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Mature Models Over 30


The best hairstyles for women over 30 are shags. And, a low-maintenance shag for wavy hair is very trendy right now. The heavy fringe and lots of layers encourage curl and texture. These styles for women over 30 with thick hair are ideal. Air dry or diffuse with a texturizing cream.




mature models over 30



Medium-length beach waves for 30+ women are perfect. The length is youthful and versatile, and the lived-in waves are very on-trend. Piecey mid-lengths are a wonderful option for women aged 30 and over. Style with a texturizing spray for a tousled finish.


Consider a silver pixie cut for a 30-year-old-woman. Hair colors this bold can also be highly effective if you are transitioning into your natural gray. Being a woman over 30 does not mean you cannot wear gray hair. In fact, it means you can celebrate it! This hair color does require time and money though so be prepared for the investment of both.


Consider a cute pixie cut for thin hair. Short cuts for women over 30 are ideal, especially for fine or thin hair. The style adds fullness and the illusion of thickness. Keep in mind a pixie cut requires more frequent visits to your stylist.


Consider long layers for women over 30 with long hair. Layering around the face is more flattering as we age, and 30-year-old haircuts should feel light and have movement. Style with a big round brush or a big barrel curling iron and a volumizing spray.


Some handsome men are like wine - they get better with age. Bored Panda collected a list of handsome guys and hot older men over or just under 50 years old that might redefine the concept of good looking.


From sporty silver heads to true fashion icons, the list will cater to many tastes. Some of these "grandpa" male models actually started their modeling careers after they hit 45 or more. For example, Philippe Dumas was 60 years old and aging gracefully when his decision to grow a beard helped him get a modeling contract. Quite a career opportunity to look forward to, don't you think? That is if you turn out to be a handsome old man with age.


Most of the hot older male models featured here have Instagram accounts which you can follow by clicking on the source below each stunning picture. You'll thank me later. Also, don't forget to vote and comment on your favorite silver foxes!


Human mature erythrocytes are terminally differentiated cells of the erythroid lineage, that are devoid of mitochondria, as well as of nucleus and other organelles, and have a normal life span of 120 days that is ended by a process of senescence leading to their clearance from the peripheral blood by reticuloendothelial cells.18,19,20 Erythrocyte senescence is associated with cell shrinkage, plasma membrane microvesiculation, a progressive shape change from a discocyte to a spherocyte, cytoskeleton alterations associated with protein (spectrin) degradation, and loss of plasma membrane phospholipid asymmetry leading to the externalization of phosphatidylserine, that may represent one of the signals allowing macrophages to ingest the senescent erythrocytes.18,19,20,21,22,23 In vitro storage of erythrocytes leads to the gradual accumulation of these modifications, and ex vivo, a very small subpopulation of human erythrocytes with a senescent phenotype can be isolated from the peripheral blood.19,20,23 Despite the similarities between this senescent phenotype and some cytoplasmic features of apoptosis, mature erythrocytes have been considered as the sole mammalian cell lacking the machinery required to undergo PCD, because they survive two conditions that induce PCD in all human nucleated cells studied so far, i.e. treatment with the protein kinase inhibitory drug staurosporine, and culture in the absence of serum or other potential survival-promoting factors.14


Since erythrocyte senescence has been reported to be associated with a progressive increase in intracellular calcium (Ca2+),24,25 we decided to investigate whether Ca2+ entry into freshly isolated human erythrocytes may suffice to induce premature erythrocyte death.


Here we report that a regulated form of self-destruction, sharing several features with apoptosis, can be rapidly induced in mature erythrocytes by calcium influx, and can be prevented by inhibitors of cysteine proteinases, that allow erythrocytes to survive in vitro and in vivo. This regulated cell death process, that operates in the absence of mitochondria and cytochrome c, appears not to require caspase activation.


Flow-cytometry analysis using labeled Annexin V indicated that incubation of human mature erythrocytes with A 23187 in the presence of Ca2+, or with Ca2+ alone, induced a rapid phosphatidylserine externalization (Figure 1C), a feature characteristic of both apoptosis in nucleated cells3,28 and of senescence in erythrocytes.19,23,28 A 23187- or Ca2+-treated erythrocytes that bound labeled Annexin V, did not bind two labeled control lectins of similar molecular weight, PNA and GNA (data not shown), indicating that Annexin V binding was specific for phosphatidylserine exposure on the outer leaflet of the plasma membrane, and was not a consequence of plasma membrane damage that would allow the indiscriminate binding or entry of any labeled protein.


Together, our data indicated that a form of Ca2+-dependent apoptosis-like cell death process can be induced in mature erythrocytes, and that cysteine proteinase inhibitors are able to prevent this death process and to allow subsequent erythrocyte survival both in vitro and in vivo.


Human mature erythrocytes are terminally differentiated cells of the erythroid lineage, that are devoid of mitochondria, as well as of nucleus and other organelles, and have a normal life span of 120 days that is ended by a process of senescence leading to their clearance from the peripheral blood by reticuloendothelial cells. Mature erythrocytes have been considered as the sole human cell type unable to undergo PCD, due to their lack of mitochondria and nucleus, and to the finding that they survive two conditions that induce PCD in vitro in all nucleated human cells tested so far, i.e. treatment with the protein kinase inhibitor staurosporine, and culture in the absence of serum and of other survival factors.14


While confirming that mature erythrocytes survive staurosporine treatment and culture in the absence of serum, our findings indicate that they constitutively express death effectors allowing them to undergo a rapid process of self-destruction that shares several features with apoptosis, including cell shrinkage, plasma membrane microvesiculation, phosphatidylserine externalization, and leading to erythrocyte disintegration, or, in the presence of macrophages, to macrophage ingestion of the dying erythrocytes. This regulated form of PCD was induced by Ca2+ influx, and prevented by in vitro treatment with cysteine proteinase inhibitors, that allowed human mature erythrocytes to survive in vitro, and murine mature erythrocytes to survive in vivo. Independently of their potential implication for the control of mature erythrocyte survival and death, our findings provide the first identification, to our knowledge, that a death program can operate in the absence of mitochondria.


Mature erythrocytes represent the end stage of the erythroid lineage emerging from erythroid progenitors through a complex process of differentiation that involves the physiological loss of their nucleus, mitochondria and other organelles. Recent findings indicate that terminal differentiation into mature erythrocytes is preceded by a form of abortive apoptosis induction, that involves transient caspase activation.36 Is the apparently peculiar death program operating in mature erythrocytes a consequence of their particular process of terminal differentiation? Or is it a legacy of cryptic effectors of cytoplasmic apoptosis that are already present in their erythroid progenitors? Identification of the molecular mechanisms of self-destruction in mature erythrocytes should allow one to assess to what extent the death effectors involved may be components of the various independent death programs that have been recently suggested to exist in parallel in nucleated mammalian cells,37,38 and whose multiplicity may be related to the ancient evolutionary origins of PCD.38,39,40


While we did not identify the death effectors operating in mature erythrocytes, our findings that inhibitors of cysteine proteinases are able to prevent Ca2+-induced erythrocyte death both in vitro and in vivo has implications for therapeutic modulation of erythrocyte survival. Firstly, blood transfusion may benefit from treatments able to inhibit premature erythrocyte death in vitro. Secondly, shortened survival and accelerated clearance of erythrocytes from the blood circulation occur in several diseases.19 Provided that accelerated erythrocyte clearance in such diseases depend on a process of Ca2+-dependent PCD similar to that we have evidenced, our findings suggest the possibility that cysteine proteinase inhibitors might allow the in vivo prevention of premature erythrocyte death. Thirdly, senescence is the physiological process that ends the normal erythrocyte life span of 120 days. Erythrocyte senescence is associated with progressive Ca2+ influx,24,25 and with most, if not all, of the apoptosis-like features that characterize the rapid Ca2+-induced premature erythrocyte death process that we identified here. If senescence represents the time-dependent induction of the same self-destruction process, it is possible that the normal life span of erythrocytes might be extended through therapeutic intervention.


In summary, the findings presented here indicate that mature erythrocytes share, with all other mammalian cell types, the capacity to self-destruct in response to environmental changes. They suggest that erythrocytes may represent a useful model for the identification of effectors of PCD and senescence that are able to operate in a minimal cell devoid of nucleus, mitochondria and other organelles. They also indicate that death and survival of mature erythrocytes, as death and survival of all other mammalian cells, may be modulated by physiological regulation, pathological dysregulation, and therapeutic intervention. 041b061a72


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