bluuebunny/crossref_metadata_2025_split huggingface dataset:
From Iraq to Katrina and Back: Bureaucratic Planning as Strategic Failure, Fiction, and Fantasy
Authors: Bissell William Cunningham 
Published: July 2008

AbstractBureaucratic planning is a complex sociocultural process rife with vested interests, contradictory aims, and internal conflicts. In the wake of Hurricane Katrina and the US occupation of Iraq, contemporary media discourses on planning have downplayed this complexity and diverted attention away from a more nuanced understanding of planning as a sociological process. In this article, I show how policy and press debates regarding bureaucratic planning in Iraq and New Orleans are rooted in technocratic and rationalist perspectives, constituting a kind of modernist faith. These contemporary discourses are often one‐dimensional, failing to consider the conflicts, contradictions, and counter‐intuitive outcomes that are inherent in planning in complex situations, including urban reconstruction, military occupation, and disaster response. I show how flawed approaches in the present are deeply linked to the past, connecting Iraq and Katrina to a detailed ethnographic case study on failed urban planning in colonial Zanzibar. Even though the three cases of Iraq, Katrina, and Zanzibar differ across time, context, and conditions, they reveal that bureaucratic planning is best understood as a multidimensional strategic practice that is intrinsically shaped by sociocultural forms. Plans may ostensibly fail in one sense and yet still produce quite enduring effects. They may remain ‘fictions’ at one level but still wield real impact. And even if they are informed by fantasy, bearing little utility from a functional perspective, plans still serve as performative and persuasive acts, informed by political ends.
The Ethical Dilemma of Ethical Committees
Authors: Derbyshire Stuart 
Published: July 2008

AbstractThe Nuremberg code, a response to the 1946 Nuremberg Medical Trials, was the first attempt to formally state ethical requirements for medical research. The Code was generally ignored as a response to the peculiarly barbaric Nazi atrocities and an unnecessary fetter on normal research. A series of research scandals, however, led to more successful attempts at regulating medical research and to the introduction of various ethical committees during the 1970s. Since then, ethical committees have expanded their remit to regulate social as well as medical research and operate according to precautionary standards that far exceed what is necessary to protect public safety. Ethical committees block investigations of medical practice even when the intent is to benefit patients directly and they prevent social research entailing even far‐fetched possibilities of ‘stress’. Although purportedly designed to protect patients and civil liberties, modern ethical regulation damages the doctor–patient relationship, undermines professional responsibility, and encourages negative scientific practice.
Distinctive Features of Surface-Anchored Proteins of
Streptococcus agalactiae
Strains from Zimbabwe Revealed by PCR and Dot Blotting
Authors: Mavenyengwa Rooyen T. , Maeland Johan A. , Moyo Sylvester R. 
Published: July 2008

ABSTRACT
The distribution of capsular polysaccharide (CPS) types and subtypes (serovariants) among 121 group B streptococcus (GBS) strains from Zimbabwe was examined. PCR was used for the detection of both CPS types and the surface-anchored and strain-variable proteins Cα, Cβ, Alp1, Alp2, Alp3, R4/Rib, and Alp4. The R3 protein was detected by an antibody-based method using monoclonal anti-R3 antibody in dot blotting. The CPS types detected, Ia (15.7% of strains), Ib (11.6%), II (8.3%), III (38.8%), V (24.0%), and nontypeable (1.7%), were essentially as expected on the basis of data from Western countries. The type V strains showed distinctive features with respect to protein markers in that Alp3 was detected in only 6.9% of the isolates while R3 occurred in 75.9% and R4/Rib occurred in 37.9% of the isolates. R3 occurred nearly always in combination with one of the alpha-like (Alp) proteins, and it was the third most common of the proteins studied. These results show that type V GBS strains from Zimbabwe differed from type V strains from other geographical areas and also emphasize the importance of the R3 protein in GBS serotyping and its potential importance in the immunobiology of GBS, including a potential role in a future GBS vaccine.
Empyema Necessitatis Due to Methicillin-Resistant
Staphylococcus aureus
: Case Report and Review of the Literature
Authors: Mizell Kelly N. , Patterson Kimberley V. , Carter J. Elliot 
Published: July 2008

ABSTRACT

Empyema necessitatis is a rare complication of empyema in which the pleural infection spreads outside of the pleural space to involve the soft tissues of the chest wall. Most cases of empyema necessitatis are related to
Mycobacterium tuberculosis
and, less commonly, to
Actinomyces
spp. and
Streptococcus
spp.
Staphylococcus aureus
has rarely been reported as the causative agent of empyema necessitatis, with the majority of
S. aureus
isolates being methicillin sensitive. Only two cases of empyema necessitatis due to methicillin-resistant
S. aureus
(MRSA) have been reported in the medical literature. We report the case of a 59-year-old Caucasian male who presented to our institution with complaints of pain in and swelling of his left upper chest of 2-months duration. A computed tomography scan of the chest showed an 8.1- by 6.5-cm lesion which extended from the left upper lobe of the lung into the extrathoracic soft tissues beneath the left upper pectoralis muscle. A wedge resection of the left upper lung lobe revealed lung tissue with an organized pneumonia-like pattern associated with marked acute pleuritis. Blood and urine cultures and cultures of the left chest soft tissue mass grew MRSA. The patient was successfully treated with vancomycin followed by a 10-day outpatient course of ciprofloxacin and trimethoprim-sulfamethoxazole. This case represents an extremely rare manifestation of an increasingly dangerous bacterial pathogen.
Prevalence of Human KI and WU Polyomaviruses in Children with Acute Respiratory Tract Infection in China
Authors: Yuan Xin-hui , Jin Yu , Xie Zhi-ping , Gao Han-chun , Xu Zi-qian , Zheng Li-shu , Zhang Rong-fang , Song Jing-rong , Hou Yun-de , Duan Zhao-jun 
Published: July 2008

ABSTRACT
The KI and WU polyomaviruses were found in 11 (2.7%) and 17 (4.2%) of 406 nasopharyngeal aspirates, respectively, from children with acute respiratory tract infection (ARTI). The phylogenetic analysis indicates that they are all in the same cluster as the prototype strains. Our findings suggest that they are common in children with ARTI in China.
Mutational Evidence for a Structural Model of the Lassa Virus RNA Polymerase Domain and Identification of Two Residues, Gly1394 and Asp1395, That Are Critical for Transcription but Not Replication of the Genome
Authors: Hass Meike , Lelke Michaela , Busch Carola , Becker-Ziaja Beate , Günther Stephan 
Published: July 2008

ABSTRACT
The RNA-dependent RNA polymerase (RdRp) of arenaviruses is an integral part of the L protein, a 200-kDa multifunctional and multidomain protein. In view of the paucity of structural data, we recently proposed a model for the RdRp domain of arenaviruses based on the folding of RdRps of plus-strand viruses (S. Vieth et al., Virology 318:153-168, 2004). In the present study, we have chosen a large-scale mutagenesis approach to gain insight into the structure and function of the Lassa virus RdRp domain. A total of 180 different mutants of the domain were generated by using a novel PCR-based mutagenesis technique and tested in the context of the Lassa virus replicon system. Nearly all residues, which were essential for function, clustered in the center of the three-dimensional model including the catalytic site, while residues that were less important for function mapped to the periphery of the model. The combined bioinformatics and mutagenesis data allowed deducing candidate residues for ligand interaction. Mutation of two adjacent residues in the putative palm-thumb subdomain junction, G1394 and D1395 (strain AV), led to a defect in mRNA synthesis but did not affect antigenomic RNA synthesis. In conclusion, the data provide circumstantial evidence for the existence of an RdRp domain between residues 1040 and 1540 of the Lassa virus L protein and the folding model of the domain. A functional element within the RdRp was identified, which is important for transcription but not replication of the genome.
The DNA Damage Sensors Ataxia-Telangiectasia Mutated Kinase and Checkpoint Kinase 2 Are Required for Hepatitis C Virus RNA Replication
Authors: Ariumi Yasuo , Kuroki Misao , Dansako Hiromichi , Abe Ken-Ichi , Ikeda Masanori , Wakita Takaji , Kato Nobuyuki 
Published: July 2008

ABSTRACT
Cellular responses to DNA damage are crucial for maintaining genome integrity, virus infection, and preventing the development of cancer. Hepatitis C virus (HCV) infection and the expression of the HCV nonstructural protein NS3 and core protein have been proposed as factors involved in the induction of double-stranded DNA breaks and enhancement of the mutation frequency of cellular genes. Since DNA damage sensors, such as the ataxia-telangiectasia mutated kinase (ATM), ATM- and Rad3-related kinase (ATR), poly(ADP-ribose) polymerase 1 (PARP-1), and checkpoint kinase 2 (Chk2), play central roles in the response to genotoxic stress, we hypothesized that these sensors might affect HCV replication. To test this hypothesis, we examined the level of HCV RNA in HuH-7-derived cells stably expressing short hairpin RNA targeted to ATM, ATR, PARP-1, or Chk2. Consequently, we found that replication of both genome-length HCV RNA (HCV-O, genotype 1b) and the subgenomic replicon RNA were notably suppressed in ATM- or Chk2-knockdown cells. In addition, the RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were suppressed in these knockdown cells after inoculation of the cell culture-generated HCV. Consistent with these observations, ATM kinase inhibitor could suppress the HCV RNA replication. Furthermore, we observed that HCV NS3-NS4A interacted with ATM and that HCV NS5B interacted with both ATM and Chk2. Taken together, these results suggest that the ATM signaling pathway is critical for HCV RNA replication and may represent a novel target for the clinical treatment of patients with chronic hepatitis C.
The Kinetics of Hepatitis C Virus-Specific CD8 T-Cell Responses in the Blood Mirror Those in the Liver in Acute Hepatitis C Virus Infection
Authors: Shin Eui-Cheol , Capone Stefania , Cortese Riccardo , Colloca Stefano , Nicosia Alfredo , Folgori Antonella , Rehermann Barbara 
Published: July 2008

ABSTRACTPeripheral blood T-cell responses are used as biomarkers in hepatitis C virus (HCV) vaccine trials. However, it is not clear how T-cell responses in the blood correlate with those in the liver, the infection site. By studying serial liver and blood samples of five vaccinated and five mock-vaccinated control chimpanzees during acute HCV infection, we demonstrate a correlation between HCV-specific CD8 T-cell responses in the blood and molecular and functional markers of T-cell responses in the liver. Thus, HCV-specific CD8 T-cell responses in the blood are valid markers for intrahepatic T-cell activity.
Scrapie-Induced Defects in Learning and Memory of Transgenic Mice Expressing Anchorless Prion Protein Are Associated with Alterations in the Gamma Aminobutyric Acid-Ergic Pathway
Authors: Trifilo Matthew J. , Sanchez-Alavez Manuel , Solforosi Laura , Bernard-Trifilo Joie , Kunz Stefan , McGavern Dorian , Oldstone Michael B. A. 
Published: July 2008

ABSTRACT

After infection with RML murine scrapie agent, transgenic (tg) mice expressing prion protein (PrP) without its glycophosphatidylinositol (GPI) membrane anchor (GPI
−/−
PrP tg mice) continue to make abundant amounts of the abnormally folded disease-associated PrPres but have a normal life span. In contrast, all age-, sex-, and genetically matched mice with a GPI-anchored PrP become moribund and die due to a chronic progressive neurodegenerative disease by 160 days after RML scrapie agent infection. We report here that infected GPI
−/−
PrP tg mice, although free from progressive neurodegenerative disease of the cerebellum and extrapyramidal and pyramidal systems, nevertheless suffer defects in learning and memory, long-term potentiation, and neuronal excitability. Such dysfunction increases over time and is associated with an increase in gamma aminobutyric acid (GABA) inhibition but not loss of excitatory glutamate/
N
-methyl-
d
-aspartic acid. Enhanced deposition of abnormally folded infectious PrP (PrPsc or PrPres) in the central nervous system (CNS) localizes with GABAA receptors. This occurs with minimal evidence of CNS spongiosis or apoptosis of neurons. The use of monoclonal antibodies reveals an association of PrPres with GABAA receptors. Thus, the clinical defects of learning and memory loss in vivo in GPI
−/−
PrP tg mice infected with scrapie agent may likely involve the GABAergic pathway.
Mutations in Human Immunodeficiency Virus Type 1 Nucleocapsid Protein Zinc Fingers Cause Premature Reverse Transcription
Authors: Thomas James A. , Bosche William J. , Shatzer Teresa L. , Johnson Donald G. , Gorelick Robert J. 
Published: July 2008

ABSTRACT

Human immunodeficiency virus type 1 (HIV-1) requires that its genome be reverse transcribed into double-stranded DNA for productive infection of cells. This process requires not only reverse transcriptase but also the nucleocapsid protein (NC), which functions as a nucleic acid chaperone. Reverse transcription generally begins once the core of the virion enters the cytoplasm of a newly infected cell. However, some groups have reported the presence of low levels of viral DNA (vDNA) within particles prior to infection, the significance and function of which is controversial. We report here that several HIV-1 NC mutants, which we previously identified as being replication defective, contain abnormally high levels of intravirion DNA. These findings were further reinforced by the inability of these NC mutants to perform endogenous reverse transcription (ERT), in contrast to the readily measurable ERT activity in wild-type HIV-1. When either of the NC mutations is combined with a mutation that inactivates the viral protease, we observed a significant reduction in the amount of intravirion DNA. Interestingly, we also observed high levels of intravirion DNA in the context of wild-type NC when we delayed budding by means of a PTAP
(−)
(Pro-Thr-Ala-Pro) mutation. Premature reverse transcription is most probably occurring before these mutant virions bud from producer cells, but we fail to see any evidence that the NC mutations alter the timing of Pr55
Gag
processing. Critically, our results also suggest that the presence of intravirion vDNA could serve as a diagnostic for identifying replication-defective HIV-1.
Herpes Simplex Virus Downregulates Secretory Leukocyte Protease Inhibitor: a Novel Immune Evasion Mechanism
Authors: Fakioglu Esra , Wilson Sarah S. , Mesquita Pedro M. M. , Hazrati Ehsan , Cheshenko Natalia , Blaho John A. , Herold Betsy C. 
Published: July 2008

ABSTRACTSecretory leukocyte protease inhibitor (SLPI), an anti-inflammatory mediator of mucosal immunity, inhibits human immunodeficiency virus (HIV) and herpes simplex virus (HSV) in cell culture. Epidemiological studies demonstrate that higher concentrations of SLPI in mucosal secretions are associated with a reduced risk of HIV transmission. The current studies were designed to test the hypothesis that HSV triggers a loss of SLPI to evade innate immunity and that this response may contribute to the increased risk of HIV infection in the setting of HSV infection. Exposure of human cervical epithelial cells to HSV-1 or HSV-2, but not HIV or vesicular stomatitis virus, triggered a significant and sustained reduction in SLPI levels. The reduction persisted when cells were infected in the presence of acyclovir but not following infection with UV-inactivated virus, indicating that viral gene expression, but not replication, is required. Reverse transcriptase PCR studies demonstrated that the loss of SLPI is mediated by downregulation of gene expression. SLPI downregulation was associated with activation of NF-κB signaling pathways and upregulation of proinflammatory cytokines, consistent with the known inhibitor effects of SLPI on NF-κB pathways. The downregulation mapped to viral early-gene expression, as variants impaired in expression of the ICP4 or ICP0 immediate-early gene failed to downregulate SLPI or activate NF-κB. Together, these results identify a novel role for HSV immediate-early-gene expression in regulating mucosal immune responses.
Potent Antibody-Mediated Neutralization and Evolution of Antigenic Escape Variants of Simian Immunodeficiency Virus Strain SIVmac239 In Vivo
Authors: Sato Shuji , Yuste Eloisa , Lauer William A. , Chang Eun Hyuk , Morgan Jennifer S. , Bixby Jacqueline G. , Lifson Jeffrey D. , Desrosiers Ronald C. , Johnson Welkin E. 
Published: July 2008

ABSTRACTHere, we describe the evolution of antigenic escape variants in a rhesus macaque that developed unusually high neutralizing antibody titers to SIVmac239. By 42 weeks postinfection, 50% neutralization of SIVmac239 was achieved with plasma dilutions of 1:1,000. Testing of purified immunoglobulin confirmed that the neutralizing activity was antibody mediated. Despite the potency of the neutralizing antibody response, the animal displayed a typical viral load profile and progressed to terminal AIDS with a normal time course. Viral envelope sequences from week 16 and week 42 plasma contained an excess of nonsynonymous substitutions, predominantly in V1 and V4, including individual sites with ratios of nonsynonymous to synonymous substitution rates (dN/dS) highly suggestive of strong positive selection. Recombinant viruses encoding envelope sequences isolated from these time points remained resistant to neutralization by all longitudinal plasma samples, revealing the failure of the animal to mount secondary responses to the escaped variants. Substitutions at two sites with significantdN/dSvalues, one in V1 and one in V4, were independently sufficient to confer nearly complete resistance to neutralization. Substitutions at three additional sites, one in V4 and two in gp41, conferred moderate to high levels of resistance when tested individually. All the amino acid changes leading to escape resulted from single nucleotide substitutions. The observation that antigenic escape resulted from individual, single amino acid replacements at sites well separated in current structural models of Env indicates that the virus can utilize multiple independent pathways to rapidly achieve similar levels of resistance.
Reduced Protection from Simian Immunodeficiency Virus SIV
mac251
Infection Afforded by Memory CD8
+
T Cells Induced by Vaccination during CD4
+
T-Cell Deficiency
Authors: Vaccari Monica , Mattapallil Joseph , Song Kaimei , Tsai Wen-Po , Hryniewicz Anna , Venzon David , Zanetti Maurizio , Reimann Keith A. , Roederer Mario , Franchini Genoveffa 
Published: July 2008

ABSTRACT

Adaptive CD4
+
and CD8
+
T-cell responses have been associated with control of human immunodeficiency virus/simian immunodeficiency virus (HIV/SIV) replication. Here, we have designed a study with Indian rhesus macaques to more directly assess the role of CD8 SIV-specific responses in control of viral replication. Macaques were immunized with a DNA prime-modified vaccinia virus Ankara (MVA)-SIV boost regimen under normal conditions or under conditions of antibody-induced CD4
+
T-cell deficiency. Depletion of CD4
+
cells was performed in the immunized macaques at the peak of SIV-specific CD4
+
T-cell responses following the DNA prime dose. A group of naïve macaques was also treated with the anti-CD4 depleting antibody as a control, and an additional group of macaques immunized under normal conditions was depleted of CD8
+
T cells prior to challenge exposure to SIV
mac251
. Analysis of the quality and quantity of vaccine-induced CD8
+
T cells demonstrated that SIV-specific CD8
+
T cells generated under conditions of CD4
+
T-cell deficiency expressed low levels of Bcl-2 and interleukin-2 (IL-2), and plasma virus levels increased over time. Depletion of CD8
+
T cells prior to challenge exposure abrogated vaccine-induced protection as previously shown. These data support the notion that adaptive CD4
+
T cells are critical for the generation of effective CD8
+
T-cell responses to SIV that, in turn, contribute to protection from AIDS. Importantly, they also suggest that long-term protection from disease will be afforded only by T-cell vaccines for HIV that provide a balanced induction of CD4
+
and CD8
+
T-cell responses and protect against early depletion of CD4
+
T cells postinfection.
Apolipoprotein C1 Association with Hepatitis C Virus
Authors: Meunier Jean-Christophe , Russell Rodney S. , Engle Ronald E. , Faulk Kristina N. , Purcell Robert H. , Emerson Suzanne U. 
Published: July 2008

ABSTRACT
Accumulating evidence suggests that cellular lipoprotein components are involved in hepatitis C virus (HCV) morphogenesis, but the precise contribution of these components remains unclear. We investigated the involvement of apolipoprotein C1 (ApoC1) in HCV infection in the HCV pseudotyped particle system (HCVpp), in the recently developed cell culture infection model (HCVcc), and in authentic HCV isolated from viremic chimpanzees. Viral genomes associated with HCVcc or authentic HCV were efficiently immunoprecipitated by anti-ApoC1, demonstrating that ApoC1 was a normal component of HCV. The infectivities of HCVpp that had been mixed with ApoC1 and, more importantly, untreated HCVcc collected from lysates or media of infected Huh7.5 cells were directly neutralized by anti-ApoC1. Indeed, convalescent anti-HCV immunoglobulin G and anti-ApoC1 each neutralized over 75% of infectious HCVcc particles, indicating that many, if not all, infectious particles were recognized by both antibodies. Moreover, peptides corresponding to the C-terminal region of ApoC1 blocked infectivity of both HCVpp and HCVcc. Altogether, these results suggest that ApoC1 associates intracellularly via its C-terminal region with surface components of virions during viral morphogenesis and may play a major role in the replication cycle of HCV.