Ultrasonic Image Features under the Intelligent Algorithm in the Diagnosis of Severe Sepsis Complicated with Renal Injury.

This research was aimed at analyzing the diagnosis of severe sepsis complicated with acute kidney injury (AKI) by ultrasonic image information based on the artificial intelligence pulse-coupled neural network (PCNN) algorithm and at improving the diagnostic accuracy and efficiency of clinical severe sepsis complicated with AKI. In this research, 50 patients with sepsis complicated with AKI were collected as the observation group and 50 patients with sepsis as the control group. All patients underwent ultrasound examination. The clinical data of the two groups were collected, and the scores of acute physiology and chronic health assessment (APACHE II) and sequential organ failure assessment (SOFA) were compared. The ultrasonic image information enhancement algorithm based on artificial intelligence PCNN is constructed and simulated and is compared with the maximum between-class variance (OSTU) algorithm and the maximum entropy algorithm. The results showed that the PCNN algorithm was superior to the OSTU algorithm and maximum entropy algorithm in the segmentation results of severe sepsis combined with AKI in terms of regional consistency (UM), regional contrast (CM), and shape measure (SM). The acute physiology and chronic health evaluation (APACHE II) and sequential organ failure assessment (SOFA) scores in the observation group were substantially higher than those in the control group (P < 0.05). The interlobular artery resistance index (RI) in the observation group was substantially higher than that in the control group (P < 0.05). Moreover, the mean transit time (mTT) in the observation group was significantly higher than that in the control group (4.85 ± 1.27 vs. 3.42 ± 1.04), and the perfusion index (PI) was significantly lower than that in the control group (134.46 ± 17.29 vs. 168.37 ± 19.28), with statistical significance (P < 0.05). In summary, it can substantially increase ultrasonic image information based on the artificial intelligence PCNN algorithm. The RI, mTT, and PI of the renal interlobular artery level in ultrasound images can be used as indexes for the diagnosis of severe sepsis complicated with AKI.

High detection efficiency silicon single-photon detector with a monolithic integrated circuit of active quenching and active reset.

Silicon single-photon detectors (SPDs) are key devices for detecting single photons in the visible wavelength range. Photon detection efficiency (PDE) is one of the most important parameters of silicon SPDs, and increasing PDE is highly required for many applications. Here, we present a practical approach to increase the PDE of silicon SPDs with a monolithic integrated circuit of active quenching and active reset (AQAR). The AQAR integrated circuit is specifically designed for thick silicon single-photon avalanche diodes (SPADs) with high breakdown voltage (250 V-450 V) and then fabricated via the process of high-voltage 0.35-µm bipolar-CMOS-DMOS. The AQAR integrated circuit implements the maximum transition voltage of ∼68 V with 30 ns quenching time and 10 ns reset time, which can easily boost PDE to the upper limit by regulating the excess bias up to a high enough level. By using the AQAR integrated circuit, we design and characterize two SPDs with the SPADs disassembled from commercial products of single-photon counting modules (SPCMs). Compared with the original SPCMs, the PDE values are increased from 68.3% to 73.7% and 69.5% to 75.1% at 785 nm, respectively, with moderate increases in dark count rate and afterpulse probability. Our approach can effectively improve the performance of the practical applications requiring silicon SPDs.

A Novel Bispecific Antibody with PD-L1-assisted OX40 Activation for Cancer Treatment.

Immunotherapy using OX40 agonist antibodies shows great preclinical efficacy in mouse tumor models. But in a clinical setting, OX40 agonist antibody alone or in combination with checkpoint blockade exhibits only modest efficacy due to lack of sufficient activation. We hypothesized that the limited antitumor activity in patients may due to insufficient clustering of OX40 antibody in the tumor. To test this hypothesis, we generated a tetravalent programmed death ligand-1 (PD-L1)/OX40 BsAb by fusing two PD-L1 VHH fragments to the C-terminus of a nonblocking agonistic anti-OX40 antibody. The resulting BsAb had intact function of each parental antibody, including efficiently blocking PD1/PD-L1 interaction and inducing OX40 activation. In addition, this BsAb showed significantly enhanced potency in activation of OX40-expressing T cells when PD-L1-expressing tumor cells or dendrite cells were present, through PD-L1-mediated cross-linking of OX40. Moreover, the BsAb exhibited superior antitumor activities over the parental monospecific antibodies alone or in combination in multiple in vivo tumor models. These results demonstrated a great potential for further clinical development of the potent immunostimulatory PD-L1/OX40 bispecific antibody.

miR-93-5p Transferred by Exosomes Promotes the Proliferation of Esophageal Cancer Cells via Intercellular Communication by Targeting PTEN / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the relationship between plasma miR-93-5p and the risk of esophageal cancer, as well as the influence of miR-93-5p on the biological function of esophageal cancer cells, exerted through exosomes.</p><p><b>METHODS</b>The expression of plasma miR-93-5p in esophageal cancer patients and healthy controls was analysed by real-time quantitative PCR. The influence of miR-93-5p on the risk and prognosis of esophageal carcinoma was analyzed by conditional logistic regression and survival analysis. The effect of miR-93-5p on the biological function of recipient cells was investigated by establishing an in vitro donor cell co-culture model. The target gene of miR-93-5p was validated by luciferase reporter assay and Western Blotting.</p><p><b>RESULTS</b>Upregulation of plasma miR-93-5p expression significantly increases the risk of esophageal cancer and is associated with poor prognosis. miR-93-5p transferred by exosomes promotes the proliferation of recipient esophageal cancer cells and affects the expression of PTEN and its downstream proteins p21 and cyclin D1.</p><p><b>CONCLUSION</b>Our study provides a reference for the identification of biomarkers for the diagnosis and prognosis of esophageal cancer.</p>

The Lipocalin LPR-1 Cooperates with LIN-3/EGF Signaling To Maintain Narrow Tube Integrity in Caenorhabditis elegans.

Lipocalins are secreted cup-shaped glycoproteins that bind sterols, fatty acids, and other lipophilic molecules. Lipocalins have been implicated in a wide array of processes related to lipophilic cargo transport, sequestration, and signaling, and several are used as biomarkers for human disease, but the functions of most lipocalins remain poorly understood. Here we show that the Caenorhabditis elegans lipocalin LPR-1 is required to maintain apical membrane integrity and a continuous lumen in two narrow unicellular tubes, the excretory duct and pore, during a period of rapid lumen elongation. LPR-1 fusion protein is expressed by the duct and pore and accumulates both intracellularly and in apical extracellular compartments, but it can also function cell nonautonomously when provided from outside of the excretory system. lpr-1 mutant defects can be rescued by increased signaling through the epidermal growth factor (EGF)-Ras-extracellular signal regulated kinase (ERK) pathway, which promotes the more elongated duct vs. less elongated pore tube fate. Spatial and temporal rescue experiments indicate that Ras signaling acts within the duct and pore tubes during or prior to cell fate determination to bypass the requirement for LPR-1 lpr-1 mutations did not disrupt LIN-3/EGF-dependent duct-fate specification, prevent functioning of any specific LIN-3/EGF isoform, or alter LET-23/EGFR localization, and reduced signaling did not phenocopy or enhance lpr-1 mutant defects. These data suggest that LPR-1 protects lumen integrity through a LIN-3/EGF-independent mechanism, but that increased signaling upregulates some target(s) that can compensate for lpr-1 absence.

Integrity of Narrow Epithelial Tubes in the C. elegans Excretory System Requires a Transient Luminal Matrix.

Most epithelial cells secrete a glycoprotein-rich apical extracellular matrix that can have diverse but still poorly understood roles in development and physiology. Zona Pellucida (ZP) domain glycoproteins are common constituents of these matrices, and their loss in humans is associated with a number of diseases. Understanding of the functions, organization and regulation of apical matrices has been hampered by difficulties in imaging them both in vivo and ex vivo. We identified the PAN-Apple, mucin and ZP domain glycoprotein LET-653 as an early and transient apical matrix component that shapes developing epithelia in C. elegans. LET-653 has modest effects on shaping of the vulva and epidermis, but is essential to prevent lumen fragmentation in the very narrow, unicellular excretory duct tube. We were able to image the transient LET-653 matrix by both live confocal imaging and transmission electron microscopy. Structure/function and fluorescence recovery after photobleaching studies revealed that LET-653 exists in two separate luminal matrix pools, a loose fibrillar matrix in the central core of the lumen, to which it binds dynamically via its PAN domains, and an apical-membrane-associated matrix, to which it binds stably via its ZP domain. The PAN domains are both necessary and sufficient to confer a cyclic pattern of duct lumen localization that precedes each molt, while the ZP domain is required for lumen integrity. Ectopic expression of full-length LET-653, but not the PAN domains alone, could expand lumen diameter in the developing gut tube, where LET-653 is not normally expressed. Together, these data support a model in which the PAN domains regulate the ability of the LET-653 ZP domain to interact with other factors at the apical membrane, and this ZP domain interaction promotes expansion and maintenance of lumen diameter. These data identify a transient apical matrix component present prior to cuticle secretion in C. elegans, demonstrate critical roles for this matrix component in supporting lumen integrity within narrow bore tubes such as those found in the mammalian microvasculature, and reveal functional importance of the evolutionarily conserved ZP domain in this tube protecting activity.

Prevalence of Overweight and Obesity among Students Aged 7-22 Years in Jiangsu Province, China / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To report the prevalence and trend of overweight and obesity among students aged 7-22 years in Jiangsu, 2010 to 2013.</p><p><b>METHODS</b>This cross-sectional study was carried out as part of students physical fitness and health survey in Jiangsu province. A total of 255,581 subjects (50.03% males and 49.97% females) enrolled in 82 school and 10 universities in Jiangsu. Weights and heights were obtained for each subject and its body mass index (BMI) was calculated using the Chinese Working Group on Obesity in China (CWGO).</p><p><b>RESULTS</b>Anthropometric measurement including bodyweight, height, BMI and bust were significantly different between males in urban compared to females living rural areas (P<0.001). The total prevalence of overweight and obesity was 12.4% and 5.7%. Males had a significantly higher rate than in female's student. The prevalence of overweight and obesity by age groups was (14.5%, 10.3%) at age 7-11 years, (11.2%, 6.8%) at age 12-14 years, (11.7%, 3.1%) at age 15-17 years, and (11.4%, 2.3%) at age 18-22 years. By regions; the highest prevalence of overweight obesity reported in Taizhou (10%, 14.2%), Xuzhou (9.4%, 12.5%), and Nanjing (9.2%, 15.6%), respectively.</p><p><b>CONCLUSION</b>The finding declares that overweight and obesity are important health problems among students in Jiangsu Province. Early intervention programme are needed to address this problems.</p>

The effect of ligands on the thermal stability of sulfotransferases: a molecular dynamics simulation study.

Human cytosolic sulfotransferases (hSULTs) are important phase II metabolic enzymes. They catalyze transfer of the sulfuryl-group (-SO3) from 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to the hydroxyl or primary amine moieties of a large number of endogenous and xenobiotic substrates. Broad selectivity and specificity of binding and activity within the sulfortransferases family could be detected by thermal denaturation assays, which have been made more and more suitable for high throughput screening based on recent technical advances. Here molecular dynamics simulations were used to explore the effect of the cofactor (PAPS) and substrate (LCA) on the thermal stability of the enzyme. It was found that the apo-enzyme unfolded fastest upon heating. The holo-enzyme with bound substrate LCA unfolded slowest. This thermo-denaturation order is consistent with that observed in experiments. Further it was found that the cofactor and substrate will pronouncedly increase the thermal stability of the active pocket regions that interact directly with the ligands. In addition, cofactor and substrate show noticeable synergy effect on the thermal stability of the enzyme.

Mycobacterium tuberculosis suppresses innate immunity by coopting the host ubiquitin system.

Mycobacterium tuberculosis PtpA, a secreted tyrosine phosphatase essential for tuberculosis pathogenicity, could be an ideal target for a drug against tuberculosis, but its active-site inhibitors lack selectivity over human phosphatases. Here we found that PtpA suppressed innate immunity dependent on pathways of the kinases Jnk and p38 and the transcription factor NF-κB by exploiting host ubiquitin. Binding of PtpA to ubiquitin via a region with no homology to human proteins activated it to dephosphorylate phosphorylated Jnk and p38, leading to suppression of innate immunity. Furthermore, the host adaptor TAB3 mediated NF-κB signaling by sensing ubiquitin chains, and PtpA blocked this process by competitively binding the ubiquitin-interacting domain of TAB3. Our findings reveal how pathogens subvert innate immunity by coopting host ubiquitin and suggest a potential tuberculosis treatment via targeting of ubiquitin-PtpA interfaces.

The SAX-3 receptor stimulates axon outgrowth and the signal sequence and transmembrane domain are critical for SAX-3 membrane localization in the PDE neuron of C. elegans.

SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UNC-51 might play a role in SAX-3 membrane localization. Furthermore, we demonstrate that the N-terminal signal sequence and the transmembrane domain are essential for the subcellular localization of SAX-3 in the PDE neurons.

Isolation and characterization of an algicidal bacterium indigenous to lake Taihu with a red pigment able to lyse microcystis aeruginosa / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To isolate and characterize indigenous algicidal bacteria and their algae-lysing compounds active against Microcystis aeruginosa, strains TH1, TH2, and FACHB 905.</p><p><b>METHODS</b>The bacteria were identified using the Biolog automated microbial identification system and 16S rDNA sequence analysis. The algae-lysing compounds were isolated and purified by silica gel column chromatography and reverse-phase high performance liquid chromatography. Their structures were confirmed by Nuclear Magnetic Resonance (NMR) and Fourier Transform Infrared (FT-IR) spectroscopy. Algae-lysing activity was observed using microscopy.</p><p><b>RESULTS</b>The algae-lysing bacterium LTH-2 isolated from Lake Taihu was identified as Serratia marcescens. Strain LTH-2 secreted a red pigment identified as prodigiosin (C20H25N3O), which showed strong lytic activity with algal strains M. aeruginosa TH1, TH2, and FACHB 905 in a concentration-dependent manner. The 50% inhibitory concentration (IC50) of prodigiosin with the algal strains was 4.8 (± 0.4)× 10⁻² μg/mL, 8.9 (± 1.1)× 10⁻² μg/mL, and 1.7 (± 0.1)× 10⁻¹ μg/mL in 24 h, respectively.</p><p><b>CONCLUSION</b>The bacterium LTH-2 and its pigment had strong Microcystis-lysing activity probably related to damage of cell membranes. The bacterium LTH-2 and its red pigment are potentially useful for regulating blooms of harmful M. aeruginosa.</p>

ZnO, TiO(2), SiO(2,) and Al(2)O(3) nanoparticles-induced toxic effects on human fetal lung fibroblasts / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>This study aims to investigate and compare the toxic effects of four types of metal oxide (ZnO, TiO(2), SiO(2,) and Al(2)O(3)) nanoparticles with similar primary size (∼20 nm) on human fetal lung fibroblasts (HFL1) in vitro.</p><p><b>METHODS</b>The HFL1 cells were exposed to the nanoparticles, and toxic effects were analyzed by using MTT assay, cellular morphology observation and Hoechst 33 258 staining.</p><p><b>RESULTS</b>The results show that the four types of metal oxide nanoparticles lead to cellular mitochondrial dysfunction, morphological modifications and apoptosis at the concentration range of 0.25-1.50 mg/mL and the toxic effects are obviously displayed in dose-dependent manner. ZnO is the most toxic nanomaterials followed by TiO(2), SiO(2), and Al(2)O(3) nanoparticles in a descending order.</p><p><b>CONCLUSION</b>The results highlight the differential cytotoxicity associated with exposure to ZnO, TiO(2), SiO(2), and Al(2)O(3) nanoparticles, and suggest an extreme attention to safety utilization of these nanomaterials.</p>

Coordinated regulation of active and repressive histone methylations by a dual-specificity histone demethylase ceKDM7A from Caenorhabditis elegans.

H3K9me2 and H3K27me2 are important epigenetic marks associated with transcription repression, while H3K4me3 is associated with transcription activation. It has been shown that active and repressive histone methylations distribute in a mutually exclusive manner, but the underlying mechanism was poorly understood. Here we identified ceKDM7A, a PHD (plant homeodomain)- and JmjC domain-containing protein, as a histone demethylase specific for H3K9me2 and H3K27me2. We further demonstrated that the PHD domain of ceKDM7A bound H3K4me3 and H3K4me3 co-localized with ceKDM7A at the genome-wide level. Disruption of the PHD domain binding to H3K4me3 reduced the demethylase activity in vivo, and loss of ceKDM7A reduced the expression of its associated target genes. These results indicate that ceKDM7A is recruited to the promoter to demethylate H3K9me2 and H3K27me2 and activate gene expression through the binding of the PHD domain to H3K4me3. Thus, our study identifies a dual-specificity histone demethylase and provides novel insights into the regulation of histone methylation.

Critical role of lysosome and its associated protein cathepsin D in manganese-induced toxicity in cultured midbrain astrocyte.

Astrocyte is considered to be the initial target in manganese neurotoxicity; however, the ultra structure changes in the cells and the mechanism underlying the manganese-induced toxicity are still unclear. In this study, we conducted several assays in cultured midbrain astrocyte to determine the role of mitochondria, lysosome and its associated protein cathepsin D in the manganese-induced toxicity. We found that a mixed form of cell death in the manganese treated astrocyte. During the process of cell death, we detected extensive cytoplasmic vacuolation, mitochondrial swelling, and increased number and membrane permeability of lysosomes in the manganese treated astrocyte. Furthermore, we documented that after exposed to manganese, the Bax protein level in the astrocyte was increased, and its cellular distribution was significantly translocated from cytosol to mitochondria and lysosomes. Moreover, we demonstrated that manganese treatment caused significant increase of lysosomal enzyme cathepsin D, and pretreatment with cathepsin D inhibitor pepstatin A increased the apoptotic cell death. Collectively, our study suggests that different forms of cell death are involved in manganese-induced toxicity in the cultured midbrain astrocyte, and lysosome and its associated protein cathepsin D play a critical role in the pathological process. These results may shed new light on the mechanism of manganese exposure related neurological disorders.

Nurr1 expression and its modulation in microglia.

OBJECTIVE: Nurr1, a transcription factor essential for the differentiation and maturation of central dopaminergic cells, is primarily expressed in neurons of the central nervous system. In this study, we intend to determine the expression and modulation of Nurr1 in cultured microglia. METHODS: Nurr1 expression in cultured primary mouse microglia was measured by reverse transcription polymerase chain reaction, Western blot and immunofluorescent staining. Lipopolysaccharide (LPS) was used to activate microglia. Specific inhibitors were used to investigate whether the mitogen- activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), MAPK/Jun N-terminal kinase (JNK), P38 MAPK and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathways were involved in the modulation of Nurr1 expression. RESULTS: Nurr1 was found to be located at both the cytoplasm and the nucleus of the microglia. After LPS stimulation, the expression of Nurr1 was significantly increased, which could be partially blocked by inhibitors of ERK, JNK and PI3K/Akt, but not by the P38 MAPK inhibitor; the ERK inhibitor can partially block the translocation of Nurr1 from the cytoplasm to the nucleus. CONCLUSION: Nurr1 is found to be expressed in cultured mouse microglia. The expression of Nurr1 is increased and the protein is translocated from the cytoplasm to the nucleus after activation by LPS, which could be modulated by the ERK, JNK and PI3K/Akt pathways.

ATP depletion is the major cause of MPP+ induced dopamine neuronal death and worm lethality in alpha-synuclein transgenic C. elegans.

OBJECTIVE: To investigate the toxic effect of environmental neurotoxin MPP+ to C. elegans and identify the mechanisms that cause the toxicity. METHODS: Human alpha-synuclein transgenic C. elegans was used as the animal model, the toxic effect of MPP+ to dopamine (DA) neurons and the lifespan of worms was tested. The worms were feed with OP50 to determine whether ATP increase can rescue the worm from toxicity. ATP level and aberrant protein accumulation were analyzed in the MPP+ treated worms with or without OP50 addition. RESULTS: We found that MPP+ induced DA cell death and worm lethality, which could be prevented by OP50 treatment. OP50 exerted the protective effect by up-regulating ATP level, even though it also induced accumulation of alpha-synuclein. Despite the undefined role of protein aggregation to the cell death, our results showed that the toxicity of MPP+ was mainly caused by the ATP depletion in the alpha-synuclein transgenic C. elegans. CONCLUSION: MPP+ could induce DA neuronal death and worm lethality in alpha-synuclein transgenic C. elegans; Compared with the aggregation of alpha-synuclein, the major cause of MPP+ toxicity appeared due to ATP depletion.

ATP depletion is the major cause of MPP+ induced dopamine neuronal death and worm lethality in alpha-synuclein transgenic C. elegans / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To investigate the toxic effect of environmental neurotoxin MPP+ to C. elegans and identify the mechanisms that cause the toxicity.</p><p><b>METHODS</b>Human alpha-synuclein transgenic C. elegans was used as the animal model, the toxic effect of MPP+ to dopamine (DA) neurons and the lifespan of worms was tested. The worms were feed with OP50 to determine whether ATP increase can rescue the worm from toxicity. ATP level and aberrant protein accumulation were analyzed in the MPP+ treated worms with or without OP50 addition.</p><p><b>RESULTS</b>We found that MPP+ induced DA cell death and worm lethality, which could be prevented by OP50 treatment. OP50 exerted the protective effect by up-regulating ATP level, even though it also induced accumulation of alpha-synuclein. Despite the undefined role of protein aggregation to the cell death, our results showed that the toxicity of MPP+ was mainly caused by the ATP depletion in the alpha-synuclein transgenic C. elegans.</p><p><b>CONCLUSION</b>MPP+ could induce DA neuronal death and worm lethality in alpha-synuclein transgenic C. elegans; Compared with the aggregation of alpha-synuclein, the major cause of MPP+ toxicity appeared due to ATP depletion.</p>

Association of combined CYP2E1 gene polymorphism with the risk for esophageal squamous cell carcinoma in Huai'an population, China / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Cytochrome P450 2E1 (CYP2E1) has an important role in the metabolic activation of precarcinogens such as N-nitrosoamines and other low relative molecular mass, organic compounds. This study examined whether CYP2E1 RsaI and DraI polymorphism are associated with susceptibility to esophageal squamous cell carcinoma and the correlation between the genotypes and expression levels of CYP2E1 mRNA.</p><p><b>METHODS</b>Seventy-seven patients with newly diagnosed, untreated esophageal squamous cell carcinoma and 79 healthy controls matched in age, gender and residence were recruited for the control study. An RsaI polymorphism in the 5'-flanking region and a DraI polymorphism in the sixth intron of the CYP2E1 gene, which could possibly affect its transcription, were determined in this study by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and mRNA level of CYP2E1 was measured by quantitative real-time reverse transcription PCR.</p><p><b>RESULTS</b>No significant association of RsaI or DraI polymorphism of CYP2E1 with susceptibility of esophageal squamous cell carcinoma were demonstrated (OR = 1.67, 95% CI: 0.89 - 3.15, P = 0.11; OR = 1.11, 95% CI: 0.59 - 2.09, P = 0.74, respectively). With SHEsis software, no linkage disequilibrium was detected between RsaI and DraI polymorphism (D' = 0.528, r(2) = 0.27). When combined RsaI polymorphism with DraI polymorphism, the association between that carrying c2 allele and DD genotype and the risk for esophageal squamous cell carcinoma were found (OR = 5.77, 95% CI: 1.65 - 20.22). Compared with the normal controls, the mRNA levels with RsaI polymorphism, DraI polymorphism, or any combined genotypes in cases showed no statistical difference.</p><p><b>CONCLUSIONS</b>This study suggests that carrying c2 allele and DD genotype conferreded an elevated risk for esophageal squamous cell carcinoma. There was no significant statistical relationship between the genotypes c1/c2, D/C, or the combined allele and mRNA expression.</p>