Great article on New Scientist by the talented science journalist Clare Wilson covering the Aging Forum.
Everyday drugs could give extra years of life - health - 01 October 2014 - New Scientist
Friday 3 October 2014
Thursday 7 August 2014
How do you imagine the life of scientists?
How do you imagine the life of scientists? Boring? Every time you think so, watch this cartoon.
Source: youtube
Wednesday 2 July 2014
First magazine cover with scientists!
Humanity definitely have a future, if scientists began to appear on the the covers of popular magazines! I believe that as soon as scientists replace celebrities from fashion, movies and other pop-culture, the scientific and technological progress immediately overgrow Moore's law hundreds of times! This is especially important for biomedicine and progress in the field of life extension. Therefore, my sincere congratulations to Alex Zhavoronkov break the silence of the media!
UPGRADE magazine
UPGRADE magazine
Saturday 28 June 2014
Conference: Practical Applications of Aging Research
This conference will be very interesting for everyone, who is passionate about aging research and drug discovery! It should be top one must visit in September!
AGINGPHARMA
BIOGERONTOLOGYmeetings
AGINGPHARMA
BIOGERONTOLOGYmeetings
Sunday 23 February 2014
MIPT presented lectures on iTunes
My alma mater, Moscow Institute of Physics and Technology (MIPT) is the first among Russian Universities, which placed its lectures on iTunes University!
15 theoretical physics lectures and 12 thermodynamics lectures are available now and even more is coming soon! It is so easy now to refresh the memory!
15 theoretical physics lectures and 12 thermodynamics lectures are available now and even more is coming soon! It is so easy now to refresh the memory!
Source: MIPT news
Wednesday 5 February 2014
Convertion of somatic cells into stem cells!
Scientists from Harvard Medical School developed unique and, the most important, simple method to trig the development of somatic cells into stem cells.
Our body mostly consists from normal, somatic cells, which are fully developed and which gene expression patterns are customized for a specific tissue to perform its function. However, we also have the stem cells, which are able to differentiate into any tissue of the organism and to replace aged or ill somatic cells. The Nobel prize in medicine in 2012 was given to scientists, who can revert the process of stem cells differentiation and to produce stem cells from skin fibroblasts using 4 transcriptions factors. Although the substance consists from only four components, the technology is difficult and it is not applicable for for large amount of cells.
Now, as a major of great scientific discoveries, a very simple method for converting somatic cells into stem cells was discovered occasionally. Dr. Haruko Obokata just added acid (creating low pH) to the mouse blood, and what lead to spontaneous conversion of lymphocytes into stem cells!
This method creates the basis for development of stem cell medicine, however, we should wait until it will be tried on human cells.
image: University of Wisconsin-Madison
More information: Nature
Thursday 23 January 2014
TCF3 and TCF4 are maintainer of skin epithelial stem cells
TCF is a family of DNA binding proteins, which are participating in the overall embryo development and in particular in epithelium's development. The member of TCF family, TCF3, works together with WNT signalling in order gastrulation to proceed. However, it was thought that after development TCF3 remains only as marker of follicle stem cells and works only with combination with WNT-signaling pathway during wounding, induces the epidermis to undergo de novo hair follicle morphogenesis.
Recently the team of Dr. Nguen from the Rockefeller University Tcf3 and Tcf4 are the key transcription factors to maintain long-term epidermal homeostasis. Overall, Tcf3 and Tcf4 may be essential for establishing and maintaining all skin epithelial stem cells through Wnt-dependent and Wnt-independent roles.
Source: Nature Genetics
Saturday 18 January 2014
Telocytes
Telocytes
(TCs), a particular interstitial cell type, have been recently
described in a wide variety of mammalian organs. The TCs are identified morphologically by a small cell body and extremely long (tens to hundreds of micrometer), thin prolongations (less than 100 nm in diameter, below the resolving power of light microscopy) called telopodes www.telocytes.com.
Recently, Ceafalan et al (2012) demonstrated that TCs were present in human dermis. In particular, TCs were found in the reticular dermis and around blood vessels. Screening for antigens showed two subpopulations of dermal TCs; one of which was positive for CD34, which is hallmark of stem cells. The TCs were connected to each other by homocellular junctions, and they formed an interstitial 3D network. Moreover, TCs established atypical heterocellular junctions with stem cells (clusters of undifferentiated cells).
Probably, TC could be one of most significant parts of skin regeneration's enigma.
Source: Ceafalan et al (2012)
Image: telocytes.com
Bioinformatics analysis of aging microarray profiles
Changes in gene expression are associated with numerous biological processes, cellular responses and disease states. However, elucidating the transcriptional features of aging and how these relate to physiological, biochemical and pathological changes with age remains a critical problem.
Considering the number of aging gene expression studies conducted to date it is impossible to analyse them without means of bioinformatics. Because the underlying molecular mechanisms of aging remain a subject of debate, whether independent transcriptional programs can drive aging in different tissues is unknown. Previous results suggest that most genes differentially expressed with age in a given tissue are not genes specifically expressed in that tissue, suggesting that only a small fraction of transcriptional responses are tissue-specific.
The results of article by de Magalhães et al (2009) reveal several signatures of aging most notably involving an activation of inflammation/immune response genes. The most significant gene was APOD or apolipoprotein D, previously associated with Alzheimer's diseases. In addition, numerous genes overexpressed with age play roles in inflammation, such as CTSS, FCGR2B, IGJ, C3, C1QA and C1QB. Other genes consistently overexpressed with age included lysozyme (LYZ), clusterin (CLU), microsomal glutathione S-transferase 1 (MGST1), glutathione S-transferase A1 (GSTA1), S100 calcium binding protein A4 (S100A4) and A6 (S100A6), and annexin A3 (ANXA3) and A5 (ANXA5).B and include four genes encoding mitochondrial proteins (ATP5G3, NDUFB11, UQCRQ and UQCRFS1) and three collagen genes (COL3A1, COL1A1 and COL4A5).
These differentially expressed genes may serve as a basis for further studies, for example, for deriving reliable biomarkers of aging.
Source: Bioinformatics(Oxford journals)
Sunday 12 January 2014
Autophagy in focus
Everyone, who is interested in ageing, knows that autophagy is very important cell process, that helps to keep cell free from unnecessary or dysfunctional cellular components.
Cell research journal gives us a unique opportunity of free access to its special issue about autophagy. Enjoy!
Friday 10 January 2014
Broken heart? Let's glue it!
It is widely known that heart wounds are difficult to repair. Due to constant heart moving it is very complicated to hold wound's edges together in order to provide the contact and ability to repair the muscle. Previously threads and staples were used in such situations. Of course, they are not a best solution, because damage of the muscle occurring during theirs usage.
Now it seems that the era of threads and staples is coming to the end. Scientists from Harvard Medical School created a special glue, which is able to stick together the edges of a wound and after solidification to expand and contract with the heart muscle. Thus surgeons do not need any more threads and staples! Remarkably, that the glue can be applied not only to the heart wounds, but to intestines and blood vessels too.
p16INK4A is a biomarker of skin ageing
Senescent cells lose theirs ability to replicate mainly due to increased expression of proteins-cell cycle regulators, called cycle check point proteins. p16INK4A is one of the such proteins. Recently, a study showing a p16IK4A as a biomarker of ageing was published in Journal of investigative dermatology.
Dr. Adamus and colleagues showed that expression of the p16INK4A increases significantly in the basal layer of human epidermis and in dermal fibroblasts during the ageing process, confirming that p16INK4A is a biomarker of skin ageing. Also the scientists demonstrated the possibility to revert aged phenotype to a younger one and vice versa by controlling expression of the protein.
First, they induced over expression of p16INK4A and observed a dramatic alterations in phenotype. Cultures with increased p16INK4A expression showed significant atrophy and other signs of ageing progression.
Second, Dr. Adamus and colleagues silenced the expression of p16INK4A, after that morphology of aged culture was improved significantly and resembled that of a much younger donor.
Dr. Adamus and colleagues showed that expression of the p16INK4A increases significantly in the basal layer of human epidermis and in dermal fibroblasts during the ageing process, confirming that p16INK4A is a biomarker of skin ageing. Also the scientists demonstrated the possibility to revert aged phenotype to a younger one and vice versa by controlling expression of the protein.
First, they induced over expression of p16INK4A and observed a dramatic alterations in phenotype. Cultures with increased p16INK4A expression showed significant atrophy and other signs of ageing progression.
Second, Dr. Adamus and colleagues silenced the expression of p16INK4A, after that morphology of aged culture was improved significantly and resembled that of a much younger donor.
Source: Journal of investigative dermatology.
Wednesday 8 January 2014
Broadband Light Treatment of skin aging
Dr. Chang from Stanford School of Medicine showed the unique effectiveness of broadband light treatment on skin aging. BBL, also known as intense pulse light, is a commonly available and popular method to ‘‘rejuvenate’’ the skin. BBL uses a broad band of noncoherent light waves, ranging from 560 to 1,200, which are absorbed by different molecules in skin. According to the American Society for Aesthetic Plastic Surgery, over $215 million dollars were spent in the United States in 2009 on these procedures.
The study showed that BBL induces skin rejuvenation on molecular level, i.e., the pattern of genes' expression more closely resembles younger skin. However, the molecular changes that are induced by this treatment are still to be unclear.
Tuesday 7 January 2014
ROS and skin aging
Reactive oxygen species (ROS) is one of the by-products of cell's metabolism. They can lead to DNA, protein and even cell's organelles damaging.
However, cell does have a protection against ROS - robust pathways for maintaining intracellular homoeostasis. First, ROS will face with the one of the superoxide dismutases, for example, SOD2. SOD2 is a mitochondrial matrix protein that converts the superoxide anion (O2-) to hydrogen peroxide (H2O2), which is in turn, converted to molecular oxygen and water by catalase and peroxiredoxins.
It was shown that normal ageing in mice accompanied by impaired mitochondrial complex II activity. The similar phenotype was observed in mice with shut downed SOD2 gene: such mice exhibit significant epidermal thinning. This is caused by decreased cellular proliferation in the senescent skin tissue.
However, cell does have a protection against ROS - robust pathways for maintaining intracellular homoeostasis. First, ROS will face with the one of the superoxide dismutases, for example, SOD2. SOD2 is a mitochondrial matrix protein that converts the superoxide anion (O2-) to hydrogen peroxide (H2O2), which is in turn, converted to molecular oxygen and water by catalase and peroxiredoxins.
It was shown that normal ageing in mice accompanied by impaired mitochondrial complex II activity. The similar phenotype was observed in mice with shut downed SOD2 gene: such mice exhibit significant epidermal thinning. This is caused by decreased cellular proliferation in the senescent skin tissue.
Yet, the link between SOD2 gene and skin ageing does not seem to be direct: heterozygous for SOD2 mice shows DNA damage andpredisposition to cancer, but without any impact on the lifespan.
Source: Aging
Source: Aging
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