DNA methyltransferases-associated long non-coding RNA PRKCQ-AS1 regulate DNA methylation in myelodysplastic syndrome.

INTRODUCTION: Myelodysplastic syndrome (MDS) is a group of clonal hematopoietic stem cell disorders. DNA hypermethylation is considered to be the key mechanism of pathogenesis for MDS. Studies have demonstrated that DNA methylation can be regulated by the co-effect between long non-coding RNAs (lncRNAs) and DNA methyltransferases (DNMTs). The aim of this study was to identify DNMTs-associated differentially expressed (DE) lncRNAs, which may be a novel diagnostic and therapeutic target for MDS. METHODS: Two gene expression profile datasets (GSE4619 and GSE19429) were downloaded from the Gene Expression Omnibus (GEO) database. Systematic bioinformatics analysis was conducted. Then we verified the expression of PRKCQ-AS1 in MDS patients and features in SKM-1 cells. RESULTS: Bioinformatics analysis revealed that the DNMT-associated DE-lncRNA PRKCQ-AS1 was functionally related to DNA methylation. The target genes of PRKCQ-AS1 associated with DNA methylation are mainly methionine synthetase (MTR) and ten-eleven-translocation 1 (TET1). Moreover, the high expression of PRKCQ-AS1 was verified in real MDS cases. Further cellular analysis in SKM-1 cells revealed that overexpressed PRKCQ-AS1 promoted methylation levels of long interspersed nuclear element 1 (LINE-1) and cell proliferation, and apparently elevated both mRNA and protein levels of MTR and TET1, while knockdown of PRKCQ-AS1 showed opposite trend in SKM-1 cells. CONCLUSION: DNMT-associated DE-lncRNA PRKCQ-AS1 may affects DNA methylation levels by regulating MTR and TET1.

Pyroptosis in sepsis induced organ dysfunction.

As an uncontrolled inflammatory response to infection, sepsis and sepsis induced organ dysfunction are great threats to the lives of septic patients. Unfortunately, the pathogenesis of sepsis is complex and multifactorial, which still needs to be elucidated. Pyroptosis is a newly discovered atypical form of inflammatory programmed cell death, which depends on the Caspase-1 dependent classical pathway or the non-classical Caspase-11 (mouse) or Caspase-4/5 (human) dependent pathway. Many studies have shown that pyroptosis is related to sepsis. The Gasdermin proteins are the key molecules in the membrane pores formation in pyroptosis. After cut by inflammatory caspase, the Gasdermin N-terminal fragments with perforation activity are released to cause pyroptosis. Pyroptosis is closely related to the occurrence and development of sepsis induced organ dysfunction. In this review, we summarized the molecular mechanism of pyroptosis, the key role of pyroptosis in sepsis and sepsis induced organ dysfunction, with the aim to bring new diagnostic biomarkers and potential therapeutic targets to improve sepsis clinical treatments.

HACE1 expression in heart failure patients might promote mitochondrial oxidative stress and ferroptosis by targeting NRF2.

BACKGROUND: Heart failure is a prevalent and life-threatening medical condition characterized by abnormal atrial electrical activity, contributing to a higher risk of ischemic stroke. Atrial remodelling, driven by oxidative stress and structural changes, plays a central role in heart failure progression. Recent studies suggest that HACE1, a regulatory gene, may be involved in cardiac protection against heart failure. METHODS: Clinical data analysis involved heart failure patients, while an animal model utilized C57BL/6J mice. RT-PCR, microarray analysis, histological examination, ELISA, and Western blot assays were employed to assess gene and protein expression, oxidative stress, and cardiac function. Cell transfection and culture of mouse atrial fibroblasts were performed for in-vitro experiments. RESULTS: HACE1 expression was reduced in heart failure patients and correlated negatively with collagen levels. In mouse models, HACE1 up-regulation reduced oxidative stress, mitigated fibrosis, and improved cardiac function. Conversely, HACE1 knockdown exacerbated oxidative stress, fibrosis, and cardiac dysfunction. HACE1 also protected against ferroptosis and mitochondrial damage. NRF2, a transcription factor implicated in oxidative stress, was identified as a target of HACE1, with HACE1 promoting NRF2 activity through ubiquitination. CONCLUSIONS: HACE1 emerges as a potential therapeutic target and diagnostic marker for heart failure. It regulates oxidative stress, mitigates cardiac fibrosis, and protects against ferroptosis and mitochondrial damage. The study reveals that HACE1 achieves these effects, at least in part, through NRF2 activation via ubiquitination, offering insights into novel mechanisms for heart failure pathogenesis and potential interventions.

Fault Diagnosis of Medium Voltage Circuit Breakers Based on Vibration Signal Envelope Analysis.

In modern power systems or new energy power stations, the medium voltage circuit breakers (MVCBs) are becoming more crucial and the operation reliability of the MVCBs could be greatly improved by online monitoring technology. The purpose of this research is to put forward a fault diagnosis approach based on vibration signal envelope analysis, including offline fault feature training and online fault diagnosis. During offline fault feature training, the envelope of the vibration signal is extracted from the historic operation data of the MVCB, and then the typical fault feature vector M is built by using the wavelet packet-energy spectrum. In the online fault diagnosis process, the fault feature vector T is built based on the extracted envelope of the real-time vibration signal, and the MVCB states are assessed by using the distance between the feature vectors T and M. The proposed method only needs to handle the envelope of the vibration signal, which dramatically reduces the signal bandwidth, and then the cost of the processing hardware and software could be cut down.

Hygroscopic Tunable Multishape Memory Effect in Cellulosic Macromolecular Networks with a Supramolecular Mesophase.

Tunable multishape memory polymers offer intriguing opportunities for memorizing multiple temporary shapes with tunable transition temperatures from one material composition. However, such multishape memory effects have been exclusively correlated with the thermomechanical behaviors of polymers, significantly limiting their applications in heat-sensitive scenarios. Here we report a nonthermal tunable multishape memory effect in covalently cross-linked cellulosic macromolecular networks, which spontaneously organize into supramolecular mesophases by water evaporation induced self-assembly. The supramolecular mesophase endows the network with a broad, reversible hygromechanical response combined with a unique moisture memory effect at ambient temperature, enabling diverse multishape memory behaviors (dual-, triple-, and quadruple-shape memory) under highly tunable and independent control of relative humidity (RH) alone. Significantly, such a hygroscopic tunable multishape memory effect readily extends the implications of shape memory polymers beyond the conventional thermomechanical regimes with potential advantages for biomedical applications.

A pilot study on pyroptosis related genes in peripheral blood mononuclear cells of non-small cell lung cancer patients.

OBJECTIVE: To investigate the GSDMD, CASP1, CASP4 and CASP5 expression in peripheral blood mononuclear cells of non-small cell lung cancer patients and analyze their clinical significance. METHODS: 71 non-small cell lung cancer patients were selected as the study group and 50 healthy individuals as the control group. The GSDMD, CASP1, CASP4 and CASP5 expression in peripheral blood mononuclear cells of the two groups were detected by real-time fluorescence quantitative PCR. The GSDMD, CASP1, CASP4, CASP5 expression and their relationship with the clinical characteristics of the patients were analyzed. RESULTS: Compared with the control group, the GSDMD, CASP4 and CASP5 expression in PBMCs of lung cancer patients was significantly higher(P < 0.05). Lymph node metastasis had significant difference with the CASP4 and GSDMD expression (P < 0.05); tumor volume had significant difference with CASP1 and CASP5 expression (P < 0.05). The areas under predictive ROC curve of the GSDMD, CASP1, CASP4, and CASP5 mRNA expression were 0.629(P < 0.05), 0.574(p > 0.05), 0.701(P < 0.05) and 0.628(P < 0.05), the sensitivity values were 84.5%, 67.6% 43.7%, and 84.3%;the specificity values were 42%, 52%, 84% and 64%, respectively. CONCLUSION: GSDMD, CASP1, CASP4 and CASP5 gene expression are highly increased in PBMCs of non-small cell lung cancer patients and their expression are closely related to the clinical characteristics of patients. The early enhanced pyroptosis-related gene expression may be potential molecular markers for early diagnosis of non-small cell lung cancer.

Validation of reference genes for the normalization of the RT-qPCR in peripheral blood mononuclear cells of septic patients.

Objective: To screen and validate reference genes suitable for gene mRNA expression study in peripheral blood mononuclear cells (PBMCs) between septic patients and healthy controls (HC). Methods: Total RNA in PBMCs was extracted and RT-qPCR was used to determine the mRNA expression profiles of 9 candidate genes, including ACTB, B2M, GAPDH, GUSB, HPRT1, PGK1, RPL13A, SDHA and YWHAZ. The genes expression stabilities were assessed by both geNorm and NormFinder software. Results: YWHAZ was the most stable gene among the 9 candidate genes evaluated by both geNorm and NormFinder in mixed and sepsis groups. The most stable gene combination in mixed group analyzed by geNorm was the combination of GAPDH, PKG1 and YWHAZ, while that in sepsis group was the combination of ACTB, PKG1 and YWHAZ. Conclusion: Our first systematic analysis of the reference genes in PBMC of septic patients suggested YWHAZ was the best candidate. The combination of ACTB, PKG1 and YWHAZ could improve RT-qPCR accuracy in septic patients. Our results identified the most stable reference genes to standardize RT-qPCR of sepsis patients, which can serve as a useful tool for gene function exploration in the future.

Mechanism and intervention of murine transfusion-related acute lung injury caused by anti-CD36 antibodies.

Anti-CD36 Abs have been suggested to induce transfusion-related acute lung injury (TRALI) upon blood transfusion, particularly in Asian populations. However, little is known about the pathological mechanism of anti-CD36 Ab-mediated TRALI, and potential therapies have not yet been identified. Here, we developed a murine model of anti-CD36 Ab-mediated TRALI to address these questions. Administration of mouse mAb against CD36 (mAb GZ1) or human anti-CD36 IgG, but not GZ1 F(ab')2 fragments, induced severe TRALI in Cd36+/+ male mice. Predepletion of recipient monocytes or complement, but not neutrophils or platelets, prevented the development of murine TRALI. Moreover, plasma C5a levels after TRALI induction by anti-CD36 Abs increased more than 3-fold, implying a critical role of complement C5 activation in the mechanism of Fc-dependent anti-CD36-mediated TRALI. Administration of GZ1 F(ab')2, antioxidant (N-acetyl cysteine, NAC), or C5 blocker (mAb BB5.1) before TRALI induction completely protected mice from anti-CD36-mediated TRALI. Although no significant amelioration in TRALI was observed when mice were injected with GZ1 F(ab')2 after TRALI induction, significant improvement was achieved when mice were treated postinduction with NAC or anti-C5. Importantly, anti-C5 treatment completely rescued mice from TRALI, suggesting the potential role of existing anti-C5 drugs in the treatment of patients with TRALI caused by anti-CD36.

Atomic-Scale Engineering of CuOx-Au Interfaces over AuCu Single-Nanoparticles.

A face-centered tetragonal (fct) AuCu particle with a size of 7.1 nm and an Au/Cu molar ratio of 1/1 was coated by a silica shell of 6 nm thickness. Segregation of Cu atoms from the metal particle under an oxidative atmosphere precisely mediated the CuOx-Au interfacial structure by simply varying the temperature. As raising the temperature from 473 to 773 K, more Cu atoms emigrated from the AuCu particle and were oxidized into CuOx layers that grew up to 0.8 nm in thickness. Simultaneously, the size of the Au-rich particle lowered moderately while the crystalline structure transformed from the fct phase into the face-centered cubic (fcc) phase. The CuOx-Au interface shifted from the CuOx monolayer bound to Au single-atoms to Au@CuOx core-shell geometry, while the catalytic activity for CO oxidation at 433 K decreased dramatically. Moreover, a sharp loss in activity was observed as the crystal-phase transition occurred. This change in catalytic performance was ascribed to the geometrical configuration at the interfacial sites: the synergetic effect between the fct-AuCu particle and CuOx monolayer contributed to the much higher activity, whereas the fcc-AuCu/Au particle weakened its interaction with the thicker CuOx layer and thus decreased the activity.

Increased Dp71 in ischemia-reperfusion injured rat heart exerts anti-apoptotic role via enhancing Bcl-2.

For the first time, increased Dp71 in ischemia-reperfusion injured rat heart were identified, both Dp71 mRNA and protein reached its peak expression 8 h after reperfusion. In H2O2 stimulated H9c2 cells, Dp71 mRNA and protein gradually increased and reached a peak at 16 h. Enhanced Dp71 in H9c2 could resist H2O2-induced cell apoptosis, while Dp71 depletion accelerated the apoptosis induced by H2O2. Enhanced Bcl-2 expression and Bcl-2∕Bax protein expression ratio was identified in Dp71 overexpressed H9c2 cells, while knocking down Dp71 significantly decreased the Bcl-2 and Bcl-2∕Bax protein expression ratio. Increased Dp71 can accelerate FAK and p65 phosphorylation, which finally resulted in enhanced Bcl-2 expression and explains the highly possible cardiac protection role of Dp71.

Mechanisms and Influence Factors of Downhole Electrical Heating-Assisted Steam-Assisted Gravity Drainage Production.

Approximately 70% steam-assisted gravity drainage (SAGD) wellpairs have entered into the production phase in China, while due to the fluvial sedimentation environment with strong reservoir heterogeneity, only 53% of the horizontal well section develops a steam chamber. In order to massively recover the bypassed oil and expand the steam chamber along the horizontal section, downhole electrical heating was proposed, and its mechanisms of high temperature-induced rock mechanics change and influence factors are investigated in this study using laboratory experiments and electrical steam hybrid numerical simulation. It is found that the electrical heating-assisted SAGD has four key mechanisms, namely, localized temperature elevation, development of a fixed point steam chamber, localized oil gravity drainage, and petrophysical property improvement. The influence factors include the static and operational factors, in which the permeability ratio is the primary factor for choosing SAGD wellpairs, while the steam injection rate, steam chamber operational pressure, injector and producer pressure difference, adjacent SAGD steam chamber pressure differential, heater surface temperature, and electrical heating period integrally influence the incremental production performance. Through carefully modifying the parameters, the typical SAGD wellpair steam chamber could expand from 67 to 100% along the horizontal section, with an incremental oil rate of 3-5 m3/day, and the cumulative steam/oil ratio decreases from 6.67 to 4.17. The downhole electrical heating is particularly efficient in improving steam chamber conformance in heterogeneous reservoirs and also has significant potential in similar reservoirs developed by horizontal wells.

Fabrication of monodisperse gold-copper nanocubes and AuCu-cuprous sulfide heterodimers by a step-wise polyol reduction.

Monodisperse gold-copper nanocubes and AuCu-cuprous sulfide (Cu1.96S) heterodimers were fabricated by a step-wise polyol reduction with the aid of oleylamine and 1-dodecanethiol. The geometric configuration was mediated by simply varying the Cu/Au atomic ratio: Au-Cu cubes with sizes of 6.4 and 4.3 nm were yielded at Cu/Au atomic ratios of 1/3 and 1/1, respectively; while AuCu-Cu1.96S heterodimer, consisting of a AuCu cube of 4.6 nm and a Cu1.96S sphere of 6.3 nm was obtained at Cu/Au atomic ratio of 3/1. Detailed structural analysis on the intermediate products, collected at different intervals during the synthesis, revealed that small-sized Au seeds formed at 423 K, followed by the growth of Cu and Cu1.96S crystals at 473 K. Oleylamine coordinated to Au3+ and Cu2+ and thus mediated the particle size; while 1-dodecanethiol bonded to Au3+ and directed the cubic morphology. Excessive Cu2+, at the Cu/Au atomic ratio of 3/1, interacted with 1-dodecanethiol and formed Cu1.96S spherical particle that epitaxially grew over the AuCu cube, resulting in a heterodimer structure. Due to the enriched surficial Cu atoms and their electronic interactions with Au atoms, Au-Cu nanocubes and AuCu-Cu1.96S heterodimers showed pronounced activities for the catalytic reduction of 4-nitrophenol to 4-aminophenol with NaBH4 at 298 K.

Experimental and Numerical Investigation on Oil Displacement Mechanism of Weak Gel in Waterflood Reservoirs.

The production performance of waterflood reservoirs with years of production is severely challenged by high water cuts and extensive water channels. Among IOR/EOR methods, weak gel injection is particularly effective in improving the water displacement efficiency and oil recovery. The visualized microscopic oil displacement experiments were designed to comprehensively investigate the weak gel mechanisms in porous media and the numerical simulations coupling equations characterizing weak gel viscosity induced dynamics were implemented to understand its planar and vertical block and movement behaviors at the field scale. From experiments, the residual oil of initial water flooding mainly exists in the form of cluster, column, dead end, and membranous, and it mainly exists in the form of cluster and dead end in subsequent water flooding stage following weak gel injection. The porous flow mechanism of weak gel includes the preferential plugging of large channels, the integral and staged transport of weak gel, and the residual oil flow along pore walls in weak gel displacement. The profile-control mechanism of weak gel is as follows: weak gel selectively enters the large channels, weak gel blocks large channels and forces subsequent water flow to change direction, weak gel uses viscoelastic bulk motion to form negative pressure oil absorption, and the oil droplets converge to form an oil stream, respectively. The numerical simulation indicates that weak gel can effectively reduce the water-oil mobility ratio, preferentially block the high permeability layer and the large pore channels, divert the subsequent water to flood the low permeability layer, and improve the water injection swept efficiency. It is found numerically that a weak gel system is able to flow forward under high-pressure differences in the subsequent water flooding, which can further improve oil displacement efficiency. Unlike the conventional profile-control methods, weak gels make it possible to displace the bypassed oil in the deep inter-well regions with significant potential to enhance oil recovery.

The Emerging Role of Ferroptosis in Sepsis.

Ferroptosis is a novel form of cell death characterized by the iron-dependent accumulation of lipid peroxides and is different from other types of cell death. The mechanisms of ferroptosis are discussed in the review, including System Xc-, Glutathione Peroxidase 4 pathway, Ferroptosis Suppressor Protein 1 and Dihydroorotate Dehydrogenase pathway. Ferroptosis is associated with the occurrence of various diseases, including sepsis. Research in recent years has displayed that ferroptosis is involved in sepsis occurrence and development. Iron chelators can inhibit the development of sepsis and improve the survival rate of septic mice. The ferroptotic cells can release damage-associated molecular patterns and lipid peroxidation, which further mediate inflammatory responses. Ferroptosis inhibitors can resist sepsis-induced multiple organ dysfunction and inflammation. Finally, we reviewed ferroptosis, an iron-dependent form of cell death that is different from other types of cell death in biochemistry, morphology, and major regulatory mechanisms, which is involved in multiple organ injuries caused by sepsis. Exploring the relationship between sepsis and ferroptosis may yield new treatment targets for sepsis.

On-treatment HBV RNA dynamic predicts entecavir-induced HBeAg seroconversion in children with chronic hepatitis B.

BACKGROUND: Hepatitis B e antigen (HBeAg) seroconversion is an important intermediate outcome in HBeAg-positive chronic hepatitis B patients. This study aimed to explore whether hepatitis B virus (HBV) RNA serum levels can predict HBeAg seroconversion treated with entecavir. METHODS: Serum samples from HBeAg-positive children previously treated with entecavir were retrospectively analyzed. HBV RNA levels were measured at baseline, weeks 12, 24, 48, 72 of therapy. Ability of individual biomarkers to predict HBeAg seroconversion was evaluated using receiver operating characteristics (ROC) analyzes. RESULTS: Serum HBV RNA was detectable in 51 children with a median of 6.05 (4.04-8.29) log10 IU/mL at baseline. Patients with subsequent HBeAg seroconversion showed a significantly larger decline in median HBV RNA levels during treatment from baseline to week 12 of 1.96 (0.30-3.38) and to week 24 of 2.27 (1.20-3.38) log10 IU/mL, respectively, in comparison to HBeAg-positive patients without HBeAg seroconversion (P < 0.001). Levels of HBV RNA at treatment weeks 12 and 24 showed good ability to predict HBeAg seroconversion (area under ROC scores > 0.85, P < 0.001). CONCLUSION: On-treatment HBV RNA dynamic predicts entecavir-induced HBeAg seroconversion in children with chronic hepatitis B living in China.

Arbuscular mycorrhizal fungi promote lead immobilization by increasing the polysaccharide content within pectin and inducing cell wall peroxidase activity.

The mechanism by which arbuscular mycorrhizal (AM) fungi immobilize lead (Pb) within the cell wall is unclear. Therefore, the aim of this study was to investigate the mechanism by which AM fungi immobilize Pb within the cell wall by measuring the Pb content in the cell wall, the polysaccharide and the uronic acid contents of different cell wall fractions, and the activity of cell wall peroxidase. Mycorrhizal-associated Medicago truncatula had higher shoot and root biomass than nonmycorrhizal-associated M. truncatula. AM inoculation increased the content of Pb in the cell wall under Pb stress. The polysaccharide content in the pectin and hemicellulose fractions were increased by AM inoculation with or without Pb stress. In AM-associated roots, the cell wall peroxidase activity increased in response to Pb stress. However, Pb stress did not affect the cell wall peroxidase activity in non-AM-associated roots. Correlation analysis suggested that MtPrx05 and MtPrx10 may participate in polysaccharide cross-linking and cell wall stiffening. The Pb stress resistance mechanism of AM-associated roots may involve cell wall stiffening. Taken together, the results show that AM inoculation may improve host plant growth and increase Pb immobilization in the cell wall by increasing the polysaccharide content within pectin and hemicellulose and by inducing cell wall peroxidase activity. Both the polysaccharide composition and cell wall peroxidase have important contributions to the resistance of mycorrhizal-associated plants.

Hydrops fetalis associated with anti-CD36 antibodies in fetal and neonatal alloimmune thrombocytopenia: Possible underlying mechanism.

OBJECTIVES: In the present study, we asked whether anti-CD36 antibodies impair the maturation of erythropoietic stem cells to mature red blood cells (RBCs), leading to anaemia and hydrops fetalis (HF). BACKGROUND: Recent studies have shown the importance of anti-CD36 antibodies in the development of Fetal/Neonatal Alloimmune Thrombocytopenia (FNAIT). In comparison to other types of antibody-mediated FNAIT, anti-CD36 antibodies are frequently associated with anaemia and HF. As mature RBCs do not express CD36, the reason for this phenomenon is currently not fully understood. MATERIAL AND METHODS: A case of FNAIT with signs of HF was characterised in this study. Maternal anti-CD36 antibodies were isolated by an absorption/elution approach. We cultured haematopoietic stem cells (HSCs) with purified anti-CD36 antibodies, and the formation of burst-forming unit-erythroid and colony-forming unit-erythroid (CFU-E/BFU-E) cells was analysed. Apoptosis of HSCs was also investigated. RESULTS: Analysis of the mother showed type-1 CD36 deficiency. Anti-CD36 antibodies were found in maternal serum, as well as on fetal platelets, by ELISA, and the specificity of these antibodies was further substantiated by flow cytometry. In comparison to control IgG, incubation of HSCs with purified anti-CD36 antibodies led to a significant reduction in CFU-E/BFU-E cell formation, and this result was associated with an increased number of apoptotic CD34+ erythroid/myeloid precursor cells. Administration of intra-uterine transfusion with washed RBCs was effective in improving fetal anaemia. CONCLUSIONS: Anti-CD36 antibodies may cause anaemia and trigger HF through apoptosis of CD34+ erythroid/myeloid precursor cells. However, the contribution of other cells must also be taken into account.

Integrated Analysis of Long Non-Coding RNA and mRNA Expression Profile in Myelodysplastic Syndromes.

BACKGROUND: Myelodysplastic syndromes (MDS) are a heterogeneous group of myeloid malignancies. The incidence of MDS is gradually increasing, but the pathogenesis is still not very clear. Studies have shown that long non-coding RNAs (lncRNAs) play a critical role in both oncogenic and tumor-suppressive pathways. However, the function of lncRNAs in MDS is still unknown. The purpose of this study was to investigate the expression profiles and biological function of the aberrantly expressed lncRNAs and mRNAs in MDS. METHODS: We downloaded two data sets (GSE4619 and GSE19429) from the Gene Expression Omnibus database and obtained differentially expressed (DE) lncRNAs and DE-mRNAs between MDS cases and healthy controls. Then we performed systematic bioinformatics analysis to know the biological function of DE-lncRNAs and DE-mRNAs in MDS. RESULTS: We identified 40 DE-lncRNAs and 643 DE-mRNAs between MDS cases and healthy controls. Gene Ontology (GO) and pathway analysis revealed that DE-lncRNAs and DE-mRNAs were mainly involved in necroptosis, apoptosis, immunodeficiency, p53 and FoxO signaling pathways. LncRNA-mRNA co-expression and lncRNA functional similarity network showed that twelve down-regulated lncRNAs co-regulated the same target gene and they were similar in function. CONCLUSIONS: The comprehensive analysis of lncRNA and mRNA is helpful in understanding the pathogenesis of MDS, and the synergistically down-regulated lncRNAs may contribute to the development of new diagnostic and therapeutic strategies.

Extinction debt in local habitats: quantifying the roles of random drift, immigration and emigration.

We developed a time-dependent stochastic neutral model for predicting diverse temporal trajectories of biodiversity change in response to ecological disturbance (i.e. habitat destruction) and dispersal dynamic (i.e. emigration and immigration). The model is general and predicts how transition behaviours of extinction may accumulate according to a different combination of random drift, immigration rate, emigration rate and the degree of habitat destruction. We show that immigration, emigration, the areal size of the destroyed habitat and initial species abundance distribution (SAD) can impact the total biodiversity loss in an intact local area. Among these, the SAD plays the most deterministic role, as it directly determines the initial species richness in the local target area. By contrast, immigration was found to slow down total biodiversity loss and can drive the emergence of species credits (i.e. a gain of species) over time. However, the emigration process would increase the extinction risk of species and accelerate biodiversity loss. Finally but notably, we found that a shift in the emigration rate after a habitat destruction event may be a new mechanism to generate species credits.

Characterization of the complete plastid genome of Craniotome Rchb., a monotypic genus of Pogostemoneae, Lamiaceae.

Craniotome Rchb. is a monotypic genus of Lamiaceae. In this study, the complete plastid genome of the species C. furcata (Link) Kuntze was sequenced and assembled. The plastid genome obtained is 152,521 bp in length, including a pair of inverted repeat (IRa and IRb) regions of 25,596 bp, a large single-copy (LSC) region of 83,690 bp, and a small single-copy (SSC) region of 17,639 bp. The genome encoded 113 unique genes, including 79 protein-coding genes, 4 ribosomal RNA genes, and 30 transfer RNA genes. The overall GC content of the genome obtained is 38.29%. The phylogenetic analysis based on 37 plastid genome of Lamiaceae revealed that the genus Craniotome was sister to the Anisomeles-Pogostemon clade with strong support.