• Title/Summary/Keyword: Biological mechanism

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Engineered bioclogging in coarse sands by using fermentation-based bacterial biopolymer formation

  • Kim, Yong-Min;Park, Taehyung;Kwon, Tae-Hyuk
    • Geomechanics and Engineering
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    • v.17 no.5
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    • pp.485-496
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    • 2019
  • Sealing of leakage in waterfront or water-retaining structures is one of the major issues in geotechnical engineering practices. With demands for biological methods as sustainable ground improvement techniques, bioclogging, defined as the reduction in hydraulic conductivity of soils caused by microbial activities, has been considered as an alternative to the chemical grout techniques for its economic advantages and eco-friendliness of microbial by-products. This study investigated the feasibility of bioaugmentation and biostimulation methods to induce fermentation-based bioclogging effect in coarse sands. In the bioaugmentation experiments, effects of various parameters and conditions, including grain size, pH, and biogenic gas generation, on hydraulic conductivity reduction were examined through a series of column experiments while Leuconostoc mesenteroides, which produce an insoluble biopolymer called dextran, was used as the model bacteria. The column test results demonstrate that the accumulation of bacterial biopolymer can readily reduce the hydraulic conductivity by three-to-four orders of magnitudes or by 99.9-99.99% in well-controlled environments. In the biostimulation experiments, two inoculums of indigenous soil bacteria sampled from waterfront embankments were prepared and their bioclogging efficiency was examined. With one inoculum containing species capable of fermentation and biopolymer production, the hydraulic conductivity reduction by two orders of magnitude was achieved, however, no clogging was found with the other inoculum. This implies that presence of indigenous species capable of biopolymer production and their population, if any, play a key role in causing bioclogging, because of competition with other indigenous bacteria. The presented results provide fundamental insights into the bacterial biopolymer formation mechanism, its effect on soil permeability, and potential of engineering bacterial clogging in subsurface.

Ononis spinosa alleviated capsaicin-induced mechanical allodynia in a rat model through transient receptor potential vanilloid 1 modulation

  • Jaffal, Sahar Majdi;Al-Najjar, Belal Omar;Abbas, Manal Ahmad
    • The Korean Journal of Pain
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    • v.34 no.3
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    • pp.262-270
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    • 2021
  • Background: Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel implicated in pain sensation in response to heat, protons, and capsaicin (CAPS). It is well established that TRPV1 is involved in mechanical allodynia. This study investigates the effect of Ononis spinosa (Fabaceae) in CAPS-induced mechanical allodynia and its mechanism of action. Methods: Mechanical allodynia was induced by the intraplantar (ipl) injection of 40 ㎍ CAPS into the left hind paw of male Wistar rats. Animals received an ipl injection of 100 ㎍ O. spinosa methanolic leaf extract or 2.5% diclofenac sodium 20 minutes before CAPS injection. Paw withdrawal threshold (PWT) was measured using von Frey filament 30, 90, and 150 minutes after CAPS injection. A molecular docking tool, AutoDock 4.2, was used to study the binding energies and intermolecular interactions between O. spinosa constituents and TRPV1 receptor. Results: The ipsilateral ipl injection of O. spinosa before CAPS injection increased PWT in rats at all time points. O. spinosa decreased mechanical allodynia by 5.35-fold compared to a 3.59-fold decrease produced by diclofenac sodium. The ipsilateral pretreatment with TRPV1 antagonist (300 ㎍ 4-[3-Chloro-2-pyridinyl]-N-[4-[1,1-dimethylethyl] phenyl]-1-piperazinecarboxamide [BCTC]) as well as the β2-adrenoreceptor antagonist (150 ㎍ butoxamine) attenuated the action of O. spinosa. Depending on molecular docking results, the activity of the extract could be attributed to the bindings of campesterol, stigmasterol, and ononin compounds to TRPV1. Conclusions: O. spinosa alleviated CAPS-induced mechanical allodynia through 2 mechanisms: the direct modulation of TRPV1 and the involvement of β2 adrenoreceptor signaling.

Methanol extracts of Asarum sieboldii Miq. induces apoptosis via the caspase pathway in human FaDu hypopharynx squamous carcinoma cells

  • Lee, Seul Ah;Park, Bo-Ram;Kim, Chun Sung
    • International Journal of Oral Biology
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    • v.46 no.2
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    • pp.85-93
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    • 2021
  • Asarum sieboldii Miq. (Aristolochiaceae) is a perennial herbaceous plant and has been used as traditional medicine for treating diseases, cold, fever, phlegm, allergies, chronic gastritis, and acute toothaches. Also, it has various biological activities, such as antiallergic, antiinflammatory, antinociceptive, and antifungal. However, the anticancer effect of A. sieboldii have been rarely reported, except anticancer effect on lung cancer cell (A549) of water extracts of A. sieboldii. This study investigated the anticancer activity of methanol extracts of A. sieboldii (MeAS) and the underlying mechanism in human FaDu hypopharyngeal squamous carcinoma cells. MeAS inhibited FaDu cells grown dose-dependently without affecting normal cells (L929), as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and live and dead assay. In addition, concentration of MeAS without cytotoxicity (0.05 and 0.1 mg/mL) inhibited migration and colony formation. Moreover, MeAS treatment significantly induced apoptosis through the proteolytic cleavage of caspase-3, -7, -9, poly (ADP-ribose) polymerase, and downregulation of Bcl-2 and upregulation of Bax in FaDu cells, as determined by fluorescence-activated cell sorting analysis, 4'6-diamidino-2-phenylindole stain, and western blotting. Altogether, these results suggest that MeAS exhibits strong anticancer effects by suppressing the growth of oral cancer cells and the migration and colony formation via caspase- and mitochondrial-dependent apoptotic pathways in human FaDu hypopharyngeal squamous carcinoma cells. Therefore, MeAS can serve as a natural chemotherapeutic for human oral cancer.

Coenzyme Q10, oxidative stress, and male infertility: A review

  • Alahmar, Ahmed T.;Calogero, Aldo E.;Singh, Rajender;Cannarella, Rossella;Sengupta, Pallav;Dutta, Sulagna
    • Clinical and Experimental Reproductive Medicine
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    • v.48 no.2
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    • pp.97-104
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    • 2021
  • Male infertility has a complex etiopathology, which mostly remains elusive. Although research has claimed that oxidative stress (OS) is the most likely underlying mechanism of idiopathic male infertility, the specific treatment of OS-mediated male infertility requires further investigation. Coenzyme Q10 (CoQ10), a vitamin-like substance, has been found in measurable levels in human semen. It exhibits essential metabolic and antioxidant functions, as well as playing a vital role in mitochondrial bioenergetics. Thus, CoQ10 may be a key player in the maintenance of biological redox balance. CoQ10 concentrations in seminal plasma directly correlate with semen parameters, especially sperm count and sperm motility. Seminal CoQ10 concentrations have been shown to be altered in various male infertility states, such as varicocele, asthenozoospermia, and medical or surgical regimens used to treat male infertility. These observations imply that CoQ10 plays an important physiological role in the maintenance and amelioration of semen quality. The present article thereby aimed to review the possible mechanisms through which CoQ10 plays a role in the regulation of male reproductive function, and to concisely discuss its efficacy as an ameliorative agent in restoring semen parameters in male infertility, as well as its impact on OS markers, sperm DNA fragmentation, pregnancy, and assisted reproductive technology outcomes.

IN-VITRO STUDY OF CO2 EXTRACT OF TERMINALIA CHEBULA IN BREAST CANCER CELL LINE MD-MBA-231

  • Chandil, Shachi;Bamoriya, Harikishan;More, D.B.
    • CELLMED
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    • v.11 no.3
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    • pp.16.1-16.7
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    • 2021
  • Cancer is an abnormal growth of cells in body which leads to death. These cells are born due to imbalance in cell proliferation mechanism. In 2018, WHO released new statistics on cancer incidence, mortality, and prevalence worldwide i.e., GLOBOCAN 2018 estimates for 28 types of cancer in which more prevalence of cervix and breast cancer. According to survey, in India about 7.8 million cancer deaths and 11.5 million new cases arise in 2018, which will increase to 19.3 million new cases per year by 2025. Though breast cancer as such is not explained anywhere in Ayurvedic compendia, correlations can be done with the Stana Arbuda. Ayurveda, the ancient system of medicine came into existence 1000's of years ago with an objective of maintaining the health of people and treating diseases. Many herbs used in Ayurveda have been screened for activity against cancer and in-vitro and in-vivo studies have given promising leads. The plant, called as "Mother of Medicine", Haritaki has been extensively studied for its various ailments because of its extraordinary healing potency. Haritaki (Terminalia chebula Retz.), Family: Combretaceae have a great therapeutic value and is widely distributed in India. Dried fruit of Terminalia chebula contains high quantities phenolic compounds consist of ellagic acid, gallic acid and chebulic acid. The fruit extract of T. chebula is having different biological properties like anticancer, antioxidant, hepatic and renal protective activities etc. In this study, we focus on the use of CO2 extract of Terminalia chebula, on the breast cancer cell line MDA-MB-231. All tests proved that CO2 extract of Terminalia chebula containing active chemical component, therefore our experiment showed the positive results for CO2 extract of Terminalia chebula against breast cancer cell line cancer MDA-MB-231. The MTT assay results were used to evaluate the anti-cancer activity of the extract. The percentage of cell growth and cell viability were calculated from tabulated result values of MTT assay. Cell viability MTT assay also showed significant growth inhibition, at the same time statistical analysis of MTT assay also proved significant results.

Apoptosis induced by water extracts of Nypa fruticans wurmb via a mitochondria-dependent pathway in human FaDu hypopharyngeal squamous carcinoma cells

  • Lee, Seul Ah;Choi, Mi Suk;Park, Bo-Ram;Kim, Jin-Soo;Kim, Chun Sung
    • International Journal of Oral Biology
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    • v.46 no.4
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    • pp.160-167
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    • 2021
  • Nypa fruticans Wurmb (NFW) contains a large amount of phenolic acid and flavonoids, and is popular as a superfood in Myanmar. NFW has various biological activities, such as anti-inflammatory, anti-oxidant, and neuroprotective properties; however, the anti-cancer effect of NFW have not been reported. In this study, we investigated the anticancer activity of water extracts of NFW (WeNFW) and the underlying mechanism in human FaDu hypopharyngeal squamous carcinoma cells. The WeNFW inhibited FaDu cell growth in a dose-dependent manner without affecting normal cells (L929), as determined by an MTT assay and Live and Dead assay. In addition, the concentrations of WeNFW without cytotoxicity (0.025, 0.05, and 0.1 mg/mL) inhibited wound healing and colony formation. Furthermore, WeNFW significantly induced apoptosis through the proteolytic cleavage of caspase-3 and -9, poly (ADP-ribose) polymerase, and downregulation of Bcl-2 and upregulation of Bax in FaDu cells, as determined by DAPI staining, FACS analysis, and western blot analysis. Taken together, these results suggest that WeNFW exhibits potent anti-cancer effects by suppressing the growth of oral cancer cells, wound healing and colony formation activity. Via mitrochondrial-dependent apoptotic pathways in human FaDu hypopharyngeal squamous carcinoma cells. Therefore, WeNFW can provide a natural chemotherapeutic drug for oral cancer in humans.

Deep Neural Network Weight Transformation for Spiking Neural Network Inference (스파이킹 신경망 추론을 위한 심층 신경망 가중치 변환)

  • Lee, Jung Soo;Heo, Jun Young
    • Smart Media Journal
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    • v.11 no.3
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    • pp.26-30
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    • 2022
  • Spiking neural network is a neural network that applies the working principle of real brain neurons. Due to the biological mechanism of neurons, it consumes less power for training and reasoning than conventional neural networks. Recently, as deep learning models become huge and operating costs increase exponentially, the spiking neural network is attracting attention as a third-generation neural network that connects convolution neural networks and recurrent neural networks, and related research is being actively conducted. However, in order to apply the spiking neural network model to the industry, a lot of research still needs to be done, and the problem of model retraining to apply a new model must also be solved. In this paper, we propose a method to minimize the cost of model retraining by extracting the weights of the existing trained deep learning model and converting them into the weights of the spiking neural network model. In addition, it was found that weight conversion worked correctly by comparing the results of inference using the converted weights with the results of the existing model.

De Novo Drug Design Using Self-Attention Based Variational Autoencoder (Self-Attention 기반의 변분 오토인코더를 활용한 신약 디자인)

  • Piao, Shengmin;Choi, Jonghwan;Seo, Sangmin;Kim, Kyeonghun;Park, Sanghyun
    • KIPS Transactions on Software and Data Engineering
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    • v.11 no.1
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    • pp.11-18
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    • 2022
  • De novo drug design is the process of developing new drugs that can interact with biological targets such as protein receptors. Traditional process of de novo drug design consists of drug candidate discovery and drug development, but it requires a long time of more than 10 years to develop a new drug. Deep learning-based methods are being studied to shorten this period and efficiently find chemical compounds for new drug candidates. Many existing deep learning-based drug design models utilize recurrent neural networks to generate a chemical entity represented by SMILES strings, but due to the disadvantages of the recurrent networks, such as slow training speed and poor understanding of complex molecular formula rules, there is room for improvement. To overcome these shortcomings, we propose a deep learning model for SMILES string generation using variational autoencoders with self-attention mechanism. Our proposed model decreased the training time by 1/26 compared to the latest drug design model, as well as generated valid SMILES more effectively.

Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells

  • Kang, Kyeong-Rok;Kim, Jae-Sung;Lim, HyangI;Seo, Jeong-Yeon;Park, Jong-Hyun;Chun, Hong Sung;Yu, Sun-Kyoung;Kim, Heung-Joong;Kim, Chun Sung;Kim, Do Kyung
    • The Korean Journal of Physiology and Pharmacology
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    • v.26 no.6
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    • pp.447-456
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    • 2022
  • The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptor-mediated extrinsic pathway.

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

  • Ma, Yuhong;Li, Yuzhen;Tang, Yuanyuan;Tang, Ning;Wang, Dengke;Li, Xiaofei
    • Journal of Microbiology and Biotechnology
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    • v.31 no.8
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    • pp.1098-1108
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    • 2021
  • The literature indicates that LINC00174 promotes the growth of colorectal cancer (CRC) cells, but its research needs to be enriched. We tried to explore the function and mechanism of LINC00174 in CRC cell proliferation and migration. Bioinformatics analysis predicted the binding relationship and expressions of lncRNA, miRNA and mRNA. Clinical study analyzes the relationship between LINC00174 and clinical data characteristics of CRC patients. The expressions of LINC00174, miR-3127-5p and E2F7 were verified by RT-qPCR, and the combination of the two was verified by dual luciferase analysis and RNA immunoprecipitation as needed. Western blot was used to detect the expression of EMT-related protein and E2F7 protein. Functional experiments were used to evaluate the function of the target gene on CRC cells. LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients. High-expression of LINC00174, contrary to the effect of siLINC00174, promoted cell viability, proliferation, migration and invasion, up-regulated the expressions of N-Cadherin, Vimentin, E2F7, and inhibited the expression of E-Cadherin. MiR-3127-5p was one of the targeted miRNAs of LINC00174 and was down-regulated in CRC samples. In addition, miR-3127-5p mimic partially reversed the malignant phenotype of CRC cells induced by LINC00174. Besides, E2F7 was a target gene of miR-3127-5p, and LINC00174 repressed miR-3127-5p to regulate E2F7. Our research reveals that LINC00174 affected the biological characteristics of CRC cells through regulated miR-3127-5p/ E2F7 axis.