Lower border reducer for symphyseal and parasymphyseal fractures of mandible: a new device.
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Biomedical subjects
Publications and source records attributed to W J Peters.
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We present a case of Collet-Sicard syndrome (palsy of cranial nerves IX-XII) together with cervicofacial emphysema after cryoblockade to the mandibular division of the trigeminal nerve.
A glutamine for proline substitution at position 1098 was previously shown to result in accumulation of brush-border sucrase-isomaltase in the Golgi apparatus. The substitution is present in a highly homologous region of the protein, and results in a comparable accumulation when introduced into the same region in lysosomal alpha-glucosidase. To study the importance of the glutamine-1098, we analyzed the transport compatibility of two mutants in which glutamine-1098 is substituted by lysine or alanine. Both mutants were transported to the cell surface and processed comparable to wild type. We concluded that glutamine-1098 is not essential for transport to the cell surface.
Human lactase-phlorizin hydrolase (LPH) is a digestive enzyme that is expressed in the small intestinal brush-border membrane. After terminal glycosylation in the Golgi apparatus, the 230-kDa pro-LPH is cleaved into the 160-kDa brush-border LPHbeta and the 100-kDa profragment (LPHalpha). Since LPHbeta is not transport-competent when it is expressed separately from LPHalpha in COS-1 cells, it was suggested that LPHalpha functions as an intramolecular chaperone. What happens to LPHalpha after cleavage is still unclear. To analyze and localize LPHalpha in polarized epithelial cells, wild type and tagged LPH were stably expressed in Caco-2 cells. In tagged LPH, a vesicular stomatitis virus epitope tag was inserted into the LPHalpha region. Wild type and tagged proteins were processed at similar rates, and both cleaved LPHbeta forms were expressed at the apical cell surface. Pro-LPH was recognized by antibodies against LPH, a profragment epitope and the vesicular stomatitis virus tag. LPHalpha alone, however, could not be recovered by these antibodies. Our data suggest that LPHalpha is degraded immediately after cleavage.
Congenital sucrase-isomaltase deficiency is an example of a disease in which mutant phenotypes generate transport-incompetent molecules. Here, we analyze at the molecular level a phenotype of congenital sucrase-isomaltase deficiency in which sucrase-isomaltase (SI) is not transported to the brush border membrane but accumulates as a mannose-rich precursor in the endoplasmic reticulum (ER), ER-Golgi intermediate compartment, and the cis-Golgi, where it is finally degraded. A 6-kb clone containing the full-length cDNA encoding SI was isolated from the patient's intestinal tissue and from normal controls. Sequencing of the cDNA revealed a single mutation, A/C at nucleotide 3298 in the coding region of the sucrase subunit of the enzyme complex. The mutation leads to a substitution of the glutamine residue by a proline at amino acid 1098 (Q1098P). The Q1098P mutation lies in a region that is highly conserved between sucrase and isomaltase from different species and several other structurally and functionally related proteins. This is the first report that characterizes a point mutation in the SI gene that is responsible for the transport incompetence of SI and for its retention between the ER and the Golgi.
This retrospective study of 100 consecutive patients with inhalation injury documents that adult respiratory distress syndrome (ARDS) and pneumonia are common complications. Pulmonary complications cause or directly contribute to death in 77% of patients with combined inhalation and cutaneous burn injury. Additionally, the high fluid requirements of these patients worsens their pulmonary injury and is associated with adverse outcome. Independent factors predictive of death include ARDS and expected fluid requirements as well as age and percentage of total body surface area burned. An abnormal chest roentgenogram in the first 48 hours after injury is also associated with death. The development of ARDS is predicted by the actual volume of fluid resuscitation, despite normal pulmonary wedge pressure or normal central venous pressure reflecting increased microvascular permeability. These findings indicate a need for reevaluation of fluid resuscitation of patients with inhalation injury.
OBJECTIVES: To report a burn unit's experience with chemical burns and to discuss the fundamental principles in managing chemical burns. DESIGN: A chart review. SETTING: A burn centre at a major university-affiliated hospital. PATIENTS: Twenty-four patients with chemical burns, representing 2.6% of all burn admissions over an 8-year period at the Ross Tilley Regional Adult Burn Centre. Seventy-five percent of the burn injuries were work-related accidents. Chemicals involved included hydrofluoric acid, sulfuric acid, black liquor, various lyes, potassium permanganate and phenol. RESULTS: Fourteen patients required excision and skin grafting. Complications were frequent and included ocular chemical contacts, wound infections, tendon exposures, toe amputation and systemic reactions from absorption of chemical. One patient died from a chemical scald burn to 98% of the body surface area. CONCLUSIONS: The key principles in the management of chemical burns include removal of the chemical, copious irrigation, limited use of antidotes, correct estimation of the extent of injury, identification of systemic toxicity, treatment of ocular contacts and management of chemical inhalation injury. Individualized treatment is emphasized.
Thermal injury-associated specific immune deficiency occurs despite indicators of systemic activation of the lymphoid compartment. We investigated the possibility that postburn immune failure and T cell activation are casually related through activation-induced (apoptotic) cell death. The relationship between the cellular immune response and cell mortality was examined in cultures of peripheral blood mononuclear cells (PBMC) from 14 immunosuppressed patients with extensive burns (35-90% total body surface area). Impaired cellular immunity coincided with significantly reduced cell viability as ascertained by propidium iodide staining and dye reduction assays. Following stimulation with the mitogenic lectin, phytohemagglutinin (PHA), the majority of DNA in patient cultures was fragmented, suggesting the occurrence of apoptotic cell death. Even without stimulation a portion of patient cells was apoptotic as indicated by oligonucleosomal bands on agarose gel electrophoresis. Exogenous interleukin-2 or phorbol ester markedly reduced constitutive as well as PHA-induced DNA fragmentation. In situ demonstration of DNA strand breaks in freshly isolated patient PBMC, by a TdT-based labeling technique, confirmed that a larger fraction (up to 60%) of circulating lymphocytes was undergoing apoptosis on the periphery. These novel observations suggest that apoptosis may play a major role in thermal injury-related cellular immunodeficiency.
OBJECTIVE: To predict the daily total energy expenditure of ventilated burn patients, this study was designed to determine the contribution of different activities on energy expenditure over a 24-hr period. DESIGN: Cohort study. SETTING: Burn unit of an adult hospital. PATIENTS: Twenty clinically stable burn patients undergoing mechanical ventilation with 36.7 +/- 4.2 total % burn surface area. INTERVENTIONS: Patients were fed according to a previously validated equation which takes into account the Harris-Benedict equation, % burn surface area, caloric intake, body temperature, and the number of postburn days: Toronto Formula = -4343 + (10.5 x % burn surface area) + (0.23 x caloric intake) + (0.84 x Harris-Benedict equation) + (114 x body temperature) - (4.5 x postburn days). The total energy expenditure of patients was measured by indirect calorimetry and their activity levels were recorded over a 24-hr period. RESULTS: The calculated Toronto Formula was 2191 +/- 83 kcal/day and patients were fed 2276 +/- 40 kcal/day. The measured resting energy expenditure was 2149 +/- 102 kcal/day and was similar to the Toronto Formula (NS). The total energy expenditure was 2492 +/- 120 kcal/day. Altogether the activities contributed 27.3 +/- 1.3% to the total energy expenditure and did not correlate with the % burn surface area. The activity factor calculated as [total energy expenditure less resting energy expenditure] x 100/resting energy expenditure was 16.6 +/- 2.4% and calculated as [total energy expenditure less Toronto Formula]/Toronto Formula was 14.5 +/- 4.3%. CONCLUSIONS: These results suggest that in clinically stable, mechanically ventilated burn patients, the Toronto Formula accurately predicts the resting energy expenditure and that the Toronto Formula or the resting energy expenditure x 1.2 can be used to estimate the total daily energy requirements.
Neuropathic complications of the burn patient are frequently undiagnosed. A retrospective study was performed looking at neuropathies in patients admitted to a tertiary care burns centre from 1984 to 1991. Nineteen out of a total of 800 patients had signs and symptoms of neuropathy, confirmed on neurophysiological testing. Most patients were severely burned with 11 patients (69%) having a total burn surface area of > 20%. Twenty-eight percent were full thickness burns. Mononeuritis multiplex was the most common finding in these patients, occurring in 11 (69%). This has not been reported before. Three patients (19%) had an isolated mononeuropathy, one (6%) had a radiculopathy and one had a generalized axonal polyneuropathy. Of the patients with mononeuropathy, nine had lesions only in burned areas and four had lesions in burned and unburned areas. Eleven patients had complications of sepsis with five also having renal failure. Age, sex, serum albumin, magnesium, phosphate, creatinine, the presence of sepsis and the number or type of drug did not correlate with the number of affected nerves nor the extent of recovery. The length of hospitalization and severity of the burns were the only two factors which correlated with the number of affected nerves. Vascular occlusion of the vasa nervorum, direct thermal injury or a disseminated neurotoxin are postulated as possible aetiological mechanisms.
A series of 86 patients who underwent submandibular gland surgery were reviewed retrospectively. Of the 92 glands excised, non-neoplastic disease accounted for 96% of cases. Preoperative clinical findings were inconsistent such that early surgery should be considered for an enlarged non-tender submandibular gland. The incidence of temporary paresis of the lower branches of the facial nerve was 36% with full recovery, on average, 4 months after surgery. The low 'non-identification' approach to the submandibular gland appears to be the technique which offers the least likelihood of permanent damage to the lower branches of the facial nerve.
In the immunosuppressed burn patient serum levels of both IL-2 and a soluble form of IL-2 receptor alpha (sIL-2R alpha) are significantly elevated. Strikingly, the production of these markers by the in vitro activated patients' cells is decreased. This study examines the role of IL-2 in the decreased production of the sIL-2R alpha in vitro in patients with major burns (n = 18, 30 to greater than 70% total body surface area). Peripheral blood mononuclear cell (PBMC) cultures from patients with highly elevated serum sIL-2R alpha, and from healthy controls (n = 12) were activated with concanavalin A (Con A) at initiation. In patients' cultures mitogen-induced increments of sIL-2R alpha levels were significantly lower. There was a significant negative correlation (r = 0.64, P less than 0.001) between a high serum sIL-2R alpha level and a decreased lectin-induced sIL-2R alpha release in vitro. Low levels of sIL-2R alpha in patients' samples were not normalized by increasing the number of T lymphocytes. Also exogenous rIL-1 was without effect, whereas rIL-3 increased sIL-2R alpha release in some cultures. However, sIL-2R alpha levels were significantly increased in patients' cultures by (i) addition of exogenous IL-2; (ii) removal of adherent cells; (iii) addition of cyclooxygenase inhibitor, indomethacin; (iv) bypassing cell surface activation by the combination of the calcium ionophore A23187 and the phorbol ester 12-o-tetradecanoyl acetate. The cyclic AMP-elevating drug, forskolin, abrogated the ability of exogenous IL-2 to increase sIL-2R alpha production. Thus, in the burn patient, the reduced in vitro sIL-2R alpha release appears to relate to abnormalities in IL-2 production and action mediated through its functional surface receptor. Elevated levels of sIL-2R alpha in vivo may, therefore, reflect systemic activation of T lymphocytes in response to biologically active IL-2.
This study examines the relationship between the capacity for interleukin-2 (IL2) production and the magnitude of the in vitro and in vivo secretion of IL2R alpha in 43 patients with major burns (30-90 per cent total body surface area). Throughout the postburn period a significant (P less than 0.001-0.05) proportion of patients studied demonstrated increasingly high levels of serum IL2 ranging from 2 to over 500 U/mL. Serum IL2R alpha also increased, reaching its highest levels at 15-40 days postburn, while serum IL2 gradually declined. In this period in vitro IL2 production and IL2R alpha secretion in patient's cultures were significantly reduced compared to control. However, in parallel cultures supplemented with exogenous IL2, IL2R alpha levels could be significantly increased (2.5 fold). IL2R alpha levels also approached normal in peripheral blood mononuclear cell cultures from recovering patients whose in vitro IL2 production had improved. These observations suggest that in the burn patient altered synthesis and/or secretion of the soluble form of IL2R alpha may be related to IL2 content. Above physiological levels of IL2R alpha and its ligand in postburn serum also indicate that thermal injury induces strong in vivo activation of the lymphoid system.
During the 6 years from July 1984 to May 1990, 193 patients (30.2 per cent of all patients) were admitted to our regional adult burn centre, for treatment of work-related burn injuries. The median age of patients was 32.5 years (range 18-64 per cent), and 94 per cent were males. Fifty-nine per cent of the patients came from metropolitan Toronto, and 40 per cent from rural Ontario. Most of the patients (97.3 per cent) were referred to the burn centre within 24 h of their injury. The most common aetiology was electrical injury (29.5 per cent), followed by flame (24.4 per cent), contact (10.4 per cent), flash (9.8 per cent), tar and asphalt (9.3 per cent), scald (7.8 per cent), chemical (5.1 per cent), steam (4.7 per cent) and grease (1 per cent). Within the electrical burn group, about one-half were flash burns, one-quarter were clothing fire injuries, and one-quarter were contact injuries. These occupational burns tended to be extensive injuries. The median body surface area (BSA) was 16.5 per cent, with a median full thickness (FT) component of 5.0 per cent. The average length of stay was 20.0 days. Inhalation injury requiring intubation occurred in 14.8 per cent of patients. Sepsis--confirmed by positive blood cultures--developed in 14 per cent of the patients, at an average time of 8.8 days postburn. Staphylococcus aureus was the commonest organism isolated from blood cultures. Pneumonia occurred in 6.3 per cent of patients. A total of 207 surgical procedures was performed on 113 of the 193 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
A general consensus that thermal injury affects T lymphocyte function adversely is supported particularly by the observation that burned patients' lymphocytes secrete reduced levels of biologically active IL-2 in vitro. In the same patients, however, high serum concentrations of the low-affinity IL-2 receptor (IL2R alpha), a product of an IL-2-activated gene, have been observed. In this study a significant proportion of patients also demonstrated over-physiological levels (from 2 to 500 U/ml) of serum IL-2 ascertained by immunoassay. Increases in serum IL-2 content correlated significantly (P less than 0.02) with those of serum IL-2R alpha during the first week post-burn. Later, serum IL-2R alpha levels continued to increase up to 30 days while IL-2 eventually declined. Thus, augmented secretion of IL-2R alpha appears related to the high serum IL-2 content. Therefore refractoriness to further immune stimulation may be due to early activation of the lymphoid system, rather than to an intrinsic incapacity of T lymphocytes for generating sequential responses.
Lipid peroxides, formed as a consequence of oxygen free radical formation, are responsible for tissue damage in a great variety of pathological conditions including thermal injury. 'Cutaneous burn toxin', formed by application of heat to skin, is thought to be specific to the burn injury. It causes dose-dependent damage to mitochondrial and red cell membranes, and dose-dependent inhibition of interleukin-2-dependent growth of lymphocytes. The possibility that the toxicity of 'cutaneous burn toxin', a lipid-protein, is exerted through lipid peroxides, was examined by measuring the levels of both agents in plasmas of eight burn patients during the first week after their injury. It was observed that plasma lipid peroxides did not appear in parallel with absorption into the circulation of 'cutaneous burn toxin'. Lipid peroxide levels equally common to very low and very high burn toxin levels, were recorded. The pair of agents correlated negatively (r = -0.26) at a significance of only 0.1. In addition, isolated purified 'cutaneous burn toxin' contained no measurable lipid peroxide. No relationship was therefore demonstrated between plasma levels of 'cutaneous burn toxin' and lipid peroxides.
The high-affinity cell-surface receptor for interleukin-2 (IL-2R) consists of the 75-kilodalton (kd) chain and a 55-kd glycoprotein known as Tac. This report examines the cellular expression of IL-2R and secretion of the soluble form of Tac in immunosuppressed blunt trauma (n = 20, injury severity score -20) and thermally injured (n = 20, Total body surface area greater than 35%) patients. The percentage of IL-2R-expressing peripheral blood mononuclear cells (PBMC) in mitogen-stimulated cultures from patients and age-matched normal donors was determined by direct immunofluorescence with a monoclonal anti-Tac followed by flow cytometry analysis. Levels of soluble Tac in patient sera were measured by a monoclonal antibody-based enzyme-linked immunosorbent assay. Expression of Tac antigen by mitogen-activated PBMC cultures from blunt trauma patients was transiently reduced (by as much as 40%) in 4 of 14 patients examined. Levels of serum Tac were significantly elevated (p less than 0.05) in 15 of 20 blunt trauma patients ranging from 750 to 3000 U/mL compared with 180 to 420 U/mL in control subjects. All burn patients studied 10 to 50 days after the injury demonstrated a significant reduction (by 50% to more than 90%) in the percentage of IL-2 receptor-bearing cells. Similarly serum levels of IL-2R increased significantly (p less than 0.001 to 0.05) in all burn patients studied, reaching concentrations as high as 5500 U/mL. These results suggest that major trauma, whether mechanical or thermal, induces alterations in the T-lymphocyte activation process. However the degree and duration of such changes may vary based on the nature of the injury.