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Do you ever wonder how a parent can deny the existence of their own child?(37 Posts)
And walk away from them totally, never wondering how they are, where they are or even what they look like?
I think it's really hard to understand how anyone could happily do this. My youngest daughter has never met her father. He ran off when I was pregnant and refused to even talk to me about her. He denies that she's his to his family and anyone else. Strangely his family do believe that she's his and contact me now and then to see how she is.
When dd was a baby I thought, naively perhaps, that it would be ok that she won't ever know her real dad. But now she's nearly 4 she's started saying things like 'I want to have a dad' and I feel bad because I made the choice to have a relationship with him in the first place iyswim. I hope she doesn't try to look for him when she grows up as I fear she'll be disappointed with what she finds.
Slightly different, but my mum turned her back on me after an argument shortly after I left home. I was 18. 20 years later, all those years with no contact. She even walked past me on the street days before I emigrated (yes, she knew I was doing so) as if she didn't know me.
But she never really wanted me, so I guess she mentally walked away shortly after my birth.
i often wonder especially now im a mum, my dad left me at 10 weeks and ignored ny existence in favour of his older children from a previous relationship and the younger ones he had whilst cheating on my mum. But know what it is his loss i am happy and pretty normal my mum did just great on her own, so dont worry one brilliant mum is more than enough x
Oh I know - and sadly my daughter is not alone. I just can't comprehend why anyone willfully would ever want to cause anyone any upset - it just doesn't compute does it.
I have more than enough love of 2 parents for my daughter - his loss. And everyone who struggles on their own, I find me and my daughter are very close - I am way over protective I admit, I had the smashed windows and threats too when she was tiny so I totally understand that fear. But for all the struggle and loneliness & being skint etc, it has been worth every single minute. Being a parent is an utter privilege I reckon - and I am very proud of her and so very grateful for her. Sod him.
It does sound as if he's had a breakdown but as you say that is no excuse. For a parent to knowingly cause pain to their child is totally indefensible.
Words fail me every day too! I keep thinking he has had a breakdown - but quite frankly that isn't a good enough excuse. As for the hatred I have had from his OW who he met online on a very dodgy site, well I can't even begin to tell you.
Initially when he left my daughter didn't want to see him as she was so disgusted with his behaviour, but instead of making the effort to keep contact going he just gave up and vanished.
He told me himself the ow is a nightmare, he sobbed about what he has done, grass isn't greener, how he was so sorry - and then he vanished again, and nothing since. I even 'spoke' to the ow and told her, begged her actually, to get him to contact his daughter - and still radio silence from him. And still the charmer of an ow continues to accuse me of abusing my own daughter. You couldn't make it up could you?
I really, really wish my own life was not like a very poor EastEnders script - it wasn't meant to be like this
fergoose - words fail me I can't imagine how anyone could be so cruel - your poor dd. Herrena, my dd's 'father' is also a heavy pot smoker and was also violent towards me and was always getting into fights. I look back and just can't understand why I wanted to be with him, but then I was unwell at the time.
herrena - that is awful
Not surprised it is still raw. He doesn't deserve to be a parent if that is how he behaves.
Gosh sorry for the essay it's all a bit raw for me at the moment.
Yes fergoose I totally agree.
I stopped allowing ex to visit baby after he smashed my window, emotional abuse is one thing, smashing up my house is another.
He has bail conditions not to approach me so I cannot supervise contact and he cannot be trusted to have unsupervised contact (having 3 times endangered dds life and being a heavy pot smoker)
I contacted family mediation (the day after smashed window) and passed on details to him via family. They contacted him, no response. He spent weeks trying to intimidate and manipulate me (through my mum ) and after 13 weeks finally contacted family mediation. He then tried to guilt me into arranging contact for her 1st birthday as he had left it too late for Fmc to organise in time.
I didn't and my justification was
If I was in his position I would have been standing outside the office of Fmc when they opened and would have done literally anything to get back to her.
He had since had 5 sessions of contact (2hrs once a week) been twenty mins late for 2 and ended on 15 mins early.
My ex was a doting father for 14 years - then he just walked, and apart from a few days last autumn refuses to see his own daughter, it has been 15 months now. Daughter is heartbroken, I have tried contacting him begging him to at least speak to her - all is ignored. I am terrified what the long term effects will be for my daughter, not to mention how the heck she is going to get through her GCSEs this year. She quite wrongly blames herself. And meanwhile his lovely new girlfriend has started an online hate campaign against me accusing me of child abuse because I am 'stopping' my daughter seeing her father apparently - you couldn't make it up could you.
I cannot comprehend how any parent could ignore their child - I wouldn't be able to breathe, let alone function, if I didn't have my daughter in my life. Maybe bit melodramatic, but you know. Every instinct as a parent is to love & protect isn't it?
I left the children's father when our newborn was just 4 weeks old. He's spent a total of around 4 weeks probably with his father since he was born.
My eldest child however has a bond with her father. Although neither have heard or seen him for over a year now.
I'd like to think he has cut all contact with them because he's hurting so much that he can't see them regularly (he lives 200 miles away) so it's easier to deal with that hurt if he just abandons them emotionally altogether.
I'd like to think that ...
But in reality, he isn't a compassionate man, he is mostly unemotional anyway, he never wanted children (with me, at least), I 'ruined his life' by having them. It was a quite intense DV relationship. So my answer at least, would be that I think he denies their existence because he just simply doesn't care about them. They are dead to him. He ought as well to be dead to them. Yet the courts still think children benefit from a relationship with their father regardless that the father wants no relationship with them.
My eldest Ds's dad walked away from them 10 years ago, they were about 4 and 6 at the time. He hasn't seen them since!
He poked ds2 on Facebook a couple of years ago so I sent a short sharp MSG telling him to fuck off! Then we all blocked him!
And I did go to Csa, thank god just before he disappeared although he pays a pittance!
Yes, very true about rewriting history. He wrote me an email saying he didn't believe she was his - he knows full well that she is his.
Last night I was talking with my parents about tracing him for child maintenance via the CSA. He is working in the UK again and I am pretty sure I know where. My parents were of the opinion that if I don't want him to see dd and given his past violent tendencies, I should leave well alone and not contact him in any way, even via the CSA as it could open a can of worms.
Have you all decided to leave child maintenance?
In a lot of cases the truth of the OP's question is that they `make stuff up' and rewrite history. They have to live with themselves every day and so they have to do that, as the truth isn't very nice or acceptable to society.
As Red says, courts are very pro two parents so no excuse.
And then if it suits later down the line and they want to see their child
or give you some sh*t they rewrite history again. Just make sure you know your own truth, don't dwell on any of it and enjoy your life, they sure has hell make sure they are doing what they want to do at all times.
Beckett -I had a similar situation with no.3. Out of interest did he go off with someone else? After a year I put my foot down & said all three or none having explained to dds that it's only fair to their beloved sibling & it worked & he now sees all 3. BUT I have to say the relationship isn't overly strong!!
Bike - in this day & age there is no excuse not to see your child, courts are very sympathetic to the right of a child to see BOTH parents & I could never say I had no kids when I did so maybe take some of what he is saying with a pinch of salt!!
Yes, I also wonder how often/if they ever really think about their kids. I can't imagine they can with any clarity as they don't know what they are missing. Ex hasn't seen DD since she was 6mo and has only asked for one pic of her since moving in with his new g.f. I do always think he has no idea how much he is missing out on, but I doubt he ever will to be honest. These people just don't think like that.
DD is only 19mo and calls my dad Papa which is a bit embarrassing - he looks pretty young and I have given up explaining to people in restaurants etc that we are not a couple Any advice on how to sort that out <poster above with same issue? -Too lazy and tired to scroll up, sorry!> She also gets very upset when he walks out of the room, which she used to do to me as well, and I worry this is some attachment to males thing (he visits about once a month).
Well, I'm glad XP isn't around anymore as he was pretty bloody awful. But I do wonder how often he thinks about the dc's. They wouldn't know him if they saw him in the street and I doubt he would recognise 6yo DS these days, he has never known DD apart from when she was 6 months old.
He had endless chances to buck his ideas up and stay together as a family but he couldn't do it.
I work with someone who has not seen his (now adult) son for 20ish years I believe, but not through want of trying. He rarely talks about it, but usually tells people that he has not DC, to stop an y further questions. I was briefly his line manager and he did open up to me a bit. I understood then why he would deny having a child.
perplex of course, thats totally up to you.
i jsut think sometimes people may say that as they long to have known/know someone as a parent.
eg- id love to have a husband, and say, Im MRS Husbandsname, i have ahUsband. (if that makes any sense)..
I haven't seen my biological father (and I'll call him what I like, thanks) since I was three. I heard on the grapevine that he has 3 more daughters and is a raging alcoholic and not a very nice man. Lovely. I always knew I wasn't missing out on much.
I've never wanted to see him, couldn't care less.
I've said before, but you really don't miss what you've never had.
glad you agree, OP, sometimes i think im just Uber-sensitive.Its sad for your daughter, of course it is, OP, in an ideal world wed all be happy families, complete mum dad and kids families. but its not an ideal world and people are not perfect.
I feel angry at 'abandoners' (another word for them) but also sad, theyll never know what it is to love and be loved by a child, the greatest love there is.
DCs asked me ONCE 'do i have a daddy' and I wont lie, i wont sugar coat it, but for now i say 'its okay, you and me are family, we're a team'. i explain that 1 of my sibs is a single parent too and i say some kids have mums, some have dads, and thats better than having no one at all.
seriously, i get boiling mad when the term parent is used in sucha frivolous way, like on the news eg, baby P, the childs mother....er...no, not mother, the childs abuser.
same with 'birth' and 'biological' 'parents' too. no, a parent is the one who loves/nurtures/brings up the child.
btw, your daughter is lucky to get the attention from your other daughters dad.
marjproops - I completely agree they are not actually parents. There definitely are advantages to being a lone parent - I get to decide everything. He wouldn't be able to give meaningful input. I think I feel sad for my daughter because her sisters have a father who is involved, who pays child maintenance and takes an interest in her.
As far as DCs concerned, there was a man but thats all he was, and as lonely and longing as I am, id rather be on my own this way with DC ANYTIME.
why oh why o why do people keep calling them absent 'parents' feckless 'fathers' or 'mothers?'
These people are NOT PARENTS. they have no right or HONOUR to be called such.
PARENT/MOTHER/FATHER/MUM/DAD is NOT a label, its a verb, its a privelage, and the utmost homour anyone could have.
PLEASE stop calling them dads/fathers/mums/mothers.
they are reckless sperm donors or breeders or anything BUT a parent.....and breathe.
Pleased to help
Your dc can't have different fathers and be who they are don't feel guilty for giving them life.
We all have our crosses to bear in life, it makes us strong and gives us depth of character, every one (including our precious kids) must suffer sometimes or become an insufferable brat!
Stop looking at other families and thinking you've failed because your doing it by yourself, it's not as cut and dried as that.
I knew beyond a shadow of a doubt that I would manage as a single mum,
I didn't feel cowed into staying in an abusive relationship (and teaching my dd to expect that from future partners)
I had seen my mum do a better job as a single mum than the majority of couples bother to do
I'm waffling now but I think what I'm trying to get to is being a single parent is harder on you than on the kids.
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text:
This article, Kyle Tobias, is property of DarkStrings.
|Kyle Tobias
|5ft 11in
|Shinigami, Vizard
|Shino Nakazume (Wife)
|Previous Occupation(s)
Amalda Finn (Daughter) Shino Zankazume (Wife)
Kyle Tobias is average in appearance, with the only exception being a distinctive American appearance. Possessing blonde hair and deep blue eyes, Kyle stands out against the many other Shinigami. Kyle also has a large scar on his chest from when his soul chain was torn form his body prior top becoming a Shinigami.
Kyle has a calm and collected personality, often at odds with his young age. While young, Kyle possess an oddly high talent for battle. Kyle is usually seen with a happy or content look, showing that, depsite the threat of death, Kyle is happy with his lot in life. Kyle is a capable leader, often being able to make heat of the moment decisions without losing his head.
Kyle has shown overwhelming devotion to his squad members, and even more to his wife Shino and his daughter Amalda. Kyle has shown overwhelming grief after being forced to kill Shino and leave his daughter Amalda in the care of Yamamoto.
Before Arc
During the before arc, thirteen years before the Hollowfication Incident, Kyle was killed by a car. The Driver was killed moments before by a passing Hollow. The Hollow attacked Kyle attempting to claim a second meal. Kyle was cornered and in a fit of primal instinct attacked the Hollow. The Hollow Struck and tore the Soul CHain from Kyle's chest, causing his soul to begin disintegrating. Kyle was brought to his inner world and, after a brief ordeal, awakened his powers as a Shinigami. Shortly after slaying the Hollow, Kyle was found by the then lieutenant Sousuke Aizen.
After being brought to Seireitei, Kyle was brought before Captain-General Yamamoto. After judging his abilities Yamamoto ranked him as a low level lieutenant or a high level third seat. Kyle then meets his Captain, and future wife, Shino Nakazume.
Powers & Abilities
Zanjutsu Specialist: Kyle focuses more on using his zanpakuto than using kidou.
Shunpo Specialist: Kyle's skill with Shunpo is so great that, to anyone with lower level abilities, it appears that he is dashing in every direction at once.
Knowledge of Bakudo: Kyle leans more towards the binding nature of Kidou, forsakening Hadou.
Natural Combatant: Kyle has an almost unnerving ability to remain himself in combat, rarely if ever losing his head and panicing. However, when his speed is matched or exceeded by an opponent, Kyle begins to worry and make mistakes.
Lisianthus (Eternal Breeze) When sealed Lisianthus takes the form of a pair of identical Ninto. Lisianthus is strange compared to most Zanpakuto in that, she prefers to be adressed as Sia as opposed to Lisianthus claiming, "I hate the way that name sounds! Almost like some stupid flower!" Lisianthus takes the form of a young woman wearing a long white scarf, sckirt, shirt and a pair of ribbons, one around her right arm, the other around her left thigh.
- Shikai: Triggered by the command, "Gust Forth".
- Shikai: In it's released state, Lisianthus becomes a body length great sword with a cross guard the extends a foot before the blade begins. The blade represents the crashing force of the wind, instead of the elegant dance.
- Shikai Special Ability: Kazeheki Shikon, (lit. Wind Slicing Fang.) Kyle fires a tumbling crescent of condensed air at his oppnents.
- Shikai Special Ability 2: Distortion. By raising his right hand up and focusing, Kyle is able to disrupt the air flow between himself and an opponent, literally threading away incoming energy based attacks.
- Bankai: Yohtsu Ohindo Lisianthus (Four Eternal Breezes) When Kyle releases his bankai, his current blade shatters and stirs up the air around him, hiding him behind a veil of dust. When the dust clears, Kyle is revealed to be holding a pair of large, wave patterened sword, each the length of his leg. He also has another pair of the same blades floating behind him. These weapons are used simultaneously, within arms reach.
- Bankai Special Ability: Kazeheki Shikon and Distortion abilities are enhanced dramatically.
- Bankai Special Ability 3: Overcast. Kyle shunpos in four directions simultaneously, resulting in him splitting into four tangible Kyle's, each wielding one of his bankai swords. All for are real and can attack independantly. This abilitu is very taxing and dangerous.
- Bankai Special Ability 4: Kazeheki Ono (lit. Wind Slicing Hatchet) Effectivly a close range Kazeheki Shikon. Kyle "sheathes" his weapons behind his back and focuses his reiatsu. The four swords spin and then shatter, forming two sets of disjointed white wings. The energy then threads into Kyle's hands, forming a large white saber of pure reiatsu. Kyle then attacks at max speed, cleaving his opponents in half.
The actual story, BLEACH:Another Side, Another Story, can be found here. http://darkstrings.deviantart.com/art/BLEACH-ASAS-Ch-1-97330129

subset: commoncrawl


text:
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Ten years ago, the groundwork for the discovery of the genetic basis of chronic pancreatitis was laid by linkage analyses of large kindreds with autosomal dominant hereditary chronic pancreatitis. Subsequent candidate gene sequencing of the 7q35 chromosome region revealed a strong association of the c.365G>A (p.R122H) mutation of the PRSS1 gene encoding cationic trypsinogen with hereditary pancreatitis. In the following years, further mutations of this gene were discovered in patients with hereditary or idiopathic chronic pancreatitis. In vitro the mutations increase autocatalytic conversion of trypsinogen to active trypsin and thus probably cause premature, intrapancreatic trypsinogen activation in vivo. The clinical presentation is highly variable, but most affected mutation carriers have relatively mild disease. In this review, we summarize the current knowledge on trypsinogen mutations and their role in pancreatic diseases.
The human pancreas produces the digestive pro-enzyme trypsinogen in three highly similar isoforms. The isoenzymes are encoded by separate genes, PRSS1 (protease, serine, 1; OMIM +276000), PRSS2 (OMIM *601564) and PRSS3. On the basis of their relative isoelectric points and electrophoretic mobility, these are commonly referred to as cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), and mesotrypsinogen (PRSS3). Normally, cationic trypsinogen represents circa 2/3 of total trypsinogen in the pancreatic juice, while anionic trypsinogen makes up approximately 1/3 (Guy et al., 1978; Rinderknecht et al., 1979, 1985). Mesotrypsinogen is a minor species, accounting for 2–10 % of human trypsinogens (Rinderknecht et al., 1984). Trypsinogens are synthesized as pre-pro-enzymes containing a signal peptide of 15 amino acids, followed by the 8 amino acid long pro-peptide, the trypsinogen activation peptide (TAP). The signal-peptide is removed upon entry into the endoplasmic reticulum lumen and the pro-enzymes (also called zymogens) are packaged into zymogen granules and eventually secreted into the pancreatic juice. Activation of trypsinogen to trypsin occurs in the duodenum by the brush-border localized protease, enteropeptidase (enterokinase), which removes the TAP. Trypsin also activates trypsinogen (autoactivation), which in the duodenum may have a physiological role in facilitating zymogen activation, whereas ectopic autoactivation in the pancreas may result in pancreatitis. Genetic variants of the cationic trypsinogen (PRSS1) have been identified in patients with hereditary pancreatitis (OMIM #167800), familial or sporadic chronic pancreatitis. In contrast, mutations of anionic trypsinogen (PRSS2) or mesotrypsinogen (PRSS3) have not been found in association with chronic pancreatitis to date (Chen et al., 1999a; Nemoda et al., 2005). Classic hereditary pancreatitis follows an autosomal dominant inheritance pattern with incomplete penetrance and highly variable disease expression (Comfort and Steinberg, 1952; Le Bodic et al., 1996a; Sossenheimer et al., 1997; Keim et al., 2001; Howes et al., 2004). The mutations are located in three clusters within the trypsinogen sequence: in the TAP, in the N-terminal part of trypsin or in the longest peptide segment not stabilized by disulfide bonds between Cys64 and Cys139 (fig. 1). Thus, all pancreatitis-associated mutations discovered to date seem to cluster in the N-terminal half of the molecule encoded by exons 2 and 3. It is important to note, however, that investigation of the PRSS1 gene in patients with suspected genetically determined chronic pancreatitis is restricted to these exons in most laboratories and possible C-terminal mutations may have been missed. The discovery of pancreatitis-associated cationic trypsinogen mutations in 1996 demonstrated that trypsinogen plays a central role in the pathogenesis of human pancreatitis (Whitcomb et al., 1996a). Here we review the wealth of genetic and biochemical data that has accumulated over the past ten years of research on the role of trypsinogen mutations in chronic pancreatitis.
After genome wide linkage analyses, three independent groups reported an association of the hereditary pancreatitis phenotype with the long arm of chromosome 7 (Le Bodic et al., 1996b; Pandya et al., 1996; Whitcomb et al., 1996b). Within the same year, the c.365G>A mutation (p.R122H; p.R117H in the chymotrypsin numbering system) of the cationic trypsinogen gene was identified in all hereditary pancreatitis affected individuals and obligate carriers from five kindreds, but not in individuals who married into the families nor in 140 unrelated individuals (Whitcomb et al., 1996a). In the early literature, the mutation nomenclature was based on the chymotrypsin numbering commonly used by biochemists and crystallographers. The genetic numbering system, which designates the initiator methionine as position 1, was widely adopted in 2000 and has been in use since (Chen and Férec, 2000a; Teich, Hoffmeister and Keim, 2000).
To explain why the R122H mutation might cause pancreatitis, David Whitcomb proposed that the Arg122-Val123 autolytic peptide bond in trypsin plays an important role in the degradation of prematurely activated trypsin in the pancreas. Destruction of this "failsafe mechanism" by the R122H mutation would increase intrapancreatic trypsin activity and disturb the protease-antiprotease equilibrium and eventually precipitate pancreatitis (Whitcomb et al., 1996a). Biochemical evidence supports the notion that Arg122 is important for autolysis of trypsin and mutations of this amino-acid result in increased trypsin stability (Higaki and Light 1986; Gaboriaud et al., 1996; Várallyai et al., 1998, Sahin-Tóth and Tóth, 2000). A study using cerulein-induced zymogen activation in isolated rat acini demonstrated that autodegradation of trypsin mitigates cathepsin B-mediated trypsinogen activation, suggesting that a failsafe mechanism might be indeed operational in the mammalian pancreas (Halangk et al., 2000). The Whitcomb model in its original form has remained very popular over the years; even though more detailed biochemical analysis indicated that the R122H mutation results not only in increased trypsin stability but also in increased zymogen stability and increased autoactivation (Sahin-Tóth and Tóth, 2000, Kukor et al., 2002b). A weak trypsin-inhibitory activity associated with the Arg122 site is also lost in the R122H mutant (Kukor et al., 2002b). Thus, the pleiotropic biochemical effect of R122H raises the possibility that the pathogenic alteration is unrelated to trypsin stability. More importantly, the model fails to explain how the other pancreatitis-associated PRSS1 mutations might work, as the majority of these do not affect trypsin stability.
A few months after the R122H mutation was reported, a second hereditary pancreatitis associated mutation was identified within the N-terminal region of the cationic trypsinogen molecule. The c.86A>T mutation (p.N29I; p.N21I according to chymotrypsin numbering) was initially found in 4 families, 2 from the USA and 2 from Germany (Gorry et al., 1997; Teich, Mössner and Keim, 1998). A different c.86A>C mutation affecting the same amino-acid (p.N29T) was also reported in 2002 (Pfützer et al., 2002). Biochemical characterization of the N29I mutation using recombinant trypsinogen found no effect on trypsin or trypsinogen stability. On the other hand, moderately increased autoactivation was observed by two independent laboratories in 4 published studies (Sahin-Tóth 2000; Sahin-Tóth and Tóth 2000; Szilágyi et al., 2001; Teich et al., 2005). The N29T mutant exhibited a phenotype similar to that of R122H, both increased trypsin stability and enhanced autoactivation were documented (Sahin-Tóth 2000). Because increased autoactivation was observed with the R122H, N29I and N29T mutations, whereas N29I had no effect on trypsin stability, the logical conclusion was put forth that enhanced autoactivation is the common pathogenic mechanism of hereditary pancreatitis associated PRSS1 mutations (Sahin-Tóth and Tóth, 2000).
The R122H and the N29I mutations are the most common PRSS1 mutations worldwide. They have been frequently reported from Europe, North America and Asia (Nishimori et al., 2001) and R122H was also recently found in a family of Aboriginal descent in Australia (McGaughran et al., 2004). Neither mutation was detected in two hereditary pancreatitis families from Brazil (Bernardino et al., 2002) and no hereditary pancreatitis cases have been reported from Africa. So far, no trypsinogen mutations have been found in animals. Curiously, there is a relatively high incidence of pancreatitis in miniature Schnauzer dogs. Bishop and colleagues sequenced all exons of the canine cationic trypsinogen gene in four Schnauzers but no mutation was found (Bishop et al., 2004).
In addition to the originally reported frequently found R122H mutation (c.365G>A), a rare double nucleotide substitution variant was also found (c.365–366 GC>AT), which also results in the R122H mutation at the amino-acid level. The routinely used Afl-III restriction digestion assay for the PRSS1 R122H mutation does not detect this variant, therefore, DNA-sequencing is recommended to screen patients from hereditary pancreatitis families (Chen et al., 2000b; Howes et al., 2001). The R122H double nucleotide substitution variant was the first convincing example of a possible gene conversion event leading to a pancreatitis-causing trypsinogen mutation (see below).
A third mutation of Arg122, c.364C>T resulting in p.R122C, was discovered in 2001 by three independent groups (LeMaréchal et al., 2001; Pfützer et al., 2002; Simon et al., 2002a) and was also found in one patient from our cohort. The recombinantly expressed R122C mutant showed a complex phenotype. PRSS1 contains 10 cysteine residues, which form 5 disulfide bridges in the correctly folded protease. The introduction of the extra unpaired cysteine in the R122C mutant results in partial misfolding during expression and purification of the recombinant protein. As a result, the R122C preparation exhibits reduced activity, autolysis and autoactivation. On the other hand, when the data are normalized to the active trypsinogen fraction, the phenotype becomes very similar to that of R122H, exhibiting reduced autolysis (i.e. increased trypsin stability) and increased autoactivation (Simon et al., 2002a). The low-activity phenotype of R122C spawned the theory that a loss of trypsin function caused by a mutation could cause pancreatitis by eliminating a protective trypsin-dependent mechanism. This model has been favored by Markus Lerch's group and received additional support from their studies indicating that trypsin might play a protective role in cerulein-induced zymogen activation (Halangk et al., 2000). Although this model is thought-provoking, from a genetic point-of-view no evidence exists to support it; as so far no clear loss-of-function mutations (e.g. nonsense, splice-site or frameshift) have been found in association with chronic pancreatitis. Furthermore, results from the large majority of in vitro experiments using recombinantly expressed trypsinogen mutants favor enhanced trypsinogen activation as the key event in the pathogenesis of genetically determined chronic pancreatitis.
In addition to Arg122, mutations were also identified in the neighboring residues, Ala121 and Val123. The c.367G>A mutation, which results in p.V123M was found in a patient with chronic pancreatitis by Jian-Min Chen and Claude Férec and their co-workers (Chen et al., 2001). The c.361G>A mutation, which results in p.A121T was detected in association with hereditary pancreatitis in a German family (Felderbauer et al., 2005). Also in the vicinity of Arg122, the c.346C>T mutation resulting in p.R116C was reported by four research groups. Arg116 is unique to human cationic trypsinogen, however, its function is unclear. Unlike Arg122, it does not appear to be important for autolysis (M. S.-T., unpublished observation). The mechanism of the "Arg122-flanking" mutations described above has not been studied yet.
Taken together, the high frequency and variability of mutations in or close to Arg122 suggests that this sequence is particularly prone to mutations, for reasons that are not readily apparent. The "mutational hot-spot" idea is consistent with the worldwide distribution of R122H and and it is also supported by the direct identification of a "de novo" R122H mutation in a German patient (Simon et al., 2002b).
Gene conversion – the substitution of genetic material from another gene – is recognized as the underlying cause of a growing number of genetic diseases, as Gaucher disease (OMIM #230800), von Willebrand disease (OMIM #193400), polycystic kidney disease (OMIM #601313) and Shwachman-Diamond syndrome (OMIM #260400). In the majority of cases, the donor gene is a duplicated pseudogene, which accumulated mutations over time and recombination of the mutated sequences with the normal gene results in the pathogenic genotype. In contrast, there is growing evidence, that gene conversion between two functional paralogous trypsinogen genes can occur and cause genetically determined chronic pancreatitis. Trypsinogen genes are tandemly repeated within the T-cell-receptor beta (TCR-beta) locus (Rowen, Koop and Hood, 1996). This is a hot spot for gene conversion events to generate a broad variety of TCR-beta genes (Flajnik, 2002). Therefore, conversion mutations within the interpolated trypsinogen gene family are very likely. This mechanism is evident in case of the R122H mutation associated with the c.365–366 GC>AT di-nucleotide substitution (c.365_366conNM_002770.2:c.365_366), but remains speculative for the single-nucleotide substitutions causing mutations R122H (c.365G>A), N29I (c.86A>T) and A16V (c.47C>T) (Chen and Férec, 2000b; Chen and Férec, 2000c; Chen et al., 2000). Recently, we described the clinical, genetic and biochemical properties of a large gene conversion event between the anionic trypsinogen gene (donor gene) and the cationic trypsinogen gene (acceptor gene) in a six-year old girl with chronic pancreatitis. In this patient, the conversion created 22 heterozygous nucleotide changes affecting mostly exon 2 of the PRSS1 gene (c.41-34_c.200+236conNM_002770.2:c.41-34_c.200+236). This resulted in the N29I and N54S mutations at the amino acid level. Biochemical characterization of the N29I–N54S double mutant revealed no difference from the previously investigated N29I mutant, indicating that the N54S mutation has no additional deleterious effect. This finding provided proof for the concept, that gene conversion is a possible mechanism for the development of pancreatitis associated PRSS1 mutations (Teich et al., 2005).
In 1999, the c.47C>T mutation, which results in p.A16V was reported in 4 out of 44 pediatric patients with chronic pancreatitis (Witt, Luck and Becker, 1999). This transition gained particular interest, as it was the first indication, that trypsinogen mutations may be associated with idiopathic chronic pancreatitis. Initially, the mutation was reported in 10 percent of chronic pancreatitis patients without a family history. In subsequent European and North American studies, only a minority of patients with idiopathic chronic pancreatitis carried the PRSS1-A16V mutation (Chen et al., 1999b; Pfützer and Whitcomb, 1999; Chen et al., 2001; Howes et al., 2001; Truninger et al., 2001; Teich et al., 2002; Howes et al., 2004). This discrepancy might be explained by the strict selection of pediatric patients in the initial report, which decreased the effect of environmental risk factors of chronic pancreatitis to a large extent (Witt, Luck and Becker, 1999). Even though it has been reported in less than 20 families worldwide, the A16V mutation represents the 3rd most common cationic trypsinogen gene mutation. In contrast to the considerably more prevalent N29I and R122H mutations, A16V was almost exclusively detected in patients without a family history of chronic pancreatitis. Unfortunately, thorough clinical and functional characterization of this mutation is lacking so far. The A16V mutation affects the first amino acid of the activation peptide and thus forms part of the signal peptide cleavage site. It was proposed that enhanced trypsinogen activation or altered intracellular transport might be the relevant pathogenic phenotype. The reduced cellular viability of AR42J cells transfected with A16V-trypsinogen might support either model (Gaiser et al., 2005). On the other hand, a recent study using recombinant human cationic trypsinogen failed to demonstrate increased autoactivation in the A16V mutant (Király et al., 2006). Furthermore, secretion is typically not influenced by the amino-acid distal to the signal-peptide cleavage site and valine is frequently found in this position in other secretory proteins, including human mesotrypsinogen.
Other genetic variants of the PRSS1 gene have been found in families with suspected hereditary pancreatitis, or in chronic pancreatitis patients without a family history (table 1). Some have been reported only once (−28delTCC, D19A, D22G, K23R, N29I+N54S, P36R, V39A, G83E, K92N, D100H, L104P, A121T, V123M, C139F) or in only a few families (N29T, E79K, R116C, R122C). Despite their limited frequency, the biochemical properties caused by some of these mutations offered interesting insights into the pathophysiology of genetically-determined chronic pancreatitis. The most interesting findings will be reviewed here.
The trypsinogen activation peptide (TAP) is hydrolyzed as the first step of the trypsinogen activation process. In vertebrates, this typically 8–10 amino-acid long peptide contains an unusual and highly conserved tetra-aspartate sequence, which precedes the scissile peptide bond Lys23-Ile24 (figure 1). This acidic motif serves as a specific recognition site for enteropeptidase, the physiological activator of trypsinogen. In addition, the acidic stretch was shown to contribute to the suppression of autoactivation. Interestingly, a recent study found that in human cationic trypsinogen the tetra-aspartate motif per se is not required for enteropeptidase recognition, whereas it is essential for maximal inhibition of autoactivation (Nemoda and Sahin-Tóth, 2005). In addition to the A16V mutation (see above), 3 pancreatitis-associated TAP mutations have been detected to date. The c.68A>G and c.65A>G mutations (p.K23R and p.D22G, respectively) were identified in families with putative hereditary pancreatitis, while the c.56A>C (p.D19A) mutation was found in a patient with idiopathic chronic pancreatitis (Férec et al., 1999; Teich et al., 2000; Chen et al., 2003a). When analyzed using model peptides or recombinant trypsinogens, all 3 activation peptide mutations significantly increased autoactivation of cationic trypsinogen; particularly the D22G and K23R mutations, which lie closer to the trypsinogen activation site Lys23-Ile24 (Teich et al., 2000; Chen et al., 2003a). These data are consistent with earlier peptide studies showing that neutralization of any of the 4 aspartate residues in the activation peptide increases autoactivation of trypsinogen (Delaage et al., 1967; Abita, Delaage and Lazdunski, 1969; Radhakrishnan, Walsh and Neurath, 1969). This notion was also confirmed recently by Ala-scanning mutagenesis of the tetra-Asp motif in human cationic trypsinogen (Nemoda and Sahin-Tóth, 2005). The markedly increased autoactivation of the K23R mutant is explained by the preference of trypsin to cleave after Arg rather than Lys at the P1 position of substrates.
Conceptually, the activation peptide mutations are important, because they do not affect trypsin structure or function, indicating that pancreatitis-associated mutations exert their effect through altering the properties of the pro-enzyme trypsinogen and not the active enzyme trypsin. In this context, properties of the characterized mutants confirmed that increased autoactivation of cationic trypsinogen is a relevant pathomechanism in hereditary pancreatitis.
In one German family with putative hereditary pancreatitis and two patients with sporadic chronic pancreatitis from France (Chen et al., 2001) and Belgium, we detected the c.235G>A mutation, which results in p.E79K (Teich et al., 2004a). This mutation was also reported in a patient with alcoholic chronic pancreatitis and one healthy control from Brasil as well as 2 healthy subjects from France (Chen et al., 2001; Bernardino et al., 2003). The affected individuals in the German family exhibited late-onset chronic pancreatitis, suggesting that this mutation might have a relatively low penetrance (Teich et al., 2004a). The wild type and E79K mutant PRSS1 alleles are transcribed in the pancreas to comparable levels. In vitro analysis of recombinant cationic trypsinogen carrying the E79K mutation revealed unaltered catalytic activity, autolysis, and inhibition by pancreatic secretory trypsin inhibitor. In contrast to previously studied mutations that increased autoactivation of cationic trypsinogen, autoactivation of E79K-trypsinogen was markedly decreased. Instead, E79K-trypsin proved to be an at least 2-fold better activator of anionic trypsinogen than wild type cationic trypsin. Thus, the E79K mutation appears to conform to the common mechanism of pancreatitis-associated mutations insofar as it leads to increased trypsinogen activation. What sets E79K apart from the other mutations is that increased trypsinogen activation is the result of transactivation of anionic trypsinogen instead of autoactivation (Teich et al., 2004a). However, it remains controversial whether the decreased autoactivation or the increased transactivation is the disease-relevant phenotype of E79K.
Chen et al described the heterozygous nonsense mutation c.111C>A (p.Y37X) and the splicing site mutation IVS2+1G>A in the PRSS1 gene of alcoholics without the development of chronic pancreatitis, but not in alcoholics with chronic pancreatitis and patients with hereditary or idiopathic chronic pancreatitis. They proposed that such "loss of function" mutations might protect against chronic pancreatitis in persons with increased pancreatitis risk (Chen et al., 2003b).
Autosomal dominant hereditary chronic pancreatitis was first described after long-term follow-up of 36 members from 4 generations of a family, in which 6 members were affected (Comfort and Steinberg, 1952). The investigation of such large families was the most important prerequisite for successful genetic linkage studies, which have localized the hereditary pancreatitis gene on chromosome 7 (Le Bodic et al., 1996b; Pandya et al., 1996; Whitcomb et al., 1996b). However, in the daily clinical setting establishing such extensive pedigrees is not feasible and the inheritance pattern cannot be determined in some cases. Consequently, the criteria of hereditary pancreatitis have been changing over the years and may be somewhat different in the various clinical centers. In the recently published Europac study, the diagnosis of hereditary pancreatitis was made on the basis of two first degree relatives or three or more second degree relatives, in two or more generations with recurrent acute pancreatitis, and/or chronic pancreatitis for which there were no precipitating factors. Cases in which these strict criteria were not met, but more than one affected family members were identified, mostly within the same generation, were classified as familial chronic pancreatitis. The diagnostic value of this classification is questionable, however, and at our center we diagnose hereditary pancreatitis if the patient has no other detectable cause of chronic pancreatitis and if he/she has one first or second degree relative with proven chronic pancreatitis. Furthermore, because the post-hoc analysis reveals a positive or putative family history of chronic pancreatitis in almost all "idiopathic chronic pancreatitis" patients with the common R122H or N29I mutations (Creighton et al., 1999, Teich, Hoffmeister and Keim, 1999), we classify all chronic pancreatitis patients with these mutations as highly susceptive of hereditary pancreatitis, even if a family history is not readily available. Based on Jane Creighton's data, that a susceptive family history for chronic pancreatitis is found post-hoc in almost all patients with typical hereditary pancreatitis-associated PRSS1 mutations, one may assume that the presence of a mutation compels clinicians to obtain a full family history post-hoc, whereas in the absence of such a mutation no post-hoc analysis of the family history is done. This may misclassify chronic pancreatitis in patients with hereditary pancreatitis as "idiopathic". Therefore, exact evaluation of anamnestic and clinical data has to precede genetic testing to avoid misclassification and unnecessary molecular investigations. In most patients with a rare or unique PRSS1 mutation, the family size is small or not reported (Chen et al., 2001; Teich et al., 2002) and the inheritance pattern of chronic pancreatitis associated with these mutations remains uncertain (table 1).
Idiopathic chronic pancreatitis has been a traditional clinical diagnosis describing the lack of an identifiable cause behind the disease. Clearly, as more and more genes (PRSS1, SPINK1, CFTR) and/or mutations are identified that cause or predispose to chronic pancreatitis, the number of patients with "true idiopathic" or "familial idiopathic" (Threadgold et al., 2002) disease keeps shrinking. As recent data suggest that chronic pancreatitis may be inherited in an autosomal dominant, autosomal recessive or multigenic fashion, the differentiation between hereditary and idiopathic chronic pancreatitis also becomes obsolete.
Hereditary pancreatitis is associated with PRSS1 mutations in more than 50 percent of affected families. However, in hereditary pancreatitis families with the PRSS1 mutations N29I or R122H, only 80% of the mutation carriers suffer from chronic pancreatitis. The cause of this incomplete penetrance is uncertain. In addition to further genetic factors, smoking, alcohol consumption or the lack of antioxidants were assumed as manifestation factors (Sibert 1978; Sossenheimer et al., 1997; Amann et al., 2001; Keim et al., 2001). On the basis of a study of 60 affected and 25 non-affected persons carrying the PRSS1 mutations N29I or R122H, we suggested that the TNF-238A promotor variant could be a relevant manifestation factor for chronic pancreatitis in hereditary pancreatitis-families (Beranek et al., 2003).
As to the clinical picture, both alcoholic and PRSS1 mutation-associated chronic pancreatitis exhibit essentially identical clinical laboratory results, histopathology or morphological changes in imaging studies. On the other hand, PRSS1 mutation associated pancreatitis manifests typically at an earlier age and pancreatic calcification and diabetes are less frequent complications (Keim et al., 2003). In the first large investigation of clinical criteria in hereditary pancreatitis, the mean age of onset was 12.9 years (Sossenheimer et al., 1997). Our own investigations revealed no difference in the age of onset between carriers of the N29I or R122H PRSS1 mutations. The median was 13 years in each group, respectively. Only 4% of our patients had severe chronic pancreatitis with exocrine and endocrine insufficiency, pancreatic calcification and duct dilation as well as hospitalizations due to pancreatitis. In general, half of the mutation carriers had little or no complaints or complications (Keim et al., 2001). A recent European study revealed a mean age of onset of 10 years and 14.5 years for affected carriers of the PRSS1 mutations R122H and N29I, respectively (Howes et al., 2004), but showed no mutation-dependent differences in complications such as exocrine or endocrine insufficiency or increased pancreatic cancer risk.
As shown in an investigation of 8 patients with pancreatic cancer in a cohort of 246 hereditary pancreatitis patients, the lifetime risk of pancreatic cancer is about 50-fold higher than in the control population and corresponds with 1 per 1066 person-years. It is only 20-fold elevated in patients with chronic alcoholic pancreatitis (Lowenfels et al., 1997; Malka et al., 2002). In our cohort of 101 hereditary pancreatitis patients, pancreatic cancer was diagnosed in 3 patients with the R122H mutation with a median of 23 years after the onset of pancreatitis. This corresponds to a rate of about 1 per 1200 person-years among affected R122H-carriers (Keim et al., 2001). However, the data basis for the estimation of the pancreatic cancer risk in patients with PRSS1-associated hereditary pancreatitis is small. The largest clinical investigation in the pre-genetic era, however, revealed no pancreatic cancer in 72 patients from 7 families (Sibert 1978). Taken together, the pancreatic cancer risk in hereditary pancreatitis patients with a PRSS1 mutation seems to be elevated - with an uncertain relative risk increase. Today, there is no generally accepted protocol for screening hereditary pancreatitis patients for early pancreatic cancer. However, affected mutation carriers should be strongly advised to stop smoking, as it is an additional risk factor for pancreatic cancer (Lowenfels et al., 2000).
Since the first description of a trypsinogen mutation in hereditary pancreatitis (Whitcomb et al., 1996a), the experimental and clinical information on genetic alterations in chronic pancreatitis has been rapidly growing resulting in a more and more complex data set. To address this issue, in early 2001 we implemented a continuously updated database, which contains all genetic variants of the PRSS1 and SPINK1 genes (www.uni-leipzig.de/pancreasmutation). In addition to exact genetic data, this database contains PubMed links to the clinical characterization of patients with different mutations and to in vitro studies with mutant molecules. Since 2002, this database has been part of the integrated database project of the Human Genome Variation Society (HGVS). This ambitious project fosters the discovery and characterization of genomic variations including population distribution and phenotypic associations. Backed by the HGVS, the novel WayStation has been inaugurated recently (www.centralmutations.org, Teich et al., 2004b). This is a web-accessible centralized structure for the submission, peer review, publication and release of genetic variation data.
The large majority of PRSS1 variants associated with chronic pancreatitis have been catalogued and the likelihood of finding novel PRSS1 mutations that affect a significant number of patients is diminishing. Nonetheless, as most laboratories have focused their studies on exons 2 and 3, it is still possible that new variants will be identified in exons 1, 3 and 5, or in the intronic and promoter regions. From a genetic aspect, a more interesting quest in the near future will be for modifier genes that might explain the penetrance problem, i.e. why some carriers of PRSS1 mutations remain healthy, whereas their relatives with the same mutation exhibit severe disease. Despite intensive research, the disease mechanism remains poorly understood. The biochemical alterations caused by the mutations have been mostly clarified, but the significance of these phenotypic changes in the disease remains to be determined. In this respect, future development of cellular and animal models of hereditary pancreatitis will be particularly valuable.
The authors thank Cèdric Le Maréchal for providing the nationalities of patients with rare PRSS1 mutations, as reported in table 1.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Dollar Tree is the nation's leading operator of single-price-point dollar stores. We're more than 5,400 stores strong and growing, with stores in all 48 contiguous states and 5 Canadian provinces. We have roots that trace back over fifty years, yet we're still defining our company, as well as our category, and looking for creative people to help us grow!
For starters, everyone has input and everybody counts. Although our dress is "business casual," there is nothing casual about our commitment and focus on growing our business. We emphasize teams that are cross-functional and multi-layered, the kind of flexible organization that allows people to deliver the best results. We're a company where our interaction with each other is based on respect, camaraderie, and a sense of joint purpose.
We continue to add Dollar Tree stores across America and in Canada.. As we continue to grow our business and look for fresh, new ideas and concepts to develop, we're always looking for people with the drive, imagination, and intelligence to help us continue our success. Do you have what it takes to join the Dollar Tree team?
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Subsea 7 S.A. has been awarded a two-year extension to two Underwater Services Contracts (USCs) by Shell Upstream International Europe, worth approximately US$240 million.
Under these Life of Field contract extensions for Diving Support Vessel (DSV) and Remotely Operated Vehicle Support Vessel (ROVSV) services, both of which will commence in 2016, Subsea 7 will continue to provide subsea construction, inspection, repair, maintenance and decommissioning services to Shell's UK offshore fields and facilities. The DSV contract will be delivered on a 24 hour, year-round basis through to the third quarter 2018.
The ROVSV contract will cover a minimum of 100 vessel days per year and continue through to the second quarter of 2018. Subsea 7's North Sea fleet, including the Seven Atlantic for the DSV work scope, will undertake the work under the USCs. Associated project management and engineering support for the USCs will be executed from Shell's and Subsea 7's offices in Aberdeen.
Subsea 7 S.A.
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Schlumberger has announced an agreement to acquire a majority (51%) equity interest in Eurasia Drilling Company Limited.
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text: "How the Masters Dig" July 11, 2012 Get link Facebook Twitter Pinterest Google+ Email Yoda on old school 1200s. The AT-ATs of turntables. Get link Facebook Twitter Pinterest Google+ Email Comments Ben KresselJuly 12, 2012 at 6:28 AMUp, pull it, selecta! Mmm.ReplyDeleteNeutonSeptember 16, 2012 at 6:54 AMHahaha, Amazing. I wonder what kind of music does he play.ReplyDeleteCheck12October 12, 2012 at 3:19 PMSuperb, that is.ReplyDeleteAdd commentLoad more... Post a Comment


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I will not becoming back this way, our story has ended a long time ago. I don't know what I was thinking letting you come back into my life. You made your mind up a long time ago. Only to find that you where unhappy with where your life has ended up. I am happy where I am. I have given up and let life take it's course. And through that I have met many wonderful people that I would have never met if you had chosen differently.
I'm glad you were immature and ignored me because as I see it now you are still that immature little girl I met oh so many years ago. Thank you for saving me from what could have been a life of many many regrets.


text: Computers are cold, hard and uninviting. A Chumby is soft, playful and at the forefront of Web-enabled home and business-travel devices. So what exactly is a Chumby? Categorizing it has probably been one of the biggest challenges founder Steve Tomlin, 46, and his team has faced. "We call it an interactive media player," says Tomlin. "It isn't a smaller, bigger or fancier computer. It's not something you already have." The Chumby, which looks like a standalone car headrest with a built-in high-resolution touch-screen, is an always-on Internet-enabled device. It offers all sort of information. The Chumby is a clock. It's also an entertainment news feed, a calendar, a digital photo frame, a video player, a stock-quote display and nearly a thousand other things enabled from the widget applications that run on it. The $179 Chumby takes your most desired information and puts it in front of you for access at a glance, whether that's the morning surf report or pictures of your family. The Chumby, which debuted in February, has squishy sides, internal speakers and runs on an open-source Linux platform. It's not surprising that a company that avoided naming their new Internet-enabled device without a prefix "e" or "i" sees things a bit differently than other tech companies. The Chumby, unlike most other consumer electronics, gets better with age. The early adopters of Chumby, for example, didn't know they were buying an Internet radio. But one morning they looked at their device and saw a tab for music that had been pushed to their device with a software update through the Internet.


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I would like to hire a Programmer
Budget $750-1500 USD
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VideoHive ELEGANT RINGS 127329
After Effects Project Files \ Openers \ Corporate
ELEGANT RINGS 127329 by ankvfx @ VideoHive
After Effects Project Files \ Openers \ Corporate
After Effects Version: CS4 File Size: 785kb Requires Plugins: No Resolution: 1920x1080
==== Elegant Rings ====
This PROJECT FILE CAN BE USED IN CORPORATE AND BRAODCAST PRESENTAIONS .
This Project file is CS4 and CS5 compatible.
This file has 9 place holders.
Everything is customizable.
This project does not contain any pre-rendered files.
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Note: Sound is NOT included, but you can find it here:http://audiojungle.net
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American Whiskey - Blended
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Great Northern Doppelgänger Whiskey
Bottle/Rating Data
Tier/Percentile : UnratedRabble Rating : UnratedType: Blended American WhiskeyProducer and Owner: Great Northern DistillingOrigin: Wisconsin, United StatesABV: 45.0% Proof: 90.0Price (USD) : $35Age: N/A
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Proof66 Notes
Great Northern Doppelganger Whiskey is the product of distilled Dominator Doppelbock malt beer from the nearby O'so Brewing Company. It takes part in the new trend of microbreweries partnering with microdistilleries to produce a whiskey out of popular craft beers. They suggest its reminiscent of a "scotch style whiskey."
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The end destination of love's journey is you.
Jin Ying is currently experiencing two of life's most depressing moments: She is jilted by her fiancé, and her loving grandmother passes away. Heartbroken, she decides to visit the European city of Prague, and hopes to use the time to heal her inner pain. While in Prague, she meets a young Chinese man named Punk. There, she slowly unravels a secret romance her grandmother once experienced long ago.
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Welcome to the Nelson Mandela Digital Archive Project. Our aim is to locate, document, digitise, and provide access to all archival materials related to Nelson Mandela. This is a work in progress. Here is a selection of materials arranged in exhibits for your enjoyment.
Nelson Mandela Centre of Memory
Title: Long Walk Original Manuscript (Image #229)
Transcript: I raised the question whether the boycott tactic would be feasable in the new situation where the proposed Territorial Authority would consist only of nominated chiefs, headmen and councillors. Already at the sessions that took place when I was at Mthatha the government officials, with whom the members of the Select Committee were negotiating, insisted on a fully nominated Territorial Authority on the ground, they argued, that elections entailed the risk of agitators being elected and using the Territorial Authority as a platform from which to launch attacks against the government.
Secondly, I argued, we were confronted with a pyramidical structure resembling an iceberg, the base of which was as dangerous, if not more, as the apex on which the liberation movemnt was concentrating all its energies. Beneath the Territorial Authority were the Regional and Tribal Authorities which were entrusted with the actual functions of carrying out the new policy, and all of which would be based very largely on nominated members and making it difficult for the movement to penetrate them. I considered that in some areas elsewhere in the country ANC organisers were attending meetings in the rural areas called to discuss the introduction of Bantu Authorities and had done good work, but I felt that to wreck the whole system we needed more resources, human and financial, and above all, a machinery that would enable us to capture the institutions where we could not destroy them from outside.
The Working Committee did not discuss the report exhaustively but merely noted it and gave tentative comments on certain aspects. One of the most important events of 1955 which was being discussed throughout the country was the publication of the Report of the Commission for the
Reference code: 229
Extent and Medium: 1 page


text:
Macaulay Culkin
August 26, 2010 by Post Team
Macaulay Culkin, Remember Macaulay Culkin? He is an actor, best known for his role as Kevin McCallister in "Home Alone" and "Home Alone 2: Lost in New York."
I was actually very very famous in the 90s with a sweet face spying making problems for those who wanted to break down at home for Christmas, when his family forgot him home alone.
More than that was considered the most successful child actor since Shirley Temple and was good friends with the late pop star Michael Jackson. Macaulay was ranked number 2 on VH1 and E! 'S respective lists, "" 100 Greatest Kid Stars "and" Big Stars 50 children. "
As for his personal life, in 1998, he married actress Rachel Macaulay mine, but they divorced in 2000. She is currently dating Mila Kunis.
Other interesting facts about him:
* He is godfather to the son of Michael Jackson, Prince Michael and daughter Paris.
* He became the first child actor to receive and $ 1 million for a film – 1991 'My Girl'.
* Your role in 'Born on the Fourth of July was cut by director Oliver Stone.
* Her aunt is actress Bonnie Bedelia.
Today is his birthday, and although we have not seen in the movies of recent times, we are still waiting for that to happen, right?
Please feel free to send if you have any questions regarding this post , you can contact on
Disclaimer: The views expressed on this site are that of the authors and not necessarily that of U.S.S.POST.


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Content Writing
Budget $250-750 USD
Need Content Writer who able to write on recopies.
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The country town of Walpole is located in the Southern Forests region. Set on the tranquil waters of the Walpole Inlet, the town is surroundedby the Walpole Wilderness. Walpole Inlet is a small estuary connected through a narrow channel to the larger and deeper Nornalup Inlet � a designated marine park.
Make a day of it � when you visit Denmark�s iconic Tree Top Walk take the time to explore the Walpole Wilderness to the west of the Shire.
Walpole is 65km west of Denmark via the South Coast Highway (60 mins).


text: The Clinical Risk Manager (CRM) directs, develops, and coordinates the clinical risk management activities for the hospital. In doing so, the CRM will integrate information obtained from the reporting of adverse events, near misses, RCAs, and issues related to clinical risk. With this information, the CRM will analyze findings and will work collaboratively with Patient Safety and hospitals leaders to develop responsive programs that will enhance an organization culture that supports patient safety and reduces risk exposure. This position requires the full understanding and active participation in fulfilling the Mission of CHRISTUS Health, and demonstrating behavior consistent with the Core Values.


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My curly hair has always been hard to control. Got 2b curling gel kept my curls frizz free. It left my hair shinny and not heavy like other products that I tired. I would definitely recommend it.
Absolutely loved this product! Have my hair large defined curls without having to use heat and made it look very natural. Will be buying this product in the future again!
I love this product, use it on my naturally wavy hair to make it wavier. Its easy to use and I love how it makes my hair look and feel. Its priced well too
This is an okay product but it does smell to high heavens until it evaporates! I tried it on my curls, to try to get them a bit more wavy and not frizzy. It does work however, it did leave my hair feeling sticky in certain areas.
I have curly hair, period! I spray this into my hair after a shower, then run a pick through it. It keeps it all contained, frizz free, and great looking until my next shower. It smells a little different.... kind of reminds me of the guts in a pumpkin, but when it dries its not as strong and Im sure its not as bad as my mind thinks it is.
These reviews are the subjective opinions of ChickAdvisor members and not of ChickAdvisor Inc.


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|Next book >>
Space Walrus(2012)
A novel by Kevin L Donihe
Space: the final frontier... these are the voyages of... a walrus? Meet Walter. He is the first walrus in a revolutionary space program. Someday, his blubbery form will float past asteroids, stars, and planets as he journeys through the dark beyond to become a Master of Space. But for now, Walter's dream is to win the heart of his lifelong love, Dr. Stephanie, who happens to be the scientist assigned to conduct experiments on him. The problem is Dr. Stephanie does not love Walter. She views him as a test subject and nothing more. To make matters worse, Dr. Stephanie appears to be in love with the abusive head scientist, Dr. Ron. From Wonderland Book Award winner Kevin L. Donihe comes a tragic comedy of unrequited love and inspired determination.
Similar Books by other authors...
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Used availability for Kevin L Donihe's Space Walrus
See all available used copies of this book at Abebooks UK or Abebooks US
Paperback Editions
July 2012 : USA Paperback
|Title: Space Walrus
Author(s): Kevin L Donihe
ISBN: 1-62105-028-9 / 978-1-62105-028-5 (USA edition)
Publisher: Eraserhead Press
Availability: Amazon Amazon UK Amazon CA
Genre Pages


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Get an overview of this hotel4-star family-friendly hotel, walk to Tuban Beach
Popular property highlights
A family-friendly stay in Kuta awaits you at The Vira Bali Hotel. You'll be 0.7 km (0.4 mi) from Tuban Beach and 1.7 km (1 mi) from Kuta Beach. Highlights at this boutique hotel include a full-service spa, a restaurant, and an outdoor swimming pool.
LCD TVs with cable channels are featured in all 56 rooms, and you can enjoy free WiFi, balconies, and coffee/tea makers. Refrigerators and round-the-clock room service make in-room dining easy, and minibars provide refreshments. Nice touches to enhance your stay include slippers and free toiletries. Free bottled water, in-room massages, and safes are also available.Information missing or incorrect? Tell us!Opens in a new window
The Vira Bali Hotel
Hotel Amenities
Hotel Amenities
In addition to a full-service spa, The Vira Bali Hotel features an outdoor pool and a children's pool. The hotel offers a restaurant. A bar/lounge is on site where guests can unwind with a drink. A complimentary breakfast is offered each morning. Wireless Internet access is complimentary.
Business amenities at this 4-star property consist of a business center, limo/town car service, and a meeting room. Event facilities measure 1184 square feet (110 square meters). This family-friendly hotel also offers spa services, a library, and gift shops/newsstands. A roundtrip airport shuttle is complimentary to guests (available 24 hours). Onsite self parking is complimentary.
- 24-hour front desk
- Babysitting or childcare (surcharge)
- Free airport transportation
- Total number of rooms - 56
- Babysitting or childcare
- Number of floors - 4
- Bar/lounge
- Business center
- Free newspapers in lobby
- Free breakfast
- Concierge services
- Dry cleaning/laundry service
- Elevator/lift
- Full-service spa
- Gift shops or newsstand
- Free WiFi
- Library
- Shopping on site
- Luggage storage
- Hair salon
- Laundry facilities
- Limo or Town Car service available
- Restaurant
- Safe-deposit box at front desk
- Free self parking
- Conference space size (feet) - 1184
- Spa services on site
- Children's pool
- Outdoor pool
- One meeting room
- Conference space size (meters) - 110
Family Friendly Amenities
- Family Hotel
- Outdoor pool
- Children's pool
- Free Wi-Fi
- Laundry facilities
- Babysitting or childcare (surcharge)
- Refrigerator
- Cribs/infant beds (complimentary)
Available in all rooms: Free WiFi
Available in some public areas: Free WiFi
Free self parking
- Airport: Denpasar (DPS-Ngurah Rai Intl.) (2.5 km)
- Property shuttles: Free airport shuttle
- Parking: Free self parking
Room Amenities
- Premium TV channels
- Balcony
- Access via exterior corridors
- Air conditioning
- Refrigerator
- Minibar
- Coffee/tea maker
- Free bottled water
- Daily housekeeping
- Free toiletries
- Hair dryer
- Slippers
- Iron/ironing board (on request)
- Cable TV service
- Desk
- In-room safe (laptop compatible)
- In-room massage available
- Connecting/adjoining rooms available
- Free cribs/infant beds
- Rollaway/extra beds (surcharge)
- Free WiFi
- Room service (24 hours)
Where to Eat
A complimentary buffet breakfast is served each morning between 7 AM and 10 AM.
The Grill Corner - This restaurant serves breakfast, brunch, lunch, and dinner. Guests can order drinks at the bar and enjoy alfresco dining (weather permitting). Open 24 hours.
24-hour room service is available.
Nearby Activities
An outdoor pool and a children's pool are on site.
The recreational activities listed below are available either on site or nearby; fees may apply.
- Surfing/boogie boarding nearby
- Free bicycles on site
Spa Services
Guests can indulge in a pampering treatment at the hotel's full-service spa, The Anahita Spa. Services include massages, facials, body scrubs, and body treatments. A variety of treatment therapies are provided, including aromatherapy and Ayurvedic.
- Ayurvedic treatments
- Facial treatments
- Body scrubs
- Aromatherapy treatments
- Massages
- Body treatments
Hotel Policies
Check-in time starts at 2 PM
Special check-in instructions:
Check-out time is noon
Payment types
Children and extra beds
- Children are welcome.
- Kids stay free! One child 2 years old or younger stays free when using existing bedding.
- Rollaway/extra beds are available for USD 25 per night.
- Free cribs (infant beds)!
- Pets not allowed
You need to know
Extra-person charges may apply and vary depending on property policy.
Government-issued photo identification and a credit card or cash deposit are required at check-in for incidental charges.
Special requests are subject to availability upon check-in and may incur additional charges. Special requests cannot be guaranteed.
24-hour check-in
Deposit is due 7 days prior to arrival. To complete the reservation process and obtain additional information, please contact the office using the information on the reservation confirmation received after booking.
- Deposit: USD 50 per stay
- New Year's Eve (31 December) Gala Dinner per adult: USD 55.00
- New Year's Eve (31 December) Gala Dinner per child: USD 28.00 (from 5 to 11 years old)
- Resort fee
Optional extras
- Rollaway bed fee: USD 25 per night
Hotel Name
- Bali Vira
- Bali Vira Hotel
- Hotel Vira Bali
- Vira Bali
- Vira Bali Hotel
- Vira Hotel
- Vira Hotel Bali
We should mention
This property offers transfers from the airport. Guests must contact the property with arrival details before travel, using the contact information on the booking confirmation. Reservations are required for massage services and spa treatments. Reservations can be made by contacting the hotel prior to arrival, using the contact information on the booking confirmation. A resort fee is included in the total price displayed. One child 2 years old or younger stays free when occupying the parent or guardian's room, using existing bedding. The property has connecting/adjoining rooms, which are subject to availability and can be requested by contacting the property using the number on the booking confirmation.


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Verizon Wireless has announced that consumers will no longer have to worry about purchasing a smartphone or tablet on Big Red's network for full cost anymore, sort of. Consumers will now be able to activate service and pay for their smartphone or tablet in monthly payments.
Like everything in the wireless industry there is a lot of fine print. Here is an overview of what is required.
- Full retail priced smartphone or tablet price must be a minimum of $349.99.
- Pay for the full retail priced smartphone or tablet in 12 payments.
- Finance charge of $24, which is $2 per month.
- Device Payment Plan customers can take advantage of Share Everything pricing and data sharing.
- First payment, including $2 finance charge, due at time of purchase. Your next payment will appear on your next Verizon Wireless bill.
- Maximum of two open Installment Plans per customer.
- $1000 combined Installment Plan balance limit per customer
To find out more check with your local Verizon Wireless store. This program can be very beneficial to someone wanting a new phone but not qualified for an upgrade.


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Somers Point middleweight Patrick Majewski (21-1, 13 KOs) will be going to Denmark to challenge Danish prospect Patrick Nielson (19-0, 9 KOs) for the WBA Inter-Continental crown.
Majewski, a native of Poland, was originally in line to fight Mexico's Marco Antonio Rubio (54-6-1, 46 KOs) for the WBC interim world title in Mexico on July 27, but negotiations fell apart. Instead, he'll be fighting Nielson at Arena Nord in Frederikshavn, Denmark.
Boxing comes back to Atlantic City on Aug. 17 when Revel Casino-Hotel hosts its first-ever professional boxing show. The card features a pair of world title fights that will be televised on HBO Championship Boxing. IBF middlweight champion Daniel Geale (29-1, 15 KOs) will take on England's Darren Barker (25-1, 16 KOs) after IBF super-bantamweight champ Jonathan Romero (23-0, 12 KOs), of Colombia, meets Spanish challenger Kiko Martinez (28-4, 20 KOs).
In MMA news, Bellator will be coming back to Atlantic City in November.
The Chicago-based mixed martial arts organization will be staging its second card of the year at Revel Casino-Hotel on Nov. 15. Bellator, which is considered the second-best MMA company behind UFC, also held a show at Revel's Ovation Hall on April 4 after a stint at Caesars Atlantic City.
Tickets go on sale Friday at 10 a.m. through Ticketmaster. Prices have not yet been announced.
Point Pleasant MMA veteran Kurt Pellegrino (16-7) will headline the show, which will be televised on Spike TV. Pellegrino, 34, will end a two-year layoff when he faces Saul Almeida (12-4) in a lightweight (155 pounds) bout. Forked River middleweight Tom DeBlass (8-2) will be in the co-feature against an opponent to be named. Bellator will also have the finals of its welterweight (165) and featherweight (145) division tournaments.
"I've been in retirement for the last two years, but I've been in the gym every day since and the competitive fire has still been burning inside of me," Pellegrino said Monday in a statement. "Every morning I wake up I realize I had the same dream as the night before, and it's to go out the way I want. With Bellator back in Atlantic City, this is my opportunity to end my nightmare and go out the way I want, the way I deserve."
Bellator will be the second MMA organization to stage a show at Revel this year. Las Vegas-based World Series of Fighting returns on Sept. 15 with a card on NBC Sports Network.


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All of our phones, accessories and services are specifically designed for the elderly, partially sighted and hard of hearing…
Place your order before 3pm (Monday to Friday) and we'll aim to deliver the next day
"Easiphone are great to deal with, very helpful and efficient, thank you."
Stephen Tyler
"If Mum needs help in an emergency, she just presses the SOS button… you've taken away a big worry."
Barry Wilkinson
"Really quick delivery, easy to set up… excellent all round! Thank you!"
Daniel Kerstein
"I purchased one for my elderly mother before Christmas and was so impressed I purchased this one for myself due to having disabilities myself. Makes a difference. Thank you once again."
Julie | January 2016
"Very good phone – I work with gloves on and big buttons are helpful..also it's IP67 suit to my job"
Mark | July 2015
"I am writing to let you know I have received the phone I ordered and I would like to say how pleased with it and how quick it was delivered.
Thank you and best wishes"
Mrs Swindon | July 2015
"This Easiphone has nice big numbers – ideal for the visually impaired – loads of space in the phone book for all those important numbers of relatives and friends and an emergency button on the rear of the phone which when pressed will run down a list of up to 5 contacts in turn until one of them answers the call. Extra features are really handy like a Camera and a magnifier to help see small text Well done Easiphone"
Patrick | July 2014
We're not a big company, we're small and concerned.
We're motivated and influenced by our own families, and by friends who are caring for the elderly and the disabled.
We also listen and learn from leading charities, local councils, GPs and carer organisations.
And we are a family run business with 20 years experience in the telecommunications industry.
Watch our short informational video
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Who cares for the carers? If you are looking after someone don't forget to look after yourself
As a GP, I have many patients who wear themselves out trying to look after loved ones. Perhaps you are doing long hours at work…
Staying Connected To Elderly Loved Ones or Those With Dementia
As loved ones get older or develop dementia, families begin to worry more and more about their wellbeing. Whether an aging parent lives nearby or…
Easiphone Big Button Mobiles
According to research by AgeUK, nearly one in five people currently in the UK will live to see their 100th birthday. As life expectancy lengthens…
Easiphones: including everyone in a connected world
New technologies may have helped most of us live in a highly connected world – but not everyone is included.
Easiphone MedInfo USB Stick
The MedInfo USB keyring stick that can carry your medical and contact information.


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As tradition would have it, it's time again to fill you all in on what's been going on here at DGLM. In a new, never-before-seen development that will surely knock your socks off, bowl you over with a feather and land you on your seat, I'm the one who will be letting you in on all the recent book sales instead of Lauren. How's that for a plot twist? You never really do know, do you? Oh stop it, don't get too nervous, calm down. I won't do anything too crazy. Before we all lose our nerves, let's just get started.
Michael kicked things off with author and E! Executive News Editor Ken Baker's Fangirl, a very modern love story about a girl with a knack for songwriting meeting and falling for the pop star she idolizes, which he sold to Lisa Cheng at Running Press.
Bestselling cookbook author Steve Raichlen's The Hermit of Chappaquiddick, a story of love, loss and redemption followed, which Tor's Bob Gleason bought from Jane.
Then Jim sold Shannon Jamieson-Vasquez at Berkley a book called The Devil I Know by Jackie Barrett, the true story of a psychic medium's correspondence with convicted Amityville murderer Ronnie DeFeo, which leads her into an investigation of what really happened the night he killed his family.
Noted chef and entrepreneur Debra Ponzek's The Modern Cook's Survival Guide, a cookbook that highlights the go-to favorites of the American palate and provides seasoned advice on how to perfect those foods, was sold by Jane to Kristin Wiewora of Running Press.
John came in next with Shandy Lawson's debut YA novel LOOP, set in New Orleans, about two teen lovers desperately trying to break out of a time loop that always ends with them being killed in a botched robbery, which he sold to Emily Meehan at Hyperion.
Jane's next sale went to Kate Hartson at Center Street forA Funny Thing Happened on the Way to Adulthood by Marion Grodin. The daughter of actor/comedian Charles Grodin, Marion struggled growing up in the shadow of celebrity and faced down a number of demons during her bumpy road through adolescence. Her book captures Grodin's "addiction-laden, hilarious, heartbreaking, and ongoing journey toward standing on her own two feet and stepping, finally, into her own light."
Joe Oestreich's memoir Hitless Wonder: A Life in Minor League Rock and Roll, which details him coming to grips with age and realities while on a two-week tour with his long-running band Watershed, was also sold by John, this time to Mary Norris at Globe Pequot.
Following the successful Fresh from the Vegetarian Slow Cooker, Stacey sold Robin Robertson's new cookbook, Fresh from the Vegan Slow Cooker to Dan Rosenberg at Harvard Common Press. Robertson's latest will feature over 200 recipes.
Stephanie sold Anita Porterfield and Marie Sprague's In the Crosshairs, an investigative piece of narrative non-fiction that recounts the events of the Fort Hood massacre and raises questions regarding the shooter, government cover-ups, and military work environments, to Hilary Claggett at Potomac Books.
Stacey's next sale went to Mary Norris at Globe Pequot press for Peyton and Diane Goddard's I am Intlgent, which is an inspirational memoir written by a nonverbal autistic woman and her mother, describing their experiences of the girl's difficult and abusive childhood, her eventual ability to communicate with the outside world, culminating in her graduation as valedictorian of her class from college, and her work now as an advocate for disabled individuals without a voice.
Suzanne Young's The Program, in which teen suicide is an epidemic and a girl struggles to stay out of the Program—a preventative treatment that will erase her memories—in order to save herself and the boyfriend who's already forgotten her was sold by Jim to Jennifer Klonsky at Simon Pulse.
Expanding on his work in Strategic Intuition, Bill Duggan's Creative Strategy turns that concept into a method and plan that strategists can use. Michael sold this to Myles Thompson at Columbia University Press.
And finally, Jane sold author of Writing Tools, The Glamour of Grammar, and the forthcoming Help! for Writers, Roy Peter Clark's How to Write Short, a book on communicating effectively in short form writing to Tracy Behar at Little, Brown.
As you can probably see, it's been a pretty busy month here at DGLM and we really have no intention of stopping any time soon. And if you read the list above in a booming orator's voice espousing the newest great ideas and innovations, then you've matched perfectly how it sounded in my head as I was writing. It's BEA this week, so everyone's more excited than usual about new books, new writers and new ideas—I encourage you to also proclaim your work below just as proudly as we have here.


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Finding your local job centre can be a difficult task, so we've done all the hard work for you. We've got all the handy information you'll need to contact your local job centre in Wolverhampton, complete with addresses and phone numbers.
Telephone: 0845 600 3115Map
Telephone: 0845 604 3719
Nearby job centres in the West Midlands : Birmingham, Cannock, Dudley, Sutton Coldfield, West Bromwich
Don't forget, if you're looking for jobs in this area, you can find jobs in Wolverhampton at totaljobs.com
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Qualified, experienced jobseekers use totaljobs to search for jobs. Our world class search technology and tools enables them to find the most relevant job. Your job!


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Microsoft has a new mascot for Internet Explorer.
Say hello to Inori Aizawa, the anime-themed version of IE, which is based on the uniquely Japanese trend, OS-Tan. Inori has been revealed ahead of a debut event that Microsoft is hosting at the Animé Festival Asia 2013, which will take place this weekend in Singapore. Inori greeted the world for the first time on her new Facebook page, and here's what she had to say:
Hey everyone! My name is Inori and you can think of me as a personification of Internet Explorer.
When I was younger, I used to be a clumsy, slow and awkward girl.
However, just like the story of ugly duckling, people told me that I have really matured and changed over the years. I feel confident in my abilities now, and I'm eager to show you what I can do.
Why don't you get to know me a little better?
Check out the video after the break…
Yeah… so if Inori doesn't creep you out, you can download the new, Inori-themed version of IE 11 from Microsoft's FB page for the mascot once it goes live. Or, if you're really eager to get to know Inori, folks using IE9 or higher can set Internet Explorer Tan as their homepage so they can enjoy all the ridiculous cuteness.
(via io9)


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Need. Wooden. Keyboard.
Saw this in the window of a shop at the Aki-Oka artists' colony under the train tracks in Akihabara. Hacoa specializes in beautiful modern things made of wood: computer stuff (keyboards, mice), iPhone covers, pens and more.
If you'd like to visit Aki-Oka Artisan the next time you're in Tokyo, directions & maps are on my website, The Tokyo Guide I Wish I'd Had.
Jonelle Patrick is the author of the Only In Tokyo mystery series, now out for the first time in paperback
…or watch the book trailer (0:52)