Spontaneous bilateral ankle and midfoot sepsis in a nonimmunocompromised patient

We describe a 70-year-old nonimmunocompromised woman with spontaneous bilateral ankle and midfoot sepsis and a deep-space abscess of the right lower leg. Salvage of both limbs was achieved by aggressive bilateral soft-tissue and osseous debridement, including a four-compartment fasciotomy of the right lower leg, antibiotic-loaded polymethyl methacrylate bone cement implantation, delayed allogeneic bone grafting of the osseous defects impregnated with autologous platelet-rich plasma bilaterally, and external fixation immobilization, implantable bone growth stimulation, and split-thickness skin graft coverage of the right lower leg, ankle, and foot. Osseous incorporation of the bone grafts bilaterally occurred 8 weeks after surgery. No soft-tissue or osseous complications occurred during the postoperative period or at 18-month follow-up except for arthrofibrosis in the right ankle; there was no evidence of recurrent abscesses, sequestrum, or wound-related problems. A review of the literature regarding bilateral pedal sepsis and the techniques used for limb salvage in this patient are presented in detail.     

Maximal Concanavalin A-Specific Agglutinability Without Loss of Density-Dependent Growth Control

Density-inhibited 3T3 mouse fibroblasts were treated for 10 min with nine concentrations of Pronase ranging from 0.25 to 40 mug/ml. Concanavalin A-specific agglutinability increased from control values of about 25% to plateau values of about 80%. None of these Pronase concentrations brought about an increase in cell number within 84 hr. Pronase-treated cells remained responsive to growth stimulation by serum and cortisol. Therefore, the protease-mediated surface change measured by increased concanavalin A-specific agglutinability is not an event sufficient by itself to bring about cell division.     

Quantification of lidocaine and several metabolites utilizing chemical-ionization mass spectrometry and stable isotope labeling.

Quantification of the suspected metabolites of lidocaine in humans was carried out using the direct insertion probe and chemicalionization mass spectrometry. Deuterated analogs of the metabolites of lidocaine were added to serial human plasma and urine samples and were used as internal standards following oral administration of 250 mg of lidocaine hydrochloride monohydrate to two male subjects and 202 mg of lidocaine free base to one male subject. The average results after analysis of the 0-24 hr urine samples, before beta-glucuronidase-sulfatase treatment, indicated the presence of seven of the possible metabolites in the following amounts (percent of administered dose based on the free base): lidocaine, 1.95; omega-ethylamino-2,6-dimethylacetanilide, 4.90; omega-amino-2,6-dimethylacetanilide, 0.88; m- and/or p-hydroxylidocaine, 0.73; m- and/or p-hydroxy-omega-ethylamino-2,6-dimethylacetanilide, 0.56; 2,6-dimethylaniline, 0.97; and 4-hydroxy-2,6-dimethylaniline, 63.5. Both N-ethyl- and N,N-diethylglycine were detected in human and Rhesus monkey urine, although quantification was not achieved.     

Upregulation of the stress-associated gene p8 in mouse models of demyelination and in multiple sclerosis tissues

Cuprizone-induced demyelination is a mouse model of multiple sclerosis (MS) as cuprizone-fed mice exhibit neuroinflammation and demyelination in the brain. Upon removal of cuprizone from the diet, inflammation is resolved and reparative remyelination occurs. In an Affymetrix GeneChip analysis, the stress-associated gene p8 was strongly upregulated (>10x) during cuprizone-induced demyelination but not remyelination. We verified this upregulation (>15x) of p8 in the CNS during demyelination by real-time polymerase chain reaction (PCR). This upregulation is brain-specific, as p8 is not elevated in the liver, lung, kidney, spleen, and heart of cuprizone-treated mice. We also localized the cellular source of p8 during cuprizone treatment, and further found elevated expression during embryogenesis but not in normal adult brain. Compared with wild-type controls, the death of oligodendrocytes in p8-/- mice is delayed, as is microglial recruitment to areas of demyelination. The corpus callosum of p8-/- mice demyelinates at a slower rate than wild-type mice, suggesting that p8 exacerbates CNS inflammation and demyelination. Enhanced expression of p8 is also observed in the spinal cords of mice with acute experimental autoimmune encephalomyelitis (EAE) induced by PLP139-151 peptide (10x). Increased expression is detected during disease onset and expression wanes during the remission phase. Finally, p8 is found upregulated (8x) in post-mortem tissue from MS patients and is higher in the plaque tissue compared with adjacent normal-appearing white and gray matter. Thus, p8 is an excellent candidate as a novel biomarker of demyelination.     

A retrospective study of relapse in rigidly fixated sagittal split osteotomies: contributing factors

Fifty-one patients who underwent mandibular advancements with or without genioplasties were rigidly fixated with three, 2-mm bicortical screws per side. Radiographs were digitized preoperatively, immediately postoperatively, at 6 weeks, at 6 months, and at a subsequent long-term follow-up period. Location of the cephalometric landmarks, referenced to a vertical reference line (in millimeters), was used as the dependent variable. An overall inspection of the data shows that rigidly fixated mandibular advancements were very stable. The average case showed further advancement of pogonion from 6 weeks to the long-term follow-up period. However, relapse was noted in several cases. Factors that could be used as predictors of relapse were examined. Results indicated that magnitude of advancement was the only factor that successfully predicted relapse, accounting for 37.9% of the variance in the sample. Anatomic changes found to accompany such advancement are as follows: (1) when pogonion comes forward, anterior facial height and mandibular plane decrease while the proximal segment rotates forward, and (2) the maxillary central incisors flare and the mandibular incisors upright during this time period. A small degree of relapse as assessed at pogonion occurred during the first 6 weeks, followed by an advancement from 6 weeks to the longest time interval after the surgical procedure. However, these directional movements were not statistically significant.     

Tomographic assessment of nasal septal changes following surgical-orthodontic rapid maxillary expansion

Nine adult patients with transverse maxillary deficiency were examined for incidence of nasal septal deviation following surgical-orthodontic rapid maxillary expansion. The osteotomies for facilitation of maxillary expansion did not include sectioning of the nasal septum. The procedure did include sectioning of the lateral maxillary walls, the pterygomaxillary suture, and the midpalatal sutures. For each patient, four graduated coronal tomograms through the incisal, molar, tuberosity, and pterygoid areas were taken prior to and not less than 4 months after surgical intervention. Results showed no significant change in the nasal septal position from before to after surgery. Analysis of the nature of maxillary movement in the coronal plane revealed rotational as opposed to bodily expansion, with inferior rotation of the palatal vault. Significant increases in the available nasal airway space were recorded. These increases were attributed primarily to shrinkage of inflamed nasal mucosa. In view of the recorded data, surgical sectioning of the nasal septum to prevent septal deviation by surgical-orthodontic rapid maxillary expansion is not warranted.     

Postsurgical maxillary movement: a comparison study of bone plate and screw versus wire osseous fixation

This study was designed to examine amounts of postoperative maxillary movement in patients who received Lefort I osteotomies, comparing bone plate and screw fixation with conventional transosseous wire fixation. Cephalograms of 17 patients whose maxillae were fixated with wire osseous fixation and 13 patients whose maxillae were fixed with bone plates and screws were compared at four different time periods throughout the first postoperative year. Millimeters of movement of five maxillary assessment points were assessed in the horizontal and vertical planes of space by use of a line constructed 7 degrees to sella-nasion at nasion as the horizontal reference. Results indicate that the amount of maxillary movement was similar for the two groups during the two time periods subsequent to the surgical procedure. However, it appears that the maxillae fixated with bone plates and screws were more stable than those with wire osteosynthesis during the last postoperative period (6 months to 1 year) and during the overall postoperative time interval (2 days to 1 year).     

Molecular size of [3H]WB-4101-binding sites in rat cortex as determined by radiation inactivation

The molecular weight of the [3H]WB-4101-binding sites in rat cerebral cortex was estimated by the irradiation-inactivation technique. The molecular weight was found to be dependent on the assay concentrations of the radioligand in the binding assay. Assays with a [3H]WB-4101 concentration of 0.25 nM showed a molecular weight of 62,100 daltons and 5.1 nM showed 50,800 daltons. Scatchard transformation of the [3H]WB-4101-binding data shows two binding sites (high-affinity: KD = 0.09 nM, Bmax = 9.1 pmoles/g; low-affinity: KD = 20 nM, Bmax = 80 pmoles/g). It is suggested that the two binding exist at two distinct molecules and in that case the observed molecular weights of 62,100 and 50,800 daltons are not true values because the determinations are carried out on a mixture of the two molecule populations. The distribution of the two binding sites was calculated for the two radioligand concentrations, 0.25 nM and 5.1 nM; and on this background the "true" molecular weights of the two [3H]WB-4101-binding sites were estimated to be 68,300 daltons for the high-affinity molecule and 41,400 daltons for the low-affinity molecule. Competition studies with a variety of adrenergic agonists and antagonists against [3H]WB-4101 supported the hypothesis that only the high-affinity binding site is an alpha-1-adrenoceptor.