bluuebunny/crossref_metadata_2025_split huggingface dataset:
Efficacy of Quinolones against Secondary Pneumococcal Pneumonia after Influenza Virus Infection in Mice
Authors: Hayashi Katsuhiko , Kadowaki Shin-etsu , Takei Masaya , Fukuda Hideyuki 
Published: January 2006

ABSTRACT
We established a mouse model of secondary pneumococcal pneumonia after influenza virus infection and investigated the efficacy of several quinolones against pneumonia in this model. Gatifloxacin exhibited the highest efficacy among the quinolones examined and is probably useful for the treatment of secondary bacterial pneumonia.
Potentiation of Catechin Gallate-Mediated Sensitization of
Staphylococcus aureus
to Oxacillin by Nongalloylated Catechins
Authors: Stapleton Paul D. , Shah Saroj , Hara Yukihiko , Taylor Peter W. 
Published: January 2006

ABSTRACT

(−)−Epicatechin gallate (ECg) and (−)−epigallocatechin gallate (EGCg) reduce oxacillin resistance in
mecA
-containing strains of
Staphylococcus aureus
. Their binding to staphylococcal cells is enhanced by the nongalloyl analogues (−)−epicatechin (EC) and (−)−epigallocatechin (EGC). EC and EGC significantly increased the capacity of ECg and EGCg to reduce levels of staphylococcal oxacillin resistance.
In117, an Unusual In0-Like Class 1 Integron Containing CR1 and
bla
CTX-M-2
and Associated with a Tn
21
-Like Element
Authors: Valverde Aránzazu , Cantón Rafael , Galán Juan Carlos , Nordmann Patrice , Baquero Fernando , Coque Teresa M. 
Published: January 2006

ABSTRACT

An unusual In0-like class 1 integron containing a common region that includes the putative recombinase gene named orf513 (CR1) and
bla
CTX-M-2
was characterized from
Escherichia coli
. The integron contained an unusual gene cassette array,
estX-aadA1
, embedded between the 5′-conserved segment (5′-CS) and 3′-CS1 regions and was flanked by
mer
-Tn
21
sequences downstream of the
tni
truncated module. This element constitutes one of the few examples of CR1-bearing class 1 integrons that has been fully characterized.
Trematocidal Activity of Praziquantel and Artemisinin Derivatives: In Vitro and In Vivo Investigations with Adult
Echinostoma caproni
Authors: Keiser Jennifer , Brun Reto , Fried Bernard , Utzinger Jürg 
Published: January 2006

ABSTRACT

We examined the effects of praziquantel and the artemisinins on adult
Echinostoma caproni
. In vitro, both praziquantel and the artemisinins exhibited exposure-response relationships. In vivo, worm burden reductions of 100% were achieved with single oral doses of praziquantel, artesunate, and artemether at 50, 700, and 1,100 mg/kg of body weight, respectively.
In Vitro Bactericidal Activity of Human β-Defensin 3 against Multidrug-Resistant Nosocomial Strains
Authors: Maisetta Giuseppantonio , Batoni Giovanna , Esin Semih , Florio Walter , Bottai Daria , Favilli Flavia , Campa Mario 
Published: January 2006

ABSTRACT

The antimicrobial activity of human β-defensin 3 (hBD-3) against multidrug-resistant clinical isolates of
Staphylococcus aureus
,
Enterococcus faecium
,
Pseudomonas aeruginosa
,
Stenotrophomonas maltophilia
, and
Acinetobacter baumannii
was evaluated. A fast bactericidal effect (within 20 min) against all bacterial strains tested was observed. The presence of 20% human serum abolished the bactericidal activity of hBD-3 against gram-negative strains and reduced the activity of the peptide against gram-positive strains.
Pulsatile Delivery of Clarithromycin Alone or in Combination with Amoxicillin against
Streptococcus pneumoniae
Authors: Leuthner Kimberly D. , Cheung Chrissy M. , Rybak Michael J. 
Published: January 2006

ABSTRACT

We evaluated pulsatile dosing of clarithromycin and amoxicillin alone or combined against
Streptococcus pneumoniae
with various susceptibilities. When combined, pulsatile amoxicillin with clarithromycin was superior to either 8- or 12-h dosing against the intermediate strain and was identical for the susceptible strain. Pulse dosing of antimicrobials warrants further investigation.
Streptococcus pyogenes
Isolates with High-Level Macrolide Resistance and Reduced Susceptibility to Telithromycin Associated with 23S rRNA Mutations
Authors: Farrell David J. , Shackcloth Jemma , Barbadora Karen A. , Green Michael D. 
Published: January 2006

ABSTRACT

Seven high-level macrolide-resistant
Streptococcus pyogenes
isolates had reduced activity to telithromycin but were negative for methylation and efflux genes. All were of the constitutive phenotype, were clonally related (
emm
type 12 and MLST type 36), and had identical dual mutations (A2058G and U2166C) in domain V of 23S rRNA.
Levels of toxins in oral tobacco products in the UK: Table 1
Authors: McNeill A , Bedi R , Islam S , Alkhatib M N , West R 
Published: January 2006

Objective:This study examined the constituents of smokeless tobacco products available in the UK and compared them with products available in India, Sweden, and the USAMethods:Seven UK brands of smokeless tobacco, including a tooth cleaning powder, and four international brands of smokeless tobacco were tested for a range of toxins and known carcinogens, such as tobacco specific N-nitrosamines (TSNA), as well as nicotine availability.Results:Ten of the 11 brands tested had detectable levels of tobacco specific nitrosamines, which are proven carcinogens, and levels varied 130-fold. All had detectable levels of benzo(a)pyrene, another proven carcinogen (with around 175-fold variation) and several toxic metals (with nearly 150-fold variation). Nicotine availability varied in the UK products from 0.1 mg/g to 63.2 mg/g. All the tobacco products tested are likely to be hazardous to users’ health, but the data indicate that it should be possible to reduce key toxins to non-detectable levels.Conclusions:Smokeless tobacco products should be regulated and standards set for maximum levels of toxins and carcinogens.
Hypoxia reduces the output of matrix metalloproteinase-9 (MMP-9) in monocytes by inhibiting its secretion and elevating membranal association
Authors: Rahat Michal A , Marom Barak , Bitterman Haim , Weiss-Cerem Lea , Kinarty Amalia , Lahat Nitza 
Published: January 2006

Abstract
Cellular hypoxia, characterizing tumors, ischemia, and inflammation induce recruitment of monocytes/macrophages, immobilize them at the hypoxic site, and alter their function. To migrate across the extracellular matrix and as part of their inflammatory functions, monocytes and macrophages secrete proteases, including matrix metalloproteinase-9 (MMP-9), whose expression is induced by proinflammatory cytokines [e.g., tumor necrosis factor α (TNF-α)]. We show that hypoxia (&lt;0.3% O2 for 48 h) reduced the output of TNF-α-induced proMMP-9 by threefold (P&lt;0.01) in the U937 monocytic cell line and in primary human monocytes. TNF-α induced MMP-9 transcription by threefold, but no significant difference was observed in MMP-9 mRNA steady-state between normoxia and hypoxia, which inhibited the trafficking of proMMP-9 via secretory vesicles and increased the intracellular accumulation of proMMP-9 in the cells by 47% and 62% compared with normoxia (P&lt;0.05), as evaluated by zymography of cellular extracts and confocal microscopy, respectively. Secretion of proMMP-9 was reduced by the addition of cytochalazin B or nocodazole, which inhibits the polymerization of actin and tubulin fibers, or by the addition of the Rho kinase inhibitor Y27632, suggesting the involvement of the cytoskeleton and the Rho GTPases in the process of enzyme secretion. Furthermore, attachment of proMMP-9 to the cell membrane increased after hypoxia via its interactions with surface molecules such as CD44. In addition, the reduced migration of monocytes in hypoxia was shown to be mediated, at least partially, by secreted MMP-9. Thus, hypoxia post-translationally reduced the secreted amounts of proMMP-9 by using two mutually nonexclusive mechanisms: mostly, inhibition of cellular trafficking and to a lesser extent, attachment to the membrane.
CCL2 as a trigger of manifestations of compensatory anti-inflammatory response syndrome in mice with severe systemic inflammatory response syndrome
Authors: Takahashi Hitoshi , Tsuda Yasuhiro , Kobayashi Makiko , Herndon David N , Suzuki Fujio 
Published: January 2006

Abstract
Patients with compensatory anti-inflammatory response syndrome (CARS) are at a higher risk for infection with various opportunistic pathogens. CARS develops commonly in association with the manifestation of systemic inflammatory response syndrome (SIRS). In the present study, the role of SIRS-associated soluble factors on the CARS development was examined in mice with pancreatitis, a carrier of typical SIRS. Following the production of SIRS-related cytokines [tumor necrosis factor α and interleukin (IL)-1β], CC chemokine ligand 2 (CCL2), IL-4, and IL-10 (typical CARS cytokines) were detected in the sera of mice with pancreatitis. CCL2 has been described as an essential chemokine for the T helper cell type 2 manifestation. CARS effector cells (cells with an ability to produce IL-4 and IL-10) were not generated from normal T cells after stimulation with SIRS-related cytokines. However, these cells were generated from normal T cells after cultivation with peripheral blood neutrophils (PMN) from SIRS mice in a dual-chamber transwell. Normal T cells did not convert to CARS effector cells after transwell cultures with PMN from normal mice. CCL2 was detected in culture fluids of PMN from SIRS mice, and PMN from normal mice did not produce CCL2 into their culture fluids. CARS effector cells did not appear in PMN-depleted SIRS mice or SIRS mice treated with anti-CCL2 monoclonal antibody, and these cells were demonstrated in PMN-depleted SIRS mice after treatment with recombinant murine CCL2. These results indicate that CCL2 produced by PMN from SIRS mice is an active molecule on the SIRS-associated CARS manifestation.
The lectin jacalin plus costimulation with anti-CD28 antibody induces phosphorylation of p38 MAPK and IL-4 synthesis-I
Authors: Tamma Seetha M Lakshmi , Balan Satya Priya , Chung Ken Wook , Pahwa Savita 
Published: January 2006

Abstract
Costimulatory signals play an important role in the development of T helper cell type 1 (Th1) or Th2 type. Little is known about jacalin plus CD28-mediated signaling and cytokine secretion. In the present study, we analyzed the intracellular signaling events following stimulation of CD4+ T cells with jacalin plus CD28 cross-linking (CD28XL) with anti-CD28 antibody. Our results indicate enhanced phosphorylation of Tec and linker for activation of T cells when compared with stimulation with jacalin alone or CD28XL alone. Stimulation with jacalin or CD28XL appears to be insufficient to induce interleukin (IL)-4 secretion; however, CD28XL followed by stimulation with jacalin resulted in enhanced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and increased secretion of IL-4. However, compared with stimulation with phorbol 12-myristate 13-acetate plus ionomycin, jacalin plus CD28XL resulted in decreased levels of tumor necrosis factor α secretion. Addition of p38 inhibitor, SB203580, inhibited p38 phosphorylation and IL-4 secretion. These data suggest that jacalin stimulation alone appears to be insufficient for Th2 development, and addition of CD28 costimulation induced Th2 generation. We propose that jacalin plus CD28XL induces Th2 differentiation via activation of p38 MAPK.
Different effects of adiponectin isoforms in human monocytic cells
Authors: Neumeier Markus , Weigert Johanna , Schäffler Andreas , Wehrwein Gabriele , Müller-Ladner Ulf , Schölmerich Jürgen , Wrede Christian , Buechler Christa 
Published: January 2006

Abstract
Adiponectin (APM) is an adipocyte-derived adipokine with immunosuppressive, antidiabetic, and antiatherosclerotic properties. Low molecular weight (LMW)- and higher molecular weight (HMW)-APM circulate in the serum and activate different signaling pathways. We were interested to see whether LMW-APM exerts different effects on monocytic cells compared with the HMW isoform. Therefore, the effects of recombinant LMW-APM produced in insect cells and the APM from higher eukaryotic cells containing HMW forms on monocytic cells were investigated with respect to apoptosis and inflammation. LMW- and HMW-APM induce apoptosis in nondifferentiated THP-1 cells, reduce macrophage scavenger receptor (MSR) A mRNA expression, and stimulate phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). However, HMW-APM induces the secretion of interleukin (IL)-6 in human monocytes and THP-1 cells but does not suppress lipopolysaccharide (LPS)-induced IL-6 secretion. In contrast, LMW-APM reduces LPS-mediated IL-6 release and furthermore, stimulates IL-10 secretion, most likely by reducing the abundance of inhibitor of nuclear factor (NF)-κB kinase β, leading to a diminished nuclear translocation of NF-κB p65. Our data indicate that the different APM isoforms do share common effects on monocytic cells but also induce isoform-specific responses. Although apoptosis, the activation of AMPK, and the reduction of MSR are mediated by all APM isoforms, only LMW-APM displays anti-inflammatory properties.
Association of Prolactin and Its Receptor Gene Regions with Familial Breast Cancer
Authors: Vaclavicek Annika , Hemminki Kari , Bartram Claus R. , Wagner Kerstin , Wappenschmidt Barbara , Meindl Alfons , Schmutzler Rita K. , Klaes Rüdiger , Untch Michael , Burwinkel Barbara , Försti Asta 
Published: January 2006

Context: The contribution of prolactin (PRL) through its receptor (PRLR) to the pathogenesis and progression of human mammary tumors has received recent attention.
Objective: We investigated whether genetic variation in the PRL and PRLR genes is associated with the risk of breast cancer (BC).
Design: We conducted a case-control study with a total of seven single nucleotide polymorphisms (SNPs).
Setting: The study was conducted at an academic research laboratory and university clinics.
Patients and Other Participants: A total of 441 German familial, unrelated BC cases and 552 controls matched by age, ethnicity, and geographical region participated in the study.
Intervention(s): There were no interventions.
Main Outcome Measures(s): SNP genotype and haplotype distributions and haplotype interactions were correlated with the risk of BC.
Results: Two SNPs (rs1341239 and rs12210179) within the PRL promoter regions were significantly associated with increased risk in homozygotes for the variant alleles [odds ratio (OR), 1.67 and 95% confidence interval (CI), 1.11–2.50; and OR, 2.09 and 95% CI, 1.23–3.52, respectively]. The PRL haplotype containing the variant alleles of the promoter SNPs increased significantly the risk of BC (OR 1.42, 95%CI 1.07–1.90). A PRLR haplotype was associated with a significant decrease in BC risk (OR 0.69, 95% CI 0.54–0.89). An increasing number of PRL and PRLR risk haplotypes led to a significant trend of increasing risk for BC (χ2 = 12.15; P = 0.007).
Conclusions: Genetic variation in the PRL and PRLR genes was shown to influence BC risk. Additional studies are needed to further clarify the role of the PRL and PRLR genes in the risk of BC.
Increased midbrain gray matter in Tourette's syndrome
Authors: Garraux Gaëtan , Goldfine Andrew , Bohlhalter Stephan , Lerner Alicja , Hanakawa Takashi , Hallett Mark 
Published: January 2006

AbstractObjectiveTo investigate cerebral structure in Tourette's syndrome (TS).MethodsVoxel‐based morphometry study of high‐resolution MRIs in 31 TS patients compared with 31 controls.ResultsIncreased gray matter mainly in the left mesencephalon in 31 TS patients.InterpretationThis result constitutes strong and direct evidence supporting Devinsky's hypothesis (Devinsky O. Neuroanatomy of Gilles de la Tourette's syndrome. Possible midbrain involvement. Arch Neurol 1983;40:508–514) according to which midbrain disturbances play an important pathogenic role in TS. Ann Neurol 2006;59:381–385
Length dependence in polyneuropathy associated with IgM gammopathy
Authors: Franssen Hessel , Notermans Nicolette C. 
Published: January 2006

AbstractObjectiveIn polyneuropathy associated with monoclonal IgM gammopathy, nerve conduction studies may show disproportionate distal slowing consistent with segmental demyelination. This was suggested to represent a length‐dependent demyelinating process, starting in distal and proceeding to proximal segments. Because the evidence for this is incomplete, we assessed whether length dependence occurs in IgM neuropathy.MethodsIn 22 patients with IgM neuropathy, 20 disease controls with chronic inflammatory demyelinating polyneuropathy (CIDP) and 36 normal controls, we investigated motor conduction, sensory conduction, and needle electromyography for nerves with short, intermediate‐length, and long axons as well as conduction in short segments of the ulnar nerve from proximal to distal. To compare variables in nerves of different length, we normalized individual values with respect to the median in normal controls.ResultsIn IgM neuropathy, distal slowing and features of axon loss increased with nerve length, and ulnar nerve conduction became gradually slower from proximal to distal when the elbow segment was excluded. In CIDP, no clear length dependence was found except for distal amplitude.InterpretationThe disproportionate distal slowing in IgM neuropathy may be part of a length‐dependent process, assuming that this process is randomly distributed due to a generalized exposure to IgM. Ann Neurol 2006;59:365–371
Neurological impact of vasopressin dysregulation and hyponatremia
Authors: Bhardwaj Anish 
Published: January 2006

AbstractHyponatremia is frequently associated with neurological disease, neurosurgical procedures, and use of psychoactive drugs. Arginine vasopressin (AVP), or antidiuretic hormone, is the principal physiological regulator of water and electrolyte balance, and disruption of the normal AVP response to osmotic stimuli is a common cause of dilutional hyponatremia in neurological disorders. The hyponatremia‐induced shift in water from the extracellular to the intracellular compartment can lead to cerebral edema and serious neurological complications, especially if the decrease in serum sodium concentration ([Na+]) is large or rapid. Overly rapid correction of the serum [Na+] may lead to osmotic demyelination and irreversible brain injury. Fluid restriction is considered first‐line treatment and pharmacological agents currently used in the treatment of hyponatremia are limited by inconsistent response and adverse side effects. AVP receptor antagonists represent a new approach to the treatment of hyponatremia by blocking tubular reabsorption of water by binding to V2 receptors in the renal collecting ducts, resulting in aquaresis. Initial clinical experience with AVP receptor antagonists for hyponatremia has shown that these agents augment free water clearance, decrease urine osmolality, and correct serum [Na+] and serum osmolality. Controlled clinical trials now underway will help elucidate the role of AVP receptor antagonism in the treatment of hyponatremia. Ann Neurol 2006;59:229–236
Axonal neuropathy with optic atrophy is caused by mutations in mitofusin 2
Authors: Züchner Stephan , De Jonghe Peter , Jordanova Albena , Claeys Kristl G. , Guergueltcheva Velina , Cherninkova Sylvia , Hamilton Steven R. , Van Stavern Greg , Krajewski Karen M. , Stajich Jeffery , Tournev Ivajlo , Verhoeven Kristien , Langerhorst Christine T. , de Visser Marianne , Baas Frank , Bird Thomas , Timmerman Vincent , Shy Michael , Vance Jeffery M. 
Published: January 2006

AbstractObjectiveCharcot‐Marie‐Tooth (CMT) neuropathy with visual impairment due to optic atrophy has been designated as hereditary motor and sensory neuropathy type VI (HMSN VI). Reports of affected families have indicated autosomal dominant and recessive forms, but the genetic cause of this disease has remained elusive.MethodsHere, we describe six HMSN VI families with a subacute onset of optic atrophy and subsequent slow recovery of visual acuity in 60% of the patients. Detailed clinical and genetic studies were performed.ResultsIn each pedigree, we identified a unique mutation in the gene mitofusin 2 (MFN2). In three families, the MFN2 mutation occurred de novo; in two families the mutation was subsequently transmitted from father to son indicating autosomal dominant inheritance.InterpretationMFN2 is a mitochondrial membrane protein that was recently reported to cause axonal CMT type 2A. It is intriguing that MFN2 shows functional overlap with optic atrophy 1 (OPA1), the protein underlying the most common form of autosomal dominant optic atrophy, and mitochondrial encoded oxidative phosphorylation components as seen in Leber's hereditary optic atrophy. We conclude that autosomal dominant HMSN VI is caused by mutations in MFN2, emphasizing the important role of mitochondrial function for both optic atrophies and peripheral neuropathies. Ann Neurol 2006;59:276–281
Preparation and properties of core [poly(styrene‐n‐butyl acrylate)]–shell [poly(styrene–methyl methacrylate–vinyl triethoxide silane)] structured latex particles with self‐crosslinking characteristics
Authors: Guo Tianying , Chen Xi , Song Moudao , Zhang Banghua 
Published: January 2006

AbstractStructured latex particles with a slightly crosslinked poly(styrene‐n‐butyl acrylate) (PSB) core and a poly(styrene–methacrylate–vinyl triethoxide silane) (PSMV) shell were prepared by seed emulsion polymerization, and the latex particle structures were investigated with Fourier transform infrared, thermogravimetric analysis, differential scanning calorimetry, transmission electron microscopy, and dynamic light scattering. The films that were formed from the structured core (PSB)–shell (PSMV) particles under ambient conditions had good water repellency and good tensile strength in comparison with films from structured core (PSB)–shell [poly(styrene–methyl methyacrylate)] latex particles; this was attributed to the self‐crosslinking of CH2CHSi(OCH2CH3)3 in the outer shell structure. The relationship between the particle structure and the film properties was also investigated in this work. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 100: 1824–1830, 2006
Millimeter wave induced reversible externalization of phosphatidylserine molecules in cells exposed in vitro
Authors: Szabo Imre , Kappelmayer Janos , Alekseev Stanislav I. , Ziskin Marvin C. 
Published: January 2006

AbstractIn vitro exposure of refrigerated samples (4 °C) of anti‐coagulated blood with millimeter waves (MMWs) at incident power densities (IPDs) between 0.55 and 1.23 W/cm2 has been found to induce clot formation. We found a small but statistically significant change in clot size with increasing IPD value. MMW exposure of blood samples starting at room temperature (22 °C) did not induce blood coagulation; neither did conventional heating at temperatures up to 40 °C. Since cell‐free plasma did not clot upon MMW exposure, the role of blood cells was particularly analyzed. Experiments on various mixtures of blood cells with plasma revealed an important role of red blood cells (RBC) in the coagulation process. Plasma coagulation also developed within the MMW beam above dense keratinocyte (HaCaT) monolayers suggesting it lacked cell‐type specificity. We hypothesized that alteration of the membrane surface in exposed cells might be responsible for the circumscribed coagulation. The thrombogenic role of externalized phosphatidylserine (PS) molecules is well known. Therefore, we carried out experiments for immunolabeling PS molecules with fluorescein isothiocyanate (FITC)‐conjugated Annexin V on exposed cells. Fluorescence microscopy of the adherent human keratinocytes (HaCaT) and murine melanoma cells (B16F10) showed that MMW exposure at an IPD of 1.23 W/cm2 is capable of inducing reversible externalization of PS molecules in cells within the beam area without detectable membrane damage. Nonadherent Jurkat cells exposed to MMW at an IPD of 34.5 mW/cm2 also showed reversible PS externalization with flow cytometry, whether the cell temperature was held constant or permitted to rise. These results suggest that certain biological effects induced by MMWs could be initiated by membrane changes in exposed cells. Bioelectromagnetics 27:233–244, 2006. © 2006 Wiley‐Liss, Inc.