Fitting a hand-glove prosthesis to enhance the reconstructed mutilated hand

We report a unique case of tubular polyclonal immunoglobulin G (IgG) deposition disease (PIDD) superimposed on diabetic nephropathy in an 84-year-old man presenting with subacute renal failure and proteinuria. The deposits were located exclusively between the tubular epithelial cells and the tubular basement membranes (TBMs) and stained intensely with antisera to IgG heavy chain and both kappa and lambda light chains. Electron microscopy revealed large predominantly extracellular electron-dense deposits with a distinctive curvilinear substructure. The associated light microscopic findings of tubular simplification with features of acute tubular necrosis implicate this tubulopathy as the cause of the acute renal failure. This appears to represent a unique entity that does not fit into any previously described category of renal tubular immune complex or immunoglobulin deposition disease.     

Long-term evaluation of the ventricular defibrillation energy requirement

INTRODUCTION: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months after implantation. However, the stability of the defibrillation energy requirement beyond 1 year has not been reported. The purpose of this study was to characterize the defibrillation energy requirement during 2 years of clinical follow-up. METHODS AND RESULTS: Thirty-one consecutive patients with a biphasic nonthoracotomy defibrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, and 1 J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defibrillation energy requirement during these evaluations was 10.9+/-5.5 J, 12.3+/-7.3 J, 11.7+/-5.6 J, 10.2+/-4.0 J, and 11.7+/-7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased by 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defibrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defibrillation system. There were no identifiable clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defibrillation energy requirement. CONCLUSION: The mean defibrillation energy requirement does not change significantly after 2 years of biphasic nonthoracotomy defibrillator system implantation. However, approximately 15% of patients develop a 10-J or greater elevation in the defibrillation energy requirement, and 3% may require a defibrillation system revision. Therefore, a yearly evaluation of the defibrillation energy requirement may be appropriate.     

Traumatic aortic rupture: diagnosis and management

BACKGROUND: Traumatic aortic rupture is a relatively uncommon lesion that presents the cardiothoracic surgeon with unique challenges in diagnosis and management. To address controversial aspects of this disease, we reviewed our experience. METHODS: The study was performed by retrospective chart review. RESULTS: Forty-two patients with traumatic thoracic aortic ruptures were managed between January 1988 and June 1997. Nine arrived without vital signs and died in the emergency department. Admission chest radiographs were normal in 3 patients (12%) and caused significant delays in diagnosis. Four of 30 patients admitted with vital signs had rupture before thoracotomy and died. Twenty-six underwent aortic repair. In 1 patient repair was performed with simple aortic cross-clamping, whereas a second was managed with a Gott shunt. The remaining 24 patients had repair with partial left heart bypass. In 1 patient hypothermic circulatory arrest was required. Two patients (7.7%) died. There were no cases of new postoperative paraplegia in the bypass group. There was no morbidity directly attributable to the administration of heparin for cardiopulmonary bypass. CONCLUSIONS: In a discrete group of patients with traumatic rupture of the aorta, the rupture will become complete during the first few hours of hospital admission; aggressive medical treatment with beta-blockade and vasodilators in the interval before the operation is an essential aspect of management. Active distal circulatory support with partial left-heart bypass provides the optimal means of preventing spinal cord ischemia during repair of acute traumatic aortic rupture.     

Chronic fluoride exposure does not cause detrimental, extraskeletal effects in nutritionally deficient rats

On the basis of observations that endemic fluorosis occurs more often in malnourished populations, a series of studies tested the hypothesis that deficient dietary intake of calcium, protein or energy affects fluoride metabolism so that the margin of safe fluoride exposure may be reduced. The objective of the investigation was to determine whether changes in fluoride metabolism in nutritionally deficient rats resulted in manifestation of any extraskeletal toxic fluoride effects not observed in healthy animals. This investigation included two studies, one that monitored the effect of calcium deficiency on the effects of chronic fluoride exposure, and a second study that observed fluoride effects in rats that were deficient either in protein or in energy and total nutrient intake. Control and experimental rats received drinking water containing 0, 0.26 (5), 0.79 (15) or 2.63 (50) mmol fluoride/L (mg/L) for 16 or 48 wk. Control rats were fed optimal diets and experimental rats were fed diets deficient in calcium (Study 1) or protein (Study 2). An additional group of experimental rats (Study 2) was provided with a restricted amount of diet; thus these rats were deficient in energy and total nutrient intake. The intake, excretion and retention of fluoride were monitored; after the rats were killed, tissue fluoride levels and biochemical markers of tissue function were analyzed. Bone marrow cells were harvested from some of the rats, after 48 wk of treatment, for determining the frequency of sister chromatid exchange, a marker of genetic damage. Although there were significant differences among fluoride treatment groups in fluoride excretion and retention that resulted in significantly greater fluoride levels in tissues of the experimental rats, we were unable to detect any harmful, extraskeletal biochemical, physiologic or genetic effects of fluoride in the nutritionally deficient rats.     

Is it time to learn more about wireless computing? Cutting the ties that bind you to your desk

Alterations caused by hypothermal stress in neurons of pelvic plexus in rats were studied histochemically. The increase of catecholamine content in neurons and serotonin--in small intensely fluorescent cells (SIFC), suppression of acetyl cholinesterase activity in neurons were demonstrated after the short-term hypothermal stress leading to moderate hypothermia. Cooling of rats following the preliminary section of pelvic nerves does not prevent the above mentioned changes in neurons and SIFC. The participant of adrenergic nerves and SIFC in peripheral mechanisms of thermoregulation is under discussion.     

Function of the proximal stomach after Nissen fundoplication

A novel chitinase gene was isolated from Metarhizium anisopliae grown in a medium containing chitin as the sole carbon source. Comparisons of nucleotide sequence of the isolated gene with those of other fungal chitinase genes showed low sequence identity (24.4-36.4%) except for the active site of chitinase. In addition, molecular mass determination of the fused gene product separated on a gel showed that the fused chitinase seems to be about 70 kDa, while the molecular mass calculated from the deduced amino acid sequence can be about 58 kDa. These molecular masses were different from values of 33 kDa for an endochitinase and 110 kDa for an exochitinase (N-acetylglucosaminidase) from M. anisopliae published previously.     

Cytokine dysregulation in the post-Q-fever fatigue syndrome

High levels of protease inhibitors are induced in potato leaves by wounding. These inhibitors, when ingested by Colorado potato beetle (Leptinotarsa decemlineata Say) larvae, induce expression of specific proteolytic activities in the gut. Induced protease activities cannot be inhibited by potato inhibitors and thus enable the insects to overcome this defence mechanism of potato plants. The induced aminopeptidase and endoproteolytic activities both have the characteristics of cysteine proteases. Twenty-one protein inhibitors of different structural types have been examined for their ability to inhibit these activities in vitro. Members of the cystatin superfamily were found to be poor inhibitors of the induced endoproteolytic activities, except for the third domain of human kininogen, which was a fairly strong inhibitor (75% inhibition). The strongest inhibition (85%) of induced endoproteolytic activity was obtained using structurally different thyroglobulin type-1 domain-like inhibitors--equistatin and MHC class II-associated p41 invariant fragment. Experiments performed using three synthetic substrates for endoproteases gave similar results and indicate the existence of at least different endoproteolytic enzymes resistant to potato inhibitors. The induced aminopeptidase activity can be inhibited only by stefin family of inhibitors in cystatin superfamily. In in vivo experiments, Colorado potato beetle larvae fed on equistatin-coated potato leaves were strongly retarded in their growth and almost 50% died after 4 days. This demonstrated the potential of equistatin to protect crops from insect attack.