Anticancer Effects of Seaweed-Derived Bioactive Compounds

Cancer remains a major life-threatening disease worldwide. The development of anticancer drugs using natural products obtained from marine organisms has been proposed as an alternative approach. Seaweeds are the mainstay of marine ecosystems; therefore, they are highly enriched with diverse bioactive compounds. In the past decade, a vast number of natural compounds, such as polysaccharides, polyphenols, carotenoids, and terpenoids, have been isolated from seaweeds. Seaweeds have bioactive compounds that show cytotoxicity in various cancer cell lines. These compounds prevent tumor growth by inducing apoptotic cell death and arrest growth by interfering with different kinases and cell cycle pathways. This review discussed the anticancer properties of various bioactive compounds isolated from different types of seaweeds and their therapeutic potential against cancers.

Study on Transition of Stress Corrosion Cracking to Sharp Edge Corrosion for a Liquids Pipeline

Although stress corrosion cracking (SCC) growth is attributed to the synergistic effects of stress and corrosion, these two factors can just as easily become competing mechanisms, with stress cycles driving growth (hydrogen, the by-product of corrosion, may facilitate the growth), and corrosion working to blunt the crack tip and arrest growth. It follows that reducing the maximum pressure and cycling severity can slow down the crack growth or even stop it, and aggressive corrosion can further blunt the sharp crack tip. The Authors have observed, on a particular Polyethylene (PE) tape coated pipeline, instances where SCC has exhibited a propensity to corrode and convert into sharp edge corrosion. This is attributed to the combined effects of limited corrosion protection and low stresses. The focus of the paper is to assist operators in recognizing this phenomenon and integrate lessons learned into pipeline integrity management strategies.

Angiogenesis: Managing the Culprits behind Tumorigenesis and Metastasis

Deregulated angiogenesis has been identified as a key contributor in a number of pathological conditions including cancer. It is a complex process, which involves highly regulated interaction of multiple signalling molecules. The pro-angiogenic signalling molecule, vascular endothelial growth factor (VEGF) and its cognate receptor 2 (VEGFR-2), which is often highly expressed in majority of human cancers, plays a central role in tumour angiogenesis. Owing to the importance of tumour vasculature in carcinogenesis, tumour blood vessels have emerged as an excellent therapeutic target. The anti-angiogenic therapies have been shown to arrest growth of solid tumours through multiple mechanisms, halting the expansion of tumour vasculature and transient normalization of tumour vasculature which help in the improvement of blood flow resulting in more uniform delivery of cytotoxic agents to the core of tumour mass. This also helps in reduction of hypoxia and interstitial pressure leading to reduced chemotherapy resistance and more uniform delivery of cytotoxic agents at the targeted site. Thus, complimentary combination of different agents that target multiple molecules in the angiogenic cascade may optimize inhibition of angiogenesis and improve clinical benefit in the cancer patients. This review provides an update on the current trend in exploitation of angiogenesis pathways as a strategy in the treatment of cancer.

Inhibitors of Ribosome Rescue Arrest Growth of Francisella tularensis at All Stages of Intracellular Replication

Bacteria require at least one pathway to rescue ribosomes stalled at the ends of mRNAs. The primary pathway for ribosome rescue istrans-translation, which is conserved in >99% of sequenced bacterial genomes. Some species also have backup systems, such as ArfA or ArfB, which can rescue ribosomes in the absence of sufficienttrans-translation activity. Small-molecule inhibitors of ribosome rescue have broad-spectrum antimicrobial activity against bacteria grown in liquid culture. These compounds were tested against the tier 1 select agentFrancisella tularensisto determine if they can limit bacterial proliferation during infection of eukaryotic cells. The inhibitors KKL-10 and KKL-40 exhibited exceptional antimicrobial activity against both attenuated and fully virulent strains ofF. tularensisin vitroand duringex vivoinfection. Addition of KKL-10 or KKL-40 to macrophages or liver cells at any time after infection byF. tularensisprevented further bacterial proliferation. When macrophages were stimulated with the proinflammatory cytokine gamma interferon before being infected byF. tularensis, addition of KKL-10 or KKL-40 reduced intracellular bacteria by >99%, indicating that the combination of cytokine-induced stress and a nonfunctional ribosome rescue pathway is fatal toF. tularensis. Neither KKL-10 nor KKL-40 was cytotoxic to eukaryotic cells in culture. These results demonstrate that ribosome rescue is required forF. tularensisgrowth at all stages of its infection cycle and suggest that KKL-10 and KKL-40 are good lead compounds for antibiotic development.