Pyrolysis of wastewater sludge and composted organic fines from municipal solid waste: laboratory reactor characterisation and product distribution

Abstract

Sludge from municipal wastewater treatment plants and organic fines from mechanical sorting of municipal solid waste (MSW) are two common widespread waste streams that are becoming increasingly difficult to utilise. Changing perceptions of risk in food production has limited the appeal of sludge use on agricultural land, and outlets via landfilling are diminishing rapidly. These factors have led to interest in thermal conversion technologies whose aim is to recover energy and nutrients from waste while reducing health and environmental risks associated with material re-use. Pyrolysis yields three output products: solid char, liquid oils and gas. Their relative distribution depends on process parameters which can be somewhat optimised depending on the end use of product. The potential of pyrolysis for the conversion of wastewater sludge (SS) and organic fines of MSW (OF) to a combustion gas and a carbon-rich char has been investigated. Pyrolysis of SS and OF was done using a laboratory fixed-bed reactor. Herein, the physical characterisation of the reactor is described, and results on pyrolysis yields are presented. Feedstock and chars have been characterised using standard laboratory methods, and the composition of pyrolysis gases was analysed using micro gas chromatography. Product distribution (char/liquid/gas) from the pyrolysis of sewage sludge and composted MSW fines at 700°C for 10 min were 45/26/29 and 53/14/33%, respectively. The combustible fractions of pyrolysis gases range from 36 to 54% for SS feedstock and 62 to 72% from OF. The corresponding lower heating value range of sampled gases were 11.8–19.1 and 18.2–21.0 MJ m⁻³, respectively.

http://ift.tt/2ETGBOt

Ascorbic acid protects male rat brain from oral potassium dichromate-induced oxdative DNA damage and apoptotic changes: the expression patterns of caspase-3, P 53, Bax, and Bcl-2 genes

Abstract

Our study designed to study the potential of potassium dichromate (K₂Cr₂O₇) oral exposure to induce damage in male rat brain and to compare the possible protective role of vitamin C (VC) either pre and/or concurrent supply against (K₂Cr₂O₇) induced changes. Thirty male rats were divided into five groups. First control group received distilled water (C), second received 120 mg/kg b.wt (VC), third received 25 mg/kg b.wt K₂Cr₂O₇ (Cr), fourth group received VC together with K₂Cr₂O₇ by the same former doses (VC + Cr), and the fifth group received the same oral doses of VC 2 weeks prior to and along with K₂Cr₂O₇ for 6 weeks (VC + Cr pro/co treated). The obtained results revealed that K₂Cr₂O₇ induced a significant decrease in cholinergic activity, glutathione reductase GR activity, reduced glutathione content GSH and ATP levels. Furthermore, K₂Cr₂O₇ induced a significant increase in oxidative DNA damage indicated by 8-hydroxy 2′-deoxyguanosine (8OH2′dG) and formation of apoptotic DNA ladders, significant increase in malondialdehyde (MDA), protein carbonyl, and lactate dehydrogenase enzyme. Increased mRNA expression of pro-apoptotic genes, including caspase-3, p53, and Bax, unlike Bcl-2 expression, was decreased. K₂Cr₂O₇ increased caspase-3 and decreased Bcl-2 immuno-labeling. VC supply noticeably ameliorates K₂Cr₂O₇-induced changes which were more significantly in VC pro and concurrent supplement rather than VC concurrent supply only. Finally, it is concluded that K₂Cr₂O₇ oral administration induced oxidative apoptotic changes in rat brain and confirms the usefulness of VC pre and concurrent supply for the amelioration of K₂Cr₂O₇-induced events more significantly than VC concurrent supply only.

http://ift.tt/2BSpud6

A Fat Lot of Good for Wound Healing

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Alessandra Maria Casano, Michael Sixt
The insect's fat body combines metabolic and immunological functions. In this issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells of the fat body are not static, but can actively "swim" toward sites of epithelial injury, where they physically clog the wound and locally secrete antimicrobial peptides.

Teaser

The insect's fat body combines metabolic and immunological functions. In this issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells of the fat body are not static, but can actively "swim" toward sites of epithelial injury, where they physically clog the wound and locally secrete antimicrobial peptides.


http://ift.tt/2F8exWQ

Organizing Complex Tissue Architecture by Pushing and Pulling Cell Contacts

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Yixie Zhang, Tony J.C. Harris
Changes to cell shape and interaction drive animal tissue morphogenesis. Reporting now in Developmental Cell, Del Signore et al. (2018) describe active lengthening of cell-cell contacts by Arp2/3-based actin networks. Through cycles of contact lengthening and shortening, the developing Drosophila eye passes through various multicellular configurations to achieve its complex architecture.

Teaser

Changes to cell shape and interaction drive animal tissue morphogenesis. Reporting now in Developmental Cell, Del Signore et al. (2018) describe active lengthening of cell-cell contacts by Arp2/3-based actin networks. Through cycles of contact lengthening and shortening, the developing Drosophila eye passes through various multicellular configurations to achieve its complex architecture.


http://ift.tt/2sZD0ZF

Ultraviolet Rays Light Up Transcriptional Networks Regulating Plant Growth

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Eirini Kaiserli
Light and hormones tightly regulate plant growth and development by both synergistic and antagonistic actions. In the current issue of Developmental Cell, Liang et al. (2018) uncover how the UV-B photoreceptor UVR8 mediates inhibition of plant growth via direct interactions with key transcriptional regulators of brassinosteroid signaling.

Teaser

Light and hormones tightly regulate plant growth and development by both synergistic and antagonistic actions. In the current issue of Developmental Cell, Liang et al. (2018) uncover how the UV-B photoreceptor UVR8 mediates inhibition of plant growth via direct interactions with key transcriptional regulators of brassinosteroid signaling.


http://ift.tt/2CmP6jl

Dynamic Encoding in the Notch Pathway

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Sean G. Megason
A small number of signaling pathways are used ubiquitously throughout development. How can enough information be carried through such a small number of channels? Reporting in Cell, Nandagopal et al. (2018) reveal how different Notch ligands can regulate different targets through the same receptor using differences in signaling dynamics.

Teaser

A small number of signaling pathways are used ubiquitously throughout development. How can enough information be carried through such a small number of channels? Reporting in Cell, Nandagopal et al. (2018) reveal how different Notch ligands can regulate different targets through the same receptor using differences in signaling dynamics.


http://ift.tt/2t0Pws5

Ben Barres (1954–2017)

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Marc Tessier-Lavigne




http://ift.tt/2F4tABb

A Role for Ploidy in Heart Regeneration

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Zachary A. Kadow, James F. Martin
There is mounting circumstantial evidence that ploidy, a cell's relative DNA content, is in part responsible for the differential cardiac regenerative capacity observed between regenerative and non-regenerative organisms. In this issue of Developmental Cell, González-Rosa et al. (2018) provide direct evidence that polyploid cardiomyocytes have reduced proliferative and regenerative potential.

Teaser

There is mounting circumstantial evidence that ploidy, a cell's relative DNA content, is in part responsible for the differential cardiac regenerative capacity observed between regenerative and non-regenerative organisms. In this issue of Developmental Cell, González-Rosa et al. (2018) provide direct evidence that polyploid cardiomyocytes have reduced proliferative and regenerative potential.


http://ift.tt/2sXva2F

A Tribute to Ben Barres: Remembrances from Barres Lab Members

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4





http://ift.tt/2F5xLwl

Cellular Stress Associated with Aneuploidy

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Jin Zhu, Hung-Ji Tsai, Molly R. Gordon, Rong Li
Aneuploidy, chromosome stoichiometry that deviates from exact multiples of the haploid compliment of an organism, exists in eukaryotic microbes, several normal human tissues, and the majority of solid tumors. Here, we review the current understanding about the cellular stress states that may result from aneuploidy. The topics of aneuploidy-induced proteotoxic, metabolic, replication, and mitotic stress are assessed in the context of the gene dosage imbalance observed in aneuploid cells. We also highlight emerging findings related to the downstream effects of aneuploidy-induced cellular stress on the immune surveillance against aneuploid cells.

Teaser

Aneuploidy refers to chromosome stoichiometry deviating from exact multiples of the haploid compliment of an organism. Zhu et al. review our current understanding of the cellular stress states that may result from aneuploidy, including proteotoxic, metabolic, replication, and mitotic stress. They also discuss immune surveillance against aneuploid cells.


http://ift.tt/2sYjtJg

Myocardial Polyploidization Creates a Barrier to Heart Regeneration in Zebrafish

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Juan Manuel González-Rosa, Michka Sharpe, Dorothy Field, Mark H. Soonpaa, Loren J. Field, Caroline E. Burns, C. Geoffrey Burns
Correlative evidence suggests that polyploidization of heart muscle, which occurs naturally in post-natal mammals, creates a barrier to heart regeneration. Here, we move beyond a correlation by demonstrating that experimental polyploidization of zebrafish cardiomyocytes is sufficient to suppress their proliferative potential during regeneration. Initially, we determined that zebrafish myocardium becomes susceptible to polyploidization upon transient cytokinesis inhibition mediated by dominant-negative Ect2. Using a transgenic strategy, we generated adult animals containing mosaic hearts composed of differentially labeled diploid and polyploid-enriched cardiomyocyte populations. Diploid cardiomyocytes outcompeted their polyploid neighbors in producing regenerated heart muscle. Moreover, hearts composed of equivalent proportions of diploid and polyploid cardiomyocytes failed to regenerate altogether, demonstrating that a critical percentage of diploid cardiomyocytes is required to achieve heart regeneration. Our data identify cardiomyocyte polyploidization as a barrier to heart regeneration and suggest that mobilizing rare diploid cardiomyocytes in the human heart will improve its regenerative capacity.

Graphical abstract

Teaser

It remains unclear why certain non-mammalian species efficiently regenerate their hearts while mammals fail in this endeavor. González-Rosa et al. demonstrate that simply increasing the DNA content of the highly regenerative zebrafish myocardium, to more closely resemble that in mammals, is sufficient to dampen cardiomyocyte proliferative capacity and organ regeneration.


http://ift.tt/2Cny6K2

The Polyploid State Plays a Tumor-Suppressive Role in the Liver

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Shuyuan Zhang, Kejin Zhou, Xin Luo, Lin Li, Ho-Chou Tu, Alfica Sehgal, Liem H. Nguyen, Yu Zhang, Purva Gopal, Branden D. Tarlow, Daniel J. Siegwart, Hao Zhu
Most cells in the liver are polyploid, but the functional role of polyploidy is unknown. Polyploidization occurs through cytokinesis failure and endoreduplication around the time of weaning. To interrogate polyploidy while avoiding irreversible manipulations of essential cell-cycle genes, we developed orthogonal mouse models to transiently and potently alter liver ploidy. Premature weaning, as well as knockdown of E2f8 or Anln, allowed us to toggle between diploid and polyploid states. While there was no detectable impact of ploidy alterations on liver function, metabolism, or regeneration, mice with more polyploid hepatocytes suppressed tumorigenesis and mice with more diploid hepatocytes accelerated tumorigenesis in mutagen- and high-fat-induced models. Mechanistically, the diploid state was more susceptible to Cas9-mediated tumor-suppressor loss but was similarly susceptible to MYC oncogene activation, indicating that polyploidy differentially protected the liver from distinct genomic aberrations. This suggests that polyploidy evolved in part to prevent malignant outcomes of liver injury.

Graphical abstract

Teaser

Most liver cells are polyploid, but the functional role of wholesale genome duplications is unknown. To interrogate liver polyploidy function without irreversible manipulations of cell-cycle genes, Zhang et al. developed models to transiently alter ploidy, finding that polyploidy reduces tumor development by buffering against tumor-suppressor loss of heterozygosity.


http://ift.tt/2EVR4Vv

Fat Body Cells Are Motile and Actively Migrate to Wounds to Drive Repair and Prevent Infection

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Anna Franz, Will Wood, Paul Martin
Adipocytes have many functions in various tissues beyond energy storage, including regulating metabolism, growth, and immunity. However, little is known about their role in wound healing. Here we use live imaging of fat body cells, the equivalent of vertebrate adipocytes in Drosophila, to investigate their potential behaviors and functions following skin wounding. We find that pupal fat body cells are not immotile, as previously presumed, but actively migrate to wounds using an unusual adhesion-independent, actomyosin-driven, peristaltic mode of motility. Once at the wound, fat body cells collaborate with hemocytes, Drosophila macrophages, to clear the wound of cell debris; they also tightly seal the epithelial wound gap and locally release antimicrobial peptides to fight wound infection. Thus, fat body cells are motile cells, enabling them to migrate to wounds to undertake several local functions needed to drive wound repair and prevent infections.

Teaser

Adipocytes and their fly equivalent, fat body cells, have been considered immotile, but Franz et al. now show the latter can actively migrate to wounds using a peristaltic-like "swimming" motility. Once there, they multitask to clear wound cell debris, plug the epithelial gap, and upregulate AMPs to prevent infection.


http://ift.tt/2FAdRaH

Cell Extrusion: A Stress-Responsive Force for Good or Evil in Epithelial Homeostasis

Publication date: 26 February 2018
Source:Developmental Cell, Volume 44, Issue 4
Author(s): Shizue Ohsawa, John Vaughen, Tatsushi Igaki




http://ift.tt/2EVEEx6

Revisiting the Functional Impact of NK Cells

Publication date: Available online 26 February 2018
Source:Trends in Immunology
Author(s): Aurélie Poli, Tatiana Michel, Neha Patil, Jacques Zimmer
Immune responses are critical for the maintenance of homeostasis but can also upset the equilibrium, depending on the context and magnitude of the response. Natural killer (NK) cells are well known for their important roles in antiviral and antitumor immune responses, and they are currently used, mostly under optimized forms, as immunotherapeutic agents against cancer. Nevertheless, with accumulating examples of deleterious effects of NK cells, it is paramount to consider their negative contributions. Here, we critically review and comment on the literature surrounding undesirable aspects of NK cell activity, focusing on situations where they play a harmful rather than a protective role.



http://ift.tt/2FC5mvW

Consent for Pragmatic Trials in Acute Myocardial Infarction

http://ift.tt/2HNZZdu

Gadolinium-Free Cardiac MR Stress T1-Mapping to Distinguish Epicardial From Microvascular Coronary Disease

AbstractBackground

Novel cardiac magnetic resonance (CMR) stress T1 mapping can detect ischemia and myocardial blood volume changes without contrast agents and may be a more comprehensive ischemia biomarker than myocardial blood flow.

Objectives

This study describes the performance of the first prospective validation of stress T1 mapping against invasive coronary measurements for detecting obstructive epicardial coronary artery disease (CAD), defined by fractional flow reserve (FFR <0.8), and coronary microvascular dysfunction, defined by FFR ≥0.8 and the index of microcirculatory resistance (IMR ≥25 U), compared with first-pass perfusion imaging.

Methods

Ninety subjects (60 patients with angina; 30 healthy control subjects) underwent CMR (1.5- and 3-T) to assess left ventricular function (cine), ischemia (adenosine stress/rest T1 mapping and perfusion), and infarction (late gadolinium enhancement). FFR and IMR were assessed ≤7 days post-CMR. Stress and rest images were analyzed blinded to other information.

Results

Normal myocardial T1 reactivity (T1) was 6.2 ± 0.4% (1.5-T) and 6.2 ± 1.3% (3-T). Ischemic viable myocardium downstream of obstructive CAD showed near-abolished T1 reactivity (T1 = 0.7 ± 0.7%). Myocardium downstream of nonobstructive coronary arteries with microvascular dysfunction showed less-blunted T1 reactivity (T1 = 3.0 ± 0.9%). Stress T1 mapping significantly outperformed gadolinium-based first-pass perfusion, including absolute quantification of myocardial blood flow, for detecting obstructive CAD (area under the receiver-operating characteristic curve: 0.97 ± 0.02 vs. 0.91 ± 0.03, respectively; p < 0.001). A T1 of 1.5% accurately detected obstructive CAD (sensitivity: 93%; specificity: 95%; p < 0.001), whereas a less-blunted T1 of 4.0% accurately detected microvascular dysfunction (area under the receiver-operating characteristic curve: 0.95 ± 0.03; sensitivity: 94%; specificity: 94%: p < 0.001).

Conclusions

CMR stress T1 mapping accurately detected and differentiated between obstructive epicardial CAD and microvascular dysfunction, without contrast agents or radiation.

http://ift.tt/2HOawp5

JACC Instructions for Authors

http://ift.tt/2GLPQNr

Diagnosis of Microvascular Angina Using Cardiac Magnetic Resonance

AbstractBackground

In patients with angina and nonobstructive coronary artery disease (NOCAD), confirming symptoms due to coronary microvascular dysfunction (CMD) remains challenging. Cardiac magnetic resonance (CMR) assesses myocardial perfusion with high spatial resolution and is widely used for diagnosing obstructive coronary artery disease (CAD).

Objectives

The goal of this study was to validate CMR for diagnosing microvascular angina in patients with NOCAD, compared with patients with obstructive CAD and correlated to the index of microcirculatory resistance (IMR) during invasive coronary angiography.

Methods

Fifty patients with angina (65 ± 9 years of age) and 20 age-matched healthy control subjects underwent adenosine stress CMR (1.5- and 3-T) to assess left ventricular function, inducible ischemia (myocardial perfusion reserve index [MPRI]; myocardial blood flow [MBF]), and infarction (late gadolinium enhancement). During subsequent angiography within 7 days, 28 patients had obstructive CAD (fractional flow reserve [FFR] ≤0.8) and 22 patients had NOCAD (FFR >0.8) who underwent 3-vessel IMR measurements.

Results

In patients with NOCAD, myocardium with IMR <25 U had normal MPRI (1.9 ± 0.4 vs. controls 2.0 ± 0.3; p = 0.49); myocardium with IMR ≥25 U had significantly impaired MPRI, similar to ischemic myocardium downstream of obstructive CAD (1.2 ± 0.3 vs. 1.2 ± 0.4; p = 0.61). An MPRI of 1.4 accurately detected impaired perfusion related to CMD (IMR ≥25 U; FFR >0.8) (area under the curve: 0.90; specificity: 95%; sensitivity: 89%; p < 0.001). Impaired MPRI in patients with NOCAD was driven by impaired augmentation of MBF during stress, with normal resting MBF. Myocardium with FFR >0.8 and normal IMR (<25 U) still had blunted stress MBF, suggesting mild CMD, which was distinguishable from control subjects by using a stress MBF threshold of 2.3 ml/min/g with 100% positive predictive value.

Conclusions

In angina patients with NOCAD, CMR can objectively and noninvasively assess microvascular angina. A CMR-based combined diagnostic pathway for both epicardial and microvascular CAD deserves further clinical validation.

http://ift.tt/2GLoHtO

Subclinical Thrombotic Events as a Mechanism for Troponin Release?

http://ift.tt/2HNyLnj