Outbreak of nosocomial Acinetobacter baumannii bacteremia in a high risk ward

Acinetobacter baumannii is emerging as a major cause of nosocomial infections particularly in high risk patients. Being resistant to adverse environmental conditions, it can stay for prolonged periods in the hospital environment. We report an outbreak in the medical oncology ward where nine patients suspected of bacteraemia were blood culture positive forA. baumannii from the two samples each, one collected through the i.v. cannula and another through the peripheral venous puncture. The bacteria was also isolated from the environmental sources from the various samples collected. The biotype, antibiogram, cellular protein profiles on SDS-PAGE and the restriction enzyme analysis patterns of the patient isolates and the environmental isolates were similar. This points to the environment as a source of infection. With reinforcement of proper barrier nursing and use of disposable heparine ampoules it was possible to control the outbreak.     

Anti-neoplastic pharmacophore benzophenone-1 coumarin (BP-1C) targets JAK2 to induce apoptosis in lung cancer

Reigning of the abnormal gene activation associated with survival signalling in lung cancer leads to the anomalous growth and therapeutic failure. Targeting specific cell survival signalling like JAK2/STAT3 nexus has become a major focus of investigation to establish a target specific treatment. The 2-bromobenzoyl-4-methylphenoxy-acetyl hydra acetyl Coumarin (BP-1C), is new anti-neoplastic agent with apoptosis inducing capacity. The current study was aimed to develop antitumor phramacophore, BP-1C as JAK2 specific inhibitor against lung neoplastic progression. The study validates and identifies the molecular targets of BP-1C induced cell death. Cell based screening against multiple cancer cell lines identified, lung adenocarcinoma as its specific target through promotion of apoptosis. The BP-1C is able to induce, specific hall marks of apoptosis and there by conferring anti-neoplastic activity. Validation of its molecular mechanism, identified, BP-1C specifically targets JAK2^Tyr1007/1008 phosphorylation, and inhibits its downstream STAT3^Tyr705 signalling pathway to induce cell death. As a consequence, modulation in Akt/Src survival signal and altered expression of interwoven apoptotic genes were evident. The results were reproducible in an in-vivo LLC tumor model and in-ovo xenograft studies. The computational approaches viz, drug finger printing confers, BP-1C as novel class JAK2 inhibitor and molecular simulations studies assures its efficiency in binding with JAK2. Overall, BP-1C is a novel JAK2 inhibitor with experimental evidence and could be effectively developed into a promising drug for lung cancer treatment.

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Dynamic change in optical properties of a nanoparticle embedded tumor phantom for plasmonic photothermal cancer therapeutics

In this study, the temporal dynamic changes in optical properties of gold nanorods (GNR) embedded tumor phantom, during photothermal interaction, are reported for plasmonic photothermal therapeutics. Tumor mimicking bilayer phantoms were prepared by using 1% agarose incorporated with 0.1% coffee powder, 0.3% intralipid solution as epidermis layer; 3% intralipid solution and 0.3% human hemoglobin (Hb) powder as dermis layer. On incorporating GNRs of concentrations 10, 20, and 40 μg/ml within the phantom, the absorption coefficients increases 4–8 times, while there is minimal change in the reduced scattering coefficients. Further the absorption coefficient increased by ~8% with the incorporation of GNRs of concentration 40 μg/ml, while no considerable dynamic change in the optical properties is observed for the phantom embedded with GNRs of concentrations 10, and 20 μg/ml. The discussed results are useful for the selection of GNRs dose for pre-treatment planning of plasmonic photothermal cancer therapeutics.     

Omnitemporal choreographies of all five STIM/Orai and IP3Rs underlie the complexity of mammalian Ca2+ signaling

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Acceleration of epithelial cell syndecan-1 shedding by anthrax hemolytic virulence factors

Background  

It has been recently reported that major pathogens Staphylococcus aureus and Pseudomonas aeruginosa accelerate a normal process of cell surface syndecan-1 (Synd1) ectodomain shedding as a mechanism of host damage due to the production of shedding-inducing virulence factors. We tested if acceleration of Synd1 shedding takes place in vitro upon treatment of epithelial cells with B. anthracis hemolysins, as well as in vivo during anthrax infection in mice.     

Method for efficient extraction of phycocyanin from Spirulina

Summary Of several different methods tried for the extraction of phycocyanin (PC) from the cyanobacterium Spirulina, treatment with 1800 Units / ml lysozyme and 100 ppm linear alkyl benzene sulfonate afforded good PC yield with high specific content, resulting in 66 and 98% recovery of PC, respectively.     

Photosynthetic control of nitrate metabolism inPhormidium uncinatum,a cyanobaterium

The impact of 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) was studied on growth, Hill reaction, nitrate uptake, enzymes of nitrate utilization, and of oxidative pentose pathway by phototrophically growingPhormidium uncinatum and its DCMU-resistant (DCMUR) mutant. The growth-inhibitory action of DCMU was apparently the consequence of an inactivation of photosystem II (PS II) reaction and of reduction of nitrate utilization owing to an inhibition of nitrite reductase (NiR) activity. Mutation to this herbicide rendered both the processes insensitive to DCMU. Nevertheless, nitrate transport, nitrate reduction to nitrite, and ammonia assimilation of both the strains remained rather unaffected by DCMU. Photosynthetically inactive cells of the two strains exhibited higher activity levels of glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) than their phototrophic cultures.These data suggest that photosynthesis regulates nitrate utilization in this cyanobacterium at nitrite reduction level and that nitrate uptake and reduction to nitrite are relaxed from this control and conditionally sustained by oxidative breakdown of reserve glycogen.