MP-08.17

Choi, Yu-jin; Cho, N.H.; Park, Kuenyoul; Cho, K.S.; Cho, S.Y.; Han, Woog; Lee, M.S.; Lee, J.S.

doi:10.1016/j.urology.2006.08.324

Cited by 3 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More complicated systems for immediately/sustained release combinations of a drug for once-a-day administration of medicaments are consisted of osmotic devices [152][153][154][155], multilayer coating formulations [156] and multilayer beads [157]. An alternative approach is proposed, where a sustained release multiparticulate dosage form is comprised of a two-bead population of a drug (propanolol hydrochloride), one bead appropriate for immediate release and the other one for sustained release [158].…”

Section: Combination Of Immediate/sustained Rel-ease Formulationsmentioning

confidence: 99%

New Aspects in Sustained Drug Release Formulations

Bikiaris¹,

Koutris²,

Karavas

2007

DDF

View full text Add to dashboard Cite

Nowadays, pharmaceutical technology and research for new drugs and formulations is of great importance, as scientists attempt to discover even more revolutionary and efficient methods to treat various diseases. At the same time the correct dosing and site targeting are equally important for clinical success. Research in sustained drug release systems is very promising towards such a direction, while it offers advantages and potential rewards contrary to traditional therapy. The drug plasma concentrations remain inside the therapeutic range for a longer time period compared to the conventional formulations. In addition, sustained release formulations may increase the likelihood for the patient to respond to the therapy, since drug formulations are generally characterized by one daily given dose. The rate at which a drug is released from a sustained-release formulation depends upon many factors, while excipients play the most important role. Most sustained release formulations are based on biodegradable polymers in the form of a drug-encapsulating matrix or membrane. Examples range from monolithic devices, polymer-coated capsules and implant devices, hydrogels, to injectable systems based on suspensions of micro-, nanospheres or polymer solutions. The advantages and disadvantages of these different formulation systems are being extensively discussed in the present review.

show abstract

Section: Combination Of Immediate/sustained Rel-ease Formulationsmentioning

confidence: 99%

New Aspects in Sustained Drug Release Formulations

Bikiaris¹,

Koutris²,

Karavas

2007

DDF

View full text Add to dashboard Cite

show abstract

“…Acute inflammation accompanied by secretion of pro-inflammatory cytokines (TNF, IL-1, IL-8, and IL-6) and chemokines (MIP-2 and MCP-1) was reported in vivo after intratracheal instillation of silica nanoparticles in mice. 109 Similarly, elevation in levels of proinflammatory cytokines (IL-1 and TNF) was observed in the blood of mice after i.p. injection of silica nanoparticles.…”

Section: Snp Effects On Expression Of Inflammation-associated Genes-mentioning

confidence: 86%

“…Likewise, other available studies report either genotoxic effects of silica nanoparticles 5,[40][41][42][43] or their pro-inflammatory properties. 107,[109][110][111] In addition to ROS production and inflammatory response, cytotoxicity of SNPs is linked to cell membrane integrity disruption 103,104,112 , disturbed cellular calcium homeostasis 113 , aberrant clusters of topoisomerase I (topo I) formation, endothelial dysfunction, and fibrogenesis in Wistar rats. 3,54,[114][115][116][117] Figure 4 summarizes the mechanistic role of ROS and RNS induction by SNPs in cytotoxicity of these materials.…”

Section: The Direct Contribution Of Inflammation To Snp Genotoxicity-mentioning

confidence: 99%

Genotoxicity of amorphous silica nanoparticles: Status and prospects

Yazdimamaghani

Moos

Dobrovolskaia

et al. 2019

Nanomedicine: Nanotechnology, Biology and Medicine

View full text Add to dashboard Cite

Amorphous silica nanoparticles (SNPs) are widely used in biomedical applications and consumer products. Little is known, however, about their genotoxicity and potential to induce gene expression regulation. Despite recent efforts to study the underlying mechanisms of genotoxicity of SNPs, inconsistent results create a challenge. A variety of factors determine particle-cell interactions and underlying mechanisms. Further, high-throughput studies are required to carefully assess the impact of silica nanoparticle physicochemical properties on induction of genotoxic response in different cell lines and animal models. In this article, we review the strategies available for evaluation of genotoxicity of nanoparticles (NPs), survey current status of silica nanoparticle gene alteration and genotoxicity, discuss particle-mediated inflammation as a contributing factor to genotoxicity, identify existing gaps and suggest future directions for this research.

show abstract

“…Furthermore, IL-6 has been linked to the acquisition of SASP in cancer cells, contributing to a protumorigenic microenvironment by promoting in ammation, angiogenesis, and immunosuppression. A translational study on the bile acidmediated induction of HSC activation and SASP in HCC sheds new light on the intricate mechanisms of hepatocarcinogenesis, suggesting a potential link between bile acid signaling, HSC activation [22], IL-6 expression, and the development of HCC. These ndings underscore the critical role of IL-6 in orchestrating the molecular pathways that contribute to HCC progression and suggest that it is a potential target for therapeutic interventions to disrupt the hepatocarcinogenic process.…”

Section: Discussionmentioning

confidence: 99%

Bile acid-mediated activation of hepatic stellate cells and myeloid cell leukemia- 1 triggers hepatocarcinogenesis

Cho,

Lee,

Park

et al. 2024

Preprint

View full text Add to dashboard Cite

Objective Activated hepatic stellate cells (HSCs) promote hepatocellular carcinoma (HCC) cell growth and migration. Senescent and cancer-associated fibroblasts express various factors contributing to tumor progression, collectively called the senescence-associated secretory phenotype (SASP). Herein, we investigated the mechanism underlying the bile acid-mediated induction of HSC activation via SASP expression in HCC cells. Methods Serum samples from 296 patients with HCC were used to analyze IL-6 levels and survival. IL-6 mRNA levels were quantified using real-time PCR. A mouse xenograft model was used to confirm the role of the SASP. MTT and invasion assays were performed to evaluate the invasive ability of HCC cells (Huh-BAT, SNU-761, and Huh-SR) co-cultured with HSCs (LX-2 cells). Western blotting was performed to investigate the levels of survival signals. Results Bile acid increased the expression of mesenchymal markers and myeloid cell leukemia-1 (Mcl-1) and cyclooxygenase-2 (COX-2) proteins in HCC cells and HSCs. Inhibiting Mcl-1 induction or COX-2 activity decreased bile acid-mediated HCC invasion. Takeda G protein-coupled receptor 5 (TGR5) activation-dependent Mcl-1 and COX-2 expression enhanced gene transcription. Bile acid significantly increased IL-6 levels and HCC cell invasion in HSC/HCC cell co-cultures compared to HCC cell monocultures. The IL-6 + MoRAL score also showed significant discrimination in overall survival (Harrell’s c-index 0.765, p < 0.0001) of HCC patients. A mouse xenograft model revealed that Mcl-1 short hairpin RNA transfection, not celecoxib treatment, significantly suppressed Huh-SR cell growth. Conclusion Bile acid-mediated activation of HSCs enhances the proliferation and invasion of HCC cells via the expression of SASP proteins, including IL-6. TGR-5-dependent Mcl-1 overexpression may be a key factor in hepatocarcinogenesis.

show abstract

MP-08.17

Cited by 3 publications

References 0 publications

New Aspects in Sustained Drug Release Formulations

New Aspects in Sustained Drug Release Formulations

Genotoxicity of amorphous silica nanoparticles: Status and prospects

Bile acid-mediated activation of hepatic stellate cells and myeloid cell leukemia- 1 triggers hepatocarcinogenesis

Contact Info

Product

Resources

About