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  <title>DSpace Collection:</title>
  <link rel="alternate" href="http://hdl.handle.net/10400.18/19" />
  <subtitle />
  <id>http://hdl.handle.net/10400.18/19</id>
  <updated>2013-06-08T07:06:51Z</updated>
  <dc:date>2013-06-08T07:06:51Z</dc:date>
  <entry>
    <title>Natural polymorphisms of HIV type 2 pol sequences from drug-naive individuals</title>
    <link rel="alternate" href="http://hdl.handle.net/10400.18/1587" />
    <author>
      <name>Parreira, R.</name>
    </author>
    <author>
      <name>Monteiro, F.</name>
    </author>
    <author>
      <name>Pádua, E.</name>
    </author>
    <author>
      <name>Piedade, J.</name>
    </author>
    <author>
      <name>Venenno, T.</name>
    </author>
    <author>
      <name>Paixão, M.T.</name>
    </author>
    <author>
      <name>Esteves, A.</name>
    </author>
    <id>http://hdl.handle.net/10400.18/1587</id>
    <updated>2013-06-04T10:51:37Z</updated>
    <published>2006-11-01T00:00:00Z</published>
    <summary type="text">Title: Natural polymorphisms of HIV type 2 pol sequences from drug-naive individuals
Authors: Parreira, R.; Monteiro, F.; Pádua, E.; Piedade, J.; Venenno, T.; Paixão, M.T.; Esteves, A.
Abstract: Until today, the susceptibility of human immunodeficiency virus type 2 (HIV-2) to protease and nucleosidic reverse-transcriptase inhibitors (PI and NRTI, respectively) has not been clearly documented. In this report we studied HIV-2 proviral sequences (n = 30) from drug-naive patients. Our results revealed that several amino acid positions in the protease and reverse transcriptase coding sequence harbored residues that have been associated with drug resistance in HIV-1-infected patients. In particular, the M46I substitution in the protease was detected in 90% of the sequences analyzed, which, together with the other substitutions identified, may indicate a reduced susceptibility of HIV-2-infected drug-naive patients to PI. Furthermore, interpretation of genotypic data with four available algorithms, developed for interpretation of HIV-1 sequence data, suggested nonoverlapping profiles of drug resistance.</summary>
    <dc:date>2006-11-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Natural variation of the nef gene in human immunodeficiency virus type 2 infections in Portugal</title>
    <link rel="alternate" href="http://hdl.handle.net/10400.18/1586" />
    <author>
      <name>Pádua, E.</name>
    </author>
    <author>
      <name>Jenkins, A.</name>
    </author>
    <author>
      <name>Brown, S.</name>
    </author>
    <author>
      <name>Bootman, J.</name>
    </author>
    <author>
      <name>Paixão, M.T.</name>
    </author>
    <author>
      <name>Almond, N.</name>
    </author>
    <author>
      <name>Berry, N.</name>
    </author>
    <id>http://hdl.handle.net/10400.18/1586</id>
    <updated>2013-05-30T01:34:29Z</updated>
    <published>2003-05-01T00:00:00Z</published>
    <summary type="text">Title: Natural variation of the nef gene in human immunodeficiency virus type 2 infections in Portugal
Authors: Pádua, E.; Jenkins, A.; Brown, S.; Bootman, J.; Paixão, M.T.; Almond, N.; Berry, N.
Abstract: Human immunodeficiency virus type 2 (HIV-2) infections cause severe immunodeficiency in humans, although HIV-2 is associated frequently with reduced virulence and pathogenicity compared to HIV-1. Genetic determinants that play a role in HIV pathogenesis are relatively poorly understood but nef has been implicated in inducing a more pathogenic phenotype in vivo. However, relatively little is known about the role of nef in HIV-2 pathogenesis. To address this, the genetic composition of 44 nef alleles from 37 HIV-2-infected individuals in Portugal, encompassing a wide spectrum of disease associations, CD4 counts and virus load, has been assessed. All nef alleles were subtype A, with no evidence of gross deletions, truncations or disruptions in the nef-encoding sequence; all were full-length and intact. HIV-2 long terminal repeat sequences were conserved and also indicated subtype A infections. Detailed analysis of motifs that mediate nef function in HIV-1 and simian immunodeficiency virus, such as CD4 downregulation and putative SH2/SH3 interactions, revealed significant natural variation. In particular, the central P(104)xxPLR motif exhibited wide interpatient variation, ranging from an HIV-1-like tetra-proline structure (PxxP)(3) to a disrupted minimal core motif (P(104)xxQLR). The P(107)--&gt;Q substitution was associated with an asymptomatic phenotype (Fisher's exact test, P=0.026) and low virus loads. These data indicate that discrete differences in the nef gene sequence rather than gross structural changes are more likely to play a role in HIV-2 pathogenesis mediated via specific functional interactions.</summary>
    <dc:date>2003-05-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Validation of a PNA-FISH method for the detection of Helicobacter pylori</title>
    <link rel="alternate" href="http://hdl.handle.net/10400.18/1585" />
    <author>
      <name>Cerqueira, L.</name>
    </author>
    <author>
      <name>Fernandes, RM.</name>
    </author>
    <author>
      <name>Ferreira, RM.</name>
    </author>
    <author>
      <name>Oleastro, M.</name>
    </author>
    <author>
      <name>Carneiro, F.</name>
    </author>
    <author>
      <name>Brandão, C.</name>
    </author>
    <author>
      <name>Pimentel-Nunes, P.</name>
    </author>
    <author>
      <name>Dinis-Ribeiro, M.</name>
    </author>
    <author>
      <name>Figueiredo, C.</name>
    </author>
    <author>
      <name>Keevil, CW.</name>
    </author>
    <author>
      <name>Vieira, MJ.</name>
    </author>
    <author>
      <name>Azevedo, NF.</name>
    </author>
    <id>http://hdl.handle.net/10400.18/1585</id>
    <updated>2013-06-04T10:51:59Z</updated>
    <published>2013-04-17T00:00:00Z</published>
    <summary type="text">Title: Validation of a PNA-FISH method for the detection of Helicobacter pylori
Authors: Cerqueira, L.; Fernandes, RM.; Ferreira, RM.; Oleastro, M.; Carneiro, F.; Brandão, C.; Pimentel-Nunes, P.; Dinis-Ribeiro, M.; Figueiredo, C.; Keevil, CW.; Vieira, MJ.; Azevedo, NF.
Abstract: Here, we evaluated a previously established peptide nucleic acid-fluorescence in situ hybridization (PNA-FISH) method as a new&#xD;
diagnostic test for Helicobacter pylori clarithromycin resistance detection in paraffin-embedded gastric biopsy specimens. Both&#xD;
a retrospective study and a prospective cohort study were conducted to evaluate the specificity and sensitivity of a PNA-FISH&#xD;
method to determine H. pylori clarithromycin resistance. In the retrospective study (n 30 patients), full agreement between&#xD;
PNA-FISH and PCR-sequencing was observed. Compared to the reference method (culture followed by Etest), the specificity and&#xD;
sensitivity of PNA-FISH were 90.9% (95% confidence interval [CI], 57.1% to 99.5%) and 84.2% (95% CI, 59.5% to 95.8%), respectively.&#xD;
In the prospective cohort (n 93 patients), 21 cases were positive by culture. For the patients harboring clarithromycin-&#xD;
resistant H. pylori, the method showed sensitivity of 80.0% (95% CI, 29.9% to 98.9%) and specificity of 93.8% (95% CI,&#xD;
67.7% to 99.7%). These values likely represent underestimations, as some of the discrepant results corresponded to patients infected&#xD;
by more than one strain. PNA-FISH appears to be a simple, quick, and accurate method for detecting H. pylori clarithromycin&#xD;
resistance in paraffin-embedded biopsy specimens. It is also the only one of the methods assessed here that allows direct&#xD;
and specific visualization of this microorganism within the biopsy specimens, a characteristic that allowed the observation that&#xD;
cells of different H. pylori strains can subsist in very close proximity in the stomach.</summary>
    <dc:date>2013-04-17T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Chronic Q fever with no elevation of inflammatory markers: a case report</title>
    <link rel="alternate" href="http://hdl.handle.net/10400.18/1571" />
    <author>
      <name>Boattini, M.</name>
    </author>
    <author>
      <name>Almeida, A.</name>
    </author>
    <author>
      <name>Barata Moura, R.</name>
    </author>
    <author>
      <name>Abreu, J.</name>
    </author>
    <author>
      <name>Santos, A.S.</name>
    </author>
    <author>
      <name>Rico, M.T.</name>
    </author>
    <id>http://hdl.handle.net/10400.18/1571</id>
    <updated>2013-06-04T10:52:37Z</updated>
    <published>2012-06-26T00:00:00Z</published>
    <summary type="text">Title: Chronic Q fever with no elevation of inflammatory markers: a case report
Authors: Boattini, M.; Almeida, A.; Barata Moura, R.; Abreu, J.; Santos, A.S.; Rico, M.T.
Abstract: Chronic q Fever with no elevation of inflammatory markers: a case report.&#xD;
Boattini M, Almeida A, Moura RB, Abreu J, Santos AS, Toscano Rico M.&#xD;
SourceDepartment of Internal Medicine, St. Marta's Hospital, 1169-024 Lisbon, Portugal.&#xD;
&#xD;
Abstract&#xD;
We describe the case of a 55-year-old man with a biological prosthetic aortic valve who suffered from epigastrium and right hypochondrium pain associated with intermittent night sweats. Liver biopsy showed infectious hepatitis pattern without pathognomonic features. Coxiella burnetii serology was suggestive of chronic Q fever, and modified Duke's criteria for endocarditis were also fulfilled. The authors present a brief literature review concerning chronic Q fever, emphasizing absent previous reports of chronic Q fever with hepatitis and endocarditis and no increase in inflammatory markers.</summary>
    <dc:date>2012-06-26T00:00:00Z</dc:date>
  </entry>
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