These evidences point us in the direction that treatment with hir sutanol A in combination with inhibitor of JNK may pro duce synergistic effect. Conclusion In summary, hirsutanol thenthereby A is a ROS generating agent which e erts anticancer effect via up regulation of ROS level and activation of mitochondria cytochrome c sig naling pathway. Moreover, hirsutanol A could activate JNK signaling pathway. Activation of JNK signaling pathway did not mediate apoptosis. however, it could regulate ROS level in a negative feedback fashion which protects cells against o idant stress induced cell death. Our results revealed that hirsutanol A may be a promis ing lead compound in future anticancer treatments. Introduction Postnatal cardiomyocytes have a limited proliferation rate that does not suffice to replenish the CM that are mas sively lost after Myocardial Infarction.

During human life span appro imately half of the cardiomyocytes are replaced. This indicates that there is a significant level of physiological proliferation of cardiomyocytes. Thus, novel therapies that promote the proliferation of CM after acute Myocardial Infarction may alleviate post infarct complications such as heart failure. Over the past decade, mesenchymal stem cells emerged as promising candidates for cardiac therapy. Stem cells and progenitor cells from sources that vary from bone marrow to adipose tissue and the heart itself have shown to be beneficial in animal models of aMI and in clinical trials. The current dogma is that stem cells act primarily through paracrine intervention in the damaged cardiac microenvironment i.

e. through secretion of trophic factors. The secretion profile and the fate of administrated cells change upon a host microenvironment. Current research on preconditioning BM MSC with the hypo ic and the inflammatory fac tors found in post MI microenvironment improve the cardioprotective outcome of the therapeutic cells. Thus priming Adipose tissue derived stem cells for the treatment of MI with hypo ic and inflammatory conditions might result in the improvement of cardiac function. ADSC belong to the family of MSC and are derived from the adipose vascular stromal fraction as fibroblastic, spindle shaped, plastic adherent cells and co e press sev eral mesenchymal markers such as CD105, CD90, CD44, CD29 or CD73.

In vitro, ADSC secrete a plethora of factors that are cytoprotective, promote angiogenesis and induce proliferation of various cell types. In deed, in animal models of Dacomitinib myocardial infarction, the intramyocardial selleck chemicals administration of ADSC improved cardiac remodeling and function. Yet, the influence of administered stem cells on the proliferation rate of cardiomyocytes is poorly studied. In damaged tissues, interleukin 6 is both cytoprotective and anti apoptotic.

Hs02758991 g1 for GAPDH. Hs00171132 m1 for GDF15. Hs01110250 m1 for HMO 1. Hs00998018 m1 for PDGFRA. and Hs01019589 m1 for PDGFRB. Primers for mouse transcripts were Mm00487499 g1 for Cyr61. Mm99999915 g1 for GAPDH. Mm00442228 m1 for Gdf15. Mm00435546 m1 for Pdgfrb. Cell culture such information and triple SILAC labeling Primary human bladder smooth muscle cells were cultured in smooth muscle cell medium at 37 C in a humidified incubator with 5% CO2. For triple SILAC labeling, pBSMCs were grown in arginine and lysine depleted SMCM supplemented with 2% dialyzed fetal bovine serum and L arginine and L lysine, 13C6 L arginine and 4,4,5,5 D4 L lysine, or 13C615N4 L arginine and 13 ies, Andover, MA. After at least 6 population doublings, pBSMCs cultured in light, medium, and heavy SILAC media were serum starved overnight and treated with 1 nM PDGF BB for 0, 4, and 24 h, respectively.

RNA e traction and microarray analysis After triple SILAC labeling and PDGF treatment, RNAs were isolated from pBSMCs and hybridized to Human Gene 1. 0 ST arrays, which comprise 28,869 well annotated genes. A quality assess ment of the microarray data was performed essentially as described. Several diagnostic plots including histogram and scatter plots of probe intensities in the arrays were used to check systemic bias of microarray e periments, such as high level of background intensity, signal saturation, and inter and intra group variation of the arrays. After the adjustment of background signal using the Plier method, probe intensities were normal ized using the quantile normalization procedure with Affymetri E pression Console software.

The raw data were deposited in the Gene E pression Omnibus. Identification of differentially e pressed genes With the normalized intensities, DEGs in samples at 4 h or 24 h after PDGF treatment in comparison with con trol samples were identified using an integrated statis tical method previously Carfilzomib described. Briefly, two independent tests��the T test and the log2 median ratio test��were performed. For each test, an empirical distri bution of the null hypothesis that the means of the gene e pression levels are not different was estimated by random permutations of the samples. For each gene, adjusted p value was computed by performing a two tailed test using the empirical distributions. The two sets of adjusted p values were combined to compute the overall adjusted p values using Stouffers method.

In addition, to determine the cutoff value of fold changes, we computed fold changes of randomly per muted samples and fitted a Gaussian distribution to the random fold changes. The 2. 5 percentile was calculated to be less than 1. 4. Thus, the DEGs were selected based on the criteria merely that the overall p is less than 0. 05 and that the absolute fold change is larger than 1. 4. Finally, to iden tify GOBPs or major pathways represented by the DEGs, the enrichment analysis was performed using the DAVID software.

Data Analysis Data were analyzed as an incomplete block design, or a randomized block design, blocked on plate using mi ed model procedures of SAS. At least si replicates were completed for each e periment. Fishers protected least significant differences were used for separating least square differences for e per iments 1, 2, selleck chemicals 3, and a two tailed Students T test was per formed on data from e periment 4. Least square means S. E. M. are e pressed as the proportion of putative zygotes. All data were subjected to a normality test and were found to be normally distributed. Results In the first e periment addition of 5 M retinol during IVM tended to improve embryonic develop ment to the blastocyst stage, compared to controls. The control blastocyst rate was 21. 9% compared to 26. 1% in 5 M retinol.

Addition of 1 M retinol to the mat uration medium did not appear to affect embryonic devel opment compared to controls. Retinol increased blastocyst development, although not significantly. Cleavage rates did not differ among the four maturation treatments. Further analysis of the maturation data revealed that when development to the blastocyst stage of controls was below 20%, 5 M retinol dramatically improved embryo development. When e pressed as blastocyst cleaved the 5 M retinol treatment also showed a significant improvement in blastocyst development. Neither 1 M nor 10 M retinol treatment improved embryonic development when com pared to those controls that did not achieve a 20% blasto cyst rate. Further e periments were conducted during IVC under both low and atmospheric o ygen tensions.

Under low o ygen conditions concentrations of 1, 2, and 5 M retinol were not statistically different from controls, and 10 M was deleterious. Preliminary dose response studies were performed under atmospheric conditions, and additional e periments were con tinued with the 5 M retinol treatment. Under atmos pheric o ygen conditions the 5 M Dacomitinib concentration significantly improved blastocyst development compared to controls. Cleavage rates did not differ significantly among embryos treated with and with out retinol during culture under low or high o ygen. Fertilization rates did not differ signifi cantly among all e periments. Discussion In the present study, over 3000 bovine oocytes were used to evaluate effects of retinol supplementation during IVM and IVC on embryonic development to the blastocyst stage.

Retinol administration during the maturation period alone resulted in concentration dependent effects. Whereas the presence of 1 M retinol had no effect on development, 5 M retinol tended to improve blastocyst rate of development, selleck inhibitor at the p 0. 07 level, compared to controls. At a concentration of 10 M, retinol did not sig nificantly improve embryo development compared to controls. In preliminary studies, higher concentrations were observed to be cytoto ic.

As shown in Figure 4A and B, the level of Mcl 1 protein decreased dramatically after treatment with CH alone, and the half life of Mcl 1 protein was 30 min. Co treatment with ABT 263 and CH mark edly attenuated the degradation of Mcl 1 protein, and the half life of Mcl 1 protein reached to more than 4 h. These results indicated that ABT 263 enhanced Mcl 1 protein stabilization in HCC cells. Meanwhile, ABT 263 could not further upregulate Mcl 1 protein level after proteasome was inhibited by MG132, suggesting that ABT 263 might upregulate Mcl 1 protein level by de creasing proteasome mediated degradation. As to whether ABT 263 affected the ubiquitination mediated Mcl 1 degradation, the role of deubiquitinase USP9 was in vestigated.

As shown in Figure 4D and E, knockdown of USP9 didnt affect ABT 263 mediated Mcl 1 accumu lation, indicating that USP9 mediated deubiquitina tion doesnt contribute to ABT 263 enhanced Mcl 1 stability. Activation of ERK and JNK involves in ABT 263 induced stabilization of Mcl 1 protein It is known that there is a unique PEST region in Mcl 1 protein and the phosphorylation of this region is closely associated with Mcl 1 protein stability, so we ana lyzed the activity of several kinases which directly phos phorylate Mcl 1, including e tracellular regulated kinase and c Jun terminal kinase. Meanwhile, phos phorylation of mammalian target of rapamycin was also detected upon ABT 263 treatment since its acti vation through phosphorylation can regulate the trans lational process of Mcl 1 protein.

As shown in Figure 5A, ERK and Entinostat JNK were activated while mTOR was repressed after treatment with ABT 263. To further clarify the role of these kinases in ABT 263 enhanced Mcl 1 pro tein stabilization, their inhibitors were used. ERK inhibitor U0126 and JNK inhibitor SP600125, but not mTOR in hibitor rapamycin, markedly attenuated ABT 263 caused Mcl 1 upregulation. Moreover, ERK and JNK inhibitors significantly increased ABT 263 induced apop tosis in PLC and Huh7 cells revealed by anne in V FITC PI staining flow cytometry analysis, trypan blue e clusion assay and Western blot for en hanced PARP cleavage. These results indicated that activation of ERK and JNK, but not mTOR, involved in ABT 263 mediated Mcl 1 protein stabilization and drug resistance.

ABT 263 enhances ERK and JNK mediated Mcl 1Thr163 phosphorylation To further investigate the concrete mechanisms of ERK and JNK mediated Mcl 1 stabilization, the phosphoryl ation status of Mcl 1Thr163 was analyzed. As shown in Figure 5E and F, inhibition of ERK or JNK significantly attenuated ABT 263 induced Mcl 1Thr163 phosphoryl ation and Mcl 1 accumulation, suggesting that the phos phorylation of Mcl 1Thr163 may contribute to ERK and JNK mediated Mcl 1 stabilization upon ABT 263 treat ment in HCC cells.

As depicted in Figure 2C, immunoblot analysis of eluates with anti PfI2 antibodies reacted with one band at 20 kDa, corresponding to the migration of the recom binant PfI2 protein. Lane 3 confirmed the presence of His tagged PfPP1 by the use of mAb anti His antibody. To accurately follow up the distribution of PfI2 during the intraerythrocytic development cycle, we e amined 3D7 parasites transfected with a pARL2 construct medi ating the episomal e pression of full length GFP fused PfI2. The use of this vector by Kuhn et al. showed that the trafficking was attributable to the nature of the pro tein e pressed rather than to the PfCRT promoter used. Using a mAb anti GFP antibody, immunoblot ana lysis of a total e tract of blood stage parasites e pressing PfI2 GFP revealed the presence of a specific band at 37 kDa, which is the e pected molecular mass of PfI2 GFP.

This demonstrates the integrity of the fused protein in transfected parasites. E amination of live parasites showed that the signal was confined within the parasite where the distribution seemed to be nucleo cytoplasmic, as the fluorescence partially overlapped DNA staining. The distribution appeared to be diffuse in the late parasite stages with most staining in the nucleus. These results are in accordance with previous localization studies carried out on mammalian or plant cells showing a nucleo cytoplasmic localization with an accumulation in the nucleus when human cells progressed into S phase. The PfI2 GFP signal was com pletely absent from the digestive food vacuole.

Genetic manipulation of PfI2 To study whether the lack of PfI2 e pression could affect the Plasmodium blood stage life cycle, attempts to disrupt the PfI2 gene using the pCAM vector system were carried out. We transfected blood ring stage para sites of the 3D7 strain with a pCAM BSD PfI2 construct containing a 5 fragment derived from the genomic PfI2 sequence and the BSD gene conferring resistance to blasticidin. The presence of this construct in transfected parasites was checked by a plasmid rescue approach as previously described. From two independent transfection e periments, the analysis of genomic DNA obtained from resistant stable parasites by PCR, with specific primers indicated in Additional file 1 Table S1, did not evidence the interruption of the PfI2 gene.

The wild type gene was still amplified in genomic DNA even after prolonged culture and the plasmid remained episomal. The absence of knock out parasites could be attributed either to the essentiality of PfI2 or to the lack AV-951 of accessibil ity of PfI2 to genetic manipulations. To e clude the latter hypothesis and to check the accessibility for recombin ation of the PfI2 locus, we introduced a targeted modifica tion in the locus without loss of function. To this end, 3D7 ring stage parasites were transfected with a plasmid containing the 3 end of the PfI2 coding region fused to the hemagglutinin sequence.

Immunofluorescence Cells were plated in Lab Tek chamber slides and treated 4 6 hours with 1 uM adaphostin, or pre treated 30 minutes with 500 nM wortmannin, followed by 4 hour incubation with 1 uM adaphostin where indicated. Cells were fixed using cold methanol. permeabilized with 0. 1% Triton X 100. blocked in 20% goat serum. incubated with Nrf2 antibody overnight. labeled using FITC conju gated secondary antibody. and nuclei were counter stained with DAPI. Prolong Anti Fade was used to mount coverslip overnight. Samples were visualized using a Leitz Laborlux D fluores cence microscope and images were captured by Leica DFC420 camera and analyzed in Adobe Photoshop Ele ments 2. 0.

Results Although hematopoietic malignancies have been the major target of pre clinical studies with adaphostin, NCI H522, a solid tumor derived, non small lung cancer cell line, was also very sensitive to adaphostin in the NCI 60 human tumor cell line screen. From four independent experiments in the NCI 60 screen, the 50% growth inhibitory concentration for the 6 leuke mia cell lines ranged from 40 nM 630 nM, and the GI50 for NCI H522 was 79 nM, which was 10 fold more sensi tive than the average response for the whole cell line panel. Transcriptional profiling of NCI H522 in response to 1 uM adaphostin showed one of the most highly upregulated genes to be HMOX1 fold increase after 24 h which encodes for an enzyme that protects against oxidative stress. This increase in HMOX1 expression was confirmed using Q RT/PCR which also corroborated the lack of significant change in expression of the NRF2 gene.

Moreover, a small but significant increase in the Nrf2 transcriptional target gene, NAD H dehydrogenase, quinone 1 NQO1 was observed although there was no change in another Nrf2 target, the catalytic subunit of glutamate cysteine ligase GCLC. A significant increase in ROS production was observed as early as 2 h after adaphostin treatment which is confirmation of the presence of drug induced oxidative stress. Heme oxygenase 1, the protein encoded by HMOX1, was shown to be increased by adaphostin treatment at a later time point than HMOX1, being only slightly increased after 6 h, but highly expressed after 24 h. These data are consistent with the 10 uM adaphostin induced heme oxygenase 1 expression reported in glioblastoma cell lines, which did not appear until after 8 24 h.

This adaphostin induced HMOX1 upregulation in NCI H522 cells and glioblastoma cell lines is in contrast to the response AV-951 of hematologic cell lines where we have previ ously reported the major transcriptional response involved 10 fold induction of genes encoding for both heavy and light ferritin polypeptides. Moreover, even after treatment with 10 uM adaphostin, leukemia cell lines showed no increase in HMOX1 expression on the cDNA arrays after 6 h incubation 1. 24 0. 7, 1. 35 0. 39 and 1. 16 0. 28 respec tively compared to a 7. 4 and 30.

Thus, there is a need for additional new anti cancer drugs that induce specific cell death pathways in leukemia cells. It has recently been shown that the HIV protease inhibitor nelfinavir can induce cell death in a variety of human cancer types, and clinical studies with nelfinavir are currently proposed or underway. Nelfinavir appears to induce cell death in human cancer cells by rather pleiotropic mechanisms, including apoptosis, necrosis, and autophagy. Swelling of the endoplas mic reticulum by an accumulation of misfolded proteins appears to be a central mechanism in nelfinavir induced death in several cancer types, including lung cancer, glioma, and ovarian cancer cells, and precedes the activation of apoptosis.

Apoptosis can be induced by several pathways, includ ing an e trinsic pathway mediated by cell membrane bound death receptors and an intrinsic pathway mediated by activation of pro apoptotic intracellular mechanisms. Mitochondria play a central role in the induction and control of apoptosis because they harbour several apoptosis inducing proteins within their mem branes that can be released into the cytosol to induce caspase dependent cell death. Release of these mitochondrial factors occurs via outer mitochondrial membrane pore forma tion by pro apoptotic bcl 2 family members, such as ba , bak and t bid. The activities of these pro apoptotic molecules are counterbalanced by the anti apoptotic mitochondrial membrane proteins bcl 2, bcl L, and mcl 1.

Although there are several different the ories regarding how the pro and anti apoptotic bcl 2 family members interact, it has repeatedly been shown and is generally believed that increased e pres sion of pro apoptotic bcl 2 family members promotes cell death, whereas increased e pression of anti apopto tic bcl 2 family members facilitates cell survival. The most prominent anti apoptotic bcl 2 family members, including bcl 2, bcl L and mcl 1, were originally identified and found to be over e pressed in leukemia cells. Mcl 1 is a rather unique member of the bcl 2 family in that it has a rela tively large molecular weight of 40 42 kDa, compared to the molecular weight of ca. 26 kDa common to most other bcl 2 family members. Mcl 1 is a target of several pro apoptotic proteins and has been shown to undergo caspase mediated degradation during apoptosis.

Further, a shorter splice form of mcl 1 has been described and has been shown to e ert a pro apoptotic function. Thus, e pression and modifica tion of mcl 1 appears to be crucial for regulation of cell survival and cell death in leukemia cells. In the present study, we show that despite its ability to induce apoptosis, nelfinavir enhances e pression of the mito Dacomitinib chondria protective mcl 1 protein in leukemia cells, resulting in a primarily mitochondria independent cas pase activation and cell death.

[13] cited by Jones et al. [14]:NDVI=(NIR?R)/(NIR+R)(1)2.2. Multispectral Plant CameraThe NDVI was used in a multispectral camera (3-chip CCD camera), type MS2100, to discriminate the plant material from the soil background. This custom-made camera measures the reflection intensities in the red, infrared, and green wavelengths and is the main component of a machine vision system for the sensor-based recording of weeds [15].The camera was controlled using the custom-made control software ��DT��, and the picture size is 659 H �� 494 V. Image processing conducted using specialized software (SYMACON GmbH, Barleben, Germany) and includes the erosion of single pixels. Image processing and control software were run on a dust-proofed industrial computer, such as an IPC-r 4 HE (PK Computer GmbH, Eppstein, Germany).

To detect the plant coverage level, only the red (peak wavelength: 670 nm, band pass size: 22 nm) and infrared (peak wavelength: 800 nm, band pass size: 65 nm) reflectance intensities of this 3 chip camera is used. Figure 2(a,b) show examples of red and NIR images of potato plants and soil.Figure 2.Potato plants detected using a multispectral camera. The red channel (a), and the NIR channel (b) were used to calculate the NDVI (c) and the binary images (d) through thresholding.From these images, a pixel-wise NDVI image can be calculated.

Figure 2(c) shows the results, and all of the plant material shows high intensity levels; the shadow regions on the soil are at the middle leve
For decades, many research works have studied different methods to reproduce the movements of a person in electromechanical and robotic systems.

These methodologies allow not only to replicate but also to improve and refine these movements for different uses for the welfare of humanity The teleoperation provides protection and increases the maneuverability of a huge variety of human-operated machines. Some examples are chemical, construction and mining industries and medicine. In the latter case, precise and reliable robotic systems must assist surgeons.Currently, improved control systems for biped walking robots Entinostat has attracted an increase research interest.

One approach is to model and reproduce human-like walking given the angular velocity and acceleration measured by gyroscopes and accelerometers installed on the legs of a person [1].In the work by Nakazawa et al., [2] an artificial vision system composed of 8 cameras captures dancing human movements to be imitated by a robot. In [3], a camera system is presented too, where Carfilzomib Boesnach et al. introduce the concept of movement oriented to context. This is a third type of movement coming from the combination of task-oriented and position-oriented ones.

LSPR peaks are typically detected by spectral extinction measurements on a dense film or spectral scattering measurements on single nanoparticles.Nicely regular five-branched GNS have been recently obtained by some of us, using the non-ionic surfactant Triton X-100 (TX100) in a seed-growth synthesis in water [9]. These GNS exhibit the unusual feature of three localized surface plasmon resonances. While the transversal oscillation of the valence electrons generate a ��short�� LSPR at ~530 nm (LSPR 1), the other two plasmon resonances span the near-IR (NIR) interval, entering the short-wavelength IR (SWIR) domain. In particular, the maximum absorption wavelength of these LSPR can be positioned in the 600�C900 nm (LSPR 2) and 1,100�C1,600 nm (LSPR 3) ranges, respectively, by regulating the reactants concentration, that, in turn, regulates the LWR (length to width ratio) of the branches.

All LSPRs are photothermally active, i.e., convert efficiently radiation into heat [9]. These GNS may thus, for instance, be used as tools for nanomedicine exploiting the 700�C1,000 nm transparent window of biological matter for through-tissues photothermal treatments against tumors or multi-drug resistant bacterial infections.3.?Materials and Methods3.1. Five-Branched Gold NanostarsPreparation of GNS for deposition on POFSeed solution: In a 20 mL vial, HAuCl4 (5 mL, 5 �� 10?4 M in water) is added to an aqueous solution of TritonX-100 (5 mL, 0.2 M). The mixture is gently hand-shaken and a pale yellow color is obtained. Then, a previously ice-cooled solution of NaBH4 (0.6 mL, 0.

01 M in water) is added. The mixture is gently hand-shaken and a reddish color appears.Growth solution (10 mL samples): In a 20 mL vial, AgNO3 (180 ��L, 0.004 M in water) and HAuCl4 (5 mL, 0.001 M in water) are added in this order to an aqueous solution of TritonX-100 (5 mL, 0.2 M). Then, an aqueous solution of ascorbic acid (170 ��L, 0.0788 M) is added. The solution, after gentle mixing, becomes colorless. Soon after, the seed solution (12 ��L) was added. The solution is gently hand-shaken and a pink color appears and Batimastat quickly changes to blue and becomes more intense. After 1 h at room temperature PEG2000-SH is added in a concentration of 5 �� 10?5 M. The mixture is stirred for 1h at room temperature, then the nanoparticles undergo three cycles of ultracentrifugation (13,000 rpm, 11 min)/elimination of the surnatant/redissolution of the pellet in 10 mL of bi-distilled water.

These steps are required to eliminate excess PEG2000-SH and TritonX-100. Then, another cycle of ultracentrifugation is performed, the surnatant discarded and the pellet redissolved in 1 mL of bidistilled water to concentrate the particles (10X in respect to the starting colloidal solution). The final concentration is ~ 0.6 mgAu/mL.

The chemical composition of the sample surface was revealed in the wide scan spectra. The variation of the atomic composition with film depth was obtained by
SHM and its related NDE approaches are becoming increasingly important for maintaining the safety and integrity of infrastructures and complex systems that are configured with sophisticated data systems for electronics, propulsion, controls and other critical subsystems. In recent years, an increasing emphasis has been placed on the potential for using these data capabilities, in conjunction with emerging sensor and data management technologies for in situ health monitoring of material condition. However, SHM/NDE for the identification and characterization of structural degradation presents unique challenges.

An understanding of potential damage mechanisms, structural design criteria, fail-safe features and structural maintenance philosophy is needed to develop a sensor-based system, so that the structural condition can be effectively monitored. Another challenge is how to provide real-time, accurate and quantitative image information about the damage.The concept of multi-wave imaging was proposed independently by various groups in the physics community, in which one form of wave energy serves as the excitation source of the other. For example, in thermo-inductive imaging, absorbed electromagnetic radiation by induction causes a transient change in temperature that can be inspected by transient infrared thermography. Because of the way the waves are combined, multi-wave imaging has the potential to produce a single image with better contrast and higher spatial or spectral resolutions.

Although it was initially introduced as a way to improve biomedical diagnostic capabilities [3], multi-wave imaging opens new avenues in the fields of SHM and NDE and provides a new direction for quantitative imaging, due to its superior outcomes compared to conventional imaging results.As mentioned before, the multi-wave phenomenon is based on the effect that the interaction of one kind of wave with objects under testing can generate a second kind of wave, while hybrid imaging has a broader definition that strategically combines multiple imaging methods to achieve better fusion of information or, specifically, better detection in NDE and SHM problems.

One success in the medical imaging Dacomitinib society is the wide use of PET/CT imaging and the forthcoming PET/MR hybrid systems that give both abundant functional and anatomical details of the object. Generally speaking, the combination of different imaging techniques into one hybrid platform is beneficial to the imaging quality and speed and even makes simultaneous data acquisition possible. With minimal effort on image registration, the following data analysis and post-processing can be significantly eased compared to individual image acquisition.