I'm looking to find if there are any upper case letter(s) immediately following a dot in a file, except it happens to fall inside either/both of the tags <given-names>...</given-names>, <uri>...</uri>
Sample text:
The search should find only two positive matches in the above example namely .I from 1980s.In 1999
and .H from programs.However.
I have tried \.\u(?!([^<>]?</given-names>|[^<>]?</uri>)) but it doesn't work and I can't think of any other ways either.
Can anyone help?
Sample text:
Code: Select all
<title-group>
<article-title>The coreceptor mutation CCR5Δ32 influences the dynamics of HIV epidemics and is selected for by HIV</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name> <surname>Sullivan</surname> <given-names>Amy D.V</given-names> </name>
<xref ref-type="author-notes" rid="FN150">*</xref>
</contrib>
<contrib contrib-type="author">
<name> <surname>Wigginton</surname> <given-names>Janis</given-names> </name>
</contrib>
<contrib contrib-type="author">
<name> <surname>Kirschner</surname> <given-names>Denise A.K.</given-names> </name>
<xref ref-type="author-notes" rid="FN151">†</xref>
</contrib>
</contrib-group>
<aff>Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109-0620 <uri>http://www.Amazon.in/b?node=11962098031</aff>
<author-notes>
<body>
<p>Nineteen million people have died of AIDS since the discovery of HIV in the 1980s.In 1999 alone, 5.4 million people were newly infected with HIV (ref. <xref ref-type="bibr" rid="B1">1</xref> and <ext-link ext-link-type="url" xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://www.unaids.org/epidemicupdate/report/Epireport.html">http://www.unaids.org/epidemicupdate/report/Epireport.html</ext-link>). (For brevity, HIV-1 is referred to as HIV in this paper.) Sub-Saharan Africa has been hardest hit, with more than 20% of the general population HIV-positive in some countries (<xref ref-type="bibr" rid="B2">2</xref>, <xref ref-type="bibr" rid="B3">3</xref>). In comparison, heterosexual epidemics in developed, market-economy countries have not reached such severe levels. Factors contributing to the severity of the epidemic in economically developing countries abound, including economic, health, and social differences such as high levels of sexually transmitted diseases and a lack of prevention programs.However, the staggering rate at which the epidemic has spread in sub-Saharan Africa has not been adequately explained. The rate and severity of this epidemic also could indicate a greater underlying susceptibility to HIV attributable not only to sexually transmitted disease, economics, etc., but also to other more ubiquitous factors such as host genetics (<xref ref-type="bibr" rid="B4">4</xref>, <xref ref-type="bibr" rid="B5">5</xref>).</p>
<p>To exemplify the contribution of such a host genetic factor to HIV prevalence trends, we consider a well-characterized 32-bp deletion in the host-cell chemokine receptor CCR5, CCR5Δ32. When HIV binds to host cells, it uses the CD4 receptor on the surface of host immune cells together with a coreceptor, mainly the CCR5 and CXCR4 chemokine receptors (<xref ref-type="bibr" rid="B6">6</xref>). Homozygous mutations for this 32-bp deletion offer almost complete protection from HIV infection, and heterozygous mutations are associated with lower pre-AIDS viral loads and delayed progression to AIDS (<xref ref-type="bibr" rid="B7">7</xref>–<xref ref-type="bibr" rid="B14">14</xref>). CCR5Δ32 generally is found in populations of European descent, with allelic frequencies ranging from 0 to 0.29 (<xref ref-type="bibr" rid="B13">13</xref>). African and Asian populations studied outside the United States or Europe appear to lack the CCR5Δ32 allele, with an allelic frequency of almost zero (<xref ref-type="bibr" rid="B5">5</xref>, <xref ref-type="bibr" rid="B13">13</xref>). Thus, to understand the effects of a protective allele, we use a mathematical model to track prevalence of HIV in populations with or without CCR5Δ32 heterozygous and homozygous people and also to follow the CCR5Δ32 allelic frequency.</p>
<p>We hypothesize that CCR5Δ32 limits epidemic HIV by decreasing infection rates, and we evaluate the relative contributions to this by the probability of infection and duration of infectivity. To capture HIV infection as a chronic infectious disease together with vertical transmission occurring in untreated mothers, we model a dynamic population (i.e., populations that vary in growth rates because of fluctuations in birth or death rates) based on realistic demographic characteristics (<xref ref-type="bibr" rid="B18">18</xref>). This scenario also allows tracking of the allelic frequencies over time. This work considers how a specific host genetic factor affecting HIV infectivity and viremia at the individual level might influence the epidemic in a dynamic population and how HIV exerts selective pressure, altering the frequency of this mutant allele.</p>
<p>CCR5 is a host-cell chemokine receptor, which is also used as a coreceptor by R5 strains of HIV that are generally acquired during sexual transmission (<xref ref-type="bibr" rid="B6">6</xref>, <xref ref-type="bibr" rid="B19">19</xref>–<xref ref-type="bibr" rid="B25">25</xref>). As infection progresses to AIDS the virus expands its repertoire of potential coreceptors to include other CC-family and CXC-family receptors in roughly 50% of patients (<xref ref-type="bibr" rid="B19">19</xref>, <xref ref-type="bibr" rid="B26">26</xref>, <xref ref-type="bibr" rid="B27">27</xref>). CCR5Δ32 was identified in HIV-resistant people (<xref ref-type="bibr" rid="B28">28</xref>). Benefits to individuals from the mutation in this allele are as follows. Persons homozygous for the CCR5Δ32 mutation are almost nonexistent in HIV-infected populations (<xref ref-type="bibr" rid="B11">11</xref>, <xref ref-type="bibr" rid="B12">12</xref>) (see ref. <xref ref-type="bibr" rid="B13">13</xref> for review). Persons heterozygous for the mutant allele (CCR5 W/Δ32) tend to have lower pre-AIDS viral loads. Aside from the beneficial effects that lower viral loads may have for individuals, there is also an altruistic effect, as transmission rates are reduced for individuals with low viral loads (as compared with, for example, AZT and other studies; ref. <xref ref-type="bibr" rid="B29">29</xref>). Finally, individuals heterozygous for the mutant allele (CCR5 W/Δ32) also have a slower progression to AIDS than those homozygous for the wild-type allele (CCR5 W/W) (<xref ref-type="bibr" rid="B7">7</xref>–<xref ref-type="bibr" rid="B10">10</xref>), remaining in the population 2 years longer, on average. Interestingly, the dearth of information on HIV disease progression in people homozygous for the CCR5Δ32 allele (CCR5 Δ32/Δ32) stems from the rarity of HIV infection in this group (<xref ref-type="bibr" rid="B4">4</xref>, <xref ref-type="bibr" rid="B12">12</xref>, <xref ref-type="bibr" rid="B28">28</xref>). However, in case reports of HIV-infected CCR5 Δ32/Δ32 homozygotes, a rapid decline in CD4<sup>+</sup> T cells and a high viremia are observed, likely because of initial infection with a more aggressive viral strain (such as X4 or R5X4) (<xref ref-type="bibr" rid="B30">30</xref>) <uri>www.Wordmvp.com/lo</uri>, <uri>istec.com.Au</uri> and <uri>google.com</uri></p>
<sec>
<title>The Model</title>
<p>Estimates for rates that govern the interactions depicted in Fig. <xref ref-type="fig" rid="F1">1</xref> were derived from the extensive literature on HIV. Our parameters and their estimates are summarized in Tables <xref ref-type="table" rid="T2">2</xref>–<xref ref-type="table" rid="T4">4</xref>. The general form of the equations describing the rates of transition between population classes as depicted in Fig. <xref ref-type="fig" rid="F1">1</xref> are summarized as follows: <disp-formula id="E1">
<tex-math id="M1">\documentclass[12pt]{minimal} \usepackage{wasysym} \usepackage[substack]{amsmath} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage[mathscr]{eucal} \usepackage{mathrsfs} \DeclareFontFamily{T1}{linotext}{} \DeclareFontShape{T1}{linotext}{m}{n} { <-> linotext }{} \DeclareSymbolFont{linotext}{T1}{linotext}{m}{n} \DeclareSymbolFontAlphabet{\mathLINOTEXT}{linotext} \begin{document} $$ \frac{dS_{i,j}(t)}{dt}={\chi}_{i,j}(t)-{\mu}_{j}S_{i,j}(t)-{\lambda}_{\hat {\imath},\hat {},\hat {k}{\rightarrow}i,j}S_{i,j}(t), $$ \end{document} </tex-math>
</disp-formula>
</p>
</sec>
</body>
<back>
<title>Reference</title>
<ref id="ref1"><mixed-citation><string-name> <surname>Kirschner</surname> <given-names>Denise A.K.</given-names> </string-name>, <string-name> <surname>Bennet</surname> <given-names>D.K.</given-names> </string-name> <source>Insomnia</source>. <volume>2</volume> <uri>https://www.gcflearnfree.org/access2007/</uri></mixed-citation>
and .H from programs.However.
I have tried \.\u(?!([^<>]?</given-names>|[^<>]?</uri>)) but it doesn't work and I can't think of any other ways either.
Can anyone help?