Perspective of strategic plasma therapy for prognostic improvement of patients with ovarian cancer

2013 ◽  
Vol 1598 ◽  
Author(s):  
Hiroaki Kajiyama ◽  
Fumi Utsumi ◽  
Kae Nakamura ◽  
Hiromasa Tanaka ◽  
Masaru Hori ◽  
...  
Keyword(s):  
Atmospheric Pressure ◽  
Antitumor Effect ◽  
Intraperitoneal Administration ◽  
Atmospheric Pressure Plasma ◽  
Plasma Therapy ◽  
Intracellular Mechanism ◽  
Patients Experience

ABSTRACTEpithelial ovarian carcinoma (EOC) is the leading cause of cancer-related death in women in Western countries. Once patients experience recurrence, complete cure is almost impossible. We elucidated the effect of nonequilibrium atmospheric pressure plasma on the growth of EOC, particularly in plasma-activated medium (PAM). Furthermore, we examined the role of reactive oxygen species (ROS) or their scavengers in chronic antineoplastic-resistant EOC cells. As a result, we showed PAM induced the antitumor effect of EOC cells in vitro and in vivo, even in chemoresistant cells. To apply the plasma treatment for advanced or recurrent EOC, we suggest adopting indirect plasma therapy instead of direct plasma considering intraperitoneal administration in the future. However, there are several problems under investigation, including intracellular mechanism of antitumor effect by PAM and adverse event in vivo.

scholarly journals Dual oxidase 1 limits the IFNγ-associated antitumor effect of macrophages

2020 ◽  
Vol 8 (1) ◽  
pp. e000622
Author(s):  
Lydia Meziani ◽  
Marine Gerbé de Thoré ◽  
Pauline Hamon ◽  
Sophie Bockel ◽  
Ruy Andrade Louzada ◽  
...  
Keyword(s):  
Antitumor Effect ◽  
Therapeutic Strategy ◽  
Critical Role ◽  
Tumor Development ◽  
Intratumoral Injection ◽  
Histocompatibility Complex ◽  
Dual Oxidase

BackgroundMacrophages play pivotal roles in tumor progression and the response to anticancer therapies, including radiotherapy (RT). Dual oxidase (DUOX) 1 is a transmembrane enzyme that plays a critical role in oxidant generation.MethodsSince we found DUOX1 expression in macrophages from human lung samples exposed to ionizing radiation, we aimed to assess the involvement of DUOX1 in macrophage activation and the role of these macrophages in tumor development.ResultsUsing Duox1−/− mice, we demonstrated that the lack of DUOX1 in proinflammatory macrophages improved the antitumor effect of these cells. Furthermore, intratumoral injection of Duox1−/− proinflammatory macrophages significantly enhanced the antitumor effect of RT. Mechanistically, DUOX1 deficiency increased the production of proinflammatory cytokines (IFNγ, CXCL9, CCL3 and TNFα) by activated macrophages in vitro and the expression of major histocompatibility complex class II in the membranes of macrophages. We also demonstrated that DUOX1 was involved in the phagocytotic function of macrophages in vitro and in vivo. The antitumor effect of Duox1−/− macrophages was associated with a significant increase in IFNγ production by both lymphoid and myeloid immune cells.ConclusionsOur data indicate that DUOX1 is a new target for macrophage reprogramming and suggest that DUOX1 inhibition in macrophages combined with RT is a new therapeutic strategy for the management of cancers.

scholarly journals The Effects of Atmospheric Pressure Argon Plasma Treated Bovine Bone Substitute on Bone Regeneration

Coatings ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 790
Author(s):  
Jong-Ju Ahn ◽  
Ji-Hyun Yoo ◽  
Eun-Bin Bae ◽  
Gyoo-Cheon Kim ◽  
Jae Joon Hwang ◽  
...  
Keyword(s):  
Bone Regeneration ◽  
Atmospheric Pressure ◽  
Bone Substitute ◽  
Argon Plasma ◽  
Atmospheric Pressure Plasma ◽  
Regeneration Ability ◽  
Bovine Bone ◽  
Significant Difference

This study was undertaken to compare new bone formation between non-expired and expired bovine-derived xenogeneic bone substitute (expired, out-of-use period) and to evaluate the efficacy of argon (Ar)-based atmospheric pressure plasma (APP) treatment on expired bone substitute in rat calvarial defect. The groups were divided into (1) Non/Expired group (Using regular xenografts), (2) Expired group (Using expired xenografts), and (3) Ar/Expired group (Using Ar-based APP treated expired xenografts). Surface observation and cell experiments were performed in vitro. Twelve rats were used for in vivo experiment and the bony defects were created on the middle of the cranium. The bone substitute of each group was implanted into the defective site. After 4 weeks, all the rats were sacrificed, and the volumetric, histologic, and histometric analyses were performed. In the results of osteogenic differentiation and mineralization, Non/Expired and Ar/Expired groups were significantly higher than Expired group (p < 0.05). However, there was no significant difference between groups in the animal study (p > 0.05). Within the limitations of this study, the surface treatment of Ar-based APP has a potential effect on the surface modification of bone grafts. However, there was no significant difference in bone regeneration ability between groups in vivo; thus, studies on APP to enhance bone regeneration should be carried out in the future.

Regulation of prostaglandin biosynthesis in vivo by glutathione

1998 ◽  
Vol 274 (2) ◽  
pp. R294-R302 ◽  
Author(s):  
Alon Margalit ◽  
Scott D. Hauser ◽  
Ben S. Zweifel ◽  
Melissa A. Anderson ◽  
Peter C. Isakson
Keyword(s):  
Reduced Glutathione ◽  
Intraperitoneal Administration ◽  
Peritoneal Macrophages ◽  
Urate Crystal ◽  
Cox 2 ◽  
Cox 1 ◽  
Urate Crystals

Intraperitoneal administration of urate crystals to mice reduced subsequent macrophage conversion of arachidonic acid (AA) to prostaglandins (PGs) and 12-hydroxyeicosatetraenoic acid for up to 6 h. In contrast, levels of 12-hydroxyheptadecatrienoic acid (12-HHT) were markedly elevated. This metabolic profile was previously observed in vitro when recombinant cyclooxygenase (COX) enzymes were incubated with reduced glutathione (GSH). Analysis of peritoneal GSH levels revealed a fivefold elevation after urate crystal administration. The GSH synthesis inhibitorl-buthionine-[ S, R]-sulfoximine partially reversed the urate crystal effect on both GSH elevation and PG synthesis. Moreover, addition of exogenous GSH to isolated peritoneal macrophages shifted AA metabolism from PGs to 12-HHT. Urate crystal administration reduced COX-1, but induced COX-2 expression in peritoneal cells. The reduction of COX-1 may contribute to the attenuation of PG synthesis after 1 and 2 h, but PG synthesis remained inhibited up to 6 h, when COX-2 levels were high. Overall, our results indicate that elevated GSH levels inhibit PG production in this model and provide in vivo evidence for the role of GSH in the regulation of PG biosynthesis.

scholarly journals Role of SHP2 phosphatase in KIT-induced transformation: identification of SHP2 as a druggable target in diseases involving oncogenic KIT

Blood ◽  
2012 ◽  
Vol 120 (13) ◽  
pp. 2669-2678 ◽  
Author(s):  
Raghuveer Singh Mali ◽  
Peilin Ma ◽  
Li-Fan Zeng ◽  
Holly Martin ◽  
Baskar Ramdas ◽  
...  
Keyword(s):  
Systemic Mastocytosis ◽  
Myelogenous Leukemia ◽  
Myeloproliferative Disease ◽  
Growth And Survival ◽  
Intracellular Mechanism ◽  
Acute Myelogenous ◽  
Lipid Kinases

Abstract Intracellular mechanism(s) that contribute to promiscuous signaling via oncogenic KIT in systemic mastocytosis and acute myelogenous leukemia are poorly understood. We show that SHP2 phosphatase is essential for oncogenic KIT-induced growth and survival in vitro and myeloproliferative disease (MPD) in vivo. Genetic disruption of SHP2 or treatment of oncogene-bearing cells with a novel SHP2 inhibitor alone or in combination with the PI3K inhibitor corrects MPD by disrupting a protein complex involving p85α, SHP2, and Gab2. Importantly, a single tyrosine at position 719 in oncogenic KIT is sufficient to develop MPD by recruiting p85α, SHP2, and Gab2 complex to oncogenic KIT. Our results demonstrate that SHP2 phosphatase is a druggable target that cooperates with lipid kinases in inducing MPD.

scholarly journals Safety evaluation of atmospheric pressure plasma jets in in vitro and in vivo experiments

2021 ◽  
Vol 51 ◽  
Author(s):  
Ji-Yoon Lee ◽  
Shin-Young Park ◽  
Kyoung-Hwa Kim ◽  
Sung-Young Yoon ◽  
Gon-Ho Kim ◽  
...  
Keyword(s):  
Atmospheric Pressure ◽  
Safety Evaluation ◽  
Atmospheric Pressure Plasma ◽  
Plasma Jets ◽  
Pressure Plasma ◽  
In Vivo Experiments

scholarly journals Antiplasmodial Properties of Acyl-Lysyl Oligomers in Culture and Animal Models of Malaria

2011 ◽  
Vol 55 (8) ◽  
pp. 3803-3811 ◽  
Author(s):  
Fadia Zaknoon ◽  
Sharon Wein ◽  
Miriam Krugliak ◽  
Ohad Meir ◽  
Shahar Rotem ◽  
...  
Keyword(s):  
Critical Role ◽  
Intraperitoneal Administration ◽  
Parasite Growth ◽  
Developmental Cycle ◽  
Potent Inhibition ◽  
High Concentrations ◽  
High Doses

ABSTRACTOur previous analysis of antiplasmodial properties exhibited by dodecanoyl-based oligo-acyl-lysyls (OAKs) has outlined basic attributes implicated in potent inhibition of parasite growth and underlined the critical role of excess hydrophobicity in hemotoxicity. To dissociate hemolysis from antiplasmodial effect, we screened >50 OAKs forin vitrogrowth inhibition ofPlasmodium falciparumstrains, thus revealing the minimal requirements for antiplasmodial potency in terms of sequence and composition, as confirmed by efficacy studiesin vivo. The most active sequence, dodecanoyllysyl-bis(aminooctanoyllysyl)-amide (C12K-2α8), inhibited parasite growth at submicromolar concentrations (50% inhibitory concentration [IC50], 0.3 ± 0.1 μM) and was devoid of hemolytic activity (<0.4% hemolysis at 150 μM). Unlike the case of dodecanoyl-based analogs, which equally affect ring and trophozoite stages of the parasite developmental cycle, the ability of various octanoyl-based OAKs to distinctively affect these stages (rings were 4- to 5-fold more sensitive) suggests a distinct antiplasmodial mechanism, nonmembranolytic to host red blood cells (RBCs). Upon intraperitoneal administration to mice, C12K-2α8demonstrated sustainable high concentrations in blood (e.g., 0.1 mM at 25 mg/kg of body weight). InPlasmodium vinckei-infected mice, C12K-2α8significantly affected parasite growth (50% effective dose [ED50], 22 mg/kg) but also caused mortality in 2/3 mice at high doses (50 mg/kg/day × 4).

The Role of Polyphenols in the Modulation of Plasma Non-Enzymatic Antioxidant Capacity (NEAC)

2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito
Keyword(s):  
Antioxidant Capacity ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
The Body ◽  
Dietary Polyphenols ◽  
Enzymatic Antioxidant ◽  
Endogenous Antioxidant

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.

Sign in / Sign up

Export Citation Format

Share Document