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Ship-Talking Podcast
Join us weekly as we talk sh*p with guests from across the Star Trek universe who have contributed to the design, creation, and production of its ships. Red alert: Maximum punnage intended.
@shiptalkingpod
http://www.shiptalkingpod.com/
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[Ship-Talking Presents] Shuttle Scuttle #25 (Reporting Damage Reports)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, James, Alex, and George chat about how Trek has portrayed ship damage throughout the franchise and some behind-the-scenes tidbits around a couple of the more famous damage sequences. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always open at www.shiptalkingpod.com or email...
[Ship-Talking Presents] Shuttle Scuttle #24 (Warping Out of 2021)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, James pilots the shuttle and takes George and Brandon on an away mission down memory lane. The gents look back at all the great sh*p content from the franchise that was seen throughout 2021, and give some initial hopes for the coming year. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always...
[Ship-Talking Presents] Shuttle Scuttle #23 (Ships in Animation)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, Brandon and Robbie are still live in-person on Starbase 33 (aka Dublin, Ireland) to continue their chat during their visit together - this time talking about ships that appear in animated shows, including Lower Decks and Prodigy. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always open at...
[Ship-Talking x Hero Collector] Ships of the Trek Universe #10 (2399 Romulan Warbird)
Welcome to the latest episode of the collaboration podcast between Ship-Talking and Hero Collector! For this episode, which was recorded live at Destination Star Trek 2021 in London last month, Brandon is joined once again by Hero Collector's Ben Robinson and John Ainsworth. While on stage, the gents discussed the 2399 Romulan Warbird, including design insights and more. Ship models discussed in this Pod series can be purchased here. Ship-Talking Pod is also on Patreon. In return for your...
[Ship-Talking Presents] Shuttle Scuttle #22 (Discussing Disco)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, Robbie takes the ship's shuttle to visit Brandon live in-person on Starbase 33 (aka Dublin, Ireland) where the two recorded a chat about their experience watching Discovery's season 4 premiere together... oh, and of course all the new ship p*rn that came along with it. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here!...
[Ship-Talking Podcast] Episode 29: Hero Collector LIVE
Recorded in front of a live audience from the Voyager stage at Destination Star Trek London 2021, Brandon hosted this episode and was joined by Hero Collector's Ben Robinson and John Ainsworth. They chat all about the process of bringing ships seen on screen (or not...) into our hands, behind-the-scenes secrets, and much more! Very soon, our patrons at or above the Constitution-class tier on Patreon will also gain access to a couple other recordings that the Pod hosted live at the con which...
[Ship-Talking x Hero Collector] Ships of the Trek Universe #9 (Section 31 Deimos-class Ship)
Welcome to the latest episode of the collaboration podcast between Ship-Talking and Hero Collector! For this episode, special guest Ryan Dening from North Front Studio joins Brandon and Hero Collector's Ben Robinson. Ryan is a production/concept illustrator who worked on the ships from the first two seasons of Star Trek: Discovery and stopped by to discuss the Section 31 Deimos-class ship and insights behind how her design came to life. Ship models discussed in this Pod series can be...
[Ship-Talking Presents] Shuttle Scuttle #21 (LIVE from Destination Star Trek London)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this very special episode, [almost (we missed you, Alex!)] the entire Pod team reports back on their away mission to Destination Star Trek London - LIVE from the convention floor. Before they board the shuttle back to the ship, each crew member shares highlights of their experience and their favourite ship memory from the con. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle...
[Ship-Talking x Hero Collector] Ships of the Trek Universe - Holiday Bonus Episode (Borg Cube Advent Calendar)
Welcome to a special holiday bonus episode of the collaboration podcast between Ship-Talking and Hero Collector! The Pod's Community Manager James gets in the holiday spirit alongside Hero Collector's Ben Robinson as they sit by a fire in the holodeck to chat about this year's Borg Cube Advent Calendar. Not only do they discuss insights behind the development of this unique offering, but they also dive into a taste of what lucky recipients of it will experience over the 24-days of Trekmas....
[Ship-Talking Presents] Shuttle Scuttle #20 (Like Father, Like Son)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, a very special visitor is shuttled from the ship back to his home planet, and during the journey with him, Brandon discusses the inspiration and impact that Trek and the original Constitution-class have played in both of their lives... have tissues to hand! All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing...
[Ship-Talking Presents] Shuttle Scuttle #19 (That Burning, Romulan Sensation)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, Alex takes the shuttle's helm and asks James and Brandon for their thoughts and theories around how 'The Burn' may or may not have affected Romulan ships when the incident occurred during the late 3060s. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always open at www.shiptalkingpod.com or...
[Ship-Talking Presents] Shuttle Scuttle #18 (Registering Registries)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, one of the Pod's very own 'lower deckers' Ryan aka "TheTrekspert" is escorted by Brandon and Robbie in the ship's shuttle on its way to drop off Ryan at Quark's on DS9 for a pub quiz - during the journey, ship registries (e.g. NCC-1701, NCC-74656, etc.) and the theories on their numbering conventions are discussed. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle...
[Ship-Talking x Hero Collector] Ships of the Trek Universe #8 (Romulan Flagship)
Welcome to the latest episode of the collaboration podcast between Ship-Talking and Hero Collector! Brandon is joined in this episode once again by both Ben Robinson and John Ainsworth from Hero Collector to talk about the Romulan Flagship that was seen on-screen during the season one finale of Star Trek: Picard. They discuss her insights and design, along with a few special tidbits you'll just have to listen out for. Ship models discussed in this Pod series can be purchased here....
[Ship-Talking Podcast] Episode 28: Thomas Marrone
Thomas Marrone finally gets his solo episode! It is a crime it took us this long; but, we're finally glad to have one of our best-friends of the Pod and Lead Ship Designer on Star Trek Online all to ourselves to talk about ship design, bringing ships to life in STO, and a whole lot of other sh*p. An expanded chat with Thomas is exclusively available to our patrons at or above the Constitution-class tier on Patreon. Your answers to the latest Community Q were also discussed before a new...
[Ship-Talking Presents] Shuttle Scuttle #17 (The Excelsior Class: The Crown of the Great Experiment)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, George leads an away mission and is joined aboard the ship's shuttle by James and Robbie - during the journey, they discuss the crown jewel herself: The Excelsior Class. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always open at www.shiptalkingpod.com or email hello@shiptalkingpod.com.
[Ship-Talking Presents] Shuttle Scuttle #16 (Stations of the Line)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, Robbie guides the shuttle on a cargo run to Empok Nor with George and Brandon in tow. While enroute, the lads talk about the various stations seen throughout the Trek universe, including those within Federation and beyond. All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide release here! Hailing frequencies are always open at...
[Ship-Talking Podcast] Episode 27: Rob Bonchune (Part 2)
The rest of Rob Bonchune's chat takes place in this episode, alongside the return of Ship-Talking Pod founder Robbie! As a reminder: Rob is an Emmy-award winning Trek VFX legend who is most known for his CGI/VFX ship work on DS9, Voyager & Enterprise. During this half of the chat, we talk about this work as well as the amazing ship art renders he's still making today. Part 2 of the expanded chat with Rob is exclusively available to our patrons at or above the Constitution-class tier on...
[Ship-Talking Presents] Shuttle Scuttle #15 (ShipCon2021 with Mark Rademaker)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle', which was recorded in front of a live audience during last month's 'Ship-Talking Pod LIVE' show that Patrons can attend. Alex and Brandon took the ship's shuttle out for a spin to ShipCon2021 where they had a chance to talk sh*p with two friends of the Pod: Designer of the U.S.S. Aventine / Vesta-class Mark Rademaker and Vesta-Super-Fan Oliver Kühle. Oliver gets to meet his idol, we get to hear from Mark more...
[Ship-Talking x Hero Collector] Ships of the Trek Universe #7 ft. John Eaves (Wallenberg-class Tug)
Welcome to the latest episode of the collaboration podcast between Ship-Talking and Hero Collector! Special guest & legendary Ship Designer John Eaves joins this episode alongside Brandon and Ben to talk about Starfleet's Wallenberg-class Tug from season one of Star Trek: Picard. In addition to insights for this ship, the gents also talk about the process that ship designs go through to get from concept to what we see on-screen. Ship models discussed in this Pod series can be purchased here....
[Ship-Talking Presents] Shuttle Scuttle #14 (What Breed of Starship is That?)
Welcome to the latest episode of our pod-within-a-pod series: 'Shuttle Scuttle'! In this episode, you learn about what we were about to discover at the end of the last episode (spoilers: Robbie squealed when we sent him our report), as well as our thoughts on which dog breeds best represent select ship classes. Do you agree with Alex, Brandon, and James's thoughts? Let us know! All patrons of Ship-Talking's Patreon gain access to new episodes of 'Shuttle Scuttle' one week before their wide...


what do you guys make out of this"
a while ago i clicked on a bbc link and my screen started scrolling and no matter what i tried, all screens would scroll back up to the top. then it happened again, but everything was fine until today when i clicked on another uk link ["the dancing queen"], which is youtube.
this time every window started the same crazy spin and i couldn't even use the "charms" [really?!] on the side, as they were just scrolling up.
rather worriedly i then waited a while and turned it back on. it started the first screen, then drew a blank. i did that a couple of times and then just waited - and after a loooong time loki woke up.
any idea what the hell what that was about? i've never had that particular problem with any other machines i've owned. and why only the uk links?
i have scanned and i'm supposed to have live on-line scanning as well, so he ought to be squeaky clean?
Fortunately I've never run into the problem. It sounds like the kind of thing that would be a nightmare to troubleshoot. The problem can be anywhere from the YouTube channel itself to a loose memory card inside your computer, not to mention the flaky software you may or may not have installed. One thing you CAN do is to try the same links on some other computer. If the problem only happens on your computer, then it might be time to take it to your local geek shop for a check-up. If it happens on all computers, then you might want to talk to the ISP from whence you get your connection. If you send me the links, I can try it here to see what happens. The government isn't filtering the Internet content in this country ... yet.
There's one more thing that pops to mind, and that's a setting. I can't recreate it here (Linux, of course), but there is a way to set the mouse so that there is some sort of "automatic scrolling." If I remember correctly, a little icon appears to the side and, if you move the mouse above it, it scrolls up, and below it, it scrolls down. This is all without having to use any buttons on the mouse.
I used to accidentally trigger that function, and it would drive me crazy until I figured out how to disable it. Like I said, I can't remember how it worked now, and can't recreate it. It's something that you might have accidentally triggered, and something easy for you to check out.


With training in full swing the Kent Phoenix are looking forward to 2019.
Having settled in to our new facility at Shepway Green our focus is now turning towards the 2019 Season. While we still have to get through the Great British Winter next spring offers a number of opportunities for our players to put their skills to the test.
The Board and Coaching staff a putting together a packed schedule that will see all our age groups play competitive football to help their skills development.
At flag level we have see strong and sustained growth with our newer members quickly finding their feet. We are also seeing the benefit of both our full kitted squad and the developmental group and the coaching staff have some exciting plans to both keep training fresh through the winter but to continue to improve and develop skills.


Light and Sound Neurotherapy encompasses a variety of drug-free technologies designed to improve brain function. EEG biofeedback (also known as neurofeedback) is the most researched neurotherapy for treating substance abuse disorders. Neurofeedback teaches people how to strengthen desired brainwave patterns to improve their ability to relax and maintain focused.
An effective tool in treating trauma, Light and Sound Neurotherapy takes advantage of the brain's natural responses to rhythm. The process involves therapists working with patients to elicit positive neurological responses via a series of tones and LED light movements. The goal of the process is to identify the origins of dysfunctional thought patterns and form positive associations with previously traumatic experiences.
Light and Sound Neurotherapy helps improve sleep patterns, reduces anxiety, decreases heart rate and blood pressure and helps in the treatment of depression. Seaside Palm Beach's accomplished and sought-after research department have been instrumental in the innovation and implementation of this unique and cutting-edge modality.


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What Juice Has Low Carbs?
Spinach is the ideal low-carb juicing component because it contains no carbohydrates.Only one gram of carbohydrates are found in one cup of raw spinach (30g).It has almost little flavor in your juices, but it is extremely beneficial to your health.In just one ounce of spinach juice, you'll get more than 100 percent of your recommended daily allowance of vitamin K.
It is necessary for the health of your bones as well as the clotting of your blood.
Most fruit juices are high in sugar, but lemon and lime juices are low in carbohydrates and may be used to flavor various beverages in addition to their own.
What kind of juice has the least carbs&sugar?
If you want your juice sweet, light juice is a low-carb, low-sugar choice that may be suitable for you.Sugar and carbohydrate levels are kept to a minimum in these ready-to-drink fruit juices, which are sweetened with artificial sweetener.It has 13 grams of carbohydrates and 10 grams of sugar in an 8-ounce serving, which is half the amount of carbs and sugar found in a glass of conventional orange juice.
What are some good low-carb drinks?
Celery, spinach, cucumbers, lemon, lime, tomato, and kale are all good options. Also good: Because it's more difficult to know the actual carb and sugar content of fresh juice, you should restrict your serving size to 8 ounces at a time while drinking it. Low-carb and sugar combinations made from tomato, kale, and celery juice are particularly delectable.
What are some carb-free and sugar-free juice drinks?
Consider diet fruit drink, a juice-based beverage sweetened with artificial sweetener, if you're looking for a carb- and sugar-free juice drink.Using a commercially available cranberry juice drink, an 8-ounce portion has just 5 calories and has no carbohydrates or sugar.In comparison, an 8-ounce serving of 100% cranberry juice contains 31 grams of carbohydrates and 31 grams of sugar, making it the healthier choice.
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What juices are lowest in carbs?
Here Are Some Low-Calorie Vegetable Juices That You Can Include In Your Low-Carb Diet for Weight Loss:
Recipes for Tomato and Cucumber Juice, Beetroot Shots, Cucumber Kiwi Juice, Carrot Orange Detox Drink, and Green Cucumber Shots are all available online.
What drink has no carbohydrates?
For example, pure types of alcohol such as whiskey, gin, tequila, rum, and vodka are all absolutely devoid of carbohydrate content. Drinks that are keto-friendly.
Type of alcohol
Carb content
Vodka 1.5 ounces (44 ml) 0 grams
Gin 1.5 ounces (44 ml) 0 grams
Tequila 1.5 ounces (44 ml) 0 grams
Whiskey 1.5 ounces (44 ml) 0 grams
What fruit has no carbs or low carbs?
2. Berries are a kind of fruit. Berries are a popular snack for folks who are watching their carbohydrate consumption. Strawberries have the fewest carbohydrates of all the berries, and blackberries have the fewest net carbs of all the berries.
What fruit had the lowest carbs?
Watermelon. Pin it to your Pinterest board. Strawberries are the summer fruit with the lowest carbohydrate content, with just 7.55 g of carbs per 100 g of fruit. Spread the word on Pinterest.
Cantaloupe. Avocados are a delicious fruit to eat.
Honeydew Peaches are a good example of this. Pin it to your Pinterest board.
What is the healthiest juice to drink?
The 9 Most Beneficial Types of Juice
Cranberry. Cranberry juice, which is tart and bright red, has a variety of health advantages.
Tomato. A tasty and healthy drink, tomato juice is not only a fundamental ingredient in Bloody Marys, but it may also be drunk on its own as a delightful and nutritious beverage.
and acai berry
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Is cranberry juice keto friendly?
As an example, an 8-ounce glass of cranberry juice has 30 grams of carbohydrates. What about apple juice? That equates to around 24 grams of carbohydrates. Having said that, there are diet or reduced sugar juices available that contain just a little amount of carbs, making them excellent keto-friendly beverages.
Is V8 juice low-carb?
Take, for example, cranberry juice, which has 30 grams of carbohydrates per 8-ounce container. Was it made from apples? The carbohydrate content is around 24 grams. But there are certain juices that are low in carbs and hence suitable for keto diets (such as diet or reduced sugar juices).
Is there a low-carb orange juice?
In one serving of Low Sugar Orange Juice 360ml (100 ml), there are 5.7 grams of total carbohydrates, 5.7 grams of net carbs, 0 grams of fat, 0 grams of protein, and 26 calories.
Can I drink orange juice on low-carb diet?
Sugar is naturally included in fruit juice beverages such as apple and orange juice. As a result, they are particularly damaging to a conventional ketogenic diet. Some manufacturers even add additional sugar to their products in order to make them more pleasant. Juice drinks should not be taken on a conventional ketogenic diet due to the high sugar level in these beverages.
Are bananas low-carb?
Bananas are nutritious but high in carbohydrates; nonetheless, berries may be used on a Keto diet. According to the USDA, a tiny banana has more than 20 g of net carbohydrates, which implies that you could easily consume your whole carbohydrate intake from a single fruit.
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Are apples low-carb?
An apple includes just 15 grams of carbs and only 55 calories per modest, 4-ounce serving, making them an excellent choice for anyone following a low-carb diet. Apples are also high in fiber and packed with minerals such as vitamin C and potassium, among others.
Are pineapples low-carb?
100 grams of pineapple, or a half-cup of pineapple, has 11 grams of carbohydrate. It is one of the most nutritious ways to receive your daily dose of manganese, a vital mineral that has an impact on your brain system, hormones, blood sugar, and the rate at which your body absorbs calcium.
Do cucumbers have carbs?
The following are the nutrients found in one medium unpeeled, raw cucumber: 30 calories per serving. Total fat content is 0 grams. Carbohydrates: 6 grams
Are oranges low-carb?
According to the USDA, oranges are a good choice for those following a low-carb diet because a small orange has 9 g of net carbohydrates. According to Wong, oranges are a good source of potassium, which can assist to reduce blood pressure levels.
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redpajama_set_name: RedPajamaCommonCrawl


When the Vision encounters a distress signal from an orbiting station, she is tricked by the villainous organization, A.I.M., into activating a latent Gah Lak Tus module. Although they believe they control it, the Vision must stop it before it threatens Earth.
This series continues elements from Ultimate Extinction.


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The World Blind Football Championships, formerly the Football-5-a-Side World Championships, were played for the first time in 1998.

IBSA Blind Football World Championships

Men's B1

Men's B2/B3 (partially sighted)

Women's Blind Football World Championships B1/B2/B3 (together)

Blind Football at the IBSA World Games

Men's B1

Men's B2/B3 (partially sighted)

Women's B1
 not yet

Women's B2/B3
 not yet

See also
Blind soccer
Cerebral Palsy International Sports and Recreation Association
International Blind Sports Federation
Paralympic games
Paralympic sports
Paralympic association football
CP football
Amputee football

References

External links
 International Blind Sport Federation - Football 5-a-side

Blind sports
Paralympic association football
Parasports world championships
IBSA competitions
Recurring sporting events established in 1998
World championships in football variants

redpajama_set_name: RedPajamaWikipedia


It is well known that moving is one of the most stressful times in anyone's life, so leave it to the best in the business. Big Red Removals have over 10 years of experience in house and flat moves within King's Cross.
Big Red offer a range of services to suit any move, large or small. We can offer a full or partial packing service to ensure that your precious possessions reach their destination intact. Our experienced and dedicated team of professional removers will ensure that your move goes without a hitch. From offering a full site survey for larger moves to flexible hourly rates for smaller moves, Big Red have got you covered, able to offer the most competitive rates in King's Cross.
All moves with Big Red can be covered with liability insurance. As Members of the National Guild of Removers we follow their Code of Practice and you can be assured that Big Red will give you the best removals service in King's Cross.
Whatever other stresses you have with your move, you can rely on Big Red to ensure that, from start to finish, the removal process is not one of them. Call the King's Cross removals specialists now on 0207 228 7651.
Most of the roads around King's Cross are controlled parking, and either parking suspensions or dispensations are required. For larger Removals in King's Cross a parking suspension is a necessity. The suspension has to be booked 14 calendar days and 3 working days in advance of the required date. These are booked with Camden council online. For smaller King's Cross removals, using vans, we can load and unload for short periods on single yellow lines. Otherwise a dispensation would need to be booked, if we are packing and King's Cross flat moving.
The area was previously a village known as Battle Bridge or Battlebridge which was an ancient crossing of the River Fleet. The original name of the bridge was Broad Ford Bridge.
The name "Battle Bridge" led to a tradition that this was the site of a major battle in AD 60 or 61 between the Romans and the Iceni tribe led by Boudica (also known as Boudicea). The suggestion that Boudica is buried beneath platform 9 or 10 at King's Cross Station seems to have arisen as urban folklore since the end of World War II .


The City Council consists of five members elected at-large on a nonpartisan basis. Elections are held the first Tuesday after the first Monday in November of even-numbered years (coinciding with the State General Election).
Council members serve staggered, four-year terms. There are no term limits and Councilmembers serve the entire community.
The Mayor is selected from the membership of the City Council at the second regular meeting in the month of December. The Mayor presides at the City Council meetings and is recognized as the official head of the city government for ceremonial purposes.
The Vice Mayor is also chosen at that time and acts in the absence of the Mayor.
For more information, please call the City Clerk's Office at (925) 671-5237.


Statistics in cricket are finally evolving but we still have the problem of missing the trees for the forest. Landmarks, milestones, grand numbers are given weightage over in-game numbers. In the SSC Test, for example, it was debated if the one-off Bangladesh Test is indeed a series, and if India are thus on an eight-series winning streak or seven. A double of 250 wickets and 2000 Test runs was manufactured so that we could say R Ashwin is the fastest to another mark.
However, a simple statistic, right there on the scorecard was missed. On that treacherous pitch with balls exploding out of some areas and staying low out of others, Wriddhiman Saha conceded zero byes in the second innings, which lasted 116.5 overs.
Batsmen were beaten 111 times in the whole innings; a further 62 were left alone. Some of them kept low, some of them exploded off a length and turned sharply, especially when Ravindra Jadeja fired them in at around 100kmph, but none went past Saha. A member of India's support staff put on the TV after the SSC Test finished, and saw Quinton de Kock let two sets of four byes go through off the bowling of Keshav Maharaj.
"I had seen Saha keep all day, and now I was watching this," the support staff member said.
A trained wicketkeeper - Saha in this case - will tell you that this assessment of de Kock was perhaps a little harsh. "I enjoy keeping to him [Jadeja] on such wickets," Saha said. "On such wickets if a lot of balls come to the keeper it is good, otherwise we only get 10-12 balls all day coming to us. If you get more balls coming to you, then you are always more focussed, so I enjoyed keeping to Ashwin and Jadeja on this wicket."
Saha was not comparing his and de Kock's work, but it put in some perspective how it can be difficult for wicketkeepers when only a few of the balls misbehave in a day. However, it doesn't take away from the sight what Saha as a keeper was. Even thought he had two sessions when not many balls came to him. Then, towards the end of it, one lobbed well in front of him. It was an offcutter from Hardik Pandya that took the inside edge, hit Kusal Mendis' back thigh pad and ballooned up. Saha dashed forward from his station, dived full length and plucked it inches from the ground. That is a catch he holds dear.
"When he got the inner edge, I thought he will be bowled," Saha said. "The ball came in but hit the pad and lobbed up, the pace was slow so I got more time to get to the ball and I could dive because of that time based on my assumption. It was a good wicket."


I've never liked the term Requirements Specification or Software Requirements Specification even though these are widely used in the industry. There are requirements and there are specifications. The two are always different in my mind. Indeed, Webster's defines them differently.
You can specify designs. You can specify architectures. Blueprints are specifications. Source code is a specification. Pseudo-code, state diagrams, and message sequence charts are specifications.
A statement of need is never precise or detailed. It should be clear, unique, feasible, and testable, but it cannot be precise or detailed.
The user interface shall be responsive, is a requirement. It's a poor requirement, but it's still a statement of need.
Lamp X shall illuminate 100 ms after button Y is pressed, is a specification. It defines a precise description of events. It's not a requirement. No information regarding the stakeholder's need has been conveyed.
I can usually spot a specification when I see one. A good requirement is difficult to identify and even harder to write. Authors naturally tend to slip into writing specifications because they don't know how to express their needs. Requirements are also subjective. Some people might view the statement, the UI shall be responsive as failing to convey need. One can always ask, why must the UI be responsive?
I admit I'm on a holy crusade to eradicate the term Requirements Specification. Let's call it a Requirements Document or a Requirements Database. Let's save the term specification for the Software Specification that will follow the Requirements Document. Typically this is a High Level Design and Low Level Design. Those documents are worthy of the title Specification.


Conversion of linoleic acid (LA) and alpha-linolenic acid (ALA) to their higher chain homologues in humans depends on the ratio of ingested n6 and n3 fatty acids.
In order to determine the most effective ratio with regard to the conversion of ALA to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), human hepatoma cells were incubated with varying ratios of [13C] labeled linoleic acid ([13C]LA)- and alpha-linolenic acid ([13C]ALA)-methylesters. Regulative cellular signal transduction pathways involved were studied by determinations of transcript levels of the genes encoding delta-5 desaturase (D5D) and delta-6 desaturase (D6D), peroxisome proliferator-activated receptor alpha (PPARα) and sterol regulatory element binding protein 1c (SREBP-1c). Mitogen-activated protein kinase kinase 1 (MEK1) and mitogen-activated protein kinase kinase kinase 1 (MEKK1) were also examined.
Maximum conversion was observed in cells incubated with the mixture of [13C]LA/[13C]ALA at a ratio of 1:1, where 0.7% and 17% of the recovered [13C]ALA was converted to DHA and EPA, respectively. Furthermore, differential regulation of enzymes involved in the conversion at the transcript level, dependent on the ratio of administered n6 to n3 fatty acids in human hepatocytes was demonstrated.
Formation of EPA and DHA was highest at an administered LA/ALA ratio of 1:1, although gene expression of PPARα, SREBP-1c and D5D involved in ALA elongation were higher in the presence of ALA solely. Also, our findings suggest that a diet-induced enhancement of the cell membrane content of highly unsaturated fatty acids is only possible up to a certain level.
Long chain polyunsaturated fatty acids (LCPUFA) of the n6 and n3 families as well as their precursors are essential dietary components for mammalian species . LCPUFAs appear to be a necessary integral part of membrane phospholipids for optimal biological function particularly in specialized cells and tissues such as brain, retina, testes, heart, liver and kidneys . The constitutive properties of PUFA in biological membranes generally are regarded in terms of their contributions to the fluidity or integrity of membrane bilayer structures [3, 4]. Increasing evidence for competitive interactions between PUFA of the n6 and n3 fatty acid families at the level of formation and action of eicosanoids, thromboxanes, prostacyclins, prostaglandins, and leukotrienes appear to relate directly to potential benefits attributed to an eligible dietary balance of n3 and n6 fatty acids . Within the common Western diet, ALA represents the quantitatively dominant fatty acid of the n3 series. Daily ALA uptake averages 1.5 g, whereas the average daily uptake of the corresponding n6 fatty acid LA is about 10 times higher .
With this 10:1 ratio of dietary n6 to n3 LCPUFA, the formation of pro-inflammatory/aggregatory eicosanoids from LA is favored over those from n3 fatty acids showing anti-inflammatory/aggregatory effects. Controlling the synthesis of n3 LCPUFA, such as EPA and DHA from ALA, and the respective eicosanoids by consumption of the optimized ratio of n6 to n3 LCPUFA is, therefore, of particular nutritional interest.
In addition, LCPUFA and their derivatives are of increasing interest as modulators of gene expression. They are reported for example to be ligands of the nuclear transcription factors peroxisome proliferator-activated receptors (PPARs)  and suppressors of sterol regulatory element binding proteins (SREBP) . Regulating the degradation of fatty acids by mitochondrial as well as by peroxisomal and microsomal fatty acid oxidation, PPARα plays a central role in fatty acid homeostasis (reviewed in Ref. ). SREBP-1 isoforms on the other hand are more active in regulating hepatic synthesis of fatty acids . Both, PPARs and SREBPs are reported to regulate expression of delta-5-desaturase (D5D) and delta-6-desaturase (D6D) [11, 12]. SREBPs as well as PPARs are, in addition to their ligand-induced regulation activity, substrates for several kinases such as mitogen-activated protein kinases (MAPK) [13, 14]. Furthermore, ligands for the PPAR receptor family such as the essential fatty acids linoleic (LA, 18:2-n6) and alpha-linolenic (ALA, 18:3-n3) acid have recently been shown to induce MAPK phosphorylation [15, 16].
LA and ALA are converted to their longer chain homologues by a combination of subsequent reactions, involving Δ6 desaturation, elongation and Δ5 desaturation. Since members of the n6 and n3 families compete for the corresponding enzyme systems [17–19], the conversion of e.g. LA or ALA into their longer chain homologues is significantly influenced by the composition of dietary fats [20, 21]. In this context, whether incorporation of n3 fatty acids into cell membranes and their bioconversion into higher homologues depends on either the absolute amount of dietary n3 fatty acids or rather on the ratio of ingested n6/n3 fatty acids has been controversially discussed.
In a human intervention trial by Liou et al. 2007 , diets containing LA/ALA ratios of 10:1 or 4:1 were administered to healthy men. The different LA/ALA ratios were adjusted by altering the LA content in the diet (high-LA or low-LA), while the ALA content was maintained constant. As a result, the ALA as well as the EPA concentration of plasma phospholipids in the low-LA group (4:1 ratio) increased compared to the high-LA group (LA/ALA ratio 10:1), although the ALA amount administered was equal in both groups. This result clearly shows that lowering dietary LA intake increases EPA in plasma phospholipids, indicating the rate of conversion of ALA to EPA being dependent on the ratio of n3/n6 fatty acids. In contrast to that, Goyens et al. 2006  postulated that bioconversion of ALA in humans is influenced by the absolute amounts of dietary ALA and LA and not by their ratio. In this study, healthy volunteers were randomly divided into 3 experimental groups: 1) high ratio LA group (LA/ALA = 19:1), 2) low ratio low-LA group (LA/ALA = 7:1) and 3) low ratio high-ALA group (LA/ALA = 7:1). Within the latter two groups, the 7:1 ratio was adjusted by lowering the LA content or increasing the ALA content of the diet respectively, compared to the diet of the high ratio LA group. In addition to the diet, multiple tracer bolus doses of [U-13C]ALA were administered to the subjects to estimate ALA conversion by compartmental modeling. Calculations derived from this study confirmed the hypothesis that conversion of ALA is rather influenced by the absolute amounts of dietary ALA and LA than by the ratio of ALA/LA. However, analyses of plasma phospholipid fatty acid composition at the end of this dietary intervention showed that concentrations of ALA and EPA within the two low ratio groups (LA/ALA = 7:1) were significantly higher compared to the high ratio LA group. However, there was no difference between the ALA and EPA plasma phospholipid contents of the two low ratio groups. These results, on the other hand, support the hypothesis that incorporation and bioconversion of ALA are rather influenced by the ratio of dietary LA/ALA. However, no final conclusion can be drawn from the data available concerning the question, whether the conversion is rather dependent on the absolute amount of fatty acids than on the ratio of n6/n3 fatty acids. Furthermore, quantitative data on the conversion of n3 LCPUFA as affected by the ratio of n6 to n3 fatty acids are scarce. Therefore, the objective of our study was to quantify the conversion of [13C]alpha-linolenic acid to eicosapentaenoic acid and docosahexaenoic acid in the presence of varying n6/n3 fatty acid ratios in the hepatoma cell line HepG2. In addition, the transcript levels of genes encoding for enzymes involved in the fatty acid conversion were also examined after incubation of the cells with different ratios of n6/n3 LCPUFAs.
HepG2 cells were obtained from Dept. of Human and Animal Cell Cultures (DSMZ), Braunschweig, Germany. The cells were grown in T-75 cell culture flasks (Sarstedt, Germany) in 15 ml Dulbecco's modified Eagle's medium (DMEM) containing 20% fetal calf serum (FCS), 2% glutamine and 2% penicillin/streptomycin solution (Sigma). Cells were maintained at 37°C in a humidified atmosphere of 95% air/5% CO2 and were subcultured every 7 days. For the experiments carried out, cells were transferred to T-25 cell culture flasks (Sarstedt, Germany) at a density of 5 × 106 cells. After 24 hrs, the medium was replaced with 8 ml DMEM without FCS. After another 24 hrs, mixtures of [13C] labeled LA/ALA (suspended by sonication in sterile bovine serum albumin, Fraction V, Sigma) were added to give a final fatty acid concentration of 100 μM. Ratios of LA/ALA were 9:1, 4:1, 1:1, 1:0 and 0:1. Cells were incubated for 24 hrs at 37°C and the exposure in each case was carried out as a quadruplicate determination. At the end of the exposure process, cells were harvested by adding 1 ml of accutase (Sigma). The cell culture medium was collected separately for determination of [13C]LA and [13C]ALA content. After harvesting, cells were washed with 2 ml of FCS free DMEM and centrifuged at 500 × g. After adding 1 ml of sodium chloride solution (0.9%; w/v) to the cell pellet, cells were stored at -75°C.
Lipids were extracted from the cells by a modified Folch extraction , with the addition of 100 μl of internal standard (1 mg/ml of tetracosanoic acid and 3 mg/ml heptadecanoic acid, dissolved in dichlormethane:methanol, 2:1, v:v) to each sample. The extraction procedure was followed by saponification and methylation of the fatty acids according to an AOAC method . Fatty acid composition was determined via HRGC-CI/-MS . Determination of absolute contents of the several fatty acids was carried out by external calibration.
For gene expression experiments, cells were pretreated as described above. Within the scope of kinetic experiments, cells were exposed to 100 μM pure ALA-methylester for 3, 6, 12 and 24 hrs, respectively, to find out the point of maximal gene expression of D5D, D6D, PPARα, SREBP-1c, MEK1 and MEKK1 via real time PCR (MX 3000P, Stratagene).
For dose response experiments, HepG2 cells were exposed to mixtures of LA-/ALA-methylester at ratios of 4:1, 1:1, 1:0 and 0:1. Here, the 9:1 ratio was not tested since there was no difference between the 9:1 and the 4:1 mixture with regard to [13C]ALA-incorporation and the formation of [13C]EPA and [13C]DHA.
Depending on the results of kinetic experiments, expression of the several aforesaid target genes was determined after 3, 6 or 12 hrs. After incubation, cells were harvested as described earlier and RNA was isolated with RNeasy mini kit® (Qiagen). cDNA was synthesizd using StrataSkript® cDNA synthesis kit (Stratagene) according to manufacturer's instructions. For amplification of gene transcripts during the realtime PCR reactions, validated primer assays from Qiagen were used according the manufacturer's protocol. Human transferrin receptor was chosen as house keeping gene. Brilliant® SYBR® Green (Stratagene) was used for detection of amplified gene products during the PCR reaction.
Data were analyzed with SPSS for WINDOWS 14.0 (SPSS Inc, Chicago, IL). Data were tested for normal distribution using the Kolmogorov-Smirnov test. All data are expressed as mean ± SEM. Statistical significance of results was assessed using two-tailed Student's t-test for non-paired samples. A p-value of less than 0.05 was considered statistically significant.
The time-dependent effects regarding the incorporation of ALA-methylester and a resulting increase in EPA and DHA concentrations were investigated. For this purpose, Hep-G2 cells were incubated with 100 μM ALA-methylester over periods of 0 h, 6 h, 12 h, 24 h, 48 h and 72 h. Subsequently, dose response experiments were performed with ALA-methylester at concentrations of 10 μM, 100 μM and 1000 μM and an exposure time of 24 hrs. Highest incorporation of ALA methylester and the most pronounced increase in EPA and DHA were analyzed after a 24 h incubation period in the presence of 100 μM ALA-methylester (data not shown).
HepG2 cells were exposed to varying mixtures of [13C] labeled ALA and LA. Whereas the total concentration of LCPUFA administered was the same for all experiments (100 μM), the ratios of [13C]ALA to [13C]LA tested were 0:1, 1:1, 4:1, 9:1 and 1:0.
Total recoveries of [13C]LA and [13C]ALA as well as the amounts of [13C]EPA, [13C]DHA and [13C]AA at the different ratios of [13C]LA and [13C]ALA are given in Table 1.
Recovery of [13C]LA or [13C]ALA after exposure of HepG2 cells to [13C]LA-/[13C]ALA-methylester at ratios of 0:1, 1:1, 4:1, 9:1 and 1:0 for 24 hours. 1not detected, LOD: 0.13 ng/μl.
Cellular recovery of [13C]LA was highest (75.3 μmol or 74.6 μmol) in cells incubated with the mixture of a n6 to n3 ratio of 9:1 or with pure LA, respectively. Of the administered amount of [13C]LA, the highest percentage recovery as [13C]LA was detected in cells which were exposed to the mixtures of 4:1 (83%) or 9:1 (84%), respectively, whereas in cells exposed to the 1:1 mixture or to pure LA, merely 75% of the [13C]LA applied to the cells were recovered. The amount of [13C]AA quantified was highest in cells exposed to the mixtures at n6 to n3 ratios of 4:1 (5.7 μmol) or 9:1 (6.3 μmol), respectively (Table 1 and 2).
Quantification of [13C]AA, [13C]EPA and [13C]DHA after exposure of HepG2 cells to [13C] LA-/[13C]ALA-methylester at ratios of 0:1, 1:1, 4:1, 9:1 and 1:0 for 24 hours.
Of the recovered cellular amounts of [13C]LA, the amount of [13C]AA quantified was equally high in those cells which were incubated with [13C]LA/[13C]ALA at ratios of 1:1, 4:1 and 9:1, whereas treatment of the cells with pure [13C]LA resulted in a significantly lower content of [13C]AA (Fig. 1A). Total cellular recovery of [13C]LA ranging between 85 and 96% (data not shown) was calculated from the sum of quantified [13C]AA and [13C]LA in the cell culture medium and in the cells.
Percentage conversion of [ 13 C]LA and [ 13 C]ALA into [ 13 C]AA and [ 13 C]EPA/[ 13 C] after exposure of HepG2 cells to [ 13 C]LA-/[ 13 C]ALA-methylester at ratios of 0:1, 1:1, 4:1, 9:1 and 1:0. Data are expressed as mean ± SEM. Bars without a common letter are statistically significant different (*: p ≤ 0.05).
As well as incorporation of [13C]LA, effective incorporation of [13C]ALA increased with escalating amounts of administered [13C]ALA (Table 1). Percentage cellular recovery of [13C]ALA, relating to its administered amount, was 65% in cells which were exposed to pure ALA or to the mixture at a ratio of 1:1, and 69% in cells incubated with the 9:1 mixture. The highest recovery of [13C]ALA (82%) was documented in cells which were exposed o the 4:1 fatty acid mixture of [13C]LA and [13C]ALA.
The content of [13C]EPA also increased with ascending amounts of administered [13C]ALA and was the highest in cells exposed to pure [13C]ALA (10.8 μmol). On the other hand regarding cells which were exposed to mixtures of [13C]LA/[13C]ALA, the amount of [13C]DHA was highest (0.48 μmol) at a ratio of 1:1.
Of the recovered quantity of [13C]ALA, the content of [13C]EPA was highest in cells incubated with pure [13C]ALA and a mixture of [13C]LA/[13C]ALA at a ratio of 1:1 (Fig. 1B). In those cells, the amount of [13C]EPA in each case was 17% of the recovered quantity of [13C]ALA. Moreover, the highest percentage amount of DHA (0.7% of recovered [13C]ALA) was formed in cells incubated with [13C]LA/[13C]ALA at a ratio of 1:1.
Total recoveries of [13C]ALA (as a sum of cellular recovered [13C]ALA and [13C]EPA or [13C]DHA, respectively and the [13C]ALA remaining in the cell culture medium) ranged between 86% (0:1 and 1:1 mixture) and 97% (5:1 mixture) (data not shown).
Since enhanced amounts of [13C]EPA and [13C]DHA were detected in HepG2 cells after incubation with [13C]ALA, we wanted to investigate whether this conversion is associated with enhanced expression of genes encoding for proteins related to lipid metabolism. Therefore, HepG2 cells were incubated with 100 μM of ALA methylester for 3, 6, 12 and 24 hrs and the transcript levels of the genes encoding for D5D, D6D, PPARα, SREBP-1c, MEKK1 and MEK1 were determined via Real-time-PCR (Fig. 2). Maximum mRNA levels of the D5D and the D6D gene were detected after 3 and 6 hrs of cells' treatment. The mRNA levels of the genes encoding for nuclear receptor proteins PPARα and SREBP-1c were highest after an incubation period of 3 hrs. The quantity of mRNA of the kinases MEKK1-gene and MEK1-gene was the highest in those cells which were incubated with ALA-methylester for 3 and 12 hrs, respectively.
Kinetics experiments – relative mRNA levels of D5D, D6D, PPARα, SREBP-1c, MEKK1 and MEK1 after 24 hrs exposure of HEPG2 cells to ALA-methylester, relating to non-exposed control cells (mRNA levels set as 1). Data are expressed as mean ± SEM. Asterisks indicate a significant difference of the values compared to control cells (*: p ≤ 0.05 **: p ≤ 0.01, ***: p ≤ 0.001).
The kinetic experiments revealed that after 3 hrs of incubating HepG2 cells with 100 μM ALA methylester, the transcript levels of the investigated genes reached their maximum. At this point in time, a dose-response experiment was carried out in order to investigate the influence of different mixtures of LA/ALA on the mRNA levels of the genes encoding for D5D, D6D, PPARα, SREBP-1c, MEKK1 and MEK1 (Fig. 3).
Dose response experiments – relative mRNA levels of D5D, D6D, PPARα, SREBP-1c, MEKK1 and MEK1 after exposure of HEPG2 cells to LA-/ALA-methylester at ratios of 0:1, 1:0, 1:1 and 4:1, relating to non-exposed control cells (mRNA levels set as 1). Data are expressed as mean ± SEM. Asterisks indicate a significant difference of the values compared to control cells (**: p ≤ 0.01, ***: p ≤ 0.001).
Compared to non-exposed control cells, the transcript level of the MEKK1 gene was significantly increased in any of the experiments, with incubation of the cells with pure LA and the 4:1 mixture of LA-/ALA-methylester caused the most considerable effects. In contrast, the transcript level of the MEK1 gene was mainly affected by ALA and not by LA. With respect to the experiments in which HepG2 cells were exposed to pure ALA-methylester, an incubation of the cells with the 1:1 and 4:1 mixture of LA-/ALA-methylester induced a significant increase (up to 35%) of the mRNA level of the gene encoding for MEK1.
Transcript levels of genes encoding for PPARα and D5D, respectively, were only increased after exposure of HepG2 cells to pure ALA-methylester. Compared to non-exposed cells, mRNA levels of these genes were about 30–50% higher in cells that were incubated with pure ALA-methylester.
As well as PPARα and D5D, the transcript level of the SREBP 1c-gene was significantly increased after incubation with pure ALA-methylester. The relative mRNA level was about 75% higher than in non-exposed cells. Furthermore, an exposure of HepG2 cells to pure LA-methylester and the 1:1 mixture of LA-/ALA-methylester, respectively, caused a significant increase in SREBP-1c gene transcript levels of up to 30%.
In the here presented study, a human hepatoma cell line (HepG2) was used as a model system to investigate the impact of varying ratios of n6/n3 fatty acids on the conversion of alpha-linolenic acid to eicosapentaenoic acid and docosahexaenoic acid. After exposure of HepG2 cells to different ratios of [13C] labeled 18:2-n6 and 18:3-n3, those fatty acids were quantified in the cell matrix. Furthermore, conversion to the corresponding homologues was demonstrated. At this, rates of incorporation as well as the extent of conversion differed depending on the ratio of administered fatty acids.
Effective incorporated quantities of [13C]ALA as well as [13C]LA increased with increasing administered amounts of these fatty acids. Percentage quantities of cellular recovered [13C]LA or [13C]ALA, relating to the administered amount, however were lower in cells exposed to 100 μM of a single fatty acid ([13C]LA or [13C]ALA) than in cells exposed to mixtures of [13C]LA and [13C]ALA. We assume that these findings may result from a limited ability of the cells to incorporate PUFAs beyond a certain level.
A study of Robinson et al.  confirms this hypothesis. In this study, the modulating effect of dietary fish oil and of n3 fatty acid methylesters on spleen phospholipid fatty acid composition was investigated. Female NZB/W mice were fed diets containing 3.6 or 10% of EPA or DHA ethyl ester (EPA-E, DHA-E), respectively. EPA or DHA levels in phospholipids increased with increasing quantities of dietary EPA-E or DHA-E, respectively, but the total phospholipid n3 levels were highest in animals to which the lowest dose of EPA-E or DHA-E was administered. Furthermore, Venkatraman et al.  investigated the existence of a dietary maximum level for incorporation of n3 fatty acids into membrane phospholipids of weanling rats. In this study, animals were fed a diet which provided increasing amounts of C20 and C22 n3 fatty acids such as C20:5-n3 and C22:6-n3, and after 4 weeks of feeding, the fatty acid composition of membrane phospholipids of liver nuclear envelopes was analyzed. An increase in n3 dietary fatty acid administration from 1.1% to 5% of total fatty acids resulted in an increase in 20:5-n3 membrane phospholipid content. But further rise of dietary n3 fatty acids did not lead to an increased incorporation of 20:5-n3 into membrane phospholipids.
In addition to the incorporation, the administered fatty acids have also been converted to their longer chain homologues, as we could clearly demonstrate by using labeled [13C]LA and [13C]ALA. As well as rates of incorporation, the extent of conversion was affected by the ratio of administered fatty acids. Regarding the conversion of [13C]18:2-n6 to 20:4-n6, it was remarkable that the amount of AA formed was significantly lower in cells exposed to 100 μM [13C]LA than in cells which were incubated with mixtures of [13C]LA and [13C]ALA. However, when comparing the percentage rates of conversion of [13C]LA and [13C]ALA to AA and EPA/DHA, respectively, the conversion of [13C]ALA to EPA/DHA was higher than the conversion of [13C]LA to AA. This effect might be attributed to a differential effect of fatty acids of the n6 series and the n3 series on desaturase activity and/or gene expression. Since suppression of D5D and D6D activities by dietary unsaturated fatty acids was shown to be associated with decreased D5D and D6D mRNA levels [29, 30], we investigated whether these transcript levels were altered after 6 hrs of incubating the HepG2 cells with either LA and ALA or mixtures of both fatty acids.
Interestingly, exposure of HepG2 cells to 100 μM LA caused a marked (p < 0.001) increase of the transcript level of the D6D gene, whereas the exposure to 100 μM ALA did not alter the transcript levels of the D6D gene. In contrast, mRNA level of the gene encoding for D5D was significantly (p < 0.001) decreased only by exposure to 100 μM of pure LA, relating to non-exposed control cells. Administration of LA alone or as part of the mixture led to a strong decrease of the transcript level of the D5D gene, relating to non-exposed cells. Since both, Δ6- and Δ5-desaturation reactions, were shown to be rate-limiting for conversion of LA or ALA to their longer chain homologues, we assume that formation of 20:4-n6 in cells incubated with 100 μM LA was limited by reduced D5D gene expression.
Despite of high amounts of EPA formed in cells exposed to 100 μM [13C]ALA, conversion to DHA was significantly (p < 0.001) lower in those cells compared to cells incubated with lower doses of [13C]ALA in the form of [13C]LA/[13C]ALA mixtures.
Similar results regarding the conversion of EPA to DHA were described by Robinson et al. . After feeding diets containing 3%, 6% or 10% of EPA ethyl ester (EPA-E) to female mice there were no increases in spleen phospholipid DHA levels in animals fed either the 10% or the 6% EPA-E diet. Only administration of the 3% EPA-E diet was associated with an elevation of DHA levels in phospholipids. According to these findings, we assume that administration of n3 PUFAs beyond a certain level suppresses formation of DHA from EPA. However, the general extent of conversion from ALA to EPA and DHA in men was reported to be about 8% for EPA and less than 0.05% for DHA . The conversion rates in our experiments were about 16% for EPA and about 0.7% for DHA, after incubation of the cells with an [13C]LA/[13C]ALA mixture of 1:1. This result gives rise to the possibility of shifting the conversion of ALA to EPA and DHA to higher rates by adjustment of the ratio of n6/n3 fatty acids.
Since the total recovery (calculated by addition of total cellular recovery and recovery within cell culture medium) of the administered fatty acids was below 100%, it seems likely that oxidation of LA and ALA also took place since both fatty acids are known to be substrates for β-oxidation. This hypothesis of partial degradation of [13C]LA and [13C]ALA via β-oxidation in our experiments is supported by results by a study of Mayes et al. , who administered [13C] labeled ALA to preterm infants. Appearance of 13CO2 in breath, which was determined as a marker of ALA partitioning towards β-oxidation, ranged from 7.6 to 19%. In our experiments, the amount of non-recovered [13C]ALA or [13C]LA ranged between 3 and 14%, respectively. Therefore, we assume that this portion of [13C]ALA or [13C]LA was used for β-oxidation since, in addition, molecular masses of non-enzymatically generated oxidation products were not detected by HRGC-CI/-MS (data not shown).
Generally, genes of fatty acid oxidation are induced by the peroxisome proliferators-activated receptor alpha (PPARα). Furthermore, fatty acids such as alpha-linolenic acid are considered natural ligands of PPARα because they were shown to bind and activate PPARα in vitro .
The administration of 100 μM pure ALA alone effectuated a marked induction of PPARα (p < 0.001) in our experiments. Also, total recovery of [13C]ALA in cells exposed to pure [13C]ALA was considerably lower, compared to cells incubated with any of the mixtures of [13C]LA and [13C]ALA. Hence, we presume that [13C]ALA was preferentially used as substrate for PPARα-mediated β-oxidation in cells incubated with pure [13C]ALA. However, the amount of 13CO2 was not analyzed in this experiment.
The transcription factor SREBP-1c plays a pivotal role in the dietary regulation of most hepatic lipogenic genes , including the expression of D5D and D6D  and its primary role is assumed to be the regulation of highly polyunsaturated fatty (PUFA) acid supply for membrane phospholipids . Expression of SREBP-1c genes was shown to be down-regulated by dietary PUFA . In contrast to this, the here presented results demonstrate that, after 3 hrs of exposure time, the transcript level of SREBP-1c gene was significantly (p < 0.001) induced by exposition of HepG2 cells to LA or ALA at a concentration of 100 μM and the mixture of LA and ALA at a ratio of 1:1, respectively. This result may imply a dose and time dependent SREBP-1c gene regulation which has to be proven in future studies.
Besides SREBP-1c, peroxisome proliferators such as alpha-linolenic acid paradoxically are identified as activators of D6D and probably D5D gene transcription [11–13]. He et al.  hypothesized hat this up-regulation of gene transcription might be a compensatory response to increased demand in PUFAs caused by induction of fatty acid oxidation.
An intracellular activation of the mitogen-activated (MAP) kinase cascade by ectopic expression of these upstream activators had a direct stimulatory effect on the transcriptional activity of SREBP-1c via phosphorylation of MAP kinases ERK1 and ERK2 . Hence, PPARα is also reported as a substrate for several kinases such as ERK1 and ERK2 [14, 35], in addition to ligand-induced regulation, transcriptional activity of PPARα may increase via phosphorylation of certain domains of the receptor protein . In this work, the transcript levels of the MEKK1 and MEK1 genes were markedly (p < 0.001) increased after the cells' exposure to LA, ALA or mixtures of both. In clear contrast to the transcript level of MEKK1 gene, the transcript levels of the MEK1 gene were lower, the higher the LA-content in the mixture was. However, we did not measure an activation of the transcriptional activities of either PPARα or SREBP-1c via MAP kinase phosphorylation. But the enhanced transcript level could indicate an induction of the respective pathway, which may has led to the observed induction of D6D and D5D. Further investigations with regard to receptor-ligand-binding and state of phosphorylation of PPARα or SREBP-1c receptor proteins in the presence of defined ration of n6/n3 PUFAs are necessary to elucidate the mechanisms of gene expression.
Our investigations show that exposure of human hepatocytes to different mixtures of LA and ALA affected transcript levels of a portfolio of genes encoding regulating proteins involved in several stages of fatty acid metabolism. This effect strongly depends on the ratio of n6/n3 fatty acids, indicating the importance of ingesting an appropriate amount of fatty acids, but also an appropriate ratio of n6 and n3 fatty acids. This is further confirmed by the fact that maximum conversion of LA to AA was measured only in the presence of ALA. Omitting ALA seems to result in higher oxidation rates as indicated by high transcript levels of PPARα. Additionally, the n6/n3 ratio strongly influenced the elongation of ALA to EPA and DHA as well as the transcript levels of D5D and D6D.
However, from a nutritional perspective, our findings suggest that a diet-induced enhancement of the cell membrane content of highly unsaturated fatty acids is only possible up to a certain level. Increasing the administered quantity of labeled alpha-linolenic acid resulted in a reduced effectiveness of [13C]ALA incorporation. Percentage incorporation of [13C]ALA was maximal after exposure of [13C]LA/[13C]ALA at a ratio of 4:1 to HepG2 cells.
With regard to the elongation of ALA to EPA and DHA, our results clearly indicate the efficiency of altering the dietary ratio of LA to ALA in favor of ALA by increasing the concentration of n3 fatty acids in human hepatocytes. At this, administration of LA/ALA at a ratio of 1:1 led to the highest formation of LCPUFAs of the n3 series.
The present study was supported by the Federal Ministry of Education and Research (BMBF-0313637E).
KH and GA performed the analysis of the biochemical data, participated in the interpretation of the results and helped draft the manuscript. VS designed the study and assisted with data interpretation and manuscript preparation.


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Biography – ARMSTRONG, CHARLES JOHNSTONE – Volume XVI (1931-1940) – Dictionary of Canadian Biography
Source: Library and Archives Canada/MIKAN
ARMSTRONG, Charles Johnstone, engineer and militia and army officer; b. 27 Aug. 1872 in Montreal, son of Charles Newhouse Armstrong and Amelia Frances Johnstone; m. 19 April 1913 Flora Macdonald Grant Kittson in Ottawa; they had no children; d. 23 Jan. 1934 in Montreal and was buried in Mount Royal Cemetery in Outremont (Montreal).
Charles Johnstone Armstrong attended the High School of Montreal before going to the Royal Military College of Canada (RMC) in Kingston, Ont., in 1889. As cadet No.293, he graduated company sergeant-major in 1893. Three of his brothers would also study at the college. On 18 May 1894 Armstrong was commissioned a second lieutenant in the 5th Battalion of Infantry (Royal Scots of Canada), a fashionable militia unit in Montreal. The following year he was promoted lieutenant. In civilian life he became an engineer, having studied engineering at RMC, where it formed an important part of the curriculum. He probably worked with his father, a railway promoter and contractor as well as the manager of the Atlantic and Lake Superior Railway.
At the outbreak of the South African War in 1899 Armstrong volunteered for service with Canada's first contingent, and he was accepted as a lieutenant in the 2nd (Special Service) Battalion, Royal Canadian Regiment of Infantry. One of the three officers in E Company, which was recruited from the Montreal area, he embarked on 30 October for South Africa. He took part in the battle of Paardeberg, and during the final assault on 27 Feb. 1900 he was slightly wounded in the thigh. He continued the advance with his battalion through the first half of the year, seeing action at Poplar Grove, Houtnek, Zand River, Johannesburg, and Pretoria (Tshwane). After his battalion returned to Canada he remained in South Africa; from July 1900 to May 1902 he served on the staff of the Imperial Military Railways under the direction of another Canadian, Édouard Percy Cranwill Girouard. When the war ended he became divisional engineer of the Central South African Railways, the civilian organization set up to administer the same lines, and he held the position until 1910, when he went back to Canada and joined Sir John Jackson Limited, a firm of railway builders and contractors. Since 1899 Armstrong had remained an absentee officer on the strength of the 5th Regiment (Royal Highlanders of Canada), as the unit had become known. He was promoted brevet captain in 1900 and a substantive captain in 1905, and he was listed in the corps reserve.
At the outbreak of the First World War, Armstrong, like so many other militia officers, offered his services to the Department of Militia and Defence, suggesting that he raise a corps of pioneers or of construction troops. Instead, he was appointed to the command of the proposed Divisional Engineers then assembling at Valcartier, Que. At age 42, his hair now grey, he was commissioned a brevet lieutenant-colonel in the Canadian Expeditionary Force on 5 Sept. 1914, and took charge of the 28 officers and 855 troops who had been selected for overseas service. Organized into a headquarters, two field companies, and a signal company, with a third field company added just before the men sailed, Armstrong's engineers embarked for England on 28 September. On arrival his first duty was to supervise the erection of the huts being built for the Canadians on Salisbury Plain by his former employer, Sir John Jackson Limited.
Armstrong went to France as chief engineer of the 1st Canadian Division on 7 April 1915. His responsibilities expanded rapidly over the following year. He was the senior engineering officer when the division fought its first major engagement, the second battle of Ypres, in April–May 1915, and he participated in the subsequent attacks at Festubert and Givenchy-lez-La Bassée. Trench warfare made ever-increasing demands on the engineers and resulted in the deployment of such novel units as tunnelling companies and tramway troops, who became part of the chief engineer's responsibilities. When the 2nd Canadian Division arrived in France in mid September, the Canadian Corps was formed and Armstrong moved up the ranks to command the corps engineers as a temporary brigadier-general from 13 September. He had been mentioned in dispatches in June 1915 and appeared again in January 1916, when he was also awarded a cmg.
On 29 Feb. 1916, while Armstrong was carrying out the reconnaissance of a bridge near Bernay in northern France, his train was struck from behind by another and he was seriously hurt. His left leg was badly broken, 14 teeth were knocked out along with part of his upper jaw, and he sustained other injuries to his head and shoulders. A long, difficult recovery followed, initially at a French hospital in Bernay, then at No.2 Red Cross Hospital in Rouen, and from April 1917 to October 1917 at hospitals in England. He suffered through pneumonia and pleurisy while at Bernay. The leg wound became septic and the fracture, which required two operations in 1916, took time to heal. More surgery in England extracted pieces of broken bone and tooth from his jaw. Not until 16 Jan. 1918, nearly two years after the accident, did he return to the front. He would carry the effects of the injuries for the rest of his life.
In February Armstrong was back in France. William Bethune Lindsay had taken over for him as brigadier-general on 7 March 1916, and Armstrong, now chief engineer on defences, was employed by the engineer-in-chief at the general headquarters of the British Expeditionary Force. The Germans made their last great offensive the following month. When the 5th British Army front threatened to collapse, he helped to put together an ad hoc force of British, American, and Canadian engineers and other specialist troops to hold the line as infantry.
From 4 Nov. 1918 to March 1919 Armstrong was chief engineer of the British VII Corps in France, tasked with the repair and reconstruction of all canals in France and Belgium devastated by the war. He returned to England on 6 March and to Canada on 14 June. He had received further honours, being again mentioned in dispatches in December 1918 and awarded a cb in January 1919. Two others followed: the Military Order of Aviz from the Portuguese in October 1919 and the Ordre de la Couronne from the Belgians in May 1920.
Once back in Canada Armstrong was employed as a full-time staff officer within the Department of Militia and Defence (from 1923 the Department of National Defence). On 28 June 1919 he became the district officer commanding of Military District No.4, with headquarters in Montreal. He ranked as a colonel, but because of his wartime service he was allowed to wear the insignia of an honorary brigadier-general. On 1 June 1921 he became a temporary colonel commandant, a short-lived rank in the militia reserved for those in charge of military districts. In this role, he undertook to reconstitute the militia regiments of the Montreal area on a peacetime footing. He was also active as chairman of a committee of the Royal Military College Club of Canada that oversaw the construction of the Memorial Arch at the front of the college grounds. It was unveiled on 15 June 1924.
In October 1926 Armstrong became the district officer commanding of Military District No.1, with headquarters in London, Ont. In July two years later he was promoted temporary brigadier, when the rank of colonel commandant was eliminated. He received two more awards: the Colonial Auxiliary Forces Officers' Decoration and the Volunteer Officers' Decoration.
Armstrong retired in 1933 and was promoted major-general on the retired list. While at his summer home in Carillon (Saint-André-d'Argenteuil), Que., he fell ill, and he died in a Montreal hospital at age 61. His funeral, from Christ Church Cathedral, was a major military event. The cortège stretched for more than four city blocks.
Charles Johnstone Armstrong's army career occurred during a coming of age for the Canadian military establishment. Despite his studies at RMC he initially had had to earn his living as a civilian, and his appointment in 1914 seems to have owed more to his militia connections than to demonstrated military engineering or administrative skills. Yet his achievements were close to the upper limits of what was possible for a Canadian officer at the time, and he was able to carve out a lifetime military career within the expanding, but still small, Canadian militia.
Owen A. Cooke
AO, RG 80-5-0-613, no.2169. BANQ-CAM, CE601-S63, 5 oct. 1872. LAC, R180-76-5, box 225-10. Gazette (Montreal), 28 Aug. 1872; 22 April 1913; 22, 23, 24, 25, 26, 27 Jan. 1934. London Gazette, November 1915–April 1919. Can., Dept. of Militia and Defence, Militia list (Ottawa), 1895–1929; Dept. of National Defence, Defence forces list, Canada (naval, military and air forces) (Ottawa), 1930–33. Directory, Montreal, 1895–1934. A. J. Kerry and W. A. McDill, The history of the Corps of Royal Canadian Engineers (2v., Ottawa, 1962–66), 1. [Minutes of annual meeting of the Royal Military College Club of Canada., 8 April 1924], Royal Military College of Can., Rev. ([Kingston, Ont.]) (May 1924): 75–77. [Minutes of annual meeting of the Royal Military College Club of Canada., 28 Feb. 1925], Royal Military College of Can., Rev. (May 1925). "No. 293, Major-General Charles Johnstone Armstrong, c.b., c.m.g.," Royal Military College of Can., Rev. (June 1934): 93–94. "No. 376, Frederick Percy Armstrong," Royal Military College of Can., Rev. (December 1934): 64. G. R. Stevens, Canadian National Railways (2v., Toronto and Vancouver, 1960–62).
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GIROUARD, Sir ÉDOUARD PERCY CRANWILL (Vol. 16)
GIROUARD, Sir ÉDOUARD PERCY CRANWILL
Owen A. Cooke, "ARMSTRONG, CHARLES JOHNSTONE," in Dictionary of Canadian Biography, vol. 16, University of Toronto/Université Laval, 2003–, accessed February 2, 2023, http://www.biographi.ca/en/bio/armstrong_charles_johnstone_16E.html.
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Author of Article: Owen A. Cooke
Title of Article: ARMSTRONG, CHARLES JOHNSTONE
Publication Name: Dictionary of Canadian Biography, vol. 16