Return-Map Cryptanalysis Revisited

As a powerful cryptanalysis tool, the method of return-map attacks can be used to extract secret messages masked by chaos in secure communication schemes. Recently, a simple defensive mechanism was presented to enhance the security of chaotic parameter modulation schemes against return-map attacks. Two techniques are combined in the proposed defensive mechanism: multistep parameter modulation and alternative driving of two different transmitter variables. This paper re-studies the security of this proposed defensive mechanism against return-map attacks, and points out that the security was much over-estimated in the original publication for both ciphertext-only attack and known/chosen-plaintext attacks. It is found that a deterministic relationship exists between the shape of the return map and the modulated parameter, and that such a relationship can be used to dramatically enhance return-map attacks thereby making them quite easy to break the defensive mechanism.Comment: 11 pages, 7 figure

Microstructural origin for the piezoelectricity evolution in (K0.5Na0.5)NbO3-based lead-free ceramics

Chemically modified (K0.5Na0.5)NbO3 compositions with finely tuned polymorphic phase boundaries (PPBs) have shown excellent piezoelectric properties. The evolution of the domain morphology and crystal structure under applied electric fields of a model material, 0.948(K0.5Na0.5)NbO3-0.052LiSbO3, was directly visualized using in situ transmission electron microscopy. The in situ observations correlate extremely well with measurements of the electromechanical response on bulk samples. It is found that the origin of the excellent piezoelectric performance in this lead-free composition is due to a tilted monoclinic phase that emerges from the PPB when poling fields greater than 14 kV/cm are applied. 2013 AIP Publishing LLC

Astaxanthin promotes mitochondrial biogenesis and antioxidant capacity in chronic high-intensity interval training

Purpose: Reactive oxygen and nitrogen species are required for exercise-induced molecular adaptations; however, excessive exercise may cause cellular oxidative distress. We postulate that astaxanthin (ASX) can neutralize oxidative distress and stimulate mitochondrial biogenesis in high-intensity exercise-trained mice. Methods: Six-week-old mice (n = 8/group) were treated with ASX (10 mg/kg BW) or placebo. Training groups participated in 30 min/day high-intensity interval training (HIIT) for 6 weeks. Gastrocnemius muscle was collected and assayed following the exercise training period. Results: Compared to the HIIT control mice, the ASX-treated HIIT mice reduced malonaldehyde levels and upregulated the expression of Nrf2 and FOXO3a. Meanwhile, the genes NQO1 and GCLC, modulated by Nrf2, and SOD2, regulated by FOXO3a, and GPx4, were transcriptionally upregulated in the ASX-treated HIIT group. Meanwhile, the expression of energy sensors, AMPK, SIRT1, and SIRT3, increased in the ASX-treated HIIT group compared to the HIIT control group. Additionally, PGC-1α, regulated by AMPK and SIRT1, was upregulated in the ASX-treated HIIT group. Further, the increased PGC-1α stimulated the transcript of NRF1 and Tfam and mitochondrial proteins IDH2 and ATP50. Finally, the ASX-treated HIIT mice had upregulations in the transcript level of mitochondrial fusion factors, including Mfn1, Mfn2, and OPA1. However, the protein level of AMPK, SIRT1, and FOXO3a, and the transcript level of Nrf2, NQO1, PGC-1α, NRF1, Mfn1, Mfn2, and OPA1 decreased in the HIIT control group compared to the sedentary control group. Conclusion: Supplementation with ASX can reduce oxidative stress and promote antioxidant capacity and mitochondrial biogenesis during strenuous HIIT exercise in mice.</p

Do preoperative finger pressures predict early arterial steal in hemodialysis access patients? A prospective analysis

AbstractBackground: Hand ischemia resulting from arterial steal is a serious complication in patients undergoing hemodialysis access, but specific risk factors for steal remain in dispute. The purpose of this study was to determine whether plethysmographically derived finger pressures (FPs) or digital-brachial indices (DBIs) are predictive of symptomatic arterial steal. Methods: We prospectively studied 72 patients (37 men, 35 women; mean age, 57 ± 10 years) who were undergoing brachial artery-based hemodialysis access. All patients had complete pre- and postoperative hand examinations and FP determinations. Surgeons were blinded to preoperative FP results. Results: Prosthetic graft was used in 60 patients (6-mm polytetrafluoroethylene [PTFE] in 50, tapered PTFE in 10), and brachial-based arteriovenous fistulas were created in 12. Fourteen (19%) patients developed arterial steal symptoms. The mean preoperative FP was significantly lower in steal patients than in those without steal (131 ± 27 vs 151 ± 31 mm Hg, P < .03). Nine (64%) of the patients with steal had DBIs <1.0, compared to 18 (31%) of the patients without steal (P = .02). However, there was no absolute FP or DBI threshold below which steal was inevitable. The occurrence of steal was attributed to proximal arterial stenoses in seven, to distal arterial disease in five, and was unknown in two. When comparing the 14 patients who developed steal to the 58 who did not, we noted that a higher proportion of steal patients had coronary artery disease (57% vs 17%, P = .005). Steal was more likely to develop in patients with arteriovenous fistulas than in patients with prosthetic grafts (43% vs 14%, P = .009). There were no significant differences in demographic factors, atherosclerotic risks (diabetes, smoking, hypertension, dyslipidemia), prevalence of peripheral vascular disease, cerebrovascular disease, shunt location, tapered vs straight graft, or number of prior grafts placed. Conclusions: These data indicate that preoperative FPs are lower in patients who develop steal syndrome after hemodialysis access. Patients with preoperative DBIs <1.0 are more likely to develop steal, but there is no DBI threshold below which steal is inevitable. Steal is more likely in patients undergoing brachial-based arteriovenous fistulas than in those receiving prosthetic grafts. (J Vasc Surg 2002;36:351-6.

HOX gene complement and expression in the planarian Schmidtea mediterranea

Abstract Background Freshwater planarians are well known for their regenerative abilities. Less well known is how planarians maintain spatial patterning in long-lived adult animals or how they re-pattern tissues during regeneration. HOX genes are good candidates to regulate planarian spatial patterning, yet the full complement or genomic clustering of planarian HOX genes has not yet been described, primarily because only a few have been detectable by in situ hybridization, and none have given morphological phenotypes when knocked down by RNAi. Results Because the planarian Schmidtea mediterranea (S. mediterranea) is unsegmented, appendage less, and morphologically simple, it has been proposed that it may have a simplified HOX gene complement. Here, we argue against this hypothesis and show that S. mediterranea has a total of 13 HOX genes, which represent homologs to all major axial categories, and can be detected by whole-mount in situ hybridization using a highly sensitive method. In addition, we show that planarian HOX genes do not cluster in the genome, yet 5/13 have retained aspects of axially restricted expression. Finally, we confirm HOX gene axial expression by RNA deep-sequencing 6 anterior–posterior “zones” of the animal, which we provide as a dataset to the community to discover other axially restricted transcripts. Conclusions Freshwater planarians have an unappreciated HOX gene complexity, with all major axial categories represented. However, we conclude based on adult expression patterns that planarians have a derived body plan and their asexual lifestyle may have allowed for large changes in HOX expression from the last common ancestor between arthropods, flatworms, and vertebrates. Using our in situ method and axial zone RNAseq data, it should be possible to further understand the pathways that pattern the anterior–posterior axis of adult planarians

Effect of Bending Stiffness of the Electroactive Polymer Element on the Performance of a Hybrid Actuator System (HYBAS)

An electroactive polymer (EAP)-ceramic hybrid actuation system (HYBAS) was developed recently at NASA Langley Research Center. This paper focuses on the effect of the bending stiffness of the EAP component on the performance of a HYBAS, in which the actuation of the EAP element can match the theoretical prediction at various length/thickness ratios for a constant elastic modulus of the EAP component. The effects on the bending stiffness of the elastic modulus and length/thickness ratio of the EAP component were studied. A critical bending stiffness to keep the actuation of the EAP element suitable for a rigid beam theory-based modeling was found for electron irradiated P(VDF-TrFE) copolymer. For example, the agreement of experimental data and theoretical modeling for a HYBAS with the length/thickness ratio of EAP element at 375 times is demonstrated. However, the beam based theoretical modeling becomes invalid (i.e., the profile of the HYBAS movement does not follow the prediction of theoretical modeling) when the bending stiffness is lower than a critical value

The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein

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Pro- and Antiinflammatory Cytokine Signaling: Reciprocal Antagonism Regulates Interferon-gamma Production by Human Natural Killer Cells

SummaryActivated monocytes produce proinflammatory cytokines (monokines) such as interleukin (IL)-12, IL-15, and IL-18 for induction of interferon-γ (IFN-γ) by natural killer (NK) cells. NK cells provide the antiinflammatory cytokine transforming growth factor (TGF)-β, an autocrine/negative regulator of IFN-γ. The ability of one signaling pathway to prevail over the other is likely important in controlling IFN-γ for the purposes of infection and autoimmunity, but the molecular mechanism(s) of how this counterregulation occurs is unknown. Here we show that in isolated human NK cells, proinflammatory monokines antagonize antiinflammatory TGF-β signaling by downregulating the expression of the TGF-β type II receptor, and its signaling intermediates SMAD2 and SMAD3. In contrast, TGF-β utilizes SMAD2, SMAD3, and SMAD4 to suppress IFN-γ and T-BET, a positive regulator of IFN-γ. Indeed, activated NK cells from Smad3−/− mice produce more IFN-γ in vivo than NK cells from wild-type mice. Collectively, our data suggest that pro- and antiinflammatory cytokine signaling reciprocally antagonize each other in an effort to prevail in the regulation of NK cell IFN-γ production