Communication: Fragment-based Hamiltonian model of electronic charge-excitation gaps and gap closure.

Capturing key electronic properties such as charge excitation gaps within models at or above the atomic scale presents an ongoing challenge to understanding molecular, nanoscale, and condensed phase systems. One strategy is to describe the system in terms of properties of interacting material fragments, but it is unclear how to accomplish this for charge-excitation and charge-transfer phenomena. Hamiltonian models such as the Hubbard model provide formal frameworks for analyzing gap properties but are couched purely in terms of states of electrons, rather than the states of the fragments at the scale of interest. The recently introduced Fragment Hamiltonian (FH) model uses fragments in different charge states as its building blocks, enabling a uniform, quantum-mechanical treatment that captures the charge-excitation gap. These gaps are preserved in terms of inter-fragment charge-transfer hopping integrals T and on-fragment parameters U((FH)). The FH model generalizes the standard Hubbard model (a single intra-band hopping integral t and on-site repulsion U) from quantum states for electrons to quantum states for fragments. We demonstrate that even for simple two-fragment and multi-fragment systems, gap closure is enabled once T exceeds the threshold set by U((FH)), thus providing new insight into the nature of metal-insulator transitions. This result is in contrast to the standard Hubbard model for 1d rings, for which Lieb and Wu proved that gap closure was impossible, regardless of the choices for t and U.

Why are some Interfaces in Materials Stronger than others?

Grain boundaries (GBs) are often the preferred sites for void nucleation in ductile metals. However, it has been observed that all boundaries do not contribute equally to this process. We present a mechanistic rationale for the role of GBs in damage nucleation in copper, along with a quantitative map for predicting preferred void nucleation at GBs based on molecular dynamics simulations in copper. Simulations show a direct correlation between the void nucleation stress and the ability of a grain boundary to plastically deform by emitting dislocations, during shock compression. Plastic response of a GB, affects the development of stress concentrations believed to be responsible for void nucleation by acting as a dissipation mechanism for the applied stress.

Direct transformation of vacancy voids to stacking fault tetrahedra.

Defect accumulation is the principal factor leading to the swelling and embrittlement of materials during irradiation. It is commonly assumed that, once defect clusters nucleate, their structure remains essentially constant while they grow in size. Here, we describe a new mechanism, discovered during accelerated molecular dynamics simulations of vacancy clusters in fcc metals, that involves the direct transformation of a vacancy void to a stacking fault tetrahedron (SFT) through a series of 3D structures. This mechanism is in contrast with the collapse to a 2D Frank loop which then transforms to an SFT. The kinetics of this mechanism are characterized by an extremely large rate prefactor, tens of orders of magnitude larger than is typical of atomic processes in fcc metals.

Abscess related to anabolic-androgenic steroid injection.

One million individuals in the United States, predominantly males under 25 yr of age, are current or past users of anabolic-androgenic steroids. Fifty percent of these young adults administer their drugs intramuscularly, placing them at risk for infections related to injection. We present here a case report of an injection-related thigh abscess in a 26-yr-old anabolic steroid injector who did not use sterile injection technique and reported sharing multidosage vials with two other weightlifting colleagues. Reported infections associated with anabolic-androgenic steroid injection include abscesses attributable to Mycobacterium smegmatis, Staphylococcus, Streptococcus, and Pseudomonas organisms as well as HIV, hepatitis B, and hepatitis C. These infections are primarily related to nonsterile injection technique, shared injection equipment, and are avoidable with appropriate prevention techniques. Education is needed to prevent infectious complications such as abscesses and blood-borne pathogens among anabolic-androgenic steroid injectors.

Stress induction of the virulence proteins (SpvA, -B, and -C) from native plasmid pSDL2 of Salmonella dublin.

The virulence region of the wild-type plasmid pSDL2 contained in Salmonella dublin is highly conserved among plasmids from several nontyphoid Salmonella serotypes and is essential for the development of systemic infection in BALB/c mice. Polyclonal antibodies against three proteins (SpvA, -B, and -C) expressed from a 4.1-kb EcoRI subclone of the plasmid virulence region were generated. These antibodies were used to detect expression of the Spv proteins when S. dublin was grown in vitro under stress-inducing conditions, such as nutrient deprivation and increased temperature, that the bacteria may encounter during the course of infection within the host. Glucose starvation resulted in expression of all three proteins shortly after the lag phase. When the bacteria were grown to the late-log phase without glucose, heat shock strongly induced expression of SpvA but not SpvB or SpvC. The addition of 0.2% glucose to the medium resulted in loss of expression of the proteins until the late-log to stationary phase. Iron limitation or lowered pH induced expression of the proteins during exponential growth even in the presence of glucose. Insertion mutations into the positive regulator gene spvR upstream from spvABC and insertions into spvA and spvC resulted in loss of expression of SpvA, -B, and -C, suggesting a complex regulation of expression. These studies define a variety of environmental conditions that induce expression of the Spv virulence proteins from the wild-type plasmid pSDL2 in S. dublin in vitro.

Evaluation of the human epidermal keratinocyte neutral red release and neutral red uptake assay using the first 10 MEIC test materials.

Two methodologies used in vitro to estimate cytotoxicity in cell culture systems were compared: these were the neutral red uptake assay (NRU), which is used to measure toxicity caused by an extended (48-hr) exposure to the test material, and the neutral red release assay (NRR), which is used to measure toxicity caused by a short-term (1-min) exposure to the test material. Both methodologies used the normal human epidermal keratinocyte (NHEK)-based NeutralRed Bioassay supplied by Clonetics Corporation (San Diego, CA, USA). 10 materials (paracetamol, acetylsalicylic acid, ferrous sulphate, diazepam, amitriptyline, digoxin, ethylene glycol, methanol, ethanol and isopropanol), which are part of the Multicenter Evaluation of In Vitro Cytotoxicity (MEIC) panel, were tested. NRU(50) values for the 10 compounds covered more than an eight-log range from 0.004 mum (digoxin) to 1.0 x 10(6) mum (methanol). Because of solubility limits, NRR(50) values for diazepam, digoxin, ferrous sulphate and paracetamol could not be determined. NRR(50) values for the remaining six compounds covered approximately a three-log range from 3.2 x 10(3) to 7.1 x 10(6) mum. When compared with documented values for either the human acute oral lethal dose or the human acute lethal blood concentration, the NRU assay was found to be much more useful in predicting human acute toxicity than was the NRR assay.

Characterization of three proteins expressed from the virulence region of plasmid pSDL2 in Salmonella dublin.

Infection of both cattle and humans with Salmonella dublin can result in septicemia and death. Like many nontyphoid Salmonella species that cause disease, S. dublin contains a cryptic plasmid (pSDL2) that is required for the full expression of virulence. Transposon mutagenesis of pSDL2 defined a 4.1-kb EcoRI region that is necessary for the development of a systemic infection in BALB/c mice. This EcoRI fragment was cloned into an expression vector (pEL11), and three proteins produced from this region with apparent molecular weights of 30,500, 76,000, and 27,000 were identified. Because bacterial proteins that play a role in virulence are often associated with the outer membrane, we were interested in establishing whether the proteins expressed from the EcoRI fragment are located in the membrane. Transposon mutagenesis of pEL11 with TnphoA defined the order of the genes along the fragment and suggested that the proteins may be exported out of the cytoplasm. Sucrose gradient cell fractionation was done to identify the cellular location of each of the three proteins. The 30-kDa protein was identified in the outer membrane fraction, and the 76-kDa protein was located in the cytosolic fraction. The 27-kDa protein was identified in both the cytosolic and the outer membrane fractions. The outer membrane contained less than 10% of the activity of enzymes known to be located in the cytoplasm, periplasm, and inner membrane. Sequence data of the 4.1-kb EcoRI region revealed that both the 30- and the 27-kDa proteins lack a typical signal sequence for export out of the cytoplasm (M. Krause, C. Roudier, J. Fierer, J. Harwood, and D. G. Guiney, Mol. Microbiol. 5:307, 1991). The outer membrane location of these proteins suggests that they may be exported out of the cytoplasm by an unusual mechanism.

Expression of tumor necrosis factor in vitro by human mononuclear phagocytes stimulated with whole Mycobacterium bovis BCG and mycobacterial antigens.

Four mycobacterial preparations directly stimulated human blood monocytes and alveolar macrophages to produce tumor necrosis factor (TNF). Monoclonal antibody against TNF blocked (99%) TNF activity. Lipopolysaccharide was not responsible for the TNF activity generated; activity was unaffected in the presence of polymyxin B.