bluuebunny/crossref_metadata_2025_split huggingface dataset:
Narrowband UVB (311 nm, TL01) phototherapy for pityriasis lichenoides
Authors: Aydogan Kenan , Saricaoglu Hayriye , Turan Hakan 
Published: May 2008

SummaryBackground/purpose: Narrowband (NB) UVB (NB‐UVB) phototherapy has recently demonstrated high levels of efficacy and tolerability in a variety of skin diseases. The purpose of the present study was to assess the efficacy of NB‐UVB phototherapy in the management of pityriasis lichenoides (PL).Methods: The therapeutic response in 31 PL patients (23 pityriasis lichenoides et varioliformis acuta; PLEVA, eight pityriasis lichenoides chronica; PLC) treated with NB‐UVB phototherapy between 2000 and 2007 was assessed.Results: NB‐UVB treatment led to a complete response (CR) in 15 out of 23 PLEVA patients (65.2%) with a mean cumulative dose of 23 J/cm2 after a mean number of 43.4 exposures and a partial response (PR) in eight patients (34.8%) with a cumulative dose of 15.6 J/cm2 after a mean number of 32.3 exposures. NB‐UVB treatment led to CR in seven out of eight PLC patients (87.5%) with a mean cumulative dose of 18.4 J/cm2 after a mean number of 45.8 exposures and PR in one patient (12.5%) with a cumulative dose of 9.1 J/cm2 after a mean number of 19 exposures. Relapses occurred in four PL patients within a mean time period of 6 months.Conclusion: NB‐UVB therapy is an effective, safe and practical alternative treatment modality for the management of PLEVA and PLC.
Polypodium leucotomos inhibits ultraviolet B radiation‐induced immunosuppression
Authors: Siscovick Jonathan R. , Zapolanski Tamar , Magro Cynthia , Carrington Kristel , Prograis Shannon , Nussbaum Marnie , Gonzalez Salvador , Ding Wanhong , Granstein Richard D. 
Published: May 2008

SummaryBackground: An extract of the tropical fern Polypodium leucotomos (PL) administered orally to mice inhibits ultraviolet B (UVB) radiation‐induced skin cancer formation. UVB‐induced murine skin cancers occur, in part, because of UVB‐induced immunosuppression. Thus, we examined whether PL inhibits UVB‐suppression of the induction of contact hypersensitivity (CHS) locally or systemically.Methods: C57BL/6 mice received standard drinking water or water‐containing PL. In the local model, mice were shaved on the dorsum and exposed to 3500 J/m2 of UVB radiation daily for 4 days. Control mice were not irradiated. After the last irradiation they were sensitized to oxazolone topically at the irradiated site. To examine the ability of PL to inhibit systemic UVB‐induced immunosuppression, mice were given 10 000 J/m2 of UVB radiation once and immunized at a non‐exposed site 3 days later. Six days after immunization (in both models), mice were challenged on the ears with oxazolone and 24/48 h ear swelling assessed.Results: PL in drinking water significantly reduced the inhibition of CHS observed with exposure to UVB radiation in both the local and systemic models.Conclusions: The ability of PL to inhibit UVB radiation‐induced immune suppression may explain, in part, its ability to inhibit UVR‐induced skin cancer induction in mice.
Intraurban Population Estimation with Remotely Sensed Imagery: A Developing World Perspective
Authors: Hardin Perry J. , Shumway J. Matthew 
Published: May 2008

AbstractAccording to the United Nations, this year (2008) over 50% of Earth's 6.6 billion human inhabitants will be living in urban areas. Given the increasing importance of cities as human habitat, there is a critical need for accurate population count data to support urban decision‐making. Models driven by remotely sensed imagery are one of the few economically viable alternatives available to countries with developing economies needing to measure intraurban population on a repeating basis. This article discusses the current methods to gather basic intraurban population counts from remotely sensed imagery and suggests avenues for future study. More methodological development and testing are necessary before any of the discussed methods can be operationalized for use in the developing world.
Anaemia and cigarette smoking
Authors: LEIFERT J. A. 
Published: May 2008

SummaryCigarette smoking causes numerous diseases that are associated with anaemia but the resulting low haemoglobin levels may be counterbalanced by increased red blood cell production caused by chronic exposure to carbon monoxide from cigarette smoke. Diverse mechanisms are involved in influencing the development or the course of anaemic disease in smokers. This article presents an evaluation of the current literature on the impact of cigarette smoking on various forms of anaemia.
Inhibitors of Bacterial Multidrug Efflux Pumps Potentiate Antimicrobial Photoinactivation
Authors: Tegos George P. , Masago Kayo , Aziz Fatima , Higginbotham Andrew , Stermitz Frank R. , Hamblin Michael R. 
Published: May 2008

ABSTRACT

Antimicrobial photodynamic inactivation (APDI) combines a nontoxic photoactivatable dye or photosensitizer (PS) with harmless visible light to generate singlet oxygen and reactive oxygen species that kill microbial cells. Cationic phenothiazinium dyes, such as toluidine blue O (TBO), are the only PS used clinically for APDI, and we recently reported that this class of PS are substrates of multidrug efflux pumps in both gram-positive and gram-negative bacteria. We now report that APDI can be significantly potentiated by combining the PS with an efflux pump inhibitor (EPI). Killing of
Staphylococcus aureus
mediated by TBO and red light is greatly increased by coincubation with known inhibitors of the major facilitator pump (NorA): the diphenyl urea INF271, reserpine, 5′-methoxyhydnocarpin, and the polyacylated neohesperidoside, ADH7. The potentiation effect is greatest in the case of
S. aureus
mutants that overexpress NorA and least in NorA null cells. Addition of the EPI before TBO has a bigger effect than addition of the EPI after TBO. Cellular uptake of TBO is increased by EPI. EPI increased photodynamic inactivation killing mediated by other phenothiazinium dyes, such as methylene blue and dimethylmethylene blue, but not that mediated by nonphenothiazinium PS, such as Rose Bengal and benzoporphyrin derivative. Killing of
Pseudomonas aeruginosa
mediated by TBO and light was also potentiated by the resistance nodulation division pump (MexAB-OprM) inhibitor phenylalanine-arginine beta-naphthylamide but to a lesser extent than for
S. aureus
. These data suggest that EPI could be used in combination with phenothiazinium salts and light to enhance their antimicrobial effect against localized infections.
Inducible Resistance of Fish Bacterial Pathogens to the Antimicrobial Peptide Cecropin B
Authors: Sallum Ulysses W. , Chen Thomas T. 
Published: May 2008

ABSTRACT

Cecropin B is a cationic antimicrobial peptide originally isolated from the diapausing pupae of the giant silk moth,
Hylphora cecropia
. Cecropin B elicits its antimicrobial effects through disruption of the anionic cell membranes of gram-negative bacteria. Previous work by our laboratory demonstrated that a constitutively expressed cecropin B transgene conferred enhanced resistance to bacterial infection in medaka. The development of antibiotic resistance by pathogenic bacteria is a growing problem. The potential for fish bacterial pathogens to develop resistance to cecropin B was addressed in this study. Four fish bacterial pathogens were selected for the study based on their importance in aquaculture.
Vibrio anguillarum
,
Vibrio vulnificus
, and
Yersinia ruckeri
all exhibited inducible resistance to cecropin B. The inducible resistance of these three pathogens was correlated with reversible changes in their ultrastructures, as observed by scanning electron microscopy.
V. anguillarum
was demonstrated to become more adhesive to a CHSE-214 cell monolayer and to cause increased cumulative mortality in medaka following exposure to cecropin B. This work demonstrates that the resistance of fish bacterial pathogens to cecropin B is inducible and suggests that resistance to other cationic antimicrobial peptides may occur through similar means. The observed changes in ultrastructure and infectivity suggest that resistance to antimicrobial peptides is an integral part of the pathogenesis of fish gram-negative bacterial pathogens.
Epidemiological Cutoffs and Cross-Resistance to Azole Drugs in
Aspergillus fumigatus
Authors: Rodriguez-Tudela Juan Luis , Alcazar-Fuoli Laura , Mellado Emilia , Alastruey-Izquierdo Ana , Monzon Araceli , Cuenca-Estrella Manuel 
Published: May 2008

ABSTRACT

Antifungal susceptibility testing of molds has been standardized in Europe and in the United States.
Aspergillus fumigatus
strains with resistance to azole drugs have recently been detected and the underlying molecular mechanisms of resistance characterized. Three hundred and ninety-three isolates, including 32 itraconazole-resistant strains, were used to define wild-type populations, epidemiological cutoffs, and cross-resistance between azole drugs. The epidemiological cutoff for itraconazole, voriconazole, and ravuconazole for the wild-type populations of
A. fumigatus
was ≤1 mg/liter. For posaconazole, the epidemiological cutoff was ≤0.25 mg/liter. Up till now, isolates susceptible to itraconazole have not yet displayed resistance to other azole drugs. Cross-resistance between azole drugs depends on specific mutations in
cyp51A
. Thus, a substitution of glycine in position 54 of Cyp51A confers cross-resistance between itraconazole and posaconazole. A substitution of methionine at position 220 or a duplication in tandem of a 34-bp fragment in the
cyp51A
promoter combined with a substitution of leucine at position 98 for histidine confers cross-resistance to all azole drugs tested. The results obtained in this study will help to develop clinical breakpoints for azole drugs and
A. fumigatus
.
Assessment of
Aspergillus fumigatus
Burden in Pulmonary Tissue of Guinea Pigs by Quantitative PCR, Galactomannan Enzyme Immunoassay, and Quantitative Culture
Authors: Vallor Ana C. , Kirkpatrick William R. , Najvar Laura K. , Bocanegra Rosie , Kinney Marsha C. , Fothergill Annette W. , Herrera Monica L. , Wickes Brian L. , Graybill John R. , Patterson Thomas F. 
Published: May 2008

ABSTRACT

Early diagnosis of invasive pulmonary aspergillosis is problematic in some patient groups due to the lack of rapid, sensitive, specific, and reliable diagnostic tests. Fungal burden and therapeutic efficacy were assessed by survival, quantitative culture (CFU counts), galactomannan enzyme immunoassay (GM-EIA), and quantitative PCR (qPCR) in a new guinea pig model of invasive pulmonary aspergillosis using an aerosol challenge. At 1 day postinfection, qPCR determined that the pulmonary fungal burden was 2 log
10
higher than that determined by CFU counting and increased significantly (
P
< 0.03) over time. In contrast, the tissue burden assessed by CFU counting did not rise over the course of the study. Therapy with the antifungal drug voriconazole produced statistically significant decreases in pulmonary fungal burden, as detected by CFU counting (
P
< 0.02), qPCR, and GM-EIA (both
P
< 0.0002). Daily assessment of the progression of fungal infection in serum was performed by qPCR and GM-EIA. GM-EIA demonstrated a statistically significant reduction in the fungal load on days 6 and 7 in voriconazole-treated animals compared to time-matched controls (
P
< 0.02). Confirmation of fungal tissue burden by two or more methods should provide a more precise account of the burden, allowing improved assessment of diagnostic and therapeutic strategies in invasive pulmonary aspergillosis.
Zidovudine Impairs Adipogenic Differentiation through Inhibition of Clonal Expansion
Authors: Stankov Metodi V. , Schmidt Reinhold E. , Behrens Georg M. N. 
Published: May 2008

ABSTRACTLipoatrophy is a prevalent side effect of treatment with thymidine analogues. We wished to confine the time point of the antiadipogenic effect of zidovudine (AZT) during adipogenesis and to evaluate the antiproliferative effect of AZT on adipocyte homeostasis. We investigated the effects of AZT on adipogenesis in 3T3-F442A cells and studied their proliferation, differentiation, viability, and adiponectin expression. Cells were exposed to AZT (1 μM, 3 μM, 6 μM, and 180 μM), stavudine (d4T; 3 μM), or dideoxycytosine (ddC; 0.1 μM) for up to 15 days. Differentiation was assessed by real-time PCR and quantification of triglyceride accumulation. Proliferation and clonal expansion were determined by a [3H]thymidine incorporation assay. When they were induced to differentiate in the presence of AZT at the maximum concentration in plasma (Cmax) and lower concentrations, 3T3-F442A preadipocytes failed to accumulate cytoplasmic triacylglycerol and failed to express normal levels of the later adipogenic transcription factors, CCAAT/enhancer-binding protein α and peroxisome proliferator-activated receptor γ. AZT exerted an inhibitory effect on the completion of the mitotic clonal expansion, which resulted in incomplete 3T3-F442A differentiation and, finally, a reduction in the level of adiponectin expression. In addition, AZT impaired the constitutive proliferation in murine and primary human subcutaneous preadipocytes. In contrast, incubation with d4T and ddC at theCmaxdid not affect either preadipocyte proliferation or clonal expansion and differentiation. We conclude that the antiproliferative and antiadipogenetic effects of AZT on murine and primary human preadipocytes reveal the impact of the drug on fat tissue regeneration. These effects of the drug are expected to contribute to disturbed adipose tissue homeostasis and to be influenced by differential drug concentration and penetration in individual patients.
A Genome-Wide Proteome Array Reveals a Limited Set of Immunogens in Natural Infections of Humans and White-Footed Mice withBorrelia burgdorferi
Authors: Barbour Alan G. , Jasinskas Algimantas , Kayala Matthew A. , Davies D. Huw , Steere Allen C. , Baldi Pierre , Felgner Philip L. 
Published: May 2008

ABSTRACTHumans and other animals with Lyme borreliosis produce antibodies to a number of components of the agentBorrelia burgdorferi, but a full accounting of the immunogens during natural infections has not been achieved. Employing a protein array produced in vitro from 1,292 DNA fragments representing ∼80% of the genome, we compared the antibody reactivities of sera from patients with early or later Lyme borreliosis to the antibody reactivities of sera from controls. Overall, ∼15% of the open reading frame (ORF) products (Orfs) ofB. burgdorferiin the array detectably elicited an antibody response in humans with natural infections. Among the immunogens, 103 stood out on the basis of statistical criteria. The majority of these Orfs were also immunogenic with sera obtained from naturally infectedPeromyscus leucopusmice, a major reservoir. The high-ranking set included severalB. burgdorferiproteins hitherto unrecognized as immunogens, as well as several proteins that have been established as antigens. The high-ranking immunogens were more likely than nonreactive Orfs to have the following characteristics: (i) plasmid-encoded rather than chromosome-encoded proteins, (ii) a predicted lipoprotein, and (iii) a member of a paralogous family of proteins, notably the Bdr and Erp proteins. The newly discovered antigens included Orfs encoded by several ORFs of the lp36 linear plasmid, such as BBK07 and BBK19, and proteins of the flagellar apparatus, such as FliL. These results indicate that the majority of deduced proteins ofB. burgdorferido not elicit antibody responses during infection and that the limited sets of immunogens are similar for two different host species.
MglA and Igl Proteins Contribute to the Modulation ofFrancisella tularensisLive Vaccine Strain-Containing Phagosomes in Murine Macrophages
Authors: Bönquist Linda , Lindgren Helena , Golovliov Igor , Guina Tina , Sjöstedt Anders 
Published: May 2008

ABSTRACTTheFrancisella tularensislive vaccine strain (LVS), in contrast to itsiglCmutant, replicates in the cytoplasm of macrophages. We studied the outcome of infection of the murine macrophagelike cell line J774A.1 with LVS and withiglC,iglD, andmglAmutants, the latter of which is deficient in a global regulator. Compared to LVS, all of the mutants showed impaired intracellular replication up to 72 h, and the number of themglAmutant bacteria even decreased. Colocalization with LAMP-1 was significantly increased for all mutants compared to LVS, indicating an impaired ability to escape into the cytoplasm. A lysosomal acidity-dependent dye accumulated in approximately 40% of the vacuoles containing mutant bacteria but not at all in vacuoles containing LVS. Preactivation of the macrophages with gamma interferon inhibited the intracellular growth of all strains and significantly increased acidification of phagosomes containing the mutants, but it only slightly increased the LAMP-1 colocalization. The intracellular replication and phagosomal escape of theiglCandiglDmutants were restored by complementation intrans. In conclusion, the IglC, IglD, and MglA proteins each directly or indirectly critically contribute to the virulence ofF. tularensisLVS, including its intracellular replication, cytoplasmic escape, and inhibition of acidification of the phagosomes.
A Triacylated Lipoprotein fromMycoplasma genitaliumActivates NF-κB through Toll-Like Receptor 1 (TLR1) and TLR2
Authors: Shimizu Takashi , Kida Yutaka , Kuwano Koichi 
Published: May 2008

ABSTRACTMycoplasma genitaliumis a sexually transmitted bacterial pathogen that causes nongonococcal chlamydia-negative urethritis, mucopurulent cervicitis, endometritis, pelvic inflammatory disease, and tubal factor infertility in humans. However, pathogenic agents that induce inflammatory responses have not been identified inM. genitalium. In this study, we examined the involvement of Toll-like receptors (TLRs) in activation of the immune response by a lipoprotein fromM. genitaliumand their active component responsible for NF-κB activation. The Triton X-114 detergent phase ofM. genitaliumwas found to induce NF-κB through TLR2. The active component of the Triton X-114 detergent phase was a lipoprotein precursor, MG149. The activation of NF-κB by MG149 was inhibited by a dominant negative (DN) construct of TLR1 but not by a DN construct of TLR6. These results indicate that the activation of NF-κB by MG149 is dependent on TLR1 and TLR2. A synthetic lipopeptide derived from MG149 containing three acyl chains also induced NF-κB through TLR1 and TLR2. Thus, the results show that MG149, a triacylated lipoprotein fromM. genitalium, activates NF-κB through TLR1 and TLR2.
Interaction of
Porphyromonas gingivalis
with Oral Streptococci Requires a Motif That Resembles the Eukaryotic Nuclear Receptor Box Protein-Protein Interaction Domain
Authors: Daep Carlo Amorin , Lamont Richard J. , Demuth Donald R. 
Published: May 2008

ABSTRACT

Porphyromonas gingivalis
initially colonizes the oral cavity by interacting with organisms in supragingival plaque, such as the oralis group of oral streptococci. This interaction involves the association of the streptococcal antigen I/II with the minor fimbrial antigen (Mfa1) of
P. gingivalis
. Our previous studies showed that a peptide (BAR) derived from antigen I/II inhibits
P. gingivalis
adherence and subsequent biofilm formation on streptococcal substrates. In addition, screening a combinatorial peptide library identified select amino acid substitutions in the NITVK active region of BAR that increased the adherence of
P. gingivalis
to streptococci. Here we report that incorporating these residues in a synthetic peptide results in more-potent inhibition of
P. gingivalis
adherence and biofilm formation (I
50
[50% inhibition] at 0.52 μM versus I
50
at 1.25 μM for BAR). In addition, a second structural motif in BAR, comprised of the amino acids KKVQDLLKK, was shown to contribute to
P. gingivalis
adherence to streptococci. Consistent with this, the KKVQDLLKK and NITVK motifs are conserved only in antigen I/II proteins expressed by the oralis group of streptococci, which interact with
P. gingivalis
. Interestingly, the primary and secondary structures and the functional characteristics of the amphipathic VQDLL core α-helix resemble the consensus nuclear receptor (NR) box protein-protein interacting domain sequence (LXXLL) of eukaryotes. BAR peptides containing amino acid substitutions with the potential to disrupt the secondary structure of VQDLL were less-effective inhibitors of
P. gingivalis
adherence and biofilm formation, suggesting that the α-helical character of VQDLL is important. Furthermore, replacing the lysines that flank VQDLL with acidic amino acids also reduced inhibitory activity, suggesting that the association of VQDLL with Mfa1 may be stabilized by a charge clamp. These results indicate that the Mfa1-interacting interface of streptococcal antigen I/II encompasses both the KKVQDLLKK and NITVK motif and suggest that the adherence of
P. gingivalis
to streptococci is driven by a protein-protein interaction domain that resembles the eukaryotic NR box. Thus, both motifs must be taken into account in designing potential peptidomimetics that target
P. gingivalis
adherence and biofilm formation.
d
-Alanylation of Lipoteichoic Acid Contributes to the Virulence of
Streptococcus suis
Authors: Fittipaldi Nahuel , Sekizaki Tsutomu , Takamatsu Daisuke , Harel Josée , Domínguez-Punaro María de la Cruz , Von Aulock Sonja , Draing Christian , Marois Corinne , Kobisch Marylène , Gottschalk Marcelo 
Published: May 2008

ABSTRACT

We generated by allelic replacement a Δ
dltA
mutant of a virulent
Streptococcus suis
serotype 2 field strain and evaluated the contribution of lipoteichoic acid (LTA)
d
-alanylation to the virulence traits of this swine pathogen and zoonotic agent. The absence of LTA
d
-alanylation resulted in increased susceptibility to the action of cationic antimicrobial peptides. In addition, and in contrast to the wild-type strain, the Δ
dltA
mutant was efficiently killed by porcine neutrophils and showed diminished adherence to and invasion of porcine brain microvascular endothelial cells. Finally, the Δ
dltA
mutant was attenuated in both the CD1 mouse and porcine models of infection, probably reflecting a decreased ability to escape immune clearance mechanisms and an impaired capacity to move across host barriers. The results of this study suggest that LTA
d
-alanylation is an important factor in
S. suis
virulence.
The Capsule Sensitizes
Streptococcus pneumoniae
to α-Defensins Human Neutrophil Proteins 1 to 3
Authors: Beiter Katharina , Wartha Florian , Hurwitz Robert , Normark Staffan , Zychlinsky Arturo , Henriques-Normark Birgitta 
Published: May 2008

ABSTRACT

Streptococcus pneumoniae
is a major cause of morbidity and mortality worldwide. Its polysaccharide capsule causes resistance to phagocytosis and interferes with the innate immune system's ability to clear infections at an early stage. Nevertheless, we found that encapsulated pneumococci are sensitive to killing by a human neutrophil granule extract. We fractionated the extract by high-performance liquid chromatography and identified α-defensins by mass spectrometry as the proteins responsible for killing pneumococci. Analysis of sensitivity to the commercial α-defensins human neutrophil proteins 1 to 3 (HNP1-3) confirmed these findings. We analyzed the sensitivities of different pneumococcal strains to HNP1-3 and found that encapsulated strains are efficiently killed at physiological concentrations (7.5 μg/ml). Surprisingly, nonencapsulated, nonvirulent pneumococci were significantly less sensitive to α-defensins. The proposed mechanisms of α-defensin resistance in nonencapsulated pneumococci is surface charge modification, e.g., by introduction of positive charge by
d
-alanylation of surface-exposed lipoteichoic acids. These mechanisms are surmounted by the presence of the capsule, which we hypothesize is masking these charge modifications. Hence, α-defensins in the phagolysosome of neutrophils possibly contribute to intracellular killing after antibody-mediated opsonophagocytosis of encapsulated pneumococci.