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The purpose of this study was to determine whether autophagy regulates the expression of human cytomegalovirus (HCMV) immediately early two viral protein (IE2). Rapamycin and 3-methyladenine (3-MA) were used to stimulate or suppress autophagy during HCMV infection. UL122 recombinant plasmid was transfected to overexpress IE2 and small interference RNA against autophagy-related protein 3 (ATG3) was used to knockdown ATG3. Western blot was performed to measure the expression of viral proteins and autophagy levels. Immunofluorescence was used to detect the immediately early 1 viral protein (IE1) expression. In human embryonic lung fibroblasts, infection of HCMV promotes the lipidation of light chain 3 (LC3) at 6 and 24 hours post infection (hpi), which was accompanied by the increased expression of viral protein IE2. When only IE2 was overexpressed via UL122 recombinant plasmid transfection without HCMV infection, the autophagy hallmarks LC3II and ATG3 were upregulated. Furthermore, viral protein IE2 expression was reduced at 24 and 48 hpi either by the treatment of autophagy inducer rapamycin or by the inhibitor 3-MA before HCMV infection. At the same time, small interference ATG3 transient transfection, used to suppress autophagy, significantly inhibited IE2 expression. However, when 3-MA was used to regulate autophagy levels after HCMV infection, expression of IE2 and IE1 were both decreased, while autophagy inducer rapamycin treatment after HCMV infection increased IE2 expression slightly. IE2 was involved in autophagy induced by HCMV infection and blocking autophagy could inhibit the expression of HCMV viral protein IE2, which might be one way for autophagy to restrict HCMV replication.

Background Early detection of urothelial carcinoma (UC) by noninvasive diagnostic methods with high accuracy is still underscored. This study aimed to develop a noninvasive assay incorporating both enrichment of urine exfoliated cells and immunoassays for UC detection. Methods Polystyrene dishes were exposed to oxygen plasma and modified with 3‐aminopropyltriethoxysilane to prepare amine‐functionalized nanostructured substrates (NS). Performance characterization of NS was evaluated by atomic force microscope and X‐ray photoelectron spectroscopy. Urine exfoliated cells were captured by NS and then immunostained to detect urinary tumor cells (UTCs), which was called UTC assay. The receiver operating characteristic (ROC) curve, area under ROC curve (AUC), and Youden index were used to find the cutoff value of UTC assay. ROC analysis and McNemar test were used to compare the diagnostic accuracy of UTC assay with cytology. Kappa test was used to analyze the agreement of UTC assay and cytology with pathological diagnosis. Results Nanostructured substrates had good cell binding yields of nucleated cells and tumor cells. CK20+CD45−CD11b− cells were considered as UTCs. UTC number ≥ 1 per sample could be considered as a positive result. By AUC and Kappa analysis, UTC assay showed good performance in UC detection. McNemar test demonstrated that UTC assay had a superior sensitivity even in low‐grade subgroup and a similar specificity compared to cytology in UC diagnosis. Conclusions Nanostructured substrates could be used to enrich the exfoliated cells from urine samples. UTC assay with NS has the potential to play a role in UC detection. The value of this assay still needs additional validation by large, multi‐center studies., Nanostructured Substrates (NS) could be used to enrich exfoliated nucleate cells from urine samples. The assay based on NS enrichment and immunocytology could be a novel non‐invasive diagnostic tool for urothelial carcinoma (UC).

Prussian blue analogs (PBAs) are considered as efficient catalysts for energy-related applications due to their porous nanoscale architectures containing finely disseminated active sites. Their catalytic capability can be greatly boosted by the rational design and construction of complex PBA hybrid nanostructures. However, present-day structure engineering inevitably involves additional etchant or procedure. Herein, a facile, yet controllable one-pot self-assembly strategy is introduced to prepare hierarchical core-shell polymetallic PBAs (featuring bimetallic FeMn PBAs cores and CoNi PBAs shells) with hollow nano-cages/solid nano-cube architectures. The detailed characterization of material morphology/composition, assisted with theoretical simulations, reveals the underlying formation mechanism where the key factor is the control of the nucleation rate via the use of chelating agent (citrates) and reaction kinetics. The resulting FeMn@CoNi-H compound is found to accelerate the oxygen evolution reaction activity with a low overpotential (236 mV at a current density 10 mA cm

Metastasis is a serious risk that may occur during the treatment of hepatocellular carcinoma (HCC), preventing many patients from being surgical candidates and contributing to poor prognosis. Hypoxia has been proved an important factor of metastasis through the epithelial–mesenchymal transition (EMT) pathway. Acetyl‐CoA synthase 2 (ACSS2) provides an acetyl group for the acetylation of hypoxia‐inducible factor (HIF)‐2α, and this epigenetic modification affects the activity of HIF‐2α and the subsequent EMT process. Here, we showed that ACSS2 expression was negatively correlated with HCC malignancy. Knockdown of ACSS2 increased the invasion and migration ability of HCC cells and promoted EMT without increasing the total protein level of HIF‐2α, even in hypoxic conditions. The immunoprecipitation assay revealed downregulated acetylation levels of HIF‐2α after ACSS2 knockdown in hypoxic conditions, which resulted in enhanced HIF‐2α activity. Finally, decreased expression of ACSS2 was found to be related to advanced stage and poor overall survival and disease‐free survival rates in a cohort of patients with HCC. In conclusion, ACSS2 plays an important role in the acetylation process of HIF‐2α, which effectively modifies the activity of HIF‐2α under hypoxic conditions and greatly impacts on the prognosis of patients with HCC.

Objective Although transforming growth factor β (TGFβ) is recognized as being a key trigger of fibroblast activation in systemic sclerosis (SSc), prominent innate immunity suggests that additional pathways contribute to disease persistence. Toll-like receptor 9 (TLR9) is implicated in autoimmunity and fibrosis; however, the expression, mechanism of action, and pathogenic role of TLR9 signaling in SSc remain uncharacterized. The aim of this study was to explore the expression, activity, and potential pathogenic role of TLR9 in the context of skin fibrosis in SSc and in mouse models of experimental fibrosis. Methods Expression and localization of TLR9 were evaluated in SSc skin biopsy specimens and explanted skin fibroblasts. Fibrotic responses elicited by type A CpG oligonucleotide and mitochondrial DNA (mtDNA) were examined in human skin fibroblasts by a combination of real-time quantitative polymerase chain reaction, Western blot analysis, transient transfection, immunofluorescence microscopy, and functional assays. Expression of TLR9 was examined in 2 distinct mouse models of experimental fibrosis. Results Skin biopsy specimens obtained from 2 independent cohorts of SSc patients showed up-regulation of TLR9, and myofibroblasts were the major cellular source. Moreover, SSc skin biopsy specimens showed evidence of TLR9 pathway activation. CpG induced robust TLR9-dependent fibrotic responses in explanted normal fibroblasts that could be blocked by bortezomib and were mediated through the action of endogenous TGFβ. Mice with experimental fibrosis showed a time-dependent increase in TLR9 localized primarily to myofibroblasts in the dermis. Conclusion In isolated fibroblasts, TLR9 elicits fibrotic responses mediated via endogenous TGFβ. In patients with SSc, mtDNA and other damage-associated TLR9 ligands in the skin might trigger localized activation of TLR9 signaling, TGFβ production, and consequent fibroblast activation. Disrupting this fibrotic process with inhibitors targeting TLR9 or its downstream signaling pathways might therefore represent a novel approach to SSc therapy.

Background: Timely harvest is critical for hybrid rice to achieve maximum seed viability, vigor and yield. However, how to predict the optimum harvest time has been rarely reported so far.; Results: The seed vigor of Zhuliangyou 06 (ZLY06) increased and reached the highest level at 20 days after pollination (DAP), when seed moisture content had a lower value, which was maintained until final seed maturation. For Chunyou 84 (CY84), seed vigor, fresh and dry weight had relatively high values at 25 DAP, when seed moisture content reached the lowest value and changed slightly from 25 to 55 DAP. In both hybrid rice varieties, seed glume chlorophyll content declined rapidly from 10 to 30 DAP and remained at a very low level after 35 DAP. Starch content exhibited an increasing trend during seed maturation, while both soluble sugar content and amylase activity decreased significantly at the early stages of seed development. Moreover, correlation analyses showed that seed dry weight, starch content and superoxide dismutase activity were significantly positively correlated with seed vigor. In contrast, chlorophyll content, moisture content, soluble sugar, soluble protein, abscisic acid, gibberellin content, electrical conductivity, catalase and ascorbate peroxidase activities were significantly negatively correlated with seed vigor. Physiological and biochemical parameters were obviously more closely related with seed vigor than with seed germinability during seed development.; Conclusion: Seed vigor could be better used as a comprehensive factor to predict the optimum seed harvest time. It is suggested that for ZLY06 seeds could be harvested as early as 20 DAP, whereas for CY84 the earliest optimum harvest time was 25 DAP. © 2016 Society of Chemical Industry.; © 2016 Society of Chemical Industry.

The site preference of Mn in alloyed cementite is investigated by using X-ray diffraction (XRD) and first-principles calculations. First-principles calculations of the cohesive energies and formation energies of Mn-alloyed cementite indicate that Mn atoms prefer to substitute the 8d sites of cementite. The calculation results of density of states (DOS) and charge-density difference show that the more stable outermost electron orbital of Mn(3d54s2) may be the main reason for the site preference of Mn at 8d sites in Mn-alloyed cementite. In addition, the experimental XRD spectrum of 25 at.% Mn-alloyed cementite, which is prepared by using mechanical alloying combined with spark plasma sintering, highly coincides with the calculated XRD spectrum of Mn 8d-substituted cementite, verifying that Mn atoms prefer to substitute the 8d sites of alloyed cementite.

An ultra-low carbon grain-oriented silicon steel as-cast strip is produced by twin-roll strip casting process, and subsequently subjected to one-pass hot rolling, one-stage cold rolling, primary annealing, and secondary annealing. The effect of hot rolling process on microstructure, texture, and inhibitor evolution is studied. It is shown that the precipitation behavior of AlN particles is significantly affected by the hot rolling temperature and the optimal precipitation temperature is ≈1100 °C. On the other hand, the intensity of Goss texture in hot-rolled sheets is determined by hot rolling reduction, which is limited in the strip casting process and the hot-rolled Goss texture is relatively weak compared to the conventional process. The primary annealed Goss texture can originate from the cold rolling process and this texture is homogeneous through the thickness, besides the inherited hot-rolled Goss texture mainly presented in the subsurface layer. Thus, relatively strong Goss texture in primary annealed sheets is obtained. The results indicate that the hot rolling process is an efficient way to optimize the texture and precipitation in strip-cast silicon steel, and relatively good magnetic properties can be obtained by the strip casting process.

Summary Erectile dysfunction is a common complication following cryotherapy for prostate cancer. In this study, we investigated the efficacy of adipose-derived stem cells (ADSC) in improving erectile function in a rat model of cavernous nerve (CN) cryoinjury and the possible mechanisms. Male rats were intracavernous (IC) injected with EdU-labeled ADSC after bilateral CN cryoinjury. Penile tissues were harvested for histology and protein level detection at 1 and 4 weeks after ADSC administration. Erectile function was assessed prior to tissue harvest. We found that erectile function was significantly improved after ADSC treatment via promoting nNOS-positive nerve regeneration and cavernous tissue recovery. The expression of cleaved caspase 3 (an apoptotic marker) reduced after ADSC treatment. Although few EdU-labeled ADSCs were visualized within the penis 4 weeks after administration, plenty of EdU-labeled ADSCs were found around penile dorsal vessels and nerves 1 week after treatment. Furthermore, three neurotrophic factors (NGF, VEGF, and Neurturin) were significantly decreased in Cryo group, and were partially recovered 1 week after ADSC injection. These results suggested that IC injection of ADSC resulted in substantial recoveries of erectile function after CN cryoinjury. The effects may be achieved through the elevated level of neurotrophic factors in penile tissue and subsequent neuroregenerative effects.

The Earth has entered into Anthropocene, a new epoch dominated by people. The world’s urban population has grown more than four times during the past 60 years to 3.9 billion. Today, more people are living in the cities than in the countryside in most nations. Cities are growing bigger and faster than ever before (United Nations, 2014). Cities that have a population >10 million are commonly considered as megacities as defined by UN-HABITAT (Li et al., 2015b). Globally, there are about 28 megacities with approximately 13% of the world’s urban population (United Nations, 2014). Most of these megacities are found in Asia. By 2030 the world is projected to have 41 megacities with cities in Africa and Asia growing the fastest (United Nations, 2014). Megacities face many emerging challenges, from economic development and social stability to environmental changes in the 21st Century. Obviously, many of the water resource challenges in megacities are rooted in the rapid rise in competing water demands by people for multiple uses. Water problems arise when water demand cannot be met by water supply due to either natural (e.g., surface or groundwater exhaustion), socioeconomic (e.g., financial and governance), water quality, or environmental constraints. Meeting rapidly growing water demand in megacities often means sacrificing the environment such as water quality degradation, ecosystem damage, and/or unsustainable water use such as groundwater depletion and salt water intrusion. Competing water use by irrigated agriculture, thermoelectric power generation, and industrial and residential water use are common causes of water shortages for megacities, especially in arid or semiarid regions or during extreme drought years. Water pollution alone from megacities can turn a “water rich” city into a “water poor” one as demonstrated by megacities in many developing countries. Climate change affects water availability everywhere, but megacities are most vulnerable simply because of the large water demand by people (Li et al., 2015a, b). Growing extreme weather events (e.g., hurricane, droughts, and floods) associated with climate change and variability pose some of the biggest challenges to water supply infrastructures in megacities. It is

Excessive extracellular matrix synthesis and accumulation in systemic sclerosis (SSc) is due to persistent activation of myofibroblasts triggered by transforming growth factor β (TGFβ) and platelet-derived growth factor (PDGF), as well as reactive oxygen species (ROS) and tissue hypoxia (1). TGFβ-induced transcription of fibrotic genes is critically dependent on histone acetylation catalyzed by acetyltransferases such as p300 (2–4). Several observations implicate p300-dependent histone and nonhistone protein acetylation in fibrosis (5). We had demonstrated significantly elevated lesional tissue p300 levels in experimental models of skin and pulmonary fibrosis in mice as well as in SSc skin biopsy samples and explanted fibroblasts (4,6). In cell-based assays, augmenting p300 expression or activity promotes histone H4 hyperacetylation and collagen transcription, whereas pharmacologic inhibition of p300 activity abrogates TGFβ-induced responses (4). These observations implicate p300 as a critical mediator of fibrosis, but the mechanisms governing p300 expression and activity are not well understood (5). Sirtuins (SIRTs) are mammalian orthologs of yeast silent information regulator 2 (Sir2) linked to regulation of lifespan. The SIRTs function as class III histone deacetylases with pleiotropic effects on cell survival, cell cycle, metabolism, and processes of aging (7). While SIRT-mediated histone deacetylation is generally associated with transcriptional repression, SIRTs also target nonhistone proteins, including transcription factors and signaling molecules (8). In particular, SIRT1 has been shown to suppress both the expression and acetyltransferase function of p300 (9–11). In view of the fundamental role that epigenetic and posttranslational mechanisms play in regulating the process of fibrosis, in the present studies we sought to investigate the expression and function of SIRT1 and its links with p300 in the context of SSc and fibrosis. The results show that SIRT1 expression was significantly reduced in SSc skin biopsy samples and explanted skin fibroblasts, as well as in lesional skin from mice with bleomycin-induced scleroderma. Pharmacologic activation of SIRT1, or its ectopic expression in normal fibroSblasts, abrogated TGFβ-induced stimulation of collagen synthesis and myofibroblast differentiation through disruption of canonical TGFβ/Smad signaling. Treatment of mice with a SIRT1 activator ameliorated bleomycin-induced skin fibrosis and reversed the suppression of SIRT1. Taken together, our results identify SIRT1 as a cell-autonomous negative regulator of the fibrotic process in skin fibroblasts, and they suggest that its deficiency in SSc may contribute to progression of skin fibrosis.

BACKGROUND The root bark of Aralia is a rich source of bioactive components that may improve glycemic control and lipid status. In this study, 148 patients with type 2 diabetes mellitus (T2DM) were assigned randomly to receive either glipizide alone or glipizide plus Aralia root bark extract (ARBE) for 8 weeks to test the effects of ARBE plus glipizide therapy on glycemic control and lipid profiles in these patients. RESULTS Levels of HbA1c, fasting plasma glucose (FPG) and 2 h postprandial plasma glucose (2-h PPG) in both groups significantly decreased from baseline. Glycated hemoglobin (HbA1c) decreased marginally significantly in participants taking glipizide plus ARBE compared with the glipizide group (P = 0.06). Participants in the combination group had significant decreases in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), and the between-group difference achieved statistical significance for LDL-C (P = 0.04). Reduction in HbA1c in the combination group was significantly associated with changes in TC (r = 0.32; P = 0.006) and LDL-C (r = 0.34; P = 0.005), and the change in FPG was inversely correlated with LDL-C reduction (r = 0.34; P = 0.004). CONCLUSIONS In patients with T2DM, combination therapy with glipizide and ARBE resulted in moderately lowering HbA1c and LDL-C levels compared with glipizide alone. © 2014 Society of Chemical Industry

The blending of a block copolymer into the membrane matrix is a convenient and efficient way to modify membranes. In this study, high-density polyethylene/polyethylene-b-poly(ethylene glycol) (PEG) membranes were prepared via a thermally induced phase separation process, and the extractant effect was investigated. An interesting finding was that the nonpolar extractant (n-hexane) was more conducive to the surface enrichment of the PEG chains than the polar solvent (ethanol). The reason was deemed to be the combined effect of the entropy drive, interfacial energy, and swelling behavior. In addition, the membrane performance related to the surface chemical properties was studied. The results suggest that the prepared blend membranes extracted by n-hexane showed enhanced the hydrophilicity, antifouling properties, and water flux. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 130: 3816–3824, 2013

Blending the block copolymer into the membrane matrix is a convenient and efficient way for membrane modification. In this study, HDPE/PE-b-PEG membranes were prepared via TIPS process, and the extractant effect was investigated. An interesting finding was that a non-polar extractant (n-hexane) was more conducive to the surface enrichment of PEG chains than a polar solvent (ethanol). The reason was deemed to be the combined effect of entropy drive, interfacial energy, and the swelling behavior. Besides, membrane performances related to the surface chemical properties were studied. Results suggested that the prepared blend membranes extracted by n-hexane showed enhanced hydrophilicity, anti-fouling property and water flux. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 130: 2680–2687, 2013

This study investigated the effects of allitridin compound on murine cytomegalovirus (MCMV)-induced regulatory T cell (Treg; CD4(+) CD25(+) Foxp3(+) ) amplification in vivo and in vitro. One hundred twenty MCMV-infected mice were allocated at random into two groups for treatment with allitridin or placebo. Another 120 mock-infected mice were randomly allocated as controls for the allitridin treatment and placebo treatment groups. The mice were euthanized at various time points after infection (out to 120 days) to evaluate the effects of treatment on Treg presence and function, as well as MCMV infective load. Co-culture with mouse embryo fibroblasts (MEF) and MCMV was performed to evaluate allitridin-mediated Treg and anti-CMV effects. The maximum tolerance concentration (MTC) of allitridin was used to treat cells for 3 days. Changes in Foxp3 mRNA and protein levels, percentages of T cell subsets, and Treg-related cytokines (IL-10 and TGF-β) were measured. Allitridin treatment did not influence Foxp3 expression and Treg proportion in uninfected mice, but did down-regulate each in infected mice during the chronic infection period. Additionally, allitridin treatment reduced the MCMV load in salivary glands. MTC allitridin treatment of co-cultures partially blocked MCMV induction of Foxp3 mRNA and protein expression. In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-β1, and significantly suppressed viral loads. In conclusion, allitridin can promote MCMV-induced Treg expansion and Treg-mediated anti-MCMV immunosuppression. Therefore, allitridin may be useful as a therapeutic agent to enhance the specific cellular immune responses against CMV.

Fibroblasts and myofibroblasts are the key effector cells executing physiological tissue repair leading to regeneration on the one hand, and pathological fibrogenesis leading to chronic fibrosing conditions on the other. Recent studies identify the multifunctional transcription factor early growth response-1(Egr-1) as an important mediator of fibroblast activation triggered by diverse stimuli. Egr-1 has potent stimulatory effects on fibrotic gene expression, and aberrant Egr-1 expression or function is associated with animal models of fibrosis and human fibrotic disorders, including emphysema, pulmonary fibrosis, pulmonary hypertension and systemic sclerosis. Pharmacological suppression or genetic targeting of Egr-1 blocks fibrotic responses in vitro and ameliorates experimental fibrosis in the skin and lung. In contrast, Egr-1 appears to act as a negative regulator of hepatic fibrosis in mouse models, suggesting a context-dependent role in fibrosis. The Egr-1-binding protein Nab2 is an endogenous inhibitor of Egr-1-mediated signalling and abrogates the stimulation of fibrotic responses induced by transforming growth factor-β (TGFβ). Moreover, mice deficient in Nab2 show excessive collagen accumulation in the skin. These observations highlight a previously unsuspected fundamental physiological function for the Egr-1-Nab2 signalling axis in regulating fibrogenesis, and suggest that Egr-1 may be a potential novel therapeutic target in human diseases complicated by fibrosis. This review summarizes recent advances in understanding the regulation and complex functional role of Egr-1 and its related proteins and inhibitors in pathological fibrosis.

BACKGROUND: The so-called factor that binds to inducer of short transcripts-1 (FBI-1) purportedly plays an important role in tumorigenesis; however, its role in hepatocellular carcinoma (HCC) remains unknown. The objective of this study was to investigate the expression level, clinical relevance, and biologic function of FBI-1 in HCC. METHODS: Real-time quantitative reverse transcriptase-polymerase chain reaction analysis, Western blot analysis, and immunohistochemical staining were used to detect expression levels of FBI-1 and to analyze its relation to clinicopathologic parameters and to the prognosis of patients with HCC. In addition, the biologic functions of FBI-1 in regulating cell proliferation, migration, and reaction to chemotherapy were detected by using HepG2 cells and SMMC-7721 cells; subsequently, the molecular mechanism of FBI-1 also was investigated. Finally, a xenograft mouse model was used to validate the observations obtained from in vitro studies. RESULTS: Expression levels of FBI-1 messenger RNA and protein were elevated significantly in HCC tissues compared with adjacent nontumorous liver tissues (ANLTs). Increased FBI-1 expression was correlated with multiple tumor nodes, Edmondson-Steiner grade, and a poor prognosis in patients with HCC (P < .05). In vitro studies revealed that FBI-1 was capable of promoting cell proliferation (but not cell migration) by regulating the cell cycle regulation proteins p53, p21, and p27. In addition, FBI-1 could inhibit cell death induced by 5-fluorouracil or doxorubicin through suppressing the activation of p53. Consistent with the in vitro data, FBI-1 was capable of promoting cell proliferation and enhancing chemotherapy resistance of HCC in vivo. CONCLUSIONS: The current findings indicated that FBI-1 plays an important role in HCC carcinogenesis and chemotherapy tolerance, and FBI-1 may served as a novel prognostic marker and therapeutic target for HCC. Cancer 2012;. © 2011 American Cancer Society.

Background: Intrathecal or epidural morphine used for post-operative analgesia frequently induces central type pruritus. The purpose of this study was to investigate the association between the severity of central type pruritus induced by epidural morphine for post-cesarean analgesia and the A118G polymorphism of the human μ-opioid receptor gene (OPRM1). Methods: Pregnant women (212) received pure epidural morphine (2 mg) twice per day for post-cesarean analgesia. Blood samples were collected and sequenced with high-resolution melting analysis to detect three different genotypes of OPRM1 (AA, AG and GG). We interviewed all candidates 24 h post-operatively to record the clinical phenotype with subjective complaints and objective observations. Results: The genotyping revealed that 99 women (46.7%) were AA, 88 (41.5%) were AG and 25 (11.8%) were GG. Sixty-two of 212 women suffered from significant pruritus (29.2%), and 150 of 212 women had non-significant pruritus (70.8%). In genotype AA, 33 patients (53.2%) experienced significant pruritus, 26 (41.9%) in genotype AG and 3 (4.8%) in genotype GG. The G allele was a statistically independent protective factor for individuals developing pruritus, and the multivariate-adjusted odds ratio was 0.27. There was a trend for progressively decreasing severity scores among the three groups, with the lowest severity score (0.72) for pruritus in the GG group. Conclusions: The incidence of significant pruritus in the recessive type (GG) was significantly lower compared with the dominant types (AA+AG). The recessive G allele in the A118G polymorphism may have protective effects against significant pruritus after epidural morphine for post-cesarean analgesia.