How effective are UV opaque face shields in UVB phototherapy cabins?

A few hours after servicing illuminated lamps inside a whole body ultraviolet radiation B (UVB) phototherapy cabin, a technician developed erythema to the anterior neck with subsequent peeling, despite wearing a UV-opaque face shield. Measurements using polysulphone film badges attached to various sites on the head and neck of a mannikin were carried out to explore the spatial distribution of UVB exposure. It was found that the lower face and neck can receive sufficient exposure to result in erythema, the reason being that the fluorescent lamps will extend to about 1.5 m inferior to the head of an upright person and so result in irradiation from below. It is important, therefore, that if operators or service personnel need to be in an illuminated UVB cabin for several minutes or more, adequate protection should be provided to the chin and neck, in addition to a UV-opaque face shield.     

Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists

The antagonist pharmacology of glutamate neurotoxicity was quantitatively examined in murine cortical cell cultures. Addition of 1-3 mM DL-2-amino-5-phosphonovalerate (APV), or its active isomer D-APV, acutely to the exposure solution selectively blocked the neuroexcitation and neuronal cell selectively blocked the neuroexcitation and neuronal cell loss produced by N-methyl-D-aspartate (NMDA), with relatively little effect on that produced by either kainate or quisqualate. As expected, this selective NMDA receptor blockade only partially reduced the neuroexcitation or acute neuronal swelling produced by the broad-spectrum agonist glutamate; surprisingly, however, this blockade was sufficient to reduce glutamate-induced neuronal cell loss markedly. Lower concentrations of APV or D-APV had much less protective effect, suggesting that the blockade of a large number of NMDA receptors was required to acutely antagonize glutamate neurotoxicity. This requirement may be caused by the amplification of small amounts of acute glutamate-induced injury by subsequent release of endogenous NMDA agonists from injured neurons, as the "late" addition of 10-1000 microM APV or D-APV (after termination of glutamate exposure) also reduced resultant neuronal damage. If APV or D-APV were present both during and after glutamate exposure, a summation dose-protection relationship was obtained, showing substantial protective efficacy at low micromolar antagonist concentrations. Screening of several other excitatory amino acid antagonists confirmed that the ability to antagonize glutamate neurotoxicity might correlate with ability to block NMDA-induced neuroexcitation: The reported NMDA antagonists ketamine and DL-2-amino-7-phosphono-heptanoate, as well as the broad-spectrum antagonist kynurenate, were all found to attenuate glutamate neurotoxicity substantially; whereas gamma-D-glutamylaminomethyl sulfonate and L-glutamate diethyl ester, compounds reported to block predominantly quisqualate or kainate receptors, did not affect glutamate neurotoxicity. The present study suggests that glutamate neurotoxicity may be predominantly mediated by the activation of the NMDA subclass of glutamate receptors--occurring both directly, during exposure to exogenous compound, and indirectly, due to the subsequent release of endogenous NMDA agonists. Given other studies linking NMDA receptors to channels with unusually high calcium permeability, this suggestion is consistent with previous data showing that glutamate neurotoxicity depends heavily on extracellular calcium.     

Contribution of neo-electroencephalography in adult functional and psychiatric disorders]

Two comparative studies of the basic activity at rest, with closed eyes taken in conventional EEG and analysed in Neo-EEG are carried out in adults showing functional or psychiatric disorders. The first open study involves 18 subjects suffering from a affection called "neurodystony" and 24 depressed subjects. The second study made in double-blind compares the results of the conventional EEG with the Neo-EEG in 19 depressed patients, 28 alcoholic patients and 26 psychotic patients. The Neo-EEG discloses abnormalities in about 60% of the cases when the conventional EEG is normal. The conventional EEG as well as the Neo-EEG diagnose a greater number of low voltage in alcoholic subjects and clear abnormalities in psychotic subjects. Low voltage is never detected in psychotic patients. In depressives, the Neo-EEG shows about 65% of abnormalities of which an asymmetry of the basic frequency in the center of the two hemispheres when they are analysed separately. That asymmetry develops in parallel with the clinical state. The asymmetry is also found in psychotic patients. In nervous or neurodystonic subjects, the Neo-EEG only discloses 25% of abnormalities. The Neo-EEG appears as an easy method, able to detect dysfunctions which cannot be disclosed with the conventional EEG and useful to follow their developments. Moreover, the result of this technique brings to the fore abnormalities not detected with the conventional EEG: this eventually leads to prescribe other therapies than those initially considered.     

The interferon in TLR signaling: more than just antiviral

The Toll-like receptor (TLR) system is responsible for the recognition of infectious agents leading to initiation of the primary innate, and later adaptive, immune response. Genetic technologies have enabled the discovery of new factors involved in these systems, their genetic manipulation and the global analyses of their effects on gene expression. Furthermore, this increased understanding has resulted in the need to reassess our preconceptions about the functions of well-known molecules. For example, type I interferons (IFNs), which were discovered as antiviral proteins, are now known to be produced in response to TLR activation by many pathogens, including bacteria. Should we be surprised? Has the inflammatory response unexpectedly highjacked the body's antiviral system? Or are we too easily blinkered by preconceptions from how a compound was discovered?     

Energy translocation across cell membranes and membrane models

Fatty acid transport is an important process in cellular energy distribution and storage in both normal and pathological states, especially obesity-linked type 2 diabetes mellitus. Fatty acid transport has been studied by the complementary approaches of cell biology and biophysics. According to the latter approach, specific proteins that enhance the uptake and storage of fatty acids are posited as fatty acid translocases, which facilitate fatty acid movement from the outer to inner leaflets of the plasma membrane. According to biophysical studies conducted in vitro, fatty acid translocation occurs by a rapid diffusive process that does not require a protein. Herein, we critically review these two mechanisms and their importance in the regulation of fatty acid uptake in vivo.     

Role of Escherichia coli K capsular antigens during complement activation, C3 fixation, and opsonization.

Escherichia coli strains with K capsular polysaccharides are relatively resistant to phagocytosis by polymorphonuclear leukocytes, in contrast to E. coli strains without K antigens. This inhibition of phagocytosis is related to an impaired recognition of the K+ strains by the phagocytes due to ineffective opsonization. All five strains without K antigens were readily phagocytized after opsonization in 5% normal serum, compared with no uptake of the K+ strains. Evidence is presented that the decreased opsonization of the K+ strains in normal serum is caused by a low rate of complement activation of the strains, with subsequent absence of C3b fixation or C3d fixation or both to the cell wall of the bacteria. After removal of the K+ antigens by heating of a K+ E. coli strain, the strain was able to activate complement, to bind C3b or C3d or both, and to become opsonized. Complement was then activated via the classical and alternative pathways, which was comparable to the complement consumption by K- E. coli.     

Inhibitability and enhanceability of basophil histamine release in asthmatic and normal subjects

Circulating human basophils contain histamine, a potent mediator of inflammation. Previous in vitro studies have shown that histamine 'releasability' in asthmatic subjects differs from normal subjects but have not evaluated possible differences in the immunopharmacological control of the release of this mediator which might account for these differences. The purpose of the present study was to examine the immunopharmacologic control of basophil histamine release in 14 asthmatics and 10 normal subjects who were characterized by pulmonary function tests, allergic status (skin tests and serum IgE levels) and nonspecific airways reactivity to methacholine and histamine. Basophils were stimulated with anti-IgE, and the inhibitory effects of the H2 agonist, dimaprit, and dibutyryl cyclic AMP (dbcAMP), as well as the enhancing properties of 5-hydroperoxyeicosatetraenoic acid (5-HPETE) and indomethacin on the modulation of histamine release, were investigated. Although no statistically significant differences were seen in the percent histamine release triggered by anti-IgE in these two groups, enhancement of histamine release by 5-HPETE was more consistent in the asthmatic subjects (10 of 10) than in control subjects (6 of 8). The percent increase in histamine release produced by 5-HPETE in asthmatic subjects averaged 3.9 +/- 1.3% using 0.03 micrograms anti-IgE/ml and 4.8 +/- 3.2% using 0.1 microgram anti-IgE/ml (p less than 0.002, Wilcoxon's signed rank test), and averaged 3.0 +/- 4.3 and 3.1 +/- 5.3%, respectively, in control subjects (p greater than 0.10).(ABSTRACT TRUNCATED AT 250 WORDS)     

Defibrination with ancrod in experimental chronic immune complex nephritis

The role of fibrin deposition in experimental (crescentic) nephritis in rabbits, due to chronic immune complex deposition induced by BSA, has been studied. Fibrin deposition was prevented and in such animals crescent formation inhibited, suggesting that, as in experimental nephritis due to anti-GBM antibodies, fibrin deposition plays a major pathogenetic role in epithelial cell proliferation. However, in defibrinated animals, mesangial and endothelial cell proliferation, polymorpho-nuclear leucocyte infiltration and impairment of renal function could still occur. These studies are further evidence that defibrination may be of benefit in the treatment of rapidly progressive glomerulonephritis in man.     

Controlling the statistics of action: obstacle avoidance

Task optimization in the presence of signal-dependent noise (TOPS) has been proposed as a general framework for planning goal-directed movements. Within this framework, the motor command is assumed to be corrupted by signal-dependent noise, which leads to a distribution of possible movements. A task can then be equated with optimizing some function of the statistics of this distribution. We found the optimal trajectory for obstacle avoidance by minimizing the mean-squared error at the end of the movement while keeping the probability of collision with the obstacle below a fixed limit. The optimal paths accurately predicted the empirical trajectories. This demonstrates that controlling the statistics of movements in the presence of signal-dependent noise may be a fundamental and unifying principle of goal-directed movements.