•This paper provides a basis for capacity management and operation management of shared bikes from the perspective of environment.•Based on whole life cycle accounting method, carbon emissions of ...each stage of production, use, and disposal are calculated.•In the disposal process, the possibility of reducing carbon emissions by different bikes disposal methods is discussed in detail.•In China, carbon emissions generated from solid waste disposal by landfilling are significantly higher than those from incineration power.
Recent global environmental initiatives designed to achieve a more sustainable society include the United Nations’ sustainable development goals (SDGs) and the Paris Agreement. While the shared economic model has long been linked to the creation of the sustainable use of resources, one problem encountered by the bike sharing is whether the current management model can maintain the focus on sustainability in China. Based on the amount of resources consumed during bike production, operation, and recycling, this paper aims to use life cycle carbon emission assessment to calculate an emission reduction threshold for bike-sharing industry. The research obtained energy consumption data from the OFO Curve bike, which is the most commonly used type of bike sharing in China. Calculating the average distance traveled and number of times each bike was used per day via the Baidu Map Application Program Interface, we found that the average number of times each bike was used per day was 4.552, and the average riding distance was 0.356 km. Additionally, the overall utilization of shared bikes averages about 50%. Further results show that the whole life cycle carbon footprint of one bike is 34.56 kg CO2. The power generation by incineration produces 1.9916 kg CO2 in less than a landfill. If a bike is deposited directly in a landfill, it will take 31 years to degrade. The final calculations show that based on the current number of bikes, each used at least 686 days to achieve a net positive reduction in emissions. This paper provides a basis for capacity management and operation management of shared bikes from the perspective of pro-environment and provides a new angle for the research on environmental impact of sharing economy.
In recent years, cardiac patches have been developed for the treatment of myocardial infarction. However, the fixation approaches onto the tissue through suture or phototriggered reaction inevitably ...cause new tissue damage. Herein, a paintable hydrogel is constructed based on Fe3+‐triggered simultaneous polymerization of covalently linked pyrrole and dopamine in the hyperbranched chains where the in situ formed conductive polypyrrole also uniquely serves to crosslink network. This conductive and adhesive hydrogel can be conveniently painted as a patch onto the heart surface without adverse liquid leakage. The functional patch whose conductivity is equivalent to that of normal myocardium is strongly bonded to the beating heart within 4 weeks, accordingly efficiently boosting the transmission of electrophysiological signals. Eventually, the reconstruction of cardiac function and revascularization of the infarct myocardium are remarkably improved. The translatable suture‐free strategy reported in this work is promising to address the human clinical challenges in cardiac tissue engineering.
A paintable conductive hydrogel is constructed based on Fe3+‐triggered polymerization of pyrrole and dopamine chemically linked to hyperbranched polymer chains. The freshly formed hydrogels can be conveniently painted as a suture‐free adhesive patch strongly bondable to the beating heart, thus efficiently boosting the reconstruction of cardiac function after myocardial infarction.
Abstract
Protein kinase A (PKA) is a central regulator of cardiac performance and morphology. Myocardial PKA activation is induced by a variety of hormones, neurotransmitters, and stress signals, ...most notably catecholamines secreted by the sympathetic nervous system. Catecholamines bind β-adrenergic receptors to stimulate cAMP-dependent PKA activation in cardiomyocytes. Elevated PKA activity enhances Ca2+ cycling and increases cardiac muscle contractility. Dynamic control of PKA is essential for cardiac homeostasis, as dysregulation of PKA signalling is associated with a broad range of heart diseases. Specifically, abnormal PKA activation or inactivation contributes to the pathogenesis of myocardial ischaemia, hypertrophy, heart failure, as well as diabetic, takotsubo, or anthracycline cardiomyopathies. PKA may also determine sex-dependent differences in contractile function and heart disease predisposition. Here, we describe the recent advances regarding the roles of PKA in cardiac physiology and pathology, highlighting previous study limitations and future research directions. Moreover, we discuss the therapeutic strategies and molecular mechanisms associated with cardiac PKA biology. In summary, PKA could serve as a promising drug target for cardioprotection. Depending on disease types and mechanisms, therapeutic intervention may require either inhibition or activation of PKA. Therefore, specific PKA inhibitors or activators may represent valuable drug candidates for the treatment of heart diseases.
•The effects of different substitution rates of N-fertilizer by green manures were evaluated in double rice cropping system.•Six years data revealed greater yield sustainability of partial ...substitution of N fertilizer by green manure (i.e., 20–40%) than sole N-fertilizer or complete substitution.•Substitution of higher rates of fertilizer-N by green manure did not show very promising results.
Rice–rice rotation is the most important intensive cropping system for food security in China. So far, few studies have examined sustainability of double-rice cropping system using partial substitution of fertilizer N (FN) by green manure (GM). The effects of 100% FN (N100) and different substitution rates of FN by GM (80%, 60%, 40% and 20% FN plus 20%, 40%, 60% and 80% N through GM, and represented respectively by N80M20, N60M40, N40M60 and N20M80) on the rice productivity and N-supplying capacity of paddy soil were evaluated in double-rice system from 2008 to 2013. Soil organic matter and total N content in the 0–15cm layer and rice grain yield of early and late rice annually increased in N80M20 and N60M40 plots, but decreased in N100, N40M60 and N20M80 plots. Compared with N100 plots, the NH4+-N content and agronomic efficiency of applied N significantly increased in N80M20 and N60M40 plots. The grain yield and sustainable yield index of rice crops were improved in N80M20 and N60M40 plots, while declined in N40M60 and N20M80. Soil NO3−-N content decreased significantly under partial substitutions of GM for FN. It can be concluded that the appropriate substitution of GM for FN (e.g., 20–40%) is beneficial for improving the productivity and sustainability of paddy field under double-rice cropping system.
Recent clinical investigations indicate that anthracycline-based chemotherapies induce early decline in heart mass in cancer patients. Heart mass decline may be caused by a decrease in cardiac cell ...number because of increased cell death or by a reduction in cell size because of atrophy. We previously reported that an anthracycline, doxorubicin (DOX), induces apoptotic death of cardiomyocytes by activating cyclin-dependent kinase 2 (CDK2). However, the signaling pathway downstream of CDK2 remains to be characterized, and it is also unclear whether the same pathway mediates cardiac atrophy. Here we demonstrate that DOX exposure induces CDK2-dependent phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcription of its proapoptotic target gene, Bcl-2–interacting mediator of cell death (Bim). In cultured cardiomyocytes, treatment with the FOXO1 inhibitor AS1842856 or transfection with FOXO1-specific siRNAs protected against DOX-induced apoptosis and mitochondrial damage. Oral administration of AS1842856 in mice abrogated apoptosis and prevented DOX-induced cardiac dysfunction. Intriguingly, pharmacological FOXO1 inhibition also attenuated DOX-induced cardiac atrophy, likely because of repression of muscle RING finger 1 (MuRF1), a proatrophic FOXO1 target gene. In conclusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyocyte apoptosis and atrophy. Our results identify FOXO1 as a promising drug target for managing DOX-induced cardiotoxicity. We propose that FOXO1 inhibitors may have potential as cardioprotective therapeutic agents during cancer chemotherapy.
Cervical cancer (CC) is one of the most common malignancies affecting female worldwide. Long non-coding RNAs (lncRNAs) are increasingly indicated as crucial participants and promising therapeutic ...targets in human cancers. The main objective of this study was to explore the functions and mechanism of LINC00885 in CC.
RT-qPCR and western blot were used to detect RNA and protein levels. Functional and mechanism assays were respectively done for the analysis of cell behaviors and molecular interplays.
Long intergenic non-coding RNA 885 (LINC00885) was discovered to be upregulated in CC tissues and cell lines through bioinformatics analysis and RT-qPCR. Overexpression of LINC00885 promoted proliferation and inhibited apoptosis, whereas its silence exerted opposite effects. The cytoplasmic localization of LINC00885 was ascertained and furthermore, LINC00885 competitively bound with miR-3150b-3p to upregulate BAZ2A expression in CC cells. Rescue assays confirmed that LINC00885 regulated CC proliferation and apoptosis through miR-3150b-3p/BAZ2A axis. Finally, we confirmed that LINC00885 aggravated tumor growth through animal experiments.
LINC00885 exerted oncogenic function in CC via regulating miR-3150b-3p/BAZ2A axis. These findings suggested LINC00885 might serve as a potential promising therapeutic target for CC patients.
With the rapid increase in cancer survival because of improved diagnosis and therapy in the past decades, cancer treatment–related cardiotoxicity is becoming an urgent healthcare concern. The ...anthracycline doxorubicin (DOX), one of the most effective chemotherapeutic agents to date, causes cardiomyopathy by inducing cardiomyocyte apoptosis. We demonstrated previously that overexpression of the cyclin-dependent kinase (CDK) inhibitor p21 promotes resistance against DOX-induced cardiomyocyte apoptosis. Here we show that DOX exposure provokes cardiac CDK2 activation and cardiomyocyte cell cycle S phase reentry, resulting in enhanced cellular sensitivity to DOX. Genetic or pharmacological inhibition of CDK2 markedly suppressed DOX-induced cardiomyocyte apoptosis. Conversely, CDK2 overexpression augmented DOX-induced apoptosis. We also found that DOX-induced CDK2 activation in the mouse heart is associated with up-regulation of the pro-apoptotic BCL2 family member BCL2-like 11 (Bim), a BH3-only protein essential for triggering Bax/Bak-dependent mitochondrial outer membrane permeabilization. Further experiments revealed that DOX induces cardiomyocyte apoptosis through CDK2-dependent expression of Bim. Inhibition of CDK2 with roscovitine robustly repressed DOX-induced mitochondrial depolarization. In a cardiotoxicity model of chronic DOX exposure (5 mg/kg weekly for 4 weeks), roscovitine administration significantly attenuated DOX-induced contractile dysfunction and ventricular remodeling. These findings identify CDK2 as a key determinant of DOX-induced cardiotoxicity. CDK2 activation is necessary for DOX-induced Bim expression and mitochondrial damage. Our results suggest that pharmacological inhibition of CDK2 may be a cardioprotective strategy for preventing anthracycline-induced heart damage.
Gut microbiota has been reported to be disrupted by cisplatin, as well as to modulate chemotherapy toxicity. However, the precise role of intestinal microbiota in the pathogenesis of cisplatin ...hepatotoxicity remains unknown.
We compared the composition and function of gut microbiota between mice treated with and without cisplatin using 16S rRNA gene sequencing and via metabolomic analysis. For understanding the causative relationship between gut dysbiosis and cisplatin hepatotoxicity, antibiotics were administered to deplete gut microbiota and faecal microbiota transplantation (FMT) was performed before cisplatin treatment.
16S rRNA gene sequencing and metabolomic analysis showed that cisplatin administration caused gut microbiota dysbiosis in mice. Gut microbiota ablation by antibiotic exposure protected against the hepatotoxicity induced by cisplatin. Interestingly, mice treated with antibiotics dampened the mitogen-activated protein kinase pathway activation and promoted nuclear factor erythroid 2-related factor 2 nuclear translocation, resulting in decreased levels of both inflammation and oxidative stress in the liver. FMT also confirmed the role of microbiota in individual susceptibility to cisplatin-induced hepatotoxicity.
This study elucidated the mechanism by which gut microbiota mediates cisplatin hepatotoxicity through enhanced inflammatory response and oxidative stress. This knowledge may help develop novel therapeutic approaches that involve targeting the composition and metabolites of microbiota.
Electrospun polycaprolactone (PCL) vascular grafts showed good mechanical properties and patency. However, the slow degradation of PCL limited vascular regeneration in the graft. Polydioxanone (PDS) ...is a biodegradable polymer with high mechanical strength and moderate degradation rate in vivo. In this study, a small-diameter hybrid vascular graft was prepared by co-electrospinning PCL and PDS fibers. The incorporation of PDS improves mechanical properties, hydrophilicity of the hybrid grafts compared to PCL grafts. The in vitro/vivo degradation assay showed that PDS fibers completely degraded within 12 weeks, which resulted in the increased pore size of PCL/PDS grafts. The healing characteristics of the hybrid grafts were evaluated by implantation in rat abdominal aorta replacement model for 1 and 3 months. Color Doppler ultrasound demonstrated PCL/PDS grafts had good patency, and did not show aneurysmal dilatation. Immunofluorescence staining showed the coverage of endothelial cells (ECs) was significantly enhanced in PCL/PDS grafts due to the improved surface hydrophilicity. The degradation of PDS fibers provided extra space, which facilitated vascular smooth muscle regeneration within PCL/PDS grafts. These results suggest that the hybrid PCL/PDS graft may be a promising candidate for the small-diameter vascular grafts.
Background The postmitotic state of adult cardiomyocytes, maintained by the cell cycle repressor Rbl2 (retinoblastoma‐like 2), is associated with considerable resistance to apoptosis. However, ...whether Rbl2 regulates cardiomyocyte apoptosis remains unknown. Methods and Results Here, we show that ablation of Rbl2 increased cardiomyocyte apoptosis following acute myocardial ischemia/reperfusion injury, leading to diminished cardiac function and exaggerated ventricular remodeling in the long term. Mechanistically, ischemia/reperfusion induced expression of the proapoptotic protein BCL2 interacting protein 3 (Bnip3), which was augmented by deletion of Rbl2. Because the Bnip3 promoter contains an adenoviral early region 2 binding factor (E2F)‐binding site, we further showed that loss of Rbl2 upregulated the transcriptional activator E2F1 but downregulated the transcriptional repressor E2F4. In cultured cardiomyocytes, treatment with H 2 O 2 markedly increased the levels of E2F1 and Bnip3, resulting in mitochondrial depolarization and apoptosis. Depletion of Rbl2 significantly augmented H 2 O 2 ‐induced mitochondrial damage and apoptosis in vitro. Conclusions Rbl2 deficiency enhanced E2F1‐mediated Bnip3 expression, resulting in aggravated cardiomyocyte apoptosis and ischemia/reperfusion injury. Our results uncover a novel antiapoptotic role for Rbl2 in cardiomyocytes, suggesting that the cell cycle machinery may directly regulate apoptosis in postmitotic cardiomyocytes. These findings may be exploited to develop new strategies to limit ischemia/reperfusion injury in the treatment of acute myocardial infarction.
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