Ninety-five patients with severe open tibial fractures (96 fractures) were treated with nonoperative treatment alone (NO group, n = 16), immediate internal fixation (I group, n = 22), delayed ...internal fixation (D group, n = 34), or external fixation (EF group, n = 24). The D group was divided into a delayed internal fixation group following nonoperative treatment (D1 group, n = 14), and a delayed internal fixation group following external fixation (D2 group, n = 20). Using the classification system of Gustilo, there were 43 type IIIA, 42 type IIIB, and 11 type IIIC open tibial fractures.There were 17 deep infections (type IIIA, n = 3; IIIB, n = 12; IIIC, n = 2). The difference in the deep infection rate (DIR) between the type IIIA and type IIIB fractures was statistically significant (7.0% vs. 28.0%, p < 0.05). The DIRs in groups NO, I, D1, D2, and EF were 12.5, 27.3, 7.1, 35, and 4%, respectively. There was a significant difference in DIR between the D2 group and the EF group. The DIR in the D (D1 + D2) group and group I showed no significant difference. There was no relationship between the DIR and either Injury Severity Score or skin closure time.The authors of this study, therefore, do not feel there is an advantage to immediate internal fixation over delayed procedures for Gustilo type III open fractures of the tibia. However, careful attention must be given to the application of delayed internal fixation, especially intramedullary nailing, after external fixation.
NF-kappaB is activated by various stimuli including inflammatory cytokines and stresses. A key step in the activation of NF-kappaB is the phosphorylation of its inhibitors, IkappaBs, by an IkappaB ...kinase (IKK) complex. Recently, two closely related kinases, designated IKKalpha and IKKbeta, have been identified to be the components of the IKK complex that phosphorylate critical serine residues of IkappaBs for degradation. A previously identified NF-kappaB-inducing kinase (NIK), which mediates NF-kappaB activation by TNFalpha and IL-1, has been demonstrated to activate IKKalpha. Previous studies showed that mitogen-activated protein kinase/ERK kinase kinase-1 (MEKK1), which constitutes the c-Jun N-terminal kinase/stress-activated protein kinase pathway, also activates NF-kappaB by an undefined mechanism. Here, we show that overexpression of MEKK1 preferentially stimulates the kinase activity of IKKbeta, which resulted in phosphorylation of IkappaBs. Moreover, a catalytically inactive mutant of IKKbeta blocked the MEKK1-induced NF-kappaB activation. By contrast, overexpression of NIK stimulates kinase activities of both IKKalpha and IKKbeta comparably, suggesting a qualitative difference between NIK- and MEKK1-mediated NF-kappaB activation pathways. Collectively, these results indicate that NIK and MEKK1 independently activate the IKK complex and that the kinase activities of IKKalpha and IKKbeta are differentially regulated by two upstream kinases, NIK and MEKK1, which are responsive to distinct stimuli.
1. The relation between workload and the antihypertensive effect of exercise therapy in hypertensive patients, and the mechanism of that effect, were investigated. 2. Twenty-six patients participated ...in the study and were randomly assigned to 10 weeks of either low or high workload exercise. In the low workload group, 16 mild hypertensive patients were treated with bicycle ergometer exercise at approximately 50% of their maximum oxygen consumption (VO2max) for 60 min three times a week for 10 weeks. In the high workload group, 10 mild hypertensive patients exercised on the same schedule, but at approximately 75% of VO2max. 3. After 10 weeks of exercise, the low workload group had significantly lower systolic (9 mmHg), mean (6 mmHg) and diastolic (6 mmHg) blood pressures. In the high workload group, decreases in systolic (3 mmHg), mean (4 mmHg) and diastolic (5 mmHg) blood pressure were not statistically significant. 4. In the low workload group, changes in haemodynamic and humoral variables were not significant, except for a reduction in plasma norepinephrine at week 7. Cardiac index and plasma norepinephrine tended to decrease. In the high workload group, plasma norepinephrine and the renin-angiotensin system were transiently stimulated after 4 weeks of exercise. Stroke volume significantly increased (+26.4%) after 10 weeks of high workload exercise. 5. Based on these results and better patient compliance with the exercise programme in the low workload group than in the high workload group, low workload exercise therapy was recommended to mild hypertensive patients.
The purpose of this investigation was to examine the validity of the exercise intensity of which lactate increased 0.1 mmol/l from baseline level (METs@LAr+0.1), as for the practical assessment of ...lactate threshold (LT), in younger adults. Thirty-two apparently healthy younger adults (21±1yr., 167.5±10.2cm, 58.2±9.4kg) performed submaximal bench stepping test, in order to determine the LT and METs@LAr+0.1. The LT (8.6±1.1METs) and METs@LAr+0.1 (8.7±1.4METs) were not significantly different, with the strong correlation (r=0.925, p<0.001). The mean error (%), the standard error of estimation (%) and the total error were -0.1±0.6 METs (-0.5±6.7%), 0.44 METs (5.1%) and 0.53 METs, respectively. Furthermore the lower and upper limit of agreement were -1.1 METs (-13.2%) and 1.0 METs (11.6%), respectively. These results suggest that METs@LAr+0.1 can estimate the LT with ±15% of error. Thus the METs@LAr+0.1 may be a valid and useful assessment of LT in younger adults.
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