Flexible dye-sensitized solar cells (DSSCs) often face the dilemma of the high temperature sintering of TiO2 photoanode to achieve superior performance and low thermal durability of the flexible substrate. Herein, we report a photoanode that combines the flexibility and high-temperature durability, which circumvents the long-standing challenge in flexible photoanode of DSSC. A hybrid mat consisting of anatase-phased TiO2 nanofibers and structurally amorphous SiO2 nanofibers is first prepared via the method of dual-spinneret electrospinning followed by pyrolysis. The hybrid fibrous mat is then impregnated with binder-free TiO2 nanoparticles and sintered at 480 °C to form a flexible composite photoanode for DSSC. The DSSC based on this composite photoanode achieves a power conversion efficiency of 6.74 ± 0.33% on FTO/glass substrate. Device characterization and phototransient measurement, dye-loading experiment, and structural characterization indicate that, in the composite photoanode, the TiO2 nanoparticles enhance the dye loading, the TiO2 nanofibers improve the electron transport, and the SiO2 nanofibers provide the mechanical strength/flexibility. The freestanding composite mat of TiO2 nanoparticles and electrospun TiO2/SiO2 nanofibers, as well as the preparation methods reported herein, not only is ideal for flexible DSSCs, but also can be applied for a broad range of flexible and low-cost energy conversion devices.
A dynamic attitude measurement system (DAMS) is developed based on a laser inertial navigation system (LINS). Three factors of the dynamic attitude measurement error using LINS are analyzed: dynamic error, time synchronization and phase lag. An optimal coning errors compensation algorithm is used to reduce coning errors, and two-axis wobbling verification experiments are presented in the paper. The tests indicate that the attitude accuracy is improved 2-fold by the algorithm. In order to decrease coning errors further, the attitude updating frequency is improved from 200 Hz to 2000 Hz. At the same time, a novel finite impulse response (FIR) filter with three notches is designed to filter the dither frequency of the ring laser gyro (RLG). The comparison tests suggest that the new filter is five times more effective than the old one. The paper indicates that phase-frequency characteristics of FIR filter and first-order holder of navigation computer constitute the main sources of phase lag in LINS. A formula to calculate the LINS attitude phase lag is introduced in the paper. The expressions of dynamic attitude errors induced by phase lag are derived. The paper proposes a novel synchronization mechanism that is able to simultaneously solve the problems of dynamic test synchronization and phase compensation. A single-axis turntable and a laser interferometer are applied to verify the synchronization mechanism. The experiments results show that the theoretically calculated values of phase lag and attitude error induced by phase lag can both match perfectly with testing data. The block diagram of DAMS and physical photos are presented in the paper. The final experiments demonstrate that the real-time attitude measurement accuracy of DAMS can reach up to 20? (1?) and the synchronization error is less than 0.2 ms on the condition of three axes wobbling for 10 min.
Tagged magnetic resonance imaging (TMRI) provides a direct and noninvasive way to visualize the in-wall deformation of the myocardium. Due to the through-plane motion, the tracking of 3D trajectories of the material points and the computation of 3D strain field call for the necessity of building 3D cardiac deformable models. The intersections of three stacks of orthogonal tagging planes are material points in the myocardium. With these intersections as control points, 3D motion can be reconstructed with a novel meshless deformable model (MDM). Volumetric MDMs describe an object as point cloud inside the object boundary and the coordinate of each point can be written in parametric functions. A generic heart mesh is registered on the TMRI with polar decomposition. A 3D MDM is generated and deformed with MR image tagging lines. Volumetric MDMs are deformed by calculating the dynamics function and minimizing the local Laplacian coordinates. The similarity transformation of each point is computed by assuming its neighboring points are making the same transformation. The deformation is computed iteratively until the control points match the target positions in the consecutive image frame. The 3D strain field is computed from the 3D displacement field with moving least squares. We demonstrate that MDMs outperformed the finite element method and the spline method with a numerical phantom. Meshless deformable models can track the trajectory of any material point in the myocardium and compute the 3D strain field of any particular area. The experimental results on in vivo healthy and patient heart MRI show that the MDM can fully recover the myocardium motion in three dimensions.
Through a simple doping route with zinc ion as a dopant in cadmium sulfide nanobelts, a bright yellow-colored light was obtained. The detailed chromaticity and brightness of the light can be engineered by the dopant concentration and the pumping power, which are used to control the dominant wavelength to any fine yellow color, and even cover the sodium-yellow-line of 589 nm. The nanobelts were synthesized through a chemical vapor deposition method. The peak shift of the XRD result proves that the zinc ions as a dopant exist in the nanobelts rather than in the ZnCdS alloy formation. Time-resolved photoluminescence of the nanobelt reveals the existence of the defect-related state, which induces a red band to further mix with green band-edge emission to form the yellow light. Moreover, low-threshold two-photon excitation was observed in the proper Zn-doped cadmium sulfide nanobelts. The dopant and pumping power-tuned generation and engineering of the yellow light makes it possible to use this kind of material as yellow light-emitting source.
Pancreatic ductal adenocarcinoma is refractory to available therapies. We have previously shown that these tumors have elevated autophagy and that inhibition of autophagy leads to decreased tumor growth. Using an autochthonous model of pancreatic cancer driven by oncogenic Kras and the stochastic LOH of Trp53, we demonstrate that although genetic ablation of autophagy in the pancreas leads to increased tumor initiation, these premalignant lesions are impaired in their ability to progress to invasive cancer, leading to prolonged survival. In addition, mouse pancreatic cancer cell lines with differing p53 status are all sensitive to pharmacologic and genetic inhibition of autophagy. Finally, a mouse preclinical trial using cohorts of genetically characterized patient-derived xenografts treated with hydroxychloroquine showed responses across the collection of tumors. Together, our data support the critical role of autophagy in pancreatic cancer and show that inhibition of autophagy may have clinical utility in the treatment of these cancers, independent of p53 status.
Autophagy is a catabolic pathway that permits cells to recycle intracellular macromolecules, and its inhibition reduces pancreatic cancer growth in model systems. We evaluated hydoxychloroquine (HCQ), an inhibitor of autophagy, in patients with pancreatic cancer and analyzed pharmacodynamic markers in treated patients and mice.
A Neisseria strain, Neisseria sp. AH-N10, was isolated from liver of a Chinese Peking duck and characterized using a number of phenotypic and genotypic approaches. Based on scanning electron microscopy examination, the isolated strain has the typical structure of Neisseria species. Sequence comparison of 16S rRNA gene and phylogenetic analysis suggest that Neisseria sp. AH-N10 is closely related to Neisseria canis, which was previously isolated from a human dog bite wound. Animal infection experiments demonstrated that the isolated Neisseria sp. AH-N10 is pathogenic in ducks and mice. The pathogenicity to humans and evolutional origin of this Neisseria strain should be further investigated.
Streptococcus suis (S. suis) type 2 is an extremely important Gram-positive bacterial pathogen that can cause human or swine endocarditis, meningitis, bronchopneumonia, arthritis and sepsis. Catabolite control protein A (CcpA) is a major transcriptional regulator in S. suis type 2 that functions in catabolite control, specifically during growth on glucose or galactose. The regulation of central metabolism can affect the virulence of bacteria. In the present study, a metabolomics approach was used along with principal components analysis (PCA) and partial least-squares-discriminant analysis (PLS-DA) models and 37 metabolites were found that differed substantially between native S. suis and a mutant lacking CcpA. These results showed that CcpA is an important protein in S. suis type 2 for studying bacterial protein function.
Brucellosis is a worldwide human and animal infectious disease, and the effective methods of its control are immunisation of animals by vaccination and elimination. Brucella abortus S19 is one of the popular vaccines with virulence in the control of cattle Brucellosis. In the present study, allelic exchange plasmids of wzm and wzt genes and partial knockout mutants of wzm and wzt were constructed to evaluate the resulting difference in virulence of B. abortus S19. PCR analysis revealed that the target genes were knocked out. The mutants were rough mutants and they could be differentiated from natural infection by the Rose Bengal plate and standard agglutination tests. The molecular weights of lipopolysaccharides of the ?wzm and ?wzt mutants were clustered between 25 and 40 kDa, and 30 and 35 kDa separately, and were markedly different from those in B. abortus S19. The virulence of B. abortus ?wzm and ?wzt was decreased compared with that of B. abortus S19 in mice. All these results identified that there were several differences between the wzm and wzt genes on lipopolysaccharide synthesis and on the virulence of B. abortus.
Autophagy, the process by which proteins and organelles are sequestered in double-membrane structures called autophagosomes and delivered to lysosomes for degradation, is critical in diseases such as cancer and neurodegeneration. Much of our understanding of this process has emerged from analysis of bulk cytoplasmic autophagy, but our understanding of how specific cargo, including organelles, proteins or intracellular pathogens, are targeted for selective autophagy is limited. Here we use quantitative proteomics to identify a cohort of novel and known autophagosome-enriched proteins in human cells, including cargo receptors. Like known cargo receptors, nuclear receptor coactivator 4 (NCOA4) was highly enriched in autophagosomes, and associated with ATG8 proteins that recruit cargo-receptor complexes into autophagosomes. Unbiased identification of NCOA4-associated proteins revealed ferritin heavy and light chains, components of an iron-filled cage structure that protects cells from reactive iron species but is degraded via autophagy to release iron through an unknown mechanism. We found that delivery of ferritin to lysosomes required NCOA4, and an inability of NCOA4-deficient cells to degrade ferritin led to decreased bioavailable intracellular iron. This work identifies NCOA4 as a selective cargo receptor for autophagic turnover of ferritin (ferritinophagy), which is critical for iron homeostasis, and provides a resource for further dissection of autophagosomal cargo-receptor connectivity.
Male mice were given drinking water alone or containing 0.5, 1.0 and 1.5g/L Pb acetate for 60 days. After the treatment, the concentrations of Pb were determined in the serum and testis of mice by ICP-MS. The gene transcription of Usp9y, Ddx3y and Uty and their protein levels in the testis were examined by real-time PCR, Western blotting and immunohistochemistry. The sperm quality, spermatogenesis, and histological alteration of the testis and epididymis were observed by microscope. The probability of impregnating female mice by lead-exposed male was evaluated. It was shown that the concentrations of Pb in serum and testis of mice significantly increased in the groups exposed to Pb in a dose-dependent manner. The male fertility significantly decreased in the groups exposed to 1.0 and 1.5g/L Pb acetate. Moreover, exposure to Pb also inhibited spermatogenesis and sperm development, and significantly downregulated expressions of Ddx3y gene expression in testis of mice, but Usp9y and Uty expressions unaffected.
The LKB1/STK11 tumor suppressor encodes a serine/threonine kinase, which coordinates cell growth, polarity, motility, and metabolism. In non-small cell lung carcinoma, LKB1 is somatically inactivated in 25% to 30% of cases, often concurrently with activating KRAS mutations. Here, we used an integrative approach to define novel therapeutic targets in KRAS-driven LKB1-mutant lung cancers. High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetically lethal with Lkb1 deficiency in mouse and human lung cancer lines. Global metabolite profiling showed that Lkb1-null cells had a striking decrease in multiple nucleotide metabolites as compared with the Lkb1-wild-type cells. Thus, LKB1-mutant lung cancers have deficits in nucleotide metabolism that confer hypersensitivity to DTYMK inhibition, suggesting that DTYMK is a potential therapeutic target in this aggressive subset of tumors.
Using a simple in situ seeding chemical vapor deposition (CVD) process, comb-like (branched) monolithic CdS micro/nanostructures were grown. Efficient optical coupling between the backbone and the teeth of the branched architecture is demonstrated by distributing light from an UV-laser-excited spot at one end of the backbone to all branch tips. By varying the deposition conditions, the orientation of the branches with respect to the backbone, their size and density can be tuned as well as the size of the backbone. This in situ seeding CVD method has the potential for a low-cost single-step fabrication of high-quality, micro/nanointegrated photonic devices, with tunable complex waveguiding possibilities.
In this article, high-affinity single-stranded DNA (ssDNA) aptamer-targeting F(ab)? fragments of saxitoxin (STX) antibodies were selected from a random ssDNA library by the SELEX strategy. After 16 rounds of repeated selection, the enriched ssDNA library was sequenced, and all of the sequences were carefully identified by indirect enzyme-linked assay and indirect competitive enzyme-linked assay (icELISA). The candidate aptamers in the above identification were selected for further characterization by icELISA and the equilibrium filtration method. We successfully obtained an aptamer that mimics STX in antibody binding, and a substitute for STX in aptamer form has been developed. Further work is in progress aimed at using this aptamer substitute to replace the STX standard in an antibody-based, nontoxic detection method for field determination of STX in seafood products.
DNA damage elicits a cellular signaling response that initiates cell cycle arrest and DNA repair. Here, we find that DNA damage triggers a critical block in glutamine metabolism, which is required for proper DNA damage responses. This block requires the mitochondrial SIRT4, which is induced by numerous genotoxic agents and represses the metabolism of glutamine into tricarboxylic acid cycle. SIRT4 loss leads to both increased glutamine-dependent proliferation and stress-induced genomic instability, resulting in tumorigenic phenotypes. Moreover, SIRT4 knockout mice spontaneously develop lung tumors. Our data uncover SIRT4 as an important component of the DNA damage response pathway that orchestrates a metabolic block in glutamine metabolism, cell cycle arrest, and tumor suppression.
Cancer cells have metabolic dependencies that distinguish them from their normal counterparts. Among these dependencies is an increased use of the amino acid glutamine to fuel anabolic processes. Indeed, the spectrum of glutamine-dependent tumours and the mechanisms whereby glutamine supports cancer metabolism remain areas of active investigation. Here we report the identification of a non-canonical pathway of glutamine use in human pancreatic ductal adenocarcinoma (PDAC) cells that is required for tumour growth. Whereas most cells use glutamate dehydrogenase (GLUD1) to convert glutamine-derived glutamate into ?-ketoglutarate in the mitochondria to fuel the tricarboxylic acid cycle, PDAC relies on a distinct pathway in which glutamine-derived aspartate is transported into the cytoplasm where it can be converted into oxaloacetate by aspartate transaminase (GOT1). Subsequently, this oxaloacetate is converted into malate and then pyruvate, ostensibly increasing the NADPH/NADP(+) ratio which can potentially maintain the cellular redox state. Importantly, PDAC cells are strongly dependent on this series of reactions, as glutamine deprivation or genetic inhibition of any enzyme in this pathway leads to an increase in reactive oxygen species and a reduction in reduced glutathione. Moreover, knockdown of any component enzyme in this series of reactions also results in a pronounced suppression of PDAC growth in vitro and in vivo. Furthermore, we establish that the reprogramming of glutamine metabolism is mediated by oncogenic KRAS, the signature genetic alteration in PDAC, through the transcriptional upregulation and repression of key metabolic enzymes in this pathway. The essentiality of this pathway in PDAC and the fact that it is dispensable in normal cells may provide novel therapeutic approaches to treat these refractory tumours.
Electrospun anatase-phase TiO2 nanofibers with desired morphological structure and relatively high specific surface area are expected to outperform other nanostructures (e.g., powder and film) of TiO2 for various applications (particularly dye-sensitized solar cell and photo-catalysis). In this study, systematic investigations were carried out to prepare and characterize electrospun anatase-phase TiO2 nanofibers with different morphological structures (e.g., solid, hollow/tubular, and porous) and specific surface areas. The TiO2 nanofibers were generally prepared via electrospinning of precursor nanofibers followed by pyrolysis at 500°C. For making hollow/tubular TiO2 nanofibers, the technique of co-axial electrospinning was utilized; while for making porous TiO2 nanofibers, the etching treatment in NaOH aqueous solution was adopted. The results indicated that the hollow/tubular TiO2 nanofibers (with diameters of ~300-500 nm and wall-thickness in the range from tens of nanometers to ~200 nm) had the BET specific surface area of ~27.3 m(2)/g, which was approximately twice as that of the solid TiO2 nanofibers (~15.2 m(2)/g) with diameters of ~200-300 nm and lengths of at least tens of microns. Porous TiO2 nanofibers made from the precursor of Al2O3/TiO2 composite nanofibers had the BET specific surface area of ~106.5 m(2)/g, whereas porous TiO2 nanofibers made from the precursor of ZnO/TiO2 composite nanofibers had the highest BET specific surface area of ~148.6 m(2)/g.
One-dimensional Mn-ZnSe nanostructures with high crystallite quality were synthesized by the CVD method. Transmission electron microscopy was used to study the defect state, crystal lattice and growth direction of as-prepared nanostructures. Raman spectra under varied excitation wavelengths confirmed the dopant modes of Mn(II) and the inhomogeneity. The micro-photoluminescence (PL) spectra of individual nanostructures under CW laser excitation with different powers showed the dominant trapped state emission with periodic multi-peaks. The selected peak mapping indicated that there were many integrated Fabry-Perot cavities and whispering gallery mode cavities within the nanowires/nanoneedles and nanobelts, respectively, which can be accounted for by inhomogeneous optical phases in the Mn-ZnSe nanostructure. The phase may be introduced by both Mn doping and structural relaxation. The micro-PL spectra under nanosecond pulse laser excitation produce low threshold lasing lines near the band edge of Mn-ZnSe nanostructures. The lasing occurs due to the dominant interaction between bound excitons at high density, evidenced by its appearance close to the LO phonon replica. The belts show much stronger lasing emission due to larger 2D coherent space than the wires due to the inhomogeneity induced by the doping process. The different optical behavior with changing excitation pulses may find applications in future photonic devices of II-VI nanostructures.
Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer is complex and may differ depending on tumor type or context. Here we show that pancreatic cancers have a distinct dependence on autophagy. Pancreatic cancer primary tumors and cell lines show elevated autophagy under basal conditions. Genetic or pharmacologic inhibition of autophagy leads to increased reactive oxygen species, elevated DNA damage, and a metabolic defect leading to decreased mitochondrial oxidative phosphorylation. Together, these ultimately result in significant growth suppression of pancreatic cancer cells in vitro. Most importantly, inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models. These results suggest that, unlike in other cancers where autophagy inhibition may synergize with chemotherapy or targeted agents by preventing the up-regulation of autophagy as a reactive survival mechanism, autophagy is actually required for tumorigenic growth of pancreatic cancers de novo, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on autophagy. As chloroquine and its derivatives are potent inhibitors of autophagy and have been used safely in human patients for decades for a variety of purposes, these results are immediately translatable to the treatment of pancreatic cancer patients, and provide a much needed, novel vantage point of attack.
Chondrocytes from the lateral trochlear ridge of the distal femur taken from 1-day-old piglets were cultured in medium supplemented with 0, 7.8, 15.6, 31.2, and 62.5 ?mol/L copper. Insulin-like growth factor-1 (IGF-1) and IGF-binding protein 3 (IGFBP-3) levels in culture medium were determined by radioimmunoassay. DNA synthesis in chondrocytes was measured by tritiated thymidine ((3)H-TdR) incorporation. Proliferation-promoting activity and incorporation of (3)H-TdR in chondrocytes were increased in all culture media supplemented with copper and 15% fetal calf serum (FCS). The contents of IGF-1 and IGFBP-3 were also enhanced significantly in culture media containing 15% FCS and supplemented with copper at 15.6, 31.2, and 62.5 ?mol/L. The optimal copper concentration for promoting chondrocyte proliferation and autocrine secretion of IGF-1 and IGFBP-3 was 31.2 ?mol/L.
This experiment was conducted to measure the effect of copper supplementation on TGF-? gene expression in chondrocytes of newborn pigs. Chondrocytes were cultured in media containing 15% fetal calf serum supplemented with 0, 15.6, 31.2, and 62.5 ?mol/L copper in 90-mm culture plate. Total RNA was isolated from chondrocytes, and TGF-? cDNA was synthesized, amplified, and sequenced. The expression level of TGF-? was examined by reverse transcription polymerase chain reaction. The results showed that the sequence of the cloned TGF-? gene was 99.4% identical to that in GenBank. The expression of TGF-? increased in culture media added with final concentration of 15.6, 31.2, and 62.5 ?mol/L copper. In this study, the optimal copper concentration and optimal culture time for the highest level of TGF-? expression were 31.2 ?mol/L and 48 h, respectively.
This experiment was conducted to examine the effect of dietary copper supplementation on somatostatin (SS) and growth hormone-releasing hormone (GHRH) mRNA expression levels in the hypothalami of growing pigs. A total of 45 crossbred pigs were randomly assigned to three groups of 15 pigs each; five replicates of three animals comprised each group. Pigs were allocated to diets that contained 5 mg/kg copper (control), 125 mg/kg copper sulfate, or 125 mg/kg copper methionine. At the end of the experiment, five pigs were selected at random from each group and slaughtered, and hypothalami were collected for determination of SS and GHRH mRNA expression levels. The results showed that the SS expression levels were lower and the GHRH levels were higher in pigs fed the diets with 125 mg/kg copper methionine (P<0.05) and 125 mg/kg copper sulfate (P<0.05), respectively, than in pigs fed the diet with 5 mg/kg copper. Furthermore, the relationship between SS mRNA and GHRH mRNA abundance had a significantly negative correlation (P<0.05). The data indicated that high dietary copper could enhance GHRH mRNA expression levels and suppress SS mRNA expression levels in the hypothalami of pigs. High lever dietary copper (125 mg/kg copper sulfate or 125 mg/kg copper methionine) increased pigs growth performance and feed efficiency but had no significant effect on daily feed intake; 125 mg/kg copper sulfate or 125 mg/kg copper methionine at the same lever had no difference on growth promoting in pigs.
Noisy chaotic neural network (NCNN), which can exhibit stochastic chaotic simulated annealing (SCSA), has been proven to be a powerful tool in solving combinatorial optimization problems. In order to retain the excellent optimization property of SCSA and improve the optimization performance of the NCNN using hysteretic dynamics without increasing network parameters, we first construct an equivalent model of the NCNN and then control noises in the equivalent model to propose a novel hysteretic noisy chaotic neural network (HNCNN). Compared with the NCNN, the proposed HNCNN can exhibit both SCSA and hysteretic dynamics without introducing extra system parameters, and can increase the effective convergence toward optimal or near-optimal solutions at higher noise levels. Broadcast scheduling problem (BSP) in packet radio networks (PRNs) is to design an optimal time-division multiple-access (TDMA) frame structure with minimal frame length, maximal channel utilization, and minimal average time delay. In this paper, the proposed HNCNN is applied to solve BSP in PRNs to demonstrate its performance. Simulation results show that the proposed HNCNN with higher noise amplitudes is more likely to find an optimal or near-optimal TDMA frame structure with a minimal average time delay than previous algorithms.
Tagged magnetic resonance imaging (tagged MRI or tMRI) provides a means of directly and noninvasively displaying the internal motion of the myocardium. Reconstruction of the motion field is needed to quantify important clinical information, e.g., the myocardial strain, and detect regional heart functional loss. In this paper, we present a three-step method for this task. First, we use a Gabor filter bank to detect and locate tag intersections in the image frames, based on local phase analysis. Next, we use an improved version of the robust point matching (RPM) method to sparsely track the motion of the myocardium, by establishing a transformation function and a one-to-one correspondence between grid tag intersections in different image frames. In particular, the RPM helps to minimize the impact on the motion tracking result of 1) through-plane motion and 2) relatively large deformation and/or relatively small tag spacing. In the final step, a meshless deformable model is initialized using the transformation function computed by RPM. The model refines the motion tracking and generates a dense displacement map, by deforming under the influence of image information, and is constrained by the displacement magnitude to retain its geometric structure. The 2D displacement maps in short and long axis image planes can be combined to drive a 3D deformable model, using the moving least square method, constrained by the minimization of the residual error at tag intersections. The method has been tested on a numerical phantom, as well as on in vivo heart data from normal volunteers and heart disease patients. The experimental results show that the new method has a good performance on both synthetic and real data. Furthermore, the method has been used in an initial clinical study to assess the differences in myocardial strain distributions between heart disease (left ventricular hypertrophy) patients and the normal control group. The final results show that the proposed method is capable of separating patients from healthy individuals. In addition, the method detects and makes possible quantification of local abnormalities in the myocardium strain distribution, which is critical for quantitative analysis of patients clinical conditions. This motion tracking approach can improve the throughput and reliability of quantitative strain analysis of heart disease patients, and has the potential for further clinical applications.
In this paper we present a novel method for left ventricle (LV) endocardium motion reconstruction using high resolution CT data and tagged MRI. High resolution CT data provide anatomic details on the LV endocardial surface, such as the papillary muscle and trabeculae carneae. Tagged MRI provides better time resolution. The combination of these two imaging techniques can give us better understanding on left ventricle motion. The high resolution CT images are segmented with mean shift method and generate the LV endocardium mesh. The meshless deformable model built with high resolution endocardium surface from CT data fit to the tagged MRI of the same phase. 3D deformation of the myocardium is computed with the Lagrangian dynamics and local Laplacian deformation. The segmented inner surface of left ventricle is compared with the heart inner surface picture and show high agreement. The papillary muscles are attached to the inner surface with roots. The free wall of the left ventricle inner surface is covered with trabeculae carneae. The deformation of the heart wall and the papillary muscle in the first half of the cardiac cycle is presented. The motion reconstruction results are very close to the live heart video.
The interactions of toxic metals with essential metals may result in disturbances in the homeostasis of essential elements. However, there are few reports about toxic effect of arsenic (As) on the levels of essential trace elements in the central nervous system. To investigate whether subchronic exposure to As disturbs levels of main essential trace elements in the brain of mice and whether the gender difference in the response to As are altered, the concentrations of As, Iron (Fe), copper (Cu), selenium (Se), zinc (Zn) and Chromium (Cr) in the cerebrum and cerebellum of mice exposed to As subchronically were examined by inductively coupled plasma-mass spectrometry (ICP-MS). The gender difference in the changed levels of these essential trace elements was also statistically analyzed. The concentration of As was significantly higher in the cerebrum or cerebellum of mice exposed to As than that in control group (P < 0.05). It indicates that As can accumulate in brain of mice after subchronic exposure. The concentrations of Fe, Se and Cr in the cerebrum or cerebellum were significantly lower in mice exposed to As than those in control group (P < 0.05). On the contrary, the concentration of Cu in the cerebrum or cerebellum was significantly higher in mice exposed to As (P < 0.05). Our results indicate that subchronic exposure to As may decrease the levels of Fe, Se and Cr or increase the level of Cu in the brain of mice. Moreover, the significant gender difference was found relative to the effect of As on concentration of Se in cerebrum and concentrations of Cu and Se in cerebellum of mice. Therefore, more experiments are required to further understand mechanisms whereby As interacts with essential elements in brain and induces the gender difference.
Phosphatase and tensin homolog (PTEN) is a potent tumor suppressor gene that also plays a vital role in regulating fatty acid metabolism. Here we attempted to elucidate the role of PTEN in the regulation of fatty acid oxidation and the assembly and secretion of very low density lipoprotein (VLDL) in dairy cow liver.
Ultraviolet (UV) light has a potent effect on biological organisms. Hemoglobin, an oxygen-transport protein, plays an irreplaceable role in sustaining life of all vertebrates. In this study we scrutinize the effects of ultraviolet irradiation (UVI) as well as visible irradiation on the fluorescence characteristics of bovine hemoglobin (BHb) in vitro. Data show that UVI results in fluorescence enhancement of BHb in a dose-dependent manner. Furthermore, UVI-induced fluorescence enhancement is significantly increased when BHb is pretreated with hydrogen peroxide (H(2)O(2)), a type of reactive oxygen species (ROS). Meanwhile, The water-soluble antioxidant vitamin C suppresses this UVI-induced fluorescence enhancement. In contrast, green light irradiation does not lead to fluorescence enhancement of BHb no matter whether H(2)O(2) is acting on the BHb solution or not. Taken together, these results indicate that catalysis of ROS and UVI-dependent irradiation play two key roles in the process of UVI-induced fluorescence enhancement of BHb.
Pancreatic ductal adenocarcinoma (PDAC) is amongst the deadliest of human cancers, due to its late diagnosis as well as its intense resistance to currently available therapeutics. To identify mechanisms as to why PDAC are refractory to DNA damaging cytoxic chemotherapy and radiation, we performed a global interrogation of the DNA damage response of PDAC. We find that PDAC cells generally harbor high levels of spontaneous DNA damage. Inhibition of Non-Homologous End Joining (NHEJ) repair either pharmacologically or by RNAi resulted in a further accumulation of DNA damage, inhibition of growth, and ultimately apoptosis even in the absence of exogenous DNA damaging agents. In response to radiation, PDAC cells rely on the NHEJ pathway to rapidly repair DNA double strand breaks. Mechanistically, when NHEJ is inhibited there is a compensatory increase in Homologous Recombination (HR). Despite this upregulation of HR, DNA damage persists and cells are significantly more sensitive to radiation. Together, these findings support the incorporation of NHEJ inhibition into PDAC therapeutic approaches, either alone, or in combination with DNA damaging therapies such as radiation.
The transition period is a severe challenge to dairy cows. Glucose supply cannot meet demand and body fat is mobilized, potentially leading to negative energy balance (NEB), ketosis, or fatty liver. Propionate produces glucose by gluconeogenesis, which depends heavily on the number and species of microbes. In the present study, we analyzed the rumen microbiome composition of cows in the transition period, cows with ketosis, and nonperinatal cows by terminal restriction fragment length polymorphism (TRFLP) analysis of 16S rRNA genes and quantitative PCR. TRFLP analysis indicated that the quantity of Veillonellaceae organisms was reduced and that of Streptococcaceae organisms was increased in rumen samples from the transition period and ketosis groups, with the number of Lactobacillaceae organisms increased after calving. Quantitative PCR data suggested that the numbers of the main propionate-producing microbes, Megasphaera elsdenii and Selenomonas ruminantium, were decreased, while numbers of the main lactate-producing bacterium, Streptococcus bovis, were increased in the rumen of cows from the transition period and ketosis groups, with the number of Lactobacillus sp. organisms increased after calving. Volatile fatty acid (VFA) and glucose concentrations were decreased, but the lactic acid concentration was increased, in rumen samples from the transition period and ketosis groups. Our results indicate that the VFA concentration is significantly related to the numbers of Selenomonas ruminantium and Megasphaera elsdenii organisms in the rumen.
We have investigated the effects of surface passivation on the dye-sensitized solar cell (DSSC) based on a donor-(?-spacer)-acceptor organic dye. A major challenge for donor-(?-spacer)-acceptor molecules as sensitizers in DSSCs is the fast recombination reactions that occur at both the photoanode (e.g. TiO2) surface and the fluorine doped tin oxide (FTO) electrode, which presents unfavorable effects on the DSSC performance. The two interfaces of TiO2/electrolyte and FTO/electrolyte were passivated selectively in a DSSC using an organic dye with Naphtho[2,1-b:3,4-b]dithiophene as the conjugated linker and the I-/I3- electrolyte. The current density-voltage characteristics, the dark current analysis, the Voc-light intensity dependence, and the transient photovoltage/photocurrent results indicated that the recombination processes were affected strongly by surface passivation under various light intensity. At high light intensity, the recombination reaction at the TiO2 surface is dominant. In this case, silane passivation of the TiO2 surface can suppress recombination significantly, while the c-TiO2 layer makes little contribution to the reduction of the recombination. At low illumination intensity, the recombination at FTO becomes significant, and the recombination can be reduced by applying a c-TiO2 layer.
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