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	<title>CiteULike: xingxu's review</title>
	<description>CiteULike: xingxu's review</description>


	<link>http://www.citeulike.org/user/xingxu/tag/review</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/xingxu/article/1758579"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/xingxu/article/2759075"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/xingxu/article/2759065"/>
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<item rdf:about="http://www.citeulike.org/user/xingxu/article/2838231">
    <title>Selection of human antibody fragments by phage display</title>
    <link>http://www.citeulike.org/user/xingxu/article/2838231</link>
    <description>&lt;i&gt;Nat. Protocols, Vol. 2, No. 11. (November 2007), pp. 3001-3008.&lt;/i&gt;</description>
    <dc:title>Selection of human antibody fragments by phage display</dc:title>

    <dc:creator>Carol Lee</dc:creator>
    <dc:creator>Niccolo Iorno</dc:creator>
    <dc:creator>Frederic Sierro</dc:creator>
    <dc:creator>Daniel Christ</dc:creator>
    <dc:identifier>doi:10.1038/nprot.2007.448</dc:identifier>
    <dc:source>Nat. Protocols, Vol. 2, No. 11. (November 2007), pp. 3001-3008.</dc:source>
    <dc:date>2008-05-27T20:27:40-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nat. Protocols</prism:publicationName>
    <prism:volume>2</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>3001</prism:startingPage>
    <prism:endingPage>3008</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>methods</prism:category>
    <prism:category>phage_display</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2562889">
    <title>Heritability in the genomics era — concepts and misconceptions</title>
    <link>http://www.citeulike.org/user/xingxu/article/2562889</link>
    <description>&lt;i&gt;Nature Reviews Genetics, Vol. 9, No. 4. (04 March 2008), pp. 255-266.&lt;/i&gt;</description>
    <dc:title>Heritability in the genomics era — concepts and misconceptions</dc:title>

    <dc:creator>Peter Visscher</dc:creator>
    <dc:creator>William Hill</dc:creator>
    <dc:creator>Naomi Wray</dc:creator>
    <dc:identifier>doi:10.1038/nrg2322</dc:identifier>
    <dc:source>Nature Reviews Genetics, Vol. 9, No. 4. (04 March 2008), pp. 255-266.</dc:source>
    <dc:date>2008-03-19T16:33:41-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nature Reviews Genetics</prism:publicationName>
    <prism:issn>1471-0056</prism:issn>
    <prism:volume>9</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>255</prism:startingPage>
    <prism:endingPage>266</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>genomics</prism:category>
    <prism:category>heritability</prism:category>
    <prism:category>population</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1758579">
    <title>Constructing the landscape of the mammalian transcriptome.</title>
    <link>http://www.citeulike.org/user/xingxu/article/1758579</link>
    <description>&lt;i&gt;J Exp Biol, Vol. 210, No. Pt 9. (May 2007), pp. 1497-1506.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The principal route to understanding the biological significance of the genome sequence comes from discovery and characterization of that portion of the genome that is transcribed into RNA products. We now know that this ;transcriptome' is unexpectedly complex and its precise definition in any one species requires multiple technical approaches and an ability to work on a very large scale. A key step is the development of technologies able to capture snapshots of the complexity of the various kinds of RNA generated by the genome. As the human, mouse and other model genome sequencing projects approach completion, considerable effort has been focused on identifying and annotating the protein-coding genes as the principal output of the genome. In pursuing this aim, several key technologies have been developed to generate large numbers and highly diverse sets of full-length cDNAs and their variants. However, the search has identified another hidden transcriptional universe comprising a wide variety of non-protein coding RNA transcripts. Despite initial scepticism, various experiments and complementary technologies have demonstrated that these RNAs are dynamically transcribed and a subset of them can act as sense-antisense RNAs, which influence the transcriptional output of the genome. Recent experimental evidence suggests that the list of non-protein coding RNAs is still largely incomplete and that transcription is substantially more complex even than currently thought.</description>
    <dc:title>Constructing the landscape of the mammalian transcriptome.</dc:title>

    <dc:creator>P Carninci</dc:creator>
    <dc:identifier>doi:10.1242/jeb.000406</dc:identifier>
    <dc:source>J Exp Biol, Vol. 210, No. Pt 9. (May 2007), pp. 1497-1506.</dc:source>
    <dc:date>2007-10-12T04:14:07-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Exp Biol</prism:publicationName>
    <prism:issn>0022-0949</prism:issn>
    <prism:volume>210</prism:volume>
    <prism:number>Pt 9</prism:number>
    <prism:startingPage>1497</prism:startingPage>
    <prism:endingPage>1506</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>transcriptome</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2759075">
    <title>Chapter 4 beta-Globin Regulation and Long-Range Interactions.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2759075</link>
    <description>&lt;i&gt;Advances in genetics, Vol. 61 (2008), pp. 107-142.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Transcriptional activation in higher eukaryotes frequently involves the long-range action of a number of regulatory DNA elements. One of the main questions in transcriptional regulation is how cis-regulatory elements communicate with the promoter of a gene over large distances. There has been a lively debate in recent years whether this communication takes place via a noncontact mechanism (linking, tracking) or via a contact mechanism (looping). The demonstration that the major regulatory element of the beta-globin locus, the locus control region (LCR), is in close proximity to the active beta-globin genes validates the contact model for long-range activation. Here, we will review the beta-globin locus as a model system to study long-range activation, briefly describe the different models for long-range activation, and summarize the recent findings that the LCR of the beta-globin locus is in close proximity to the active promoters. Although it is now firmly established that looping takes place within the beta-globin locus (and other loci), it is not clear how these long-range contacts are established and what the precise role is of the LCR. We will argue that the main action of the LCR takes place at the promoter and open reading frame of the gene itself and we will discuss key rate-limiting steps in transcriptional activation and the possible mechanisms by which they are influenced by the LCR.</description>
    <dc:title>Chapter 4 beta-Globin Regulation and Long-Range Interactions.</dc:title>

    <dc:creator>RJ Palstra</dc:creator>
    <dc:creator>W de Laat</dc:creator>
    <dc:creator>F Grosveld</dc:creator>
    <dc:identifier>doi:10.1016/S0065-2660(07)00004-1</dc:identifier>
    <dc:source>Advances in genetics, Vol. 61 (2008), pp. 107-142.</dc:source>
    <dc:date>2008-05-05T19:48:49-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Advances in genetics</prism:publicationName>
    <prism:issn>0065-2660</prism:issn>
    <prism:volume>61</prism:volume>
    <prism:startingPage>107</prism:startingPage>
    <prism:endingPage>142</prism:endingPage>
    <prism:category>beta_globin</prism:category>
    <prism:category>long_range</prism:category>
    <prism:category>regulation</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2759065">
    <title>Blurring cis and trans in Gene Regulation</title>
    <link>http://www.citeulike.org/user/xingxu/article/2759065</link>
    <description>&lt;i&gt;Cell, Vol. 126, No. 2. (28 July 2006), pp. 248-250.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In this issue of Cell, Axel and colleagues (Lomvardas et al., 2006) report that a single enhancer of an odorant receptor (OR) gene cluster interacts with multiple OR gene promoters on different chromosomes. This study suggests a mechanism that allows olfactory sensory neurons to choose randomly and express only one out of more than 1000 OR genes.</description>
    <dc:title>Blurring cis and trans in Gene Regulation</dc:title>

    <dc:creator>Fabio Savarese</dc:creator>
    <dc:creator>Rudolf Grosschedl</dc:creator>
    <dc:identifier>doi:10.1016/j.cell.2006.07.008</dc:identifier>
    <dc:source>Cell, Vol. 126, No. 2. (28 July 2006), pp. 248-250.</dc:source>
    <dc:date>2008-05-05T19:43:01-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Cell</prism:publicationName>
    <prism:volume>126</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>248</prism:startingPage>
    <prism:endingPage>250</prism:endingPage>
    <prism:category>breakthrough</prism:category>
    <prism:category>long_range</prism:category>
    <prism:category>neuroscience</prism:category>
    <prism:category>regulation</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2733224">
    <title>The genetics of glycosylation in Gram-negative bacteria</title>
    <link>http://www.citeulike.org/user/xingxu/article/2733224</link>
    <description>&lt;i&gt;FEMS Microbiology Letters, Vol. 218, No. 2. (2003), pp. 211-222.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract In recent years there has been a dramatic increase in reports of glycosylation of proteins in various Gram-negative systems including Neisseria meningitidis, Neisseria gonorrhoeae, Campylobacter jejuni, Pseudomonas aeruginosa, Escherichia coli, Caulobacter crescentus, Aeromonas caviae and Helicobacter pylori. Although this growing list contains many important pathogens (reviewed by Benz and Schmidt [Mol. Microbiol. 45 (2002) 267-276]) and the glycosylations are found on proteins important in pathogenesis such as pili, adhesins and flagella the precise role(s) of the glycosylation of these proteins remains to be determined. Furthermore, the details of the glycosylation biosynthetic process have not been determined in any of these systems. The definition of the precise role of glycosylation and the mechanism of biosynthesis will be facilitated by a detailed understanding of the genes involved.</description>
    <dc:title>The genetics of glycosylation in Gram-negative bacteria</dc:title>

    <dc:creator>Power</dc:creator>
    <dc:creator>Jennings</dc:creator>
    <dc:identifier>doi:10.1111/j.1574-6968.2003.tb11520.x</dc:identifier>
    <dc:source>FEMS Microbiology Letters, Vol. 218, No. 2. (2003), pp. 211-222.</dc:source>
    <dc:date>2008-04-29T09:24:55-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>FEMS Microbiology Letters</prism:publicationName>
    <prism:volume>218</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>211</prism:startingPage>
    <prism:endingPage>222</prism:endingPage>
    <prism:category>glycosylation</prism:category>
    <prism:category>microbiology</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2681757">
    <title>Genomics and Biology Come Together to Fight HIV</title>
    <link>http://www.citeulike.org/user/xingxu/article/2681757</link>
    <description>&lt;i&gt;PLoS Biology, Vol. 6, No. 3. (1 March 2008), e76.&lt;/i&gt;</description>
    <dc:title>Genomics and Biology Come Together to Fight HIV</dc:title>

    <dc:creator>David Goldstein</dc:creator>
    <dc:identifier>doi:10.1371%2Fjournal.pbio.0060076</dc:identifier>
    <dc:source>PLoS Biology, Vol. 6, No. 3. (1 March 2008), e76.</dc:source>
    <dc:date>2008-04-17T12:27:45-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>PLoS Biology</prism:publicationName>
    <prism:volume>6</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>e76</prism:startingPage>
    <prism:category>genomics</prism:category>
    <prism:category>gwa</prism:category>
    <prism:category>hiv</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2626641">
    <title>Review article: exploring the link between Helicobacter pylori and gastric cancer.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2626641</link>
    <description>&lt;i&gt;Alimentary pharmacology &#38; therapeutics, Vol. 13 Suppl 1 (March 1999), pp. 3-11.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Cancer of the distal stomach, both of the intestinal and diffuse type, is strongly associated with Helicobacter pylori colonization. This bacterium causes chronic active inflammation of the gastric mucosa in the majority of colonized subjects. In a considerable number of them, this will eventually lead to a loss of gastric glands, and thus the establishment of atrophic gastritis, which is associated with the development of intestinal metaplasia and dysplasia. Development of atrophy and metaplasia of the gastric mucosa are thus strongly associated with H. pylori infection, instead of a direct and inevitable consequence of ageing. Approximately 40-50% of infected subjects develop these conditions, but they are rare in non-infected subjects. The presence of these consecutive disorders leads to a 5-90-fold increased risk for cancer of the distal stomach, in particular of the intestinal type. This sequence explains the increased risk for gastric cancer in H. pylori-infected subjects, as has been shown in various cross-sectional and longitudinal studies. In a combined analysis of three longitudinal studies, a significant trend was observed towards an increased odds ratio with longer intervals between (retrospective) serological diagnosis of H. pylori infection and observation of gastric cancer, this risk being more than eight-fold increased if the interval had been at least 15 years. This is thought to reflect development of atrophic gastritis and intestinal metaplasia with loss of H. pylori colonization in the years prior to development of cancer. Atrophic gastritis and gastric cancer thus appear closely associated with the presence of H. pylori, yet not all infected subjects will eventually develop atrophy and only a small minority develop gastric cancer. Factors that influence the risks for atrophy and cancer in the presence of infection may be related to the time that infection occurred and to characteristics of the bacterial strain and the host. Evidence for the role of these factors is now increasing. Recognition of the causal role of H. pylori in the induction of gastric cancer theoretically presents tools for cancer prevention. The efficacy of screening and bacterial eradication for prevention of distal gastric cancer is being studied in a number of large-scale intervention studies in different populations. It is hoped that these studies will also provide answers to the potential preventive role of H. pylori colonization in the development of gastro-oesophageal reflux disease and associated conditions, in particular development of cancer of the proximal stomach. Infection with H. pylori plays an important role in the aetiology of atrophic gastritis and gastric cancer. Studies suggest an eight-fold increased risk for both conditions in the presence of infection. Factors that influence the risk for both conditions in the presence of infection are the age at which infection occurred and the presence of cagA as a marker for more pathogenetic H. pylori strains. The efficacy and side-effects of intervention for the prevention of distal gastric cancer has yet to be established.</description>
    <dc:title>Review article: exploring the link between Helicobacter pylori and gastric cancer.</dc:title>

    <dc:creator>EJ Kuipers</dc:creator>
    <dc:source>Alimentary pharmacology &#38; therapeutics, Vol. 13 Suppl 1 (March 1999), pp. 3-11.</dc:source>
    <dc:date>2008-04-03T16:05:23-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Alimentary pharmacology &#38; therapeutics</prism:publicationName>
    <prism:issn>0269-2813</prism:issn>
    <prism:volume>13 Suppl 1</prism:volume>
    <prism:startingPage>3</prism:startingPage>
    <prism:endingPage>11</prism:endingPage>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2626640">
    <title>The prevalence of Helicobacter pylori in peptic ulcer disease.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2626640</link>
    <description>&lt;i&gt;Alimentary pharmacology &#38; therapeutics, Vol. 9 Suppl 2 (1995), pp. 59-69.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Both duodenal and gastric ulcer disease are closely associated with Helicobacter pylori infection. An infected individual has an estimated lifetime risk of 10-20% for the development of peptic ulcer disease, which is at least 3-4 fold higher than in non-infected subjects. H. pylori infection can be diagnosed in 90-100% of duodenal ulcer patients and in 60-100% of gastric ulcer patients. Subjects infected with a cytotoxin-producing bacterial strain, or a strain possessing cagA, are at a higher risk of duodenal ulcer. Other factors that may influence the peptic ulcer risk in infected subjects are the amount of gastric acid production (which is increased in duodenal ulcer disease and decreased in gastric ulcer disease), the presence of gastric metaplasia in the duodenal bulb, smoking, and genetic factors (e.g. blood group O and lack of the secretor gene). After eradication of the infection, the risk of recurrence of ulcer disease is reduced to below 10% for gastric ulcer disease and to approximately 0% for duodenal ulcer disease.</description>
    <dc:title>The prevalence of Helicobacter pylori in peptic ulcer disease.</dc:title>

    <dc:creator>EJ Kuipers</dc:creator>
    <dc:creator>JC Thijs</dc:creator>
    <dc:creator>HP Festen</dc:creator>
    <dc:source>Alimentary pharmacology &#38; therapeutics, Vol. 9 Suppl 2 (1995), pp. 59-69.</dc:source>
    <dc:date>2008-04-03T16:05:12-00:00</dc:date>
    <prism:publicationYear>1995</prism:publicationYear>
    <prism:publicationName>Alimentary pharmacology &#38; therapeutics</prism:publicationName>
    <prism:issn>0269-2813</prism:issn>
    <prism:volume>9 Suppl 2</prism:volume>
    <prism:startingPage>59</prism:startingPage>
    <prism:endingPage>69</prism:endingPage>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2625796">
    <title>H. pylori infection: bacterial virulence factors and cytokine gene polymorphisms as determinants of infection outcome.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2625796</link>
    <description>&lt;i&gt;Critical reviews in clinical laboratory sciences, Vol. 41, No. 3. (2004), pp. 313-337.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The gram negative bacterium H. pylori infects the human stomach worldwide, invariably causing mucosal inflammation. In the majority of cases, H. pylori-associated gastritis remains the only clinical manifestation of the infection, which might cause, otherwise, peptic ulcer, gastric adenocarcinoma. or MALToma. The balance between the bacterial virulence machinery and the host response to the infection determines the different clinical outcomes. The main bacterial virulence factors comprise adhesins (BabA, SabA), the vacuolating cytotoxin VacA, and the products of cag pathogenicity island. The pattern of cytokine production in response to the infection is one of the main host determinants involved in limiting the infection outcome to gastritis or in favoring peptic ulcer or cancer onset. The polymorphisms of some cytokine genes (IL-1beta IL-1RN, TNF-alpha, IFN-gamma) have been correlated with H. pylori-associated gastric adenocarcinoma or peptic ulcer, possibly because they influence the amount of cytokine production in response to H. pylori infection. This review focuses on the role of H. pylori virulence genes and on host cytokines' genes polymorphisms in determining clinical outcome to H. pylori infection.</description>
    <dc:title>H. pylori infection: bacterial virulence factors and cytokine gene polymorphisms as determinants of infection outcome.</dc:title>

    <dc:creator>D Basso</dc:creator>
    <dc:creator>M Plebani</dc:creator>
    <dc:source>Critical reviews in clinical laboratory sciences, Vol. 41, No. 3. (2004), pp. 313-337.</dc:source>
    <dc:date>2008-04-03T11:20:23-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Critical reviews in clinical laboratory sciences</prism:publicationName>
    <prism:issn>1040-8363</prism:issn>
    <prism:volume>41</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>313</prism:startingPage>
    <prism:endingPage>337</prism:endingPage>
    <prism:category>cytokine</prism:category>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2625788">
    <title>Polymorphism and gastric cancer</title>
    <link>http://www.citeulike.org/user/xingxu/article/2625788</link>
    <description>&lt;i&gt;Journal of Gastroenterology and Hepatology, Vol. 20, No. 5. (2005), pp. 793-794.&lt;/i&gt;</description>
    <dc:title>Polymorphism and gastric cancer</dc:title>

    <dc:creator>Roberts Thomson</dc:creator>
    <dc:creator>WJ Butler</dc:creator>
    <dc:identifier>doi:10.1111/j.1440-1746.2005.03938.x</dc:identifier>
    <dc:source>Journal of Gastroenterology and Hepatology, Vol. 20, No. 5. (2005), pp. 793-794.</dc:source>
    <dc:date>2008-04-03T11:18:09-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Journal of Gastroenterology and Hepatology</prism:publicationName>
    <prism:volume>20</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>793</prism:startingPage>
    <prism:endingPage>794</prism:endingPage>
    <prism:category>cancer</prism:category>
    <prism:category>gastric</prism:category>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2625637">
    <title>Pathogenesis of Helicobacter pylori infection.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2625637</link>
    <description>&lt;i&gt;Clinical microbiology reviews, Vol. 19, No. 3. (July 2006), pp. 449-490.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.</description>
    <dc:title>Pathogenesis of Helicobacter pylori infection.</dc:title>

    <dc:creator>JG Kusters</dc:creator>
    <dc:creator>AH van Vliet</dc:creator>
    <dc:creator>EJ Kuipers</dc:creator>
    <dc:identifier>doi:10.1128/CMR.00054-05</dc:identifier>
    <dc:source>Clinical microbiology reviews, Vol. 19, No. 3. (July 2006), pp. 449-490.</dc:source>
    <dc:date>2008-04-03T09:53:28-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Clinical microbiology reviews</prism:publicationName>
    <prism:issn>0893-8512</prism:issn>
    <prism:volume>19</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>449</prism:startingPage>
    <prism:endingPage>490</prism:endingPage>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2625298">
    <title>Demystified... recombinant antibodies</title>
    <link>http://www.citeulike.org/user/xingxu/article/2625298</link>
    <description>&lt;i&gt;J Clin Pathol, Vol. 57, No. 9. (1 September 2004), pp. 912-917.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Recombinant antibodies are important tools for biomedical research and are increasingly being used as clinical diagnostic/therapeutic reagents. In this article, a background to humanised antibodies is given, together with details of the generation of antibody fragments--for example, single chain Fv fragments. Phage antibody fragments are fast becoming popular and can be generated by simple established methods of affinity enrichment from libraries derived from immune cells. Phage display methodology can also be used for the affinity enrichment of existing antibody fragments to provide a reagent with a higher affinity. Here, phage antibodies are demystified to provide a greater understanding of the potential of these reagents and to engage clinicians and biomedical scientists alike to think about potential applications in pathology and clinical settings. 10.1136/jcp.2003.014407</description>
    <dc:title>Demystified... recombinant antibodies</dc:title>

    <dc:creator>KA Smith</dc:creator>
    <dc:creator>PN Nelson</dc:creator>
    <dc:creator>P Warren</dc:creator>
    <dc:creator>SJ Astley</dc:creator>
    <dc:creator>PG Murray</dc:creator>
    <dc:creator>J Greenman</dc:creator>
    <dc:identifier>doi:10.1136/jcp.2003.014407</dc:identifier>
    <dc:source>J Clin Pathol, Vol. 57, No. 9. (1 September 2004), pp. 912-917.</dc:source>
    <dc:date>2008-04-03T07:11:15-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>J Clin Pathol</prism:publicationName>
    <prism:volume>57</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>912</prism:startingPage>
    <prism:endingPage>917</prism:endingPage>
    <prism:category>methods</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2612066">
    <title>Helicobacter pylori adhesins: review and perspectives.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2612066</link>
    <description>&lt;i&gt;Helicobacter, Vol. 5, No. 4. (December 2000), pp. 183-195.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;It is highly unlikely that chronic infection with H. pylori could occur in the absence of adhesin-host cell interactions. Also, there is no evidence that any of the serious outcomes of H. pylori infection such as gastric and duodenal ulcers, gastric cancer or mucosa-associated lymphoid tissue (MALT) lymphoma could occur without prior colonization of the gastric epithelium mediated by H. pylori adhesins. H. pylori is highly adaptable, as evidenced by the fact that it can occupy a single host for decades. An important facet of this adaptability is its ability to physically interact with various types of host cells and also with host mucins and extracellular matrix proteins using a number of different adhesins displaying a variety of unique receptor specificities. Thus it is highly unlikely that any one particular H. pylori adhesin will ever be proven responsible for a particular outcome such as duodenal ulcer, MALT lymphoma, or adenocarcinoma. Also, while the search for additional H. pylori adhesins should and certainly will continue, we suggest that the scope of this effort should be expanded to include investigations into the patterns of expression and interaction between individual outer membrane proteins. Which of the numerous H. pylori outer membrane proteins (OMPs) actually function as adhesins (i.e., have receptor-binding sites) and which OMPs are simply necessary for optimal display of the adhesive OMPs? There are many other important questions about H. pylori adhesins waiting to be answered. For example, which adhesins are responsible for loose adherence to host cells and which adhesins are responsible for intimate, or membrane-to-membrane, adherence, and do these adhesins normally work in concert or in a sequential fashion? Also, is a specific type of adhesin necessary for type IV protein translocation into host cells and, if so, is adhesin expression coregulated with the effector protein export?</description>
    <dc:title>Helicobacter pylori adhesins: review and perspectives.</dc:title>

    <dc:creator>DJ Evans</dc:creator>
    <dc:creator>DG Evans</dc:creator>
    <dc:source>Helicobacter, Vol. 5, No. 4. (December 2000), pp. 183-195.</dc:source>
    <dc:date>2008-03-30T05:00:12-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Helicobacter</prism:publicationName>
    <prism:issn>1083-4389</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>183</prism:startingPage>
    <prism:endingPage>195</prism:endingPage>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2564402">
    <title>Epidemiology of Helicobacter pylori infection.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2564402</link>
    <description>&lt;i&gt;Helicobacter, Vol. 9 Suppl 1 (2004), pp. 1-6.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This review summarizes key results of epidemiologic studies published in peer-reviewed journals between April 2003 and March 2004. The prevalence of H. pylori infection continues to vary strongly between developing countries and developed countries, and according to ethnicity, place of birth and socioeconomic factors among people living in the same country. Intrafamilial spread appears to play a central role in transmission of the infection in both developing and developed countries. The role of H. pylori infection in development of noncardia gastric cancer appears to be even much stronger than previously assumed, whereas the lack of an association with cardia cancer and an inverse association with adenocarcinoma of the esophagus could be confirmed. Suggestions for an inverse association of the infection with atopic diseases have recently received further support, whereas evidence concerning the role of the infection (or its eradication) in GERD and a large variety of other extragastric diseases, including cardiovascular disease, remains inconclusive.</description>
    <dc:title>Epidemiology of Helicobacter pylori infection.</dc:title>

    <dc:creator>GI Perez-Perez</dc:creator>
    <dc:creator>D Rothenbacher</dc:creator>
    <dc:creator>H Brenner</dc:creator>
    <dc:identifier>doi:10.1111/j.1083-4389.2004.00248.x</dc:identifier>
    <dc:source>Helicobacter, Vol. 9 Suppl 1 (2004), pp. 1-6.</dc:source>
    <dc:date>2008-03-19T23:27:05-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Helicobacter</prism:publicationName>
    <prism:issn>1083-4389</prism:issn>
    <prism:volume>9 Suppl 1</prism:volume>
    <prism:startingPage>1</prism:startingPage>
    <prism:endingPage>6</prism:endingPage>
    <prism:category>epidemiology</prism:category>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1302512">
    <title>Helicobacter pylori evolution and phenotypic diversification in a changing host</title>
    <link>http://www.citeulike.org/user/xingxu/article/1302512</link>
    <description>&lt;i&gt;Nature Reviews Microbiology, Vol. 5, No. 6., pp. 441-452.&lt;/i&gt;</description>
    <dc:title>Helicobacter pylori evolution and phenotypic diversification in a changing host</dc:title>

    <dc:creator>Sebastian Suerbaum</dc:creator>
    <dc:creator>Christine Josenhans</dc:creator>
    <dc:identifier>doi:10.1038/nrmicro1658</dc:identifier>
    <dc:source>Nature Reviews Microbiology, Vol. 5, No. 6., pp. 441-452.</dc:source>
    <dc:date>2007-05-17T15:09:42-00:00</dc:date>
    <prism:publicationName>Nature Reviews Microbiology</prism:publicationName>
    <prism:issn>1740-1526</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>441</prism:startingPage>
    <prism:endingPage>452</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>evolution</prism:category>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2485963">
    <title>Membrane Topology and Insertion of Membrane Proteins: Search for Topogenic Signals</title>
    <link>http://www.citeulike.org/user/xingxu/article/2485963</link>
    <description>&lt;i&gt;Microbiol. Mol. Biol. Rev., Vol. 64, No. 1. (1 March 2000), pp. 13-33.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Integral membrane proteins are found in all cellular membranes and carry out many of the functions that are essential to life. The membrane-embedded domains of integral membrane proteins are structurally quite simple, allowing the use of various prediction methods and biochemical methods to obtain structural information about membrane proteins. A critical step in the biosynthetic pathway leading to the folded protein in the membrane is its insertion into the lipid bilayer. Understanding of the fundamentals of the insertion and folding processes will significantly improve the methods used to predict the three-dimensional membrane protein structure from the amino acid sequence. In the first part of this review, biochemical approaches to elucidate membrane protein topology are reviewed and evaluated, and in the second part, the use of similar techniques to study membrane protein insertion is discussed. The latter studies search for signals in the polypeptide chain that direct the insertion process. Knowledge of the topogenic signals in the nascent chain of a membrane protein is essential for the evaluation of membrane topology studies. 10.1128/MMBR.64.1.13-33.2000</description>
    <dc:title>Membrane Topology and Insertion of Membrane Proteins: Search for Topogenic Signals</dc:title>

    <dc:creator>Marleen van Geest</dc:creator>
    <dc:creator>Juke Lolkema</dc:creator>
    <dc:identifier>doi:10.1128/MMBR.64.1.13-33.2000</dc:identifier>
    <dc:source>Microbiol. Mol. Biol. Rev., Vol. 64, No. 1. (1 March 2000), pp. 13-33.</dc:source>
    <dc:date>2008-03-07T17:04:33-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Microbiol. Mol. Biol. Rev.</prism:publicationName>
    <prism:volume>64</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>13</prism:startingPage>
    <prism:endingPage>33</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>transmembrane</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/562745">
    <title>Evaluation of methods for the prediction of membrane spanning regions.</title>
    <link>http://www.citeulike.org/user/xingxu/article/562745</link>
    <description>&lt;i&gt;Bioinformatics, Vol. 17, No. 7. (July 2001), pp. 646-653.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;MOTIVATION: A variety of tools are available to predict the topology of transmembrane proteins. To date no independent evaluation of the performance of these tools has been published. A better understanding of the strengths and weaknesses of the different tools would guide both the biologist and the bioinformatician to make better predictions of membrane protein topology. RESULTS: Here we present an evaluation of the performance of the currently best known and most widely used methods for the prediction of transmembrane regions in proteins. Our results show that TMHMM is currently the best performing transmembrane prediction program.</description>
    <dc:title>Evaluation of methods for the prediction of membrane spanning regions.</dc:title>

    <dc:creator>S Möller</dc:creator>
    <dc:creator>MD Croning</dc:creator>
    <dc:creator>R Apweiler</dc:creator>
    <dc:identifier>doi:10.1093/bioinformatics/17.7.646</dc:identifier>
    <dc:source>Bioinformatics, Vol. 17, No. 7. (July 2001), pp. 646-653.</dc:source>
    <dc:date>2006-03-24T20:51:38-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Bioinformatics</prism:publicationName>
    <prism:issn>1367-4803</prism:issn>
    <prism:volume>17</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>646</prism:startingPage>
    <prism:endingPage>653</prism:endingPage>
    <prism:category>bioinformatics</prism:category>
    <prism:category>review</prism:category>
    <prism:category>transmembrane</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2445319">
    <title>Systematic analyses of the cancer genome: lessons learned from sequencing most of the annotated human protein-coding genes.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2445319</link>
    <description>&lt;i&gt;Curr Opin Oncol, Vol. 20, No. 1. (January 2008), pp. 66-71.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;PURPOSE OF REVIEW: The availability of a reference human genome sequence has enabled unbiased mutational analyses of tumor genomes to identify the mutated genes that cause cancer. This review discusses recent insights from such analyses of protein-coding genes in breast and colorectal cancers. RECENT FINDINGS: Mutational analyses of approximately 18,000 human protein-coding genes in breast and colorectal cancers have identified 280 candidate cancer genes. These include known cancer genes, but most had not previously been linked to cancer. There are few frequently mutated cancer genes among hundreds of less frequently mutated candidate cancer genes, and the compendium of mutated genes differs among tumors of the same tissue origin. SUMMARY: Recent work has shown the feasibility of coding cancer genome sequencing, and new technologies promise to facilitate these mutational analyses. Whereas cancer genetics can identify candidate genes in a rapid and scalable fashion, careful functional studies of mutated genes are required for ultimate proof of cancer gene status and translation into clinical utility. The rapid progress of cancer genetics has yielded novel diagnostic and therapeutic modalities, and cancer genome sequencing will accelerate this development to the benefit of cancer patients.</description>
    <dc:title>Systematic analyses of the cancer genome: lessons learned from sequencing most of the annotated human protein-coding genes.</dc:title>

    <dc:creator>T Sjöblom</dc:creator>
    <dc:identifier>doi:10.1097/CCO.0b013e3282f31108</dc:identifier>
    <dc:source>Curr Opin Oncol, Vol. 20, No. 1. (January 2008), pp. 66-71.</dc:source>
    <dc:date>2008-02-28T22:00:28-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Curr Opin Oncol</prism:publicationName>
    <prism:issn>1040-8746</prism:issn>
    <prism:volume>20</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>66</prism:startingPage>
    <prism:endingPage>71</prism:endingPage>
    <prism:category>cancer</prism:category>
    <prism:category>genomics</prism:category>
    <prism:category>review</prism:category>
    <prism:category>somatic</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2409622">
    <title>Communication modules in bacterial signaling proteins.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2409622</link>
    <description>&lt;i&gt;Annu Rev Genet, Vol. 26 (1992), pp. 71-112.&lt;/i&gt;</description>
    <dc:title>Communication modules in bacterial signaling proteins.</dc:title>

    <dc:creator>JS Parkinson</dc:creator>
    <dc:creator>EC Kofoid</dc:creator>
    <dc:identifier>doi:10.1146/annurev.ge.26.120192.000443</dc:identifier>
    <dc:source>Annu Rev Genet, Vol. 26 (1992), pp. 71-112.</dc:source>
    <dc:date>2008-02-21T23:01:16-00:00</dc:date>
    <prism:publicationYear>1992</prism:publicationYear>
    <prism:publicationName>Annu Rev Genet</prism:publicationName>
    <prism:issn>0066-4197</prism:issn>
    <prism:volume>26</prism:volume>
    <prism:startingPage>71</prism:startingPage>
    <prism:endingPage>112</prism:endingPage>
    <prism:category>microbiology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2409617">
    <title>Two-component signal transduction.</title>
    <link>http://www.citeulike.org/user/xingxu/article/2409617</link>
    <description>&lt;i&gt;Annu Rev Biochem, Vol. 69 (2000), pp. 183-215.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Most prokaryotic signal-transduction systems and a few eukaryotic pathways use phosphotransfer schemes involving two conserved components, a histidine protein kinase and a response regulator protein. The histidine protein kinase, which is regulated by environmental stimuli, autophosphorylates at a histidine residue, creating a high-energy phosphoryl group that is subsequently transferred to an aspartate residue in the response regulator protein. Phosphorylation induces a conformational change in the regulatory domain that results in activation of an associated domain that effects the response. The basic scheme is highly adaptable, and numerous variations have provided optimization within specific signaling systems. The domains of two-component proteins are modular and can be integrated into proteins and pathways in a variety of ways, but the core structures and activities are maintained. Thus detailed analyses of a relatively small number of representative proteins provide a foundation for understanding this large family of signaling proteins.</description>
    <dc:title>Two-component signal transduction.</dc:title>

    <dc:creator>AM Stock</dc:creator>
    <dc:creator>VL Robinson</dc:creator>
    <dc:creator>PN Goudreau</dc:creator>
    <dc:identifier>doi:10.1146/annurev.biochem.69.1.183</dc:identifier>
    <dc:source>Annu Rev Biochem, Vol. 69 (2000), pp. 183-215.</dc:source>
    <dc:date>2008-02-21T23:00:26-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Annu Rev Biochem</prism:publicationName>
    <prism:issn>0066-4154</prism:issn>
    <prism:volume>69</prism:volume>
    <prism:startingPage>183</prism:startingPage>
    <prism:endingPage>215</prism:endingPage>
    <prism:category>microbiology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
    <prism:category>textbook</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2353649">
    <title>Modulated receptor interactions in bacterial transmembrane signaling</title>
    <link>http://www.citeulike.org/user/xingxu/article/2353649</link>
    <description>&lt;i&gt;Trends in Cell Biology, Vol. 14, No. 9. (September 2004), pp. 478-482.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Bacteria can detect and respond to a remarkably diverse set of environmental conditions. This ability enables motile species to integrate stimuli, to compare current surroundings with those of the recent past, and to adjust swimming behavior to move up gradients of attractants and avoid repellents. Many of the molecular details involved in the bacterial chemotaxis system have been elucidated. Several models have been proposed recently to explain how cells process external information through a patch of highly interactive transmembrane receptors and transduce this information to other components in the cytoplasm that, in turn, function to regulate motility.</description>
    <dc:title>Modulated receptor interactions in bacterial transmembrane signaling</dc:title>

    <dc:creator>Daniel Webre</dc:creator>
    <dc:creator>Peter Wolanin</dc:creator>
    <dc:creator>Jeffry Stock</dc:creator>
    <dc:identifier>doi:10.1016/j.tcb.2004.07.015</dc:identifier>
    <dc:source>Trends in Cell Biology, Vol. 14, No. 9. (September 2004), pp. 478-482.</dc:source>
    <dc:date>2008-02-08T15:17:11-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Trends in Cell Biology</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>478</prism:startingPage>
    <prism:endingPage>482</prism:endingPage>
    <prism:category>interactions</prism:category>
    <prism:category>microbiology</prism:category>
    <prism:category>receptor</prism:category>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
    <prism:category>transmembrane</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2231309">
    <title>Polymorphisms in Toll-like receptor genes and risk of cancer</title>
    <link>http://www.citeulike.org/user/xingxu/article/2231309</link>
    <description>&lt;i&gt;Oncogene, Vol. 27, No. 2. (0000), pp. 244-252.&lt;/i&gt;</description>
    <dc:title>Polymorphisms in Toll-like receptor genes and risk of cancer</dc:title>

    <dc:creator>EM El-Omar</dc:creator>
    <dc:creator>MT Ng</dc:creator>
    <dc:creator>GL Hold</dc:creator>
    <dc:identifier>doi:10.1038/sj.onc.1210912</dc:identifier>
    <dc:source>Oncogene, Vol. 27, No. 2. (0000), pp. 244-252.</dc:source>
    <dc:date>2008-01-14T18:02:11-00:00</dc:date>
    <prism:publicationYear>0000</prism:publicationYear>
    <prism:publicationName>Oncogene</prism:publicationName>
    <prism:volume>27</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>244</prism:startingPage>
    <prism:endingPage>252</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cancer</prism:category>
    <prism:category>gastric</prism:category>
    <prism:category>pylori</prism:category>
    <prism:category>review</prism:category>
    <prism:category>toll</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2220583">
    <title>Next generation sequencing technologies</title>
    <link>http://www.citeulike.org/user/xingxu/article/2220583</link>
    <description>&lt;i&gt;Drug Discovery Today: Technologies, Vol. 2, No. 3. ( 2005), pp. 255-260.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;From the investigation of disease-associated loci in humans, to monitoring the changing genomes of pathogenic viruses and bacteria, sequencing is a powerful and versatile tool. A new generation of sequencing technologies will increase the speed and lower the cost of sequencing, and promises to expand the utility of sequencing in drug discovery and development.</description>
    <dc:title>Next generation sequencing technologies</dc:title>

    <dc:creator>Thomas Jarvie</dc:creator>
    <dc:identifier>doi:10.1016/j.ddtec.2005.08.003</dc:identifier>
    <dc:source>Drug Discovery Today: Technologies, Vol. 2, No. 3. ( 2005), pp. 255-260.</dc:source>
    <dc:date>2008-01-11T19:22:25-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Drug Discovery Today: Technologies</prism:publicationName>
    <prism:volume>2</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>255</prism:startingPage>
    <prism:endingPage>260</prism:endingPage>
    <prism:category>prospective</prism:category>
    <prism:category>review</prism:category>
    <prism:category>sequencing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2216185">
    <title>Advanced sequencing technologies and their wider impact in microbiology</title>
    <link>http://www.citeulike.org/user/xingxu/article/2216185</link>
    <description>&lt;i&gt;J Exp Biol, Vol. 210, No. 9. (1 May 2007), pp. 1518-1525.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In the past 10 years, microbiology has undergone a revolution that has been driven by access to cheap high-throughput DNA sequencing. It was not long ago that the cloning and sequencing of a target gene could take months or years, whereas now this entire process has been replaced by a 10 min Internet search of a public genome database. There has been no single innovation that has initiated this rapid technological change; in fact, the core chemistry of DNA sequencing is the same as it was 30 years ago. Instead, progress has been driven by large sequencing centers that have incrementally industrialized the Sanger sequencing method. A side effect of this industrialization is that large-scale sequencing has moved out of small research labs, and the vast majority of sequence data is now generated by large genome centers. Recently, there have been advances in technology that will enable high-throughput genome sequencing to be established in research labs using bench-top instrumentation. These new technologies are already being used to explore the vast microbial diversity in the natural environment and the untapped genetic variation that can occur in bacterial species. It is expected that these powerful new methods will open up new questions to genomic investigation and will also allow high-throughput sequencing to be more than just a discovery exercise but also a routine assay for hypothesis testing. While this review will concentrate on microorganisms, many of the important arguments about the need to measure and understand variation at the species, population and ecosystem level will hold true for many other biological systems. 10.1242/jeb.001370</description>
    <dc:title>Advanced sequencing technologies and their wider impact in microbiology</dc:title>

    <dc:creator>Neil Hall</dc:creator>
    <dc:identifier>doi:10.1242/jeb.001370</dc:identifier>
    <dc:source>J Exp Biol, Vol. 210, No. 9. (1 May 2007), pp. 1518-1525.</dc:source>
    <dc:date>2008-01-10T21:05:28-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>J Exp Biol</prism:publicationName>
    <prism:volume>210</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>1518</prism:startingPage>
    <prism:endingPage>1525</prism:endingPage>
    <prism:category>microbiology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>sequencing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2179247">
    <title>Next-generation sequencing transforms today's biology</title>
    <link>http://www.citeulike.org/user/xingxu/article/2179247</link>
    <description>&lt;i&gt;Nature Methods, Vol. 5, No. 1. (19 December 2007), pp. 16-18.&lt;/i&gt;</description>
    <dc:title>Next-generation sequencing transforms today's biology</dc:title>

    <dc:creator>Stephan Schuster</dc:creator>
    <dc:identifier>doi:10.1038/nmeth1156</dc:identifier>
    <dc:source>Nature Methods, Vol. 5, No. 1. (19 December 2007), pp. 16-18.</dc:source>
    <dc:date>2007-12-29T05:58:24-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nature Methods</prism:publicationName>
    <prism:issn>1548-7091</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>16</prism:startingPage>
    <prism:endingPage>18</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>news</prism:category>
    <prism:category>opinion</prism:category>
    <prism:category>review</prism:category>
    <prism:category>sequencing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2179248">
    <title>Primer: Sequencing—the next generation</title>
    <link>http://www.citeulike.org/user/xingxu/article/2179248</link>
    <description>&lt;i&gt;Nature Methods, Vol. 5, No. 1. (19 December 2007), pp. 15-15.&lt;/i&gt;</description>
    <dc:title>Primer: Sequencing—the next generation</dc:title>

    <dc:creator>Nicole Rusk</dc:creator>
    <dc:creator>Veronique Kiermer</dc:creator>
    <dc:identifier>doi:10.1038/nmeth1155</dc:identifier>
    <dc:source>Nature Methods, Vol. 5, No. 1. (19 December 2007), pp. 15-15.</dc:source>
    <dc:date>2007-12-29T05:58:24-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nature Methods</prism:publicationName>
    <prism:issn>1548-7091</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>15</prism:startingPage>
    <prism:endingPage>15</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>review</prism:category>
    <prism:category>sequencing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1160439">
    <title>Viral metagenomics</title>
    <link>http://www.citeulike.org/user/xingxu/article/1160439</link>
    <description>&lt;i&gt;Reviews in Medical Virology, Vol. 17, No. 2. (March 2007), pp. 115-131.&lt;/i&gt;</description>
    <dc:title>Viral metagenomics</dc:title>

    <dc:creator>Delwart</dc:creator>
    <dc:creator>L Eric</dc:creator>
    <dc:identifier>doi:10.1002/rmv.532</dc:identifier>
    <dc:source>Reviews in Medical Virology, Vol. 17, No. 2. (March 2007), pp. 115-131.</dc:source>
    <dc:date>2007-03-14T15:32:59-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Reviews in Medical Virology</prism:publicationName>
    <prism:issn>1052-9276</prism:issn>
    <prism:volume>17</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>115</prism:startingPage>
    <prism:endingPage>131</prism:endingPage>
    <prism:publisher>John Wiley &#38; Sons, Ltd.</prism:publisher>
    <prism:category>metagenomics</prism:category>
    <prism:category>review</prism:category>
    <prism:category>virology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/2051896">
    <title>The influence of genetic variation on gene expression</title>
    <link>http://www.citeulike.org/user/xingxu/article/2051896</link>
    <description>&lt;i&gt;Genome Res., Vol. 17, No. 12. (1 December 2007), pp. 1707-1716.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The view that changes to the control of gene expression rather than alterations to protein sequence are central to the evolution of organisms has become something of a truism in molecular biology. In reality, the direct evidence for this is limited, and only recently have we had the ability to look more globally at how genetic variation influences gene expression, focusing upon inter-individual variation in gene expression and using microarrays to test for differences in mRNA levels. Here, we review the scope of these experimental analyses, what they are designed to tell us about genetic variation, and what are their limitations from both a technical and a conceptual viewpoint. We conclude that while we are starting to understand the impact of this class of genetic variation upon steady-state mRNA levels, we are still far from identifying the potential phenotypic and evolutionary outcomes. 10.1101/gr.6981507</description>
    <dc:title>The influence of genetic variation on gene expression</dc:title>

    <dc:creator>Rohan Williams</dc:creator>
    <dc:creator>Eva Chan</dc:creator>
    <dc:creator>Mark Cowley</dc:creator>
    <dc:creator>Peter Little</dc:creator>
    <dc:identifier>doi:10.1101/gr.6981507</dc:identifier>
    <dc:source>Genome Res., Vol. 17, No. 12. (1 December 2007), pp. 1707-1716.</dc:source>
    <dc:date>2007-12-03T18:49:51-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Genome Res.</prism:publicationName>
    <prism:volume>17</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1707</prism:startingPage>
    <prism:endingPage>1716</prism:endingPage>
    <prism:category>expression</prism:category>
    <prism:category>review</prism:category>
    <prism:category>variability</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1307464">
    <title>Network motifs: theory and experimental approaches</title>
    <link>http://www.citeulike.org/user/xingxu/article/1307464</link>
    <description>&lt;i&gt;Nature Reviews Genetics, Vol. 8, No. 6., pp. 450-461.&lt;/i&gt;</description>
    <dc:title>Network motifs: theory and experimental approaches</dc:title>

    <dc:creator>Uri Alon</dc:creator>
    <dc:identifier>doi:10.1038/nrg2102</dc:identifier>
    <dc:source>Nature Reviews Genetics, Vol. 8, No. 6., pp. 450-461.</dc:source>
    <dc:date>2007-05-19T03:15:41-00:00</dc:date>
    <prism:publicationName>Nature Reviews Genetics</prism:publicationName>
    <prism:issn>1471-0056</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>450</prism:startingPage>
    <prism:endingPage>461</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>network</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1928086">
    <title>Evolutionary developmental biology and genomics</title>
    <link>http://www.citeulike.org/user/xingxu/article/1928086</link>
    <description>&lt;i&gt;Nature Reviews Genetics, Vol. 8, No. 12., pp. 932-942.&lt;/i&gt;</description>
    <dc:title>Evolutionary developmental biology and genomics</dc:title>

    <dc:creator>Cristian Cañestro</dc:creator>
    <dc:creator>Hayato Yokoi</dc:creator>
    <dc:creator>John Postlethwait</dc:creator>
    <dc:identifier>doi:10.1038/nrg2226</dc:identifier>
    <dc:source>Nature Reviews Genetics, Vol. 8, No. 12., pp. 932-942.</dc:source>
    <dc:date>2007-11-16T20:59:31-00:00</dc:date>
    <prism:publicationName>Nature Reviews Genetics</prism:publicationName>
    <prism:issn>1471-0056</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>932</prism:startingPage>
    <prism:endingPage>942</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>development</prism:category>
    <prism:category>evolution</prism:category>
    <prism:category>genomics</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1927977">
    <title>Multimetal resistance and tolerance in microbial biofilms</title>
    <link>http://www.citeulike.org/user/xingxu/article/1927977</link>
    <description>&lt;i&gt;Nature Reviews Microbiology, Vol. 5, No. 12., pp. 928-938.&lt;/i&gt;</description>
    <dc:title>Multimetal resistance and tolerance in microbial biofilms</dc:title>

    <dc:creator>Joe Harrison</dc:creator>
    <dc:creator>Howard Ceri</dc:creator>
    <dc:creator>Raymond Turner</dc:creator>
    <dc:identifier>doi:10.1038/nrmicro1774</dc:identifier>
    <dc:source>Nature Reviews Microbiology, Vol. 5, No. 12., pp. 928-938.</dc:source>
    <dc:date>2007-11-16T20:56:46-00:00</dc:date>
    <prism:publicationName>Nature Reviews Microbiology</prism:publicationName>
    <prism:issn>1740-1526</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>928</prism:startingPage>
    <prism:endingPage>938</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>biofilms</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1411336">
    <title>How Ebola and Marburg viruses battle the immune system</title>
    <link>http://www.citeulike.org/user/xingxu/article/1411336</link>
    <description>&lt;i&gt;Nature Reviews Immunology, Vol. 7, No. 7., pp. 556-567.&lt;/i&gt;</description>
    <dc:title>How Ebola and Marburg viruses battle the immune system</dc:title>

    <dc:creator>Mansour Mohamadzadeh</dc:creator>
    <dc:creator>Lieping Chen</dc:creator>
    <dc:creator>Alan Schmaljohn</dc:creator>
    <dc:identifier>doi:10.1038/nri2098</dc:identifier>
    <dc:source>Nature Reviews Immunology, Vol. 7, No. 7., pp. 556-567.</dc:source>
    <dc:date>2007-06-25T17:04:21-00:00</dc:date>
    <prism:publicationName>Nature Reviews Immunology</prism:publicationName>
    <prism:issn>1474-1733</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>556</prism:startingPage>
    <prism:endingPage>567</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>immunology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>virology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1572693">
    <title>The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?</title>
    <link>http://www.citeulike.org/user/xingxu/article/1572693</link>
    <description>&lt;i&gt;Trends Genet, Vol. 23, No. 5. (May 2007), pp. 219-224.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Pseudogenes have long been considered to be 'dead', nonfunctional by-products of genome evolution. However, several lines of evidence now show that some pseudogenes are transcriptionally 'alive', and a few might even have biochemical roles. Therefore, the boundary between genes (often considered to be 'living') and pseudogenes (often considered to be 'dead') might be ambiguous and difficult to define. Here, we examine the evidence for and against pseudogene functionality, and we argue that the time is ripe for revising the definition of a pseudogene. Furthermore, we suggest a classification system to accommodate pseudogenes with various levels of functionality.</description>
    <dc:title>The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?</dc:title>

    <dc:creator>D Zheng</dc:creator>
    <dc:creator>MB Gerstein</dc:creator>
    <dc:identifier>doi:10.1016/j.tig.2007.03.003</dc:identifier>
    <dc:source>Trends Genet, Vol. 23, No. 5. (May 2007), pp. 219-224.</dc:source>
    <dc:date>2007-08-17T16:28:03-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Trends Genet</prism:publicationName>
    <prism:issn>0168-9525</prism:issn>
    <prism:volume>23</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>219</prism:startingPage>
    <prism:endingPage>224</prism:endingPage>
    <prism:category>pseudogene</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1184077">
    <title>Inflammation in prostate carcinogenesis</title>
    <link>http://www.citeulike.org/user/xingxu/article/1184077</link>
    <description>&lt;i&gt;Nature Reviews Cancer, Vol. 7, No. 4., pp. 256-269.&lt;/i&gt;</description>
    <dc:title>Inflammation in prostate carcinogenesis</dc:title>

    <dc:creator>Angelo De Marzo</dc:creator>
    <dc:creator>Elizabeth Platz</dc:creator>
    <dc:creator>Siobhan Sutcliffe</dc:creator>
    <dc:creator>Jianfeng Xu</dc:creator>
    <dc:creator>Henrik Grönberg</dc:creator>
    <dc:creator>Charles Drake</dc:creator>
    <dc:creator>Yasutomo Nakai</dc:creator>
    <dc:creator>William Isaacs</dc:creator>
    <dc:creator>William Nelson</dc:creator>
    <dc:identifier>doi:10.1038/nrc2090</dc:identifier>
    <dc:source>Nature Reviews Cancer, Vol. 7, No. 4., pp. 256-269.</dc:source>
    <dc:date>2007-03-24T18:09:46-00:00</dc:date>
    <prism:publicationName>Nature Reviews Cancer</prism:publicationName>
    <prism:issn>1474-175X</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>256</prism:startingPage>
    <prism:endingPage>269</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>inflammation</prism:category>
    <prism:category>prostate</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1333516">
    <title>Morphogens, morphostats, microarchitecture and malignancy</title>
    <link>http://www.citeulike.org/user/xingxu/article/1333516</link>
    <description>&lt;i&gt;Nature Reviews Cancer, Vol. 7, No. 6., pp. 464-474.&lt;/i&gt;</description>
    <dc:title>Morphogens, morphostats, microarchitecture and malignancy</dc:title>

    <dc:creator>John Potter</dc:creator>
    <dc:identifier>doi:10.1038/nrc2146</dc:identifier>
    <dc:source>Nature Reviews Cancer, Vol. 7, No. 6., pp. 464-474.</dc:source>
    <dc:date>2007-05-25T19:44:16-00:00</dc:date>
    <prism:publicationName>Nature Reviews Cancer</prism:publicationName>
    <prism:issn>1474-175X</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>464</prism:startingPage>
    <prism:endingPage>474</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cancer</prism:category>
    <prism:category>microenvironment</prism:category>
    <prism:category>morphogens</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1333517">
    <title>Nuclear microenvironments in biological control and cancer</title>
    <link>http://www.citeulike.org/user/xingxu/article/1333517</link>
    <description>&lt;i&gt;Nature Reviews Cancer, Vol. 7, No. 6., pp. 454-463.&lt;/i&gt;</description>
    <dc:title>Nuclear microenvironments in biological control and cancer</dc:title>

    <dc:creator>Sayyed Zaidi</dc:creator>
    <dc:creator>Daniel Young</dc:creator>
    <dc:creator>Amjad Javed</dc:creator>
    <dc:creator>Jitesh Pratap</dc:creator>
    <dc:creator>Martin Montecino</dc:creator>
    <dc:creator>Andre van Wijnen</dc:creator>
    <dc:creator>Jane Lian</dc:creator>
    <dc:creator>Janet Stein</dc:creator>
    <dc:creator>Gary Stein</dc:creator>
    <dc:identifier>doi:10.1038/nrc2149</dc:identifier>
    <dc:source>Nature Reviews Cancer, Vol. 7, No. 6., pp. 454-463.</dc:source>
    <dc:date>2007-05-25T19:44:16-00:00</dc:date>
    <prism:publicationName>Nature Reviews Cancer</prism:publicationName>
    <prism:issn>1474-175X</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>454</prism:startingPage>
    <prism:endingPage>463</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>cancer</prism:category>
    <prism:category>microenvironment</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1541317">
    <title>Uridine insertion/deletion RNA editing in trypanosome mitochondria -- a review</title>
    <link>http://www.citeulike.org/user/xingxu/article/1541317</link>
    <description>&lt;i&gt;Gene, Vol. 240, No. 2. (29 November 1999), pp. 247-260.&lt;/i&gt;</description>
    <dc:title>Uridine insertion/deletion RNA editing in trypanosome mitochondria -- a review</dc:title>

    <dc:creator>Antonio Estevez</dc:creator>
    <dc:creator>Larry Simpson</dc:creator>
    <dc:identifier>doi:10.1016/S0378-1119(99)00437-0</dc:identifier>
    <dc:source>Gene, Vol. 240, No. 2. (29 November 1999), pp. 247-260.</dc:source>
    <dc:date>2007-08-07T16:12:44-00:00</dc:date>
    <prism:publicationYear>1999</prism:publicationYear>
    <prism:publicationName>Gene</prism:publicationName>
    <prism:volume>240</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>247</prism:startingPage>
    <prism:endingPage>260</prism:endingPage>
    <prism:category>parasitology</prism:category>
    <prism:category>review</prism:category>
    <prism:category>rna-editing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1530871">
    <title>Hedgehog Signaling Pathway</title>
    <link>http://www.citeulike.org/user/xingxu/article/1530871</link>
    <description>&lt;i&gt;Cell, Vol. 130 (2007)&lt;/i&gt;</description>
    <dc:title>Hedgehog Signaling Pathway</dc:title>

    <dc:creator>Miao-Hsueh Chen</dc:creator>
    <dc:source>Cell, Vol. 130 (2007)</dc:source>
    <dc:date>2007-08-02T15:01:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Cell</prism:publicationName>
    <prism:volume>130</prism:volume>
    <prism:category>diagram</prism:category>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/xingxu/article/1530797">
    <title>Notch signaling: control of cell communication and cell fate</title>
    <link>http://www.citeulike.org/user/xingxu/article/1530797</link>
    <description>&lt;i&gt;Development, Vol. 131, No. 5. (1 March 2004), pp. 965-973.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Notch is a transmembrane receptor that mediates local cell-cell communication and coordinates a signaling cascade present in all animal species studied to date. Notch signaling is used widely to determine cell fates and to regulate pattern formation; its dysfunction results in a tremendous variety of developmental defects and adult pathologies. This primer describes the mechanism of Notch signal transduction and how it is used to control the formation of biological patterns. 10.1242/dev.01074</description>
    <dc:title>Notch signaling: control of cell communication and cell fate</dc:title>

    <dc:creator>Eric Lai</dc:creator>
    <dc:identifier>doi:10.1242/dev.01074</dc:identifier>
    <dc:source>Development, Vol. 131, No. 5. (1 March 2004), pp. 965-973.</dc:source>
    <dc:date>2007-08-02T14:54:50-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Development</prism:publicationName>
    <prism:volume>131</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>965</prism:startingPage>
    <prism:endingPage>973</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>signaling</prism:category>
</item>



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