Algunos Webcast para publicar
http://www.elsevier.com/wps/find/authorsview.authors/trainingwebcasts
Monday, February 27, 2012
Saturday, February 25, 2012
Monday, February 20, 2012
Microarreglos no tan exactos
Concerning the Affymetrix™ human genotyping array, we detected 25 differences (5 in different chromosomes), of which 10 (40%) were in different genes. These 25 discrepancies lead to 61,916 SNPs being in a different genomic order, with 89% being less or equal than 2 indexes away (Data S5). By checking manually a subset of those alignment discrepancies, we found that the Affymetrix™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned. With the Illumina's™ human beadchip, 271 SNPs have different genomic positions (with 22 on different chromosomes), of which 59 (22%) are on different genes. The 271 discrepancies lead to 131,378 SNPs being in a different genomic order, although 98% are less or equal than two indexes away (Data S6). By checking manually a subset of those alignment discrepancies, we found that the Illumina™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned.
Fuente
2012 Genomic Position Mapping Discrepancies of Commercial SNP Chips. PLoS ONE 7(2): e31025. doi:10.1371/journal.pone.0031025
Concerning the Affymetrix™ human genotyping array, we detected 25 differences (5 in different chromosomes), of which 10 (40%) were in different genes. These 25 discrepancies lead to 61,916 SNPs being in a different genomic order, with 89% being less or equal than 2 indexes away (Data S5). By checking manually a subset of those alignment discrepancies, we found that the Affymetrix™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned. With the Illumina's™ human beadchip, 271 SNPs have different genomic positions (with 22 on different chromosomes), of which 59 (22%) are on different genes. The 271 discrepancies lead to 131,378 SNPs being in a different genomic order, although 98% are less or equal than two indexes away (Data S6). By checking manually a subset of those alignment discrepancies, we found that the Illumina™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned.
Fuente
2012 Genomic Position Mapping Discrepancies of Commercial SNP Chips. PLoS ONE 7(2): e31025. doi:10.1371/journal.pone.0031025
Wednesday, January 04, 2012
Ciencia en México (y el mundo)
Aunque el mapa de como estamos en producción científica es poco halagador, lo interesante es que hemos crecido, sobre todo comparando a otros países (incluído EU). Compare la primera foto con la segunda. Este tipo de gráficas se parecen al homúnculo de Penfield (http://es.wikipedia.org/wiki/Homúnculo) :)
PRODUCCION CIENTIFICA
CRECIMIENTO PRODUCCION CIENTIFICA
fuente http://www.worldmapper.org
Molecular definitions of cell death subroutines
In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including ‘apoptosis’, ‘necrosis’ and ‘mitotic catastrophe’. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.
http://www.nature.com/cdd/journal/v19/n1/pdf/cdd201196a.pdf
http://www.nature.com/cdd/journal/v19/n1/pdf/cdd201196a.pdf
Video animation: RNA interference
RNA interference (RNAi) is an important pathway that is used in many different organisms to regulate gene expression. This animation introduces the principles of RNAi involving small interfering RNAs (siRNAs) and microRNAs (miRNAs).
Friday, December 30, 2011
Notable advance for 2011 (from Nature Medicine)
Cancer biology: BET-ting on chromatin
Tumor development often involves genomic changes that affect protein expression, so chromatin alterations have received a lot of attention as possible therapeutic targets. A handful of recent studies support this idea by identifying a role for the bromodomain and extraterminal (BET) family of transcriptional regulators, which bind and recognize histone acetylation, in several human hematological malignancies.
Four independent groups—from Boston's Dana-Farber Cancer Institute, New York state's Cold Spring Harbor Laboratory, the UK's Cambridge University and Massachusetts's Constellation Pharmaceuticals—started from different points and used different models, but they all converged on the finding that interfering with the function of BET proteins reduces the transcription of key oncogenes such as Myc, arrests cell-cycle progression and leads to apoptosis (Cell 146, 904–917, 2011; Nature 478, 524–528 & 529–533, 2011; Proc. Natl. Acad. Sci. USA 108, 16669–16674, 2011).
Crucially, the four studies highlighted the clinical implications of this finding by showing that small-molecule inhibitors of BET family members had therapeutic effects in mouse models of leukemia, lymphoma and myeloma, as well as in primary cells isolated from people with cancer. —JCL
Tumor development often involves genomic changes that affect protein expression, so chromatin alterations have received a lot of attention as possible therapeutic targets. A handful of recent studies support this idea by identifying a role for the bromodomain and extraterminal (BET) family of transcriptional regulators, which bind and recognize histone acetylation, in several human hematological malignancies.
Four independent groups—from Boston's Dana-Farber Cancer Institute, New York state's Cold Spring Harbor Laboratory, the UK's Cambridge University and Massachusetts's Constellation Pharmaceuticals—started from different points and used different models, but they all converged on the finding that interfering with the function of BET proteins reduces the transcription of key oncogenes such as Myc, arrests cell-cycle progression and leads to apoptosis (Cell 146, 904–917, 2011; Nature 478, 524–528 & 529–533, 2011; Proc. Natl. Acad. Sci. USA 108, 16669–16674, 2011).
Crucially, the four studies highlighted the clinical implications of this finding by showing that small-molecule inhibitors of BET family members had therapeutic effects in mouse models of leukemia, lymphoma and myeloma, as well as in primary cells isolated from people with cancer. —JCL
Wednesday, November 30, 2011
Man-made flu virus with potential to wipe out many millions if it ever escaped is created in research lab
A group of scientists is pushing to publish research about how they created a man-made flu virus that could potentially wipe out civilisation.
The deadly virus is a genetically tweaked version of the H5N1 bird flu strain, but is far more infectious and could pass easily between millions of people at a time.
The research has caused a storm of controversy and divided scientists, with some saying it should never have been carried out.
Tuesday, May 03, 2011
Apoptosis promotes early tumorigenesis
One hallmark of cancer is intrinsic or acquired resistance
to apoptosis. Surprisingly, recent studies demonstrate that
CD95/Fas/Apo1 and p53 upregulated mediator of apoptosis/
PUMA (potent inducers of the death receptor and the
mitochondrial apoptotic pathways, respectively) promote
tumorigenesis. These findings provide important insights
into the multifaceted roles of apoptosis in tumorigenesis.
http://www.nature.com/onc/journal/v30/n16/pdf/onc2010573a.pdf
to apoptosis. Surprisingly, recent studies demonstrate that
CD95/Fas/Apo1 and p53 upregulated mediator of apoptosis/
PUMA (potent inducers of the death receptor and the
mitochondrial apoptotic pathways, respectively) promote
tumorigenesis. These findings provide important insights
into the multifaceted roles of apoptosis in tumorigenesis.
http://www.nature.com/onc/journal/v30/n16/pdf/onc2010573a.pdf
Wednesday, April 20, 2011
EMT theory for metastases challenged during AACR
It can't be easy to stand in front of hundreds of colleagues and tell them that ten years of research has led them in the wrong direction. But at the annual meeting of the American Association for Cancer Research (AACR) earlier this month, pathologist David Tarin did just that, by challenging a leading hypothesis on how cancers metastasize...
PARA VER EL TEXTO COMPLETO GRATUITO
PARA VER EL TEXTO COMPLETO GRATUITO
Saturday, April 02, 2011
Academic bias & biotech failures
The unspoken rule is that at least 50% of the studies published even in top tier academic journals – Science, Nature, Cell, PNAS, etc… – can’t be repeated with the same conclusions by an industrial lab.
Artículo completo (libre acceso):
Artículo completo (libre acceso):
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