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A simple and selective method was validated for the determination of nitrates (V) and (III) by ion chromatography technique. Efficient ion separation was achieved on a column IonPacTM AG-9HC, (4 × 50 mm). A conductometric detector was used for the detection of the analyte. The mobile phase consisted of 9.0 mM sodium carbonate (Na2CO3) and was delivered in a isocratic mode at a flow rate of 1.0 ml·min-1 at 30 °C. The method was validated for linearity, selectivity, precision, limit of detection LOD, limit of quantitation LOQ and uncertainty. The method demonstrates good linearity, with r = 0.998. The uncertainty is 29.0% and 35.0% for nitrates (V) and (III), respectively. The limit of detection (LOD) values are 0.080 mg·dm-3 and 0.040 mg·dm-3 for nitrates (V) for nitrates (III), respectively. Limit of quantitation (LOQ) values are 0.240 mg·dm-3 and 0.120 mg·dm-3 for nitrates (V) and (III), respectively. The low limit of detection and limit of quantitation of nitrate and nitrite ions enables the detection and quantitation of these ions at low concentrations. This method is characterized by high selectivity.
The results of investigations on infection of P. nigra by Dothistroma septospora in seed plantation of the Miechów Forest District are presented in this paper. Disease symptoms were analized and the infection intensity depending on the needle age and location in the tree crown was estimated. The differences between individual progenies, and between individual plantation plots with respect to the disease intensity were also analized. The danger created for Pinus sylvestris by the inoculum of D. septospora accumulated on P. nigra was pointed out in the discussion.
BACKGROUND AND AIMS: Alzheimer’s disease (AD) develops for decades, but the molecular mechanism of pathogenesis is poorly understood. In result, an effective AD cure is still missing. According to the cell cycle (CC) hypothesis, one of the AD causes is CC reactivation in mature neurons. We aimed at elucidation if similar CC alterations occur in AD brain neurons and in peripheral blood cells. METHODS: As the study materials, we used 40 lines of immortalized lymphoblasts from sporadic AD (SAD) patients and 40 lines from healthy non-demented individuals (controls)1-4. CC in lymphocytes was analyzed by real-time PCR-arrays, immunoblotting, and flow cytometry. Human post mortem brain tissue from AD patients was prepared by paraffin embedding and microscopic tissue slides of hippocampus and enthorinal cortex was analyzed by antip21 immunohistochemical staining. RESULTS: Our data demonstrated aberrant CC in SAD lymphoblasts that involved a prolongation of the G1 phase driven by a marked increase of levels of p21 protein (Walf1/Cip1/Sid1), the key regulator of the G1/S CC checkpoint and of apoptosis. Consistently, we also found differences in p21 levels and its signaling pathway in apoptotic response of SAD lymphoblasts to redox stess. The analysis of p21 protein levels and related signaling in AD brain neurons will also be presented. CONCLUSIONS: In summary, these studies indicate that p21-related molecular changes underlie altered cell cycle and apoptosis in AD pathology and may represent novel therapeutic targets. Moreover, our data show that AD have a features of a systemic disease with CC alterations in peripheral lymphoblasts which thus have a potential diagnostic value. Support: CEPT, Polish National Science Centre grant NN401 596840, and JPND grant 2/BIOMARKAPD/JPND/2012.
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