Lunate silicone replacement arthroplasty in Kienb?ck's disease: a long-term follow-up

We report a long-term follow-up (average, 5 years) of 10 patients who had lunate silicone replacement arthroplasty for treatment of Kienb?ck's disease. Clinical results were assessed on relief of pain, return to normal occupation, and range of motion. At 18- to 20-months follow-up, eight patients had satisfactory results, whereas at final follow-up only five of the patients had satisfactory results. Three of five patients with radiographs averaging 57 months after operation had evidence of particulate synovitis. Contrary to our previous publications on silicone replacement arthroplasty, it was concluded that the success rate for silicone replacement arthroplasty and the incidence of particulate synovitis do not warrant the continued use of silicone replacement arthroplasty as a primary treatment modality for Kienb?ck's disease.     

Cannabinoid Transmission and Pain Perception

The use of cannabis for the management of a wide range of painful disorders has been well documented in case reports throughout history. However, clinical evaluations of cannabis and its psychoactive constituent THC have not led to a consensus regarding their analgesic effectiveness. On the other hand, THC and its synthetic derivatives have been shown to be effective in most animal models of pain. These antinociceptive effects are mediated through cannabinoid receptors in the brain that in turn appear to interact with noradrenergic and kappa opioid systems in the spinal cord to modulate the perception of painful stimuli. The endogenous ligand, anandamide, is also an effective antinociceptive agent. The extent to which the endogenous cannabinoid system is involved in the modulation of pain is currently unknown.     

SR 141716 (Rimonabant) precipitates withdrawal in marijuana-dependent mice

Repeated marijuana use is known to lead to physical dependence in humans; however, its dependence liability has yet to be adequately assessed in laboratory animals. The goals of the present study were to: assess whether the CB(1) antagonist SR 141716 (rimonabant) precipitates withdrawal in mice that had been repeatedly exposed to marijuana smoke, and to compare these precipitated withdrawal effects to those elicited following intravenous administration of its chief psychoactive component Delta(9)-tetrahydrocannabinol (Delta(9)-THC). SR 141716 elicited a significant increase in paw tremors in mice that were repeatedly dosed with either marijuana or Delta(9)-THC. Unexpectedly, the blood and brain concentrations of Delta(9)-THC following marijuana exposure were considerably lower than those found following Delta(9)-THC injection when comparing an equivalent magnitude of paw tremors in both conditions. Finally, Delta(9)-THC dose-dependently alleviated SR 141716-induced paw tremors in marijuana-dependent mice, but marijuana itself failed to reverse the precipitated withdrawal effect. It is likely that marijuana exposure generated insufficient Delta(9)-THC brain levels (i.e., 203+/-19 ng/g) to reverse the withdrawal signs compared with the brain levels following intravenous injection (i.e., 1862+/-82 ng/g). These findings taken together indicate that mice exposed repeatedly to marijuana smoke exhibit similar precipitated withdrawal effects as Delta(9)-THC-injected mice.     

Alpha-aminoisobutyric acid transport in human leukemic lymphocytes: in vitro characteristics and inhibition by cortisol and cycloheximide

We have studied the transport of alpha-aminoisobutyric acid (AIB)-3-(14)C and its response to cortisol and cycloheximide in vitro in blood lymphocytes from untreated patients with chronic lymphocytic leukemia. The accumulation of AIB-3-(14)C increased in a linear fashion for 60 min, and reached an apparent steady state in 120 min. The initial rate of AIB accumulation (V(o)) varied from 1.1 to 10.2 mumoles/kg cell H(2)O per min in cells from 16 different patients; however, V(o) was reproducible in cells from five of six patients which were studied repeatedly over 1-9 months, and correlated positively with the lymphocyte count (r = 0.51, P = < 0.01).Virtually total inhibition of protein synthesis with cycloheximide was found to decrease the accumulation of AIB in cells from four patients which had high rates of AIB transport, but had no effect on transport in cells from four patients which accumulated AIB more slowly. These results indicate that active transport depends, in part, upon the presence of labile protein with a turnover rate which varies among different cell populations.Treatment with 10 muM cortisol for 240 min in vitro reduced the initial rate of AIB-3-(14)C accumulation (V(o)) by 43.4+/-4.1% (SE) (range, 9-66%) in cells from 16 patients. The degree of inhibition did not vary appreciably over a 9 month period in four of five patients. The effect of cortisol was proportional to its starting concentration, and developed at low concentrations (0.1-1.0 muM). Cortisol appears to decrease AIB accumulation by inhibiting active uptake, since it neither enhanced the exodus of AIB, nor inhibited apparently nonsaturable transport. Inhibition was noncompetitive in type, suggesting that cortisol decreases the total capacity of the active transport mechanism.Cortisol inhibited AIB transport indirectly by a process which involved de novo protein synthesis, since inhibition (a) appeared only after 60 min of treatment, (b) was present in treated cells which were subsequently incubated for 60 min in cortisol-free medium, and (c) failed to develop during simultaneous blockade of protein synthesis with cycloheximide, even when cycloheximide itself did not decrease AIB transport.     

Understanding midcarpal instability

This article outlines the historical development of midcarpal instability observations and terminology and places them in the broader context of currently accepted theories of wrist pathomechanics. Such an understanding may help resolve the following questions: Are there 1 or more entities under the current designation of midcarpal instability? What are the underlying pathogenesis and pathomechanics of the disorder(s)? What are the recommended treatment options? What further research needs to be done to better answer these questions?     

Randomized controlled trial of calcaneal taping, sham taping, and plantar fascia stretching for the short-term management of plantar heel pain

STUDY DESIGN: Prospective, experimental, randomized, single-factor, pretest/posttest design. OBJECTIVES: To examine the effects of a calcaneal and Achilles-tendon-taping technique, utilizing only 4 pieces of tape and not involving the medial arch, on the symptoms of plantar heel pain. BACKGROUND: Plantar fasciitis is one of the most common causes of heel and foot pain. Physical therapists have applied many techniques in an attempt to relieve the symptoms of plantar heel pain, including various taping methods for which there is little existing evidence. METHODS AND MEASURES: Subjects (n=41) were randomly assigned into 4 groups: (1) stretching of the plantar fascia, (2) calcaneal taping, (3) control (no treatment), and (4) sham taping. A visual analog scale (VAS) for pain and a patient-specific functional scale (PSFS) for functional activities were measured pretreatment and after 1 week of treatment (posttreatment). Results: A significant difference was found posttreatment among the groups for the VAS (P < .001). Specifically, significant differences were found between stretching and calcaneal taping (mean + SD, 4.6 +/- 0.7 versus 2.7 +/- 1.8; P = .006), stretching and control (mean +/- SD, 4.6 +/- 0.7 versus 6.2 +/- 1.0; P = .026), calcaneal taping and control (mean +/- SD, 2.7 +/- 1.8 versus 6.2 +/- 1.0; P < .001), and calcaneal taping and sham taping (mean +/- SD, 2.7 +/- 1.8 versus 6.0 +/- 0.9; P < .001). No significant difference among groups was found for posttreatment PSFS (P = .078). Conclusions: Calcaneal taping was shown to be a more effective tool for the relief of plantar heel pain than stretching, sham taping, or no treatment.     

Evidence for interaction between platelet fibrinogen receptors

Previous analysis of fibrinogen binding to human aspirin-treated gel- filtered platelets yielded upwardly concave Scatchard plots. To ascertain whether this was due to the presence of independent heterogeneous receptor populations binding fibrinogen with different affinities, the dissociation of purified 125I-fibrinogen from ADP- treated gel-filtered platelets was evaluated as a function of receptor occupancy. Dissociation of bound labeled fibrinogen was measured after 50-fold dilution with buffer containing O, 0.2, 0.8, and 2.0 mg/ml unlabeled fibrinogen. Dissociation of labeled fibrinogen increased with increasing receptor occupancy and was biphasic. With buffer alone, 76.0% +/- 5.8% (SD) of labeled fibrinogen dissociated in 30 min, with an initial rate of 0.392 +/- 0.175 min-1; with 0.2 mg/ml fibrinogen, 83.7% +/- 3.9% dissociated, with an initial rate of 0.589 +/- 0.044 min- 1; with 0.8 mg/ml, 91.8% +/- 1.3% of the labeled fibrinogen dissociated, with an initial rate of 0.910 +/- 0.028 min-1; and with 2.0 mg/ml fibrinogen, 97.3% +/- 2.3% of label dissociated, with an initial rate of 1.06 +/- 0.257 min-1 (n=5). The final rates of fibrinogen dissociation were unaffected by unlabeled fibrinogen in the dilution buffer and were not statistically different from the final dissociation rate of 0.015 +/- 0.10 min-1 observed following dilution with buffer alone. These results were neither an artifact of aspirin treatment or gel filtration, as similar observations were made using non-aspirin-treated washed platelets, nor were they an artifact of the purified fibrinogen preparations, because binding studies using whole plasma as the major source of fibrinogen also yielded upwardly concave Scatchard plots. Since the data demonstrate that the initial rate and extent of fibrinogen dissociation are dependent on fibrinogen receptor occupancy, they suggest receptor interactions possibly resulting from receptor clustering or crosslinking. Because the dissociation was biphasic, the results also suggest some heterogeneity among platelet- fibrinogen interactions.     

Acute, severe noncardiac conditions in patients with acute myocardial infarction

Purpose

The study’s purpose was to determine the prevalence and prognostic importance of acute, severe, noncardiac conditions present at the time of an acute myocardial infarction (AMI).

Methods

We identified consecutive patients with AMI who were discharged from Yale-New Haven Hospital between January 1, 1997, and June 30, 2000. Acute, noncardiac conditions that were present at admission were abstracted from patient records and graded by severity (imminent threat to life; other significant condition that would warrant admission). We examined the prognostic importance of these conditions on hospital mortality in multivariable logistic models. The study included 1145 patients with AMI, of whom 8.5% (n = 97) presented with an acute, life-threatening, noncardiac condition at admission and 19.5% (n = 223) presented with another significant noncardiac condition.

Results

Hospital mortality was 25.8% and 9.0%, respectively, for patients who presented with life-threatening and other significant noncardiac conditions, compared with 4.6% for patients without either of these conditions. In multivariable analysis, life-threatening noncardiac conditions were associated with increased hospital mortality after adjusting for demographic factors, medical history, clinical presentation, cardiac severity, and initial therapy (odds ratio 2.5; 95% confidence interval [CI], 1.2-5.2). No increased hospital mortality risk was found for other significant noncardiac conditions in the risk-adjusted analyses (odds ratio 1.0; 95% CI, 0.5-1.7).

Conclusions

A subgroup of patients with AMI presented with a life-threatening noncardiac condition, which was associated with a marked increase in the risk of death during the hospitalization. Despite the excessive mortality risk associated with concomitant noncardiac conditions, this subset of patients with AMI are poorly described in current literature.