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PMC1134660
15862124
1
1471-2288-5-15-1
null
Figure 1 UK Hip trial: results for any treatment in strong-suspicion and moderate-suspicion subgroups. Points on the red diagonal line indicate lack of effect; points on the other lines indicate the same risk difference (RD), risk ratio for harm (RR(H)), risk ratio for benefit (RR(B)) or odds ratio (OR) as in the strong-suspicion subgroup.
CC BY
no
2022-01-12 14:34:15
BMC Med Res Methodol. 2005 Apr 29; 5:15
PMC1134661
15865626
1
1471-2202-6-31-1
null
Figure 1 Schematic representations (redrawn from Paxinos and Watson's Atlas, 1997) of the cerebral areas implanted with dialysis probes.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
2
1471-2202-6-31-2
null
Figure 2 A: microphotograph showing the electrode localization into the locus coeruleus. B: schematic representation of locus coeruleus stimulation parameters; each vertical line represent a stimulus (700 μA, 250 μs), burst were delivered in 250 ms.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
3
1471-2202-6-31-3
null
Figure 3 Effect of locus coeruleus stimulation on extracellular NA and DA levels in the medial prefrontal and occipital cortex . Stimuli were delivered in bursts, as described in Methods, for a duration of 20 min (horizontal solid lines). Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test)
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
4
1471-2202-6-31-4
null
Figure 4 Effect of locus coeruleus stimulation on extracellular NA and DA levels in the medial prefrontal and occipital cortex locally perfused with TTX . TTX perfusion started after collection of basal samples, as indicated by the dashed line. Burst stimuli were delivered 40 min (two samples) after the beginning of TTX perfusion, for a duration 20 min (horizontal solid line). Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test).
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
5
1471-2202-6-31-5
null
Figure 5 Effect of repeated locus coeruleus stimulation on extracellular NA and DA levels in the medial prefrontal and occipital cortex . Stimuli were delivered in bursts, as described in Methods (horizontal solid lines). Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test).
CC BY
no
2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
6
1471-2202-6-31-6
null
Figure 6 Effect of TTX perfusion during repeated locus coeruleus stimulation on extracellular NA and DA levels in the occipital cortex . Stimuli were delivered in bursts, as described in Methods (horizontal solid lines). TTX perfusion started with the third stimulation administration, as indicated by the dashed line. Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test).
CC BY
no
2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
7
1471-2202-6-31-7
null
Figure 7 Effect of repeated locus coeruleus stimulation on extracellular NA and DA levels in the medial prefrontal cortex and caudate nucleus. Stimuli were delivered in bursts, as described in Methods (horizontal solid lines). Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test).
CC BY
no
2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
8
1471-2202-6-31-8
null
Figure 8 Effect of repeated locus coeruleus stimulation on extracellular NA and DA levels in the medial prefrontal and occipital cortex locally perfused with DMI . 100 μM DMI was administered through reverse dialysis for at least 2 h before stimulation, as represented by the dotted line. Stimuli were delivered in bursts, as described in Methods, for a duration 20 min (horizontal solid lines). Data are means ± SE, expressed as percent of mean basal value. Filled symbols indicate p < 0.05 with respect to basal values (Dunnett test).
CC BY
no
2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134661
15865626
9
1471-2202-6-31-9
null
Figure 9 Effect of stimulation outside the locus coeruleus on extracellular NA and DA levels in the medial prefrontal cortex and caudate nucleus . Stimuli were delivered in bursts, as described in Methods (horizontal solid lines). Data are means ± SE, expressed as percent of mean basal value.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 2; 6:31
PMC1134662
15869709
1
1471-2202-6-32-1
null
Figure 1 Composite of injection sites shown on the medial (A), lateral (B) and orbital (C) surfaces of the right cerebral hemisphere . The injection sites are superimposed on an architectonic map of the prefrontal cortex [38]. Different cortical types are depicted in shades of grey as follows: 1 (darkest grey) agranular areas with three distinguishable layers; 2, dysgranular areas with four distinguishable layers, including a poorly developed layer IV; 3–5, eulaminate areas with increasing cellular density and thickness of layer IV from levels 3 to 5. In A-C, small dashed lines demarcate architectonic areas indicated by numbers; large dashed lines depict the cortex buried in sulci. MPAll, OPAll, OPro, OLF indicate architectonic areas. Letters before architectonic areas designated by letters or numbers denote: C, caudal; L, lateral; M, medial; O, orbital; R, rostral. Other letter combinations refer to cases. Abbreviations: A, arcuate sulcus; Cg, cingulate sulcus; LF, lateral fissure; ST, superior temporal sulcus.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
2
1471-2202-6-32-2
null
Figure 2 Comparison of contralateral to ipsilateral projections . Cases on the abscissa are identified by the area of the injection of neural tracer. Multiple cases with injection of tracers in the same area are identified by the number in parenthesis after each case. (A) Ratios of contralateral to ipsilateral projection densities. Values were calculated as the total number of contralateral neurons retrogradely labeled by an injection, divided by all labeled neurons ipsilaterally. (B) Ratios of contralateral to ipsilateral projection frequencies. Values were determined as the total number of areas with projection neurons on the contralateral side, divided by all areas with projection neurons in the ipsilateral hemisphere. Projections were included independently of their density and matching origins in the two hemispheres. (C) Strength of correlation between contralateral and ipsilateral projection patterns.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
3
1471-2202-6-32-3
null
Figure 3 Non-metric multidimensional scaling (NMDS), assessing the pairwise similarities of projection patterns among cases . Cases are identified by the area of tracer injection. Multiple cases with injection of tracer in the same area are identified by the number in parenthesis after each case. Since NMDS configurations are invariant to rotation, the coordinate axes provide a scale of relative similarity, but do not prescribe specific dimensions, and are left unlabeled. (A) ipsilateral cases; (B) contralateral cases. Similarity was defined as the correlation of relative retrograde projection patterns resulting from the injections. The two main projection systems apparent in the diagram consist of predominantly mediodorsal areas (to the left), and basoventral areas (to the right) for both ipsilateral (A) and contralateral (B) projections.
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
4
1471-2202-6-32-4
null
Figure 4 Regional average for ratios of contralateral to ipsilateral projection densities . The apparent trend of progressively smaller contralateral projection densities in medial prefrontal, orbital and lateral prefrontal cortices was significant (rank correlation ρ, p < 0.01).
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
5
1471-2202-6-32-5
null
Figure 5 Bilateral distribution of projections neurons directed to orbitofrontal cortices . Coronal sections through the prefrontal cortex showing labeled neurons in ipsilateral (ipsi) and contralateral (contra) hemispheres after infection of tracers in three cases. Rostral to caudal sections are shown from left to right (case AF), and top to bottom (cases BCb and AM). (Top) The injection of HRP was in area OPro (A, B, black area) and labeled neurons are seen in layers II-III (blue dots) and layers V and VI (red dots); (Left) Injection of fast blue was in area OPro (C), blue area). (Right) Injection of HRP was in the rostral part of area 11 (not shown). Dotted lines through the cortex in the coronal sections show the bottom of layer IV. Architectonic areas indicated by letters include: OPAll, orbital periallocortex; OPro, orbital proisocortex. Other architectonic areas are indicated by numbers. Abbreviations: A, arcuate sulcus; Cg, cingulate sulcus; LF, lateral fissure; LO, lateral orbital sulcus; MO, medial orbital sulcus; P, principal sulcus.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
6
1471-2202-6-32-6
null
Figure 6 Bilateral distribution of projection neurons directed to medial prefrontal and lateral prefrontal cortices . Coronal sections through the prefrontal cortex showing labeled neurons in ipsilateral (ipsi) and contralateral (contra) hemispheres after infection of tracers in three cases. Labeled neurons were found in layers II-III (blue dots) and in layers V-VI (red dots). In all cases rostral sections are shown on the left, and caudal on the right. (Top) Injection of HRP-WGA (A, black area) was in medial area 32. (Center) Injection of HRP-WGA was in medial area 9 (not shown). (Bottom) Injection of fast blue was in dorsal area 46 (not shown). Dotted lines through the cortex in the coronal sections show the bottom of layer IV. Abbreviations as in Figure 5.
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
7
1471-2202-6-32-7
null
Figure 7 Comparison of border distance and structural type (Δ) as determinants of the pattern of contralateral projections . (A) Frequency of contralateral projections depending on border distance, defined as the number of borders between the contralateral area of projection origin and the area homotopic to the injection site. (B) The relationship of the density of contralateral projections to border distance (Spearman's ρ = -0.87; p (two-tailed) < 0.0002). (C) Frequency of contralateral projections as a function of the absolute structural type difference of the linked areas, delta (|Δ|). (D) The relationship of the density of contralateral projections to the type similarity between the contralateral area of origin and the ipsilateral target area, |Δ| (Spearman's ρ = -0.96; p (two-tailed) < 0.0005). Note that in panels A and C data were pooled over adjacent intervals to avoid artificial variance from sparsely filled categories. In these cases, a distance or Δ of '2', for instance, included data for distance or Δ for 2 proper as well as for 2.5.
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
8
1471-2202-6-32-8
null
Figure 8 Average proportion of laminar origins in superficial layers II-III for ipsilateral and contralateral projections . Data from all cases were included, except for instances where a projection resulted in fewer than 20 neurons. The black and white bars, respectively, add up to 1.0.
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
9
1471-2202-6-32-9
null
Figure 9 Comparison of the relative origin of projection neurons in superficial cortical layers II-III in ipsilateral and contralateral areas . Relative laminar origin of: (A) ipsilateral; (B) contralateral projections. The x-axis shows the proportion of projection neurons found in the upper cortical layers II-III, plotted into intervals of 10% (e.g., in the interval '.8,.9', 80%–90% of projection neurons were located in layers II-III, and the remaining 10%–20% were found in the deep layers, V-VI). Projections originating predominantly from layers V-VI are shown on the left, and projections originating in layers II-III are shown on the right. Projection neurons found in approximately equal proportions in superficial and deep layers are shown in the center. Ipsilateral projections (A) showed a broad Gaussian distribution of laminar origin patterns. By contrast, the distribution of contralateral projection origins (B) was more restricted and skewed towards the superficial layers.
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
10
1471-2202-6-32-10
null
Figure 10 Comparison of the relationship of laminar origin of contralateral projection neurons to structural type and border distance . (A) The x-axis represents the type level difference, Δ), calculated as level (projection origin) – level (projection target, that is, injection site). Normalized origins of contralateral projection neurons varied significantly with Δ (Spearman's ρ, = 0.70; p < 0.04). (B) The x-axis represents the border distance from the injection site on the contralateral side (Spearman's ρ, = -0.04, p > 0.91).
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1134662
15869709
11
1471-2202-6-32-11
null
Figure 11 Comparison of the distribution of projection neurons in the supragranular layers II-III in matched areas on the contralateral and ipsilateral hemispheres for individual cases . (A-C) Areal distribution of projection neurons in cases with injection of tracer in orbitofrontal areas (area OPro, case ALy; area 13, case ALb; area 11, case AM); (D) In a case with injection of tracer in medial area 9 (case AO); (E) In a case with injection in dorsal area 46 (case BFb). In all cases the prevalence of projection neurons in layers II-III in most areas is higher on the contralateral side (silhouette bars) than on the ipsilateral side (black bars).
CC BY
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2022-01-12 14:24:44
BMC Neurosci. 2005 May 3; 6:32
PMC1135295
15901208
1
pbio.0030192.g001
null
Figure 1 Architecture of the Liver Sinusoid Liver sinusoids (S) are lined by fenestrated endothelia (EC) and interspersed Kupffer cells (KC), the resident macrophages of the liver. Stellate cells (SC), the major producers of liver ECM, are located inside the narrow space of Disse (D), which is formed by the sinusoidal cell layer and cords of hepatocytes (H).
CC BY
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
2
pbio.0030192.g002
null
Figure 2 Distribution of GFP-Expressing Endothelia and Kupffer Cells in the Liver (A) Confocal microscopy demonstrates the GFP distribution in sinusoidal endothelia from a Tie2-GFP mouse. GFP is most prominent in the perinuclear region (arrowheads) of endothelia located in the periphery of the liver lobule. (B) A still image from an intravital movie shows GFP-expressing endothelia lining the sinusoids of a Tie2-GFP mouse. Kupffer cells can be identified by their orange autofluorescent lysosomes (arrowheads). (C) Star-shaped Kupffer cells (arrowheads) are located in sinusoids of a lys-EGFP-ki mouse liver. (D) Round blood granulocytes (arrows), traveling with the bloodstream or crawling along the sinusoidal cell layer, exhibit a stronger GFP signal than Kupffer cells (still image extracted from an intravital movie). Note the orange autofluorescence of the Kupffer cell lysosomes (arrowheads). Bar = 10 μm. See Videos S1 and S2 .
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
3
pbio.0030192.g003
null
Figure 3 Sporozoite Gliding along the Sinusoidal Endothelium (A) A P. berghei sporozoite expressing fluorescent RedStar protein glides with and against the bloodstream inside a liver sinusoid of a Tie2-GFP mouse. The arrow indicates the overall movement of the parasite. (B) The projection through the same area of the liver visualizes the outline of the highly branched sinusoids. The direction of the blood flow is indicated by the dashed arrows. Bar = 10 μm. See Videos S3 and S4 .
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
4
pbio.0030192.g004
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Figure 4 Sporozoite Passage into the Liver Parenchyma (A–E) show individual frames extracted from an intravital movie; (F) is a projection visualizing the transmigration path of the GFP P. berghei sporozoite in a Tie2-GFP mouse liver. (G–I) show projections from an intravital movie demonstrating the path of the parasite; its overall direction is indicated by arrows (dotted lines). (A) After gliding along a sinusoid, a sporozoite has encountered a Kupffer cell, which it faces with its apical cell pole. (B and C) Following a pause, the parasite slowly enters the Kupffer cell. (D and E) Sporozoite passage into the liver parenchyma occurs at a slow speed and involves the formation of a constriction in the parasite (arrow). (F) Once inside the liver tissue, the sporozoite increases its speed and transmigrates through several hepatocytes. (G) A projection from an intravital movie shows the path of a GFP P. berghei sporozoite gliding against the bloodstream along a sinusoid in a lys-EGFP-ki mouse liver. Eventually, the parasite encounters a Kupffer cell. (H) The sporozoite stops, facing the phagocyte with its apical cell pole. The outline of the two Kupffer cells in the image is indicated by dotted lines. (I) After slowly passing through the Kupffer cell, the sporozoite enters the liver parenchyma and migrates through several hepatocytes. Bars = 10 μm. See Videos S5 and S6 .
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
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pbio.0030192.g005
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Figure 5 P. berghei Sporozoite Transmigration Is Independent of the Species of the Infected Host Projections of typical GFP P. berghei sporozoite paths show that the parasites transmigrate in a similar fashion through many hepatocytes in mouse ([A] Tie2-GFP mouse; [B] lys-EGFP-ki mouse) and also in rat livers (C and D). Bars = 10 μm. See Videos S7 and S8 .
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
6
pbio.0030192.g006
null
Figure 6 Unsuccessful Attempts of Liver Infection (A) The composite image of ten selected frames from an intravital movie shows a paralyzed or dead P. berghei sporozoite that is eventually dislodged and flushed out of the liver lobule (short arrows). The parasite maintains a fixed crescent shape, fails to cling to the sinusoidal cell layer, and makes no attempt to glide against the bloodstream. The long arrow (dotted line) indicates the direction of the blood flow. (B) Projection composed of 14 selected frames extracted from an intravital movie showing a GFP P. berghei sporozoite that initially transmigrates in the liver parenchyma (dotted lines), but then reenters a sinusoid (arrow) and is swept away with the bloodstream (solid lines). Bars = 10 μm. See Videos S9 and S10 .
CC BY
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
7
pbio.0030192.g007
null
Figure 7 Transmigrating Plasmodium Sporozoites Leave Behind a Trail of Dead Hepatocytes (A) Three hours after infection with 5 × 10 6 P. berghei salivary gland sporozoites, a mouse liver contains small clusters of necrotic hepatocytes that have been infiltrated by inflammatory cells (arrows). (B) Four hours after intravenous infection with 5 × 10 6 P. yoelii sporozoites, a mouse liver contains individual or small clusters of necrotic hepatocytes (arrows). (C) Six hours after infection, the signs of hepatocytic damage appear more severe in another mouse liver (arrow). (D) Forty hours after inoculation of 2 × 10 6 P. yoelii sporozoites, small infiltrates of inflammatory cells (arrows) block the lumina of some sinusoids, while maturing EEFs are free of any inflammatory reaction. (E) Fifty hours after infection with 2 × 10 6 P. yoelii sporozoites, the size of the inflammatory infiltrates (arrows) has increased. Stains used: (A) paraffin section stained with H&E, (B and C) frozen sections stained with Evans blue, (D and E) semithin Epon sections stained with Toluidine blue. Bars = 20 μm.
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
8
pbio.0030192.g008
null
Figure 8 Sporozoites, Surrounded by a Parasitophorous Vacuole Membrane, Can Be Found in Intact Hepatocytes (A) Six hours after infection by bite of 50 P. yoelii –infected mosquitoes, electron microscopic examination of a mouse liver shows a sporozoite inside an intact hepatocyte. Note that the parasite is enclosed in a parasitophorous vacuole (insert). The neighboring hepatocyte shows signs of cytoplasmic swelling. (B and C) P. yoelii –infected mouse livers contain hepatocytes that exhibit various degrees of necrosis, ranging from hydropic swelling to near-complete disintegration of the cell, adjacent to parenchymal cells with a normal ultrastructure (arrows). The normal hepatocytes did not contain a sporozoite in the plane of the section. L, lipid droplet; M, mitochondrium; N, nucleus; S, sinusoid. Bars = 1 μm.
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
9
pbio.0030192.g009
null
Figure 9 Sporozoite Transmigration Causes Histopathological Changes in the Liver Mouse livers were removed 2 d (A–D) or 7 d (E–H) after daily infection with P. yoelii by bite of 150 mosquitoes and stained with H&E (A and E) or Masson's trichrome (B and F). Other sections were subjected to immunohistochemistry using mAb PC10 against proliferating cell nuclear antigen (C and G) or mAb HHF35 against smooth muscle actin (D and H). In contrast to the livers fixed after 2 d of infection, in which only a few cells reacted with mAb PC10 and mAb HHF35 (arrows in C and D), livers examined after 7 d of infection showed (E) increased numbers of nonparenchymal cells lining the sinusoids (arrow), (F) a focal deposition of collagen (blue) in some spaces of Disse, (G) large numbers of proliferating nonparenchymal cells and hepatocytes (brown, arrows), and (H) a focal increase in the concentration of smooth muscle actin (brown, arrow).
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
10
pbio.0030192.g010
null
Figure 10 Sporozoite Infection Increases the Serum ALT Activity (A) Three mice were inoculated with salivary gland extract from 100 uninfected mosquitoes each (labeled “0” on the x -axis). Another three mice were infected by intravenous inoculation into the tail vein of 0.7 × 10 6 , 1.2 × 10 6 , or 1.8 × 10 6 purified P. yoelii sporozoites (indicated as “0.7,” “1.2,” and “1.8” on the x- axis). The ALT activity in the serum was determined before and after infection at the indicated time points. In comparison to the control serum drawn before infection, the ALT levels increased significantly and depended on the number of inoculated sporozoites in all mice during the observation period of 52 h. Uninfected salivary gland extract had only a temporary effect on the serum ALT level (9 h). The indicated values represent the average ± standard deviation of triplicate measurements. *, p < 0.005 in relation to the corresponding control sera. (B) No change in the serum ALT activity was detectable when three mice were infected with P. berghei by bite of 150 mosquitoes. The indicated values represent the average ± standard deviation of duplicate measurements. For ready comparison, the data were normalized for each animal prior to statistical analysis.
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135295
15901208
11
pbio.0030192.g011
null
Figure 11 Model of Plasmodium Sporozoite Infection of the Mammalian Liver The dual blood supply of the liver, consisting of branches of the portal vein and the hepatic artery, merges upon entry into the liver lobule at the portal field. The blood flows along the sinusoid and exits at the central vein. First sporozoites enter the liver lobule either via the portal vein or the hepatic artery, and then are abruptly arrested by binding to the sinusoidal cell layer. The initial binding is presumably mediated by stellate-cell-derived ECM proteoglycans that protrude from the space of Disse across the endothelial sieve plates into the sinusoidal lumen. After a pause, the parasites begin to glide along the sinusoid, frequently moving against the bloodstream, until they then encounter a Kupffer cell, on the surface of which they recognize selected chondroitin and heparan sulfate proteoglycans. Sporozoites position themselves with their apical cell pole facing the phagocyte. After a considerable pause, they slowly pass through the Kupffer cell and cross the space of Disse beyond it, exhibiting a clearly visible constriction. Once inside the liver parenchyma, the parasites increase their velocity and migrate for many minutes through several hepatocytes, before they eventually settle down in a final one for EEF development. Sporozoite transmigration results in a trail of necrotic hepatocytes, whose remains are subsequently removed by infiltrating inflammatory cells.
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2022-01-13 00:07:27
PLoS Biol. 2005 Jun 24; 3(6):e192
PMC1135296
15907155
1
pbio.0030196.g001
null
Figure 1 Levels of Polymorphism for Different Classes of Sites Levels of polymorphism were quantified using two different estimators of the neutral mutation rate θ : θ^ S , which uses the number of polymorphic sites, and θ^ P , which uses the average number of pairwise differences [ 3 ].
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
15907155
2
pbio.0030196.g002
null
Figure 2 Population Structure and Genomic Distributions of Various Statistics (A) Results from Structure under different assumptions about the number of clusters ( K = 2,..., 8). Each individual is represented by a line, which is partitioned into K colored segments according to the individual's estimated membership fractions in each of the K clusters. The assignment of each individual is the average across the genome. (B) Results from Structure across Chromosome 1 for K = 3. Each chromosomal segment is colored according to the cluster in which it had the highest probability of membership. (C) A plot showing those fragments that appear to be monophyletic with respect to each of the three clusters identified by Structure. (D) F ST with respect to the same three clusters (blue solid line) and the lower 95th percentile of F ST obtained through 1,000 random permutations of the accessions (red dotted line). (E) θ^ P within each of the three clusters. (F) Tajima's D statistic within each of the three clusters. (G) Results from Structure across Chromosome 1 for K = 8. (H) A plot showing those fragments that appear to be monophyletic with respect to each of these eight clusters. (I) F ST with respect to these eight clusters.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
15907155
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pbio.0030196.g003
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Figure 3 Population Structure in A. thaliana Each pie chart represents an accession, and is placed on the map according to origin (some of the population samples were too densely sampled and have been shifted for clarity). Accessions sampled outside Europe have been placed at the correct latitude. The exact origin of the standard lab accession Col-0 is not known. The colors and proportions within each pie chart correspond to the output of Structure in Figure 2 . (A) K = 3; (B) K = 8.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
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pbio.0030196.g004
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Figure 4 The Distribution of Pairwise Differences (SNPs Only) between All Pairs of Accessions (A) An example of the distribution we would expect to see in the absence of population structure, obtained by randomizing genotypes with respect to individuals for each sequenced fragment. (B) The observed distribution. (C) The observed distribution with accessions Cvi-0 and Mr-0 removed.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
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pbio.0030196.g005
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Figure 5 Haplotype Sharing on Chromosome 4 among Pairs of Individuals in the Population Samples from Northern Sweden, Central Europe, and the US The lines indicate regions where the particular pair of accessions share at least five identical adjacent fragments. Within-population comparisons are highlighted in red. The patterns in southern Sweden and in the UK are similar to that in central Europe.
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no
2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
15907155
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pbio.0030196.g006
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Figure 6 The Decay of LD as a Function of Distance between the Polymorphisms
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135296
15907155
7
pbio.0030196.g007
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Figure 7 Characteristics of the Pattern of Polymorphism (A) The allele frequency distribution for synonymous and nonsynonymous SNPs using a sample size of 90 individuals (loci with less than 90 individuals were not used; loci with greater than 90 individuals were randomly culled). For a sample of size n, the expected frequency of SNP loci with a minor allele frequency of i under a standard constant-size population genetics model is . The excess of rare alleles is largely limited to frequencies one and two. (B) The distribution of Tajima's D statistic [ 27 ] across the sequenced fragments, along with its expected distribution in a constant population (estimated by simulating 1,000 datasets matching the real one in terms of exon/nonexon composition and sample size). (C) The distribution of the level of polymorphism (θ^ S ) across the sequenced fragments along with its expected distribution (estimated the same way). (D) The level of polymorphism in nonexon sequences as a function of the local gene density (measured in open reading frames per centimorgan). (E) The level of polymorphism in nonexon sequences as a function of the degree of duplication in each fragment (measured as the negative log 10 of the BLAST significance for the second-best hit in the genome). The patterns in (D) and (E) are also seen in exons.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e196
PMC1135297
0
1
pbio.0030215.g001
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Tagged with red fluorescent protein, the malarial parasites in the sporozoite stage can be seen migrating along the sinusoids in a mouse liver
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2022-01-13 00:01:43
PLoS Biol. 2005 Jun 24; 3(6):e215
PMC1135298
15907156
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pbio.0030201.g001
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Figure 1 adgf-a Mutant Phenotype (A and B) Fat body disintegration visualized by GFP expression driven by Cg-Gal4 driver in the fat body. While adgf-a/+ heterozygous third instar larvae have normal flat layers of fat body (A), adgf-a mutant showed extensive fat body disintegration into small pieces of tissue (B). (C) Multiple melanotic tumors present in adgf-a mutant third-instar larva. (D) An adgf-a mutant pupa with typical abdominal curvature.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
PMC1135298
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pbio.0030201.g002
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Figure 2 Rescue of the adgf-a Mutant Phenotype by Expression of ADGF-A in Different Tissues (A) Percentage of pupae (blue bars) and adult flies (purple bars) demonstrating the larval and pupal survival, respectively, of the adgf-a mutant flies rescued by expression of transgenic ADGF-A in different tissues. Along the x -axis (which is shared with [B]), the rescue experiments are shown (marked by the Gal4 driver used for expression of ADGF-A except for first three sets of bars—the first set presents only an adgf-a mutant, the second an adgf-a mutant carrying HS-ADGF-A construct without heat shock, and the third with heat shock) and the y -axis represents percentage of pupae and adult flies out of the total number of transferred first-instar larvae of particular genotype. Each experiment was repeated at least four times (with 20–30 animals in each vial) and the standard error is shown. (B) Percentage of late third-instar larvae with melanotic tumors. The x -axis is shared with (A) (described above). The y -axis shows the percentage of larvae with tumors out of all larvae of each genotype examined for (A).
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
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Figure 3 Number of Circulating Hemocytes in Late Third-Instar Larvae Genotypes are shown along the x -axis, and the number of hemocytes/larva along the y -axis. Each bar shows the number of all circulating hemocytes, and the gray part of the bars represent the lamellocyte population. Each count was repeated five to ten times and the standard error is shown.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
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Figure 4 Hemocyte Abnormalities in adgf-a Mutant Larvae (A–E) Differential interference contrast microscopy of living circulating hemocytes (magnification 200×; scale bar, 10 μm). Round, nonadhesive plasmatocytes from wild-type larva (A). Hemocytes from the adgf-a mutant developing filamentous extensions (B and C) or membranous extension surrounding the cell (D). Large flat lamellocyte from the adgf-a mutant (E). (F and G) Differential interference contrast and fluorescent microscopy (merged image) of living circulating hemocytes stained by the Hml-GFP marker (magnification 100×; scale bar, 10 μm). While most of the cells from wild-type larvae are GFP-positive (F), just few of the cells from late third instar adgf-a larvae are stained by GFP at this stage (G). (H–J) Fluorescence microscopy of living larvae with Hml-GFP stained hemocytes (magnification 40×; scale bar, 100 μm). Posterior part of late third-instar wild-type larva (H). Middle sections of early third-instar larvae of wild type (I) and adgf-a mutant (J).
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
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Figure 5 Crystal Cells in Late Third Instar Larvae Crystal cells were visualized by heating larvae of different genotypes at 60 °C for 10 min [ 46 ]. (A) Wild-type larva, (B) adgf-a single mutant, (C) adoR adgf-a double mutant (scale bar, 0.5 mm).
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
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Figure 6 Suppression of the adgf-a Mutant Phenotype by Mutations in Other Genes (A) Percentage of late third-instar larvae with melanotic tumors (black bars) and fat body disintegration (green bars). The x -axis (which is shared with [B]), shows the genotype. The y -axis shows the percentage of larvae with tumors and fat body disintegration. (B) Survival rate of double mutants compared to single adgf-a mutant. The y -axis shows the percentage of the pupae (blue bars) and adult flies (purple bars) demonstrating the larval and pupal survival, respectively. Each experiment was repeated at least four times (with 20–30 animals in each vial) and the standard error is shown.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
PMC1135298
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pbio.0030201.g007
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Figure 7 Ecdysone Regulation of Development in adgf-a (A) Larvae of different genotypes were collected after L2/L3 molt, and the number of puparia was counted at different time points ( x -axis: hours after egg laying). The y -axis shows the percentage of puparia out of all collected third-instar larvae (three vials each with 30 animals; the standard error is shown). (B and C) Ring gland morphology in arrested adgf-a larvae. Approximately 8-d old mutant larva (i.e., 3 d after normal pupariation) with very extensive fat body disintegration (note the transparency of larva in the middle part with small white pieces of fat body) (B). The ring gland dissected from this larva (C) shows morphology of the normal ring gland before the degenerative changes of prothoracic gland starts (compare to schematic diagram to the left of [C], from [ 28 ]). (D–F) Expression of GFP-marked glue protein (SgsΔ3-GFP) in salivary gland of the adgf-a mutant larvae and pupae. All late third-instar larvae express the glue protein as shown on dissected salivary gland (D). Some mutants show typical expulsion from the glands with GFP totally external to the puparial case (E), while others do not expel glue proteins even after puparium formation (F).
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
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Figure 8 Genetic Interactions of Toll Signaling and ADGF-A Survival rate and melanotic tumor formation were compared in mutants in the Toll signaling pathway and in similar mutants with overexpression of ADGF-A using the HS-ADGF-A construct. (A) The bar graph shows the percentage of the pupae (blue bars) and adult flies (purple bars) demonstrating the larval and pupal survival of each genotype. The x -axis shows the genotypes and is shared with (B). Flies heterozygous for the cact mutation were used as a control. (B) Percentage of late third instar larvae presenting melanotic tumor formation.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
PMC1135298
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Figure 9 Schematic Map of the ADGF-A Gene with Promoter Analysis The ADGF-A gene contains four exons and two transcriptional starts [ 17 , 47 ]. We analyzed sequences preceding both transcriptional starts for the presence of known transcriptional factor binding sites using the software program Gene2Promoter (Genomatix Software GmbH). Selected sites are represented by color bars in approximate positions of promoter regions. The legend under the sequence show the names of transcription factors binding to matching colored binding sites.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 24; 3(7):e201
PMC1135299
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pbio.0030231.g001
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The global geographic structure of variation in Arabidopsis is shown by the clusters of similar pie charts signifying patterns of isolation (each chart represents an Arabidopsis accession)
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2022-01-13 00:07:28
PLoS Biol. 2005 Jul 24; 3(7):e231
PMC1135300
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pbio.0030232.g001
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Drosophila adgf-a mutant larvae with melanotic tumors in their body cavities
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2022-01-13 00:07:28
PLoS Biol. 2005 Jul 24; 3(7):e232
PMC1140679
15913420
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pbio.0030203.g001
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Figure 1 Expression Levels Are Allowed to Evolve toward Any Point in the Triangle For example, the circle corresponds to the additive case, where heterozygotes are equally likely to express either A only or a only and so have fitness halfway between the fitnesses of AA and aa individuals. The evolution of expression levels predicted by the quasi-linkage equilibrium analysis is indicated by the direction of arrows. Double-headed arrows indicate that the quasi-linkage equilibrium analysis predicts an outcome that depends on allele frequencies. Results from numerical simulations are shown as percentages of total parameter combinations that resulted in evolution of expression levels in the direction shown. Entries labelled “neutral” are cases where no change in modifier frequency occured. The range of parameter values used in these simulations is described in the main text. Predicted patterns for the host are shown in (A), and those for the parasite are shown in (B).
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e203
PMC1140679
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Figure 2 Co-Evolutionary Dynamics of Parasite Gene Expression In both panels, the frequency of a modifier allele that increases the expression of the B allele in the parasite population is shown in orange. The frequency of the B allele in the parasite population is shown in blue, and the frequency of the A allele in the host population is shown in maroon. Both panels considered an expression modifier introduced at an initial frequency of 0.5 with the following effects: ρ 1 [ MM ] = 0.75, ρ 1 [ Mm ] = 0.50, ρ 1 [ mm ] = 0.25, ρ 3 [ MM ] = 0.25, ρ 3 [ Mm ] = 0.5, ρ 3 [ mm ] = 0.75, and ρ 2 [ i ] = 1 − ρ 1 [ i ] − ρ 3 [ i ]. Parameters for the IMA model (A) were α h = 0.15, α p = 0.20, r h = 0.25, and r p = 0.25. Parameters for the GFG model (B) were γ h = 0.15, γ p = 0.20, C h = 0.075, C p = 0.10, c h = 0.0075, c p = 0.01, r h = 0.25, and r p = 0.25. In both panels, the initial frequency of the A allele and the B allele was 0.55.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e203
PMC1140680
16000018
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pbio.0030223.g001
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Figure 1 Feeding Rates of Female Drosophila on Food Media with Different Nutrient Concentrations Feeding rates were recorded by direct observation as the proportion of time flies spent on the surface of the media with their proboscis extended and touching the food ( y -axis). Replicate measurements of the proportion of females feeding versus those not feeding were recorded during a 2-h period on the days shown. No significant different was seen between flies fed different diets on days 3, 7, 11, and 24 as assessed by chi-squared tests ( p > 0.01, Bonferroni correction for multiple comparisons). There was a significant difference in feeding rates on day 17 ( p = 0.0068) with flies on the DR yeast/control sugar media eating less. These data show that Drosophila does not exhibit compensatory feeding behaviour for the DR regime imposed.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e223
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Figure 2 Survivorship (l x ) Analysis of Life Span of Female Drosophila on Different Food Regimes Colour/Symbol of the curves shows yeast level while the line type represents sugar levels in the respective foods. (A) and (B) are independent repeats. In both cases, changing caloric content of the food by altering yeast levels had a much greater effect on life span than that seen when the same change in caloric content was brought about by manipulating sugar levels.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e223
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Figure 3 Plot of Median Life Span of Female Drosophila against the Estimated Caloric Content of the Food Medium (A) and (B) represent independent repeats. Red arrows link pairs of food types where differences in caloric content are due to different yeast concentrations. Blue arrows link pairs of food types where differences in caloric content are due to different sugar concentrations. Green arrow links food types where differences in caloric content are due to both different sugar and yeast concentrations. Life span is extended to a greater extent per calorie by reducing yeast concentration from control to DR levels than by reducing sugar. This is in contrast to what would be predicted if calorie intake were the key mediator of life-span extension by DR in fruit flies.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e223
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Figure 4 Effect of Tetracycline on Life Span of Female D. melanogaster The addition of the antibiotic tetracycline to the food media did not have a significant effect on life span at either control or DR concentration food media.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e223
PMC1140680
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pbio.0030223.g005
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Figure 5 The Acute Effects on Age-Specific Mortality in Drosophila of Changes in Nutritional Content of the Food Midway through Life Vertical line represents switch day. Mortality trajectories were truncated when n < 40. (A) Switching between control and DR yeast (Y) diets midway though life results in rapid changes in age-specific mortality rates within 48 h similar to those seen previously for whole food dilutions [ 24 ]. Control yeast intake caused no irreversible damage since flies switched from control yeast to DR yeast at day 25 rapidly became no more likely to die than those flies given DR yeast levels throughout adulthood. Flies with a history of DR yeast levels showed rapid increases in mortality rate when moved to control yeast levels at day 25, but mortality rates did not become as high as those of flies that had been maintained on control yeast levels permanently. (B) Changing caloric intake to the same extent via changes to sugar (S) levels rather than yeast did not cause rapid changes in mortality rate. Despite flies chronically fed control sugar and DR yeast having increased mortality rate compared to the DR control, switching from DR to control sugar late in life did not increase mortality rate.
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e223
PMC1140681
0
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pbio.0030237.g001
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Contrary to popular belief, life span extension by dietary restriction in Drosophila is not explained by calories
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2022-01-13 00:07:28
PLoS Biol. 2005 Jul 31; 3(7):e237
PMC1140682
0
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pbio.0030252.g001
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Interactions between hosts and parasites shape changes in gene expression, potentially maximizing parasite recognition for hosts while minimizing detection for parasites (such as red blood cells and trypanosomes)
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2022-01-13 00:01:43
PLoS Biol. 2005 Jul 31; 3(7):e252
PMC1140752
15885138
1
1471-2156-6-22-1
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Figure 1 Birthweight SD score (A) and cord blood IGF-II levels at birth (B) in the ALSPAC cohort, by mother's H19 2992 genotype, and stratified by birth order ("Primip" = mother's first child; "Non-primip" = second or subsequent child). Mean ± 95% CI. First-born infants had lower birthweights than infants of subsequent pregnancies (Ref. 5). Associations with mother's genotype (CC vs. T* [CT or TT]) were only seen in first pregnancies.
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2022-01-12 14:36:03
BMC Genet. 2005 May 10; 6:22
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1471-2156-6-22-2
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Figure 2 Postnatal weight gain (change in weight SD score 0–3 years) in the ALSPAC cohort, by offspring's (A) or mother's (B) H19 2992 genotype, and stratified by birth order ("Primip" = mother's first child; "Non-primip" = second or subsequent child). Mean ± 95% CI. The overall association between weight gain and offspring genotype (CC vs. T* [CT or TT], P = 0.01; Table 5) was only apparent in first-born offspring.
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2022-01-12 14:36:03
BMC Genet. 2005 May 10; 6:22
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1471-2156-6-22-3
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Figure 3 Birthweight SD score (A) and mother's glucose levels one hour post-oral glucose load at 27 to 32 weeks gestation (B) in the Cambridge cohort, by mother's H19 2992 genotype, and stratified by birth order ("Primip" = mother's first child; "Non-primip" = second or subsequent child). Mean ± 95% CI. Associations with mother's genotype (CC vs. T* [CT or TT]) were only seen in first pregnancies.
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2022-01-12 14:36:03
BMC Genet. 2005 May 10; 6:22
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1471-2164-6-63-1
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Figure 1 Venn diagram with number of genes present in each platform, genes in common between platforms, and genes in common among all three platforms.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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1471-2164-6-63-2
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Figure 2 a-f . Scatter plot analysis to determine correlation coefficients between and within platforms using Jurkat RNA as an example. Correlations for all cell lines are given in Table 4 . (a) Operon versus Incyte (b) Affymetrix versus Incyte (c) Affymetrix versus Operon (d) GEM2 versus GEM2 replicate correlation (e) Operon versus Operon (f) HG-U133A versus HG-U133A
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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Figure 3 Principal Component Analysis (PCA) of the three microarray platforms and six cell lines using expression of the 3186 genes with signals above background.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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1471-2164-6-63-4
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Figure 4 a-c . Correlation of correlations of platforms for all cell lines. Correlation values R for each pair of platforms are given in the figures. (a) Operon versus Incyte (b) Affymetrix versus Incyte (c) Affymetrix versus Operon.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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1471-2164-6-63-5
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Figure 5 a-b . Clustered image maps showing patterns of expression relationship among genes, platforms, and cell lines. The axes were ordered by hierarchical clustering using an uncentered correlation and the average linkage algorithm for 909 genes expressed at a two-fold or greater level in at least two of the six cell lines. (a) Clustering of all 909 genes (b) A subcluster of 41 genes to show correct clustering and congruence of expression values. As indicated by the cluster trees, all three platforms gave essentially the same relationships among the six cell lines.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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1471-2164-6-63-6
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Figure 6 Quantitative real-time RT-PCR analysis of 12 genes matched for direction of expression relative to the reference RNA for all three platforms. Log2 ratios are given in table below the graph. This example is a comparison between LnCaP and MCF-10A.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
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1471-2164-6-63-7
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Figure 7 a-f . Quantitative RT-PCR analysis of 10 mismatched genes in the six cells lines for all three platforms. (a) MCF10A, (b) LnCaP, (c) OCI-Ly3, (d) Jurkat, (e) SUDHL-6 and (f) L428.
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2022-01-12 14:36:30
BMC Genomics. 2005 May 5; 6:63
PMC1140939
15916456
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pmed.0020107.g001
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Health care practitioners in developing countries need the most appropriate evidence to guide their practice (Photo: World Health Organization/P. Virot)
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2022-01-13 02:39:25
PLoS Med. 2005 May 31; 2(5):e107
PMC1140940
15916458
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pmed.0020109.g001
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Figure 1 Global Variation in the Density of Health Workers In a report by the Joint Learning Initiative, 186 countries were designated as having low, medium, and high worker density clusters (below 2.5, between 2.5 and 5.0, and above 5.0 workers per 1,000 population, respectively), with the low- and high-density clusters further subdivided according to high and low under-five mortality [ 9 ]. Among low-density countries, 45 are in the low-density/high-mortality cluster; these are predominantly sub-Saharan countries experiencing rising death rates and weak health systems. (Illustration: Giovanni Maki, adapted from [ 9 ])
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e109
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Figure 2 Association between Mortality and Health Worker Density (Illustration: Giovanni Maki, adapted from [ 9 ])
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e109
PMC1140941
15916462
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pmed.0020122.g001
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Corridor of the clinic in Riga's Central Prison (Photo: Melanie Zipperer)
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e122
PMC1140942
15916463
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pmed.0020123.g001
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Figure 1 Use of Statins and All Lipid-Lowering Medications among United States Ambulatory Visits by Patients Diagnosed with Hyperlipidemia Data from NAMCS and NHAMCS, 1992–2002.
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2022-01-13 02:09:31
PLoS Med. 2005 May 31; 2(5):e123
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Figure 2 Share of Total Statin Use among United States Ambulatory Visits by Individual Statin Medications Data from NAMCS and NHAMCS, 1992–2002.
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2022-01-13 02:09:31
PLoS Med. 2005 May 31; 2(5):e123
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Figure 3 Use of Statins among United States Ambulatory Visits, by CHD Risk Category Data from NAMCS and NHAMCS, 1992–2002.
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2022-01-13 02:09:31
PLoS Med. 2005 May 31; 2(5):e123
PMC1140944
15916465
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pmed.0020127.g001
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A nurse at Malipur Maternity Home (Delhi, India) prepares to vaccinate a child (Photo: the WHO/P. Virot)
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2022-01-13 02:39:25
PLoS Med. 2005 May 31; 2(5):e127
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pmed.0020127.g002
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Figure 1 Primary Vaccine Suppliers to the Indian EPI in the Last Four Decades The data were compiled from the annual reports of Health Information of India (1970–1971 to 2001–2002), and the Ministry of Health and Family Welfare, Government of India, New Delhi.
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2022-01-13 02:39:25
PLoS Med. 2005 May 31; 2(5):e127
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pmed.0020127.g003
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Figure 2 The Growth of the Private Sector in the Indian Vaccine Market The data were compiled from the annual reports of Health Information of India (1970–1971 to 2001–2002), the Ministry of Health and Family Welfare (Government of India) and MIMS India ( www.mims-india.com ), Nov 2001, New Delhi.
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2022-01-13 02:39:25
PLoS Med. 2005 May 31; 2(5):e127
PMC1140945
15916466
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pmed.0020128.g001
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Figure 1 The IRR for Malaria in HbAS versus HbAA Children by Age and Genotypic Group Infants less than 3 mo old were excluded from the baseline group.
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2022-01-13 02:09:29
PLoS Med. 2005 May 31; 2(5):e128
PMC1140949
15916457
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pmed.0020138.g001
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(Illustration: Margaret Shear, Public Library of Science)
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2022-01-13 02:09:30
PLoS Med. 2005 May 17; 2(5):e138
PMC1140952
15916472
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pmed.0020141.g001
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Figure 1 Flow Diagram (Selection Strategy) of Included Studies Double asterisk indicates exclusion categories (number studies excluded in parentheses). Double asterisk indicates numbers that are not mutually exclusive. A few studies provided rates for more than one group (11 studies provided data for both core and migrant [ n = 3] or both core and other special groups [ n = 8]; details in Results). LOTE, language other than English.
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 2 Cumulative Plots of the Point Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 7 Cumulative Plots of the Inpatient-Census-Derived Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 3 Cumulative Plots of the Period Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 4 Cumulative Plots of the Lifetime Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 5 Cumulative Plots of the LMR Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 6 Cumulative Plots of the NOS Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 8 Cumulative Plots of Combined Prevalence Estimates per 1,000 by Sex
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 9 Cumulative Plots of the Male:Female Prevalence Estimate Ratio of Schizophrenia
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 10 Cumulative Plots of Combined Prevalence Estimates per 1,000 for Persons by Urbanicity
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2022-01-13 02:09:30
PLoS Med. 2005 May 31; 2(5):e141
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Figure 11 Cumulative Plots of the Migrant:Native-Born Prevalence Estimate Ratio for Persons
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Figure 12 Cumulative Plots of the Combined Prevalence Estimates per 1,000 for Persons by Economic Status of Country
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Figure 13 Cumulative Plots of the Male:Female Prevalence Estimate Ratio of Schizophrenia by Economic Status of Country
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Figure 14 Cumulative Plots of Combined Prevalence Estimates per 1,000 for Persons by Tercile of Quality Score
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Women at a Microbicides Development Programme phase III trial site (Photo: Frank Herholdt; Copyright: © 2005 Microbicides Development Programme. This is an open-access photo distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.)
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2022-01-13 02:09:33
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Figure 1 Sites of Action of Candidate Microbicides (Illustration: Giovanni Maki)
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Figure 1 Plot of the Detectable Rate Ratio as a Function of Sample Size Assuming power of 90% at the 95% significance level [ 11 ], a rate ratio of 2.27 or greater would have achieved a significant result given the 5,500 years of observation in the sample: where u = 1.28, which is the one-sided percentage point of the normal distribution corresponding to 100% minus the power; v = 1.96, which is the percentage point of the normal distribution corresponding to the two-sided significance level; and μ 1 and μ 2 are the seroconversion rates in exposed and unexposed individuals, respectively.
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2022-01-13 02:39:26
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Psychiatric Research by Ted Watson—this painting, representing collaborative research between people with schizophrenia and mental health professionals, is by an aboriginal mental health service user and was commissioned by the Queensland Centre for Mental Health Research, Australia
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PLoS Med. 2005 May 31; 2(5):e151