bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ecological proportion of indigenous bacterial populations in saliva is correlated with oral health status
Authors: Takeshita Toru , Nakano Yoshio , Kumagai Takashi , Yasui Masaki , Kamio Noriaki , Shibata Yukie , Shiota Susumu , Yamashita Yoshihisa 
Published: October 2008

Abstract
To obtain deeper insights into the etiology of oral disease, an understanding of the composition of the surrounding bacterial environments that lead to health or disease is required, which is attracting increasing attention. In this study, the bacterial compositions in the saliva of 200 subjects aged 15–40 years were depicted as peak patterns by terminal restriction fragment length polymorphism (T-RFLP) analysis of 16S rRNA genes. The subjects were classified into three clusters by partitioning around medoids clustering based on their T-RFLP profiles, and the clinical oral health parameters of the clusters were compared. The clustering of the T-RFLP profiles in this study was mainly based on differences in the abundance distribution of the dominant terminal restriction fragments (TRFs) detected in most of the subjects. Predicted from the sizes of the TRFs, the characteristically more predominant members of each were Prevotella and Veillonella species in cluster I; Streptococcus species in cluster II and Neisseria, Haemophilus or Aggregatibacter species and Porphyromonas species in cluster III. The parameters associated with periodontal disease were significantly different among the clusters. Clusters I and II had a higher percentage of sites of periodontal pockets greater than 4 mm than cluster III, and cluster I contained sites exhibiting bleeding on probing more often than cluster II or III; no significant differences were observed in other parameters. These results suggest that the abundance distribution of commensal bacteria in saliva is correlated with periodontal health, and might be involved in the susceptibility of an individual to periodontal disease.
Activation of a nuclear-localized SIPK in tobacco cells challenged by cryptogein, an elicitor of plant defence reactions
Authors: Dahan Jennifer , Pichereaux Carole , Rossignol Michel , Blanc Sabrina , Wendehenne David , Pugin Alain , Bourque Stéphane 
Published: October 2008

When a plant cell is challenged by a well-defined stimulus, complex signal transduction pathways are activated to promote the modulation of specific sets of genes and eventually to develop adaptive responses. In this context, protein phosphorylation plays a fundamental role through the activation of multiple protein kinase families. Although the involvement of protein kinases at the plasma membrane and cytosolic levels are now well-documented, their nuclear counterparts are still poorly investigated. In the field of plant defence reactions, no known study has yet reported the activation of a nuclear protein kinase and/or its nuclear activity in plant cells, although some protein kinases, e.g. MAPK (mitogen-activated protein kinase), are known to be translocated into the nucleus. In the present study, we investigated the ability of cryptogein, a proteinaceous elicitor of tobacco defence reactions, to induce different nuclear protein kinase activities. We found that at least four nuclear protein kinases are activated in response to cryptogein treatment in a time-dependent manner, some of them exhibiting Ca2+-dependent activity. The present study focused on one 47 kDa protein kinase with a Ca2+-independent activity, closely related to the MAPK family. After purification and microsequencing, this protein kinase was formally identified as SIPK (salicyclic acid-induced protein kinase), a biotic and abiotic stress-activated MAPK of tobacco. We also showed that cytosolic activation of SIPK is not sufficient to promote a nuclear SIPK activity, the latter being correlated with cell death. In that way, the present study provides evidence of a functional nuclear MAPK activity involved in response to an elicitor treatment.
ERRATUM: “MEETING THE COOL NEIGHBORS. X. ULTRACOOL DWARFS FROM THE 2MASS ALL-SKY DATA RELEASE” (2008, AJ, 136, 1290)
Authors: Reid I. Neill , Cruz Kelle L. , Kirkpatrick J. Davy , Allen Peter R. , Mungall F. , Liebert James , Lowrance Patrick , Sweet Anne 
Published: October 2008

IOP Publishing sincerely regrets that an error was made in the acknowledgements section of this article. This has been amended in the online journal and the corrected text is reproduced below.The NStars research described in this paper was partially supported by a grant awarded as part of the NASA Space Interferometry Mission Science Program, administered by the Jet Propulsion Laboratory, Pasadena. Support for K.L.C. is provided by NASA through theSpitzer Space TelescopeFellowship Program, through a contract issued by the Jet Propulsion Laboratory, California Institute of Technology under a contract with NASA. P.R.A. acknowledges support from grant NAG5-11627 to Kevin Luhman from the NASA Long-Term Space Astrophysics program. This publication makes use of data products from the Two Micron All Sky Survey (2MASS), which is a joint project of the University of Massachusetts and the Infrared Processing and Analysis Center/California Institute of Technology, funded by NASA and the National Science Foundation. We acknowledge use of the NASA/IPAC Infrared Source Archive (IRSA), which is operated by the Jet Propulsion Laboratory, California Institute of Technology, under contract with NASA. We also acknowledge making extensive use of the SIMBAD database, maintained by Strasbourg Observatory, and of the ADS bibliographic service. This research has made extensive use of the M-, L-, and T-dwarf compendium housed at DwarfArchives.org and maintained by Chris Gelino, Davy Kirkpatrick, and Adam Burgasser. This program has also profited from extensive allocations of telescope time at both Kitt Peak Observatory and Cerro Tololo Inter-American Observatory (CTIO). We thank the National Optical Astronomy Observatory (NOAO) Telescope Allocation Committees for their support of this project and acknowledge the courteous and efficient assistance of the technical support staff: John Glaspey, Darryl Willmarth, Diane Harmer, Bill Gillespie, Hillary Mathis, and Hal Halbedel at KPNO, and Alberto Alvarez, Angel Guerra, and Patricio Ugarte at CTIO.We apologize to the authors of the article and to readers of the journal for this unfortunate error.
Lipophilic and Stereospecific Interactions of Amino-amide Local Anesthetics with Human Kv1.1 Channels
Authors: Punke Mark A. , Friederich Patrick 
Published: October 2008

Background
This study's aim was to investigate the interaction of amino-amide local anesthetics with human Kv1.1 potassium channels. These channels were chosen because of their proven physiologic role. By using a homolog series of local anesthetics with different lengths of the N-substituent, it was intended to elucidate the role of lipophilic interactions with Kv1.1. The use of stereoisomers allowed testing of the role of polar drug actions.

Methods
Human Kv1.1 channels were measured with the patch clamp technique. Concentration-response data were described by Hill functions. Gating changes were described by Boltzmann functions.

Results
Inhibition of Kv1.1 channels by dextrobupivacaine, bupivacaine, levobupivacaine, dextroropivacaine, levoropivacaine, and mepivacaine was concentration dependent, reversible, stereoselective, voltage dependent, and frequency independent. The IC(50) values were (mean +/- SEM) 41 +/- 3 microm (n = 20), 56 +/- 3 microm (n = 26), 76 +/- 8 microm (n = 24), 135 +/- 29 microm (n = 23), 313 +/- 32 microm (n = 25), and 1,451 +/- 351 microm (n = 23), respectively. The midpoint of current activation was shifted into the hyperpolarizing direction. The inhibitory potency as well as the potency to induce gating changes correlated with the number of CH(2) groups in the side chain of the drugs (r > 0.9, P < 0.05).

Conclusions
Kv1.1 channels constitute an important biophysical model for elucidating molecular mechanisms underlying local anesthetic drug effects. Inhibition likely results from an open state-dependent blocking mechanism. Interaction of local anesthetics with the ion channel protein is determined by lipophilic drug properties.
Helium-induced Preconditioning in Young and Old Rat Heart
Authors: Heinen Andre , Huhn Ragnar , Smeele Kirsten M. A. , Zuurbier Coert J. , Schlack Wolfgang , Preckel Benedikt , Weber Nina C. , Hollmann Markus W. 
Published: October 2008

Background
The noble gas helium induces cardiac preconditioning. Whether activation of mitochondrial K(+) channels is involved in helium preconditioning (He-PC) is unknown. The authors investigated whether He-PC (1) is mediated by activation of Ca(2+) -sensitive potassium channels, (2) results in mitochondrial uncoupling, and (3) is age dependent.

Methods
Anesthetized Wistar rats were randomly assigned to six groups (n = 10 each). Young (2-3 months) control (Con) and aged (22-24 months) control animals (Age Con) were not treated further. Preconditioning groups (He-PC and Age He-PC) inhaled 70% helium for 3 x 5 min. The Ca(2+) -sensitive potassium channel blocker iberiotoxin was administered in young animals, with and without helium (He-PC+Ibtx and Ibtx). Animals underwent 25 min of regional myocardial ischemia and 120 min of reperfusion. In additional experiments, cardiac mitochondria were isolated, and the respiratory control index was calculated (state 3/state 4).

Results
Helium reduced infarct size in young rats from 61 +/- 7% to 36 +/- 14% (P < 0.05 vs. Con). Infarct size reduction was abolished by iberiotoxin (60 +/- 11%; P < 0.05 vs. He-PC), whereas iberiotoxin alone had no effect (59 +/- 8%; not significant vs. Con). In aged animals, helium had no effect on infarct size (Age Con: 59 +/- 7% vs. Age He-PC: 58 +/- 8%; not significant). Helium reduced respiratory control index in young animals (2.76 +/- 0.05 to 2.43 +/- 0.15; P < 0.05) but not in aged animals (Age Con: 2.87 +/- 0.17 vs. Age He-PC: 2.87 +/- 0.07; not significant). Iberiotoxin abrogated the helium effect on respiratory control index (2.73 +/- 0.15; P < 0.05 vs. He-PC) but had no effect itself on mitochondrial respiration (2.75 +/- 0.05; not significant vs. Con).

Conclusion
Helium causes mitochondrial uncoupling and induces preconditioning in young rats via Ca(2+) -sensitive potassium channel activation. However, these effects are lost in aged rats.
Reversal of Profound Rocuronium-induced Blockade with Sugammadex
Authors: Jones R Kevin , Caldwell James E. , Brull Sorin J. , Soto Roy G. 
Published: October 2008

Background
Traditionally, reversal of nondepolarizing neuromuscular blocking agents was achieved using acetylcholinesterase inhibitors, but these are unable to adequately reverse profound blockade. Sugammadex is a novel reversal agent, reversing the effects of rocuronium by encapsulation. This study assessed the efficacy and safety of sugammadex versus neostigmine for reversal of profound rocuronium-induced neuromuscular blockade.

Methods
This phase III, randomized study enrolled surgical patients, aged 18 yr or older with American Society of Anesthesiologists physical status I-IV. Patients were randomized to receive sugammadex (4.0 mg/kg) or neostigmine (70 microg/kg) plus glycopyrrolate (14 microg/kg). Anesthetized patients received an intubating dose of rocuronium (0.6 mg/kg), with maintenance doses (0.15 mg/kg) as required. Neuromuscular monitoring was performed by acceleromyography. Sugammadex or neostigmine was administered at reappearance of 1-2 posttetanic counts (profound neuromuscular blockade). The primary efficacy parameter was the time from sugammadex or neostigmine-glycopyrrolate administration to return of the train-of-four ratio to 0.9.

Results
In the intent-to-treat population (n = 37 in each group), geometric mean time to recovery to a train-of-four ratio of 0.9 with sugammadex was 2.9 min versus 50.4 min with neostigmine-glycopyrrolate (P < 0.0001) (median, 2.7 min vs. 49.0 min). Most sugammadex patients (97%) recovered to a train-of-four ratio of 0.9 within 5 min after administration. In contrast, most neostigmine patients (73%) recovered between 30 and 60 min after administration, with 23% requiring more than 60 min to recover to a train-of-four ratio of 0.9.

Conclusions
Recovery from profound rocuronium-induced neuromuscular blockade was significantly faster with sugammadex versus with neostigmine, suggesting that sugammadex has a unique ability to rapidly reverse profound rocuronium neuromuscular blockade.
Long-term Outcome in Chest Trauma
Authors: Leone Marc , Brégeon Fabienne , Antonini François , Chaumoître Kathia , Charvet Aude , Ban Leang H. , Jammes Yves , Albanèse Jacques , Martin Claude 
Published: October 2008

Background
Currently, there are limited data available describing the long-term outcomes of chest trauma survivors. Here, the authors sought to describe chest trauma survivor outcomes 6 months and 1 yr after discharge from the intensive care unit, paying special attention to pulmonary outcomes.

Methods
A cohort of 105 multiple trauma patients with blunt chest trauma admitted to the intensive care unit was longitudinally evaluated. After 6 months, a chest computed tomography scan, pulmonary function testing (PFT), and quality of life were collected in 55 of these patients. A subgroup of 38 patients was followed up for 1 yr.

Results
At least one abnormal PFT result was found in 39 patients (71%). Compared with normalized data of the age- and sex-matched population, physical function was decreased in 38 patients (70%). The 6-min walk distance was reduced for 29 patients (72%). Although pathologic images were observed on the chest computed tomography scan from 33 patients (60%), no relation was found between PFT and computed tomography. A ratio of arterial oxygen pressure to inspired oxygen fraction less than 200 at admission to the intensive care unit predicted an abnormal PFT result at 6 months. One year after discharge from the intensive care unit, paired comparisons showed a significant increase in forced vital capacity (P = 0.02) and Karnofsky Performance Status (P < 0.001).

Conclusions
Survivors of multiple traumas including chest trauma demonstrate a persistent decrease in the 6-min walk distance, impairment on PFT, and reduced pulmonary-specific quality of life.
Antitumor activities of synthetic and natural stilbenes through antiangiogenic action
Authors: Kimura Yoshiyuki , Sumiyoshi Maho , Baba Kimiye 
Published: October 2008

We reported that the antitumor and antimetastatic actions of resveratrol might be due to the inhibition of tumor‐induced angiogenesis. To search for anticancer agents with stronger activity than resveratrol, we examined the antiangiogenic effects of 21 synthetic and/or natural stilbenes. Among these 21 stilbenes, 2,3‐, 3,4‐, and 4,4′‐dihydroxystilbene inhibited the pro‐matrix metalloproteinase (pro‐MMP)–9 production in colon 26 cells at 5–25 µM, vascular endothelial growth factor (VEGF)–induced human umbilical vein endothelial cell (HUVEC) migration at 10 and 25 µM, and VEGF‐induced angiogenesis at 5–50 µM. Resvertarol inhibited the pro‐MMP‐9 production and VEGF‐induced angiogenesis at 25 or 50 µM. Thus, the inhibition of pro‐MMP‐9 production in colon 26 cells and VEGF‐induced angiogenesis by three dihydroxystilbenes were greater than those of resveratrol. The three dihydroxystilbenes (8 mg/kg, intraperitoneal injection) inhibited the tumor‐induced neovascularization in colon 26–packed chamber‐bearing mice and the tumor growth in colon 26–bearing mice. Furthermore, the three dihydroxystilbenes inhibited VEGF‐induced VEGFR‐2 phosphorylation. On the other hand, the three dihydroxystilbenes had no effect on VEGFR‐1 and‐2 expression, and VEGF‐induced VEGFR‐1 phosphorylation in HUVECs. These findings suggest that the inhibition of tumor‐induced neovascularization by these three dihydroxystilbenes may be due to the inhibition of VEGF‐induced endothelial cell migration and VEGF‐induced angiogenesis through the inhibition of VEGF‐induced VEGFR‐2 phosphorylation in endothelial cells and pro‐MMP‐9 expression in colon 26 cells. (Cancer Sci 2008; 99: 2083–2096)
Structural and functional diversity in the PAR1b/MARK2‐binding region of Helicobacter pylori CagA
Authors: Lu Huai‐Sheng , Saito Yasuhiro , Umeda Mayumi , Murata‐Kamiya Naoko , Zhang Hong‐Mei , Higashi Hideaki , Hatakeyama Masanori 
Published: October 2008

Helicobacter pylori (H. pylori) cagA‐positive strains are associated with gastritis, peptic ulcerations, and gastric adenocarcinoma. Upon delivery into gastric epithelial cells, the cagA‐encoded CagA protein specifically binds and aberrantly activates SHP‐2 oncoprotein in a manner that is dependent on CagA tyrosine phosphorylation. CagA‐deregulated SHP‐2 then elicits aberrant Erk activation while causing an elongated cell shape known as the hummingbird phenotype. In polarized epithelial cells, CagA also binds to PAR1b/MARK2 and inhibits the PAR1b kinase activity, thereby disrupting tight junctions and epithelial cell polarity independent of CagA tyrosine phosphorylation. We show here that the CagA‐multimerization (CM) sequence that mediates interaction of CagA with PAR1b is not only essential for the CagA‐triggered junctional defects but also plays an important role in induction of the hummingbird phenotype by potentiating CagA‐SHP‐2 complex formation. We also show that the CM sequence of CagA isolated from East Asian H. pylori (referred to as the E‐CM sequence) binds PAR1b more strongly than that of CagA isolated from Western H. pylori (referred to as the W‐CM sequence). Within Western CagA species, the ability to bind PAR1b is proportional to the number of W‐CM sequences. Furthermore, the level of PAR1b‐binding activity of CagA correlates with the magnitude of junctional defects and the degree of hummingbird phenotype induction. Our findings reveal that structural diversity in the CM sequence is an important determinant for the degree of virulence of CagA, a bacterial oncoprotein that is associated with gastric carcinogenesis. (Cancer Sci 2008; 99: 2004–2011)
Oviposition preferences of Maculinea alcon as influenced by aphid (Aphis gentianae) and fungal (Puccinia gentianae) infestation of larval host plants
Authors: ÁRNYAS ERVIN , BERECZKI JUDIT , TÓTH ANDREA , VARGA KATALIN , PECSENYE KATALIN , TARTALLY ANDRÁS , KÖVICS GYÖRGY , KARSA DÓRA , VARGA ZOLTÁN 
Published: October 2008

Abstract 1. The influence of infestation of the larval host plant Gentiana cruciata on the egg‐laying preferences of the xerophilous ecotype of Alcon Blue butterfly (Maculinea alcon) was studied in a semi‐dry grassland area (Aggtelek Karst Region, Northern Hungary).2. We examined whether oviposition patterns of females differed when G. cruciata stems were uninfested compared with when they were infested by an aphid (Aphis gentianae) or a rust (Puccinia gentianae) species.3. Females laid more than 90% of their eggs on fertile, uninfested G. cruciata stems, although these stems comprised only ∼ 50% of the total stems available. Stems infested by aphids were similar to uninfested ones in properties that had a strong correlation with egg numbers, and yet there were significantly fewer eggs on infested stems than on intact ones.4. Females never laid eggs on parts of Gentiana stems infested by aphids, and the presence of Lasius paralienus ants, which have a mutualistic interaction with Aphis gentianae, did not increase the repulsive effect of aphids. Infection of Gentiana by Puccinia did not influence the egg‐laying behaviour of females, even though the flowers and buds of infested stems exhibited a delayed development.5. Aphid infestation can influence butterfly oviposition patterns through both direct and indirect effects. The presence of aphids directly excluded oviposition, but our data also indicated the possibility of an indirect effect of aphid infestation. Stems that had no aphids at the last egg counting, but were infested prior to it, had significantly fewer eggs than those that were never infested.
Deriving effects of pressure depletion on elastic framework moduli from sonic logs
Authors: Furre Anne‐Kari , Andersen Mona , Moen Anita Smalø , Tønnessen Randi Kristin 
Published: October 2008

ABSTRACTWe have developed a method to determine the effect of pore pressure depletion on elastic framework moduli, by utilizing sonic logs from wells drilled at different locations through a reservoir at varying depletion stages. This is done by first inverting the sonic logs for elastic framework bulk and shear moduli, thus carefully removing pressure dependent fluid effects. By crossplotting these elastic framework moduli against an increase in net stress (which is directly related to depletion), we derive the stress sensitivity of the elastic framework moduli. We found that the observed stress sensitivity was consistent with time‐lapse seismic results and that the sensitivity derived from the sonic logs was much smaller than predicted by hydrostatic measurements on core samples. This method is applicable to depletion scenarios in mature fields and can be used both for modelling and inverting time‐lapse seismic data for effects of pore pressure depletion on seismic data.
NUCLEAR FACTOR‐κB MEDIATES CYTOPROTECTION OF HYDROGEN PEROXIDE PRECONDITIONING AGAINST APOPTOSIS INDUCED BY OXIDATIVE STRESS IN PC12 CELLS
Authors: Zhang Mei , Guo Rui‐Xian , Mo Li‐Qiu , Liao Xin‐Xue , Li Wei , Zhi Jun‐Li , Sun Sheng‐Nan , Wang Yan‐Li , Cui Yu , Liu Wei , Feng Jian‐Qiang , Chen Pei‐Xi 
Published: October 2008

SUMMARY

Cytoprotection by H2O2 preconditioning against oxidative stress‐induced apoptosis of PC12 cells has been demonstrated previously. In the present study, we investigated the effects of H2O2 preconditioning on nuclear factor (NF)‐κB activation and the role of NF‐κB in the adaptive cytoprotection of H2O2 preconditioning in PC12 cells.
The PC12 cells were preconditioned with 100 µmol/L H2O2 for 90 min, followed by 24 h recovery and subsequent exposure to 300 µmol/L H2O2 for a further 12 h.
The results showed that preconditioning with 100 µmol/L H2O2 upregulated NF‐κB expression and enhanced its nuclear translocation and DNA binding activity. In addition to its own effects on NF‐κB expression, H2O2 preconditioning also promoted the overexpression of NF‐κB induced by a lethal concentration of H2O2 (300 µmol/L).
N‐Tosyl‐l‐phenylalanine chloromethyl ketone (TPCK; 20 µmol/L), an inhibitor of NF‐κB, was administered 20 min before preconditioning with 100 µmol/L H2O2. At this concenteration, TPCK blocked the overexpression of NF‐κB induced by H2O2 preconditioning, accompanied by attenuation of H2O2 preconditioning‐induced cytoprotection. The inhibition of NF‐κB by TPCK enhanced caspase 3 activity induced by 300 µmol/L H2O2.
5. The findings of the present study provide novel evidence for the effects of preconditioning with H2O2 on constitutive activation of NF‐κB, which contributes to the adaptive cytoprotection of H2O2 preconditioning against PC12 cells apoptosis.