bluuebunny/crossref_metadata_2025_split huggingface dataset:
A population-based study examining the emergence of community-associated methicillin-resistant Staphylococcus aureus USA300 in New York City
Authors: Bratu Simona , Landman David , Gupta Jyoti , Trehan Manoj , Panwar Monica , Quale John 
Published: November 2006

Abstract

Background
Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is a serious pathogen in several regions in the United States. It is unclear which populations are at high risk for the emergence of these strains.

Methods
All unique patient isolates of S. aureus were collected from hospitals in Brooklyn, NY over a three-month period. Isolates of MRSA that were susceptible to clindamycin underwent SCCmec typing. Isolates with the SCCmec type IV (characteristic of CA-MRSA strains) underwent ribotyping. Demographic information involving the neighborhoods of Brooklyn was also gathered and correlated with the prevalence of CA-MRSA strains.

Results
Of 1316 isolates collected during the surveillance, 217 were MRSA susceptible to clindamycin. A total of 125 isolates possessed SCCmec type IV; 72 belonged to the USA300 strain and five belonged to the USA400 strain. Hospitals in the eastern part of the city had the highest prevalence of USA300 strain. Individuals in the eastern region, when compared to the western region, were more likely to be Black, Hispanic, female, and < 18 years of age, and to have households of ≥ 3 persons. In addition, the median household income was lower, and the proportion of individuals on public assistance was higher, for the population in the eastern region.

Conclusion
The USA300 strain of CA-MRSA is emerging in New York City. In this population-based study, urban regions of lower socioeconomic status and with evidence of overcrowding appear to be at higher risk for the emergence of this pathogen.
Cerebral edema in a patient following cytoreductive surgery and hyperthermic intraoperative intraperitoneal chemoperfusion
Authors: Nair Rajalakshmi L , Tobias Jonathan , Stemmerman Grant , Lowy Andrew M 
Published: November 2006

Abstract

Background
Cytoreductive surgery and intraoperative, intraperitoneal hyperthermic chemoperfusion (HIPEC) is increasingly used to treat peritoneal surface metastases. We describe a fatal case of cerebral edema in a patient with appendiceal carcinoma and an underlying seizure disorder who underwent cytoreductive surgery and HIPEC.

Case presentation
A case of fatal postoperative cerebral edema is presented in a patient with an underlying seizure disorder and recurrent mucinous adenocarcinoma of the appendix. The patient was treated with cytoreductive surgery and intraoperative intraperitoneal hyperthermic chemoperfusion. The details and implications of this complication are discussed.

Conclusion
The recognition of this potential complication is important for physicians performing cytoreductive surgery and HIPEC. Special caution should be taken when patients with seizure disorders are being considered for this treatment.
Atlas of Salivary Gland Tumor Cytopathology, Oral & Surgical Pathology - CD-ROM Disk 2: by Kini S. & Dardick I. Pathology Images Inc, 2006
Authors: Basir Zainab 
Published: November 2006

This CD-ROM version of Atlas of Salivary Gland Tumor Cytopathology, Oral & Surgical Pathology is an excellent and concise tool for easy reference during sign out of cytology and surgical cases. It is also invaluable as a teaching tool for residents and fellows.
Atlas of Salivary Gland Tumor Cytopathology, Oral & Surgical Pathology CD-ROM (ISBN 0-9736518-0-7), Published by Pathology images Inc Ottawa, Ontario K2B 7L4, Canada
Single-Walled Carbon Nanotube (SWCNT)-induced interstitial fibrosis in the lungs of rats is associated with increased levels of PDGF mRNA and the formation of unique intercellular carbon structures that bridge alveolar macrophages In Situ
Authors: Mangum James B , Turpin Elizabeth A , Antao-Menezes Aurita , Cesta Mark F , Bermudez Edilberto , Bonner James C 
Published: November 2006

Abstract

Background
Nanotechnology is a rapidly advancing industry with many new products already available to the public. Therefore, it is essential to gain an understanding of the possible health risks associated with exposure to nanomaterials and to identify biomarkers of exposure. In this study, we investigated the fibrogenic potential of SWCNT synthesized by chemical vapor deposition using cobalt (Co) and molybdenum (Mo) as catalysts. Following a single oropharyngeal aspiration of SWCNT in rats, we evaluated lung histopathology, cell proliferation, and growth factor mRNAs at 1 and 21 days post-exposure. Comparisons were made to vehicle alone (saline containing a biocompatible nonionic surfactant), inert carbon black (CB) nanoparticles, or vanadium pentoxide (V2O5) as a known inducer of fibrosis.

Results
SWCNT or CB caused no overt inflammatory response at 1 or 21 days post-exposure as determined by histopathology and evaluation of cells (>95% macrophages) in bronchoalveolar lavage (BAL) fluid. However, SWCNT induced the formation of small, focal interstitial fibrotic lesions within the alveolar region of the lung at 21 days. A small fraction of alveolar macrophages harvested by BAL from the lungs of SWCNT-exposed rats at 21 days were bridged by unique intercellular carbon structures that extended into the cytoplasm of each macrophage. These "carbon bridge" structures between macrophages were also observed in situ in the lungs of SWCNT-exposed rats. No carbon bridges were observed in CB-exposed rats. SWCNT caused cell proliferation only at sites of fibrotic lesion formation as measured by bromodeoxyuridine uptake into alveolar cells. SWCNT increased platelet-derived growth factor (PDGF)-A, PDGF-B, and PDGF-C mRNA levels significantly at 1 day as measured by Taqman quantitative real-time RT-PCR. At 21 days, SWCNT did not increase any mRNAs evaluated, while V2O5 significantly increased mRNAs encoding PDGF-A, -B, and -C chains, PDGF-Rα, osteopontin (OPN), connective tissue growth factor (CTGF), and transforming growth factor (TGF)-β1.

Conclusion
Our findings indicate that SWCNT do not cause lung inflammation and yet induce the formation of small, focal interstital fibrotic lesioins in the alveolar region of the lungs of rats. Of greatest interest was the discovery of unique intercellular carbon structures composed of SWCNT that bridged lung macrophages. These "carbon bridges" offer a novel and easily identifiable biomarker of exposure.
Association study of the vesicular monoamine transporter 1 (VMAT1) gene with schizophrenia in a Japanese population
Authors: Richards Misty , Iijima Yoshimi , Kondo Hitomi , Shizuno Tomoko , Hori Hiroaki , Arima Kunimasa , Saitoh Osamu , Kunugi Hiroshi 
Published: November 2006

Abstract

Background
Vesicular monoamine transporters (VMATs) mediate accumulation of monoamines such as serotonin, dopamine, adrenaline, and noradrenaline from the cytoplasm into storage organelles. The VMAT1 (alternatively solute carrier family 18: SLC18A1) regulates such biogenic amines in neuroendocrine systems. The VMAT1 gene maps to chromosome 8p21.3, a locus with strong evidence of linkage with schizophrenia. A recent study reported that a non-synonymous single nucleotide polymorphism (SNP) of the gene (Pro4Thr) was associated with schizophrenia.

Methods
We attempted to replicate this finding in a Japanese sample of 354 schizophrenics and 365 controls. In addition, we examined 3 other non-synonymous SNPs (Thr98Ser, Thr136Ile, and Val392Leu). Genotyping was performed by the TaqMan allelic discrimination assay.

Results
There was no significant difference in genotype or allele distribution of the three SNPs of Pro4Thr, Thr136Ile, or Val392Leu between patients and controls. There was, however, a significant difference in genotype and allele distributions for the Thr98Ser polymorphism between the two groups (P = 0.01 for genotype and allele). When sexes were examined separately, significant differences were observed in females (P = 0.006 for genotype, P = 0.003 for allele), but not in males. The Thr98 allele was more common in female patients than in female controls (odds ratio 1.69, 95% CI 1.19–2.40, P = 0.003). Haplotype-based analyses also provided evidence for a significant association in females.

Conclusion
We failed to replicate the previously reported association of Pro4Thr of the VMAT1 gene with schizophrenia. However, we obtained evidence for a possible role of the Thr98Ser in giving susceptibility to schizophrenia in women.
Characterization of ovine hepatic gene expression profiles in response to Escherichia coli lipopolysaccharide using a bovine cDNA microarray
Authors: Cao Honghe , Kabaroff Leah C , You Qiumei , Rodriguez Alexander , Boermans Herman J , Karrow Niel A 
Published: November 2006

AbstractBackgroundDuring systemic gram-negative bacterial infections, lipopolysaccharide (LPS) ligation to the hepatic Toll-like receptor-4 complex induces the production of hepatic acute phase proteins that are involved in the host response to infection and limit the associated inflammatory process. Identifying the genes that regulate this hepatic response to LPS in ruminants may provide insight into the pathogenesis of bacterial diseases and eventually facilitate breeding of more disease resistant animals. The objective of this research was to profile the expression of ovine hepatic genes in response toEscherichia coliLPS challenge (0, 200, 400 ng/kg) using a bovine cDNA microarray and quantitative real-time PCR (qRT-PCR).ResultsTwelve yearling ewes were challengedivwithE. coliLPS (0, 200, 400 ng/kg) and liver biopsies were collected 4–5 hours post-challenge to assess hepatic gene expression profiles by bovine cDNA microarray and qRT-PCR analyses. The expression ofCD14,C3,IL12R, NRAMP1,SODandIGFBP3genes was down regulated, whereas the expression ofACTHR,IFNαR,CD1,MCP-1andGHwas increased during LPS challenge. With the exception of C3, qRT-PCR analysis of 7 of these genes confirmed the microarray results and demonstrated that GAPDH is not a suitable housekeeping gene in LPS challenged sheep.ConclusionWe have identified several potentially important genes by bovine cDNA microarray and qRT-PCR analyses that are differentially expressed during the ovine hepatic response to systemic LPS challenge. Their potential role in regulating the inflammatory response to LPS warrants further investigation.
Viral and Bacterial Pathogens in Bovine Respiratory Disease in Finland
Authors: Härtel H , Nikunen S , Neuvonen E , Tanskanen R , Kivelä S-L , Aho P , Soveri T , Saloniemi H 
Published: November 2006

AbstractPathogens causing bovine respiratory tract disease in Finland were investigated. Eighteen cattle herds with bovine respiratory disease were included. Five diseased calves from each farm were chosen for closer examination and tracheobronchial lavage. Blood samples were taken from the calves at the time of the investigation and from 86 calves 3–4 weeks later. In addition, 6–10 blood samples from animals of different ages were collected from each herd, resulting in 169 samples. Serum samples were tested for antibodies to bovine parainfluenza virus-3 (PIV-3), bovine respiratory syncytial virus (BRSV), bovine coronavirus (BCV), bovine adenovirus-3 (BAV-3) and bovine adenovirus-7 (BAV-7). About one third of the samples were also tested for antibodies to bovine virus diarrhoea virus (BVDV) with negative results. Bacteria were cultured from lavage fluid and in vitro susceptibility to selected antimicrobials was tested. According to serological findings, PIV-3, BAV-7, BAV-3, BCV and BRSV are common pathogens in Finnish cattle with respiratory problems. A titre rise especially for BAV-7 and BAV-3, the dual growth ofMycoplasma disparandPasteurella multocida, were typical findings in diseased calves.Pasteurellasp. strains showed no resistance to tested antimicrobials.Mycoplasma bovisandMannheimia haemolyticawere not found.
Effect of infliximab on mRNA expression profiles in synovial tissue of rheumatoid arthritis patients
Authors: Lindberg Johan , af Klint Erik , Catrina Anca Irinel , Nilsson Peter , Klareskog Lars , Ulfgren Ann-Kristin , Lundeberg Joakim 
Published: November 2006

AbstractWe examined the gene expression profiles in arthroscopic biopsies retrieved from 10 rheumatoid arthritis patients before and after anti-TNF treatment with infliximab to investigate whether such profiles can be used to predict responses to the therapy, and to study effects of the therapy on the profiles. Responses to treatment were assessed using European League Against Rheumatism response criteria. Three patients were found to be good responders, five patients to be moderate responders and two patients to be nonresponders. The TNF-α status of the biopsies from each of the patients before treatment was also investigated immunohistochemically, and it was detected in biopsies from four of the patients, including all three of the good responders. The gene expression data demonstrate that all patients had unique gene expression signatures, with low intrapatient variability between biopsies. The data also revealed significant differences between the good responding and nonresponding patients (279 differentially expressed genes were detected, with a false discovery rate < 0.025). Among the identified genes we found that MMP-3 was significantly upregulated in good responders (log2 fold change, 2.95) compared with nonresponders, providing further support for the potential of MMP-3 as a marker for good responses to therapy. An even more extensive list of 685 significantly differentially expressed genes was found between patients in whom TNF-α was found and nonresponders, indicating that TNF-α could be an important biomarker for successful infliximab treatment. Significant differences were also observed between biopsies taken before and after anti-TNF treatment, including 115 differentially expressed genes in the good responding group. Interestingly, the effect was even stronger in the group in which TNF-α was immunohistochemically detected before therapy. Here, 1,058 genes were differentially expressed, including many that were novel in this context (for example, CXCL3 and CXCL14). Subsequent Gene Ontology analysis revealed that several 'themes' were significantly over-represented that are known to be affected by anti-TNF treatment in inflammatory tissue; for example, immune response (GO:0006955), cell communication (GO:0007154), signal transduction (GO:0007165) and chemotaxis (GO:0006935). No genes reached statistical significance in the moderately responding or nonresponding groups. In conclusion, this pilot study suggests that further investigation is warranted on the usefulness of gene expression profiling of synovial tissue to predict and monitor the outcome of rheumatoid arthritis therapies.
Genome-wide identification of functionally distinct subsets of cellular mRNAs associated with two nucleocytoplasmic-shuttling mammalian splicing factors
Authors: Gama-Carvalho Margarida , Barbosa-Morais Nuno L , Brodsky Alexander S , Silver Pamela A , Carmo-Fonseca Maria 
Published: November 2006

Abstract
Background
Pre-mRNA splicing is an essential step in gene expression that occurs co-transcriptionally in the cell nucleus, involving a large number of RNA binding protein splicing factors, in addition to core spliceosome components. Several of these proteins are required for the recognition of intronic sequence elements, transiently associating with the primary transcript during splicing. Some protein splicing factors, such as the U2 small nuclear RNP auxiliary factor (U2AF), are known to be exported to the cytoplasm, despite being implicated solely in nuclear functions. This observation raises the question of whether U2AF associates with mature mRNA-ribonucleoprotein particles in transit to the cytoplasm, participating in additional cellular functions.

Results
Here we report the identification of RNAs immunoprecipitated by a monoclonal antibody specific for the U2AF 65 kDa subunit (U2AF65) and demonstrate its association with spliced mRNAs. For comparison, we analyzed mRNAs associated with the polypyrimidine tract binding protein (PTB), a splicing factor that also binds to intronic pyrimidine-rich sequences but additionally participates in mRNA localization, stability, and translation. Our results show that 10% of cellular mRNAs expressed in HeLa cells associate differentially with U2AF65 and PTB. Among U2AF65-associated mRNAs there is a predominance of transcription factors and cell cycle regulators, whereas PTB-associated transcripts are enriched in mRNA species that encode proteins implicated in intracellular transport, vesicle trafficking, and apoptosis.

Conclusion
Our results show that U2AF65 associates with specific subsets of spliced mRNAs, strongly suggesting that it is involved in novel cellular functions in addition to splicing.
MCP-1 deficiency causes altered inflammation with impaired skeletal muscle regeneration
Authors: Shireman Paula K , Contreras-Shannon Verónica , Ochoa Oscar , Karia Bijal P , Michalek Joel E , McManus Linda M 
Published: November 2006

AbstractWe examined the role of MCP-1, a potent chemotactic and activating factor for macrophages, in perfusion, inflammation, and skeletal muscle regeneration post-ischemic injury. MCP-1−/− or C57Bl/6J control mice [wild-type (WT)] underwent femoral artery excision (FAE). Muscles were collected for histology, assessment of tissue chemokines, and activity measurements of lactate dehydrogenase (LDH) and myeloperoxidase. In MCP-1−/− mice, restoration of perfusion was delayed, and LDH and fiber size, indicators of muscle regeneration, were decreased. Altered inflammation was observed with increased neutrophil accumulation in MCP-1−/− versus WT mice at Days 1 and 3 (P≤0.003), whereas fewer macrophages were present in MCP-1−/− mice at Day 3. As necrotic tissue was removed in WT mice, macrophages decreased (Day 7). In contrast, macrophage accumulation in MCP-1−/− was increased in association with residual necrotic tissue and impaired muscle regeneration. Consistent with altered inflammation, neutrophil chemotactic factors (keratinocyte-derived chemokine and macrophage inflammatory protein-2) were increased at Day 1 post-FAE. The macrophage chemotactic factor MCP-5 was increased significantly in WT mice at Day 3 compared with MCP-1−/− mice. However, at post-FAE Day 7, MCP-5 was significantly elevated in MCP-1−/− mice versus WT mice. Addition of exogenous MCP-1 did not induce proliferation in murine myoblasts (C2C12 cells) in vitro. MCP-1 is essential for reperfusion and the successful completion of normal skeletal muscle regeneration after ischemic tissue injury. Impaired muscle regeneration in MCP-1−/− mice suggests an important role for macrophages and MCP-1 in tissue reparative processes.
Prostaglandin I2 analogs inhibit Th1 and Th2 effector cytokine production by CD4 T cells
Authors: Zhou Weisong , Blackwell Timothy S , Goleniewska Kasia , O’Neal Jamye F , FitzGerald Garret A , Lucitt Margaret , Breyer Richard M , Peebles R Stokes 
Published: November 2006

AbstractAn anti-inflammatory effect of PGI2 has been suggested by increased inflammation in mice that are deficient in the PGI2 receptor (IP) or in respiratory syncytial viral- or OVA-induced CD4 T cell-associated responses. To determine the mechanism of the anti-inflammatory effect, we hypothesized that PGI2 analogs inhibit CD4 T cell effector cytokine production. To test this hypothesis, we activated purified CD4 T cells with anti-CD3 and anti-CD28 antibodies under Th1 and Th2 polarizing conditions for 4 days and restimulated the T cells with anti-CD3 in the presence of PGI2 analogs for 2 days. We found that PGI2 analogs (cicaprost and iloprost) inhibited the production of Th1 cytokines (IFN-γ) and Th2 cytokines (IL-4, IL-10, and IL-13) in a dose-dependent pattern. The inhibitory effect was partially dependent on the IP receptor signaling and was correlated with elevated intracellular cAMP and down-regulated NF-κB activity. Pretreatment of the CD4 T cells with 8-bromoadenosine-3′,5′-cyclic monophosphorothioate, Rp-isomer, to inhibit a key signaling molecule in the cAMP pathway, protein kinase A (PKA), attenuated the suppressive effect of PGI2 analogs significantly, suggesting that PKA, in part, mediates the inhibition of the cytokine production. These data indicate that PGI2 analogs have an immune-suppressive effect on previously activated and differentiated CD4 T cells in vitro and suggest that PGI2 may have a similar function in vivo.
Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1
Authors: Tang Daolin , Shi Yongzhong , Kang Rui , Li Tong , Xiao Weimin , Wang Haichao , Xiao Xianzhong 
Published: November 2006

AbstractHigh mobility group box 1 (HMGB1) can be actively secreted by macrophages/monocytes in response to exogenous and endogenous inflammatory stimuli (such as bacterial endotoxin, TNF-α, IL-1, and IFN-γ) or passively released by necrotic cells and mediates innate and adaptive inflammatory responses to infection and injury. Here, we demonstrated that a reactive oxygen species, hydrogen peroxide (H2O2), induces active and passive HMGB1 release from macrophage and monocyte cultures in a time- and dose-dependent manner. At nontoxic doses (e.g., 0.0125–0.125 mM), H2O2 induced HMGB1 cytoplasmic translocation and active release within 3–24 h. At higher concentrations (e.g., 0.25 mM), however, H2O2 exhibited cytotoxicity to macrophage and monocyte cell cultures and consequently, triggered active and passive HMGB1 release. In addition, H2O2 stimulated potential interaction of HMGB1 with a nuclear export factor, chromosome region maintenance (CRM1), in macrophage/monocyte cultures. Inhibitors specific for the JNK (SP600125) and MEK (PD98059), but not p38 MAPK (SB203580), abrogated H2O2-induced, active HMGB1 release. Together, these data establish an important role for oxidative stress in inducing active HMGB1 release, potentially through a MAPK- and CRM1-dependent mechanism.
Treatment options in moderate and severe depression: decision
analysis supporting a clinical guideline
Authors: Simon Judit , Pilling Stephen , Burbeck Rachel , Goldberg David 
Published: November 2006

BackgroundTreatment options for depression include antidepressants, psychological
therapy and a combination of the two.AimsTo develop cost-effective clinical guidelines.MethodSystematic literature reviews were used to identify clinical, utility and
cost data. A decision analysis was then conducted to compare the benefits
and costs of antidepressants with combination therapy for moderate and
severe depression in secondary care in the UK.ResultsOver the 15-month analysis period, combination therapy resulted in higher
costs and an expected 0.16 increase per person in the probability of
remission and no relapse compared with antidepressants. The cost per
additional successfully treated patient was £4056 (95% CI 1400–18 300);
the cost per quality-adjusted life year gained was £5777 (95% CI 1900–33
800) for severe depression and £14 540 (95% CI 4800–79 400) for moderate
depression.ConclusionsCombination therapy is likely to be a cost-effective first-line secondary
care treatment for severe depression. Its cost-effectiveness for moderate
depression is more uncertain from current evidence. Targeted combination
therapy could improve resource utilisation.