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The article presents an interview with crime and thriller writer Michael Connelly who discusses his initial thoughts about the terrorist attacks on the U.S. on September 11, 2001, the impact of the September 11 terrorist attack on his writing and his books titled "City of Bones" and "Lost Light."

Michael Connelly's 2002 crime novel, City of Bones, follows an investigation by LAPD Detective Harry Bosch into the unsolved murder of a 12 year old boy, registered missing in 1980. Bosch's investigation to uncover the circumstances that led to the boy's murder, and therein uncover the hidden identity of the killer, is transposed against 'the struggle everyone had to find meaning after such a catastrophic event, literally witnessed first-hand through television'1. An early entrant in what quickly blossomed into a rich tapestry of cultural material critically (and not so critically) engaged with the politics of 9/11 and the unfolding war on terror, City of Bones questions the extent to which an absolute truth can be arrived it in the narrativisation of a trauma by its immediate experiencers. Moreover, in a narrative of crime where the political imperatives of the LAPD consistently assert control over trauma's narrativising -- a consequence of which is an unfolding sequence of further traumatic deaths -- City of Bones explores how the imperatives of a political hegemon may militate against trauma's abatement by hijacking post-trauma narrativisation to create a record of trauma that confers legitimacy upon the recurrence of violence as the response to trauma. Read within the post 9/11 context into which the novel emerged, my paper contends that City of Bones offers an allegorical microcosm of the Bush administration's efforts to manage the narrativising of 9/11 into a position directly relational to the 9/11 attacks; a position from which revanchist counter-violence emerged as a legitimate response to the trauma of 9/11. [ABSTRACT FROM AUTHOR]

The problem of understanding how Earth's magnetic field is generated is one of the foremost challenges in modern science. It is believed to be generated by a dynamo process, where the complex motions of an electrically conducting fluid provide the inductive action to sustain the field against the effects of dissipation. Current dynamo simulations, based on the numerical approximation to the governing equations of magnetohydrodynamics, cannot reach the very rapid rotation rates and low viscosities (i.e. low Ekman number) of Earth due to limitations in available computing power. Using a pseudospectral method, the most widely used method for simulating the geodynamo, computational requirements needed to run simulations in an 'Earth-like' parameter regime are explored theoretically by approximating operation counts, memory requirements and communication costs in the asymptotic limit of large problem size. Theoretical scalings are tested using numerical calculations. For asymptotically large problems the spherical transform is shown to be the limiting step within the pseudospectral method; memory requirements and communication costs are asymptotically negligible. Another limitation comes from the parallel implementation, however, this is unlikely to be threatened soon and we conclude that the pseudospectral method will remain competitive for the next decade. Extrapolating numerical results based upon the code analysis shows that simulating a problem characterizing the Earth with Ekman number E = 10 would require at least 13 000 days per magnetic diffusion time with 54 000 available processors, a formidable computational challenge. At E = 10 an allocation of around 350 million CPU hours would compute a single diffusion time, many more CPU hours than are available in current supercomputing allocations but potentially reachable in the next decade. Exploration of the 10⩽ E⩽10 regime could be performed at the present time using a substantial share of national supercomputing facilities or a dedicated cluster. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Abstract: The alkylation of (ArHNCH2CH2)2NH with RX [RX=MeI, (2-C5H4N)CH2Cl] under basic conditions gives (ArHNCH2CH2)2NMe (Ar=2,6-Me2C6H3 L1a, 2,4-Me2C6H3 L1b) and (ArHNCH2CH2)2{(2-C5H4N)CH2}N (Ar=2,4,6-Me3C6H2 L2a, 2,4-Me2C6H3 L2b) in moderate yield, respectively. Alternatively, L1a and L1b can be accessed by the arylation (with Ar–Br) of (H2NCH2CH2)2NMe in the presence of a catalytic quantity of Pd2(dba)3. Treatment of L1 with CoCl2 in n-BuOH gave high-spin [{(ArHNCH2CH2)2NMe}CoCl2] (Ar=2,6-Me2C6H3 1a, 2,4-Me2C6H3 1b) in good yield; no reaction occurred with FeCl2. The molecular structure of 1a reveals a distorted trigonal bipyramidal geometry with the L1a adopting a mer-configuration. Reaction of L2 with MCl2 affords the cobalt and iron complexes, [{ArNHCH2CH2}2{(2-C5H4N)CH2}NMCl2] (M=Co, Ar=2,4,6-Me3C6H2 2a, 2,4-Me2C6H3 2b; M=Fe, Ar=2,4,6-Me3C6H2 3a, 2,4-Me2C6H3 3b); the octahedral frameworks in 2a and 3a are found to be considerably distorted with one of the two M-N(mesityl-substituted) distances noticeably elongated [M-N 2.597(4)–2.795(2)Å]; no such inequivalence is observed in solution at room temperature. On activation with methylaluminoxane, complexes 1a and 1b display some activity for the oligomerisation of ethylene. [Copyright &y& Elsevier]

This paper interrogates the aesthetic signature of CSI: Crime Scene Investigation (2000-2015). Utilizing a selection of representative episodes airing during George W. Bush's first term, I analyze how CSI mobilizes a particular aesthetic of wounding in which wound sites,bodily and geographic,may be understood to serve as vulnerable apertures through which underlying threads of critical engagement with the direction of the 9/11 discourse may be aspirated from within the body of the text. Specifically, I approach the wound sites of CSI as sources of war-on-terror critique that serve political double-duty. On the one hand, CSI's injury-centric narratives and accompanying wound aesthetic provide a canvas against which the traumatizing realities of 9/11 could be mediated and moderated for a newly death-anxious audience. On the other hand, the wound aesthetic ironically provides a recuperative narrative about the state's ability to respond to political violence and prosecute its perpetrators. [ABSTRACT FROM AUTHOR]

Zika virus (ZIKV) causes no-to-mild symptoms or severe neurological disorders. To investigate the importance of viral and host genetic variations in determining ZIKV infection outcomes, we created three full-length infectious cDNA clones as bacterial artificial chromosomes for each of three spatiotemporally distinct and genetically divergent ZIKVs: MR-766 (Uganda, 1947), P6-740 (Malaysia, 1966), and PRVABC-59 (Puerto Rico, 2015). Using the three molecularly cloned ZIKVs, together with 13 ZIKV region-specific polyclonal antibodies covering nearly the entire viral protein-coding region, we made three conceptual advances: (i) We created a comprehensive genome-wide portrait of ZIKV gene products and their related species, with several previously undescribed gene products identified in the case of all three molecularly cloned ZIKVs. (ii) We found that ZIKV has a broad cell tropism in vitro, being capable of establishing productive infection in 16 of 17 animal cell lines from 12 different species, although its growth kinetics varied depending on both the specific virus strain and host cell line. More importantly, we identified one ZIKV-non-susceptible bovine cell line that has a block in viral entry but fully supports the subsequent post-entry steps. (iii) We showed that in mice, the three molecularly cloned ZIKVs differ in their neuropathogenicity, depending on the particular combination of viral and host genetic backgrounds, as well as in the presence or absence of type I/II interferon signaling. Overall, our findings demonstrate the impact of viral and host genetic variations on the replication kinetics and neuropathogenicity of ZIKV and provide multiple avenues for developing and testing medical countermeasures against ZIKV. [ABSTRACT FROM AUTHOR]

Abstract: Dendritic cell antigen targeting primes robust immune responses in mouse models. Optimizing this immunization strategy in the actual hosts that require protection will advance development of efficacious contemporary vaccines. In a proof-of-concept study, we tested the immunogenicity of a single, low dose of a novel multi-component DNA construct expressing a CD205-targeted antigen fused to a CD40L minimal functional domain for linked DC activation. The DNA construct was formulated with DNA-encoded Flt3L and GM-CSF for DC recruitment and the formulation was evaluated in MHC class II-matched calves. Immunization of the calves with the CD205 antigen-targeting construct mixed with the cytokine constructs induced significant IFN-γ-secreting CD4+ T-cells, CD4+ T-cell proliferation, and antibody responses detectable within one week post-immunization. CD205 antigen-targeting significantly expanded IFN-γ-secreting CD4+ T-cells, CD4+ T-cell proliferation, and IgG antibody responses three weeks post-immunization. Nineteen weeks post-priming, the IFN-γ-secreting CD4+ T-cells, CD4+ T-cell proliferation, and the IgG titers were waning, but they remained significant. Following boosting at nineteen weeks post-immunization, the immune responses primed by the CD205-targeted antigen underwent rapid recall and the mean response tripled within one week post-boost. Comparative analysis of the immune responses observed one week post-priming versus the responses detected one week post-boost revealed that the average number of the IFN-γ-secreting CD4+ T-cells observed in the calves immunized with the CD205 antigen targeting construct increased five-fold, the mean CD4+ T-cell proliferation increased three-fold, whereas the mean IgG antibody titer increased two hundred-fold. These promising outcomes support testing the protective efficacy of CD205-targeted antigens in the calf model. [Copyright &y& Elsevier]

In an attempt to express and isolate BoLA-NC3*00101, a bovine, non-classical, major histocompatibility complex (MHC) class I protein, the mouse mastocytoma cell line P815 was transfected with the NC3*00101 transgene. The transfected cells were checked for expression by flow cytometry and positive stable transfectants were sorted using a fluorescence-activated cell sorter (FACS). A large amount of purified protein is required for the generation of monoclonal antibodies in order to immunize the mice and then boost the host for several months to get highly-specific antibodies. To avoid using a large number of cell culture flasks and shorten the time required to obtain a sufficient quantity of protein, stably-transfected BoLA-NC3*00101 -expressing cells were grown in a pitched-blade bioreactor. One week of culturing in the bioreactor yielded a large cell mass which was used to isolate and purify the protein. [ABSTRACT FROM AUTHOR]

Trophoblast cells from bovine somatic cell nuclear transfer (SCNT) conceptuses express major histocompatibility complex class I (MHC-I) proteins early in gestation, and this may be one cause of the significant first-trimester embryonic mortality observed in these pregnancies. MHC-I homozygous-compatible (n = 9), homozygous-incompatible (n = 8), and heterozygous-incompatible (n = 5) SCNT pregnancies were established. The control group consisted of eight pregnancies produced by artificial insemination. Uterine and placental samples were collected on Day 35 ± 1 of pregnancy, and expression of MHC-I, leukocyte markers, and cytokines were examined by immunohistochemistry. Trophoblast cells from all SCNT pregnancies expressed MHC-I, while trophoblast cells from age-matched control pregnancies were negative for MHC-I expression. Expression of MHC-I antigens by trophoblast cells from SCNT pregnancies was associated with lymphocytic infiltration in the endometrium. Furthermore, MHC-I-incompatible conceptuses, particularly the heterozygous-incompatible ones, induced a more pronounced lymphocytic infiltration than MHC-I-compatible conceptuses. Cells expressing cluster of differentiation (CD) 3, gamma/deltaTCR, and MHC-II were increased in the endometrium of SCNT pregnancies compared to the control group. CD4(+) lymphocytes were increased in MHC-I-incompatible pregnancies compared to MHC-I-compatible and control pregnancies. CD8(+), FOXP3(+), and natural killer cells were increased in MHC-I heterozygous-incompatible SCNT pregnancies compared to homozygous SCNT and control pregnancies., (© 2016 by the Society for the Study of Reproduction, Inc.)

Structural remodeling in chronic atrial fibrillation (AF) occurs over weeks to months. To study the electrophysiological, structural, and functional changes that occur in chronic AF, the selection of the best animal model is critical. AF was induced by rapid atrial pacing (50-Hz stimulation every other second) in pigs (n = 4), dogs (n = 8), and goats (n = 9). Animals underwent MRIs at baseline and 6 mo to evaluate left ventricular (LV) ejection fraction (EF). Dogs were given metoprolol (50-100 mg po bid) and digoxin (0.0625-0.125 mg po bid) to limit the ventricular response rate to <180 beats/min and to mitigate the effects of heart failure. The pacing leads in pigs became entirely encapsulated and lost the ability to excite the heart, often before the onset of sustained AF. LV EF in dogs dropped from 54 ± 11% at baseline to 33 ± 7% at 6 mo (P < 0.05), whereas LV EF in goats did not drop significantly (69 ± 8% at baseline vs. 60 ± 9% at 6 mo, P = not significant). After 6 mo of AF, fibrosis levels in dog atria and ventricles increased, whereas only atrial fibrosis levels increased in goats compared with control animals. In our experience, the pig model is not appropriate for chronic rapid atrial pacing-induced AF studies. Rate-controlled chronic AF in the dog model developed HF and LV fibrosis, whereas the goat model developed only atrial fibrosis without ventricular dysfunction and fibrosis. Both the dog and goat models are representative of segments of the patient population with chronic AF.

Previously, our laboratory showed that Holstein cattle experimentally infected with Neospora caninum develop parasite-specific CD4+ cytotoxic T lymphocytes (CTL) that lyse infected, autologous target cells through a perforin-granzyme pathway. To identify specific parasite antigens inducing bovine CTL and helper T-lymphocyte responses for vaccine development against bovine neosporosis, the tachyzoite major surface proteins NcSAG1 and NcSRS2 were targeted. In whole tachyzoite antigen-expanded bovine T-lymphocyte lines, recombinant NcSRS2 induced potent memory CD4+- and CD8+-T-lymphocyte activation, as indicated by proliferation and gamma interferon (IFN-gamma) secretion, while recombinant NcSAG1 induced a minimal memory response. Subsequently, T-lymphocyte epitope-bearing peptides of NcSRS2 were mapped by using overlapping peptides covering the entire NcSRS2 sequence. Four experimentally infected cattle with six different major histocompatibility complex (MHC) class II haplotypes were the source of immune cells used to identify NcSRS2 peptides presented by Holstein MHC haplotypes. NcSRS2 peptides were mapped by using IFN-gamma secretion by rNcSRS2-stimulated, short-term T-lymphocyte cell lines, IFN-gamma enzyme-linked immunospot (ELISPOT) assay with peripheral blood mononuclear cells, and 51Cr release cytotoxicity assay of rNcSRS2-stimulated effector cells. Four N. caninum-infected Holstein cattle developed NcSRS2 peptide-specific T lymphocytes detected ex vivo in peripheral blood by IFN-gamma ELISPOT and in vitro by measuring T-lymphocyte IFN-gamma production and cytotoxicity. An immunodominant region of NcSRS2 spanning amino acids 133 to 155 was recognized by CD4+ T lymphocytes from the four cattle. These findings support investigation of subunit N. caninum vaccines incorporating NcSRS2 gene sequences or peptides for induction of NcSRS2 peptide-specific CTL and IFN-gamma-secreting T lymphocytes in cattle with varied MHC genotypes.

Johne's disease of cattle is widespread and causes significant economic loss to producers. Control has been hindered by limited understanding of the immune response to the causative agent, Mycobacterium avium subsp. paratuberculosis, and lack of an effective vaccine and sensitive specific diagnostic assays. The present study was conducted to gain insight into factors affecting the immune response to M. avium subsp. paratuberculosis. A persistent proliferative response to M. avium subsp. paratuberculosis purified protein derivative and soluble M. avium subsp. paratuberculosis antigens was detected in orally infected neonatal calves 6 months postinfection (p.i.) by flow cytometry (FC). CD4(+) T cells with a memory phenotype (CD45R0(+)) expressing CD25 and CD26 were the predominant cell type responding to antigens. Few CD8(+) T cells proliferated in response to antigens until 18 months p.i. gammadelta T cells did not appear to respond to antigen until 18 months p.i. The majority of WC1(+) CD2(-) and a few WC1(-) CD2(+) gammadelta T cells expressed CD25 at time zero. By 18 months, however, subsets of gammadelta T cells from both control and infected animals showed an increase in expression of CD25, ACT2, and CD26 in the presence of the antigens. Two populations of CD3(-) non-T non-B null cells, CD2(+) and CD2(-), proliferated in cell cultures from some control and infected animals during the study, with and without antigen. The studies clearly show multicolor FC offers a consistent reliable way to monitor the evolution and changes in the immune response to M. avium subsp. paratuberculosis that occur during disease progression.