A toolkits’ main purpose is to guide the user to useful resources for their specific program and researching needs. They are built specifically to help students find the necessary material for their classes, including: eBooks, journals, databases, useful websites, and helpful video tutorials.
Library toolkits are not static products. They are constantly being edited and updated based on the acquisition of new material and requests from students and faculty alike. There are plans to add evidence-based practice resources, as well as to create more tutorial videos on how to use PubMed, Clinical Key, DynaMed Plus and many other databases.
When you have the time, look at your toolkit specific to your program. It is your one stop shop to find all your necessary resources.
The CRISPR-Cas9 system represents a remarkable breakthrough in genome editing technology. With relative ease and amazing precision, investigators may now alter or replace genes in the genomes of organisms across the evolutionary spectrum. The potential for human disease treatment or prevention is incredible – an observation not lost on the pharmaceutical companies that have invested heavily in the approach.
All the excitement notwithstanding, some problems have arisen with the technology that may limit its usefulness going forward. Specifically, two papers from the journal Nature Medicine, suggest that the “genome guardian” protein, p53, is activated in response to employment of CRISPR-Cas9. To understand what p53 is responding to, a brief description of how the CRISPR-Cas 9 system works is warranted.
The CRISPR (clustered regularly interspaced short palindromic repeats)-Cas9 (CRISPR associated protein 9) system employs specific enzymes and carefully designed RNA guides to seek out distinct genomic DNA sequences for editing, removal, or replacement. The process involves the cleavage of DNA – an action not unnoticed by the human cell. Indeed, it is at this step that the cell takes exception to indiscriminate cutting of its DNA and turns on the (DNA) damage response pathway – orchestrated by p53. The aforementioned papers document the effects in human cells of such initiation of the p53-mediated reaction to DNA strand breaks.
In the paper by Haapaniemi and colleagues, the authors observe that CRISPR-Cas9 activates the p53 pathway in human cells, and limits the efficiency of the gene editing process. In contrast, inhibiting the damage response pathway allows for greater effectiveness of the CRISPR-Cas9 genomic modification apparatus. The obvious problem is that any attempts to down-regulate p53, or to select for cells that have reduced activity of the pathway, by definition create cells potentially susceptible to cancerous transformation. The authors suggest that in future work, mechanisms by which the DNA repair pathway could be modulated – perhaps turned off during gene editing, but reinitiated shortly thereafter, represent an appropriate work around.
In the study by Ihry and colleagues, attempts are made to employ CRISPR-Cas9 to reprogram pluripotent stem cells. Once again, the gene editing procedure elicits a p53-mediated DNA damage response, and the cells undergo programmed cell death (~apoptosis). Cells that survive are very much at risk as they may harbor down-regulated p53 – potentiating the possibility of an accumulation of offsite mutations. As above, the answer seems to point to modulating p53 activity – turning it off for the editing step, but reactivating immediately following.
Much has been written about these results, both in the scientific literature and popular press. No one is calling for the technique to be abandoned; rather, additional research will be required before it can be expected that the human cell’s sophisticated and evolutionarily developed capacity for protecting itself can be sidestepped. Expect a wealth of research to be published on the topic in coming months. Stay tuned!
SRT – August 2018
References:  E. Haapaniemi et al., Nat Med. (2018) doi: 10.1038/s41591-018-0049-z. [Epub ahead of print] (Link to Text)
 R.J. Ihry et al., Nat Med. (2018) doi: 10.1038/s41591-018-0050-6. Epub 2018 Jun 11. (Link to Text).
IHS faculty, students, and staff have full access to IHS Library resources including scholarly articles, books (both online and print), and databases like AccessMedicine and ClinicalKey. We encourage users to bookmark the following pages:
For searching PubMed, we encourage you to bookmark this link to PubMed. This specific link enables the Find@SHU button (screenshot below), which you can click to easily access PDFs (if we have online access) or to request the article for free using SHU’s interlibrary loan service.
As you’re starting your studies at the IHS Campus, you’ll be getting acquainted with a range of new information resources and tools. You’re going to have lots of questions, and lots of new terminology to learn. While Google is an easy place to start when looking up a definition or researching a concept, we’ve licensed another easy-to-use resource for IHS Campus users called DynaMed Plus.
DynaMed Plus is a clinical reference tool that is designed to help you quickly look up answers to your questions about diseases, drugs, diagnostic tests, and other patient care topics. Other useful features of DynaMed Plus include:
Hundreds of medical calculators, equations, and decision trees
A DynaMed Plus mobile app you can download and install on your phone.
Medical students may find DynaMed Plus particularly handy for researching answers to questions identified during Monday morning PPPC sessions.
While DynaMed Plus probably can’t answer EVERY question you might have, it comes pretty close, and we’re confident you’ll find it useful. Next time you’re tempted to reach for Google, try DynaMed Plus.
Hello all and welcome to this corner of the Interprofessional Health Sciences Library and Information Commons website, an area devoted to bringing you what we hope you find interesting and exciting stories of innovation in biomedical science. Thank you for joining us!
This first installment focuses on malaria – a worldwide health problem that, according to the Centers for Disease Control and Prevention, killed some 445,000 people in 2016. Malaria is caused by parasites, carried by mosquitos which introduce the microorganisms into humans’ blood. Infection results in flu-like fever/chills, headache, and respiratory problems. Left untreated – progression to more serious and life-threatening complications is rapid. The parasite most responsible for this scourge is the protozoan Plasmodium falciparum. Pharmacological interventions exist – but have been thwarted by the unicellular organisms’ ability to acquire resistance. For example, chloroquine and related compounds were employed for decades to disable the parasite’s lysosome-like digestive vacuole. With the organism unable to completely metabolize the host red blood cells’ hemoglobin, toxic metabolites amass and the parasites die. The more recent drug of choice is artemisinin, a natural product derived from the plant Artemisia annua. Compounds containing artemisinin, or related semi-synthetic derivatives, reduce the number of parasites in the bloodstream through what is thought to involve formation of highly reactive free radical species. Unfortunately, identification of other safe drugs with efficacy in killing the microorganism has not been successful.
Which brings us to the new approach – pioneered by a team of investigators of the University of South Florida and Wellcome Trust Sanger Institute and described in a research article entitled “Uncovering the essential genes of the human malarial parasite Plasmodium falciparum by saturation mutagenesis”. Here, a technique called piggyback transposition mutagenesis was used to insert crippling DNA stretches into genes across the organism’s genome. Non-essential genes were so-identified by their ability to withstand the random insertions. Essential genes, in contrast, resulted in the parasite’s death. Illumina-based deep sequencing allowed for identification of the insertion sites – and the analysis was on!
Of the 5399 genes that exist in the P. falciparum genome, 2680 were found to be essential for the parasite’s disease propagation processes. Powerful bioinformatic analyses revealed that essential gene clusters exist encoding proteins involved in, among other functions – lipid metabolic pathways, proteasomal degradation, cell cycle control, and RNA stability. Naturally, these genes and their associated proteins/pathways now are the molecular targets for future antimalarial drug development. It is certain that sophisticated drug screens are currently being employed and we can only hope that safe and efficacious compounds are found in a timely manner. With the dearth of currently available antimalarials and the disease’s continued health toll, advances cannot come too soon.
SRT – June 2018
Reference:  M. Zhang et al., Science360, eaap7847 (2018). DOI: 10:1126/science.aap7847 (Link to Text)
Welcome to the brand new website for the Interprofessional Health Sciences Library!
The IHS Library is a critical component of the learning environment at the IHS campus. Located on the ground floor of the campus, the IHS library includes a spacious Information Commons with access to numerous desktop computers, lounge seating, a quiet study room, and a numerous areas to plug in personal devices. There are twenty study rooms throughout the library for both individual and group study. Study rooms can be reserved through an online reservation system.
Welcome to the webpage for the Interprofessional Health Sciences Library and Information Commons (IHSLIC)! A unit of Seton Hall University Libraries, the IHSLIC serves students, faculty and staff at the Inter-Professional Health Sciences Campus of Seton Hall University. This website will serve as the access-point for scholarly resources and services provided by the library.
Through this webpage, SHU-affiliated students, faculty and staff can access all of our databases, electronic journals, point-of-care tools, e-books, and more.
The librarians at the IHSLIC will support learning, research, and the spirit of inquiry at the IHS campus by providing resources and services that promote evidence-based practice and foster the life-long learning skills that ultimately lead to excellence in patient-care. Our mission is to provide outstanding service and innovative support to help students achieve these goals.
We invite you to explore this website, and we look forward to meeting you on campus soon!
Christopher Duffy, MLIS, Associate Dean and Founding Director, IHSLIC