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"systems biology"

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11 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results:

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

These pubmed results were generated on 2018/02/21

PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Do Cancer Drugs Counteract Neurodegeneration? Repurposing for Alzheimer's Disease.

J Alzheimers Dis. 2017;55(4):1295-1306

Authors: Monacelli F, Cea M, Borghi R, Odetti P, Nencioni A

Abstract
In spite of in depth investigations in the field of the amyloid cascade hypothesis, so far, no disease modifying therapy has been developed for Alzheimer's disease (AD). The pathophysiology provides some evidence of the inverse correlation between cancer and AD. Both AD and cancer are characterized by abnormal cellular behaviors; trigger factors along with a meta synchronously action is expected to drive cancer or neurodegeneration, supporting, respectively, progressive neuronal loss or uncontrolled cell proliferation in cancer cells. So far, cancer and AD are seemingly two opposite ends of the same biological spectrum. Basic science increasingly indicates shared molecular mechanisms between cancer and AD and gives weight to key relevant biological theories; according to them, the inverse tuning of clustered gene expression, the sharing of mutual independent pathway or the deregulated unfolded proteins system (UPR) may count for this inverse association. Additionally, the common biological background gave credibility to the recent discovery of a repurposing role for cancer drugs in AD. It refers to the development of new uses for existing pharmaceuticals having the same role as the original mechanism or to the discovery of a new drug action with disease modifying effects. The present review summarizes the most important biological theories that link neurodegeneration and cancer and provides an up-to-date revision of the repurposing cancer agents for AD. The review also addresses the gap of knowledge, since drug cancer repositioning holds an important promise but further investigations are warranted to ascertain the clinical relevance of such attractive clinical candidate compounds for AD.

PMID: 27834781 [PubMed - indexed for MEDLINE]

Repurposing phenformin for the targeting of glioma stem cells and the treatment of glioblastoma.

Oncotarget. 2016 Aug 30;7(35):56456-56470

Authors: Jiang W, Finniss S, Cazacu S, Xiang C, Brodie Z, Mikkelsen T, Poisson L, Shackelford DB, Brodie C

Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor with poor prognosis. Here, we studied the effects of phenformin, a mitochondrial complex I inhibitor and more potent chemical analog of the diabetes drug metformin on the inhibition of cell growth and induction of apoptosis of glioma stem cells (GSCs) using both in vitro and in vivo models. Phenformin inhibited the self-renewal of GSCs, decreased the expression of stemness and mesenchymal markers and increased the expression of miR-124, 137 and let-7. Silencing of let-7 abrogated phenformin effects on the self-renewal of GSCs via a pathway associated with inhibition of H19 and HMGA2 expression. Moreover, we demonstrate that phenformin inhibited tumor growth and prolonged the overall survival of mice orthotopically transplanted with GSCs. Combined treatments of phenformin and temozolomide exerted an increased antitumor effect on GSCs in vitro and in vivo. In addition, dichloroacetate, an inhibitor of the glycolysis enzyme pyruvate dehydrogenase kinase, that decreases lactic acidosis induced by biguanides, enhanced phenformin effects on the induction of cell death in GSCs and prolonged the survival of xenograft-bearing mice. Our results demonstrate for the first time that phenformin targets GSCs and can be efficiently combined with current therapies for GBM treatment and GSC eradication.

PMID: 27486821 [PubMed - indexed for MEDLINE]

FATCO Syndrome (Fibular Aplasia, Tibial Campomelia, Oligosyndactyly with Talar Aplasia). A Case Study.

Ortop Traumatol Rehabil. 2017 Jan 26;19(1):75-78

Authors: Ahmad K, Ahmad Malla H, Dawood S

Abstract
FATCO syndrome consists of fibular hemimelia, tibial campomelia and oligosyndactyly. FATCO syndrome can also be associated with other congenital anomalies; therefore, every case needs thorough evaluation so as to make the management of the patient easier. A few cases of this syndrome have been described in literature but only two cases have been reported in India so far. We present a 3-year-old male child born of a non-con-sanguinous marriage with FATCO syndrome and ipilateral talar aplasia without any other congenital anomalies.

PMID: 28436373 [PubMed - indexed for MEDLINE]

Evaluating the Calling Performance of a Rare Disease NGS Panel for Single Nucleotide and Copy Number Variants.

Mol Diagn Ther. 2017 Jun;21(3):303-313

Authors: Cacheiro P, Ordóñez-Ugalde A, Quintáns B, Piñeiro-Hermida S, Amigo J, García-Murias M, Pascual-Pascual SI, Grandas F, Arpa J, Carracedo A, Sobrido MJ

Abstract
INTRODUCTION: Variant detection protocols for clinical next-generation sequencing (NGS) need application-specific optimization. Our aim was to analyze the performance of single nucleotide variant (SNV) and copy number (CNV) detection programs on an NGS panel for a rare disease.
METHODS: Thirty genes were sequenced in 83 patients with hereditary spastic paraplegia. The variant calls obtained with LifeScope, GATK UnifiedGenotyper and GATK HaplotypeCaller were compared with Sanger sequencing. The calling efficiency was evaluated for 187 (56 unique) SNVs and indels. Five multiexon deletions detected by multiple ligation probe assay were assessed from the NGS panel data with ExomeDepth, panelcn.MOPS and CNVPanelizer software.
RESULTS: There were 48/51 (94%) SNVs and 1/5 (20%) indels consistently detected by all the calling algorithms. Two SNVs were not detected by any of the callers because of a rare reference allele, and one SNV in a low coverage region was only detected by two algorithms. Regarding CNVs, ExomeDepth detected 5/5 multi-exon deletions, panelcn.MOPs 4/5 and only 3/5 deletions were accurately detected by CNVPanelizer.
CONCLUSIONS: The calling efficiency of NGS algorithms for SNVs is influenced by variant type and coverage. NGS protocols need to account for the presence of rare variants in the reference sequence as well as for ambiguities in indel calling. CNV detection algorithms can be used to identify large deletions from NGS panel data for diagnostic applications; however, sensitivity depends on coverage, selection of the reference set and deletion size. We recommend the incorporation of several variant callers in the NGS pipeline to maximize variant detection efficiency.

PMID: 28290094 [PubMed - indexed for MEDLINE]

[The place of neuropathy in the early diagnosis of Cockayne syndrome: Report on two siblings].

Arch Pediatr. 2017 Apr;24(4):353-359

Authors: Blin-Rochemaure N, Allani-Essid N, Carlier R, Laugel V, Quijano-Roy S

Abstract
Two siblings affected with Cockayne syndrome (CS) are described: this diagnosis was suggested by the finding of a demyelinating neuropathy on electromyography in both children and consistent clinical features. CS is a rare genetic disorder with severe prognosis and a highly varied phenotype, making early diagnosis difficult. Taking into account these two cases and the literature, the current diagnosis criteria are insufficiently specific and appear late: the diagnosis may be delayed because multi-organ involvement and sensorial impairment suggests more frequent neurometabolic disorders. Neuroradiologic abnormalities are suggestive but may occur later. The finding of a demyelinating peripheral neuropathy seems to be a more useful marker to suspect this disorder in the presence of other clinical features. Further studies are required to better define the chronology of the symptoms, not only for adequate genetic counseling and eventual prenatal diagnosis, but also to assess the efficacy of future therapies.

PMID: 28258862 [PubMed - indexed for MEDLINE]

[Chronic vulvar lymphedema revealing Crohn disease in a teenage girl].

Arch Pediatr. 2017 Apr;24(4):346-349

Authors: Aounallah A, Ghariani Fetoui N, Ksiaa M, Boussofara L, Saidi W, Mokni S, Sriha B, Belajouza C, Denguezli M, Ghariani N, Nouira R

Abstract
INTRODUCTION: Cutaneous Crohn disease is a rare cutaneous manifestation of Crohn disease in children. Herein is reported a case of persistent vulvar lymphedema revealing Crohn disease in a teenage girl.
CASE REPORT: A 14-year-old girl presented with an 8-month history of persistent vulvar swelling associated with chronic macrocheilia. Dermatologic examination showed an inflammatory vulvar lymphedema, associated with perianal fissures and hypertrophic gingivitis. Vulvar skin biopsy revealed non-necrotizing granulomatous inflammation. Gastrointestinal endoscopy yielded no significant findings. The diagnosis of Crohn disease presenting as vulvar lymphedema was established. Oral metronidazole therapy resulted in partial improvement of cutaneous lesions beginning the 1st week.
CONCLUSION: The originality of this case lies in the presentation of chronic macrocheilia with persistent vulvar lymphedema in a child, revealing Crohn disease without gastrointestinal involvement.

PMID: 28233720 [PubMed - indexed for MEDLINE]

[A Rare Form of Oral Leukoplakia].

Laryngorhinootologie. 2017 01;96(1):43-44

Authors: Steinbichler TB, Moser P, Dudas J, Gassner R, Riechelmann H

PMID: 27978585 [PubMed - indexed for MEDLINE]

Design and Implementation of e-Health System Based on Semantic Sensor Network Using IETF YANG.

Sensors (Basel). 2018 Feb 20;18(2):

Authors: Jin W, Kim DH

Abstract
Recently, healthcare services can be delivered effectively to patients anytime and anywhere using e-Health systems. e-Health systems are developed through Information and Communication Technologies (ICT) that involve sensors, mobiles, and web-based applications for the delivery of healthcare services and information. Remote healthcare is an important purpose of the e-Health system. Usually, the eHealth system includes heterogeneous sensors from diverse manufacturers producing data in different formats. Device interoperability and data normalization is a challenging task that needs research attention. Several solutions are proposed in the literature based on manual interpretation through explicit programming. However, programmatically implementing the interpretation of the data sender and data receiver in the e-Health system for the data transmission is counterproductive as modification will be required for each new device added into the system. In this paper, an e-Health system with the Semantic Sensor Network (SSN) is proposed to address the device interoperability issue. In the proposed system, we have used IETF YANG for modeling the semantic e-Health data to represent the information of e-Health sensors. This modeling scheme helps in provisioning semantic interoperability between devices and expressing the sensing data in a user-friendly manner. For this purpose, we have developed an ontology for e-Health data that supports different styles of data formats. The ontology is defined in YANG for provisioning semantic interpretation of sensing data in the system by constructing meta-models of e-Health sensors. The proposed approach assists in the auto-configuration of eHealth sensors and querying the sensor network with semantic interoperability support for the e-Health system.

PMID: 29461493 [PubMed - in process]

Semantic network analysis of vaccine sentiment in online social media.

Vaccine. 2017 Jun 22;35(29):3621-3638

Authors: Kang GJ, Ewing-Nelson SR, Mackey L, Schlitt JT, Marathe A, Abbas KM, Swarup S

Abstract
OBJECTIVE: To examine current vaccine sentiment on social media by constructing and analyzing semantic networks of vaccine information from highly shared websites of Twitter users in the United States; and to assist public health communication of vaccines.
BACKGROUND: Vaccine hesitancy continues to contribute to suboptimal vaccination coverage in the United States, posing significant risk of disease outbreaks, yet remains poorly understood.
METHODS: We constructed semantic networks of vaccine information from internet articles shared by Twitter users in the United States. We analyzed resulting network topology, compared semantic differences, and identified the most salient concepts within networks expressing positive, negative, and neutral vaccine sentiment.
RESULTS: The semantic network of positive vaccine sentiment demonstrated greater cohesiveness in discourse compared to the larger, less-connected network of negative vaccine sentiment. The positive sentiment network centered around parents and focused on communicating health risks and benefits, highlighting medical concepts such as measles, autism, HPV vaccine, vaccine-autism link, meningococcal disease, and MMR vaccine. In contrast, the negative network centered around children and focused on organizational bodies such as CDC, vaccine industry, doctors, mainstream media, pharmaceutical companies, and United States. The prevalence of negative vaccine sentiment was demonstrated through diverse messaging, framed around skepticism and distrust of government organizations that communicate scientific evidence supporting positive vaccine benefits.
CONCLUSION: Semantic network analysis of vaccine sentiment in online social media can enhance understanding of the scope and variability of current attitudes and beliefs toward vaccines. Our study synthesizes quantitative and qualitative evidence from an interdisciplinary approach to better understand complex drivers of vaccine hesitancy for public health communication, to improve vaccine confidence and vaccination coverage in the United States.

PMID: 28554500 [PubMed - indexed for MEDLINE]

N-acetylcysteine in a Double-Blind Randomized Placebo-Controlled Trial: Toward Biomarker-Guided Treatment in Early Psychosis.

Schizophr Bull. 2018 Feb 15;44(2):317-327

Authors: Conus P, Seidman LJ, Fournier M, Xin L, Cleusix M, Baumann PS, Ferrari C, Cousins A, Alameda L, Gholam-Rezaee M, Golay P, Jenni R, Woo TW, Keshavan MS, Eap CB, Wojcik J, Cuenod M, Buclin T, Gruetter R, Do KQ

Abstract
Biomarker-guided treatments are needed in psychiatry, and previous data suggest oxidative stress may be a target in schizophrenia. A previous add-on trial with the antioxidant N-acetylcysteine (NAC) led to negative symptom reductions in chronic patients. We aim to study NAC's impact on symptoms and neurocognition in early psychosis (EP) and to explore whether glutathione (GSH)/redox markers could represent valid biomarkers to guide treatment. In a double-blind, randomized, placebo-controlled trial in 63 EP patients, we assessed the effect of NAC supplementation (2700 mg/day, 6 months) on PANSS, neurocognition, and redox markers (brain GSH [GSHmPFC], blood cells GSH levels [GSHBC], GSH peroxidase activity [GPxBC]). No changes in negative or positive symptoms or functional outcome were observed with NAC, but significant improvements were found in favor of NAC on neurocognition (processing speed). NAC also led to increases of GSHmPFC by 23% (P = .005) and GSHBC by 19% (P = .05). In patients with high-baseline GPxBC compared to low-baseline GPxBC, subgroup explorations revealed a link between changes of positive symptoms and changes of redox status with NAC. In conclusion, NAC supplementation in a limited sample of EP patients did not improve negative symptoms, which were at modest baseline levels. However, NAC led to some neurocognitive improvements and an increase in brain GSH levels, indicating good target engagement. Blood GPx activity, a redox peripheral index associated with brain GSH levels, could help identify a subgroup of patients who improve their positive symptoms with NAC. Thus, future trials with antioxidants in EP should consider biomarker-guided treatment.

PMID: 29462456 [PubMed - in process]

The Impact of NOD2 Variants on Fecal Microbiota in Crohn's Disease and Controls Without Gastrointestinal Disease.

Inflamm Bowel Dis. 2018 Feb 15;24(3):583-592

Authors: Kennedy NA, Lamb CA, Berry SH, Walker AW, Mansfield J, Parkes M, Simpkins R, Tremelling M, Nutland S, UK IBD Genetics Consortium, Parkhill J, Probert C, Hold GL, Lees CW

Abstract
Background/Aims: Current models of Crohn's disease (CD) describe an inappropriate immune response to gut microbiota in genetically susceptible individuals. NOD2 variants are strongly associated with development of CD, and NOD2 is part of the innate immune response to bacteria. This study aimed to identify differences in fecal microbiota in CD patients and non-IBD controls stratified by NOD2 genotype.
Methods: Patients with CD and non-IBD controls of known NOD2 genotype were identified from patients in previous UK IBD genetics studies and the Cambridge bioresource (genotyped/phenotyped volunteers). Individuals with known CD-associated NOD2 mutations were matched to those with wild-type genotype. We obtained fecal samples from patients in clinical remission with low fecal calprotectin (<250 µg/g) and controls without gastrointestinal disease. After extracting DNA, the V1-2 region of 16S rRNA genes were polymerase chain reaction (PCR)-amplified and sequenced. Analysis was undertaken using the mothur package. Volatile organic compounds (VOC) were also measured.
Results: Ninety-one individuals were in the primary analysis (37 CD, 30 bioresource controls, and 24 household controls). Comparing CD with nonIBD controls, there were reductions in bacterial diversity, Ruminococcaceae, Rikenellaceae, and Christensenellaceae and an increase in Enterobacteriaceae. No significant differences could be identified in microbiota by NOD2 genotype, but fecal butanoic acid was higher in Crohn's patients carrying NOD2 mutations.
Conclusions: In this well-controlled study of NOD2 genotype and fecal microbiota, we identified no significant genotype-microbiota associations. This suggests that the changes associated with NOD2 genotype might only be seen at the mucosal level, or that environmental factors and prior inflammation are the predominant determinant of the observed dysbiosis in gut microbiota.

PMID: 29462388 [PubMed - in process]

Improving stability of prediction models based on correlated omics data by using network approaches.

PLoS One. 2018;13(2):e0192853

Authors: Tissier R, Houwing-Duistermaat J, Rodríguez-Girondo M

Abstract
Building prediction models based on complex omics datasets such as transcriptomics, proteomics, metabolomics remains a challenge in bioinformatics and biostatistics. Regularized regression techniques are typically used to deal with the high dimensionality of these datasets. However, due to the presence of correlation in the datasets, it is difficult to select the best model and application of these methods yields unstable results. We propose a novel strategy for model selection where the obtained models also perform well in terms of overall predictability. Several three step approaches are considered, where the steps are 1) network construction, 2) clustering to empirically derive modules or pathways, and 3) building a prediction model incorporating the information on the modules. For the first step, we use weighted correlation networks and Gaussian graphical modelling. Identification of groups of features is performed by hierarchical clustering. The grouping information is included in the prediction model by using group-based variable selection or group-specific penalization. We compare the performance of our new approaches with standard regularized regression via simulations. Based on these results we provide recommendations for selecting a strategy for building a prediction model given the specific goal of the analysis and the sizes of the datasets. Finally we illustrate the advantages of our approach by application of the methodology to two problems, namely prediction of body mass index in the DIetary, Lifestyle, and Genetic determinants of Obesity and Metabolic syndrome study (DILGOM) and prediction of response of each breast cancer cell line to treatment with specific drugs using a breast cancer cell lines pharmacogenomics dataset.

PMID: 29462177 [PubMed - in process]

SNPs and STRs in forensic medicine. A strategy for kinship evaluation.

Arch Med Sadowej Kryminol. 2017;67(3):226-240

Authors: Pontes L, Sousa JC, Medeiros R

Abstract
Some emerging technologies are used as strategies for the analyses of single nucleotide polymorphisms (SNPs) that have attracted much interest in recent years, applied to various scientific areas. They have been extensively used as markers to identify genes that underlie complex diseases and also to realize the potential of pharmacogenomics in relation to different drug responses. Additionally, SNPs have been shown to be very useful in forensic genetics resolving all kinds of legal problems, namely crime cases, disaster victim identification and paternity and kinship investigation testing. The low mutation rate of SNPs, makes these markers very suitable for relationship testing. In the great majority of the cases, analyses with the widely used sets of STR markers provide powerful statistical evidence but some of them remain with ambiguous results. Those include cases with complex pedigrees or cases with some problems, like mutations, that are inherent to the use of STRs. At this time several forensic laboratories are using SNPs especially to complement the study of STRs in some of their casework cases. This paper intends to analyze some of our casework examples and to providea data update on the joint use of STRs and autosomal SNPs in the evaluation and kinship calculation, one of the strategies currently used for this purpose, namely reviewing and comparing results published by various working groups.

PMID: 29460612 [PubMed - in process]

Research directions in the clinical implementation of pharmacogenomics - An Overview of US programs and projects.

Clin Pharmacol Ther. 2018 Feb 20;:

Authors: Volpi S, Bult C, Chisholm RL, Deverka PA, Ginsburg GS, Jacob HJ, Kasapi M, McLeod HL, Roden DM, Williams MS, Green ED, Lyman Rodriguez L, Aronson S, Cavallari LH, Denny JC, Dressler L, Johnson JA, Klein TE, Steven Leeder J, Piquette-Miller M, Perera M, Rasmussen-Torvik LJ, Rehm HL, Ritchie MD, Skaar TC, Wagle N, Weinshilboum R, Weitzel KW, Wildin R, Wilson J, Manolio TA, Relling MV

Abstract
Response to a drug often differs widely among individual patients. This variability is frequently observed not only with respect to effective responses but also with adverse drug reactions. Matching patients to the drugs that are most likely to be effective and least likely to cause harm is the goal of effective therapeutics. Pharmacogenomics (PGx) holds the promise of precision medicine through elucidating the genetic determinants responsible for pharmacological outcomes and using them to guide drug selection and dosing. Here, we survey the US landscape of research programs in PGx implementation, review current advances and clinical applications of PGx, summarize the obstacles that have hindered PGx implementation, and identify the critical knowledge gaps and possible studies needed to help to address them. This article is protected by copyright. All rights reserved.

PMID: 29460415 [PubMed - as supplied by publisher]

Pharmacogenetic information in clinical guidelines - the European perspective.

Clin Pharmacol Ther. 2018 Feb 20;:

Authors: Swen JJ, Nijenhuis M, van Rhenen M, de Boer-Veger NJ, Buunk AM, Houwink EJF, Mulder H, Rongen GA, van Schaik RHN, van der Weide J, Wilffert B, Deneer VHM, Guchelaar HJ, Dutch Pharmacogenetics Working Group (DPWG) of the Royal Dutch Pharmacists Association (KNMP)

PMID: 29460273 [PubMed - as supplied by publisher]

Operationalizing the Reciprocal Engagement Model of Genetic Counseling Practice: a Framework for the Scalable Delivery of Genomic Counseling and Testing.

J Genet Couns. 2018 Feb 19;:

Authors: Schmidlen T, Sturm AC, Hovick S, Scheinfeldt L, Scott Roberts J, Morr L, McElroy J, Toland AE, Christman M, O'Daniel JM, Gordon ES, Bernhardt BA, Ormond KE, Sweet K

Abstract
With the advent of widespread genomic testing for diagnostic indications and disease risk assessment, there is increased need to optimize genetic counseling services to support the scalable delivery of precision medicine. Here, we describe how we operationalized the reciprocal engagement model of genetic counseling practice to develop a framework of counseling components and strategies for the delivery of genomic results. This framework was constructed based upon qualitative research with patients receiving genomic counseling following online receipt of potentially actionable complex disease and pharmacogenomics reports. Consultation with a transdisciplinary group of investigators, including practicing genetic counselors, was sought to ensure broad scope and applicability of these strategies for use with any large-scale genomic testing effort. We preserve the provision of pre-test education and informed consent as established in Mendelian/single-gene disease genetic counseling practice. Following receipt of genomic results, patients are afforded the opportunity to tailor the counseling agenda by selecting the specific test results they wish to discuss, specifying questions for discussion, and indicating their preference for counseling modality. The genetic counselor uses these patient preferences to set the genomic counseling session and to personalize result communication and risk reduction recommendations. Tailored visual aids and result summary reports divide areas of risk (genetic variant, family history, lifestyle) for each disease to facilitate discussion of multiple disease risks. Post-counseling, session summary reports are actively routed to both the patient and their physician team to encourage review and follow-up. Given the breadth of genomic information potentially resulting from genomic testing, this framework is put forth as a starting point to meet the need for scalable genetic counseling services in the delivery of precision medicine.

PMID: 29460110 [PubMed - as supplied by publisher]

Leptospirosis in human: Biomarkers in host immune responses.

Microbiol Res. 2018 Mar;207:108-115

Authors: Vk C, Ty L, Wf L, Ywy WS, An S, S Z, A M

Abstract
Leptospirosis remains one of the most widespread zoonotic diseases caused by spirochetes of the genus Leptospira, which accounts for high morbidity and mortality globally. Leptospiral infections are often found in tropical and subtropical regions, with people exposed to contaminated environments or animal reservoirs are at high risk of getting the infection. Leptospirosis has a wide range of clinical manifestations with non-specific signs and symptoms and often misdiagnosed with other acute febrile illnesses at early stage of infection. Despite being one of the leading causes of zoonotic morbidity worldwide, there is still a gap between pathogenesis and human immune responses during leptospiral infection. It still remains obscure whether the severity of the infection is caused by the pathogenic properties of the Leptospira itself, or it is a consequence of imbalance host immune factors. Hence, in this review, we seek to summarize the past and present milestone findings on the biomarkers of host immune response aspects during human leptospiral infection, including cytokine and other immune mediators. A profound understanding of the interlink between virulence factors and host immune responses during human leptospirosis is imperative to identify potential biomarkers for diagnostic and prognostic applications as well as designing novel immunotherapeutic strategies in future.

PMID: 29458845 [PubMed - in process]

[Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis].

Adv Gerontol. 2016;29(4):646-650

Authors: Kozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VK, Dyakonov MM, Kozina LS

Abstract
Peptide KED (Lys-Glu-Asp) has vasoprotective effects and is effective substance in treatment of of atherosclerosis and other cardio-vascular disorders in elderly people. One of the probable mechanisms of biological activity of this peptide is epigenetic genes regulation. These genes can coding proteins, which are markers of endothelium functional activity. The goal of investigation was to study the KED peptide effect on signal molecules expression in normal, atherosclerotic and restenotic endothelium in vitro. It was shown, that KED peptide has normalized endothelin-1 expression, which increased during atherosclerosis and restenosis. KED peptide also restorates cells interactions by connexin expression. Geroprotective effect of KED peptide is realized by increasing of sirtuin1 expression, which has took part in DNA reparation.

PMID: 28539025 [PubMed - indexed for MEDLINE]