Hauer E.,Apt Therapeutics, Inc.
Accident Analysis and Prevention | Year: 2010
Researchers use various ways to determine what change in safety is caused by some treatment. One way is to fit regression equations to cross-section data. Can this work? Another way is to do a before-after study. Is this better? I examine these questions in the setting of a case study. The treated units are rail-highway grade crossings, the treatment is the replacement of 'crossbucks' by 'flashers', and as evidence serve published papers and reports. The results of regression studies are all over the place. Still, one cannot be sure whether this is a sign that the regression failed to capture cause and effect or a sign that the effect of this treatment depends strongly on the conditions in which it is applied. As different regressions use different variables, they cannot corroborate or negate each other's results. This is deeply troubling. The results of before-after studies, in this case, are very consistent. Unfortunately the results do not apply to specific conditions and are therefore of limited practical use. In this respect crash modification functions derived from regressions would have an inherent advantage over those from before-after studies provided they captured cause and effect. There is, at present, little ground for the belief that they do. © 2009 Elsevier Ltd. Source
Goldstein M.,Apt Therapeutics, Inc.
Journal of Non-Crystalline Solids | Year: 2011
A short overview is given of the discovery of the Johari-Goldstein (JG) relaxation. The current perception that it plays an important role in the molecular processes leading to the alpha relaxation is due to K. L. Ngai and associates. Recently it has become apparent that the activation barriers for the JG relaxation are too high to be consistent with an intra-basin process, and the relaxation must involve an inter-basin one, contrary to the original view of Johari and this author. © 2010 Elsevier B.V. All rights reserved. Source
Hsin-I Feng C.,Apt Therapeutics, Inc.
Comprehensive Reviews in Food Science and Food Safety | Year: 2012
This article is an exploration of the history of sushi consumption in the United States and how the ingredients of sushi are regulated. The article delineates the course of sushi's culinary history in Japan, and will attempt to present an overview on the incremental process by which sushi as a cuisine evolved from a humble street food with scarce recognition to an immensely sophisticated popular cuisine in Japan and America. After describing and analyzing the historical background of sushi, the article will present the underpinnings of the confounding set of etiquettes that center the art of consuming sushi. This article will also examine sushi as an exemplary form of successful, multi-directional product of globalization. It is intriguing to observe sushi as a circulating global commodity that internalizes and promotes regional dietary preferences and cultural practices. The second half of the article will discuss both the health benefits and health hazards associated with the sushi cuisine. While the seafood, seaweed, and seasoning involved with eating sushi have high nutritional value, sushi consumers need to be aware of the perilous nature of mercury poisoning and the biological contaminants that are embedded in improperly processed sushi fish. The FDA's current consumer advisory scheme on mercury poisoning is incomprehensible, conflicts with the guidelines that Environmental Protection Agency (EPA) delineates, and its inspection and surveillance guidelines are in practice difficult to enforce. The last section of the article will trace the development of the Seafood Hazard Analysis and Critical Control Point (HACCP) plan and compare its prospective policy visions and practical guidelines with the Hong Kong Food and Environmental Hygiene Department's (FEHD) Sushi Surveillance Guidelines. © 2012 Institute of Food Technologists ®. Source
Agency: Department of Health and Human Services | Branch: National Institutes of Health | Program: SBIR | Phase: Phase I | Award Amount: 299.79K | Year: 2015
DESCRIPTION provided by applicant Neuropathic pain such as diabetic neuropathic pain DNP can be difficult to treat with only of patients achieving meaningful andgt pain relief Current therapies e g duloxeline mainly address symptoms by focusing on blocking neurotransmission in the pain pathway with limited efficacy potentially severe side effects and narrow therapeutic index Hence novel therapies are needed to safely manage symptoms and also target the underlying pathophysiological mechanisms that will improve the functional status and life quality of affected patients APT an optimized human apyrase selectively scavenges excess pro inflammatory and algogenic extracellular ATP eATP and ADP eADP and metabolizes them to eAMP thereby attenuating vascular or central inflammation and pain Ubiquitous CD further metabolizes eAMP to adenosine which has been shown to reduce neuropathic pain in animals and humans It has been shown that administration of APT exhibited a long lasting days anti hyperalgesic effect in the model of Complete Freudandapos s Adjuvant induced inflammatory pain with no noticeable side effects In the proposed studies we will evaluate the dose response of APT in both the chronic constriction injury CCI model of neuropathy and the model of STZ induced diabetic neuropathy We also will determine the potential side effects of APT using the rotarod and functional observational battery assays in healthy rats Specific Aim To determine whether APT s c will abrogate neuropathic pain in the CCI model in rats without behavioral side effects Specific Aim To determine whether APT s c will abrogate neuropathic pain in the STZ induced diabetic model in rats without significant side effects The long term goal is to develop APT as a safe and disease modifying analgesic therapy Weekly or monthly dosing will provide sustained pain relief for neuropathic pain patients without significant side effects tolerance or addiction PUBLIC HEALTH RELEVANCE We will determine whether an optimized human apyrase will abrogate diabetic neuropathic pain without behavioral side effects in animal models
Agency: Department of Health and Human Services | Branch: National Institutes of Health | Program: SBIR | Phase: Phase I | Award Amount: 298.49K | Year: 2015
DESCRIPTION provided by applicant Type diabetes is an immune mediated disease in which insulin producing beta cells are destroyed resulting in life long dependence on exogenous insulin The number of patients being diagnosed is increasing each year particularly in the very young Despite advances in glucose monitoring and insulin delivery there is a compelling need to identify therapies that may safely alter the course of immune mediated beta cell destruction and preserve and even increase beta cell function It is well established that patients with type diabetes are marked by defects in regulatory T cells and or interleukin IL or its receptor signaling that controls autoimmunity Transient treatment with low dose recombinant IL increased regulatory T cell number and induced the persistence of repaired IL responsiveness in diabetic patients These clinical data strongly support further development of IL based therapy However current low dose rIL therapy has a very short half life with an unwanted increase in several innate immune cells types such as natural killer cells and eosinophils To obtain ideal outcomes in patients who are mostly young and feel otherwise healthy and have little short term morbidity we have designed a long acting IL analog that promises to generate low and stable circulating levels of IL related agonist The IL analog effectively binds to high affinity trimolecular IL R complex but not the intermediate affinity bimolecular IL R complex e g natural killer cells eosinophils Only regulatory T cells and newly activated previously na ve T cells express the high affinity IL R While IL is essential for the viability and functional integrity of regulatory T cells IL is actually a death factor fr newly activated T effector cells Hence the innovative drug candidate at low dose will enable selective stimulation of regulatory T cells and transient or intermittent administration while minimizing negative clinical effects Importantly a better efficacy and safety profile has been demonstrated in multiple animal models The specific aim of this Phase I SBIR proposal is to determine whether twice weekly treatment with the innovative IL analog for weeks will more effectively restore euglycemia for weeks of follow up than daily treatment of rIL for weeks in spontaneous new onset onset of andlt hours diabetic NOD mice PUBLIC HEALTH RELEVANCE The innovative approach involves the treatment with a novel IL analog to restore regulatory T cell function in Type diabetes mellitus that will arrest the autoimmune process and thereby preserve residual insulin production