Cerebellar and Spinal Direct Current Stimulation

Neuroscience and Behavioral Physiology - This review presents neurophysiological and behavioral data obtained in experimental and clinical studies in recent years based on noninvasive treatments of...     

Restoration of Motor Functions in Spinal Rats by Electrical Stimulation of the Spinal Cord and Locomotor Training

Neuroscience and Behavioral Physiology - The recovery of motor functions in chronic spinal rats with locomotor training on a treadmill combined with electrical stimulation of the spinal cord was...     

Male andropause: A myth or reality

Male andropause, male climacteric or viropause is a condition in which men suffer from complex symptomatology due to low androgen level with aging. After the age of 40 years testosterone level starts declining and andropause corresponds to the age at which a pathogenic threshold is reached. This review summarizes the etiology, consequences, screening, diagnosis, monitoring of androgen deficiency in aging male (ADAM). The pros and cons of testosterone replacement therapy (TRT) in elderly male have been discussed. Currently oral, transdermal, transbuccal, intramuscular, and subcutaneous implants are available for clinical use. The choice is made by physicians based on therapeutic indication and patient preferences.     

Spongiadioxins A and B, two new polybrominated dibenzo-p-dioxins from an Australian marine sponge Dysidea dendyi.

Two new cytotoxic tetrabromodibenzo-p-dioxins, spongiadioxins A (1) and B (2), were isolated from an Australian marine sponge Dysidea dendyi. The structures of these compounds were established by 1D and 2D NMR spectroscopy, X-ray analysis of the methyl ether of spongiadioxin A (3), and synthesis of the methyl ether of spongiadioxin B (4) from diphenyl ether (9) isolated from Dysidea herbacea.