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Circadian rhythm disorder (CRD) in space flight can lead to memory impairment, performance decrements and adverse health outcomes, the main manifestations of which are circadian desynchronization, sleep loss and insomnia. Sleep deprivation (SD) provide the means to evaluate these effects and the risks associated with CRD on ground. Gastrodia elata Blume (GEB) has beneficial effects on the treatment of sleep disturbances and memory loss. Fresh GEB (FG), an unprocessed raw tuber of GEB, has been used as functional health food in Asian countries for a long time. However, the research report of FG to ameliorate memory impairment caused by insomnia or lack of sleep is meager. In this study, ICR male mice were sleep-deprived continuously and water extract of FG (WFG) was orally administrated (3 and 9 g/kg/d, i.g) during the SD process lasted for 25 days, except control and model groups gavage administration with water, positive control group with modafinil (MOD, 0.1 g/kg/d, i.g). We studied the effect of WFG on CRD-induced learning and memory impairment using a set of behavioral analyses including the object location recognition test (OLRT), novel object recognition test (NORT), and the passive avoidance test (PAT). In addition, oxidative stress parameters were assessed by measuring the malondialdehyde (MDA) and superoxide dismutase (SOD) reactivity in serum and hippocampus. Our results revealed that SD decreased discrimination index (DI) in OLRT and NORT, with shorter latency into the dark chamber in PAT. Both WFG and MOD treatment can reverse these changes (P0.05). We concluded that WFG treatment improve CRD-induced learning and memory impairment and oxidative stress damage which makes FG a promising candidate as herbal health product of memory decline in CRD.

Placenta-specific protein 9 (PLAC9) is a putative secretory protein that was initially identified in the placenta and is involved in cell proliferation and motility. Bioinformatics analyses revealed that PLAC9 is repressed in lung cancers (LCs), especially lung adenocarcinomas, compared to that in the paired adjacent normal tissues, indicating that PLAC9 might be involved in the pathogenesis of pulmonary diseases. To investigate the potential role of PLAC9 in the abnormal reprogramming of airway epithelial cells (AECs), a key cause of pulmonary diseases, we constructed a stable PLAC9-overexpressing human bronchial epithelial cell line (16HBE-GFP-Plac9). We utilized the proteomic approach isobaric tag for relative and absolute quantification (iTRAQ) to analyze the effect of PLAC9 on cellular protein composition. Gene ontology (GO) and pathway analyses revealed that GO terms and pathways associated with cell proliferation, cell cycle progression, and cell motility and migration were significantly enriched among the proteins regulated by PLAC9. Our in vitro results showed that PLAC9 overexpression reduced cell proliferation, altered cell cycle progression, and increased cell motility, including migration and invasion. Our findings suggest that PLAC9 inhibits cell proliferation through S phase arrest by altering the expression levels of cyclin/cyclin-dependent kinases (CDKs) and promotes cell motility, likely via the concerted actions of cyclins, E-cadherin, and vimentin. Since these mechanisms may underlie PLAC9-mediated abnormal human bronchial pathogenesis, our study provides a basis for the development of molecular targeted treatments for LCs.

Objective. To investigate and study the related risk factors of gastric cancer (GC) patients, to establish a high-risk scoring model of GC by multiple logistic regression analysis, and to explore the establishment of a GC screening mode with clinical opportunistic screening as the main method, and by using the pattern of opportunistic screening to establish the screening of high-risk GC patients and the choice of screening methods in the clinical outpatient work. Methods. Collected the epidemiological questionnaire of 99 GC cases and 284 non-GC patients (other chronic gastric diseases and normal) diagnosed by the General Hospital of Ningxia Medical University from October 2017 to March 2019. Serum pepsinogen (PG) levels were measured by enzyme-linked immunosorbent assay (ELISA) and confirmed Helicobacter pylori (Hp) infection in gastric mucosa tissues by Giemsa staining. Determined the high-risk factors and established a scoring model through unconditional logistic regression model analysis, and the ROC curve determined the cut-off value. Then, we followed up 26 patients of nongastric cancer patients constituted a validation group, which validated the model. Results. The high-risk factors of GC included age≥55, male, drinking cellar or well water, family history of GC, Hp infection, PGI≤43.6 μg/L, and PGI/PGII≤2.1. Established the high-risk model: Y=A×age+30×gender+30×drinking water+30×Hp infection+50×family history of GC+B×PG level. The ROC curve determined that the cut-off value for high-risk GC population was ≥155, and the area under the curve (AUC) was 0.875, the sensitivity and specificity were 87.9% and 71.5%. Conclusions. According to the risk factors of GC, using statistical methods can establish a high-risk scoring model of GC, and the score≥155 is divided into the screening cut-off value for high-risk GC population. Using this model for clinical outpatient GC screening is cost-effective and has high sensitivity and specificity.

Symbiosis is a ubiquitous phenomenon in the biological world. A typical example of mutualism is gut microbiota and their host, especially human. Host use the gut microbiota to consume food to get the energy and nutrients necessary for survival, while the gut microbiota gains habitat and nutrition. Gut microbiota interacts with host to form a balance state that is closely related to host health, and the dysequilibrium can result in many diseases in host such as obesity, high blood pressure, inflammatory bowel disease, and cancer. The gut microbiota participates in host metabolism, organism immunity, gene expression, disease development, and drug efficacy, while it is also affected by diet, antibiotics, lifestyle, inheritance, and time. We systematically reviewed the interaction between host and gut microbiota, analyzed the application status of the gut microbiota in the treatment of host diseases, described the main problems in the treatment, and provided new ideas for the application of gut microbiota in the treatment of human diseases.

Candidate oncogene placenta specific 8 (PLAC8) has been identified to participate in different cellular process and human diseases. However, the effects of PLAC8 on cell proliferation and migration in human kidney cancer (KC) remained unclear. In current study, physiological effects of PLAC8 in immortalized human embryonic kidney cell line (HEK293T) were investigated in vitro. Two PLAC8 knockout (KO) cell lines were established via CRISPR/Cas9-mediated methods combined with fluorescence activated single cell sorting. To classify the characteristic of PLAC8 during cell proliferation and migration in HEK293T, cellular proliferative activity was analyzed by cell counting and colony formation assay. Cell cycle distribution was analyzed by flow cytometry. Cellular motile activity was analyzed by wound-healing and migration assay. Further underlying molecular mechanism was explored via western blot. With the KO cell lines, it was found that PLAC8 KO could decrease cell proliferation. Moreover, the inhibitory effects of PLAC8 KO on cell proliferation were associated with a G2/M arrest in cell cycle progression concomitant with a remarkable inhibition of Cyclin B1 and elevation of Cyclin A. The alteration of cell cycle proteins and E-cadherin might further associate with the enhancement of cell motility. Our study revealed a novel role for PLAC8 in cell proliferation and migration of HEK293T cells, which might shed light on further study of PLAC8 on human KC.

Isoflurane/surgery (I/S) may induce neurocognitive disorders, but detailed mechanisms and appropriate treatment remain largely unknown. This experiment was designed to determine whether ginsenoside Rg1 could attenuate I/S-induced neurocognitive disorders and Sirtuin3 (Sirt3) dysfunction. C57BL/6J male mice received 1.4% isoflurane plus abdominal surgery for 2 h. Ginsenoside Rg1 10 mg/kg was intraperitoneally given for 8 days before surgery. Neurocognitive function was assessed by the Barnes Maze test. Levels of reactive oxygen species (ROS), oxygen consumption rate (OCR), mitochondrial membrane potential (MMP), expression and deacetylation activity of Sirt3 in the hippocampus tissues were measured. Results showed that I/S induced hippocampus-dependent learning and memory impairments, with increased ROS levels, and reduced OCR, MMP, and expression and deacetylation activity of Sirt3 in hippocampus tissues. Ginsenoside Rg1 treatment before I/S intervention significantly ameliorated learning and memory performance, reduced ROS levels and improved the OCR, MMP, expression and deacetylation activity of Sirt3. In conclusion, this experiment demonstrates that ginsenoside Rg1 treatment can attenuate I/S-induced neurocognitive disorders and Sirt3 dysfunction.

An aptamer-based electrochemical biosensor was successfully developed and applied in the rapid detection of pathogenic Escherichia coli (E. coli) in licorice extract. The thiolated capture probes were firstly immobilized on a gold electrode, and then the biotinylated aptamer probes for E. coli were introduced by hybridization with the capture probes. Due to the stronger interaction between the aptamer and the E. coli, a part of the biotinylated aptamers will dissociate from the capture probes in the presence of E. coli. The residual biotinylated aptamer probes can quantitatively bind with streptavidin-alkaline phosphatase. Subsequently, α-naphthyl phosphate substrate was catalytically hydrolyzed to generate electrochemical response, which could be recorded by a differential pulse voltammetry. The dependence of the peak current on the logarithm of E. coli concentration in the range from 5.0 × 102 colony forming units (CFU)/mL to 5.0 × 107 CFU/mL exhibited a linear trend with a detection limit of 80 CFU/mL. The relative standard deviation of 5 successive scans was 5.3%, 4.5% and 1.1% for 5.0 × 102, 5.0 × 105 and 5.0 × 107 CFU/mL E. coli, respectively. In the detection of the licorice extract samples, the results obtained from the proposed strategy and traditional culture counting method were close to each other, but the time consumption was only ~1/30 compared with the traditional method. These results demonstrate that the designed biosensor can be potentially utilized for rapid microbial examination in traditional Chinese medicine and relevant fields.

γ-Tocotrienol (γ-T3) exhibits the activity of anticancer via regulating cell signaling pathways. Nuclear factor-κB (NF-κB), one of the crucial pro-inflammatory factors, is involved in the regulation of cell proliferation, apoptosis, invasion, and migration of tumor. In the present study, NF-κB activity inhibited by γ-T3 was investigated in gastric cancer cells. Cell proliferation, NF-κB activity, active protein phosphatase type 2A (PP2A), and ataxia-telangiectasia mutated (ATM) protein were explored using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT), methylene blue, enzyme-linked immunosorbent assay (ELISA), malachite green, luciferase, and Western blotting assays. The effects of γ-T3 on tumor growth and the expression of NF-κB and PP2A proteins were also further examined by implanting human gastric cancer cells in a BALB/c nude mouse model. The results showed that γ-T3 significantly inhibited the cell proliferation and attenuated the NF-κB activity in vitro and in vivo. γ-T3 dramatically increased PP2A activity and protein expression, which suppressed ATM phosphorylation and its translocation to the cytoplasm in gastric cancer cells. Thus, our findings may provide mechanistic insight into effects of γ-T3 on the regulation of NF-κB activity by a PP2A-dependent mechanism and suggest that PP2A may serve as a molecular target for a potential chemopreventive agent.

Tocotrienols (T3s) are a subgroup of vitamin E and they have been widely tested to inhibit cell growth in various tumor types. Previous studies have shown that T3s inhibit cancer cell growth by targeting multiple signaling transduction and cellular processes. However, the role of T3s in the regulation of cellular bioenergetic processes remains unclear. In this study, we found that γ-T3 interacts with mitochondrial electron transfer chain NDUFB8 (a subunit of complex I) and SDHB (a subunit of complex II) and inhibits oxidative phosphorylation (OXPHOS), and triggers the production of reactive oxygen species (ROS). In addition, we observed that γ-T3 upregulates the glycolytic capacity in cells, but it did not compensate for cellular ATP generation and decreased the ATP levels in cells. Furthermore, we performed western blots and RT-PCR to measure the mRNA and protein levels of mitochondrial electron transfer chain (ETC) proteins and complex V (ATP synthase), where the results indicated that γ-T3 specifically inhibited the levels of NDUFB8 and SDHB, whereas it had little effect on UQCRC2 (a subunit of complex III), COX4I1 (a subunit of complex IV), and ATP5F1A (a subunit of complex V). The inhibition of NDUFB8 and SDHB by γ-T3 led to the overproduction of ROS and the depletion of ATP, which may be responsible for inducing apoptosis in cancer cells. Our results suggest that mitochondrial respiration may be an effective target for anticancer treatments based on γ-T3.

Pathogenic Escherichia coli (E. coli) widely exist in Nature and have always been a serious threat to the human health. Conventional colony forming units counting-based methods are quite time consuming and not fit for rapid detection for E. coli. Therefore, novel strategies for improving detection efficiency and sensitivity are in great demand. Aptamers have been widely used in various sensors due to their extremely high affinity and specificity. Successful applications of aptamers have been found in the rapid detection of pathogenic E. coli. Herein, we present the latest advances in screening of aptamers for E. coli, and review the preparation and application of aptamer-based biosensors in rapid detection of E. coli. Furthermore, the problems and new trends in these aptamer-based biosensors for rapid detection of pathogenic microorganism are also discussed.

γ-tocotrienol (γ-T3), a tocotrienol isoform belonging to the vitamin E family, has been revealed to exert inhibitory effects on proliferation, migration and invasion in human gastric cancer cells. However, its precise mechanism of action is still unclear and needs to be further tested. Cyclooxygenase-2 (COX-2) is well known for its key role in promoting the migration and invasion abilities of human gastric cancer cells. In light of these data, our study aimed to validate whether the inhibitory actions of γ-T3 could be achieved by downregulation of COX-2 activity in vitro. In the present study, a Cell Counting Kit-8 (CCK-8) assay was performed to observe proliferation in human gastric cancer cells (SGC-7901 and MGC-803 cells), and wound healing and Transwell chamber assays were performed to detect migration and invasion. Western blot analyses were performed to analyse the relative expression of COX-2, matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) proteins, and enzyme-linked immunosorbent assays (ELISA) were used to determine the exocrine roles of MMP-2 and MMP-9. The results revealed that γ-T3 exerted significant inhibitory effects on proliferation, migration, invasion and COX-2 protein expression, as well as on exocrine functions of MMP-2 and MMP-9 in SGC-7901 and MGC-803 cells. Therefore, our results indicated that γ-T3 exerts inhibitory effects on migration and invasion, which may be mediated through downregulation of COX-2 expression in SGC-7901 and MGC-803 cells.

Introduction: The etiological and clinical characteristics of patients with infectious diarrhea have changed during the last decade in Shanghai. Methodology: The records of 29,210 patients with infectious diarrhea in the outpatient department of the Jinshan Hospital (Shanghai, China) between January 1998 and December 2013 were analyzed. Results: A total of 2,849 samples were positive for intestinal pathogenic bacteria including Vibrio parahaemolyticus (2,489; 84.0%), Salmonella spp. (235; 8.3%), and Shigella spp. (125; 4.4%). V. parahaemolyticus infections are mainly characterized by abdominal pain, nausea, and vomiting, whereas Shigella spp. infections can, in addition, induce fever. In contrast, Salmonella infections can produce all of these symptoms but in a smaller percentage of patients. During the 16-year study, both the number of patients and the positive infection rate declined. Notably, the rate of infections by V. parahaemolyticus decreased while the detection rates of Salmonella spp. increased year by year from 2006 on with the introduction of a new detection method. Conclusions: Salmonella has been identified as the third-most frequent cause of diarrhea from 1998–2006, as the second-most frequent cause from 2006–2010, and as the most frequent cause from 2011–2013, which was mainly due to a sharp decrease of V. parahaemolyticus infections in 2011–2013. Salmonella strains collected in 2011–2013 showed high susceptibility to imipenem (100%) and meropenem (100%), whereas susceptibilities for ampicillin (39%) and piperacillin (40%) were low.

Distal myopathy with rimmed vacuoles is an autosomal recessive genetic disease characterized by weakness of the anterior compartment of the lower limbs, sparing the quadriceps muscle, and rimmed vacuoles in muscle biopsies. The disease is caused by a mutation in the UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) gene located on chromosome 9p13.3. We present two cases of Chinese patients with progressive lower extremity weakness. Clinical presentation, laboratory evaluation, electrodiagnostic testing, muscle pathology, and genetic analysis are described. Patient 1 was found to have heterozygous missense mutations (p.C13S and p.G576R) in the GNE gene and patient 2 had a homozygous missense mutation (p.C13S). The mutation p.C13S has been reported previously in China, Japan, and South Korea; however, the mutation p.G576R has not been described previously.

Ottelia cordata (Wallich) Dandy (Hydrocharitaceae) is an endangered aquatic macrophyte. The complete chloroplast genome sequence of O. cordata was generated by de novo assembly using whole genome n...

The Bcr-Abl oncoprotein is the cause of chronic myelogenous leukemia (CML). Crystal structure analysis suggests that Bcr30-63 is the core of the Bcr-Abl oligomerization interface for aberrant kinase activity; however, the precise role of other residues of Bcr1-72 excluding Bcr30-63 have not been evaluated. In this study, Bcr30-63 was named OD2 and other residues of Bcr1-72 were named OD1. Cytoplasmic transduction peptide (CTP) was used to carry molecules into cytoplasm. CTP-OD1 and CTP-OD2 fusion peptides were expressed from a cold-inducible expression system. Our results demonstrated that both fusion peptides could localize into the cytoplasm, specifically interact with the Bcr-Abl protein and further inhibit growth, induce apoptosis, and decrease the phosphorylation of Bcr-Abl in K562 cell lines. However, the viability of THP-1, a Bcr-Abl negative cell line, was unaffected. These results suggested that CTP-OD1 and CTP-OD2 may be an attractive therapeutic option to inhibit the activation of Bcr-Abl kinase in CML.

Kruppel-like factor 7 (Klf7) has been extensively studied in the mammalian species, but its function in avian species is unclear. The objective of this study was to reveal the function of chicken Klf7 (Gallus gallus Klf7, gKlf7) in adipogenesis. The results of real-time reverse transcription polymerase chain reaction demonstrated that the relative mRNA level of chicken Klf7 (gKlf7/gβ-Actin) in the abdominal adipose tissue was significantly associated with the abdominal fat content and the age of broilers (P < 0.05), and gKlf7 was more highly expressed in preadipocytes than in mature adipocytes (P < 0.05). In addition, Oil red O staining showed that gKlf7 inhibited chicken preadipocyte differentiation, and MTT assay indicated that gKlf7 overexpression promoted preadipocyte proliferation. Additionally, luciferase assays showed that gKlf7 overexpression suppressed the chicken CCAAT/enhancer-binding protein α (C/ebpα), fatty acid synthase (Fasn), and lipoprotein lipase (Lpl) promoter activities (P < 0.05), and gKlf7 knockdown increased the chicken peroxisome proliferator-activated receptor γ (Pparγ), C/ebpα and fatty acid-binding protein 4 (Fabp4) promoter activities (P < 0.05). Together, our study demonstrated that chicken Klf7 inhibits preadipocyte differentiation and promotes preadipocyte proliferation.

A moderately halophilic, Gram-stain-negative, non-endospore-forming endophytic bacterium designated strain ST307T was isolated from the euhalophyte Suaeda salsa in Dongying, China. Strain ST307T was aerobic, rod-shaped, motile and orange–yellow-pigmented. The organism grew at NaCl concentrations of 0.6–20 % (w/v) (optimum 5–6 %, w/v), at temperatures of 5–45 °C (optimum 35 °C) and at pH 5–9 (optimum pH 7–8). It accumulated poly-β-hydroxybutyric acid and produced exopolysaccharides. The major fatty acids were C18 : 1 ω7c/C18 : 1 ω6c, C16 : 0 and C16 : 1 ω7c/C16 : 1 ω6c. The predominant lipoquinone was ubiquinone Q-9. The polar lipids consisted of phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, a glycoaminolipid and a phosphoglycoaminolipid. The DNA G+C content was 60.5 mol%. Phylogenetic analyses of 16S rRNA gene sequences and concatenated atpA, rpoD and secA gene sequences revealed that the strain represents a member of the genus Larsenimonas . The closest related type strain was Larsenimonas salina M1-18T. Mean DNA–DNA relatedness values between strain ST307T and the related species L. salina M1-18T, Chromohalobacter beijerinckii DSM 7218T, C. canadensis DSM 6769T, C. israelensis DSM 6768T, C. marismortui CGMCC 1.2321T, C. nigrandesensis DSM 14323T, C. salexigens DSM 3043T and C. sarecensis DSM 15547T were 15±2−45±1 %. On the basis of phenotypic, chemotaxonomic and molecular features, strain ST307T clearly represents a novel species of the genus Larsenimonas . The name Larsenimonas suaedae sp. nov. is proposed, with ST307T (=CGMCC 1.8902T=DSM 22428T) as the type strain.

Emergence of resistance to imatinib mesylate complicates the treatment of chronic myeloid leukemia (CML). Second-generation tyrosine kinase inhibitors are capable to overcome resistance mediated by most mutations except T315I. As this mutation is causative for 20% of clinically observed resistances, the need for novel treatment strategies becomes obvious and urgent. The autophosphorylated BCR/ABL Tyr177 recruits Grb2 via its SH2 domain, which is required for efficient induction of the myeloproliferative disease by BCR/ABL. The death effector domain (DED) is the critical factor for activation of caspase-8 induced apoptosis signal. We thus speculated that transduction of an exogenous SH2-DED (SD) fragment into the CML cells may inhibit the binding of BCR/ABL Tyr177 and Grb2, activate caspase-8 induced apoptosis and serve as a novel CML treatment strategy. The infection of the recombinant adenovirus Ad5/F35-SD was verified to show both cell proliferation-inhibitory and apoptosis-inducing effect. Further exploration into the underlying mechanisms revealed that Ad5/F35-SD exerted its function by binding to the phospho-BCR/ABL Tyr177 site, reducing Ras, MAPK and AKT kinase activities, and activating caspase-8 induced apoptosis signal by DED protein binding to DED domain of precursor caspase-8. Moreover, high anti-proliferative activity of Ad5/F35-SD was observed in nude mice and its leukemia-protective effect was evident in chronic myeloid leukemia model mice injected with BCR/ABL+ BaF3 cells. In conclusion, Ad5/F35-SD exhibits anti-proliferative and pro-apoptotic activity on BCR/ABL positive leukemia cells in vitro and in vivo through disruption of Grb2 SH2-phospho-BCR/ABL Tyr177 complex formation and induction of caspase-8 activation.

bcr/abl fusion gene is thought to be a promising target for chronic myelogenous leukemia (CML) patients to enhance immune response after attaining complete remission. In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form. The successfully constructed plasmid pBudCE4.1-BCR/ABL-GPI-mIL12 resulted in high levels of splenocyte proliferative responses, significant levels of IL-2 and IFNγ, and strong cytotoxic T-lymphocyte (CTL) responses in vitro. In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells. Results of the present study indicated that this novel immunization strategy is useful in enhancing immune protection in mice, which would provide new insights into the development of effective vaccines for treating CML.

There was an obvious relationship between seed testa structure, storage material and resistance to A. flavus of peanut. Results showed that seed testa of peanut germplasm with high resistance (HR) to A. flavus infection had thicker wax layer, integrated and tight epidermis layer, regular vascular tissue range. However, the seed testa of peanut germplasm with high sensitivity (HS) to A. flavus had the reverse results, and results of those with medium resistance (MR) to A. flavus lay in between, but changes of testa thickness were not significant among different resistance kinds. Results also showed that some seed storage materials were closely related with resistance potential to A. flavus. It seemed that varieties with higher resistance to A. flavus had higher oleic acid and protein content, lower linoleic acid and fat content. Content of palm acid, total sugar and VE did not show positive relationship with the resistance to A. flavus.

Arsenic produces liver disease through the oxidative stress. While lutein can alleviate cytotoxic and oxidative injury, nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays a critical role in defending oxidative species. However, the mechanisms by which lutein protects the liver against the effect of arsenic are not known. Therefore, this study aims to investigate the mechanisms involved in the action of lutein using mice model in which hepatotoxicity was induced by arsenic. We found that mice treatment with lutein could reverse changes in morphological and liver indexes and result in a significant improvement in hepatic function comparing with arsenic trioxide group. Lutein treatment improved the activities of antioxidant enzymes and attenuated increasing of ROS and MDA induced by arsenic trioxide. Lutein could increase the mRNA and protein expression of Nrf2 signaling related genes (Nrf2, Nqo1, Ho-1, and Gst). These findings provide additional evidence that lutein may be useful for reducing reproductive injury associated with oxidative stress by the activation of Nrf2 signaling. Our findings suggest a possible mechanism of antioxidant lutein in preventing the hepatotoxicity, which implicate that a dietary lutein may be a potential treatment for liver diseases, especially for arsenicosis therapy.

Hepatitis B virus X protein (HBx) plays an important role in the development of hepatocellular carcinoma (HCC). Emerging evidence has shown the association between aberrantly expressed miR-221 and cancer development; however, little is known concerning its potential role in hepatitis B virus (HBV)-related HCC. In the present study, functional studies demonstrated that HBx leads to the promotion of cell proliferation and cell growth viability. Obviously overexpressed miR-221 was found in HBx-transfected cells compared with the mock counterparts. Suppression of miR-221 significantly inhibited HCC cell proliferation. Western blot analysis indicated that estrogen receptor-α (ERα) was downregulated in HCC tissues and cell lines. Bioinformatic analysis combined with validation experiments identified ERα as a direct target of miR-221. The present study suggests that miR-221 modulates HCC cancer cell proliferation by suppressing ERα, functioning as a tumor promoter. Moreover, our data imply that miR-221 has potential as an miRNA-based therapeutic target for HBV-related HCC.

Background The chicken (Gallus gallus) is an important model organism that bridges the evolutionary gap between mammals and other vertebrates. Copy number variations (CNVs) are a form of genomic structural variation widely distributed in the genome. CNV analysis has recently gained greater attention and momentum, as the identification of CNVs can contribute to a better understanding of traits important to both humans and other animals. To detect chicken CNVs, we genotyped 475 animals derived from two broiler chicken lines divergently selected for abdominal fat content using chicken 60 K SNP array, which is a high-throughput method widely used in chicken genomics studies. Results Using PennCNV algorithm, we detected 438 and 291 CNVs in the lean and fat lines, respectively, corresponding to 271 and 188 CNV regions (CNVRs), which were obtained by merging overlapping CNVs. Out of these CNVRs, 99% were confirmed also by the CNVPartition program. These CNVRs covered 40.26 and 30.60 Mb of the chicken genome in the lean and fat lines, respectively. Moreover, CNVRs included 176 loss, 68 gain and 27 both (i.e. loss and gain within the same region) events in the lean line, and 143 loss, 25 gain and 20 both events in the fat line. Ten CNVRs were chosen for the validation experiment using qPCR method, and all of them were confirmed in at least one qPCR assay. We found a total of 886 genes located within these CNVRs, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed they could play various roles in a number of biological processes. Integrating the results of CNVRs, known quantitative trait loci (QTL) and selective sweeps for abdominal fat content suggested that some genes (including SLC9A3, GNAL, SPOCK3, ANXA10, HELIOS, MYLK, CCDC14, SPAG9, SOX5, VSNL1, SMC6, GEN1, MSGN1 and ZPAX) may be important for abdominal fat deposition in the chicken. Conclusions Our study provided a genome-wide CNVR map of the chicken genome, thereby contributing to our understanding of genomic structural variations and their potential roles in abdominal fat content in the chicken. Electronic supplementary material The online version of this article (doi:10.1186/1471-2164-15-517) contains supplementary material, which is available to authorized users.

Chimeric T cell receptors (chTCRs), composed of the single-chain variable fragments (scFv) of murine antibodies and human signaling molecules, are used to redirect the specificity of autologous or allogeneic T lymphocytes. To develop novel therapeutic agents for treatment of chronic myeloid leukemia (CML), we engineered a scFv from the hybridoma cell line CMA1 which produces monoclonal antibody specific against CML. The genes encoding the heavy and light chain variable regions were amplified from CMA1 cDNA and a humanized chTCR was constructed. Expression of the novel hchTCR was verified in NIH3T3 cells transduced with retroviral vectors. The results demonstrated that hchTCR can be expressed and presented on cell surface normally. These results suggest that retroviral vectors expressing hchTCR specific for CML cells may be used to redirect human T lymphocytes.