Displaced intra-articular fractures of the calcaneus treated non-operatively. Clinical results and analysis of motion and ground-reaction and temporal forces

Twenty-seven patients who had a unilateral displaced intra-articular fracture of the calcaneus were managed with a cast instead of with reduction or an operation. The clinical result after a mean of six years (range, two to ten years) was excellent in five patients, good in five, fair in seven, and poor in ten. The sixteen patients who were re-examined for this study and for whom the gait was analyzed demonstrated abnormalities in ground-reaction force with regard to vertical force (F3) and temporal force factors (T2, T3, T6, and T9). Analysis of temporal and distance factors showed a trend toward a decreased proportion of single-limb support on the involved side. Three-dimensional motion analysis of the ankle and hindfoot was performed with electrogoniometers as the subject walked on a level surface, on a 10-degree side-slope, and up and down stairs. Motion was decreased in the sagittal, coronal, and transverse planes during walking on level ground and on a side-sloping surface. Significant decreases in motion in these planes were also seen during walking up and down stairs. Although these patients did not have a subsequent reconstructive operation, most had a residual functional deficit.     

Clearance of technetium 99m N-NOET in normal, ischemic-reperfused, and membrane-disrupted myocardium

BACKGROUND: Technetium 99m-labeled bis(N-ethoxy, N-ethyl dithiocarbamato) nitrido technetium(v) (99mTcN-NOET) is a new neutral cardiac perfusion imaging agent that has been shown to have very high uptake and retention in vitro. The purpose of this study was to determine the clearance kinetics of 99mTcN-NOET in control, ischemic-reperfused, and membrane-disrupted myocardium. METHODS AND RESULTS: After a 100 microCi (3.7 x 10(6) Bq) bolus of 99mTcN-NOET was injected, myocardial clearance was monitored for 1 hour by the use of a sodium iodide detector in 30 isolated, Krebs-Henseleit (KH) perfused rat hearts. Seven hearts were used as controls (group 1). In seven ischemic-reperfused hearts, tracer administration and uptake was followed by 30 minutes of no flow and 1 hour of reflow (group 2). In six additional ischemic-reperfused hearts, tracer administration was followed by deprivation of flow for 1 hour followed by 1 hour of reflow (group 3). Six hearts were perfused with a 0.5% Triton X-100 KH perfusate for 1 hour (group 4). Four hearts were perfused with KH for 10 minutes, followed by cyanide for 10 minutes (group 5). This cycle was repeated three times. Activities remaining in each heart at the end of each experiment were quantitated, and activity at peak uptake was calculated. The 99mTcN-NOET myocardial clearance was near linear in the control (0.6 +/- 0.4) and both ischemic-reperfused groups with virtually no fractional clearance (1.2% +/- 0.6% and 2.1% +/- 0.6%, respectively; p = NS). In the Triton X-100 membrane-disrupted hearts, clearance was substantial (94.2% +/- 4.0%; p < 0.0001 compared with the control and ischemic-reperfused groups). Cyanide treatment produced rapid clearance, which was arrested by a return to the standard KH perfusate. Peak uptake as a percentage of injected dose was 74.9% +/- 1.4% for all groups combined. CONCLUSION: Thus 99mTcN-NOET has extremely high myocardial retention after 1 hour in normal myocardium and is not significantly affected by ongoing myocardial ischemia or reperfusion injury in this model. Clearance is increased markedly in extreme conditions of membrane disruption. These data are consistent with the concept that 99mTc-NOET is localized predominantly in or on cell membranes. 99mTcN-NOET is a promising, new myocardial perfusion imaging agent that exhibits a stable myocardial distribution in the setting of acute developing injury.     

Effect of hypotension preceding death on the function of lungs from donors with nonbeating hearts

BACKGROUND: A shortage of suitable brain-dead donors continues to severely limit lung transplantation. Use of donors with nonbeating hearts has been suggested as a solution. Lungs are unique, in that aerobic metabolism can continue in the absence of blood circulation because oxygen is present in airways and alveoli. Animal studies have shown reasonable cadaveric graft function up to several hours after sudden death by drug administration. However, hemodynamic instability before death may worsen lung function through activation and pulmonary sequestration of neutrophils and release of inflammatory mediators. Because many potential cadaveric donors experience hypotension before death, this study was undertaken to assess the effect of hypotensive shock on cadaveric lung viability. METHODS: A rat isolated lung reperfusion model was used to assess pulmonary function over 3 hours of reperfusion or until gross pulmonary edema developed. Twenty-five rats were randomly allocated to the following study groups, which were based on status before lung harvest: (1) control: no interventions; (2) hypotensive: 1 hour of hypotension by exsanguination to a mean blood pressure of 30 to 40 mm Hg; (3) cadaver: death by cervical dislocation followed by 3 hours of in situ lung ischemia; (4) hypotensive + 3 hours cadaver: 1 hour of hemorrhagic shock, followed by death and 3 hours of in situ ischemia; (5) hypotensive + 2 hours cadaver: similar to group 4, except the in situ ischemia was abbreviated to 2 hours. RESULTS: No significant differences were found among group 1, 2, or 3 lungs with regard to wet to dry weight ratios, gas exchange, and pulmonary arterial or airway pressures. However, all group 4 lungs became grossly hemorrhagic and developed severe pulmonary edema within 10 minutes of reperfusion. Group 5 lungs fared only marginally better, with two of five lungs tolerating 3 hours of reperfusion. CONCLUSIONS: A period of hypotension before death severely impairs cadaveric lung viability.     

Effects of midazolam on the differentiation of murine myeloid leukemia cells

The effects of midazolam (MID) on the in vitro growth and differentiation of two murine myeloid leukemia WEHI 3B (JCS) and M1 cells were studied. MID inhibits the proliferation of both M1 and JCS cells in a dose-dependent manner. At the concentration of 10 micrograms/ml, MID was found to induce both monocytic and granulocytic differentiation of the JCS but not M1 cells. Induction of morphological differentiation of the JCS cells was also associated with the enhanced expression of the differentiation antigens Mac-1, F4/80, and Gr-1 for the cells. Results from mRNA phenotyping experiments also indicated that the expression of tumor necrosis factor (TNF-alpha) and neutrophil-specific J11d differentiation marker was significantly upregulated in MID-treated JCS cells. In addition, the phagocytic activity of MID-treated JCS cells was increased towards opsonized yeast cells. Results from this investigation suggested that MID may be used as an inducer for further study on the mechanisms of differentiation in these myeloid leukemia cells.     

The free radicals--the hidden culprits--an update

Free radicals are normally produced as a by-product of cellular metabolism. Free radicals are capable of killing bacteria, damage biomolecules, provoke immune response, activate oncogens, cause atherogenesis and enhance ageing process. However, in healthy conditions nature has endowed human body with enormous antioxidant potential. Subtle balance exists between free radical generation and antioxidant defence system to cope with oxidative stress by various enzymes and vitamins at cellular level which prevent the occurrence of disease. However, factors tilting the balance in favour of excess free radicals generation lead to widespread oxidative tissue damage and diseases. Therefore, trouble starts when there is an excess of free radicals and the defence mechanism lags behind. Overwhelming production of free radicals in response to exposure to toxic chemicals and ageing may necessitate judicious antioxidant supplement to help alleviate free radical mediated damage.     

Health assessment in the rheumatic diseases of childhood

Assessment of children and adults with rheumatic diseases, both in clinical practice and controlled clinical trials in rheumatology, has traditionally focused on the measurement of disease activity. More recently emphasis has been placed on the need to incorporate estimates of physical, social, and mental functioning into health assessment. Thus there has been a tremendous growth in the development of measurement instruments that evaluate health status, functional status, disability, and quality of life. This type of measurement has become essential, particularly for clinical trials in adults with rheumatic diseases, for which the AIMS (Arthritis Impact Measurement Scales), the HAQ (Health Assessment Questionnaire), and the MACTAR (McMaster-Toronto arthritis) patient preference questionnaire have been the most widely used. In the past few years, similar measures have been developed for application in children with rheumatic diseases. These include the CHAIMS (Childhood Arthritis Impact Measurement Scales), the CHAQ (Childhood Health Assessment Questionnaire), the JAFAR (Juvenile Arthritis Functional Assessment Report), the JASI (Juvenile Arthritis Self-report Index), the JAQQ (Juvenile Arthritis Quality of Life Questionnaire), and the CAHP (Childhood Arthritis Health Profile). In this review, the development and measurement properties of these childhood instruments are discussed, with particular emphasis on their potential roles as supported by recent literature.