MicroRNA Hsa-miR-370-3p Suppresses the Expression and Induction of CYP2D6 by Facilitating mRNA Degradation.

Biochem Pharmacol. 2017 May 25;:

Authors: Zeng L, Chen Y, Wang Y, Yu LR, Knox B, Chen J, Shi T, Chen S, Ren Z, Guo L, Wu Y, Liu D, Huang K, Tong W, Yu D, Ning B

Abstract
Cytochrome P450 2D6 (CYP2D6) participates in the metabolism of approximately 20-25% of prescribed drugs. Genetic polymorphisms influence the expression and/or activity of CYP2D6, and inter-individual differences in drug activation and elimination caused by CYP2D6 genetic variants were reported. However, little is known about the potential modulation of CYP2D6 expression by microRNAs (miRNAs). In the current study, by using in silico prediction of the stabilities of miRNA/mRNA complexes, we screened 38 miRNA candidates that may interact with the transcript of CYP2D6. An inverse correlation between the expression of miRNA hsa-miR-370-3p and the expression of CYP2D6 was observed in human liver tissue samples. Electrophoretic mobility shift assays confirmed that hsa-miR-370-3p was able to directly bind to its cognate target within the coding region of the CYP2D6 transcript. The transfection of hsa-miR-370-3p mimics into the HepG2(CYP2D6) cell line, a genetically modified cell line that overexpresses exogenous CYP2D6, was able to suppress the expression of CYP2D6 significantly at both mRNA and protein levels. The transfection of hsa-miR-370-3p mimics was also able to inhibit endogenous mRNA expression and/or protein production of CYP2D6 in HepaRG cells. Furthermore, in HepaRG, HepG2, and Huh7 cells, dexamethasone-induced expression of CYP2D6 was inhibited by hsa-miR-370-3p mimics. To investigate whether the miRNA mediated suppression is caused by inhibiting protein translation or promoting mRNA degradation, an actinomycin D assay was used to measure the stability of CYP2D6 transcripts. The results indicated that hsa-miR-370-3p mimics facilitated significantly the degradation of CYP2D6 mRNA. In addition, proteomics analyses of proteins isolated from the miRNA/mRNA/protein complex suggested that a group of multifunctional proteins facilitated the interaction between hsa-miR-370-3p and CYP2D6, thereby promoting mRNA degradation.

PMID: 28552654 [PubMed - as supplied by publisher]

Thiopurine S-Methyltransferase as a Pharmacogenetic Biomarker: Significance of Testing and Review of Major Methods.

Cardiovasc Hematol Agents Med Chem. 2017 May 28;:

Authors: Asadov C, Aliyeva G, Mustafayeva K

Abstract
Thiopurine S-methyltransferase (TPMT) enzyme metabolizes thiopurine drugs which are widely used in various disciplines as well as in leukemias. Individual enzyme activity varies depending on the genetic polymorphisms of TPMT gene located at chromosome 6. Up to 14% of population is known to have a decreased enzyme activity, and if treated with standard doses of thiopurines, these individuals are at the high risk of severe adverse drug reactions (ADR) as myelosuppression, gastrointestinal intolerance, pancreatitis and hypersensitivity. However, TPMT-deficient patients can successfully be treated with decreased thiopurine doses if enzyme status is identified by a prior testing. TPMT status identification is a pioneering experience in an application of a pharmacogenetic testing in clinical settings. 4 TPMT (*2,*3A, *3B, *3C) alleles are known to account for 80-95% of a decreased enzyme activity, and therefore, identifying the presence of these alleles supported by phenotypic measurement of the enzyme activity can reveal patient's TPMT status. Evaluation of the levels of thiopurine metabolites further supports the practice of appropriate dose adjustment by providing the efficient monitoring of drug cytotoxicity. We hereby review the thiopurine pharmacogenetics and the methods applied in common practice to evaluate patient's TPMT status.

PMID: 28552060 [PubMed - as supplied by publisher]

ABCB1 Polymorphisms and Cold Pressor Pain Responses: Opioid-Dependent Patients on Methadone Maintenance Therapy.

Nurs Res. 2017 Mar/Apr;66(2):134-144

Authors: Zahari Z, Lee CS, Ibrahim MA, Musa N, Mohd Yasin MA, Lee YY, Tan SC, Mohamad N, Ismail R

Abstract
BACKGROUND: Methadone is a substrate of the P-glycoprotein efflux transporter, which is encoded by ABCB1 (MDR1), and thus, ABCB1 polymorphisms may influence the transport of methadone at the blood-brain barrier, affecting its adverse effects.
OBJECTIVES: This study investigated the association between ABCB1 polymorphisms and cold pressor pain responses among opioid-dependent patients on methadone maintenance therapy (MMT).
METHODS: Malay male opioid-dependent patients receiving MMT (n = 148) were recruited. Cold pressor pain responses (pain threshold, pain tolerance, and pain intensity) were measured at 0, 2, 4, 8, 12, and 24 hours post-methadone dose. DNA was extracted from whole blood and genotyped for ABCB1 polymorphisms including 1236C>T (rs1128503), 2677G>T/A (rs2032582), and 3435C>T (rs1045642) using the allelic discrimination real-time polymerase chain reaction. Repeated-measure analysis of variance between-group analysis was used to compare the three cold pressor pain responses and ABCB1 polymorphisms (1236C>T, 2677G>T/A, and 3435C>T) according to genotypes and allelic additive models, genotype dominant and recessive models, haplotypes, and diplotypes.
RESULTS: Patients with 2677 GG or 2677G allele had the lowest pain threshold compared with 2677G>T/A genotypes or alleles (p = .007 and .002, respectively). Haplotype analysis showed a significant association between ABCB1 haplotypes and pain threshold (p = .02). Patients with 2677G allele had the lowest pain tolerance compared to those with 2677T and 2677A alleles (2677G < 2677T < 2677A allele carriers; p = .05). In terms of pain intensity scores, patients with 2677 GG or 2677G allele had the highest scores compared to other 2677G>T/A genotypes or alleles (p = .04 and .008, respectively). Haplotype analysis revealed a significant difference between patients with CGC haplotype and those without this haplotype (p = .02).
DISCUSSION: To the best of our knowledge, this study provides the first evidence that ABCB1 polymorphisms are associated with cold pressor pain responses among Malay male patients with opioid dependence on MMT. The results may provide an initial prediction on heightened pain sensitivity or hyperalgesia for individuals who are carriers of the ABCB1 polymorphisms.

PMID: 28252574 [PubMed - indexed for MEDLINE]

Designer Drugs 2.0.

Clin Pharmacol Ther. 2017 Feb;101(2):152-157

Authors: Huestis MA, Tyndale RF

Abstract
This "Designer Drugs 2.0" issue of Clinical Pharmacology & Therapeutics focuses on novel psychoactive substances, primarily cannabinoids and cathinones, and the repurposing of established psychoactive compounds (e.g., modafinil, psilocybin, lysergic acid diethylamide, and 3,4-methylenedioxymethamphetamine) that simultaneously offer new pharmacotherapies and pose serious health problems. Novel psychoactive substances were initially used as potent tools to investigate endogenous neurotransmitter systems; for example, synthetic cannabinoids have much higher potency than Δ9-tetrahydrocannabinol at the cannabinoid receptors. However, they are now being used illicitly as well as being tested for their efficacy in numerous clinical indications. Likewise, previously established psychoactive drugs are being repurposed as treatments for a wide variety of indications where currently approved medications are ineffective. This set of papers examines the arising problems associated with designer drugs (e.g., adverse events, psychosis, rapid new synthesis, abuse liability testing, internet sales, scheduling) as well as the potential therapeutic promises in areas as diverse as cognition enhancement, exercise-mimetics, epilepsy, multiple sclerosis, and posttraumatic stress disorder.

PMID: 28084644 [PubMed - indexed for MEDLINE]

Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer's disease.

Brain. 2017 Mar 01;140(3):813-825

Authors: Hayes JP, Logue MW, Sadeh N, Spielberg JM, Verfaellie M, Hayes SM, Reagan A, Salat DH, Wolf EJ, McGlinchey RE, Milberg WP, Stone A, Schichman SA, Miller MW

Abstract
Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. Whole-genome polygenic risk scores for the development of Alzheimer's disease were calculated using summary statistics from the largest Alzheimer's disease genome-wide association study to date. Results showed that mild traumatic brain injury moderated the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions. Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease was associated with cortical thinning as a function of time since injury. A moderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced episodic memory performance through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechanism for reduced memory performance. Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of causal effects cannot be inferred from cross-sectional studies. These results underscore the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.

PMID: 28077398 [PubMed - indexed for MEDLINE]

H2S-Donating Doxorubicins May Overcome Cardiotoxicity and Multidrug Resistance.

J Med Chem. 2016 May 26;59(10):4881-9

Authors: Chegaev K, Rolando B, Cortese D, Gazzano E, Buondonno I, Lazzarato L, Fanelli M, Hattinger CM, Serra M, Riganti C, Fruttero R, Ghigo D, Gasco A

Abstract
Doxorubicin (DOXO) is one of the most effective antineoplastic agents in clinical practice. Its use is limited by acute and chronic side effects, in particular by its cardiotoxicity and by the rapid development of resistance to it. As part of a program aimed at developing new DOXO derivatives endowed with reduced cardiotoxicity, and active against DOXO-resistant tumor cells, a series of H2S-releasing DOXOs (H2S-DOXOs) were obtained by combining DOXO with appropriate H2S donor substructures. The resulting compounds were studied on H9c2 cardiomyocytes and in DOXO-sensitive U-2OS osteosarcoma cells, as well as in related cell variants with increasing degrees of DOXO-resistance. Differently from DOXO, most of the products were not toxic at 5 μM concentration on H9c2 cells. A few of them triggered high activity on the cancer cells. H2S-DOXOs 10 and 11 emerged as the most interesting members of the series. The capacity of 10 to impair Pgp transporter is also discussed.

PMID: 27120394 [PubMed - indexed for MEDLINE]

β-Sitosterol Reduces the Expression of Chemotactic Cytokine Genes in Cystic Fibrosis Bronchial Epithelial Cells.

Front Pharmacol. 2017;8:236

Authors: Lampronti I, Dechecchi MC, Rimessi A, Bezzerri V, Nicolis E, Guerrini A, Tacchini M, Tamanini A, Munari S, D'Aversa E, Santangelo A, Lippi G, Sacchetti G, Pinton P, Gambari R, Agostini M, Cabrini G

Abstract
Extracts from Nigella arvensis L. seeds, which are widely used as anti-inflammatory remedies in traditional medicine of Northern Africa, were able to inhibit the expression of the pro-inflammatory neutrophil chemokine Interleukin (IL)-8 in Cystic Fibrosis (CF) bronchial epithelial IB3-1 cells exposed to the Gram-negative bacterium Pseudomonas aeruginosa. The chemical composition of the extracts led to the identification of three major components, β-sitosterol, stigmasterol, and campesterol, which are the most abundant phytosterols, cholesterol-like molecules, usually found in plants. β-sitosterol (BSS) was the only compound that significantly reproduced the inhibition of the P. aeruginosa-dependent expression of IL-8 at nanomolar concentrations. BSS was tested in CF airway epithelial CuFi-1 cells infected with P. aeruginosa. BSS (100 nM), showed a significant and consistent inhibitory activity on expression of the P. aeruginosa-stimulated expression chemokines IL-8, GRO-α GRO-β, which play a pivotal role in the recruitment of neutrophils in CF inflamed lungs. Preliminary mechanistic analysis showed that BSS partially inhibits the P. aeruginosa-dependent activation of Protein Kinase C isoform alpha, which is known to be involved in the transmembrane signaling activating IL-8 gene expression in bronchial epithelial cells. These data indicate BSS as a promising molecule to control excessive lung inflammation in CF patients.

PMID: 28553226 [PubMed - in process]

β1-Integrin Accumulates in Cystic Fibrosis Luminal Airway Epithelial Membranes and Decreases Sphingosine, Promoting Bacterial Infections.

Cell Host Microbe. 2017 May 25;:

Authors: Grassmé H, Henry B, Ziobro R, Becker KA, Riethmüller J, Gardner A, Seitz AP, Steinmann J, Lang S, Ward C, Schuchman EH, Caldwell CC, Kamler M, Edwards MJ, Brodlie M, Gulbins E

Abstract
Chronic pulmonary colonization with bacterial pathogens, particularly Pseudomonas aeruginosa, is the primary cause of morbidity and mortality in patients with cystic fibrosis (CF). We observed that β1-integrins accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with CF. β1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap β1-integrins on the luminal pole of bronchial epithelial cells. β1-integrins downregulate acid ceramidase expression, resulting in further accumulation of ceramide and consequent reduction of surface sphingosine, a lipid that kills bacteria. Interrupting this vicious cycle by triggering surface β1-integrin internalization via anti-β1-integrin antibodies or the RGD peptide ligand-or by genetic or pharmacological correction of ceramide levels-normalizes β1-integrin distribution and sphingosine levels in CF epithelial cells and prevents P. aeruginosa infection in CF mice. These findings suggest a therapeutic avenue to ameliorate CF-associated bacterial infections.

PMID: 28552668 [PubMed - as supplied by publisher]

Spirometry-Assisted High Resolution Chest Computed Tomography in Children: Is it Worth the Effort?

Curr Probl Diagn Radiol. 2017 Apr 07;:

Authors: Otjen JP, Swanson JO, Oron A, DiBlasi RM, Swortzel T, van Well JAM, Gommers EAE, Rosenfeld M

Abstract
BACKGROUND: Image quality of high resolution chest computed tomographies (HRCTs) depends on adequate breath holds at end inspiration and end expiration. We hypothesized that implementation of spirometry-assisted breath holds in children undergoing HRCTs would improve image quality over that obtained with voluntary breath holds by decreasing motion artifact and atelectasis.
METHODS: This is a retrospective case-control study of HRCTs obtained at a tertiary care children's hospital before and after implementation of a spirometry-assisted CT protocol, in which children ≥8 years of age are first trained in supine slow vital capacity maneuvers and then repeat the maneuvers in the CT scanner, coached by a respiratory therapist. Spirometry-assisted CT scans (cases) were matched by age, gender and diagnosis (cystic fibrosis vs other) to CT scans obtained with voluntary breath holds in the 6 years before implementation of the spirometry assistance protocol (controls), and evaluated by 2 blinded pediatric radiologists.
RESULTS: Among both cases and controls (N = 50 each), 10 carried the diagnosis of cystic fibrosis and 40 had other diagnoses. Mean age was 12.9 years (range: 7.5-20.1) among cases and 13.0 (7.1-19.7) among controls. Mean (SD) inspiratory image density among cases was -852 (37) Hounsfield units (HU) and -828 (43) among controls (p = 0.006). Mean (SD) expiratory image density was -629 (95) HU among cases and -688 (83) HU among controls (p = 0.002). Mean (SD) change in image density between inspiratory and expiratory images was +222 (85) HU among cases and +140 (76) HU among controls (p < 0.001). Motion artifact was present on inspiratory images in 5 cases and 9 controls (p = 0.39 by Fisher's exact test), and on expiratory images in 20 cases and 18 controls (p > 0.80). Atelectasis was present on inspiratory images in 8 cases and 9 controls and on expiratory images in 9 cases and 10 controls (p > 0.80).
CONCLUSIONS: Spirometry-assisted CTs had a significantly greater difference in lung density between inspiratory and expiratory scans than those performed with voluntary breath holds, likely improving the ability to detect air trapping. No appreciable difference in image quality was detected for the presence of motion artifact or atelectasis.

PMID: 28552547 [PubMed - as supplied by publisher]

Bacteriology and treatment of infections in the upper and lower airways in patients with primary ciliary dyskinesia: adressing the paranasal sinuses.

Dan Med J. 2017 May;64(5):

Authors: Alanin MC

Abstract
The respiratory tract is lined with motile cilia that transport respiratory mucus. Primary ciliary dyskinesia (PCD) is a chronic genetic disease caused by mutations in genes responsible for ciliary structure and function. Non-functional airway cilia impair the mucociliary clearance (MCC), causing mucostasis, lung infections and destruction, chronic rhinosinusitis (CRS) and hearing impairment. It is of paramount importance to postpone chronic lung infection mainly with Gram-negative bacteria (GNB) in patients with an impaired MCC. When successful, lung function can be stabilized and quality of life (QoL) improved. In this thesis, we evaluated whether PCD patients can benefit from the experience we have gained from our operative approach towards the paranasal sinuses in cystic fibrosis (CF) patients. In CF, it has been established that bacterial sinusitis can be a focus for initial lung colonization and chronic lung infection. Combined endoscopic sinus surgery (ESS) and adjuvant therapy can eradicate sinus bacteria, reduce pulmonary infections and improve quality of life (QoL).      Currently, approximately 120 patients are diagnosed with PCD in Denmark and all are affiliated with the Danish PCD Centre. Patients included in this thesis were recruited from this cohort. In papers (I, IV), we found that the most frequent sinus pathogen was P. aeruginosa, which was isolated in 12 out of 31 (39%) patients who underwent ESS. In searching for a non-pulmonary infectious focus, we observed simultaneous sinus and lung infec-tions with identical pathogens in two out of three patients. This supports our hypothesis of a bacterial reservoir in the sinuses. Next (II), we examined the bacterial flora associated with acute and chronic pulmonary infections in PCD. A high prevalence of chronic infections encouraged a search for new treatment regimens, including ESS with adjuvant therapy, to impact the course of infection. We revealed that P. aeruginosa frequently colonizes the airways in PCD and during the 11-year study period a total of 42 out of 107 (39%) patients fulfilled the definition of chronic lung infection at some point. Importantly, 10 out of 12 patients (83%) with chronic lung infection had the same clone type of P. aeruginosa for years, as determined by pulsed field gel-electrophoresis (PFGE), thus substantiating factual chronic airway infection. Further, we found an increase in the prevalence of P. aeruginosa with age and observed a negative association between early PCD diagnosis and prevalence of P. aeruginosa. This indicates a positive effect of early diagnosis and initiation of therapy. In paper (III), we performed whole genome sequencing (WGS) of P. aeruginosa isolated from the same 12 patients who were included in the PFGE analysis in paper II. By sequencing and phenotypically characterizing multiple isolates from the same patients we were able to study the with-in host bacterial evolution for the first time in PCD. The analyses provided detailed insight into how P. aeruginosa evolves in PCD when they are stressed by the host immune system and antibiotics. We verified the persistence of clonal lineages and confirmed that different clone types of P. aeruginosa can establish persistent infections in PCD patients. Further, we showed that P. aeruginosa acclimatizes grad-ually to the PCD airway by accumulating pathoadaptive mutations and phenotypic characteristics similar to those of CF. Such information may provide valuable clinical information, and as an example we identified mutations in genes responsible for the development of antibiotic resistance. Based on our research we conclude that P. aeruginosa is a major pathogen in PCD and that future research should focus on pre-venting or eradicating these bacteria. Implementing ESS with adjuvant therapy to PCD patients (I, IV) significantly ameliorated CRS symptoms. Further, postoperatively patients tended to have fewer positive lower airway cultures and better lung function; approximately one out of four operated patients, in search of an infectious focus, remained free of lung colonization with P. aeruginosa during follow-up for at least six months. Based on these results, it is tempting to speculate that ESS with adjuvant therapy can eradicate sinus bacteria and thereby reduce lung re-colonization from the sinuses. However, further evidence is needed to support this hypothesis, preferably from a multicentre randomized controlled trial.

PMID: 28552099 [PubMed - in process]

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"Rare Diseases"[Mesh] OR "orphan disease"

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(exome OR "exome sequencing") AND disease

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"systems biology"

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("drug-induced" OR "drug-related") AND ("adverse events" OR "side effects" OR "side-effects")

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Low-dose methotrexate in myeloproliferative neoplasm models.

Haematologica. 2017 May 26;:

Authors: Chinnaiya K, Lawson MA, Thomas S, Haider MT, Down J, Chantry AD, Hughes D, Green A, Sayers JR, Snowden JA, Zeidler MP

PMID: 28550185 [PubMed - as supplied by publisher]

"gnparser": a powerful parser for scientific names based on Parsing Expression Grammar.

BMC Bioinformatics. 2017 May 26;18(1):279

Authors: Mozzherin DY, Myltsev AA, Patterson DJ

Abstract
BACKGROUND: Scientific names in biology act as universal links. They allow us to cross-reference information about organisms globally. However variations in spelling of scientific names greatly diminish their ability to interconnect data. Such variations may include abbreviations, annotations, misspellings, etc. Authorship is a part of a scientific name and may also differ significantly. To match all possible variations of a name we need to divide them into their elements and classify each element according to its role. We refer to this as 'parsing' the name. Parsing categorizes name's elements into those that are stable and those that are prone to change. Names are matched first by combining them according to their stable elements. Matches are then refined by examining their varying elements. This two stage process dramatically improves the number and quality of matches. It is especially useful for the automatic data exchange within the context of "Big Data" in biology.
RESULTS: We introduce Global Names Parser (gnparser). It is a Java tool written in Scala language (a language for Java Virtual Machine) to parse scientific names. It is based on a Parsing Expression Grammar. The parser can be applied to scientific names of any complexity. It assigns a semantic meaning (such as genus name, species epithet, rank, year of publication, authorship, annotations, etc.) to all elements of a name. It is able to work with nested structures as in the names of hybrids. gnparser performs with ≈99% accuracy and processes 30 million name-strings/hour per CPU thread. The gnparser library is compatible with Scala, Java, R, Jython, and JRuby. The parser can be used as a command line application, as a socket server, a web-app or as a RESTful HTTP-service. It is released under an Open source MIT license.
CONCLUSIONS: Global Names Parser (gnparser) is a fast, high precision tool for biodiversity informaticians and biologists working with large numbers of scientific names. It can replace expensive and error-prone manual parsing and standardization of scientific names in many situations, and can quickly enhance the interoperability of distributed biological information.

PMID: 28549446 [PubMed - in process]

Incidence and triggers of Stevens-Johnson syndrome and toxic epidermal necrolysis in a large cancer patient cohort.

J Invest Dermatol. 2017 May 23;:

Authors: Gillis NK, Hicks JK, Bell GC, Daly AJ, Kanetsky PA, McLeod HL

PMID: 28549953 [PubMed - as supplied by publisher]