Special Issue "Feature Papers"
A special issue of Diseases (ISSN 2079-9721).
Deadline for manuscript submissions: closed (30 October 2013)
Prof. Dr. Frank Lee Schwartz
331 Academic Research Center, Department of Specialty Medicine, Ohio University Heritage College of Osteopathic Medicine, Athens, OH 45701, USA
Phone: +1 740 593 2424
Interests: Basic research: inflammation; innate immune response; toll like receptors (TLR); autoimmune disease; toll like receptor antagonists; Clinical research: artificial intelligence; case-based reasoning; insulin pumps; artificial pancreas; socioeconomic stress; Appalachia; chronic disease
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. Diseases is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. For the first couple of issues the Article Processing Charge (APC) will be waived for well-prepared manuscripts. English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
Diseases 2013, 1(1), 36-50; doi:10.3390/diseases1010036
Received: 10 September 2013; in revised form: 30 September 2013 / Accepted: 12 October 2013 / Published: 21 October 2013| Download PDF Full-text (205 KB) | Download XML Full-text
Review: Effect of Cardio-Metabolic Risk Factors Clustering with or without Arterial Hypertension on Arterial Stiffness: A Narrative Review
Diseases 2013, 1(1), 51-72; doi:10.3390/diseases1010051
Received: 20 June 2013; in revised form: 9 November 2013 / Accepted: 14 November 2013 / Published: 20 November 2013| Download PDF Full-text (299 KB) | Download 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.
Type of the Paper: Review article
Title: The nervous system cytoskeleton under oxidative stress
Authors: John Gardiner
Affiliations: The School of Biological Sciences, The University of Sydney; E-Mail: firstname.lastname@example.org
Abstract: Oxidative stress is a key mechanism causing protein aggregation, cell death and neurodegeneration in the nervous system. The neuronal cytoskeleton, that is microtubules, actin filaments and neurofilaments, plays a key role in defending the nervous system against oxidative stress-induced damage and is also a target for this damage itself. Microtubules appear particularly susceptible to damage, with oxidative stress downregulating key microtubule-associated proteins (MAPs) and affecting tubulin through aberrant post-translational modifications. Actin filaments utilise oxidative stress for their reorganisation and thus may be less susceptible to deleterious effects. However, because cytoskeletal components are interconnected through cross-linking proteins, damage to one component affects the entire cytoskeletal network. Neurofilaments are phosphorylated under oxidative stress, leading to the formation of protein aggregates reminiscent of those seen in neurodegenerative diseases. Drugs that target the cytoskeleton may thus be of great use in treating various neurodegenerative diseases caused by oxidative stress.
Type of the Paper: Review
Title: Trypanosomatid Aquaporins: role in physiology and drug response
Authors: Jose F. Orta 1, Goutam Mandal 1, Mansi Sharma1, 2, and Rita Mukhopadhyay 1,*
Affiliations: 1 Herbert Wertheim College of Medicine, Florida International University, 11200 SW 8th Street
Miami, FL, 33199, USA; E-Mail: email@example.com; Tel.: +1-305-348-1472
2 Department of Biological Sciences, Florida International University, 11200 SW 8th Street
Miami, FL, 33199, USA;
Abstract: In the class Kinetoplastida we find an order of parasitic protozoans classified as
Trypanosomatids. Three major pathogens form part of this order, Trypanosoma cruzi, Trypanosoma
brucei, and Leishmania, which are responsible for disease and fatalities in millions of humans
worldwide, especially in non-industrialized countries of tropical and sub-tropical regions. In order
to develop new drugs and treatments, the physiology of these pathogenic protozoans has been studied
in detail, specifically the significance of membrane transporters in host parasites interactions.
Aquaporins and Aquaglyceroporins (AQPs) are a part of the major intrinsic proteins (MIPs) super-
family. AQPs are characterized for their ability to facilitate the diffusion of water (aquaporin),
glycerol (aquaglyceroporin), and other small-uncharged solutes. Furthermore, AQPs have been shown to
allow the ubiquitous passage of some metalloids, such as trivalent arsenic and antimony. These
trivalent metalloids are the active ingredient of a number of chemotherapeutic agents used against
certain cancers and protozoan parasitic infections. Recently, it has been reported the importance of
the AQPs not only in osmotic adaptations, but also as a factor in drug resistance of the
trypanosomatid parasites. In this review, we will describe the physiological functions of aquaporins
and their effect in drug response across the different trypanosomatids.
Last update: 2 September 2013