Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence.

Telomeres, TTAGGGn DNA repeat sequences located at the ends of eukaryotic chromosomes, play a pivotal role in aging and are targets of DNA damage response. Although we and others have demonstrated presence of short telomeres in genetic cardiomyopathic and heart failure cardiomyocytes, little is known about the role of telomere lengths in cardiomyocyte. Here, we demonstrate that in heart failure patient cardiomyocytes, telomeres are shortened compared to healthy controls. We generated isogenic human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) with short telomeres (sTL-CMs) and normal telomeres (nTL-CMs) as model. Compared to nTL-CMs, short telomeres result in cardiac dysfunction and expression of senescent markers. Using Hi-C and RNASeq, we observe that short telomeres induced TAD insulation decrease near telomeric ends and this correlated with a transcription upregulation in sTL-CMs. FOXC1, a key transcription factor involved in early cardiogenesis, was upregulated in sTL-CMs and its protein levels were negatively correlated with telomere lengths in heart failure patients. Overexpression of FOXC1 induced hiPSC-CM aging, mitochondrial and contractile dysfunction; knockdown of FOXC1 rescued these phenotypes. Overall, the work presented demonstrate that increased chromatin accessibility due to telomere shortening resulted in the induction of FOXC1-dependent expression network responsible for contractile dysfunction and myocardial senescence.

Prognostic value of coronary CT angiography in heart failure patients with preserved ejection fraction.

OBJECTIVES: To investigate the prognostic value of coronary CT angiography (CCTA) in heart failure patients with preserved ejection fraction (HFpEF). METHODS: Between January 2009 and December 2013, 6497 participants (mean age 63 ± 9.4 [range 32-86] years; 4111 men) who underwent CCTA and echocardiography were prospectively included. Participants were divided into HFpEF group and without HFpEF group. The primary endpoint was major adverse cardiovascular events (MACEs), including cardiovascular mortality, nonfatal myocardial infarction (MI), or hospitalization for heart failure (HF). RESULTS: Among those participants, 3096 were identified with HFpEF and 3401 were without HFpEF. Higher prevalence of coronary atherosclerosis was observed in HFpEF group than those without (78.3% vs. 64.9%, p < 0.001). During a median of 11.0 [IQR: 9.0-12.0] years follow-up, participants with HFpEF exhibit a heightened risk of MACEs in CAD-RADS = 0, 1-2, and ≥ 3 respectively (p < 0.001 for all). In the risk-adjusted hazard analysis among participants with HFpEF, CAD-RADS = 1-2 increased a 2.5-time risk for non-fatal MI (adjusted HR: 2.5, 95% CI: 1.5 to 4.3, p < 0.001), while CAD-RADS ≥ 3 conferred 3.9-fold and 3.1-fold higher risk for cardiovascular mortality (adjusted HR: 3.9, 95% CI: 2.2 to 7.1, p < 0.001) and hospitalization due to HF (adjusted HR: 3.1, 95% CI: 1.9 to 5.3, p < 0.001) with reference to CAD-RADS = 0 respectively. CONCLUSIONS: Coronary artery disease is common in participants with HFpEF and associated with MACEs. Among those participants, the presence of CAD-RADS = 1-2 increased the risk of nonfatal MI, while CAD-RADS ≥ 3 were correlated with cardiovascular mortality and hospitalization due to HF. KEY POINTS: • Higher median of CACS and higher CAD-RADS categories were observed in the HFpEF group than those without (p < 0.001 for both). • Participants with HFpEF exhibit a heightened risk of MACEs in CAD-RADS = 0, 1-2, and ≥ 3 respectively (p < 0.001 for all). • In the risk-adjusted hazard analysis among participants with HFpEF, CAD-RADS =1-2 increased a 2.5-time risk for non-fatal MI (adjusted HR: 2.5, 95% CI: 1.5 to 4.3, p < 0.001) with reference to CAD-RADS = 0 respectively.

Genetic polymorphisms and phylogenetic characteristics of Tibeto-Burman-speaking Lahu population from southwest China based on 41 Y-STR loci.

BACKGROUND: Male sex-linked Y-chromosome short tandem repeats (Y-STRs) have been widely used in forensic cases and population genetics research. At present, the forensic-related Y-STR data in the Chinese Lahu population are still poorly understood. AIM: To enrich the available Y-STR data of this Chinese minority population and investigate its phylogenetic relationships with other reported populations. SUBJECTS AND METHODS: The genetic polymorphisms of 41 Y-STR loci were analysed in 299 unrelated healthy Lahu male individuals from Southwest China. Phylogenetic analyses were performed by multidimensional scaling analysis and neighbor-joining phylogenetic tree construction. RESULTS: A total of 379 alleles were observed at the 41 Y-STR loci. The allele frequencies ranged from 0.0033 to 0.9666. The genetic diversity values ranged from 0.0653 to 0.9072. A total of 254 different haplotypes of the 41 Y-STR loci were observed in 299 individuals. The values of haplotype diversity, haplotype match probability, and discrimination capacity were 0.9987, 0.0047, and 0.8495, respectively. The phylogenetic analysis indicated that the Tibeto-Burman-speaking Lahu population showed a close genetic relationship with the Yunnan Yi population. CONCLUSIONS: The haplotype data of the present study can enrich the forensic databases of this Chinese minority population and will be useful for population genetics and forensic DNA application.

Hydrothermal oxidation degradation of dioxins in fly ash with water-washing and added Ce-Mn catalyst.

A comprehensive analysis of the effects of the temperature, reaction time, liquid-solid ratio (L/S), and initial pH on the hydrothermal degradation of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) (which are both PCDD/Fs) in municipal solid waste incineration (MSWI) fly ash is presented. Consequently, the hydrothermal degradation reaction is catalyzed using Ce-Mn catalyst under low-temperature conditions to study the effect of the catalyst on the degradation efficiency of PCDD/Fs. The experimental results show that temperature is the most critical factor for the reaction. When the hydrothermal oxidation temperature reaches 280 °C (reaction time = 120 min, original pH = 8.5, L/S = 4 mL/g), the toxicity equivalent (I-TEQ) of PCDD/Fs is only 5.4 ng TEQ/kg, and the degradation efficiency reaches 99.71%. Under these conditions, 2,3,4,7,8-P5CDF makes the highest contribution to I-TEQ degradation, reaching 37.4%. There are four main pathways for the reaction of 2,3,4,7,8-P5CDF with hydroxyl radicals. A comparison of the PCDD/F concentrations of different products shows that the addition of 0.5%, 1.0%, and 1.5% of the Ce-Mn catalyst reduces the degradation efficiency by 8.79%, 1.40%, and 0.07%, respectively, which indicates that the addition of a small quantity of Ce-Mn catalyst does not facilitate the degradation of PCDD/Fs. The addition of the catalyst significantly decreases the degradation efficiency of low-chlorinated homologs but has a relatively small effect on that of high-chlorinated homologs. Therefore, it is concluded that Ce-Mn catalysts are more likely to promote resynthesis than degradation of PCDD/Fs.

Cell-specific expression of lung disease risk-related genes in the human small airway epithelium.

BACKGROUND: The human small airway epithelium (SAE) plays a central role in the early events in the pathogenesis of most inherited and acquired lung disorders. Little is known about the molecular phenotypes of the specific cell populations comprising the SAE in humans, and the contribution of SAE specific cell populations to the risk for lung diseases. METHODS: Drop-seq single-cell RNA-sequencing was used to characterize the transcriptome of single cells from human SAE of nonsmokers and smokers by bronchoscopic brushing. RESULTS: Eleven distinct cell populations were identified, including major and rare epithelial cells, and immune/inflammatory cells. There was cell type-specific expression of genes relevant to the risk of the inherited pulmonary disorders, genes associated with risk of chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis and (non-mutated) driver genes for lung cancers. Cigarette smoking significantly altered the cell type-specific transcriptomes and disease risk-related genes. CONCLUSIONS: This data provides new insights into the possible contribution of specific lung cells to the pathogenesis of lung disorders.

Exaggerated BMP4 signalling alters human airway basal progenitor cell differentiation to cigarette smoking-related phenotypes.

Airway remodelling in chronic obstructive pulmonary disease (COPD) originates, in part, from smoking-induced changes in airway basal stem/progenitor cells (BCs). Based on the knowledge that bone morphogenetic protein 4 (BMP4) influences epithelial progenitor function in the developing and adult mouse lung, we hypothesised that BMP4 signalling may regulate the biology of adult human airway BCs relevant to COPD.BMP4 signalling components in human airway epithelium were analysed at the mRNA and protein levels, and the differentiation of BCs was assessed using the BC expansion and air-liquid interface models in the absence/presence of BMP4, BMP receptor inhibitor and/or small interfering RNAs against BMP receptors and downstream signalling.The data demonstrate that in cigarette smokers, BMP4 is upregulated in ciliated and intermediate undifferentiated cells, and expression of the BMP4 receptor BMPR1A is enriched in BCs. BMP4 induced BCs to acquire a smoking-related abnormal phenotype in vitro mediated by BMPR1A/Smad signalling, characterised by decreased capacity to differentiate into normal mucociliary epithelium, while generating squamous metaplasia.Exaggerated BMP4 signalling promotes cigarette smoking-relevant airway epithelial remodelling by inducing abnormal phenotypes in human airway BCs. Targeting of BMP4 signalling in airway BCs may represent a novel target to prevent/treat COPD-associated airway disease.

Ontogeny and Biology of Human Small Airway Epithelial Club Cells.

RATIONALE: Little is known about human club cells, dome-shaped cells with dense cytoplasmic granules and microvilli that represent the major secretory cells of the human small airways (at least sixth-generation bronchi). OBJECTIVES: To define the ontogeny and biology of the human small airway epithelium club cell. METHODS: The small airway epithelium was sampled from the normal human lung by bronchoscopy and brushing. Single-cell transcriptome analysis and air-liquid interface culture were used to assess club cell ontogeny and biology. MEASUREMENTS AND MAIN RESULTS: We identified the club cell population by unbiased clustering using single-cell transcriptome sequencing. Principal component gradient analysis uncovered an ontologic link between KRT5 (keratin 5)+ basal cells and SCGB1A1 (secretoglobin family 1A member 1)+ club cells, a hypothesis verified by demonstrating in vitro that a pure population of human KRT5+ SCGB1A1- small airway epithelial basal cells differentiate into SCGB1A1+KRT5- club cells on air-liquid interface culture. Using SCGB1A1 as the marker of club cells, the single-cell analysis identified novel roles for these cells in host defense, xenobiotic metabolism, antiprotease, physical barrier function, monogenic lung disorders, and receptors for human viruses. CONCLUSIONS: These observations provide novel insights into the molecular phenotype and biologic functions of the human club cell population and identify basal cells as the human progenitor cells for club cells.

EGF-Amphiregulin Interplay in Airway Stem/Progenitor Cells Links the Pathogenesis of Smoking-Induced Lesions in the Human Airway Epithelium.

The airway epithelium of cigarette smokers undergoes dramatic remodeling with hyperplasia of basal cells (BC) and mucus-producing cells, squamous metaplasia, altered ciliated cell differentiation and decreased junctional barrier integrity, relevant to chronic obstructive pulmonary disease and lung cancer. In this study, we show that epidermal growth factor receptor (EGFR) ligand amphiregulin (AREG) is induced by smoking in human airway epithelium as a result of epidermal growth factor (EGF)-driven squamous differentiation of airway BC stem/progenitor cells. In turn, AREG induced a unique EGFR activation pattern in human airway BC, distinct from that evoked by EGF, leading to BC- and mucous hyperplasia, altered ciliated cell differentiation and impaired barrier integrity. Further, AREG promoted its own expression and suppressed expression of EGF, establishing an autonomous self-amplifying signaling loop in airway BC relevant for promotion of EGF-independent hyperplastic phenotypes. Thus, EGF-AREG interplay in airway BC stem/progenitor cells is one of the mechanisms that mediates the interconnected pathogenesis of all major smoking-induced lesions in the human airway epithelium. Stem Cells 2017;35:824-837.

POU2AF1 Functions in the Human Airway Epithelium To Regulate Expression of Host Defense Genes.

In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU domain class 2-associating factor 1 (POU2AF1), a known transcription cofactor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of upregulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation, and analysis of differentiating single basal cell clones. Lentivirus-mediated upregulation of POU2AF1 in airway basal cells induced upregulation of host defense genes, including MX1, IFIT3, IFITM, and known POU2AF1 downstream genes HLA-DRA, ID2, ID3, IL6, and BCL6. Interestingly, expression of these genes paralleled changes of POU2AF1 expression during airway epithelium differentiation in vitro, suggesting POU2AF1 helps to maintain a host defense tone even in pathogen-free condition. Cigarette smoke, a known risk factor for airway infection, suppressed POU2AF1 expression both in vivo in humans and in vitro in human airway epithelial cultures, accompanied by deregulation of POU2AF1 downstream genes. Finally, enhancing POU2AF1 expression in human airway epithelium attenuated the suppression of host defense genes by smoking. Together, these findings suggest a novel function of POU2AF1 as a potential regulator of host defense genes in the human airway epithelium.

Smoking-Dependent Distal-to-Proximal Repatterning of the Adult Human Small Airway Epithelium.

RATIONALE: Small airways are the primary site of pathologic changes in chronic obstructive pulmonary disease (COPD), the major smoking-induced lung disorder. OBJECTIVES: On the basis of the concept of proximal-distal patterning that determines regional specialization of the airway epithelium during lung development, we hypothesized that a similar program operates in the adult human lung being altered by smoking, leading to decreased regional identity of the small airway epithelium (SAE). METHODS: The proximal and distal airway signatures were identified by comparing the transcriptomes of large and small airway epithelium samples obtained by bronchoscopy from healthy nonsmokers. The expression of these signatures was evaluated in the SAE of healthy smokers and smokers with COPD compared with that of healthy nonsmokers. The capacity of airway basal stem cells (BCs) to maintain region-associated phenotypes was evaluated using the air-liquid interface model. MEASUREMENTS AND MAIN RESULTS: The distal and proximal airway signatures, containing 134 and 233 genes, respectively, were identified. These signatures included known developmental regulators of airway patterning, as well as novel regulators such as epidermal growth factor receptor, which was associated with the proximal airway phenotype. In the SAE of smokers with COPD, there was a dramatic smoking-dependent loss of the regional transcriptome identity with concomitant proximalization. This repatterning phenotype was reproduced by stimulating SAE BCs with epidermal growth factor, which was up-regulated in the SAE of smokers, during differentiation of SAE BCs in vitro. CONCLUSIONS: Smoking-induced global distal-to-proximal reprogramming of the SAE represents a novel pathologic feature of COPD and is mediated by exaggerated epidermal growth factor/epidermal growth factor receptor signaling in SAE BCs.

Role of GPR30 in estrogen-induced prostate epithelial apoptosis and benign prostatic hyperplasia.

Several studies have implicated estrogen and the estrogen receptor (ER) in the pathogenesis of benign prostatic hyperplasia (BPH); however, the mechanism underlying this effect remains elusive. In the present study, we demonstrated that estrogen (17ß-estradiol, or E2)-induced activation of the G protein-coupled receptor 30 (GPR30) triggered Ca2+ release from the endoplasmic reticulum, increased the mitochondrial Ca2+ concentration, and thus induced prostate epithelial cell (PEC) apoptosis. Both E2 and the GPR30-specific agonist G1 induced a transient intracellular Ca2+ release in PECs via the phospholipase C (PLC)-inositol 1, 4, 5-triphosphate (IP3) pathway, and this was abolished by treatment with the GPR30 antagonist G15. The release of cytochrome c and activation of caspase-3 in response to GPR30 activation were observed. Data generated from the analysis of animal models and human clinical samples indicate that treatment with the GPR30 agonist relieves testosterone propionate (TP)-induced prostatic epithelial hyperplasia, and that the abundance of GPR30 is negatively associated with prostate volume. On the basis of these results, we propose a novel regulatory mechanism whereby estrogen induces the apoptosis of PECs via GPR30 activation. Inhibition of this activation is predicted to lead to abnormal PEC accumulation, and to thereby contribute to BPH pathogenesis.

EGF shifts human airway basal cell fate toward a smoking-associated airway epithelial phenotype.

The airway epithelium of smokers acquires pathological phenotypes, including basal cell (BC) and/or goblet cell hyperplasia, squamous metaplasia, structural and functional abnormalities of ciliated cells, decreased number of secretoglobin (SCGB1A1)-expressing secretory cells, and a disordered junctional barrier. In this study, we hypothesized that smoking alters airway epithelial structure through modification of BC function via an EGF receptor (EGFR)-mediated mechanism. Analysis of the airway epithelium revealed that EGFR is enriched in airway BCs, whereas its ligand EGF is induced by smoking in ciliated cells. Exposure of BCs to EGF shifted the BC differentiation program toward the squamous and epithelial-mesenchymal transition-like phenotypes with down-regulation of genes related to ciliogenesis, secretory differentiation, and markedly reduced junctional barrier integrity, mimicking the abnormalities present in the airways of smokers in vivo. These data suggest that activation of EGFR in airway BCs by smoking-induced EGF represents a unique mechanism whereby smoking can alter airway epithelial differentiation and barrier function.

Effects of temperature and composite alumina on pyrolysis of sewage sludge.

An interactive dual-circulating fluidized bed system has been proposed in which the pyrolysis of sewage sludge (SS) and incineration of biomass proceed simultaneously, and alumina is used as the bed material and heat carrier. The alumina coated with biomass ash would mix with sewage sludge in the pyrolysis reactor of this device. It is important to know the influence of composite alumina (CA) on the pyrolysis progress. Sewage sludge was pyrolyzed in a fixed bed reactor from 400 to 600°C using CA as catalyst. The effects of temperature and CA additive ratio on the products were investigated. The product yields and component distribution of non-condensable gas were more sensitive to the change of temperature, and the maximum liquid yield of 48.44 wt.% and maximum Useable Energy of Liquid of 3871 kJ/kg sludge were observed at 500°C with 1/5 CA/SS (mass ratio). The gas chromatography-mass spectrometry results showed that the increase of temperature enhanced devolatilization of organic matter and promoted cyclization and aromatization of aliphatics. The presence of CA could strengthen secondary cracking and interaction among primary products from different organic compounds, such as acid-amine condensation, and reduce the content of oxygenated compounds. When the CA additive amount exceeded a certain proportion, the aromatization was clearly strengthened. The effects of CA on decomposition of fatty acids and formation of aromatics were similar to that of temperature. This means that the reaction temperature could be lowered by introducing CA, which has a positive effect on reducing energy consumption.

A study of the stabilization and solidification of heavy metals in co-vitrification of medical waste incineration ash and coal fly ash.

Medical waste incineration ash (MWIA) has significant concentrations of heavy metals, dioxins, and chlorine that, if handled incorrectly, might cause permanent damage to the environment and humans. The low content of calcium (Ca), silicon (Si), and aluminum (Al) is a brand-new challenge for the melting technique of MWIA. This work added coal fly ash (CFA) to explore the effect of melting on the detoxication treatment of MWIA. It was found that the produced vitrification product has a high vitreous content (98.61%) and a low potential ecological risk, with an initial ash solidification rate of 67.38%. By quantitatively assessing the morphological distribution features of heavy metals in ashes before melting and molten products, the stabilization and solidification rules of heavy metals during the melting process were investigated. This work ascertained the feasibility of co-vitrification of MWIA and CFA. In addition, the high-temperature melting and vitrification accelerated the detoxification of MWIA and the solidification of heavy metals.

Attempts to obtain clean biochar from hyperaccumulator through pyrolysis: Removal of heavy metals and transformation of phosphorus.

The sound disposal of the ensuing heavy metal-rich plants can address the aftermath of phytoremediation. In this study, the first attempt was made to obtain heavy metals-free and phosphorus-rich biochar from phytoremediation residue (PR) by pyrolysis, and the effects of chlorinating agent type, chlorine dosage, and pyrolysis residence time on heavy metal removal, phosphorus (P) transformation, and biochar properties were investigated. The results showed that as chlorine dosage and pyrolysis residence time increased, added polyvinyl chloride (PVC) reduced the concentration of Zn in biochar to one-tenth of that in PR by intensified chlorination, where both Zn concentration (2727.50 mg/kg) and its leaching concentration (29.13 mg/L) met the utilization requirements, in which the acid-base property of biochar plays a key role in heavy metal leaching. Meanwhile, more than 90% of P in PR remained in biochar and the bioavailability of P in biochar enhanced with the decomposition of organic P to inorganic P, where the concentration of plant-availability P (Pnac) expanded from 1878.40 mg/kg in PR to 8454.00 mg/kg in biochar. This study demonstrated that heavy metal hyperaccumulator can be converted into heavy metal-free and phosphorus-rich biochar with promising applications, which provides new perspectives for the treatment of such hazardous wastes.

Smoking-induced CXCL14 expression in the human airway epithelium links chronic obstructive pulmonary disease to lung cancer.

CXCL14, a recently described epithelial cytokine, plays putative multiple roles in inflammation and carcinogenesis. In the context that chronic obstructive pulmonary disease (COPD) and lung cancer are both smoking-related disorders associated with airway epithelial disorder and inflammation, we hypothesized that the airway epithelium responds to cigarette smoking with altered CXCL14 gene expression, contributing to the disease-relevant phenotype. Using genome-wide microarrays with subsequent immunohistochemical analysis, the data demonstrate that the expression of CXCL14 is up-regulated in the airway epithelium of healthy smokers and further increased in COPD smokers, especially within hyperplastic/metaplastic lesions, in association with multiple genes relevant to epithelial structural integrity and cancer. In vitro experiments revealed that the expression of CXCL14 is induced in the differentiated airway epithelium by cigarette smoke extract, and that epidermal growth factor mediates CXCL14 up-regulation in the airway epithelium through its effects on the basal stem/progenitor cell population. Analyses of two independent lung cancer cohorts revealed a dramatic up-regulation of CXCL14 expression in adenocarcinoma and squamous-cell carcinoma. High expression of the COPD-associated CXCL14-correlating cluster of genes was linked in lung adenocarcinoma with poor survival. These data suggest that the smoking-induced expression of CXCL14 in the airway epithelium represents a novel potential molecular link between smoking-associated airway epithelial injury, COPD, and lung cancer.

Experimental study on adsorption of PbCl2 and CdCl2 on kaolin modified by leachates from municipal solid waste incineration power plant.

Six kinds of waste liquids produced in the treatment process of leachate in a waste incineration plant were used to improve the adsorption effect of raw kaolin on heavy metal chloride. The capture performances of these modified kaolin on PbCl2 and CdCl2 vapor were investigated in a two-stage fixed bed combustor. The results indicated that the adsorption effects of raw kaolin on PbCl2 and CdCl2 were improved in some experimental groups, main effective component was Na+ in the leachate, but the influences did not change regularly with the increase in the concentration of Na + introduced into kaolin. The adsorbents formed by modifying 10 g kaolin with 21.25 ml leachate 2 were the best adsorbents for PbCl2 and CdCl2. The capture efficiencies of PbCl2 and CdCl2 can reach 95% and 63.88%, with the increase of 36% and 53%, respectively. Using leachate as modifying agent had the same effect as directly using Na+. Adsorptions of PbCl2 and CdCl2 were still mainly chemical adsorptions. After adsorption of PbCl2, the modified kaolin not only generated PbA12Si2O8, but also produced other chemical compounds. The adsorption of CdCl2 by modified kaolin did not generate CdAl2Si2O8, but other chemical reactions occurred to generate CdAl2O4 and Pb8Cd (Si2O7)3.

Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy.

With aging, abnormalities during oocyte meiosis become more prevalent. However, the mechanisms of aging-related oocyte aneuploidy are not fully understood. Here we performed Hi-C and SMART-seq of oocytes from young and old mice and reveal decreases in chromosome condensation and disrupted meiosis-associated gene expression in metaphase I oocytes from aged mice. Further transcriptomic analysis showed that meiotic maturation in young oocytes was correlated with robust increases in mevalonate (MVA) pathway gene expression in oocyte-surrounding granulosa cells (GCs), which was largely downregulated in aged GCs. Inhibition of MVA metabolism in GCs by statins resulted in marked meiotic defects and aneuploidy in young cumulus-oocyte complexes. Correspondingly, supplementation with the MVA isoprenoid geranylgeraniol ameliorated oocyte meiotic defects and aneuploidy in aged mice. Mechanically, we showed that geranylgeraniol activated LHR/EGF signaling in aged GCs and enhanced the meiosis-associated gene expression in oocytes. Collectively, we demonstrate that the MVA pathway in GCs is a critical regulator of meiotic maturation and euploidy in oocytes, and age-associated MVA pathway abnormalities contribute to oocyte meiotic defects and aneuploidy.

Population data and phylogenetic structure of 19 STR loci in Chinese Hui ethnic group residing in Yunnan province of China.

Allele frequency distributions and statistical forensic parameters of 19 autosomal STR loci in a sample of 535 unrelated healthy Hui individuals from Yunnan province were estimated. A total of 236 alleles at these loci were identified and their corresponding allele frequencies ranged from 0.000935 to 0.527103. Penta E is the most informative in Hui population, whereas TPOX showed the lowest. All of the STR loci reached the Hardy-Weinberg equilibrium after Bonferroni correction. The combined discrimination power and probability of excluding paternity of the 19 STR loci were 0.999 999 999 999 999 999 999 984 47 16 and 0.999 999 988, respectively. Furthermore, the genetic relationship between the Yunnan Hui population and other 8 different Hui groups or 25 previously investigated groups residing in other areas of China were also estimated based on pairwise genetic distance. These results suggest that the 19 STR loci are highly polymorphic, which is suitable for forensic personal identification and paternity testing.

Preparation of Alkali Activated Cementitious Material by Upgraded Fly Ash from MSW Incineration.

Utilization of municipal solid waste incineration fly ash (MSWI-FA) can avoid land occupation and environmental risks of landfill. In this paper, MSWI-FA was used to prepare alkali activated cementitious materials (AACMs) after two-step pretreatment. The ash calcination at 450 °C removed 93% of dioxins. The alkali washing with 0.2 g NaOH/g ash removed 89% of chlorine and retained almost 100% of calcium. The initial setting time of AACMs was too short to detect for 20% of MSWI-FA addition, and the prepared block had extensive cracks and expansion for CaClOH and CaSO4 inside. Alkaline washing pretreatment increased the initial setting time by longer than 3 min with 30% ash addition and eliminated the cracks and expansion. The significance of the factors for compressive strength followed the modulus of alkali activator > silica fume amount > alkaline washing MSWI fly ash (AW-MSWI-FA) amount. When the activator modulus was 1.2, 1.4 and 1.6, the blocks with 30% of AW-MSWI-FA had a compressive strength of up to 36.73, 32.61 and 16.06 MPa, meeting MU15 grade. The leaching test shows that these AACM blocks were not hazardous waste and almost no Zn, Cu, Cd, Pb, Ba, Ni, Be and Ag were released in the leaching solution.