Adult Niche Amateur
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If you are going to start a new adult website then you need to choose your niche. It is really the first thing you should do before you launch any porn site. The biggest mistake that you could make as an new adult webmaster is to create a general video tube website. There are millions of sites like this one and you have a very very low chances that you will outrank the top competitors. You will only waste your money and your time by doing it. Instead I recommend you to find a one porn niche that you like the most.
A niche is simply what topic you will focus on for your new adult site. Nowadays when you are starting as a newbie, the only real solution to make a lot of money is a niche site. You focus on the one small topic that is not so much saturated.
When I look at all the big adult sites, they are all promoting the same sites and same content and I think it is rather boring. Just give them what you personally love and find interesting, and I am sure you will find a lot of people who share your tastes. You might see it as just writing about the things that interest you, but you are adding your personality to it, and that is what makes a blog successful and gains actual followers rather than just passing clickers.
It all makes money, but for longevity I say you need to promote something you like. Otherwise you get burned out on what you are doing and then go look for a new niche to promote. I think it is best to stick with the one thing then promote the fuck out of it.
I can write about all kinds of action and all niches, but when you are doing it for yourself rather than as I do for paying customers, it is far too easy to abandon projects if you have little interest.
There are many more porn niches. If you are a straight dude and like big juicy boobs then you should thing about launching a tube video site or blog site that is filled daily with hot busty models. Or maybe you are a gay guy who loves big uncut dicks, I think you should focus on this niche. But it does not necessarily work that way, I know many hetero-oriented webmasters that have a lot of luck in promoting gay paysites. It depends only on you and you will have to make that decision which thousands of new webmasters make everyday.
If you still did not decide then you can go to any popular tube website and you will see all the existing niches listed there. I suggest you to watch a few videos from all of them. It will help you to determine which niches you like and you are interested in the most. So now you have a list of several categories from which you should choose only the one.
I have found myself getting into some of the fetishes on niche sites I work on. I do not know if this is due to prolonged exposure or a natural evolution of my sexuality as I have been doing this for a long time. On the flip side an editor I was working with on one of our hardcore fetish sites began as a total gay sub and working on the site for a long time turned him into a dominant straight guy. So it effects different people in different ways. I know some people who prefer to work in niches which do not float their boat as they say working with material they find hot spoils it for them.As long as you can understand what is sexy about the niche I do not think it maters whether you are into it or not. It depends on the scale you are working on as well. If you only have a personal blog around a certain fetish it is going to be a lot easier to maintain if it is coming from a genuine place and you will naturally attract followers who are into the same thing. I always thought that niche or fetishes would be easier to sell as it is more rare, the only downside is getting enough content to do something.
You should start with the niche you have the most interest in because even if you start a site in the most profitable niche, you will most likely fail because you will quickly lose the interest in maintaining that site. If you like milf women, then create an adult site in that niche. If you need a more detailed response, please open your own thread on my forum. I will be happy to reply there.
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A schematized, limb bud stage mouse embryo with arrows indicating the flow of macrophage progenitors, which are all initially derived from the yolk sac and aorta-gonad-mesonephros (AGM), but with some populations moving directly onto their eventual tissues and others bypassing and differentiating further in the liver. In Drosophila (right), as in vertebrates, hematopoiesis occurs in two waves. The first during early embryogenesis gives rise to embryonic macrophages (red) that disperse throughout the embryo and later populate the larva organizing into sessile patches and circulating blood cells; these can be considered the fly equivalent of tissue macrophages. A second population arise from the larval lymph gland (green); these cells are released during pupal development, make up most of the population of blood cells in both the pupa and the adult, and can be considered the fly equivalent of bone marrow-derived macrophages.
A second wave of hematopoiesis in flies occurs post-embryonically in a specialist larval organ called the lymph gland (Figure 1). This organ supplies blood cells at the beginning of metamorphosis (Crozatier et al., 2007, Jung et al., 2005, Lanot et al., 2001) and gives rise to all three types of Drosophila blood cell: macrophages (plasmatocytes), crystal cells, and lamellocytes. These macrophages can be considered the fly equivalent of vertebrate bone marrow-derived macrophages (Gold and Bruckner, 2015), and studies have revealed a number of signaling pathways that play key roles in directing this hematopoietic program. A pool of progenitor blood cells is maintained within the larval lymph gland under the control of a posterior signaling center (PSC), which expresses the fly homolog of the vertebrate EBF-1 transcription factor, Collier (Krzemien et al., 2007). This signaling center operates as a stem cell niche to control blood cell homeostasis acting in a non-cell-autonomous manner to maintain the activity of the Hedgehog (Hh) and JAK-STAT pathways in the progenitor cells, which maintains their multipotency (Mandal et al., 2007). Wingless (Wg), the fly ortholog of vertebrate Wnt signaling, has also been shown to control the maintenance of hematopoietic progenitor cells within the lymph gland (Sinenko et al., 2009). The activity of the PSC niche in the fly can be modulated by physiological constraints reminiscent of the interactions described in vertebrates between hematopoietic stem cells and their microenvironment. A key study established reactive oxygen species (ROS) as a regulator of fly hematopoiesis by revealing that ROS levels in progenitor cells sensitize these progenitors to differentiate (Owusu-Ansah and Banerjee, 2009). The maintenance of hematopoietic progenitor cells can also be directly influenced by the nutritional state of the fly as well as by levels of sensory perception in the animal (Shim et al., 2012, Shim et al., 2013).
Following infection in the fly, macrophages do not act exclusively as phagocytic cells to clear the invading microorganism but also carry out signaling roles to coordinate systemic immune responses across different tissues. In part this role is needed because of the absence of an adaptive immune response in flies. For example, septic injury to adult flies has been shown to induce the production of the cytokine Unpaired 3 (Upd3) in macrophages, which then activates JAK/STAT signaling in the fly equivalent of the liver, the fat body (Agaisse et al., 2003). Following gut infection with the phytopathogen Erwinia carotovora (Ecc15), macrophages are required for the induction of the expression of the antimicrobial peptide, Diptericin, in the fat body (Basset et al., 2000), and macrophages have been shown to relay Ecc15 infection-induced oxidative stress signals in the gut to the fat body to trigger antimicrobial peptide production (Wu et al., 2012). Expression of another antimicrobial peptide, defensin, in the fat body has been shown to be dependent on pathogen degradation within macrophages via the lysosomal protein Psidin (Brennan et al., 2007), and antimicrobial peptide production in the fat body following septic injury has also been shown to require a signal relayed by macrophages through secretion of the Toll pathway ligand Spatzle (Shia et al., 2009).
Right: F480 immunostaining of a wound made to the back skin of an adult mouse with multiphoton second harmonics revealing collagen (white) to reveal the wound margin running from top left to bottom right of the field of view. Macrophages (green) are clustered at the wound edge. Left: similarly, laser ablation wounds made in the epithelium of a fly embryo trigger a rapid chemotactic response from macrophages (green), which are recruited to the wound within minutes and remain at the wound site throughout closure. Wounds are marked with an asterisk. Mouse wound image courtesy of Jenna Cash, and fly image courtesy of Helen Weavers.
Macrophages are not absolutely critical for mammalian healing per se, because embryonic tissues can repair at stages before the first macrophages are born, and neonatal mice null for PU.1 that have no macrophages can repair wounds very efficiently; indeed, they do this without leaving any trace of a scar, just as in the embryo, which is suggestive that macrophages mediate wound fibrosis (Martin et al., 2003). However, adult tissue repair appears much more dependent on macrophages, with classic antimacrophage serum knockdown experiments in rabbits exhibiting poor healing (Leibovich and Ross, 1975), and more recent temporally regulated diphtheria toxin killing of macrophages in mice revealing different healing defects depending on which phase of healing is targeted: early knockdown of macrophages results in retarded re-epithelialization and reduces the extent of wound granulation tissue and eventual scar size, whereas mid-stage knockdown leads to a failure of granulation tissue maturation and contraction and to severe wound hemorrhaging, suggesting that macrophages may be orchestrating key behaviors at different times and in several cell lineages within the healing wound (Lucas et al., 2010). 781b155fdc