5). Incubation with a suprapharmacological dose of the drug (100 ��M), two orders of magnitude higher than the maximum concentration of total selleck catalog rosiglitazone reached in human plasma after an 8-mg oral dose (14), led to a significant increase in apical Na+/H+ activity, but this increase was not different in control and lipid-loaded cells (Fig. 5). DISCUSSION One renal manifestation of the metabolic syndrome in both humans and ZDF rats is an excessively acidic urine, attributed in part to impaired urinary NH4+ excretion (6, 9, 16, 27, 28). Decreased NHE3 expression and activity in the proximal tubule brush border contribute to this defect in ZDF rats, although other factors such as decreased glutamine metabolism due to mitochondrial substrate competition by excess intracellular FFA could also play a role (6).

Impaired luminal acid extrusion via NHE3 could also explain the reduced excretion of urinary citrate in ZDF rats, since intracellular acidification in the proximal tubule upregulates both citrate reabsorption and citrate metabolism (1, 29). Hypocitraturia in these animals cannot be attributed to differences in acid or alkali intestinal absorption, given that urinary sulfate and potassium were not different in ZDF and lean rats. These functional abnormalities are accompanied by renal steatosis with predominant tubular localization in ZDF rats and can be reproduced in part in a cell culture model of proximal tubule lipotoxicity, OKP cells incubated with FFA (6). Renal steatosis and lipotoxicity may thus be an important factor in the pathophysiology of renal acidification defects associated with the metabolic syndrome.

We have shown that TZD treatment in ZDF rats reduces renal steatosis. The antisteatotic action of TZD has been described in humans and animal models of the metabolic syndrome in the liver, heart, and skeletal muscle (4, 22, 38, 47, 52, 57), but to our knowledge the effect of TZD on renal triglyceride content has not been previously examined. Reduction of renal fat with TZD in ZDF rats was accompanied by a shift in urinary NH4+, pH, TA, and citrate to levels comparable to their lean littermates and led to a commensurate increase in brush-border NHE3 protein and activity. No effect of TZD on urinary acidification parameters was noted in lean control rats, in the absence of renal steatosis.

The concurrent reduction in renal triglycerides and normalization of NHE3 and urinary parameters strongly suggest correction of functional abnormalities with renal lipid mobilization, and thus support the causal relationship between renal steatosis and urinary acidification defects in vivo. The effect of TZD on renal steatosis and GSK-3 functional abnormalities is likely attributable to PPAR�� activation in the adipose tissue, which in turn decreases nonadipose tissue lipotoxicity by redistributing lipids to adipocytes (44, 55).

Some of the derivatives exhibited potency in the nanomolar range, with one (2-phenoxy-1,4-naphthoquinone, B6 in Figure 1) displaying an ED50 value of 80 nM against Trypanosoma brucei selleck Belinostat rhodesiense, as assessed in experiments using in vitro cultured parasites. It also showed a selectivity index (ratio of the compound’s ED50 values on mammalian cell lines and trypanosomes) of 74 [24], which is very close to the specifications required by WHO/TDR to be considered an anti-trypanosomatid hit [25]. However, the molecular mechanism and the target(s) responsible for the biological profile of this class of compounds have remained undisclosed. Figure 1 Chemical structures. Here, by means of a chemical proteomics approach, we aimed at identifying the putative molecular target(s) of B6.

In particular, using its immobilized derivative 1 (Fig. 1), we isolated its targets from parasite extracts. Then, by means of biochemical experiments, we verified the ability of the molecule to bind to recombinant forms of the identified targets. In light of the general property of naphthoquinones to generate free radicals, we finally analyzed oxygen consumption in permeabilized trypanosomes and production of reactive oxygen species (ROS) in trypanosome mitochondrial cell fractions. This allowed us to elucidate additional B6 potential mechanisms of action, as chemical proteomics is not suited to identify non-protein targets. Methods Chemical synthesis and anti-trypanosomal activity of B6-derivatives 1�C3 Before covalently attaching B6 to the solid support through a linker, we analyzed which site(s) of the molecule were more appropriate for linking purposes.

To this end we synthesized derivatives 1�C3 (Fig. 1), which carry in different positions amino or hydroxyl groups that can be easily exploited as anchor points. The synthesis was carried out according to the procedure reported for B6 [24], and which relies on the substitution of a 2-bromonaphthoquinone with the corresponding phenol. Synthesis of 2-(4-amino-phenoxy)-[1], [4]naphthoquinone (1). To a stirred solution of 4-amino-phenol (0.46 g, 4.2 mmol) in 90 ml dimethylformamide (DMF) potassium carbonate (1.70 g, 12.3 mmol) was added. After stirring for 1 h at room temperature, 2-bromo-[1], [4]-naphthoquinone (1.0 g, 4.2 mmol) was added. After stirring for further 3 h, the reaction was diluted with water and ice (500 ml) and the resulted brownish solid was collected by filtration to give 0.

49 g of crude 1, which was crystallized by EtOH/water (40% yield). IR (Nujol) 3421, 3382, 1680, 1635, 1609, 1508, 1204, 980, 718 cm?1; 1H NMR (300 MHz, CDCl3) �� 8.25-8.22 (m, 1H), 8.12-8.09 (m, 1H), 7.80-7.78 (m, 2H), 6.95 (d, 2H, J=8.5 Hz), 6.76 (d, 2H, J=8.5 Hz), 6.04 (s, 1H), 3.77 (br s, 2H, exchangeable with D2O); HRMS (ES) m/z calculated for C16H11NO3Na 288.0637, found 288.0639 [M++Na+]. Synthesis of 5-hydroxy-2-phenoxy-[1], [4]naphthoquinone Entinostat (2).

Figure 2 Conserved increase in expression of the miR-17�C92 polycistron and miR-21 in both human and woodchuck HCCs. Northern blot analysis of the expression of miRNAs in human and woodchuck peri-tumor liver and primary HCCs. A: Human samples. B: Woodchuck selleck … Interestingly, expression of the major liver miRNA, miR-122, which is down-regulated in a rat HCC model,28 was maintained in all of the human HCCs samples. Although miR-122 expression was substantially reduced in some of the HBV-positive HCCs (Figure 2A), there was no statistically significant difference in matched tumor and peri-tumor samples (P = 0.86) (supplemental Figure 1, see http://ajp.amjpathol.org).

HBV-Associated Cirrhotic Livers Overexpresses Members of the miR-17�C92 Polycistron and miR-21 Compared to Normal Liver Cirrhosis is considered to be a significant aetological factor that precedes HCC in humans, whether it is associated with chronic HBV infection or not. qRT-PCR analysis of human liver and human HCC (Ambion) demonstrates that miR-17�C92 polycistron and miR-21 were overexpressed in HCC, a result that is consistent with our Northern blot and cloning data (Figure 3). To determine whether these miRNAs are overexpressed in precancerous liver, we analyzed their levels in three cirrhotic human livers from individuals that were undergoing human liver transplant surgery, and in which primary HCC had not been identified. The severe nodular cirrhosis of these patients was reflected in their liver function tests (supplemental Table 2, see http://ajp.amjpathol.org).

Each of the three cirrhotic livers showed variable levels of elevation of the miRNAs as compared with normal liver (Figure 3). Out of the four members of the miR-17�C92 polycistron (miR-17, miR-19a, miR-20, and miR-92), each cirrhotic liver has statistically significant over-expression of at least two of the miRNAs; however, although miR-19a showed a trend of increased expression in cirrhotic liver these changes were not statistically significant (Figure 3). As expected, the expression of these oncogenic miRNAs was variable and not generally as high as that determined for HCC. We attribute this miRNA expression pattern to the multinodular precancerous nature of the liver cirrhosis samples that were used to make the RNAs. For example, in liver cirrhosis 1, miR-17 and miR-20 exhibited respective 3.

5- and 12-fold increases over liver (Figure 3). Furthermore, miR-21 expression was significantly enhanced in all of the cirrhotic livers (~ 15-fold Dacomitinib increase) (Figure 3). However, the fold increase (relative to normal liver) of these miRNAs in cirrhotic livers was less than that observed for the same miRNAs in HCC. These data support the hypothesis that activation of the miR-17�C92 miRNAs and miR-21 precedes HCC, and suggests that these genetic elements may represent important etiological agents in tumor initiation or progression and not just products of the transformed state.

Our main findings suggest that positive expression of EpCAM and ABCG5 within tumor buds is a frequent event selleck chemicals llc and may confer a significant and adverse prognosis in patients with colorectal cancer, particularly in lymph node-negative patients expressing ABCG5. Several of these putative CSC markers have previously been evaluated in tumor buds. Horst et al[31] assessed CD133 in colorectal cancers using 3 different antibodies. They reported pronounced expression of CD133 in tumor glands close to the invasive margin but restricted to glandular differentiated cells and a general lack of CD133 in the tumor buds themselves. They further found that nuclear ��-catenin expression and CD133 were not correlated and that the 2 protein markers may stain different, yet overlapping populations of tumor cells[32].

Our results of only a few CD133-positive tumor budding cases and no prognostic differences between patients with CD133-positive and -negative tumor budding are in line with these findings. Investigating rectal cancers, Gosens et al[33] found strong membranous EpCAM staining in the tumor center and a progressive loss at the tumor front associated with high tumor grade, tumor budding, and a poor local and distant recurrence-free survival. This was also accompanied by a concomitant increase in cytoplasmic EpCAM staining as well as overexpression of ��-catenin. We also observed a pronounced loss of EpCAM toward the invasive tumor front, particularly in tumors with infiltrating margins, as well as a shift in localization of EpCAM expression from membrane to cytoplasm.

The findings of this study indicate that despite this loss towards the border, patients with EpCAM-positive tumor buds have a most unfavorable survival time, a result which was maintained in multivariable analysis. Although EpCAM, like CD44, is known for its cell-adhesion function, it seems to have versatile roles in signaling, cell migration, proliferation, and differentiation depending on the microenvironment[34]. In the normal epithelium, EpCAM supports adhesion, whereas in carcinoma it seems to prevent strong cell-cell adhesion, enabling cell migration and metastasis similar to E-cadherin. The intracellular localization of EpCAM and its identification by immunohistochemistry may represent differential roles of this protein in colorectal cancer progression and partially explain why, despite loss of expression from normal at tumor center to tumor border, the positive expression in buds is linked to a poorer patient outcome.

Masaki et al[35] have also described associations between membranous CD44 and CD44v6 expression and a higher degree of tumor budding. However, Batimastat it is unclear from these studies whether expression was evaluated in the tumor center, then correlated with tumor budding or whether expression was evaluated in buds themselves.

However, the basal level of cleaved PARP was also higher in SKOV3 cells as compared with the other cell lines. To quantitatively investigate the apoptotic effect of 11a, Annexin V/PI double staining was performed. Consistent with the cleaved-PARP assays, 11a only modestly induced www.selleckchem.com/products/MDV3100.html apoptosis in SKOV3 cells but not in A2780 or OVCAR3 cells using etoposide as the positive control (Figure 4B and Figure S7). Similar effects were observed in MCF7 breast cancer cell line, where both doxorubicin and staurosporine induced significant apoptosis while 11a did not induce apoptosis at the tested concentrations (Figure 4C and 4D). Collectively, these data indicate that apoptosis is not the main mechanism accounting for 11a-induced cytotoxicity. Figure 4 11a induces minimal cell apoptosis in ovarian cancer cell lines and a breast cancer cell line.

11a induces G1/S cell cycle arrest in a p53-dependent manner Since 11a failed to induce significant apoptosis in any of the cell lines tested, we hypothesized that 11a-induced cytotoxicity may be attributed to cell cycle arrest, which could induce growth inhibition as determined by the sulforhodamine B (SRB) colorimetric assay used for the NCI-60 cell line cytotoxicity screening. To further discern whether 11a cytotoxicity correlated with p53 status, colorectal cancer isogenic HCT116 p53+/+ and HCT116 p53-/- cell lines were used [35]. Interestingly, these isogenic cell lines exhibited differential sensitivity to 11a. The p53 wild type cell line (IC50 = 0.0337 ��M) was about 10-fold more sensitive than p53 null cell line (IC50 = 0.

3188 ��M) in a pilot screen performed by the Small Molecule Screening and Synthesis Facility (SMSSF) of University of Wisconsin (Figure 5A). The differential sensitivity was later confirmed using the MTT proliferation assay where p53 wild type cells (IC50 = 0.36 ��M) were more sensitive than p53 null cells (IC50 = 1.76 ��M) (Figure 5B). To further investigate the mechanism by which the two isogenic cell lines showed differential sensitivities to 11a, we assessed the apoptotic effects of 11a in these two cell lines. The cells were treated with increasing concentrations of 11a for 24 hours, and apoptosis was measured using a PARP-cleavage assay, in which the PARP cleavage ratio indicates the apoptotic status. Figure 5C shows that only modest PARP cleavage was observed in either p53+/+ or p53-/- HCT116 cells.

To examine whether PARP played a role in 11a mediated cytotoxicity, we co-treated cells with 11a and 3-aminobenzamide (3-AB), a specific PARP inhibitor [51]. PARP inhibition did not affect the cytotoxicity of 11a (Figure 5D), indicating that 11a mediated Brefeldin_A cytotoxicity was independent of PARP activity. The apoptotic effect of 11a was further examined by Annexin V/PI staining. While staurosporine caused severe apoptosis, 11a did not induce any apoptosis in the isogenic cell lines as compared with DMSO control (Figure 5E).

3F). Sox9-EGFP High cells were also highly enriched (+3.46-+101.8-fold change vs. Sox9-EGFP Negative cells) in multiple genes encoding gastrointestinal hormones including neurotensin, substance P, ChgA, chromogranin-B, cholecystokinin, glucagon, secretin, gastric inhibitory peptide, and ghrelin (Table 3). These findings strongly support prior data (17, thereby 21) that the Sox9-EGFP High cells are highly enriched for EECs (Table 3). Unexpectedly, microarray data also revealed that BMI1 and HOPX, which mark +4 slowly cycling or quiescent ISCs (54, 61), were significantly and exclusively enriched in Sox9-EGFP High cells vs. all other Sox9-EGFP cell types (+2.65- and +4.15-fold change vs. Sox9-EGFP Negative cells, respectively; P = 4.04E-11 and P = 9.25E-15, respectively) (Table 3).

Several lines of evidence suggest that Dclk1, also called DCAMKL-1, may represent another putative marker of slowly cycling/quiescent ISCs (39). Immunofluorescence studies clearly demonstrated that DCAMKL-1 colocalized with cells expressing high levels of Sox9-EGFP (Fig. 4) and quantitative PCR revealed that DCAMKL-1 mRNA was dramatically enriched in Sox9-EGFP High cells (+147.0 �� 61.9-fold change vs. Sox9-EGFP Negative cells; P < 0.05). Table 3. Genes upregulated specifically in Sox9-EGFP High cells Fig. 4. DCAMKL-1 colocalizes with Sox9-EGFP High cells. Immunostaining for Sox9-EGFP (green) and DCAMKL-1 (red) demonstrates that in intestinal epithelial crypts, DCAMKL-1 colocalizes with high levels of Sox9-EGFP [nuclei staining, 4,6-diamidino-2-phenylindole ... Sox9-EGFP Negative cells and phenotype of differentiated IEC lineages.

A number of genes that were specifically expressed at significantly higher levels in Sox9-EGFP Negative cells vs. all other Sox9-EGFP cell populations are known markers of absorptive enterocytes including trehalase, lactase, aminopeptidase N, alkaline phosphatase, and glucoamylase, which are all enterocyte brush border enzymes (Table 4). Furthermore, Sox9-EGFP Negative cells exhibited specific upregulation of FABP1, FABP2, and SLC2A5 genes, coding for liver and intestinal fatty acid-binding protein and GLUT5, which are all well-accep
Malaria is a major disease burden in 106 countries, causing an estimated 225 million cases and, as reported for 2010, 665,000 to 1,133,000 human deaths each year in tropical and sub-tropical regions [1].

Despite recent progress [2], drug resistance remains a major obstacle to the effective and sustainable control of malaria. Cellular redox Cilengitide reactions play important roles not only in redox regulatory processes and antioxidant defense but also in the mechanisms of drug action and drug resistance in malaria parasites [3], [4]. Recent advances in parasite biology suggest a compartmentalization of redox metabolism [5] as well as of cellular processes that are sites of drug action [6]. Indeed, several antimalarial drugs have been reported to act through the induction of oxidative [7] or nitrosative stress [8].

Thus cuckoo birds are always looking for a better place in order to decrease the chance of their eggs to be discovered. The process customer reviews can be approximated by the fraction pa of the NP nests which are displaced by new nests (with new random solutions). Consequently, it will enhance the original quality of the candidate solution. Thus, the more cuckoos a UCAV path is passed by, the bigger possibility that a path can be selected by the other cuckoos. This process can guarantee nearly all cuckoos walk along the shortest UCAV path in the end.Based on the above analysis, the pseudocode of improved CS-DE/CS for UCAV three-dimension path planning is described as follows (Algorithm 5).Algorithm 5Algorithm of DE/CS for UCAV three-dimension path planning.5.

Path-Smoothing StrategiesThe generated UCAV optimal three-dimension path using the proposed hybrid metaheuristic method DE/CS is usually hard for exact flying. There are some turning points on the optimized path [20, 21]. In this section, we adopt a class of dynamically feasible trajectory smooth strategy called B-Spline curves smoothing strategy [17]. B-Splines are adopted to define the UCAV desired path, providing at least first-order derivative continuity. B-Spline curves are well fitted in the evolutionary procedure; they need a few variables (the coordinates of their control points) in order to define complicated curved paths. Each control point has a very local effect on the curve’s shape and small perturbations in its position produce changes in the curve only in the neighborhood of the repositioned control point.

B-Spline curves are parametric curves, with their construction based on blending functions [22]. Their parametric construction provides the ability to produce nonmonotonic curves. If the number of control points of the corresponding curve is n + 1, with coordinates w0(x0, y0, z0),��, wn(xn, yn, zn), the coordinates of the B-Spline curve may be written asx(u)=��i=1nxi?Ni,p(u),y(u)=��i=1nyi?Ni,p(u),z(u)=��i=1nzi?Ni,p(u),(11)where u is the free parameter of the curve, Ni,p(u) are the blending functions of the curve, and p is its degree, which is associated with curve’s smoothness (p + 1 being its order). Higher values of p correspond to smoother curves. The blending functions are defined recursively in terms of a knot vector U = u0,��, um, which is a nondecreasing sequence of real numbers, with the most common form being the uniform nonperiodic one, defined asui={0if??i Brefeldin_A functions Ni,p are computed, using the knot values defined above, asNi,0={1ui��u��ui+1,0otherwise,Ni,p(u)=u?uiui+p?uiNi,p?1(u)+ui+p+1?uui+p+1?ui+1Ni+1,p?1(u).(13)If the denominator of either of the fractions is zero, that fraction is defined to have zero value.

2. Materials and Methods2.1. Plant MaterialThe ground seed powder of Garcinia kola was obtained from the plant www.selleckchem.com/products/epz-5676.html material collection of the Applied and Environmental Microbiology Research Group (AEMREG) laboratory, University of Fort Hare Alice. South Africa.2.2. Preparation of ExtractsThe extracts were prepared following the descriptions of Basri and Fan [19]. A 100-gram measurement of the seed powder was steeped in 500mL of methanol solvent for a 48h period with shaking in an orbital shaker (Stuart Scientific Orbital Shaker, UK). The resultant extract was centrifuged at 3000rpm for 5min at 4��C (Beckman Model TJ-6RS Centrifuge, Great Britain), the supernatant was then filtered through Whatman No.1 filter paper, while the residue was then used in the second extraction process involving 300mL of the solvent.

The combined extracts were concentrated using a rotary evaporator at 65��C (Steroglass S.R.L, Italy), after which they were dried to a constant weight under a stream of air in a fume cupboard at room temperature. Dimethyl sulphoxide (DMSO) at a concentration equal to 5% of the total volume which was made up with sterile distilled water was used to aid the reconstitution of the dried extract when making test concentrations.2.3. Test Listeria StrainsThe 42 test Listeria isolates used in this study were obtained from the culture collection of the Applied and Environmental Microbiology Research Group (AEMREG) laboratory at the University of Fort Hare, Alice, South Africa. The bacteria were previously isolated from wastewater effluents in the Eastern Cape Province of South Africa and belonged to three species groups which are L.

ivanovii, L. grayi, and L. monocytogenes [20].2.4. Preparation of the Inoculum The EUCAST [21] colony suspension method was used to prepare the inoculums of the test organisms. In brief, colonies picked from 24h old cultures were suspended in saline solution (0.85% NaCl) to give an optical density of approximately 0.1 at 600nm after which the suspension was then diluted a hundredfold before use.2.5. Antibacterial Susceptibility TestThe agar well diffusion method according to Irobi et al. [22] with modifications was used to determine the sensitivity of the test Listeria to the extract. The prepared bacterial suspension (100��L) was inoculated into sterile molten Mueller-Hinton agar medium at 50��C in a MacCarthney bottle, mixed gently, and then poured into a sterile petri dish and allowed to solidify. A sterile 6mm diameter cork borer was used to Carfilzomib bore wells into the agar medium after which the wells were filled up with approximately 100��L of 10mg/mL extract solution.

05 was taken as statistically significant.3. Results3.1. Patient Demographics18 patients, including 12 males and 6 females, aged 3�C24 years (mean 11.5) at the time of surgery, underwent resective surgery. Preoperative characteristics of these subjects, selleckchem Ixazomib including etiology, seizure type, EEG patterns, and imaging findings are shown in Table 1. Age at seizure onset ranged from 2 months to 6 years, with an average 3.5 years. The time period between epilepsy onset and surgery ranged from 2 to 21 years (average 8 years). Patients experienced, on average, 3.6 different seizure types prior to surgery. Patients had been using AEDs for a period of 1 to 19 years; the average number of AEDs tried was 4 and the average number of AEDs used was 2.8 at the time of surgery.

Antiepileptic drugs were continued after surgery and gradually withdrawn if the patients were seizure-free and had marked improvement in EEG pattern. The follow-up period was between 1 to 9 years with a mean of 5.4 years.Table 1Patient profiles��number 1. As shown in Table 1, four patients experienced pre- or perinatal hypoxic-ischemic insult; two cases had a history of head injury; two showed damage resulting from postnatal encephalitis; two, focal cortical dysplasia; and two, small vascular malformations. One was diagnosed with tuberous sclerosis. Five patients showed hemispheric or focal atrophy without a recognizable cause.3.2. EEG and Image FindingsResults of routine EEG, and/or ambulatory EEG, and/or long-term video EEG monitoring were abnormal in all patients, and indicated an abnormal slow background activity/diffuse slowing.

All patients showed symmetrical or asymmetrical 1.5 to 2.5Hz SSW activity in the interictal EEG (primary bilateral synchrony in seven and secondary bilateral synchrony in 11 subjects) (Figures 1(a), 2(d), and 3(f)). PFA was noted in sleep EEGs in 17 patients (Figures 1(b), 2(c), and 3(e)). The epileptic discharges were characterized by bilateral symmetrical synchronous generalized discharge or bilateral asymmetrical discharge or bilateral asynchronous discharge or focal discharge. Hemispheric dominant discharges, that is, at least Dacomitinib 70% of all discharges originating from one hemisphere, were noted in all patients in ictal and interictal EEGs.

More details were explained by Lee et al. [7].The proposed vision-based system can support two cameras at the subsystem level with 30 frames per second (fps), so it can be appropriate to track the motion of civil structures with the maximum frequency of less than 15Hz (Nyquist frequency). In phase 3 reality, civil structures usually have a natural frequency of lower than 4-5Hz [8], thus the proposed system can be applicable to measuring the dynamic displacement of large-scale structures. However, for the purpose of real-time processing, the processing time per frame should be less than 33.3 milliseconds (ms). To verify the performance of the proposed system, processing time per frame at a subsystem PC was checked as shown in Figure 9. A total of 2300 frames were captured by camcorders and processed at the subsystem.

The averaged and maximum processing time per frame are 17ms and 21.5ms, respectively, which is fast enough for real-time processing.Figure 9Processing time per frame.3. Experimental VerificationsSeveral laboratory tests were conducted to verify the proposed multipoint vision-based system and the time synchronization algorithm. To ensure good data transaction between the slave subsystems and the master PC, all the PCs and their components should be stable without viruses and spywares before conducting the verification tests. 3.1. Shaking Table TestIn order to evaluate the performance and the stability of the proposed synchronized multipoint vision-based system, several shaking table tests were performed. Figure 10 shows the shaking table and the target used in the experiments.

The results of this system were compared with those measured using LVDT. Figure 10Shaking table and target size.The testing system consisted of two laptops, one Lenovo-R61 (Intel Core Duo 2.4MHz, 2GB of RAM), and one Acer-Asprire 5580 (Intel Core 2-Duo 1.66MHz, 3GB of RAM), Lenovo was used as the slave PC. Two JVC GZ-MS120 camcorders with an optical zooming capability of 40 times, a resolution of 640 �� 480 pixels, and a frame rate of 30 fps were used. In addition, GSK-3 two myVision USB frame grabbers, two telescopic lenses, and one wireless LAN router complying with the 802.11g wireless standard were implemented to transfer data between the master PC and slave PCs. The target size is 15mm in vertical and horizontal directions. The camera was placed at 16 meters apart from the target. The number of pixels between the uppermost white spot and the lowermost white spot was 284, thus the physical resolution was 0.053mm/pixel. The schematic of the testing configuration is given in Figure 11.Figure 11Experimental location setup.