Effect of number of burst assemblers on TCP performance in optical burst switching networks

Burst assembly mechanism is one of the fundamental factors that determine the performance of an optical burst switching (OBS) network. In this paper, we investigate the influence of number of burstifiers on TCP performance for an OBS network. An ns2-based OBS network simulator is developed for simulating the optical network. The goodput of TCP flows between an ingress and an egress nodes traveling through an optical network is studied for different values of the number of assembly buffers per destination. First, the losses resulting from the congestion in the core OBS network are modeled using a burst independent Bernoulli loss model. Then, a background burst traffic is generated to create contention at a core node in order to realize a burst dependent loss model. Simulation results show that for an OBS network employing timer-based assembly algorithm, TCP goodput increases as the number of burst assemblers is increased for both types of loss models. The improvement from one burstifier to moderate number of burst assemblers is significant (15-50% depending on the burst loss probability, processing delay and the TCP version), but the goodput difference between moderate number of buffers andperflow aggregation is relatively small, implying that a cost-effective OBS edge switch implementation should use moderate number of assembly buffers per destination for enhanced TCP performance. © 2006 IEEE

Using multiple per egress burstifiers for enhanced TCP performance in OBS networks

Burst assembly mechanism is one of the fundamental factors that determine the performance of an optical burst switching (OBS) network. In this paper, we investigate the influence of the number of burstifiers on TCP performance for an OBS network. The goodput of TCP flows between an ingress node and an egress node traveling through an optical network is studied as the number of assembly buffers per destination varies. First, the burst-length independent losses resulting from the contention in the core OBS network using a non-void-filling burst scheduling algorithm, e.g., Horizon, are studied. Then, burst-length dependent losses arising as a result of void-filling scheduling algorithms, e.g., LAUC-VF, are studied for two different TCP flow models: FTP-type long-lived flows and variable size short-lived flows. Simulation results show that for both types of scheduling algorithms, both types of TCP flow models, and different TCP versions (Reno, Newreno and Sack), TCP goodput increases as the number of burst assemblers per egress node is increased for an OBS network employing timer-based assembly algorithm. The improvement from one burstifier to moderate number of burst assemblers is significant (15-50% depending on the burst loss probability, per-hop processing delay, and the TCP version), but the goodput difference between moderate number of buffers and per-flow aggregation is relatively small, implying that an OBS edge switch should use moderate number of assembly buffers per destination for enhanced TCP performance without substantially increasing the hardware complexity. © 2008 Springer Science+Business Media, LLC

NOBS: An ns2 based simulation tool for performance evaluation of TCP traffic in OBS networks

Performance evaluation of TCP traffic in OBS networks has been under intensive study, since TCP constitutes the majority of Internet traffic. As a reliable and publicly available simulator, ns2 has been widely used for studying TCP/IP networks; however ns2 lacks many of the components for simulating optical burst switching networks. In this paper, an ns2 based OBS simulation tool (nOBS), which is built for studying burst assembly, scheduling and contention resolution algorithms in OBS networks is presented. The node and link objects in OBS are extended in nOBS for developing optical nodes and optical links. The ingress, core and egress node functionalities are combined into a common optical node architecture, which comprises agents responsible for burstification, routing and scheduling. The effects of burstification parameters, e.g., burstification timeout, burst size and number of burstification buffers per egress node, on TCP performance are investigated using nOBS for different TCP versions and different network topologies

Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the Prostate Cancer Prevention Trial

BACKGROUND: A previous analysis of the placebo arm of the Prostate Cancer Prevention Trial (PCPT) reported 82% overall prevalence of intraprostatic inflammation and identified a link between inflammation and higher-grade prostate cancer and serum PSA. Here we studied these associations in the PCPT finasteride arm. METHODS: Prostate cancer cases (N=197) detected either on a clinically indicated biopsy or on protocol-directed end-of-study biopsy, and frequency-matched controls (N=248) with no cancer on an end-of-study biopsy were sampled from the finasteride arm. Inflammation in benign prostate tissue was visually assessed using digital images of H&E stained sections. Logistic regression was used for statistical analysis. RESULTS: In the finasteride arm, 91.6% of prostate cancer cases and 92.4% of controls had at least one biopsy core with inflammation in benign areas; p < 0.001 for difference compared to placebo arm. Overall, the odds of prostate cancer did not differ by prevalence (OR=0.90, 95% CI 0.44-1.84) or extent (P-trend=0.68) of inflammation. Inflammation was not associated with higher-grade disease (prevalence: OR=1.07, 95% CI 0.43-2.69). Furthermore, mean PSA concentration did not differ by the prevalence or extent of inflammationin either cases or controls. CONCLUSION: The prevalence of intraprostatic inflammation was higher in the finasteride than placebo arm of the PCPT, with no association with higher-grade prostate cancer. IMPACT: Finasteride may attenuate the association between inflammation and higher-grade prostate cancer. Moreover, the missing link between intraprostatic inflammation and PSA suggests that finasteride may reduce inflammation-associated PSA elevation

Bluetooth Broadcasting Performance: Reliability and Throughput

This paper studies the performance of Bluetooth broadcasting scheme. The transmission of a Bluetooth broadcast packet is repeated several times to increase the reliability of broadcast. We have analyzed the effects of baseband ACL packet type preference, on the broadcast performance in terms of reliability and effective throughput, over different channel characteristics (i.e. bit error rate). As the result of our analysis, we determined the optimal packet type and re-transmission count combinations that can provide the highest effective throughput values for various practical BER ranges. These results can be used at Bluetooth baseband layer to dynamically adapt to varying channel conditions and to achieve a good broadcast performance. © Springer-Verlag Berlin Heidelberg 2006

Omacetaxine may have a role in chronic myeloid leukaemia eradication through downregulation of Mcl-1 and induction of apoptosis in stem/progenitor cells

Chronic myeloid leukaemia (CML) is maintained by a rare population of tyrosine kinase inhibitor (TKI)-insensitive malignant stem cells. Our long-term aim is to find a BcrAbl-independent drug that can be combined with a TKI to improve overall disease response in chronic-phase CML. Omacetaxine mepesuccinate, a first in class cetaxine, has been evaluated by clinical trials in TKI-insensitive/resistant CML. Omacetaxine inhibits synthesis of anti-apoptotic proteins of the Bcl-2 family, including (myeloid cell leukaemia) Mcl-1, leading to cell death. Omacetaxine effectively induced apoptosis in primary CML stem cells (CD34&lt;sup&gt;+&lt;/sup&gt;38&lt;sup&gt;lo&lt;/sup&gt;) by downregulation of Mcl-1 protein. In contrast to our previous findings with TKIs, omacetaxine did not accumulate undivided cells &lt;i&gt;in vitro&lt;/i&gt;. Furthermore, the functionality of surviving stem cells following omacetaxine exposure was significantly reduced in a dose-dependant manner, as determined by colony forming cell and the more stringent long-term culture initiating cell colony assays. This stem cell-directed activity was not limited to CML stem cells as both normal and non-CML CD34&lt;sup&gt;+&lt;/sup&gt; cells were sensitive to inhibition. Thus, although omacetaxine is not leukaemia stem cell specific, its ability to induce apoptosis of leukaemic stem cells distinguishes it from TKIs and creates the potential for a curative strategy for persistent disease

Betatrophin levels are related to the early histological findings in nonalcoholic fatty liver disease

Betatrophin, a liver hormone, regulates glucose and lipid metabolism. We investigated the betatrophin levels in nonalcoholic fatty liver disease (NAFLD) and searched for any relationship with histological severity and metabolic parameters. Fifty males with NAFLD [Nonalcoholic Steatohepati-tis (NASH) (n = 32); non-NASH (n = 18)] and 30 healthy controls were included. Plasma betatrophin was measured by ELISA method. Insulin sensitivity was assessed by HOMA-IR index. Histological features were scored by the semi quantitative classification and combined as the NAFLD activity score (NAS). Betatrophin levels in the non-NASH group were significantly higher than the controls. Betatrophin was positively correlated to the age, waist circumference, total cholesterol, triglycerides, LDL cholesterol, glucose, insulin, HOMA-IR index and gamma glutamyl transpeptidase levels, and negatively correlated to the steatosis and NAS. In the stepwise linear regression analysis, the triglyceride (β = 0.457, p &lt; 0.001), glucose (β = 0.281, p = 0.02) and NAS (β = −0.260, p = 0.03) were the independent determinants of betatrophin. Betatrophin levels are higher in the early stages of NAFLD and tend to decrease when the disease progresses. This could be an important preliminary mechanistic finding to explain the increased frequency of glucose intolerance during the course of NAFLD

Model for the hydration of non-polar compounds and polymers

We introduce an exactly solvable statistical-mechanical model of the hydration of non-polar compounds, based on grouping water molecules in clusters where hydrogen bonds and isotropic interactions occur; interactions between clusters are neglected. Analytical results show that an effective strengthening of hydrogen bonds in the presence of the solute, together with a geometric reorganization of water molecules, are enough to yield hydrophobic behavior. We extend our model to describe a non-polar homopolymer in aqueous solution, obtaining a clear evidence of both ``cold'' and ``warm'' swelling transitions. This suggests that our model could be relevant to describe some features of protein folding.Comment: REVTeX, 6 pages, 3 figure

Peginterferon alfa-2a alone, lamivudine alone, and the two in combination in patients with HBeAg-negative chronic hepatitis B

BACKGROUND: Available treatments for hepatitis B e antigen (HBeAg)-negative chronic hepatitis B are associated with poor sustained responses. As a result, nucleoside and nucleotide analogues are typically continued indefinitely, a strategy associated with the risk of resistance and unknown long-term safety implications. METHODS: We compared the efficacy and safety of peginterferon alfa-2a (180 microg once weekly) plus placebo, peginterferon alfa-2a plus lamivudine (100 mg daily), and lamivudine alone in 177, 179, and 181 patients with HBeAg-negative chronic hepatitis B, respectively. Patients were treated for 48 weeks and followed for an additional 24 weeks. RESULTS: After 24 weeks of follow-up, the percentage of patients with normalization of alanine aminotransferase levels or hepatitis B virus (HBV) DNA levels below 20,000 copies per milliliter was significantly higher with peginterferon alfa-2a monotherapy (59 percent and 43 percent, respectively) and peginterferon alfa-2a plus lamivudine (60 percent and 44 percent) than with lamivudine monotherapy (44 percent, P=0.004 and P=0.003, respectively; and 29 percent, P=0.007 and P=0.003, respectively). Rates of sustained suppression of HBV DNA to below 400 copies per milliliter were 19 percent with peginterferon alfa-2a monotherapy, 20 percent with combination therapy, and 7 percent with lamivudine alone (P<0.001 for both comparisons with lamivudine alone). Loss of hepatitis B surface antigen occurred in 12 patients in the peginterferon groups, as compared with 0 patients in the group given lamivudine alone. Adverse events, including pyrexia, fatigue, myalgia, and headache, were less frequent with lamivudine monotherapy than with peginterferon alfa-2a monotherapy or combination therapy. CONCLUSIONS: Patients with HBeAg-negative chronic hepatitis B had significantly higher rates of response, sustained for 24 weeks after the cessation of therapy, with peginterferon alfa-2a than with lamivudine. The addition of lamivudine to peginterferon alfa-2a did not improve post-therapy response rates. Copyright 2004 Massachusetts Medical Societypublished_or_final_versio

Structural basis for tunable control of actin dynamics by myosin-15 in mechanosensory stereocilia

The motor protein myosin-15 is necessary for the development and maintenance of mechanosensory stereocilia, and mutations in myosin-15 cause hereditary deafness. In addition to transporting actin regulatory machinery to stereocilia tips, myosin-15 directly nucleates actin filament (“F-actin”) assembly, which is disrupted by a progressive hearing loss mutation (p.D1647G, “jordan”). Here, we present cryo–electron microscopy structures of myosin-15 bound to F-actin, providing a framework for interpreting the impacts of deafness mutations on motor activity and actin nucleation. Rigor myosin-15 evokes conformational changes in F-actin yet maintains flexibility in actin’s D-loop, which mediates inter-subunit contacts, while the jordan mutant locks the D-loop in a single conformation. Adenosine diphosphate–bound myosin-15 also locks the D-loop, which correspondingly blunts actin-polymerization stimulation. We propose myosin-15 enhances polymerization by bridging actin protomers, regulating nucleation efficiency by modulating actin’s structural plasticity in a myosin nucleotide state–dependent manner. This tunable regulation of actin polymerization could be harnessed to precisely control stereocilium height