Special Issue "Antivenom and Venom Therapeutics"
Deadline for manuscript submissions: closed (30 June 2014)
Prof. Dr. Bryan Fry
Venom Evolution Laboratory, School of Biological Sciences, University of Queensland, St. Lucia, QLD, 4072, Australia
Interests: venom molecular evolution; phylogenetics and structure-function relationships; toxins
Antivenom is the only scientifically-validated treatment against snakebite and is formulated as either purifyed IgGs or as pepsin (F(ab/)2)/papain (Fab) cleaved fragments raised against venoms of single (monospecific) or multiple snake species (polyspecific). Although the treatment aims to neutralize the toxic components of snake venom, its formulation frequently fails to take into account their distinct variation in representation and immunogenicity. Consequently, the often low, clinically-relevant fraction needed to achieve reversal of envenoming frequently leads to the administration of life-threatening volumes that compromise the effectiveness of the treatment and further increase its cost and availability. This Special Issue of Toxins aims to provide a comprehensive look at the challenges of antivenom therapy and the current strategies for improving such therapy.
Dr. Bryan Fry
Dr. Camila Renjifo
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed Open Access monthly journal published by MDPI.
- snake venom
Toxins 2014, 6(5), 1667-1695; doi:10.3390/toxins6051667
Received: 13 March 2014; in revised form: 9 May 2014 / Accepted: 14 May 2014 / Published: 23 May 2014| PDF Full-text (2036 KB) | HTML Full-text | XML Full-text
Article: Ophiophagus hannah Venom: Proteome, Components Bound by Naja kaouthia Antivenin and Neutralization by N. kaouthia Neurotoxin-Specific Human ScFv
Toxins 2014, 6(5), 1526-1558; doi:10.3390/toxins6051526
Received: 15 February 2014; in revised form: 20 April 2014 / Accepted: 5 May 2014 / Published: 13 May 2014| PDF Full-text (1418 KB) | HTML Full-text | XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Author: Jin Tae Hong
Affiliation: College of Pharmacy, Chungbuk National University
Abstract: Our studies and others have demonstrated bee venom (BV) have anti-cancer activity in several cancer cells. However, the effects of BV on the lung cancer cell growth have not been reported. Cell viability was determined with trypan blue uptake, soft agar formation as well as DAPI and TUNEL assay. Cell death related protein expression was determined with Western blotting. EMSA was used nuclear factor kappaB (NF-kappaB) activity assay. BV (1-5 μg/ml) inhibited growth of lung cancer cells by induction of apoptosis in a dose dependent manner in A549 and NCI-H460. Consistent with apoptotic cell death, expression of DR3 and DR6 was significantly increased. However, deletion of DRs by small interfering RNA significantly reversed BV induced cell growth inhibitory effects. Expression of pro-apoptotic proteins (caspase-3 and Bax) were concomitantly increased, but the nuclear factor kappaB (NF-kB) activity and expression of Bcl-2 were inhibited. Combination treatment of tumor necrosis factor (TNF)-like weak inducer of apoptosis, TNF-related apoptosis-inducing ligand, docetaxel and cisplatin, with BV synergistically inhibited the both lung cancer cell growth with further down regulation of NF-kB activity. These results show that BV induces apoptotic cell death in lung cancer cells through enhancement of DR3 expression and inhibition of NF-kappaB pathway.
Last update: 31 March 2014