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1.
J Environ Manage ; 345: 118832, 2023 Nov 01.
Article in English | MEDLINE | ID: mdl-37619382

ABSTRACT

The global economy has accelerated the transition to a green, low-carbon economy. An enterprise's green innovation (GI) is directly related to its capacity for sustainable production as a micro-subject of economic development. This study examined the impact of managerial capacity on enterprise green innovation and changes of green innovation targeting. We used data collected manually from 423 Chinese A-share companies from 2010 to 2017. The effect of various external impact signals was then investigated. This study's findings are as follows: (1) Managerial ability stimulated green enterprise innovation. The marginal effect was 0.0696. While quality targeting has focused more on green invention innovation, managerial capacity significantly improved the marginal impact of green substantial innovation by 0.0375; (2) The clean production link targeting analysis confirmed that enterprises focused on end-of-pipe governance innovation (0.0466), along with new energy innovation (0.0495) rather than energy-saving innovation (-0.0227); (3) The multi-period DDD (Difference in Difference in Difference) model revealed that low-carbon city policy promoted green innovation with a diminishing trend; (4) The voluntary environmental regulation signals, ISO14001 certification, displayed a substitute effect for managerial capacity on enterprise green innovation. This paper provides recommendations, including that enterprises should improve the utilization of new and renewable energy while improving and optimizing production processes. The government should also improve innovation incentive policies and strengthen environmental information disclosure.


Subject(s)
Biological Products , Economic Development , Carbon , Certification , Disclosure , China
2.
J Alzheimers Dis Rep ; 7(1): 51-76, 2023.
Article in English | MEDLINE | ID: mdl-36777330

ABSTRACT

Background: Alzheimer's disease (AD) is a multifactorial disorder characterized by cognitive decline. Current available therapeutics for AD have limited clinical benefit. Therefore, preventive therapies for interrupting the development of AD are critically needed. Molecules targeting multifunction to interact with various pathlogical components have been considered to improve the therapeutic efficiency of AD. In particular, herbal medicines with multiplicity of actions produce cognitive benefits on AD. Bugu-M is a multi-herbal extract composed of Ganoderma lucidum (Antler form), Nelumbo nucifera Gaertn., Ziziphus jujuba Mill., and Dimocarpus longan, with the ability of its various components to confer resilience to cognitive deficits. Objective: To evaluate the potential of Bugu-M on amyloid-ß (Aß) toxicity and its in vitro mechanisms and on in vivo cognitive function. Methods: We illustrated the effect of Bugu-M on Aß25-35-evoked toxicity as well as its possible mechanisms to diminish the pathogenesis of AD in rat cortical neurons. For cognitive function studies, 2-month-old female 3×Tg-AD mice were administered 400 mg/kg Bugu-M for 30 days. Behavioral tests were performed to assess the efficacy of Bugu-M on cognitive impairment. Results: In primary cortical neuronal cultures, Bugu-M mitigated Aß-evoked toxicity by reducing cytoskeletal aberrations and axonal disruption, restoring presynaptic and postsynaptic protein expression, suppressing mitochondrial damage and apoptotic signaling, and reserving neurogenic and neurotrophic factors. Importantly, 30-day administration of Bugu-M effectively prevented development of cognitive impairment in 3-month-old female 3×Tg-AD mice. Conclusion: Bugu-M might be beneficial in delaying the progression of AD, and thus warrants consideration for its preventive potential for AD.

3.
Front Psychol ; 13: 938918, 2022.
Article in English | MEDLINE | ID: mdl-36118501

ABSTRACT

"Carbon neutrality, carbon peaking" is China's national commitment to the whole world about its plans to manage global climate change. China faces many severe challenges in fulfilling its commitments to reduce emissions. China's digital economy is currently booming, and whether it can provide opportunities for reducing regional carbon emissions is worth exploring. This study constructed a comprehensive system to evaluate the development of its digital economy based on China's regional data and empirically tested the direct, indirect, and spatial effects of the comprehensive development of digital economy on regional carbon emissions. In addition, it examined the special stage characteristics using a Hansen threshold model. This study found the following: first, the digital economy significantly suppresses carbon emissions in general, notably with a spatial spillover effect to neighboring provinces. Secondly, an analysis of the mechanism shows that the comprehensive development of a digital economy can restrain regional carbon emissions through industrial progress and the optimization of energy consumption. Third, there are double thresholds, special driving trends and an "inverted N-type" relationship with development. Fourth, a spatial heterogeneity analysis revealed that significant "local" and "neighboring" impacts on the reduction of carbon emissions only exist in the central and eastern areas. This study has a reference value for releasing the dividend of digital economy development and reducing carbon emissions.

4.
Oxid Med Cell Longev ; 2020: 7353618, 2020.
Article in English | MEDLINE | ID: mdl-32047579

ABSTRACT

Cisplatin chemotherapy causes myelosuppression and often limits treatment duration and dose escalation in patients. Novel approaches to circumvent or lessen myelotoxicity may improve clinical outcome and quality of life in these patients. Chlorella sorokiniana (CS) is a freshwater unicellular green alga and exhibits encouraging efficacy in immunomodulation and anticancer in preclinical studies. However, the efficacy of CS on chemoprotection remains unclear. We report here, for the first time, that CS extract (CSE) could protect normal myeloid cells and PBMCs from cisplatin toxicity. Also, cisplatin-induced apoptosis in HL-60 cells was rescued through reservation of mitochondrial function, inhibition of cytochrome c release to cytosol, and suppression of caspase and PARP activation. Intriguingly, cotreatment of CSE attenuated cisplatin-evoked hypocellularity of bone marrow in mice. Furthermore, we observed the enhancement of CSF-GM activity in bone marrow and spleen in mice administered CSE and cisplatin, along with increased CD11b levels in spleen. In conclusion, we uncovered a novel mechanism of CSE on myeloprotection, whereby potentially supports the use of CSE as a chemoprotector against cisplatin-induced bone marrow toxicity. Further clinical investigation of CSE in combination with cisplatin is warranted.


Subject(s)
Antineoplastic Agents/adverse effects , Bone Marrow Cells/drug effects , Cisplatin/adverse effects , Drug-Related Side Effects and Adverse Reactions/drug therapy , Mitochondria/metabolism , Myeloid Cells/drug effects , Plant Extracts/therapeutic use , Bone Marrow Cells/pathology , CD11b Antigen/metabolism , Chlorella , Cisplatin/therapeutic use , Granulocyte-Macrophage Colony-Stimulating Factor/metabolism , HL-60 Cells , Humans , Immunomodulation , Immunosuppression Therapy , Myeloid Cells/pathology
5.
Int J Offender Ther Comp Criminol ; 62(2): 551-570, 2018 02.
Article in English | MEDLINE | ID: mdl-29301468

ABSTRACT

Job burnout has long been recognized as a common occupational hazard among correctional workers. Although past studies have investigated the effects of job-related characteristics on correctional staff burnout in Western societies, this line of research has largely been absent from the literature on community corrections in China. Using data collected from 225 community correction workers in a Chinese province, this study assessed the effects of positive and negative job characteristics on occupational burnout. Positive job characteristics included job autonomy, procedural justice, and role clarity. Negative characteristics included role conflict, job stress, and job dangerousness. As expected, role clarity tended to reduce burnout, whereas role conflict, job stress, and job dangerousness were likely to produce greater burnout among Chinese community correction workers. Male correctional officers were also subjected to a higher level of burnout than their female coworkers. Implications for future research and policy were discussed.


Subject(s)
Burnout, Professional/psychology , Prisons , Adult , China , Female , Humans , Male , Occupational Stress/psychology , Professional Autonomy , Professional Role
6.
Oxid Med Cell Longev ; 2017: 5414297, 2017.
Article in English | MEDLINE | ID: mdl-29181126

ABSTRACT

Neuroinflammation plays a central role in the pathophysiology of Alzheimer's disease (AD). Compounds that suppress neuroinflammation have been identified as potential therapeutic targets for AD. Rhinacanthin C (RC), a naphthoquinone ester found in Rhinacanthus nasutus Kurz (Acanthaceae), is currently proposed as an effective molecule against inflammation. However, the exact role of RC on neuroinflammation remains to be elucidated. In the present study, we investigated RC effect on modulating lipopolysaccharides (LPS), amyloid-ß peptide (Aß), or interferon-γ- (IFN-γ-) evoked pathological events in neurons and glia. Our findings demonstrated that RC prevented Aß-induced toxicity in rat hippocampal neurons and attenuated LPS-activated nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) expression, and NF-κB signaling in rat glia. Likewise, RC suppressed LPS-induced neuroinflammation by reducing NO production and iNOS, IL-1ß, CCL-2, and CCL-5 mRNA levels in rat microglia. Further studies using BV-2 microglia revealed that RC inhibited LPS-, Aß-, and IFN-γ-stimulated IL-6 and TNF-α secretion. Of note, NF-κB and ERK activation was abrogated by RC in BV-2 cell response to Aß or IFN-γ. Moreover, RC protected neurons from Aß-stimulated microglial conditioned media-dependent toxicity. Collectively, these data highlight the beneficial effects of RC on neuroprotection and support the therapeutic implications of RC to neuroinflammation-mediated conditions.


Subject(s)
Amyloid beta-Peptides/metabolism , Inflammation/drug therapy , Lipopolysaccharides/metabolism , Naphthoquinones/therapeutic use , Neurons/metabolism , Animals , Interferon-gamma/metabolism , Mice , Naphthoquinones/pharmacology , Neuroglia/metabolism , Rats , Rats, Sprague-Dawley
7.
Am J Chin Med ; 43(7): 1401-17, 2015.
Article in English | MEDLINE | ID: mdl-26477794

ABSTRACT

Antrodia cinnamomea (A. cinnamomea) is a Chinese medicinal herb that possesses a broad range of bioactivities, including anti-inflammation. Given that the proinflammatory cytokine IL-17 plays a critical role in the pathogenesis of autoimmune diseases, we investigated whether A. cinnamomea could inhibit the development of Th17 cells, the main producer of IL-17, and exhibit therapeutic effects on an animal model of psoriasis. We found that A. cinnamomea extract (AC) inhibited the differentiation of Th17 cells as well as the production of IL-17A, IL-21, and IL-22 from these cells. This effect was associated with the inhibition of STAT3 phosphorylation and RORγt expression. Notably, the oral administration of AC reduced psoriasis-like inflammation in imiquimod-mediated dermal damage, repressed the expression of IL-17A, IL-22, and TNF-α in skin lesions, and decreased the infiltration of CD4⁺ T cells, CD8⁺ T cells, and neutrophils into the dermis. Finally, serum levels of IL-17A were decreased in AC-treated mice with psoriasis-like skin inflammation. Taken together, these findings indicate that AC inhibits Th17 cell differentiation, suggesting a role for A. cinnamomea in the treatment of psoriasis and other Th17 cell-mediated inflammatory diseases.


Subject(s)
Antrodia/chemistry , Cell Differentiation/drug effects , Phytotherapy , Psoriasis/chemically induced , Psoriasis/drug therapy , Th17 Cells/drug effects , Administration, Oral , Aminoquinolines/pharmacology , Animals , Anti-Inflammatory Agents/pharmacology , Autoimmunity , Cells, Cultured , Depression, Chemical , Disease Models, Animal , Drugs, Chinese Herbal/administration & dosage , Drugs, Chinese Herbal/pharmacology , Imiquimod , Interleukin-17/immunology , Interleukin-17/metabolism , Male , Mice, Inbred C57BL , Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism , Phosphorylation/drug effects , Psoriasis/immunology , Psoriasis/metabolism , STAT3 Transcription Factor/metabolism , Skin/immunology , Skin/metabolism , Th17 Cells/metabolism
8.
Mol Biol Cell ; 19(10): 4521-33, 2008 Oct.
Article in English | MEDLINE | ID: mdl-18685083

ABSTRACT

The glial fibrillary acidic protein (GFAP) gene is alternatively spliced to give GFAP-alpha, the most abundant isoform, and seven other differentially expressed transcripts including GFAP-delta. GFAP-delta has an altered C-terminal domain that renders it incapable of self-assembly in vitro. When titrated with GFAP-alpha, assembly was restored providing GFAP-delta levels were kept low (approximately 10%). In a range of immortalized and transformed astrocyte derived cell lines and human spinal cord, we show that GFAP-delta is naturally part of the endogenous intermediate filaments, although levels were low (approximately 10%). This suggests that GFAP filaments can naturally accommodate a small proportion of assembly-compromised partners. Indeed, two other assembly-compromised GFAP constructs, namely enhanced green fluorescent protein (eGFP)-tagged GFAP and the Alexander disease-causing GFAP mutant, R416W GFAP both showed similar in vitro assembly characteristics to GFAP-delta and could also be incorporated into endogenous filament networks in transfected cells, providing expression levels were kept low. Another common feature was the increased association of alphaB-crystallin with the intermediate filament fraction of transfected cells. These studies suggest that the major physiological role of the assembly-compromised GFAP-delta splice variant is as a modulator of the GFAP filament surface, effecting changes in both protein- and filament-filament associations as well as Jnk phosphorylation.


Subject(s)
Alexander Disease/genetics , Glial Fibrillary Acidic Protein/chemistry , alpha-Crystallin B Chain/chemistry , Alexander Disease/metabolism , Astrocytes/metabolism , Cell Line , Cell Line, Tumor , Humans , MAP Kinase Kinase 4/metabolism , Models, Biological , Mutation , Phosphorylation , Protein Binding , Protein Isoforms , Spinal Cord/metabolism , Transfection
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