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Multi-constrained QoS routing is one of the challenging problems of the upcoming next-generation networks. Taking into account the local optimization of some QoS routing algorithms, this paper introduced a new combinatorial optimization algorithm, which combines the simulated annealing and k-shortest path algorithm. It is a good method to jump out to other useful space, and find the feasible paths. It can achieve good convergence. The simulation shows that the algorithm is efficient and has a good scalability in both network scale and weight number. [ABSTRACT FROM AUTHOR]

Abstract: Hypoxia inducible factor-1 (HIF-1) is an important transcription activator involved in cell responses to hypoxic stress. Previous studies demonstrated that HIF-1 exerts both pro- and anti-survival effects under hypoxia. The mechanisms underlying these contrary effects of HIF-1 remain unclear. Transcription co-activator p300 is necessary for HIF-1-induced transcriptional activation. Many factors inhibit HIF-1 activity by competitively binding to p300, which suggests that p300 is a key player in the modulation of HIF-1 function. To examine the alteration of p300 expression under hypoxia and its role in hypoxia-induced neuronal damage, neuronal-like PC12 cells were cultured with cobalt chloride (CoCl2), a hypoxia mimic reagent. The results showed that CoCl2 treatment-induced p300 expression along with an increase in cell damage. Furthermore, CoCl2-induced cell damage was attenuated by suppression of p300 expression with short hairpin RNA (shRNA). The data suggests that CoCl2-induced up-regulation of p300 expression promotes neuronal-like PC12 cell damage. [Copyright &y& Elsevier]

Objective: To analyze the long non-coding RNA (lncRNA) and messenger RNA (mRNA) co-expression network changes induced by mtDNA3010A/G mutation in acute hypoxia, and to investigate the role of key lncRNA and mRNA in the regulation of gene expression induced by hypoxia. Methods: The genotype combinations A-C-C and G-C-C of mitochondrial DNA 3010-5178-10400 were screened, and genotypes of mtDNA3010A and mtDNA3010G fusion cells were constructed by using osteosarcoma cell treated by ethidium bromide without mitochondrion (ρ 0 206 cell) as donors. After treatment with 1% O 2 24 h, the lncRNA - mRNA expression chip was applied to detect the differently expressed lncRNA and mRNA in two kinds of fusing cells, and fluorescence quantitative polymerase chain method was used to verify differently expressed mRNA. Bioinformatics methods were applied to build co-expression network of lncRNA-mRNA, predict target genes of differently expressed lncRNA, and the functions of differently expressed mRNA and target genes predicted by lncRNA were also analyzed based on gene ontology (GO) and the Kyoto encyclopedia of genes and genomes (KEGG) forecast analysis. Results: After treatment with 1% O 2 for 24 h, compared with mtDNA3010G fusion cells: 688 lncRNAs were up-regulated, 21 were more than 2 times; 1098 were down-regulated, and 4 were more than 2 times. There were 1151 mRNA expressions up-regulated, 14 were more than 2 times, 539 mRNA expressions were down-regulated, and 3 were more than 2 times. Conclusion: MtDNA3010A/G genotype mutation under hypoxia is able to affect the lncRNA-mRNA regulatory network, and the differentially expressed lncRNA and mRNA may play an important role in regulation network of gene expression induced by hypoxia, which is expected to be a target for the regulation of hypoxia reaction from the perspective of mitochondria.

Objective: To investigate the relationship between mitochondrial DNA (mtDNA) variation and high altitude essential hypertension(HAEH) in the Chinese Tajik population. Methods: Fifty-three patients with HAEH and 46 healthy subjects were enrolled from the Chinese Tajik population. The mtDNA fragments were amplificated by polymerase chain reaction, and products were sequenced to acquire full sequence of mtDNA. The mtDNA sequences of all subjects were compared to the Cambridge sequence to explore mtDNA variations and analyze difference between HAEH and healthy controls. Online softwares were applied to predict function changes caused by positive associated mtDNA variations. Results: Compared to the control group, the frequency of haplogroup U4b was significant higher in HAEH group( P =0.023,OR=7.062,CI(95%)=1.306-38.182), and the frequencies of 8 mutations from haplogroup U4b showed a significant difference between the HAEH group and control group (all with P values below 0.05). The mt DNA15693T＞C mutation was the only missense mutation, which affected amino acid 316 in mitochondrial cytochrome b (MTCYB) by changing it from methionine to threonine. Bioinformatics analysis indicated that the mutation in MTCYB may play a biological role through affecting the second structure of protein. Conclusion: MtDNA subhaplogroup U4b is a genetic factor for HAEH in the Chinese Tajik population, and mtDNA15693T＞C mutation may be an important molecular mechanism of HAEH.

Mitochondrial division inhibitor 1 (Mdivi-1) is a selective cell-permeable inhibitor of dynamin-related protein-1 (Drp1) and mitochondrial division. To investigate the effect of Mdivi-1 on cells treated with glutamate, cerebral cortex neurons isolated from neonatal rats were treated with 10 mM glutamate for 24 hours. Normal cultured cells and dimethyl sulfoxide-cultured cells were considered as controls. Apoptotic cells were detected by flow cytometry. Changes in mitochondrial morphology were examined by electron microscopy. Drp1, Bax, and caspase-3 expression was evaluated by western blot assays and immunocytochemistry. Mitochondrial membrane potential was detected using the JC-1 probe. Twenty-four hours after 10 mM glutamate treatment, Drp1, Bax and caspase-3 expression was upregulated, Drp1 and Bax were translocated to mitochondria, mitochondrial membrane potential was decreased and the rate of apoptosis was increased. These effects were inhibited by treatment with 50 μM Mdivi-1 for 2 hours. This finding indicates that Mdivi-1 is a candidate neuroprotective drug that can potentially mitigate against neuronal injury caused by glutamate-induced excitotoxicity., Competing Interests: None declared

Objective: Highland natives adapt well to the hypoxic environment at high altitude (HA). Several genes have been reported to be linked to HA adaptation. Previous studies showed that the endothelial ni- tric oxide synthase (ENOS) G894T polymorphism contributed to the physiology and pathophysiology of hu- mans at HA by regulating the production of NO. In this meta-analysis, we evaluate the association between the ENOS G894T polymorphism and HA adaptation through analyzing the published data., Methods: We searched all relevant literature about the ENOS G894T polymorphism and HA adaptation in PubMed, Med- line, and Embase before Step 2015. A random-effects model was applied (Revman 5.0), and study quality was assessed in duplicate. Six studies with 634 HA native cases and 621 low-altitude controls were included in this meta-analysis., Results: From the results, we observed that the wild-type allele G was significantly overrepresented in the HA groups (OR = 1.85; 95% Cl, 1.47-2.33; P < 0.0001). In addition, the GG genotype was significantly associated with HA adaptation (OR = 1.99; 95% Cl, 1.54-2.57; P < 0.0001)., Conclusion: Our results showed that in 894 G allele carriers, the GG genotype might be a beneficial factor for HA adaptation through enhancing the level of NO. However, more studies were needed to confirm our findings due to the limited sample size.

Aim: To study whether over-starvation aggravates intestinal mucosal injury and promotes bacterial and endotoxin translocation in a high-altitude hypoxic environment., Methods: Sprague-Dawley rats were exposed to hypobaric hypoxia at a simulated altitude of 7000 m for 72 h. Lanthanum nitrate was used as a tracer to detect intestinal injury. Epithelial apoptosis was observed with terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Serum levels of diamino oxidase (DAO), malondialdehyde (MDA), glutamine (Gln), superoxide dismutase (SOD) and endotoxin were measured in intestinal mucosa. Bacterial translocation was detected in blood culture and intestinal homogenates. In addition, rats were given Gln intragastrically to observe its protective effect on intestinal injury., Results: Apoptotic epithelial cells, exfoliated villi and inflammatory cells in intestine were increased with edema in the lamina propria accompanying effusion of red blood cells. Lanthanum particles were found in the intercellular space and intracellular compartment. Bacterial translocation to mesenteric lymph nodes (MLN) and spleen was evident. The serum endotoxin, DAO and MDA levels were significantly higher while the serum SOD, DAO and Gln levels were lower in intestine (P < 0.05). The bacterial translocation number was lower in the high altitude hypoxic group than in the high altitude starvation group (0.47 ± 0.83 vs 2.38 ± 1.45, P < 0.05). The bacterial translocation was found in each organ, especially in MLN and spleen but not in peripheral blood. The bacterial and endotoxin translocations were both markedly improved in rats after treatment with Gln., Conclusion: High-altitude hypoxia and starvation cause severe intestinal mucosal injury and increase bacterial and endotoxin translocation, which can be treated with Gln.