 desperate to do it I sometimes have to limit them to a paragraph each so we can get to lunch on time. It also helps them to spot mistakes they'd never notice if you just handed them the book and asked them to edit away.
Beyond proofreading, are all the ticklists and highlighters and peer-editing sessions really improving the writing skills of most children? Can children honestly rewrite a piece of work to improve its tone and make it "flow" without intensive adult support?
For a start, the medium is all wrong. Editing on a laptop, where you can rewrite the same sentence seven times, is pretty satisfying. Doing the same on a crammed page of already-marked work is plain miserable. It's no wonder children who pride themselves on their neatness recoil at the prospect of all that crossing out and insertion.
And I haven't even touched on the emotional cost. Editing can feel like an act of betrayal. I still remember being handed back my carefully constructed "Diary from the Trenches" by my Year 9 teacher who had angrily crossed out the sentence "the French were shelling us again" and written in triple underlined red pen "We were fighting the Germans not the French!". She had completely missed the fact I was writing as a German soldier. This was nearly 30 years ago and I still haven't recovered.
Writing is personal. Children invest in it. Many of them find it incredibly hard to do and when you've put a lot of effort into something, it's disheartening to have that effort scrawled over with different coloured pens and comments for improvement. If they haven't put the effort in, then asking them to throw in some expanded noun phrases is unlikely to improve matters.
Getting children to edit before they're ready is counterproductive - a bit like trying to teach an emergent swimmer more advanced techniques while they're spluttering in the deep end. As all good swimming teachers know, you don't look back. You keep on swimming and improve your technique as you go.
Sometimes children's creative-writing efforts should be celebrated for what they are - with a round of applause and a sticker. Because editing your own writing is never easy. If it was, I wouldn't be emailing this off to a lovely Tes sub-editor who will work their magic on it until it's fit for your eyes.
The shares of T-Mobile Us Inc (NASDAQ:TMUS) are up 0.3% at $123.76 at last check, after announcing TVision, the wireless carrier's live television service, will stop operating at the end of April. Customers will now be offered discounts to subscribe to Google's YouTube TV service, which is part of an expansive new multi-year deal between T-Mobile and Alphabet (GOOGL) -owned Google. The company's CEO, Mike Sievert, called the move a "big upgrade," noting that YouTube TV has twice as many channels as TVision Live.
The security has struggled for direction on the charts since claiming a record-high close of $135.54 on Jan. 11. The 200-day moving average, an area of long-term support, acted as a floor for the equity's February pullback, and TMUS is up 48.5% year-over-year.
The options pits lean bullish, per T-Mobile stock's 50-day call/put volume ratio of 3.11 at the International Securities Exchange (ISE), Cboe Options Exchange (CBOE), and NASDAQ OMX PHLX (PHLX). This ratio stands higher than 94% of readings from the past year, indicating a healthier-than-usual appetite for long calls over the last 10 weeks.
Echoing this, TMUS's Schaeffer's put/call open interest ratio (SOIR) of 0.45 stands in the low 6th percentile of readings from the past year. In other words, short-term option traders have rarely been more call-biased.
Plus, these premiums are attractively priced at the moment. The stock's Schaeffer's Volatility Index (SVI) of 25% stands higher than just 12% of all other readings in its annual range, implying options players are pricing in relatively low volatility expectations at the moment.The results of Dr. Jana Bogum (MDC/FMP) from the MDC research group led by Professor Walter Rosenthal and PD Dr. Enno Klußmann could be important in the future for the treatment of excessive fluid retention in patients with chronic heart failure. Using a novel approach, the researchers have also discovered a new molecular mechanism controlling water homeostasis in the kidneys (Journal of the American Society of Nephrology, doi:10.1681/ASN.2012030295)*.
Every day around 1 500 liters of blood flow through the kidneys. Of this total volume, the kidneys initially filter 180 liters of primary urine, which they concentrate to two liters and then excrete as the final urine. A key regulatory step of the concentration mechanism is the release of the hormone AVP (arginine-vasopressin) from the brain. This hormone triggers a multi-step signaling cascade in the kidneys which affects water channels (aquaporins) and in particular aquaporin-2. “The water channels, specifically aquaporin-2, and their redistribution play a key role in the regulation of the water balance,” said Dr. Klußmann.
AVP, which is released from the brain upon thirst, induces aquaporin-2 located in the renal collecting duct principal cells to redistribute from the cell interior to the plasma membrane. The renal cells can then filter out the water from the primary urine flowing past the membrane via aquaporin-2. Dr. Klußmann explained: “To keep the renal cell from bursting and the body from dehydrating, the water is directed back via another group of water channels, aquaporin 3 and 4, into the bloodstream and body tissue. In contrast to aquaporin-2, these water channels are located in another domain of the plasma membrane in the renal principal cells and stay there permanently.” Once the thirst is quenched, the levels of the hormone AVP are reduced and aquaporin-2 is shuttled back into the interior of the renal cell until it is needed again.
However, if the AVP level is too high, as is the case in patients with chronic heart failure, aquaporin-2 remains permanently in the plasma membrane of the renal principal cell and directs the water continuously from the primary urine into the renal collecting duct principal cells. These cells funnel the excess water into the body tissue. “This process contributes to edema,” Dr. Klußmann said.
How can aquaporin-2 be prevented from settling permanently in the plasma membrane and thus triggering diseases or making them worse? Using a new research approach, the scientists were able to identify an inhibitor which prevents the translocation of the water channel aquaporin-2 into the cell membrane. At the same time they discovered a new regulatory mechanism of water homeostasis at the molecular level.
The researchers used “small molecules“, low molecular weight organic compounds, which penetrate well into cells. They tested 17 700 such substances in renal cells and ultimately filtered out a substance that blocks the redistribution of aquaporin-2 to the plasma membrane. The substance (4-acetyldiphyllin) prevents phosphorylation, an important biological and regulatory activation step. In particular, the compound prevents a phosphorylation reaction that is catalyzed by a protein termed protein kinase A. This protein is activated in the signaling cascade that is triggered by AVP in the renal principal cells. In the presence of 4-acetyldiphillin protein kinase A cannot add a phosphate group to aquaporin-2, with the result that the water channels can no longer redistribute to the plasma membrane.
The new research findings may not only be of interest for the treatment of edema but also for the treatment of depression. Here, by contrast, medical researchers are seeking a way to shuttle aquaporin-2 to the plasma membrane of the renal principal cell, because lithium, which is often used to treat depression, prevents aquaporin-2 from redistributing to the plasma membrane, thus causing diabetes insipidus. If AVP is not released from the brain, or if the receptor for AVP in the renal cell is defective, this likewise results in diabetes insipidus, as Professor Rosenthal discovered several years ago. The affected individuals excrete 20 liters of urine every day. A similar effect, but not quite as drastic, is caused by alcohol. Drinking lots of beer causes the body to excrete large amounts of urine. The reason – alcohol prevents the brain from releasing the hormone AVP and thus prevents the redistribution of aquaporin-2 to the plasma membrane.
M&amp;B only does less damage on a "drag" (quoted because they aren't really referenced like that in M&amp;B) if you walk away from the direction of force of the impact or hit very late in the swing. M&amp;B also gave a damage boost for held swings.

Warband wasn't as inconsistent as you're saying either. Honestly, that last claim in kind of garbage. Near one-shots from "veterans" would very often be a held hilt-slash to the face. 

Drags and accels didn't really matter that much in Warband anyway: if you could see/read the released swing, you could hold the block in the correct direction. There were some rare corner-cases with left-to-right hitting on the victim's right side (and the mirrored situation), but they were rare.

The nice thing about Warband is that 95% of the hits that looked like they should do no damage