Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets

Mitochondria are the centrol hub for cellular energy metabolisms. They regulate fuel metabolism by oxygen levels, participate in physiological signaling pathways, and act as oxygen sensors. Once oxygen deprived, the fuel utilizations can be switched from mitochondrial oxidative phosphorylation to glycolysis for ATP production. Notably, mitochondria can also adapt to hypoxia by making various functional and phenotypes changes to meet the demanding of oxygen levels. Hypoxic pulmonary hypertension is a life-threatening disease, but its exact pathgenesis mechanism is still unclear and there is no effective treatment available until now. Ample of evidence indicated that mitochondria play key factor in the development of hypoxic pulmonary hypertension. By hypoxia-inducible factors, multiple cells sense and transmit hypoxia signals, which then control the expression of various metabolic genes. This activation of hypoxia-inducible factors considered associations with crosstalk between hypoxia and altered mitochondrial metabolism, which plays an important role in the development of hypoxic pulmonary hypertension. Here, we review the molecular mechanisms of how hypoxia affects mitochondrial function, including mitochondrial biosynthesis, reactive oxygen homeostasis, and mitochondrial dynamics, to explore the potential of improving mitochondrial function as a strategy for treating hypoxic pulmonary hypertension

Secured green communication scheme for interference alignment based networks

In this paper, a new security and green communication scheme is proposed to the Interference-Alignment (IA) based networks. To achieve a secured communication, full-duplex receivers are utilized to transmit artificial noise (AN). Both the signals and the ANs are used to harvest energy to realize green communication. For these reasons, the feasible conditions of this scheme are analyzed first. Secondly, the average transmission rate, the secrecy performance and the harvested energy are investigated. Thirdly, an optimization scheme of simultaneous wireless information and power transfer (SWIPT) is given to optimize the information transmission and the energy harvesting efficiency. Meanwhile, an improved IA iteration algorithm is designed to eliminate both the AN and the interference. Furthermore, relay cooperation is considered and its system performance is analyzed. The simulations show that the target average transmission rate is not affected by AN, while the secrecy performance can be greatly improved. The energy harvesting efficiency is also better than the traditional schemes. As expected, the average transmission rate further is improved with the relay cooperation

Soil N-oxide emissions decrease from intensive greenhouse vegetable fields by substituting synthetic N fertilizer with organic and bio-organic fertilizers

In order to reduce soil and environmental quality degradation associated with the use of synthetic nitrogen (N), substituting chemical fertilizer with organic or bio-organic fertilizer has become an increasingly popular option. However, components of this fertilizer strategy related to mitigation of soil N-oxide emissions and maintenance of crop yield remain uncertain. Here, we evaluated the effects of three different fertilizer strategies, with equal amounts of N, on nitrous oxide (N2O) and nitric oxide (NO) emissions, vegetable yield, and yield-scaled N2O and NO emissions under three consecutive cucumber growing seasons. The three treatments were chemical fertilizer (NPK, urea), organic fertilizer (O, composted cattle manure), and bio-organic fertilizer (O + T, O combined with Trichoderma.spp). Results showed that the NPK plot had the highest area-scaled emissions of N2O (13.1 ± 0.48 kg N ha−1 yr−1) and NO (5.01 ± 0.34 kg N ha−1 yr−1), which were 1.3–1.4 and 3.1–3.7 times greater than the O and O + T plots, respectively. The annual direct emission factors for N2O and NO were 2.08% and 0.92% for the NPK plot, which declined to 1.34% and 0.09% in the O plot, and 1.12% and 0.03% in the O + T plot, respectively. The annual vegetable yield was 117 ± 2.9 t ha−1 for NPK plot and 122 ± 2.0 t ha−1 for O + T plot, which was higher than 111 ± 1.7 t ha−1 for O plot. The yield-scaled N2O + NO emissions differed significantly with fertilization treatment, with the lowest value observed in the O + T plot. We attributed the lower soil N-oxide emissions following organic fertilizer application to the slow release of available N and enhanced denitrification caused by the increase of soil dissolved organic carbon and pH. Compared with the use of organic fertilizer alone, the addition of Trichoderma.spp significantly increased the potential denitrification rate but decreased N2O emissions, which may have promoted the reduction of N2O to N2. Therefore, our results suggest that adopting composted organic fertilizer mixtures with microbial inoculants could be a win-win practice to mitigate gaseous N losses and simultaneously improve crop yield in intensively managed vegetable cropping systems

The Epigenetic Modifier PRDM5 Functions as a Tumor Suppressor through Modulating WNT/β-Catenin Signaling and Is Frequently Silenced in Multiple Tumors

BACKGROUND: PRDM (PRDI-BF1 and RIZ domain containing) proteins are zinc finger proteins involved in multiple cellular regulations by acting as epigenetic modifiers. We studied a recently identified PRDM member PRDM5 for its epigenetic abnormality and tumor suppressive functions in multiple tumorigeneses. METHODOLOGY/PRINCIPAL FINDINGS: Semi-quantitative RT-PCR showed that PRDM5 was broadly expressed in human normal tissues, but frequently silenced or downregulated in multiple carcinoma cell lines due to promoter CpG methylation, including 80% (4/5) nasopharyngeal, 44% (8/18) esophageal, 76% (13/17) gastric, 50% (2/4) cervical, and 25% (3/12) hepatocellular carcinoma cell lines, but not in any immortalized normal epithelial cell lines. PRDM5 expression could be restored by 5-aza-2'-deoxycytidine demethylation treatment in silenced cell lines. PRDM5 methylation was frequently detected by methylation-specific PCR (MSP) in multiple primary tumors, including 93% (43/46) nasopharyngeal, 58% (25/43) esophageal, 88% (37/42) gastric and 63% (29/46) hepatocellular tumors. PRDM5 was further found a stress-responsive gene, but its response was impaired when the promoter was methylated. Ectopic PRDM5 expression significantly inhibited tumor cell clonogenicity, accompanied by the inhibition of TCF/β-catenin-dependent transcription and downregulation of CDK4, TWIST1 and MDM2 oncogenes, while knocking down of PRDM5 expression lead to increased cell proliferation. ChIP assay showed that PRDM5 bound to its target gene promoters and suppressed their transcription. An inverse correlation between the expression of PRDM5 and activated β-catenin was also observed in cell lines. CONCLUSIONS/SIGNIFICANCE: PRDM5 functions as a tumor suppressor at least partially through antagonizing aberrant WNT/β-catenin signaling and oncogene expression. Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker