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1.  Developmental Status of Children of Teen Mothers: Contrasting Objective Assessments with Maternal Reports 
Introduction
Descriptive study compared adolescent mothers’ subjective perceptions of their children’s development with objective developmental assessments.
Method
Volunteer sample of mother/child pairs was recruited from urban high school. Thirty-three mothers completed Ages and Stages Questionnaire (A&SQ). Children were administered Bayley Scales of Infant Development (BSID).
Results
On the BSID, group mean scores all fell within the normal range. However, almost 20% of individual children had one or more delays. Almost 73% of mothers accurately assessed their children’s development on the (A&SQ) when compared to BSID results. Eighteen percent of mothers suspected delays when there were none objectively identified. A single mother identified delay in a different domain than that identified on the BSID.
Discussion
Findings that almost 20% of these children had developmental delays support other research that children of adolescent mothers are at risk for delays. Findings that teen mothers varied in their abilities to assess their children’s development reinforce the need for education of teen mothers about child development. Further study needed to determine the best models of this education in school and community settings.
doi:10.1016/j.pedhc.2008.09.001
PMCID: PMC3561665  PMID: 19720265
2.  HLA Alleles Associated with Delayed Progression to AIDS Contribute Strongly to the Initial CD8+ T Cell Response against HIV-1 
PLoS Medicine  2006;3(10):e403.
Background
Very little is known about the immunodominance patterns of HIV-1-specific T cell responses during primary HIV-1 infection and the reasons for human lymphocyte antigen (HLA) modulation of disease progression.
Methods and Findings
In a cohort of 104 individuals with primary HIV-1 infection, we demonstrate that a subset of CD8+ T cell epitopes within HIV-1 are consistently targeted early after infection, while other epitopes subsequently targeted through the same HLA class I alleles are rarely recognized. Certain HLA alleles consistently contributed more than others to the total virus-specific CD8+ T cell response during primary infection, and also reduced the absolute magnitude of responses restricted by other alleles if coexpressed in the same individual, consistent with immunodomination. Furthermore, individual HLA class I alleles that have been associated with slower HIV-1 disease progression contributed strongly to the total HIV-1-specific CD8+ T cell response during primary infection.
Conclusions
These data demonstrate consistent immunodominance patterns of HIV-1-specific CD8+ T cell responses during primary infection and provide a mechanistic explanation for the protective effect of specific HLA class I alleles on HIV-1 disease progression.
A subset of CD8+ T cell epitopes within HIV-1 are consistently targeted early after infection. This could explain some of the protective effect of certain HLA class I alleles on HIV-1 disease progression.
Editors' Summary
Background.
Nearly 15,000 new HIV infections occur each day. There is no cure for HIV, and the treatments currently used to prevent people with HIV from dying are expensive and unavailable to many who need them. There is also no vaccine to prevent HIV. An effective vaccine would somehow induce the immune system to prevent the virus from reaching destructive levels in the body, but how to design such a vaccine is unknown.
In most people infected with HIV, the immune system doesn't keep the AIDS virus in check over the long term. It has been known for a long time, however, that the body somehow brings the virus under control within a few weeks following infection, after which, in the absence of treatment, the amount of virus gradually increases again over time. Exactly why the amount of virus drops after initial infection is not fully understood, but there is good evidence that the white blood cells called CD8 T lymphocytes, which can kill other cells infected with viruses, are at least partially responsible for initially bringing HIV infection under control.
In order for a CD8 T lymphocyte to recognize and kill an infected cell, that cell has to display some part of the infecting virus on its surface. There are many possible fragments of HIV that can activate CD8 T cells, although some of these fragments appear more effective than others at provoking a strong killer response. Also, in order to activate CD8 T cells the viral fragments must bind to and be presented by a particular kind of protein called HLA on the surface of the infected cells. There are hundreds of varieties of HLA in the human population, allowing our immune systems to recognize many parts of many different viruses. (Each person can have up to six different kinds of HLA class I on the surface of his or her cells). A few specific types of HLA have been found to provide some advantage in keeping the AIDS virus under control, possibly because they present fragments of the virus that are particularly good at activating CD8 T cells.
Why Was This Study Done?
The researchers wanted to find out whether specific HLA types and specific protein fragments (peptides) of the AIDS virus are particularly important in helping CD8 T cells control HIV. Specifically, they wanted to find out the very earliest protein fragments recognized, since these might be particularly important in keeping the virus in check. They also wanted to see if these particular HLA-peptide combinations might affect the long-term health of people with HIV infection. Finding specific combinations of peptide and HLA that give rise to strong control of HIV could help in the design of an effective AIDS vaccine.
What Did the Researchers Do and Find?
The researchers studied CD8 T cells in blood samples from 104 people in the early stages of HIV infection. They used DNA analysis to determine which HLA types were present in each participant, and then chose, from among 173 different protein fragments of HIV, the peptides that are known to bind to and be presented by the participant's HLA types. The ability of these peptides to activate the participant's CD8 T cells was measured in the laboratory.
These studies found that for many types of HLA, there were a few specific viral peptides that triggered most of the CD8 T cell activity found in early HIV infection, when the amount of virus in the blood is being lowered by this response. A few types of HLA were found to contribute more strongly than others to CD8 T-cell activity in early HIV infection. These same types of HLA are also found in people who tend to remain healthier for a longer time after becoming infected with HIV.
What Do These Findings Mean?
This study provides evidence that ability of CD8 T cells to keep HIV under control in the first few months following infection depends on a person's HLA composition, and that this early CD8 T cell activity sets the stage for the long-term balance between the body and the virus. Knowing the particular peptide–HLA combinations that dominate the early immune response (when the immune system appears to be bringing the virus under control) might be of use in designing an HIV vaccine. Because this study was done in people already infected with HIV, however, it remains unclear whether a vaccine based on this knowledge would actually prevent new HIV infection or improve health after infection, even in people with “good” HLA types.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030403.
The UCSF Center for HIV Information's HIV InSite includes resources on HIV immunology and vaccine development
The Los Alamos Natural Laboratory HIV Molecular Immunology Database contains information for researchers on HIV peptides, HLA, and CD8 T cell responses
The International AIDS Vaccine Initiative (IAVI) Web site provides policy and scientific information on the global AIDS vaccine effort
The Massachuetts General Hospital Web site contains information about their HIV-1 research programs
doi:10.1371/journal.pmed.0030403
PMCID: PMC1626551  PMID: 17076553
3.  An XML standard for the dissemination of annotated 2D gel electrophoresis data complemented with mass spectrometry results 
BMC Bioinformatics  2004;5:9.
Background
Many proteomics initiatives require a seamless bioinformatics integration of a range of analytical steps between sample collection and systems modeling immediately assessable to the participants involved in the process. Proteomics profiling by 2D gel electrophoresis to the putative identification of differentially expressed proteins by comparison of mass spectrometry results with reference databases, includes many components of sample processing, not just analysis and interpretation, are regularly revisited and updated. In order for such updates and dissemination of data, a suitable data structure is needed. However, there are no such data structures currently available for the storing of data for multiple gels generated through a single proteomic experiments in a single XML file. This paper proposes a data structure based on XML standards to fill the void that exists between data generated by proteomics experiments and storing of data.
Results
In order to address the resulting procedural fluidity we have adopted and implemented a data model centered on the concept of annotated gel (AG) as the format for delivery and management of 2D Gel electrophoresis results. An eXtensible Markup Language (XML) schema is proposed to manage, analyze and disseminate annotated 2D Gel electrophoresis results. The structure of AG objects is formally represented using XML, resulting in the definition of the AGML syntax presented here.
Conclusion
The proposed schema accommodates data on the electrophoresis results as well as the mass-spectrometry analysis of selected gel spots. A web-based software library is being developed to handle data storage, analysis and graphic representation. Computational tools described will be made available at . Our development of AGML provides a simple data structure for storing 2D gel electrophoresis data.
doi:10.1186/1471-2105-5-9
PMCID: PMC341449  PMID: 15005801

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