Lever action henry 22

The place for all your lever-lovin' needs

2014.06.17 21:04 The place for all your lever-lovin' needs

A subreddit for those that love Levers, and things that go bang, together. A place to enjoy Levers without competitive shooting taking it all over.

2015.12.08 19:46 Lever Action Rifles

For pictures and discussions about the OG cowboy gun

2010.05.03 20:39 leftnode Gun Deals - Deals for firearms, ammunition, and accessories

/GunDeals is a community dedicated to the collection and sharing of firearm related deals.

2023.05.28 18:22 chadowan A Comprehensive Guide to Pro Football Video Game Covers

Another Madden $70 re-skin is upon us, so let's take a moment to explore the history of all the people who have been featured on the cover of an pro football video game.
While the selection of the Madden cover athlete is now an event, there was a wild wild west period of football games from the 80s to the mid-2000s where anybody with a computer could and would build football games, with the selection of the cover being all over the place. Roger Craig was the first cover athlete in 1985 on NFL Challenge for MS-DOS. Madden's first game was in 1988, then by the mid-90s getting a cover athlete or spokesman for your football game was pretty standard.
I wanted to compile those games and covers based on this Wiki article (and a few that it was missing from that list) and see who was on the main cover of all of those games (some games were almost completely irrelevant, so I left them off this list). Some of these may have more alternates with other people, but I'll stick with the main cover.

Covers by Position

*These are heavily boosted by John Madden being on 10 Madden covers
Obviously QBs dominate here, but I didn't realize how little defensive players have been on football game covers (9%), with none being on a cover since Richard Sherman in 2014. I'd love to see more defensive players on the Madden cover. Who would be the most likely defensive guy in the near future? Aaron Donald, TJ Watt, Nick Bosa, Myles Garrett, or Sauce Gardner?

Covers by Team

If a team's player was not a lead on the cover or was not any identifiable player, I gave them a *
The Re-skins/Commanders?, Jags, Panthers, and Bills have appeared on a cover but never with an athlete as the lead or with a real person. Only the Texans have never appeared at all on the cover of any football video game. I'd say the Bills are most likely to get one next (Josh Allen), then the Jags (Trevor Lawrence), then the Panthers/Texans if either hits a home run with Young or Stroud. The Commanders have a long road ahead to getting a feature cover athlete, unless you ask Sam Howell who thinks he should be this year's Madden cover athlete.

Most Prolific Cover People

Kordell Stewart, Daunte Culpepper, and Donovan McNabb (and possibly Lamar Jackson, still too early for him) are the only players with multiple appearances that are either not or are unlikely to make the Hall of Fame. McNabb is the only guy to appear in multiple covers in the same year. Also of note, 7 athletes were on a cover without ever making a pro bowl in their careers: Brad Muster, Pat Terrell, Gordon Laro, Chris Zorich, Albert Fontenot, William Floyd, and Peyton Hillis (Hillis was the only one to be the primary cover athlete).
I'll list all the games and their respective covers by their era below. I'll also attach some of my favorite covers from each era. If the cover person was a Hall of Famer, I'll mark them with a \). If they're very likely to make the HoF but they're not yet eligible, I'll mark them with a +

Covers by Era

Decade # of Games # of Games w/Cover Athletes # of Cover Athletes
60s 1 0 0
70s 4 0 0
80s 11 2 (18%) 2
90s 36 32 (89%) 21
00s 40 38 (95%) 36
10s 14 10 (71%) 12
20s 8 4 (50%) 5
Total 114 86 (75%) 76
We didn't see the first cover athlete until 1985 with Roger Craig. They didn't really become standard until the early to mid-90s after Madden became a big selling point for the early Madden games. The dip in the last 2 decades is because there's just less games, so any generic football games will have a large effect.

The Early Days: 1965-1982

1978: Football! for the Magnavox Odyssey 2 was the first football video game with a cover, but obviously the cover athletes are generic.
Year Game Cover Athlete Team Position
1972 Football (Magnavox) NA NA NA
1978 Football! Generic players NA NA
1978 Football (Atari) Generic players NA NA
1979 NFL Football Generic players NA NA
1982 Realsports: Football Generic players NA NA

The 2D Era: 1983-1996

1985: NFL Challenge was the first football game with a real cover athlete (Roger Craig). This was the original bar for realism in football simulation, to where it was used in a 1988 ESPN Program \"NFL Dream Season\" where they simulated the greatest teams of all time against each other.
1988: John Madden Football released on the Apple II, MS-DOS, and Commodore 64/128 (partly being developed by Bethesda), which was the beginning of the most dominant franchise in football video games. They featured no NFL teams due to a lack of an NFL license.
1991: Tecmo Super Bowl is probably still my personal favorite football video game. It's totally timeless, and if you pick the Raiders then you're a cheater.
Year Game Cover Athlete Team Position
1983 10-Yard Fight Generic Jersey NA NA
1984 Super Action Football Generic player NA NA
1985 NFL Challenge Roger Craig 49ers RB
1987 4th & Inches Generic players NA NA
1987 Tecmo Bowl Generic players NA NA
1988 TV Sports: Football Generic player NA NA
1988 John Madden Football ('88) John Madden* None John Madden
1989 ABC Monday Night Football Generic player NA NA
1989 NFL Generic players 49ers, Raiders, Oilers, Broncos, Re-skins NA
1989 PlayMaker Football Equipment NA NA
1990 Joe Montana Football Joe Montana* None QB
1990 John Madden Football ('90) John Madden* None John Madden
1991 John Madden Football II (or '92) John Madden* None John Madden
1991 Tecmo Super Bowl Generic player NA NA
1992 NFL Sports Talk Football '93 Joe Montana* 49ers QB
1992 Front Page Sports Football Generic players NA NA
1993 Capcom's MVP Football Brad Muster Bears FB
1993 Madden NFL '94 John Madden* NA HC/Announcer
1993 NFL Football '94 Starring Joe Montana Joe Montana* Chiefs QB
1993 Mutant League Football Mutant NA NA
1994 ESPN Sunday Night NFL Chris Berman NA Announcer
1994 Madden NFL '95 John Madden* NA John Madden
1994 Tecmo Super Bowl II: Special Edition Generic player Cowboys NA
1994 Troy Aikman NFL Football Troy Aikman* Cowboys QB
1995 Emmitt Smith Football Emmitt Smith* None RB
1995 Madden NFL '96 John Madden*, Pat Terrell, Gordon Laro NA, Panthers, Jags John Madden, DB, TE
1995 NFL Quarterback Club 96 Steve Young*, Chris Zorich, Albert Fontenot 49ers, Bears QB, DL
1995 Sterling Sharpe: End 2 End Sterling Sharpe None WR
1995 Tecmo Super Bowl III: Final Edition Generic players Raiders, Bills NA
1995 NFL GameDay William Floyd 49ers FB
1996 Madden NFL 97 John Madden* NA John Madden
1996 NFL '97 Kordell Stewart Steelers QB
1996 NFL Quarterback Club 97 Dan Marino* Dolphins QB
1996 NFL GameDay '97 Daryl "Moose" Johnston Cowboys FB

The Parity Era: 1997-2004

1997: NFL Blitz came from Midway studios and was a breath of fresh air for football games. They had mostly been stagnant trying to hone in on realistic simulation in 2D form, whereas Blitz came out in 3D and threw realism out the window. I definitely spent too much money on the arcade version of this game.
2000: Madden 2001 started the tradition of having their games feature a cover athlete in this format, which consolidated into nearly everyone following this trend.
2001: Backyard Football 2002 was a more kid-friendly version of a football video game, and they also had other games for other professional sports. I definitely played this a lot on my old Windows Me computer, and Pablo Sanchez is a god.
2002: NFL Fever was Microsoft's foray into football video games on the original Xbox. All 3 of their games featured Peyton Manning as the cover athlete.
2002: NFL GameDay 2003 was 989 Sports' exclusive for Sony on the PlayStation platform.
2004: ESPN NFL 2K5 was the last great football game before the NFL exclusively gave their license to the EA. It was this game that definitely led to NFL's decision though, as they slashed their release price to an unheard of $20, which forced Madden 2004 to release at $30 instead of the typical $50. This pissed off the NFL, who decided to have less competition instead.
Year Game Cover Athlete Team Position
1997 NFL Blitz Kordell Stewart Steelers QB
1997 NFL Quarterback Club 98 Brett Favre* Packers QB
1997 NFL GameDay '98 Jerome Bettis* Steelers RB
1997 Madden NFL 98 (64) John Madden* NA John Madden
1998 NFL Xtreme Mike Alstott Bucs FB
1998 NFL Quarterback Club 99 Brett Favre* Packers QB
1998 NFL GameDay '99 Terrell Davis* Broncos RB
1998 Madden NFL 99 John Madden* NA John Madden
1999 NFL Xtreme 2 John Randle* Vikings DL
1999 NFL Quarterback Club 2000 Brett Favre* Packers QB
1999 NFL GameDay 2000 Terrell Davis* Broncos RB
1999 NFL 2K Randy Moss* Vikings WR
1999 Madden NFL 2000 John Madden* NA John Madden
1999 Backyard Football Steve Young)*, Jocinda Smith, Amir Khan 49ers, Generic QB
2000 NFL Quarterback Club 2001 Brett Favre* Packers QB
2000 NFL GameDay 2001 Marshall Faulk* Rams RB
2000 NFL 2K1 Randy Moss* Vikings WR
2000 Madden NFL 2001 Eddie George Titans RB
2001 NFL Quarterback Club 2002 Brett Favre*, Rich Gannon Packers, Raiders QB
2001 NFL GameDay 2002 Donovan McNabb Eagles QB
2001 NFL Fever 2002 Peyton Manning* Colts QB
2001 NFL 2K2 Randy Moss* Vikings WR
2001 Madden NFL 2002 Daunte Culpepper Vikings QB
2001 Backyard Football 2002 Drew Bledsoe or Donovan McNabb Pats or Eagles QB
2001 ESPN NFL PrimeTime 2002 Edgerrin James* Colts RB
2002 NFL GameDay 2003 Tom Brady+ Pats QB
2002 NFL Fever 2003 Peyton Manning* Colts QB
2002 NFL 2K3 Brian Urlacher* Bears LB
2002 Madden NFL 2003 Marshall Faulk* Rams RB
2003 NFL GameDay 2004 LaDainian Tomlinson* Chargers RB
2003 NFL Fever 2004 Peyton Manning* Colts QB
2003 Madden NFL 2004 Michael Vick Falcons QB
2003 ESPN NFL Football Warren Sapp* Bucs DL
2003 Backyard Football 2004 Jeff Garcia 49ers QB
2004 NFL GameDay 2005 Derrick Brooks* Bucs LB
2004 Madden NFL 2005 Ray Lewis* Ravens LB
2004 ESPN NFL 2K5 Terrell Owens* Eagles WR
2004 NFL Street Ricky Williams Dolphins RB

The Madden Era: 2005-Present

2005: NFL Street 2 was the second in the NFL Street series as a kind of spiritual successor to NFL Blitz. EA tried to have some diversity in their football video games outside of the Madden franchise, so they had the short-lived Street franchise under \"EA BIG\"
2006: NFL Head Coach was a new perspective on NFL Games where you play as the coach instead of the players. I enjoyed these although they could get a little boring.
2007: All Pro Football 2K8 was 2K's attempt at keeping the 2K football franchise alive without the coveted NFL license. They got three HoF players on the cover in Elway, Barry, and Rice, but not the actual license to any NFL team. This game received praise for its mechanics, but poor sales showed that a non-NFL licensed game would always struggle to make it.
2011: Madden 12 was maybe the last good Madden game. Also, Peyton Hillis. The only guy on a NFL football game cover to never make a Pro Bowl. This guy is an actual hero though, so good for him.
2019: Doug Flutie's Maximum Football was a mix of american and CFL football as another attempt at making a football game without the NFL license to poor results. They have announced a new game as a free to play title on new platforms, but no games in this franchise have released since 2020.
2020: Retro Bowl is a mobile game more in the style of Tecmo Super Bowl than Madden. It's probably the most successful non-Madden game since ESPN NFL 2K5, and it's pretty fun. People should definitely give this one a try since it's free to play on any mobile platform.
2022: Madden 23 gave the cover back to Madden for the first time since 1999 to honor the passing of the legend John Madden. Unfortunately the game inside the cover was crap, has been the style of Madden games for over a decade.
Year Game Cover Athlete Team Position
2005 Madden NFL 06 Donovan McNabb Eagles QB
2005 NFL Street 2 Jeremy Shockey, Xzibit Giants, Pimp My Ride TE, Rapper
2005 Blitz: The League Generic players NA NA
2005 Backyard Football 2006 Daunte Culpepper Vikings QB
2006 Madden NFL 07 Shaun Alexander Seahawks RB
2006 NFL Head Coach Bill Cowher* Steelers HC
2006 NFL Street 3 Chad Johnson Bengals WR
2007 Backyard Football '07 Ben Roethlisberger+ Steelers QB
2007 Madden NFL 08 Vince Young Titans QB
2007 All-Pro Football 2K8 John Elway*, Barry Sanders*, Jerry Rice* Generic QB, RB, WR
2007 Backyard Football '08 Tom Brady+ Pats QB
2008 NFL Tour Shawne Merriman Chargers LB
2008 NFL Head Coach 09 Tony Dungy* Colts HC
2008 Backyard Football '09 Tom Brady+ Pats QB
2009 Madden NFL 10 Troy Polamalu*, Larry Fitzgerald+ Steelers, Cards DB, WR
2009 Backyard Football '10 Frank Gore+, Eli Manning+, Kurt Warner*, Peyton Manning*, Adrian Peterson+, Jason Witten+ 49ers, Giants, Cards, Colts, Vikings, Cowboys RB, QB, TE
2010 Quick Hit Football Logo NA NA
2010 Madden NFL 11 Drew Brees+ Saints QB
2010 Backbreaker Generic player NA NA
2011 Madden NFL 12 Peyton Hillis Browns RB
2012 Madden NFL 13 Calvin Johnson* Lions WR
2013 Madden NFL 25 Barry Sanders* or Adrian Peterson+ Lions or Vikings RB
2014 Madden NFL 15 Richard Sherman+ Seahawks DB
2015 Madden NFL 16 Odell Beckham Jr. Giants WR
2016 Madden NFL 17 Rob Gronkowski+ Pats TE
2016 Axis Football 2016 Generic player NA NA
2017 Madden NFL 18 Tom Brady+ Pats QB
2017 Axis Football 17 Generic player NA NA
2018 Madden NFL 19 Antonio Brown+ Steelers WR
2019 Doug Flutie's Maximum Football 2019 Doug Flutie Generic (Stampeders) QB
2020 Sunday Rivals Helmet NA NA
2020 Retro Bowl Generic player NA NA
2020 Legend Bowl Silhouette NA NA
2019 Madden NFL 20 Patrick Mahomes+ Chiefs QB
2020 Madden NFL 21 Lamar Jackson Ravens QB
2021 Madden NFL 22 Tom Brady+, Patrick Mahomes+ Bucs, Chiefs QB
2022 Madden NFL 23 John Madden* NA John Madden
2023 NFL Pro Era Lamar Jackson Ravens QB
submitted by chadowan to nfl [link] [comments]

2023.05.28 18:22 PanzerBirb [BATTLE] Taming the Welsh Dragon

While Richard de la Pole secured his reign over England proper, the situation of Wales hung over his head like a sore thumb. While the Welsh rebels led by Rhys ap Thomas had been unable to assert Prince Henry’s claim to the English throne, they proved too resilient for the Marcher Lords to handle after years of warfare. As such, the question of Wales was deferred as neither side had the strength to do more than launch small raids. However, with some of the devastation in England proper repaired and with an army raised, Richard began his march into Wales in order to bring the Welsh rebels to heel by iron and blood.
After an extensive preparation period in Cardiff and Bristol, the English army makes its slow march across southern Wales, hampered by its relatively large artillery train and the region's poor infrastructure. With this slow movement along the southern coast, the Welsh rebels are able to muster their forces. While small compared to the total English force, the Welsh force forces the England army to stay more or less unified in its march across Wales. The towns of Tenbye, Penebrok, and Haverford fall without bloodshed to the English army, but as the English march north, several other towns such as Cardigan and Aberystroth refuse to surrender instantly to the English army, resulting in the aforementioned towns to be looted.
Only after Richard pushes north to siege down the citadel at Caernarvon do the Welsh rebels act, splitting their forces and attacking the recently established English garrisons in western and south-western Wales. While these attacks are relatively successful, fears of the English army and the Marcher Lords force the Welsh rebels to retreat to their mountain strongholds with moderate losses. With Rhys ap Thomas unwilling, or unable, to face off against Richard, his efforts in northwest Wales are successful.
With the capture of Caernarvon, Conwy, Penbrock, and Harlech Castles, Richard’s army moves East where they link up with the forces of George Talbot at the town of Mold in mid-October. While Talbot was told to secure their own holdings, the Earl of Shrewsbury took personal initiative in the latter half of the campaign, aiming to take advantage of the split Welsh forces and concluding that the best defense of the Earldom was offensive action.
While the Welsh rebels still remain a potent force, the control of Rhys ap Thomas over the rebels has fractured in the wake of Richard’s campaign. While Rhys ap Thomas is still the nominal leader of the rebels, more Welsh rebels have signaled a willingness to break with Rhys, viewing his personal insistence of Prince Henry's claim to be self-destructive to their cause. Warfare in Wales has begun to devolve into guerilla warfare, but the Welsh rebels still have a good portion of their forces should they be forced to take the battlefield.
Map of Wales at the end of 1518
~500 men
submitted by PanzerBirb to empirepowers [link] [comments]

2023.05.28 18:14 Schuckman [RECRUITING] Inferno Blitz Level 22 TH13+ #JCVULJGL Capital/CWL/Farming CWL: Masters II Capital: Champion I

Are you wanting to join a high level clan, but you're tired of filling out applications and looking for passwords just to be put on a waiting list? Are you wanting something that's a little more laid-back and fun? Join us at Inferno Blitz!

Inferno Blitz

About the Clan: Inferno Blitz was our first clan started on November 11, 2017. We have grown stronger over the years and have many talented veterans still with us since the beginning. We declare wars 2-3 times a well and CWL is usually 30v30 so everyone can earn those juicy CWL Medals.
About the People: Inferno Blitz is full of experienced and competitive players. If you’re an above-average attacker and have a good knowledge of the game, then you’ll fit right in. An important aspect in both of our clans is that we want you to be active and participate, but we understand Clash isn’t (and shouldn’t be!) a full-time job. We’ll help you play the game the way you want to play it. We have players that focus on wars, trophy pushing, donations, and Clan Games. We also have progression styles that range from strategic-rushing to maxing.

Inferno Blitz fun facts

Why should you join our clan?

What do we need from you?

How do you join?

Does this sound like the type of clan you want to join? Great! Tap on the link below, tell us you’re from Reddit and a little bit about yourself!
Inferno Blitz Clan Link: https://link.clashofclans.com/en?action=OpenClanProfile&tag=JCVULJGL
submitted by Schuckman to ClashOfClansRecruit [link] [comments]

2023.05.28 18:04 dagibaus Peaking his rating in YA.

Peaking his rating in YA.
Player that was in the club when I arrive. (SC Verl in 3. Liga)
submitted by dagibaus to FifaCareers [link] [comments]

2023.05.28 18:03 UnDead_Ted Daily Light Sunday, May 28th 2023

Daily Light Sunday, May 28th 2023


We await a Savior. — Phil 3:20
For the grace of God has appeared, bringing salvation for all people, training us to renounce ungodliness and worldly passions, and to live self-controlled, upright, and godly lives in the present age, waiting for our blessed hope, the appearing of the glory of our great God and Savior Jesus Christ, who gave himself for us to redeem us from all lawlessness and to purify for himself a people for his own possession who are zealous for good works (Titus 2:11-14).— But according to his promise we are waiting for new heavens and a new earth in which righteousness dwells. Therefore, beloved, since you are waiting for these, be diligent to be found by him without spot or blemish, and at peace (2 Peter 3:13-14).
Christ, having been offered once to bear the sins of many, will appear a second time, not to deal with sin but to save those who are eagerly waiting for him (Hebrews 9:28).— It will be said on that day, “Behold, this is our God; we have waited for him, that he might save us. This is the Lord; we have waited for him; let us be glad and rejoice in his salvation.” (Isa 25:9).


So run that you may obtain it. — 1 Cor 9:24
The sluggard says, “There is a lion outside (Prov 22:13).—Therefore, since we are surrounded by so great a cloud of witnesses, let us also lay aside every weight, and sin which clings so closely, and let us run with endurance the race that is set before us, looking to Jesus, the founder and perfecter of our faith (Heb 12:1-2).
Let us cleanse ourselves from all filthiness of the flesh and spirit, perfecting holiness in the fear of God (2 Corinthians 7:1).
I press toward the mark (Philippians 3:14).— So I do not run aimlessly ; But I discipline my body and keep it under control...I myself should be disqualified (1 Corinthians 9:26-27).
For the present form of this world is passing away (1 Cor 7:31).
But according to his promise we are waiting for new heavens and a new earth in which righteousness dwells. Therefore, beloved, since you are waiting for these, be diligent (2 Pet 3:13-14).—Therefore, preparing your minds for action, and being sober-minded, set your hope fully on the grace that will be brought to you at the revelation of Jesus Christ (1 Pet 1:13).
submitted by UnDead_Ted to TheDailyDose [link] [comments]

2023.05.28 17:59 Suspicious_Gold1283 Jurassic World: Worldwide Coexistence Recruitment and RP Links

Dinosaurs are now living in our world.
The solution has been made and put into action after the events of Jurassic World Dominion.
Help me create roleplaying stories with OCs and existing characters from the franchise and encounter never before seen extinct animals and hybrids.

Welcome to Jurassic World!

Hi, tourists.
Now that dinosaurs are learning to co-exist with humans and modern-day animals like horses and elephants, De-Extinction is becoming something more and more advanced.

Dinosaurs are not the only animals that are back.

Marine reptiles and Ice age animals are here as well.

Every extinct animal has rights now.

The roleplay is always open for new people as well as help is always wanted.

I may be the host of this roleplay, but after suffering from memory issues from 4 seizures, My knowledge is cursed to be limited.

Welcome to Jurassic World!

I need people to play any character they want.

I am also new as well on here, to be honest.

The Plot is simple as well.

Plot: After the film, Owen, Alan, Claire, and many old and original characters travel the world to help bring balance between De-Extinct animals and Humans from America, South America, and the rest of the globe!

Welcome to Jurassic World!


  1. Play as both a Human and a Prehistoric Animal.
  2. OCs are welcome as well.
  3. Deaths are allowed for both humans and animals.
  4. Help make coexistence between Humans and Animals more likely.
  5. Characters like Owen, Henry, Claire, and other existing characters are allowed to be played by more than just one person.

Also, you are welcome to ask questions or give notes or reminders in the roleplay.
Recruitment Link Below

Actual RP link Below
submitted by Suspicious_Gold1283 to JurassicPark [link] [comments]

2023.05.28 17:56 alex2003super HomeKit app crashes on Mac

I've been trying for a while to use the Home app on Mac, but to no avail, it always crashes. I'm on Ventura 13.4, MacBook Pro 16" (2019) (MBP 16,1)
When launching it from Terminal, here's the output I get:
❯ /System/Applications/Home.app/Contents/MacOS/Home 2023-05-28 17:52:16.089 Home[34635:1248076] XType: XTFontStaticRegistry is enabled by Info.plist. 2023-05-28 17:52:16.732 Home[34635:1248076] *** Assertion failure in +[NSCollectionLayoutDimension absoluteDimension:], NSCollectionLayoutItem.m:1742 2023-05-28 17:52:16.751 Home[34635:1248076] *** Terminating app due to uncaught exception 'NSInternalInconsistencyException', reason: 'Invalid absolute dimension: -inf. The dimension must be a finite value.' *** First throw call stack: ( 0 CoreFoundation 0x00007ff8073d718a __exceptionPreprocess + 242 1 libobjc.A.dylib 0x00007ff806efd42b objc_exception_throw + 48 2 Foundation 0x00007ff8082add28 -[NSCalendarDate initWithCoder:] + 0 3 CollectionViewCore 0x00007ffb0d891c34 +[NSCollectionLayoutDimension absoluteDimension:] + 294 4 HomeUI 0x00007ffc10308ab0 block_destroy_helper.23 + 14240 5 HomeUI 0x00007ffc10306641 block_destroy_helper.23 + 4913 6 HomeUI 0x00007ffc10311501 block_destroy_helper + 1745 7 HomeUI 0x00007ffc103cb5d1 block_destroy_helper + 27313 8 HomeUI 0x00007ffc103cb740 block_destroy_helper + 27680 9 HomeUI 0x00007ffc106a07cb -[HUItemCollectionViewController _layoutSectionForSection:layoutEnvironment:] + 245 10 HomeUI 0x00007ffc1069ddf2 __78-[HUItemCollectionViewController initUsingCompositionalLayoutWithItemManager:]_block_invoke + 84 11 UIKitCore 0x00007ff9150c051e __51-[UICollectionViewCompositionalLayout _fullResolve]_block_invoke + 349 12 UIKitCore 0x00007ff9150d8b6c -[_UICollectionCompositionalLayoutSolver _queryClientForSectionDefinitionForSectionIndex:] + 315 13 UIKitCore 0x00007ff9150d173a -[_UICollectionCompositionalLayoutSolver _solveRetainingPreferredSizes:] + 313 14 UIKitCore 0x00007ff9150c5a33 -[_UICollectionCompositionalLayoutSolver initWithContainer:traitCollection:layoutAxis:dataSourceSnapshot:options:sectionProvider:] + 576 15 UIKitCore 0x00007ff9150bfdfe -[UICollectionViewCompositionalLayout _fullResolve] + 1092 16 UIKitCore 0x00007ff9150bc23c -[UICollectionViewCompositionalLayout prepareLayout] + 204 17 UIKitCore 0x00007ff914d192a2 -[UICollectionViewData _prepareToLoadData] + 163 18 UIKitCore 0x00007ff914d1c37f -[UICollectionViewData collectionViewContentRect] + 29 19 UIKitCore 0x00007ff914c93bab -[UICollectionView setFrame:] + 924 20 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 21 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) _resizeWithOldSuperviewSize:] + 286 22 UIKitCore 0x00007ff914cf42f8 -[UIScrollView(_UIOldConstraintBasedLayoutSupport) _resizeWithOldSuperviewSize:] + 46 23 CoreFoundation 0x00007ff807354377 __NSARRAY_IS_CALLING_OUT_TO_A_BLOCK__ + 7 24 CoreFoundation 0x00007ff807354328 -[__NSArrayM enumerateObjectsWithOptions:usingBlock:] + 505 25 UIKitCore 0x00007ff914c1f6f2 -[UIView(Geometry) resizeSubviewsWithOldSize:] + 132 26 UIKitCore 0x00007ff914bf506c -[UIView(Geometry) setFrame:] + 693 27 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 28 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) _resizeWithOldSuperviewSize:] + 286 29 CoreFoundation 0x00007ff807354377 __NSARRAY_IS_CALLING_OUT_TO_A_BLOCK__ + 7 30 CoreFoundation 0x00007ff807368511 -[__NSSingleObjectArrayI enumerateObjectsWithOptions:usingBlock:] + 80 31 UIKitCore 0x00007ff914c1f6f2 -[UIView(Geometry) resizeSubviewsWithOldSize:] + 132 32 UIKitCore 0x00007ff914bf506c -[UIView(Geometry) setFrame:] + 693 33 UIKitCore 0x00007ff914c54417 -[UIViewControllerWrapperView setFrame:] + 86 34 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 35 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) _resizeWithOldSuperviewSize:] + 286 36 CoreFoundation 0x00007ff807354377 __NSARRAY_IS_CALLING_OUT_TO_A_BLOCK__ + 7 37 CoreFoundation 0x00007ff807368511 -[__NSSingleObjectArrayI enumerateObjectsWithOptions:usingBlock:] + 80 38 UIKitCore 0x00007ff914c1f6f2 -[UIView(Geometry) resizeSubviewsWithOldSize:] + 132 39 UIKitCore 0x00007ff914bf506c -[UIView(Geometry) setFrame:] + 693 40 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 41 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) _resizeWithOldSuperviewSize:] + 286 42 CoreFoundation 0x00007ff807354377 __NSARRAY_IS_CALLING_OUT_TO_A_BLOCK__ + 7 43 CoreFoundation 0x00007ff807354328 -[__NSArrayM enumerateObjectsWithOptions:usingBlock:] + 505 44 UIKitCore 0x00007ff914c1f6f2 -[UIView(Geometry) resizeSubviewsWithOldSize:] + 132 45 UIKitCore 0x00007ff914bf506c -[UIView(Geometry) setFrame:] + 693 46 UIKitCore 0x00007ff914c106f3 -[UILayoutContainerView setFrame:] + 70 47 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 48 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) _resizeWithOldSuperviewSize:] + 286 49 CoreFoundation 0x00007ff807354377 __NSARRAY_IS_CALLING_OUT_TO_A_BLOCK__ + 7 50 CoreFoundation 0x00007ff807368511 -[__NSSingleObjectArrayI enumerateObjectsWithOptions:usingBlock:] + 80 51 UIKitCore 0x00007ff914c1f6f2 -[UIView(Geometry) resizeSubviewsWithOldSize:] + 132 52 UIKitCore 0x00007ff914bf506c -[UIView(Geometry) setFrame:] + 693 53 UIKitCore 0x00007ff914c54417 -[UIViewControllerWrapperView setFrame:] + 86 54 UIKitCore 0x00007ff914c42730 -[UIView(Geometry) _applyAutoresizingMaskWithOldSuperviewSize:] + 750 55 UIKitCore 0x00007ff914c4242b -[UIView(Geometry) 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_DPSNextEvent + 858 137 AppKit 0x00007ff80a3f147a -[NSApplication(NSEvent) _nextEventMatchingEventMask:untilDate:inMode:dequeue:] + 1214 138 AppKit 0x00007ff80a3e3ae8 -[NSApplication run] + 586 139 AppKit 0x00007ff80a3b7d02 NSApplicationMain + 817 140 AppKit 0x00007ff80a675255 _NSApplicationMainWithInfoDictionary + 16 141 UIKitMacHelper 0x00007ff81f658231 UINSApplicationMain + 1413 142 UIKitCore 0x00007ff914bc043b UIApplicationMain + 144 143 Home 0x000000010f201572 Home + 320882 144 dyld 0x00007ff806f2a41f start + 1903 ) libc++abi: terminating due to uncaught exception of type NSException [1] 34635 abort /System/Applications/Home.app/Contents/MacOS/Home 
submitted by alex2003super to HomeKit [link] [comments]

2023.05.28 17:53 BossFresh34 [The Boss Fresh Chronicle] Week 21, 2023

A few months ago I posted my progress so far in 2023, largely to check if the gains I was seeing were a fluke. While they have not kept pace, I have continued this income strategy and it appears to be working. I need to state that what I share here is not the entirety of my portfolio. In recent days my brokerage account has utterly ripped as I have a large position in NVDA. The growth in that position last week alone is greater than all of the premiums I have collected so far this year. I figured I could document progress here going forward and you can all laugh at me when I screw up, or cheer me on, or give me pointers.

YTD Results by Week
Week 21 Action:
Assigned - MDB
On 5/22, Bought 100 shares at $279.47, Sold 1 CC @ $280 exp 5/26 for $744.33. Total gain: $797.34
Closed - NVDA
On 5/18, Sold 1 CSP @ $312.50 exp 5/26 for $1,129.33, bought to close for $9.66. Total gain: $1,119.67
Rolled - BURL
On 5/16, Sold 3 CC @ $197.50 exp 5/26 for $268.01, bought to close for $6.03. Total gain: $261.98
Rolled - BILL
On 5/22, Sold 5 CC @ $100.00 exp 5/26 for $723.68, bought to close for $103.30. Total gain: $620.38
Rolled - WBD
On 5/10, Sold 16 CC @ $15.50 exp 6/9 for $197.40, bought to close for $48.16. Total gain: $149.24
Disclaimer: I do not provide personal investment advice and I am not a qualified licensed investment advisor. I am an amateur investor.
submitted by BossFresh34 to CoveredCalls [link] [comments]

2023.05.28 17:44 pylori pylori's Physiology Bites - Kidney function, acute kidney injury, and acid-base disorders

This is a series I am going to be working on where I endeavour to cover various topics in physiology intermixed with clinical pearls to impart some knowledge that doctors of most specialties and grades will hopefully find useful when looking after acutely unwell patients. Join me as we dredge through the depths of anaesthetic exam revision to answer important questions like "why do CT ask for a pink cannula", "why frusemide is okay to give in AKI", "why is hypoxic drive a bunch of horse manure" and many more. Pick up some of this material and you'll be well on your way to becoming a pernickety anaesthetist, whether you like it or not!
Questions, comments, feedback, and suggestions are both encouraged and welcome.

Previous installments:

Kidney function, acute kidney injury, and acid-base disorders

Next stop along our systems review are the mighty kidneys. I won't talk to you about Lupus nephritis or renal tubular acidosis, however I will try my best to cover some more typical things you might encounter like acute kidney injury (AKI) and drug dosing in renal impairment while trying to avoid embarrassing myself as a non-renal doctor.

What do the kidneys do?

An obvious question, they allow us to get rid of waste substances in urine. They are so much more than that however, they:
  • Regulate electrolyte concentrations, water balance and plasma volume, plasma osmolality
  • Regulate red blood cell production
  • Regulate blood pressure via RAA system influencing vascular resistance
  • Maintain acid-base homeostasis
  • Control Vitamin D production
  • Produce glucose from proteins and triglycerides (gluconeogenesis)
We will focus on only a few of these in this post, but the kidney's multiple roles and complex biochemical signalling deserves as mention as it can make diagnosing and understanding disease states difficult. It can also make us forget what other consequences there might be for patients in these disease states.

How do we measure kidney function?

In some respects knowing the heart or the brain aren't working is easy. Low blood pressure and infection? Septic shock. Low blood pressure + STEMI? Cardiogenic shock. Unconsciounsess or coma? Well whatever it is, it ain't working. So what about the kidneys, well we have creatinine, right? WRONG.
Although the kidney has many functions as we noted before, the easiest methods to quantify function look at the obvious: waste production. Its function is the sum of filtration through all the glomeruli in the kidneys, the glomerular filtration rate (GFR). When a substance is freely filtered through the kidneys and is neither secreted nor reabsorbed (which occur in the tubules rather than the glomeruli), the rate at which that substance is removed or cleared from the plasma can be used to measure GFR (in mL/min).
This substance is inulin and not creatinine. Because inulin isn't naturally present in our bodies, it has to be infused and then its concentration and the rate of decay measured. This is impractical clinically, so creatinine was selected as a practical alternative. The correlation between serum creatinine and measured GFR was researched and various formulas like MDRD and CKD-EPI were developed to estimate GFR (eGFR). This is why labs report eGFR as opposed to GFR. (There are also other methods to determine GFR like radionuclide scintigraphy...)

What's the problem?

The estimation of the GFR relies on assumptions that are not without problems. This review covers the topic at length, however the main points are:
  • Creatinine is secreted, unlike inulin. As mentioned this occurs in the tubules, so changes in secretion will affect serum creatinine level despite a static filtration rate. As renal diseases progress, more and more creatinine is secreted, making serum concentrations less reflective of actual filtration.
  • To truly reflect instrinsic renal function creatinine has to be in a steady state with stable generation and serum concentration. Creatinine is produced as a waste product of protein breakdown mainly from muscles. Therefore anything affecting catabolism, muscle activity, dietary protein intake, can alter this steady state. Frail sarcopenic patients will have artificially low creatinines and may not get as significant of a rise as a young muscular person in AKI.
  • There has to be adequate delivery of creatinine to the glomeruli. The kidneys receive ~20% of the cardiac output, so the heart has to be pumping out effectively with healthy blood vessels, good volume and blood flow. A hypovolaemic patient with an MI may have a high creatinine despite working kidneys, they're just not being adequately perfused. Chronic diseases like hypertension, diabetes, heart failure, lead to upset of autoregulation of normal afferent (entering) arterioles, whereas ACE inhibitors and ARBs block AT-II from causing vasoconstriction of efferent (outgoing) arterioles, an imbalance can lead to renal impairment if perfusion isn't maintained, or improved blood flow and urine output if it is.
  • The studies from which eGFR formulas are derived were conducted in mostly European and North American populations with elderly, black and CKD patients being significantly underrepresented. They only measured GFR a few times a year. With increasingly older, frailer, sicker patients, leading more sedentary industrialized diets and lifestyles, will the accuracy of these formulas hold up with time?
  • eGFR correlates loosely with important indicators like proteinuria, fluid status, blood pressure, acidosis, anaemia, bone disease, iron deficiency, tubular function, etc. In the absence of those indicators, the elderly often have decreased GFR without increases in morbidity and mortality.
The takeaway is that creatinine and eGFR are tools developed from the assessment and monitoring of long term renal function. It is not designed for use in patients with acute fluctuations or those with zero kidney function (eg, anuric dialysis dependent).

What else we can monitor?

The example of the heart earlier was misleading. Blood pressure is influenced by many factors. Septic shock is actually a high cardiac output state with low systemic vascular resistance (SVR). Patients with heart failure can have normal blood pressures despite severe systolic dysfunction and poor exercise tolerance. Blood pressure is an easy surrogate marker because determining cardiac output and SVR is invasive and complex (of course we have focused echocardiography to help us these days).
A surrogate marker we can use for the kidneys is urine output (UO). After all the end product of glomerular filtration is the ultrafiltrate which will become the urine. If there is adequate urine output despite raised or increasing creatinine levels, we can be reasonably satisfied the kidneys are actually receiving enough blood flow to get rid of waste and perform its other functions.

Acute Kidney Injury

This leads us into one of the most commonly encountered entities in hospitalised patients: AKI. Let's look at the KDIGO criteria seen in the table below.
AKI Stage Serum creatinine criteria Urine output criteria
1 SeCr increase ≥26 umol/L <48hrs or SeCr increase ≥1.5 - 2x from baseline <0.5mL/kg/hr for ≥6hrs
2 SeCr increase ≥2-3x from baseline <0.5mL/kg/hr for ≥12hrs
3 SeCr increase ≥354 umol/L <48hrs or SeCr increase ≥3x from baseline or started on renal replacement therapy (any stage) <0.3mL/kg/hr for ≥24hrs or anuria for ≥12hrs
Note: UO <0.5mL/kg/hr is the definition of oliguria.
Definining by creatinine is a more practical screening test in most situations, allowing earlier diagnosis and intervention. UO can be monitored during the course of the day to identify patients who are borderline or not responding to treatment, may need re-evaluation of the cause, or escalation of care. This way a combination of the two can help offset the limitations of each method.
NICE guidance already exists on the diagnosis and management of AKI, most hospitals will have care bundles or even 'AKI nurses', so I'll run over a few important points.
  • Pre-renal - This only means the cause lies outside the kidneys, and in at least in the early stages there is no histological change in the kidneys. In many cases like sepsis, diarrhoea, haemorrhage, there can be a relative or absolute fluid deficit and IV fluids are generally indicated. However excessive fluids can result in interstitial oedema in the kidneys, reducing the glomerular pressure gradient and so also reducing filtration. Similarly in poor cardiac output states where there is venous congestion there is a problem with the outflow of blood from the kidneys, so this is not a cause to reflexively withhold diuretics.
  • Intrinsic - Here there are structural histological changes in the kidney, caused by many intrinsic renal diseases or nephrotoxic agents like aminoglycosides, vancomycin, NSAIDs, etc. If this is suspected, stopping the offending agent generally resolves AKI without needing a biopsy. Furosemide is not mentioned here as it is not inherently nephrotoxic. Acute tubular necrosis is often mentioned as a specific clinical entity, either due to nephrotoxic agents or sustained hypoperfusion from pre-renal causes. It is not a very helpful term since histological tubular damage has rarely been proven in studies, nor does it help with treatment.
  • Post-renal - Obstruction may be incomplete, acute on chronic, with a normal ultrasound, no oligo/anuria, and may be associated with other pathologies like a kidney stone with pyelonephritis or sepsis. Catheters can get blocked too so don't forget a bladder scan if anuric, and obstruction can rarely be external such as by tumours or abdominal compartment syndrome.

When do I refer to renal or ICU?

Local protocols aside, advice should be sought when the patient does not appear to be responding to medical management and there may be a need for renal replacement therapy (RRT). This is often in the form of intermittent haemodialysis (iHD) on renal wards, and continuous venovenous haemodiafiltration (CVVHDF) in ICU. There are small differences in mechanism, efficacy, and indications of the many forms of RRT, the details of which aren't important for most non specialists. Generally accepted indications for RRT include:
  • Symptomatic uraemia - Encephalopathy, neuropathy, pericarditis. Elevated urea on its own is not generally an indication.
  • Hyperkalaemia - Persistent hyperkalaemia (>6.5) despite insulin/dextrose. Severe hyperkalaemia (>8 ) with arrhythmias, requiring pacing or isoprenaline. This can occur even without anuria and should be escalated as it obviously can be life threatening.
  • Severe metabolic acidosis, pH <7.1 - This will depend upon the cause and patient's condition. Patients with DKA and pH <7 can almost always quickly be turned around with insulin and fluids. Severely septic patients may not be able to tolerate medical management long enough to improve without RRT.
  • Toxins or overdose - Some medications and toxins may be removed by RRT (eg, lithium, vancomycin), with specific type of RRT better for some drugs than others. This is uncommon and decisions will depend on the input from renal, clinical state of the patient, and advice from toxbase or national poisons service. A drug may not be removed by RRT but if it leads to another entity such as acidosis it may still warrant RRT.
  • Fluid overload or pulmonary oedema refractory to diuretics - If patient is anuric despite diuretics then it's more likely they'll end up requiring RRT. In contrast pulmonary oedema in decompensated heart failure with worsening renal function is not helped more by RRT than by adequate diuresis.
Absent from above include oligo/anuria or specific values of urea and creatinine. This doesn't exclude them as considerations, however the whole picture should be taken together to make decisions on an individualised basis. It might be that the patient improves despite a creatinine of 700, it might be they become acidotic and hyperkalaemic with a creatinine of 400. Even on the ICU we still don't know when the right time is to start RRT.
This is a reason why renal and ICU often advise the generic "monitor I/O" rather than taking over care. We do appreciate accurate monitoring is unrealistic on the wards, but we also don't have the ability to admit everyone when few will need a specific intervention like RRT. An adequate UO to aim for is above 0.5mL/kg/hr. As AKI resolves some patients enter a polyuric phase, this will resolve but watch that they don't become hypovolaemic in the process, it may require further fluids matching what is lost.

Renal vs ICU referral

This will depend on local arrangements and acuity. Refer to renal if:
  • Single organ kidney failure - Normotensive haemodynamically stable patients, not septic or comorbid with poor cardiac function. The principal reason haemodialysis is intermittent because fluid is more rapidly removed therefore borderline hypotensive patients may not tolerate large volumes of blood and fluid being rapidly withdrawn from their intravascular space. I have seen patients arrest from starting dialysis!
  • Unclear cause of AKI - ICU can offer RRT as a bridge, but the underlying cause has to be treated, if the cause is unclear or there is persistent renal dysfunction, this will require renal input. We refer for this from the ICU too.
  • Diagnosis requiring specialist treatment - Immunosuppressive therapy for vasculitis.
  • Renal transplant patients - Even with a clear cause and response to treatment, the precarious nature of immunosuppression, renal impairment and graft function mean these usually merit a call to transplant renal physicians.
Refer to ICU if:
  • Multiorgan failure - Borderline blood pressure, high oxygen requirements, fluctuating consciousness level, coagulopathy, these patients are unlikely to tolerate iHD, but more importantly it suggests they are critically ill and may need rapid escalation of care (if appropriate) beyond what renal can provide (intubation, vasopressors, etc).
  • No on-site dialysis service - In hours there may be arrangements to transfer to partnetertiary hospital particularly for complex patients. However hospitalised dialysis patients known to the renal team may require more urgent RRT than this allows. Some ICUs have the plumbing to offer dialysis (this will need a dialysis nurse however).
  • Patient in extremis - ICU may be able to offer more timely input in patients needing urgent intervention especially if prior to surgery. A patient with bowel perforation and severe AKI will usually be septic and in multiorgan failure anyway, but a 70 year old with obstructive pathology may benefit from being close to theatre to offer RRT while awaiting a nephrostomy (or exchange). If it's reversible and there is somebody willing to operate, I would even dialyse a patient with a DNACPR we wouldn't otherwise admit.

Specific considerations

  • AKI in heart failure
    • The heart-kidney interaction is complex and works both ways (see this review). Volume status and cardiac function needs to be carefully evaluated. Seeing CCF documented in the notes is meaningless. What does their most recent echo show? What did they present with? Stable HF with reasonable ventricular function and sepsis with no signs of overload can receive fluids. Acute cardiogenic pulmonary oedema with severe ventricular dysfunction probably has AKI rooted in the decompensation of heart failure (type 1 cardio-renal syndrome) and would benefit from diuresis.
    • Acute decompensated HF is usually a hypervolaemic state. Elevated right atrial pressures reduce the arteriovenous pressure gradient in the kidney leading to venous congestion, poor outflow. Inflow is also limited adding to the poor cardiac output so glomerular filtration is reduced, leading to a vicious cycle. Aggressive diuresis with furosemide reduces this congestion, improves glomerular pressure gradient and increasing filtration (as long as the patient does not become hypovolaemic). Furosemide's initial beneficial effects in venous congestion is preceded by its diuretic action and is thought to be due to it causing venodilation, reducing preload. The addition of acetazolamide may improve decongestion further.
    • Creatinine rising is not an indication to stop diuresis, it may in fact signify adequate decongestion with improved patient outcomes.
  • AKI in liver disease
    • Like in heart failure this is a complicated topic (see this recent review). AKI is very common, occuring in up to 50% of hospitalised patients with cirrhosis. While we hear things like hepatorenal syndrome thrown around, common things being common we have to look at all the usual causes we've discussed first (so don't just throw terlipressin at everyone!)
    • Pre-renal causes are most common: Discontinue nephrotoxic drugs. Look for and cover for infections and spontaneous bacterial peritonitis. Hypovolaemia from diuretics or GI bleeds, resuscitate with crystalloids and blood as needed until euvolaemic (careful to avoid overload). Albumin has been found to improve survival in patients with SBP and can be considered if worsening renal function despite resuscitation (or following paracetensis for large volume >5L ascites). Hypervolaemia from congestion (cirrhotic cardiomyopathy leading to right heart failure can benefit from diuretics, abdominal compartment syndrome from tense ascites should be drained).
    • Intrinsic leaves us with tubulointerstitial causes and hepatorenal syndrome (HRS). Low fractional excretion of sodium and urine microscopy can help confirm HRS which offers a grim prognosis. Terlipressin may improve renal function at the cost of significant pulmonary oedema so regular volume assessment and avoidance of overload is paramount. RRT would only expected to be offered if waiting, or under consideration, for liver transplantation. If not, palliation will be the most likely alternative course.
  • Drug dosing
    • I would avoid using the BNF in renal impairment. Many of its recommendations are different than common guidelines and frankly weird. Do talk to your pharmacist (also microbiologist where appropriate), they'll often refer to The Renal Drug Handbook which is a good resource and covers scenarios like RRT. Most drugs will be dosed based on creatinine clearance not eGFR so arm yourself with an app or calculator.
  • Sodium bicarbonate
    • Bicarbonate infusions offer temporary extra buffering capacity, mopping up excess hydrogen ions resulting in a higher pH. This is beneficial in hyperkalaemia as a higher pH favours potassium moving intracellularly (for this reason saline is more harmful and Hartmann's more beneficial in hyperkalaemia). It also has accepted roles in tricyclic antidepressant overdose with adverse ECG findings (QRS, QT prolongation), urinary alkalinization (in salicylate poisonining, poor evidence in rhabdomyolysis), and normal anion gap metabolic acidosis (there is high cloride to replace loss of bicarbonate, see later).
    • Its use outside these indications is contentious. There is no evidence of benefit in DKA over conventional fluids even if normal saline's tendancy for acidosis may slow resolution of the acidaemia in DKA. It may be actively harmful in lactic acidosis and respiratory failure as the increased pH shifts the O2Hb dissociation curve to the left, causing reduced oxygen offloading. It also results in net CO₂ production (HCO₃⁻ + H⁺ → H₂CO₃ → H₂O + CO₂) which will have to be blown off with excess minute ventilation.
    • So why do ICU and renal advise it or use it themselves even with a lack of solid indications? Well, essentially it's a temporising measure. Severe acidaemia contributes to myocardial dysfunction, arrhythmias, and catecholamine resistance. In the critically ill it can be useful as a delay while you insert lines or in the hope it will avoid the need for RRT. The BICAR-ICU trial did find it delays the need for RRT and may even possibly reduce the need. I'm not entirely sold on the latter, but it can be reasonable to try if there are positive indicators like good UO.
    • How? Usually available in concentrated (8.4% with 1000mmol/L of each ion) or dilute (1.26% with 150mmol/L) forms. Due to the high tonicity of the former, 1.26% is generally preferrable especially if you can or want to give larger volumes. 8.4% should be reserved for fluid restricted states and should be given slowly via a central line except in an emergency. Slow infusions help combat significant CO₂ rises and hypernatraemia (especially with 8.4%). Dosing is 1 mmol/kg which is 1mL/kg of 8.4% or 6-7mL/kg of 1.26%. For real simplicity most patients can take a 50mL vial of 8.4% or 500mL bag of 1.26%.
  • Iodinated contrast
    • The entity contrast induced nephropathy, better termed contrast associated acute kidney injury, is a contentious topic. There are many good reviews already on this topic.
    • The evidence is from old studies using high osmolality agents during PCI. Fluctuations in creatinine may not be indicative of actual renal function and may simply reflect the underlying illness requiring a scan rather than the contrast itself. Patients are not more likely to need long term RRT.
    • IV contrast with modern low osmolality agents isn't associated with AKI in patients who aren't and even those who are critically ill. There was no association in patients even with pre-existing AKI. Prophylaxis with intravenous saline nor sodium bicarbonate have been found to make a difference even in CKD patients with eGFR >30.
    • The tl;dr is unless you're in cath lab or IR suite bolusing large quantities of dye arterially it is probably irrelevant. The benefit of a quality contrast enhanced scan in diagnosing and treating the patient are likely to outweigh any miniscule risk. RCR guidelines mention appropriate consent and identification of patients at risk (eGFR <40) they do not exclude the use of contrast or require hydration, at any renal function. You are the doctor, it's up to you to discuss and determine need and benefit. (It's the radiographer's job to ask, don't @ them, but they shouldn't refuse either).

Acid-base disturbances

Now it would seem we are forced to consider the fundamental concept of what acid-base physiology even is. You might have heard about strong ion difference and become lost in confusion. You're not alone. Put simply, there are two competing theories that try to explain how pH changes occur in the body: the traditional model that uses the Henderson-Hasselbalch equation to mathematically explain pH with bicarbonate, and the Stewart model that uses the concept of strong ion difference to explain why changes in bicarbonate occur. The bottom line is that these are detailed explorations of physiology more useful for bed time reading than the bedside. For the interested details can be read elsewhere.
More practically, we can work through a blood gas in a systematic fashion to help decipher the type of acid-base disturbance. Start with pH → PO₂ (always check oxygenation) → PCO₂ (respiratory component) → HCO₃⁻ (metabolic component). I've reproduced this in a simple but limited table below for reference, but this is a more intuitive flowchart to work through.
pH PCO₂ HCO₃⁻ Disturbance
<7.35 >6 Acute respiratory acidosis
Chronic respiratory acidosis
↔ /↓ <22 Metabolic acidosis
>7.45 <4.5 Acute respiratory alkalosis
Chronic respiratory alkalosis
↔ /↑ >26 Metabolic alkalosis
Numbers indicate primary abnormalities, arrows indicate compensatory changes. Respiratory compensation by altering ventilation occurs quickly, while renal compensation by altering bicarbonate excretion is a much slower process.


With the topic being the kidney, I won't discuss respiratory acidosis here (see this earlier physiology bite). Acute respiratory alkalosis is due to hyperventilation blowing off CO₂. This can be due to obvious things like pain or anxiety, a compensation for hypoxaemia (eg, high altitude climbing), pregnancy (increased minute ventilation stimulated by progesterone), or salicylate poisoning (direct stimulation of respiratory centre).


Dipping back into some physiology, we can consider two concepts that can give us more information: base excess and anion gap. The purpose of these concepts is help narrow our differential diagnosis, rather than serve as pathophysiological explanations of illness.
  • Base excess (BE) - This idea comes from Danish physicians during the polio epidemic where patients often experienced chronic CO₂ retention. For a standardised numerical way of gauging the degree of disturbance Siggaard-Andersen proposed BE to represent the quantity of acid in a lab that needed to be added to a solution of blood to normalise it to a pH to 7.40 and PCO₂ of 5.3. Not because the plan was to literally add acid, but this way you could easily quantify the degree of disturbance. Rather than use this concept Americans appear obsessed with the more complicated Winter's formula instead. Most blood gas analysers will calculate BE for us, often reported as standardised base excess (SBE), with a normal range of +/- 3. A negative base excess is sometimes described as a base deficit, they're the same thing.
    • SBE <-3 - There is a metabolic acidosis, alone or as compensation for a respiratory alkalosis.
    • SBE >3 - There is a metabolic alkalosis, alone or as compensation for a respiratory acidosis.
    • Mild -4 to -9, moderate -10 to -14, and severe <-15 (same but positive values for alkalosis)
    • It is especially helpful with mixed disorders or causes. A lactate of 4 doesn't explain a BE of -12 alone, are there other contributors to the acidosis? A bicarb of 30 doesn't explain a BE of +10, what else can be causing alkalosis?
  • Anion gap (AG) - I have a more detailed reply here explaining anion gap. It is a theoretical number that exploits the body's need to maintain electroneutrality: we have a bunch of positively charged ions (cations) that are evenly matched with negatively charged ions (anions), and we measure some of these. When we have an excess of some anions that we don't measure like lactate this calculated number rises because one of the measured anions (bicarbonate) drops to compensate to maintain electroneutrality. Like BE, most blood gas analysers will calculate AG for you.
There are far too many causes and detailed physiology to discuss here exhaustively. If you want to read about the Cori cycle, Type A and B lactic acidosis, helpful mnemonics and more, head to this review or this section on Deranged Physiology.

Metabolic acidosis

Symptoms are non-specific, with the most obvious being hyperventilation for compensation. In severely acidotic states (pH <7) seek early ICU help. Awake patients will hyperventilate sometimes down to PCO₂ <2 which can dramatically increase work of breathing. Initiating invasive ventilation in this stage or patient fatigue can be very dangerous if hyperventilation isn't maintained, the acidosis can worsen and precipitate cardiac arrest. Hypotension from vasodilation and reduced cardiac contractility can occur, as well as arrhythmias, confusion, delirium, coma.
  • High anion gap metabolic acidosis - The presence of unmeasured anions including: lactate, ketones (diabetes, starvation, alcoholic), salicylates, formate (metabolite of methanol), oxalate and glycolate (metabolites of ethylene glycol), other toxins.
  • Normal anion gap metabolic acidosis - Losses of base (bicarbonate loss in GI tract via high ouput ileostomy or diarrhoea, renal loss via acetazolamide) or excess of acid (renal tubular acidosis, hyperchloraemia, adrenal insufficiency).
  • Pitfalls: Albumin is an unmeasured anion, so low albumin can mask a high anion gap. Albumin corrected formulas have been developed. Similarly excessively high unmeasured cations like magnesium, calcium, and even lithium, can also lower the gap.
Treatment is aimed at eliminating the underlying cause with specific therapies as required like insulin in DKA, fomepizole for ethylene glycol poisoning, folinic acid in methanol poisoning, etc.

Metabolic alkalosis

Despite metabolic acidosis being the usual focus, metabolic alkalosis is actually the more common abnormality of the two in hospitalised patients and is frequently seen as a mixed disorder (like as a response to prolonged CO2 retention as seen in mechanically ventilated patients). In severe states it can lead to delirium, seizures, obtundation, arrhythmias.
The 'opposite' of acidosis, here we see a gain of alkali or loss of acid, with impaired bicarbonate excretion required to maintain this (via chloride or potassium depletion, impaired renal function, or volume depletion).
  • Gain of alkali - Iatrogenic from bicarbonate infusions, citrate in transfused blood.
  • Loss of acid - From the kidneys via diuretic therapy, or mineralocorticoid excess, hypokalaemia. From the GI tract by vomiting especially with pyloric stenosis or obstruction as there is gastric acid loss (with chloride) only, laxative abuse diarrhoea.
Treating the underlying cause is important as always. Where there is low chloride and hypovolaemia, this usually responds well to fluid replacement with saline and potassium as required. Acetazolamide can be given if there is hypervolaemia although in practice this is rarely required unless continued diuresis with other diuretics is required. Alkalosis results in low ionised calcium that can cause paraesthesias, but as calcium is buffered by albumin this rarely requires treatment and resolves with correction of the alkalosis.


This is another large topic where there was plenty to talk about. I had to cut down the scope significantly as it rapidly spun out of control, however I thought the nuances deserved a detailed writeup. Nothing is ever absolute so don't take any of this as incontrovertible evidence of the incompetence of a hated colleague (or their brilliance)! It will hopefully have given you some ideas to think about and research further when you see patients with AKI yourself.
Until next time!
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2023.05.28 17:39 SnooGuavas1126 AITA for yelling at my roommate after weeks of being corrected on how i live?

I had got asked out on a date and at 22 had to tell my 26 year old date i have only 2 hours to be out because my roommate will not let me sleep if i dont. ( he unmatched me after this but he was a loser so silver lining) however after literally just leaving the house and we arrived at the restaurant at 9:30 i got a message asking me to come back at 10ish 11 because of there on own going issues. I got mad. After keeping my mouth shut for weeks, doing whatever i can to be quiet, and polite and non confrontational i snapped. I went home and just yelled. I told then they cant control me, they cant tell me when to come home, they are only responsible for themselves. As someone who grow up in a very controling, abusive family that i moved away from to not deal with this i was just not doing it for me. I will admit i did curse and call them a psycho bitch but like... i felt like i was being trapped again. They then told me how i was too loud around the house, i wasnt doing things around the house ( i clean our bathroom and when i tried to take out the garbage i was stoped by them) said i should be greatful to live in there space and that they let me live here and have the decency to stay at a friend's place if i am coming home late. Compared me to my abusive family and that ive been harassing they. ( i barely have time to buy bedsheets or a pillow but apparently walking up stairs and washing my face after work is harassment) told them to leave me alone slammed the door to my room and they just kept talking till they finally left to get into there room. Next day I felt bad about the whole situation. I also at one point pulled my other roommates from downstairs to ask if i have been loud because i was that fed up and they also said i wasnt loud and just thought i was always home because they never hear me come or go. I went down to apologize. I should also make note i am a very non-confrontational black girl that is very anxious so i do my best to stay out of peoples way. But that incident broke me and just stayed in my room to quietly cry. However they had different plans. Every couple of hours they would come and say something to me which i wouldn't respond. Then they threatened me by saying im lucky my other roommate wasn't here because he wouldn't have let that slide they way i yelled at her ( this is a bf bestie) i then saw that as doable action to contact my landlords which they said they will do nothing to resolve the situation and if i feel threatened to file a police report. I took a nap and as soon as i got up the harassing started again. I was so done i open the door and just said i will file a police report of they didn't stop which they also said they would file a report for me yelling and it was just a back and forth till i broke down crying and just come up with something that will make my life less of a hell fire and brimstone. I said to compromise i will be sleeping on the couch whenever i come home late form work ( i work 5 out of the 7 days of the week and i always close) so i will be using my bed 2 days of the week and maybe for 4-5 hours before i have work. We split up the chores and i took full responsibility for the bathroom they do kitchen and the other dose outside lawn maintenance. I eat my cold meal prep food in our backyard while i have a smoke and then i sleep on our couch.
submitted by SnooGuavas1126 to AmItheAsshole [link] [comments]

2023.05.28 17:33 AutoModerator Where To Watch Evil Dead Rise Online Free Reddit

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2023.05.28 17:23 zenpartymix Stolen: 44cm Soma Saga Disc touring bike, burnt orange

Hi everyone,
New here but not to biking in the city, and posting on the recommendation of a friend. My bike was stolen in Bed-Stuy last night—it was custom built and fairly distinctive, so I’m hoping against hope it turns up.
It was stolen out of my apartment vestibule on Monroe St. between 3:30 and 11:30pm on Saturday, 5/27. It’s a 44cm burnt orange Soma Saga Disc touring/road bike with 26-inch wheels. It was custom built and features drop bars, a rather tall seatpost with a weathered Brooks saddle, and an attached black trunk rack. At the time it was stolen, it also had silvertone plastic front and back fenders in so-so consition, cork tape on the handlebars, and a dark grey Ortlieb pannier attached containing my Kryptonite U-lock and a beach towel.
A very distinctive feature on this bike: there is a short piece of seatpost pipe attached vertically to the back of the cargo rack (this was for mounting a light so it would be visible despite a fully loaded rack).
Here’s a craigslist post (same text): https://newyork.craigslist.org/brk/bik/d/brooklyn-stolen-soma-saga-disc-cm-burnt/7626151571.html . Photo is not my bike but looks very similar and is the same model; I will update the post when I track down some good ones of my own.
Hoping against hope it turns up—any leads appreciated, and if found and returned I will pay you a cash reward.
Please, please get in touch if you see a bike like this out there.
Here are the parts it was built with: - Shimano Dura-Ace BS77 Double/Triple 9-Speed Bar End Shift Levers - Shimano Deore M590 9-Speed 170mm 22/32/44t Crankset, Black, with Bottom Bracket - Dimension Threadless Stem: 80mm~ 107 Degree~ Black~ 1-1/8"~ 26.0 - Nitto Noodle 177 Handlebar: 42cm Width 26.0mm Bar Clamp 140mm Drop 95mm Reach Alloy Silver - Tektro RL520 Ergo Brake Lever Set for Linear pull Black/Black - Shimano Deore M591 9-Speed Down-Swing Dual-Pull Multi-Clamp Front Derailleur - Shimano Deore M591-SGS 9-Speed Long Cage Rear Derailleur Black - Avid BB7 MTB 180mm G2 Rotor Graphite Front/Rear - Avid BB7 Mtn Disc Brake Caliper and 160mm G2 Rotor Graphite Front or Rear - CaneCreek 10 Thrdless Headset EC34/ 28.6 EC34/30 Blk - Brooks B17 Standard Electric Blue w/Black Rail - Dimension 27.2 x 350mm Seatpost Black - Shimano Deore M525A 32h Rear 6-Bolt Disc Hub, Black - Shimano Deore M525A 32h Front Disc Hub Black DT Swiss XR400 Rim 32h Mountain Disc 26" Black x 2 - KMC X9.93 Chain: 9 Speed 116 Links SilveGray - Shimano HG50 9-Speed 11-32t Cassette
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2023.05.28 17:14 Gullible-Big7231 Hello I’m looking .22 lever action air rifle that uses a spring instead of c02 ideally in the UK

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2023.05.28 17:09 beturass Today's Action

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2023.05.28 17:08 beturass Today's Action

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2023.05.28 17:00 mcfcbot [Match Thread] Brentford vs Manchester City (Premier League)

Premier League


Brentford 0 - 0 Manchester City

Kick Off: 16:30
Referee: John Brooks, England
Venue: Gtech Community Stadium
Brentford (5-3-2)
Coach: T. Frank
Pos # Name
G 1 David Raya
D 2 Aaron Hickey
D 13 Zanka
D 5 Ethan Pinnock
D 16 Ben Mee
D 3 Rico Henry
M 24 Mikkel Damsgaard
M 27 Vitaly Janelt
M 15 Frank Onyeka
F 19 Bryan Mbeumo
F 11 Yoane Wissa
Pos # Name
G 22 Thomas Strakosha
D 33 Finley Stevens
D 20 Kristoffer Ajer
M 26 Shandon Baptiste
M 10 Joshua Dasilva
M 35 Ryan Trevitt
D 30 Mads Roerslev Rasmussen
F 14 Saman Ghoddos
M 9 Kevin Schade
Manchester City (3-2-4-1)
Coach: Pep Guardiola
Pos # Name
G 31 Ederson
D 2 Kyle Walker
D 14 Aymeric Laporte
D 6 Nathan Aké
M 82 Rico Lewis
M 4 Kalvin Phillips
F 26 Riyad Mahrez
M 80 Cole Palmer
M 47 Phil Foden
F 21 Sergio Gómez
F 19 Julián Álvarez
Pos # Name
G 18 Stefan Ortega
D 5 John Stones
M 8 İlkay Gündoğan
M 16 Rodri
M 62 Shea Charles
M 20 Bernardo Silva
M 96 Ben Knight
M 93 Alex Robertson
F 9 Erling Haaland
Events not available
Match Stats:
Brentford Manchester City
1 Shots on Goal 1
2 Shots off Goal 2
5 Total Shots 6
2 Blocked Shots 3
4 Shots insidebox 3
1 Shots outsidebox 3
4 Fouls 3
1 Corner Kicks 2
3 Offsides None
32% Ball Possession 68%
None Yellow Cards None
None Red Cards None
1 Goalkeeper Saves 1
137 Total passes 306
106 Passes accurate 270
77% Passes % 88%
0.46 expected_goals 0.38
Player Stats:
player mins rating goals assists shots (on) passes key passes tackles blocks & interceptions duels (won) dribbles (success) fouled fouls offsides saves
David Raya (C) 45 6.9 - - - (-) 21 - - -/- - (-) - (-) - - - 1
Aaron Hickey 45 6.5 - - - (-) 12 - - -/- 2 (1) - (-) - - - -
Zanka 45 6.9 - - - (-) 17 2 1 -/1 3 (1) - (-) - 1 - -
Ethan Pinnock 45 6.9 - - - (-) 14 - - 2/- - (-) - (-) - - - -
Ben Mee 45 6.9 - - 2 (1) 13 - - -/1 2 (-) - (-) - - - -
Rico Henry 45 6.9 - - - (-) 10 - 1 -/1 3 (2) - (-) 1 - - -
Mikkel Damsgaard 45 6.9 - - - (-) 13 - 1 -/- 3 (3) 1 (1) - - - -
Vitaly Janelt 45 6.7 - - 1 (-) 12 - 1 -/- 5 (2) - (-) 1 1 - -
Frank Onyeka 45 6.6 - - - (-) 8 - - 1/2 1 (-) 1 (-) - - - -
Bryan Mbeumo 45 6.3 - - - (-) 12 1 - -/2 7 (1) 3 (1) - 1 1 -
Yoane Wissa 45 6.6 - - - (-) 9 - - -/- 4 (3) - (-) 1 1 2 -
Manchester City
player mins rating goals assists shots (on) passes key passes tackles blocks & interceptions duels (won) dribbles (success) fouled fouls offsides saves
Ederson 45 6.9 - - - (-) 25 - - -/- - (-) - (-) - - - 1
Kyle Walker (C) 45 6.6 - - - (-) 40 - - -/- 1 (1) - (-) - - - -
Aymeric Laporte 45 6.9 - - - (-) 30 - 1 -/- 5 (3) 1 (1) 1 1 - -
Nathan Aké 45 7 - - - (-) 39 1 1 -/1 4 (3) - (-) 1 - - -
Rico Lewis 45 6.6 - - - (-) 32 2 - 1/- 2 (-) - (-) - 1 - -
Kalvin Phillips 45 6.9 - - 1 (-) 35 - - -/- 3 (2) - (-) 1 1 - -
Riyad Mahrez 45 7.2 - - - (-) 23 2 - 1/- 1 (1) - (-) - - - -
Cole Palmer 45 6.6 - - 1 (1) 20 - - -/- 5 (2) 4 (2) - - - -
Phil Foden 45 6.7 - - - (-) 17 - - -/- 2 (1) 1 (1) - - - -
Sergio Gómez 45 6.9 - - 1 (-) 32 - 1 -/- 4 (2) - (-) 1 - - -
Julián Álvarez 45 6.5 - - - (-) 13 - 1 -/- 5 (2) 1 (1) - - - -


Brentford 0 - 0 Manchester City

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2023.05.28 16:56 sclkoma Open Letter to the DOTA 2 Community Regarding My Permanent Ban from the Competitive Scene

Hello everyone. My name is Kamil "Koma`" Biktimirov, I’m 20 years old and I'm a professional Dota 2 player who was banned for account sharing in December 2022. I'm writing this post today to express my deepest regret for my actions and to ask for consideration in reviewing my case. I am hoping this post gets enough attention so that it might reach PGL and Valve but more importantly I want to shed some light on the situation.
Firstly, I want to say outright that I accept full responsibility for my actions. I was involved in account sharing, and it was an enormous mistake on my part. I won't make excuses for my behavior, but I want to assure you that I was not fully aware of the gravity of my actions at the time. I now understand the damage I've caused to the integrity of the esports scene and the trust of everyone in the Dota 2 community.
Please allow me to explain the situation and my actions. In September 2022, I played for team Luna Gaming in a tournament called Dota 2 Champions League (D2CL). One day, my manager, Lil_skrip, told me we had tournament games to play on 22 September, although there were not supposed to be any games on that day based on our team schedule. He then told me that I needed to play from the account of another person, who was in team S9, participating in that same tournament. I was unsure about it, but I was then told that this was only for us to get more games to use as practice for more competitions in the future, and that no match fixing was involved. I was naive, so I did not think any further and said okay, and went ahead to play since it was just more practice for me. Suddenly, I saw news about 10 banned players, with myself being included. After this, I found out more about this situation, and realized that some players received money for those games. I was not persuaded to play on the basis of money, just practice, so I did not receive any money from this incident which I can prove with bank statements. I have since washed my hands off of this issue, but some others who were banned alongside myself were found to have committed more offenses, namely Kirill “deihra” Haritonov and Yaroslav “Limitless” Parshin. They were found to have played with fake nicknames and fake accounts in EU DPC Qualifiers, stuff that I am 100% not involved in. (https://cyberscore.live/en/news/lefitan-mog-igrat-za-swat-ix-vchera-diskvalificirovali/)
I now fully understand how severe my actions were. I was very naive and I am sincerely regretful for what I have done.
Dota 2 is my passion, and nothing can replace it, and I am fully committed to doing whatever it takes to prove that I deeply regret my actions and making amends. I hope that the community is able to forgive me as I did not act on malicious intent or financial greed, I am just a kid who wants to play Dota. Moreover, this is my first and only offense, and I can promise that I will not repeat the same mistakes.
Since the ban, I've reflected on my actions, and their severity. However, I have not given up on my Dota 2 career and have continued grinding MMR (currently top 30 ranked in EU servers at 11000+ MMR). I am still playing in order to improve as a player, and I have taken up streaming on Twitch to stay in touch and involved with the Dota 2 community. (https://www.twitch.tv/sclkoma)
Dota 2 has been a major part of my life since I was 13 years old, I have nearly 20000 hours in the game and more than 15000 games. It will continue to be a major part of my life regardless of the ban because I just simply love Dota. I just hope to be given a second chance to fulfill my dream of a professional career in Dota. Just as I had the opportunity to properly partake in the professional scene, my life was turned upside down because of a severe lapse of judgment on my part. I am young, and I cannot express how deeply regretful I am for my actions and how much despair I am in due to the severity of the punishment. It took me a really long time to accept and deal with this situation and it has already been 5 months since the ban.
There have been other players in the scene who were given second chances in the past and have grown to be an integral part of the Dota 2 esports scene, such as Noone (account sharing) and Solo (match fixing) who are now regarded as Dota 2 legends. I just ask for empathy and forgiveness for my mistakes. I greatly hope to be able to continue my career in the future.
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2023.05.28 16:32 jaddf Brentford XI [28.05.2023][GW38][22/23] vs MCI

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2023.05.28 16:30 Loki2298 [A3][RECRUITING] USMC SPMAGTF-22 Quarantine Company[EST/PST][Semi-Realism]

[A3][RECRUITING] USMC SPMAGTF-22 Quarantine Company[EST/PST][Semi-Realism]
When the world dials 911, the United States Marine Corps is the first on the scene. For this purpose, the Marines have developed a combined arms approach to maintaining its presence globally, a task organization known as the Marine Air-Ground Task Force, or MAGTF, consisting of ground, air, logistics, and command elements.
There are several types of MAGTFs. The most common are Marine Expeditionary Units(MEUs), Marine Expeditionary Brigades(MEBs), and Marine Expeditionary Forces(MEFs). But there are times when specialized units must be stood up temporarily. These are known as Special Purpose MAGTFs.
We are SPMAGTF-22, a handpicked reconnaissance and direct action unit, stationed between US Central Command and US Pacific Command. From the deserts of Iraq to the islands of Taiwan, we are dedicated to protecting America's interests wherever they may be threatened.
Our Operations are expected to take place Saturdays at 5pm PST/8pm EST. We offer a large variety of MOS and roles from Rifleman to Mortarman. We play semi-realism and ask that you attend at least every other operation to maintain activity. For those with more hectic schedules, we do offer a reserve and attendance not required MOS options.
As always, if joining us from a Sister Unit, give us the heads up when joining the discord and ask if there are any special promotions going on. Otherwise, please speak with a Recruiter in our Discord for more information!
Quarantine 6, OUT!
Discord: https://discord.gg/CySQpKvkqB
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2023.05.28 16:09 Ok-Role-4987 AITA for telling my employee to pay himself for studies he randomly decided and complaining about a coffee pot he broke out of anger?

As a manager at a startup, I recently encountered a challenging situation with one of my employees, David. I'd like to share some details and seek insights from others. Last fall, I hired David, a 22-year-old male, and initially assigned him tasks that he struggled to deliver on for about six months. Recognizing his difficulties, I reassigned him to different projects hoping for improvement. However, in his new role, David independently initiated costly studies without prior consultation, leaving me unaware until after the fact. Unfortunately, these studies contained significant errors, rendering them ineffective and a waste of valuable resources. I expressed my concern to David, explaining the importance of discussing such initiatives beforehand to prevent unnecessary expenses. Consequently, I declined to cover the expenses, which upset him. Regrettably, he vented his frustration by breaking a coffee pot I had brought for the team, negatively impacting everyone's ability to enjoy coffee in the office. Realizing the stress this situation caused David, I reconsidered my decision and offered to cover the costs of the studies as a gesture of goodwill. I also requested that he consult with me in the future before proceeding with any similar initiatives. He appeared appreciative, apologized to me personally, and we seemed to reconcile. However, David's behavior took a concerning turn as he began consistently missing work, failing to deliver assignments, and skipping important meetings where his presence and contributions were expected. This resulted in a poor impression of our team among our partners. Subsequently, my superior called me in to discuss a complaint filed by David. According to my superior, I was in the wrong for refusing to pay for David's studies. Additionally, they suggested I should not have made a big deal about the broken coffee pot. Their insinuation was that I was being frugal or overly concerned about a seemingly trivial matter. I firmly expressed that David's action was inappropriate and went beyond what should be tolerated in a professional setting. To address the situation, David was reassigned to another team within the startup. However, this experience left me questioning whether my actions were justified. I would appreciate any insights or perspectives on this matter. Personally, I believe that setting boundaries and ensuring responsible conduct are essential in maintaining a productive and respectful work environment. Looking back, I now regret my decision to cover the expenses for David's studies, as it might have reinforced a lack of accountability on his part. Additionally, David left without properly transferring his work, further impacting the team. Thank you for your understanding and any guidance you can provide in this situation.
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2023.05.28 15:21 beturass Yesterday's Grade

Yesterday's Grade submitted by beturass to SportsPicksChat [link] [comments]

2023.05.28 15:20 Electrical-Food9136 What type am i?

  1. What's your biggest fear?
I would say failing. Failing life/failing the goals i have set for myself. Why failing? Next question explains it.
  1. What’s your biggest desire?
To succeed in life. And what i mean by that is being a good person, getting a good job, care for my family and be kind to others. And i am religious aswell so just pass the test of life.
  1. What are you ‘’the best’’ at?
Hard to say, i don't wanna come across weirdly but i couldn't say to be honest. I have some good traits but the best? Not sure sorry.
  1. How do you see yourself right now?
Someone who has been in a bad spiral for years and destroying himself. Now on the way to rebuilding himself.
  1. How do you see yourself 5 years from now?
Hopefully happy, enjoying life and having a study course i enjoy and a job i enjoy. And just that everything is going at least much better then now hopefully.
  1. How do you express yourself?
I can be very expressive but on the other hand i can be private. With friends and family i can be much more expressive and if i am annoyed or angry for example, they will know. But with random people i will hide it alot more since i don't wanna be weird and keep my emotions under control.
  1. How do you feel about those near you (family, friends)?
Not really close to be honest. I speak with modt of direct/close family. Theres some farther family (aunts, nephews etc.) i speak with here and there but most of them are just not worth speaking to and if i explained then i would make more sense but i can't.
  1. How do you feel about strangers?
Depends on the strangers themselves. But mostly i am skeptical and doubtful of them 100%. If they are nice tho or chill then my view can change very quickly :)
  1. How do you view change/uncertainty?
That is something i can struggle witn, especially uncertainty. Its scary. Its anxious making. But i am trying to deal with it more and just accept it.
  1. How do you make decisions?
Depends on what the decision is for. If its not that serious, then i may just look at my will/feelings more. If its serious then i will analyze and look at it more logically.
  1. How do you solve logical problems?
Analyze what the problem is, look what i could do to fix it. If that doesn't work then try other solutions and if nothings works. I either think creatively/out of the box or i just get help maybe.
  1. How do you deal with your emotions?
I def feel them. And i can feel them pretty deep/strong.
  1. What drives you in life? What do you look for?
Like i said i am religious. So my goal is to pass the test of life. Why would i make nothing of this?
  1. What do you hope to accomplish in your life?
Success (in the multiple things i already listed).
  1. What do you hope to avoid doing or being? What values are important to you?
Being a bad person or doing bad things. Also just failing miserabelly and only f***ing around. Especially when i know i can just succeed.
Values, i would say just respectfulness, kindness, honestly, loyalty and intelligence (idk if that counts xD).
  1. How do you want others to see you? How do you see yourself?
I see myself as like i said, not very good since i destroyed myself. I am trying to better myself tho so i hope other see me well, as a kind person who is doing a good job in his life etc.
  1. Describe how you experience each of:
Anger: 2nd most, if not the most. I can get pretty annoyed/angry fast but i am trying recently to work it out more.
Shame: I don't like this. I want to avoid it and if it happens, i feel bad (also depends on the action ofcourse).
Anxiety: Basically my whole life. I was always shy but also could be nervous/anxious for multiple things.
  1. What do you do as a job or as a career (if you have one)? Do you like it? Why or why not?
I don't have a job yet. I did have one but it sucked ass (staff were jerks, too much pressure, etc.). I just don't have one because there is nothing that speaks to me. I am not gonna take i job that i don't enjoy and feel misarable going to.
  1. If you had to spend an entire weekend by yourself, how would you feel? Would you feel lonely or refreshed?
Depends on the week. Normally (school or with events) i would like it, so i can chill and recharge. But if the week was dry. I would be bored and lonely.
  1. What kinds of activities do you prefer? Do you like, and are you good at sports? Do you enjoy any other outdoor or indoor activities?
I like sports (football, not american. And also a bit of basketball aswell). I like gaming and reading!
  1. How curious are you? Do you have more ideas then you can execute? What are your curiosities about? What are your ideas about - is it environmental or conceptual, and can you please elaborate?
Very curious. I can be curious about even just small trivial matters. I have more ideas then i execute yes. But i am working on executing some ideas. I don't understand the environmental/conceptual?
  1. Would you enjoy taking on a leadership position? Do you think you would be good at it?
Hmm, sure. I may not take it all the time immediately, but i can take it if no one else does or i know that it will go wrong if i don't take it. I can be quite a good leader but my shyness sometimes doesn't let me take it.
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