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        <title>BioMed Central - Most accessed articles</title>
        <link>http://www.biomedcentral.com/</link>
        <description>The most accessed research articles published by BioMed Central</description>
        <dc:date>2009-11-24T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.virologyj.com/content/6/1/207" />
                                <rdf:li rdf:resource="http://www.virologyj.com/content/6/1/197" />
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2377/9/35" />
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                                <rdf:li rdf:resource="http://www.virologyj.com/content/5/1/29" />
                                <rdf:li rdf:resource="http://www.ijbnpa.org/content/1/1/3" />
                                <rdf:li rdf:resource="http://ccforum.com/content/8/4/R204" />
                                <rdf:li rdf:resource="http://breast-cancer-research.com/content/11/6/R78" />
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        <item rdf:about="http://www.virologyj.com/content/6/1/207">
        <title>From where did the 2009 &apos;swine-origin&apos; influenza A virus (H1N1) emerge?</title>
        <description>The swine-origin influenza A (H1N1) virus that appeared in 2009 and was first found in human beings in Mexico, is a reassortant with at least three parents. Six of the genes are closest in sequence to those of H1N2 &apos;triple-reassortant&apos; influenza viruses isolated from pigs in North America around 1999-2000. Its other two genes are from different Eurasian &apos;avian-like&apos; viruses of pigs; the NA gene is closest to H1N1 viruses isolated in Europe in 1991-1993, and the MP gene is closest to H3N2 viruses isolated in Asia in 1999-2000. The sequences of these genes do not directly reveal the immediate source of the virus as the closest were from isolates collected more than a decade before the human pandemic started. The three parents of the virus may have been assembled in one place by natural means, such as by migrating birds, however the consistent link with pig viruses suggests that human activity was involved. We discuss a published suggestion that unsampled pig herds, the intercontinental live pig trade, together with porous quarantine barriers, generated the reassortant. We contrast that suggestion with the possibility that laboratory errors involving the sharing of virus isolates and cultured cells, or perhaps vaccine production, may have been involved. Gene sequences from isolates that bridge the time and phylogenetic gap between the new virus and its parents will distinguish between these possibilities, and we suggest where they should be sought. It is important that the source of the new virus be found if we wish to avoid future pandemics rather than just trying to minimize the consequences after they have emerged. Influenza virus is a very significant zoonotic pathogen. Public confidence in influenza research, and the agribusinesses that are based on influenza&apos;s many hosts, has been eroded by several recent events involving the virus. Measures that might restore confidence include establishing a unified international administrative framework coordinating surveillance, research and commercial work with this virus, and maintaining a registry of all influenza isolates.</description>
        <link>http://www.virologyj.com/content/6/1/207</link>
                <dc:creator>Adrian Gibbs</dc:creator>
                <dc:creator>John Armstrong</dc:creator>
                <dc:creator>Jean Downie</dc:creator>
                <dc:source>Virology Journal 2009, 6:207</dc:source>
        <dc:date>2009-11-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-6-207</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>207</prism:startingPage>
        <prism:publicationDate>2009-11-24T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.virologyj.com/content/6/1/197">
        <title>Anti-viral properties and mode of action of standardized Echinacea purpurea extract against highly pathogenic avian Influenza virus (H5N1, H7N7) and swine-origin H1N1 (S-OIV) </title>
        <description>Background:
Influenza virus (IV) infections are a major threat to human welfare and animal health worldwide. Anti-viral therapy includes vaccines and a few anti-viral drugs. However vaccines are not always available in time, as demonstrated by the emergence of the new 2009 H1N1-type pandemic strain of swine origin (S-OIV) in April 2009, and the acquisition of resistance to neuraminidase inhibitors such as Tamiflu&#174; (oseltamivir) is a potential problem. Therefore the prospects for the control of IV by existing anti-viral drugs are limited. As an alternative approach to the common anti-virals we studied in more detail a commercial standardized extract of the widely used herb Echinacea purpurea (Echinaforce&#174;, EF) in order to elucidate the nature of its anti-IV activity.
Results:
Human H1N1-type IV, highly pathogenic avian IV (HPAIV) of the H5- and H7-types, as well as swine origin IV (S-OIV, H1N1), were all inactivated in cell culture assays by the EF preparation at concentrations ranging from the recommended dose for oral consumption to several orders of magnitude lower. Detailed studies with the H5N1 HPAIV strain indicated that direct contact between EF and virus was required, prior to infection, in order to obtain maximum inhibition in virus replication. Hemagglutination assays showed that the extract inhibited the receptor binding activity of the virus, suggesting that the extract interferes with the viral entry into cells. In sequential passage studies under treatment in cell culture with the H5N1 virus no EF-resistant variants emerged, in contrast to Tamiflu&#174;, which produced resistant viruses upon passaging. Furthermore, the Tamiflu&#174;-resistant virus was just as susceptible to EF as the wild type virus.
Conclusion:
As a result of these investigations, we believe that this standard Echinacea preparation, used at the recommended dose for oral consumption, could be a useful, readily available and affordable addition to existing control options for IV replication and dissemination.</description>
        <link>http://www.virologyj.com/content/6/1/197</link>
                <dc:creator>Stephan Pleschka</dc:creator>
                <dc:creator>Michael Stein</dc:creator>
                <dc:creator>Roland Schoop</dc:creator>
                <dc:creator>James Hudson</dc:creator>
                <dc:source>Virology Journal 2009, 6:197</dc:source>
        <dc:date>2009-11-13T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-6-197</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>197</prism:startingPage>
        <prism:publicationDate>2009-11-13T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://jbiol.com/content/8/10/88">
        <title>The nature of cell-cycle checkpoints: facts and fallacies</title>
        <description>The concept of checkpoint controls revolutionized our understanding of the cell cycle. Here we revisit the defining features of checkpoints and argue that failure to properly appreciate the concept is leading to misinterpretation of experimental results. We illustrate, using the mitotic checkpoint, problems that can arise from a failure to respect strict definitions and precise terminology.</description>
        <link>http://jbiol.com/content/8/10/88</link>
                <dc:source>Journal of Biology 2009, 8:88</dc:source>
        <dc:date>2009-11-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/jbiol195</dc:identifier>
        <prism:publicationName>Journal of Biology</prism:publicationName>
        <prism:issn>1475-4924</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>88</prism:startingPage>
        <prism:publicationDate>2009-11-16T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.nutritionj.com/content/4/1/24">
        <title>Childhood obesity, prevalence and prevention</title>
        <description>Childhood obesity has reached epidemic levels in developed countries. Twenty five percent of children in the US are overweight and 11% are obese. Overweight and obesity in childhood are known to have significant impact on both physical and psychological health. The mechanism of obesity development is not fully understood and it is believed to be a disorder with multiple causes. Environmental factors, lifestyle preferences, and cultural environment play pivotal roles in the rising prevalence of obesity worldwide. In general, overweight and obesity are assumed to be the results of an increase in caloric and fat intake. On the other hand, there are supporting evidence that excessive sugar intake by soft drink, increased portion size, and steady decline in physical activity have been playing major roles in the rising rates of obesity all around the world. Consequently, both over-consumption of calories and reduced physical activity are involved in childhood obesity.Almost all researchers agree that prevention could be the key strategy for controlling the current epidemic of obesity. Prevention may include primary prevention of overweight or obesity, secondary prevention or prevention of weight regains following weight loss, and avoidance of more weight increase in obese persons unable to lose weight. Until now, most approaches have focused on changing the behaviour of individuals in diet and exercise. It seems, however, that these strategies have had little impact on the growing increase of the obesity epidemic. While about 50% of the adults are overweight and obese in many countries, it is difficult to reduce excessive weight once it becomes established. Children should therefore be considered the priority population for intervention strategies. Prevention may be achieved through a variety of interventions targeting built environment, physical activity, and diet. Some of these potential strategies for intervention in children can be implemented by targeting preschool institutions, schools or after-school care services as natural setting for influencing the diet and physical activity. All in all, there is an urgent need to initiate prevention and treatment of obesity in children.</description>
        <link>http://www.nutritionj.com/content/4/1/24</link>
                <dc:creator>Mahshid Dehghan</dc:creator>
                <dc:creator>Noori Akhtar-Danesh</dc:creator>
                <dc:creator>Anwar Merchant</dc:creator>
                <dc:source>Nutrition Journal 2005, 4:24</dc:source>
        <dc:date>2005-09-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1475-2891-4-24</dc:identifier>
        <prism:publicationName>Nutrition Journal</prism:publicationName>
        <prism:issn>1475-2891</prism:issn>
        <prism:volume>4</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2005-09-02T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/35">
        <title>Diagnostic accuracy of the vegetative and minimally conscious state: Clinical consensus versus standardized neurobehavioral assessment</title>
        <description>Background:
Previously published studies have reported that up to 43% of patients with disorders of consciousness are erroneously assigned a diagnosis of vegetative state (VS). However, no recent studies have investigated the accuracy of this grave clinical diagnosis. In this study, we compared consensus-based diagnoses of VS and MCS to those based on a well-established standardized neurobehavioral rating scale, the JFK Coma Recovery Scale-Revised (CRS-R).
Methods:
We prospectively followed 103 patients (55 &#177; 19 years) with mixed etiologies and compared the clinical consensus diagnosis provided by the physician on the basis of the medical staff&apos;s daily observations to diagnoses derived from CRS-R assessments performed by research staff. All patients were assigned a diagnosis of &apos;VS&apos;, &apos;MCS&apos; or &apos;uncertain diagnosis.&apos;
Results:
Of the 44 patients diagnosed with VS based on the clinical consensus of the medical team, 18 (41%) were found to be in MCS following standardized assessment with the CRS-R. In the 41 patients with a consensus diagnosis of MCS, 4 (10%) had emerged from MCS, according to the CRS-R. We also found that the majority of patients assigned an uncertain diagnosis by clinical consensus (89%) were in MCS based on CRS-R findings.
Conclusion:
Despite the importance of diagnostic accuracy, the rate of misdiagnosis of VS has not substantially changed in the past 15 years. Standardized neurobehavioral assessment is a more sensitive means of establishing differential diagnosis in patients with disorders of consciousness when compared to diagnoses determined by clinical consensus.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/35</link>
                <dc:creator>Caroline Schnakers</dc:creator>
                <dc:creator>Audrey Vanhaudenhuyse</dc:creator>
                <dc:creator>Joseph Giacino</dc:creator>
                <dc:creator>Manfredi Ventura</dc:creator>
                <dc:creator>Melanie Boly</dc:creator>
                <dc:creator>Steve Majerus</dc:creator>
                <dc:creator>Gustave Moonen</dc:creator>
                <dc:creator>Steven Laureys</dc:creator>
                <dc:source>BMC Neurology 2009, 9:35</dc:source>
        <dc:date>2009-07-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-35</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>35</prism:startingPage>
        <prism:publicationDate>2009-07-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ijbnpa.org/content/2/1/8">
        <title>Increasing weight-bearing physical activity and calcium-rich foods to promote bone mass gains among 9-11 year old girls: outcomes of the Cal-Girls study</title>
        <description>Background:
A two-year, community-based, group-randomized trial to promote bone mass gains among 9&#8211;11 year-old girls through increased intake of calcium-rich foods and weight-bearing physical activity was evaluated.
Methods:
Following baseline data collection, 30 5th-grade Girl Scout troops were randomized to a two-year behavioral intervention program or to a no-treatment control group. Evaluations were conducted at baseline, one year, and two years. Measures included bone mineral content, density, and area (measured by DXA), dietary calcium intake (24-hour recall), and weight-bearing physical activity (physical activity checklist interview). Mixed-model regression was used to evaluate treatment-related changes in bone mineral content (g) for the total body, lumbar spine (L1-L4), proximal femur, one-third distal radius, and femoral neck. Changes in eating and physical activity behavioral outcomes were examined.
Results:
Although the intervention was implemented with high fidelity, no significant intervention effects were observed for total bone mineral content or any specific bone sites. Significant intervention effects were observed for increases in dietary calcium. No significant intervention effects were observed for increases in weight-bearing physical activity.
Conclusion:
Future research needs to identify the optimal dosage of weight-bearing physical activity and calcium-rich dietary behavior change required to maximize bone mass gains in pre-adolescent and adolescent girls.</description>
        <link>http://www.ijbnpa.org/content/2/1/8</link>
                <dc:creator>Simone French</dc:creator>
                <dc:creator>Mary Story</dc:creator>
                <dc:creator>Jayne Fulkerson</dc:creator>
                <dc:creator>John Himes</dc:creator>
                <dc:creator>Peter Hannan</dc:creator>
                <dc:creator>Dianne Neumark-Sztainer</dc:creator>
                <dc:creator>Kristine Ensrud</dc:creator>
                <dc:source>International Journal of Behavioral Nutrition and Physical Activity 2005, 2:8</dc:source>
        <dc:date>2005-07-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1479-5868-2-8</dc:identifier>
        <prism:publicationName>International Journal of Behavioral Nutrition and Physical Activity</prism:publicationName>
        <prism:issn>1479-5868</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2005-07-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.virologyj.com/content/5/1/29">
        <title>On the epidemiology of influenza</title>
        <description>The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, &quot;seemingly unmindful of traditional infectious disease behavioral patterns.&quot; Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify &#8211; and attempt to explain &#8211; nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D&apos;s effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D&apos;s seasonal and population effects on innate immunity, and the presence of a subpopulation of &quot;good infectors.&quot; If true, our revision of Edgar Hope-Simpson&apos;s theory has profound implications for the prevention of influenza.</description>
        <link>http://www.virologyj.com/content/5/1/29</link>
                <dc:creator>John Cannell</dc:creator>
                <dc:creator>Michael Zasloff</dc:creator>
                <dc:creator>Cedric Garland</dc:creator>
                <dc:creator>Robert Scragg</dc:creator>
                <dc:creator>Edward Giovannucci</dc:creator>
                <dc:source>Virology Journal 2008, 5:29</dc:source>
        <dc:date>2008-02-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-422X-5-29</dc:identifier>
        <prism:publicationName>Virology Journal</prism:publicationName>
        <prism:issn>1743-422X</prism:issn>
        <prism:volume>5</prism:volume>
        <prism:startingPage>29</prism:startingPage>
        <prism:publicationDate>2008-02-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ijbnpa.org/content/1/1/3">
        <title>Food Advertising and Marketing Directed at Children and Adolescents in the US</title>
        <description>In recent years, the food and beverage industry in the US has viewed children and adolescents as a major market force. As a result, children and adolescents are now the target of intense and specialized food marketing and advertising efforts. Food marketers are interested in youth as consumers because of their spending power, their purchasing influence, and as future adult consumers. Multiple techniques and channels are used to reach youth, beginning when they are toddlers, to foster brand-building and influence food product purchase behavior. These food marketing channels include television advertising, in-school marketing, product placements, kids clubs, the Internet, toys and products with brand logos, and youth-targeted promotions, such as cross-selling and tie-ins. Foods marketed to children are predominantly high in sugar and fat, and as such are inconsistent with national dietary recommendations. The purpose of this article is to examine the food advertising and marketing channels used to target children and adolescents in the US, the impact of food advertising on eating behavior, and current regulation and policies.</description>
        <link>http://www.ijbnpa.org/content/1/1/3</link>
                <dc:creator>Mary Story</dc:creator>
                <dc:creator>Simone French</dc:creator>
                <dc:source>International Journal of Behavioral Nutrition and Physical Activity 2004, 1:3</dc:source>
        <dc:date>2004-02-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1479-5868-1-3</dc:identifier>
        <prism:publicationName>International Journal of Behavioral Nutrition and Physical Activity</prism:publicationName>
        <prism:issn>1479-5868</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2004-02-10T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://ccforum.com/content/8/4/R204">
        <title>Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group</title>
        <description>IntroductionThere is no consensus definition of acute renal failure (ARF) in critically ill patients. More than 30 different definitions have been used in the literature, creating much confusion and making comparisons difficult. Similarly, strong debate exists on the validity and clinical relevance of animal models of ARF; on choices of fluid management and of end-points for trials of new interventions in this field; and on how information technology can be used to assist this process. Accordingly, we sought to review the available evidence, make recommendations and delineate key questions for future studies.
Methods:
We undertook a systematic review of the literature using Medline and PubMed searches. We determined a list of key questions and convened a 2-day consensus conference to develop summary statements via a series of alternating breakout and plenary sessions. In these sessions, we identified supporting evidence and generated recommendations and/or directions for future research.
Results:
We found sufficient consensus on 47 questions to allow the development of recommendations. Importantly, we were able to develop a consensus definition for ARF. In some cases it was also possible to issue useful consensus recommendations for future investigations. We present a summary of the findings. (Full versions of the six workgroups&apos; findings are available on the internet at http://www.ADQI.net)
Conclusion:
Despite limited data, broad areas of consensus exist for the physiological and clinical principles needed to guide the development of consensus recommendations for defining ARF, selection of animal models, methods of monitoring fluid therapy, choice of physiological and clinical end-points for trials, and the possible role of information technology.</description>
        <link>http://ccforum.com/content/8/4/R204</link>
                <dc:creator>Rinaldo Bellomo</dc:creator>
                <dc:creator>Claudio Ronco</dc:creator>
                <dc:creator>John Kellum</dc:creator>
                <dc:creator>Ravindra Mehta</dc:creator>
                <dc:creator>Paul Palevski</dc:creator>
                <dc:source>Critical Care 2004, 8:R204</dc:source>
        <dc:date>2004-05-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/cc2872</dc:identifier>
        <prism:publicationName>Critical Care</prism:publicationName>
        <prism:issn>1364-8535</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>R204</prism:startingPage>
        <prism:publicationDate>2004-05-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://breast-cancer-research.com/content/11/6/R78">
        <title>A selective eradication of human nonhereditary breast cancer cells by phenanthridine-derived polyADP-ribose polymerase inhibitors</title>
        <description>IntroductionPARP-1 (polyADP-ribose polymerase-1) is known to be activated in response to DNA damage, and activated PARP-1 promotes DNA repair. However, a recently disclosed alternative mechanism of PARP-1 activation by phosphorylated externally regulated kinase (ERK) implicates PARP-1 in a vast number of signal-transduction networks in the cell. Here, PARP-1 activation was examined for its possible effects on cell proliferation in both normal and malignant cells.
Methods:
In vitro (cell cultures) and in vivo (xenotransplants) experiments were performed.
Results:
Phenanthridine-derived PARP inhibitors interfered with cell proliferation by causing G2/M arrest in both normal (human epithelial cells MCF10A and mouse embryonic fibroblasts) and human breast cancer cells MCF-7 and MDA231. However, whereas the normal cells were only transiently arrested, G2/M arrest in the malignant breast cancer cells was permanent and was accompanied by a massive cell death. In accordance, treatment with a phenanthridine-derived PARP inhibitor prevented the development of MCF-7 and MDA231 xenotransplants in female nude mice. Quiescent cells (neurons and cardiomyocytes) are not impaired by these PARP inhibitors.
Conclusions:
These results outline a new therapeutic approach for a selective eradication of abundant nonhereditary human breast cancers.</description>
        <link>http://breast-cancer-research.com/content/11/6/R78</link>
                <dc:creator>Dana Inbar-Rozensal</dc:creator>
                <dc:creator>Asher Castiel</dc:creator>
                <dc:creator>Leonid Visochek</dc:creator>
                <dc:creator>David Castel</dc:creator>
                <dc:creator>Francoise Dantzer</dc:creator>
                <dc:creator>Shai Izraeli</dc:creator>
                <dc:creator>Malka Cohen-Armon</dc:creator>
                <dc:source>Breast Cancer Research 2009, 11:R78</dc:source>
        <dc:date>2009-11-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/bcr2445</dc:identifier>
        <prism:publicationName>Breast Cancer Research</prism:publicationName>
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