224 research outputs found
Lifestyle factors and lumbar disc disease: results of a German multi-center case-control study (EPILIFT)
Introduction: In the large-scale case-control study EPILIFT, we investigated the dose-response relationship between lifestyle factors (weight, smoking amount, cumulative duration of different sports activities) and lumbar disc disease. Methods: In four German study regions (Frankfurt am Main, Freiburg, Halle/Saale, Regensburg), 564 male and female patients with lumbar disc herniation and 351 patients with lumbar disc narrowing (chondrosis) aged 25 to 70 years were prospectively recruited. From the regional population registers, 901 population control subjects were randomly selected. In a structured personal interview, we enquired as to body weight at different ages, body height, cumulative smoking amount and cumulative duration of different sports activities. Confounders were selected according to biological plausibility and to the change-in-estimate criterion. Adjusted, gender-stratified odds ratios with 95% confidence intervals were calculated using unconditional logistic regression analysis. Results: The results of this case-control study reveal a positive association between weight and lumbar disc herniation as well as lumbar disc narrowing among men and women. A medium amount of pack-years was associated with lumbar disc herniation and narrowing in men and women. A non-significantly lowered risk of lumbar disc disease was found in men with high levels of cumulative body building and strength training. Conclusions: According to our multi-center case-control study, body weight might be related to lumbar disc herniation as well as to lumbar disc narrowing. Further research should clarify the potential protective role of body building or strength training on lumbar disc disease
Functional characterization of P2Y and P2X receptors in human eosinophils
Activation of purinoceptor by ATP induces in eosinophils various cell responses including calcium transients, actin polymerization, production of reactive oxygen metabolites, CD11b-expression, and chemotaxis. Here, the effect of ion channel-gated P2X and/or G protein-coupled P2Y receptor agonists ATP, ATPgammaS, alpha,beta-meATP, 2-MeSATP, BzATP, ADP, CTP, and UTP on the intracellular Ca(2+)-mobilization, actin polymerization, production of reactive oxygen metabolites, CD11b expression and chemotaxis of human eosinophils were measured and the biological activity was analyzed. Although all tested nucleotides were able to induce all these cell responses, the biological activity of the analyzed nucleotides were distinct. Agonists of the G protein-coupled P2Y receptors such as 2-MeSATP, UTP, and ADP have a higher biological activity for production of reactive oxygen metabolites, actin polymerization and chemotaxis in comparison to the ion channel-gated P2X agonists alphabeta-meATP, BzATP, and CTP. In contrast, P2Y and P2X agonist showed similar potencies in respect to intracellular calcium transient and CD11b up-regulation. This conclusion was further supported by experiments with receptor iso-type antagonist KN62, EGTA or with the G(i) protein-inactivating pertussis toxin. These findings indicate participation of different purinorecptors in the regulation of cell responses in eosinophils
Neural control of curved walking in people with stroke
Presented at the International Society of Posture and Gait Research Congress, Bologna, Italy (June 21-25, 2009).
During curved walking, muscle activity and foot pressure distribution must be adapted according to path curvature in order to accommodate to the specific demands of turning.
The purpose of this study was to assess whether stroke participants would adapt to the task of turning by modulating muscle activity and foot pressure distribution with changes to path curvature as seen in able-bodied individuals.Not peer reviewedposter
Adenosine triphosphate-induced oxygen radical production and CD11b up- regulation: Ca++ mobilization and actin reorganization in human eosinophils
Eosinophils are major effector cells in cellular inflammatory conditions such as parasitic infections, atopic diseases, bullous dermatoses, and vasculitis. Biological activities of adenosine triphosphate (ATP) were characterized in human eosinophils and compared with those of other eosinophil activators such as complement fragment product C5a, platelet-activating factor (PAF), and eotaxin. ATP initiated production of reactive oxygen metabolites, as demonstrated by lucigenin-dependent chemiluminescence. Furthermore, ATP caused up-regulation of the integrin CD11b. In addition, fluorescence microscope measurements labeled with fura-2 (1-[2-(5-carboxy-oxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2' -amino-5' -methyl-phenoxy)-ethane-N, N, N, N'-tetraacetic acid, pentaacetoxymethyl ester) eosinophils in the presence or absence of ethyleneglycotetraacetic acid (EGTA) indicated that there was Ca(++) mobilization from intracellular stores by ATP. Flow cytometric studies showed transient actin polymerization upon stimulation with ATP and its stable analogues adenosine 5'-0-(3-thiotriphosphate) and 2-methylthioadenosine triphosphate tetrasodium (met-ATP). The reactions induced by ATP were comparable to those obtained by C5a, PAF, and eotaxin. Production of reactive oxygen metabolites and actin polymerization after stimulation with ATP was inhibited by pertussis toxin, which indicated involvement of receptor-coupled guanine nucleotide-binding proteins (G(i) proteins). In addition, experiments with oxidized ATP also suggest involvement of P2X receptors in this activation process. The results show that ATP is a strong activator of eosinophils and has biological activity comparable to those of the eosinophil chemotaxins C5a, PAF, and eotaxin. The findings strongly suggest a role of ATP in the pathogenesis of eosinophilic inflammation as an activator of proinflammatory effector functions
P2 purinergic receptors of human eosinophils: characterization and coupling to oxygen radical production
Extracellular nucleotides elicit multiple responses in eosinophils but no information on expression of purinergic receptors in these cells is available so far. In the present study we show that human eosinophils express the following P2Y and P2X subtypes: P2Y(1), P2Y(2), P2Y(4), P2Y(6), P2Y(11), and P2X(1), P2X(4), P2X(7), whose stimulation results in intracellular Ca(2+) increase and production of large amounts of reactive oxygen intermediates. These events are stimulated or inhibited, respectively, by P2 receptor agonists or antagonists
Luttmann, Louise (Death, 1886-03-19)
Address: Moore & LibertyAge at death: 6Pg.167/1886/340/F W S/Cinti/Dr. E.E.Sattler/Meyer/St. MarysOriginal record filed in drawer labeled 'LUCKER-LUTUHA'
Luttmann, Emil J. (Death, 1892-02-04)
Address: 61 Calhoun St.Age at death: 22 yrs.Pg 17/1892/126/MW S/Germany/Dr. A. T. Juettner/Geo. Meyer/St.Mary'sOriginal record filed in drawer labeled 'LUCKER-LUTUHA'
P2 receptors-mediated responses in human eosinophils.
Although it is increasing appreciated that P2 receptors play a pivotal role in macrophage and dendritic cell functions, little is known about expression and function of P2 receptors in human eosinophils (1, 2). We have investigated expression and function of P2 receptors expressed in these cells, with the following results:
A) Human eosinophils express mRNA for the following P2 receptor subtypes: P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, and P2X1, P2X4, P2X7.
B) Stimulation with extracellular nucleotides results in:
a) Intracellular Ca2+ increases.
b) Actin polymerization.
c) Production of large amounts of reactive oxygen intermediates. These events were inhibited by P2 receptors antagonists.
d) CD11b-expression.
e) Chemotaxis.
Although all tested nucleotides (ATP, ATPgammaS, alpha,beta-meATP, 2-MeSATP, BzATP, ADP, CTP and UTP) are able to induce all the reported responses, agonists that preferentially activate G protein-coupled P2Y receptors (2-MeSATP, UTP and ADP) are more potent than the P2X agonists alpha,beta-meATP and BzATP in inducing the production of reactive oxygen metabolites, actin polymerization and chemotaxis. On the contrary, both P2Y and P2X agonists show similar potency in inducing intracellular calcium transients and CD11b up-regulation. These conclusions are further supported by experiments with pertussis toxin, KN-62 or by experiments performed in Ca2+-free conditions, indicating participation of different P2 receptor subtypes in the regulation of eosinophils responses (3, 4).
Bibliography:
1) Saito et al., 1991. Int Arch Allergy Appl Immunol 94:68-70.
2) Mohanty et al., 2001. J Allergy Clin Immunol 107:849-855.
3) Ferrari et al., 2000. FEBS Lett 486:217-224.
4) Idzko et al., 2001. J Cell Physiol 188:329-336
Luttmann, Edmund (Death, 1886-07-11)
Address: 593 WalnutAge at death: 2 mo204/Pg.207/1886/M W S/Cinti/Dr. A. Schwagemeyer/Geo. Meyer/St. MarysOriginal record filed in drawer labeled 'LUCKER-LUTUHA'
Plasma and fibroblasts of Tangier disease patients are disturbed in transferring phospholipids onto apolipoprotein A-I
Plasmas of patients with Tangier disease (TD) lack lipid-rich alpha-HDL which, in normal plasma, constitutes the majority of high density lipoprotein (HDL). Residual amounts of apolipoprotein (apo)A-I in TD plasma occur as lipid-poor or even lipid-free prebeta-HDL. By contrast to normal plasma, TD plasma does not convert prebeta-HDL into alpha-HDL. Moreover, fibroblasts of TD patients were found to be defective in secreting cholesterol or phospholipids in the presence of lipid-free apoA-I. We have therefore hypothesized that both defective conversion of prebeta-HDL into alpha-HDL and defective lipid efflux from TD cells onto lipid-free apoA-I result from a disturbance in phospholipid transfer occurring in both cellular and extracellular compartments. To test this hypothesis we established an assay that measures the activity of plasma, cells, and cell culture media to transfer radiolabeled phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylinositol (PI) from vesicles onto apoA-I, apoA-II, albumin, or reconstituted HDL. Plasmas, HDL, and lipoprotein-depleted plasma of normolipidemic probands as well as cell homogenates and culture media of normal fibroblasts were active at 37 degrees C but not at 4 degrees C in transferring radiolabeled PC, PI, and PE dose- and time-dependently onto either lipid-free apoA-I or reconstituted HDL. Transfer of glycerophospholipids onto apoA-II was much lower than onto apoA-I; transfer onto albumin was close to background. Compared to ten normolipidemic plasmas and four apoA-I-deficient plasmas, plasmas of six TD patients were significantly reduced by 40-50% in their glycerophospholipid transfer activities. Compared to eight normal fibroblast cell lines, homogenates and culture media of four TD fibroblast cell lines were reduced by 40-50% and 30-35%, respectively, in their activity to transfer PC, PI, or PE onto apoA-I. Our data suggest that in TD the same mechanism underlies both defective conversion of prebeta-HDL into alpha-HDL and impaired efflux of cellular lipids, namely a defective phospholipid transfer
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