Removing a Bent Femoral Intramedullary Nail Cost Effectively: A Case Report.

A bent intramedullary (IM) nail becomes challenging and technically demanding to the orthopaedic surgeon for nail extraction. A broken nail can be easily removed through the fracture site. However, a bent nail has to be broken before it can be removed. Several studies and case reports outline the strategies and techniques for removing a bent IM nail. However, there is a paucity of guidelines and standard protocol describing the best and inexpensive strategy. We report a case where two years following surgery for intramedullary nailing of the right femur, the IM mail was bent following secondary trauma. We used a technique based on the principles of an ability to fully cut the nail and extract it in two pieces by using a Jumbo cutter which is available in the orthopaedic armamentarium. This technique is simple yet economical, with the likelihood of causing less soft tissue damage and thermal necrosis.

Cyclooxygenases-1 and -2 differentially modulate leukocyte recruitment into the inflamed brain.

Peripheral leukocyte recruitment in neuroinflammatory conditions can exacerbate brain tissue damage by releasing cytotoxic mediators and by increasing vascular permeability. Cyclooxygenase (COX)-derived prostaglandins promote the migration of several immune cells in vitro, however, the specific roles of COX-1 and -2 on leukocyte recruitment in vivo have not been investigated. To examine the specific effects of COX-1 or COX-2 deficiency on neuroinflammation-induced leukocyte infiltration, we used a model of intracerebroventricular lipopolysaccharide (LPS)-induced neuroinflammation in COX-1(-/-), COX-2(-/-), and their respective wild-type (WT) ((+/+)) mice. After LPS, leukocyte infiltration and inflammatory response were attenuated in COX-1(-/-) and increased in COX-2(-/-) mice, compared with their respective WT controls. This influx of leukocytes was accompanied by a marked disruption of blood-brain barrier and differential expression of chemokines. These results indicate that COX-1 and COX-2 deletion differentially modulate leukocyte recruitment during neuroinflammation, and suggest that inhibition of COX-1 activity is beneficial, whereas COX-2 inhibition is detrimental, during a primary neuroinflammatory response.

The brain expression of genes involved in inflammatory response, the ribosome, and learning and memory is altered by centrally injected lipopolysaccharide in mice.

Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipopolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 microg) was administered into the lateral ventricle of mice and, 24 h later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not in the hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation.

Dietary docosahexaenoic acid [22: 6(n-3)] as a phospholipid or a triglyceride enhances the potassium chloride-evoked release of acetylcholine in rat hippocampus.

We demonstrated previously that a dietary-induced depletion of docosahexaenoic acid (DHA) in cerebral phospholipids increases the spontaneous release of acetylcholine (Ach) in the rat hippocampus and reduces its potassium chloride evoked-release. In the present study, we investigated the effects in rats of DHA-enriched diets supplied by egg phospholipids (E-PL) or tuna oil (TO) on the PUFA in hippocampus membranes and on the synaptic release of Ach. Control rats were fed 3 g/kg of the DHA precursor, alpha-linolenic acid (LNA). Chronically (n-3) PUFA-deficient females were fed, starting 2 wk before mating, the deficient diet, a control diet, or a purified diet supplying 1, 2, or 3 g DHA/kg diet as E-PL or TO. Experiments were performed on the adult male progeny fed the same diet as their dams throughout life. The form of dietary DHA (TO or E-PL) did not influence its incorporation into the hippocampus. The 1 g DHA/kg diets allowed maximal incorporation into phosphatidylethanolamine (PE), but 2 g DHA/kg diet was needed for phosphatidylcholine (PC). A minimum of 2 g DHA/kg was needed to decrease the basal Ach release and to enhance the stimulated release to that of the control; the Ach release of the 1 g/kg DHA-groups did not differ from that of the deficient group. This suggests that >1 g DHA/kg diet is needed to ensure PUFA incorporation into PE and PC, and basal and stimulated Ach release in the rat hippocampus equivalent to the control group fed only LNA. PUFA incorporation into the hippocampus depends mainly on the PUFA concentration of the diet, not on the form of dietary DHA.