Press Release | Bentham Science launches new journal, ‘Current Dentistry’


Bentham Science is pleased to announce the launch of new subscription-based journal, Current Dentistry. The first issue of the journal is available online and can be obtained from: For more details, please visit the journal homepage:


Prof. Alvaro Della Bona is the Editor-in-Chief of this journal. He is a Senior Professor and Dean of Dental School, University of Passo Fundo, Brazil. The information for the Editorial Board of the journal can be viewed from:

Current Dentistry, a peer-reviewed journal, publishes original research, expert reviews, and thematic issues in all areas of dental, oral and craniofacial sciences including biological, clinical, materials engineering and bioengineering aspects of dental research. The journal will be of interest to researchers, healthcare professionals and medical / dental professionals.


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Press Release | Bentham science’s latest book ‘Frontiers in Anti-Cancer Drug Discovery Volume 10’


This eBook is authored by Dr. Atta-ur-Rahman, published on June; this book is authored by Atta-ur-Rahman and M. Iqbal Choudhary; published on May 31, 2019. For Further Details, Please Visit :


Frontiers in Anti-Cancer Drug Discovery is a book series devoted to publishing the latest advances in anti-cancer drug design and discovery. In each volume, eminent scientists contribute reviews relevant to all areas of rational drug design and drug discovery including medicinal chemistry, in-silico drug design, combinatorial chemistry, high-throughput screening, drug targets, recent important patents, and structure-activity relationships. The book series should prove to be of interest to all pharmaceutical scientists involved in research in anti-cancer drug design and discovery. The book series is essential reading to all scientists involved in drug design and discovery who wish to keep abreast of rapid and important developments in the field. The tenth volume of the series features chapters covering the following topics:

  • Challenges in the Management of Hepatoblastoma
  • The Emerging Role of Monocarboxylate Transporter-1 in Cancer
  • In-vitro Anti-Proliferative Assays and Techniques Used in Pre-Clinical Anti-Cancer Drug Discovery
  • Recent Advances in the Development of Mesoporous Anti-Cancer Drug Nanocarriers
  • Polyphenols and Cancer
  • Glioblastoma Multiforme
  • Cutting Edge Targeting Strategies Utilizing Nanotechnology in Breast Cancer Therapy
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Press Release | Treatment of Parkinson’s disease: Separating hope from hype


Parkinson’s disease is a neurodegenerative disorder characterized by motor and nonmotor deficits majorly caused by the loss of dopaminergic cells in the Substantia Nigra pars compacta (SNc) as well as the destruction of nigrostriatal pathway. Despite the numerous advances in cutting-edge approaches for the treatment or prevention of PD, there still exists some obstacles that have incapacitated the definitive treatment of this disease.

New therapeutic strategies have emerged over recent years to treat PD, including gene- and stem cell- based therapies, targeted delivery of neurotrophic factors, and brain stimulation techniques such as Transcranial Magnetic Stimulation (TMS), transcranial Direct Current Stimulation (tDCS), and Deep Brain Stimulation (DBS).

The review covers various gene therapy strategies including Adeno-Associated Virus-Glutamic Acid Decarboxylase (AAV-GAD), AAV-Aromatic L-Amino Acid Decarboxylase (AAV-AADC), Lenti-AADC/Tyrosine Hydroxylase/Guanosine Triphosphate- Cyclohydrolase I (Lenti-AADC/TH/GTP-CH1), AAV-Neurturin (AAV-NRTN), α-Synuclein silencing, and PRKN gene delivery. The review also covers the advantages and disadvantages of these treatments along with the results of relevant trials. With many advances in treatments for PD, there still exist some hurdles that have resulted in treatment failure; the reasons for failure of treatment were described, with hope separated from hype. Read full press release to find out more at:




The article by Dr. Alireza Mohammadi et al. is published in Current Gene Therapy, Volume 18, Issue 4, 2018. To obtain the article please visit:



Press Release | Vitamin D intake and obesity in occupational asthma patients and need for supplementation

Occupational asthma is common occurrence in a significant number of adults suffering from the disease. Even after the cessation of exposure, the asthma remains dominant. Previously, Vitamin D intake was rarely evaluated in cases of occupational asthma regardless of it being an important part of nutrition. The main objective of this study is to assess the Vitamin D intake in occupational asthma patients and its relation with body mass index, co-morbidities related to Vitamin D deficit, lung function and quality of life.

The researchers found a reduced Vitamin D intake in both irritant and allergic asthma both in obese and non-obese patients. Even though the average intake levels were comparably higher in non-obese patients than obese patients, it did not reach to a significant level. Lower intake was also found in mild asthma group compared to severe asthma group, marginally reaching significance level at the median test. Regression analysis revealed a different pattern in the asthma groups. The Impact score in irritant asthma indicated a stronger relationship with BMI while the symptom score in allergic asthma group was closely associated with the Vitamin D intake. Read full press release to find out more at:





The article by Dr. Marina Ruxandra Otelea and Dr. Agripina Rascu is published in Endocrine, Metabolic & Immune Disorders – Drug Targets, Volume 18, Issue 6, 2018. To obtain the article, please visit:

Press Release | Coenzyme Q10 supplementation on metabolic profiles of patients with chronic kidney disease


Chronic Kidney disease (CKD) is highly associated with all-cause mortality, Diabetic Nephropathy (DN), cardiovascular events and hospitalization whether the patient has an existing risk or current cardiovascular disease or not. CKD can increase the chances of cardiovascular disease by two to fifty times and 50% mortality of patients with end stage renal disease (ESRD) on dialysis attributed to CVD and its complications. In this review, Co-enzyme Q10 (CoQ10) was tested as a potential treatment for CKD. The systemic review and meta-analysis of randomized control trials (RCTs) was conducted to evaluate the effects of CoQ10 supplementation on metabolic profiles of patients diagnosed with CKD.

CoQ10 is a potent lipophilic antioxidant that couple’s electron transport to oxidative phosphorylation in mitochondria. It is generally used as an alternative and complementary therapy for diseases with metabolic disorders. The supplementary protein has shown beneficial effects during the treatment of heart failure. It was found that the circulating concentration in patients with CKD had been decreased. This suggested that the CoQ10 antioxidant treatment would be an ideal solution for the disease. The results accumulated during meta-analysis proved that the CoQ10 supplementation significantly reduced total-cholesterol, malondialdehyde, and creatinine levels in patients diagnosed with CKD. It did not affect Triglycerides, HDL-cholesterol, fasting glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), and C-reactive protein (CRP) concentrations. Read full press release to find out more at:



The article by Dr. Zatollah Asemi et al. is published in Current Pharmaceutical Design, Volume 24, Issue 31, 2018. To obtain the article, please visit:

Press Release | Computational advances in the label-free quantification of cancer proteomics data


In recent years, proteomics research has become a popular method for characterizing the functional proteins driving the transformation of malignancy, tracing the large-scale protein alterations induced by anti-cancer drug, as well as discovering the innovative targets and first-in-class drugs for oncologic disorders. Proteomics became popular due to its ability to provide quantitative and dynamic information on tumor genesis and development by directly profiling protein expression. Label-free Quantification (LFQ) is an important method for quantifying protein expression in cancer proteomics. However, the main challenge in using this method for discovering anti-cancer targets and drugs is the low precision, poor reproducibility, and inaccuracy of the LFQ of proteomics data.




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Press Release | Fighting to Find Relief: A new study shows decrease in depression in cancer patients


A New Study Published by Bentham Science Shows Support Groups and Educational Resources Can Decrease Depression in Breast Cancer Patients


1 in 8 women in the US will be diagnosed with breast cancer in their lifetime.

In 2018 alone, an estimated 266,120 new cases of breast cancer were diagnosed nationwide. As the numbers of new cases grow, the support network of women who suffer from breast cancer grows. In their ever-increasing numbers, the many women diagnosed with this disease face an arduous physical and emotional journey on their road to recovery, and along the way, many suffer from depression, anxiety, and body image issues.

Regardless of the prevalence of body image issues, anxiety, and depression in women who are suffering from breast cancer, there aren’t a lot of resources available for those afflicted. A recent study suggests it’s time to right that wrong. The study, published by Bentham Science, focused on Dr. Fausto Meriggi and his team at Fondazione Poliambulanza di Brescia who studied the effects of psychotherapeutic and educational groups on depression, anxiety, and body image issues among women suffering from breast cancer.


This study was published in Reviews on Recent Clinical Trials, a journal published by Bentham Science.  Bentham Science continues their work in the Middle East and North Africa, bringing education materials and increased accessibility to the region.


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Press Release | Tumor necrosis associate with atherosclerotic lipid accumulation


The article by Dr. Alexander N. Orekhov et al. is published in Current Pharmaceutical Design, 2018

Inflammation is currently a well-documented component of atheroslcerosis pathogenesis, which plays a role at each stage of the disease development. Local activation of endothelial cells causing increase endothelial permeability, infiltration of intima with atherogenic low-density lipoprotein (LDL), and recruitment of circulating immune cells is regarded as a first step of atherosclerotic plaque development. Circulating modified LDL is immunogenic, and forms highly atherogenic aggregates with antibodies that are later accumulated in the arterial wall. In growing plaques, circulating monocytes are attracted to the lesions site by cytokine signalling. In the arterial wall, monocyte-derived macrophages play an active role in lipid accumulation, internalizing large associates of lipoprotein particles by means of phagocytosis. Phagocytic cells with cytoplasm filled by stored lipid droplets called foam cells can be found in developing plaques in large quantities. There is evidence that lipid accumulation in the arterial wall cells in its turn activates cytokine signalling leading to a vicious cycle and further aggravating the disease. However, the immune response in atherosclerosis is not limited to enhanced inflammation, since anti-inflammatory cytokines and alternatively-activated (M2) macrophages are also present in atherosclerotic plaques. Anti-inflammatory M2 macrophages are likely to be responsible for hte resolution of the inflammatory response and tissue remodelling observed in advancing plaques. At later stages of lesion development, lipofibrous plaquest with high lipid contents and cell counts give rise to fibrous plaques that contain less cells and lipids, but more extracellular matrix material.

Although the involvement of cytokines in atherosclerotic lesion development is currently beyond doubt, quantitative evaluation of the expression of pro- and anti-inflammatory cytokines in the plaque remains to be studied in detail. In this study, we analyzed the distribution of two cytokines, pro-inflammatory TNFα and anti-inflammatory CCL18, in sections of human carotid atherosclerotic plaques at different stages of development. Our results demonstrated that both pro- and anti-inflammatory cytokines were present in the plaques, although differently distributed and likely expressed by different cells, and appeared to be enriched as compared to grossly normal intima taken as a control. To test whether the expression of TNFα and CCL18 is increased in atherosclerotic lesions, we performed gene expression analysis by means of quantitative PCR. We found that the expression of both cytokines was indeed increased in different types of atherosclerotic lesions. Moreover, it followed a bell-shaped distribution across the 4 studied plaque stages, gradually increasing from the early initial lesions to fatty streaks, reaching maximum in lipofibrous plaques, and decreasing again in fibrous plaques. This distribution was consistent with our previously published observations of bell-shaped changes of atherosclerotic lesion cellularity, proliferative activity, collagen synthesis and lipid content at different stages of the development. For TNFα, the maximal increase in atherosclerotic lesions reached 2 folds as compared to normal tissue, while for CCL18, this number was 1.5 folds.

We next investigated the relationship between pro- and anti-inflammatory cytokine production and lipid accumulation in cells. To that end, we used cultured human monocyte-derived macrophages with lipid accumulation induced by incubation with atherogenic LDL obtained from atheroslcerosis patients’ blood serum. Non-atherogenic LDL obtained from healthy donors, which did not cause cholesterol accumulation in cultured cells, was used as a control. We found that cholesterol accumulation in macrophages caused by atherogenic LDL treatment was associated with up-regulation of both TNFα and CCL18. The increase in relative gene expression was statistically significant (p=0.05 for TNFα and p=0.023 for CCL18) as compared to non-atherogenic LDL treatment.

In this work, we report the increased expression of pro-inflammatory cytokine TNFα and anti-inflammatory CCL18 in human atherosclerotic lesions, which could be observed microscopically and in gene expression analysis by means of quantitative PCR. Furthermore, we demonstrate that the increase of pro- and anti-inflammatory cytokines expression is associated with cholesterol accumulation caused by atherogenic LDL in cultured cells. It is likely that lipid accumulation is the trigger of cytokine expression in atherosclerotic lesions, since the maximum of expression is observed in atherosclerotic lesions most enriched in lipids. We discuss the implications of these findings for atheroslcerosis pathogenesis, postulating that a splash of cytokine signalling occurs in lesions with the highest lipid contents. We hypothesize that both pro- and anti-inflammatory responses take place in human atherosclerotic lesions, but are probably characterized by different dynamics. While pro-inflammatory signalling occurs rapidly in response to triggering stimuli and is transient, anti-inflammatory response is relatively slow and long-lasting. Under favorable conditions, resolution of inflammation should lead to a healing process and plaque stabilization, while chronic inflammation may aggravate the disease development.

Browse the Article at:

Press Release | A role for circadian enhancers to prevent myocardial injury in the perioperative setting

The article by Dr. Tobias Eckle et al. is published in Current Pharmaceutical Design, 2018


Innovative cardioprotective strategies are of imminent demand. Nonfatal myocardial ischemia (MI) poses a significant risk to patients undergoing major non-cardiac surgery and these non-cardiac surgeries account for around 8 million myocardial injuries per year. Considering perioperative MI is the most common major cardiovascular complication, identifying factors that lead to cardiac disease onset and finding solutions to prevent potential cardiac damage are of critical importance. Previous work revealed that anesthetics used in the perioperative setting alter cellular circadian biology and furthermore, a critical role for the circadian rhythm protein Period 2 (PER2) was revealed in promoting cardioprotection through metabolic pathway mediation. The current studies intended to answer this question: does anesthetic administration lead to increased susceptibility to MI, and if so, does targeting circadian PER2 provide a cardioprotective effect?

The starting point of the study was a screening test for the effects of frequently administered anesthetics on cardiac PER2. This screening demonstrated that only the benzodiazepine, midazolam, significantly downregulated PER2 levels in the heart tissue. Considering loss of PER2 is known to be detrimental during myocardial ischemia and reperfusion (IR)-injury, the study next addressed whether administration of midazolam prior to the occurrence of an MI would increase severity of such an incident. Using a well-established mouse model of myocardial IR-injury, the study team found that mice exposed to midazolam had an approximate 28.8% increase in infarct size compared to the control group. In agreement, Troponin-I levels were on average 198.9% greater in the mice given midazolam compared to the control mice. Indeed, mice administered midazolam were associated with deleterious consequences upon myocardial IR-injury.

The second part of the study sought to reverse the deleterious effects of midazolam when administered prior to myocardial ischemia. Recently, a large-scale screen identified nobiletin, a flavonoid from citrus peels, as a potent circadian PER2 enhancer. Not only was nobiletin found to increase cardiac PER2 and reduce infarct sizes by 47.4%, but nobiletin also abolished the deleterious effects of midazolam as demonstrated by a 28.9% decrease in infarct sizes and 55.4% decrease in Troponin-I levels in mice given both midazolam and nobiletin compared to mice given solely midazolam prior to myocardial ischemia. Furthermore, nobiletin provided cardioprotection in a PER2 dependent manner during IR-injury. This was demonstrated by nobiletin treatment prior to myocardial ischemia in mice with a genetic deletion of PER2, which revealed no cardioprotection.

This publication reports how midazolam mediated alterations of PER2 expression may have functional consequences during myocardial ischemia and identifies circadian biology as a potential consideration in translational studies and in the perioperative setting to prevent or treat myocardial ischemia.

Browse the Article at: The Circadian PER2 Enhancer Nobiletin Reverses the Deleterious Effects of Midazolam in Myocardial Ischemia and Reperfusion Injury


News release date: November 19, 2018

Dr. Atta-ur-Rahman, FRS, appointed as Executive Editor for Current Molecular Medicine. Dr. Rahman won the UNESCO Science Prize and was elected Fellow of Royal Society (London). He was conferred honorary doctorate degrees by many universities including Cambridge University. He was elected Honorary Life Fellow of Kings College, Cambridge University, and the Austrian government honoured him with its high civil award (“Grosse Goldene Ehrenzeischen am Bande”) (2007) .He is Foreign Fellow (“Academician”) of Chinese and Korean Academies of Sciences..

Current Molecular Medicinal (Impact factor 2.254), is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews, original research articles, short communications/letters and drug clinical trial studies on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. More information about the journal can be found here.


For  ore details, please visit:

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