Graded responses of human neutrophils induced by serum-treated zymosan

A modified zymosan preparation was used to probe the interaction of particulate stimuli with human neutrophils (PMNs). After extraction with alkali and detergent, the zymosan particles retained their ability to be opsonized in serum and to stimulate PMNs. Serum-treated zymosan (STZ) induced dose-dependent superoxide (O2-) production and membrane potential depolarization in the range of 1 to 10 mg/mL of STZ. The rate and extent of secretion of lysozyme and beta-glucuronidase were also dose-dependent in the range of 1 to 10 mg/mL of STZ. Cytochemical studies using nitroblue tetrazolium, however, showed that 92% of PMNs were stimulated to produce O2- at 0.1 mg/mL of STZ. The dose response of O2- production induced by STZ is therefore due to increasing O2- production by individual PMNs and not to the stimulation of more PMNs to produce O2-. Evidence for O2- production was found only in the area of PMN-zymosan contact, suggesting a mechanism for the graded responses of PMNs treated with particulate stimuli. In order to determine the nature of the dose dependence of depolarization (a measure of PMN activation), PMNs equilibrated with the fluorescent probe 3,3'- dipentyloxacarbocyanine were analyzed by flow cytometry. The results demonstrate that STZ induces a dose-dependent depolarization of the membrane potential of individual PMNs. These results also demonstrate that increasing concentrations of STZ can induce increasing PMN responses even when all of the PMNs have been activated. These results are consistent with the hypothesis that receptor-mediated particulate stimulation of PMNs is a phenomenon that results in graded PMN responses.     

Abnormal renal vasodilation to an amino acid infusion in congestive heart failure: normalization by enalapril

In congestive heart failure (CHF), the neurohormonal mechanisms that cause renal vasoconstriction, particularly those depending on the renin-angiotensin system, could interfere with renal vasodilating mechanisms. To elucidate this issue, we studied the kidney response to an amino acid infusion (known to cause renal vasodilation in healthy individuals) in eight patients with CHF. We found that the amino acid infusion (0.7 mL/kg/h of a 10% solution) elicited no renal hemodynamic response, in marked contrast to healthy subjects. We next hypothesized that the renin-angiotensin system (known to be activated in heart failure) has a role in the lack of response to the amino acid infusion. To test this hypothesis, we repeated the study after two 5-mg doses of enalapril, an inhibitor of the angiotensin-converting enzyme, administered 12 hours apart. After enalapril treatment, the amino acid infusion caused a 45% increase in mean renal blood flow (RBF) from 383 +/- 55 to 557 +/- 51 mL/min at the fifth hour (P < 0.05). This normalization of the renal response to the amino acid infusion occurred without changes in cardiac output or in systemic vascular resistance. Hence, the renal fraction of the cardiac output increased during the amino acid infusion. The recovery of the renal vascular response was not accompanied by an increase in glomerular filtration rate (GFR; filtration fraction decreased), suggesting a predominant efferent arteriole dilatation. Our study shows that, in heart failure, the kidney loses its ability to increase RBF in response to an amino acid load. This lack of renal vascular response can be restored by inhibiting the renin-angiotensin system and is unrelated to changes in systemic hemodynamics.     

Umbilical endometriosis

Tumors of the papillary region are an unusual and heterogeneous group of neoplasms that arise from the major papilla, the ampulla of Vater, and the peripapillary duodenum. Benign adenomas of the papilla of Vater are an increasingly recognized condition in those with familial adenomatous polyposis syndromes as well as sporadic cases. Papillary adenoma is a recognized but rare cause of acute pancreatitis. We describe a patient who presented with acute recurrent pancreatitis that was attributed to an intrapapillary pedunculated villous adenoma. Following diagnosis by endoscopic needle knife sphincterotomy and endoscopic retrograde cholangiopancreatography, endoscopic snare resection of the adenoma resulted in symptomatic improvement.     

Vertebroplasty increases compression of adjacent IVDs and vertebrae in osteoporotic spines

Background contextApproximately 25% of vertebroplasty patients experience subsequent fractures within 1 year of treatment, and vertebrae adjacent to the cemented level are up to three times more likely to fracture than those further away. The increased risk of adjacent fractures postaugmentation raises concerns that treatment of osteoporotic compression fractures with vertebroplasty may negatively impact spine biomechanics.PurposeTo quantify the biomechanical effects of vertebroplasty on adjacent intervertebral discs (IVDs) and vertebral bodies (VBs).Study designA biomechanics study was conducted using cadaveric thoracolumbar spinal columns from elderly women (age range, 51–98 years).MethodsFive level motion segments (T11–L3) were assigned to a vertebroplasty treated or untreated control group (n=10/group) such that bone mineral density (BMD), trabecular architecture, and age were similar between groups. Compression fractures were created in the L1 vertebra of all specimens, and polymethylmethacrylate bone cement was injected into the fractured vertebra of vertebroplasty specimens. All spine segments underwent cyclic axial compression for 115,000 cycles. Microcomputed tomography imaging was performed before and after cyclic loading to quantify compression in adjacent VBs and IVDs.ResultsCyclic loading increased strains 3% on average in the vertebroplasty group when compared with controls after 115,000 cycles. This global strain manifested locally as approximately fourfold more compression in the superior VB (T12) and two- to fourfold higher axial and circumferential deformations in the superior IVD (T12–L1) of vertebroplasty-treated specimens when compared with untreated controls. Low BMD and high cement fill were significant factors that explained the increased strain in the vertebroplasty-treated group.ConclusionsThese data indicate that vertebroplasty alters spine biomechanics resulting in increased compression of adjacent VB and IVD in severely osteoporotic women and may be the basis for clinical reports of adjacent fractures after vertebroplasty.