text:
|Topic Review (Newest First)
We checked the system and found no problems. Kitted one of the alternators and it has been running fine. I think it was a combination of a run-down battery and good old Bakersfield 105F summer that was too much heat load on the units trying to recharge an almost dead battery. Keep my fingers X'd!
Now our problem is a 'blown' engine. Troy fired it up last week and it literally exploded - spark set off explosive mixture in the crank case and he blew out the valve cover gaskets, belled the valve covers, probably belled the oil pan. I was hoping beyond hope the blowby we were experiencing would mend but I think we have a hole in a piston due to hitting the valves. After we rebuilt the engine we broke pushrods on all the cylinders. Turns out I thought he timed the cam and he thought I did. We hadn't, it was ~15deg out. We pulled the heads, had them gone over replaced a couple bent valves and put it all back together. We have had not-right engine problems ever since - low power, hard starting, excessive crankcase blowby. This explosion tells me we have a cracked piston.
Out comes the engine again for a tear down parts inspection and build up. We are getting so good taking the enginge out, working on it, and getting it back in the car, I want to do a run against a Top Fuel team to see if we can beat them!!!!!
Ain't hot rodding fun?
Did you get anywhere on this?
Couple of questions: What amperage alternator and what is this crimp you speak of?
Poor crimps on high power circuits can lead excess heat and corrosion causing failure at the crimp point. If the crimp is bad enough to cause a voltage drop across it, moving your exciter wire to the choke would have only made the problem worse. The alt would push it's output voltage higher to make the voltage from the dash 12v. Possible burning out the alt faster that way?
|Good point. I matched colors on the harness but I'll double check that.
|EOD Guy
|I had a very simular problem........ It ended up that I had mistakenly mixed up the exciter and sense leads on the alt plug...... I just knew I had them correct, but after a cont test....nope I had reversed them. I corrected the problem and the new alt has run flawlessly for over a year now
I've burned up two alternators in a month
Have a SBC with EZ harness, GM alternator, pretty plain vanilla setup. We ran the car for a couple months and the battery started running down. Checked the alternator and the white wire connector on the alternator was melted. I put on a new plug and moved the red exciter wire from the hot lead on the alternator to the unused electric choke wire on the EZ harness (keyed 12V). Thought the lead might be over voltage being hooked directly to the alternator out. Had another chrome alternator in the shop so installed that one at the same time. That ran for less than a week and it fried too. It melted the white wire this time but just 3" back to the blue wire splice I used to install it. The rest of thst wire was fine. I took the splice apart and the end farthest from the alternator was blue on the very tip but clean copper the rest of the way. Almost looks like a bad crimp? I got a repair kit and rebuilt the first one and found the internal regulator fried and one diode out, the windings were fine, no sign of other problems.
Anyone have any ideas why I am burning the idiot light lead and internal regulator?
My thoughts;
1) bad crimp on the white wire connector causing high impedence in that circuit? Doesn't make sense 'cause the circuit is designed to have resisitance in it (light bulb).
2) run down battery requiring the alternator to recharge it and in our 100F summer weather overheating the regulator?
3) other?
Thanx in advance for the help!
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text: I saw today that Miranda Kerr said her son's middle name of Christopher is in honor of her high school boyfriend who died. They had been dating two years when he died and Miranda said she would name her son after him in some way. Would you name your child after an ex girlfriend or boyfriend?


text:
Massage Very little hot water, no safety deposit box, didn't pick us up from port as promised, staff had a poor attitude, over-priced food menu, dirty swimming pool (dead frog in), no gym, no adaptors for overseas plugs, shower was a wet room-not big enough for 4 people, ceiling fell in due to leak-no compensation offered, door didn't lock properly, food took ages to be cooked, service at breakfast was very slow, they asked for money up front, bad service when checking out-they charged us for things that we hadn't even had, no receipt given to show us what we had been charged for, no hairdryer, over priced taxis arranged into Phangan.
We had a fantastic stay at the Sunset Hill Resort & Spa. Our room was huge with a big balcony overlooking the nice pool and the ocean. We also loved the breakfast area with the same nice view. The staff is friendly and helpfull. If we go back to Koh Phanang we will defenitely stay here again. No
The staff was very friendly and helpful in all matters. Very peaceful place, not on the party side of the island. Good place for those who just want to relax. The massage service the resort provided was excellent! Construction work was in progress but id didn't disturb at all. There were some problems with water pressure and supply on a couple of days, though shower/toilet worked every day, so no showers were interrupted. The resort staff recommended a dutch tour guide who didn't deliver as promised so we recommend to explore the island on your own.
Absolutely nothing. Worst experience of my life. From the moment we arrived at the Sunset Hill Resort and "Spa" untill the moment we left there was not one thing I can honestly say that corresponded with the desciption of the hotel on Booking.com or on the hotels own website. The hotel was a complete let-down.
The apartment we stayed in was lovely with beautiful views, great air con and cleaned very well, everyday. Staff were helpful & friendly. The resort is situated on a hill so you need to hire a car/motorbike or get a taxi everywhere.The facilities were poor and the very few staff that were there are not very organized, just little things like the breakfast tables not laid ready for you in the morning so you get your breakfast before the knives and forks...by this time the food is cold! Couldnt have any cocktails one night as ''the girl that makes them has gone home'' lounge and restaurant is only open from 8am - 11pm. I would have imagined a spa resort to be packed full of things to do but all we had was a jacuzzi and a pool. The place is only half built at the moment, but I can imagine will be great in a few years when all is up and running.
nice view of surroundings
Close to the beach. Newly designed bungalows. Completely over priced. Staff very slack and lazy. Had to ask for things a number of times. Food orders always wrong.
The bungalow rooms were cheap enough however they where old and not as clean as they should have been. Our friends stayed in the nicer sea view bungalows however we think they were not good value for the price. Only one member of staff was competent - she seems to run the place- everyone else, (at least 10 members) are hanging/running around disorganised. Our booking didnt exist when we arrived. Food in restaurant was not good - no room service. a serious trek down to the nice bungalows at the sea. Front entrance needs tidying up. Furniture dated in rooms, bathrooms in need of maintenance - old. better value further into haad yao.


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tuf-duc wrote:
I think they cll that a "SHART"!
Ahhhhh! You beat me to it.
As far as fragrances go it's tough to beat cabbage and guiness the night before. I chased myself out of the blind last year with one of those.
Moderators: Tealer, Indaswamp, Dep6, Preacher1011, lostpup, La. Hunter, steve-o
tuf-duc wrote:
I think they cll that a "SHART"!
TNAL45 wrote:I like my beer like I like my violence....Domestic.
Swamp Puppy wrote:gunman wrote:I'm waiting for HW to comment on this thread..... :laughing:
Bah...Wimmin don't fart. just ask one. :toofunny:
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text:
Something Different
Week of: September 1, 2014
Download 300 dpi photo
Contact: Alice Bender, (202) 328-7744
How To Enjoy the Perfect Pear
By Dana Jacobi
for the American Institute for Cancer Research
Fragrant with perfume, the best pear I ever ate announced its perfection as the waiter set it in front of me. It was served as dessert at The Café at Chez Panisse, Alice Waters's more casual restaurant in Berkeley, California. My plate arrived bearing just the pear, presented whole, with a modest slab of Italian sweet Gorgonzola cheese beside it.
It was a Bartlett variety called a Butter Pear, with almost liquid flesh that is too fragile to make it to the supermarket. But supermarkets have other kinds of Bartletts. Treat them with the same care as they get at Chez Panisse and they, too, can deliver exquisite aroma, abundant juice and sugar-sweetness.
Treating a pear properly is simple. Pears are picked when mature but not fully ripe. If left to ripen on the tree, they develop a gritty texture. So let your pears sit at room temperature for two to three days. Ripening from the inside out, they will be at their peak of flavor, juice and sweetness when the stem end yields to gentle pressure. By the time the body of a pear feels soft, it is likely to be mushy.
If they ripen before you are ready to eat them, pears keep in the refrigerator for two or three days. Bring cold pears to room temperature to fully enjoy them.
Supermarkets carry several varieties of pears. The ones you find nearly any time are:
- Green and Red Bartletts: The green-skinned ones turn yellow when ripe. Aromatic and tender, both kinds are good for eating, cooking and canning. Try them accompanied by shavings of good Parmigiano-Reggiano cheese.
- Bosc: With russet skin over spicy flesh, their crispness makes them good for eating, poaching and canning. Hardy enough to carry in a lunch box, Bosc pears are delicious peeled, cubed or sliced in salads.
- Green or Red Comice: Tough, thick skin covers their tender, grainy yet meltingly juicy flesh. Serve them for dessert, either cut into wedges and peeled, or baked like an apple at 400 degrees F. for an hour.
- Forelle: With red freckles on green skin, this small pear is ideal for snacking.
- Seckel: Russet skinned with a red cheek, a ripe Seckel is a crisp, spicy little sugar bomb. Delicious eaten fresh, it is also excellent poached in apple cider or canned.
This salsa shows how pears are good in savory dishes as well as desserts.
Pear and Jicama Salsa
- 1/3 cup cubed jicama, peeled and cut into 1/4-inch cubes
- Juice of 1/2 lime
- 1/2 tsp. salt
- 1 small garlic clove, very finely chopped
- 1 medium Bartlett pear
- 2 large mint leaves, finely chopped
- 1 tsp. finely chopped cilantro
In medium mixing bowl add jicama, lime juice, salt and garlic. Using fork, mix to combine.
Peel, core and cut pear into 1/4-inch cubes. Add to bowl with mint and cilantro, gently mixing to distribute them evenly.
Serve salsa within 4 hours, chilled or cool.
Makes 6 servings.
Per 1/4 cup serving: 22 calories, 0 g total fat (0 g saturated fat),
5 g carbohydrate, 0 g protein, 1.5 g dietary fiber, 195 mg sodium.
Something Different is written by Dana Jacobi, author of 12 Best Foods Cookbook and contributor to AICR's New American Plate Cookbook: Recipes for a Healthy Weight and a Healthy Life.
Our Mission: The American Institute for Cancer Research champions the latest and most authoritative scientific research from around the world on cancer prevention and survival through diet, weight and physical activity, so that we can help people make informed lifestyle choices to reduce their cancer risk.
We have contributed over $105 million for innovative research conducted at universities, hospitals and research centers across the country. Find evidence-based tools and information for lowering cancer risk, including AICR's Recommendations for Cancer Prevention, at www.aicr.org.
All active news articles


text:
Kristin Chenoweth has some advice for Anthony Weiner, and she's delivered it in song.
The Tony-award winning Broadway performer and actress appeared on
The Tonight Show with Jay Leno
Tuesday night
to perform Popular from the musical
Wicked –
but with a twist: she changed the lyrics to reflect Weiner's current sexting controversy.
"I'll teach you to zip your fly, you won't be that guy with a camera down his pants," Chenoweth sang on
The Tonight Show
. "I'll teach you what tweets to tweet, something clean and sweet."
Before appearing on Leno, the singer herself tweeted that she had some music for Weiner.
Weiner made headlines on Thursday of last week when he admitted to having engaged in lewd online correspondence with as many as three women after having resigned from U.S. Congress in 2011 for similar behaviour.
Chenoweth is known for her portrayal of Glinda in
a role for which she has earned a Tony nomination. Coincidentally, the actress was also a guest star on
The Good Wife
, a show that focuses on the wife of a politician caught in a sex scandal.
You can watch the video of Chenoweth's performance of
The Tonight Show
below — and you'll want to follow along with the lyrics, which we've posted after the clip.
Whenever I meet someone who's in the public eye And let's face it, Mr. Weiner, you're in the public eye My tender heart tends to start to bleed But may I suggest a makeover I simply need to takeover You know I know exactly what you need Can't you see it in my face? This is the toughest case I've yet to face Don't worry, Carlos Danger is no more He's out the door And now for sure you will be popular, the right kind of popular I'll teach you to zip your fly, you won't be that guy with a camera down his pants I'll teach you what tweets to tweet, something clean and sweet We'll make sure you get your chance to be popular, the right kind of popular They'll think you've become a monk, though they've seen your junk Now you'll play a different show So let's start cause you've got an awfully long way to go (spoken) Long, well, hmm Please pay attention to my frank analysis Think of it as social media dialysis Now that you'll running I'll become your pal, a sister, an advisor, you need someone wiser Someone to make you popular, the right kind of popular There'll be no more sexy pics with your biceps flexed You're roaming, you will roam no more You want to be the mayor, stop acting like a big old wh-re We'll try to make you popular Oh think about your dear wife, Huma, hope she's got a sense of humour She should take a page from Hillary, and become independent of her hubby While you score that chatroom chubby With all her brains and knowledge she should be free to be popular Please, I know she'd be popular The voters want leadership, not some sexting drip There's no question she would be, very very popular like me (spoken) Seriously Huma, woman to woman, if that guy doesn't zip up and unplug, just kick him to the curb And to Anthony Carlos Danger Weiner or whatever your name is You may have guessed my disinterest in your running NYC Don't know if I can bear it, your porno-popularity Sure you're popular, just not quite as popular as me


text:
Figure 1: Age-standardised incidence rates (ASIR, 1992-2007) and age-standardised mortality rates (ASMR, 1992-2006) for all cancers among adolescents, 15-19 years, Canada
Source: The Canadian Cancer Registry and the Canadian Vital Statistics Death Database, Statistics Canada.
Formerly known as the Canadian Childhood Cancer Surveillance and Control Program, the Cancer in Young People in Canada Program (CYP-C) aims to fill gaps in knowledge and ultimately reduce the burden of childhood cancer in Canada. CYP-C is a partnership between the Public Health Agency of Canada and the C17 Council, a network of all the seventeen pediatric cancer centers across the country. For more information, please contact the manager of the CYP-C program at email@example.com 10


text:
Welcome to the award-winning restaurant Taste of Thai. Thank you for stopping by. Please take a look around and see what we offer. Be sure to go to our Contact Us page and receive a coupon for 15% off on your next visit!
Thai cuisine is a subtle interplay of five taste sensations: sweet, sour, hot, salty, and neutral. Southeastern Asian spices and seasonings imprint Thai cooking with their distinctive flavors.
These include: lemongrass, coriander root and leaves, the kaffir lime, kha root and some of the hottest and flavorful chilies. Their unique flavors give way for many appetizing dishes.
Please note that Thai food is very highly seasoned. We will be happy to accommodate individual tastes as much as we can without losing the integrity of a dish.Also, please alert your server if you have any special preferences such as food allergies and sensitivities to specific foods.We have taken great pride in preparing the Thai cuisine you are about to experience and hope you find it as enjoyable as we do. We welcome and appreciate your patronage and we encourage you to tell a friend about your dining experience with us.


text:
Malone KE, Daling JR, Thompson JD, O'Brien CA, Francisco LV, Ostrander EA. BRCA1 Mutations and Breast Cancer in the General PopulationAnalyses in Women Before Age 35 Years and in Women Before Age 45 Years With First-Degree Family History. JAMA. 1998;279(12):922-929. doi:10.1001/jama.279.12.922
© 2017
From the Public Health Sciences Division (Drs Malone and Daling and Ms O'Brien) and Clinical Research Division (Mss Thompson and Francisco and Dr Ostrander), Fred Hutchinson Cancer Research Center, Seattle, Wash.
Context.— Studies of high-risk families with multiple early-onset cases of breast
cancer have been useful for assessing the type and spectrum of germline mutations
on the BRCA1 gene, but do not provide guidance to
women with modest family history profiles. Thus, studies of women from the
general population are needed to determine the BRCA1
mutation frequency in women perceived to be at high risk, and to develop profiles
of those most likely to be carriers.
Objective.— To characterize frequency and spectrum of germline BRCA1 mutations in 2 categories of women identified via population-based
studies hypothesized to be at increased risk of carrying such mutations: those
diagnosed as having breast cancer before age 35 years and those diagnosed
before age 45 years who have first-degree breast cancer family history.
Design.— Study subjects were drawn from 2 population-based case-control studies
of breast cancer in young women on the basis of their family history or their
age of diagnosis. Cases were younger than 35 years or were younger than 45
years with first-degree family history at the time of breast cancer diagnosis
and were ascertained via a population-based cancer registry, and controls
(women without breast cancer) were identified via random-digit dialing.
Setting.— Three counties in western Washington State.
Main Outcome Measure.— BRCA1 germline mutations in study subjects
identified in DNA from peripheral blood lymphocytes by single-strand conformation
polymorphism analysis using primer pairs that span the BRCA1 coding region and intron-exon boundaries.
Results.— Of 193 women diagnosed as having breast cancer before age 35 years,
none of whom were selected on the basis of family history status, 12 (6.2%,
95% confidence interval [CI], 3.2%-10.6%) had germline BRCA1 mutations. In 208 women diagnosed before age 45 years who had
first-degree breast cancer family history, 15 (7.2%, 95% CI, 4.1%-11.6%) had
germline mutations in BRCA1. In both groups, there
were variations in mutation frequency noted by age and by family history.
Mutation frequency decreased with increasing age of diagnosis. Higher proportions
of mutations were seen in cases with at least 1 relative diagnosed as having
breast cancer before age 45 years, in cases with greater numbers of affected
relatives, and those with ovarian cancer family history. Mutation frequency
did not vary by bilateral breast cancer family history. No frameshift or nonsense
mutations were observed in 71 control women with a first-degree family history,
although missense changes of unknown significance were seen in cases and controls.
Conclusions.— Women with BRCA1 germline mutations lacked
a common family history profile. Also, a large proportion of the women with
a first-degree breast cancer family history and women diagnosed as having
breast cancer before age 35 years did not carry germline BRCA1 mutations. Hence, while early-onset disease and a strong breast
cancer family history may be useful guidelines for checking BRCA1 status, these findings on women drawn from the general population
suggest that it may be difficult to develop BRCA1
mutation screening criteria among women with modest family history profiles.
ABOUT 5% to 10% of breast cancer patients carry germline mutations that
predispose them to inherited disease.1,2
Through genetic linkage studies, BRCA1, a breast
and ovarian cancer susceptibility gene,3,4
was identified on chromosome 17q. Cloning and sequencing of BRCA1 revealed 24 exons and 5592 nucleotides.5
Over 130 germline mutations in the coding region are reported in the Breast
Cancer Information Core database to date.6
The majority of these result in truncation of the message, leading to absence
of functional protein.6
Chromosomal mapping of BRCA1 relied exclusively
on the analysis of rare, high-risk families, each of which had multiple members
affected with breast and/or ovarian cancer.3,4
Subsequent studies of the number and type of germline BRCA1 mutations or mutation-related breast and ovarian cancer risk also
almost exclusively involved high-risk families.7- 11
Two analyses, each involving over 100 families, suggest that 80% of high-risk
breast and/or ovarian cancer families and nearly half of high-risk breast
cancer families have inherited mutations in BRCA1,12,13 although a recent review of high-risk
families ascertained worldwide suggests that proportions of such families
may be more modest than prior estimates suggest.11
The one exception has been the mutation screening of women of Ashkenazi Jewish
descent, where analyses suggest 0.9% of Ashkenazi Jewish women have BRCA1 germline mutations.14- 16
The question of how well data derived from relatively rare high-risk
families helps to predict BRCA1 mutation status in
women in the general population poses an obstacle to the development of comprehensive
screening strategies. Many of the families used to generate the frequency
and penetrance estimates have as many as 10 affected members. We wished to
assess whether the type and frequency of mutations in the general population
differ significantly from those seen in women from high-risk families and
the degree to which family history profiles of the type seen in the general
population are predictive of BRCA1 status.
In a prior analysis of 80 breast cancer cases diagnosed in women younger
than 35 years from a population-based breast cancer case-control study and
unselected for family history status, 6 (7.5%) had germline BRCA1 mutations.17 Two of the 6 women
reported little or no breast cancer family history and the other 4 mutation
carriers had relatively modest family history profiles. Similar results were
found elsewhere in 30 women diagnosed as having breast cancer before age 30
years.18 In this study, we examined the frequency
and spectrum of BRCA1 germline mutations in 2 categories
of women drawn from 2 population-based studies hypothesized to be at increased
risk of carrying BRCA1 mutations: those with a first-degree
(mother or sister) breast cancer family history and breast cancer cases diagnosed
in women younger than 35 years.
Cases (women diagnosed as having breast cancer before age 45 years)
and controls (similarly aged women without breast cancer) were drawn from
2 population-based case-control studies of breast cancer conducted in western
Washington State. The methods of the studies were similar and have been reported.19,20 Cases were identified via the Cancer
Surveillance System of western Washington, a population-based registry that
participates in the National Cancer Institute Surveillance, Epidemiology,
and End Results Program. Controls were identified through random-digit dialing.21 The first study identified all incident first primary
breast cancer cases diagnosed between January 1, 1983, and April 30, 1990,
in white women born after 1944 living in the 3-county metropolitan Seattle
area at the time of diagnosis. Interviews were completed on 845 cases (83.6%
of eligible cases) and 961 controls(75.5% of those eligible). Supplemental
funding allowed for subsequent blood collection in 563 cases and a subset
of controls (n=113).
The second study identified all incident first primary breast cancer
cases diagnosed before age 45 years, from May 1, 1990, to December 31, l992,
in women of all races living in the 3-county area. Interviews were completed
on 648 (87.0%) of eligible cases and 610 (78.7%) of eligible controls. As
part of the original study and of a subsequent investigation, blood was collected
from 523 cases and 450 controls.
In both studies, data regarding potential breast cancer risk factors
were obtained via structured in-person interviews. Each subject was asked
to enumerate all first-degree (mothers, sisters, daughters) and second-degree
(aunts and grandmothers) female blood relatives. For each relative enumerated,
the interviewer asked for birth year, vital status, death year, history and
type of cancer, and laterality (if breast cancer). Follow-up with all previously
interviewed women (or proxies) for updated pedigree information was initiated
as part of a large, ongoing genetic-epidemiologic study. Information on vital
status was obtained from the Cancer Surveillance System and from our ongoing
follow-up tracing activities. The institutional review board at the Fred Hutchinson
Cancer Research Center approved the study, and all subjects signed an informed
consent document before participation.
Three subgroups from the 2 case-control studies were targeted for initial
molecular analyses: cases with first-degree breast cancer family history (ie,
affected mother and/or sister), cases diagnosed before age 35 years, and controls
with first-degree breast cancer family history. We are also screening controls
from the same 2 population-based case control studies who were not selected
on the basis of family history; this ongoing work is part of larger population-based
mutation analyses. Thus, we briefly report results of testing 1 subset of
the controls: all women aged 40 to 44 years from our second case-control study
for whom blood was available.
Genomic DNA was purified from either frozen buffy coats or immortalized
lymphoblastoid cell lines. The polymerase chain reaction (PCR) and subsequent
single-strand conformation polymorphism analyses were carried out as described
with only minor modifications, including the addition of several new primer
pairs constructed to allow for redundant screening.17
Results were visualized by autoradiography. Variant bands were cut from the
gel, rehydrated, and all alterations seen in less than 10% of subjects were
sequenced as described.17
Haplotypes were constructed for the BRCA1 region
using microsatellites D17S855 (AFM248yg9), D17S1322 (s754), D17S1323 (s975),
and D17S1327 (ED2) by inspection of segregation patterns.22
Because of potentially limiting numbers, we used the Fisher exact test
to assess whether age, stage, vital status, and family history varied between
those tested and not tested for BRCA1 mutations.
In tested women, the Fisher exact test was used to compare whether proportions
of those with a BRCA1 mutation varied by age group,
stage, vital status, and family history. We calculated the binomial exact
95% confidence interval (CI) for proportion of those with a BRCA1 mutation. P values for the Fisher exact
tests and the 95% CIs and 97.5% CIs (where there were zero mutations) were
attained using Stata statistical software (Stata Corp, College Station, Tex).
BRCA1 mutation status was determined for women
in 3 categories hypothesized to have increased probability of carrying a mutation:
208 cases with first-degree breast cancer family history, 193 cases diagnosed
before age 35 years (80 of whom were previously reported17
), and 71 controls with first-degree family history. Also, 199 controls aged
40 to 44 years (not selected on basis of family history) were tested. Groups
were not mutually exclusive. Thirty-eight cases studied had both positive
first-degree family history and breast cancer diagnosis before age 35 years;
similarly, 18 controls with first-degree family history were also members
of the age 40 to 44 years control group. Of the total 363 cases studied, 350
(96.4%) were white, 4 (1.1%) African American, 6 (1.7%) Asian, and 1 (0.3%)
American Indian; of 251 controls studied, 227 (90.4%) were white, 10 (4%)
African American, 8 (3.2%) Asian, and 7 (2.8%) American Indian.
Table 1, Table 2, and Table 3
present characteristics of all eligible women from the population-based studies
in each of the 3 potentially high-risk categories targeted. In both case groups
studied, proportions available for molecular analysis did not vary substantially
by age of diagnosis or family history (Table 1 and Table 2).
Compared with all eligible cases, the subgroup of cases tested was more likely
to be alive at last follow-up and to have been diagnosed as having earlier-stage
breast cancer. This was largely attributable to a lag between interviewing
and blood collection (median, 42 months in women tested) in our first case-control
study that resulted from initial lack of funding for blood collection. The
controls with first-degree family history who were available for analysis
were slightly older than the entire group of controls with first-degree family
history (Table 3). In controls
aged 40 to 44 years, higher proportions were available for analysis in those
with a positive family history (Table 4).
In the 208 breast cancer cases aged 21 through 44 years with a first-degree
family history, 15 (7.2%, 95% CI, 4.1%-11.6%) had germline BRCA1 mutations (Table 5).
Mutation frequency decreased by age of diagnosis, from 23.1% in cases diagnosed
before age 30 years to 3.4% in the cases diagnosed at age 40 to 44 years.
Although mutation frequency did not differ substantially by vital status,
there was variation by disease stage. Specifically, the highest proportion
of mutations was seen in women with regional or distant disease (11.3%).
There were 12 (6.2%, 95% CI, 3.2%-10.6%) germline BRCA1 mutations detected in 193 cases diagnosed before age 35 years
(Table 6). Similar to the findings
in cases with first-degree family history, mutation frequency was higher in
this group in those diagnosed at a younger age (11.4% in cases diagnosed before
age 30 years vs 4.7% in those diagnosed at ages 30 to 34 years) and in those
diagnosed as having more advanced disease (12.7% in cases with regional or
distant disease, 3.9% in those with local disease, and none in 27 in situ
cases). All 12 mutations in cases diagnosed before age 35 years were in the
179 cases still alive at last follow-up; none were detected in 14 cases now
In both groups of cases, mutation frequency varied to some extent according
to features of family history. In 208 cases studied because of at least 1
first-degree relative with breast cancer, mutations were seen in 10.0% of
cases with an affected sister and 6.8% of cases with an affected mother (Table 5). There were 2 mutations (11.1%)
in 18 cases with an affected sister and mother. Mutation frequency in cases
with a mother and/or sister diagnosed as having breast cancer before age 45
years was 13.2% vs 4.4% in those with an affected mother and/or sister diagnosed
at or after age 45 years. A similar pattern was seen regarding early age of
diagnosis in aunts and/or grandmothers.
In cases diagnosed before age 35 years and not selected on the basis
of family history, those with a mother and/or sister with breast cancer had
a greater proportion of mutations (13.2%) than did cases with only an aunt
and/or grandmother affected (7.2%) (Table
6). Of 104 women diagnosed before age 35 years with no breast cancer
family history, 3 (2.9%) had mutations, one of whom, although she did not
have breast cancer family history, did have a maternal aunt with ovarian cancer.
Similar to findings in cases selected for first-degree family history, in
cases diagnosed before age 35 years, those with a mother and/or sister diagnosed
as having breast cancer before age 45 years had a mutation frequency of 16.7%
vs those with an affected mother and/or sister diagnosed at age 45 years and
older (10.5%). Mutations were also more common in cases with an aunt and/or
grandmother diagnosed before age 45 years (15.4%) vs cases with an affected
aunt and/or grandmother diagnosed at age 45 years or older (5.3%).
Family history of ovarian cancer was also indicative of BRCA1 mutation status among cases, although there were few subjects
with such history. A high proportion of those with first-degree breast cancer
family history and ovarian cancer history in a mother and/or sister or in
an aunt and/or grandmother had a BRCA1 mutation (25.0%
and 23.1%, respectively). In cases diagnosed as having breast cancer before
age 35 years, 2 (25.0%) of 8 women with an aunt and/or grandmother with ovarian
cancer had BRCA1 mutations.
Mutation frequency varied by number of relatives affected in each case
group (Table 5 and Table 6) and in the aggregate of all cases tested. In all 363 cases
tested, there were 3 mutations (2.9%) in 104 women with no breast cancer–affected
relatives, 15 mutations (6.4%) in 235 cases with 1 to 3 such relatives, and
4 mutations (20.0%) in 20 cases with 4 or more affected relatives. Results
were similar when we considered both breast and ovarian cancer in the families.
Mutation frequency did not vary noticeably by presence or absence of
bilateral breast cancer family history (data not shown). In all cases with
at least 1 relative with breast cancer (n=255), mutations were seen in 3 (4.8%)
of 63 cases with at least 1 relative with bilateral breast cancer, 8 (6.3%)
of 126 cases with no relatives affected with bilateral disease, and 8 (12.1%)
of 66 cases unsure of relatives' laterality status.
No disease-associated mutations were observed in the 71 controls with
first-degree breast cancer family history or in the 199 controls aged 40 to
44 years.
Molecular mutations observed in this study are listed in Table 7 and mutation location and frequency are shown in Figure 1. The most common mutation seen was
the 185delAG mutation, which was seen in 6 cases and no controls. DNA from
the 6 cases with this mutation was tested with markers spanning the BRCA1 region to determine haplotype. All 6 shared the same
haplotype in this region that has been observed repeatedly in women of Ashkenazi
Jewish descent. For markers D17S855, D17S1322, and D17S1323, all women carried
alleles of 146, 128, and 157 base pairs (bp), respectively. For marker 17S1327,
varying allele sizes were observed, although a 133-bp allele was seen in 4
of the 6 cases, as is commonly reported in Ashkenazi women.23
Of the 25560 PCR reactions required for this study, 25558 (99.99%) were
completed and scored. For 2 women, however, there was 1 reaction that never
yielded a product, likely reflecting polymorphism within the PCR primers for
both alleles.
Twenty of the 22 disease-associated mutations observed have been seen
previously in studies of high-risk families, and are listed in the Breast
Cancer Information Core database.6 Two mutations
were novel: a deletion of 4 bp at nucleotide 2911 causing a stop codon at
amino acid 999 and a 28-bp deletion at nucleotide 5489 causing a stop codon
at amino acid 1825.
Missense mutations, which change only a single amino acid, were seen
in cases and controls. Rare polymorphisms occurring in less than 5% of cases
and controls were seen that did not change the protein in substantial ways
and are not likely of molecular significance. The distribution of genetic
alterations (disease-associated mutations, missense mutations of unknown significance,
and rare polymorphisms) is given in Table
Much of what is known about the frequency and distribution of germline BRCA1 mutations derives from studies of rare families with
large numbers of affected women and many living family members available for
sampling.6- 8,13,24
While detailed analysis of these mapping families has proven invaluable in
studies aimed at determining the initial mutation spectrum, additional studies
are now needed to clarify the role of germline BRCA1
mutations outside the selected venue of high-risk families.
Hospital-based case series partially meet that need; for instance, Krainer
et al25 recently reported 9 (12.3%) BRCA1 germline mutations in 73 women diagnosed as having breast cancer
before age 32 years. There was no information regarding family history, but
this was part of a larger cohort originally collected because of early-onset
breast cancer. Similarly, 12.8% of 798 women who presented at high-risk clinics
because of their presumed elevated risk were found to be BRCA1 positive.26 Mutation status was
related to several factors, including early age of onset, number of relatives
with breast or ovarian cancer, Ashkenazi ancestry, and bilateral disease.
Similar results were reported by Couch et al27
in 94 women diagnosed as having breast cancer before age 40 years identified
from general oncology practices, and in 169 women with breast cancer referred
to a breast cancer clinic because of family history. These studies provide
useful data but have limited generalizability to those with more modest family
histories for 2 reasons: the average number of affected women was substantial,
with some families having as many as 11 affected women, and as many as 25%
of families had both breast and ovarian cancer. Studies of broader scope are
therefore needed to provide data for the large number of women with a modest
to minimal family history of disease.
The analysis described here has several strengths. First, all women
were drawn from the general population as part of 2 population-based case-control
studies, the proportion of eligible cases interviewed was high, and no specific
ethnic groups were targeted. Second, 2 factors believed relevant to BRCA1 mutation status, family history, and early age of
onset were examined separately and together. Also, because detailed breast
and/or ovarian cancer family history was available, we could assess contributions
of additional family history characteristics that might affect probability
of being a carrier. For example, mutation frequency was not noticeably different
for those with a bilateral breast cancer family history vs those without such
history. However, our data suggest that having relatives diagnosed as having
breast cancer early in life, larger numbers of relatives affected with breast
cancer, and ovarian cancer family history may be important factors in assessing
risk. Also, as in the study by Couch et al,27
mutation frequency was greater in those with both breast and ovarian cancer
family history vs those with only breast cancer family history.27
In all cases,BRCA1 mutations were found in 2 (2.1%)
of 97 cases with no family history of breast or ovarian cancer, 14 (6.1%)
of 230 cases with breast but not ovarian cancer family history, 1 (14.3%)
of 7 cases with ovarian but not breast cancer family history, and 5 (20.0%)
of 25 cases with both breast and ovarian cancer family history.
Also, our analysis provides information about the number of BRCA1 mutations in the general population in groups of women whose
risk of being a carrier is uncertain but could be expected to be elevated.
In the absence of population-based molecular studies, guidance regarding mutation
frequency in autosomal dominant genes in those with fewer than 4 affected
relatives or those diagnosed in specific age ranges has been largely drawn
from statistical analyses of interview data from population-based studies.
Initial estimates based on a large population-based case-control breast cancer
study suggested that mutations in autosomal dominant genes were responsible
for 36% of breast cancer in women younger than 30 years, decreasing to 1%
in cases age 80 years or older.2 By comparison,
Whittemore et al28 using data pooled from 3
population-based case-control studies of ovarian cancer estimated that in
young women diagnosed before age 40 years, 11% of breast cancer and 18% of
ovarian cancer are due to autosomal dominant germline mutations. Finally,
data from 2 population-based studies of cancer mortality in relatives of breast
and ovarian cancer patients were used to estimate the proportion of breast
cancer cases in the general population due to autosomal dominant breast cancer
susceptibility genes and the results showed it to be 5.3% in those younger
than age 40 years, 2.2% between ages 40 and 49 years, and 1.1% between ages
50 and 70 years.29
Collectively, these 3 studies offered upper-boundary estimates of BRCA1 mutation frequency in women in the general population.
Variation among these studies is likely due, at least in part, to distinctions
in the data sets used (eg, extent to which women with both breast and ovarian
cancer were included). Also, contributions of BRCA1
could not be distinguished from those of other autosomal dominant breast cancer
genes (eg, BRCA2).
The frequency of BRCA1 mutation in this study
in women younger than 35 years (6.2%) approximates those predicted,28,29 with 11.4% of women diagnosed as
having breast cancer younger than 30 years and 4.7% of women diagnosed from
31 to 34 years carrying germline mutations. Mutation frequency increased to
23.1% among cases with a first-degree breast cancer history diagnosed before
age 30 years and was 8.0% in cases with such history diagnosed from 30 to
34 years, suggesting that a first-degree breast cancer family history along
with young age at diagnosis may increase the risk of being a carrier.
Since the family history profiles seen in our series of cases are considerably
less pronounced than those in studies of high-risk families,27,30,31
the BRCA1 mutation frequency is, as expected, much
lower. It has been suggested that cancer in most families with fewer than
4 cases of breast and no ovarian cancer is not due to highly penetrant genes
like BRCA1.27 Excluding
the study participants, the mean number of relatives affected with breast
cancer in this series was 1.7, and the mean number with breast or ovarian
cancer was 1.85. Although the number of families in our study with 4 or more
affected women is small, as in Ford et al,29
we did find that mutation frequency varied by combination of 4 or more relatives
with breast cancer and ovarian cancer family history. There were mutations
in 14 (4.5%, 95% CI, 2.5%-7.4%) of 312 women with fewer than 4 affected relatives
and no ovarian cancer family history, 4 (14.8%, 95% CI, 4.2%-33.7%) of 27
women with fewer than 4 affected relatives and ovarian family history, 2 (10.5%,
95% CI, 1.3%-33.1%) of 19 women with more than 4 affected relatives and no
ovarian cancer family history, and 2 (40.0%, 95% CI, 5.3%-85.3%) of 5 women
with 4 affected relatives and this history (for difference in groups, P=.005).
Of 22 women with disease-associated BRCA1 mutations,
6 (27.8%) had the 185delAG mutation and associated haplotype, frequently seen
in those of Ashkenazi descent.6,14- 16
Data regarding ethnic background were not collected in the original interview;
thus, no data are available regarding the ancestry of the 6 women with this
mutation or its frequency in western Washington. Of originally interviewed
controls (n=1571) and cases (n=1489), 1.5% and 2.4%, respectively, indicated
their religion as Jewish.
Those with modest breast cancer family history present the biggest challenge
for development of BRCA1 testing strategies in women
from the general population. This will be further complicated by lack of knowledge
about the BRCA1 protein and uncertainty regarding
most rare missense mutations (sometimes referred to as "rare variants" or
"missense changes of unknown consequence"). Only the missense mutation characterized
by a Cys→Gly change at amino acid 61, which destroys the protein RING
finger, and which was seen in 1 woman in this study, is known to be disease
associated as it has been seen to segregate with affected women in many high-risk
families.7,8 Functional assays
will be useful for addressing significance of missense mutations such as the
Ile→Met at nt 1256 or Met→Thr at nt 5002 described herein (thus
far seen only in unaffected persons); such changes may represent rare events
of no significance or disease-associated mutations of varying penetrance.
Characteristics that suggest that a missense mutation may predispose to disease
include absence in a control group of sufficient size, cosegregation with
disease in some families, or occurrence in a highly conserved area of the
protein or in a putative functional domain. Previously, because it was seen
only in cases, we considered the 12-bp insertion in intron 20 likely to be
disease associated.17 However, as it is seen
in controls herein and as proposed,32 it is
likely to be a polymorphism.
Studies of the relationship between first-degree breast cancer family
history and survival and between BRCA1 mutation status
and histopathologic prognostic factors are suggestive, but not conclusive.33- 36 Our
finding of higher proportions of mutations in women with more advanced disease
and no mutations in women with in situ disease is provocative but needs replication.
Generalizability of our findings may be influenced by the extent to
which the women whose samples were available for testing are not representative
of the otherwise eligible women in the categories studied, and, if there were
an association between BRCA1 mutations and increased
(or decreased) survival from breast cancer, our study could overestimate (underestimate)
overall mutation frequency due to inclusion of women more (less) likely to
survive. It is reassuring that in cases younger than 35 years, there is no
evidence of bias in blood collection by family history (Table 2). Although we cannot directly assess potential bias for
blood collection by family history in women selected for testing on the basis
of first-degree family history, the overall proportion of women aged 35 to
44 years with a first-degree family history (19.4%) interviewed in original
case-control studies is similar to that (20.5%) having blood drawn.
The overall small number of mutations seen in 363 cases makes interpretation
of their relationship with features of family history preliminary; some differences
in frequency observed according to specific characteristics could be due to
chance, as demonstrated by the wide CIs accompanying observed mutation frequencies.
No mutations were observed in the 252 controls studied. Estimates of general
population BRCA1 mutation frequency range from 1
in 500 to 1 in 1500 women.2,28,29
Thus, we would not necessarily have expected to detect even a single mutation
in the control subgroup studied. Larger population-based studies will be needed
to elucidate the role of specific family history features in predicting mutation
status and for assessment of factors influencing risk of disease.
In addition, sensitivity of our mutational screening strategy could
have influenced findings. When performed correctly, single-strand conformation
polymorphism and techniques like it can detect over 80% of mutations.37 To further optimize our ability to detect mutations,
most primers were designed to produce PCR fragments that were no larger than
280 bp, gels were run as long as 24 hours to maximize detection of subtle
variants, and additional primer pairs were constructed to allow for redundant
screening of parts of the gene, particularly exon 11. However, a few mutations,
likely missense changes, that tend to produce more subtle gel pattern perturbations
will be missed even in an optimal setting. One additional limitation that
is not unique to this or other commonly used screening methods is that mutations
affecting expression, splicing, or stability of the transcript are difficult
to detect. Yet, they likely account for as much as 15% to 20% of BRCA1 mutations.11
Several issues raised in this report have implications for women and
their clinicians who are considering genetic counseling. First, many women
in the general population with a positive family history of breast cancer
who may believe they are at high risk for carrying a mutation in an autosomal
dominant breast cancer susceptibility gene are not BRCA1 carriers. Second, some women with family histories may have mutations
in genes other than BRCA1. Third, some women may
be BRCA1 mutation carriers in the absence of strong
family history, perhaps reflecting paternal origin, few assessable family
members, or variability in mutation penetrance; a mechanism for identifying
these women is needed. Finally, the role of missense mutations or unclassified
variants in disease causation is unclear and testing strategies targeting
only known or common mutations will miss novel or rare mutations.
In light of such complexities, it is critical that genetic testing be
undertaken only after careful counseling by skilled health care providers.
While the information presented here suggests that overall the risk of carrying
a BRCA1 mutation for women with modest breast cancer
family history is much lower than that for women with extreme family histories,
sufficient data do not yet exist to devise the optimal stratifications for
deciding who, specifically, should be offered carrier testing. In the face
of such uncertainties, it may be recalled that breast cancer is a disease
of high frequency in Western women. While the research community continues
to probe questions of genetic susceptibility, there remains no substitute
for access to high-quality, affordable health care that provides for vigilant
screening and early diagnosis for all women.


text:
Looking for a new sound system for the Jeepster
I do realize people have made plenty of threads about this, but no one ever has the precise answer I'm looking for.
Well let me start off with that my 2001 Jeep Wrangler was broken into. Some punk had the balls to go and slash open my soft top window, and steal my radio and car charger. Way to go. Who steals and sells radios anymore?
Anyways with that, the person cut the wires from the Jeep that plugged into the radio and the wires that connected to the sound bar. So everything is done. Now I am in the market for a new sound bar and speakers, and was also thinking of putting a Jeep JK radio in my jeep because I like the way they look plus bluetooth.
Any feedback is great I'm all ears for speaker brands, and a new sound bar (preferably with no speakers so I can add my own)
Thanks everyone :)
I use a head unit with a detachable faceplate, works wonders, cant steal what you cant see. In dash speakers are Boston's, I have a VDP 6 speaker soundbar, the VDP Sound pods with 6.5 Boston marines, and 2x 10" subs in the "trunk"; all hooked up to a 5channel marine amp. Everything Is bolted down and I also have a safe under the passenger seat for when I lock my watch/wallet up at the gym and also for when im carrying. Sound is great, even on the highway topless/doorless with wicked tire noise. Comes in handy too for outdoor get toghethers.
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text:
The Open Group Architecture Framework
The Open Group Architecture Framework (TOGAF) is a framework for enterprise architecture that provides an approach for designing, planning, implementing, and governing an enterprise information technology architecture.[2] TOGAF has been a registered trademark of The Open Group in the United States and other countries since 2011.[3]
TOGAF is a high level approach to design. It is typically modeled at four levels: Business, Application, Data, and Technology. It relies heavily on modularization, standardization, and already existing, proven technologies and products.
An architecture framework is a set of tools which can be used for developing a broad range of different architectures.[4] It should:
- describe a method for defining an information system in terms of a set of building blocks
- show how the building blocks fit together
- contain a set of tools
- provide a common vocabulary
- include a list of recommended standards
- include a list of compliant products that can be used to implement the building blocks
TOGAF is such an architecture framework.
The ANSI/IEEE Standard 1471-2000 specification of architecture (of software-intensive systems) may be stated as: "the fundamental organization of a system, embodied in its components, their relationships to each other and the environment, and the principles governing its design and evolution."
However TOGAF has its own view, which may be specified as either a "formal description of a system, or a detailed plan of the system at component level to guide its implementation", or as "the structure of components, their interrelationships, and the principles and guidelines governing their design and evolution over time."
The Architecture Development Method (ADM) is core of TOGAF which describes a method for developing and managing the lifecycle of enterprise architecture.
TOGAF was initiated in the early 1990s as methodology for the development of technical architecture, and has been developed by The Open Group into an extensive enterprise architecture framework.[6] In 1995, the first version of TOGAF (TOGAF 1.0) was presented. This version was mainly based on the Technical Architecture Framework for Information Management (TAFIM), developed since the late 1980s by the US Department of Defense
In December 2001 TOGAF 7, the "Technical Edition", was published.[7] TOGAF 8 ("Enterprise Edition") was first published in December 2002 and republished in updated form as TOGAF 8.1 in December 2003. Around 2005 TOGAFTM became a registered trademark of The Open Group.[8] In November 2006 the Open Group released TOGAF 8.1.1. According to The Open Group, as of February 2011, over 15,000 individuals are TOGAF Certified.[9] As of September 2012 the official register has over 20,000 certified individuals.
The latest version is TOGAF 9.1, launched on 1 December 2011. An evolutionary development from TOGAF 8, TOGAF 9[10] includes many new features including:[citation needed]
- Increased rigor, including a formal Content Metamodel that links the artifacts of TOGAF together (although there are some problems with the Metamodel)[11]
- Elimination of unnecessary differences
- Many more examples and templates
Additional guidelines and techniques include:[citation needed]
- A formal business-driven approach to architecture
- Business capability-based planning
- Guidance on how to use TOGAF to develop a Security Architecture or SOA
The Open Group provides TOGAF free of charge to organizations for their own internal noncommercial purposes.[12]
TOGAF topics[edit]
Enterprise architecture domains[edit]
TOGAF is based on four interrelated areas of specialization called architecture domains:
- Business architecture which defines the business strategy, governance, organization, and key business processes of the organization
- Applications architecture which provides a blueprint for the individual systems to be deployed, the interactions between the application systems, and their relationships to the core business processes of the organization with the frameworks for services to be exposed as business functions for integration
- Data architecture which describes the structure of an organization's logical and physical data assets and the associated data management resources
- Technical architecture, or technology architecture, which describes the hardware, software, and network infrastructure needed to support the deployment of core, mission-critical applications
Architecture Development Method[edit]
The Architecture Development Method (ADM) is applied to develop an enterprise architecture which will meet the business and information technology needs of an organization. It may be tailored to the organization's needs and is then employed to manage the execution of architecture planning activities.[13]
The process is iterative and cyclic. Each step checks with Requirements. Phase C involves some combination of both Data Architecture and Applications Architecture. Additional clarity can be added between steps B and C in order to provide a complete information architecture.
Performance engineering working practices are applied to the Requirements phase, and to the Business Architecture, Information System Architecture, and Technology architecture phases. Within Information System Architecture, it is applied to both the Data Architecture and Application Architecture.
Enterprise Continuum[edit]
The Enterprise Continuum is a way of classifying solutions and architectures on a continuum that ranges from generic foundation architectures through to tailored organization-specific both within and outside the Architecture Repository.[14] These include architectural models, architectural patterns, architecture descriptions, and other artifacts. These artifacts may exist within the enterprise and also in the IT industry at large.
The Enterprise Continuum consists of both the Architecture Continuum and the Solutions Continuum. The Architecture Continuum specifies the structuring of reusable architecture assets and includes rules, representations, and relationships of the information system(s) available to the enterprise. The Solutions Continuum describes the implementation of the Architecture Continuum by defining reusable solutions building blocks.
TOGAF Certified Tools[edit]
The Open Group has a certification program for TOGAF 8 Tools, and as of early 2011 plans to extend that to cover TOGAF 9 Tools. For the latest register of certified tools see The Open Group register.[15]
The Open Group oversees formal qualifications in TOGAF at two levels, which can be taken following formal training or self-study.[16]
(Level I) Ensures that an individual understands Enterprise Architecture along with core concepts and terminology of TOGAF.[16]
(Level II) Further to the Foundation qualification, this establishes that the candidate is able to analyse and apply their knowledge.[16]
Gaining TOGAF Certified status automatically confers free membership of the Association of Enterprise Architects.[17]
- ^ Stephen Marley (2003). "Architectural Framework," at aiwg.gsfc.nasa.gov, NASA /SCI. Retrieved 10 Dec 2008 (webarchive.org).
- ^ Dirk Draheim, Gerald Weber eds. (2007) Trends in Enterprise Application Architecture: 2nd International Conference, TEAA 2006, Berlin, Germany, November 29 - Dezember 1, 2006, Revised Selected Papers. p. 260
- ^ Garry Doherty, The Open Group (2011) "TOGAF Trademark Success". on blog.opengroup.org. 8 February 2011
- ^ TOGAF Introduction The Open Group Architecture Framework. Accessed 22 Jan 2009.
- ^ Department of Defense (1996). Technical Architecture Framework for Information Management. Vol. 4. April 1996
- ^ Marc Lankhorst (2013) Enterprise Architecture at Work: Modelling, Communication and Analysis p. 23
- ^ Jaap Schekkerman (2003) How to Survive in the Jungle of Enterprise Architecture. p. 119
- ^ Tom van Sante, Hans Van Den Bent (2007) Togaf the Open Group Architectural Framework: A Management Guide. p. iv
- ^ 15,000 certifications
- ^ TOGAF 9.1 White Paper An Introduction to TOGAF Version 9.1 http://www.opengroup.org/togaf/
- ^ Gerber A; Van der Merwe, A; Kotze, P: 2010. Towards the Formalisation of the TOGAF Contenet Metamodel using Ontlogies. To appear in: Proceedings of The 12th International Conference on Enterprise Information Systems (ICEIS 2010). INSTICC
- ^ The Open Group (2011). TOGAF® Version 9 - Download. Architecture Forum. Retrieved on 2011-11-17 from http://www.opengroup.org/architecture/togaf9/downloads.htm.
- ^ The process flow can be seen as an image located here: Architecture Development Cycle
- ^ "Enterprise Continuum". The Open Group. Retrieved 4 January 2014.
- ^ The Open Group Certification Register
- ^ a b c "TOGAF 9 Certification". The Open Group. Retrieved 11 January 2014.
- ^ "TOGAF Certification FAQ". The Open Group. Retrieved 11 January 2014.
External links[edit]
|Wikimedia Commons has media related to TOGAF.
- Official website
- TOGAF 9.1 Online
- TOGAF 8.1.1 Online
- The TOGAF information site
- Developer.com: TOGAF: Establishing Itself As the Definitive Method for Building Enterprise Architectures in the Commercial World (June 2004)
- TOGAF or not TOGAF: Extending Enterprise Architecture beyond RUP (January 2007)
- Practical advice: How to bring TOGAF to life (October 2007)
- Togaf Modeling using UML and BPMN (May 2010)


text:
Windows used to have a long sidebar which is a vertical bar that is displayed on the side of your desktop. It contains mini-programs called gadgets, which offer information at a glance and provide easy access to frequently used tools. These gadgets were available in Windows 7 and Vista. But with the release of Windows 8, Microsoft has completely removed the concept of gadgets and sidebar.
Now if you were using gadgets in Windows 7 and want to get it back in Windows 8, then you can probably try 8GadgetPack.
This app works on Windows 8 (32/64-bit). This app will install all those original Windows gadgets available in Windows 7.
The app comes with almost all popular gadgets like clock, calendar, CPU, disk usage, weather, slideshow, sticky notes etc.
If you love gadget on your Windows desktop, then this free app is for you.


text:
Arsenal is delighted to confirm that a squad comprising the Club's young professionals will participate in the Dr Pepper Dallas Cup 2011.
The tournament, which is taking place at the Pizza Hut Park complex, the home of MLS Side FC Dallas, from April 17th – 24th 2011, will see Arsenal's young side coming up against opponents from top Italian, German, Mexican and Brazilian sides, with the Gunners participating in the 'Super Group' section of the competition.
The young crop of players, which will be formed from the Club's young professionals and Scholars from the Youth Development section, will travel out to Dallas for the international youth tournament which has been running for over 30 years. The structure of the tournament starts with an initial group stage format where teams play their opposing three group sides, with the winner progressing to a semi-final against another group winner, with the respective victors meeting in the final.
Liam Brady, Arsenal's Head of Youth Development said of the tournament: "The Dallas Cup gives our boys great competition against clubs from all over the world by which we can measure ourselves. It also of course gives the players an opportunity to go to the United States and sample the culture, which in itself is an education for the young players. Travelling and representing the Club is an important part of a player's development, and appearing at a prestigious tournament like this will be a great test for our young players. We're very thankful for the invitation to participate and look forward to the challenge next April. We know Arsenal has a huge following in the United States and we hope many fans will come to see our young talent."
Executive Director of the tournament Gordon Jago added: "Our thanks to Arsenal FC and Head of Youth Development Liam Brady for making it possible for his young men to compete in the Super Group next April. This being the first appearance for the club at the tournament, we are all very excited and want the team to know that we will make this an experience the young men will remember for many years to come. One of the most famous soccer clubs in the world, the "Gunners" are renowned for their exciting and highly skilled style of play that has made them one of the most popular teams in the English Premier League. Their academy teams follow that style of play and have won the EPL U18 Academy League for the past two seasons."
"We are delighted to have Arsenal FC come to the Dallas Cup next year" stated Tournament Manager Randy Jones. "All the reports on their championship success have been highly praised and I am certain that the Dallas soccer fans will enjoy the opportunity to see such an exciting team in action plus I know that for Gordon having made his debut as a professional footballer in the English First Division against Arsenal many, many years ago, the club holds a special place in his heart."
Arsenal.com and the Dallas Cup website (www.dallascup.com) will have the latest information on the Super Group as it develops. Full tournament information and match reports will feature on Arsenal.com when the tournament is up and running.Copyright 2017 The Arsenal Football Club plc. Permission to use quotations from this article is granted subject to appropriate credit being given to www.arsenal.com as the source


text:
Hundreds of new jobs are also being created at the German-owned car-maker's plants, in Oxford, Swindon and Birmingham.
The Oxford plant will build the 100,000th Mini later this month, 13 months after production on the redesigned model started.
'The Mini is clearly an international success story,' Dr Norbert Reithofer, BMW board member for production said during a visit to the Oxford factory today.
Americans bought 1,559 Minis in April, which was the first full month of Mini sales in the US.
- More about:
- Manufacturing
- Oxford
- Swindon


text:
It's time! I may be back to blogging regularly, but I have yet to reestablish my routine visits to other bloggers. I have never felt that blogging is just about me. The blog-blessing is in the sharing and exchange.
I am calling this FORAGE FRIDAY where I will visit fellow bloggers and then share five finds. I love the thrill of the hunt! Don't you?
"Where Bloggers...Uh...Create"
With no apologies, this blogger shares her creative chaos and the vices that see her through.
"Vintage Clip Art - Engraved Roses - Printable Labels"
Karen is a go-to source for vintage and copyright free clipart.
"Bird Notes"
Susy's charming home doubles as a bird sanctuary.
"Apple Crisp Breakfast Muffins"
Cherry Menlove, author of The Handmade Home, has a website brimming with enticing photos and sparks of inspiration.
Cherry Menlove, author of The Handmade Home, has a website brimming with enticing photos and sparks of inspiration.
"Our Hummingbirds"
My previous post celebrated my very first hummingbird feeder. At Bailiwick Studios, Jill shares some incredible photos of a hummingbird nest in her own backyard. I learned a few things.
[NOTE: Scroll down one post to read more about hummingbirds.]


text:
Imagine turning Labour and Wait — that temple to utilitarian good taste — into a wine bar, and you have something of the atmosphere of Canela. The Portuguese café, which opened 11 years ago a few doors down from the Donmar Warehouse in Earlham Street, has just been extended with an extra room that opens onto Shorts Gardens, completely redecorated and relaunched as a restaurant-cum-wine-bar.
With its restrained décor of petrol-blue tongue-and-groove panelling, polished white marble tables, dark leather banquettes, window stools and simple pendant lighting (the only frivolities being a glittering chandelier and a wall of vintage radios), you might expect restrained food to match.
But the menu, devised by owners Suzanna Pascoal and Suki Lam, is surprisingly ambitious, the dishes quite elaborate. Choose between the small "petisco" platters or larger dishes, which are perfect for sharing. We began with pataniscas — bacalhau fritters (£7), three small patties of salt-cod fried with onions and flour which were hot, salty and oily, and came with a herby mayonnaise which tasted of salad cream.
Squid Boat with chorizo, peppers and spiced tomatoes (£6) was a single plump pillow of squid, stuffed with a smokey-sweet ragu of chorizo, tomato and pepper and generously garnished with stems of fresh thyme, while the marinated seafood with tomato and capers (£11) consisted of chopped-up pieces of octopus, squid and whole prawns cooked in tomatoes, garlic, ginger, capers and spring onions, and was served warm. Both dishes were delicious.
The only real disappointment was the creamy black rice (£12), an unctuous, glistening black mound studded with three huge tiger prawns and topped with sunflower seeds that was like an emulsion on the verge of splitting, with the oil just beginning to seep back out again. The pink-on-black combination looked dramatic but it was oddly tasteless. We longed for something green, crunchy and simple but even the green bean salad (£7) came overly complicated with shredded green olives, radicchio and raw fennel dressed in a sweet orange zest and mustard dressing.
Of the puddings, quindim, a Brazilian speciality of coconut and lemon custard (£3), was intensely rich and sweet thanks to it being made with condensed milk and honey, its coconutty base oozing syrup, while the banana and cinnamon cake (£5) was an unexpected pleasure: layers of caramelised banana sandwiched between a sweet thick cinammon "goo" , which we were told, by one of the two friendly young waitresses serving us, was made "according to chef's secret recipe". A tiny glass of cinnamon-topped single cream arrived with it.
From the wine list, the most expensive single thing we tried was a glass of fruity, mineral-crisp Campolargo Cercial 2011. It was complex and unusual, but still, pretty steep at £13.20. There are plenty of cheaper wines from boutique Portuguese vineyards available by the glass, which is all the more reason to treat this as a drop-in place for a drink and a plate rather than a full-blown meal — and the deli counter still serves takeaways throughout the day.
33 Earlham Street, WC2 (020 7240 6926, canelacafe.com). Open Mon- Sat 11am-11pm, Sun 11am-9pm. A meal for two with service, about £75
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50 terms
Biology 01
Biology 1
Compound Light Microscope
- requires contrast between cells and cell structures
- contrast is obtained through staining techniques that results in cell death
- use various stains and dyes
ex: hematoxylin (reveals the distribution of DNA and RNA within a cell due to its affinity for negatively charged molecules)
Phase Contrast Microscope
- a type of light microscope
- allows study of living cells
- differences in refractive index are used to produce contrast between cellular structures
-this technique doesn't kill the specimen
Electron Microscope
- uses a beam of electrons to allow a thousandfold higher magnification compared to light microscopy
- can only examine dead specimens
- preparation: fix & section tissues, sometimes stained with solutions of heavy metals
- uses radioactive molecules to trace and identify cell structures and biochemical activity
- can be used to study protein synthesis
- similar techniques are used to study mechanisms of DNA & RNA synthesis
Autoradiography Preparation
- cells are exposed to a radioactive compound for a brief, measured period of time
- cells are incubated, fixed at various intervals and processed for microscopy
- each preparation is covered with a film of photographic emulsion
- preparations must be kept in the dark for several days while radioactive compound decays
- the emulsion is then developed
- dark silver grains reveal the distribution of radioactivity within the specimen
- used to separate cells or mixtures of cells without destroying them in process
- lower speed: cell mixtures separate into layers on the basis of cell type
- high speed: fragmented cells' components will sediment at different levels based on their densities
ex: ribosomes (high density) will end up at the bottom of the test tube, mitochondria & lysosomes (low density) remain on top
- unicellular organisms with a simple cell structure
ex: bacteria and cyanobacteria (blue-green algae)
- have an outer cell membrane but do not contain any membrane-bound organelles
- have a cell wall, cell membrane, cytoplasm, ribosomes (30S & 50S) & flagella
- have no true nucleus
- in prokayrotes
- where the genetic material is concentrated as a single molecule of DNA
- in prokayrotes
- smaller rings of DNA, consisting of just a few genes, replicate independently from main chromosome, often contain genes to survive adverse conditions
- typically bounded by cell membrane and contains cytoplasm
- Cytosol: fluid component of the cytoplasm and consist free proteins, nutrients & other solutes
- genetic material (linear strands of DNA) organized into chromosomes, located in the nucleus
- Centrioles: found in animal cells but not in plant cells
- found in the cytosol
- composed of microtubules, microfilaments, intermediate fibers
- give cell shape and anchor organelles
- aid intracellular transport
Cell/Plasma Membrane
- encloses the cell and composed of phospholipid bilayer
- outside: hydrophillic (polar) phosphoric acid
- inside: hydrophobic (non-polar) fatty acid
- selective permeability: small non-polar molecules pass through/diffuse freely, charged ions, proteins & carbohydrates don't (need carrier proteins to cross)
- cholesterol molecules: often embedded in hydrophobic interior & contribute to fluidity
- receptors: complex proteins/glycoproteins embedded in - membrane with biding sites, may carry molecule into the cell via pinocytosis
- controls activity of the cell, including division
- surrounded by a nuclear membrane/envelope that maintains distinct environment from cytoplasm
- nuclear membranes have nuclear pores for two way material exchange
- contains DNA
- histones: structural proteins that form chromosomes
- nucleolus: dense structure in the nucleus where ribosomal RNA (rRNA) synthesis occurs
- sites of protein production
- synthesized by nucleolus
- two subunits: one large and one small
- each subunit is composed of rRNA and proteins
- free ribosomes: found in cytoplasm
- bound ribosomes: line the outer membrane of endoplasmic reticulum
Endoplasmic Reticulum
- a network of membrane-enclosed spaces connected at points with the nuclear membrane
- function: transport materials throughout the cell, mainly secretion
- smooth ER: lipid synthesis
- rough ER: protein synthesis
- these proteins cross to smooth ER, secreted into cytoplasmic vesicles & transported to golgi apparatus
Golgi Apparatus
- stack of membrane-enclosed sacs
- receives vesicles from smooth ER, modifies them, repackages into vesicles & distributes them
- usually active in distributing new materials to cell surface
- exocytosis: when golgi apparatus' secretory vesicles release their contents to the cell's exterior
Vesicles and Vacuoles
- membrane-bound sacs involved in the transport and storage of materials that are ingested, secreted, processed or digested by the cell
- vacuoles are larger than vesicles and are more likely to be found in plant cells
- membrane-bound vesicles that contain hydrolytic enzymes involved in intracellular digestion
- enzymes are maximally effective at pH 5, thrives in lysosmes
- lysosome is an acidic environment distinct from neutral pH of cytosol
- fuse with endocytotic vacuoles and break down materials ingested by the cell
- aid in renewing cell's own components by breaking down old ones to be recycled in the cytosol
- autolysis: injured/dying cell may commit suicide by rupturing the lysosome membrane & releasing its hydrolytic enzymes, which will digest cellular contents
- membrane-bound organelles specialized as containers for metabolic reactions
- two types: peroxisomes and glyoxysomes
- a type of microbodies
- contain oxidative enzymes that produce hydrogen peroxide by the transfer of hydrogen from a substrate to oxygen
- break fats down into smaller molecules that can be used for fuel
- smaller fat molecules also used in the liver to detoxify compounds harmful to the body (ex: alcohol)
- a type of microbodies
- usually found in fat tissue of germinating seedlings
- used by the seedling to convert fats into sugars until the seedling is mature enough to make its own sugar through photosynthesis
- sites of aerobic respiration within the cell
- suppliers of energy
- each mitochondrion is bound by an outer and inner phospholipid bilayer membrane
- is semiautonomous: contain own (circular) DNA and ribosomes, can produce own proteins and self replicate by binary fission
- believed to have been early prokaryotic cells that evolved a symbiotic relationship with ancestors of eukaryotic cells
Mitochondria's Membrane
- outer membrane: smooth, acts as a sieve, allows molecule through based on size
- intermembrane space: area between the inner and outer membrane
- inner membrane: has cristaes (convolutions) and high protein content that includes the proteins of electron transport chain
- matrix: area bounded by inner membrane, site of many reactions in cell respiration
Cell Wall
- tough outer cell wall
- protects the cell from external stimuli and desiccation
- only on plant cells
- specialized type of microtubule involved in spindle organization during cell division
- not bound by a membrane
- only on animal cells
- oriented at right angles to each other and lie in a region called the centrosome
- direct separation of chromosomes during cell division
- composed of microtubules
- gives cell mechanical support, maintains it's shape and functions in cell motility
- composed of microtubules, mirofilaments and intermediate filaments
- hollow rods made up of polymerized tubulins
- radiate throughout the cell and provide it with support
- provide a framework for organelle movement within the cell
- tubulins make up mirotubules, which make up centrioles
- solid rods of actin
- involved in cell movement and support
ex: muscle contraction is based on interaction of actin with myosin in muscle cells
- move materials across the plasma membrane in amoeboid movement
Intermediate filaments
- collection of fibers involved in maintenace of cytoskeletal integrity
- diameter falls between microtubules and microfilaments
Movements across the cell membrane
a) simple diffusion
b) facilitated diffusion
c) active transport
d) endocytosis
e) exocytosis
Simple Diffusion
- net movement of dissolved particles down their concentration gradients
- from high concentration to low
- passive process
- types of molecules transported: small/non polar (O₂, CO2, etc)
- simple diffusion of water from a region of lower solute concentration to a region of a higher solute concentration
- if membrane is impermeable to a particular solute, water will flow across membrane until solute concentration differences are equal
- types of molecules transported: H₂O
Hypertonic (in respect to another liquid)
- has a higher solute concentration
- water will flow into the hypertonic liquid
Hypotonic (in respect to another liquid)
- has a lower solute concentration
- water will flow out of hypotonic liquid, into the higher concentrated liquid
- solute concentration between two liquids are equal
- no net flow of water in either direction
Faciliated Diffusion
- passive transport
- net movement of dissolved particles down their concentration gradient
- need help from carrier molecules
- types of molecules transported: large/non-polar (glucose)
Active Transport
- net movement of dissolved particles against their concentration gradient
- need help from transport proteins
- requires energy
- required to maintain membrane potentials in specialized cells (ex: neurons)
- types of molecules transported: polar molecules/ions (Na+, Cl-, K+, etc)
- process in which the cell membrane invaginates, forming a vesicle that contains extracellular medium
ingestion of fluids or small particles
engulfing of large particles
- a vesicle within the cell fuses with the cell membrane and releases its contents to the outside
- in both endocytosis and exocytosis, the material never actually crosses through the cell membrane
- groups of morphologically and functionally related cells
- types of tissues: epithelial, connective, nervous and muscle
Epithelial Tissue
- covers the surfaces of the body
- lines the cavities
- protects against injury, invasion and dessication
- involved in absorption, secretion and sensation
Connective Tissue
- involved in body support
- specialized connective tissues: bone, cartilage, tendons, ligaments, adipose tissue and blood
Nervous Tissue
- composed of specialized cells called neurons
- these neurons are involved in the perception, processing and storage of information concerning the internal and external environments
Muscle Tissue
- has great contractile capability
- involved in body movement
- three types: skeletal, cardiac and smooth
- acellular structures composed of nucleic acid enclosed by a protein coat
- range in size from 20-300 nm (prokaryotes are 1-10 nm & eukaryotes are 10-100 nm)
- nucleic acid can be either linear or circular and has four varieties: single-stranded & double-stranded DNA, single-stranded and double-stranded RNA
- virus' protein coat
- composed of many protein subunits
- may be enclosed by a membranous envelope
"obligate intracellular parasite"
- viruses can only reproduce in a living host cell
- lack structures for independent activity & reproduction
- virus attaches itself to a host cell, injects its nucleic acid, take control of protein synthesis within the cell
- viral genome replicates itself, produce protein coats and assembles new virions that leave host cells
- antiviral meds work by interfering with enzymatic reactions involved in viral replication. it's easier to vaccinate to combat viruses
- viruses that exclusively infect bacteria
- injects its nucleic acid into a bacterial cell, the phage capsid doesn't enter the cell
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I would like to thank audio-jungle for allowing me to merge in to this community. It is exactly what I have been seeking for months!
Do check out my music and leave comments on the track for feedback.http://audiojungle.net/item/the-presence-of-evil/2544895
Great work! I like heavy atmosphere you've created with it. Congrats on your first sale! You're definitely gonna like it here. I've been a member for around a month now and I've been lovin every minute of it.
Congrats! The first sale is the best!
Congratulations! It's a great feeling
Congrats! Great feeling isn't it?
Congrats KaezerMusik!!!
Heck ya man, big Congratulations. My first sale was an awesome feeling. When someone likes your music enough to pay for it, its the ultimate compliment. And also its as if they are paying you to keep going!
Congrats friend!!!


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Automatically Disconnect Remote Access Callers (Windows NT/2000/XP)
Specifies the amount of idle time in minutes to wait before disconnecting the remote access client.
|This tweak can be easily applied using WinGuides Tweak Manager.
Download a free trial now!
Open your registry and find or create the key below.
Create a new DWORD value, or modify the existing value, called "AutoDisconnect" and set it according to the value data below.
Exit your registry; you may need to restart or log out of Windows for the change to take effect.
|(value not set)
|0x00000005 (5)
Value Name: AutoDisconnect
Data Type: REG_DWORD (DWORD Value)
Value Data: Time in Minutes
>> Recommended Download - check, repair and optimize your registry now with Registry Mechanic <<
Disclaimer: Modifying the registry can cause serious problems that may require you to reinstall your operating system. We cannot guarantee that problems resulting from modifications to the registry can be solved. Use the information provided at your own risk.
Last modified: April 3, 2002
|More Guides »
|Security Guide
|Support Forums
|Software Guide
|Scripting Guide


text:
Store Locator
S8 Note - This prescription item is Schedule 8 and can only be supplied on a script from a registered doctor in Queensland. Any prescriptions from any other state cannot be filled and will be returned in the mail
Note: Private, PBS and our prices are available to the general public. Concession and Safety Net prices are only available to people with the appropriate concession or Safety Net cards. See Prescriptions for more details.
We can no longer accept signed authority forms from your doctor as permission to dispense more than one pack. Please contact our pharmacist for more information.
If you order this item as Private, NO PBS stickers will be issued. Once any prescription order has been sent the product cannot be returned for a refund even if your doctor changes your medication or you have an adverse reaction.
Pharmacist Only Medicine
This EXTRA WIDE Magnetic Back Support is designed to provide protective support and warmth for all physical activities. Helps to keep muscles supple and assists to relieve muscular aches and painsand may provide temporary pain relief from ailments like arthritis and rheumatism. Enjoy greater flexibility without feeling like you are wearing a support or brace. Wear it over or under clothing, where it remains undetectable. Made from lightweight anti-sweat material and completely hand washable. Ideal for a larger framed person, for men and women alike. Contains 45 Magnets - Total Gauss 22,500.
Medium: 32 to 36 Inches, 80cm to 90cmLarge: 36 to 40 Inches, 90cm to 100cmExtra Large: 40 to 44 Inches, 100cm to 110cmDouble Extra Large: 44 to 48+ Inches, 110cm to 120cm+


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24 inch long
5 inch wide
Worsted weight yarn: 1 skein
I used Red Heart Super Saver Pink Camo
Elastic hair band (ponytail holder) or rubber band
Size G & H crochet hooks
Pattern Notes
Beg ch 3 counts as first dc in each rnd.
Sl st to 3rd ch of beg ch 3 to join each rnd unless other wise stated.
The main pattern is worked in the spaces.
The main pattern is worked in the spaces.
Rnd 1) With H hook, attach yarn to elastic hair band. Ch 3, 20 dc around hair band.
Rnd 2) Ch 3, dc in same st, (2 dc in next st) repeat around.
Rnds 3-4) Ch 3, (dc in next st) repeat around.
Rnd 5) Ch 3, dc in same st, (dc in next st, 2 dc in next st) repeat around.
Rnd 6) Repeat Rnd 3.
Rnd 7) Ch 3, dc in next 2 st, ch 1, skip next st, (dc in next 3 st, ch 1, sk next st) repeat around.
Rnd 8)* Ch 4, sc in 1st space, (ch 3, sk next 3 st, sc in next sp) repeat around, sl st to 1st st of beg ch 4.
Rnd 9)* Sl st in 1st sp, ch 3, 2 dc in same sp, (ch 1, 3 dc in next sp) repeat around.
Rnds 10-33) Alternate repeating Rnds 8 & 9. Increase the number of Rnds if you would like to make the bag holder longer. Rnd 10 is the same as Rnd 8, Rnd 11 is like Rnd 9 ect.
Rnds 34-36) Repeat Rnd 3.
Rnd 37) Ch 1, sc in each st around, fasten off.
* Rnds of main design.
Rnd 1) With G hook, ch 100, sc in 2nd ch from hook, sc in each ch across.
To attach: Weave the drawstring through 1st row of dc on top of the bag holder body. I weaved the string behind one dc post, skipped three dc, and then weaved the string behind another dc post. You can weave the drawstring any way you would like.
Hanging Loop
Rnd 1) Attach yarn to top of bag holder body, ch 5, sl st to bag holder body, fasten off.
I crocheted a custom hanger for my grocery bag holder. I wanted to hang from a towel bar and wanted to be able to easily detached the holder from the bar. You can use a variety of ways to hang your holder. What you decide to use depends on where you are going to use it. You can attach another hair band, a metal or plastic loop, or an old key ring.
Please let me know if there are any problems with this pattern, or if you have questions. Email me at email@example.com. I hope you enjoy this free crochet pattern!
Pattern Abbreviations
beg beginning
ch chain
dc double crochet
rnd(s) round(s)
sc single crochet
sk skip
sl st slip stitch
sp space
beg beginning
ch chain
dc double crochet
rnd(s) round(s)
sc single crochet
sk skip
sl st slip stitch
sp space