300 research outputs found

    Discrimination of Helicobacter pullorum and Campylobacter lari by analysis of whole cell fatty acid extracts

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    Helicobacter pullorum and Campylobacter lari are rarely isolated from humans with acute enteritis. Hitherto the two species could only be identified by genotypic techniques. Gas liquid chromatography of whole cell fatty acid extracts is described as the first phenotypic method for discrimination of the two species. Cholesteryl glucoside, a characteristic feature of the genus Helicobacter, but seldom found in other bacteria, could not be detected in Helicobacter pullorum. Therefore, rapid determination of this glycolipid may serve as a discrimination marker for Helicobacter pullorum from most other Helicobacter specie

    Discrimination of Helicobacter pullorum and Campylobacter lari by analysis of whole cell fatty acid extracts

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    Helicobacter pullorum and Campylobacter lari are rarely isolated from humans with acute enteritis. Hitherto the two species could only be identified by genotypic techniques. Gas liquid chromatography of whole cell fatty acid extracts is described as the first phenotypic method for discrimination of the two species. Cholesteryl glucoside, a characteristic feature of the genus Helicobacter, but seldom found in other bacteria, could not be detected in Helicobacter pullorum. Therefore, rapid determination of this glycolipid may serve as a discrimination marker for Helicobacter pullorum from most other Helicobacter species

    Superação da insuficiĂȘncia de frio hibernal em ameixeiras (prunus domestica L.) cv D'agen.

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    bitstream/item/31592/1/comunicado79.pd

    Thermoelectric effects in a strongly correlated model for Nax_xCoO2_2

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    Thermal response functions of strongly correlated electron systems are of appreciable interest to the larger scientific community both theoretically and technologically. Here we focus on the infinitely correlated t-J model on a geometrically frustrated two-dimensional triangular lattice. Using exact diagonalization on a finite sized system we calculate the dynamical thermal response functions in order to determine the thermopower, Lorenz number, and dimensionless figure of merit. The dynamical thermal response functions is compared to the infinite frequency limit and shown to be very weak functions of frequency, hence, establishing the validity of the high frequency formalism recently proposed by Shastry for the thermopower, Lorenz number, and the dimensionless figure of merit. Further, the thermopower is demonstrated to have a low to mid temperature enhancement when the sign of the hopping parameter tt is switched from positive to negative for the geometrically frustrated lattice considered.Comment: 16 pages, 10 figures, color version available at http://physics.ucsc.edu/~peterson/mrpeterson-condmat-NCO.pdf. V.2 has fixed minor typos in Eq. 11, 19, 25, and 26. V.3 is a color versio

    Responses of Solanum tuberosum L. to Water Deficit by Matric or Osmotic Induction.

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    Toselectpotatogenotypestoleranttowaterdeficit,systemstosimulatethisstresshavebeen used. Polyethylene glycol (PEG) is the main osmotic agent used for this purpose, but it causes an excessively severe stress. However, it is difficult to carry out an experiment that aims to compare plant responses under water deficit by osmotic or matric induction, and, thus,fewstudiescomparethesestress-inducingmechanisms.Therefore,theobjectiveofthis studywas to compare the responses of Agata, BRS Clara,C2406-03andCota genotypes to water deficit in both induction methods (matric or osmotic). The tests were carried out in a greenhouse, one using hydroponics (osmotic induction) and the other in pots with soil (matric induction). In both tests, the application of stressful conditions occurred at the beginning of tuberization. Assessments of gas exchange and shoot temperature were made throughout the exposure to stress. Also, samples were collected from leaves for analysis of osmotic potential and leaves and tubers for analysis of metabolite content. At the end of the potatoplantcycle,thenumberandweightoftuberswereevaluated.Inbothstressconditions, there were significant reductions in photosynthesis and transpiration rate compared to the respective normal hydration conditions. In addition, indicators such as metabolite levels (proline and soluble sugars) were significantly altered in plants exposed to different stress inductions. These data, together with the significant limitations in the growth of stressed plants, indicate that the experimental models induce similar responses. However, the water deficit by osmotic induction was more severe for the potato plants when compared to stress due to matric induction, mainly affecting tuber production. Therefore, the water deficit osmotic induction model can be recommended for phenotyping tolerance to this stress, due to the hydroponic system inducing greater tuber production per plant under optimal cultivation conditions

    Pharmacological inhibition of Akt and downstream pathways modulates the expression of COX-2 and mPGES-1 in activated microglia

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    <p>Abstract</p> <p>Background</p> <p>Microglia are considered a major target for modulating neuroinflammatory and neurodegenerative disease processes. Upon activation, microglia secrete inflammatory mediators that contribute to the resolution or to further enhancement of damage in the central nervous system (CNS). Therefore, it is important to study the intracellular pathways that are involved in the expression of the inflammatory mediators. Particularly, the role of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and glycogen synthase kinase-3 (GSK-3) pathways in activated microglia is unclear. Thus, in the present study we investigated the role of Akt and its downstream pathways, GSK-3 and mTOR, in lipopolysaccharide (LPS)-activated primary rat microglia by pharmacological inhibition of these pathways in regard to the expression of cyclooxygenase (COX)-2 and microsomal prostaglandin E synthase-1 (mPGES-1) and to the production of prostaglandin (PG) E<sub>2 </sub>and PGD<sub>2</sub>.</p> <p>Findings</p> <p>We show that inhibition of Akt by the Akt inhibitor X enhanced the production of PGE<sub>2 </sub>and PGD<sub>2 </sub>without affecting the expression of COX-2, mPGES-1, mPGES-2 and cytosolic prostaglandin E synthase (cPGES). Moreover, inhibition of GSK-3 reduced the expression of both COX-2 and mPGES-1. In contrast, the mTOR inhibitor rapamycin enhanced both COX-2 and mPGES-1 immunoreactivity and the release of PGE<sub>2 </sub>and PGD<sub>2</sub>. Interestingly, NVP-BEZ235, a dual PI3K/mTOR inhibitor, enhanced COX-2 and reduced mPGES-1 immunoreactivity, albeit PGE<sub>2 </sub>and PGD<sub>2 </sub>levels were enhanced in LPS-stimulated microglia. However, this compound also increased PGE<sub>2 </sub>in non-stimulated microglia.</p> <p>Conclusion</p> <p>Taken together, we demonstrate that blockade of mTOR and/or PI3K/Akt enhances prostanoid production and that PI3K/Akt, GSK-3 and mTOR differently regulate the expression of mPGES-1 and COX-2 in activated primary microglia. Therefore, these pathways are potential targets for the development of novel strategies to modulate neuroinflammation.</p

    Diffusion on networked systems is a question of time or structure

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    Network science investigates the architecture of complex systems to understand their functional and dynamical properties. Structural patterns such as communities shape diffusive processes on networks. However, these results hold under the strong assumption that networks are static entities where temporal aspects can be neglected. Here we propose a generalized formalism for linear dynamics on complex networks, able to incorporate statistical properties of the timings at which events occur. We show that the diffusion dynamics is affected by the network community structure and by the temporal properties of waiting times between events. We identify the main mechanism—network structure, burstiness or fat tails of waiting times—determining the relaxation times of stochastic processes on temporal networks, in the absence of temporal–structure correlations. We identify situations when fine-scale structure can be discarded from the description of the dynamics or, conversely, when a fully detailed model is required due to temporal heterogeneities

    Migraine headaches in Chronic Fatigue Syndrome (CFS): Comparison of two prospective cross-sectional studies

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    <p>Abstract</p> <p>Background</p> <p>Headaches are more frequent in Chronic Fatigue Syndrome (CFS) than healthy control (HC) subjects. The 2004 International Headache Society (IHS) criteria were used to define CFS headache phenotypes.</p> <p>Methods</p> <p>Subjects in Cohort 1 (HC = 368; CFS = 203) completed questionnaires about many diverse symptoms by giving nominal (yes/no) answers. Cohort 2 (HC = 21; CFS = 67) had more focused evaluations. They scored symptom severities on 0 to 4 anchored ordinal scales, and had structured headache evaluations. All subjects had history and physical examinations; assessments for exclusion criteria; questionnaires about CFS related symptoms (0 to 4 scale), Multidimensional Fatigue Inventory (MFI) and Medical Outcome Survey Short Form 36 (MOS SF-36).</p> <p>Results</p> <p>Demographics, trends for the number of diffuse "functional" symptoms present, and severity of CFS case designation criteria symptoms were equivalent between CFS subjects in Cohorts 1 and 2. HC had significantly fewer symptoms, lower MFI and higher SF-36 domain scores than CFS in both cohorts. Migraine headaches were found in 84%, and tension-type headaches in 81% of Cohort 2 CFS. This compared to 5% and 45%, respectively, in HC. The CFS group had migraine without aura (60%; MO; CFS+MO), with aura (24%; CFS+MA), tension headaches only (12%), or no headaches (4%). Co-morbid tension and migraine headaches were found in 67% of CFS. CFS+MA had higher severity scores than CFS+MO for the sum of scores for poor memory, dizziness, balance, and numbness ("Neuro-construct", p = 0.002) and perceived heart rhythm disturbances, palpitations and noncardiac chest pain ("Cardio-construct"; p = 0.045, t-tests after Bonferroni corrections). CFS+MO subjects had lower pressure-induced pain thresholds (2.36 kg [1.95-2.78; 95% C.I.] n = 40) and a higher prevalence of fibromyalgia (47%; 1990 criteria) compared to HC (5.23 kg [3.95-6.52] n = 20; and 0%, respectively). Sumatriptan was beneficial for 13 out of 14 newly diagnosed CFS migraine subjects.</p> <p>Conclusions</p> <p>CFS subjects had higher prevalences of MO and MA than HC, suggesting that mechanisms of migraine pathogenesis such as central sensitization may contribute to CFS pathophysiology.</p> <p>Clinical Trial Registration</p> <p>Georgetown University IRB # 2006-481</p> <p>ClinicalTrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT00810329">NCT00810329</a></p

    Potential Role of Aromatase over Estrogen Receptor Gene Polymorphisms in Migraine Susceptibility: A Case Control Study from North India

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    BACKGROUND: The present study was undertaken to find out the role of estrogen pathway related gene polymorphisms in susceptibility to migraine in Northern Indian population. Aromatase, CYP19A1 (rs10046 and rs4646); estrogen receptors, ESR1 (rs2234693, rs1801132, rs2228480 and rs9340799) and ESR2 (rs1271572 and rs1256049) polymorphisms were selected for the present study. METHODOLOGY/PRINCIPAL FINDINGS: The patients were recruited in two cohorts - primary (207) and replicative (127) along with 200 healthy controls and genotyped for various polymorphisms. Logistic regression analysis was applied for statistical analyses. The results were validated in the replicative cohort and pooled by meta analysis using Fisher's and Mantel-Haenszel test. Furthermore, Benjamini - Hochberg false discovery rate test was used to correct for multiple comparisons. CYP19A1 rs10046 and CYP19A1 rs4646 polymorphisms were found to confer risk and protective effect, respectively. Out of four ESR1 polymorphisms, only rs2234693 variant allele was significantly associated in migraine with aura. No significant associations were observed for ESR2 polymorphisms. Significant haplotypes were identified for CYP19A1 and ESR1 polymorphisms. Gene- gene interactions of genotypes as well as haplotypes were observed for CYP19A1- ESR1 showing both risk and protective combinations. CONCLUSION: We strongly suggest CYP19A1 polymorphisms to be the major contributing factors in migraine susceptibility instead of genetic variants of estrogen receptors

    Differential expression of presynaptic genes in a rat model of postnatal hypoxia: relevance to schizophrenia

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    Obstetric complications play a role in the pathophysiology of schizophrenia. However, the biological consequences during neurodevelopment until adulthood are unknown. Microarrays have been used for expression profiling in four brain regions of a rat model of neonatal hypoxia as a common factor of obstetric complications. Animals were repeatedly exposed to chronic hypoxia from postnatal (PD) day 4 through day 8 and killed at the age of 150 days. Additional groups of rats were treated with clozapine from PD 120–150. Self-spotted chips containing 340 cDNAs related to the glutamate system (“glutamate chips”) were used. The data show differential (up and down) regulations of numerous genes in frontal (FR), temporal (TE) and parietal cortex (PAR), and in caudate putamen (CPU), but evidently many more genes are upregulated in frontal and temporal cortex, whereas in parietal cortex the majority of genes are downregulated. Because of their primary presynaptic occurrence, five differentially expressed genes (CPX1, NPY, NRXN1, SNAP-25, and STX1A) have been selected for comparisons with clozapine-treated animals by qRT-PCR. Complexin 1 is upregulated in FR and TE cortex but unchanged in PAR by hypoxic treatment. Clozapine downregulates it in FR but upregulates it in PAR cortex. Similarly, syntaxin 1A was upregulated in FR, but downregulated in TE and unchanged in PAR cortex, whereas clozapine downregulated it in FR but upregulated it in PAR cortex. Hence, hypoxia alters gene expression regionally specific, which is in agreement with reports on differentially expressed presynaptic genes in schizophrenia. Chronic clozapine treatment may contribute to normalize synaptic connectivity
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