A more efficient biofeedback procedure for the treatment of nocturnal bruxism

This study describes a novel approach in the use of a conditioning procedure for the treatment of nocturnal bruxism. The effectiveness of the procedure is demonstrated through its application with two nocturnal bruxists in controlled case study designs. Subject 1 received several variations of this procedure and the results indicated that using a loud tone which she manually reset after awakening was the most effective approach to this treatment. The second study was designed to compare the effectiveness of relaxation training to the conditioning technique. Subject 2 failed to show any decrease in her bruxing behaviour when taught relaxation. However, she showed immediate decreases in both frequency and duration of bruxing responses when treated with the biofeedback procedure. The need for future research in this area is discussed with emphasis on the development of low cost, home treatment units.     

Immune-mediated adherence of eosinophils to Toxocara canis infective larvae: the role of excretory-secretory antigens

The participation of Toxocara canis larval excretory-secretory antigens in immune-mediated adherence was determined in vitro. Adsorption of immune sera with excretory-secretory antigens removed some complement components, removed IgG antibody directed against larval surfaces, and abrogated all adherence observed with untreated immune serum. At least four antigens could be implicated in adherence, by Western blot analysis of adherence mediating sera. Scanning and transmission electron microscopic examination of larval-eosinophil interactions revealed that eosinophils adhered to a membranous sheath-like layer that was frequently detached from the larval epicuticle. The layers appeared to be composed of surface antigens and antibody, and may provide larvae with protection against antibody and eosinophil toxins by preventing their contact with the epicuticle. The release of surface antigens also may be important in allowing larvae to evade the host's immune response by facilitating the removal of antibody and eosinophils from the larval surface.     

Increased expression of urokinase-type plasminogen activator in colorectal carcinoma and in adenomatous polyps

Human plasminogen activators (HPA) comprise the tissue type produced mainly by endothelial cells of 66 000 molecular weight (MW) which is principally involved in fibrinolysis (HPA66) and the urokinase type of 52 000 MW (HPA52) which is implicated in the invasion process of malignancy. The purpose of this study was to elucidate the pattern of HPA expression in histologically normal colonic mucosa, sporadic polyps, polyposis coli polyps, and in colon cancer tissue, to determine whether the expression of HPA52 is a correlate of neoplastic transformation of colonic epithelial cells. Homogenates of colonoscopic biopsies and resected colon tissue were subjected to polyacrylamide gel electrophoresis and the HPA activity was detected by a fibrin overlay gel. In histologically normal mucosal biopsies from non-cancer-bearing colons and in uninvolved mucosa from cancer-bearing colons, only HPA66 was detected. By contrast, all 19 colon cancer specimens expressed HPA52 and 16 of these also showed HPA66 activity. Two of three colon cancer cell lines showed HPA52 activity, but none expressed HPA66. HPA52 activity was observed in 17 of 20 adenomatous polyps, all of which displayed HPA66 activity. No correlation was found between polyp size, degree of epithelial dysplasia or the type of polyp architecture, and the semiquantitative estimates of HPA52 activity as judged by the areas of fibrinolysis generated.
This study of HPA52 in the colon epithelial neoplasms comprising adenomatous polyps, colon cancer tissue and colon cancer cell lines suggests that the transformation of the colon epithelial cell correlates with increased expression of HPA52, an enzyme that has been implicated in the invasive process of malignancy.     

The Mode of Inheritance of PTA Deficiency: Evidence for the Existence of Major PTA Deficiency and Minor PTA Deficiency

Plasma thromboplastin antecedent (PTA) activity was measured with aquantitative assay in the available members of the families of eight propositiwith severe PTA deficiency. PTA deficiency was found to exist in two forms:major PTA deficiency, characterized by PTA levels of up to 20 per cent of ourstandard reference plasma and by the potential for serious surgical bleeding,and minor PTA deficiency, characterized by PTA levels between 30 and 65per cent of our standard reference plasma and by the absence of significantsurgical bleeding. Minor PTA deficiency was found in parents and childrenof subjects with major PTA deficiency.

It would appear that the gene for PTA deficiency is an incompletely recessive or "intermediate" gene which produces major PTA deficiency in the homozygote and minor PTA deficiency in the heterozygote.

Submitted on March 27, 1961 Accepted on May 16, 1961     

Blood Coagulation Factors in Total Body Irradiation

Investigation of the clotting factors in five humans accidentally exposed tototal body irradiation disclosed no deficiencies. There was no evidence of acirculating anticoagulant in any case. Moderate fibrinolysis was seen in twoinstances in the same individual but was not evident in the others. At theeleventh day there was uniformly a moderate increase in the levels of fibrinogen. At the twenty-ninth day there was observed an increase in the levels offactors V and VIII coincidental with thrombocytopenia. This change reverseditself with recovery. A similar increase in the levels of factor VIII and less soof factor V was seen in cases of idiopathic thrombocytopenic purpura andsecondary thrombocytopenia. An increase in level of factor VIII was observedin patients on oral coumarin anticoagulation. It is concluded that the supernormal levels of factors V and VIII are secondary to lowered thrombin levelsin the circulating plasma as a result of the thrombocytopenia and not duedirectly to the effect of irradiation.

Submitted on June 12, 1961 Accepted on September 15, 1961