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Multi-rotor UAVs suffer from a restricted range and flight duration due to limited battery capacity. Autonomous landing on a 2D moving platform offers the possibility to replenish batteries and offload data, thus increasing the utility of the vehicle. Classical approaches rely on accurate, complex and difficult-to-derive models of the vehicle and the environment. Reinforcement learning (RL) provides an attractive alternative due to its ability to learn a suitable control policy exclusively from data during a training procedure. However, current methods require several hours to train, have limited success rates and depend on hyperparameters that need to be tuned by trial-and-error. We address all these issues in this work. First, we decompose the landing procedure into a sequence of simpler, but similar learning tasks. This is enabled by applying two instances of the same RL based controller trained for 1D motion for controlling the multi-rotor’s movement in both the longitudinal and the lateral directions. Second, we introduce a powerful state space discretization technique that is based on i) kinematic modeling of the moving platform to derive information about the state space topology and ii) structuring the training as a sequential curriculum using transfer learning. Third, we leverage the kinematics model of the moving platform to also derive interpretable hyperparameters for the training process that ensure sufficient maneuverability of the multi-rotor vehicle. The training is performed using the tabular RL method Double Q-Learning. Through extensive simulations we show that the presented method significantly increases the rate of successful landings, while requiring less training time compared to other deep RL approaches. Furthermore, for two comparison scenarios it achieves comparable performance than a cascaded PI controller. Finally, we deploy and demonstrate our algorithm on real hardware. For all evaluation scenarios we provide statistics on the agent’s performance. Source code is openly available at . [ABSTRACT FROM AUTHOR]

Arsenic trioxide (ATO), an inorganic arsenical, is a toxic environmental contaminant. It is also a widely used chemical with industrial and medicinal uses. Significant public health risk exists from its intentional or accidental exposure. The pulmonary pathology of acute high dose exposure is not well defined. We developed and characterized a murine model of a single inhaled exposure to ATO, which was evaluated 24 h post-exposure. ATO caused hypoxemia as demonstrated by arterial blood-gas measurements. ATO administration caused disruption of alveolar-capillary membrane as shown by increase in total protein and IgM in the bronchoalveolar lavage fluid (BALF) supernatant and an onset of pulmonary edema. BALF of ATO-exposed mice had increased HMGB1, a damage-associated molecular pattern (DAMP) molecule, and differential cell counts revealed increased neutrophils. BALF supernatant also showed an increase in protein levels of eotaxin/CCL-11 and MCP-3/CCL-7 and a reduction in IL-10, IL-19, IFN-γ, and IL-2. In the lung of ATO-exposed mice, increased protein levels of G-CSF, CXCL-5, and CCL-11 were noted. Increased mRNA levels of TNF-a, and CCL2 in ATO-challenged lungs further supported an inflammatory pathogenesis. Neutrophils were increased in the blood of ATO-exposed animals. Pulmonary function was also evaluated using flexiVent. Consistent with an acute lung injury phenotype, respiratory and lung elastance showed significant increase in ATO-exposed mice. PV loops showed a downward shift and a decrease in inspiratory capacity in the ATO mice. Flow-volume curves showed a decrease in FEV0.1 and FEF50. These results demonstrate that inhaled ATO leads to pulmonary damage and characteristic dysfunctions resembling ARDS in humans. [ABSTRACT FROM AUTHOR]

Esophageal cancer (EC) is frequently considered a lethal malignancy and is often identified at a later stage. It is one of the major causes of cancer-related deaths globally. The conventional treatment methods like chemotherapy, radiotherapy, and surgery offer limited efficacy and poor clinical outcome with a less than 25% 5-year survival rate. The poor prognosis of EC persists despite the growth in the development of diagnostic and therapeutic modalities to treat EC. This underlines the need to elucidate the complex molecular mechanisms that drive esophageal oncogenesis. Apart from the role of the tumor microenvironment and its structural and cellular components in tumorigenesis, mounting evidence points towards the involvement of the esophageal microbiome, inflammation, and their cross-talk in promoting esophageal cancer. The current review summarizes recent research that delineates the underlying molecular mechanisms by which the microbiota and inflammation promote the pathophysiology of esophageal cancer, thus unraveling targets for potential therapeutic intervention. [ABSTRACT FROM AUTHOR]

The tumor microenvironment (TME) comprises of components that exist within the immediate vicinity of tumor cells, including fibroblasts, immune cells, the extracellular matrix, and more. Significant advances have been made in recent years in our understanding of the components of TME and their mutual interactions. Part of the focus of this research has been on epigenetic events, which are increasingly being recognized for their importance in gene regulation and cancer progression. The Collection represents the gradual growth in our understanding of the overall process of how cancer progresses, along with the factors that play a decisive role in this progression. It features studies conducted on models representing many different cancers, and includes mechanistic reports conducted using appropriate in vitro models, studies that analyzed human cancer patients-derived specimens, clinical trials and, additionally, studies involving bioinformatics, metabolomics, chemical libraries screening, next-generation sequencing, and single-cell analysis approaches. [ABSTRACT FROM AUTHOR]

The ever-growing perception of cancer stem cells (CSCs) as a plastic state rather than a hardwired defined entity has evolved our understanding of the functional and biological plasticity of these elusive components in malignancies. Pancreatic cancer (PC), based on its biological features and clinical evolution, is a prototypical example of a CSC-driven disease. Since the discovery of pancreatic CSCs (PCSCs) in 2007, evidence has unraveled their control over many facets of the natural history of PC, including primary tumor growth, metastatic progression, disease recurrence, and acquired drug resistance. Consequently, the current near-ubiquitous treatment regimens for PC using aggressive cytotoxic agents, aimed at "tumor debulking" rather than eradication of CSCs, have proven ineffective in providing clinically convincing improvements in patients with this dreadful disease. Herein, we review the key hallmarks as well as the intrinsic and extrinsic resistance mechanisms of CSCs that mediate treatment failure in PC and enlist the potential CSC-targeting 'natural agents' that are gaining popularity in recent years. A better understanding of the molecular and functional landscape of PCSC-intrinsic evasion of chemotherapeutic drugs offers a facile opportunity for treating PC, an intractable cancer with a grim prognosis and in dire need of effective therapeutic advances. [ABSTRACT FROM AUTHOR]

A social networking site (SNS) is a platform for building social networks or social relations with those who share similar profiles, career, interests, activities, backgrounds, etc. Social networking site serves for communication purposes to specific interest groups, but they do not have a searching option where we can search for individuals or groups with obvious features. A user can be found on social network only if we know the name of the person. With the help of this paper, we aim at presenting a searching method using natural language processing and query optimization and classification for searching people by name or any distinct characteristic. These concepts can be together used to constitute and process social network information so that searching user through their name or some distinguished characteristics is feasible. This paper handles some of the present limitations of accessing social network data by natural language processing technique. We have used PHP for programming and algorithm implementation and MySQL for storing sample data. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the mechanism of action involved in the anti-cancer activity of daidzein and identification of cancer specific micro-environment as therapeutic target of this secondary metabolite derived from soy. Our data indicated that daidzein induces cellular DNA breakage, anti-proliferative effects and apoptosis in a concentration-dependent manner. We demonstrated that such a daidzein-induced anti-cancer action involves a copper-dependant pathway in which endogenous copper is mobilized by daidzein and redox-cycled to generate reactive oxygen species which act as an upstream signal leading to pro-oxidant cell death. Further in the context of hypoxia being a resistant factor against standard therapies and that an effect secondary to hypoxia is the intracellular acidification, we show that the anticancer activity of daidzein is modulated positively in acidic pH but copper-specific chelator is still able to inhibit daidzein activity. Moreover, an experimental setup of hypoxia mimic (cobalt chloride) revealed an enhanced sensitivity of cancer cells to the cytotoxic effects of daidzein which was neutralized in the presence of neocuproine. The findings support a paradigm shift from the conventional antioxidant property of dietary isoflavones to molecules capable of initiating a pro-oxidant signaling mediated by reactive oxygen species. Further, the clinical relevance of such an action mechanism in cancer chemoprevention is also proposed. This study identified endogenous copper as a molecular target and acidic pH as a modulating factor for the therapeutic activity of daidzein against cancer. The evidence presented highlights the potential of dietary agents as adjuvants to standard therapeutic regimens. [ABSTRACT FROM AUTHOR]

Purpose: The 4,5-diarylimidazole brimamin is an analog of the natural vascular-disrupting agent combretastatin A-4 (CA-4) with improved water solubility, tolerance by animals and efficacy in multidrug-resistant tumors. Here, we aimed at identifying the major mechanisms underlying the in vitro and in vivo actions of brimamin on endothelial and carcinoma cells, including vascularization. Methods: The contribution of specific signaling kinases to the effects of brimamin on cytoskeleton organization and the viability and differentiation of endothelial cells was assessed by MTT and tube formation assays in the presence or absence of specific kinase inhibitors. Changes in DNA affinity and expression of NF-κB in endothelial and carcinoma-derived cells and their solid tumors (xenografts) treated with brimamin were ascertained by electrophoretic mobility shift assays and Western blotting. The anti-vascular effect of brimamin in solid tumors was verified by CD31 immunostaining. Results: We found that brimamin can inhibit tubulin polymerization and cause a reorganization of F-actin in Ea.hy926 endothelial cells. Its inhibitory effect on tube formation was found to depend on functional Rho kinase and JNK. JNK inhibition was found to suppress the induction of endothelial cell apoptosis by brimamin. In CA-4-refractory human BxPC-3 pancreas carcinoma-derived and triple-negative MDA-MB-231 breast carcinoma-derived cells brimamin was found to inhibit growth and to induce apoptosis at low nanomolar concentrations by blocking NF-κB activation in a dose-dependent manner. Brimamin was also found to reduce the in vivo growth rate and vascularization of MDA-MB-231 xenografts in mice. Residual tumor cells of these treated xenografts showed a relatively low expression of the p65 subunit of NF-κB. Conclusions: Our data indicate that cellular JNK and Rho kinase activities are crucial for the cytotoxic and cytoskeleton reorganizing effects of brimamin on endothelial cells. In addition, we found that in resistant carcinoma cells and xenografts brimamin can induce down-regulation of anti-apoptotic NF-κB expression and signaling. Its chemical properties and efficacy against clinically relevant cancer entities make brimamin a promising candidate vascular-disrupting agent. [ABSTRACT FROM AUTHOR]

We have earlier elucidated a pathway for the anticancer action of plant polyphenolic compounds against malignant cells involving mobilisation of endogenous copper ions and the consequent prooxidant action. To further confirm our hypothesis in vivo, we induced hepatocellular carcinoma (HCC) in rats by diethylnitrosamine (DEN). We show that in such carcinoma cells, there is a progressive elevation in copper levels at various intervals after DEN administration. Concurrently with increasing copper levels, epigallocatechin-3-gallate (EGCG; a potent anticancer plant polyphenol found in green tea) mediated DNA breakage in malignant cells is also increased. The cell membrane permeable copper chelator neocuproine inhibited the EGCG-mediated cellular DNA degradation, whereas the membrane impermeable chelator bathocuproine was ineffective. Iron and zinc specific chelators desferoxamine mesylate and histidine, respectively, were also ineffective in inhibiting EGCG mediated DNA breakage. Through the use of specific scavengers, the mechanism of DNA breakage was determined to be mediated by reactive oxygen species. In summary, we provide an in vivo evidence of accumulating copper in hepatocellular carcinoma that is targeted by EGCG, leading to its anticancer role in a prooxidant manner. Our findings confirm a novel mechanism of anticancer activity of EGCG in particular and plant derived nutraceuticals in general. [ABSTRACT FROM AUTHOR]

The poor survival statistics of the fatal cancer diseases highlight the need for multiple alternative treatment options. An impressive embodiment of evidence shows that naturally occurring herbal products contain a wide variety of phytochemicals that are regarded as effective cancer protective agents, possessing the ability to retard, block or reverse carcinogenesis. These include dietary agents often termed as nutraceuticals and also the components of non-dietary plants. Many studies in different cell lines, animal models and human epidemiological trials suggest a protective role of a large number of medicinal molecules of herbal origin against different types of cancers. The standard chemotherapeutic regime against cancer faces an unequivocal challenge due to the severity of the side-effects and the post therapeutic management of the disease. Cancer control may therefore benefit from the anti-cancer potential of alternative therapies that may include herbal treatment which nonetheless has been an effective curative strategy reported for a number of diseases since ancient times. In congruence of the above idea, it has been observed that in recent years the demand to utilize alternative approaches to the treatment of cancer is escalating. Additionally, the emergence of resistance to cancer chemotherapy has forced researchers to turn to natural products of herbal and marine origin. Currently, in the armamentarium of anti-cancer pharmaceuticals there are effective plant-derived drugs such as paclitaxel (a complex taxane diterpene isolated from the bark of Taxus brevifolia) which acts as microtubule disruptor. Further there are plant-based dietary agents such as sulphoraphane (an isothiocyanate derived from cruciferous vegetables) and non-dietary agents such as pomiferin (an isoflavonoid from Maclura pomifera) which strongly mimic chemotherapeutic drugs such as vorinostat (suberoylanilidehydroxamic acid) possessing histone diacetylase inhibition activity. In this review we provide a comprehensive outline of the translational potential of plant-based herbal medicine for complementing the current treatment modalities as an adjuvant or alternative therapy for cancer patients. [ABSTRACT FROM AUTHOR]

Recently, nutraceuticals have received increasing attention as the agents for cancer prevention and supplement with conventional therapy. Prostate cancer (PCa) is the most frequently diagnosed cancer and second leading cause of cancer-related death in men in the US. Growing evidences from epidemiological studies, in vitro experimental studies, animal studies, and clinical trials have shown that nutraceuticals could be very useful for the prevention and treatment of PCa. Several nutraceuticals including isoflavone, indole-3-carbinol, 3,3′-diindolylmethane, lycopene, (−)-epigallocatechin-3-gallate, and curcumin are known to downregulate the signal transductions in AR, Akt, NF-κB, and other signal transduction pathways which are vital for the development of PCa and the progression of PCa from androgen-sensitive to castrate-resistant PCa. Therefore, nutraceutical treatment in combination with conventional therapeutics could achieve better treatment outcome in prostate cancer therapy. Interestingly, some nutraceuticals could regulate the function of cancer stem cell (CSC)-related miRNAs and associated molecules, leading to the inhibition of prostatic CSCs which are responsible for drug resistance, tumor progression, and recurrence of PCa. Hence, nutraceuticals may serve as powerful agents for the prevention of PCa progression and they could also be useful in combination with chemotherapeutics or radiotherapy. Such strategy could become a promising newer approach for the treatment of metastatic PCa with better treatment outcome by improving overall survival. [ABSTRACT FROM AUTHOR]

Plant-derived dietary antioxidants have attracted considerable interest in recent past for their ability to induce apoptosis and regression of tumors in animal models. While it is believed that the antioxidant properties of these agents may contribute to lowering the risk of cancer induction by impeding oxidative injury to DNA, it could not account for apoptosis induction and chemotherapeutic observations. In this article, we show that dietary antioxidants can alternatively switch to a prooxidant action in the presence of transition metals such as copper. Such a prooxidant action leads to strand breaks in cellular DNA and growth inhibition in cancer cells. Further, the cellular DNA breakage and anticancer effects were found to be significantly enhanced in the presence of copper ions. Moreover, inhibition of antioxidant-induced DNA strand breaks and oxidative stress by Cu(I)-specific chelators bathocuproine and neocuproine demonstrated the role of endogenous copper in the induction of the prooxidant mechanism. Since it is well established that tissue, cellular, and serum copper levels are considerably elevated in various malignancies, such a prooxidant cytotoxic mechanism better explains the anticancer activity of dietary antioxidants against cancer cells. [ABSTRACT FROM AUTHOR]

Isoflavones have been investigated in detail for their role in the prevention and therapy of prostate cancer. This is primarily because of the overwhelming data connecting high dietary isoflavone intake with reduced risk of developing prostate cancer. A number of investigations have evaluated the mechanism(s) of anticancer action of isoflavones such as genistein, daidzein, biochanin A, equol, etc., in various prostate cancer models, both in vitro and in vivo. Genistein quickly jumped to the forefront of isoflavone cancer research, but the initial enthusiasm was followed by reports on its contradictory prometastatic and tumor-promoting effects. Use of soy isoflavone mixture has been advocated as an alternative, wherein daidzein can negate harmful effects of genistein. Recent research indicates a novel role of genistein and other isoflavones in the potentiation of radiation therapy, epigenetic regulation of key tumor suppressors and oncogenes, and the modulation of miRNAs, epithelial-to-mesenchymal transition, and cancer stem cells, which has renewed the interest of cancer researchers in this class of anticancer compounds. This comprehensive review article summarizes our current understanding of the role of isoflavones in prostate cancer research. [ABSTRACT FROM AUTHOR]

A planar, polycyclic and aromatic hydrocarbon ligand, namely 9,10-phenanthrenequinone semicarbazone, and its transition metal complexes have been synthesized and structurally characterized. The in vitro antiproliferative activity of these compounds against five human cancer cell lines revealed that they were effective against androgen receptor-positive/negative prostate cancer cells as well as COX-positive pancreatic BxPC-3 cancer cell line. The driving force behind such antiproliferative activity seems to be the up-regulated COX expression in these cells, which was amenable for targeting through metal complexation. These structural motifs can, therefore, serve as a starting point for developing novel cytotoxic agents against the growing number of prostate and pancreatic cancers. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSCs) are cells that exist within a tumor with a capacity of self-renewal and an ability to differentiate, giving rise to heterogeneous populations of cancer cells. These cells are increasingly being implicated in resistance to conventional therapeutics and have also been implicated in tumor recurrence. Several cellular signaling pathways including Notch, Wnt, phosphoinositide-3-kinase-Akt-mammalian target of rapamycin pathways, and known markers such as CD44, CD133, CD166, ALDH, etc. have been associated with CSCs. Here, we have reviewed our current understanding of self-renewal pathways and factors that help in the survival of CSCs with special emphasis on those that have been documented to be modulated by well characterized natural agents such as curcumin, sulforaphane, resveratrol, genistein, and epigallocatechin gallate. With the inclusion of a novel derivative of curcumin, CDF, we showcase how natural agents can be effectively modified to increase their efficacy, particularly against CSCs. We hope that this article will generate interest among researchers for further mechanistic and clinical studies exploiting the cancer preventive and therapeutic role of nutraceuticals by targeted elimination of CSCs. [ABSTRACT FROM AUTHOR]

Purpose: Several formulations have been proposed to improve the systemic delivery of novel cancer therapeutic compounds, including cyclodextrin derivatives. We aimed to synthesize and characterize of CDF-β-cyclodextrin inclusion complex (1:2) (CDFCD). Methods: The compound was characterized by Fourier transform infrared, differential scanning calorimetry, powder X-ray diffraction studies, H1 & C13 NMR studies and scanning electron microscopic analysis. Its activity was tested against multiple cancer cell lines, and in vivo bioavailability was checked. Results: CDF-β-cyclodextrin was found to lower IC value by half when tested against multiple cancer cell lines. It preferentially accumulated in the pancreas, where levels of CDF-β-cyclodextrin in mice were 10 times higher than in serum, following intravenous administration of an aqueous CDF-β-cyclodextrin preparation. Conclusions: Novel curcumin analog CDF preferentially accumulates in the pancreas, leading to its potent anticancer activity against pancreatic cancer cells. Synthesis of such CDF-β-cyclodextrin self-assembly is an effective strategy to enhance its bioavailability and tissue distribution, warranting further evaluation for CDF delivery in clinical settings for treatment of human malignancies. [ABSTRACT FROM AUTHOR]

To account for the observed anticancer properties of plant polyphenols, we have earlier proposed a mechanism which involves the mobilization of endogenous copper ions by polyphenols leading to the generation of reactive oxygen species (ROS) that serve as proximal DNA cleaving agents and lead to cell death. Over the last decade we have proceeded to validate our hypothesis with considerable success. As a further confirmation of our hypothesis, in this paper we first show that oral administration of copper to rats leads to elevated copper levels in lymphocytes. When such lymphocytes with a copper overload were isolated and treated with polyphenols EGCG, genistein and resveratrol, an increased level of DNA breakage was observed. Further, preincubation of lymphocytes having elevated copper levels with the membrane permeable copper chelator neocuproine, resulted in inhibition of polyphenol induced DNA degradation. However, membrane impermeable chelator of copper bathocuproine, as well as iron and zinc chelators were ineffective in causing such inhibition in DNA breakage, confirming the involvement of endogenous copper in polyphenol induced cellular DNA degradation. It is well established that serum and tissue concentrations of copper are greatly increased in various malignancies. In view of this fact, the present results further confirm our earlier findings and strengthen our hypothesis that an important anticancer mechanism of plant polyphenols could be the mobilization of intracellular copper leading to ROS-mediated cellular DNA breakage. In this context, it may be noted that cancer cells are under considerable oxidative stress and increasing such stress to cytotoxic levels could be a successful anticancer approach. [ABSTRACT FROM AUTHOR]

Platelet-derived growth factor-D (PDGF-D) has been linked with several human malignancies; however, its role in breast cancer progression is not known. We found that PDGF-D expressing breast cancer cell lines MDA-MB-231 and SUM-149 are more invasive compared to cell lines with little or no expression of PDGF-D such as MDA-MB-468 and MCF-7 cells. Over-expression of PDGF-D in PDGF-D low expressing MDA-MB-468 and MCF-7 cells by cDNA transfection showed increased cell proliferation while silencing the expression of PDGF-D by siRNA in PDGF-D high expressing MDA-MB-231 and SUM-149 cells showed decreased cell proliferation and increased apoptosis. Moreover, PDGF-D over-expression was positively correlated with the expression of Notch-1 and Jagged-1, and the expression of mesenchymal markers (Vimentin and ZEB-2) with concomitant decreased expression of epithelial marker E-cadherin. Since NF-κB activation plays a crucial role in Notch signaling as well as in epithelial-mesenchymal transition and tumor aggressiveness, we determined the DNA binding activity of NF-κB and our findings are consistent showing that PDGF-D over-expression led to increased DNA binding activity of NF-κB while it was found to be decreased by inactivation of PDGF-D. These results were also consistent with the expression and activity of MMP-9 and VEGF, as well as invasive characteristics. Further, forced expression of Notch-1/Jagged-1 by cDNA transfection de-repressed the effects of PDGF-D silencing on NF-κB activity and invasion. From these results, we conclude that PDGF-D plays an important role in breast tumor aggressiveness and this process is mechanistically linked with the activation of Notch and NF-κB signaling. [ABSTRACT FROM AUTHOR]

Forkhead box M1 (FoxM1) transcription factor is known to play important role in human cancers which, in part, is mediated by its ability to modulate cell cycle regulatory proteins as well as genes involved in cell proliferation and differentiation. In breast cancer, FoxM1 down-regulation is increasingly being recognized as an important mechanism for the targeted activity of anti-cancer agents. However, the mechanistic insight in support of the role of FoxM1 in aggressive breast cancer is poorly understood. We have tested the biological consequence of FoxM1 down-regulation and up-regulation in breast cancer cell lines and found that the down-regulation of FoxM1 in MDA-MB-231 and SUM149 cells by siRNA approach inhibited cell growth, clonogenicity, migration, and invasion. We also found decreased expression of CDK2 and E2F1 with concomitant increase in p21 and p27 proteins, suggesting an important role of FoxM1 in cell cycle progression. In contrast, over-expression of FoxM1 by cDNA transfection, in breast cancer cells (SUM102 and SKBR3) expressing low levels of FoxM1, resulted in increased cell proliferation, migration, and invasion. Moreover, down-regulation of FoxM1 inhibited the expression of many factors that are involved in the degradation of extra cellular matrix and angiogenesis such as uPA, uPAR, MMP-2, MMP-9, and vascular endothelial growth factor (VEGF) as well as inhibited the activity of MMP-9 and VEGF. Interestingly, over-expression of uPA by cDNA transfection abrogated the cellular effects that were observed by the down-regulation of FoxM1. Taken together, these results suggest the potential application of FoxM1 down-regulation as a novel approach for the treatment of aggressive breast cancer. [ABSTRACT FROM AUTHOR]

Pancreatic cancer remains the fourth most common cause of cancer-related death in the United States. Therefore, novel strategies for the prevention and/or treatment are urgently needed. Genistein has been found to be responsible for lowering the rate of pancreatic cancer. However, the molecular mechanisms by which genistein elicits its effects on pancreatic cancer cells has not been fully elucidated. Therefore, the purpose of the current study was to elucidate the anti-cancer mechanism(s) of genistein. Multiple molecular techniques, such as Real-time RT-PCR, Western blot analysis, invasion assay, immunofluorescence assay, gene transfection, MTT assay, and Histone/DNA ELISA, were used. We found that genistein inhibited cell growth accompanied by induction of apoptosis with concomitant attenuation of FoxM1 and its downstream genes, such as survivin, cdc25a, MMP-9, and VEGF, resulting in the inhibition of pancreatic cancer cell invasion. We also found that down-regulation of FoxM1 by siRNA prior to genistein treatment resulted in enhanced cell growth inhibition and induction of apoptosis. This is the first report showing the molecular role of FoxM1 in mediating the biological effects of genistein in pancreatic cancer cells, suggesting that FoxM1 could be a novel target for the treatment of pancreatic cancer. [ABSTRACT FROM AUTHOR]

Endoscopic retrograde cholangiopancreatography (ERCP) is an accepted and accurate procedure that combines the advantage of diagnosis of biliary obstruction with possible therapeutic endobiliary intervention. However, it is an operator-dependent and invasive procedure that is associated with complications and limitations. Magnetic resonance cholangiopancreatography (MRCP) is a unique noninvasive technique for the diagnosis of biliary obstruction. It is well suited to provide the information required to plan the optimal therapeutic approach for these patients. MRCP has the potential to replace or at least precede ERCP as the first-line imaging effort in the evaluation of suspected biliary obstruction. Significant advantages and some notable limitations inherent to the modality dictate its judicious use in appropriate circumstances. The present article reviews the utility of MRCP in evaluation of biliary obstruction, with brief reference to its principles and techniques. [ABSTRACT FROM AUTHOR]

An abstract of the article "Helicobacter Pylori in Patients is Killed by Visible Light," by Robert A. Ganz, Michael Hamblin, Josh Tolkoff, Norman Nishioka, Aamir Ahmad, Jennifer Viveiros and Ayesha Khalil is presented.