Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling

Cryptanalysis of the Hillery-Buzek-Berthiaume quantum secret-sharing protocol

The participant attack is the most serious threat for quantum secret-sharing protocols. We present a method to analyze the security of quantum secret-sharing protocols against this kind of attack taking the scheme of Hillery, Buzek, and Berthiaume (HBB) [Phys. Rev. A 59 1829 (1999)] as an example. By distinguishing between two mixed states, we derive the necessary and sufficient conditions under which a dishonest participant can attain all the information without introducing any error, which shows that the HBB protocol is insecure against dishonest participants. It is easy to verify that the attack scheme of Karlsson, Koashi, and Imoto [Phys. Rev. A 59, 162 (1999)] is a special example of our results. To demonstrate our results further, we construct an explicit attack scheme according to the necessary and sufficient conditions. Our work completes the security analysis of the HBB protocol, and the method presented may be useful for the analysis of other similar protocols.Comment: Revtex, 7 pages, 3 figures; Introduction modifie

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies

Threshold quantum cryptograph based on Grover's algorithm

Grover's operator in the two-qubit case can transform a basis into its conjugated basis. A permutation operator can transform a state in the two conjugated bases into its orthogonal state. These properties are included in a threshold quantum protocol. The proposed threshold quantum protocol is secure based the proof that the legitimate participators can only eavesdrop 2 bits of 3 bits operation information on one two-qubit with error probability 3/8. We propose a scheme to detect the Trojan horse attack without destroying the legal qubit.Comment: 7 pages, 1 figure

Fake one-time pad cannot be used to improve the efficiency of quantum communication

Two misuses of one-time pad in improving the efficiency of quantum communication are pointed out. One happens when using some message bits to encrypt others, the other exists because the key bits are not truly random. Both of them result in the decrease of security. Therefore, one-time pad should be used carefully in designing quantum communication protocols.Comment: 6 pages, no figure

Sleep duration and patterns in Chinese older adults: A comprehensive meta-analysis

This meta-analysis examined the mean sleep duration and patterns in Chinese older adult population. A literature search was systematically conducted covering major English (PubMed, Embase and PsycINFO) and Chinese (Chinese National Knowledge Infrastructure (CNKI), WanFang and SinoMed) databases. Data in studies with the mean and standard deviation of sleep duration and/or the proportion of short and long sleep durations in Chinese older adults were extracted and pooled using random-effects models. Subgroup analyses were conducted according to gender, region, area, survey time and sample size. A total of 36 studies with 150,616 subjects were included for analyses. The pooled mean sleep duration of 21 studies with available data was 6.82 hours/day (95% CI: 6.59–7.05 hours/day). The estimated proportions of sleep duration \u3c5 hours/day, \u3c6 hours/day, \u3c7 hours/day were 18.8% (95% CI: 1.7%–35.9%), 26.7% (95% CI: 19.7%–33.7%) and 42.3% (95% CI: 34.8%–49.8%), respectively. The pooled proportions for long sleepers were 22.6% (95% CI: 13.9%–31.4%) (\u3e8 hours/day) and 17.6% (95% CI: 12.4%–22.9%) (\u3e9 hours/day). Given the adverse effects of unhealthy sleep patterns, health professionals should pay more attention to sleep patterns in this population in China