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Loss of the retinoblastoma protein (pRb) induces a cell‐nonautonomous defect in both erythroid and neuronal differentiation. It has previously been thought that this reflects a requirement for pRb function in cells that normally support erythropoiesis and neurogenesis, rather than in the erythrocytes or neurons themselves. However, recent studies have challenged this interpretation, and it appears that erythrocytes and neurons themselves have the intrinsic requirement for pRb function. This requirement can be bypassed by signals supplied by wild‐type erythroid or neuronal cells. The existence of such a signalling mechanism has implications not only in understanding pRb function but also in the interpretation of other cell‐nonautonomous phenotypes.
The pRb protein
The retinoblastoma protein (pRb) is the founding member of the family of so‐called pocket proteins, which also includes the proteins p107 and p130 (Lipinski and Jacks, 1999). Although pRb plays a pivotal role in controlling gene expression to regulate cellular proliferation, apoptosis and differentiation (Lipinski and Jacks, 1999; Vooijs and Berns, 1999; Nevins, 2001; Zhang and Dean, 2001), it lacks a DNA‐binding domain and is tethered to promoters through its interaction with other transcription factors (Zhang and Dean, 2001). The interaction of pRb with such factors is inhibited by its phosphorylation (Sherr, 1996), a process that is mediated by cyclin‐dependent kinases (CDKs), which are themselves regulated by the CDK inhibitors (Sherr and Roberts, 1999). The E2F family of transcription factors is among those bound and regulated by hypophosphorylated pRb (Nevins, 2001). The latter acts both by directly inhibiting E2F transactivating activity and by recruiting transcriptional repression complexes to promoters containing E2F sites (Lipinski and Jacks, 1999). In fact, pRb phosphorylation results in disruption of pRb/E2F complexes and is thought to be a crucial event in the G1 to S phase transition (Sherr, 1996; Sherr and Roberts, 1999). Hypophosphorylated pRb also binds to and regulates the function of other proteins, including the helix–loop–helix protein Id2 (Lasorella et al., 2000), CAAT/enhancer binding proteins (Chen et al., 1996) the HMG family member HBP1 (Shih et al., 1998) and, possibly, basic‐helix–loop–helix proteins such as MyoD (Gu et al., 1993). pRb also appears to regulate gene transcription by recruiting chromatin remodelling factors such as histone deacetylases, the SWI/SNF complex, DNA methyltransferases and histone methyltransferases (Ferreira et al., 2001; Nielsen et al., 2001; Zhang and Dean, 2001).
Loss of pRb in mice
Recent work on the role of pRb in erythropoiesis has revealed a novel link between this cell cycle regulatory protein and intercellular signalling. pRb regulates the development and differentiation of various tissues, including central and peripheral nervous system, muscle, retina, lens and blood (Lipinski and Jacks, 1999; Vooijs and Berns, 1999). However, pRb does not induce a simple cell‐autonomous defect in some of these tissues, i.e. the phenotype of the cell does not directly correlate with its genotype. This was demonstrated by the finding that, in pRb null chimeric animals, the mutant cells contributed signficantly to both the erythroid and neuronal lineages (Maandag et al., 1994; Williams et al., 1994). It is important to understand how pRb functions in this cell‐nonautonomous manner in these lineages.
The requirement for pRb function was demonstrated by gene disruption experiments in mice. Complete loss of pRb resulted in lethality during gestation at around 14 days post coitum (d.p.c.). pRb null embryos displayed excessive neuronal cell death and were anemic. The latter effect appears to have been due to the disruption of fetal liver erythropoiesis. Normally, at this stage in development, definitive (or adult) enucleated erythrocytes replace primitive (or embryonic) nucleated yolk‐sac derived erythrocytes in the circulation. The first and major site of definitive erythropoiesis at this stage is the fetal liver. Definitive erythropoiesis in the fetal liver (and later in the spleen and bone marrow) occurs in erythroblastic islands (Bessis et al., 1983). These contain a central macrophage surrounded by erythroid cells at different stages of maturation. The latter are arranged in a characteristic pattern, with immature cells close to the centre and mature cells near the edge (Figure 1) (Bessis et al., 1983; Bernard, 1991). In pRb null embryos, the number of the definitive erythrocytes was dramatically reduced. Instead, immature (nucleated) fetal liver derived cells were present in the circulation in high numbers (Clarke et al., 1992; Jacks et al., 1992; Lee et al., 1992). Furthermore, erythroid colonies grown from pRb null fetal livers were defective in differentiation, i.e. the colonies were more numerous and the cells were paler and failed to enucleate efficiently (Jacks et al., 1992).
From these experiments, it is unclear whether pRb is intrinsically required in the erythroid cells for their normal differentiation or in a cell type that supports erythropoiesis, such as a growth factor producing stromal cell. Chimeric mice are usually generated to determine whether a gene functions autonomously or nonautonomously in a particular lineage. Gene function is considered cell autonomous when a cell displays a phenotype corresponding to its genotype, regardless of the genotype of surrounding cells (Figure 2A). In the case of the pRb null chimeric mice (Maandag et al., 1994; Williams et al., 1994), the function of pRb in the erythroid lineage would be considered cell autonomous if pRb null cells failed to differentiate and the surrounding wild‐type erythroid cells differentiated normally. Gene function is defined as cell nonautonomous when a cell displays a phenotype that does not correspond to its genotype (Figure 2B) (Apfeld and Kenyon, 1998): in other words, where wild‐type cells display the phenotype of mutant cells or mutant cells display the phenotype of wild‐type cells. In the chimeric animals, pRb null cells contributed highly to the erythroid compartment (Maandag et al., 1994; Williams et al., 1994). Importantly, the differentiation of pRb null erythroid cells was indistinguishable from that of wild‐type cells. The only phenotypic change in a few mice was a transient persistence of nucleated cells (both wild‐type and pRb null) in the circulation of chimeras with a relatively higher contribution of pRb null cells (Maandag et al., 1994). Since genotypically pRb null erythroid cells display a wild‐type phenotype, the function of pRb in erythropoiesis is, by definition, cell nonautonomous.
The cell that requires pRb
These observations beg the question: in which cell type is the function of the pRb gene required for normal erythropoiesis? If the defect had been cell autonomous, the interpretation would have been that the pRb gene is required in the erythroid cells themselves for their normal development and/or differentiation. Conversely, when cell nonautonomy occurs, as is the case in the pRb chimeras, the gene is thought to function in cells other than those that exhibit the original phenotype (Rossant and Spence, 1998). In principle, if a cell‐nonautonomous phenotype is displayed by cell A, then the function of gene X is required in cell B (Figure 3). In such a model, cell B could be supplying a signal that is required for the wild‐type phenotype of cell A. Cell A then responds to this signal by displaying a wild‐type phenotype, regardless of whether or not gene X is present in its own genome. In the case of the erythroid pRb phenotype, it was proposed that pRb is required in a stromal cell (cell B), which supports erythroid differentiation, and that pRb is not intrinsically required by the erythroid cells themselves (cell A) (Figure 3A) (Maandag et al., 1994; Williams et al., 1994; Vooijs and Berns, 1999). This interpretation is a heterotypic signalling model, where cell A is of a different lineage to cell B. However, subsequent experiments cast doubt on this interpretation. When lethally irradiated wild‐type animals (all hematopoietic cells essentially eliminated) were repopulated with pRb null hematopoietic cells, all hematopoietic lineages examined appeared normal, with the exception of the erythroid lineage. In this case, the erythoid cells failed to differentiate normally, showing increased proliferation and a block in differentiation, manifest as a stable persistence of nucleated erythroid cells in the circulation and extensive erythropoiesis outside the bone marrow (Hu et al., 1997). There are two possible outcomes of the irradiation relevant to this experiment, i.e. the stromal cells in the recipient animal survive or not. If the host stromal cells did not survive the irradiation, all donor derived hematopoietic cell lineages requiring stromal cells would be affected, regardless of their pRb requirement (i.e. the same would be observed with wild‐type donor tissue). In contrast, if the host stromal cells (pRb positive) persisted after irradiation, the heterotypic model described above predicts that all hematopoietic lineages (pRb negative) would be normal. Neither of these possibilities occurred. This indicates that pRb function must be required in a critical transplantable cell that is lost in the recipient during the lethal irradiation. This cell, in turn, expresses a signal that is required for the normal differentiation of pRb null erythroid cells. This may be a non‐erythroid cell, consistent with a heterotypic signalling model. However, such a critical non‐erythroid cell has not been identified, making this model unsubstantiated.
In contrast to a heterotypic model, one can propose a homotypic signalling model (Figure 3B). In this case, cell B, which supplies the signal required by cell A, has differentiated further along the same lineage. According to this model, in the pRb null chimeric mice, the surrounding wild‐type erythroid cells would supply the signal that activates the differentiation of less mature pRb null erythroid cells. This is distinct from a heterotypic model, as it is based on the premise that pRb functions in the erythroid cell itself. In a homotypic model, loss of pRb in erythroid cells disrupts the expression of the signal required for the differentiation of pRb null cells. If the gene disrupted is, for example, a paracrine growth factor expressed and required by cells of a particular lineage, such a homotypic model is intuitively obvious. However, pRb is not a paracrine growth factor and it is unlikely that it would regulate only the expression of such factors by erythroid cells. Nevertheless, pRb may indirectly affect the expression of paracrine factors by regulating the differentiation process itself. Indeed, many studies suggest that pRb plays an intrinsic role in regulating the proliferation and differentiation of erythroid cells. During hematopoiesis, pRb is expressed in the erythroid lineage and down‐regulated in other lineages (Condorelli et al., 1995). Accumulation of hypophosphorylated pRb is characteristically observed during erythroid differentiation (Sehy et al., 1992; Kiyokawa et al., 1994; Zhuo et al., 1995; Hseih et al., 2000). pRb‐mediated G1 arrest is thought to be important in chemically induced differentiation of virally transformed murine erythroleukemia (MEL) cells (Zhuo et al., 1995) and in activin‐A induced differentiation of human erythroleukemia cells (Sehy et al., 1992). Inhibition of MEL cell differentiation by the overexpression of the erythroid transcription factor GATA‐1 is also associated with reduced levels of hypophosphorylated pRb and the inhibition of differentiation‐associated G1 arrest (Whyatt et al., 1997). Antisense experiments suppressing pRb activity have suggested that pRb regulates erythropoiesis (Condorelli et al., 1995; Bergh et al., 1997; Konishi et al., 1999). Various studies have proposed functional cross‐regulation between pRb and factors such as Fli‐1, PU.1, PML and Tal‐1 during erythropoiesis (Konishi et al., 1999; Labbaye et al., 1999; Tamir et al., 1999; Vitelli et al., 2000). When considered alongside the transplantation experiment (Hu et al., 1997), these studies argue that erythroid cells have an intrinsic requirement for pRb activity. A homotypic signalling model reconciling this with the cell nonautonomy found in the chimeras is shown in Figure 3B. In this model, when an erythroid cell is pRb null, the requirement for pRb activity can be bypassed by signals supplied by cells that have already undergone the maturation process.
In support of the above, a similar model has already been proposed that is based on an experiment in which the transcription factor GATA‐1 was overexpressed in erythroid cells (Whyatt et al., 2000). GATA‐1 is a zinc‐finger‐like transcription factor required for erythroid differentiation, and loss of this factor induced cell‐autonomous apoptosis in immature erythroid cells (Pevny et al., 1991; Weiss and Orkin, 1995). Interestingly, mice overexpressing GATA‐1 under erythroid‐specific activating sequences had an erythroid phenotype similar to that of the pRb null mice (Whyatt et al., 2000). The mice were anemic due to a failure in fetal liver derived erythropoiesis and died at around 13.5 d.p.c. Erythroid cells overexpressing GATA‐1 were intrinsically defective and failed to differentiate in mice overexpressing GATA‐1 in all erythroid cells. However, this defect was also cell nonautonomous. It is postulated that GATA‐1 overexpressing erythroid cells differentiate in response to a signal (designated REDS, for red cell differentiation signal) that is supplied by relatively mature erythroid cells (Whyatt et al., 2000) in the erythroblastic island (Figure 4). In mosaic animals, immature erythroid cells overexpressing GATA‐1 would be juxtaposed with wild‐type 'mature' cells in the same erythroblastic island and/or the neighbouring island, making REDS signalling possible and thereby reversing the defects induced by high GATA‐1 levels. In mice overexpressing GATA‐1 in all cells there would be no such juxtaposition, explaining the failure of erythroid differentiation (Whyatt et al., 2000).
Nonautonomous pRb function in the nervous system
Although pRb null neurons in chimeric mice autonomously display ectopic S‐phase entry, the neuronal apoptosis that otherwise occurs in the absence of pRb is suppressed (Lipinski et al., 2001). Thus, the effect of pRb loss is partially cell nonautonomous in neuronal tissues. Theoretically, pRb null cells could secrete an apoptosis‐inducing factor that is diluted in chimeras (Lipinski et al., 2001). However, it is unlikely that pRb would specifically regulate the expression of such a secreted factor by neurons. In fact, loss of pRb in the neuronal cells themselves is likely to disrupt their differentiation and thereby lead to apoptosis (Lee et al., 1994; Macleod et al., 1996; Tsai et al., 1998). It has been suggested that a signal supplied by wild‐type cells might inhibit the apoptosis of pRb null neurons (Lipinski et al., 2001). If this were the case and the cells supplying the signal were wild‐type neurons, homotypic signalling would again be the factor that overcomes the loss of pRb in neurogenesis.
Homotypic signalling in other systems
Homotypic signalling mechanisms also appear to explain cell‐nonautonomous phenomena in other systems. One precedent for the homotypic model presented here exists in the nematode Caenorhabditis elegans. In this organism, the insulin/IGF receptor homologue DAF‐2 regulates adult development and ageing. A mild decrease in daf‐2 activity can lengthen lifespan, and a more severe decrease in activity can cause larvae to enter a state of diapause (dauer formation) rather than progressing to adulthood. Mosaic analysis demonstrated that daf‐2 functions cell nonautonomously in both processes. For example, during development, larvae null for daf‐2 become dauers. In contrast, larvae mosaic for daf‐2 can become adults and all cells, regardless of genotype, display an adult phenotype. Importantly, an adult phenotype was not associated with a requirement for daf‐2 activity in any particular cell. It is thought that secondary signals operate to ensure that all cells adopt the same developmental fate (Apfeld and Kenyon, 1998). Similarly, in mice, homotypic signalling between neural crest cells has been proposed to explain the cell‐nonautonomous defect in colonization of the lower gut by endothelin‐receptor B null enteric neuroblasts (Kapur et al., 1995).
Homotypic signalling potentially activates pathways that allow defects, such as pRb loss or GATA‐1 overexpression, to be tolerated. However, what would be the function of such a signalling mechanism during erythropoiesis when such defects are not present? Mature erythroid cells regularly leave the erythroblastic island and must be replaced. Signals, such as the postulated REDS, may normally regulate the balance of proliferating and differentiating cells within the island. REDS produced by mature cells may activate the maturation and differentiation (at the expense of proliferation) of more immature cells. This would lead to the reinforcement or acceleration of maturation among all responsive cells in the island. This, in turn, would create a feedback mechanism in which the departure of mature cells would allow immature cells to proliferate and expand, whereas the accumulation of mature cells would inhibit the proliferation and activate the differentiation of immature cells. In addition to a normal role in regulating the balance between differentiation and proliferation, REDS could also provide a mechanism to activate differentiation during periods of rapid proliferation, e.g. during Epo‐induced erythroid expansion following hypoxia (Krantz, 1991). As immature cells moved towards the source of REDS, i.e. relatively mature cells on the periphery of the island, differentiation would become synchronized, maintaining the distribution of mature cells on the periphery. This could explain the observation that the process of erythroid differentiation within islands, including the timing of cell division, can be highly synchronous (Allen and Testa, 1991). Such synchronization may be functionally important in the efficient release of mature cells into the circulation, as it would result in a large proportion of cells being at the same late stage of maturation (Allen and Testa, 1991).
In conclusion, it appears that the intrinsic requirement for pRb function in the differentiation of some cell types can be bypassed by signals supplied by wild‐type cells, particularly in systems in which mature and immature cells are often in contact with one another. This phenomenon has implications in cancer, as loss of signal responsiveness could contribute to the tumorigenecity of cells that have lost pRb function. Furthermore, the existence of such a signalling mechanism indicates that previous interpretations of cell‐nonautonomous defects may, in fact, attribute gene function to incorrect cell types.
We would like to thank D. Meijer, S. Philipsen, G. Zafarana and L. Gutierrez for critically reviewing the manuscript. The authors are supported by the Dutch Cancer Society.
- Copyright © 2002 European Molecular Biology Organization


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Oil spill-Triumph departure delayed to 9:00 p.m.
Someone asked a few days ago so when I heard this, thought I should post. It seems that Triumph has to delay it's departure until 9:00 tonight, because it takes about 8 hours to reach the mouth of the Mississippi and they are not allowing ships to navigate the oil in the dark.
If that doesn't make them late to any ports I have no issue with it. If it is out of kilter, I likely won't be too thrilled when we sail in two weeks.
Your kidding! That sucks! I don't cruise on her again until October - and I have a feeling it will be cancelled.
Triumph did delay - will we ever know the real reason?
Please read the posted port notice:
Long before October the leak will be sealed. Are you serious? It already has been reduced and may be sealed within days and certainly will be within a couple of months.
Triumph did delay - will we ever know the real reason?
Please read the posted port notice:
A day or two old, but no restrictions.
Long before October the leak will be sealed. It already has been reduced and may be sealed within days and certainly will be within a couple of months.
My understanding is that the passenger's who boarded yesterday were told it was because they were not allowed to navigate the spill area during the darkness and could only do so during the daylight hours.
What no one knows is who or what entity imposed that restriction. Perhaps the Captain or Carnival itself. It may also be a restriction of the ports they are going to, where they cannot dock if they have oil on their hull. Who knows?
I started thinking about it and really I doubt a 5 hour delay will mean much to our upcoming cruise on June 5. Since there are 2 full sea days before we'll arrive in Belize, I would think there should be plenty of time.
Cheryl I would not worry too much about a trip so far out in October. If they don't have this menace plugged by then, a cruise will be the least of everyone's worries. At the point that Carnival's schedule is consistently or substantially impacted by these conditions, they would move the Triumph to a different port and make appropriate changes. Lord knows we love New Orleans and want ships sailing from there year round, so let's pray they can stop that oil flow and get this mess cleaned up. I fear for the Gulf Coast and hope that BP can get this oil stopped before it does more damage. My advice is, do what you would normally do, buy trip insurance, book hotels and flights with generous change/cancellation policies and just keep a watchful eye on it.
We have a B2B booked for October.....and I don't think we will have any issues.
The Mississippi River is to vital an import/export commodity for it to be closed....and that would be the only way the Triumph would not sail.
I'm sailing on the Triumph in September and I hope it leaves from NO. I remember years ago I was booked on the Conquest that was scheduled to leave from NO, but was repositioned to TX because of Hurricane Katrina.
It just leaves you to wonder how much of a whack can the people of the gulf take? First Katrina, now this? I feel sick just thinking about all the damage being done and people that are being financially impacted, if not ruined, again! :mad:
Long before October the leak will be sealed. It already has been reduced and may be sealed within days and certainly will be within a couple of months.
Are you holding your breath? I'm not! Please consider that, even when they stop the leak, there will still be a HUGE amount of oil floating around to deal with. I heard a report recently that said there are still problems from the Valdes spill. How many years ago was that?
Even if the leak is stoped tomorrow, the impact it will have will be long lasting - they have already closed some beach resorts in the lower Parishes...not to mention fishing. People are loosing money everyday.
The oil that makes it to the wetlands will be a problem for a while
Yes, it is a catastrophe, but nothing like what some people are making it out to be.
Yes, some areas are closed to fishing - but they have opened some oyster beds that were previously closed.
I have to agree with you. The media is having a field day with it. I have seen the same brown pelican for days now on the news. Just like the Swine Flu. You would have thought the entire population of the US as well as the world was dying. I feel for those folks that are taking the direct brunt right now. The fisherman, the coastal communities that rely on tourism, the shrimpers, etc. Their economy will suffer. However, I think this problem will go away and in time fade into the past. Just my humble opinion.
Some things are true and some things are probably not true. I live in South Louisiana and happen to work for an oil company. (Not BP) I do have to say that most of my immediate family and plenty of other relatives works as commercial fishermen in the area known as the inside waters of the State of Louisiana. The thing about working the inside areas is you have to follow the rules of fishing seasons that are set by the state. Shrimping in the inside waters normally runs from the 1st week in May to the middle of June. Then again opens in the 1st week of August to around December 1st. Being someone whos actually done this right out of high school you have to make enough money in the 1st season to last until August. Then make enough in the 2nd season to get you through the winter until next May. These fishermen make there money in shorts periods of time. If you take one of those times away it is devastating to them. It being said it could take years for the areas to be fishable again. This means lots of people will suffer in ways unamaginable. I understand that BP is trying to help most of them out, but at a small monthly basis according to when they narmally work. This will not cover what actually needs to be made for one month, since one month might have to over 3 to 4 months. Praying for everyone affected by this catastrophe. Yes it is a catastrophe in more ways than one.
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subset: commoncrawl


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TORONTO, Jan. 13, 2016 /CNW/ - Canadian governments need to spend wisely in order to maximize their infrastructure dollars, according to a new C.D. Howe Institute report. In "Getting More Buildings for our Bucks: Canadian Infrastructure Policy in 2016," author Benjamin Dachis provides Canada's federal, provincial and municipal governments with a blueprint for sound infrastructure investment.
"Billions will be committed to infrastructure spending in 2016," commented Dachis. "It is critical that governments invest in smart projects and do so using best practices." The report has recommendations for all three levels of government:
"Financing infrastructure with deficits has an economic cost," Dachis concludes, "As governments expand their investments in critical infrastructure, they should ensure they are investing in the right projects with highest long-run returns, not necessarily the shovel-ready ones."
For the report go to: https://www.cdhowe.org/public-policy-research/getting-more-buildings-our-bucks-canadian-infrastructure-policy-2016
The C.D. Howe Institute is an independent not-for-profit research institute whose mission is to raise living standards by fostering economically sound public policies. Widely considered to be Canada's most influential think tank, the Institute is a trusted source of essential policy intelligence, distinguished by research that is nonpartisan, evidence-based and subject to definitive expert review.
SOURCE C.D. Howe Institute
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Loot Crate May 2016 Spoiler + Coupon!
We have the latest spoiler for the May 2016 Loot Crate! There is 1 day left to sign up (it closes on the 19th at 9PM PT) and get this box!
Thanks to Letita on Instagram – Each box will include:
WOW! I love QFigs, and this one is incredible (excellent box use!)
In the comments, we get a hint at what all the items might be. Here's what we think is in the box:
- World of Warcraft Shirt
- Dragonball Z Plush
- Hulk QFig
- Marvel Glove (Oven Mitt?)
UPDATE – The oven mitt is Thanos's Infinity Gauntlet!!!!
If you haven't signed up yet, use coupon code SAVE3 to save $3 off your first Loot Crate box, or use ADDICTION to save 10% off any length subscription!
What do you think of the May 2016 Loot Crate spoiler?
Check out our Loot Crate reviews to see what has been in past subscription boxes!


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The title of this tumblr says it all
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Andy and Pee-wee
Beasts of the Southern Wild now has a great interactive site and tumblr.
related: How to Recreate an Animated GIF on a Pizza
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IVC (Inter-Vehicle Communication) is a promising technology for the The proposed service employs a distributed algorithm to build an approximate congestion perimeter. This task is carried out by dissemination of positioning data of vehicles vertices of a polygon that is a close approximation of the congestion area. Given the polygon and its current location, a vehicle can then plan its escape-way route from the traffic jam.
http://www.lbd.dcc.ufmg.br/colecoes/sbrc/2006/st1_2.pdfCaso o link acima esteja inválido, faça uma busca pelo texto completo na Web: Buscar na Web


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Over the weekend, actress Michelle Rodriguez came across TMZ's camera people in Hollywood and when asked if she was taking over the Green Lantern role, she gave an interesting reply.
"That's the dumbest thing I ever heard," she the reporter. "I think it's so stupid because of this whole minorities in Hollywood thing. It's so stupid. Stop stealing all the white people's superheroes. Make up your own. What's up with that?"
That comment was met with a ton of backlash online, especially since people have complained about Hollywood's lack of diversity. Many people felt that as a Latina, Rodriguez's comments were asinine and problematic. Rodriguez posted a video on Facebook to clarify her comments.
"I guess it got taken out of context, because a lot of people got offended or whatever," she said. "What I really meant was that ultimately at the end of the day, there's a language. And the language that you speak in Hollywood is successful franchise. And I think there are many cultures in Hollywood that are not white that can come up with their own mythology. I think it's time for us to write our own mythology."
On one hand, we all know Hollywood is lazy. So turning a white superhero character into a female or non-white character is the easy way out, and doesn't require Hollywood to actually 'make' something new. Hollywood is known for reinventing the wheel with remakes, reboots, and stealing from other countries.
But on the other hand, until Hollywood actually gets some type of originality, I'm all for reboots and remakes using women and people of color in the roles. But don't hold your breath for Hollywood to all of a sudden become filled with originality. Until then, we're stuck with Rodriguez playing the same type of roles, in a black tank top.
Image Credit: Michelle Rodriguez Twitter


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We recently threw a birthday party for Brooke. This is my second attempt at a kid birthday party since becoming a mother 5 years ago. My first attempt was when Brooke was 1.
Every new mom is pretty much obligated to throw a first birthday party for their first child. Some decide to continue to regularly throw birthday parties after that. Others, like me, decide that it's a ridiculous amount of effort to put forth for someone who doesn't understand any of it and would just as soon chew on a stick as appreciate the the sentiment.
Don't get me wrong, Brooke's first party was adorable, the food was wonderful, and lots of beautiful friends and family turned out and brought tons of love and cheer to the day. However, I spent at least $500, and it poured buckets of rain for hours, mid-way through. Did I mention it was an outdoor party? I was pretty over it when it was all said and done.
Since then, I vowed only to throw birthday parties for people who specifically asked for them. Here we are 4 years later, and Brooke took her cute little blonde head out of the sand and requested a Care Bears party. Ironically, the new Care Bears series premiered on the day BEFORE the party. Thus, there was not a single Care Bear licensed product to be found in all the land. In two weeks, there will be a Care Bears extravaganza for all to enjoy at every iParty in the world.
But, we made do with what we had, and some very special ladies in my life came through with Care Bears support.
Allie made absolutely gorgeous and delicious cookies, which happened to be gluten, dairy, nut and soy free, which our allergic friends really appreciated. Brooke was overjoyed.
My mom brought my old Care Bears toys from back in the day to decorate. It was neat to see my 5 year old playing with toys that I received on my own 5th birthday. Crazy!
And our friend, Miss Dawne, who owns this amazing place called The Bright Spot, created a Care Bears craft for the kids. They made their own Care Bear bellies! Such cuteness!
And yes, this time around I had the party at a facility rather than open my home to a bajillion (lovely and well-mannered, but young) children. This was a lifesaver. It was so nice to show up at this place, have another person handle the ins and outs of the day, plan activities for the kids, make sure everyone is fed and happy, while I mingled with my parent-friends and took pictures of the kids. I actually got to enjoy my own (I mean my daughter's) party. I wish Dawne could clone herself because she's so amazing with kids. Literally, there were many moments where parents were tearing up because she was creating such a magical time for them, and their little faces were completely lit up with joy. What a beautiful thing.
So all in all, this party made up for all the shit that went wrong in my first kid birthday party experience. A good time was had by all, and I left feeling extremely grateful for my family and all of our beautiful, intelligent and most importantly, good looking friends. 😉


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Microsoft, along with every other company out there are now free to use the term "Netbook" after winning the right back from Psion.
Psion claimed that they had copyright of the term for one of it's old products. But even after the tern netbook can be freely used, Microsoft want to change it to something else.
Clearly not happy with the many other terms such as netbook, smartbook, ultra-portable, thin-and-light and MID, Microsoft want to introduce a new term; Low cost small notebook PCs.
It doesn't exactly roll well off of the tongue. I can't exactly picture two friends saying "Hey, I just bought a new low cost small notebook PC".
The new term is meant to show the fact that netbooks now do much more than just Internet browsing.
As the phrase netbook came around from both users and netbook manufacturers, we think, and hope it sticks around!


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Mullah Abdul Salam Zaeef said the civilians had all died in the Kabul area. He refused to give details.
"Unfortunately rockets landed on several dwelling places," he declared. The American planes had made no attempt to distinguish between civilian and military targets, the ambassador said.
Speaking at a press conference in Islamabad in the Taliban's last remaining embassy, Mullah Zaeef said that Osama bin Laden had survived Sunday's bombardment unscathed. "He is still alive. He is still in Afghanistan," he added. "In the present circumstances we have not taken any talks with Osama."
Reuters carried an interview with a 16-year-old ice-cream vendor from Jalalabad who said he had lost his leg and two fingers in a missile strike on an airfield near his home.
"There was just a roaring sound, and then I opened my eyes and I was in a hospital," said the boy, called Assadullah, speaking in Peshawar after being taken across the border for medical help . "I lost my leg and two fingers. There were other people hurt. People were running all over the place."
Earlier Donald Rumsfeld, US defence secretary, and Geoff Hoon, his British opposite number, said the raids had been entirely successful, striking with precision at enemy assets and avoiding civilian deaths.
Avoiding civilian casualties is crucial to maintaining international support for the US action against the Taliban and Bin Laden, particularly among Muslim allies uneasy with the use of force.
Mr Rumsfeld said the opening sorties of Operation Enduring Freedom had been a complete success and that only military targets had been hit. "Every single target which the coalition forces hit was a military target," he said. "There was an attack on the military airport near Kabul but certainly not on anything relating to other targets near the city."
Mr Hoon moved to halt speculation that civilians had been killed by elaborating on the locations of some of the targets, emphasising that most of them were in isolated parts of the country away from the major population centres.
Despite the prospect of further American bombing, which began again last night, the Taliban yesterday continued to strike a defiant pose. At an emergency cabinet meeting in Kabul, Taliban ministers agreed to declare jihad against the United States. Troops were now reinforcing defensive positions, they said.
In an assertion immediately rejected by the Pentagon, the Taliban also claimed yesterday to have shot down an American plane in the remote western province of Farah. Officials said there were unconfirmed reports that two more allied planes had also been shot down.
"It was a night-time sky. It was dark. Rockets attacked the plane and one plane was shot down," Mullah Zaeef said. Asked whether the wreckage would soon be displayed, officials said Farah was a long way away.
Ordinary Afghans described how the attacks had caused widespread panic. "All night I was with my four children. We were very afraid. We didn't sleep," said Mirza Mohammed, who lives near Kabul airport. "I don't understand why the people of Afghanistan are such unlucky people."
Hamid Jalil, 12, said shrapnel had broken the windows of his home, while witnesses con firmed that at least one private house in Kabul suffered a direct hit. A deep crater was visible yesterday.
"All the night we were in the basement with our neighbours," Hamid Jalil said.
Refugees trickling into Pakistan yesterday said residents in Kandahar had fled into the streets as plumes of black smoke enveloped the city. They confirmed that Kandahar airport had been hit, together with the house of the Taliban leader, Mullah Mohammed Omar.
Noor Mohammed, a nurse who lives three alleys away, said people started running out of the house as soon as the attacks started. About 20 cars left the compound. Seconds later three missiles struck, he said.
Nematollah, another Kandahar resident, who reached the Pakistani border town of Chaman yesterday, said: "I was standing on my roof when I heard planes overhead, and the next thing I knew there were explosions and panic everywhere. The electricity went out, and people were running in the streets in the darkness."
Other refugees reported seeing at least four wounded.
There was no sign last night that the seemingly accurate bombing had prompted any change of heart from the Taliban leadership. Mullah Zaeef described the attacks as a "terrorist action" and said the "violation" of the Islamic Emirate of Afghanistan amounted to an attack on the whole Muslim world. He described the opposition, who are expected soon to advance on Kabul, as "America's slaves".
In Kabul, the Taliban minister Amir Khan Muttaqi said the Afghan people would "forcefully resist" the US-British attacks. "We resist America as we resisted the Russians," he added. The extremist militia's policy on Bin Laden had not changed, he said.
Western diplomats in Islamabad last night said that the eight foreign aid workers on trial in Kabul charged with preaching Christianity had so far survived the bombardment unhurt. They were in a secluded place with their Pakistani lawyer, officials said.


text: tag:blogger.com,1999:blog-7931726123533399648.post6425928697126279906..comments2016-06-08T13:43:04.569-04:00Comments on Bonnaroo Bound: Leohttp://firstname.lastname@example.com:blogger.com,1999:blog-7931726123533399648.post-72714303025157624972010-06-06T07:16:25.565-04:002010-06-06T07:16:25.565-04:00Generally it is one spot for one vehicle. You mig...Generally it is one spot for one vehicle. You might get lucky and get parked on the end of a row or some other place where you have more room but chances are not. They pack the cars in pretty tight.Leohttps://firstname.lastname@example.com:blogger.com,1999:blog-7931726123533399648.post-18730433418617116702010-06-04T16:21:28.579-04:002010-06-04T16:21:28.579-04:00I have a similar question about camping. I believe...I have a similar question about camping. I believe I will be carpooling with some friends, however I do not think we will be camping together. Is it possible to get an additional spot near my friends (so we can stay somewhat close) without having an additional car for the next spot? I would like to keep close to the people I know, and would prefer not to go into the campsite-only areas without them. I guess my question would be this- Can a large group of people who rode in one car get more than one camping firstname.lastname@example.com


text:
8/17/2011 1:55pm, #1
tactical firearms training bullshido
This video clip has been passing through the gun blog-discussion board world like wildfire lately.
The safety violations are too numerous to list, but the one that stuck out most in my mind was the "room clearing" segment where one person was firing directly in front of a team member as he was moving to enter the next room.
This training group calls themslves American Defense Enterprises, and the following is their promotional video.
"We do dangerous things"...uhhh yeah. And stupid things too.
Word on the net is that the guy running the show, one Bill Beasley, is supposed to be former "Special Operations".
It's interesting how "Bullshido" doesn't apply only to the traditional/asian martial arts. The increase in these tactical/defensive firearms courses draw the exact same type of personas...both as students and instructors.
8/17/2011 1:59pm, #2
What should scare all of us firearms owners is the media splash yahoos like this will make when someone eventually gets killed at one of these places. Can you just imagine the picture of the American gun owner MSNBC will paint with a trove of fail like this to draw from?
8/17/2011 2:31pm, #3
Hey they do the same slow synchronized scan like Ralph Severe
8/17/2011 2:36pm, #4
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Why wait till someone gets killed? Frankly, I think these assholes should be all over the news right now. It'd certainly get to the bottom of his "Special Forces" credentials right quick.Originally Posted by Sarcastro
8/17/2011 2:43pm, #5
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damn, you said it first.
Edit: Lindz
Last edited by Homernoid; 8/17/2011 2:43pm at . Reason: being to slow
8/17/2011 2:48pm, #6
The thing that we all seem to take for granted in this "YouTube" age is the cameraman...in some of these clips dont miss the fact that it looks like some numbnut was standing in front of these turkeys shooting video.
8/17/2011 6:21pm, #7
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I watched pretty carefully, and I think that most times the camera was down range it was on a stand and still. Still though, this is fucking retarded.Originally Posted by Sarcastro
8/21/2011 2:49pm, #8
I like how the graphic for the 2nd video had him Sabrina ing.Lone Wolf McQuade Final Fight: https://www.youtube.com/watch?v=VmrDe_mYUXg
8/22/2011 2:36am, #9
There are no words for how stupidly dangerous that is, and their promotional video is downright repugnant.
You wanna go where people know
safety isn't a game.
You wanna go where
everything points down range.
8/31/2011 10:04am, #10
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There is a difference between "Special Operations" and "Special Forces"
Special Forces is a US Army Green Beret.
Special Operations is a much larger umbrella. It encompasses everything for US Army Rangers and Navy SEALs to Civil Affairs and PsyOps. First two are direct action type (ie door kicky shooty type) the others are still dangerous (especially CA) but not direct action types.
So with that said he could easily be SpecOps but that doesn't mean he was superninja commando.______
Xiao Ao Jiang Hu Zhi Dong Fang Bu Bai (Laughing Proud Warrior Invincible Asia) Dark Emperor of Baji!!!
Didn't anyone ever tell him a fat man could never be a ninja
You can't practice Judo just to win a Judo Match! You practice so that no matter what happens, you can win using Judo!The key to fighting two men at once is to be much tougher than both of them.