Dynamics of hip joint effusion after posterior soft tissue repair in total hip arthroplasty

Dislocation after total hip replacement is more common in the early, postoperative period. Postoperative intraarticular haematoma and remaining seroma fluid and/or weakened posterior soft tissue wall may be contributing factors. Our purpose was to compare and follow with sonography the resorption of the postoperative volume of intraarticular fluid/synovial oedema after total hip arthroplasty (THA) with or without posterior soft tissue repair. Thirty-three consecutive patients with hip osteoarthritis were admitted for THA. All of them received the same type of cemented implant. Patients were randomised for posterior soft tissue repair or not. Sonography, measuring the anterior capsular distension, indicating the volume of intraarticular fluid/synovial oedema in the prosthetic hip joints, was performed after six and 12 months in all patients. At six months postoperatively greater capsular distension, i.e., remaining volume of intraarticular fluid/synovial oedema, was observed in the group with posterior soft tissue repair than in the group without. After one year the capsular distension had decreased in both groups and there was no significant difference between the groups. Our results show that posterior soft tissue repair after THA is associated with increased capsular distension during the first six months. After 12 months the volume of intraarticular fluid/synovial oedema is the same with or without posterior soft tissue repair.     

The proto-oncogene Cot kinase participates in CD3/CD28 induction of NF-kappaB acting through the NF-kappaB-inducing kinase and IkappaB kinases

The proto-oncogene Cot/Tpl-2 encodes a MAP3K-related serine-threonine kinase. Expression of wild type Cot activates the IkappaB kinases (IKK) leading to induction of NF-kappaB. Conversely, expression of kinase-deficient Cot inhibits CD3/CD28 but not TNF alpha induction of NF-kappaB. These findings suggest the selective involvement of Cot/Tpl-2 or a closely related kinase in the CD3/CD28 costimulatory pathway leading to induced nuclear expression of NF-kappaB. In contrast, a kinase-deficient mutant of the NF-kappaB-inducing kinase (NIK) inhibits both CD3/CD28 and TNF alpha signaling, indicating that these pathways converge at or prior to the action of NIK. Consistent with such a sequential function of these two kinases, Cot physically assembles with and phosphorylates NIK in vivo.     

Specific binding of human corticosteroid-binding globulin to cell membranes.

Specific binding sites for corticosteroid-binding globulin were detected on membranes prepared from human prostates. The binding sites are typical of membrane receptors: they are saturable and specific and have high affinity. There was little specific binding at 4 degrees C and 23 degrees C. Maximal specific binding was obtained at 37 degrees C. Scatchard analysis revealed the presence of a single set of binding sites with an apparent dissociation constant of 8.7 X 10(-7) M and a binding capacity of 22 pmol/mg of membrane protein. The sites were specific for corticosteroid-binding globulin; binding was not inhibited by human testosterone/estradiol-binding globulin, by albumin, or by transferrin. The density of specific binding sites in membranes obtained from several organs from the rhesus monkey is consistent with the hypothesis that corticosteroid-binding globulin is involved in the transport of steroid hormones into target tissues.     

Autoantibodies to neutrophil cytoplasmic (ANCA) and endothelial cell surface antigens (AECA) in chronic inflammatory bowel disease

Sera from 103 patients with chronic inflammatory bowel disease (IBD) were tested prospectively for antibodies against neutrophil cytoplasmic antigens (anti-neutrophil cytoplasm antibodies, ANCA) and endothelial cell surface antigens (anti-endothelial cell antibodies, AECA) by indirect immunofluorescence (IIF) and assays based on whole fixed neutrophils, purified neutrophil enzyme substrates and human umbilical vein endothelial cells. Using IIF, ANCA were found in 26 IBD sera (25%) and in none of 51 controls. Twenty-two positive sera (85%) were from patients with ulcerative colitis (UC). The pattern of distribution of immunofluorescence was always perinuclear (P-ANCA). A majority of UC patients positive for these autoantibodies (68%) had active colitis, but none had evidence of vasculitis. Using a whole neutrophil ELISA, binding was demonstrable in 73% of UC sera compared to 27% of Crohn's (CD) sera and only 4% of controls. Unlike vasculitis sera, UC sera with P-ANCA did not bind strongly to myeloperoxidase (MPO). Forty-five per cent of IBD sera tested positive for IgG AECA in an endothelial cell ELISA, compared to seven of 51 (14%) controls. Binding correlated with both active and extensive colitis. A type of P-ANCA, in most cases distinct from MPO-specific P-ANCA observed in vasculitis, is detected in a significant proportion of patients with UC, but rarely Crohn's colitis and therefore may be of differential diagnostic value. IgG AECA are also frequent in CIBD sera but are less disease specific than ANCA. (Aust NZ J Med 1992; 22: 652ndash;659.)     

Bone loss in inflammatory arthritis: mechanisms and therapeutic approaches with bisphosphonates

The inflammatory process in rheumatoid arthritis provokes intense bone resorption, evidenced as bone erosions, juxta-articular osteopenia and generalized osteoporosis. These types of bone loss share a common pathogenesis, and the role of osteoclasts in focal bone erosion was verified in elegant animal studies. The tumour necrosis factor (TNF) family of cytokines and receptors--specifically TNF-alpha, RANKL, RANK and OPG--are dominant regulators of osteoclastic bone resorption in rheumatoid arthritis. The confirmation of the osteoclast mechanism provides new insight into the structural joint protection afforded by disease-modifying drugs and suggests innovative approaches to limit bone destruction. Emerging treatment strategies for bone disease in rheumatoid arthritis are the use of monoclonal antibodies to neutralize RANKL, and powerful bisphosphonates that target pathogenic osteoclasts.