bluuebunny/crossref_metadata_2025_split huggingface dataset:
Who Was Who? Race and Jews in Turn-of-the-Century Britain
Authors: Cohen Deborah 
Published: January 2003

Race—as a category—has commonly been understood as a response to difference. In the first instance, race offered a means of ordering unfamiliar peoples, whether encountered in the empire or at home. In the European historiography, the notion of “biological” race, defined by an inherited set of characteristics passed through the blood, possesses a particular genealogy: its roots can be found in the eighteenth century, its fullest articulation came in the late nineteenth century, and its twentieth-century decline was hastened by the Holocaust.This article sets out a different, if not completely incompatible, thesis. It takes the case of British Jews to argue that racial categories could arise as a response to the apparent similarities, as well as the perceived differences, between Jews and other Britons. Put differently, in the late nineteenth century, Jews came increasingly to be identified as a race precisely because they were difficult to differentiate from their fellow citizens. Class proved a critical determinant. Jews became ever more invisible as they scaled the social ladder. “East End” Jews—poor and newly immigrated—might be readily detectable, but their middle- and upper-middle-class “West End” counterparts confounded observers. Notions of race, I will argue, emerged in part as a consequence of assimilation, delimiting difference in a nation where formal legal barriers to Jewish integration had been eliminated and social obstacles largely overcome.Race was a staple term of the late nineteenth century. It proliferated throughout the language of the time.
Wars in the Wards: The Social Construction of Medical Work in First World War Britain
Authors: Watson Janet S. K. 
Published: January 2003

When the Imperial War Museum was founded in early 1917, the subcommittee in charge of collections related to “Women's Work” solicited contributions from Dr. Flora Murray of the Military Hospital at Endell Street in London. Murray and Dr. Louisa Garrett Anderson had formed the Women's Hospital Corps and, with the French Red Cross, opened hospitals in Paris and Wimereux in the early stages of the war. After successful cooperation with British military and medical authorities overseas, they were asked to open the Endell Street facility, the only hospital operating under the auspices of the War Office to be staffed entirely by women. Murray refused to cooperate with the museum committee “because she wished her hospital to be considered purely professionally as a military hospital and not as women's war work.”This was not just rhetoric of women's equality from someone who described herself as “one of Mrs. Pankhurst's lot,” but reflected the new emphasis on professionalism that had developed in the preceding fifty years. The First World War provided new opportunities for work in a variety of fields more or less closely related to the perpetuation and advancement of the armed conflict; scholars have recently focused in particular on working-class women in industry and paramilitary organizations. Though opportunities for educated women increased throughout civil society, my focus here is on work that was perceived as explicitly on behalf of the war effort, with a special concentration on three populations of women working in hospitals: doctors, trained nurses, and volunteers.
Regulation of Expression of the
Borrelia burgdorferi
β
3
-Chain Integrin Ligand, P66, in Ticks and in Culture
Authors: Cugini Carla , Medrano Melisa , Schwan Tom G. , Coburn Jenifer 
Published: January 2003

ABSTRACT

Borrelia burgdorferi
is maintained in an infection cycle between mammalian and arthropod hosts. Appropriate gene expression by
B. burgdorferi
at different stages of this cycle is probably essential for transmission and establishment of infection. The
B. burgdorferi
β
3
integrin ligand P66 is expressed by the bacteria in mammals, laboratory culture, and engorged but not unfed ticks. No in vitro culture conditions in which P66 expression reflected that in the unfed tick were found, suggesting that there are aspects of
B. burgdorferi
-tick interaction that remain unexplored.
Modulation of J774.1 Macrophage
l-
Arginine Metabolism by Intracellular
Mycobacterium bovis
BCG
Authors: Peteroy-Kelly Marcy A. , Venketaraman Vishwanath , Talaue Meliza , Seth Anjali , Connell Nancy D. 
Published: January 2003

ABSTRACT

Using a
Mycobacterium bovis
BCG mutant (AS1) lacking a
Bacillus subtilis
l
-arginine transporter homolog, we demonstrate here that the interaction between intracellular mycobacteria and the macrophage with respect to
l-
arginine transport and metabolism is quite complex. Intracellular AS1 stimulates macrophage
l-
arginine transport and accumulates 2.5-fold more
3
H label derived from
l-
arginine than does the wild type. These studies suggest that the accumulation of
3
H label reflects the acquisition of metabolites of
l-
arginine produced by the macrophage.
Pathogenic Potential of Environmental
Vibrio cholerae
Strains Carrying Genetic Variants of the Toxin-Coregulated Pilus Pathogenicity Island
Authors: Faruque Shah M. , Kamruzzaman M. , Meraj Ismail M. , Chowdhury Nityananda , Nair G. Balakrish , Sack R. Bradley , Colwell Rita R. , Sack David A. 
Published: January 2003

ABSTRACT

The major virulence factors of toxigenic
Vibrio cholerae
are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTXΦ. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of
V. cholerae
carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTXΦ, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the
tcpA
gene, 9 strains carrying a new allele of the
toxT
gene, and 2 strains carrying conventional
tcpA
and
toxT
genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of
V. cholerae
O1. Five of the 14 strains were susceptible to CTXΦ, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the
tcpA
and
toxT
genes found in environmental strains of
V. cholerae
encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of
V. cholerae
.
UreR, the Transcriptional Activator of the
Proteus mirabilis
Urease Gene Cluster, Is Required for Urease Activity and Virulence in Experimental Urinary Tract Infections
Authors: Dattelbaum Jonathan D. , Lockatell C. Virginia , Johnson David E. , Mobley Harry L. T. 
Published: January 2003

ABSTRACT

Proteus mirabilis
, a cause of complicated urinary tract infection, produces urease, an essential virulence factor for this species. UreR, a member of the AraC/XylS family of transcriptional regulators, positively activates expression of the
ure
gene cluster in the presence of urea. To specifically evaluate the contribution of UreR to urease activity and virulence in the urinary tract, a
ureR
mutation was introduced into
P. mirabilis
HI4320 by homologous recombination. The isogenic
ureR
::
aphA
mutant, deficient in UreR production, lacked measurable urease activity. Expression was not detected in the UreR-deficient strain by Western blotting with monoclonal antibodies raised against UreD. Urease activity and UreD expression were restored by complementation of the mutant strain with
ureR
expressed from a low-copy-number plasmid. Virulence was assessed by transurethral cochallenge of CBA mice with wild-type and mutant strains. The isogenic
ureR
::
aphA
mutant of HI4320 was outcompeted in the urine (
P
= 0.004), bladder (
P
= 0.016), and kidneys (
P
≤ 0.001) 7 days after inoculation. Thus, UreR is required for basal urease activity in the absence of urea, for induction of urease by urea, and for virulence of
P. mirabilis
in the urinary tract.
Human Eosinophil Peroxidase Induces Surface Alteration, Killing, and Lysis ofMycobacterium tuberculosis
Authors: Borelli Violetta , Vita Francesca , Shankar Sandeep , Soranzo Maria Rosa , Banfi Elena , Scialino Giuditta , Brochetta Cristiana , Zabucchi Giuliano 
Published: January 2003

ABSTRACTThe antimycobacterial role of eosinophil peroxidase (EPO), one of the most abundant granule proteins in human eosinophils, was investigated. Our data indicate that purified EPO shows significant inhibitory activity towardsMycobacterium tuberculosisH37Rv. On a molar basis, this activity was similar to that exhibited by neutrophil myeloperoxidase (MPO) and was both dose and time dependent. In contrast to the activity of MPO, which requires H2O2, EPO also exhibited anti-M. tuberculosisactivity in the absence of exogenously added peroxide. Morphological evidence confirmed that the mechanism of action of EPO against mycobacteria differs from that of MPO. While MPO killsM. tuberculosisH37Rv exclusively in the presence of hydrogen peroxide, it does not induce morphological changes in the pathogen. In contrast, EPO-treated bacteria frequently had cell wall lesions and eventually underwent lysis, either in the presence or in the absence of H2O2.
Induction of Proinflammatory Cytokines in Human Lung Epithelial Cells duringChlamydia pneumoniaeInfection
Authors: Yang Jun , Hooper W. Craig , Phillips Donald J. , Tondella Maria L. , Talkington Deborah F. 
Published: January 2003

ABSTRACTChlamydia pneumoniaeis an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established thatC. pneumoniaecan induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment ofC. pneumoniaesignificantly reduced its ability to induce interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α) mRNA in human lung carcinoma cells, indicating that cytadherence is an important early stimulus for induction of proinflammatory mediators. Although the IL-8, gamma interferon, and TNF-α message was consistently induced by infection of A549 cells not treated with heparin, only an elevation of IL-8 protein was detected in A549 supernatants. A549 IL-β and IL-6 mRNA and supernatant protein profiles were not significantly changed by infection. Heat or UV inactivation ofC. pneumoniaeonly partially reduced the cytokine response, and inhibition ofC. pneumoniaeprotein or DNA synthesis did not affect its ability to induce cytokine gene expression. To prevent stress-induced cytokine release by the A549 cells, centrifugation was not utilized for infection experiments. These experiments establish the importance of cytadherence in cytokine release by cells of respiratory epithelial origin and suggest that further work in the area of cytokine mediators is warranted to gain valuable pathogenic and therapeutic insights.
Clostridium sordellii
Phospholipase C: Gene Cloning and Comparison of Enzymatic and Biological Activities with Those of
Clostridium perfringens
and
Clostridium bifermentans
Phospholipase C
Authors: Karasawa Tadahiro , Wang Xingmin , Maegawa Tsuneo , Michiwa Yoshio , Kita Hiroyuki , Miwa Koichi , Nakamura Shinichi 
Published: January 2003

ABSTRACT

The gene encoding
Clostridium sordellii
phospholipase C (Csp) was cloned and expressed as a histidine-tagged (His-tag) protein, and the protein was purified to compare its enzymatic and biological activities with those of
Clostridium perfringens
phospholipase C (Cpa) and
Clostridium bifermentans
phospholipase C (Cbp). Csp was found to consist of 371 amino acid residues in the mature form and to be more homologous to Cbp than to Cpa. The egg yolk phospholipid hydrolysis activity of the His-tag Csp was about one-third of that of His-tag Cpa, but the hemolytic activity was less than 1% of that of His-tag Cpa. His-tag Csp was nontoxic to mice. Immunization of mice with His-tag Cbp or His-tag Csp did not provide effective protection against the lethal activity of His-tag Cpa. These results indicate that Csp possesses similar molecular properties to Cbp and suggest that comparative analysis of toxic and nontoxic clostridial phospholipases is helpful for characterization of the toxic properties of clostridial phospholipases.
The
msbB
Mutant of
Neisseria meningitidis
Strain NMB Has a Defect in Lipooligosaccharide Assembly and Transport to the Outer Membrane
Authors: Post Deborah M. B. , Ketterer Margaret R. , Phillips Nancy J. , Gibson Bradford W. , Apicella Michael A. 
Published: January 2003

ABSTRACT

A deletion-insertion mutation in
msbB
, a gene that encodes a lipid A acyltransferase, was introduced into encapsulated
Neisseria meningitidis
serogroup B strain NMB and an acapsular mutant of the same strain. These mutants were designated NMBA11K3 and NMBA11K3cap-, respectively. Neither lipooligosaccharide (LOS) nor lipid A could be isolated from NMBA11K3 although a number of techniques were tried, but both were easily extracted from NMBA11K3cap-. Immunoelectron microscopy using monoclonal antibody (MAb) 6B4, which recognizes the terminal Galβ1-4GlcNAc of LOS, demonstrated that NMB, NMBcap-, and NMBA11K3cap- expressed LOS circumferentially, while MAb 6B4 did not bind to the surface of NMBA11K3. However, cytoplasmic staining of NMBA11K3 with MAb 6B4 was a consistent observation. Mass-spectrometric analyses demonstrated that the relative amounts of the lipid A-specific C12:0 3-OH and C14:0 3-OH present in the membrane preparations (MP) from NMBA11K3 were substantially decreased (25- and 23-fold, respectively) compared to the amount in MP from its parent strain, NMB. Western blot analyses of MP from NMBA11K3 demonstrated that the levels of porin in the outer membrane of NMBA11K3 were also substantially decreased. These studies suggest that the lipid A acylation defect in encapsulated NMBA11K3 influences the assembly of the lipid A and consequently the incorporation of porin in the outer membrane.
A/J Mice Are Susceptible and C57BL/6 Mice Are Resistant toListeria monocytogenesInfection by Intragastric Inoculation
Authors: Czuprynski Charles J. , Faith Nancy G. , Steinberg Howard 
Published: January 2003

ABSTRACTPrevious studies demonstrated that the innate resistance of mice toListeria monocytogenesinfection by intravenous or intraperitoneal inoculation is regulated principally by theHclocus on mouse chromosome 2. The A/J and C57BL/6 mouse strains were identified as prototypeL. monocytogenes-susceptible and -resistant strains, respectively. In the present study, we compared the relative susceptibilities of A/J and C57BL/6 mice to intragastric (i.g.) inoculation withL. monocytogenes. The results of our study indicate that A/J mice are significantly more susceptible than C57BL/6 mice to an i.g. challenge withL. monocytogenes. This was reflected in the estimated 50% lethal doses for the two strains (106and 108CFU for A/J and C57BL/6 mice, respectively) and a more rapid and severe dissemination of the infection to the spleen and liver in A/J mice than in C57BL/6 mice. Histopathological examination of tissues from the infected mice confirmed the greater severity of disease in A/J mice. Clearance of a primary infection enhanced the resistance of both A/J and C57BL/6 mice to reinfection withL. monocytogenesvia the gastrointestinal tract. However, the relative difference in susceptibility between the two strains was evident even after immunization. The A/J mouse holds promise as a model for investigating the pathogenesis of gastrointestinal listeriosis because of its ability to develop systemic infection following challenge with numbers of organisms similar to those recovered from someL. monocytogenes-contaminated food products.
Lon, a Stress-Induced ATP-Dependent Protease, Is Critically Important for Systemic
Salmonella enterica
Serovar Typhimurium Infection of Mice
Authors: Takaya Akiko , Suzuki Masato , Matsui Hidenori , Tomoyasu Toshifumi , Sashinami Hiroshi , Nakane Akio , Yamamoto Tomoko 
Published: January 2003

ABSTRACT

Studies on the pathogenesis of
Salmonella enterica
serovar Typhimurium infections in mice have revealed the presence of two prominent virulence characteristics—the invasion of the nonphagocytic cells to penetrate the intestinal epithelium and the proliferation within host phagocytic cells to cause a systemic spread and the colonization of host organs. We have recently demonstrated that the ATP-dependent Lon protease of
S. enterica
serovar Typhimurium negatively regulates the efficiency of invasion of epithelial cells and the expression of invasion genes (A. Takaya et al., J. Bacteriol.
184:
224-232, 2002). This study was performed to reveal the contribution of the Lon protease to the virulence of
S. enterica
serovar Typhimurium in mice. Determination of 50% lethal doses for the
lon
disruption mutant and wild-type strain revealed that the mutant was highly attenuated when administered either orally or intraperitoneally to BALB/c mice. The mutant was also found to be able to reach extraintestinal sites but unable to proliferate efficiently within the spleen and cause lethal systemic disease of mice. Macrophage survival assays revealed that the
lon
disruption mutant could not survive or proliferate within murine macrophages. In addition, the mutant showed extremely increased susceptibility to hydrogen peroxide, which contributes to the bactericidal capacity of phagocytes. The mutant also showed increased sensitivity to acidic conditions. Taken together, the impaired ability of the
lon
disruption mutant to survive and grow in macrophages could be due to the enhanced susceptibility to the oxygen-dependent killing mechanism associated with respiratory burst and the low phagosomal pH. These results suggest that the Lon protease is essentially involved in the systemic infection of mice with
S. enterica
serovar Typhimurium, which can be fatal. Of further interest is the finding that the
lon
disruption mutant persists in the BALB/c mice for long periods without causing an overwhelming systemic infection.
Mycobacterium bovis
BCG Vaccines Exhibit Defects in Alanine and Serine Catabolism
Authors: Chen Jeffrey M. , Alexander David C. , Behr Marcel A. , Liu Jun 
Published: January 2003

ABSTRACT

Mycobacterium bovis
BCG is the only accepted vaccine for the prevention of tuberculosis (TB) in humans. BCG is a live vaccine, and induction of immunity to TB requires productive infection of the host by BCG. However, BCG is not a satisfactory vaccine, because it fails to protect against pulmonary TB in adults. In this study, we found that BCG strains cannot utilize many naturally occurring amino acids as the sole nitrogen source for growth. This defect is caused, at least partially, by the lack of functional metabolic enzymes. All BCG strains are unable to catabolize
l
-alanine or
d
-alanine due to a frameshift mutation in the
l
-alanine dehydrogenase gene (
ald
). Some BCG strains, such as BCG-Pasteur and BCG-Frappier, cannot catabolize
l
-serine, apparently due to inadequate expression of
l
-serine deaminase (
sdaA
). We also found that undegraded alanine and serine inhibit the growth of BCG through blockage of glutamine synthetase. These results suggest that BCG strains are limited in nitrogen metabolic capacity and predict defects that may restrict multiplication and persistence of the live vaccine within the host.
Protective Levels of Diphtheria-Neutralizing Antibody Induced in Healthy Volunteers by Unilateral Priming-Boosting Intranasal Immunization Associated with Restricted Ipsilateral Mucosal Secretory Immunoglobulin A
Authors: Mills Kingston H. G. , Cosgrove Catherine , McNeela Edel A. , Sexton Amy , Giemza Rafaela , Jabbal-Gill Inderjit , Church Anne , Lin Wu , Illum Lisbeth , Podda Audino , Rappuoli Rino , Pizza Mariagrazia , Griffin George E. , Lewis David J. M. 
Published: January 2003

ABSTRACT

Subunit intranasal vaccines offer the prospect of inducing combined systemic-mucosal immunity against mucosally transmitted infections such as human immunodeficiency virus. However, although human studies have demonstrated the induction of active immunity, secretory immunoglobulin A (sIgA) responses are variable, and no study has demonstrated protection by accepted vaccine-licensing criteria as measured by direct toxin-neutralizing activity. Using the genetically inactivated mutant diphtheria toxoid CRM
197
in a bioadhesive polycationic polysaccharide chitosan delivery system, we found that a single nasal immunization was well tolerated and boosted antitoxin neutralizing activity in healthy volunteers, which could be further boosted by a second immunization. The neutralizing activity far exceeded accepted protective levels and was equivalent to that induced by standard intramuscular vaccine and significantly greater than intranasal immunization with CRM
197
in the absence of chitosan. A striking but unexpected observation was that although unilateral intranasal immunization induced circulating antitoxin antibody-secreting cells, a nasal antitoxin sIgA response was seen only after the second immunization and only in the vaccinated nostril. If these data are reproduced in larger studies, an intranasal diphtheria vaccine based on CRM
197
-chitosan could be rapidly licensed for human use. However, a restricted sIgA response suggests that care must be taken in the priming-boosting strategy and clinical sampling techniques when evaluating such vaccines for the induction of local mucosal immunity.
Role of Systemic and Mucosal Immune Responses in Reciprocal Protection against
Bordetella pertussis
and
Bordetella parapertussis
in a Murine Model of Respiratory Infection
Authors: Watanabe Mineo , Nagai Masaaki 
Published: January 2003

ABSTRACT

The roles of systemic humoral immunity, cell-mediated immunity, and mucosal immunity in reciprocal protective immunity against
Bordetella pertussis
and
Bordetella parapertussis
were examined by using a murine model of respiratory infection. Passive immunization with serum from mice infected with
B. pertussis
established protective immunity against
B. pertussis
but not against
B. parapertussis
. Protection against
B. parapertussis
was induced in mice that had been injected with serum from mice infected with
B. parapertussis
but not from mice infected with
B. pertussis
. Adoptive transfer of spleen cells from mice infected with
B. pertussis
or
B. parapertussis
also failed to confer reciprocal protection. To examine the role of mucosal immunity in reciprocal protection, mice were infected with preparations of either
B. pertussis
or
B. parapertussis
, each of which had been incubated with the bronchoalveolar wash of mice that were convalescing after infection with
B. pertussis
or
B. parapertussis
. Such incubation conferred reciprocal protection against
B. pertussis
and
B. parapertussis
on infected mice. The data suggest that mucosal immunity including secreted immunoglobulin A in the lungs might play an important role in reciprocal protective immunity in this murine model of respiratory infection.