The University of Malaya Library encompasses a network of libraries and through this network the Library is able to provide comprehensive services and facilities using the discipline-based approach. Through the Library’s home page at, one is able to explore the multitude of services as well as the various facilities available to the users. The collection within the Library has been developed in line with the teaching, learning and research needs of the University. The Library now holds more than 1.4 million titles with over 2.1 million items in various formats. In addition to that the Library provides access to more than 85 online databases comprising of more than 46,000 e-journal titles and more than 150,000 e-book titles.



Alzaytoonah University of Jordan, founded in 1993, is a private university located in Amman, Jordan. It is accredited by the Jordanian Ministry of Higher Education & Scientific Research. As of 2008 there were 8,000 students enrolled in the university of whom 14% are international students from 28 countries. As is the case in all other Jordanian universities, the credit-hour system is used in the university.


PRESS RELEASE – Metabolomics, a promising tool for advancing in treatment personalization of oncological patients

This article by Dr. Leonor Puchades-Carrasco and Dr. Antonio Pineda- Lucena is published in Current Topics in Medicinal Chemistry, Volume 17 , Issue 24 , 2017

Graphical Abstract:


Metabolomics, the analysis of the complete set of metabolites in a defined biological compartment, is a relatively novel approach. Metabolomics studies have been successfully applied to get a better understanding of many diseases, including a number of neoplastic processes. In this context, it is important to underline that cancer patients exhibit metabolic profiles that are different from those of healthy individuals and patients with benign diseases. Moreover, the site, the stage, and the location of the tumors have been shown to further alter the metabolic composition.

Currently, tumors are defined not only by their location but also by their molecular characteristics. The identification of specific mutations in tumors has started to play a critical role when determining therapeutic treatments. However, that information is not currently available for the majority of cancers, and the existing biomarkers are far from being optimal. Furthermore, there is considerable heterogeneity within the current definitions of pathological process, exemplified by the fact that patients who are given an identical diagnosis react differently to the same therapy and have different outcomes. In this context, metabolomics, in combination with other “omics” approaches, could contribute to get a deeper insight into the molecular mechanisms underlying pathological processes, thus facilitating the classification of patients and their therapeutic treatment.

Precision medicine promises to tailor therapies for each individual by delivering more effective drug treatments, while avoiding or reducing adverse drug reactions. Towards this end, considerable efforts have been made over the last few years in the field of pharmacogenomics, with a focus on genotyping and identifying specific genetic variations associated with drug response. However, clinical pharmacology would benefit from the introduction of new methodologies capable of providing information that could complement this genomic information. This is necessary because drug metabolism and utilization involves many different enzymes, multiple organs, several compartments and even the microbiome, being not always possible to screen for all possible genetic or tissue variants. Furthermore, because drug metabolism varies with ethnicity, age, gender, weight, height and diet – as well as other environmental and physiological variables – it can be particularly challenging to predict how an individual will respond to a drug based on their genotype alone.

In this context, the ability to directly and accurately assess the biological phenotype of patients will be a critical component in determining the correct drug treatment or in predicting the response following a therapeutic treatment. Metabolites are the final products of cellular regulatory processes and their levels can be regarded as the ultimate response of biological systems to genetic and environmental changes. Similarly, to the terms ‘transcriptome’ or ‘proteome’, the set of metabolites synthetized by a biological system constitutes its ‘metabolome’. Since the metabolome is closely tied to the genotype of an individual as well as its physiology and the surrounding environment, metabolomics offers a unique opportunity to look at genotype-phenotype and genotype-environment relationships. Metabolomics is closely linked to the overall physiopathological status of an individual. Thus, metabolomics may incorporate the biochemical events of thousands of small molecules in cells, tissues, organs, or biological fluids. Disease state or drug exposure could alter such metabolite composition in qualitative and quantitative terms generating complex metabolic signatures. The analysis of these signatures can potentially provide useful information for the diagnosis and prognosis of patients as well as for predicting pharmacological responses to specific interventions. Additionally, specific metabolic signatures occur after drug treatment, thus providing information from pathways targeted or affected by drug therapy.

This review provides specific examples of metabolomics applications in the field of clinical pharmacology and precision medicine with a focus on the therapeutic management of cancer and in the translation of these results to the clinics.

EDITOR’S CHOICE – Environment and Neurodegenerative Diseases – MicroRNA

Journal: MicroRNA 

Author(s): Margherita Ferrante*, Gea Oliveri Conti

Graphical Abstract:



Introduction: The importance of neurodegenerative diseases on the management of public health is growing and the real role of the environment and miRNA in their occurrence is still unclear. miRNA can significantly affect the regulatory network. The complex variety and gene-regulatory capacity of miRNAs are particularly valuable in the brain, being a very complex organ with a functional specialization of neurons highly adaptable to environmental stimuli. In particular, an miRNAs role is demonstrated in neurological diseases as an effect to toxic and mutagenic substances exposure by the environment.

Objective: The focus was on the three most important neurodegenerative diseases: Alzheimer, Parkinson and Amyotrophic lateral sclerosis.

Materials and Methods: A brief critical review on scientific papers of the last ten years using PuBMED, Scopus, Web of Science and Cochrane databases was carried out.

Results: Several studies have shown that miRNAs may contribute to neurodegeneration process in response to environmental risks. The miRNAs are known to play a dynamic role in many biochemical pathways of mammalian’s brain, including neuroplasticity, stress responses, cellular signaling, etc. miRNAs have a role in neurodegenerative phenotype of AD, PD and ALS.

The environmental chemicals such as metals and pesticides and then behavior can cause miRNA alterations via increasing oxidative stress and/or triggering inflammatory responses.

Conclusion: A discussion with theoretical and possible future research directions is provided and it is clear that the need is not only of longitudinal population studies and of better knowledge of epigenetics markers but, especially, of environmental policy interventions based on the green economy.


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MOST ACCESSED ARTICLE – Glucose Oxidase Production from Sustainable Substrates – Current Biotechnology

Journal: Current Biotechnology

Author(s): Daniel P. Kiesenhofer, Robert L. Mach, Astrid R. Mach-Aigner*

Graphical Abstract:



Background: Glucose oxidase (GoxA) catalyzes the reaction from β-D-glucose to gluconic acid. It has a wide range of applications, for example as a sugar sensor for diabetes monitoring or as a prominent additive in food industry. The fungus Aspergillus niger naturally expresses and secretes GoxA. Currently, GoxA is produced by A. niger on yeast peptone dextrose media or by yeasts on media containing sugars in high concentration.

Objective: Trichoderma reesei is a well-studied, saprotrophic fungus that is used for industry-scale enzyme production due to its high secretory capacity. GoxA production in T. reesei could combine two promising aspects: high expression and secretion on the one hand, and the utilization of a sustainable and inexpensive carbon source, such as wheat straw or chitin, on the other hand.

Method: To evaluate if this is a feasible concept for GoxA production we applied four different expression systems: the constitutive promoter of the pyruvate kinase-encoding gene pki1 of T. reesei, the inducible promoters of the xylanase II-encoding gene xyn2 and of the cellobiohydrolase I-encoding gene cbh1, which is considered as one of the strongest promoters known in T. reesei, and finally, the promoter of the N-acetylglucosaminidase-encoding gene nag1 of Trichoderma harzianum.
Result: We discovered that an engineered variant of the cbh1 promoter led to higher yields of GoxA than the wild-type promoter did. This could be demonstrated in shake flask and bioreactor cultivation experiments. The obtained yields (between 28.90 U/ml and 39.00 U/ml) from wheat straw even exceeded the ones reported for A. niger.


PRESS RELEASE – Getting a GRiP on Chemoresistance: A Review of GRP78 as a Therapeutic

Review Article: GRP78 Influences Chemoresistance and Prognosis in Cancer

Innate or acquired resistance to current standard-of-care therapies is a major hindrance to successful chemotherapeutic intervention. There is a critical need to elucidate the underlying mechanisms responsible for chemoresistance in order to accelerate the development of more efficacious treatment strategies.

Endoplasmic Reticulum (ER) stress response proteins are produced by cells undergoing periods of stress and facilitate the folding of proteins. The studies highlighted in this review article by researchers from the Hill Lab at the University of Notre Dame, show that ER stress response proteins are also overexpressed in cancer cells, and are often associated with high resistance to chemotherapy and poor prognosis. Specifically, elevated expression of GRP78, the master regulator of the unfolded protein response, has been shown to induce chemoresistance and serves as a indictor of poor prognosis in patients with a variety of cancers.

This review focuses on the role of GRP78 in regulating signaling pathways that control cell survival and draw attention to its value as a prognostic marker and therapeutic target. It shows that elevated GRP78 expression is predictive of resistance to chemotherapy and tumor resurgence in many cancers. Moreover, GRP78 regulates chemoresistance through several branches of the unfolded protein response as well as through modulation of the PI3K/AKT pathway.

Elevated GRP78 expression has been linked to the failure of a growing number of current standard-of-care therapies, which suggest that it is necessary to identify strategies to inhibit GRP78 function in order to sensitize chemotherapy-resistant tumors to currently available treatment regimens.


Cardiovascular & Hematological Disorders-Drug Targets Volume 17, Issue 3

Current Clinical Pharmacology Volume 12, Issue 2

Current Pharmaceutical Design Volume 23, Issue 39

Current Drug Metabolism Volume 18, Issue 12

Current Medicinal Chemistry Volume 25, Issue 4

Current Medicinal Chemistry Volume 25, Issue 5


EDITOR’S CHOICE – Big Data and Genome Editing Technology – Current Cardiology Reviews

Journal: Current Cardiology Reviews

Author(s):Chayakrit Krittanawong*, Tao Sun, Eyal Herzog

Graphical Abstract:



Opinion Statements: Cardiovascular diseases (CVDs) encompass a range of conditions extending from congenital heart disease to acute coronary syndrome most of which are heterogenous in nature and some of them are multiple genetic loci. However, the pathogenesis of most CVDs remains incompletely understood. The advance in genome-editing technologies, an engineering process of DNA sequences at precise genomic locations, has enabled a new paradigm that human genome can be precisely modified to achieve a therapeutic effect. Genome-editing includes the correction of genetic variants that cause disease, the addition of therapeutic genes to specific sites in the genomic locations, and the removal of deleterious genes or genome sequences. Site-specific genome engineering can be used as nucleases (known as molecular scissors) including zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9) systems to provide remarkable opportunities for developing novel therapies in cardiovascular clinical care. Here we discuss genetic polymorphisms and mechanistic insights in CVDs with an emphasis on the impact of genome-editing technologies. The current challenges and future prospects for genomeediting technologies in cardiovascular medicine are also discussed.


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OPEN ACCESS ARTICLE – Sulfonamides as Inhibitors of Leishmania – Anti-Infective Agents

Journal: Anti-Infective Agents

Author(s): Jade Katinas*, Rachel Epplin, Christopher Hamaker, Marjorie A. Jones

Graphical Abstract:



Introduction: Leishmaniasis is an endemic disease caused by the protozoan parasite Leishmania. Current treatments for the parasite are limited by cost, availability and drug resistance as the occurrence of leishmaniasis continues to be more prevalent. Sulfonamides are a class of compounds with medicinal properties which have been used to treat bacterial and parasitic disease via various pathways especially as antimetabolites for folic acid.

Methods: New derivatives of sulfonamide compounds were assessed for their impact on Leishmania cell viability and potential pathways for inhibition were evaluated. Leishmania tarentolae (ATCC Strain 30143) axenic promastigote cells were grown in brain heart infusion (BHI) medium and treated with varying concentrations of the new sulfonamide compounds. Light microscopy and viability tests were used to assess the cells with and without treatment.

Discussion: A non-water soluble sulfonamide was determined to have 90-96% viability inhibition 24 hours after treatment with 100 μM final concentration. Because Leishmania are also autotrophs for folate precursors, the folic acid pathway was identified as a target for sulfonamide inhibition. When folic acid was added to untreated Leishmania, cell proliferation increased. A water soluble derivative of the inhibitory sulfonamide was synthesized and evaluated, resulting in less viability inhibition with a single dose (approximately 70% viability inhibition after 24 hours with 100 μM final concentration), but additive inhibition with multiple doses of the compound.
Results: However, the potential mechanism of inhibition was different between the water-soluble and non-water soluble sulfonamides. The inhibitory effects and potential pathways of inhibition indicate that these compounds may be new treatments for this disease.