| 1. |
- Alavi, Y., et al.
(författare)
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The dynamics of interactions between Plasmodium and the mosquito : a study of the infectivity of Plasmodium berghei and Plasmodium gallinaceum, and their transmission by Anopheles stephensi, Anopheles gambiae and Aedes aegypti
- 2003
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Ingår i: International Journal of Parasitology. - : Elsevier. - 0020-7519 .- 1879-0135. ; 33:9, s. 933-943
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Tidskriftsartikel (refereegranskat)abstract
- Knowledge of parasite–mosquito interactions is essential to develop strategies that will reduce malaria transmission through the mosquito vector. In this study we investigated the development of two model malaria parasites, Plasmodium berghei and Plasmodium gallinaceum, in three mosquito species Anopheles stephensi, Anopheles gambiae and Aedes aegypti. New methods to study gamete production in vivo in combination with GFP-expressing ookinetes were employed to measure the large losses incurred by the parasites during infection of mosquitoes. All three mosquito species transmitted P. gallinaceum; P. berghei was only transmitted by Anopheles spp. Plasmodium gallinaceum initiates gamete production with high efficiency equally in the three mosquito species. By contrast P. berghei is less efficiently activated to produce gametes, and in Ae. aegypti microgamete formation is almost totally suppressed. In all parasite/vector combinations ookinete development is inefficient, 500–100,000-fold losses were encountered. Losses during ookinete-to-oocyst transformation range from fivefold in compatible vector parasite combinations (P. berghei/An. stephensi), through >100-fold in poor vector/parasite combinations (P. gallinaceum/An. stephensi), to complete blockade (>1,500 fold) in others (P. berghei/Ae. aegypti). Plasmodium berghei ookinetes survive poorly in the bloodmeal of Ae. aegypti and are unable to invade the midgut epithelium. Cultured mature ookinetes of P. berghei injected directly into the mosquito haemocoele produced salivary gland sporozoites in An. stephensi, but not in Ae. aegypti, suggesting that further species-specific incompatibilities occur downstream of the midgut epithelium in Ae. aegypti. These results show that in these parasite–mosquito combinations the susceptibility to malarial infection is regulated at multiple steps during the development of the parasites. Understanding these at the molecular level may contribute to the development of rational strategies to reduce the vector competence of malarial vectors.
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| 2. |
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| 3. |
- Hines, C J, et al.
(författare)
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Characterization of endotoxin and 3-hydroxy fatty acid levels in air and settled dust from commercial aircraft cabins.
- 2003
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Ingår i: Indoor Air. - : Hindawi Limited. - 0905-6947. ; 13:2, s. 166-173
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Tidskriftsartikel (refereegranskat)abstract
- Endotoxin was measured in air and dust samples collected during four commercial aircraft flights. Samples were analyzed for endotoxin biological activity using the Limulus assay. 3-hydroxy fatty acids (3-OH FA) of carbon chain lengths C10:0-C18:0 were determined in dust by gas chromatography-ion trap tandem mass spectrometry. The geometric mean (geometric standard deviation) endotoxin air level was 1.5 EU/m3 (1.9, n = 28); however, significant differences were found by flight within aircraft type. Mean endotoxin levels were significantly higher in carpet dust than in seat dust (140 ± 81 vs. 51 ± 25 EU/mg dust, n = 32 each, P < 0.001). Airborne endotoxin levels were not significantly related to either carpet or seat dust endotoxin levels. Mean 3-OH FA levels were significantly higher in carpet dust than in seat dust for C10:2, C12:0, and C14:0 (P < 0.001 for each), while the mean level of C16:0 was significantly higher in seat dust than in carpet dust (P < 0.01). Carpet dust endotoxin was significantly, but moderately, correlated with 3-OH-C12:0 and 3-OH-C14:0 (Pearson r = 0.52 and 0.48, respectively), while correlation of seat dust endotoxin with individual 3-OH FAs depended on the test statistic used. Mean endotoxin potency was significantly higher for carpet dust than for seat dust (6.3 ± 3.0 vs. 3.0 ± 1.4 EU/pmol LPS, P < 0.0001). Mean endotoxin levels in the air and dust of commercial aircraft cabins were generally higher than mean levels reported in homes and office buildings. These results suggest that exposure route and dust source are important considerations when relating endotoxin exposure to specific health outcomes.
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| 5. |
- Chen, QJ, et al.
(författare)
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Untitled
- 2004
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Ingår i: MOLECULAR AND BIOCHEMICAL PARASITOLOGY. - : Elsevier BV. - 0166-6851. ; 134:1, s. 1-1
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Waters, DD, et al.
(författare)
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Effects of atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction : A myocardial ischemia reduction with aggressive cholesterol lowering (MIRACL) substudy
- 2002
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Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 106:13, s. 1690-1695
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Tidskriftsartikel (refereegranskat)abstract
- Background - This report describes the effect of intensive cholesterol lowering with atorvastatin on the incidence of nonfatal stroke, a secondary end point, in a randomized, placebo-controlled trial of patients with unstable angina or non-Q-wave myocardial infarction. The primary end point, a composite of death, nonfatal myocardial infarction, resuscitated cardiac arrest, or recurrent symptomatic myocardial ischemia with objective evidence requiring emergency rehospitalization, was reduced from 17.4% in the placebo group to 14.8% in the atorvastatin group over the 16 weeks of the trial (P=0.048). Methods and Results - Strokes were adjudicated by a blinded end-point committee using standard clinical and imaging criteria. The outcomes of nonfatal stroke and fatal plus nonfatal stroke were analyzed by time to first occurrence during the 16-week trial. Of 38 events (in 36 patients) adjudicated as fatal or nonfatal strokes, 3 were classified as hemorrhagic, one as embolic, and 29 as thrombotic or embolic, 5 could not be categorized. Nonfatal stroke occurred in 9 patients in the atorvastatin group and 22 in the placebo group (relative risk, 0.40, 95% confidence intervals, 0.19 to 0.88, P=0.02). Fatal or nonfatal stroke occurred in 12 atorvastatin patients and 24 placebo patients (relative risk, 0.49, 95% confidence intervals, 0.24 to 0.98, P=0.04). All 3 hemorrhagic strokes occurred in the placebo group. Conclusion - Intensive cholesterol lowering with atorvastatin over 16 weeks in patients with acute coronary syndromes reduced the overall stroke rate by half and did not cause hemorrhagic stroke. These findings need to be confirmed in future trials.
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