Cellular and circuit architecture of the lateral septum for reward processing.

The lateral septum (LS) is composed of heterogeneous cell types that are important for various motivated behaviors. However, the transcriptional profiles, spatial arrangement, function, and connectivity of these cell types have not been systematically studied. Using single-nucleus RNA sequencing, we delineated diverse genetically defined cell types in the LS that play distinct roles in reward processing. Notably, we found that estrogen receptor 1 (Esr1)-expressing neurons in the ventral LS (LSEsr1) are key drivers of reward seeking via projections to the ventral tegmental area, and these neurons play an essential role in methamphetamine (METH) reward and METH-seeking behavior. Extended exposure to METH increases the excitability of LSEsr1 neurons by upregulating hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, thereby contributing to METH-induced locomotor sensitization. These insights not only elucidate the intricate molecular, circuit, and functional architecture of the septal region in reward processing but also reveal a neural pathway critical for METH reward and behavioral sensitization.

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro.

The increase of circulating galactose-deficient IgA1 (Gd-IgA1) is caused by excessive activation of IgA-positive secretory cells in the process of mucosal immune responses, which is a critical link in the pathogenesis of IgA nephropathy (IgAN). Peyer's patch, the prominent place where B lymphocytes are transformed into IgA-secreting plasma cells, is the primary source of IgA. In addition, the lower expression of core 1ß-1,3-galactosyltransferase (C1GalT1) and its molecular chaperone, C1GalT1-specific molecular chaperone (Cosmc), is related to abnormal glycosylation of IgA1 in IgAN patients. Our clinical experience shows that Dioscoreae Nipponicae Rhizoma's (DNR) herbal medicine can relieve proteinuria and hematuria and improve renal function in IgAN patients. Dioscin (DIO) is one of the main active ingredients of DNR, which has various pharmacological activities. This study explores DIO's possible mechanism in treating IgAN.The IgAN model mouse was established by mucosal immune induction. The mice were divided into the control, model, and DIO gavage groups. The glomerular IgA deposition in mice, renal pathological changes, and B cell markers CD20 and CXCR5 expression in Peyer's patch were detected by immunofluorescence and immunohistochemistry. After lipopolysaccharide (LPS) stimulation, DIO's effects on DAKIKI cells proliferation, IgA and Gd-IgA1 secretion, C1GalT1, and Cosmc expression were studied by cell counting kit-8 (CCK-8) assay, enzyme-linked immunosorbent assay (ELISA) test, quantitative real-time polymerase chain reaction (QRT-PCR), and western blotting (WB). In in vivo studies, IgA deposition accompanied by glomerular mesangial hyperplasia and increased expression of CD20 and CXCR5 in Peyer's patch in the IgAN model mouse was alleviated by DIO. In vitro studies showed 0.25 µg/mL to 1.0 µg/mL DIO inhibited LPS-induced DAKIKI cell proliferation, IgA and Gd-IgA1 secretion, and up-regulated the mRNA and protein expression of C1GalT1 and Cosmc. This study demonstrates that DIO may reduce Gd-IgA1 production by inhibiting excessive activation of IgA-secreting cells and up-regulating C1GALT1/Cosmc expression.

Chaperonin co-expression and chemical modification enables production of active microbial transglutaminase from E. coli cytoplasm.

Microbial transglutaminase (MTG) is a usable enzyme for biomacromolecule modification. In the present study, a "molecular chaperonin" strategy was developed to produce MTG in E. coli cytoplasm with high expression level and a "small molecule-mediated chemical modification" strategy was adopted to strip propeptide chaperonin efficiently during purification. Propeptide (Pro) was expressed separately as a chaperonin to facilitate MTG expression in E. coli cytoplasm with a yield up to 300 mg or about 9 kU from 1 L fed-batch culture. Furthermore, small molecular chemicals were applied to interfere the interaction between MTG and Pro. Chemical acetylation was identified as a suitable method to strip Pro resulting in pure MTG with high specific activity up to 49.6 U/mg. The purified acetylated MTG was characterized by MS analysis. The deconvoluted mass and Peptide Sequence Tags analysis confirmed acetylation on amino groups of MTG protein. Finally, the applications of obtained MTG were demonstrated via protein polymerization of bovine serum albumin and PEGylation of human interferon-α2b. Our method provides MTG with high purity and specific activity as well as unique merit with masked amino groups thus avoiding self-polymerization and cross-linking between MTG and substrates.

A potential immunotherapeutic and prognostic biomarker for multiple tumors including glioma: SHOX2.

BACKGROUND: Short stature homeobox 2 (SHOX2) is significant gene in the development and progression of multiple types of tumors. Nonetheless, the biological role of SHOX2 within pan-cancer datasets has not been investigated. Thus, comprehensive bioinformatics analyses of pan-cancer datasets were conducted to explore how SHOX2 regulates tumorigenesis. METHODS: A variety of tumor datasets and online analytical tools, including SangerBox, TIMER2, LinkedOmic, GEPIA2 and cBioPortal, were applied to explore SHOX2 expression in various tumors. To ascertain the connections between SHOX2 expression and genetic alterations, SHOX2-related genes and tumor immunity, the pan-cancer datasets were examined. In vitro assays were applied to verify the biological functions of SHOX2 in glioma cells via CCK-8, wound healing, Transwell and colony formation assays. RESULTS: Analyses found that SHOX2 was overexpressed in multiple cancer types. SHOX2 expression level was significantly correlated with isocitrate dehydrogenase (IDH), 1p/19q, O6-methylguanine DNA methyltransferase (MGMT) status and new types of glioma patients. High mRNA expression levels of SHOX2 were associated with a poor prognosis in multiple tumor patients. KEGG enrichment analysis showed that SHOX2-related genes were associated with cell cycle and DNA damage repair. Genetic alterations of SHOX2 were identified in multiple types of cancers, including duplications and deep mutations. Immune analysis showed that SHOX2 was closely correlated with the tumor mutation burden (TMB), microsatellite instability (MSI), neoantigen and neoantigens and immune checkpoint (ICP) in a variety of tumors and could influence the immunotherapy sensitivity of cancers. CCK-8, wound healing, Transwell and colony formation experiments showed that SHOX2 knockdown inhibited glioma cell proliferation, migration, invasion and colony formation abilities. CONCLUSION: SHOX2 was overexpressed in multiple cancer types in TCGA cohort. SHOX2 knockdown inhibited glioma cell proliferation, migration and colony formation ability. Our study showed that SHOX2 may be an immunotherapeutic and promising prognostic biomarker in certain types of tumors.

The Gut Microbiota-Brain Axis: Potential Mechanism of Drug Addiction.

As a chronic encephalopathy, drug addiction is responsible for millions of deaths per year around the world. The gut microbiome is a crucial component of the human microbiome. Through dynamic bidirectional communication along the 'gut-brain axis,' gut bacteria cooperate with their hosts to regulate the development and function of the immune, metabolic, and nervous systems. These processes may affect human health because some brain diseases are related to the composition of gut bacteria, and disruptions in microbial communities have been implicated in neurological disorders. We review the compositional and functional diversity of the gut microbiome in drug addiction. We discuss intricate and crucial connections between the gut microbiota and the brain involving multiple biological systems and possible contributions by the gut microbiota to neurological disorders. Finally, the treatment of probiotics and fecal transplantation was summarized. This was done to further understand the role of intestinal microecology in the pathogenesis of drug addiction and to explore new methods for the treatment of drug addiction.

A novel gene therapy for methamphetamine- induced cognitive disorder with a hyper-acidified fusion variant of DnaJB1.

Methamphetamine (MA) is spread worldwide and is a highly addictive psychostimulant that can induce neurodegeneration and cognitive disorder, which lacks effective treatments. We and other researchers have found that the crucial member of Hsp70 chaperone machinery, DnaJ, is liable to be co-aggregated with aberrant proteins, which has been confirmed a risk factor to promote neurodegeneration. In the current study, we demonstrated that tailing with a hyper-acidic fusion partner, tua2, human DnaJB1 could resist the formation of toxic mutant Tau aggregates both in prokaryote and eukaryote models. We found that aberrant Tau aggregates could deplete the antioxidant enzyme pool and disturb Hsp70 molecular chaperone system by co-aggregating with the principal members of these systems. Stability-enhanced DnaJB1-tua2 could stop the chain reaction of Tau aggregates as well as maintain redox balance and protein homeostasis. With an MA-induced cognitive disorder mouse model, we found that the cognitive disorder of MA mice was rescued and the overactivated inflammatory response was relieved by the expression of DnaJB1-tua2 in the hippocampus. Furthermore, the Tau neurofibrillary tangles and apoptotic neurons were diminished with the escorting of DnaJB1-tua2. These findings demonstrate that delivering DnaJB1-tua2 in hippocampus may have a therapeutic potential in the treatment of MA-induced cognitive disorder.

A New Strategy on Designing Fluxes for Aluminum Alloy Melt Refinement.

With the aim of obtaining a refining flux that is stable and provides effective refining of aluminum melt, a new strategy of designing the flux composition has been proposed. Ten fluxes were designed, by selecting ten molten salt compounds according to their thermophysical parameters, physical properties, and thermodynamic analysis. The melting points of the ten fluxes, and the phases transformation of the fluxes after melting, were studied by DSC and XRD, respectively. The contact angles between four groups of fluxes and alumina at refinement temperatures were studied, and the effect of refinement was characterized by a metallographic microscope. The process of the fluxes removing inclusions and degassing was analyzed thermodynamically. The research findings indicate that flux #10 (11.0 wt.%NaF, 29.5 wt.%NaCl, 46.5 wt.%Na2CO3, 3.0 wt.%CaF2, 10.0 wt.%Na3AlF6) has a melting point (562.2 °C) below the refining temperature. At the refining temperature (760 °C), flux #10 has the lowest contact angle, of 12.78°. In addition, compared to that of flux STJ-A3, currently used in practice, flux #10 has a better refining effectiveness, with the pores and inclusions content of the sample being reduced to 1.11% from 2.96%.

Distinct reward processing by subregions of the nucleus accumbens.

The nucleus accumbens (NAc) plays an important role in motivation and reward processing. Recent studies suggest that different NAc subnuclei differentially contribute to reward-related behaviors. However, how reward is encoded in individual NAc neurons remains unclear. Using in vivo single-cell resolution calcium imaging, we find diverse patterns of reward encoding in the medial and lateral shell subdivision of the NAc (NAcMed and NAcLat, respectively). Reward consumption increases NAcLat activity but decreases NAcMed activity, albeit with high variability among neurons. The heterogeneity in reward encoding could be attributed to differences in their synaptic inputs and transcriptional profiles. Specific optogenetic activation of Nts-positive neurons in the NAcLat promotes positive reinforcement, while activation of Cartpt-positive neurons in the NAcMed induces behavior aversion. Collectively, our study shows the organizational and transcriptional differences in NAc subregions and provides a framework for future dissection of NAc subregions in physiological and pathological conditions.

Exercise modulates central and peripheral inflammatory responses and ameliorates methamphetamine-induced anxiety-like symptoms in mice.

Anxiety-like symptoms are common symptoms of methamphetamine (METH) users, especially in the acute withdrawal period, which is an important factor for the high relapse rate during METH acute withdrawal. Exercise has been demonstrated to relieve anxiety-like symptoms during METH withdrawal, but the underlying mechanisms of this anti-anxiety effect are still unclear. Activated microglia and abnormal neuroinflammation play an important role in the pathogenesis of anxiety-like symptoms after METH withdrawal. Moreover, peripheral immune factors were also significantly associated with anxiety symptoms. However, the effects of treadmill exercise on microglial function and neuroinflammation in the striatum and hippocampus during acute METH withdrawal have not been reported. In the current study, we found severe peripheral immune dysfunction in METH users during acute withdrawal, which may in part contribute to anxiety symptoms during METH acute withdrawal. We also showed that 2 weeks of METH exposure induced anxiety-like symptoms in the acute withdrawal period. Additionally, METH exposure resulted in increased microglial activation and proinflammatory cytokines released in the mouse striatum and hippocampus during acute withdrawal. We next evaluated the effects of treadmill exercise in countering anxiety-like symptoms induced by METH acute withdrawal. The results showed that anxiety-like symptoms induced by acute METH withdrawal were attenuated by coadministration of treadmill exercise. In addition, treadmill exercise counteracted METH-induced microglial activation in the mouse striatum and various subregions of the hippocampus. Furthermore, treadmill exercise also reversed the increase in proinflammatory cytokines induced by acute METH withdrawal in the mouse striatum, hippocampus and serum. Our findings suggest that the anti-anxiety effect of treadmill exercise may be mediated by reducing microglial activation and regulating central and peripheral inflammatory responses.

Effects and associated transcriptomic landscape changes of methamphetamine on immune cells.

BACKGROUND: Methamphetamine (METH) abuse causes serious health problems, including injury to the immune system, leading to increased incidence of infections and even making withdrawal more difficult. Of course, immune cells, an important part of the immune system, are also injured in methamphetamine abuse. However, due to different research models and the lack of bioinformatics, the mechanism of METH injury to immune cells has not been clarified. METHODS: We examined the response of three common immune cell lines, namely Jurkat, NK-92 and THP-1 cell lines, to methamphetamine by cell viability and apoptosis assay in vitro, and examined their response patterns at the mRNA level by RNA-sequencing. Differential expression analysis of two conditions (control and METH treatment) in three types of immune cells was performed using the DESeq2 R package (1.20.0). And some of the differentially expressed genes were verified by qPCR. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of differentially expressed genes by the clusterProfiler R package (3.14.3). And gene enrichment analysis was also performed using MetaScape ( www.metascape.org ). RESULTS: The viability of the three immune cells was differentially affected by methamphetamine, and the rate of NK-cell apoptosis was significantly increased. At the mRNA level, we found disorders of cholesterol metabolism in Jurkat cells, activation of ERK1 and ERK2 cascade in NK-92 cells, and disruption of calcium transport channels in THP-1 cells. In addition, all three cells showed changes in the phospholipid metabolic process. CONCLUSIONS: The results suggest that both innate and adaptive immune cells are affected by METH abuse, and there may be commonalities between different immune cells at the transcriptome level. These results provide new insights into the potential effects by which METH injures the immune cells.

Long-term exercise at different intensities can reduce the inflammatory response in the brains of methamphetamine-treated mice.

Methamphetamine (METH) is a highly addictive psychoactive drug that is used worldwide. Various approaches have been used to address METH dependence, but many of them have little effect. Previous studies have shown that exercise on a treadmill could reduce METH dependence in mice, but the intensity and duration of exercise that was needed to be effective was unknown. This study investigated the effects of low- and medium-intensity treadmill exercise on methamphetamine reward in male mice via conditioned place preference (CPP) training, and the levels of the inflammatory factors IL-1ß, IL-6 and TNF-α in three brain regions (cerebral cortex, hippocampus and striatum) were determined. The results showed that long-term medium-intensity exercise reduced the effects of methamphetamine on inflammation markers in the brain and CPP scores. In addition, long-term medium-intensity exercise decreased IL-1ß concentrations in the cerebral cortex and hippocampus, reduced IL-6 concentrations in the striatum, and reduced TNF-α concentrations in the cerebral cortex, hippocampus, and striatum in methamphetamine-treated mice; low-intensity exercise was less effective. The results indicated that long-term medium-intensity exercise could reduce concentrations of methamphetamine-induced encephalitis factors in male mice, while low-intensity exercise was less effective in alleviating dependence and inflammatory responses. It is suggested that exercise intensity is an important factor affecting the dependence level and inflammatory responses in the brain in mice administered methamphetamine.

Associations of Dietary Inflammatory Index With Prediabetes and Insulin Resistance.

BACKGROUND AND AIMS: Previous studies suggested that dietary inflammatory index (DII) was associated with a variety of adverse health conditions. However, less is known about the role of DII in prediabetes and insulin resistance (IR). Therefore, this study aimed to investigate whether DII is associated with prediabetes and IR in American adults. METHOD AND RESULTS: DII scores were calculated using the average of two 24-hour dietary recalls. Linear regression models were performed to evaluate the associations of DII with markers of Type 2 diabetes (T2D) risk, and the associations of DII with prediabetes and IR were estimated using logistic regression model. The diet of the participants showed an anti-inflammatory potential, with a mean DII score of -0.14 (range: -5.83 to +5.32). After controlling for multiple potential confounders, DII scores were positively associated with fasting plasma glucose (FPG) (ß: 0.009; 95%CI: 0.005 to 0.012), fasting serum insulin (FSI) (ß: 0.083; 95%CI: 0.067 to 0.099) and homeostatic model assessment of insulin resistance (HOMA-IR) (ß: 0.092; 95%CI: 0.075 to 0.109). Participants in the highest tertile of DII score have increased odds of prediabetes (OR: 1.40; 95%CI: 1.17 to 1.69; P for trend <0.001) and IR (OR: 1.79; 95%CI: 1.49 to 2.14; P for trend <0.001) compared with those in the first tertile of DII score. CONCLUSIONS: This study indicates that DII was positively associated with FPG, FSI, and HOMA-IR, and a more pro-inflammatory diet was related to increased odds of insulin resistant and prediabetes.

Research on Total Ionizing Dose Effect and Reinforcement of SOI-TFET.

Since the oxide/source overlap structure can improve the tunneling probability and on-state current of tunneling field effect transistor (TFET) devices, and the silicon-on-insulator (SOI) structure has the effect of resisting the single event effect, SOI-TFET with the oxide/source overlap structure is a device with development potential. The total ionizing dose (TID) effect on SOI-TFET was studied by discussing the switching ratio, band-band tunneling rate, threshold voltage, sub-threshold swing and bipolar effect of the device under different doses of irradiation. At the same time, simulations prove that selecting the proper thickness of the buried oxide (BOX) layer can effectively reduce the influence of the TID effect. This provides a way of direction and method for research on the irradiation effects on the device in the future.

Parallel implementation of w-projection wide-field imaging.

w-Projection is a wide-field imaging technique that is widely used in radio synthesis arrays. Processing the wide-field big data generated by the future Square Kilometre Array (SKA) will require significant updates to current methods to significantly reduce the time consumed on data processing. Data loading and gridding are found to be two major time-consuming tasks in w-projection. In this paper, we investigate two parallel methods of accelerating w-projection processing on multiple nodes: the hybrid Message Passing Interface (MPI) and Open Multi-Processing (OpenMP) method based on multicore Central Processing Units (CPUs) and the hybrid MPI and Compute Unified Device Architecture (CUDA) method based on Graphics Processing Units (GPUs). Both methods are successfully employed and operated in various computational environments, confirming their robustness. The experimental results show that the total runtime of both MPI + OpenMP and MPI + CUDA methods is significantly shorter than that of single-thread processing. MPI + CUDA generally shows faster performance when running on multiple nodes than MPI + OpenMP, especially on large numbers of nodes. The single-precision GPU-based processing yields faster computation than the double-precision processing; while the single- and double-precision CPU-based processing shows consistent computational performance. The gridding time remarkably increases when the support size of the convolution kernel is larger than 8 and the image size is larger than 2,048 pixels. The present research offers useful guidance for developing SKA imaging pipelines.

Manipulating Microrobots Using Balanced Magnetic and Buoyancy Forces.

We present a novel method for the three-dimensional (3D) control of microrobots within a microfluidic chip. The microrobot body contains a hollow space, producing buoyancy that allows it to float in a microfluidic environment. The robot moves in the z direction by balancing magnetic and buoyancy forces. In coordination with the motion of stages in the xy plane, we achieved 3D microrobot control. A microgripper designed to grasp micron-scale objects was attached to the front of the robot, allowing it to hold and deliver micro-objects in three dimensions. The microrobot had four degrees of freedom and generated micronewton-order forces. We demonstrate the microrobot's utility in an experiment in which it grips a 200 µm particle and delivers it in a 3D space.

The novel truncated isoform of human manganese superoxide dismutase has a differential role in promoting metastasis of lung cancer cells.

Growing evidences have demonstrated alternative splicing makes great contribution to tumor metastasis since multiple protein isoforms from a single gene that often display different functions in the cell. Human manganese superoxide dismutase (hMnSOD) was revealed dysregulation in progress of tumor metastasis, while the effect of hMnSOD isoforms on metastasis remained unclear. In this study, we showed a novel truncated hMnSOD isoform hMnSOD183, which lacked 39 amino acids compared with hMnSOD222. We expressed two hMnSOD protein isoforms in Escherichia coli, respectively, and found that the MnSOD activity of truncated hMnSOD isoform was especially weaker. In 95-D cells, mRNA levels of hMnSOD variants and MnSOD activity were significantly increased than that in A549 cells. Furthermore, the hMnSODc exhibited lower mRNA level than hMnSODa/b in A549 and 95-D cells. Additionally, the effects of two isoforms were assessed about cell invasion, overexpression of hMnSOD222 but not hMnSOD183 promoted 95-D cells metastasis, and hMnSOD knockdown significantly reduced cells invasive behavior. Overexpression of hMnSOD isoforms also caused changes of metastasis associated proteins, such as up-regulation of MMPs, VEGF and Vimentin and down-regulation of E-cadherin. Moreover, overexpression of hMnSOD183 had weaker effect on metastasis related signaling proteins, such as Akt, JNK and IKKß, compared to hMnSOD222. In conclusion, our study identified that hMnSOD isoforms induced lung cancer cells invasion through Akt-JNK-IKKß signaling pathways and the hMnSOD183 isoform played a weaker role than hMnSOD222. Characterization of hMnSOD isoforms is useful for future investigation on metastasis of lung cancer cells.

EPB41L3 is a potential tumor suppressor gene and prognostic indicator in esophageal squamous cell carcinoma.

Although there have been reports about the role of erythrocyte membrane protein band 4.1 like 3 (EPB41L3) in several types of cancer, primarily in non-small-cell lung carcinoma, the molecular function and modulatory mechanisms of EPB41L3 remain unclear. In specific, the functional and clinical significance of EPB41L3 in esophageal squamous cell carcinoma (ESCC) has not been explored to date. In the present study, reduced EPB41L3 expression was demonstrated in ESCC cell lines and tissues, which was due to its high methylation rate. Ectopic expression of EPB41L3 in ESCC cells inhibited cell proliferation in vivo and in vitro. In addition, EPB41L3 overexpression induced apoptosis and G2/M cell cycle arrest by activating Caspase-3/8/9 and Cyclin-dependent kinase 1/Cyclin B1 signaling, respectively. Notably, patients with higher EPB41L3 expression had markedly higher overall survival rates compared with patients with lower EPB41L3 expression. In summary, the present results suggest that EPB41L3 may be a tumor suppressor gene in ESCC development, representing a potential therapeutic target and a prognostic indicator for ESCC.

Detection and analysis of 12 heavy metals in blood and hair sample from a general population of Pearl River Delta area.

To detect the content of 12 heavy metals in blood and hair sample from a general population of Pearl River Delta area, and to analyze the influence of duration of residence, gender, age, smoking and drinking on the heavy metal content. Use inductively coupled plasma mass spectrometry to detect the content of 12 heavy metals lead (Pb), mercury (Hg), cadmium (Cd), aluminum (Al), arsenic (As), copper (Cu), chrome (Cr), manganese (Mn), nickel (Ni), zinc (Zn), tin (Sn) and antimony (Sb) in blood and hair samples of a total of 50 subjects from a general population, collected by multistage stratified cluster random sampling method. The geometric mean of heavy metal content in blood samples of general population (µg/L): blood aluminum 214.00; blood chrome 92.82; blood manganese 21.43; blood nickel 20.59; blood copper 0.67; blood zinc 11.50; blood arsenic 0.55; blood cadmium 2.45; blood tin 0.00; blood antimony 1.92; blood lead 158.84; and blood mercury 1.19. The geometric mean of heavy metal content in hair samples of general population (µg/g): hair aluminum is 84.65; hair chrome 0.00; hair manganese 2.44; hair nickel 0.61; hair copper 28.49; hair zinc 136.65; hair arsenic 0.75; hair cadmium 0.46; hair tin 1.04; hair antimony 0.05; hair lead 8.97; and hair mercury 0.69. Some heavy metals were correlated with duration of residence, gender, age, smoking and drinking. This was the first time that simultaneously detecting heavy metal content in blood and hair was used to analyze the internal heavy metal burden in resident population of Pearl River Delta area. These data can serve as reference for further research.

A systems biology approach to study the biology characteristics of esophageal squamous cell carcinoma by integrating microRNA and messenger RNA expression profiling.

Esophageal squamous cell carcinoma (ESCC) is one of the most malignant tumors. The aim of this study was to investigate the biology characteristics of ESCC by analyzing microRNA and mRNA expression profile. We used BRB-array tools to analyze the deregulated microRNA and mRNA between esophageal squamous cell carcinomas and paired normal adjacent tissues. We used miRTrail and protein-protein interaction methods to explore the related pathways and networks of deregulated microRNA and mRNA. By combining the results of pathways and networks, we found that the deregulated microRNA and their deregulated target mRNA are enriched in the following pathways: DNA replication, cell cycle, ECM-receptor interaction, focal adhesion, mismatch repair, and pathways in cancer. The results showed that many deregulated microRNAs and mRNAs may play a vital role in the pathogenesis of ESCC, and the systems biology approach is very helpful to explore molecular mechanism of ESCC.