Search

This study aims to improve the evaluation of residual oil saturation in water flooded zones based on the material balance model (MBM) with variable multiple for injected water. We investigated the change patterns of rock-electro parameters during waterflooding through the analysis of displacement tests. Our work differentiated the waterflooding into numerous displacement processes and accordingly propose an improved time-differentiated variable multiple MBM. The calculation results of the improved model are more consistent with the displacement experiment data of cores. Furthermore, the improved method was integrated into the comprehensive interpretation platform of offshore logging to analyze water flooded zones of a well in the A oilfield. As a result, the residual oil saturation calculated is in close agreement with the results of experiments on cores. Our results indicate that the time-differentiation and variable multiplier for injected water can effectively enhance the assessment accuracy of the residual oil saturation of water-flooded zones. [ABSTRACT FROM AUTHOR]

At a particular aquaculture facility in Zhangjiajie in China, the Chinese giant salamander (Andrias davidianus) exhibited analogous clinical manifestations, culminating in sequential mortalities. This study used rigorous aseptic sampling methods to isolate bacteria from the affected liver of salamanders to determine the causative agent behind the decline in amphibians. A bacterial pathogen was isolated from diseased A. davidianus, and the strain was named DN-3. This isolate was subjected to bacterial identification, antibiotic susceptibility assays, reinfection experiments, and biochemical profiling. The isolated bacterial strain was definitively identified as Acinetobacter schindleri using 16S rRNA sequence analysis and biochemical identification. Antibiotic susceptibility testing revealed that this isolate was susceptible to neomycin, macrolides, doxycycline, piperacillin, nitrofurantoin, and carbenicillin. Subsequent reinfection assays, in which varying concentrations of the bacterial inoculum were administered to healthy salamanders, confirmed that the pathogen elicited varying degrees of morbidity or mortality within an eight-day observation period. The median lethal dose (LD50) of A. schindleri DN-3 for A. davidianus was calculated to be 6.25×104 CFU/mL. This result supports the significant pathogenicity of the strain for A. davidianus. The findings of this study provide empirical insights into the clinical management and epidemiological control of diseases affecting A. davidianus. [ABSTRACT FROM AUTHOR]

Soundscape is a sound environment that emphasizes the awareness of auditory perception and social or cultural understandings. The case of spatial perception is significant to soundscape. However, previous studies on the auditory spatial perception of the soundscape environment have been limited. Based on 21 native binaural-recorded soundscape samples and a set of auditory experiments for subjective spatial perception (SSP), a study of the analysis among semantic parameters, the inter-aural-cross-correlation coefficient (IACC), A-weighted-equal sound-pressure-level (Leq), dynamic (D), and SSP is introduced to verify the independent effect of each parameter and to re-determine some of their possible relationships. The results show that the more noisiness the audience perceived, the worse spatial awareness they received, while the closer and more directional the sound source image variations, dynamics, and numbers of sound sources in the soundscape are, the better the spatial awareness would be. Thus, the sensations of roughness, sound intensity, transient dynamic, and the values of Leq and IACC have a suitable range for better spatial perception. A better spatial awareness seems to promote the preference slightly for the audience. Finally, setting SSPs as functions of the semantic parameters and Leq-D-IACC, two linear multivariate evaluation models of subjective spatial perception are proposed. [ABSTRACT FROM AUTHOR]

Experimental and epidemiologic evidence suggests that dysregulation of proteins involved in iron metabolism plays a critical role in cancer. The mechanisms by which cancer cells alter homeostatic iron regulation are just beginning to be understood. Here, we demonstrate that iron regulatory protein 2 (IRP2) plays a key role in iron accumulation in breast cancer. Although both IRP1 and IRP2 are overexpressed in breast cancer, the over-expression of IRP2, but not IRP1, is associated with decreased ferritin H and increased transferrin receptor 1 (TfR1). Knockdown of IRP2 in triple-negative MDA-MB-231 human breast cancer cells increases ferritin H expression and decreases TfR1 expression, resulting in a decrease in the labile iron pool. Further, IRP2 knockdown reduces growth of MDA-MB-231 cells in the mouse mammary fat pad. Gene expression microarray profiles of patients with breast cancer demonstrate that increased IRP2 expression is associated with high-grade cancer. Increased IRP2 expression is observed in luminal A, luminal B, and basal breast cancer subtypes, but not in breast tumors of the ERBB2 molecular subtype. These results suggest that dysregulation of IRP2 is an early nodal point underlying altered iron metabolism in breast cancer and may contribute to poor outcome of some patients with breast cancer. [ABSTRACT FROM AUTHOR]

Radiation-induced normal brain injury is associated with acute and/or chronic inflammatory responses, and has been a major concern in radiotherapy. Recent studies suggest that microglial activation is a potential contributor to chronic inflammatory responses following irradiation; however, the molecular mechanism underlying the response of microglia to radiation is poorly understood. c-Jun, a component of AP-1 transcription factors, potentially regulates neural cell death and neuroinflammation. We observed a rapid increase in phosphorylation of N-terminal c-Jun (on serine 63 and 73) and MAPK kinases ERK½, but not JNKs, in irradiated murine microglial BV2 cells. Radiation-induced c-Jun phosphorylation is dependent on the canonical MEK-ERK signaling pathway and required for both ERK1 and ERK2 function. ERK½ directly interact with c-Jun in vitro and in cells; meanwhile, the JNK binding domain on c-Jun is not required for its interaction with ERK kinases. Radiation-induced reactive oxygen species (ROS) potentially contribute to c-Jun phosphorylation through activating the ERK pathway. Radiation stimulates c-Jun transcriptional activity and upregulates c-Jun-regulated proinflammatory genes, such as tumor necrosis factor-a, interleukin-1b, and cyclooxygenase-2. Pharmacologic blockade of the ERK signaling pathway interferes with c-Jun activity and inhibits radiation-stimulated expression of c-Jun target genes. Overall, our study reveals that the MEK-ERK½ signaling pathway, but not the JNK pathway, contributes to the c-Jun-dependent microglial inflammatory response following irradiation. [ABSTRACT FROM AUTHOR]

Background: In prostate cancer (PCa), the common treatment involving androgen ablation alleviates the disease temporarily, but results in the recurrence of highly aggressive and androgen-independent metastatic cancer. Therefore, more effective therapeutic approaches are needed. It is known that aberrant epigenetics contributes to prostate malignancy. Unlike genetic changes, these epigenetic alterations are reversible, which makes them attractive targets in PCa therapy to impede cancer progression. As a histone methyltransferease, Ezh2 plays an essential role in epigenetic regulation. Since Ezh2 is overexpressed and acts as an oncogene in PCa, it has been proposed as a bona fide target of PCa therapy. MicroRNAs (miRNAs) regulate gene expression through modulating protein translation. Recently, the contribution of miRNAs in cancer development is increasingly appreciated. In this report, we present our study showing that microRNA-101 (miR-101) inhibits Ezh2 expression and differentially regulates prostate cancer cells. In addition, the expression of miR-101 alters upon androgen treatment and HIF-1α/HIF-1β induction. Result: In our reporter assays, both miR-101 and miR-26a inhibit the expression of a reporter construct containing the 3'-UTR of Ezh2. When ectopically expressed in PC-3, DU145 and LNCaP cells, miR-101 inhibits endogenous Ezh2 expression in all three cell lines, while miR-26a only decreases Ezh2 in DU145. Ectopic miR-101 reduces the invasion ability of PC-3 cells, while restored Ezh2 expression rescues the invasiveness of PC-3 cells. Similarly, miR-101 also inhibits cell invasion and migration of DU145 and LNCaP cells, respectively. Interestingly, ectopic miR-101 exhibits differential effects on the proliferation of PC-3, DU-145 and LNCaP cells and also causes morphological changes of LNCaP cells. In addition, the expression of miR-101 is regulated by androgen receptor and HIF-1α/HIF-1β. While HIF-1α/HIF-1β induced by deferoxamine mesylate (DFO) decreases miR-101 levels, the overall effects of R-1881 on miR-101 expression are stimulatory. Conclusions: This study indicates that miR-101 targets Ezh2 and decreases the invasiveness of PCa cells, suggesting that miR-101 introduction is a potential therapeutic strategy to combat PCa. MiR-101 differentially regulates prostate cell proliferation. Meanwhile, the expression of miR-101 is also modulated at different physiological conditions, such as androgen stimulation and HIF-1α/HIF-1β induction. [ABSTRACT FROM AUTHOR]

Water transport through the cell membranes is regulated largely by a family of proteins known as aquaporins (AQPs). In this study, six novel aquaporin genes, TaAQP1~TaAQP6, were isolated from the common wheat Triticum aestivum L. var. Changle 5. These six TaAQPs share common features with other plant AQPs. Three of them (TaAQP2, 3, and 4) phylogenetically belong to plant PIP2 group, and the other three resemble proteins from PIP1(TaAQP1), TIP1(TaAQP6), and TIP2 (TaAQP5) groups, respectively. The subcellular localization assay, determined by onion epidermal cell transient expression system, indicated that TaAQP6 is a membrane-associated protein. Transformation of TaAQP6 into Xenopus oocytes demonstrated that it facilitated water uptake, suggesting that this TaAQP is an active membrane-associated protein. The expression of TaAQP6 was upregulated in shoots of wheat seedlings, but downregulated in roots under polyethylene glycol (PEG) stress. In split-root experiment, the amount of TaAQP6 transcripts decreased in dry roots (cultured in PEG solution), but increased in wet roots (cultured in water), and remained unchanged in shoots. It is interesting to note that the osmolality changes of different pans in PEG-treated and split-root seedlings were related to the expression of TaAQP6. Taken together, we proposed that TaAQP6 participates in internal water redistribution of wheat seedlings during osmotic stress by regulating outflow of water from water-rich organs to the parts with poor water status under water deficit condition. [ABSTRACT FROM AUTHOR]

Air pollution significantly impacts lung cancer progression, but there is a lack of a comprehensive molecular characterization of clinical samples associated with air pollution. Here, we performed a proteogenomic analysis of lung adenocarcinoma (LUAD) in 169 female never-smokers from the Xuanwei area (XWLC cohort), where coal smoke is the primary contributor to the high lung cancer incidence. Genomic mutation analysis revealed XWLC as a distinct subtype of LUAD separate from cases associated with smoking or endogenous factors. Mutational signature analysis suggested that Benzo[a]pyrene (BaP) is the major risk factor in XWLC. The BaP-induced mutation hotspot, EGFR-G719X, was present in 20% of XWLC which endowed XWLC with elevated MAPK pathway activations and worse outcomes compared to common EGFR mutations. Multi-omics clustering of XWLC identified four clinically relevant subtypes. These subgroups exhibited distinct features in biological processes, genetic alterations, metabolism demands, immune landscape, and radiomic features. Finally, MAD1 and TPRN were identified as novel potential therapeutic targets in XWLC. Our study provides a valuable resource for researchers and clinicians to explore prevention and treatment strategies for air-pollution-associated lung cancers. [ABSTRACT FROM AUTHOR]

This study aimed to identify the primary pathogenic bacteria responsible for the mortality of the Chinese giant salamander (Andriasd davidianus). A pathogenic bacterium was isolated from a diseased Chinese giant salamander exhibiting typical symptoms under aseptic conditions and then identified by morphological examinations, biochemical analysis, and the sequence analysis of bacterial 16S rRNA. Artificial infection testing was then conducted to determine the pathogenicity of the isolated bacteria strain. Drug susceptibility tests were conducted using the agar diffusion method. The isolated pathogenic bacteria, named DN-2, was successfully identified as Acinetobacter lwoffii. The artificial infection showed that the typical symptoms of the disease could be replicated as the ones originally occurred, and this bacterium exhibited high pathogenicity to the Chinese giant salamander. In the Chinese giant salamander, the median lethal dosage (LD50) of A. lwoffii DN-2 for A. davidianus was determined to be 4.63*104 CFU/g. Drug sensitivity testing showed that these bacteria were highly sensitive to erythromycin, gentamicin, neomycin, streptomycin, midecamycin, ciprofloxacin, piperacillin, florfenicol, doxycycline, carbenicillin, and sulfanilamide. In summary, A. lwoffii was identified as the primary pathogen responsible for the demise of A. davidianus. Our study first presents how these bacteria harm Chinese giant salamanders. [ABSTRACT FROM AUTHOR]

L-type voltage-gated calcium (Ca2+) channels (L-VGCC) dysfunction is implicated in several neurological and psychiatric diseases. While a popular therapeutic target, it is unknown whether molecular mechanisms leading to disrupted L-VGCC across neurodegenerative disorders are conserved. Importantly, L-VGCC integrate synaptic signals to facilitate a plethora of cellular mechanisms; however, mechanisms that regulate L-VGCC channel density and subcellular compartmentalization are understudied. Herein, we report that in disease models with overactive mammalian target of rapamycin complex 1 (mTORC1) signaling (or mTORopathies), deficits in dendritic L-VGCC activity are associated with increased expression of the RNA-binding protein (RBP) Parkinsonism-associated deglycase (DJ-1). DJ-1 binds the mRNA coding for the alpha and auxiliary Ca2+ channel subunits CaV1.2 and a2d2, and represses their mRNA translation, only in the disease states, specifically preclinical models of tuberous sclerosis complex (TSC) and Alzheimer's disease (AD). In agreement, DJ-1-mediated repression of CaV1.2/a2d2 protein synthesis in dendrites is exaggerated in mouse models of AD and TSC, resulting in deficits in dendritic L-VGCC calcium activity. Finding of DJ-1-regulated L-VGCC activity in dendrites in TSC and AD provides a unique signaling pathway that can be targeted in clinical mTORopathies. [ABSTRACT FROM AUTHOR]

As a multifunctional protein, Yin Yang 1 (YY1) has been demonstrated to regulate both gene expression and protein posttranslational modifications. However, gaps still exist in our knowledge of how YY1 can be modified and what the consequences of its modifications are. Here we report that YY1 protein can be sumoylated both in vivo and in vitro. We have identified lysine 288 as the major sumoylation site of YY1. We also discovered that PIASy, a SUMO E3 ligase, is a novel YY1-interacting protein and can stimulate the sumoylation of YY1 both in vitro and in vivo. Importantly, the effects of PIASy mutants on in vivo YY1 sumoylation correlate with the YY1-PIASy interaction but do not depend on the RING finger domain of PIASy. This regulation is unique to YY1 sumoylation because PIASy-mediated p53 sumoylation still relies on the integrity of PIASy, which is also true of all of the previously identified substrates of PIASy. In addition, PIASy colocalizes with YY1 in the nucleus, stabilizes YY1 in vivo, and differentially regulates YY1 transcriptional activity on different target promoters. This study demonstrates that YY1 is a target of SUMOs and reveals a novel feature of a SUMO E3 ligase in the PIAS family that selectively stimulates protein sumoylation independent of the RING finger domain. [ABSTRACT FROM AUTHOR]

Previous studies have reported that STAT4 rs7574865 conferred the susceptibility to systemic lupus erythematosus (SLE). In this study, a meta-analysis (including 32 comparative studies of 11384 patients and 17609 controls) was conducted to investigate the role of STAT4 polymorphism in SLE in a comprehensive way. We found that the Asian population had the highest prevalence of the T allele than any other study population at 32.2% and that STAT4 rs7574865 polymorphism was associated with SLE in the overall population (OR = 1.579 , 95 % CI = 1.497 -1.665, P < 0.001). In the subgroup analysis by ethnicity, STAT4 rs7574865 T allele was shown to be risk factor in SLE in Asian, European, and American origins. Our results do support STAT4 rs7574865 polymorphism as a susceptibility factor for SLE in populations of different ethnic and that its prevalence is ethnicity dependent. [ABSTRACT FROM AUTHOR]

Considerable progress has been made in understanding the function of receptor-like kinase (RLK) genes in model plants. However, much less is known about these genes in crop species. Here we report the characterization of three new wheat RLK genes ( TaRLK-R1, 2 and 3). The primary structure of the putative proteins TaRLK-R1, 2 and 3 contained a signal peptide, a cysteine-rich extracellular domain, a transmembrane domain, and a predicted intracellular kinase domain. The fusions between TaRLK-R1, 2 or 3 and the green fluorescence protein (GFP) were targeted to the plasma membrane; such targeting required the signal peptide, extracellular domain and transmembrane domain. Transcription of TaRLK-R1, 2 and 3 was found mainly in the green organs, and was regulated by light. Transcript levels of TaRLK-R1, 2 and 3 increased during the hypersensitive reaction (HR) to stripe rust fungus. In addition, the TaRLK-R3 transcript level was also upregulated by abiotic stresses. Further experiments revealed that the recombinant kinase domain of TaRLK-R3 exhibited auto-phosphorylation activity in vitro. Knocking down the transcript levels of TaRLK-R1, 2 or 3 individually or all together by virus-induced gene silencing compromised the wheat HR to stripe rust fungus. The demonstration of TaRLK-R1, 2 and 3 as positive contributors in the wheat HR to stripe rust fungus suggests a new direction for further functional studies of this important family of RLK genes, and may facilitate the breeding of wheat varieties resistant to stripe rust disease. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a devastating incident that induces neuronal loss and dysfunction. Notoginsenoside R1 (NGR1) has been reported to exhibit a neuro-protective role after SCI. In this study, the effect and molecular mechanisms of NGR1 in models of SCI were further investigated. Rat adrenal pheochromocytoma cell line (PC-12) were stimulated with lipopolysaccharide (LPS) to establish a cell model of SCI-like condition. The changes of proinflammatory cytokines and associated proteins were analyzed using enzyme linked immunosorbent assay (ELISA) and western blotting. A rat model of SCI was established. Nissl staining were used to observe the morphological characteristics of spinal cord tissues. reverse transcription-quantitative PCR (RT-qPCR) was used to measure the expression of miR-301a and Krüppel-like factor 7 (KLF7). Our results showed that NGR1 alleviated LPS-triggered apoptosis and inflammation in PC-12 cells. MiR-301a was upregulated in LPS-stimulated PC-12 cells and was downregulated by NGR1 treatment. MiR-301a overexpression reversed the effect of NGR1 in LPS-treated PC-12 cells. KLF7 was verified to be targeted by miR-301a. NGR1 activated Wnt/β-catenin signaling in LPS-treated PC-12 cells by inhibiting miR-301a and upregulating KLF7. Moreover, blocking wingless/integrated (Wnt)/β-catenin signaling eliminated the protective effect of NGR1 against SCI in vitro and in vivo. Overall, NGR1 could reduce inflammation and apoptosis and promote functional recovery of SCI rats by activating Wnt/β-catenin pathway. [ABSTRACT FROM AUTHOR]

Background: SIX homeobox 3 (SIX3) is a member of the sine oculis homeobox transcription factor family. It plays a vital role in the nervous system development. Our previous study showed that the SIX3 gene is hypermethylated, and its expression is decreased in astrocytoma, but the role of SIX3 remains unknown. Methods: Chromatin-immunoprecipitation (ChIP) and luciferase reporter assay were used to confirm the binding of SIX3 to the promoter regions of aurora kinase A (AURKA) and aurora kinase B (AURKB). Confocal imaging and coimmunoprecipitation (Co-IP) were used to detect the interaction between AURKA and AURKB. Flow cytometry was performed to assess the effect of SIX3 on cell cycle distribution. Colony formation, EdU incorporation, transwell, and intracranial xenograft assays were performed to demonstrate the effect of SIX3 on the malignant phenotype of astrocytoma cells. Results: SIX3 is identified as a novel negative transcriptional regulator of AURKA and AURKB, and it decreases the expression of AURKA and AURKB in a dose-dependent manner in astrocytoma cells. Importantly, interactions between AURKA and AURKB stabilize and protect AURKA/B from degradation, and overexpression of SIX3 does not affect these interactions; SIX3 also acts as a tumor suppressor, and it increases p53 activity and expression at the post-translational level by the negative regulation of AURKA or AURKB, reduces the events of numerical centrosomal aberrations and misaligned chromosomes, and significantly inhibits the proliferation, invasion, and tumorigenesis of astrocytoma in vitro and in vivo. Moreover, experiments using primary cultured astrocytoma cells indicate that astrocytoma patients with a low expression of SIX3 and mutant p53 are more sensitive to treatment with aurora kinase inhibitors. Conclusion: SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA and AURKB in astrocytoma. For the first time, the functional interaction of AURKA and AURKB has been found, which aids in the protection of their stability, and partially explains their constant high expression and activity in cancers. SIX3 is a potential biomarker that could be used to predict the response of astrocytoma patients to aurora kinase inhibitors. [ABSTRACT FROM AUTHOR]

Hepatic apolipoprotein A-IV (apoA-IV) expression is correlated with hepatic triglyceride (TG) content in mouse models of chronic hepatosteatosis, and steatosis-induced hepatic apoA-IV gene expression is regulated by nuclear transcription factor cAMP-responsive element-binding protein H (CREBH) processing. To define what aspects of TG homeostasis regulate hepatic CREBH processing and apoA-IV gene expression, several mouse models of attenuated VLDL particle assembly were subjected to acute hepatosteatosis induced by an overnight fast or short term ketogenic diet feeding. Compared with chow-fed C57BL/6 mice, fasted or ketogenic diet-fed mice displayed increased hepatic TG content, which was highly correlated (r²= 0.95) with apoA-IV gene expression, and secretion of larger, TG-enriched VLDL, despite a lower rate of TG secretion and a similar or reduced rate of apoB100 secretion. When VLDL particle assembly and secretion was inhibited by hepatic shRNA-induced apoB silencing or genetic or pharmacologic reduction in microsomal triglyceride transfer protein (MTP) activity, hepatic TG content increased dramatically; however, CREBH processing and apoA-IV gene expression were attenuated compared with controls. Adenovirus-mediated reconstitution of MTP expression proportionately restored CREBH processing and apoA-IV expression in liver-specific MTP knock-out mice. These results reveal that hepatic TG content, per se, does not regulate CREBH processing. Instead, TG mobilization into the endoplasmic reticulum for nascent VLDL particle assembly activates CREBH processing and enhances apoA-IV gene expression in the setting of acute steatosis. We conclude that VLDL assembly and CREBH activation play key roles in the response to hepatic steatosis by up-regulating apoA-IV and promoting assembly and secretion of larger, more TG-enriched VLDL particles. [ABSTRACT FROM AUTHOR]

Hepcidin is a circulating peptide hormone made by the liver that is a central regulator of systemic iron uptake and recycling. Here, we report that prostate epithelial cells also synthesize hepcidin, and that synthesis and secretion of hepcidin are markedly increased in prostate cancer cells and tissue. Prostatic hepcidin functions as an autocrine hormone, decreasing cell surface ferroportin, an iron exporter, increasing intracellular iron retention, and promoting prostate cancer cell survival. Synthesis of hepcidin in prostate cancer is controlled by a unique intersection of pathways that involves BMP4/7, IL6, Wnt, and the dual BMP and Wnt antagonist, SOSTDC1. Epigenetic silencing of SOSTDC1 through methylation is increased in prostate cancer and is associated with accelerated disease progression in patients with prostate cancer. These results establish a new connection between iron metabolism and prostate cancer, and suggest that prostatic dysregulation of hepcidin contributes to prostate cancer growth and progression. [ABSTRACT FROM AUTHOR]

Primary Sjögren's syndrome (pSS) is a common autoimmune disease involving abnormal Th17 activation. The aim of the current study was to investigate the immunosuppression effect of Cyclosporine A (Cys A), a potent immunosuppressor on the proliferation and activation of T cells, on the activation of Th17 cells. Blood samples from both inactive and active pSS patients as well as healthy controls were collected and serum and peripheral blood mononuclear cells (PBMCs) were collected and tested for IL-17 and RORγt expression. Subsequently, PBMCs were treated in vitro with Cys A in a series of doses and incubation time and the effect of Cys A on inhibiting Th17 activation was tested by measuring IL-17 and RORγt expression. IL-17 in both serum and PBMCs as well as RORγt in PBMCs from active pSS patients were significantly elevated on both the mRNA and protein levels comparing to those from both inactive pSS patients and healthy controlCys A in the final concentration of 80ng/ml and the treatment time of 24h showed strong inhibition effect on the expression of IL-17 and RORγt in PBMCs from active pSS patients. However, Cys A in various doses and incubation times did not show much impact on inhibiting IL-17 as well as RORγt expression in PBMCs from healthy donors and inactive pSS patients. Cys A possesses the capability in immunosuppressing the activation of Th17 cells, suggesting that Cys A may be a potential treatment for pSS and maybe other autoimmune diseases. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are small, endogenous RNAs that regulate gene expression in both plants and animals. A large number of miRNAs has been identified from various animals and model plant species such as Arabidopsis thaliana and rice ( Oryza sativa); however, characteristics of wheat ( Triticum aestivum) miRNAs are poorly understood. Here, computational identification of miRNAs from wheat EST sequences was preformed by using the in-house program GenomicSVM, a prediction model for miRNAs. This study resulted in the discovery of 79 miRNA candidates. Nine out of 22 miRNA representatives randomly selected from the 79 candidates were experimentally validated with Northern blotting, indicating that prediction accuracy is about 40%. For the 9 validated miRNAs, 59 wheat ESTs were predicted as their putative targets. [ABSTRACT FROM AUTHOR]