Infratentorial subdural empyema: clinical and computerized tomography findings. Report of three cases

Infratentorial subdural empyemas are rare. The authors report three cases encountered between 1979 and 1988, representing a 3% incidence among all subdural empyemas. The common source was an ear infection. Clinical presentation encompassed a systemic febrile illness, headaches, and a stiff neck. Only one patient had an inconspicuous focal neurological deficit that suggested a cerebral location. Initial diagnosis was acute meningitis in each case. A lumbar puncture was ordered in all three cases but was actually performed in two without developing tonsillar herniation. Cerebrospinal fluid analysis confirmed the diagnosis of meningitis in one but was normal in the other. Computerized tomography allowed a precise diagnosis and localization of the pathology. All three patients received aggressive antibiotic therapy plus suboccipital craniectomy and aspiration of pus; catheter drainage was performed in two. Cultures were positive in one case and negative in the others. Two patients were cured without sequelae; the third patient was moribund at surgery and died. Although it is known that subdural empyemas may localize in the posterior fossa, only one previous report was found. Infratentorial subdural empyema may sometimes be an unrecognized companion of acute meningitis and is cured with antibiotic therapy alone.     

Differential contribution of chemotaxins and opsonins to neutrophil-mediated killing of Schistosoma mansoni larvae.

In neutrophil-mediated killing of schistosomula, antibody and serum complement serve two functions: (i) opsonization of the target pathogen and (ii) generation of cell-activating, chemotactic peptides. We studied neutrophil-mediated schistosomulum killing in experiments designed to isolate these functions of antibody and complement in the cell activation response of neutrophils to external pathogens. Schistosomula opsonized by antibody or antibody plus complement induced neutrophil-mediated killing, while complement-opsonized larvae did not. Antibody enhancement of cell-mediated killing correlated with increased cell-to-parasite adherence, while cell-mediated killing in the presence of fresh normal human serum (providing chemotactic factor stimulation and complement opsonization of larvae) demonstrated a dissociation between neutrophil adhesive and killing responses. Exogenous chemotactic stimuli were found to enhance significantly neutrophil-mediated killing of both opsonized and unopsonized larvae. Experiments involving parabiotic chambers confirmed that chemotactic-factor-stimulated neutrophils may cause significant parasite mortality without direct cell-parasite contact. In further analysis of the neutrophil response to surface and fluid-phase stimulation, release of neutrophil cytotoxic mediators was found to vary according to the type of stimulus provided: cell exposure to either larvae opsonized by antibody plus complement or to chemotactic factors provoked low-to-moderate cell release of superoxide anion, granule enzymes, and arginase; when opsonic and chemotactic stimuli were combined, a greater-than-additive secretory response was noted. Under such maximal stimulation, oxidative and nonoxidative mediators were synergistic in effecting neutrophil-mediated parasite killing. The primary function of complement in cell-mediated parasite killing appears to be to promote chemotactic-factor-mediated cellular release of toxic agents and not cell-target linkage, whereas antibody-mediated adherence is associated with concurrent cellular activation. Both neutrophils adherent to the antibody-opsonized schistosomulum and chemotactic-factor-stimulated cells (adherent and not adherent to the parasite) appear to contribute significantly to its demise.     

Lipoplastics of Legs: Our Experience with a New Cannula Compared with Classical Technique

The Authors compare the results obtained between two groups of patients suffering from leg lipodystrophy, who were subjected to a reducing lipoplasty. In the first group, surgeons made use of a new sort of cannula, deprived of the classical grip, whereas in the second group, they employed the traditional probe. The best results, achieved with the first group, prove this new operating system is really effective, particularly on legs, for the following reasons: (1) Higher precision and better control of the instrument (2) Swan-neck cannula abolition (3) Opportunity to operate with both hands (4) Halved operating time (5) No tiredness after the operation.     

Annuloplasty in children and young adolescents with severe rheumatic mitral insufficiency

Eleven patients aged 8 to 15 years underwent measured asymmetrical annuloplasty for severe mitral regurgitation in the years 1961 through 1966. They had had a total of 20 attacks of acute rheumatic fever. The intervals between the last attack of acute rheumatic fever and operation ranged from 2 to 8 years. The criteria for surgery were congestive failure and progressive cardiac enlargement. Using the hydraulic formula of Gorlin, a mitral annuloplasty was tailored to the size of each patient so that insufficiency was eliminated without producing hemodynamically significant stenosis. In this group of 11 children there has been one death. The majority of our 11 patients reacquired murmurs of mitral regurgitation. Satisfactory results, however, are not dependent on complete hemodynamic correction. All patients have improved remarkably and have sustained this improvement up to 7 years. These results suggest that mitral annuloplasty should be the operation of choice in children with severe mitral regurgitation.     

HMGB1 promotes CXCL12-dependent egress of murine B cells from Peyer's patches in homeostasis

High mobility group box-1 protein (HMGB1) is an alarmin that, once released, promotes inflammatory responses, alone and as a complex with the chemokine CXCL12. Here, we report that the HMGB1–CXCL12 complex plays an essential role also in homeostasis by controlling the migration of B lymphocytes. We show that extracellular HMGB1 is critical for the CXCL12-dependent egress of B cells from the Peyer's patches (PP). This promigratory function of the complex was restricted to the PPs, since HMGB1 was not required for B-cell migratory processes in other locations. Accordingly, we detected higher constitutive levels of the HMGB1–CXCL12 complex in PPs than in other lymphoid organs. HMGB1–CXCL12 in vivo inhibition was associated with a reduced basal IgA production in the gut. Collectively, our results demonstrate a role for the HMGB1–CXCL12 complex in orchestrating B-cell trafficking in homeostasis, and provide a novel target to control lymphocyte migration in mucosal immunity.     

Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis

The junctional membrane protein vascular endothelial (VE)-cadherin mediates contact inhibition of growth and inhibits apoptosis of endothelial cells. In this article we show that VE-cadherin induces expression of growth arrest-specific 1 (Gas1), an integral membrane protein up-regulated in nonproliferating cells. By comparing syngenic endothelial cell lines, we found that Gas1 mRNA was increased by 3-fold in VE-cadherin-positive cells in comparison to VE-cadherin-null cells. Ectopic expression of Gas1 in endothelial or 293 cells strongly reduced apoptosis without affecting cell growth. Addition of vascular endothelial growth factor (VEGF) also up-regulated Gas1 and this effect was augmented more so in confluent nonproliferating cells than in sparse cultures. VE-cadherin-blocking antibody partially inhibited VEGF-induced Gas1, suggesting that VE-cadherin clustering is required for an optimal response to this stimulus. Inhibition of phosphoinositole-3-OH kinase (PI3-kinase) pathway by Wortmannin prevented Gas1 synthesis and the antiapoptotic effect of VEGF, but, in cells ectopically expressing Gas1, Wortmannin was ineffective. Furthermore, inhibition of Gas1 expression by short interfering RNA (siRNA) both in vitro and in allantois organ cultures made endothelial cells refractory to the antiapoptotic effect of VEGF. Overall these data indicate that Gas1 induction by VE-cadherin and VEGF in endothelial cells requires activation of PI3-kinase. Gas1 expression positively correlates with inhibition of endothelial cell apoptosis and may contribute to the integrity of resting endothelium.     

Bioavailability and toxicity of pentachlorophenol in contaminated soil evaluated on coelomocytes of Eisenia andrei (Annelida: Lumbricidae).

Pentachlorophenol (PCP) is widely distributed and highly persistent in soil, and represents a threat to the health of ecosystems. The present study aimed to assess the toxicity and bioavailability of PCP in soils as a function of different aging periods with the attempt to select a good toxicological assay for Eisenia andrei Bouché (Annelida: Lumbricidae). The experiments were performed on soil contaminated with PCP at 15 and 150ppm. After different aging periods (20, 60 and 120 days from spiking), bioavailability and toxicity were evaluated on E. andrei kept for 7 and 14 days in treated soils. The actual bioavailability decreased in relation to the aging for both PCP concentrations. No membrane damage was observed on coelomocytes collected by ethanol extrusion. Modifications in distribution of coelomocyte subpopulations were detected by flow cytometry on samples aged for 60 and 120 days at 150ppm PCP contamination. The reduction of lysosomal membrane stability, measured by neutral red retention time, was observed in all treatments. Worm mortality increased with aging in soils spiked with 150ppm of PCP. In conclusion, aging did not seem to reduce PCP cytotoxicity. This is the first report on in vivo toxicity of PCP evaluated on coelomocytes of E. andrei using different assays.