18 research outputs found
Characterizing the Opportunity Space for Sustainable Hydrothermal Valorization of Wet Organic Wastes
Resource
recovery from wet organic wastes can support
circular
economies by creating financial incentives to produce renewable energy
and return nutrients to agriculture. In this study, we characterize
the potential for hydrothermal liquefaction (HTL)-based resource recovery
systems to advance the economic and environmental sustainability of
wastewater sludge, FOG (fats, oils, and grease), food waste, green
waste, and animal manure management through the production of liquid
biofuels (naphtha, diesel), fertilizers (struvite, ammonium sulfate),
and power (heat, electricity). From the waste management perspective,
median costs range from −193 ·tonne–1 (green waste), and
median carbon intensities range from 367 kg CO2 eq·tonne–1 (wastewater sludge) to 769 kg CO2 eq·tonne–1 (green waste). From the fuel production perspective,
the minimum selling price of renewable diesel blendstocks are within
the commercial diesel price range (2.37 to 5.81 $·gal–1) and have a lower carbon intensity than petroleum diesel (101 kg
CO2 eq·MMBTU–1). Finally, through
uncertainty analysis and Monte Carlo filtering, we set specific targets
(i.e., achieve wastewater sludge-to-biocrude yield >0.440) for
the
future development of hydrothermal waste management system components.
Overall, our work demonstrates the potential of HTL-based resource
recovery systems to reduce the costs and carbon intensity of resource-rich
organic wastes
Down-regulation of STC1 promoted CaSki cells growth and invasion.
<p>(A) Knock down of STC1 in CaSki cells. CaSki cells were transfected by STC1 targeting siRNA, and knockdown efficiency was shown by RT-PCR and western blotting. (B) MTT assays showed that the effect of decreased STC1 on CaSki cell growth. Following a 7-day period, the growth of CaSki/siRNA cells was much faster than CaSki/NC cells (*<i>p</i><0.05). (C) Colony formation assay demonstrated the large number of cell colonies from CaSki/siRNA cells compared to CaSki/NC cells (<i>p</i><0.05). (D) Wound healing assays showed the effect of STC1 on the migration of CaSki cells. CaSki/siRNA cells migrated faster compared to CaSki/NC cells (left panel). The relative migration distance of CaSki cells was calculated (right panel) (<i>p</i><0.05). Bar size: 100 µm. (E) Matrigel invasion assays showed the effect of STC1 on the invasion of CaSki cells. The number of CaSki/siRNA cells on the filter surface was larger than CaSki/NC cells (left panel) (<i>p</i><0.05). The mean value of invaded cells was shown in right panel. Bar size: 100 µm. (F) The growth curves of the xenografts were determined by tumor volume (left panel) (*<i>p</i><0.05). The growth rates of the xenografts were valuated by tumor volume/days (right panel) (*<i>p</i><0.05). CaSki/siRNA or CaSki/NC cells were injected subcutaneously into nude mice. (G) At end of experimental period, the final xenograft tumors were shown. (H) RT-PCR analyzed the expression of STC1 in representative xenograft tumors. (I) Representative images of histological inspection of xenograft tumors. The sections of xenograft tumors were stained with H&E. Bar size: 20 µm. Data was expressed as mean ± SEM of three separated experiments. Data was expressed as mean ± SEM of three separated experiments. A value of P<0.05 was considered as statistical significance.</p
Stanniocalcin1 (STC1) Inhibits Cell Proliferation and Invasion of Cervical Cancer Cells
<div><p>STC1 is a glycoprotein hormone involved in calcium/phosphate (Pi) homeostasis. There is mounting evidence that STC1 is tightly associated with the development of cancer. But the function of STC1 in cancer is not fully understood. Here, we found that STC1 is down-regulated in Clinical tissues of cervical cancer compared to the adjacent normal cervical tissues (15 cases). Subsequently, the expression of STC1 was knocked down by RNA interference in cervical cancer CaSki cells and the low expression promoted cell growth, migration and invasion. We also found that STC1 overexpression inhibited cell proliferation and invasion of cervical cancer cells. Moreover, STC1 overexpression sensitized CaSki cells to drugs. Further, we showed that NF-κB p65 protein directly bound to STC1 promoter and activated the expression of STC1 in cervical cancer cells. Thus, these results provided evidence that STC1 inhibited cell proliferation and invasion through NF-κB p65 activation in cervical cancer.</p> </div
STC1 sensitized CaSki cells to drugs.
<p>(A) Effect of cisplatin on CaSki cells growth. CaSki cells were treated with with or without cisplatin (0, 1, 2, and 3 mg/L) for 96 h, removing aliquots every 24 h to evaluate cell viability. (B) Effect of thapsigargin on CaSki cells growth. CaSki cells were treated with with or without thapsigargin (0, 1, 3, 6, and 9 µM) for 72 h, removing aliquots every 24 h to evaluate cell viability. (C) Effect of rapamycin on CaSki cells growth. CaSki cells were treated with with or without rapamycin (0, 0.01, 0.1, 0.5, and 1 mg/L) for 72 h, removing aliquots every 24 h to evaluate cell viability. (D) STC1 sensitized CaSki cells to cisplatin. CaSki/STC1 or CaSki/NC cells were treated with cisplatin (2 mg/L) for 96 h. MTT assays detected the cell growth of CaSki/STC1 or CaSki/NC cells in the face of cisplatin (*<i>p</i><0.05). (E) STC1 sensitized CaSki cells to thapsigargin. CaSki/STC1 or CaSki/NC cells were treated with thapsigargin (3 µM) for 72 h. MTT assays detected the cell growth of CaSki/STC1 or CaSki/NC cells in the face of thapsigargin (*<i>p</i><0.05). (F) STC1 sensitized CaSki cells to rapamycin. CaSki/STC1 or CaSki/NC cells were treated with rapamycin (0.5 mg/L) for 72 h. MTT assays detected the cell growth of CaSki/STC1 or CaSki/NC cells in the face of rapamycin (*<i>p</i><0.05). Data was expressed as mean ± SEM of three separated experiments. A value of P<0.05 was considered as statistical significance.</p
Overexpression of STC1 inhibited cell proliferation and invasion of CaSki cells.
<p>(A) Overexpression of STC1 in CaSki cells. STC1 expression vector was transfected into CaSki cells, and increased expression of STC1 was shown by RT-PCR and western blotting. (B) MTT assays showed that the growth of CaSki/STC1 cells was much slower than CaSki/NC cells (*<i>p</i><0.05). (C) Colony formation assay showed that a small amount of cell colonies from CaSki/STC1 cells demonstrated a low activity (<i>p</i><0.05). (D) Matrigel invasion assay revealed that up-regulation of STC1 mitigated the invasion of cells in vitro. Bar size: 100 µm. (E) STC1 overexpressed tumors emerged later and slowly grew compared to control tumors (*<i>p</i><0.05). (F) At end of experimental period, the final weights of STC1 overexpressed tumors were found to be lower than controls. (G) RT-PCR of STC1 in xenograft tumors indicated that increased STC1 expression had been maintained throughout experimental time course. (H) H&E staining of STC1 overexpressed tumors showed a low nuclear/cytoplasmic ratio, and limited to the cancer nests compared to control tumors. Bar size: 20 µm. Data was expressed as mean ± SEM of three separated experiments. A value of P<0.05 was considered as statistical significance.</p
Exploring the Mechanism of Yiwei Decoction in the Intervention of a Premature Ovarian Insufficiency Rat Based on Network Pharmacology and the miRNA-mRNA Regulatory Network
Objective: our aim
is to explore the mechanism of action
of Yiwei
decoction (YWD) in addressing premature ovarian insufficiency (POI)
through a combination of transcriptomics and network pharmacology.
By doing so, we hope to identify important pathways of action, key
targets, and active components that contribute to the efficacy of
YWD. Materials and Methods: group A comprised of the model + traditional
Chinese medicine group, while group B was the model control group
and group C was the normal control group. After gavage, serum AMH
and E2 levels were measured by using ELISA. HE staining was used to
study the impact of YWD on ovarian follicle recovery in POI rats.
Additionally, RNA-seq sequencing technology was employed to analyze
the transcription levels of mRNAs and miRNAs in the ovarian tissues
of each group, and the resulting data were examined using R. YWD used
UPLC-Q-TOF-HRMS to analyze its active ingredients. Upon obtaining
the sequencing results, the miRWalk database was utilized to forecast
the targets of DEmiRNAs. Network pharmacology was then applied to
predict the targets of active ingredients present in YWD, ultimately
constructing a regulatory network consisting of active ingredients-mRNA-miRNA.
The coexpression relationship between mRNAs and miRNAs was calculated
using the Pearson correlation coefficient, and high correlation coefficients
between miRNA-mRNA were confirmed through miRanda sequence combination.
Results: the application of YWD resulted in improved serum levels
of AMH and E2, as well as an increased number of ovarian follicles
in rats with POI. However, there was a minimal impact on the infiltration
of ovarian lymphocytes. Through GSEA pathway enrichment analysis,
we found that YWD may have a regulatory effect on PI3K-Akt, ovarian
steroidogenesis, and protein digestion and absorption, which could
aid in the treatment of POI. Additionally, our research discovered
a total of 6 DEmiRNAs between groups A and B, including 2 new DEmiRNAs.
YWD contains 111 active compounds, and our analysis of the active
component-mRNA regulatory network revealed 27 active components and
73 mRNAs. Furthermore, the coexpression network included 5 miRNAs
and 18 mRNAs. Our verification of MiRanda binding demonstrated that
12 of the sequence binding sites were stable. Conclusions: our research
has uncovered the regulatory network mechanism of active ingredients,
mRNA, and miRNA in YWD POI treatment. However, further research is
needed to determine the effect of the active ingredients on key miRNAs
and mRNAs
Direct binding of NF-κB p65 protein to STC1 promoter and regulated the expression of STC1.
<p>(A) The binding sites of STC1 were tested in CaSki cells by chromatin coimmunoprecipitation. The site was found to bind to NFκB p65. (B) Western blotting detected the activity of PARP, caspase-3, STC1, and NF-κB p65 in CaSki cells. CaSki cells were treated with thapsigargin (3 µM) for 12 h. (C) Western blotting detected the activity of p65, STC1, and caspase-3 in CaSki cells. CaSki cells were treated with increasing time of TNFα (10 mg/L) for 2.5 h. (D) Western blotting detected the activity of p65 and STC1 in CaSki cells. CaSki cells were treated with PDTC (10 µM) for 60 min. (E) Subcellular activity of p65 and STC1 in CaSki cells was analyzed by Western blotting. CaSki cells were treated with siRNA knockdown of p65 for 72 h. (F) The expression of p65 and STC1 in CaSki was detected by RT-PCR at mRNA level. CaSki cells were treated with siRNA knockdown of p65 for 48 h. (G) Schematic representation of some findings in this work.</p
Exploring the Mechanism of Yiwei Decoction in the Intervention of a Premature Ovarian Insufficiency Rat Based on Network Pharmacology and the miRNA-mRNA Regulatory Network
Objective: our aim
is to explore the mechanism of action
of Yiwei
decoction (YWD) in addressing premature ovarian insufficiency (POI)
through a combination of transcriptomics and network pharmacology.
By doing so, we hope to identify important pathways of action, key
targets, and active components that contribute to the efficacy of
YWD. Materials and Methods: group A comprised of the model + traditional
Chinese medicine group, while group B was the model control group
and group C was the normal control group. After gavage, serum AMH
and E2 levels were measured by using ELISA. HE staining was used to
study the impact of YWD on ovarian follicle recovery in POI rats.
Additionally, RNA-seq sequencing technology was employed to analyze
the transcription levels of mRNAs and miRNAs in the ovarian tissues
of each group, and the resulting data were examined using R. YWD used
UPLC-Q-TOF-HRMS to analyze its active ingredients. Upon obtaining
the sequencing results, the miRWalk database was utilized to forecast
the targets of DEmiRNAs. Network pharmacology was then applied to
predict the targets of active ingredients present in YWD, ultimately
constructing a regulatory network consisting of active ingredients-mRNA-miRNA.
The coexpression relationship between mRNAs and miRNAs was calculated
using the Pearson correlation coefficient, and high correlation coefficients
between miRNA-mRNA were confirmed through miRanda sequence combination.
Results: the application of YWD resulted in improved serum levels
of AMH and E2, as well as an increased number of ovarian follicles
in rats with POI. However, there was a minimal impact on the infiltration
of ovarian lymphocytes. Through GSEA pathway enrichment analysis,
we found that YWD may have a regulatory effect on PI3K-Akt, ovarian
steroidogenesis, and protein digestion and absorption, which could
aid in the treatment of POI. Additionally, our research discovered
a total of 6 DEmiRNAs between groups A and B, including 2 new DEmiRNAs.
YWD contains 111 active compounds, and our analysis of the active
component-mRNA regulatory network revealed 27 active components and
73 mRNAs. Furthermore, the coexpression network included 5 miRNAs
and 18 mRNAs. Our verification of MiRanda binding demonstrated that
12 of the sequence binding sites were stable. Conclusions: our research
has uncovered the regulatory network mechanism of active ingredients,
mRNA, and miRNA in YWD POI treatment. However, further research is
needed to determine the effect of the active ingredients on key miRNAs
and mRNAs
Exploring the Mechanism of Yiwei Decoction in the Intervention of a Premature Ovarian Insufficiency Rat Based on Network Pharmacology and the miRNA-mRNA Regulatory Network
Objective: our aim
is to explore the mechanism of action
of Yiwei
decoction (YWD) in addressing premature ovarian insufficiency (POI)
through a combination of transcriptomics and network pharmacology.
By doing so, we hope to identify important pathways of action, key
targets, and active components that contribute to the efficacy of
YWD. Materials and Methods: group A comprised of the model + traditional
Chinese medicine group, while group B was the model control group
and group C was the normal control group. After gavage, serum AMH
and E2 levels were measured by using ELISA. HE staining was used to
study the impact of YWD on ovarian follicle recovery in POI rats.
Additionally, RNA-seq sequencing technology was employed to analyze
the transcription levels of mRNAs and miRNAs in the ovarian tissues
of each group, and the resulting data were examined using R. YWD used
UPLC-Q-TOF-HRMS to analyze its active ingredients. Upon obtaining
the sequencing results, the miRWalk database was utilized to forecast
the targets of DEmiRNAs. Network pharmacology was then applied to
predict the targets of active ingredients present in YWD, ultimately
constructing a regulatory network consisting of active ingredients-mRNA-miRNA.
The coexpression relationship between mRNAs and miRNAs was calculated
using the Pearson correlation coefficient, and high correlation coefficients
between miRNA-mRNA were confirmed through miRanda sequence combination.
Results: the application of YWD resulted in improved serum levels
of AMH and E2, as well as an increased number of ovarian follicles
in rats with POI. However, there was a minimal impact on the infiltration
of ovarian lymphocytes. Through GSEA pathway enrichment analysis,
we found that YWD may have a regulatory effect on PI3K-Akt, ovarian
steroidogenesis, and protein digestion and absorption, which could
aid in the treatment of POI. Additionally, our research discovered
a total of 6 DEmiRNAs between groups A and B, including 2 new DEmiRNAs.
YWD contains 111 active compounds, and our analysis of the active
component-mRNA regulatory network revealed 27 active components and
73 mRNAs. Furthermore, the coexpression network included 5 miRNAs
and 18 mRNAs. Our verification of MiRanda binding demonstrated that
12 of the sequence binding sites were stable. Conclusions: our research
has uncovered the regulatory network mechanism of active ingredients,
mRNA, and miRNA in YWD POI treatment. However, further research is
needed to determine the effect of the active ingredients on key miRNAs
and mRNAs
Table_1_Acute stress induces an inflammation dominated by innate immunity represented by neutrophils in mice.xls
It is well known that psychological stress could affect the immune system and then regulate the disease process. Previous studies mostly focused on the effects of chronic stress on diseases and immune cells. How acute stress affects the immune system remains poorly understood. In this study, after 6 hours of restraint stress or no stress, RNA was extracted from mouse peripheral blood followed by sequencing. Through bioinformatics analysis, we found that when compared with the control group, differentially expressed genes in the stress group mainly displayed up-regulated expression. Gene set enrichment analysis results showed that the enriched gene terms were mainly related to inflammatory response, defense response, wounding response, wound healing, complement activation and pro-inflammatory cytokine production. In terms of cell activation, differentiation and chemotaxis, the enriched gene terms were related to a variety of immune cells, among which neutrophils seemed more active in stress response. The results of gene set variation analysis showed that under acute stress, the inflammatory reaction dominated by innate immunity was forming. Additionally, the concentration of serum IL-1β and IL-6 increased significantly after acute stress, indicating that the body was in an inflammatory state. Importantly, we found that acute stress led to a significant increase in the number of neutrophils in peripheral blood, while the number of T cells and B cells decreased significantly through flow cytometric analysis. Through protein-protein interaction network analysis, we screened 10 hub genes, which mainly related to inflammation and neutrophils. We also found acute stress led to an up-regulation of Ccr1, Ccr2, Xcr1 and Cxcr2 genes, which were involved in cell migration and chemotaxis. Our data suggested that immune cells were ready to infiltrate into tissues in emergency through blood vessels under acute stress. This hypothesis was supported in LPS-induced acute inflammatory models. After 48 hours of LPS treatment, flow cytometric analysis showed that the lungs of mice with acute stress were characterized by increased neutrophil infiltration, decreased T cell and B cell infiltration. Immunohistochemical analysis also showed that acute stress led to more severe lung inflammation. If mice received repeat acute stress and LPS stimulation, the survival rate was significantly lower than that of mice only stimulated by LPS. Altogether, acute stress led to rapid mobilization of the immune system, and the body presented an inflammatory state dominated by innate immune response represented by neutrophils.</p