Association between monocyte-to-lymphocyte ratio and prostate cancer in the U.S. population: a population-based study.

Introduction: Monocyte-to-lymphocyte ratio (MLR) is a convenient and noninvasive inflammatory biomarker, and inflammation has been reported to be associated with prostate cancer (PCa). Our objective was to ascertain any possible correlation between PCa and MLR. Methods: We utilized data from the 1999-2020 cycles of the National Health and Nutrition Examination Survey (NHANES) regarding MLR and PCa. The independent associations of MLR and other inflammatory biomarkers (platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), system inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI)) with PCa was investigated using weighted multivariate logistic regression and generalized additive models. Receiver operating characteristic (ROC) curves were conducted to evaluate and contrast their diagnostic capabilities. Results: The analysis we conducted comprised 25,367 persons in total. The mean MLR was 0.31 ± 0.14. The prevalence of PCa was 3.1%. A positive association was found between MLR and PCa (OR = 2.28; 95% CI: 1.44, 3.62). According to the interaction tests, age, body mass index (BMI), hypertension, diabetes, and smoking status did not significantly impact the relationship between MLR and PCa (all p for interaction >0.05). ROC analysis showed that MLR had a stronger discriminative ability and accuracy in predicting PCa than other inflammatory biomarkers (NLR, SII, AISI, PLR, and SIRI). Conclusion: MLR might be better than other inflammatory biomarkers (NLR, SIRI, AISI, PLR, and SII) in predicting PCa. American adults who have elevated levels of MLR, NLR, PLR, SII, and AISI should be aware that they have a greater risk of PCa.

Survival and clinicopathological significance of B7-H3 in bladder cancer: a systematic review and meta-analysis.

BACKGROUND: B7-H3 has been implicated in clinical pathological features and prognosis across various cancer types, suggesting its potential as a cancer biomarker. Nevertheless, consensus remains elusive regarding its clinical-pathological and prognostic significance in bladder cancer. To address this gap, we conducted a systematic review and meta-analysis. METHODS: We systematically searched PubMed, Embase, Web of Science, Cochrane, and CNKI databases from their inception up to October 6, 2022. We evaluated the literature's quality using the Newcastle-Ottawa Scale. We performed meta-analysis using Review Manager 5.3 and STATA 12.0, synthesizing data and calculating odds ratios (ORs) or hazard ratios (HRs) with corresponding 95% confidence intervals (CIs). RESULTS: After applying eligibility criteria and conducting assessments, we included data from 8 studies, encompassing 1622 bladder cancer patients. Bladder tumor tissues exhibited significantly elevated B7-H3 protein expression compared to normal bladder tissues. Elevated B7-H3 expression was notably associated with patient age, tumor infiltration, and recurrence in bladder cancer. However, no significant correlations were observed with other clinical characteristics. Our pooled HR analysis indicated no significant association between B7-H3 expression and overall survival in bladder cancer patients. CONCLUSION: Our meta-analysis unveils the complex role of B7-H3 in bladder cancer progression. It appears to be directly involved in tumor infiltration and recurrence but cannot definitively serve as a prognostic biomarker for bladder cancer. To validate these findings, further well-designed studies, encompassing larger sample sizes and diverse racial backgrounds, are warranted. PROSPERO REGISTRATION: No. CRD42022364688.

circPVT1 Inhibits the Proliferation and Aids in Prediction of the Prognosis of Bladder Cancer.

Background: Circular RNA PVT1 (circPVT1) is aberrantly expressed in several cancers, but its functional role and clinical relevance in bladder urothelial carcinoma (BLCA) remain unknown. This study aimed to identify the expression level of circPVT1 in BLCA and investigated its functional relevance with BLCA progression both in vitro and in vivo. Methods: GEPIA, UALCAN, and OncoLnc were referred to presented data. Quantitative real-time PCR (qPCR) was used for the measurement of transnational expression of genes in BLCA specimens and cell lines. Immunohistochemistry (IHC) and fluorescence in situ hybridization analysis (FISH) assays were performed to detect HER2 amplification, Pearson's correlation analysis to analyze the correlation between circPVT1 expression and clinical characteristics, Cox regression and K-M survival analyses to analyze prognostic factors. A nomogram was constructed for predicting prognosis. The proliferation of cells was measured by CCK-8 and colony formation assay, and the proliferation in vivo was evaluated using nude mouse models. qPCR was used to detect the expression of proliferation-related genes. Results: circPVT1 was but mRNA PVT1 was not significantly overexpressed in BLCA. A high circPVT1 expression was associated with a better survival and negative HER2, but not with age, gender, and T stage. circPVT1 was an independent prognostic factor for the overall survival of BLCA patients. Knocking down circPVT1 promoted BLCA proliferation in vitro and in vivo. Knocking down circPVT1 upregulated ERBB2, MKI67, and PCNA expression and downregulated TP53 expression, but exerted no influence on CCND1 and CCNB1 expression. Conclusion: circPVT1 is a tumor suppressor and novel prognostic biomarker for BLCA.

Crosstalk of disulfidptosis-related subtypes, establishment of a prognostic signature and immune infiltration characteristics in bladder cancer based on a machine learning survival framework.

Background: Bladder cancer (BLCA) is the most common malignancy of the urinary tract. On the other hand, disulfidptosis, a mechanism of disulfide stress-induced cell death, is closely associated with tumorigenesis and progression. Here, we investigated the impact of disulfidptosis-related genes (DRGs) on the prognosis of BLCA, identified various DRG clusters, and developed a risk model to assess patient prognosis, immunological profile, and treatment response. Methods: The expression and mutational characteristics of four DRGs were first analyzed in bulk RNA-Seq and single-cell RNA sequencing data, IHC staining identified the role of DRGs in BLCA progression, and two DRG clusters were identified by consensus clustering. Using the differentially expressed genes (DEGs) from these two clusters, we transformed ten machine learning algorithms into more than 80 combinations and finally selected the best algorithm to construct a disulfidptosis-related prognostic signature (DRPS). We based this selection on the mean C-index of three BLCA cohorts. Furthermore, we explored the differences in clinical characteristics, mutational landscape, immune cell infiltration, and predicted efficacy of immunotherapy between high and low-risk groups. To visually depict the clinical value of DRPS, we employed nomograms. Additionally, we verified whether DRPS predicts response to immunotherapy in BLCA patients by utilizing the Tumour Immune Dysfunction and Rejection (TIDE) and IMvigor 210 cohorts. Results: In the integrated cohort, we identified several DRG clusters and DRG gene clusters that differed significantly in overall survival (OS) and tumor microenvironment. After the integration of clinicopathological features, DRPS showed robust predictive power. Based on the median risk score associated with disulfidptosis, BLCA patients were divided into low-risk (LR) and high-risk (HR) groups, with patients in the LR group having a better prognosis, a higher tumor mutational load and being more sensitive to immunotherapy and chemotherapy. Conclusion: Our study, therefore, provides a valuable tool to further guide clinical management and tailor the treatment of BLCA patients, offering new insights into individualized treatment.

Preparation of REE-doped NaY(WO4)2 single crystals for quantitative determination of rare earth elements in REE:NaY(WO4)2 laser crystals by LA-ICP-MS.

In REE:NaY(WO4)2 laser crystals, optical properties like laser conversion efficiency are dependent on the doped rare earth element (REE) concentration, which necessitates the importance for accurate determination of the REE concentration in these precious samples. However, in situ microanalysis of these samples by laser ablation-inductively coupled plasma-mass spectrometry (LA-ICP-MS) is often hampered by the lack of matrix-matched reference materials. In this work, a REE-doped NaY(WO4)2 single crystal (NaYW-500) that has a nominal REE concentration of 500 µg g-1 was synthesized and employed as a candidate reference material. Its homogeneity (1 RSD of elemental concentration or 89Y-normalized signal intensity) was measured by electron probe microanalysis (EPMA) and LA-ICP-MS to be less than 2% for major elements and mainly <3% for REEs, respectively. Then, an LA-ICP-MS analytical method was developed by using 89Y as the internal standard and using NaYW-500 as the external calibrator under the optimal operating conditions. Quantitative determination of the REE concentration in the other two REE:NaY(WO4)2 single crystals NaYW-50 and NaYW-5000 show that these samples can be accurately measured with relative deviations (Dr) of -6.00 to 12.33% and -9.86 to 6.94%, respectively. Further application of the proposed analytical method to quantitative determination of the Ho concentration in a Ho:NaY(WO4)2 laser crystal shows that desirable accuracy was obtained with a Dr of 4.62%. It demonstrates that the proposed method by preparing REE-doped NaY(WO4)2 single crystals for quantitative determination of the REE concentration in NaY(WO4)2 laser crystals is valid and robust.

The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in central nervous system diseases.

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a member of the immunoglobulin superfamily and is mainly expressed on the surface of myeloid cells such as monocytes, macrophages, and neutrophils. It plays an important role in the triggering and amplification of inflammatory responses, and it is involved in the development of various infectious and non-infectious diseases, autoimmune diseases, and cancers. In recent years, TREM-1 has also been found to participate in the pathological processes of several central nervous system (CNS) diseases. Targeting TREM-1 may be a promising strategy for treating these diseases. This paper aims to characterize TREM-1 in terms of its structure, signaling pathway, expression, regulation, ligands and pathophysiological role in CNS diseases.

Characteristics and clinical significance of CD163+/CD206+M2 mono-macrophage in the bladder cancer microenvironment.

The tumor microenvironment may recruit monocytes, with a protumoral macrophage phenotype (M2) that plays an important role in solid tumor progression and metastasis. Therefore, it is necessary to understand the characteristics of these cells for cancer prevention and treatment. Bladder cancer tissue samples and paracarcinoma tissues samples were collected, and the expression of CD163+ cells in tumor tissues was observed. Then, we observed the expression of infiltrating CD45+CD14+CD163+ cell subset and analyzed the molecular expressions related to immunity and angiogenesis. C57/BL6 mice were inoculated subcutaneously, and dynamic changes of CD11b+F4/80+CD206+ mononuclear macrophages expression for tumor-bearing mice were detected. The results showed that the proportion of CD45+CD14+CD163+ mono-macrophage subset infiltrated by tumor tissue was significantly higher than that in paracarcinoma tissues. In bladder cancer tissue, the expression rate of CD40 in CD45+CD14+CD163- mono-macrophage subset was significantly lower than that in CD45+CD14+CD163+ mono-macrophage subset. Similar results were found in the paracarcinoma tissues. We found that, as the proportion of CD11b+F4/80+CD206+ mono-macrophages increased gradually, the difference was statistically significant. CD163+/CD206+ mono-macrophages in bladder cancer microenvironment are abnormally elevated, and these cells are closely related to tumor progression. CD40 may be an important molecule that exerts biological function in this subset.

Knockdown of MCM8 inhibits development and progression of bladder cancer in vitro and in vivo.

BACKGROUND: Bladder cancer is a frequently diagnosed urinary system tumor, whose mortality remains rising. Minichromosome maintenance eight homologous recombination repair factor (MCM8), a newly discovered MCM family member, has been shown to be required for DNA replication. Unfortunately, little is known concerning the roles of MCM8 in bladder cancer. METHODS: The present study, we aimed at probing into the impacts and detailed mechanisms of MCM8 in bladder cancer progression. In this study, MCM8 expression level was detected through immunohistochemistry staining (IHC), qRT-PCR and Western blot assay. Silenced MCM8 cell models were constructed by lentivirus transfection. In vitro, the cell proliferation was evaluated by the MTT assay. The wound-healing assay and the transwell assay were utilized to assess the cell migration. Also, the cell apoptosis and the cell cycle were determined by flow cytometry. Moreover, the Human Apoptosis Antibody Array assay was performed to analyze the alterations of apoptosis-related proteins. The in vivo experiments were conducted to verify the effects of MCM8 knockdown on the tumor growth of bladder cancer. RESULTS: The results demonstrated that compared with normal adjacent tissues, MCM8 expression in bladder cancer tissues was strongly up-regulated. The up-regulation of MCM8 expression in bladder cancer may be a valuable independent prognostic indicator. Of note, MCM8 inhibition modulated the malignant phenotypes of bladder cancer cells. In terms of mechanism, it was validated that MCM8 knockdown made Akt, P-Akt, CCND1 and CDK6 levels down-regulated, as well as MAPK9 up-regulated. CONCLUSIONS: Taken together, our study demonstrated an important role of MCM8 in bladder cancer and created a rationale for the therapeutic potential of MCM8 inhibition in human bladder cancer therapy.

Integrating transcriptome and metabolome reveals molecular networks involved in genetic and environmental variation in tobacco.

Tobacco (Nicotiana tabacum) is one of the most widely cultivated commercial non-food crops with significant social and economic impacts. Here we profiled transcriptome and metabolome from 54 tobacco samples (2-3 replicates; n = 151 in total) collected from three varieties (i.e. genetic factor), three locations (i.e. environmental factor), and six developmental stages (i.e. developmental process). We identified 3,405 differentially expressed (DE) genes (DEGs) and 371 DE metabolites, respectively. We used quantitative real-time PCR to validate 20 DEGs, and confirmed 18/20 (90%) DEGs between three locations and 16/20 (80%) with the same trend across developmental stages. We then constructed nine co-expression gene modules and four co-expression metabolite modules , and defined seven de novo regulatory networks, including nicotine- and carotenoid-related regulatory networks. A novel two-way Pearson correlation approach was further proposed to integrate co-expression gene and metabolite modules to identify joint gene-metabolite relations. Finally, we further integrated DE and network results to prioritize genes by its functional importance and identified a top-ranked novel gene, LOC107773232, as a potential regulator involved in the carotenoid metabolism pathway. Thus, the results and systems-biology approaches provide a new avenue to understand the molecular mechanisms underlying complex genetic and environmental perturbations in tobacco.

Docetaxel promotes cell apoptosis and decreases SOX2 expression in CD133­expressing hepatocellular carcinoma stem cells by suppressing the PI3K/AKT signaling pathway.

Docetaxel is a front­line standard­of­care chemotherapeutic drug for the treatment of cancers. However, the underlying function and mechanism of docetaxel in human hepatocellular carcinoma (HCC) are uncertain. Therefore, the present study aimed to determine the effects of docetaxel on cell apoptosis and SOX2 expression in cultured human HCC stem cells. After human HCC stem cells were treated with docetaxel, cell proliferation was assessed by methyl thiazolyl tetrazolium (MTT) method, the cell apoptotic rate was evaluated by flow cytometry, the expression of CD133 and sex determining region Y­box 2 (SOX2) was determined by RT­PCR and immunohistochemistry, and the protein levels of CD133, SOX2, phosphoinositide 3­kinases (PI3K), AKT and phosphorylated AKT (p­AKT) were analyzed by western blotting. The results indicated that SOX2 and CD133 were highly expressed in patients with HCC while their expression was significantly decreased after patients with HCC were treated with docetaxel. In vitro, docetaxel inhibited the proliferation while it enhanced the apoptosis of human CD133­expressing HCC stem cells. Furthermore, lower expression of p­AKT and SOX2 were revealed in the presence of docetaxel. Notably, docetaxel­inhibited SOX2 expression and growth of human CD133­expressing HCC stem cells were partially restricted following the block of the PI3K/AKT signaling pathway using the inhibitor LY294002. The present study collectively indicated that docetaxel promoted apoptosis and upregulated SOX2 expression of human HCC stem cells through the suppression of the PI3K/AKT signaling pathway.

MiR-130a-3p inhibits migration and invasion by regulating RAB5B in human breast cancer stem cell-like cells.

Breast cancer stem cells (BCSCs) constitute a subpopulation of tumor cells that express stem cell-associated markers and have a high capacity for tumor generation in vivo. MicroRNAs (miRNAs) are involved in tumorigenesis by regulating specific oncogenes and tumor suppressor genes, and their roles in BCSCs are becoming more apparent. We try to reveal the mechanism by which specific miRNA plays its function in BCSCs. Herein, we show that miR-130a-3p is down-regulated in human breast cancer tissues and exosomes from circulating blood. Overexpression of miR-130a-3p in BCSCs inhibited cellular proliferation, migration, and invasion, and silencing of miR-130a-3p had the opposite effects. We also confirmed that RAB5B is directly down-regulated by miR-130a-3p. Knockdown of RAB5B also inhibited cell proliferation, migration and invasion. Furthermore, we found that lower levels of exosome-derived miR-130a-3p are associated with lymph node metastasis and advanced TNM stage. Taken together, our results demonstrate that miR-130a-3p may act as a disease progression monitoring indicator and therapeutic target in breast cancer.

Genetic Variations in the 3'-untranslated Regions of Genes Involved in the Cell Cycle and Apoptosis Pathways Affect Bladder Cancer Risk.

BACKGROUND: Key genes related to cell cycle and apoptosis pathways play critical roles in bladder cancer. Single nucleotide polymorphisms (SNPs) in the 3'-untranslated regions (3'-UTR) of genes may impact microRNA (miRNA)-messenger RNA (mRNA) binding capacity and alter gene expression to contribute to the susceptibility of cancers. However, an association of genetic variations in cell cycle and apoptosis pathways with bladder cancer risk, has not been reported. MATERIALS AND METHODS: We selected SNPs in the 3'-UTR of cell cycle and apoptosis pathways genes and genotyped them with a case-control study consisting of 578 bladder cancer patients and 1,006 cancer-free subjects. Dual luciferase reporter gene assay was performed to validate the biological function of important SNPs. RESULTS: We found that 5 SNPs might change the binding ability of miRNA to their target genes, among which PPP3CC rs7431 A>G located in the 3'-untranslated regions with the minimum p-value (p=5.75×10-4). Analysis revealed that the rs7431 disrupted miR-212 and miR-132 targeting sites. Logistic regression revealed a significantly decreased risk of bladder cancer associated with the PPP3CC rs7431 A>G polymorphism with an odds ratio (OR) of 0.76 [95% confidence interval (CI)=0.66-0.89, p=5.75×10-4]. Luciferase report assay showed that both miR-212 and miR-132 could lead to significantly increased PPP3CC expression levels in the construct with the G allele compared to the A allele. CONCLUSION: PPP3CC rs7431 may alter miRNA binding ability of miR-212 and miR-132, and thus decrease bladder cancer risk.

Molecular cloning and expression analysis of duplicated polyphenol oxidase genes reveal their functional differentiations in sorghum.

Polyphenol oxidase (PPO) is believed to play a role in plant growth, reproduction, and resistance to pathogens and pests. PPO causes browning of grains in cereals. In this study, genetic mapping of sorghum grain for phenol color reaction (PHR) was performed using a recombinant inbred line population. Only one locus was detected between SSR markers SM06072 and Xtxp176 on chromosome 6. Two linked orthologous genes (Sb06PPO1 and Sb06PPO2) within the mapped region were discovered and cloned. Transformation experiments using Nipponbare (a PHR negative rice cultivar) showed that Sb06PPO1 from LTR108 and two Sb06PPO2 alleles from both varieties could complement Nipponbare, whereas Sb06PPO1 from 654 could not. Subsequent quantitative real-time PCR (qPCR) experiments showed that Sb06PPO1 and Sb06PPO2 functioned diversely, Sb06PPO1 was mainly expressed in young panicles before flowering. Sb06PPO2 was strongly expressed in flowering panicles, especially in hulls and branches at filling stage. Moreover, the expression of Sb06PPO1 was found to be significantly up-regulated by exogenous ABA and salt, whereas Sb06PPO2 was not changed significantly, further demonstrating functional differentiation between the two genes.

OspTAC2 encodes a pentatricopeptide repeat protein and regulates rice chloroplast development.

Functional chloroplast generation depends on the precise coordination of gene expression between the plastid and the nucleus and is essential for plant growth and development. In this study, a rice (Oryza sativa) mutant that exhibited albino and seedling-lethal phenotypes was isolated from a60Co-irradiated rice population. The mutant gene was identified as an ortholog of the Arabidopsis plastid transcriptionally active chromosome protein 2 (pTAC2) gene, and the mutant strain was designated osptac2. Sequence and transcription analyses showed that OspTAC2 encodes a putative chloroplast protein consisting of 10 pentratricopeptide repeat (PPR) domains and a C-terminal small MutS-related (SMR) domain. Cytological observations via microscopy showed that the OspTAC2-green fluorescent fusion protein is localized in the chloroplasts. Transmission electron microscopy revealed that the chloroplast of the osptac2 mutant lacks an organized thylakoid membrane. The transcript levels of all investigated PEP (plastid-encoded RNA polymerase)-dependent genes were dramatically reduced in the osptac2 mutant, whereas the transcript levels of NEP (nuclear-encoded polymerase)-dependent genes were increased. These results suggest that OspTAC2 plays a critical role in chloroplast development and indicate that the molecular function of the OspTAC2 gene is conserved in rice and Arabidopsis.

Decreased IDE and IGF2 expression but increased Aß40 in the cerebral cortex of mouse pups by early life lead exposure.

As the abbreviation of plumbum and a chemical symbol for lead, Pb produces neurotoxic effects, which result into an impairment of learning and memory and other neurological dysfunctions. However, the mechanism of neurotoxicity of Pb exposure is unclear. The present study was undertaken to investigate the effects of maternal lead exposure on expression of insulin-degrading enzyme (IDE),insulin-like growth factor 2 (IGF2) and beta amyloid protein 40 (Aß40) in the cerebral cortex of mice offspring. Lead exposure initiated from beginning of gestation to weaning. Lead acetate administered in drinking solutions was dissolved in distilled deionized water at the concentrations of 0.1%, 0.2% and 0.5% groups respectively. On the 21st postnatal day, On the PND21, the learning and memory ability were tested by water maze test and the Pb levels were also determined by graphite furnace atomic absorption spectrometry. The expression of IDE, IGF2 and Aß40 in cerebral cortex was examined by immunohistochemistry, immunofluorescence and western blotting. The lead levels in blood and cerebral cortex of all lead exposure groups were significantly higher than that of the control group (P<0.05). In water maze test, the performances of 0.5% and 1% lead exposure groups were worse than that of the control group (P<0.05).The expression of IDE and IGF2 was decreased, but Aß40 was increased in lead exposed groups than that of the control group (P<0.05). The decreased expression of IDE and IGF2 and increased expression of Aß40 in the cerebral cortex of pups may contribute to the neurotoxicity associated with maternal Pb exposure.

Characterization and molecular cloning of a serine hydroxymethyltransferase 1 (OsSHM1) in rice.

Serine hydroxymethyltransferase (SHMT) is important for one carbon metabolism and photorespiration in higher plants for its participation in plant growth and development, and resistance to biotic and abiotic stresses. A rice serine hydroxymethyltransferase gene, OsSHM1, an ortholog of Arabidopsis SHM1, was isolated using map-based cloning. The osshm1 mutant had chlorotic lesions and a considerably smaller, lethal phenotype under natural ambient CO2 concentrations, but could be restored to wild type with normal growth under elevated CO2 levels (0.5% CO2 ), showing a typical photorespiratory phenotype. The data from antioxidant enzymes activity measurement suggested that osshm1 was subjected to significant oxidative stress. Also, OsSHM1 was expressed in all organs tested (root, culm, leaf, and young panicle) but predominantly in leaves. OsSHM1 protein is localized to the mitochondria. Our study suggested that molecular function of the OsSHM1 gene is conserved in rice and Arabidopsis.

The effects of early life lead exposure on the expression of P2X7 receptor and synaptophysin in the hippocampus of mouse pups.

The present study was undertaken to investigate the effects of maternal lead exposure on expression of P2X7 receptor and synaptophysin in the hippocampus of mice offspring. Lead exposure initiated from beginning of gestation to weaning. Lead acetate administered in drinking solutions was dissolved in distilled deionized water at the concentrations of 0.1%, 0.5% and 1% groups, respectively. On the 21st postnatal day, the Pb levels were also determined by graphite furnace atomic absorption spectrometry. The expression of P2X7 receptor and synaptophysin in hippocampus was examined by immunohistochemistry and Western blotting. The lead levels in blood and hippocampus of all lead exposure groups were significantly higher than that of the control group (P<0.05). Compared with the control group, the expression of P2X7 receptor was increased in lead exposed groups (P<0.05), but the expression of synaptophysin was decreased (P<0.05). The high expression of P2X7 receptor and low expression of synaptophysin in the hippocampus of pups may contribute to the neurotoxicity associated with maternal Pb exposure.

The effects of early life lead exposure on the expression of insulin-like growth factor 1 and 2 (IGF1, IGF2) in the hippocampus of mouse pups.

The present study was undertaken to investigate the effects of maternal lead exposure on expression of IGF1 and IGF2 in the hippocampus of mice offspring. Lead exposure initiated from beginning of gestation to weaning. Lead acetate administered in drinking solutions was dissolved in distilled deionized water at the concentrations of 0.1%, 0.5% and 1% groups respectively. On the 21st postnatal day, the learning and memory ability was tested by Water Maze test and the Pb levels were also determined by graphite furnace atomic absorption spectrometry. The expression of IGF1 and IGF2 in hippocampus was examined by immunohistochemistry and western blotting. The lead levels in blood and hippocampus of all lead exposure groups were significantly higher than that of the control group (P<0.05). In Water Maze test, the performances of 0.5% and 1% lead exposure groupswere worse than that of the control group (P<0.05). The expression of IGF1 and IGF2 was decreased in lead exposed groups than that of the control group (P<0.05). The low expression of IGF1 and IGF2 in the hippocampus of pups may contribute to the impairment of learning and memory associated with maternal Pb exposure.

Light exposure inhibiting tissue browning and improving antioxidant capacity of fresh-cut celery (Apium graveolens var. dulce).

Fresh-cut celery is perishable and susceptible to tissue browning during storage. In this study, the effect of continuous light exposure (2000 lux) on browning related enzyme activity of fresh-cut celery was investigated during 8d storage at 7 °C using darkness (0.2 lux) as control. Light exposure significantly suppressed polyphenol oxidase (PPO) and peroxidase (POD) activities, and subsequently decreased soluble quinone accumulation and browning index (BI) evolution during storage. In addition, phenylalanine ammonia lyase (PAL) activity, total phenol (TP) content, and antioxidant capacity (AC) values were all higher when the fresh-cut celery samples were exposed to light than in darkness during storage. A significant positive correlation between TP and AC was observed at both light (R=0.884, P<0.01) and dark (R=0.705, P<0.01) conditions.

SNR of DNA sequences mapped by general affine transformations of the indicator sequences.

The identification of gene coding regions of DNA sequences through digital signal processing techniques based on the so-called 3-base periodicity has been an emerging problem in bioinformatics. The signal to noise ratio (SNR) of a DNA sequence is computed after mapping the DNA symbolic sequence into numerical sequences. Typical mapping schemes include the Voss, Z-curve and tetrahedron representations and the like, which have been used to construct gene coding region detecting algorithms. In this paper, an extended definition of SNR is proposed, which has less computational cost and wider applicability than its original ones. Furthermore, we analyze the SNRs of different mapping schemes and derive the general relationship between Voss based SNR and that of its general affine transformations. We conclude that the SNRs of Z-curve and tetrahedron map are also linearly proportional to that of Voss map. Not only is our conclusion instructional for the design of other affine transformations, but it is also of much significance in understanding the role of the symbolic-to-numerical mapping in the detection of gene coding regions.