The need to control asbestos fibers in potable water supply systems

Occupational studies have shown that asbestos is a human carcinogen. Becausemany inhaled asbestos fibers deposited in the lung are cleared and swalloed workers are also exposed through ingestion. Of the millions of current and former workers who have been heavily exposed to asbestos, one in ten will die from cancer of the gastrointestinal tract. A number on the order of 1 in 1,000 ingested asbestos fibers penetrate the digestive tract and ingested fibers have been recovered in such tissues as kidney, intestine, liver, and urine. One animal study showed tumor production related to ingestion of asbestos-containing material but, in general, the results of seven animal feeding studies have been inconclusive. A statistically significant relationship between male lung and stomach cancer and female peritoneal, gall bladder, and esophageal cancer and asbestos counts in drinking water was determined in one epidemiology study. Increased rates for male stomach and lung, and female pancreatic cancer related to asbestos in drinking water were reported in another study but possible occupational exposure made it difficult to draw conclusions. Data on excess gastrointestinal cancer among occupational groups has been used to estimate that drinking water containing 300,000 asbestos fibers per liter over a lifetime will result in one additional cancer among 100,000 people.     

Effect of deposition rates on overlay coating structure

Surface alloys were fabricated by the implantation of 25 keV chromium and nickel ions into polycrystalline iron in doses ranging from 1.0 × 10¹⁶ to 4.0 × 10¹⁶ ions cm^-2. The alloy distribution as a function of depth (depth profile) was determined for the Fe-Cr and Fe-Ni surface alloys, and the results were compared with theoretical predictions. The resistance of the surface alloys to environmental attack was evaluated both by determining their anodic polarization behavior under potentiostatic conditions in a buffered boric acid solution and by determining their gaseous oxidation characteristics. The results of the electrochemical studies showed that the general corrosion resistances of the surface alloys are comparable with those of nominally equivalent bulk alloys and that the pitting-corrosion resistances of the surface alloys are superior to that of iron, although generally they are not as good as those of most equivalent bulk alloys. The gaseous oxidation studies showed that surface and bulk Fe-Cr alloys exhibit essentially identical oxidation kinetics, with a much higher rate of oxidation being observed for iron. In both the aqueous corrosion and the gaseous oxidation studies the quantity of the alloying element in the surface alloys was six to seven orders of magnitude less than that in the equivalent bulk alloys.     

Iodine diffusion and gettering in solid electrolyte batteries

The diffusion of iodine in batteries based on Ag₄RbI₅ has been treated on the basis of a simple mathematical model, and comparison has been made with data from cell stored for various lengths of time.     

Supraceliac, but not infrarenal, aortic cross-clamping upregulates neutrophil integrin CD11b

OBJECTIVE: To evaluate the effects of supraceliac and infrarenal aortic cross-clamping on the expression of neutrophil integrin in CD11b (a marker of systemic cytokine release). DESIGN: Two groups, determined by anatomic placement of aortic cross-clamp. Laboratory personnel were blinded as to group assignment. SETTING: University teaching and community hospitals. Laboratory facilities used were university and Veteran's Affairs medical centers. PARTICIPANTS: Patients scheduled for aortic surgery. INTERVENTIONS: Blood sampling was performed at baseline, after 30 minutes of aortic cross-clamp duration, 30 and 90 minutes after reperfusion (for tumor necrosis factor-alpha plasma levels in infrarenal cross-clamp group), and at baseline and 90 minutes reperfusion (for neutrophil CD11b expression quantification) in both groups. MEASUREMENTS AND MAIN RESULTS: Tumor necrosis factor-alpha measured by ELISA technique did not change at any time period in the infrarenal clamping group. Neutrophil CD11b expression, measured by double antibody staining and FACScan analysis, did not change significantly at 90 minutes of reperfusion in the infrarenal group, but increased significantly (p < 0.05) in the supraceliac aortic cross-clamp group. CONCLUSION: Neutrophil integrin CD11b has been demonstrated to be the primary adhesive glycoprotein responsible for neutrophil organ entrapment and subsequent neutrophil-mediated reperfusion injury. These results suggest that upregulation of neutrophil integrin CD11b after supraceliac aortic clamping may in part be responsible for the higher incidence of acute lung injury after thoracic aortic aneurysm repair requiring supraceliac clamping when compared with infrarenal aneurysm surgery.     

Erosion of conventional and ultrafine-grained materials

The erosion behavior was investigated of wear-resistant coatings of SiSiC and WWC applied to steel and graphite substrates using the controlled nucleation thermochemical deposition (CNTD) process, a refinement of the chemical vapor deposition (CVD) process. This process produces ultrafine equiaxed crystallites with average grain sizes of the order of tens to hundreds of ångströms.The room temperature erosion behavior of these materials was determined and compared with that of other conventional ceramic and metallic composite wear-resistant materials. The effects of various erodents, impingement angles and post-deposition heat treatments were investigated. The CNTD process produces materials with greater erosion resistance than that of conventional CVD materials and can be modified to deposit coatings onto ferrous alloys at low deposition temperatures. The erosion mechanism for CNTD materials is of the brittle type where the erosion rate is determined by the rate of initiation and propagation of cracks. It was found that post-deposition heat treatment of the CNTD WWC deposited at low temperatures improved the material's erosion resistance.     

Rat blood neutrophils express very late antigen 4 and it mediates migration to arthritic joint and dermal inflammation

Blood neutrophils contribute to joint injury in human and experimental models of arthritis. Neutrophil migration out of the blood in joint inflammation involves both the CD18 (beta2) integrins and a CD18 integrin-independent pathway. To investigate this migration, radiolabeled rat blood neutrophils were used to measure neutrophil accumulation in the inflamed joints of rats with adjuvant arthritis and the role of leukocyte integrins in migration to these joints and to dermal inflammation was determined. Neutrophils migrated rapidly (<2 h) to the inflamed joints 14-18 d after immunization with adjuvant. Blocking monoclonal antibodies (mAbs) to both LFA-1 and Mac-1 together, as well as a mAb to CD18, inhibited neutrophil accumulation in the inflamed joints by 50-75%. However, migration to dermal inflammation induced by C5a(des Arg)' tumor necrosis factor alpha, lipopolysaccharide, and poly-inosine:cytosine was inhibited by approximately 90%. Flow cytometry revealed the expression of low levels of very late antigen 4 (VLA-4) on nearly all rat blood neutrophils. Treatment with anti-VLA-4 plus anti-LFA-1 but neither mAb alone, strongly (60-75%) inhibited neutrophil accumulation in arthritic joints. This mAb combination also inhibited neutrophil migration to dermal inflammatory reactions by 30-70%. Blocking VLA-4 together with the CD18 integrins inhibited neutrophil accumulation by 95-99%, virtually abolishing neutrophil accumulation in cutaneous inflammation. A similar blockade of VLA-4 and CD18 decreased neutrophil accumulation in the inflamed joints by 70-83%, but a significant portion of the neutrophil accumulation to these joints still remained. In conclusion, rat blood neutrophils express functional VLA-4 that can mediate neutrophil migration to both inflamed joints and dermal inflammatory sites. VLA-4 appears to be able to substitute for LFA-1 in this migration and is particularly important for accumulation in inflamed joints. However, there exists an additional CD18- and VLA-4-independent pathway of neutrophil migration to arthritic joints that is not involved in acute dermal inflammation.     

Optical amplification of ligand-receptor binding using liquid crystals

Liquid crystals (LCs) were used to amplify and transduce receptor-mediated binding of proteins at surfaces into optical outputs. Spontaneously organized surfaces were designed so that protein molecules, upon binding to ligands hosted on these surfaces, triggered changes in the orientations of 1- to 20-micrometer-thick films of supported LCs, thus corresponding to a reorientation of approximately 10(5) to 10(6) mesogens per protein. Binding-induced changes in the intensity of light transmitted through the LC were easily seen with the naked eye and could be further amplified by using surfaces designed so that protein-ligand recognition causes twisted nematic LCs to untwist. This approach to the detection of ligand-receptor binding does not require labeling of the analyte, does not require the use of electroanalytical apparatus, provides a spatial resolution of micrometers, and is sufficiently simple that it may find use in biochemical assays and imaging of spatially resolved chemical libraries.     

Laminin directs growth cone navigation via two temporally and functionally distinct calcium signals

During development, growth cones navigate to their targets via numerous interactions with molecular guidance cues, yet the mechanisms of how growth cones translate guidance information into navigational decisions are poorly understood. We have examined the role of intracellular Ca2+ in laminin (LN)-mediated growth cone navigation in vitro, using chick dorsal root ganglion neurons. Subsequent to contacting LN-coated beads with filopodia, growth cones displayed a series of stereotypic changes in behavior, including turning toward LN-coated beads and a phase of increased rates of outgrowth after a pause at LN-coated beads. A pharmacological approach indicated that LN-mediated growth cone turning required an influx of extracellular Ca2+, likely in filopodia with LN contact, and activation of calmodulin (CaM). Surprisingly, fluorescent Ca2+ imaging revealed no LN-induced rise in intracellular Ca2+ in filopodia attached to their parent growth cone. However, isolation of filopodia by laser-assisted transection unmasked a rapid, LN-specific rise in intracellular Ca2+ (+73 +/- 11 nM). Additionally, a second, sustained rise in intracellular Ca2+ (+62 +/- 8 nM) occurred in growth cones, with a distinct delay 28 +/- 3 min after growth cone filopodia contacted LN-coated beads. This delayed, sustained Ca2+ signal paralleled the phase of increased rates of outgrowth, and both events were sensitive to the inhibition of Ca2+/CaM-dependent protein kinase II (CaM-kinase II) with 2 microM KN-62. We propose that LN-mediated growth cone guidance can be attributed, in part, to two temporally and functionally distinct Ca2+ signals linked by a signaling cascade composed of CaM and CaM-kinase II.