Biomedical subjects
Publications and source records attributed to H Rode.
A spectrophotometric method is described for the quantitative biochemical assay of total cholinesterase in rectal biopsy tissue. Significantly increased enzyme activity was found in this tissue from patients with Hirschsprung's disease, suggesting that the assay has diagnostic value.
One-way mixed leukocyte cultures, supplemented by the daily addition of small numbers of fresh stimulating cells between days 5 and 15 of incubation, failed to give a secondary proliferative or cell-mediated lympholytic response upon challenge with activating concentrations of the same stimulating. cells. However, these cultures could be fully activated by blastogenic factor (BF). The unresponsiveness induced was immunologically specific: when responding cells were primed simultaneously with stimulating cells from two donors and one stimulator was added daily, the cultures were unresponsive to challenge with cells of the stimulator which were added daily, but good secondary responses were elicited both by cells of the other stimulator used in priming and by BF. The induced unresponsiveness may be a consequence of specific inactivation of helper cells.
Citrate lyase deacetylase or acetyl-S-(acyl-carrier protein) enzyme thioester hydrolase (acetate) (EC 3.1.2-), was purified 3100-fold with a yield of 3.8% from cell extracts of Rhodopseudomonas gelatinosa. The final enzyme preparation gave a single protein band upon polyacrylamide-gel electrophoresis in the absence or in the presence of sodium dodecylsulfate. The molecular weight of the native enzyme was estimated by gel filtration to be 14 300 +/- 1000. Sodium dodecylsulfate/polyacrylamide gel electrophoresis yielded a molecular weight of 7300 +/- 600 indicating that the enzyme consisted of two subunits. Citrate lyase deacetylase acted as an S-acetyl enzyme thioesterhydrolase because it catalyzed the conversion of citrate lyase (S-acetyl form) into citrate lyase (sulfhydryl form) and acetate. Citrate lyase deacetylase was strongly inhibited by L-glutamate. The half-maximal inhibitor concentration was 7.5 X 10(-4) M. and a Ki-value of 1.2 X 10(-4) M was determined. The mode of inhibition appeared to be of the linear mixed type. L-Glutamate was bound by citrate lyase deacetylase but not by citrate lyase. The pool concentrations of L-glutamate in R. gelatinosa were 10 mM when citrate was present in substrate amounts and 2.7 mM after total consumption of citrate. Simulation of conditions in vivo using homogeneous enzyme preparations of citrate lyase and citrate lyase deacetylase, and glutamate concentrations of 10 mM and 2.7 mM respectively, revealed that the rate of citrate lyase inactivation increased from 8% within 15 min during growth on citrate to 50% within 15 min in the absence of citrate.
Posterolateral diaphragmatic hernias and cystic hamartomatous malformations of the lung can cause actue respiratory distress in the immediate postnatal period. The clinical and radiological features of these two conditions can be similar. Owing to misdiagnosis, the surgical approach was inappropriate in 2 of 26 patients diagnosed as having posterolateral diaphragmatic hernias on admission. During the same period, 5 cases of congenital cystic lung disease were treated surgically. Three of these patients were admitted in severe respiratory failure within 48 hours of birth, and in 2 of these cases the wrong diagnosis was made. The clinical features of these two easily confused congenital anomalies are discussed, and the main differentiating points on the chest radiographs are presented.
Congenital anorectal deformities present a therapeutic challenge to the paediatric surgeon. The anomalies encountered range in complexity from the most simple to the most intricate. It is for this reason that three clear phases in management are defined and applied in every instance, i.e. absolute clarification of the anatomy of the defect, its appropriate operative correction, and, finally, a protracted postoperative period of care during which time voluntary stool control is acquired. Anal continence is the ultimate functional objective. The meticulous treatment required by the unfortunate baby born with this correctable abnormality is emphasized.
The anomalous false-positive results often found in the primed lymphocyte typing (PLT) test seem to be partially due to the release of blastogenic factor (BF) from the stimulating cell, resulting in back stimulation of the primed lymphocyte. These anomalous responses can be greatly reduced by treating the stimulator cell with high doses of irradiation or with puromycin.
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Primary failure of host defense mechanisms has been associated with increased infection and mortality. Anergy, the failure of delayed hypersensitivity response, has been shown to identify surgical patients at increased risk for sepsis and related mortality. The anergic and relatively anergic patients whose skin tests failed to improve had a mortality rate of 74.4%, whereas those who improved their responses had a mortality rate of 5.1% (P < 0.001). This study documents abnormalities of neutrophil chemotaxis, T-lymphocyte rosetting in anergic patients and the effect of autologous serum. These abnormalities may account for the increased infection and mortality rates in anergic patients. Skin testing with five standard antigens has identified 110 anergic (A) or relatively anergic (RA) patients in whom neutrophil chemotaxis (CTX) and bactericidal function (NBF), T-lymphocyte rosettes, mixed lymphocyte culture (MLC), cell-mediated lympholysis (CML), and blastogenic factor (BF) were studied. The MLC, CML and BF were normal in the patients studied, and were not clinically helpful. Neutrophil CTX in 19 controls was 117.5 +/- 1.6 u whereas in 40 A patients, neutrophils migrated 81.7 +/- 2.3 u and in 15 RA patients 97.2 +/- 3.8 u (P < 0.01). In 14 patients whose skin tests converted to normal, neutrophil migration improved from 78.2 +/- 5.4 u to 107.2 +/- 4.0 u (P < 0.01). Incubation of A or control neutrophils in A serum reduced migration in A patients from 93 +/- 3.7 u to 86.2 +/- 3.5 u (P < 0.01) and in normals from 121.2 +/- 1.6 u to 103.6 +/- 2.6 u (P < 0.001). The per cent rosette forming cells in 66 A patients was 42.5 +/- 3.1 compared to 53.6 +/- 2.8 in normal responders (P < 0.02). Incubation of normal lymphocytes in anergic serum further reduced rosetting by 30%. Restoration of delayed hypersensitivity responses and concurrent improvement in cellular and serum components of host defense were correlated with maintenance of adequate nutrition and aggressive surgical drainage.
During a 5-year period, 1970 to 1974, a total of 2 118 new patients were admitted to the Burns Unit of the Red Cross War Memorial Children's Hospital in Cape Town. There were 35 deaths. The main complications and causes of death in these 35 patients are critically analysed and standard management methods are reviewed to highlight mistakes in the management of burns.
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