bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sudden Headache Associated With Unilateral Asterixis
Authors: Alvarez‐Cermeño J.C. , Martinez‐Castrillo J.C. , Gobernado J.M. 
Published: June 2005

SYNOPSISIn a patient presenting with sudden headache and right unilateral asterixis, a computed tomography scan (CT) showed a left thalamic hematoma. This and other four similar cases reported previously, indicate that the acute development of headache and focal asterixis should alert the clinician to the possibility of an intracranial hemorrhage.
The Controlled Application of Cold and Heat by a New Device (Migra‐lief Apparatus) in the Treatment of Headache
Authors: Lance J.W. 
Published: June 2005

SYNOPSISAn apparatus which incorporates a cooling compartment encircling the head, extending down the neck, and a separate warming compartment applied to the vertex, was employed in 28 patients with recurrent headaches (20 with migraine, 7 with tension headaches, and I with cluster headaches) who had had inadequate relief from prophylactic and acute medications. This Migra‐lief apparatus reduced severity of headache in 15 of the migraine patients, 6 of the tension headache patients, and in the one cluster headache patient.
Autonomic Dysfunction in Migraine: A Survey of 188 Patients
Authors: Havanka‐Kanniainen H. , Tolonen U. , Myllylä V.V. 
Published: June 2005

SYNOPSISAutonomic nervous system functions were studied in 188 patients with migraine during headache free intervals by measuring cardiovascular reflex responses. Eighty‐five healthy subjects served as a control group.Pulse rate (R‐R‐ interval) variation in normal and deep breathing, during Valsalva manoeuvre and orthostatic test was diminished in migraine patients. Diastolic blood pressure rises in orthostatic test and isometric work test were lower than in the controls. The results of patients with classic and common migraine did not deviate from each other. The same was true for the results of the female and male patients.The results of the patients with frequent migraine attacks (>4/month) showed more severe disturbance than those with infrequent attacks. Disturbances gradually developed with age, being minimal or totally lacking in young migraine patients. The results confirm the development of sympathetic and parasympathetic hypofunction in migraine patients during the course of the disorder.
A Diagnostic Test for Migraine Using the Visual Evoked Potential
Authors: Marsters J.B. , Good P.A. , Mortimer M.J. 
Published: June 2005

SYNOPSISTraditionally the diagnosis of migraine has been made by clinical history, examination and investigation to exclude other ophthalmological and neurological diseases. To date there has been no simple objective test for the diagnosis of migraine on an individual basis. Patients were subjected to both flash and pattern light stimuli, and measurements were made from the resultant visual evoked potential (VEP) charted as a waveform. Calculations based on the parameters of the waveforms produced a Coefficient which correlated well with the medical diagnosis. This study demonstrates that electro‐diagnostic methods can be utilised to provide a fast, reliable and accurate diagnosis for migraine on an individual basis, and which will also differentiate between the Common and Classical varieties.
Visual Evoked Potential in Patients with Migraine
Authors: Raudino Francesco 
Published: June 2005

SYNOPSISUsing pattern reversal stimuli, visual evoked potentials (VEP) were measured between attacks in 40 (6 classic and 34 common) migraine sufferers, and in 20 control subjects. While there were no statistically significant differences between the groups in mean P wave latency or in mean P wave amplitude, there were some intriguing individual findings in some of the migraine patients. Nine had P wave latencies more than 2 SD above the control mean; 6 had more than 2 SD increases above control in P wave amplitude; 3 had simultaneous increases in both latencies and amplitudes. In almost all the cases with these unusual values, the tracing had been done close in time to a migraine attack.
Clinical Characterization of Patients with Chronic Tension Headache
Authors: Langemark Michael , Olesen Jes , Poulsen Dorte Loldrup , Bech Per 
Published: June 2005

SYNOPSISOne hundred and forty‐eight patients with tension headaches at least 10 days per month were studied prospectively with a standardized interview, neurological examination and evaluation of muscle tenderness and jaw movements. Patients with migraine attacks oftener than once per month were excluded. Ninety‐three had daily headache. Median age at onset was 23 yrs. (quartiles 15–23 yrs.). Half of the patients had headache predominating in one part of the head. In the other half, headache was diffuse or with changing pattern. Fifty‐eight reported migraine attacks 1–12 times per year; twenty‐seven of these did not remember onset, 15 initially had migraine later developing into chronic headache, and 16 started with tension headache and developed migraine attacks later in life. Photophobia was reported as frequently associated with tension headache (migraine attacks not included) in 13 percent, infrequently in 38 percent and absent in 49 percent. Corresponding figures for phonophobia were 7, 35 and 57 percent. Characteristics of chronic tension headache were similar in patients with and without migraine attacks. The components included in the usual indices of temporo‐mandibular joint dysfunction showed little mutual correlation. Pericranial tenderness scores were elevated compared to previously studied controls. Tenderness in paravertebral muscles was significantly correlated to pericranial tenderness, and patients indicating influence by environmental factors had the highest pericranial tenderness scores. The findings are suggestive of a generalized muscular reaction to environmental stress in the majority of patients.
Trafficking Pathways and Characterization of CD4 and CD8 Cells Recruited to the Skin of Humans Experimentally Infected withHaemophilus ducreyi
Authors: Humphreys Tricia L. , Baldridge Lee Ann , Billings Steven D. , Campbell James J. , Spinola Stanley M. 
Published: June 2005

ABSTRACTT-cell homing to infected skin is not well studied in humans. We examined sites experimentally infected withHaemophilus ducreyiby immunohistochemistry and flow cytometry for expression of receptors and ligands involved in cutaneous T-cell homing and determined the phenotypes of the T cells that trafficked to skin. Endothelial cells expressed E-selectin in infected but not uninfected skin, while peripheral node addressin (PNAd) was minimally expressed in all samples. CC chemokine ligand 27 (CCL27) was expressed in the epidermis and endothelium of both infected and uninfected skin. Interestingly, CCL21, a chemokine thought to be associated principally with T-cell trafficking in the lymphatic compartment, was highly expressed on the endothelium of infected skin. Few naive cells were present in experimental lesions, emphasizing the combined role of PNAd and CCL21 in trafficking of this subset. Memory cells (CD45RA−) dominated both CD4 and CD8 T-cell populations at the site of infection. Effector memory (CD45RA−CD27−) CD4+and CD8+T cells were enriched in lesions. Although the CC chemokine receptor 7-positive (CCR7+) population of both central memory (CD45RA−CD27+) and effector memory cells was not enriched in the skin compared to peripheral blood, CCR7+cells were not precluded from entering infected skin. Taken together with our previous work (D. Soler, T. L. Humphreys, S. M. Spinola, and J. J. Campbell, Blood 101:1677-1683, 2003), these studies led us to propose a model of memory T-cell trafficking to skin in response to experimentalH. ducreyiinfection.
Antagonizing Deactivating Cytokines To Enhance Host Defense and Chemotherapy in Experimental Visceral Leishmaniasis
Authors: Murray Henry W. , Flanders Kathleen C. , Donaldson Debra D. , Sypek Joseph P. , Gotwals Philip J. , Liu Jianguo , Ma Xiaojing 
Published: June 2005

ABSTRACTIn experimental visceral leishmaniasis, inhibition of interleukin 10 (IL-10) signaling enhances Th1-cell-associated responses, promoting gamma interferon (IFN-γ) secretion, granuloma assembly, macrophage activation with substantial liver parasite killing, and synergy with pentavalent antimony (Sb) chemotherapy. To determine if inhibiting other suppressive cytokines has similar therapeutic potential,Leishmania donovani-infected BALB/c mice were injected with anti-IL-4 monoclonal antibody or receptor fusion antagonists of IL-13 or transforming growth factor β (TGF-β). Targeting IL-13 or TGF-β enabled inhibition ofL. donovanireplication but little parasite killing; anti-IL-4 had no effect. None of the three antagonists promoted IFN-γ production, granuloma maturation, or Sb efficacy. Excess IL-13 and TGF-β exacerbated liver infection; however, effects were transient. Among IL-10, IL-4, IL-13, and TGF-β, cytokines capable of disabling Th1-cell mechanisms (including those which support chemotherapy), IL-10 appears to be the appropriate target for therapeutic inhibition in visceralL. donovaniinfection.
Local Peroxynitrite Formation Contributes to Early Control of
Cryptosporidium parvum
Infection
Authors: Gookin Jody L. , Allen Jessica , Chiang Sophia , Duckett Laurel , Armstrong Martha U. 
Published: June 2005

ABSTRACT

In intestinal inflammation, mucosal injury is often exacerbated by the reaction of NO with neutrophil-derived superoxide to form the potent oxidant peroxynitrite. Peroxynitrite also has antimicrobial properties that aid in the killing mechanism of macrophages and neutrophils.
Cryptosporidium parvum
parasitizes intestinal epithelium, resulting in loss of epithelial cells and mucosal inflammation. Synthesis of NO is significantly increased and arises from the induced expression of inducible nitric oxide synthase (iNOS) by the infected epithelium. Inhibition of iNOS results in intensified epithelial parasitism and oocyst excretion. We hypothesized that formation of peroxynitrite is restricted to sites of iNOS expression by the epithelium and contributes to host defense in
C. parvum
infection. Accordingly, the location and biological effects of peroxynitrite formation were examined in neonatal piglets infected with
C. parvum
. Infected piglets were treated daily with a selective iNOS inhibitor [
L
-N6-(1-iminoethyl)-lysine] or one of two peroxynitrite scavengers [5,10,15,20-tetrakis(
N
-methyl-4′-pyridyl)porphyrinato iron(III) or uric acid] or received vehicle. At peak infection, peroxynitrite formation was restricted to sites of iNOS expression by parasitized epithelium and lamina propria of the apical villi. Peroxynitrite formation was dependent on iNOS activity and was inhibited by treatment with peroxynitrite scavengers. Scavengers increased the number of intracellular parasites and the number of infected epithelial cells present per villus and significantly exacerbated oocyst excretion. Recovery from infection was not delayed by ongoing treatment with scavenger. The present results are the first to demonstrate an in vivo role for peroxynitrite formation in acute mucosal defense against a noninvasive intestinal epithelial pathogen.
Short Fimbriae of
Porphyromonas gingivalis
and Their Role in Coadhesion with
Streptococcus gordonii
Authors: Park Yoonsuk , Simionato M. Regina , Sekiya Kachiko , Murakami Yukitaka , James Deanna , Chen Weibin , Hackett Murray , Yoshimura Fuminobu , Demuth Donald R. , Lamont Richard J. 
Published: June 2005

ABSTRACT

Porphyromonas gingivalis
, one of the causative agents of adult periodontitis, attaches and forms biofilms on substrata of
Streptococcus gordonii
. Coadhesion and biofilm development between these organisms requires the interaction of the short fimbriae of
P. gingivalis
with the SspB streptococcal surface polypeptide. In this study we investigated the structure and binding activities of the short fimbriae of
P. gingivalis
. Electron microscopy showed that isolated short fimbriae have an average length of 103 nm and exhibit a helical structure with a pitch of ca. 27 nm. Mfa1, the major protein subunit of the short fimbriae, bound to SspB protein, and this reaction was inhibited by purified recombinant Mfa1 and monospecifc anti-Mfa1 serum in a dose-dependent manner. Complementation of a polar Mfa1 mutant with the
mfa1
gene restored the coadhesion phenotype of
P. gingivalis
. Hence, the Mfa1 structural fimbrial subunit does not require accessory proteins for binding to SspB. Furthermore, the interaction of Mfa1 with SspB is necessary for optimal coadhesion between
P. gingivalis
and
S. gordonii
.
Role of Mitogen-Activated Protein Kinases and NF-κB in the Regulation of Proinflammatory and Anti-Inflammatory Cytokines byPorphyromonas gingivalisHemagglutinin B
Authors: Zhang Ping , Martin Michael , Michalek Suzanne M. , Katz Jannet 
Published: June 2005

ABSTRACTHemagglutinin B (HagB) is a nonfimbrial adhesin expressed on the surface ofPorphyromonas gingivalisand has been implicated as a potential virulence factor involved in mediating the attachment of the bacteria to host cells. However, the molecular mechanisms underlying host responses to HagB and their roles in pathogenesis have yet to be elucidated. Mitogen-activated protein kinases (MAPKs) are activated following engagement of a variety of cell surface receptors via dual tyrosine and threonine phosphorylation and are thought to be involved in various cellular responses. The purpose of this study was to determine the role of intracellular signaling pathways including the MAPKs and NF-κB in regulating the production of proinflammatory and anti-inflammatory cytokines following stimulation of murine macrophages with recombinant HagB (rHagB). Stimulation of peritoneal macrophages with rHagB resulted in the production of the proinflammatory cytokines interleukin-12p40 (IL-12p40), gamma interferon (IFN-γ), and tumor necrosis factor alpha, as well as the anti-inflammatory cytokine IL-10. We also demonstrated the activation of extracellular signal-related kinase (ERK), c-Jun NH2-terminal protein kinase (JNK), and p38 MAPKs by rHagB-stimulated macrophages. Furthermore, blocking of the ERK and p38 signaling pathways by using specific inhibitors revealed differential regulatory roles in the rHagB-mediated production of proinflammatory and anti-inflammatory cytokines. ERK and p38 were important in down-regulation of IL-12p40 and IFN-γ production and up-regulation of IL-10 production. The enhanced levels of IL-12p40 in rHagB-stimulated macrophages by inhibition of ERK or p38 activity were partially attributable to the inhibition of IL-10 production. Moreover, NF-κB was found to be critical for up-regulation of IL-12p40 and down-regulation of IL-10 production in rHagB-stimulated macrophages. Taken together, our results demonstrate a role for the p38 and ERK pathways and the transcription factor NF-κB in modulating key immunoregulatory cytokines involved in the development of immune responses toP. gingivalisHagB.
Activation of Lipid Metabolism Contributes to Interleukin-8 Production duringChlamydia trachomatisInfection of Cervical Epithelial Cells
Authors: Fukuda Elaine Y. , Lad Sonya P. , Mikolon David P. , Iacobelli-Martinez Milena , Li Erguang 
Published: June 2005

ABSTRACTChlamydia trachomatisinfection is the most common cause of bacterial sexually transmitted diseases. Infection of the urogenital tract byC. trachomatiscauses chronic inflammation and related clinical complications. Unlike other invasive bacteria that induce a rapid cytokine/chemokine production, chlamydial infection induces delayed inflammatory response and proinflammatory chemokine production that is dependent on bacterial growth. We present data here to show that the lipid metabolism required for chlamydial growth contributes toChlamydia-induced proinflammatory chemokine production. By gene microarray profiling, validated with biochemical studies, we found thatC. trachomatisLGV2 selectively upregulated PTGS2 (COX2) and PTGER4 (EP4) in cervical epithelial HeLa 229 cells. COX2 is an enzyme that catalyzes the rate-limiting step of arachidonic acid conversion to prostaglandins, including prostaglandin E2 (PGE2) and other eicosanoids, whereas EP4 is a subtype of cell surface receptors for PGE2. We show thatChlamydiainfection induced COX2 protein expression in both epithelial cells and peripheral blood mononuclear cells and promoted PGE2 release. Exogenous PGE2 was able to induce interleukin-8 release in HeLa 229 epithelial cells. Finally, we demonstrated that interleukin-8 induction byChlamydiainfection or PGE2 treatment was dependent on extracellular signal-regulated kinase/mitogen-activated protein activity. Together, these data demonstrate that the host lipid remodeling process required for chlamydial growth contributes to proinflammatory chemokine production. This study also highlights the importance of maintaining a balanced habitat for parasitic pathogens as obligate intracellular organisms.
Regulatory T Cells Modulate Th2 Responses Induced byBrugia pahangiThird-Stage Larvae
Authors: Gillan Victoria , Devaney Eileen 
Published: June 2005

ABSTRACTInfection of BALB/c mice withBrugia pahangithird-stage larvae (L3) results in the production of interleukin-4 (IL-4), IL-5, and IL-10 with a resultant down-regulation in Th1 responses. Previously, this was thought to reflect a skewing of immune responses towards a Th2 phenotype by the infective stage of the parasite. In this study, we show that exposure to the L3 ofBrugiaalso induces the expansion of a population of CD4 cells that express CD25 and cytotoxic-T-lymphocyte-associated antigen 4 in an IL-4-independent fashion. By quantitative reverse transcription-PCR, we show that the CD25+population is highly enriched in mRNA for theFoxp3transcription factor and that these cells express significantly moreIL-10mRNA than the CD25−population, suggesting a likely regulatory phenotype. The functional capacity of these cells was demonstrated using a neutralizing CD25 monoclonal antibody (MAb). Mice treated with this MAb demonstrated elevated levels of antigen (Ag)-specific proliferation in vitro, and levels of Ag-specific Th2 cytokines were significantly increased. These results suggest a complex network of regulation in L3-infected mice with Th2 cells limiting the Th1 response, while T-regulatory cells modulate Th2 responses.
Characterization of a Human Monoclonal Antibody against Shiga Toxin 2 Expressed in Chinese Hamster Ovary Cells
Authors: Akiyoshi D. E. , Rich C. M. , O'Sullivan-Murphy S. , Richard L. , Dilo J. , Donohue-Rolfe A. , Sheoran A. S. , Chapman-Bonofiglio S. , Tzipori S. 
Published: June 2005

ABSTRACTShiga toxin-producingEscherichia coliinfections can often lead to the development of hemolytic-uremic syndrome (HUS) in a small percentage of infected humans. Patients with HUS receive only supportive treatment as the benefit of antibiotic therapy remains uncertain. We have previously reported the generation and preclinical evaluation of neutralizing human monoclonal antibodies (HuMAbs) against the Shiga toxins (Stx). In this paper, we describe the expression in Chinese hamster ovary (CHO) cells of 5C12 HuMAb, which is directed against the A subunit of Stx2. The cDNAs of the light and heavy chain immunoglobulin (Ig) variable regions of 5C12 HuMAb were isolated and cloned into an expression vector containing human IgG1 constant regions. The vector was transfected into CHO cells, and transfectants secreting Stx2-specific antibody were screened by an Stx2-specific enzyme-linked immunosorbent assay. The CHO-produced recombinant 5C12 (r5C12) showed similar specificity and binding affinity to Stx2 as the parent hybridoma-produced 5C12. More significantly, the r5C12 displayed the same neutralizing activity as the parent 5C12 in vitro and in vivo. In the mouse toxicity model, both antibodies significantly and equally prolonged survival at a dose of 0.312 μg/mouse. The data showed that since r5C12, produced in CHO cells, was equally effective as the parent 5C12, it is our choice candidate as a potential prophylactic or therapeutic agent against hemolytic-uremic syndrome.
Thymidine-Dependent
Staphylococcus aureus
Small-Colony Variants Are Associated with Extensive Alterations in Regulator and Virulence Gene Expression Profiles
Authors: Kahl Barbara C. , Belling Gunnar , Becker Petra , Chatterjee Indranil , Wardecki Katrin , Hilgert Karin , Cheung Ambrose L. , Peters Georg , Herrmann Mathias 
Published: June 2005

ABSTRACT

Chronic airway infection is a hallmark of cystic fibrosis (CF) and many CF patients are infected persistently by
Staphylococcus aureus
. Thymidine-dependent trimethoprim-sulfamethoxazole (SXT)-resistant
S. aureus
small-colony variants (SCVs), often in combination with isogenic normal
S. aureus
phenotypes, are highly prevalent and persistent in airway secretions of CF patients due to long-term SXT therapy (B. Kahl, M. Herrmann, A. S. Everding, H. G. Koch, K. Becker, E. Harms, R. A. Proctor, and G. Peters, J. Infect. Dis.
177:
1023-1029, 1998). In this report, SCVs were compared to normal
S. aureus
by transcription analysis of important regulator (
sigB
,
sarA
, and
agr
) and virulence (α-hemolysin,
hla
, and protein A,
spa
) genes. Growth curve analyses revealed longer doubling times and lower final densities for SCVs than for normal strains.
sigB
activity was measured by transcription analysis of the
sigB
target gene
asp23
. For nearly all SCVs, expression of all regulators was decreased as assessed by
asp23
reverse transcription-PCR for
sigB
and Northern analysis for
sarA
and
agr
. These results are in agreement with diminished
hla
signals in all SCVs and increased
spa
signals in 5 of 10 SCVs compared to the isogenic normal
S. aureus
. Both supplementation of SCVs with thymidine and activation of the
agr
quorum-sensing system by the supernatant of the isogenic normal strain reversed transcription to almost normal levels. In conclusion, multiple changes in growth characteristics and in regulator and virulence gene expression render SCVs less virulent and allow them to survive in the hostile environment present in the airways of CF patients, thereby illustrating adaptation of the bacteria during long-term persistence.
Regulation of a Type III and a Putative Secretion System in
Edwardsiella tarda
by EsrC Is under the Control of a Two-Component System, EsrA-EsrB
Authors: Zheng J. , Tung S. L. , Leung K. Y. 
Published: June 2005

ABSTRACT

Edwardsiella tarda
is a gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and gastro- and extraintestinal infections in humans. A type III secretion system (TTSS) and a putative secretion system (EVP) have been found to play important roles in
E. tarda
pathogenesis. Our previous studies suggested that the TTSS and EVP gene clusters were regulated by a two-component system of EsrA-EsrB. In the present study, we characterized another regulator, EsrC, which showed significant sequence similarity to the AraC family of transcriptional regulators. Mutants with in-frame deletions of
esrC
increased the 50% lethal doses in blue gourami fish, reduced extracellular protein production, and failed to aggregate. Complementation of
esrC
restored these three phenotypes. Two-dimensional gel electrophoresis showed that EsrC regulated the expression of secreted proteins encoded by the TTSS (such as EseB and EseD) and EVP (EvpC) gene clusters. The expression of
esrC
required a functional two-component system of EsrA-EsrB. EsrC in turn regulated the expression of selected genes encoded in TTSS (such as the transcriptional unit of
orf29
and
orf30
, but not
esaC
) and genes encoded in the EVP gene cluster. The present study sheds light on the regulation of these two key virulence-associated secretion systems and provides greater insight into the pathogenic mechanisms of this bacterium.