Few U.S. public health schools offer courses on palliative and end-of-life care policy

Background: Palliative care has been identified by the World Health Organization (WHO) as a critical policy element for the relief of suffering, yet palliative care policy receives minimal attention in mainstream U.S. public health journals, conferences, or textbooks. In the ’90s, documentation of the lack of attention to end-of-life and palliative care in medical and nursing curricula led to concerted efforts to improve medical and nursing education in palliative care. No such educational effort has yet been directed toward public health professionals. Objective: This study\u27s objective was to quantify current course offerings covering palliative and end-of-life care from a public health and health policy perspective at accredited schools of public health. Design: Using a list of keywords about palliative and end-of-life care, the research team searched publicly accessible websites of all CEPH accredited and affiliated U.S. schools of public health to identify courses that included relevant content about palliative care. Results: For academic years 2011/12 and 2012/13, 3 (6%) of the 49 accredited U.S. schools of public health offered a full course covering public health issues in palliative care. Six schools (12%) included some palliative care content in related courses such as gerontology policy. Conclusions: Schools of public health are not preparing future policy experts with a basic knowledge of the components and systems of palliative care and hospice. Development and dissemination of appropriate curricular material to address the public health and policy aspects of palliative care is needed to address this gap

Molecular targets in the discovery and development of novel antimetastatic agents: current progress and future prospects

Tumour invasion and metastasis have been recognized as major causal factors in the morbidity and mortality among cancer patients. Many advances in the knowledge of cancer metastasis have yielded an impressive array of attractive drug targets, including enzymes, receptors and multiple signalling pathways. The present review summarizes the molecular pathogenesis of metastasis and the identification of novel molecular targets used in the discovery of antimetastatic agents. Several promising targets have been highlighted, including receptor tyrosine kinases, effector molecules involved in angiogenesis, matrix metalloproteinases (MMPs), urokinase plasminogen activator, adhesion molecules and their receptors, signalling pathways (e.g. phosphatidylinositol 3-kinase, phospholipase Cγ1, mitogen-activated protein kinases, c-Src kinase, c-Met kinases and heat shock protein. The discovery and development of potential novel therapeutics for each of the targets are also discussed in this review. Among these, the most promising agents that have shown remarkable clinical outcome are anti-angiogenic agents (e.g. bevacizumab). Newer agents, such as c-Met kinase inhibitors, are still undergoing preclinical studies and are yet to have their clinical efficacy proven. Some therapeutics, such as first-generation MMP inhibitors (MMPIs; e.g. marimastat) and more selective versions of them (e.g. prinomastat, tanomastat), have undergone clinical trials. Unfortunately, these drugs produced serious adverse effects that led to the premature termination of their development. In the future, third-generation MMPIs and inhibitors of signalling pathways and adhesion molecules could form valuable novel classes of drugs in the anticancer armamentarium to combat metastasis

Temporal profiles of neuronal degeneration, glial proliferation, and cell death in hNFL(+/+) and NFL(-/-)mice

10.1002/glia.20218GLIA52159-69GLIA

RNA and Protein Interactors with TDP-43 in Human Spinal-Cord Lysates in Amyotrophic Lateral Sclerosis

The TAR DNA-binding protein of 43 kDa (TDP-43) is a dual function RNA- and DNA-binding protein with varied cellular functions. In degenerating motor neurons in amyotrophic lateral sclerosis (ALS), TDP-43 relocalizes from the nucleus to the cytosol, where it is sequestered into inclusions. It is likely that the pathogenic role of TDP-43 in ALS can involve either a gain or a loss of function, depending on the nature of its RNA or protein interactor. However, while TDP-43 binding partners have been identified in a range of model systems and from the human brain, interactors from human spinal-cord tissue have not. In this study, we have characterized both protein and RNA TDP-43 interactors from neuropathologically normal (control) and ALS-affected ventral lumbar spinal cord, including sporadic ALS (sALS) and familial cases harboring either a A4T mutant SOD1 or a 3′ UTR *c.41G>A mutant <i>FUS/TLS</i> or expressing pathological <i>c9orf72</i> expanded repeats. RNA interactors with TDP-43 were similar between the control and ALS spinal cords examined regardless of genotype. In contrast, protein interactors with TDP-43 did demonstrate differences, with the sALS and mtSOD1 harboring cases examined differing from the protein interactors identified in the <i>FUS</i> 3′ UTR mutation and <i>c9orf72</i> repeat-positive cases