bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparative tissue transcriptomics reveal prompt inter-organ communication in response to local bacterial kidney infection
Authors: Boekel Jorrit , Källskog Örjan , Rydén-Aulin Monica , Rhen Mikael , Richter-Dahlfors Agneta 
Published: February 2011

AbstractBackgroundMucosal infections elicit inflammatory responses via regulated signaling pathways. Infection outcome depends strongly on early events occurring immediately when bacteria start interacting with cells in the mucosal membrane. Hitherto reported transcription profiles on host-pathogen interactions are strongly biased towardsin vitrostudies. To detail the localin vivogenetic response to infection, we here profiled host gene expression in a recent experimental model that assures high spatial and temporal control of uropathogenicEscherichia coli(UPEC) infection within the kidney of a live rat.ResultsTranscriptional profiling of tissue biopsies from UPEC-infected kidney tissue revealed 59 differentially expressed genes 8 h post-infection. Their relevance for the infection process was supported by a Gene Ontology (GO) analysis. Early differential expression at 3 h and 5 h post-infection was of low statistical significance, which correlated to the low degree of infection. Comparative transcriptomics analysis of the 8 h data set and online available studies of early local infection and inflammation defined a core of 80 genes constituting a "General tissue response to early local bacterial infections". Among these, 25% were annotated as interferon-γ (IFN-γ) regulated. Subsequent experimental analyses confirmed a systemic increase of IFN-γ in rats with an ongoing local kidney infection, correlating to splenic, rather than renalIfnginduction and suggested this inter-organ communication to be mediated by interleukin (IL)-23. The use of comparative transcriptomics allowed expansion of the statistical data handling, whereby relevant data could also be extracted from the 5 h data set. Out of the 31 differentially expressed core genes, some represented specific 5 h responses, illustrating the value of comparative transcriptomics when studying the dynamic nature of gene regulation in response to infections.ConclusionOur hypothesis-free approach identified components of infection-associated multi-cellular tissue responses and demonstrated how a comparative analysis allows retrieval of relevant information from lower-quality data sets. The data further define marked representation of IFN-γ responsive genes and a prompt inter-organ communication as a hallmark of an early local tissue response to infection.
Role of a Fur homolog in iron metabolism in Nitrosomonas europaea
Authors: Vajrala Neeraja , Sayavedra-Soto Luis A , Bottomley Peter J , Arp Daniel J 
Published: February 2011

Abstract

Background
In response to environmental iron concentrations, many bacteria coordinately regulate transcription of genes involved in iron acquisition via the ferric uptake regulation (Fur) system. The genome of Nitrosomonas europaea, an ammonia-oxidizing bacterium, carries three genes (NE0616, NE0730 and NE1722) encoding proteins belonging to Fur family.

Results
Of the three N. europaea fur homologs, only the Fur homolog encoded by gene NE0616 complemented the Escherichia coli H1780 fur mutant. A N. europaea fur:kanP mutant strain was created by insertion of kanamycin-resistance cassette in the promoter region of NE0616 fur homolog. The total cellular iron contents of the fur:kanP mutant strain increased by 1.5-fold compared to wild type when grown in Fe-replete media. Relative to the wild type, the fur:kanP mutant exhibited increased sensitivity to iron at or above 500 μM concentrations. Unlike the wild type, the fur:kanP mutant was capable of utilizing iron-bound ferrioxamine without any lag phase and showed over expression of several outer membrane TonB-dependent receptor proteins irrespective of Fe availability.

Conclusions
Our studies have clearly indicated a role in Fe regulation by the Fur protein encoded by N. europaea NE0616 gene. Additional studies are required to fully delineate role of this fur homolog.
In-hospital outcome of patients with culture-confirmed tuberculous pleurisy: clinical impact of pulmonary involvement
Authors: Shu Chin-Chung , Wang Jann-Tay , Wang Jann-Yuan , Lee Li-Na , Yu Chong-Jen 
Published: February 2011

Abstract

Background
Outcomes for hospitalized patients with tuberculous pleurisy (TP) have rarely been reported, and whether or not pulmonary involvement affects outcomes is uncertain. This study aimed to analyze the in-hospital mortality rate of culture-confirmed TP with an emphasis on the clinical impact of pulmonary involvement.

Methods
Patients who were hospitalized for pleural effusion (PE) of unconfirmed diagnosis and finally diagnosed as TP were identified. We classified them according to the disease extent: isolated pleurisy (isolated pleurisy group) and pleurisy with pulmonary involvement (pleuro-pulmonary group).

Results
Among the 205 patients hospitalized before the diagnosis was established, 51 (24.9%) belonged to the isolated pleurisy group. Compared to the pleuro-pulmonary group, patients in the isolated pleurisy group were younger, had fewer underlying co-morbidities, and presented more frequently with fever and chest pain. Fewer patients in the isolated pleurisy group had hypoalbuminemia (< 3.5 g/dL) and anemia. The two groups were similar with regards to PE analysis, resistance pattern, and timing of anti-tuberculous treatment. Patients who had a typical pathology of TP on pleural biopsy received anti-tuberculous treatment earlier than those who did not, and were all alive at discharge. The isolated pleurisy group had a lower in-hospital mortality rate, a shorter length of hospital stay and better short-term survival. In addition, the presence of underlying comorbidities and not receiving anti-tuberculous treatment were associated with a higher in-hospital mortality rate.

Conclusion
In culture-confirmed tuberculous pleurisy, those with pulmonary involvement were associated with a higher in-hospital mortality rate. A typical pathology for TP on pleura biopsy was associated with a better outcome.
Methylenetetrahydrofolate reductase C677T polymorphism in patients with lung cancer in a Korean population
Authors: Cui Lian-Hua , Shin Min-Ho , Kim Hee Nam , Song Hye-Rim , Piao Jin-Mei , Kweon Sun-Seog , Choi Jin-Su , Yun Woo-Jun , Kim Young-Chul , Oh In-Jae , Kim Kyu-Sik 
Published: February 2011

Abstract

Background
This study was designed to investigate an association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and the risk of lung cancer in a Korean population.

Methods
We conducted a large-scale, case-control study involving 3938 patients with newly diagnosed lung cancer and 1700 healthy controls. Genotyping was performed with peripheral blood DNA for MTHFR C677T polymorphisms. Statistical significance was estimated by logistic regression analysis.

Results
The MTHFR C677T frequencies of CC, CT, and TT genotypes were 34.5%, 48.5%, and 17% among lung cancer patients, and 31.8%, 50.7%, and 17.5% in the controls, respectively. The MTHFR 677CT and TT genotype showed a weak protection against lung cancer compared with the homozygous CC genotype, although the results did not reach statistical significance. The age- and gender-adjusted odds ratio (OR) of overall lung cancer was 0.90 (95% confidence interval (CI), 0.77-1.04) for MTHFR 677 CT and 0.88 (95% CI, 0.71-1.07) for MTHFR 677TT. However, after stratification analysis by histological type, the MTHFR 677CT genotype showed a significantly decreased risk for squamous cell carcinoma (age- and gender-adjusted OR, 0.78; 95% CI, 0.64-0.96). The combination of 677 TT homozygous with 677 CT heterozygous also appeared to have a protection effect on the risk of squamous cell carcinoma. We observed no significant interaction between the MTHFR C677T polymorphism and age and gender or smoking habit.

Conclusions
This is the first reported study focusing on the association between MTHFR C677T polymorphisms and the risk of lung cancer in a Korean population. The T allele was found to provide a weak protective association with lung squamous cell carcinoma.
A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation
Authors: Valentine Jane M , Kumar Sonia , Moumen Abdeladim 
Published: February 2011

Abstract

Background
The mammalian DNA-damage response (DDR) has evolved to protect genome stability and maximize cell survival following DNA-damage. One of the key regulators of the DDR is p53, itself tightly regulated by MDM2. Following double-strand DNA breaks (DSBs), mediators including ATM are recruited to the site of DNA-damage. Subsequent phosphorylation of p53 by ATM and ATM-induced CHK2 results in p53 stabilization, ultimately intensifying transcription of p53-responsive genes involved in DNA repair, cell-cycle checkpoint control and apoptosis.

Methods
In the current study, we investigated the stabilization and activation of p53 and associated DDR proteins in response to treatment of human colorectal cancer cells (HCT116p53+/+) with the MDM2 antagonist, Nutlin-3.

Results
Using immunoblotting, Nutlin-3 was observed to stabilize p53, and activate p53 target proteins. Unexpectedly, Nutlin-3 also mediated phosphorylation of p53 at key DNA-damage-specific serine residues (Ser15, 20 and 37). Furthermore, Nutlin-3 induced activation of CHK2 and ATM - proteins required for DNA-damage-dependent phosphorylation and activation of p53, and the phosphorylation of BRCA1 and H2AX - proteins known to be activated specifically in response to DNA damage. Indeed, using immunofluorescent labeling, Nutlin-3 was seen to induce formation of γH2AX foci, an early hallmark of the DDR. Moreover, Nutlin-3 induced phosphorylation of key DDR proteins, initiated cell cycle arrest and led to formation of γH2AX foci in cells lacking p53, whilst γH2AX foci were also noted in MDM2-deficient cells.

Conclusion
To our knowledge, this is the first solid evidence showing a secondary role for Nutlin-3 as a DDR triggering agent, independent of p53 status, and unrelated to its role as an MDM2 antagonist.
Spontaneous hyaline cartilage regeneration can be induced in an osteochondral defect created in the femoral condyle using a novel double-network hydrogel
Authors: Yokota Masashi , Yasuda Kazunori , Kitamura Nobuto , Arakaki Kazunobu , Onodera Shin , Kurokawa Takayuki , Gong Jian-Ping 
Published: February 2011

Abstract

Background
Functional repair of articular osteochondral defects remains a major challenge not only in the field of knee surgery but also in tissue regeneration medicine. The purpose is to clarify whether the spontaneous hyaline cartilage regeneration can be induced in a large osteochondral defect created in the femoral condyle by means of implanting a novel double-network (DN) gel at the bottom of the defect.

Methods
Twenty-five mature rabbits were used in this study. In the bilateral knees of each animal, we created an osteochondral defect having a diameter of 2.4-mm in the medial condyle. Then, in 21 rabbits, we implanted a DN gel plug into a right knee defect so that a vacant space of 1.5-mm depth (in Group I), 2.5-mm depth (in Group II), or 3.5-mm depth (in Group III) was left. In the left knee, we did not apply any treatment to the defect to obtain the control data. All the rabbits were sacrificed at 4 weeks, and the gross and histological evaluations were performed. The remaining 4 rabbits underwent the same treatment as used in Group II, and real-time PCR analysis was performed at 4 weeks.

Results
The defect in Group II was filled with a sufficient volume of the hyaline cartilage tissue rich in proteoglycan and type-2 collagen. The Wayne's gross appearance and histology scores showed that Group II was significantly greater than Group I, III, and Control (p < 0.012). The relative expression level of type-2 collagen, aggrecan, and SOX9 mRNAs was significantly greater in Group II than in the control group (p < 0.023).

Conclusions
This study demonstrated that spontaneous hyaline cartilage regeneration can be induced in vivo in an osteochondral defect created in the femoral condyle by means of implanting the DN gel plug at the bottom of the defect so that an approximately 2-mm deep vacant space was intentionally left in the defect. This fact has prompted us to propose an innovative strategy without cell culture to repair osteochondral lesions in the femoral condyle.
Effects of Green Tea Catechins and Theanine on Preventing Influenza Infection among Healthcare Workers: A Randomized Controlled Trial
Authors: Matsumoto Keiji , Yamada Hiroshi , Takuma Norikata , Niino Hitoshi , Sagesaka Yuko M 
Published: February 2011

Abstract

Background
Experimental studies have revealed that green tea catechins and theanine prevent influenza infection, while the clinical evidence has been inconclusive. This study was conducted to determine whether taking green tea catechins and theanine can clinically prevent influenza infection.

Methods

Design, Setting, and Participants: A randomized, double-blind, placebo-controlled trial of 200 healthcare workers conducted for 5 months from November 9, 2009 to April 8, 2010 in three healthcare facilities for the elderly in Higashimurayama, Japan.

Interventions: The catechin/theanine group received capsules including green tea catechins (378 mg/day) and theanine (210 mg/day). The control group received placebo.

Main Outcome Measures: The primary outcome was the incidence of clinically defined influenza infection. Secondary outcomes were (1) laboratory-confirmed influenza with viral antigen measured by immunochromatographic assay and (2) the time for which the patient was free from clinically defined influenza infection, i.e., the period between the start of intervention and the first diagnosis of influenza infection, based on clinically defined influenza infection.

Results
Eligible healthcare workers (n = 197) were enrolled and randomly assigned to an intervention; 98 were allocated to receive catechin/theanine capsules and 99 to placebo. The incidence of clinically defined influenza infection was significantly lower in the catechin/theanine group (4 participants; 4.1%) compared with the placebo group (13 participants; 13.1%) (adjusted OR, 0.25; 95% CI, 0.07 to 0.76, P = 0.022). The incidence of laboratory-confirmed influenza infection was also lower in the catechin/theanine group (1 participant; 1.0%) than in the placebo group (5 participants; 5.1%), but this difference was not significant (adjusted OR, 0.17; 95% CI, 0.01 to 1.10; P = 0.112). The time for which the patient was free from clinically defined influenza infection was significantly different between the two groups (adjusted HR, 0.27; 95% CI, 0.09 to 0.84; P = 0.023).

Conclusions
Among healthcare workers for the elderly, taking green tea catechins and theanine may be effective prophylaxis for influenza infection.

Trial Registration
ClinicalTrials (NCT): NCT01008020
Pro-inflammatory cytokine/chemokine production by reovirus treated melanoma cells is PKR/NF-κB mediated and supports innate and adaptive anti-tumour immune priming
Authors: Steele Lynette , Errington Fiona , Prestwich Robin , Ilett Elizabeth , Harrington Kevin , Pandha Hardev , Coffey Matt , Selby Peter , Vile Richard , Melcher Alan 
Published: February 2011

Abstract

Background
As well as inducing direct oncolysis, reovirus treatment of melanoma is associated with activation of innate and adaptive anti-tumour immune responses.

Results
Here we characterise the effects of conditioned media from reovirus-infected, dying human melanoma cells (reoTCM), in the absence of live virus, to address the immune bystander potential of reovirus therapy. In addition to RANTES, IL-8, MIP-1α and MIP-1β, reovirus-infected melanoma cells secreted eotaxin, IP-10 and the type 1 interferon IFN-β. To address the mechanisms responsible for the inflammatory composition of reoTCM, we show that IL-8 and IFN-β secretion by reovirus-infected melanoma cells was associated with activation of NF-κB and decreased by pre-treatment with small molecule inhibitors of NF-κB and PKR; specific siRNA-mediated knockdown further confirmed a role for PKR. This pro-inflammatory milieu induced a chemotactic response in isolated natural killer (NK) cells, dendritic cells (DC) and anti-melanoma cytotoxic T cells (CTL). Following culture in reoTCM, NK cells upregulated CD69 expression and acquired greater lytic potential against tumour targets. Furthermore, melanoma cell-loaded DC cultured in reoTCM were more effective at priming adaptive anti-tumour immunity.

Conclusions
These data demonstrate that the PKR- and NF-κB-dependent induction of pro-inflammatory molecules that accompanies reovirus-mediated killing can recruit and activate innate and adaptive effector cells, thus potentially altering the tumour microenvironment to support bystander immune-mediated therapy as well as direct viral oncolysis.
Nanoscaled carborane ruthenium(II)-arene complex inducing lung cancer cells apoptosis
Authors: Zhang Gen , Wu Chunhui , Ye Hongde , Yan Hong , Wang Xuemei 
Published: February 2011

Abstract

Background
The new ruthenium(II)-arene complex, which bearing a carborane unit, ruthenium and ferrocenyl functional groups, has a novel versatile synthetic chemistry and unique properties of the respective material at the nanoscale level. The ruthenium(II)-arene complex shows significant cytotoxicity to cancer cells and tumor-inhibiting properties. However, ruthenium(II)-arene complex of mechanism of anticancer activity are scarcely explored. Therefore, it is necessary to explore ruthenium(II)-arene complex mechanism of anticancer activity for application in this area.

Results
In this study, the ruthenium(II)-arene complex could significantly induce apoptosis in human lung cancer HCC827 cell line. At the concentration range of 5 μM-100 μM, ruthenium(II)-arene complex had obvious cell cytotoxicity effect on HCC827 cells with IC50 values ranging 19.6 ± 5.3 μM. Additionally, our observations demonstrate that the ruthenium(II)-arene complex can readily induce apoptosis in HCC827 cells, as evidenced by Annexin-V-FITC, nuclear fragmentation as well as DNA fragmentation. Treatment of HCC827 cells with the ruthenium(II)-arene complex resulted in dose-dependent cell apoptosis as indicated by high cleaved Caspase-8,9 ratio. Besides ruthenium(II)-arene complex caused a rapid induction of cleaved Caspase-3 activity and stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP) in vitro and in vivo.

Conclusion
In this study, the ruthenium(II)-arene complex could significantly induce apoptosis in human lung cancer HCC827 cell line. Treatment of HCC827 cells with the ruthenium(II)-arene complex resulted in dose-dependent cell apoptosis as indicated by high cleaved Caspase-8,9 ratio. Besides ruthenium(II)-arene complex caused a rapid induction of cleaved Caspase-3 activity and stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP) in vitro and in vivo. Our results suggest that ruthenium(II)-arene complex could be a candidate for further evaluation as a chemotherapeutic agent for human cancers, especially lung cancer.
Mono- and bi-functional arenethiols as surfactants for gold nanoparticles: synthesis and characterization
Authors: Vitale Floriana , Fratoddi Ilaria , Battocchio Chiara , Piscopiello Emanuela , Tapfer Leander , Russo Maria Vittoria , Polzonetti Giovanni , Giannini Cinzia 
Published: February 2011

AbstractStable gold nanoparticles stabilized by different mono and bi-functional arenethiols, namely, benzylthiol and 1,4-benzenedimethanethiol, have been prepared by using a modified Brust's two-phase synthesis. The size, shape, and crystalline structure of the gold nanoparticles have been determined by high-resolution electron microscopy and full-pattern X-ray powder diffraction analyses. Nanocrystals diameters have been tuned in the range 2 ÷ 9 nm by a proper variation of Au/S molar ratio. The chemical composition of gold nanoparticles and their interaction with thiols have been investigated by X-ray photoelectron spectroscopy. In particular, the formation of networks has been observed with interconnected gold nanoparticles containing 1,4-benzenedimethanethiol as ligand.
Advanced materials nanocharacterization
Authors: Giannazzo Filippo , Eyben Pierre , Baranowski Jacek , Camassel Jean , Lányi Stefan 
Published: February 2011

AbstractThis special issue of Nanoscale Research Letters contains scientific contributions presented at the Symposium D "Multidimensional Electrical and Chemical Characterization at the Nanometer-scale of Organic and Inorganic Semiconductors" of the E-MRS Fall Meeting 2010, which was held in Warsaw, Poland from 13th to 17th September, 2010.
Fabrication of ordered nanoporous anodic alumina prepatterned by mold-assisted chemical etching
Authors: Lai Kuan-Liang , Hon Min-Hsiung , Leu Ing-Chi 
Published: February 2011

AbstractIn this article, a simple and cost-effective method to create patterned nanoindentations on Al surface via mold-assisted chemical etching process is demonstrated. This report shows the reaction-diffusion method which formed nanoscale shallow etch pits by the absorption/liberation behaviors of chemical etchant in poly(dimethylsiloxane) stamp. During subsequent anodization, it was possible to obtain the ordered nanopore arrays with 277 nm pitch that were guided by the prepatterned etch pits. The prepatterned etch pits obtained can guide the growth of AAO nanopores during anodization and facilitate the preparation of ordered nanopore arrays.
Spinal Toll like Receptor 3 is Involved in Chronic Pancreatitis-Induced Mechanical Allodynia of Rat
Authors: Qian Nian-Song , Liao Yong-Hui , Feng Quan-Xing , Tang Yu , Dou Ke-Feng , Tao Kai-Shan 
Published: February 2011

Background: Mechanisms underlying pain in chronic pancreatitis (CP) are incompletely understood. Our previous data showed that astrocytes were actively involved. However, it was unclear how astrocytic activation was induced in CP conditions. In the present study, we hypothesized that toll-like receptors (TLRs) were involved in astrocytic activation and pain behavior in CP-induced pain. Results: To test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Western blot showed that after TNBS infusion, TLR3, but not TLR2 or TLR4, was increased gradually and maintained at a very high level for up to 5 w, which correlated with the changing course of mechanical allodynia. Double immunostaining suggested that TLR3 was highly expressed on astrocytes. Infusion with TLR3 antisense oligodeoxynucleotide (ASO) dose-dependently attenuated CP-induced allodynia. CP-induced astrocytic activation in the spinal cord was also significantly suppressed by TLR3 ASO. Furthermore, real-time PCR showed that IL-1β, TNF-α, IL-6 and monocyte chemotactic protein-1 (MCP-1) were significantly increased in spinal cord of pancreatic rats. In addition, TLR3 ASO significantly attenuated CP-induced up-regulation of IL-1β and MCP-1. Conclusions: These results suggest a probable “TLR3-astrocytes-IL-1β/MCP-1“ pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients.