Publications by authors named "Reza Ghasemi"

30 Publications

  • Page 1 of 1

Isolation of in oral candidiasis: First report among cancer patients in Iran.

Curr Med Mycol 2020 Jun;6(2):58-62

Center for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran.

Background And Purpose: Oropharyngeal candidiasis (OPC) is a fungal infection of the oral cavity caused by the members of complex. Although , as a part of the complex, is considered to be mostly responsible for the development of vulvovaginal candidiasis, it may be associated with a wider clinical spectrum.

Case Report: This report described two cases diagnosed with oral candidiasis during the receipt of treatment for malignancies. Conventional and molecular tests were performed on the samples collected from the patients' oral cavities. The test results revealed as the causative agent of oral candidiasis. Furthermore, in vitro antifungal susceptibility test indicated the full susceptibility of all isolates to caspofungin. However, the data were also suggestive of the resistance against fluconazole and amphotericin B. Caspofungin was used as the main antifungal agent for the treatment of oral candidiasis, resulting in the improvement of thrush in patients. The resistance of to fluconazole and amphotericin B suggests the necessity of performing in vitro susceptibility testing on the isolates for the selection of appropriate antifungal agents.

Conclusion: As the findings indicated, the achievement of knowledge regarding as an emerging non-albicans Candida species and its antifungal susceptibility profile is crucial to select antifungal prophylaxis and empirical therapy for oral candidiasis in cancer patients undergoing chemotherapy.

None: non.
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http://dx.doi.org/10.18502/CMM.6.2.2695DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7888514PMC
June 2020

Multidrug-resistant Trichophyton mentagrophytes genotype VIII in an Iranian family with generalized dermatophytosis: report of four cases and review of literature.

Int J Dermatol 2020 Oct 13. Epub 2020 Oct 13.

Center for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran.

Background: The global spread of terbinafine-resistant Trichophyton mentagrophytes with point mutations in the squalene epoxidase (SQLE) gene is a big concern.

Aim: The present study presents a series of unusual familial cases of generalized dermatophytosis caused by multidrug-resistant T. mentagrophytes genotype VIII.

Methods: Initially, the skin samples of each patient were taken and then subjected to direct microscopy and culture in Mycosel Agar. The molecular identification of Trichophyton species (spp.) was performed for all family members. In addition, the immunologic tests were requested, and an antifungal susceptibility test was carried out using the broth microdilution protocol based on the Clinical and Laboratory Standards Institute M38, third edition. The SQLE gene for a terbinafine-resistant T. mentagrophytes genotype VIII was sequenced and confirmed its nucleotide sequence to KU242352 as a susceptible strain.

Results: Based on the results of mycological examination and ITS rDNA sequencing, the etiologic agent was identified as T. mentagrophytes as a zoophilic dermatophyte. This species showed multiple drug resistance in vitro against terbinafine (minimum inhibitory concentration (MICs ≥8 µg/ml), itraconazole (MIC ≥4), and fluconazole (MIC ≥16). The SQLE gene of the isolate was subjected to sequencing for mutation, which showed a point mutation as TTC/TTA in the gene leading to Phe397Leu amino acid substitution in the enzyme. Only one of the family members responded to itraconazole and was cured after the long-term use of itraconazole. Other family members were treated with oral voriconazole with no recurrence.

Conclusion: The transmission of this resistant T. mentagrophytes to other countries due to globalization is a serious issue to be considered.
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http://dx.doi.org/10.1111/ijd.15226DOI Listing
October 2020

The effect of bio/organic fertilizers on the phytotoxicity of sulfadiazine to Echium amoenum in a calcareous soil.

Ecotoxicol Environ Saf 2021 Jan 7;208:111408. Epub 2020 Oct 7.

Soil Science, Julius Kühn-Institut, Braunschweig, Germany. Electronic address:

The fate of antibiotics and their effects on plant growth may be changed by the application of fertilizers. The present study was carried out to investigate the effect of sulfadiazine (SDZ), rice husk compost (RHC), rice husk biochar (RHB), and mycorrhiza (MR) on the growth attributes of Iranian Echium amoenum Fisch & C.A. Mey. A greenhouse experiment as a completely randomized design with six treatments of bio/organic-fertilizers (no bio-fertilizer (NF), RHB, RHC, MR, RHB+MR, and RHC+MR) and three levels of SDZ application (0, 100, and 200 mg kg) was performed for 7months with three replicates. Shoot and root SDZ concentrations were determined using high-pressure liquid chromatography-diode array detection (HPLC-DAD) instrumentation. The results revealed that the application of RHC, RHB, and MR had a significant impact on the reduction of the toxicity effects of SDZ on plant properties. The lowest values of growth parameters belonged to the 200 mg kg of SDZ with no bio-fertilizers, while the highest growth parameters were observed in the treatments of RHB+MR, and RHC+MR with no SDZ application. Also, chlorophyll pigments content was affected by used treatments and the lowest rates of chlorophyll a (4.24), chlorophyll b (2.99), and carotenoids (2.88) were related to the 200 mg kg of SDZ with no biofertilizers application. The co-application of bio-fertilizers and SDZ (at both levels of 100 and 200 mg kg) decreased SDZ uptake by both shoot and root in comparison with the control. The same results were obtained with macro (NPK) and micro (Fe, Zn, Cu, and Mn) nutrients uptake by the shoot in which the lowest values of nutrients uptake were observed in treatment of 200 mg kg of SDZ with no bio-fertilizers. Furthermore, in the case of the effect of the used treatments on root colonization, the results showed that the lowest value (7.26%) belonged to the 200 mg kg application of SDZ with no bio-fertilizers. Generally, this study demonstrated that bio-fertilizers could be considered as an effective strategy in controlling the negative effects of antibiotics on the growth properties and nutrients status of the plants grown in such contaminated soils.
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http://dx.doi.org/10.1016/j.ecoenv.2020.111408DOI Listing
January 2021

Investigating conformational changes of Prefoldin β1 as result of applying external mechanical force without any position constraint.

IET Nanobiotechnol 2020 Aug;14(6):491-500

Department of Mechanical Engineering, Ferdowsi University of Mashhad, Mashhad, Iran.

Manipulating molecular scale bio-nanorobots and influencing their behaviour is one of the major challenges of new researches. Many coiled coil type proteins are involved in important biological functions due to physical properties that make them ideal for both nanoscale manipulation and sensing. The Prefoldin beta subunit from strain KS-1(Prefoldin β1) is one of the possible proteins that can serve as a new bio-nano-actuator. Besides having a balanced architecture, Prefoldin β1 can exhibit a wide range of exclusive authorities. In this study, steered molecular dynamics simulation is applied along with the centre of mass pulling and analyses of Prefoldin β1 conformational changes to characterise some of those abilities. Thus, applying external mechanical force without any position constraint shows that it has no movement throughout simulations. This proposes a novel method to capture different sizes and shapes of cargoes. During simulations, each arm was found to be very flexible, allowing it to enlarge its central cavity and capture different cargoes. For a more accurate analysis, the variations in the cavity of nano-actuator are investigated qualitatively and quantitatively with different parameters. Also, the force analysis of the arms can provide us with decent information about the performance of this nano-actuator.
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http://dx.doi.org/10.1049/iet-nbt.2019.0265DOI Listing
August 2020

Comparison of Patient's Kidney Function Based on Kidney Disease Improving Global Outcomes (KDIGO) Criteria and Clinical Parameters in Isolated Coronary Artery Bypass Graft (CABG) Surgery in On-Pump and Off-pump Methods in Patients with Low Cardiac Output Syndrome (LCOS) After Surgery.

Anesth Pain Med 2020 Apr 19;10(2):e100517. Epub 2020 Apr 19.

Department of Extra-Corporeal Circulation (ECC), Razavi Hospital, Imam Reza International University, Mashhad, Iran.

Background: Acute kidney injury (AKI) is one of the serious complications of cardiac surgery. It is worsened when accompanied by low cardiac output syndrome.

Objectives: In this study, we compared kidney function based on the KDIGO criteria in isolated on-pump and off-pump coronary artery bypass graft (CABG) surgery.

Methods: In this cohort study, 52 patients with LCOS were enrolled after on-pump (28 patients) and off-pump (24 patients) CABG. In the first six hours after ICU entrance, blood samples were taken for serum creatinine based on routine. For determining AKI after surgery, we used the KDIGO criteria as a primary endpoint. Also, some clinical parameters were recorded before, during, and after surgery. The data were analyzed by SPSS software, version 24, using paired and independent -test, ANOVA, and Pearson correlation test and non-parametric tests such as Mann-Whitney and Kruskal-Wallis tests at a significance level of P < 0.05.

Results: There was no significant difference in age (P = 0.3) and gender (P = 0.57) between the two groups. Among cardiac disease risk factors, only hypertension (P = 0.02) had a significant difference between the two groups, but AKI in patients with hypertension did not show a significant difference (P = 0.09). In paraclinical parameters, serum creatinine showed a significant difference before and after surgery in on-pump (P < 0.001) and off-pump (P = 0.007) groups. Also, this parameter had a significant difference at 6 h, 12 h, 24 h, and 48 h after surgery between the on-pump and on-pump groups. The AKI incidence showed a significant difference between the two groups (P < 0.001).

Conclusions: The incidence of AKI was more in on-pump patients than in off-pump patients. Also, a significant difference was observed between their clinical parameters. Thus, to improve the patients' clinical outcomes and lower the health costs, we suggest that patients with a high risk of LCOS be followed up after CABG, especially on-pump CABG.
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http://dx.doi.org/10.5812/aapm.100517DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352649PMC
April 2020

Epilepsy control using a fixed time integral super twisting sliding mode control for Pinsky-Rinzel pyramidal model through ion channels with optogenetic method.

Comput Methods Programs Biomed 2020 Oct 22;195:105665. Epub 2020 Jul 22.

Department of Electrical & Electronics Engineering, University of Qom, Qom, Iran.

Background And Objective: Epilepsy is a dynamic disease of neuronal networks and epileptic activity in the brain should be suppressed quickly in the shortest possible time with minimum control signal. Thus, a closed-loop feedback control by using the fixed-time integral super-twisting sliding-mode controller via an optogenetic method is employed for suppressing seizures in the Pinsky-Rinzel (PR) model as a dynamic model of the hippocampus CA3 region where epileptic seizures occur. The control signal is applied to the PR model through the ChR2 channel model in the form of light photons using the optogenetic method. The present study aimed to determine the controller robustness against parameter changes and disturbances in order to reduce the control time, approach the zero tracking error of the normal desired state in a fixed time, and finally, converge the epileptic state to the normal desired state.

Method: In order to apply the control signal to the Pinsky-Rinzel model in the optogenetic method, the dynamic model of the ion current generated by channelrhodopsin 2 (ChR2) as a light-sensitive protein model in the optogenetic method was first applied to the PR model. Then, a fixed-time integral super-twisting sliding-mode controller was designed for the system, which is the combination of PR and ChR2 models.

Results: After applying the proposed controller, the simulation results indicated that the control signal was -0.7 mV, the tracking error of the normal desired state could reach zero within 1.5 milliseconds, and the problems of singularity and chattering were solved.

Conclusions: A reduction occurred in the control signal reduced regarding the objectives of the study and comparing the proposed controller with the classical sliding-mode controller. Thus, this method can produce a safe control input for brain. In addition, both types of sliding mode controllers are robust against the parameters variations and external disturbances. Thus, they are superior to non-robust and simple controllers. Finally, based on the results, the validity of the fixed-time integral super-twisting sliding mode controller is confirmed for epilepsy control.
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http://dx.doi.org/10.1016/j.cmpb.2020.105665DOI Listing
October 2020

Design and Simulation of a DNA Origami Nanopore for Large Cargoes.

Mol Biotechnol 2020 Sep 4;62(9):423-432. Epub 2020 Jul 4.

Department of Mechanical Engineering, Hakim Sabzevari University, 397, Sabzevar, Iran.

Since less than a decade ago, the DNA origami technique has become an important tool in nanopore fabrication. DNA origami nanopores are highly efficient because of their compatibility with biomolecules and the possibility to precisely engineer their dimensions and designs. However, accurate comprehension of their molecular behavior under various conditions is still unsatisfactory. In this study, a thin plate DNA origami nanopore is designed and investigated using molecular dynamics simulation. The thin plate is designed using caDNAno software along with the square lattice method and the molecular dynamics simulation is performed using GROMACS software. The model is simulated in a wide temperature range and its stability is investigated. The shape and dimensions of the nanopore are also compared at these temperatures. The results indicate that the designed nanopore exhibits decent stability at these temperatures and no breakdown was observed despite some distortions in the structure at high temperatures. In addition, the effect of the number of staple strands on the structure, stability, and deformation of the DNA origami plate is investigated and it is found that addition of staple strands have a significant positive effect on the stability of nanopore's shape. By the results of analyzing the shape of the nanopore, it suggests that the proposed nanopore can be used to pass a wide range of molecules, macromolecules, and drug cargoes.
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http://dx.doi.org/10.1007/s12033-020-00261-zDOI Listing
September 2020

Contribution of CTCF binding to transcriptional activity at the HOXA locus in NPM1-mutant AML cells.

Leukemia 2021 02 12;35(2):404-416. Epub 2020 May 12.

Division of Oncology, Department of Medicine, Section of Stem Cell Biology, Washington University School of Medicine, St. Louis, MO, USA.

Transcriptional regulation of the HOXA genes is thought to involve CTCF-mediated chromatin loops and the opposing actions of the COMPASS and Polycomb epigenetic complexes. We investigated the role of these mechanisms at the HOXA cluster in AML cells with the common NPM1c mutation, which express both HOXA and HOXB genes. CTCF binding at the HOXA locus is conserved across primary AML samples, regardless of HOXA gene expression, and defines a continuous chromatin domain marked by COMPASS-associated histone H3 trimethylation in NPM1-mutant primary AML samples. Profiling of the three-dimensional chromatin architecture in primary AML samples with the NPM1c mutation identified chromatin loops between the HOXA cluster and loci in the SNX10 and SKAP2 genes, and an intergenic region located 1.4 Mbp upstream of the HOXA locus. Deletion of CTCF binding sites in the NPM1-mutant OCI-AML3 AML cell line reduced multiple long-range interactions, but resulted in CTCF-independent loops with sequences in SKAP2 that were marked by enhancer-associated histone modifications in primary AML samples. HOXA gene expression was maintained in CTCF binding site mutants, indicating that transcriptional activity at the HOXA locus in NPM1-mutant AML cells may be sustained through persistent interactions with SKAP2 enhancers, or by intrinsic factors within the HOXA gene cluster.
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http://dx.doi.org/10.1038/s41375-020-0856-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657955PMC
February 2021

The effect of structure on improvement of the PNA Young modulus: A study of steered molecular dynamics.

Comput Biol Chem 2019 Dec 25;83:107133. Epub 2019 Sep 25.

Master of Science, Department of Engineering, Hakim Sabzevari University, Sabzevar, Iran.

Prefoldin is a molecular chaperone and acts as a nano-actuator in cargo carriage and drug delivery for disease treatment. Investigating the mechanical properties of nano-actuator helps predict its behavior and measure its performance under various environmental conditions, like external forces that are applied. Accordingly, this paper investigates the elastic properties of the Prefoldin nano-actuator (PNA), specifically its Young modulus and the structural changes on a microscopic scale. For this purpose, three structurally different PNAs obtained from Protein Data Bank (PDB) and previous studies of our research team have been used. The selected three-tentacles Prefoldin are analyzed via the series of steered molecular dynamics simulations (SMD) based on the theory of Two Springs in Series. The simulation is applied in the velocity of 0.1, 0.05, and 0.01. Due to differences in the structure of the Prefoldin, PNAs exhibited different behaviours at various pull rates. Also, the analysis showed different values of Young's modulus for the PNA tentacles in the interval of (2.5-4 GPa). Understanding the mechanical properties of a Prefoldin nano actuator allows for a closer examination of its application in transportation the pathogenic cargos and intelligent drug delivery.
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http://dx.doi.org/10.1016/j.compbiolchem.2019.107133DOI Listing
December 2019

Quetiapine versus Haloperidol in Controlling Conversion Disorder Symptoms; a Randomized Clinical Trial.

Emerg (Tehran) 2018 2;6(1):e47. Epub 2018 Aug 2.

Department of Epidemiology, Faculty of Health, Iran University of Medical Sciences, Tehran, Iran.

Introduction: About 5% of visits to emergency departments are made up of conversion disorder cases. This study was designed with the aim of comparing the effectiveness of quetiapine and haloperidol in controlling conversion disorder symptoms.

Methods: The present single-blind clinical trial has been performed on patients with conversion disorder (based on the DSM-IV definition) presenting to emergency department of 9-Day Hospital, Torbat Heydariyeh, Iran, from January 2017 until May 2018.

Results: 73 patients were allocated to haloperidol and 71 to quetiapine group. Mean age of these patients was 32.03 ± 12.80 years (62.50% female). Two groups were similar regarding the baseline characteristics. Within 30 minutes, 90.41% of haloperidol cases and 91.55% of quetiapine cases were relieved (p=0.812). The most common side effects after 30 minutes were extrapyramidal symptoms (9.59%) in the haloperidol group and fatigue and sleepiness (7.04%) in the quetiapine group. Extrapyramidal symptoms was significantly higher than the quetiapine group (p=0.013).

Conclusion: The results of the present study showed that although quetiapine and haloperidol have a similar effect in relieving the patients from conversion disorder symptoms, the prevalence of extrapyramidal symptoms is significantly lower in the group under treatment with quetiapine. Therefore, it seems that quetiapine is a safer drug compared to haloperidol.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6289155PMC
August 2018

Technologies in the Treatment of Bone Marrow Edema Syndrome.

Orthop Clin North Am 2019 Jan;50(1):131-138

Tehran University of Medical Science, Number 21, Dameshgh Street, Vali-e Asr Avenue, Tehran 1416753955, Iran.

Bone marrow edema syndrome is a rare and self-limited syndrome with an unknown cause. The natural time course for improvement of clinical symptoms and normalization in MRI lasts from 3 to 18 months. This entity must be distinguished from other causes of marrow abnormality, such as stress fractures and osteonecrosis, for the best treatment options. Various treatments from conservative to surgical have been made to provide pain relief and accelerate the natural course of the disease. This article reviews bone marrow edema syndrome with a focus on treatment in the foot and ankle.
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http://dx.doi.org/10.1016/j.ocl.2018.08.008DOI Listing
January 2019

Trifascicular block as primary presentation of the cardiac amyloidosis; A rare case report.

ARYA Atheroscler 2018 Mar;14(2):101-104

Assistant Professor, Department of Cardiology, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.

Background: Amyloidosis is a severe systemic disorder produces by the accumulation of inappropriately amyloid deposition in tissues. Cardiac involvement, as a main type of amyloidosis, has a major impact on prognosis. We describe a biopsy-proven cardiac amyloidosis in an old man with unexpected presentation.

Case Report: A 70-year-old man, with a complaint of severe weakness, lightheadedness, and lower limb paresthesia, was admitted to the emergency department. Electrocardiography revealed right bundle branch block and Trifascicular block. Echocardiography study showed a moderately increased thickness of left ventricular wall with concentric pattern as well. Laboratory investigations including serum and urine electrophoresis, and serum free light chain examination as immunofixation assay revealed that κ chains predominated over λ chains in a ratio of 3:2. Our patient with final diagnosis of amyloid light-chain (AL) amyloidosis underwent chemotherapy with melphalan combined with high-dose dexamethasone, CPHPC and monoclonal antibodies for 2 weeks.

Conclusion: It shows that rapid diagnosis of AL amyloidosis can enhance the prognosis. Applying an optimal strategy for the treatment leads to effective therapy, too.
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http://dx.doi.org/10.22122/arya.v14i2.1676DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6087624PMC
March 2018

Eccentric exercise increases circulating fibroblast activation protein α but not bioactive fibroblast growth factor 21 in healthy humans.

Exp Physiol 2018 06;103(6):876-883

School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.

New Findings: What is the central question of this study? The role of FGF21 as an exercise-induced myokine remains controversial. The aim of this study was to determine whether eccentric exercise would augment the release of FGF21 and/or its regulatory enzyme, fibroblast activation protein α (FAP), from skeletal muscle tissue into the systemic circulation of healthy human volunteers. What is the main finding and its importance? Eccentric exercise does not release total or bioactive FGF21 from human skeletal muscle. However, exercise releases its regulatory enzyme, FAP, from tissue(s) other than muscle, which might play a role in the inactivation of FGF21.

Abstract: The primary aim of the investigation was to determine whether eccentric exercise would augment the release of the myokine fibroblast growth factor 21 (FGF21) and/or its regulatory enzyme, fibroblast activation protein α (FAP), from skeletal muscle tissue into the systemic circulation of healthy human volunteers. Physically active young healthy male volunteers (age 25.0 ± 10.7 years; body mass index 23.1 ± 7.9 kg m ) completed three sets of 25 repetitions (with 5 min rest in between) of single-leg maximal eccentric contractions using their non-dominant leg, whilst the dominant leg served as a control. Arterialized blood samples from a hand vein and deep venous blood samples from the common femoral vein of the exercised leg, along with blood flow of the superficial femoral artery using Doppler ultrasound, were obtained before and after each exercise bout and every 20 min during the 3 h recovery period. Muscle biopsy samples were taken at baseline, immediately and 3 and 48 h postexercise. The main findings showed that there was no significant increase in total or bioactive FGF21 secreted from skeletal muscle into the systemic circulation in response to exercise. Furthermore, skeletal muscle FGF21 protein content was unchanged in response to exercise. However, there was a significant increase in arterialized and venous FAP concentrations, with no apparent contribution to its release from the exercised leg. These findings raise the possibility that the elevated levels of FAP might play a role in the inactivation of FGF21 during exercise.
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http://dx.doi.org/10.1113/EP086669DOI Listing
June 2018

Aftermath of bustamante attack on genomic beacon service.

BMC Med Genomics 2017 07 26;10(Suppl 2):43. Epub 2017 Jul 26.

Department of Computer Science, University of Manitoba, Winnipeg, Canada.

Background: With the enormous need for federated eco-system for holding global genomic and clinical data, Global Alliance for Genomic and Health (GA4GH) has created an international website called beacon service which allows a researcher to find out whether a specific dataset can be utilized to his or her research beforehand. This simple webservice is quite useful as it allows queries like whether a certain position of a target chromosome has a specific nucleotide. However, the increased integration of individuals genomic data into clinical practice and research raised serious privacy concern. Though the answer of such queries are yes or no in Bacon network, it results in serious privacy implication as demonstrated in a recent work from Shringarpure and Bustamante. In their attack model, the authors demonstrated that with a limited number of queries, presence of an individual in any dataset can be determined.

Methods: We propose two lightweight algorithms (based on randomized response) which captures the efficacy while preserving the privacy of the participants in a genomic beacon service. We also elaborate the strength and weakness of the attack by explaining some of their statistical and mathematical models using real world genomic database. We extend their experimental simulations for different adversarial assumptions and parameters.

Results: We experimentally evaluated the solutions on the original attack model with different parameters for better understanding of the privacy and utility tradeoffs provided by these two methods. Also, the statistical analysis further elaborates the different aspects of the prior attack which leads to a better risk management for the participants in a beacon service.

Conclusions: The differentially private and lightweight solutions discussed here will make the attack much difficult to succeed while maintaining the fundamental motivation of beacon database network.
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http://dx.doi.org/10.1186/s12920-017-0278-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547468PMC
July 2017

Dacomitinib, a pan-inhibitor of ErbB receptors, suppresses growth and invasive capacity of chemoresistant ovarian carcinoma cells.

Sci Rep 2017 06 23;7(1):4204. Epub 2017 Jun 23.

Haematology/Oncology and Stem Cell Transplantation Research Centre, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Epithelial ovarian cancer (EOC) is the most lethal gynaecological malignancy worldwide. Development of chemoresistance and peritoneal dissemination of EOC cells are the major reasons for low survival rate. Targeting signal transduction pathways which promote therapy resistance and metastatic dissemination is the key to successful treatment. Members of the ErbB family of receptors are over-expressed in EOC and play key roles in chemoresistance and invasiveness. Despite this, single-targeted ErbB inhibitors have demonstrated limited activity in chemoresistant EOC. In this report, we show that dacomitinib, a pan-ErbB receptor inhibitor, diminished growth, clonogenic potential, anoikis resistance and induced apoptotic cell death in therapy-resistant EOC cells. Dacominitib inhibited PLK1-FOXM1 signalling pathway and its down-stream targets Aurora kinase B and survivin. Moreover, dacomitinib attenuated migration and invasion of the EOC cells and reduced expression of epithelial-to-mesenchymal transition (EMT) markers ZEB1, ZEB2 and CDH2 (which encodes N-cadherin). Conversely, the anti-tumour activity of single-targeted ErbB agents including cetuximab (a ligand-blocking anti-EGFR mAb), transtuzumab (anti-HER2 mAb), H3.105.5 (anti-HER3 mAb) and erlotinib (EGFR small-molecule tyrosine kinase inhibitor) were marginal. Our results provide a rationale for further investigation on the therapeutic potential of dacomitinib in treatment of the chemoresistant EOC.
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http://dx.doi.org/10.1038/s41598-017-04147-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482808PMC
June 2017

Huge mass in right side of the heart: A rare case report.

ARYA Atheroscler 2016 Nov;12(6):291-294

Department of Cardiac Anesthesiology, School of Medicine, Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran.

Background: The presence of primary intracardiac tumors are scarce, and most of them are myxomas. We reported, in this paper, a case with huge mass in the right side of the heart.

Case Report: A 45-year-old man, with a complaint of bilateral lower limbs edema and exertional dyspnea, was admitted to intensive cardiac care unit. Cardiac auscultation revealed soft grade systolic murmur without any evidence of "tumor plop." Echocardiography showed a huge mobile mass in right side of the heart that suggested myxoma. Our patient underwent cardiac surgery with excision of 13 cm mass. Histopathological study was confirmed the diagnosis of mass type.

Conclusion: In this case report, it shows that in the differential diagnosis of right-sided heart failure, the right sided myxoma must be considered. The preferable approach in patient with cardiac myxomas is surgical excision to alleviate symptoms, early identification, and removal.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5455328PMC
November 2016

Increasing skeletal muscle carnitine availability does not alter the adaptations to high-intensity interval training.

Scand J Med Sci Sports 2018 Jan 12;28(1):107-115. Epub 2017 May 12.

MRC/ARUK Centre for Musculoskeletal Ageing Research, School of Life Sciences, University of Nottingham, Nottingham, UK.

Increasing skeletal muscle carnitine availability alters muscle metabolism during steady-state exercise in healthy humans. We investigated whether elevating muscle carnitine, and thereby the acetyl-group buffering capacity, altered the metabolic and physiological adaptations to 24 weeks of high-intensity interval training (HIIT) at 100% maximal exercise capacity (Watt ). Twenty-one healthy male volunteers (age 23±2 years; BMI 24.2±1.1 kg/m ) performed 2 × 3 minute bouts of cycling exercise at 100% Watt , separated by 5 minutes of rest. Fourteen volunteers repeated this protocol following 24 weeks of HIIT and twice-daily consumption of 80 g carbohydrate (CON) or 3 g l-carnitine+carbohydrate (CARN). Before HIIT, muscle phosphocreatine (PCr) degradation (P<.0001), glycogenolysis (P<.0005), PDC activation (P<.05), and acetylcarnitine (P<.005) were 2.3-, 2.1-, 1.5-, and 1.5-fold greater, respectively, in exercise bout two compared to bout 1, while lactate accumulation tended (P<.07) to be 1.5-fold greater. Following HIIT, muscle free carnitine was 30% greater in CARN vs CON at rest and remained 40% elevated prior to the start of bout 2 (P<.05). Following bout 2, free carnitine content, PCr degradation, glycogenolysis, lactate accumulation, and PDC activation were all similar between CON and CARN, albeit markedly lower than before HIIT. VO , Watt , and work output were similarly increased in CON and CARN, by 9, 15, and 23% (P<.001). In summary, increased reliance on non-mitochondrial ATP resynthesis during a second bout of intense exercise is accompanied by increased carnitine acetylation. Augmenting muscle carnitine during 24 weeks of HIIT did not alter this, nor did it enhance muscle metabolic adaptations or performance gains beyond those with HIIT alone.
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http://dx.doi.org/10.1111/sms.12885DOI Listing
January 2018

Targeting of IL-2 to cytotoxic lymphocytes as an improved method of cytokine-driven immunotherapy.

Oncoimmunology 2017;6(2):e1265721. Epub 2017 Jan 10.

Department of Surgery, University of Virginia , Charlottesville, VA, USA.

The use of high-dose interleukin-2 (IL-2) has fallen out of favor due to severe life-threatening side effects. We have recently described a unique way of directly targeting IL-2 to cytotoxic lymphocytes using a virally encoded immune evasion protein and an IL-2 mutant that avoids off-target side effects such as activation of regulatory T cells and vascular endothelium.
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http://dx.doi.org/10.1080/2162402X.2016.1265721DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5353927PMC
January 2017

Deficiency of the adaptor protein SLy1 results in a natural killer cell ribosomopathy affecting tumor clearance.

Oncoimmunology 2016;5(12):e1238543. Epub 2016 Sep 27.

Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA; The Alvin Siteman Cancer Center of Washington University School of Medicine, St. Louis, MO, USA; The John Cochran VA Medical Center, St. Louis, MO, USA.

Individuals with robust natural killer (NK) cell function incur lower rates of malignancies. To expand our understanding of genetic factors contributing to this phenomenon, we analyzed NK cells from cancer resistant and susceptible strains of mice. We identified a correlation between NK levels of the X-chromosome-located adaptor protein SLy1 and immunologic susceptibility to cancer. Unlike the case for T or B lymphocytes, where SLy1 shuttles between the cytoplasm and nucleus to facilitate signal transduction, in NK cells SLy1 functions as a ribosomal protein and is located solely in the cytoplasm. In its absence, ribosomal instability results in p53-mediated NK cell senescence and decreased clearance of malignancies. NK defects are reversible under inflammatory conditions and viral clearance is not impacted by SLy1 deficiency. Our work defines a previously unappreciated X-linked ribosomopathy that results in a specific and subtle NK cell dysfunction leading to immunologic susceptibility to cancer.
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http://dx.doi.org/10.1080/2162402X.2016.1238543DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215235PMC
September 2016

Private and Efficient Query Processing on Outsourced Genomic Databases.

IEEE J Biomed Health Inform 2017 09 4;21(5):1466-1472. Epub 2016 Nov 4.

Applications of genomic studies are spreading rapidly in many domains of science and technology such as healthcare, biomedical research, direct-to-consumer services, and legal and forensic. However, there are a number of obstacles that make it hard to access and process a big genomic database for these applications. First, sequencing genomic sequence is a time consuming and expensive process. Second, it requires large-scale computation and storage systems to process genomic sequences. Third, genomic databases are often owned by different organizations, and thus, not available for public usage. Cloud computing paradigm can be leveraged to facilitate the creation and sharing of big genomic databases for these applications. Genomic data owners can outsource their databases in a centralized cloud server to ease the access of their databases. However, data owners are reluctant to adopt this model, as it requires outsourcing the data to an untrusted cloud service provider that may cause data breaches. In this paper, we propose a privacy-preserving model for outsourcing genomic data to a cloud. The proposed model enables query processing while providing privacy protection of genomic databases. Privacy of the individuals is guaranteed by permuting and adding fake genomic records in the database. These techniques allow cloud to evaluate count and top-k queries securely and efficiently. Experimental results demonstrate that a count and a top-k query over 40 Single Nucleotide Polymorphisms (SNPs) in a database of 20 000 records takes around 100 and 150 s, respectively.
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http://dx.doi.org/10.1109/JBHI.2016.2625299DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498255PMC
September 2017

Selective targeting of IL-2 to NKG2D bearing cells for improved immunotherapy.

Nat Commun 2016 09 21;7:12878. Epub 2016 Sep 21.

Department of Surgery, Washington University in St Louis, 660 South Euclid Avenue, St Louis, Missouri 63110, USA.

Despite over 20 years of clinical use, IL-2 has not fulfilled expectations as a safe and effective form of tumour immunotherapy. Expression of the high affinity IL-2Rα chain on regulatory T cells mitigates the anti-tumour immune response and its expression on vascular endothelium is responsible for life threatening complications such as diffuse capillary leak and pulmonary oedema. Here we describe the development of a recombinant fusion protein comprised of a cowpox virus encoded NKG2D binding protein (OMCP) and a mutated form of IL-2 with poor affinity for IL-2Rα. This fusion protein (OMCP-mutIL-2) potently and selectively activates IL-2 signalling only on NKG2D-bearing cells, such as natural killer (NK) cells, without broadly activating IL-2Rα-bearing cells. OMCP-mutIL-2 provides superior tumour control in several mouse models of malignancy and is not limited by mouse strain-specific variability of NK function. In addition, OMCP-mutIL-2 lacks the toxicity and vascular complications associated with parental wild-type IL-2.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5036003PMC
http://dx.doi.org/10.1038/ncomms12878DOI Listing
September 2016

Neurocysticercosis presenting as a 'Stroke Mimic'.

Acute Med 2016 ;15(2):79-83

MBChB MRCP PhD, Vascular Medicine, School of Medicine, Royal Derby Hospital Centre, University of Nottingham.

A 62 year old Nepalese gentleman presented with left sided weakness and sensory loss. Initial brain CT scanning was suggestive of acute infarction but a subsequent MRI scan showed cysts with oedema. Cysticercosis serology was positive and a diagnosis of neurocysticercosis was made. The patient made almost a complete recovery after treatment with albendazole, praziquantel and steroids. Neurocysticercosis should be considered in the diffierential diagnosis when patients originating from endemic areas present with focal neurological deficit.
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February 2017

Over-expression of the miR-483-3p overcomes the miR-145/TP53 pro-apoptotic loop in hepatocellular carcinoma.

Oncotarget 2016 May;7(21):31361-71

Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.

The miR-145-5p, which induces TP53-dependent apoptosis, is down-regulated in several tumors, including hepatocellular carcinomas (HCCs), but some HCCs show physiological expression of this miR. Here we demonstrate that in HCC cells carrying wild-type TP53 the steady activation of the miR-145 signaling selects clones resistant to apoptosis via up-regulation of the oncogenic miR-483-3p. Expression of the miR-145-5p and of the miR-483-3p correlated negatively in non-neoplastic liver (n=41; ρ=-0.342, P=0.028), but positively in HCCs (n=21; ρ=0.791, P<0.0001), which we hypothesized to be due to impaired glucose metabolism in HCCs versus normal liver. In fact, when liver cancer cells were grown in low glucose, miR-145-5p lowered miR-483-3p expression, allowing apoptosis, whereas when cells were grown in high glucose the levels of miR-483-3p increased, reducing the apoptotic rate. This indicates that depending on glucose availability the miR-145-5p has double effects on the miR-483-3p, either inhibitory or stimulatory. Moreover, resistance to apoptosis in clones overexpressing both miR-145-5p and miR-483-3p was abrogated by silencing the miR-483-3p. Our data highlight a novel mechanism of resistance to apoptosis in liver cancer cells harbouring wild type TP53 and suggest a potential role of miR-145-5p and miR-483-3p as druggable targets in a subset of HCCs.
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http://dx.doi.org/10.18632/oncotarget.8913DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5058762PMC
May 2016

Effects of silibinin on growth and invasive properties of human ovarian carcinoma cells through suppression of heregulin/HER3 pathway.

Tumour Biol 2016 Mar 19;37(3):3913-23. Epub 2015 Oct 19.

Hematology/Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Epithelial ovarian cancer (EOC) is the most fatal gynecological malignancy due to its high proliferative and invasive capacities. A heregulin (HRG)/HER3 autocrine loop increases proliferative and metastatic properties of EOC cells, suggesting that modulators of this signaling pathway may prove effective to trammel growth and motility of these cells. This study aimed to evaluate the effects of multi-tyrosine kinase inhibitor silibinin on proliferative and invasive characteristics of EOC cell lines OVCAR8 and SKOV3 through suppression of the HRG/HER3 pathway. To achieve this, the effects of silibinin on proliferation, DNA synthesis, clonogenicity, cell cycle progression, cathepsin B enzymatic activity, and migration and invasion were explored in vitro. Silibinin suppressed proliferation, DNA synthesis, and clonogenic abilities of OVCAR8 and SKOV3 cells through inhibition of the autocrine HRG/HER3 circuit. Silibinin-mediated attenuation of the HER3 signaling disabled the HER3/AKT/survivin axis and thereby, induced G1/S cell cycle arrest. Furthermore, silibinin reduced invasive potentials of the EOC cells through quelling the HRG/HER3 pathway and suppression of cathepsin B activity. Altogether, these results suggest that silibinin is a potential anti-cancer drug to inhibit proliferative and invasive characteristics of the EOC cells that exhibit an autocrine HRG/HER3 pathway.
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http://dx.doi.org/10.1007/s13277-015-4220-6DOI Listing
March 2016

EV20, a Novel Anti-ErbB-3 Humanized Antibody, Promotes ErbB-3 Down-Regulation and Inhibits Tumor Growth In Vivo.

Transl Oncol 2013 Dec 1;6(6):676-84. Epub 2013 Dec 1.

MediaPharma srl, Chieti, Italy ; Department of Experimental and Clinical Sciences, G. D'Annunzio University Foundation, Chieti, Italy.

ErbB-3 (HER-3) receptor is involved in tumor progression and resistance to therapy. Development of specific inhibitors impairing the activity of ErbB-3 is an attractive tool for cancer therapeutics. MP-RM-1, a murine monoclonal antibody targeting human ErbB-3, has shown anticancer activity in preclinical models. With the aim to provide novel candidates for clinical use, we have successfully generated a humanized version of MP-RM-1. The humanized antibody, named EV20, abrogates both ligand-dependent and ligand-independent receptor signaling of several tumor cell types, strongly promotes ErbB-3 down-regulation, and efficiently and rapidly internalizes into tumor cells. Furthermore, treatment with EV20 significantly inhibits growth of xenografts originating from prostatic, ovarian, and pancreatic cancers as well as melanoma in nude mice. In conclusion, we provide a novel candidate for ErbB-3-targeted cancer therapy.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890702PMC
http://dx.doi.org/10.1593/tlo.13475DOI Listing
December 2013

Multitargeting and antimetastatic potentials of silibinin in human HepG-2 and PLC/PRF/5 hepatoma cells.

Nutr Cancer 2013 ;65(4):590-9

Hematology, Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Hepatocellular carcinoma (HCC) is the most common sort of primary liver malignancy with poor prognosis. This study aimed at examining the effects of silibinin (a putative antimetastatic agent) on some transcriptional markers mechanistically related to HCC recurrence and metastasis in HepG-2 [hepatitis B virus (HBV)-negative and P53 intact) and PLC/PRF/5 (HBV-positive and P53 mutated) cells. The expression of 27 genes in response to silibinin was evaluated by real-time RT-PCR. The MMP gelatinolytic assay and microculture tetrazolium test (MTT) were tested. Silibinin was capable of suppressing the transcriptional levels of ANGPT2, ATP6L, CAP2, CCR6, CCR7, CLDN-10, cortactin, CXCR4, GLI2, HK2, ID1, KIAA0101, mortalin, PAK1, RHOA, SPINK1, and STMN1 as well as the enzymatic activity of MMP-2 but promoted the transcripts of CREB3L3, DDX3X, and PROX1 in both cells. Some significant differences between the cells in response to silibinin were detected that might be related to the differences of the cells in terms of HBV infection and/or P53 mutation, suggesting the possible influence of silibinin on HCC through biological functions of these 2 prognostic factors. In conclusion, our findings suggest that silibinin could potentially function as a multitargeting antimetastatic agent and might provide new insights for HCC therapy particularly for HBV-related and/or P53-mutated HCCs.
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http://dx.doi.org/10.1080/01635581.2013.770043DOI Listing
December 2013

Tumor-derived microvesicles: the metastasomes.

Med Hypotheses 2013 Jan 21;80(1):75-82. Epub 2012 Nov 21.

Department of Biomedical Sciences, University of "G. D'Annunzio" of Chieti-Pescara, Italy.

Metastasis is the leading cause of cancer death, yet it is mechanistically considered a very inefficient process suggesting the presence of some sort of (e.g. systemic) routes for fuelling the process. The pre-metastatic niche formation is described as one such metastasis promoting route. Now, the emerging potentials of tumor-derived microvesicles (TDMVs), not only in formulating the pre-metastatic niche, but also conferring neoplastic phenotypes onto normal cells, has integrated new concepts into the field. Here, we note as an ancillary proposition that, exerting functional disturbances in other sites, TDMVs (we have termed them metastasomes) may aid foundation of the secondary lesions via two seemingly interrelated models: (i) tumor-organ-training (TOTr), training a proper niche for the growth of the disseminated tumor cells; (ii) tumor-organ-targeting (TOTa), contribution to the propagation of the transformed phenotype via direct or indirect (TOTr-mediated disturbed stroma) transformation and/or heightened growth/survival states of the normal resident cells in the secondary organs. Respecting the high content of the RNA molecules (particularly microRNAs) identified in the secretory MVs, they may play crucial parts in such "malignant trait" spreading system. That is, the interactions between tumor tissue-specific RNA signatures, being transferred via metastasomes, and the cell-type/tissue-specific RNA stockrooms in other areas may settle a unique outcome in each organ. Thus, serving as tumor-organ matchmakers, the RNA molecules may also play substantial roles in the seeding and tropism of the process.
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http://dx.doi.org/10.1016/j.mehy.2012.10.011DOI Listing
January 2013

Silibinin inhibits invasive properties of human glioblastoma U87MG cells through suppression of cathepsin B and nuclear factor kappa B-mediated induction of matrix metalloproteinase 9.

Anticancer Drugs 2010 Mar;21(3):252-60

Hematology, Oncology and Bone Marrow Transplantation Research Center, Tehran, Iran.

Glioblastoma multiforme remains one of the most devastating human malignancies because of its high infiltrative capacity. This study aimed to investigate the effects of silibinin on human glioblastoma U87MG cells. The microculture tetrazolium test, bromodeoxyuridine cell proliferation assay, cell-based nuclear factor kappa B (NF-[kappa]B) activation assessment, cathepsin B activity assay, gelatin zymography, and quantitative real-time reverse transcription-PCR were performed to appraise the effects of silibinin on the metabolic activity, DNA synthesis, NF-[kappa]B phosphorylation, cathepsin B activity, and gelatinolytic activity of U87 cells. Silibinin inhibited metabolic activity, cell proliferation, NF-[kappa]B activation, cathepsin B enzymatic levels, and gelatinase B activity in U87 cells. In addition, an expressive decrease in mRNA levels of matrix metalloproteinase-9, cathepsin B, urokinase plasminogen activator receptor, urokinase plasminogen activator, and intercellular adhesion molecule 1 coupled with a significant induction in transcriptional levels of stefin A was observed. Altogether, these issues show for the first time that silibinin treatment could trammel invasive features of a highly invasive human glioma cell line, U87, through suppression of NF-[kappa]B-mediated stimulation of matrix metalloproteinase-9. Furthermore, silibinin might cripple the activation of gelatinase B by cramping transcriptional and enzymatic activities of cathepsin B in U87 cells.
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http://dx.doi.org/10.1097/cad.0b013e3283340cd7DOI Listing
March 2010

Arsenic trioxide induces apoptosis in NB-4, an acute promyelocytic leukemia cell line, through up-regulation of p73 via suppression of nuclear factor kappa B-mediated inhibition of p73 transcription and prevention of NF-kappaB-mediated induction of XIAP, cIAP2, BCL-XL and survivin.

Med Oncol 2010 Sep 10;27(3):833-42. Epub 2009 Sep 10.

Hematology, Oncology and Bone Marrow Transplantation Research Center, Shariati Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

The purpose of the present study is to evaluate the effects of arsenic trioxide (ATO) on human acute promyelocytic leukemia NB-4 cells. Microculture tetrazolium test, bromodeoxyuridine (BrdU) cell proliferation assay, caspase 3 activity assay, cell-based nuclear factor kappa B (NF-kappaB) phosphorylation measurement by ELISA and real-time RT-PCR were employed to appraise the effects of ATO on metabolic activity, DNA synthesis, induction of programmed cell death and NF-kappaB activation. The suppressive effects of ATO on metabolic potential, cell proliferation and NF-kappaB activation were associated with induction of apoptosis in NB-4 cells. In addition, an expressive enhancement in mRNA levels of p73, cyclin-dependent kinase inhibitor 1A (p21), tumor protein 53-induced nuclear protein 1 (TP53INP1), WNK lysine deficient protein kinase 2 (WNK2) and lipocalin 2 coupled with a significant reduction in transcriptional levels of NF-kappaB inhibitor beta (IKK2), Nemo, BCL2-like 1 (BCL-X(L)), inhibitor of apoptosis protein 1 (cIAP2), X-linked inhibitor of apoptosis protein (XIAP), survivin, Bcl-2, TIP60, ataxia telangiectasia (ATM), SHP-2 and sirtuin (SIRT1) were observed. Altogether, these issues show for the first time that ATO treatment could trammel cell growth and proliferation as well as induces apoptosis in NB-4 cells through induction of transcriptional levels of p73, TP53INP1, WNK2, lipocalin 2 as well as suppression of NF-kappaB-mediated induction of BCL-X(L), cIAP2, XIAP and survivin. Furthermore, the inductionary effects of ATO on transcriptional stimulation of p73 might be through cramping the NF-kappaB module (through suppression of p65 phosphorylation as well as transcriptional hindering of IKK2, ATM and Nemo) along with diminishing the mRNA expression of TIP60, SHP-2 and SIRT1.
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http://dx.doi.org/10.1007/s12032-009-9294-9DOI Listing
September 2010