Summer 2019 transfer thread

[sammyspurs]

Trippier was absolutely not first choice in our third and second place seasons of 17/16 and 16/17 respectively.

Don’t know what you mean with your seasons.
16/17 he played the last months of the season and we finished 2nd so he was clearly not a step down from Walker.

17/18 he played 24 PL, 6 FA Cup, 3 CL and 2 Carabou cups.

Mind telling me who was first choice RB that season then?

 

[Incomplete_usernam]

Everyone knows it's Omega3 and Bacteria based now... But stress will definitely strain the adrenals and set the scene.

H.Pylori, for example, is demonstrated to be regulated down by ALA and L.Plantarum, deep stuff.

"Physiological functions of CLA and HYA. CLA and HYA are produced from linoleic acid by intestinal bacteria. c9,t11-CLA ameliorates insulin sensitivity and prevents atherosclerosis, t10,c12-CLA deteriorates insulin sensitivity and promotes atherosclerosis, and t9,t11-CLA prevents atherosclerosis. HYA enhances intestinal barrier function by increasing occludin expression and inhibiting intestinal inflammation in a GPR40-dependent manner. HYA inhibits atopic dermatitis by increasing claudin-1 expression and enhancing skin barrier function. HYA also inhibits gastric Helicobacter infections by blocking the bacterial futalosine pathways. "

Host- and Microbe-Dependent Dietary Lipid Metabolism in the Control of Allergy, Inflammation, and Immunity – Choose Life

chooselife.co.uk

Not deep enough and wrong in conclusion = https://www.researchgate.net/public...ogical_factors_of_duodenal_and_gastric_ulcers

"The most common cause of duodenal and gastric ulcer was Helicobacter pylori, and it was responsible for three-fourths of the cases. About half of the patients had a history of nonsteroidal antiinflammatory drug use, and nonsteroidal antiinflammatory drug and Helicobacter pylori were both responsible for the ulcer in three-fourths of these patients. In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic. "

Given the above, you can see the H.Pylori blaming is foolish, dated thinking. Trigger yes, cause no. Béchamp looking pretty smug nowadays, to me.

(Bored on nights)

You're Lemon from SC aren't you? Did you get banned or something? lol.

 

[Incomplete_usernam]

So I can understand where you're coming from, could you tell me what you want?

 

[Zest]

You're Lemon from SC aren't you? Did you get banned or something? lol.

I posted a load of Flax seed based scientific studies in Random, just scientific studies, was told it could be construed that I was giving medical advice, crock of shit but their choice.

Here are some of the studies I posted = Flax – Choose Life

 

[todd1882]

Everyone knows it's Omega3 and Bacteria based now... But stress will definitely strain the adrenals and set the scene.

H.Pylori, for example, is demonstrated to be regulated down by ALA and L.Plantarum, deep stuff.

"Physiological functions of CLA and HYA. CLA and HYA are produced from linoleic acid by intestinal bacteria. c9,t11-CLA ameliorates insulin sensitivity and prevents atherosclerosis, t10,c12-CLA deteriorates insulin sensitivity and promotes atherosclerosis, and t9,t11-CLA prevents atherosclerosis. HYA enhances intestinal barrier function by increasing occludin expression and inhibiting intestinal inflammation in a GPR40-dependent manner. HYA inhibits atopic dermatitis by increasing claudin-1 expression and enhancing skin barrier function. HYA also inhibits gastric Helicobacter infections by blocking the bacterial futalosine pathways. "

Host- and Microbe-Dependent Dietary Lipid Metabolism in the Control of Allergy, Inflammation, and Immunity – Choose Life

chooselife.co.uk

Not deep enough and wrong in conclusion = https://www.researchgate.net/public...ogical_factors_of_duodenal_and_gastric_ulcers

"The most common cause of duodenal and gastric ulcer was Helicobacter pylori, and it was responsible for three-fourths of the cases. About half of the patients had a history of nonsteroidal antiinflammatory drug use, and nonsteroidal antiinflammatory drug and Helicobacter pylori were both responsible for the ulcer in three-fourths of these patients. In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic. "

Given the above, you can see the H.Pylori blaming is foolish, dated thinking.

I don't know exactly what your background is but if you were ever in some sort of research you would know the folly and futility of pulling 1 study to support one's assertion. One study does not make science (not even commenting on the results of this particular study as they are not germane to my point here).

Given that H pylori is the most common etiological agent that is where you start. When you hear hoofbeats think horse not zebra.

Everyone knows it's Omega3 and Bacteria based now

Don't really know what to do with this. It's been H pylori for like 30 years and IDK why you are implicating Omega 3 fatty acids.

EDIT: looks like you've edited a bit. Let's see how these match up now.

 

[Hotspurpaul]

There 'is' still hope for you in this world.... Possibly.

You obviously haven't got an answer to the question, so you keep on this merry go round of calling me thick to get out of it. I'll leave it there then if you can't answer and bow to the superior knowledge of the forums very own Stephen Hawking.

 

[Zest]

I don't know exactly what your background is but if you were ever in some sort of research you would know the folly and futility of pulling 1 study to support one's assertion. One study does not make science (not even commenting on the results of this particular study as they are not germane to my point here).

Given that H pylori is the most common etiological agent that is where you start. When you hear hoofbeats think horse not zebra.


Don't really know what to do with this. It's been H pylori for like 30 years and IDK why you are implicating Omega 3 fatty acids.

EDIT: looks like you've edited a bit. Let's see how these match up now.

"HYA also inhibits gastric Helicobacter infections by blocking the bacterial futalosine pathways. "

N6 is actually what the body converts into HYA = 10-hydroxy-cis-12-octadecenoic acid.

If you are medical, of course you will look at H.Pylori, but looking at it from a biochemistry viewpoint it is further back along the regulatory chain which makes the host susceptible, or as I see it the real cause.

I'm a very, very amateur scientist (emphasis very, very)...

Edit : Fledgling research areas, but here are some further:

Supplemental feeding of a gut microbial metabolite of linoleic acid, 10-hydroxy-cis-12-octadecenoic acid (HYA), alleviates spontaneous atopic dermatitis and modulates intestinal microbiota in NC/nga mice.

https://www.tandfonline.com/doi/abs/10.1080/09637486.2017.1318116?journalCode=iijf20

Japan leading on this stuff it seems.

More:

Highlights

• A gut microbial metabolite of linoleic acid (HYA) elicits anti-inflammatory effects in vitro

.• HYA down-regulates the Lipopolysaccharide-induced maturation of bone marrow dendritic cells (DCs).

• HYA treatment associated with an anti-inflammatory profile in murine enterocyte and in mature DCs.

• HYA up-regulates cytoprotections in murine enterocyte and in mature DCs.

• HYA is considered a functional component in foods and pharmaceutical products.

Immunomodulatory activity of a gut microbial metabolite of dietary linoleic acid, 10-hydroxy-cis-12-octadecenoic acid, associated with improved antioxidant/detoxifying defences

Various hydroxy-, oxo-, and conjugated fatty acids are generated by gut microbes throughout the metabolism of dietary PUFAs. Specifically, 10-Hydroxy-…

www.sciencedirect.com

Anyway, hope NDombele has a good dietary lipid profile...

 

[Thin Lilywhite Duke]

Don’t know what you mean with your seasons.
16/17 he played the last months of the and we finished 2nd so he was clearly not a step down from Walker.

17/18 he played 24 PL, 6 FA Cup, 3 CL and 2 Carabou cups.

Mind telling me who was first choice RB that season then?

Apologies - I mistyped and meant 15/16 (and 16/17).

As for Trippier apparently playing the last months of that 16/17 season, here's a list of the final 17 Premier League games of that year and the starting RB/RWB...

Man City - Walker
Sunderland -Walker
Middlesborough - Walker
Liverpool - Walker
Stoke - Walker
Everton - Walker
Southampton - Walker
Burnley - Trippier
Swansea - Walker
Watford - Trippier
Bournemouth - Walker
Palace - Walker
Woolwich - Trippier
West Ham – Walker
United - Trippier
Leicester - Sissoko
Hull - Trippier

It took until April 1st for Trippier to take any foothold as our starting right back, probably in no small part because by that point we didn't have many cup games to use him. Even then, they still alternated - 5 Trippier starts to Walker's 4 and bloody Sissoko ended up being wheeled out as a RWB against Leicester.

According to Poch's book, it was after the Watford game that Walker came to him and asked to leave. Again, this makes me very unsure as to what exactly the motivation was over team selection at RB from that point on. My best bet is rotation for fitness with Trippier getting the more prestigious games.

Regardless, our best performing league season - that of 16/17 - came with Walker as our clear first choice RB and it's erroneous to use that 2nd place finish as any justification as to why Trippier is good enough.

 

[Nabil Bentaleb]

Trippier is worst than Toby from the office. There I said it

 

[Yorkshire Yid]

I haven't seen it reported anywhere that we need to sell to spend £60m?!?

Looking our our financials for the past 2-3 years, along with the debt levels and speculated pay back time I think it's evident that we definitely have at least that to spend without being reliant on outgoings IMO. Where did this £60m but need to sell before we buy come from pal?

I was replying to someone who said it seems like we need to sell before paying fees. I to agree we should have at least 100 to spend without any outgoings. Stadium is financed and the payments structured in a safe manner by all accounts. It shouldnt be effecting our transfers

 

[todd1882]

"HYA also inhibits gastric Helicobacter infections by blocking the bacterial futalosine pathways. "

N6 is actually what the body converts into HYA = 10-hydroxy-cis-12-octadecenoic acid.

What does this have to do with anything? I asked about the implication of Omega 3s. N6 would be for Omega 6s. And thus if you are suggesting that since an N6 inhibits (probably in vitro) these things then N3s must be bad? But even taking this as 'fact' for now that wouldn't support the statement that Omega 3s are an etiological agent. ie if one thing is protective it doesn't automatically mean the other detrimental. And to claim that something is an etiological agent then by definition it has to be detrimental. And again, I would like to add that this looks to all have been done IN VITRO and 1 study. If you only knew how many types of cancer I 'cured' in cell culture by soaking them in different eicosanoids you would be amazed...except that every grad student in the biomedical sciences has done similar. None of this actually means anything in vivo and it's a far cry from being accepted scientific fact to suggest etiology.

If you are medical, of course you will look at H.Pylori, but looking at it from a biochemistry viewpoint it is further back along the regulatory chain which makes the host susceptible, or as I see it the real cause.

This is not how anyone would do this in a disease state situation. How is it do you think someone gets H pylori in their gut?

I'm a very, very amateur scientist (emphasis very, very)...

Actually the jig was up when you capitalized the 'p' in pylori. The use of individual studies from questionable journals was just confirmatory. You'd be surprised what gets published and why. Quite frequently things get published because they are the first to do it/demonstrate a certain thing. That thing may not be useful or further science much but the important thing is that now it is 'known'. In the publish or perish world of big academia there is a lot of noise to sift through to get to the real science.

 

[bus-conductor]

'Poch's own words'. Disputed by Walker, interestingly (I'm not necessarily saying that Walker is the correct party). It's not outside the realms of possibility that Trippier's promotion was based on Poch's upset with Walker rather than being a decision based on quality.

Midfielders are key, I wouldn't disagree, but we did achieve better with Rose and Walker on the pitch than with Trippier as our starter. Aside from improving markedly in the CL (possibly with more and more experience in the competition) we've regressed over the last two years.

Will sorting the midfield out help that? Of course.

Would sorting our full backs help further? I'm sure of it.

But we didn't achieve better with Walker/Rose. Our results with Trippier were 2nd in 16/17 (played the latter 3rd of the season and we absolutely smashed everyone, same/better results - I'm pretty sure - than first 2/3rds). 3rd in 17/18 (equaling the 3rd in 15/16 with Walker/Rose) and 4th in 18/19 beating the 5th in 14/15 with Walker/Rose. And in 13/14 we were 6th, 12/13 5th.

In reality, it's much to over simplistic to try and attribute a set of results to one particular player, but there is unequivocally no evidence in terms of results and league position or even cup success, that supports your theory. And to further support that, Trippier's offensive stats - chances created and assists etc - absolutely smash Walker's out the park. In 16/17 he bettered Walker's in a third of the pitch time and didn't cost us anything defensively at all.

It's evident to me that the gradual deterioration of "us" and the weakest link is down to deterioration of our midfield. It improved when we replaced Dier with Wanyama and paired him with a fit and firing Dembele, then both Wanyama and Dembele degrade and disappear - and our performances decline. To the point where we end up with a kid who's had 8 league starts in two years before this season, and even he can't stay fit, a failed AM with the technical dexterity of rhino on mogodon, Wanyama in his wheelchair with star turns from our two 10's.


1. Midfield. Midfield. Midfield.
.
.
.
.
2. Composure final third
.
.
.
.
.
.
3. RB and LB

 

[Claud601]

This squad has so much muck to unload I’m realizing what levy is seeing. It’s going to a long summer

 

[pleb]

I was replying to someone who said it seems like we need to sell before paying fees. I to agree we should have at least 100 to spend without any outgoings. Stadium is financed and the payments structured in a safe manager by all accounts. It shouldnt be effect our transfers

Good post-We will get two players and have to sell at least 3 players to fund 2-3 more in-comings, projected total of new players 5-6!

 

[Zest]

What does this have to do with anything? I asked about the implication of Omega 3s. N6 would be for Omega 6s. And thus if you are suggesting that since an N6 inhibits (probably in vitro) these things then N3s must be bad? But even taking this as 'fact' for now that wouldn't support the statement that Omega 3s are an etiological agent. ie if one thing is protective it doesn't automatically mean the other detrimental. And to claim that something is an etiological agent then by definition it has to be detrimental. And again, I would like to add that this looks to all have been done IN VITRO and 1 study. If you only knew how many types of cancer I 'cured' in cell culture by soaking them in different eicosanoids you would be amazed...except that every grad student in the biomedical sciences has done similar. None of this actually means anything in vivo and it's a far cry from being accepted scientific fact to suggest etiology.


This is not how anyone would do this in a disease state situation. How is it do you think someone gets H pylori in their gut?


Actually the jig was up when you capitalized the 'p' in pylori. The use of individual studies from questionable journals was just confirmatory. You'd be surprised what gets published and why. Quite frequently things get published because they are the first to do it/demonstrate a certain thing. That thing may not be useful or further science much but the important thing is that now it is 'known'. In the publish or perish world of big academia there is a lot of noise to sift through to get to the real science.

Got a bit defensive at the end, it's not one study and not my fault you are not aware of this emerging field of research. It's a really solid collation of studies, think you are being mean spirited towards it.

I edited the original post to say Omega3/6 (as that paricular point in that study was N6, but they are a tandem as I am sure you are aware, but it is not as simple as N3 good, N6 bad.

I've worked with a Nobel winner, on their prize winning work, as it happens, not that it makes me any more informed than anyone else on these new study areas.

Next you'll be saying the terrain pH doesn't matter either...

Here is further proof this is a solid study area:

However, we identified an alternative pathway, the futalosine pathway, operating in some microorganisms including Helicobacter pylori and Campylobacter jejuni, which cause gastric carcinoma and diarrhea, respectively. Because some useful intestinal bacteria, such as lactobacilli, use the canonical pathway, the futalosine pathway is an attractive target for development of chemotherapeutics for the abovementioned pathogens. In this mini-review, we summarize compounds that inhibit Mqn enzymes involved in the futalosine pathway discovered to date.

...

Polyunsaturated fatty acids (PUFAs) and siamycin
Matsui et al. screened for specific inhibitors of the futalosine pathway in culture broth samples of 6183 microbes including 2160 fungi, 3783 actinomycetes, and 240 lactobacilli. They employed a paper disk method using two indicator microorganisms, B. halodurans C-125 (the futalosine pathway) and B. subtilis H17 (the canonical pathway). Isolation and structural elucidation of active compounds from screening hits revealed that ω-3 and ω-6 PUFAs, including α-linoleic acid, γ-linoleic acid, arachidonic acid, eicosapentaenoic acid (EPA, 20), and docosahexaenoic acid (DHA, 21), as well as, siamycin I (22), a lasso peptide natural product, specifically inhibited the futalosine pathway [28]. They next showed that compounds 20–22 suppressed the growth of H. pylori strains SS1 and TN2GF4 in a dose-dependent manner. They also evaluated the effect of these compounds using a mouse model of H. pyloriinfection. Treatment of mice with EPA (30 μg/ml), DHA (30 μg/ml), or siamycin I (5 μg/ml) in drinking water significantly reduced the colonization of H. pylori by 96, 78, and 68%, respectively.

Searching for potent and specific antibiotics against pathogenic Helicobacter and Campylobacter strains - Journal of Industrial Microbiology & Biotechnology

Menaquinone is an obligatory component of the electron-transfer pathway in microorganisms. Its biosynthetic pathway was established by pioneering studies with Escherichia coli and it was revealed to be derived from chorismate by Men enzymes. However, we identified an alternative pathway, the...

link.springer.com

Actually EPA (N3), beats the absolute crap out of it (96% colonisation reduction) It's cool stuff.

I love learning on these posts, thanks Todd.

Sorry todd

Edit 2 : Actually this data is in the originally posted collation study :

Furthermore, HYA prevents Helicobacter infections by blocking their futalosine pathways, which is an alternative menaquinone biosynthetic pathway and an essential metabolic pathway for the growth of Helicobacter. Moreover, HYA treatment suppresses the formation of lymphoid follicles in the gastric mucus layer after H. suis infection, and therefore HYA treatment protects mice against the formation of gastric mucosa-associated lymphoid tissue lymphoma induced by infection with Helicobacter (74).

 

[5purs]

OK, so I've read back. You want Levy to compete with Manchester City and Liverpool in the transfer window to win trophies. If they're not willing to do that thwn they can sell up to someone who will.

Right?

 

[Thin Lilywhite Duke]

But we didn't achieve better with Walker/Rose. Our results with Trippier were 2nd in 16/17 (played the latter 3rd of the season and we absolutely smashed everyone, same/better results - I'm pretty sure - than first 2/3rds). 3rd in 17/18 (equaling the 3rd in 15/16 with Walker/Rose) and 4th in 18/19 beating the 5th in 14/15 with Walker/Rose. And in 13/14 we were 6th, 12/13 5th.

See my post here:

Apologies - I mistyped and meant 15/16 (and 16/17).

As for Trippier apparently playing the last months of that 16/17 season, here's a list of the final 17 Premier League games of that year and the starting RB/RWB...

Man City - Walker
Sunderland -Walker
Middlesborough - Walker
Liverpool - Walker
Stoke - Walker
Everton - Walker
Southampton - Walker
Burnley - Trippier
Swansea - Walker
Watford - Trippier
Bournemouth - Walker
Palace - Walker
Woolwich - Trippier
West Ham – Walker
United - Trippier
Leicester - Sissoko
Hull - Trippier

It took until April 1st for Trippier to take any foothold as our starting right back, probably in no small part because by that point we didn't have many cup games to use him. Even then, they still alternated - 5 Trippier starts to Walker's 4 and bloody Sissoko ended up being wheeled out as a RWB against Leicester.

According to Poch's book, it was after the Watford game that Walker came to him and asked to leave. Again, this makes me very unsure as to what exactly the motivation was over team selection at RB from that point on. My best bet is rotation for fitness with Trippier getting the more prestigious games.

Regardless, our best performing league season - that of 16/17 - came with Walker as our clear first choice RB and it's erroneous to use that 2nd place finish as any justification as to why Trippier is good enough.

Trippier did not 'play the latter third of the season', he started 5 PL games out of 10 during the run in. I absolutely will not credit him for that 2nd place finish. Walker was our first choice for the vast majority of games.

In reality, it's much to over simplistic to try and attribute a set of results to one particular player, but there is unequivocally no evidence in terms of results and league position or even cup success, that supports your theory. And to further support that, Trippier's offensive stats - chances created and assists etc - absolutely smash Walker's out the park. In 16/17 he bettered Walker's in a third of the pitch time and didn't cost us anything defensively at all.

Except for that 2nd place finish where Trippier only made 12 league appearances (including substitute appearances). Whoops.

And yes, while 17/18's third placed finish did match that of 15/16, it was regression from our peak during 16/17. I'm no fool, I wouldn't attribute it to one player. Along with the upheaval of the stadium build and issues in midfield, I see our deterioration at full back as a contributing factor.

But hey, you see, I agree with you that we need to upgrade midfield...

It's evident to me that the gradual deterioration of "us" and the weakest link is down to deterioration of our midfield. It improved when we replaced Dier with Wanyama and paired him with a fit and firing Dembele, then both Wanyama and Dembele degrade and disappear - and our performances decline. To the point where we end up with a kid who's had 8 league starts in two years before this season, and even he can't stay fit, a failed AM with the technical dexterity of rhino on mogodon, Wanyama in his wheelchair with star turns from our two 10's.

Why the fuck else do you think I'm hanging my liver out for Ndombele? Regardless of CM being priority over RB, the latter can still be discussed.

I really don't get this defence of Trippier, to be quite honest. People are waxing lyrical about him as if Man City could have picked him over Walker. Bollocks would they. The guy can whip in a nice cross (explaining your assist stat from before), but his defensive mistakes this season have been fucking dreadful at times - and this is from a 28 year old, not a 21 year old prospect who is ironing out his game.

Fuck me, if Juve (for whatever reason) want to buy him for a good price then we should be biting their hands off. If Aurier was to be shipped out instead, then fine, but we shouldn't be rolling into the 19/20 season with Trippier as our first choice RB.

 

[todd1882]

1. Midfield. Midfield. Midfield.
.
.
.
.
2. Composure final third
.
.
.
.
.
.
3. RB and LB

Wouldn't mind another midfielder or 2...or 3 if you're feeling generous.

 

[Spaniel]

Idiotic post.

Maybe to you......

 

[bus-conductor]

See my post here:

Trippier did not 'play the latter third of the season', he started 5 PL games out of 10 during the run in. I absolutely will not credit him for that 2nd place finish. Walker was our first choice for the vast majority of games.

Except for that 2nd place finish where Trippier only made 12 league appearances (including substitute appearances). Whoops.

And yes, while 17/18's third placed finish did match that of 15/16, it was regression from our peak during 16/17. I'm no fool, I wouldn't attribute it to one player. Along with the upheaval of the stadium build and issues in midfield, I see our deterioration at full back as a contributing factor.

But hey, you see, I agree with you that we need to upgrade midfield...



Why the fuck else do you think I'm hanging my liver out for Ndombele? Regardless of CM being priority over RB, the latter can still be discussed.

I really don't get this defence of Trippier, to be quite honest. People are waxing lyrical about him as if Man City could have picked him over Walker. Bollocks would they. The guy can whip in a nice cross (explaining your assist stat from before), but his defensive mistakes this season have been fucking dreadful at times - and this is from a 28 year old, not a 21 year old prospect who is ironing out his game.

Fuck me, if Juve (for whatever reason) want to buy him for a good price then we should be biting their hands off. If Aurier was to be shipped out instead, then fine, but we shouldn't be rolling into the 19/20 season with Trippier as our first choice RB.

I’m just disagreeing with the notion that it’s “evident” that RB/Trippier is our biggest problem/weakness. It isn’t. Having a RB that isn’t the best in the league but is still decent (you do realise Walker was shelved by Guardiola midway for repetitive mistakes and poor performances) is much less of a weakness than having one of the shittest midfields in this league.