On the Gaussian Many-to-One X Channel

In this paper, the Gaussian many-to-one X channel (XC), which is a special case of general multiuser XC, is studied. In the Gaussian many-to-one XC, communication links exist between all transmitters and one of the receivers, along with a communication link between each transmitter and its corresponding receiver. As per the XC assumption, transmission of messages is allowed on all the links of the channel. This communication model is different from the corresponding manyto- one interference channel (IC). Transmission strategies, which involve using Gaussian codebooks and treating interference from a subset of transmitters as noise, are formulated for the above channel. Sum-rate is used as the criterion of optimality for evaluating the strategies. Initially, a 3 x 3 many-to-one XC is considered and three transmission strategies are analyzed. The first two strategies are shown to achieve sum-rate capacity under certain channel conditions. For the third strategy, a sum-rate outer bound is derived and the gap between the outer bound and the achieved rate is characterized. These results are later extended to the K x K case. Next, a region in which the many-to-one XC can be operated as a many-to-one IC without the loss of sum-rate is identified. Furthermore, in the above region, it is shown that using Gaussian codebooks and treating interference as noise achieve a rate point that is within K/2 -1 bits from the sum-rate capacity. Subsequently, some implications of the above results to the Gaussian many-to-one IC are discussed. Transmission strategies for the many-to-one IC are formulated, and channel conditions under which the strategies achieve sum-rate capacity are obtained. A region where the sum-rate capacity can be characterized to within K/2 -1 bits is also identified. Finally, the regions where the derived channel conditions are satisfied for each strategy are illustrated for a 3 x 3 many-to-one XC and the corresponding many-to-one IC.

High-throughput miniaturized microfluidic microscopy with radially parallelized channel geometry

In this article, we present a novel approach to throughput enhancement in miniaturized microfluidic microscopy systems. Using the presented approach, we demonstrate an inexpensive yet high-throughput analytical instrument. Using the high-throughput analytical instrument, we have been able to achieve about 125,880 cells per minute (more than one hundred and twenty five thousand cells per minute), even while employing cost-effective low frame rate cameras (120 fps). The throughput achieved here is a notable progression in the field of diagnostics as it enables rapid quantitative testing and analysis. We demonstrate the applicability of the instrument to point-of-care diagnostics, by performing blood cell counting. We report a comparative analysis between the counts (in cells per mu l) obtained from our instrument, with that of a commercially available hematology analyzer.

Quercetin, a Natural Flavonoid Interacts with DNA, Arrests Cell Cycle and Causes Tumor Regression by Activating Mitochondrial Pathway of Apoptosis

Naturally occurring compounds are considered as attractive candidates for cancer treatment and prevention. Quercetin and ellagic acid are naturally occurring flavonoids abundantly seen in several fruits and vegetables. In the present study, we evaluate and compare antitumor efficacies of quercetin and ellagic acid in animal models and cancer cell lines in a comprehensive manner. We found that quercetin induced cytotoxicity in leukemic cells in a dose-dependent manner, while ellagic acid showed only limited toxicity. Besides leukemic cells, quercetin also induced cytotoxicity in breast cancer cells, however, its effect on normal cells was limited or none. Further, quercetin caused S phase arrest during cell cycle progression in tested cancer cells. Quercetin induced tumor regression in mice at a concentration 3-fold lower than ellagic acid. Importantly, administration of quercetin lead to -5 fold increase in the life span in tumor bearing mice compared to that of untreated controls. Further, we found that quercetin interacts with DNA directly, and could be one of the mechanisms for inducing apoptosis in both, cancer cell lines and tumor tissues by activating the intrinsic pathway. Thus, our data suggests that quercetin can be further explored for its potential to be used in cancer therapeutics and combination therapy.