Throughput Analysis of CSMA Wireless Networks with Finite Offered-load

This paper proposes an approximate method, equivalent access intensity (EAI), for the throughput analysis of CSMA wireless networks in which links have finite offered-load and their MAC-layer transmit buffers may be empty from time to time. Different from prior works that mainly considered the saturated network, we take into account in our analysis the impacts of empty transmit buffers on the interactions and dependencies among links in the network that is more common in practice. It is known that the empty transmit buffer incurs extra waiting time for a link to compete for the channel airtime usage, since when it has no packet waiting for transmission, the link will not perform channel competition. The basic idea behind EAI is that this extra waiting time can be mapped to an equivalent "longer" backoff countdown time for the unsaturated link, yielding a lower link access intensity that is defined as the mean packet transmission time divided by the mean backoff countdown time. That is, we can compute the "equivalent access intensity" of an unsaturated link to incorporate the effects of the empty transmit buffer on its behavior of channel competition. Then, prior saturated ideal CSMA network (ICN) model can be adopted for link throughput computation. Specifically, we propose an iterative algorithm, "Compute-and-Compare", to identify which links are unsaturated under current offered-load and protocol settings, compute their "equivalent access intensities" and calculate link throughputs. Simulation shows that our algorithm has high accuracy under various offered-load and protocol settings. We believe the ability to identify unsaturated links and compute links throughputs as established in this paper will serve an important first step toward the design and optimization of general CSMA wireless networks with offered-load control.Comment: 6 pages. arXiv admin note: text overlap with arXiv:1007.5255 by other author

Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell, Leading to Bohring-Opitz-like Syndrome in Mice

De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood mortality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models, we found that Asxl1 global loss as well as conditional deletion in osteoblasts and their progenitors led to significant bone loss and a markedly decreased number of bone marrow stromal cells (BMSCs) compared with wild-type littermates. Asxl1(-/-) BMSCs displayed impaired self-renewal and skewed differentiation, away from osteoblasts and favoring adipocytes. RNA-sequencing analysis revealed altered expression of genes involved in cell proliferation, skeletal development, and morphogenesis. Furthermore, gene set enrichment analysis showed decreased expression of stem cell self-renewal gene signature, suggesting a role of Asxl1 in regulating the stemness of BMSCs. Importantly, re-introduction of Asxl1 normalized NANOG and OCT4 expression and restored the self-renewal capacity of Asxl1(-/-) BMSCs. Our study unveils a pivotal role of ASXL1 in the maintenance of BMSC functions and skeletal development

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Markov approximation for combinatorial network optimization

Many important network design problems can be formulated as a combinatorial optimization problem. A large number of such problems, however, cannot readily be tackled by distributed algorithms. The Markov approximation framework studied in this paper is a general technique for synthesizing distributed algorithms. We show that when using the log-sum-exp function to approximate the optimal value of any combinatorial problem, we end up with a solution that can be interpreted as the stationary probability distribution of a class of time-reversible Markov chains. Certain carefully designed Markov chains among this class yield distributed algorithms that solve the log-sum-exp approximated combinatorial network optimization problem. By three case studies, we illustrate that Markov approximation technique not only can provide fresh perspective to existing distributed solutions, but also can help us generate new distributed algorithms in various domains with provable performance. We believe the Markov approximation framework will find applications in many network optimization problems, and this paper serves as a call for participation

Obstructive Sleep Apnea and Obesity Are Associated with Hypertension in a Particular Pattern: A Retrospective Study

Obstructive sleep apnea (OSA) and obesity can increase the risk of hypertension, but the combined effects of these two conditions on hypertension are not yet known. We collected the basic characteristics, sleep parameters, and glucose levels of subjects with a polysomnography test and divided them into four groups, according to whether they had severe OSA and obesity or not. The main effects of severe OSA and obesity and the interactions of the two on systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels were detected using analysis of covariance. The association between obesity and severe OSA and abnormal blood pressure and their combined effects were detected with logistic regression. In total, 686 subjects were included. After adjusting for multiple confounding factors, the strong main effects of obesity and severe OSA were detected in the SBP and DBP levels, with no combined effects from the two conditions on SBP or DBP. Obesity was independently associated with the presence of hyper-systolic blood pressure (hyper-SBP) and hypertension, and severe OSA was independently associated with the presence of hyper diastolic blood pressure (hyper-DBP) and hypertension. No effects of the interaction between severe OSA and obesity on the presence of abnormal blood pressure were observed. Both severe OSA and obesity were associated with hypertension, while obesity was closely associated with hyper-SBP, and severe OSA was associated with hyper-DBP. No effects of the interaction between these two on hypertension were observed