Genome-wide analysis of the peanut CaM/CML gene family reveals that the AhCML69 gene is associated with resistance to Ralstonia solanacearum.

BACKGROUND: Calmodulins (CaMs)/CaM-like proteins (CMLs) are crucial Ca2+-binding sensors that can decode and transduce Ca2+ signals during plant development and in response to various stimuli. The CaM/CML gene family has been characterized in many plant species, but this family has not yet been characterized and analyzed in peanut, especially for its functions in response to Ralstonia solanacearum. In this study, we performed a genome-wide analysis to analyze the CaM/CML genes and their functions in resistance to R. solanacearum. RESULTS: Here, 67, 72, and 214 CaM/CML genes were identified from Arachis duranensis, Arachis ipaensis, and Arachis hypogaea, respectively. The genes were divided into nine subgroups (Groups I-IX) with relatively conserved exon‒intron structures and motif compositions. Gene duplication, which included whole-genome duplication, tandem repeats, scattered repeats, and unconnected repeats, produced approximately 81 pairs of homologous genes in the AhCaM/CML gene family. Allopolyploidization was the main reason for the greater number of AhCaM/CML members. The nonsynonymous (Ka) versus synonymous (Ks) substitution rates (less than 1.0) suggested that all homologous pairs underwent intensive purifying selection pressure during evolution. AhCML69 was constitutively expressed in different tissues of peanut plants and was involved in the response to R. solanacearum infection. The AhCML69 protein was localized in the cytoplasm and nucleus. Transient overexpression of AhCML69 in tobacco leaves increased resistance to R. solanacearum infection and induced the expression of defense-related genes, suggesting that AhCML69 is a positive regulator of disease resistance. CONCLUSIONS: This study provides the first comprehensive analysis of the AhCaM/CML gene family and potential genetic resources for the molecular design and breeding of peanut bacterial wilt resistance.

Shock lung is not "wet" but characterized as necroptotic inflammation in a mouse model of hypotension.

OBJECTIVES: Hypotension episodes before or after donor brain death are assumed to trigger hypoxia-reoxygenation, causing diffuse alveolar-capillary damage via necrosis. However, alveolar-capillary membranes have direct access to oxygen in alveoli. We hypothesized hypotension-induced lung injury is not diffuse alveolar-capillary damage but interstitial inflammation resulting from nonhypoxic lung ischemia and systemic responses to hypoxic extrapulmonary ischemia. METHODS: The 4-hour hypotension model was established by subjecting C57BL/6J mice to 4-hour hypotension at 15 ± 5 mm Hg of mean artery pressure and resuscitated with whole shed blood and norepinephrine. Nonhypoxic lung ischemia model was established by 4-hour left pulmonary artery ligation. At 24 hours postprocedure, an arterial blood gas analysis and a gastroduodenal occult blood test were conducted. Lung samples were assessed for histology, cytokine transcripts, regulated cell death, and alveolar-capillary permeability. RESULTS: The 4-hour hypotension model had an intraoperative mortality rate of 17.7% (41/231) and a stress-ulcer bleeding rate of 15.3% (29/190). No signs of alveolar flooding were observed in both models. Four-hour hypotension without stress ulcer showed normal oxygenation and permeability but increased interstitial infiltration, transcription of Tnf and Il1b, phosphorylation of MLKL and RIPK3, and cleaved caspase 3 compared with 4-hour pulmonary artery ligation and naïve control. Animals that developed stress ulcer presented with worse pulmonary infiltration, intracellular edema, and oxygenation but just slightly increased permeability. Immunoblotting showed significant upregulations of protein expression and phosphorylation of MLKL and RIPK3, cleaved Caspase-3, but not its prototype in 4-hour hypotension with stress ulcer. CONCLUSIONS: Hypotensive lung injury is essentially a nonhypoxic ischemia-reperfusion injury enhanced by systemic responses. It is predominated by necroptosis-induced inflammation rather than necrosis-induced diffuse alveolar-capillary damage.

Cancer-associated fibroblasts-derived lncRNA signature as a putative biomarker in breast cancer.

Long noncoding RNAs (lncRNAs) have been reported to play a key role in regulating tumor microenvironment and immunity. Cancer-associated fibroblasts (CAFs) are abundant in many tumors. However, the functional and clinical significance of lncRNAs specifically expressed in CAFs has not been fully elucidated. In this study, we identified a list of 95 CAF-specific lncRNAs (FibLnc), including HHLA3, TP53TG1, ST7-AS1, LINC00536, ZNF503-AS1, MIR22HG, and MAPT-AS1, based on immune cell transcriptome expression profiling data. Based on the Cancer Genome Atlas and Gene Expression Omnibus datasets, we found that the FibLnc score predicted differences in overall patient survival and performed well in multiple datasets. FibLnc score was associated with the clinical stage of patients with breast cancer but did not significantly correlate with the PAM50 classification. Functional analysis showed that FibLnc was positively correlated with signaling pathways associated with malignant tumor progression. In addition, FibLnc was positively correlated with tumor mutational load and could predict immunotherapy response in patients with breast cancer receiving anti-PD-1 or anti-CTLA4 therapy. Our proposed FibLnc score was able to reflect the status of the immune environment and immunotherapeutic response in breast cancer, which could help explore potential therapeutic decisions and regulatory mechanisms of CAF-specific lncRNAs.

LncRNA PSR Regulates Vascular Remodeling Through Encoding a Novel Protein Arteridin.

RATIONALE: Vascular smooth muscle cells (VSMCs) phenotype switch from contractile to proliferative phenotype is a pathological hallmark in various cardiovascular diseases. Recently, a subset of long noncoding RNAs was identified to produce functional polypeptides. However, the functional impact and regulatory mechanisms of long noncoding RNAs in VSMCs phenotype switching remain to be fully elucidated. OBJECTIVES: To illustrate the biological function and mechanism of a VSMC-enriched long noncoding RNA and its encoded peptide in VSMC phenotype switching and vascular remodeling. RESULTS: We identified a VSMC-enriched transcript encoded by a previously uncharacterized gene, which we called phenotype switching regulator (PSR), which was markedly upregulated during vascular remodeling. Although PSR was annotated as a long noncoding RNA, we demonstrated that the lncPSR (PSR transcript) also encoded a protein, which we named arteridin. In VSMCs, both arteridin and lncPSR were necessary and sufficient to induce phenotype switching. Mechanistically, arteridin and lncPSR regulate downstream genes by directly interacting with a transcription factor YBX1 (Y-box binding protein 1) and modulating its nuclear translocation and chromatin targeting. Intriguingly, the PSR transcription was also robustly induced by arteridin. More importantly, the loss of PSR gene or arteridin protein significantly attenuated the vascular remodeling induced by carotid arterial injury. In addition, VSMC-specific inhibition of lncPSR using adeno-associated virus attenuated Ang II (angiotensin II)-induced hypertensive vascular remodeling. CONCLUSIONS: PSR is a VSMC-enriched gene, and its transcript IncPSR and encoded protein (arteridin) coordinately regulate transcriptional reprogramming through a shared interacting partner, YBX1. This is a previously uncharacterized regulatory circuit in VSMC phenotype switching during vascular remodeling, with lncPSR/arteridin as potential therapeutic targets for the treatment of VSMC phenotype switching-related vascular remodeling.

Iliosacral screw fixation of pelvic ring disruption with tridimensional patient-specific template guidance.

INTRODUCTION: Posterior pelvic ring disruption includes sacral fractures, sacroiliac joint fracture dislocations and ilium fractures. Percutaneous iliosacral screw fixation of sacral fractures and sacraoiliac joint fracture dislocations have been prevailing, it has the advantages of minimal invasiveness, less blood loss and low wound infection rate. HYPOTHESIS: This study was to evaluate the application of three-dimensional (3D) printed patient-specific guide template in closed reduction and iliosacral screw fixation of posterior pelvic ring disruption. MATERIAL AND METHODS: The data of patients, who were treated with closed reduction and iliosacral screw fixation of posterior pelvic ring disruption with the assistance of 3D printed guide template from December 2014 to September 2018, were collected. The screw placement time, fluoroscopy time, intraoperative blood loss, fracture reduction, screw position, and functional assessment were recorded. RESULTS: There were 17 cases of unstable pelvic fractures,and 20 screws were inserted for fixation of sacral fractures or sacroiliac joint dislocations, with bilateral screw placement in 3 cases. The average time for each screw placement was 45.9±8.6min (30-60min). The average fluoroscopy time for each screw insertion was 50.3±19.7s (24-96 s). The mean blood loss for each screw placement was 32.0±11.1ml (20-50ml). According to Matta scale, the fracture reduction was graded as excellent in all the 17 cases. According to the modified Gras classification, the 3D CT reconstruction of the pelvis demonstrated Grade 1 for 18 screws and Grade 2 for 2 screw. Functional outcome 1 year postoperatively was rated as 15 excellent and 2 good, according to the Majeed functional scale. DISCUSSION: It is feasible and safe to stabilize the posterior pelvic ring disruption using iliosacral screw fixation under assistance of the 3D printed guide template. It could reduce fluoroscopy time, screw placement time and intraoperative blood loss and achieve good postoperative recovery. LEVEL OF PROOF: IV; Retrospective study.

Screening and prioritizing substances in groundwater in the Beijing-Tianjin-Hebei region of the North China Plain based on exposure and hazard assessments.

Screening and prioritizing hazardous substances in groundwater is crucial to monitor and control groundwater quality. Total of 283 substances were determined in 213 groundwater samples from the Beijing-Tianjin-Hebei region during 2019-2020. 184 substances were screened as candidates. 22 prioritizing indicators were evaluated and scored for the candidates to reflect their occurrence, mobility, persistence, bioaccumulation, acute and chronic ecotoxicities with different trophic levels, and long-term human health effects. Multi-attribute decision-making technologies were applied to prioritize these candidates, including analytic hierarchy process (AHP), TOPSIS and VIKOR. Greater weightings in AHP were assigned to attributes of occurrence and acute toxicity by experts' judgment. Hierarchical cluster analysis and principal component analysis were used to transform initial matrix with the 22 indicators into an orthogonalized matrix with 6 principal components, which represented general toxicity to aquatic organism and mammal, bioaccumulation, carcinogenicity & mutagenicity, persistence, and teratogenicity & endocrine, respectively. VIKOR and TOPSIS results were similar, but different from the AHP ranking. Two filter criteria harmonized their difference. Twenty-three substances were proposed as the priority substance with high hazard and potential exposure, and nitrate-nitrogen and ammonia-nitrogen were selected as additional priority substance frequently and extensively exceeding official groundwater quality standard on the regional scale.

Novel Design of the Chimeric Deep Inferior Epigastric Artery Perforator Flap that Provides for Three-Dimensional Reconstruction of Composite Tissue Defects of the Heel in Children.

OBJECTIVE: The aim of the present study was to report a novel design of the chimeric deep inferior epigastric artery perforator flap (DIEP) to achieve dead space filling, Achilles tendon bridging, and skin resurfacing simultaneously with minimal donor-site morbidity. METHODS: From September 2012 to May 2016, a retrospective study was carried out on six pediatric patients with composite soft tissue defects of the heel that were repaired with the chimeric DIEP flap. The chimeric flap design included a flap of the anterior sheath of the rectus, a block of rectus muscle, and a large skin paddle. All the parts were supplied by a common artery. After harvesting the flap, all element parts were inserted at the corresponding sites in a tension-free manner. With one set of vessel anastomoses at the recipient site, accurate repair with tendon reconstruction, dead space elimination, and wound covering were accomplished. The donor site incisions were closed initially. Data on patient age, medical history, injury severity, defect size, flap dimensions, recipient vessels, donor site closure, complications, and follow-up were collected and reviewed. RESULTS: Five of the six chimeric DIEP flaps survived without complications. The remaining one case experienced partial necrosis of the skin paddle caused by venous congestion, which healed after routine dressing changes. Primary donor site closure was accomplished in all cases. The mean follow-up was 18.6 months (range, 10-36 months). Five patients had satisfactory aesthetic and functional outcomes; one patient needed a secondary debulking procedure. Compared to the unaffected side, the affected side showed no obvious difference for ankle movement, tiptoe function, and patient gait during the follow-up period. Good ankle function was observed in all patients. There was no donor site breakdown, with only a slightly noticeable linear scar. CONCLUSION: The chimeric DIEP flap reduced the operative time, solved the problem of deficiency of recipient vessels, and attained satisfactory functional and aesthetic outcomes with low donor site morbidity. Therefore, it is a promising option for three-dimensional reconstruction of composite defects with dead space and Achilles tendon defects as well as skin loss in children.

Long Noncoding RNA Ahit Protects Against Cardiac Hypertrophy Through SUZ12 (Suppressor of Zeste 12 Protein Homolog)-Mediated Downregulation of MEF2A (Myocyte Enhancer Factor 2A).

BACKGROUND: Long noncoding RNA (lncRNA) can regulate various physiological and pathological processes through multiple molecular mechanisms in cis and in trans. However, the role of lncRNAs in cardiac hypertrophy is yet to be fully elucidated. METHODS: A mouse lncRNA microarray was used to identify differentially expressed lncRNAs in the mouse hearts following transverse aortic constriction-induced pressure overload comparing to the sham-operated samples. The direct impact of one lncRNA, Ahit, on cardiomyocyte hypertrophy was characterized in neonatal rat cardiomyocytes in response to phenylephrine by targeted knockdown and overexpression. The in vivo function of Ahit was analyzed in mouse hearts by using cardiac-specific adeno-associated virus, serotype 9-short hairpin RNA to knockdown Ahit in combination with transverse aortic constriction. Using catRAPID program, an interaction between Ahit and SUZ12 (suppressor of zeste 12 protein homolog) was predicted and validated by RNA immunoprecipitation and immunoblotting following RNA pull-down. Chromatin immunoprecipitation was performed to determine SUZ12 or H3K27me3 occupancy on the MEF2A (myocyte enhancer factor 2A) promoter. Finally, the expression of human Ahit (leukemia-associated noncoding IGF1R activator RNA 1 [LUNAR1]) in the serum samples from patients of hypertrophic cardiomyopathy was tested by quantitative real-time polymerase chain reaction. RESULTS: A previously unannotated lncRNA, antihypertrophic interrelated transcript (Ahit), was identified to be upregulated in the mouse hearts after transverse aortic constriction. Inhibition of Ahit induced cardiac hypertrophy, both in vitro and in vivo, associated with increased expression of MEF2A, a critical transcriptional factor involved in cardiac hypertrophy. In contrast, overexpression of Ahit significantly attenuated stress-induced cardiac hypertrophy in vitro. Furthermore, Ahit was significantly upregulated in serum samples of patients diagnosed with hypertensive heart disease versus nonhypertrophic hearts (1.46±0.17 fold, P=0.0325). Mechanistically, Ahit directly bound and recruited SUZ12, a core PRC2 (polycomb repressive complex 2) protein, to the promoter of MEF2A, triggering its trimethylation on H3 lysine 27 (H3K27me3) residues and mediating the downregulation of MEF2A, thereby preventing cardiac hypertrophy. CONCLUSIONS: Ahit is a lncRNA with a significant role in cardiac hypertrophy regulation through epigenomic modulation. Ahit is a potential therapeutic target of cardiac hypertrophy.

SODs involved in the hormone mediated regulation of H2O2 content in Kandelia obovata root tissues under cadmium stress.

Cadmium (Cd) pollution in mangrove wetlands has received increasing attention as urbanization expands rapidly. As a dominant mangrove species, Kandelia obovata is highly tolerant to Cd toxicity. Plant hormones and superoxide dismutase (SODs) play critical roles in the response to heavy metal stress in K. obovata roots. Although theirs important influence have been reported, the regulation mechanism between SODs and plant hormones in Cd detoxification by K. obovata roots remains limited. Here, we investigated relationships among SOD, plant hormones, and Cd tolerance in K. obovata roots exposed to Cd. We found that Cd was retained in the epidermis and exodermis of roots, and the epidermis and exodermis had highest hydrogen peroxide (H2O2) content and SOD activity. Similarly, SOD isozymes also exhibited distinct activity in the different parts of root. Overexpressed KoCSD3 and KoFSD2 individually in Nicotiana benthamiana revealed that different SOD members contributed to H2O2 content regulation by promote the activity of downstream antioxidant enzymes under Cd treatment. In addition, assays on the effects of hormones showed that increased endogenous indole-3-acetic acid (IAA) was observed in the cortex and stele, whereas the abscisic acid (ABA) content was enhanced in the epidermis and exodermis in roots during Cd treatment. The results of exogenous hormones treatment indicated that KoFSD2 upregulated under ABA and IAA treatment, but KoCSD3 only induced by ABA stimulation. Taken together, our results reveal the relationship between SODs and plant hormones, which expands the knowledge base regarding KoSODs response to plant hormones and mediating H2O2 concentration under Cd stress.

Analysis of anatomical changes and cadmium distribution in Aegiceras corniculatum (L.) Blanco roots under cadmium stress.

Heavy metal stress changes the morphological and anatomical structure of plant organs. In this study, we determined the anatomical changes and Cd distribution in the roots of Aegiceras corniculatum (L.) Blanco (Black mangrove) under Cd stress. The results showed that Cd levels in A. corniculatum root tissues decreased in the following order: endodermis > pith > xylem > epidermis and exodermis > phloem > cortex. The endodermis secondary casparian strip replaces exodermis casparian strip and plays a role in the "retardation mechanism", which sort of compensates for the missing exodermis retardation effect. The xylem and pith both show high affinity for Cd and contain enriched Cd. This creates a low-Cd environment for phloem and protects the nutrient transport function of the vasculature against Cd toxicity. The present study provides new evidences suggesting that Cd regional enrichment and anatomical structure changes are an adaptive strategy of mangrove plants to HM tolerance.

Regulation of Cholesterol Homeostasis by a Novel Long Non-coding RNA LASER.

Genome-wide association studies (GWAS) have identified many genetic variants in genes related to lipid metabolism. However, how these variations affect lipid levels remains elusive. Long non-coding RNAs (lncRNAs) have been implicated in a variety of biological processes. We hypothesize lncRNAs are likely to be located within disease or trait-associated DNA regions to regulate lipid metabolism. The aim of this study was to investigate whether and how lncRNAs in lipid- associated DNA regions regulate cholesterol homeostasis in hepatocytes. In this study, we identified a novel long non-coding RNA in Lipid Associated Single nucleotide polymorphism gEne Region (LASER) by bioinformatic analysis. We report that LASER is highly expressed in both hepatocytes and peripheral mononuclear cells (PBMCs). Clinical studies showed that LASER expression is positively related with that of cholesterol containing apolipoprotein levels. In particular, we found that LASER is positively correlated with plasma PCSK9 levels in statin free patients. siRNAs mediated knock down of LASER dramatically reduces intracellular cholesterol levels and affects the expression of genes involved in cholesterol metabolism. Transcriptome analyses show that knockdown of LASER affects the expression of genes involved in metabolism pathways. We found that HNF-1α and PCSK9 were reduced after LASER knock-down. Interestingly, the reduction of PCSK9 can be blocked by the treatment of berberine, a natural cholesterol-lowering compound which functions as a HNF-1α antagonist. Mechanistically, we found that LASER binds to LSD1 (lysine-specific demethylase 1), a member of CoREST/REST complex, in nucleus. LASER knock-down enhance LSD1 targeting to genomic loci, resulting in decreased histone H3 lysine 4 mono-methylation at the promoter regions of HNF-1α gene. Conversely, LSD1 knock-down abolished the effect of LASER on HNF-1α and PCSK9 expressions. Finally, we found that statin treatment increased LASER expression, accompanied with increased PCSK9 expression, suggesting a feedback regulation of cholesterol on LASER expression. This observation may partly explain the statin escape during anti-cholesterol treatment. These findings identified a novel lncRNA in cholesterol homeostasis. Therapeutic targeting LASER might be an effective approach to augment the effect of statins on cholesterol levels in clinics.

Prolonged Cold Ischemia Induces Necroptotic Cell Death in Ischemia-Reperfusion Injury and Contributes to Primary Graft Dysfunction after Lung Transplantation.

Primary graft dysfunction (PGD) is a major cause of morbidity and mortality after lung transplantation. Ischemia-reperfusion injury (IRI) is a key event that contributes to PGD, though complex interactions affect donor lungs status, such as preceding brain death (BD), hemorrhagic shock (HS), and pre-engraftment lung management, the latter recognized as important risk factors for PGD. We hypothesized that a multi-hit isogenic mouse model of lung transplantation is more closely linked to PGD than IRI alone. Left lung transplants were performed between inbred C57BL/6 mice. A one-hit model of IRI was established by inducing cold ischemia (CI) of the donor lungs at 0°C for 1, 72, or 96 hours before engraftment. Multi-hit models were established by inducing 24 hours of HS and/or 3 hours of BD before 24 hours of CI. The recipients were killed at 24 hours after transplant and lung graft samples were analyzed. In the one-hit model of IRI, up to 72-hour CI time resulted in minimal cellular infiltration near small arteries after 24-hour reperfusion. Extension of CI time to 96 hours led to increased cellular infiltration and necroptotic pathway activation, without evidence of apoptosis, after 24-hour reperfusion. In a multi-hit model of PGD, "HS + BD + IRI" demonstrated increased lung injury, cellular infiltration, and activation of necroptotic and apoptotic pathways compared with IRI alone. Treatment with an inhibitor of receptor-interacting protein kinase 1 kinase, necrostatin-1, resulted in a significant decrease of downstream necroptotic pathway activation in both single- and multi-hit models of IRI. Thus, activation of necroptosis is a central event in IRI after prolonged CI, though it may not be sufficient to cause PGD alone. Pathological evaluation of donor lungs after CI-induced IRI, in conjunction with pre-engraftment donor lung factors in our multi-hit model, demonstrated early evidence of lung injury consistent with PGD. Our findings support the premise that pre-existing donor lung status is more important than CI time alone for inflammatory pathway activation in PGD, which may have important clinical implications for donor lung retrieval.

Humanin analog enhances the protective effect of dexrazoxane against doxorubicin-induced cardiotoxicity.

The chemotherapeutic effect of doxorubicin (Dox) is limited by cumulative dose-dependent cardiotoxicity in cancer survivors. Dexrazoxane (DRZ) is approved to prevent Dox-induced cardiotoxicity. Humanin and its synthetic analog HNG have a cytoprotective effect on the heart. To investigate the cardioprotective efficacy of HNG alone or in combination with DRZ against Dox-induced cardiotoxicity, 80 adult male mice were randomly divided into 8 groups to receive the following treatments via intraperitoneal injection: saline dailym HNG (5 mg/kg) daily, DRZ (60 mg/kg) weekly, Dox (3 mg/kg) weekly, DRZ + HNG, Dox + HNG, Dox + DRZ, and Dox + HNG + DRZ. Echocardiograms were performed before and at 4, 8, and 9.5 wk after the beginning of treatment. All mice were euthanized at 10 wk. In the absence of Dox, HNG, DRZ, or DRZ + HNG had no adverse effect on the heart. Dox treatment caused decreases in ejection fraction and cardiac mass and increases in cardiomyocyte apoptosis and intracardiac fibrosis. HNG or DRZ alone blunted the Dox-induced decrease in left ventricle posterior wall thickness and modestly ameliorated the Dox-induced decrease in ejection fraction. HNG + DRZ significantly ameliorated Dox-induced decreases in ejection function, cardiac fibrosis, and cardiac mass. Using a targeted analysis for the mitochondrial gene array and protein expression in heart tissues, we demonstrated that HNG + DRZ reversed DOX-induced altered transcripts that were biomarkers of cardiac damage and uncoupling protein-2. We conclude that HNG enhances the cardiac protective effect of DRZ against Dox-induced cardiotoxicity. HNG + DRZ protects mitochondria from Dox-induced cardiac damage and blunts the onset of cardiac dysfunction. Thus, HNG may be an adjuvant to DRZ in preventing Dox-induced cardiotoxicity. NEW & NOTEWORTHY Doxorubicin (Dox) is commonly used for treating a wide range of human cancers. However, cumulative dosage-dependent carditoxicity often limits its clinical applications. We demonstrated in this study that treating young adult male mice with synthetic humanin analog enhanced the cardiac protective effect of dexrazoxane against chemotherapeutic agent Dox-induced cardiac dysfunction. Thus, humanin analog can potentially serve as an adjuvant to dexrazoxane in more effectively preventing Dox-induced cardiac dysfunction and cardiomyopathy.

Distribution correlations of cadmium to calcium, phosphorus, sodium and chloridion in mangrove Aegiceras corniculatum root tissues.

Nutriment distributions might influence Cd distribution and Cd tolerance in mangrove plant roots. To demonstrate this, Aegiceras corniculatum was stressed by Cd, and the distributions of Cd, Ca, P, Na and Cl in plant roots were detected with the aid of SEM-EDX. It was found that endodermis, pith and xylem were the predominant tissues for retardation and regional enrichment of Cd. Na and Cl distributions suggest a critical role of salt resistance tissues on Cd tolerance in roots. P participated in Cd retardation and regional enrichment of endodermis and xylem. P, Na, Cl and Ca distribution had a high correlation to that of Cd in roots. The synergetic accumulation between Ca and Cd could be a crucial mechanism for Cd tolerance in A. corniculatum roots. In conclusion, the research of Cd and nutriment distributions in A. corniculatum roots deepens the understanding on Cd tolerance in mangrove plants.

Co-effect of phosphorus and cadmium interaction on fraction distribution and accumulation of phosphorus in mangrove-sediment system.

Mangrove [Kandelia obovata (S. L.)] seedlings were cultivated in rhizoboxes under different rates of phosphorus (P) and cadmium (Cd) level. The speciation distributions of P both in the rhizosphere and non-rhizosphere sediments were examined using sequential extraction procedures. P contents in different K. obovata (S.L.) tissues were also determined. Results showed that considerable differences existed in P speciation distribution between rhizosphere and bulk sediments. A higher proportion of iron-bound phosphate (Fe-P) was found in the rhizosphere sediments, while a relatively higher concentration of exchangeable phosphate (Ex-P) and Aluminum-bound phosphate was found in the bulk sediments. P accumulation in plant tissues was significantly positively correlated to Ex-P and Fe-P. Results indicated that root activities play an important role in the P cycling. And the coexistence of P and Cd induced higher P accumulation in mangrove plants. It is suggested that the root-induced chemical and biological changes in the rhizosphere environment play an important role in enhancing the bioavailability of soil P.

Circulating 'lncRNA OTTHUMT00000387022' from monocytes as a novel biomarker for coronary artery disease.

AIMS: Long non-coding RNAs (lncRNAs) have been found to be involved in the pathogenesis of coronary artery disease (CAD). However, it remains to be established whether or not circulating lncRNAs can serve as biomarkers of CAD. METHODS AND RESULTS: Using a microarray-based lncRNA expression profiling, we found 86 lncRNAs that were differentially expressed in circulating peripheral blood monocytes and plasma from 15 CAD patients and 15 control subjects. After choosing a consistent criterion (average normalized intensity ≥7 with significance <0.005) and confirmed by quantitative PCR, only three lncRNAs (CoroMarker, BAT5, and IL21R-AS1) remained as candidate CAD biomarkers. Using the analysis of area under the curve (AUC) of the receiver-operating characteristic in another pilot group and another larger cohort, CoroMarker was found to be the best candidate biomarker for CAD with an AUC of 0.920 and 95% confidence interval of 0.892-0.947. CoroMarker was independent from known CAD risk factors and other cardiovascular diseases. In a prospective study, we found that the sensitivity and specificity of CoroMarker were 76 and 92.5%, respectively. Functional enrichment analysis showed CoroMarker to be clustered with genes positively associated with signal transduction, transmembrane transport, synaptic transmission, and innate immunity and negatively associated with inflammation. These findings were validated in THP-1 cells; CoroMarker siRNA treatment decreased the concentrations of proinflammatory cytokines [interleukin (IL)-1ß, IL-6, and tumour necrosis factor α] in the culture medium. CONCLUSION: The present study suggests that CoroMarker is a novel and specific biomarker of CAD.

Influence of the phenols on the biogeochemical behavior of cadmium in the mangrove sediment.

Phenols exert a great influence on the dynamic process of Cd in the soil-plant interface. We investigated the influence of phenols on the biogeochemical behavior of cadmium in the rhizosphere of Avicennia marina (Forsk) Vierh. All combinations of four levels of cadmium (0, 1, 2 and 4 mg/kg DW) and two levels of phenol (0 and 15 mg/kg DW) were included in the experimental design. We found that phenols facilitated increasing concentrations of exchangeable cadmium (Ex-Cd), acid volatile sulfide (AVS) and reactive solid-phase Fe (II) in sediments, and iron in plants, but inhibited Cd accumulation in iron plaque and roots. The concentrations of AVS and reactive solid-phase Fe (II) were significantly positively correlated with Cd treatment. As for the biogeochemical behavior of Cd in mangrove sediments, this research revealed that phenols facilitated activation and mobility of Cd. They disturbed the "source-sink" balance of Cd and turned it into a "source", whilst decreasing Cd absorption in A. marina. Additionally, phenols facilitated iron absorption in the plant and alleviated the Fe limit for mangrove plant growth.

[Experimental study of the transferred keratinocytes transplanted on biomembrane].

OBJECTIVE: To search an ideal carrier of transferred keratinocytes for transplantation. METHODS: The transferred keratinocytes were seeded on the surfaces of the artificial dermis and the silicone membrane and cultured in vitro for 2 weeks. The growth of the keratinocytes was observed by microscope and scanning electron microscope. RESULTS: The keratinocytes implanted on the artificial dermis began to rupture and died after 2 to 3 days. While the keratinocytes adhered well on the surface of silicone membrane with pseudopodia formation after 1 week under scanning electron microscope, and the cells kept normal morphological and proliferative properties 2 weeks later. CONCLUSION: The silicone membrane can be applied as an useful carrier for the keratinocytes transplantation.