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1.
Fig. 4

Fig. 4. From: Suppression of Aging in Mice by the Hormone Klotho.

Rescue of aging-like phenotypes in KL−/− mice by genetic intervention in insulin and IGF1 signaling. (A and B) Life-span extension in KL−/− mice by reducing IRS-1 expression. KL−/− mice heterozygous for an IRS-1 null allele (IRS-1+/−) lived longer than those without the mutation (IRS-1+/+) both in males (P = 0.0005 by log-rank test) and females (P = 0.01 by log-rank test). [(C) to (N)] Rescue of aging-like phenotypes in KL−/− IRS-1+/− mice at the histological level. Typical findings from four 8-week-old males of each genotype are shown. (C and D) Aorta (von Kossa staining). Calcification of arterial walls [black deposits in (C)] was decreased in KL−/− IRS-1+/− mice (D). (E and F) Kidney (von Kossa staining). Calcification of small arteries and renal tubules [black deposits in (E)] was decreased in KL−/− IRS-1+/− mice (F). (G and H) Stomach (von Kossa staining). Ectopic calcification in gastric mucosa and small arteries [black deposits in (G)] was alleviated in KL−/− IRS-1+/− mice (H). (I and J) Cross-sections of the skin. Hematoxylin-eosin (HE) staining. Reduction in epidermal layer (e) thickness observed in KL−/− mice (I) was improved and subcutaneous fat (s) was restored in KL−/− IRS-1+/− mice (J). (K and L) Lung (HE staining). Emphysematous changes, including enlargement of air spaces and destruction of the normal alveolar architecture were observed in KL−/− mice (K), but were alleviated in KL−/− IRS-1+/− mice (L). (M and N) Testis (HE staining). Seminiferous tubules were atrophic and no mature sperm was observed in KL−/− mice (M). Spermatogenesis was restored in KL−/− IRS-1+/− mice (N). All panels were shown in the identical magnification (×200). Scale bar, 200 μm.

Hiroshi Kurosu, et al. Science. ;309(5742):1829-1833.
2.
Figure 1.

Figure 1. From: Klotho Regulates Retinal Pigment Epithelial Functions and Protects Against Oxidative Stress.

Klotho knock-out mice exhibit degenerative phenotypes in the retina. A, B, Light microscopy images of the retina of adult Kl+/+ and Kl−/− mice. The number of pigmentation granules in RPE cells is reduced by 30%. Eyes from four 6-week-old Kl−/− (B) and four age-matched Kl+/+ (A) mice were dissected for histological analysis. The number of melanin granules was counted in 10 RPE cells from each mouse; the statistical analysis of the results is presented in Table 1. The choroid (Ch) of the Kl−/− mice showed deformed layers separated by dilated blood vessels (BV; B). POS, Photoreceptor outer segments. C–H, Electron microscopy images of the retinal region of adult Kl+/+ and Kl−/− mice: choroid, RPE, and outer segments of the photoreceptors of wild-type mice (C); choroid and RPE of Kl−/− mice (D; the choroidal region appears grossly deformed with tissue layers that have been separated by severely dilated BVs; RPE (R) of Kl+/+ mice, showing normal cytoplasmic content, normal mitochondria, and Bruch's membrane (E); the RPE (R) of Kl−/− mice are degenerated with light cytoplasmic content, damaged mitochondria (H, red arrowheads), and melanosomes with disorganized distribution (F, white arrowheads). BM is thinner, deformed by dilated blood vessels, showing significant degeneration; F, black arrowhead). The POSs are thinner, showing signs of degeneration (F, H) compared with the Kl+/+ photoreceptors (E, G); phagocytosis of the POSs is observed in the RPE cells of Kl+/+ mice (G); arrows indicate presumptive phagocytotic vesicles at different stages of the phagocytosis process. White arrowheads show the mature lysosomes. Red arrowheads show normal mitochondria. H, No signs of phagocytosis of the outer segments of photoreceptors were observed in the RPE cells of Kl−/− mice. Red arrowheads show damaged mitochondria.

Maria Kokkinaki, et al. J Neurosci. 2013 October 9;33(41):16346-16359.
3.
Fig. 7

Fig. 7. From: Use of RNA structure flexibility data in nanostructure modeling.

A tectosquare built out of MD states of four kissing loop models and one MD state of the L-shaped monomer used four times. (A) The KL states come from the following points in their respective trajectories: A1D2 – 4.0 ns, A2B1 – 4.5 ns, B2C1 – 18.9 ns, and C2D1 – 1.8 ns. Listed under each KL label are the actual KL torsion angles measured for each of them. The MD state of the L-shaped monomer comes from the 3.2 ns point in its trajectory. The color-coded KL fragments were truncated for display purposes to include only the two base pairs closest to the interacting hairpin loops, which were used as reference points in a chain-fitting of the building blocks together. The last KL in this procedure, C2D1, was fit to the monomer C and the gap between the KL and the D monomer was used as a measure of the overall closure quality. The gap distances were measured for the corresponding KL complex’s and L-shaped monomer’s 5′ and 3′-side P atoms of the second base pairs from the KL’s H-loops (L-KL interface points). A perfect fit would measure 0 Å for both gaps. The RMSD values of each fit in the chain assembly are listed next to each side of every KL. (B) A plot of the KL bending angle (red) and the KL torsion angle (black) in the MD simulation of the KL complex B2C1. A point in the trajectory corresponding to 18.917 ns is marked with the blue vertical line for which the KL bending angle is 177.9° and the KL torsion angle is 17.4°. This MD state was used as one of the kissing loops yielding the closed full tectosquare shown in (A).

Wojciech Kasprzak, et al. Methods. ;54(2):239-250.
4.
Figure 4.

Figure 4. From: Mechanism of human Hb switching: a possible role of the kit receptor/miR 221-222 complex.

Analysis of miR-221/222 expression in CD34+ HPCs. (A) miR-221/222 expression in pre-term CBs (white), mid-full-term CBs (gray) and APB (black). Fold increase of miR-221 and miR-222 levels as compared to pre-term CBs (set as 1) is indicated. Mean ± SEM (n=9 pre-term CB; n=12 mid-full-term CB; n=20 APB). ***P<0.001 when compared to pre-term CB group, **P<0.01 when compared to mid-full-term group. (B) Growth curve (left panel) and percentage of HbF (right panel) in HPC erythroid cultures untransfected (C) or transfected with a control miR (CmiR) or with miR-221 and miR-222 alone or in combination (miR-221+222). Cells were grown in absence (upper panels) or in the presence (lower panels) of KL. Mean ± S.E.M. (n=3). (Upper panels) P<0.05 when miR-221 and -222 growth curves are compared to C groups (left panel) and **P<0.01 when miR 221 and -222 HbF contents are compared to C groups (right panel). (Lower panels) P<0.01 when miR-221 and -222 growth curves are compared to C groups (left panel) and ***P<0.001 when miR 221 and -222 HbF contents are compared to C groups (right panel). (C) Growth curve (left panel) and percentage of HbF (right panel) in HPC erythroid cultures untransfected (C) or transfected with a control antagomiR (C antagomiR), antagomiR 221 or antagomiR 222. Cells grown in the presence of KL are included (KL). Mean ± SEM (n=3). **P<0.01 when compared to C groups (right panel). (D) Growth curve (left panel) and percentage of HbF content (right panel) in HPC erythroid cultures untransfected (C) or transfected with c-kit siRNA and grown in the presence of KL. Cells grown in the presence of KL alone or in combination with imatinib are included as positive and negative controls of HbF induction. Mean ± SEM (n=3). P<0.001 when KL+ siRkit growth curve is compared to KL curve (left panel) and ***P<0.001 when compared to KL HbF content (right panel).

Marco Gabbianelli, et al. Haematologica. 2010 August;95(8):1253-1260.
5.
Fig. 3

Fig. 3. From: Complex chemoattractive and chemorepellent Kit signals revealed by direct imaging of murine mast cells in microfluidic gradient chambers.

BMMC cells exhibit a bimodal chemotactic response to Kit ligand (KL) gradients. (A) The tracks of individual BMMC with initial positions located in Q1–Q4 in the presence (+KL) or absence (−KL) of a KL gradient. Individual cell tracks were plotted with the starting position of each cell at the graph origin. Cell tracks that possessed a positive net displacement towards the source channel are plotted in black, while absolute movement away from the source are in red. The total number of observed cells with net movement towards or away from the source is given in black and red fonts, respectively. A yellow star indicates the center of mass of all tracks. (B) Chemotactic indices of each individual cell (black dots) and population averages (red line) for cells in Q1–Q4 with (top) or without (bottom) exposure to a KL gradient. (C) Individual cell speeds (black dots) and population averages (red line) for each condition. Three individual trials were run; n ≥ 143 cells for each +KL quadrant, and n ≥ 60 for each −KL quadrant.

Amir Shamloo, et al. Integr Biol (Camb). 2013 August;5(8):1076-1085.
6.
Figure 6

Figure 6. FGF23 functional assay. From: Identification of novel small molecules that elevate Klotho expression.

KL and FGFR function as co-receptors for FGF23 signalling. (A) Assay validation. bFGF stimulates ERK phosphorylation, indicating that cells express ERK and are able to transduce a signal from the cell surface. Upon transfection of KL and FGFR into HEK-293 cells, FGF23 signalling induces ERK phosphorylation. Shown is a representative blot of pERK and total ERK. (B) HEK-293 cells transfected with control plasmid were treated with compounds G–I for 24 h and processed similarly to the FGF23 assay, although no protein stimulus was added to the medium. Although phosphorylation was detected in bFGF controls, no pERK was detected as a result of compound stimulation alone. (C) HEK-293 cells were transfected with FGFR1c or control plasmid pcDNA3.1. Following transfection, KL-activating compounds G–I were added to the medium overlaying cells (1 µM) for 24 h. FGF23 was subsequently added to the medium for 20 min to determine whether increased KL protein would result in elevated pERK signalling. Increases in pERK were observed in all of the compound-treated wells. Shown is a blot representative of three independent experiments. (D) HEK-293 cells were transfected with a plasmid expressing KL alone or in combination with KL siRNA or a scrambled control siRNA. Although no effects were observed on β-tubulin control proteins, KL siRNA reduced KL expression to nearly undetectable levels. (E) HEK-293 cells were co-transfected with FGFR and either KL or scrambled control siRNA. Cells were then exposed to compound and processed for FGF23 signalling as above. Fold change of pERK expression was normalized to total ERK in the cell and quantified across multiple experiments. All three compounds tested showed elevated levels of pERK (white bars, G–I) unless transfected with KL siRNA which blocked FGF23 signalling (black bars, G–I). Hatched bars represent cells alone or cells treated with FGF23 as controls for background levels of pERK in HEK-293 cells. Each compound was tested in three independent experiments and results are means ± S.E.M. (*P < 0.01, **P < 0.001, ANOVA). Dividing lines indicate where the image was spliced together; all samples were run on the same gel. Molecular masses are indicated in kDa.

Gwendalyn D. King, et al. Biochem J. ;441(1):453-461.
7.
Figure 3.

Figure 3. From: Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease.

The levels of calcium content in the kidneys and the aortas of Sham and CKD mice are correlated with genetic levels of Klotho. (A and B) Calcium content was assayed using OCPC in the aortas (A) and the kidneys (B) of Sham and CKD mice at different genetic Klotho levels: Kl+/− (red) and Tg-Kl (blue) and their WT littermates (black). The data are represented as the means ± SEM (n = 7). *P < 0.05; **P < 0.01 versus Sham WT mice of Kl+/− group; ¥P < 0.05; ¥¥P < 0.01 Sham Kl+/− mice; #P < 0.05; ##P < 0.01 versus CKD Kl+/− mice; $P < 0.05, $$P < 0.01 versus Sham WT mice of Tg-Kl group; §P < 0.05; §§P < 0.01 versus Sham Tg-Kl mice; £P < 0.05; ££P < 0.01 versus CKD Tg-Kl mice by one-way ANOVA followed by Student-Newman-Keul's test. (C) Relationship of calcium content in the aortas and the kidneys with blood Pi and blood Cr, respectively, in Sham (triangles) and in CKD (circles) mice at three different genetic Klotho levels: Kl+/− (red) and Tg-Kl (blue) and their WT littermates (black). C, CKD; S, Sham.

Ming Chang Hu, et al. J Am Soc Nephrol. 2011 January;22(1):124-136.
8.
Figure 3

Figure 3. From: Klotho is silenced through promoter hypermethylation in gastric cancer.

KL downregulation in gastric cancer cells was mediated by promoter hypermethylation. The schematic structure of the KL CGI was shown in (A) CGI was plotted by GeneTool program. Black triangles indicate BstU I sites. Promoter methylation of KL were analyzed by Cobra (B) and MSP (C), respectively. M: methylation specific PCR; U: un-methylation specific PCR. N1 and N2 are normal stomach tissues. (D) The expression of KL before and after Aza treatment were analyzed by RT-PCR. GAPDH was used as the loading control.

Liangjing Wang, et al. Am J Cancer Res. 2011;1(1):111-119.
9.
Figure 2.

Figure 2. From: Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease.

Klotho levels and soft tissue calcification in CKD mice are associated with genetic levels of Klotho. (A) Representative blots of Klotho protein in plasma (n = 3), urine (n = 4), and kidney (n = 4) of CKD compared with Sham mice of Kl+/−, Tg-Kl, and their WT littermate mice, respectively. (B and C) Plasma PTH (B) and 1,25-(OH)2 vitamin D3 (C) from Sham and CKD mice with different genetic Klotho background: Kl+/− (red) and Tg-Kl (blue) and their WT (black) littermates for measurement. The data are represented as the means ± SEM (n = 6). *P < 0.05; **P < 0.01 versus Sham WT mice of Kl+/− group; ¥P < 0.05; ¥¥P < 0.01 Sham Kl+/− mice; #P < 0.05; ##P < 0.01 versus CKD Kl+/− mice; $P < 0.05; $$P < 0.01 versus Sham WT mice of Tg-Kl group; §P < 0.05; §§P < 0.01 versus Sham Tg-Kl mice; £P < 0.05; ££P < 0.01 versus CKD Tg-Kl mice by one-way ANOVA followed by Student-Newman-Keul's test. (D) Von Kossa staining of calcification (arrow) in the aortas (low amplification in top panel and high amplification in middle panel) and kidneys (bottom panel) of Kl+/− CKD mice, Tg-Kl CKD mice, and their WT CKD mice, respectively. No Von Kossa staining was found in the tissues of Sham mice (data not shown).

Ming Chang Hu, et al. J Am Soc Nephrol. 2011 January;22(1):124-136.
10.
Figure 4

Figure 4. Cartoon showing extrapolations of the zeroth order KL divergences and entropies (see Eqs. (9) and (11)).. From: Pairwise Maximum Entropy Models for Studying Large Biological Systems: When They Can Work and When They Can't.

These extrapolations illustrate why the two natural quantities derived from them, and , occur beyond the point at which the extrapolation is meaningful. (A) Extrapolations on a log-log scale. Black: ; green: ; cyan: . The red points are the data. The points and label the intersections of the two extrapolations with the independent entropy, . (B) Extrapolation of the entropies rather than the KL divergences, plotted on a linear-linear scale. The data, again shown in red, is barely visible in the lower left hand corner. Black: ; solid orange: ; solid maroon: . The dashed orange and maroon lines are the extrapolations of the true entropy and true pairwise “entropy”, respectively.

Yasser Roudi, et al. PLoS Comput Biol. 2009 May;5(5):e1000380.
11.
Figure 1

Figure 1. Isolation of KSL, KL, SL, and CD34+ cells by FACS and EPC-CFA.. From: CD34+ Cells Represent Highly Functional Endothelial Progenitor Cells in Murine Bone Marrow.

a, Lineage depleted BMMNCs were stained with APC anti-c-kit and PE anti-Sca-1 antibodies followed by FACS sorting. The cell fractions gated with black, red, and blue frames were defined as KSL, KL, and SL cells, respectively. Also BMMNCs were stained with a FITC anti-CD34 antibody followed by FACS sorting for CD34 positive cells. b, The number of colonies was counted in each group. Small EPC colony count in each group and large EPC colony count in each group. c, EPC-CFA was performed with KSL, KL, SL, and CD34+ cells, and the morphologies of small EPC colony and large EPC colony were dispalyed. The framed areas were magnified in lower panels. d, Representative double staining for Fluorescein isolectin B4 (ILB4) and DiI-acLDL in KSL cell-formed colonies. All assays were triplicated and demonstrated similar results.

Junjie Yang, et al. PLoS One. 2011;6(5):e20219.
12.
Figure 1

Figure 1. From: Direct interaction between Kit and the interleukin-7 receptor.

KL stimulation of Jurkat-K7 cells results in the activation of IL-7R, Jak3, and Stat5. (A) γc and IL-7Rα are tyrosine phosphorylated by and associated with Kit after KL stimulation and γc-associated Jak3 is tyrosine phosphorylated in response to KL stimulation. Jurkat-K7 cells were stimulated with KL for the times indicated and γc and IL-7Rα were immunoprecipitated. Bound fractions of the γc IPs were analyzed for tyrosine phosphorylation and protein amounts of γc, γc-associated Kit, and γc-associated Jak3 (top panels). Bound fractions of the IL-7Rα IPs were analyzed for tyrosine phosphorylation of IL-7Rα, and IL-7Rα-associated Kit (middle panels). Lysates were analyzed for tyrosine-phosphorylated Kit and the presence of equal amounts of Kit protein at each time point of KL stimulation (bottom panels). (B) KL-induced tyrosine phosphorylation of Jak3 and Stat5. Immunoprecipitations of Jak3 and Stat5 were analyzed for tyrosine phosphorylation and protein amounts of Jak3 (top 2 panels) and Stat5 (bottom 2 panels). (C) Quantification of the relative change in KL-induced protein phosphorylation (γc, IL-7Rα, Jak3, and Stat5) between baseline (0 minutes) and 3 time points of KL stimulation (5, 10, and 15 minutes). Western blot signals on films from 3 independent experiments (■, ♦, ▴) were densitometrically evaluated as described in “Materials and methods, Immunoprecipitations and immunoblotting,” and fold changes were expressed as the log2 ratio. A log2 ratio of 1 is equal to a fold change of 2. The P values for the t tests (5, 10, 15 minutes versus 0 minute, respectively) are indicated by asterisks (*): *.01 ≤ P < .05; **.001 ≤ P < .01; ***P < .001. The connection from time point 0 (fold increase = 1, log2 1 = 0) to time point 5′ is indicated by a dashed line only for orientation as the 0′ value was used for normalization. Thus, mathematically it is not part of the graph anymore. (D) Quantification of the relative change in the amount of phospho-Kit associated with γc and IL-7Rα at 5, 10, and 15 minutes of KL stimulation. Data are displayed and statistically analyzed as in panel C.

Thomas Jahn, et al. Blood. 2007 September 15;110(6):1840-1847.
13.
Fig. 4.

Fig. 4. From: Targeting the protein prenyltransferases efficiently reduces tumor development in mice with K-RAS-induced lung cancer.

Simultaneous inactivation of Fntb and Pggt1b in mice with K-RASG12D-induced lung cancer. (A) Lung weight of 3-week-old KL (n = 4), Fntbfl/ΔPggt1bfl/ΔKL (n = 6), Fntbfl/ΔPggt1bfl/ΔL (n = 5), and Ctr (n = 9) mice. BW, body weight. (B) Representative hematoxylin/eosin-stained lung sections of mice from the experiment shown in A. (Scale bars, 100 μm.) (C) Kaplan–Meier curve showing survival of KL (n = 12), Fntbfl/ΔPggt1bfl/ΔKL (n = 10), and Fntbfl/ΔPggt1bfl/ΔL (n = 9) mice. Black tick marks indicate healthy Fntbfl/ΔPggt1bfl/ΔL mice that were euthanized for tissue analyses. (D) Western blots of protein extracts from the lungs of 3-week-old KL and Fntbfl/ΔPggt1bfl/ΔKL mice showing levels of phosphorylated ERK1/2. Total ERK1/2 was used as a loading control. (E) Confocal immunofluorescence micrographs showing expression of Ki-67 (pink) in cells from KL, Fntbfl/ΔPggt1bfl/ΔKL, and Ctr mice. Nuclei were visualized with DAPI (blue).

Meng Liu, et al. Proc Natl Acad Sci U S A. 2010 April 6;107(14):6471-6476.
14.
Fig. 5

Fig. 5. From: QSAR with experimental and predictive distributions: an information theoretic approach for assessing model quality.

Charts showing the order of performance of the PD methods for each model/endpoint in terms of mean KL divergence against the combined experimental test sets. Variable error estimation methods are shown in grey and uniform error estimation methods are shown in black. The variable error estimation methods must result in a reduced mean KL divergence for them to represent an improvement on the uniform error estimation methods

David J. Wood, et al. J Comput Aided Mol Des. 2013 March;27(3):203-219.
15.
Figure 1

Figure 1. From: Anharmonic Normal Mode Analysis of Elastic Network Model Improves the Modeling of Atomic Fluctuations in Protein Crystal Structures.

The results of ADP modeling for an E. Coli hppk crystal structure (PDB code: 1F9Y). (a) A cartoon representation of 1F9Y with two floppy loops (residues 45–50 and 85–90) colored black. (b) B factors (rescaled by 3/8π2) from crystallography (dotted line), modeled by NMA (gray line) and by ANMA with (black line) (the positions of the two loops shown in a are underscored). (c and d) ccmod and KL distance, respectively, for NMA (gray lines) and ANMA with (black lines). (e) B factors (rescaled by 3/8π2) from crystallography (dotted line), modeled by ANMA with (gray line) and by ANMA with (black line). (f and g) ccmod and KL distance, respectively, for ANMA with (gray lines) and ANMA with (black lines).

Wenjun Zheng. Biophys J. 2010 June 16;98(12):3025-3034.
16.
FIG. 1.

FIG. 1. From: AmpC ?-Lactamase in an Escherichia coli Clinical Isolate Confers Resistance to Expanded-Spectrum Cephalosporins.

Comparison of amino acid sequences of AmpC KL and AmpC S4 with those of other AmpC β-lactamases. The sources of the enzymes are as follows: AmpC K12 is from E. coli K12 (5), AmpC CHE is from E. cloacae CHE (2), and AmpC HD is from S. marcescens (15). β-Lactamases AmpC KL, AmpC CHE, and AmpC HD confer resistance to cefepime. The arrow indicates cleavage of the peptide leader site for AmpC K12. Amino acid residues of AmpC CHE and AmpC HD that were deleted compared to those of the wild-type cephalosporinase appear in black dashes on a grey background (2, 15). Dashes have been introduced to optimize the alignment, and dots indicate amino acid residues identical to those of AmpC KL. Conserved residues of class C β-lactamases are underlined.

Hedi Mammeri, et al. Antimicrob Agents Chemother. 2004 October;48(10):4050-4053.
17.
Figure 1

Figure 1. From: Limited plasticity in the phenotypic variance-covariance matrix for male advertisement calls in the black field cricket, Teleogryllus commodus.

The location of the six populations that crickets were collected. Populations are colour coded: Western Australia (WA, green), South Australia (SA, yellow), Tasmania (TAS, orange), Australian Capital Territory (ACT, red), Kioloa (KL, blue) and Smith’s Lakes (SL, black).

W. R. Pitchers, et al. J Evol Biol. 2013 May;26(5):1060-1078.
18.
Fig. 4

Fig. 4. From: Klotho and kidney disease.

Correlation of calcium content in the kidneys, hearts and aortas in sham and chronic kidney disease (CKD) mice. Calcium content was assayed using o-cresolphthalein complexone (OCPC) in the kidney, heart and aortas of sham and CKD mice at different genetic Klotho levels: Kl+/− (light gray) and Tg-Kl (black gray) and their wild-type (WT) littermates (dark gray). For given concentration of blood creatinine (Cr) or phosphate (Pi) (vertical dotted line) Kl+/− (light gray) mice have the highest, and Tg-Kl (black) the lowest and their WT littermates (dark gray) intermediate levels of Ca content in soft tissues.

Ming-Chang Hu, et al. J Nephrol. ;23(Suppl 16):S136-S144.
19.
Figure 1

Figure 1. From: Characterization of hyaluronan and TSG-6 in skin scarring: differential distribution in keloid scars, normal scars and unscarred skin.

Haematoxylin and eosin (H&E) staining. Unscarred skin (a) with an undulating dermal-epidermal junction (white arrow) and haphazardly arranged dermal collagen bundles (black arrow). A normal scar (b) with a flattened epidermis (white arrow) and thin strand-like collagen bundles (black arrow) parallel to the epidermis. A keloid scar (c) with flattened epidermis (white arrow) and thin, parallel strand-like collagen bundles (black arrow) in the superficial dermis. Emigrant lymphocytes were seen in the dermis around vascular structures in all three tissue types (blue arrows). Hair follicles (d) consist of an internal (black arrow) and external root sheath (white arrow); a sebaceous gland (e) containing sebocytes (black arrows) filled with abundant lipid droplets and thin strands of cytoplasm; and an eccrine gland (f) with several cross sections of a coiled duct (black arrows) in unscarred skin. A low magnification view of a keloid scar (g) showing a flattened epidermis, thin strand-like collagen bundles in the SD and thick bundles of collagen arranged in a haphazard orientation within the actual KL in the reticular dermis. The central region of a KL (h) shows a high density of cells interspersed between the thick bundles of collagen (black arrows). The central region of another KL (I) shows thinner bundles of collagen arranged in a reticular pattern (black arrows). (Ep: epidermis; D: dermis). Scale bars: 100 μm (Original magnification a–f,h,i: 20×; g: 10×).

KT Tan, et al. J Eur Acad Dermatol Venereol. 2011 March;25(3):317-327.
20.
Figure 3

Figure 3. From: Geographically multifarious phenotypic divergence during speciation.

Size (area) measurements of wing pattern models approached by male Lycaeides during MP1. Circles depict the morphospace of wing pattern models presented to (gray) and approached by (black) male butterflies. Circle sizes are proportional to the frequency a wing pattern model was presented or approached. Arrows show the vector (i.e., direction and magnitude) difference in mean PC1 and PC2 scores between the presented and approached models. The arrowhead denotes the bivariate mean of the approached models. KL = Kulback–Liebler divergence measure (KL) between the presented and approached wing pattern models (P-values give the probability of obtaining the observed Kulback–Liebler divergence by chance). See Table 1 for population abbreviations.

Zachariah Gompert, et al. Ecol Evol. 2013 March;3(3):595-613.

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