Radiation Protective Effects of Baclofen Predicted by a Computational Drug Repurposing Strategy.

Pharmacol Res. 2016 Sep 21;

Authors: Ren L, Xie D, Li P, Qu X, Zhang X, Xing Y, Zhou P, Bo X, Zhou Z, Wang S

Abstract
Exposure to ionizing radiation causes damage to living tissues; however, only a small number of agents have been approved for use in radiation injuries. Radioprotector is the primary countermeasure to radiation injury and none radioprotector has indeed reached the drug development stage. Repurposing the long list of approved, non-radioprotective drugs is an attractive strategy to find new radioprotective agents. Here, we applied a computational approach to discover new radioprotectors in silico by comparing publicly available gene expression data of ionizing radiation-treated samples from the Gene Expression Omnibus (GEO) database with gene expression signatures of more than 1,309 small-molecule compounds from the Connectivity Map (cmap) dataset. Among the best compounds predicted to be therapeutic for ionizing radiation damage by this approach were some previously reported radioprotectors and baclofen (P<0.01), a chemical that was not previously used as radioprotector. Validation using a cell-based model and a rodent in vivo model demonstrated that treatment with baclofen reduced radiation-induced cytotoxicity in vitro (P<0.01), attenuated bone marrow damage and increased survival in vivo (P<0.05). These findings suggest that baclofen might serve as a radioprotector. The drug repurposing strategy by connecting the GEO data and cmap can be used to identify known drugs as potential radioprotective agents.

PMID: 27664700 [PubMed - as supplied by publisher]

In Silico Prediction and In Vitro and In Vivo Validation of Acaricide Fluazuron as a Potential Inhibitor of FGFR3 and a Candidate Anticancer Drug for Bladder Carcinoma.

Chem Biol Drug Des. 2016 Sep 24;

Authors: Ke K, Li H, Yao H, Shi XN, Dong C, Zhu Y, Liu X, Li L, Leung KS, Wong MH, Liu XD, Kung HF, Lin MC

Abstract
Bladder carcinoma (BC) is the 9(th) most common cause of cancer worldwide. Surgical resection and conventional chemotherapy and radiotherapy will ultimately fail due to tumor recurrence and resistance. Thus, the development of novel treatment is urgently needed. Fibroblast growth factor receptor 3 (FGFR3) is an important and well-established target for BC treatment. In this study, we utilized the free and open-source protein-ligand docking software idock to prospectively identify potential inhibitors of FGFR3 from 3167 worldwide approved small-molecule drugs using a repositioning strategy. Six high-scoring compounds were purchased and tested in vitro. Among them, the acaricide drug fluazuron exhibited the highest anti-proliferative effect in human BC cell lines RT112 and RT4. We further demonstrated that fluazuron treatment significantly increased the percentage of apoptosis cells, decreased the phosphorylation level of FGFR3 and its downstream proteins FRS2-α, AKT and ERK. We also investigated the anticancer effect of fluazuron in vivo in BALB/C nude mice subcutaneously xenografted with RT112 cells. Our results showed that oral treatment with fluazuron (80mg/kg) significantly inhibited tumor growth. These results suggested for the first time that fluazuron is a potential inhibitor of FGFR3 and a candidate anticancer drug for the treatment of BC. This article is protected by copyright. All rights reserved.

PMID: 27664399 [PubMed - as supplied by publisher]

Poly(ADP-ribose)polymerase is not involved in the neuroprotection exerted by azithromycin against ischemic stroke in mice.

Eur J Pharmacol. 2016 Sep 20;

Authors: Petrelli F, Muzzi M, Chiarugi A, Bagetta G, Amantea D

Abstract
Repurposing azithromycin has recently emerged as a promising strategy for the acute treatment of ischemic stroke. The mechanism of neuroprotection depends on the ability of this macrolide to promote polarization of microglia/macrophages towards beneficial M2 phenotypes. The immunomodulatory and anti-inflammatory effects of azithromycin, well documented in chronic inflammatory airway diseases, have been ascribed to the inhibition of the transcription factors nuclear factor (NF)-κB and activator protein (AP)-1. Since these inflammatory transcription factors are positively regulated by poly(ADP-ribose)polymerase (PARP)-1, an enzyme actively involved in ischemic brain injury, we have investigated whether the neuroprotective properties of azithromycin in ischemic stroke involve upstream modulation of PARP-1. Administration of a single dose of this macrolide antibiotic upon reperfusion reduced, to a similar extent in wild type and PARP-1 knockout mice, infarct brain damage produced by transient occlusion of the middle cerebral artery. Moreover, we demonstrated the lack of effects of azithromycin on PARP-dependent death of HeLa cells, as well as on activity of purified PARP-1 and PARP-2. Thus, azithromycin protects mice against ischemic stroke injury through a mechanism independent of PARP activation.

PMID: 27663279 [PubMed - as supplied by publisher]

A genetic cluster of xeroderma pigmentosum variant patients with two different founder mutations.

Br J Dermatol. 2016 Sep 24;

Authors: Munford V, Castro LP, Souto R, Lerner LK, Vilar JB, Quayle C, Asif H, Schuch AP, de Souza TA, Ienne S, Alves FI, Moura LM, Galante PA, Camargo AA, Liboredo R, Pena SD, Sarasin A, Chaibub SC, Menck CF

Abstract
BACKGROUND: Xeroderma pigmentosum (XP) is a rare human syndrome associated with hypersensitivity to sunlight and a high frequency of skin tumors at an early age. We identified a community in the state of Goias (central Brazil), a very sunny and tropical region, with a high incidence of XP (17 patients among approximately 1,000 inhabitants).
OBJECTIVES: To identify the gene mutations in the affected community and map the distribution of the affected alleles, correlating the mutations with clinical phenotypes.
METHODS: Functional analyses of DNA repair capacity and cell cycle responses after ultraviolet exposure were investigated in cells from local XP patients, allowing the identification of the mutated gene, which was then sequenced to locate the mutations. A specific assay was designed for mapping the distribution of these mutations in the community.
RESULTS: Skin primary fibroblasts showed normal DNA damage removal but abnormal DNA synthesis after ultraviolet irradiation and deficient expression of the Polη protein, which is encoded by the POLH gene. We detected two different POLH mutations: one at the splice donor site of intron 6, c.764 +1 G>A, and the other in exon 8, c.907 C>T, p.Arg303X. The mutation at intron 6 is novel, whereas the mutation at exon 8 was previously described in Europe. Thus, these mutations were likely brought to the community long ago, suggesting two founder effects for this rare disease.
CONCLUSIONS AND RELEVANCE: This work describes a genetic cluster involving the POLH gene, and, particularly unexpected, with two independent founder mutations, including one that likely originated in Europe. This article is protected by copyright. All rights reserved.

PMID: 27664908 [PubMed - as supplied by publisher]

Parathyroid carcinoma in tertiary hyperparathyroidism.

Asian J Surg. 2016 Oct;39(4):255-259

Authors: Kim BS, Ryu HS, Kang KH, Park SJ

Abstract
Parathyroid carcinoma is a rare disease of unknown etiology. This study presents a case of parathyroid carcinoma in a patient with tertiary hyperparathyroidism. Despite a successful kidney transplantation, the intact parathyroid hormone (iPTH) level of the patient was elevated consistently and could not be controlled by medical therapy. Due to the development of tertiary hyperparathyroidism with bone pain and osteoporosis, subtotal parathyroidectomy was performed 4 months after the kidney transplantation. Histological evaluation revealed that one of four parathyroid lesions was a parathyroid carcinoma, while the others were diffuse hyperplasia. Postoperative laboratory studies indicated a decreased level of iPTH. A positron emission tomography-computed tomography performed 6 months after the operation revealed no evidence of local recurrence or distant metastasis.

PMID: 27664600 [PubMed - as supplied by publisher]

The Inherited p53 Mutation in the Brazilian Population.

Cold Spring Harb Perspect Med. 2016 Sep 23;

Authors: Achatz MI, Zambetti GP

Abstract
A common criticism of studying rare diseases is the often-limited relevance of the findings to human health. Here, we review ∼15 years of research into an unusual germline TP53 mutation (p.R337H) that began with its detection in children with adrenocortical carcinoma (ACC), a remarkably rare childhood cancer that is associated with poor prognosis. We have come to learn that the p.R337H mutation exists at a very high frequency in Southern and Southeastern Brazil, occurring in one of 375 individuals within a total population of ∼100 million. Moreover, it has been determined that carriers of this founder mutation display variable tumor susceptibility, ranging from isolated cases of pediatric ACC to Li-Fraumeni or Li-Fraumeni-like (LFL) syndromes, thus representing a significant medical issue for this country. Studying the biochemical and molecular consequences of this mutation on p53 tumor-suppressor activity, as well as the putative additional genetic alterations that cooperate with this mutation, is advancing our understanding of how p53 functions in tumor suppression in general. These studies, which originated with a rare childhood tumor, are providing important information for guiding genetic counselors and physicians in treating their patients and are already providing clinical benefit.

PMID: 27663983 [PubMed - as supplied by publisher]

Familial amyloid polyneuropathy: When does it stop to be asymptomatic and need a treatment?

Rev Neurol (Paris). 2016 Sep 20;

Authors: Adams D, Beaudonnet G, Adam C, Lacroix C, Théaudin M, Cauquil C, Labeyrie C

Abstract
Transthyretin familial amyloid polyneuropathy (FAP) is a rare disease with autosomal transmission due to point mutation of the transthyretin (TTR) gene. It is the most disabling hereditary neuropathy affecting sensory, motor and autonomic nerves, and is irreversible and fatal within 7 to 12 years of onset in the absence of therapy. Diagnosis is usually delayed for 1-5 years because the onset is usually insidious, and a positive family history is lacking in 50% of late-onset cases. Penetrance is variable, and depends of the age of the carrier and age of onset in family members. Two treatments are available: liver transplantation, to suppress the main source of systemic production of mutant TTR; and TTR tetramer stabilizer drugs, to avoid the release of highly amyloidogenic monomers and oligomers. These therapies are able to stop or slow the progression of the disease in its early stages. Genetic counseling is crucial to detect carriers at risk of developing the disease. The European network for TTR-FAP recommends careful baseline assessment by questionnaire, clinical examination and neurophysiological tests, and periodic consultations to detect the onset of disease in time to start anti-amyloid therapy after biopsy findings of amyloid deposition. A therapeutic educational program is important for improving patients' awareness. Patients are considered symptomatic and ill when they themselves perceive symptoms or changes, including changes from baseline measurements on neurophysiological tests, followed by findings of amyloid deposition on biopsy. The most sensitive biopsies are from the labial salivary gland and skin.

PMID: 27663057 [PubMed - as supplied by publisher]

The environment ontology in 2016: bridging domains with increased scope, semantic density, and interoperation.

J Biomed Semantics. 2016;7(1):57

Authors: Buttigieg PL, Pafilis E, Lewis SE, Schildhauer MP, Walls RL, Mungall CJ

Abstract
BACKGROUND: The Environment Ontology (ENVO; http://www.environmentontology.org/ ), first described in 2013, is a resource and research target for the semantically controlled description of environmental entities. The ontology's initial aim was the representation of the biomes, environmental features, and environmental materials pertinent to genomic and microbiome-related investigations. However, the need for environmental semantics is common to a multitude of fields, and ENVO's use has steadily grown since its initial description. We have thus expanded, enhanced, and generalised the ontology to support its increasingly diverse applications.
METHODS: We have updated our development suite to promote expressivity, consistency, and speed: we now develop ENVO in the Web Ontology Language (OWL) and employ templating methods to accelerate class creation. We have also taken steps to better align ENVO with the Open Biological and Biomedical Ontologies (OBO) Foundry principles and interoperate with existing OBO ontologies. Further, we applied text-mining approaches to extract habitat information from the Encyclopedia of Life and automatically create experimental habitat classes within ENVO.
RESULTS: Relative to its state in 2013, ENVO's content, scope, and implementation have been enhanced and much of its existing content revised for improved semantic representation. ENVO now offers representations of habitats, environmental processes, anthropogenic environments, and entities relevant to environmental health initiatives and the global Sustainable Development Agenda for 2030. Several branches of ENVO have been used to incubate and seed new ontologies in previously unrepresented domains such as food and agronomy. The current release version of the ontology, in OWL format, is available at http://purl.obolibrary.org/obo/envo.owl .
CONCLUSIONS: ENVO has been shaped into an ontology which bridges multiple domains including biomedicine, natural and anthropogenic ecology, 'omics, and socioeconomic development. Through continued interactions with our users and partners, particularly those performing data archiving and sythesis, we anticipate that ENVO's growth will accelerate in 2017. As always, we invite further contributions and collaboration to advance the semantic representation of the environment, ranging from geographic features and environmental materials, across habitats and ecosystems, to everyday objects in household settings.

PMID: 27664130 [PubMed - as supplied by publisher]

Pediatric chemotherapy induced peripheral neuropathy: A systematic review of current knowledge.

Cancer Treat Rev. 2016 Sep 10;50:118-128

Authors: Kandula T, Park SB, Cohn RJ, Krishnan AV, Farrar MA

Abstract
BACKGROUND: The dramatic increase in the number of childhood cancer survivors over the last 60years has made monitoring and minimising long term side effects of cancer treatment increasingly important. Chemotherapy induced peripheral neuropathy (CIPN) has been described with many commonly used chemotherapy agents. This article provides a critical overview of pediatric CIPN, its incidence, clinical manifestations, late effects, and recent advances in understanding of risk factors and pharmacogenomics as well as evaluating current assessment strategies and treatment approaches.
METHODS: Neurotoxicity data was systematically collated from Medline, Embase and Pubmed and analysed for quality, relevance and originality in three stages prior to inclusion. Quality scoring was done using the QUALSYST assessment tool.
RESULTS: A total of 61 studies met inclusion criteria. Peripheral neuropathy is common and may be long lasting with characteristics specific to each chemotherapy agent. There is significant variability in reported incidence and natural history, related to challenges in clinical assessment and diagnosis. Emerging risk factors for CIPN include treatment factors such as dose, duration and concurrent medication and patient factors such as age and inherited susceptibilities. Recent identification of individual genetic variations has advanced understanding of pathomechanisms and may direct future treatment approaches.
CONCLUSION: While these studies guide suggestions for current clinical practice, further systematic research with development of strategies for amelioration and prevention of CIPN is necessary. Standardised assessment protocols and objective outcomes measures of CIPN applicable to patients of different ages are critical to enabling the development of novel treatments and facilitation of future clinical trials and treatment individualisation.

PMID: 27664395 [PubMed - as supplied by publisher]

Psychiatric Pharmacogenomics: How Close Are We?

Biol Psychiatry. 2016 Oct 15;80(8):e63-5

Authors: Hirschtritt ME, Besterman AD, Ross DA

PMID: 27663067 [PubMed - in process]

Multidrug-Resistant Pseudomonas aeruginosa Infection in a Child with Cystic Fibrosis.

Antimicrob Agents Chemother. 2016 Oct;60(10):5627-30

Authors: Ang JY, Abdel-Haq N, Zhu F, Thabit AK, Nicolau DP, Satlin MJ, van Duin D

Abstract
We describe a pediatric cystic fibrosis patient who developed a pulmonary exacerbation due to two multidrug-resistant (MDR) Pseudomonas aeruginosa isolates. In addition to these MDR organisms, the case was further complicated by β-lactam allergy. Despite the MDR phenotype, both isolates were susceptible to an antimicrobial combination.

PMID: 27664282 [PubMed - in process]

Three-base periodicity of sites of sequence variation in Pseudomonas aeruginosa and Staphylococcus aureus core genomes.

FEBS Lett. 2016 Sep 24;

Authors: Morán Losada P, Fischer S, Chouvarine P, Tümmler B

Abstract
The three-base periodicity property is characteristic of protein-coding sequences. Here we report on three-base periodicity of sequence variation in the core genome of bacteria. Single nucleotide polymorphism (SNP) syntenies were extracted from pairwise genome alignments of 41 Staphylococcus aureus or 20 Pseudomonas aeruginosa strains. The length of fragment pairs with identical nucleotides at all SNP positions showed a length-dependent overrepresentation of multiples of three nucleotides at corresponding codon positions of the AT-rich S. aureus and the GC-rich P. aeruginosa. Three-base SNP periodicity seems to be a characteristic feature of the tightly arranged bacterial core genome. This article is protected by copyright. All rights reserved.

PMID: 27664047 [PubMed - as supplied by publisher]

Correction of Lung Inflammation in a F508del CFTR murine Cystic Fibrosis model by the Sphingosine-1-Phosphate Lyase Inhibitor LX2931.

Am J Physiol Lung Cell Mol Physiol. 2016 Sep 23;:ajplung.00298.2016

Authors: Veltman M, Stolarczyk M, Radzioch D, Wojewodka G, De Sanctis JB, Dik WA, Dzyubachyk O, Oravecz T, De Kleer I, Scholte BJ

Abstract
Progressive lung disease with early onset is the main cause of mortality and morbidity in Cystic Fibrosis patients. Here we report a reduction of Sphingosine-1-Phosphate (S1P) in the lung of unchallenged Cftrtm1EUR F508del CFTR mutant mice. This correlates with enhanced infiltration by inducible nitric oxide synthase (iNOS) expressing granulocytes, B- and T-cells. Furthermore, the ratio of macrophage derived dendritic cells (MoDC) to conventional dendritic cells (cDC) is higher in mutant mouse lung, consistent with unprovoked inflammation. Oral application of a S1P-lyase inhibitor (LX2931), increases S1P levels in mutant mouse tissues. This normalizes the lung MoDC/cDC ratio, and reduces B- and T-cell counts. Lung granulocytes are enhanced, but iNOS expression is reduced in this population. Although lung LyC6+ monocytes are enhanced by LX2931, they apparently do not differentiate to MoDC and macrophages. After challenge with bacterial toxins (LPS-fMLP) we observe enhanced levels of pro-inflammatory cytokines TNF-α, KC, IFNγ and IL-12, and the inducible mucin MUC5AC in mutant mouse lung, evidence of deficient resolution of inflammation. LX2931 does not prevent transient inflammation or goblet cell hyperplasia after challenge, but it reduces MUC5AC and pro-inflammatory cytokine levels towards normal values. We conclude that lung pathology in homozygous mice expressing murine F508del CFTR, which represents the most frequent mutation in CF patients, is characterized by abnormal behavior of infiltrating myeloid cells and delayed resolution of induced inflammation. This phenotype can be partially corrected by a S1P lyase inhibitor, providing a rationale for therapeutic targeting of the S1P signaling pathway in CF patients.

PMID: 27663991 [PubMed - as supplied by publisher]

Fungal infections of the lung in children.

Pediatr Radiol. 2016 Sep 23;

Authors: Toma P, Bertaina A, Castagnola E, Colafati GS, D'Andrea ML, Finocchi A, Lucidi V, Mastronuzzi A, Granata C

Abstract
Fungal infections of the lungs are relatively common and potentially life-threatening conditions in immunocompromised children. The role of imaging in children with lung mycosis is to delineate the extension of pulmonary involvement, to assess response to therapy, and to monitor for adverse sequelae such as bronchiectasis and cavitation. The aim of this paper is to show imaging findings in a series of patients with fungal pneumonia from two tertiary children's hospitals, to discuss differential diagnoses and to show how imaging findings can vary depending on the host immune response.

PMID: 27663906 [PubMed - as supplied by publisher]

ABO incompatible Renal Transplantation following Lung Transplantation.

Transpl Immunol. 2016 Sep 20;

Authors: Snell GI, Davis AK, Menahem S, Kotecha S, Whitford HM, Levvey BJ, Paraskeva M, Webb A, Westall GW, Walker RG

Abstract
We present management strategies utilised for the first case of an urgent live-donor ABO-incompatible B blood group renal transplant, in a patient with a prior A blood group lung transplant for cystic fibrosis. Three years on, renal function is excellent and stable, while lung function has improved.

PMID: 27663090 [PubMed - as supplied by publisher]

The Power of OMICs.

Biochem Biophys Res Commun. 2016 Sep 20;

Authors: Stagljar I

Abstract
Over the past two decades, the field of systems biology, which encompasses the numerous, widely popular "OMICs" approaches, has driven many significant advances in biomedical research, enabling researchers to generate huge datasets at multiple levels of biological organization. Despite such successes, some scientists still think that "OMICs"-based research introduces a lot of chaos into the biomedical field and claim that the resultant data are often not reproducible and do not reveal deep mechanistic aspects of biological processes. In this editorial, I argue the following: first, that "OMICs" technologies have improved significantly to yield much better datasets; and second, that follow-up studies on components identified in "OMICs" analyses have yielded many valuable biological insights.

PMID: 27663662 [PubMed - as supplied by publisher]

The effect of inhibition of PP1 and TNFα signaling on pathogenesis of SARS coronavirus.

BMC Syst Biol. 2016;10(1):93

Authors: McDermott JE, Mitchell HD, Gralinski LE, Eisfeld AJ, Josset L, Bankhead A, Neumann G, Tilton SC, Schäfer A, Li C, Fan S, McWeeney S, Baric RS, Katze MG, Waters KM

Abstract
BACKGROUND: The complex interplay between viral replication and host immune response during infection remains poorly understood. While many viruses are known to employ anti-immune strategies to facilitate their replication, highly pathogenic virus infections can also cause an excessive immune response that exacerbates, rather than reduces pathogenicity. To investigate this dichotomy in severe acute respiratory syndrome coronavirus (SARS-CoV), we developed a transcriptional network model of SARS-CoV infection in mice and used the model to prioritize candidate regulatory targets for further investigation.
RESULTS: We validated our predictions in 18 different knockout (KO) mouse strains, showing that network topology provides significant predictive power to identify genes that are important for viral infection. We identified a novel player in the immune response to virus infection, Kepi, an inhibitory subunit of the protein phosphatase 1 (PP1) complex, which protects against SARS-CoV pathogenesis. We also found that receptors for the proinflammatory cytokine tumor necrosis factor alpha (TNFα) promote pathogenesis, presumably through excessive inflammation.
CONCLUSIONS: The current study provides validation of network modeling approaches for identifying important players in virus infection pathogenesis, and a step forward in understanding the host response to an important infectious disease. The results presented here suggest the role of Kepi in the host response to SARS-CoV, as well as inflammatory activity driving pathogenesis through TNFα signaling in SARS-CoV infections. Though we have reported the utility of this approach in bacterial and cell culture studies previously, this is the first comprehensive study to confirm that network topology can be used to predict phenotypes in mice with experimental validation.

PMID: 27663205 [PubMed - as supplied by publisher]

The environment ontology in 2016: bridging domains with increased scope, semantic density, and interoperation.

J Biomed Semantics. 2016;7(1):57

Authors: Buttigieg PL, Pafilis E, Lewis SE, Schildhauer MP, Walls RL, Mungall CJ

Abstract
BACKGROUND: The Environment Ontology (ENVO; http://www.environmentontology.org/ ), first described in 2013, is a resource and research target for the semantically controlled description of environmental entities. The ontology's initial aim was the representation of the biomes, environmental features, and environmental materials pertinent to genomic and microbiome-related investigations. However, the need for environmental semantics is common to a multitude of fields, and ENVO's use has steadily grown since its initial description. We have thus expanded, enhanced, and generalised the ontology to support its increasingly diverse applications.
METHODS: We have updated our development suite to promote expressivity, consistency, and speed: we now develop ENVO in the Web Ontology Language (OWL) and employ templating methods to accelerate class creation. We have also taken steps to better align ENVO with the Open Biological and Biomedical Ontologies (OBO) Foundry principles and interoperate with existing OBO ontologies. Further, we applied text-mining approaches to extract habitat information from the Encyclopedia of Life and automatically create experimental habitat classes within ENVO.
RESULTS: Relative to its state in 2013, ENVO's content, scope, and implementation have been enhanced and much of its existing content revised for improved semantic representation. ENVO now offers representations of habitats, environmental processes, anthropogenic environments, and entities relevant to environmental health initiatives and the global Sustainable Development Agenda for 2030. Several branches of ENVO have been used to incubate and seed new ontologies in previously unrepresented domains such as food and agronomy. The current release version of the ontology, in OWL format, is available at http://purl.obolibrary.org/obo/envo.owl .
CONCLUSIONS: ENVO has been shaped into an ontology which bridges multiple domains including biomedicine, natural and anthropogenic ecology, 'omics, and socioeconomic development. Through continued interactions with our users and partners, particularly those performing data archiving and sythesis, we anticipate that ENVO's growth will accelerate in 2017. As always, we invite further contributions and collaboration to advance the semantic representation of the environment, ranging from geographic features and environmental materials, across habitats and ecosystems, to everyday objects in household settings.

PMID: 27664130 [PubMed - as supplied by publisher]

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("orphan disease" OR "rare disease" OR "orphan diseases" OR "rare diseases")

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