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  • Neueste Artikel (Zeitschrifteninhaltsverzeichnisse / in press)  (13.802)
  • Artikel: DFG Deutsche Nationallizenzen
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  • 1
    Publikationsdatum: 2016-07-12
    Beschreibung: Waterborne diseases have emerged as global health problems and their rapid and sensitive detection in environmental water samples is of great importance. Bacterial identification and enumeration in water samples is significant as it helps to maintain safe drinking water for public consumption. Culture-based methods are laborious, time-consuming, and yield false-positive results, whereas viable but nonculturable (VBNCs) microorganisms cannot be recovered. Hence, numerous methods have been developed for rapid detection and quantification of waterborne pathogenic bacteria in water. These rapid methods can be classified into nucleic acid-based, immunology-based, and biosensor-based detection methods. This review summarizes the principle and current state of rapid methods for the monitoring and detection of waterborne bacterial pathogens. Rapid methods outlined are polymerase chain reaction (PCR), digital droplet PCR, real-time PCR, multiplex PCR, DNA microarray, Next-generation sequencing (pyrosequencing, Illumina technology and genomics), and fluorescence in situ hybridization that are categorized as nucleic acid-based methods. Enzyme-linked immunosorbent assay (ELISA) and immunofluorescence are classified into immunology-based methods. Optical, electrochemical, and mass-based biosensors are grouped into biosensor-based methods. Overall, these methods are sensitive, specific, time-effective, and important in prevention and diagnosis of waterborne bacterial diseases. Waterborne diseases pose constant threats to public health. Therefore, public healthcare needs rapid, sensitive, and accurate detection of pathogens for the diagnosis and treatment.
    Digitale ISSN: 2045-8827
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2016-07-13
    Beschreibung: Testicular germ cell tumors (TGCTs) are frequent solid malignant tumors and cause of death in men between 20–40 years of age. Genetic and environmental factors play an important role in the origin and development of TGCTs. Although the majority of TGCTs are responsive to chemotherapy, about 20% of patient presents incomplete response or tumors relapse. In addition, the current treatments cause acute toxicity and several chronic collateral effects, including sterility. The present mini-review collectively summarize the most recent findings on the new discovered molecular biomarkers such as tyrosine kinases, HMGAs, Aurora B kinase, and GPR30 receptor predictive of TGCTs and as emerging new possible molecular targets for therapeutic strategies. This article is protected by copyright. All rights reserved
    Digitale ISSN: 1097-4652
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2016-07-13
    Beschreibung: ABSTRACT Atrogin-1, an E3 ligase present in skeletal, cardiac and smooth muscle, down-regulates myocardin protein during skeletal muscle differentiation. Myocardin, the master regulator of smooth muscle cell (SMC) differentiation, induces expression of smooth muscle marker genes through its association with serum response factor (SRF), which binds to the CArG box in the promoter. Myocardin undergoes ubiquitylation and proteasomal degradation. Evidence suggests that proteasomal degradation of myocardin is critical for myocardin to exert its transcriptional activity, but there is no report about the E3 ligase responsible for myocardin ubiquitylation and subsequent transactivation. Here, we showed that overexpression of atrogin-1 increased contractility of cultured SMCs and mouse aortic tissues in organ culture. Overexpression of dominant-negative myocardin attenuated the increase in SMC contractility induced by atrogin-1. Atrogin-1 overexpression increased expression of the SM contractile markers while downregulated expression of myocardin protein but not mRNA. Atrogin-1 also ubiquitylated myocardin for proteasomal degradation in vascular SMCs. Deletion studies showed that atrogin-1 directly interacted with myocardin through its amino acids 284-345. Immunostaining studies showed nuclear localization of atrogin-1, myocardin and the Rpt6 subunit of the 26S proteasome. Atrogin-1 overexpression not only resulted in degradation of myocardin but also increased recruitment of RNA Polymerase II onto the promoters of myocardin target genes. In summary, our results have revealed the roles for atrogin-1 in the regulation of smooth muscle contractility through enhancement of myocardin ubiquitylation/degradation and its transcriptional activity. This article is protected by copyright. All rights reserved
    Digitale ISSN: 1097-4652
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2016-07-15
    Beschreibung: Cholesterol is an important component for cell physiology. It regulates the fluidity of cell membranes and determines the physical and biochemical properties of proteins. In the central nervous system, cholesterol controls synapse formation and function and supports the saltatory conduction of action potential. In recent years, the role of cholesterol in the brain has caught the attention of several research groups since a breakdown of cholesterol metabolism has been associated with different neurodevelopmental and neurodegenerative diseases, and interestingly also with psychiatric conditions. The aim of this review is to summarize the current knowledge about the connection between cholesterol dysregulation and various neurologic and psychiatric disorders based on clinical and preclinical studies. This article is protected by copyright. All rights reserved
    Digitale ISSN: 1097-4652
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2016-07-16
    Beschreibung: The study of cellular senescence and proliferative lifespan is becoming increasingly important because of the promises of autologous cell therapy, the need for model systems for tissue disease and the implication of senescent cell phenotypes in organismal disease states such as sarcopenia, diabetes and various cancers, among others. Here, we explain the concepts of proliferative cellular lifespan and cellular senescence, and we present factors that have been shown to mediate cellular lifespan positively or negatively. We review much recent literature and present potential molecular mechanisms by which lifespan mediation occurs, drawing from the fields of telomere biology, metabolism, NAD + and sirtuin biology, growth factor signaling and oxygen and antioxidants. We conclude that cellular lifespan and senescence are complex concepts that are governed by multiple independent and interdependent pathways, and that greater understanding of these pathways, their interactions and their convergence upon specific cellular phenotypes may lead to viable therapies for tissue regeneration and treatment of age-related pathologies, which are caused by or exacerbated by senescent cells in vivo. Replicative cellular lifespan is regulated by myriad cellular factors and processes, including telomeres, oxygen, DNA damage signaling, growth factors and metabolism. In this review, we will explain some of the molecular means by which these and other factors mediate cellular lifespan.
    Print ISSN: 0265-9247
    Digitale ISSN: 1521-1878
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 2016-07-16
    Beschreibung: Uncoupling proteins (UCPs) regulate mitochondrial function, and thus cellular metabolism. Angiotensin-converting enzyme (ACE) is the central component of endocrine and local tissue renin–angiotensin systems (RAS), which also regulate diverse aspects of whole-body metabolism and mitochondrial function (partly through altering mitochondrial UCP expression). We show that ACE expression also appears to be regulated by mitochondrial UCPs. In genetic analysis of two unrelated populations ( healthy young UK men and Scandinavian diabetic patients ) serum ACE (sACE) activity was significantly higher amongst UCP3-55C (rather than T) and UCP2 I (rather than D) allele carriers. RNA interference against UCP2 in human umbilical vein endothelial cells reduced UCP2 mRNA sixfold ( P  〈 0·01) whilst increasing ACE expression within a physiological range (〈1·8-fold at 48 h; P  〈 0·01). Our findings suggest novel hypotheses. Firstly, cellular feedback regulation may occur between UCPs and ACE. Secondly, cellular UCP regulation of sACE suggests a novel means of crosstalk between (and mutual regulation of) cellular and endocrine metabolism. This might partly explain the reduced risk of developing diabetes and metabolic syndrome with RAS antagonists and offer insight into the origins of cardiovascular disease in which UCPs and ACE both play a role. Uncoupling proteins (UCPs) regulate mitochondrial function, and thus cellular metabolism. Angiotensin-converting enzyme (ACE) is the central component of endocrine and local tissue renin–angiotensin systems, which also regulate diverse aspects of whole-body metabolism and mitochondrial function. We demonstrate that ACE expression appears to be regulated by mitochondrial UCPs.
    Print ISSN: 0265-9247
    Digitale ISSN: 1521-1878
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    facet.materialart.
    Unbekannt
    Wiley
    In: BioEssays
    Publikationsdatum: 2016-07-16
    Beschreibung: Positive transcription elongation factor (P-TEFb) plays an important role in host cell and viral gene expression. Many viruses, including Herpes Simplex Virus 1, have evolved strategies to hijack this key factor via their own regulatory proteins. The central role of P-TEFb in viral life cycles raises the possibility that Cdk9 inhibitors might be useful antiviral agents. See article “P-TEFb goes viral” by Justyna Zaborowska, Nur F. Isa and Shona Murphy in this issue.
    Print ISSN: 0265-9247
    Digitale ISSN: 1521-1878
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Publikationsdatum: 2016-07-16
    Beschreibung: Tumors are often viewed as unique entities with specific behaviors. However, tumors are a mixture of differentially evolved subpopulations of cells in constant Darwinian evolution, selecting the fittest clone and allowing it to outgrow the rest. As in the natural environment, the niche defines the properties the fittest clones must possess. Therefore, there can be multiple fit clones because of the various microenvironments inside a single tumor. Hypoxia is considered to be a major feature of the tumor microenvironment and is a potential contributor to the cancer stem cell (CSC) phenotype and its enhanced tumorigenicity. The acidic microenvironment around hypoxic cells is accompanied by the activation of a subset of proteases that contribute to metastasis. Because of aberrant angiogenesis and the inaccessibility of their locations, hypoxic cells are less likely to accumulate therapeutic concentrations of chemotherapeutics that can lead to therapeutic resistance. Therefore, the targeting of the hypoxic CSC niche in combination with chemotherapy may provide a promising strategy for eradicating CSCs. In this review, we examine the cancer stem cell hypothesis and its relationship to the microenvironment, specifically to hypoxia and the subsequent metabolic switch and how they shape tumor behavior. Tumors are a mixture of differentially evolved subpopulations of cells in constant evolution. As in the natural environment, the niche defines the properties the fittest clones must possess. Therefore, there can be multiple fit clones because of the various microenvironments inside a single tumor. Hypoxia is considered to be a major feature of the tumor microenvironment and is a potential contributor to the cancer stem cell phenotype and its enhanced tumorigenicity.
    Print ISSN: 0265-9247
    Digitale ISSN: 1521-1878
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Publikationsdatum: 2016-07-21
    Beschreibung: Eukaryotic gene expression is extensively controlled at the level of mRNA stability and the mechanisms underlying this regulation are markedly different from their archaeal and bacterial counterparts. We propose that two such mechanisms, nonsense-mediated decay (NMD) and motif-specific transcript destabilization by CCCH-type zinc finger RNA-binding proteins, originated as a part of cellular defense against RNA pathogens. These branches of the mRNA turnover pathway might have been used by primeval eukaryotes alongside RNA interference to distinguish their own messages from those of RNA viruses and retrotransposable elements. We further hypothesize that the subsequent advent of “professional” innate and adaptive immunity systems allowed NMD and the motif-triggered mechanisms to be efficiently repurposed for regulation of endogenous cellular transcripts. This scenario explains the rapid emergence of archetypical mRNA destabilization pathways in eukaryotes and argues that other aspects of post-transcriptional gene regulation in this lineage might have been derived through a similar exaptation route. mRNA turnover in eukaryotes is remarkably different from its prokaryotic counterparts and possible reasons underlying this divergence remain unclear. Here we propose that eukaryotic mRNA destabilization pathways evolved as a part of host defense against RNA pathogens and were subsequently repurposed for post-transcriptional regulation of cell-encoded genes.
    Print ISSN: 0265-9247
    Digitale ISSN: 1521-1878
    Thema: Biologie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 2016-07-21
    Beschreibung: Photodynamic therapy (PDT) is a non-thermal technique for inducing tumour damage following administration of a light-activated photosensitizing drug (PS). In a previous work we found that PDT induces cytoskeleton changes in HB4a-Ras cells (human mammary breast carcinoma HB4a cells transfected with the RAS oncogene). In the present work we have studied the migratory and invasive features and the expression of proteins related to these processes on HB4a-Ras cells after 3 successive cycles of PDT using different PSs: 5-aminolevulinic acid (ALA), Verteporfin (Verte), m -tetrahydroxyphenylchlorin ( m -THPC) and Merocyanine 540 (MC). A slight (1.25- to -2 fold) degree of resistance was acquired in cell populations subjected to the three successive PDT treatments. However, complete cell killing was achieved after a light dose increase. Regardless of the PS employed, all the PDT-treated populations had shorter stress fibres than the untreated control HB4a-Ras cells, and the number of dorsal stress fibres was decreased in the PDT-treated populations. E-Cadherin distribution, which was already aberrant in HB4a-Ras cells, became even more diffuse in the PDT-treated populations, though its expression was increased in some of them. The strong migratory and invasive ability of HB4a-Ras cells in vitro was impaired in all the PDT-treated populations, with a behaviour that was similar to the parental non-tumoral HB4a cells. MMP-2 and MMP-9 metalloproteinase activities were also impaired in the PDT-treated populations. The evidence presented herein suggests that the cells surviving PDT would be less metastatic than the initial population. These findings encourage the use of PDT in combination with other treatments such as intraoperative or post-surgery therapeutic procedures. This article is protected by copyright. All rights reserved
    Digitale ISSN: 0091-7419
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Wiley
    Standort Signatur Erwartet Verfügbarkeit
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