Patients with prosthetic joints: Are they at risk when receiving invasive dental procedures?

Most prosthetic joint infections (PJI) are due to wound contamination at the time of surgery. Some infections occur due to the hematogenous spread of bacteria from distant sites of infection. A review of the literature fails to associate PJI with transient bacteremias from invasive dental procedures. Several authors have described conditions which, they believe, render patients with prosthetic joints more at risk for infection. Prosthetic joint patients with these "high risk" conditions have the same types of infecting organisms as other patients with PJI. This indicates that the infecting bacteria are from wound contamination or distant sites of infection and not related to dental procedure bacteremias. Based on this review, antibiotic prophylaxis is not indicated for patients with prosthetic joints when receiving invasive dental procedures, since there is no proven benefit and there are known risks involved with the use of antibiotics. However, the American Dental Association (ADA) and the American Academy of Orthopaedic Surgeons (AAOS), in an advisory statement, suggest prophylaxis for "high risk" patients. The ADA and AAOS recommend a single dose of amoxicillin, cephradine, or clindamycin when prophylaxis is selected. The dentist is ultimately responsible for making treatment recommendations for his or her patients.     

The neutrophil oxidative burst in diarrhoea – associated haemolytic uraemic syndrome

. Neutrophil-mediated tissue damage has been implicated in the pathogenesis of diarrhoea-associated haemolytic uraemic syndrome (D+ HUS). This study evaluates priming and activation of the neutrophil oxidative burst in D+ HUS using chemiluminescent techniques. Peripheral blood neutrophils from 11 children with acute D+ HUS were examined. No difference was found in the oxidative burst of neutrophils from patients and controls. Serum elastase levels were measured in 8 patients and found to be significantly elevated. Although elastase results suggest neutrophil activation, chemiluminescence studies do not confirm this in the peripheral blood neutrophil. This does not support a significant role for circulating agents in priming and activating the peripheral blood neutrophil. Received August 17, 1995; received in revised form and accepted November 27, 1995     

Facilitating Perinatal Grieving Between the Mother and the Father

Society often expects mothers and fathers to share equally in the perinatal grief process because the child was a common bond between them. Unfortunately, in perinatal grief, this is not always the case. The mother and the father can experience incongruent grieving and use discordant coping mechanisms. It is important to evaluate these differences to facilitate communication between the distraught parents. Improved communication can in turn facilitate the grieving process.     

A multicentre assessment of the specificity of ten anti-HBc screening tests

SUMMARY. Samples from 1828 donations were screened for anti-HBc at seven sites in the UK using kits supplied by 10 manufacturers. Only 10 (0.55%) donations were considered to have true anti-HBc reactivity and these were detected by all 10 kits. Additional markers of HBV infection were found in nine of these 10 donations. Additional reactives were found by all kits, the number ranging from 1 to 43.
In the four more specific kits, the 10 true reactives were clearly distinguished from the 'false reactives' by the strength of the reaction. It is concluded that the reliance on a single ELISA test for anti-HBc diagnosis is unwise. The use of a second test known to be more specific than the screening ELISA is recommended.     

The characterization and localization of the glutamate receptor subunit GluR1 in the rat brain.

The cloning of cDNAs that encode functional glutamate receptors makes it possible to produce antibodies that can be used as high-affinity probes for the localization and characterization of these receptors in the mammalian brain. We have made antibodies to different regions of the first cloned member of this family, GluR1, using bacterially overproduced antigen. On Western blots, these antisera detect glycoprotein(s) of 105 kDa present in crude membranes of the hippocampus and cerebellum. The 105-kDa band is associated with postsynaptic densities, and it is observed in cultured cells upon transfection with the GluR1 cDNA. Although glutamate receptors are thought to be the most prevalent excitatory ligand-gated ion channel in the mammalian brain, immunohistochemistry reveals that the receptors recognized by these antisera are localized predominantly in neurons of the cerebellum and some structures of the limbic system, including the hippocampus, the central nucleus of the amygdala, and portions of the septum. This pattern of expression is, in general, consistent with the distribution of GluR1 mRNA as determined by in situ hybridization histochemistry. Our results suggest that glutamate excitatory circuits recognized by these antisera are predominantly found in regions of the limbic system that are reciprocally interconnected.     

Synovial fluid phospholipase A2s and inflammation.

The activation of phospholipase A2 is believed to have an important role in the inflammatory process owing to its induction of eicosanoids, platelet activating factor, and other mediators. Soluble phospholipase A2 has been associated with exudates in different inflammatory conditions. In this review the general physiology and control of this enzyme and, in particular, the most recent findings on human synovial fluid phospholipase A2s are discussed.     

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release.

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.