Subgingival colonization by Porphyromonas gingivalis

Porphyromonas gingivalis, a gram-negative anaerobe, is a major causative agent in the initiation and progression of severe forms of periodontal disease. In order to cause periodontal disease, P. gingivalis must colonize the subgingival region, a process that involves several distinct steps and multiple gene products. The organism must first navigate within the oral fluids in order to reach the hard or soft tissues of the mouth. Retention and growth of bacteria on these surfaces is facilitated by a repertoire of adhesins including fimbriae, hemagglutinins and proteinases. Once established subgingivally, P. gingivalis cells participate in intercellular communication networks with other oral prokaryotic cells and with eukaryotic cells. The establishment of these multiple interactive interfaces can lead to biofilm formation, invasion of root dentin and internalization within gingival epithelial cells. The resulting bacterial and host cellular locations, products and fate contribute to the success of P. gingivalis in colonizing the periodontal region.     

Setting up a pain management programme. The Ayrshire experience

A controlled trial of an outpatient cognitive behavioural pain management programme for sufferers of non-cancer chronic pain is described. A multidisciplinary team set up a programme of ten half day sessions for groups of ten to fourteen patients aiming to improve activity levels and control over pain; to reduce maladaptive pain behaviours and drug intake; to mitigate negative mood; to modify unhelpful beliefs and to maintain treatment gains by operant and cognitive methods. Self report questionnaires were employed before and six weeks, six months and one year after the programme. Fifty-eight patients entered the study group and 39 patients completed the programme and initial follow up with further attrition in long term follow up. There were no changes in the waiting list control group of twelve subjects but the study group made significant short and long term improvements in pain severity, activity levels, mood, coping and experienced fewer catastrophizing thoughts.     

Interleukin-2 Induced Systemic Toxicity: Induction of Mediators and Immunopharmacologic Intervention

Interleukin-2 has been tested as an anti-cancer agent, either alone or in combination with immune cells, but severe dose limiting adverse toxic effects have been observed. Because the pathogenesis c the toxicity has remained uncharacterized, it has not been possible to determine whether the therapeutic and the toxic events could be separated. We have examined immunopharmacologic regulation of IL2 induced mediator induction and toxicity syndrome and have compared this data with our earlier information on IL2 enhancement of immune function in murine systems. The results of this study have shown that treatment with recombinant human interleukin-2 induced increased cellular TNF activity in lymphoid organs and this activity was abrogated by an anti-TNF antibody. Additionally, continuous daily treatment with interleukin-2 also induced increases in serum corticosterone but no detectable increases in serum IL1 or TNF. The increases in serum corticosterone occured later in the treatment process and coincided with histopathologic changes in the adrenal glands and other tissues. Animals that died as a result of IL2 treatment had ascites and hydrothorax. Histopathologic changes were noted in the lungs, liver, adrenals, kidneys, gastrointestinal tract, heart and lymphoid organs. Cyclophosphamide, dexamethasone and anti-ASGM1 antibody were most effective in increasing survival and inhibiting immune enhancement but differentially effective in inhibiting TNF induction (or in certain cases gamma interferon induction), decreasing ascites or hydrothorax or affecting lymphoid proliferation in the lungs and spleen. Cyclosporin A and azathioprine were not as effective in enhancing survival and had differential effects on the other parameters. Possible mechanisms of both therapeutic and toxic events are discussed.     

The effects of local cooling on canine spinal cord blood flow

The internal spinal cord blood flow was measured in dogs at the site of local cooling using hydrogen polarography. Blood flow decreased to 50% of the normothermic values during cooling of the cord to a central temperature of 16 degrees Celsius. Upon cessation of cooling internal blood flow rapidly returned to normal values. Implications of this finding for the treatment of spinal cord injury are discussed.     

Amoebic liver abscess in Rhodesian Africans

Eighty-eight African patients with amoebic liver abscess are described. The diagnosis was readily made in pyrexial patients who had right-sided upper abdominal pain, an enlarged, very tender liver and signs at the right base. However, in apyrexial subjects (10%) and where abdominal pain was absent (7%), the diagnosis was considerably delayed. Five children (7%) were seen under the age of five, four of whom died because the diagnosis was not suspected. It is particularly emphasized that there should be a greater awareness of this condition in this age group.Amoebae were found in only a small percentage of stool (14%) and pus specimens (11%), while biopsy of the abscess edge yielded 40%. The relative values of a positive amoebic latex test (82%) and an elevated alkaline phosphatase (71%) are noted. In only half the aspirations was the classical anchovy sauce appearance seen. Metronidazole is the drug of choice with repeated aspirations for large abscesses. Mortality was 13·5%, occurring mainly in the extremes of life.     

HLA Antigens in a Scottish Psoriatic Population

Sixty-one patients in the Dundee area suffering from psoriasis were typed for HLA-A and HLA-B antigens. On the basis of the typing results, the patients were divided into three groups, and studied with respect to sex, age of onset and familial incidence of the disease. The frequency of HLA-A1 appeared to be increased and HLA-B7 decreased but HLA-B13 and HLA-B17 were highly significantly increased (P less than 10(-6) and P less than 10(-10) respectively) in the psoriatic group compared to 204 controls. Of particular interest was a highly significant association of HLA-A1 with HLA-B17 in psoriatic patients. Family studies showed HLA-B17 to be a useful genetic marker for psoriasis in the families of B17 positive patients. Considerations of age of onset, familial incidence and typing data suggest that there is heterogeneity of genetic susceptibility to psoriasis and that one probable mechanism is the dominant inheritance of a "disease allele" in linkage disequilibrium with the allele coding for HLA-B17.