bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of yeasts isolated from traditional Turkish cheeses by Lactobacillus spp.
Authors: DURLU‐ÖZKAYA FÜGEN , KARABIÇAK NILGÜN , KAYALI REVASIYE , ESEN BERRIN 
Published: April 2005

Antifungal activity of some Lactobacillus strains was determined. Yeasts were isolated and identified as Saccharomyces cerevisiae (10 of 17) and one each of Candida pseudotropicalis, C. krusei, C. lipolytica, C. lusitaniae, C. ciferrii, Torulopsis glabrata and Rhodotorula rubra. Lactobacillus strains were found to have fairly strong antifungal activity against S. cerevisiae. Of the 19 bacteria tested, L. plantarum Lp 21 seemed to have the most inhibitory effect against all of the S. cerevisiae strains except for S. cerevisiae 13. We suggest that L. plantarum Lp 21 can be used with starter cultures for cheese production.
Regulation of glutamate carboxypeptidase II hydrolysis ofN‐acetylaspartylglutamate (NAAG) in crayfish nervous tissue is mediated by glial glutamate and acetylcholine receptors
Authors: Urazaev Albert K. , Grossfeld Robert M. , Lieberman Edward M. 
Published: April 2005

AbstractGlutamate carboxypeptidase II (GCPII), a glial ectoenzyme, is responsible forN‐acetylaspartylglutamate (NAAG) hydrolysis. Its regulation in crayfish nervous tissue was investigated by examining uptake of [3H]glutamate derived fromN‐acetylaspartyl‐[3H]glutamate ([3H]NAAG) to measure GCPII activity. Electrical stimulation (100 Hz, 10 min) during 30 min incubation with [3H]NAAG increased tissue [3H]glutamate tenfold. This was prevented by 2‐(phosphonomethyl)‐pentanedioic acid (2‐PMPA), a GCPII inhibitor, suggesting that stimulation increased the hydrolysis of [3H]NAAG and metabolic recycling of [3H]glutamate. Antagonists of glial group II metabotropic glutamate receptors (mGLURII), NMDA receptors and acetylcholine (ACh) receptors that mediate axon–glia signaling in crayfish nerve fibers decreased the effect of stimulation by 58–83%, suggesting that glial receptor activation leads to stimulation of GCPII activity. In combination, they reduced [3H]NAAG hydrolysis during stimulation to unstimulated control levels. Agonist stimulation of mGLURIImimicked the effect of electrical stimulation, and was prevented by antagonists of GCPII or mGLURII. Raising extracellular K+to three times the normal level stimulated [3H]NAAG release and GCPII activity. These effects were also blocked by antagonists of GCPII and mGLURII. No receptor antagonist or agonist tested or 2‐PMPA affected uptake of [3H]glutamate. We conclude that NAAG released from stimulated nerve fibers activates its own hydrolysis via stimulation of GCPII activity mediated through glial mGLURII,NMDA and ACh receptors.
Energy substrate requirements for survival of rat retinal cells in culture: the importance of glucose and monocarboxylates
Authors: Wood John P. M. , Chidlow Glyn , Graham Mark , Osborne Neville N. 
Published: April 2005

AbstractThe process of metabolic coupling has been described as a means of providing additional fuel for neurons during periods of intense activity. This process has been suggested to occur in the mammalian retina, but whether retinal neurons can metabolise glial‐derived monocarboxylates remains uncertain. The present study therefore sought to define the preferred energy substrates for maintenance of different retinal cells in culture, in order to clarify whether metabolic coupling can potentially occur in this tissue. All cells in rat retinal cultures were detrimentally affected by glucose deprivation. The effect on some neurons, however, could be partially reversed by 5 mm pyruvate or lactate. Furthermore, the glycolytic inhibitor, iodoacetic acid, caused a dose‐dependent loss of all retinal cells in culture, whereas the mitochondrial inhibitor, 2,4‐dinitrophenol, only led to a decrease in the number of neurons. Finally, inhibition of transporters for glucose or monocarboxylates caused the respective loss of glia or neurons from cultures. These data together demonstrate that, although cells do preferentially metabolise glucose, monocarboxylates such as lactate or pyruvate do play an important role in neuronal maintenance. These data therefore give partial support to the notion that metabolic coupling may occur in the retina.
Transport characteristics of N‐acetyl‐l‐aspartate in rat astrocytes: involvement of sodium‐coupled high‐affinity carboxylate transporter NaC3/NaDC3‐mediated transport system
Authors: Fujita Takuya , Katsukawa Hiromi , Yodoya Etsuo , Wada Miyuki , Shimada Ayumi , Okada Naoki , Yamamoto Akira , Ganapathy Vadivel 
Published: April 2005

AbstractWe investigated in the present study the transport characteristics of N‐acetyl‐l‐aspartate in primary cultures of astrocytes from rat cerebral cortex and the involvement of NA+‐coupled high‐affinity carboxylate transporter NaC3 (formerly known as NaDC3) responsible for N‐acetyl‐l‐aspartate transport. N‐acetyl‐l‐aspartate transport was NA+‐dependent and saturable with a Michaelis–Menten constant (Km) of ∼110 µm. NA+‐activation kinetics revealed that the NA+ to‐N‐acetyl‐l‐aspartate stoichiometry was 3 : 1 and concentration of Na+ necessary for half‐maximal transport (KNAm) was 70 mm. NA+‐dependent N‐acetyl‐l‐aspartate transport was competitively inhibited by succinate with an inhibitory constant (Ki) of 14.7 µm, which was comparable to the Km value of NA+‐dependent succinate transport (29.4 µm). l‐Aspartate also inhibited NA+‐dependent [14C]N‐acetyl‐l‐aspartate transport with relatively low affinity (Ki = 2.2 mm), whereas N‐acetyl‐l‐aspartate was not able to inhibit NA+‐dependent aspartate transport in astrocytes. In addition, Li+ was found to have a significant inhibitory effect on the NA+‐dependent N‐acetyl‐l‐aspartate transport in a concentration‐dependent manner. Furthermore, RT–PCR and western blot analyses revealed that NaC3 is expressed in primary cultures of astrocytes. Taken collectively, these results indicate that NaC3 expressed in rat cerebrocortical astrocytes is responsible for NA+‐dependent N‐acetyl‐l‐aspartate transport. This transporter is likely to be an essential prerequisite for the metabolic role of N‐acetyl‐l‐aspartate in the process of myelination.
Cellular and subcellular localization of EFA6C, a third member of the EFA6 family, in adult mouse Purkinje cells
Authors: Matsuya Shigetsune , Sakagami Hiroyuki , Tohgo Akira , Owada Yuji , Shin Hye‐Won , Takeshima Hiroshi , Nakayama Kazuhisa , Kokubun Shoichi , Kondo Hisatake 
Published: April 2005

AbstractEFA6C is a third member of the EFA6 family of guanine nucleotide exchange factors (GEFs) for ADP‐ribosylation factor 6 (ARF6). In this study, we first demonstrated that EFA6C indeed activated ARF6 more selectively than ARF1 by ARF pull‐down assay. In situ hybridization histochemistry revealed that EFA6C mRNA was expressed predominantly in mature Purkinje cells and the epithelial cells of the choroid plexus in contrast to the ubiquitous expression of ARF6 mRNA throughout the brain. EFA6C mRNA was already detectable in the Purkinje cells at embryonic day 13, increased progressively during post‐natal development and peaked during post‐natal second week. In Purkinje cells, the immunoreactivity for EFA6C was localized particularly in the post‐synaptic density as well as the plasma membranes of the cell somata, dendritic shafts and spines, while the immunoreactivity in their axon terminals in the deep cerebellar nuclei was very faint. These findings suggest that EFA6C may be involved in the regulation of the membrane dynamics of the somatodendritic compartments of Purkinje cells through the activation of ARF6.
Anxiety, gingival inflammation and periodontal disease in non‐smokers and smokers – an epidemiological study
Authors: Johannsen Annsofi , Åsberg Marie , Söder Per‐Östen , Söder Birgitta 
Published: April 2005

AbstractObjectives: The aim of the present study was to investigate the influence of anxiety, measured by one single question, on gingival inflammation and periodontal disease in non‐smokers and smokers.Material and Methods: The participants were 144 subjects with untreated periodontal disease 30–40 years of age, and 26 healthy controls, 30–40 years of age. All subjects were clinically examined and answered an uncomplicated question regarding anxiety in every day life, as well as smoking habits. The periodontitis subjects were divided into; an aggressive periodontitis (AP)‐group and a chronic periodontitis (CP)‐group. Fisher's exact probability t‐test, analysis of variance (anova), Mann–Whitney U‐test and analysis of covariance (ancova) were used as statistical methods.Results: Anxious subjects had a significantly higher gingival index than non‐anxious subjects, when controlling for smoking (p<0.01). The healthy anxious non‐smokers had an average score of GI 1.6 (±0.4 SD) compared with 1.2 (±0.4 SD), p<0.05 for the non‐anxious non‐smokers. Anxious smokers with periodontits (AP‐/CP‐group) had significantly more sites with pockets 5 mm, compared with non‐anxious smokers, (p<0.05).Conclusions: The results of the present study, suggest that self‐reported anxiety was associated with an adverse affect on the gingiva. Anxiety seemed to be associated with increased severity of periodontal disease in smokers.
Pain during prophylaxis treatment elicited by two power‐driven instruments
Authors: Kocher T. , Rodemerk B. , Fanghänel J. , Meissner G. 
Published: April 2005

AbstractBackground: Sonic scalers have an elliptical and piezoceramic ultrasonic scalers a linear oscillation pattern. Thus, a sonic scaler “hammers” the tooth surface, irrespective of its alignment to the tooth, whereas a piezoceramic ultrasonic scaler may oscillate parallel to the tooth surface and gently remove calculus if the alignment is correct. The aim of this study was to measure pain on a visual analogue scale (VAS) during removal of supragingival calculus on mandibular incisors with a sonic or an ultrasonic scaler.Material and methods: Seventy‐four periodontally healthy subjects with supragingival calculus on the mandibular incisors were treated with both a sonic and a piezoceramic ultrasonic scaler in a split‐mouth design. The sequence of instrument application and allocation of instruments to jaw side were randomized. Patient comfort was assessed with a VAS after treatment.Results: The VAS results did not show any difference between the two instrumentation modalities.Conclusion: For calculus removal during prophylaxis the type of power‐driven instrument does not seem to have an impact on perceived pain. This means that the oscillation pattern does not influence the pain experience.
THE BETA‐BINOMIAL MODEL: VARIABILITY IN OVERDISPERSION ACROSS METHODS AND OVER TIME
Authors: LIGGETT RACHEL E. , DELWICHE JEANNINE F. 
Published: April 2005

ABSTRACTThe beta‐binomial model accounts for variability between samples as well as variability between judges (overdispersion), making it possible to combine responses across judges and replications. Overdispersion (measured by gamma) was examined in this 3‐part study. (1) Groups of judges (n = 53–59) performed two replications each of a paired comparison and paired preference. Results showed that extent of overdispersion could not be predicted from the method. (2) The stability of gamma across discrimination methods (2‐alternative forced choice [2‐AFC], 3‐alternative forced choice [3‐AFC], triangle and duo‐trio) was also examined (n = 103). Results indicated that gamma was largely consistent across 2‐AFC, 3‐AFC and triangle tasks, but it was higher in the duo‐trio task. (3) The stability of gamma over time was also investigated (n = 25). Results demonstrate that overdispersion varied over time with no clear pattern. In all cases, use of the beta‐binomial model allowed responses across judges and replications to be combined, increasing the power achieved for a given panel size.
SENSORY COMPARISON OF SEVERAL CHEESE VARIETIES MANUFACTURED FROM DIFFERENT MILK SOURCES
Authors: BÁRCENAS P. , PÉREZ ELORTONDO F.J. , ALBISU M. 
Published: April 2005

ABSTRACT The objectives of the present study were (1) to identify specific sensory patterns for several cheese varieties, paying special attention to ewe's milk cheeses, (2) to describe nonewe's milk cheeses (goat, cow, milk mixture) relationships within the considered ewe's milk cheese sensory space and (3) to evaluate if a lexicon specifically suited for ewe's milk cheeses’ description was useful for other sources of milk cheeses’ sensory assessment. A lexicon specifically adapted for ewe's milk cheese sensory description was employed. Results from Linear Discriminant Analysis showed that ewe's milk cheese varieties have unique sensory characteristics that are very different from each other. Cow milk variety was the closest to one of the ewe's milk cheese category; however, a deeper analysis showed both products had very specific sensory properties. The ewe's milk cheese descriptive lexicon is adequate to discriminate among nonovine varieties. However, updates may be necessary for a complete sensory characterization.
A potential role of YC-1 on the inhibition of cytokine release in peripheral blood mononuclear leukocytes and endotoxemic mouse models
Authors: Pan Shiow-Lin , Guh Jih-Hwa , Peng Chieh-Yu , Chang Ya-Ling , Cheng Fong-Chi , Chang Jau-Hsiang , Kuo Sheng-Chu , Lee Fang-Yu , Teng Che-Ming 
Published: April 2005

SummaryTo evaluate the anti-sepsis potential of YC-1, we have examined the effect of YC-1 on the regulation of cytokine production in human leukocytes and endotoxemic mice. The data demonstrated that YC-1 showed a preferential inhibition on proinflammatory cytokine production without inhibition of cell growth or induction of cytotoxicity in human leukocytes. On the other hand, in the septic mouse model, treatment with an intraperitoneal application of LPS caused a cumulative death within 27 hours. The post-treatment administration of YC-1 significantly increased the survival rate in endotoxemic mice. Furthermore, several mediators were detected and the data showed that YC-1 profoundly blocked LPS-induced NO as well as TNF-α production, and prevented lung damage by histological examination. Samples from the animal model showed that LPS-induced NF-κB/DNA binding activity and consequent up-regulation of iNOS expression in tissues were abolished by post-administration of YC-1. Furthermore, YC-1, by itself, did not modify cGMP content while significantly inhibit LPS-induced cGMP formation, suggesting that YC-1-mediated effect was not through a cGMP-elevating pathway. Taken together, it is evident that the post-treatment administration of YC-1 after LPS application significantly inhibits NF-κB activation, iNOS expression, NO over-production, and cytokine release reaction resulting in an improved survival rate in endotoxemic mice. It is suggested that YC-1 may be a potential agent for the therapeutic treatment of sepsis.
Extracellular fibrinogen binding protein, Efb, from Staphylococcus aureus as an antiplatelet agent in vivo
Authors: Shannon Oonagh , Uekötter Andreas , Flock Jan-Ingmar 
Published: April 2005

Summary
Staphylococcus aureus produces and secretes a protein, extracellular fibrinogen binding protein (Efb), which contributes to virulence in wound infection. We have previously shown that Efb is a potent inhibitor of platelet function in vitro. We confirm here that this is also the case in vivo. Pre-treatment with Efb resulted in a significant prolongation of bleeding time in a mouse model. Furthermore, Efb was capable of rescuing animals from death caused by the administration of potent platelet agonists. This antiplatelet effect may explain the retardation of wound healing associated with Efb in S. aureus wound infections. These results are important not only in terms of understanding S. aureus pathogenesis, and consequently identifying new treatment strategies, but also with regard to the development of potential, novel antiplatelet agents for the prevention of thrombosis.
B-domain deleted factor VIII is aggregated and degraded through proteasomal and lysosomal pathways
Authors: Guillet Benoit , Ducasse Cécile , Enjolras Nathalie , Rodriguez Marie-Hélène , Rolli Véronique , Négrier Claude , Plantier Jean-Luc 
Published: April 2005

SummaryFactor VIII (FVIII) processing within mammalian cells is demonstrated to be much less efficient than proteins of similar size. The deletion of the B-domain from FVIII improves the level of production, due partly to the increase in mRNA synthesis. We aimed to characterise the cellular fate and the intracellular processing of the FVIII molecule devoid of B-domain. A B-domain deleted factor VIII (BDD-FVIII) possessing a furin consensus cleavage site in the connecting segment between the heavy and the light chain, was produced in CHO cell line. In such cells, FVIII was retained as two single chain products from which a majority was aggregated. The two species were located in Triton X-100 soluble (for 60–80%) and insoluble fractions (for 20–40%). The incubation of the expressing cells with tunicamycin (5 μg/ml) and the treatment of the intracellular species with a mixture of Neuraminidase and N-glycosidase-F revealed that both intracellular species were N-glycosylated. Furin over-expression neither diminished the intracellular FVIII contents nor improved its extracellular production. Intracellular FVIII was degraded through both lysosomal and proteasomal pathways as evidenced by inhibitor treatments (e.g. NH4Cl, leupeptin, clasto-Lactacystin β-lactone and MG-132), pulse-chase analysis and confocal observations. This study demonstrates that a BDD-FVIII expressed in CHO cells is inefficiently processed consecutively to intracellular aggregation, proteasomal degradation, and routage to lysosomes.
P2Y12 ADP receptor-dependent tyrosine phosphorylation of proteins of 27 and 31 kDa in thrombin-stimulated human platelets
Authors: Fälker Knut , Lange Danica , Presek Peter 
Published: April 2005

SummaryIn thrombin-stimulated human platelets several proteins undergo rapid and transient changes in tyrosine phosphorylation. We demonstrate that a set of proteins of 27, 29, 31, 34, and 39 kDa is affected by released ADP and P2Y12 receptor signaling during platelet activation. AR-C69931MX, an antagonist of the Gi2-coupled P2Y12 ADP receptor, inhibits initial tyrosine phosphorylation of p27 and p31 and prevents subsequent dephosphorylation of p29, p34, and p39. Antagonists of the Gq-coupled P2Y1 ADP receptor have no effect. Precluding integrin αIIbβ3 outside-in signaling with RGDS or S1197 does not affect the increase in tyrosine phosphorylation of the set of proteins but inhibits their subsequent dephosphorylation. Besides the ADP analogue 2-MeS-ADP, other platelet agonists such as collagen and the TXA2-mimetic U46619 also induce p27 and p31 tyrosine phosphorylation in a P2Y12 receptor-dependent manner. Tyrosine phosphorylation of p27 and p31 in response to collagen, but not thrombin, is prevented by aspirin and the TXA2 receptor antagonist SQ29548, indicating that the effect of collagen strongly relies on TXA2 signaling. Furthermore, epinephrine, acting via inhibitory Gz-coupled α2A-adrenoceptors, bypasses the inhibitory effect of AR-C69931MX on thrombin-induced p27 and p31 tyrosine phosphorylation. Finally, we demonstrate that tyrosine phosphorylation of p27 and p31 downstream of P2Y12 receptors is due to the inhibition of adenylyl cyclase but not phosphoinositide 3-kinase (PI 3-K) activation. Elevating cAMP levels with PGI2 or forskolin precludes thrombin-induced p27 and p31 tyrosine phosphorylation. Moreover, direct inhibition of adenylyl cyclase by SQ22536 reverses the effect of AR-C69931MX. Our data indicate that the observed changes in tyrosine phosphorylation are the result of both primary Gq signaling, initiating the release of ADP, as well as subsequent P2Y12 receptor-mediated Gi coupling.
Non-invasive imaging of glycoprotein VI binding to injured arterial lesions
Authors: Konrad Ildiko , Hauser Andrea , Sauer Suzanne , Li Zhongyan , Wester Hans-Jürgen , Bengel Frank , Schwaiger Markus , Schömig Albert , Massberg Steffen , Haubner Roland , Gawaz Meinrad 
Published: April 2005

SummaryGlycoprotein VI (GPVI) is the major platelet collagen receptor and plays a critical role in the process of thrombosis at sites of atherosclerotic lesions. This study evaluates the feasibility of radiolabeled soluble GPVI to identify injured arterial lesions. Radiolabeling was carried out using the iodogen method and resulted in the radioiodinated GPVI in radiochemical yields between 97–100%. The biodistribution of [125I]GPVI was determined in normal mice and demonstrated a blood clearance halftime of approximately 5.5 hours. Vascular lesions were induced in the carotid artery in wild type and ApoE -/- mice. Immediately after injury radioiodinated GPVI was injected intravenously. Binding of [123I]GPVI to carotid lesions was assessed by szinti-graphic in vivo imaging. Carotid arteries were explanted for ex vivo autoradiography and histological characterization of the lesion. In vivo and ex vivo imaging revealed substantial accumulation of radioiodinated GPVI in the injured artery wall, with a ratio of lesion to control vessel of 3:1 and 7:1, respectively. Because GPVI is the critical collagen receptor that mediates platelet adhesion to vascular lesions, soluble radiolabeled GPVI may be an agent for non-invasive imaging of thrombogenic thus, vulnerable atherosclerotic plaques.
A novel homozygous mutation (1619delC) in GPIIb gene associated with Glanzmann thrombasthenia, the decay of GPIIb-mRNA and the synthesis of a truncated GPIIb unable to form complex with GPIIIa
Authors: Losonczy Gergely , Rosenberg Nurit , Kiss Csongor , Kappelmayer János , Vereb György , Kerényi Adrienne , Balogh István , Muszbek László 
Published: April 2005

SummaryThe absence of agonist-induced platelet aggregation and the lack of fibrinogen receptor (GPIIb/IIIa) on the platelet surface demonstrated that the severe hemorrhagic complications of a child of Romany descent were caused by Glanzmann thrombasthenia. DNA sequencing revealed a novel homozygous deletion of a cytosine (1619delC) in the GPIIb gene causing a frameshift and predicting a novel stop codon at position 533 following 24 altered amino acids. Both parents possessed the same deletion in heterozygous form. The amount of GPIIb mRNA in the patient’s platelets was 0.06% of the amount measured in control platelets. Neither GPIIb nor its truncated form could be detected in the platelets of the patient by Western blotting, while a small amount of GPIIIa was demonstrated. Quantitative flow cytometric analysis showed an elevated number of vitronectin receptors, a component of which is GPIIIa, on the patient’s platelets. The surface expression of vitronectin receptor on thrombasthenic, but not on normal platelets was further increased by activation with thrombin receptor agonist peptide. BHK cells transfected with wild type GPIIIa and mutated GPIIb failed to express any mature GPIIb or pro-GPIIb. Immunoprecipitation with a polyclonal antibody recognizing both GPIIb and GPIIIa recovered a 60 kDa truncated form of GPIIb. This band was absent when immunoprecipitation was carried out with an antibody recognizing GPIIIa, suggesting that the truncated protein, lacking calf-1, calf-2 domains and major part of the thigh domain, is unable to form complex with GPIIIa.