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  1. Han Y, Bai J, Zhang Z, Wu T, Chen P, Sun G, et al.
    Sci Total Environ, 2019 Nov 10;690:748-759.
    PMID: 31302540 DOI: 10.1016/j.scitotenv.2019.06.508
    Many species of birds gradually adapt to urbanization and colonize cities successfully. However, their nest site selection and competitive relationship in an urban community remain little known. Understanding the impact of urbanization on birds and the competitive relationship has important implications for the conservation and management of wildlife in urban ecosystems. Here, we undertook a systematic study to quantify nests in all species of birds in an urbanizing area of Nanchang, China. A total of 363 nests were detected in surveys including 340 nests of 16 bird species and 23 unidentified species nests. We mainly analyzed 5 dominant breeding birds with a sample size of >10 during the two breeding seasons (From April to July in 2016 and 2017), which included the light-vented bulbul, Chinese blackbird, scaly-breasted munia, spotted dove and grey-capped greenfinch. Most birds (93.66%) nested in the tree of artificial green belts, which seems to be the best breeding habitat for urban birds. Our results suggested that birds' breeding success relies on the trade-off between the benefit and the expense of specific stresses from habitats. The nest site selection of birds is also affected by the life habit of urban predators. Furthermore, competition among species can influence their distributions and utilization of environmental resources when birds nest in cities. We confirmed that the niche differentiation of five bird species in an urban environment makes them coexist successfully by utilizing various resources.
  2. Gao D, Guo P, Cao X, Ge L, Ma H, Cheng H, et al.
    Food Sci Nutr, 2020 Jun;8(6):2798-2808.
    PMID: 32566197 DOI: 10.1002/fsn3.1572
    Chicken plasma protein hydrolysate (CPPH) was prepared by trypsin with angiotensin I-converting enzyme (ACE) inhibitory activity of 53.5% ± 0.14% and the degree of hydrolysis (DH) of 16.22% ± 0.21% at 1 mg·ml-1; then, five proteases, including pepsin, trypsin, papain, alcalase, and neutrase, were employed to improve ACE inhibitory ability by catalyzing plastein reaction. The results indicated that trypsin-catalyzed plastein reaction showed the highest ACE inhibitory activity. The exogenous amino acids of leucine, histidine, tyrosine, valine, and cysteine were selected to modify the CPPH. The leucine-modified plastein reaction released the highest ACE inhibitory activity. The effects of four reaction parameters on plastein reaction were studied, and the optimal conditions with the purpose of obtaining the most powerful ACE inhibitory peptides from modified products were obtained by response surface methodology (RSM). The maximum ACE inhibition rate of the modified hydrolysate reached 82.07% ± 0.03% prepared at concentration of hydrolysates of 30%, reaction time of 4.9 hr, pH value of 8.0, temperature of 40°C, and E/S ratio of 5,681.62 U·g-1. The results indicated that trypsin-catalyzed plastein reaction increased ACE inhibitory activity of chicken plasma protein hydrolysates by 28.57%.
  3. Cheng YW, Chong CC, Lam MK, Ayoub M, Cheng CK, Lim JW, et al.
    J Hazard Mater, 2021 05 05;409:124964.
    PMID: 33418292 DOI: 10.1016/j.jhazmat.2020.124964
    Thriving oil palm agroindustry comes at a price of voluminous waste generation, with palm oil mill effluent (POME) as the most cumbersome waste due to its liquid state, high strength, and great discharge volume. In view of incompetent conventional ponding treatment, a voluminous number of publications on non-conventional POME treatments is filed in the Scopus database, mainly working on alternative or polishing POME treatments. In dearth of such comprehensive review, all the non-conventional POME treatments are rigorously reviewed in a conceptual and comparative manner. Herein, non-conventional POME treatments are sorted into the five major routes, viz. biological (bioconversions - aerobic/anaerobic biodegradation), physical (flotation & membrane filtration), chemical (Fenton oxidation), physicochemical (photooxidation, steam reforming, coagulation-flocculation, adsorption, & ultrasonication), and bioelectrochemical (microbial fuel cell) pathways. For aforementioned treatments, the constraints, pros, and cons are qualitatively and quantitatively (with compiled performance data) detailed to indicate their process maturity. Authors recommended (i) bioconversions, adsorption, and steam reforming as primary treatments, (ii) flotation and ultrasonication as pretreatments, (iii) Fenton oxidation, photooxidation, and membrane filtration as polishing treatments, and (iv) microbial fuel cell and coagulation-flocculation as pretreatment or polishing treatment. Life cycle assessments are required to evaluate the environmental, economic, and energy aspects of each process.
  4. Klionsky DJ, Abdel-Aziz AK, Abdelfatah S, Abdellatif M, Abdoli A, Abel S, et al.
    Autophagy, 2021 Jan;17(1):1-382.
    PMID: 33634751 DOI: 10.1080/15548627.2020.1797280
    In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
  5. Klionsky DJ, Abdelmohsen K, Abe A, Abedin MJ, Abeliovich H, Acevedo Arozena A, et al.
    Autophagy, 2016;12(1):1-222.
    PMID: 26799652 DOI: 10.1080/15548627.2015.1100356
  6. Wang W, Zhang H, Sandai D, Zhao R, Bai J, Wang Y, et al.
    Front Cell Dev Biol, 2023;11:1324213.
    PMID: 38161333 DOI: 10.3389/fcell.2023.1324213
    ATP-induced cell death has emerged as a captivating realm of inquiry with profound ramifications in the context of osteoporosis. This study unveils a paradigm-shifting hypothesis that illuminates the prospective involvement of ATP-induced cellular demise in the etiology of osteoporosis. Initially, we explicate the morphological attributes of ATP-induced cell death and delve into the intricacies of the molecular machinery and regulatory networks governing ATP homeostasis and ATP-induced cell death. Subsequently, our focus pivots towards the multifaceted interplay between ATP-induced cellular demise and pivotal cellular protagonists, such as bone marrow-derived mesenchymal stem cells, osteoblasts, and osteoclasts, accentuating their potential contributions to secondary osteoporosis phenotypes, encompassing diabetic osteoporosis, glucocorticoid-induced osteoporosis, and postmenopausal osteoporosis. Furthermore, we probe the captivating interplay between ATP-induced cellular demise and alternative modalities of cellular demise, encompassing apoptosis, autophagy, and necroptosis. Through an all-encompassing inquiry into the intricate nexus connecting ATP-induced cellular demise and osteoporosis, our primary goal is to deepen our comprehension of the underlying mechanisms propelling this malady and establish a theoretical bedrock to underpin the development of pioneering therapeutic strategies.
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