bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Conversion of Social Capital into Community Development: an Intervention in Australia's Outback
Authors: ONYX JENNY , LEONARD ROSEMARY 
Published: January 2010

AbstractThe research presented in this article employed a deliberate intervention to mobilize social capital and then studied the dynamics of the way in which it influenced community development. Whether or not social capital is able to facilitate development depends on the specific context in which it occurs. Although the general context of this study was that of small rural towns in Australia's outback that are experiencing decline, each of the four towns studied had unique features which could influence the mobilization of social capital. Rural communities have the willingness and capacity to mobilize but whether this capacity is actualized may well depend on the presence of other mobilizing factors. Specifically the intervention study found that a structure needs to be in place which can take the initiative and work across the community — engaging a range of organizations. Second, the structure needs to be supported, but not controlled, by local government. Third, it needs the kind of social entrepreneurship that can sustain a community‐wide vision and bring together the diverse groups within the community.Résumé Les recherches présentées s'appuient sur une opération destinée à mobiliser le capital social, afin d'étudier les dynamiques selon lesquelles il a influé sur le développement communautaire. L'aptitude du capital social à faciliter le développement dépend du contexte dans lequel celui‐ci se produit. Bien que cette étude se place dans de petites villes de campagnes reculées d'Australie confrontées à un déclin, chacune des quatre villes concernées présentaient des spécificités propres susceptibles d'influencer la mobilisation du capital social. Les communautés rurales ont la volonté et la capacité de se mobiliser, mais la concrétisation de cette capacité peut dépendre largement de la présence d'autres facteurs mobilisateurs. En particulier, l'analyse de l'opération montre qu'il doit exister une structure capable de prendre l'initiative et de travailler avec toute la communauté en impliquant tout un éventail d'organismes. Ensuite, il faut que la structure soit épaulée, et non contrôlée, par le gouvernement local. Enfin, elle a besoin d'une sorte d'esprit d'entreprise sociale qui puisse nourrir une vision à l'échelle communautaire et réunir les différents groupes présents dans la communauté.
Well being, psychopathology and coping strategies in psoriasis compared with atopic dermatitis: a controlled study
Authors: Leibovici V , Canetti L , Yahalomi S , Cooper‐Kazaz R , Bonne O , Ingber A , Bachar E 
Published: January 2010

AbstractBackground  There is a vast literature describing the association between psoriasis, atopic dermatitis (AD) and psychological distress. Some of these studies were uncontrolled and others used non‐dermatological diseases as control, but only a few used chronic skin diseases as controls.Objective  To compare well being, psychopathology and coping strategies of psoriatic, AD and healthy controls in a prospective case‐control study.Methods  Thirty‐seven psoriatic patients and 31 AD patients were recruited from the Hadassah Ein Karem Hospital, Jerusalem, Israel, outpatient and inward clinic. The participants in the control group were 31 healthy workers and volunteers with no dermatological diseases from Kaplan Hospital, Rehovot, Israel. We used self‐report questionnaires [Mental Health Inventory (MHI) and Adjustment to Chronic Skin Diseases Questionnaire (ACSD)], a projective technique (Hand Test) and assessment tools (Clinical Global Impression).Results  Psoriatic patients experienced reduced well being (P = 0.007) and more anxiety and depression (P = 0.018) than normal controls. Psoriatic patients also displayed more severe psychopathology (P = 0.039) a more passive attitude towards life, and loss of meaning in life (P = 0.001) as measured by the projective technique compared with AD patients and normal controls.Conclusions  We propose two explanations, derived from the psychological and the psycho‐neuro‐immunological domains. First, greater mental distress in psoriasis is because of the greater stigma it bears compared with AD. Alternatively, we hypothesize that the psoriatic inflammatory process may possibly have a direct central nervous system effect.
Preterm delivery and risk of subsequent cardiovascular morbidity and type‐II diabetes in the mother
Authors: Lykke JA , Paidas MJ , Damm P , Triche EW , Kuczynski E , Langhoff‐Roos J 
Published: January 2010

Please cite this paper as: Lykke J, Paidas M, Damm P, Triche E, Kuczynski E, Langhoff‐Roos J. Preterm delivery and risk of subsequent cardiovascular morbidity and type‐II diabetes in the mother. BJOG 2010;117:274–281.Objective  Preterm delivery has been shown to be associated with subsequent maternal cardiovascular morbidity. However, the impact of the severity and recurrence of preterm delivery on the risk of specific cardiovascular events and the metabolic syndrome in the mother, have not been investigated.Design  National registry‐based retrospective cohort study.Setting  Women delivering in Denmark from 1978 to 2007.Population  Women with a first singleton delivery (n = 782 287), and with a first and second singleton delivery (n = 536 419).Methods  Cox proportional hazard models, with the gestational age stratified into four groups as primary exposure. We made adjustments for maternal age, year of delivery, hypertensive pregnancy disorders, fetal growth deviation, placental abruption and stillbirth.Main outcome measures  Subsequent maternal hypertension, ischaemic heart diseases, thromboembolism and type‐II diabetes.Results  After a first delivery at 32–36 completed weeks of gestation, the adjusted risk of subsequent type‐II diabetes increased 1.89‐fold (1.69–2.10) and the risk of thromboembolism increased 1.42‐fold (1.24–1.62). Women having a preterm delivery in the first pregnancy and a term delivery in the second had a 1.58‐fold (1.34–1.86) increased risk of type‐II diabetes and a 1.18‐fold (0.96–1.44) increased risk of thromboembolism. Women having two preterm deliveries had a 2.30‐fold (1.71–3.10) increased risk of type‐II diabetes and a 1.80‐fold (1.29–2.50) increased risk of thromboembolism.Conclusions  Preterm delivery is independent of other pregnancy complications associated with subsequent maternal overt type‐II diabetes and thromboembolism. The recurrence of preterm delivery will augment these risks.
Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia
Authors: Masuyama H , Segawa T , Sumida Y , Masumoto A , Inoue S , Akahori Y , Hiramatsu Y 
Published: January 2010

Please cite this paper as: Masuyama H, Segawa T, Sumida Y, Masumoto A, Inoue S, Akahori Y, Hiramatsu Y. Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia. BJOG 2010;117:314–320.Objective  Circulating angiogenic factors have been shown to be important in the pathophysiology of pre‐eclampsia. Blood levels of adipocytokines differ in pre‐eclampsia relative to controls and may also play an important role in disease pathogenesis. Differences in the circulating levels of these molecules were compared between matched normotensive controls and women with pre‐eclampsia with onset before or at/after 32 weeks, and according to whether the women were of normal weight (18.5 < body mass index < 25) or overweight.Design  A cross‐sectional study of 110 pregnant Japanese women who visited the Department of Obstetrics and Gynecology, Okayama University Hospital, Okayama, Japan.Setting  Tertiary referral centre serving 2000 births.Methods  Serum concentrations of soluble fms‐like tyrosine kinase 1 (sFlt‐1), placental growth factor (PlGF), soluble endoglin (sEng), adiponectin and leptin were measured in women with pre‐eclampsia and in normotensive controls matched for age, gestational week, parity and body mass index.Main outcome measures  Serum levels of sFlt‐1, PlGF, the sFlt‐1/PlGF ratio, sEng, adiponectin and leptin.Results  The sFlt‐1/PlGF ratio in early‐onset pre‐eclampsia was significantly higher than that in late‐onset pre‐eclampsia (112.0 ± 30.2 versus 45.4 ± 43.8, P = 0.037). There was a significant elevation of leptin in both subtypes relative to controls (early: 58.6 ± 18.3 ng/ml versus 26.0 ± 6.7 ng/ml, P = 0.001; late: 39.5 ± 9.2 ng/ml versus 22.0 ± 4.3 ng/ml, P = 0.005), but adiponectin was increased only in late‐onset pre‐eclampsia (36.5 ± 13.4 μg/ml versus 12.0 ± 4.3 μg/ml, P = 0.003). Significant differences in angiogenic factors and adiponectin were found between normal and overweight women only in late‐onset pre‐eclampsia.Conclusions  These data suggest that there are different profiles of angiogenic factors and adipocytokines between women who develop early‐ and late‐onset pre‐eclampsia.
Evidence that MDMA (‘ecstasy’) increases cannabinoid CB2 receptor expression in microglial cells: role in the neuroinflammatory response in rat brain
Authors: Torres Elisa , Gutierrez‐Lopez Maria Dolores , Borcel Erika , Peraile Ines , Mayado Andrea , O’Shea Esther , Colado Maria Isabel 
Published: January 2010

J. Neurochem.(2010) 10.1111/j.1471‐4159.2010.06578.xAbstract3,4‐Methylenedioxymethamphetamine (MDMA, ‘ecstasy’) produces selective long‐lasting serotonergic neurotoxicity in rats. The drug also produces acute hyperthermia which modulates the severity of the neurotoxic response. In addition, MDMA produces signs of neuroinflammation reflected as microglial activation and an increase in the release of interleukin‐1β, the latter of which appears to be a consequence of the hyperthermic response and to be implicated in the neurotoxicity induced by the drug. Over‐expression of the cannabinoid CB2 receptor in microglia during non‐immune and immune pathological conditions is thought to be aimed at controlling the production of neurotoxic factors such as proinflammatory cytokines. Our objective was to study the pattern of CB2 receptor expression following MDMA and to examine the effect of JWH‐015 (a CB2 agonist) on the MDMA‐induced neuroinflammatory response as well as 5‐hydroxytryptamine (5‐HT) neurotoxicity. Adult Dark Agouti rats were given MDMA (12.5 mg/kg, i.p.) and killed 3 h or 24 h later for the determination of CB2 receptor expression. JWH‐015 was given 48 h, 24 h and 0.5 h before MDMA and 1 h and/or 6 h later and animals were killed for the determination of microglial activation (3 h and 24 h) and 5‐HT neurotoxicity (7 days). MDMA increased CB2 receptor expression shortly after administration and these receptors were found in microglia. JWH‐015 decreased MDMA‐induced microglial activation and interleukin‐1β release and slightly decreased MDMA‐induced 5‐HT neurotoxicity. In conclusion, CB2 receptor activation reduces the neuroinflammatory response following MDMA and provides partial neuroprotection against the drug.
Characterization of human synovial fluid cells of 26 patients with osteoarthritis knee for cartilage repair therapy
Authors: KUROSE Rie , ICHINOHE Sadafumi , TAJIMA Goro , HORIUCHI Saburo , KUROSE Akira , SAWAI Takashi , SHIMAMURA Tadashi 
Published: January 2010

AbstractAim:  To investigate the possibility of chondrogenic differentiation and cartilage repair of synovial fluid cells of osteoarthritis (OA) knee.Methods:  Synovial fluids from 26 patients with OA knee were aspirated from each knee joint and cultured in vitro. The morphology of cultured synovial fluid cells, cell proliferation rate, the phenotype, and chondrogenic differentiation were analyzed in in vitro. Also, human autologous synovial fluid cells were transplanted to OA cartilage, and the cells were traced in ex vivo.Results:  In 19 of 26 materials, the cells proliferated satisfactorily. The cell proliferation in six materials was very slow and one material contaminated. Culture‐expanded synovial fluid cells had a fibroblastic morphology and the phenotype was negative for CD10, CD14, and CD45, and positive for CD13, CD44, and CD105. Pellet culture of synovial fluid cells showed chondrogenic differentiation. In the ex vivo study, autologous transplanted synovial fluid cells were observed in repaired or enhanced regenerative cartilage areas and showed a tendency to infiltrate the original degenerative cartilage of OA.Conclusions:  This study proved the possibility of chondrogenic differentiation of synovial fluid cells of OA knee joints despite the pathologic environment within a diseased joint. Synovial fluid cells were actually heterogeneous cells but they showed chondrogenic differentiation, similar to that of bone marrow‐derived mesenchymal progenitor cells (BMMPCs). The Ex vivo study suggested that synovial fluid cells had a tendency to adhere to OA degenerative cartilage in humans.
Trailing or Paradoxical Growth of
Candida albicans
When Exposed to Caspofungin Is Not Associated with Microsatellite Genotypes
Authors: Khlif Mohamed , Bogreau Hervé , Michel-Nguyen Annie , Ayadi Ali , Ranque Stéphane 
Published: January 2010

ABSTRACT

Multilocus microsatellite polymorphisms in 27 clinical
Candida albicans
isolates were found to be clearly unrelated to
in vitro
paradoxical growth or trailing effect with caspofungin. These findings suggest that such
in vitro
phenotypes are either gained or lost too rapidly to be predicted by more stable genomic markers.
Attenuation of Cerebrospinal Fluid Inflammation by the Nonbacteriolytic Antibiotic Daptomycin versus That by Ceftriaxone in Experimental Pneumococcal Meningitis
Authors: Grandgirard Denis , Oberson Kevin , Bühlmann Angela , Gäumann Rahel , Leib Stephen L. 
Published: January 2010

ABSTRACT

Antibiotic-induced bacteriolysis exacerbates inflammation and brain damage in bacterial meningitis. Here the quality and temporal kinetics of cerebrospinal fluid (CSF) inflammation were assessed in an infant rat pneumococcal meningitis model for the nonbacteriolytic antibiotic daptomycin versus ceftriaxone. Daptomycin led to lower CSF concentrations of interleukin 1β (IL-1β), IL-10, IL-18, monocyte chemoattractant protein 1 (MCP-1), and macrophage inflammatory protein 1 alpha (MIP-1α) (
P
< 0.05). In experimental pneumococcal meningitis, daptomycin treatment resulted in more rapid bacterial killing, lower CSF inflammation, and less brain damage than ceftriaxone treatment.
Antibiotic Sensitivity Profiles Determined with an
Escherichia coli
Gene Knockout Collection: Generating an Antibiotic Bar Code
Authors: Liu Anne , Tran Lillian , Becket Elinne , Lee Kim , Chinn Laney , Park Eunice , Tran Katherine , Miller Jeffrey H. 
Published: January 2010

ABSTRACT

We have defined a sensitivity profile for 22 antibiotics by extending previous work testing the entire KEIO collection of close to 4,000 single-gene knockouts in
Escherichia coli
for increased susceptibility to 1 of 14 different antibiotics (ciprofloxacin, rifampin [rifampicin], vancomycin, ampicillin, sulfamethoxazole, gentamicin, metronidazole, streptomycin, fusidic acid, tetracycline, chloramphenicol, nitrofurantoin, erythromycin, and triclosan). We screened one or more subinhibitory concentrations of each antibiotic, generating more than 80,000 data points and allowing a reduction of the entire collection to a set of 283 strains that display significantly increased sensitivity to at least one of the antibiotics. We used this reduced set of strains to determine a profile for eight additional antibiotics (spectinomycin, cephradine, aztreonem, colistin, neomycin, enoxacin, tobramycin, and cefoxitin). The profiles for the 22 antibiotics represent a growing catalog of sensitivity fingerprints that can be separated into two components, multidrug-resistant mutants and those mutants that confer relatively specific sensitivity to the antibiotic or type of antibiotic tested. The latter group can be represented by a set of 20 to 60 strains that can be used for the rapid typing of antibiotics by generating a virtual bar code readout of the specific sensitivities. Taken together, these data reveal the complexity of intrinsic resistance and provide additional targets for the design of codrugs (or combinations of drugs) that potentiate existing antibiotics.
Penicillin-Binding Protein Gene Alterations in
Streptococcus uberis
Isolates Presenting Decreased Susceptibility to Penicillin
Authors: Haenni Marisa , Galofaro Laure , Ythier Mathilde , Giddey Marlyse , Majcherczyk Paul , Moreillon Philippe , Madec Jean-Yves 
Published: January 2010

ABSTRACT

Streptococcus uberis
is an environmental pathogen commonly causing bovine mastitis, an infection that is generally treated with penicillin G. No field case of true penicillin-resistant
S. uberis
(MIC > 16 mg/liter) has been described yet, but isolates presenting decreased susceptibility (MIC of 0.25 to 0.5 mg/liter) to this drug are regularly reported to our laboratory. In this study, we demonstrated that
S. uberis
can readily develop penicillin resistance in laboratory-evolved mutants. The molecular mechanism of resistance (acquisition of mutations in penicillin-binding protein 1A [PBP1A], PBP2B, and PBP2X) was generally similar to that of all other penicillin-resistant streptococci described so far. In addition, it was also specific to
S. uberis
in that independent resistant mutants carried a unique set of seven consensus mutations, of which only one (Q
554
E in PBP2X) was commonly found in other streptococci. In parallel, independent isolates from bovine mastitis with different geographical origins (France, Holland, and Switzerland) and presenting a decreased susceptibility to penicillin were characterized. No mosaic PBPs were detected, but they all presented mutations identical to the one found in the laboratory-evolved mutants. This indicates that penicillin resistance development in
S. uberis
might follow a stringent pathway that would explain, in addition to the ecological niche of this pathogen, why naturally occurring resistances are still rare. In addition, this study shows that there is a reservoir of mutated PBPs in animals, which might be exchanged with other streptococci, such as
Streptococcus agalactiae
, that could potentially be transmitted to humans.
Population Pharmacokinetic Comparison and Pharmacodynamic Breakpoints of Ceftazidime in Cystic Fibrosis Patients and Healthy Volunteers
Authors: Bulitta J. B. , Landersdorfer C. B. , Hüttner S. J. , Drusano G. L. , Kinzig M. , Holzgrabe U. , Stephan U. , Sörgel F. 
Published: January 2010

ABSTRACT

Despite the promising activity of ceftazidime against
Pseudomonas aeruginosa
and
Burkholderia cepacia
, there has not yet been a study that directly compared the pharmacokinetics (PK) of ceftazidime in cystic fibrosis (CF) patients and healthy volunteers by population PK methodology. We assessed the population PK and PK/pharmacodynamic (PD) breakpoints of ceftazidime in CF patients and healthy volunteers. Eight CF patients (total body weight [WT] [average ± standard deviation] = 42.9 ± 18.4 kg) and seven healthy volunteers (WT = 66.2 ± 4.9 kg) received 2 g ceftazidime as a 5-min intravenous infusion. High-performance liquid chromatography (HPLC) was used for drug analysis, and NONMEM (results reported), S-ADAPT, and NPAG were used for parametric and nonparametric population PK modeling. We considered linear and allometric body size models to scale clearance and volume of distribution. Monte Carlo simulations were based on a target time of non-protein-bound plasma concentration of ceftazidime above MIC of ≥65%, which represents near-maximal killing. Unscaled total clearance was 19% lower in CF patients, and volume of distribution was 36% lower. Total clearance was 7.82 liters/h for CF patients and 6.68 liters/h for healthy volunteers with 53 kg fat-free mass. Allometric scaling by fat-free mass reduced the between-subject variability by 32% for clearance and by 18 to 26% for volume of both peripheral compartments compared to linear scaling by WT. A 30-min ceftazidime infusion of 2 g/70 kg WT every 8 h (q8h) achieved robust (≥90%) probabilities of target attainment (PTAs) for MICs of ≤1 mg/liter in CF patients and ≤3 mg/liter in healthy volunteers. Alternative modes of administration achieved robust PTAs up to markedly higher MICs of ≤8 to 12 mg/liter in CF patients for 5-h infusions of 2 g/70 kg WT q8h and ≤12 mg/liter for continuous infusion of 6 g/70 kg WT daily.
Impact of Azithromycin Resistance Mutations on the Virulence and Fitness of
Chlamydia caviae
in Guinea Pigs
Authors: Binet Rachel , Bowlin Anne K. , Maurelli Anthony T. , Rank Roger G. 
Published: January 2010

ABSTRACT

Azithromycin (AZM) is a major drug used in the treatment and prophylaxis of infections caused by
Chlamydia
, yet no significant clinical resistance has been reported for these obligate intracellular bacteria. Nevertheless, spontaneous AZM resistance (Azm
r
) arose
in vitro
at frequencies ranging from 3 × 10
−8
to 8 × 10
−10
for clonal isolates of
Chlamydia caviae
, which is a natural pathogen of guinea pigs. Sequencing of the unique 23S rRNA gene copy in 44 independent Azm
r
isolates identified single mutations at position A
2058
or A
2059
(
Escherichia coli
numbering system). While SP
6
AZ
1
(A
2058
C) and SP
6
AZ
2
(A
2059
C) Azm
r
mutants showed growth defects in cell culture and were less pathogenic in the guinea pig ocular infection model than in the parent SP
6
, the three isogenic
C. caviae
isolates grew equally well in the animal. On the other hand, coinoculation of the
C. caviae
parent strain with one of the Azm
r
strains was detrimental for the mutant strain. This apparent lack of association between pathology and bacterial load
in vivo
showed that virulence of the two Azm
r
mutants of
C. caviae
was attenuated. While chlamydial growth
in vitro
reflects the ability of the bacteria to multiply in permissive cells, survival in the host is a balance between cellular multiplication and clearance by the host immune system. The obligate intracellular nature of
Chlamydia
may therefore limit emergence of resistance
in vivo
due to the strength of the immune response induced by the wild-type antibiotic-sensitive bacteria at the time of antibiotic treatment.
Update on
Cyclospora cayetanensis
, a Food-Borne and Waterborne Parasite
Authors: Ortega Ynés R. , Sanchez Roxana 
Published: January 2010

SUMMARY

The coccidian parasite
Cyclospora cayetanensis
is recognized as an emerging pathogen that causes protracted diarrhea in humans. The first cases of
Cyclospora
infection were reported in the late 1970s and were observed among expatriates and travelers in regions where infections are endemic. Since then,
Cyclospora
has been considered a cause of traveler's diarrhea. Epidemiological investigations were reported and examined in areas of endemicity even before the true identity of
Cyclospora
was elucidated.
Cyclospora
was fully characterized in the early 1990s, but it was not until the 1995
Cyclospora
outbreak in the United States and Canada that it caught the attention of the public and physicians. The biology, clinical presentation, epidemiology, diagnosis, treatment, and control of cyclosporiasis are reviewed, with a focus on diagnostic assays currently being used for clinical and environmental samples. Challenges and limitations in working with
Cyclospora
are also discussed.