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Posts by Benjamin Brooks2

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Betting site threatening moderators - this is absolutely bottom-tier behavior in Feedback & Suggestions · Mar 22, 2022

slycyclist342 said:Let's get off the topic of whether the mod went too far by threatening a ban against a guy calling a company fraudsters, liars, and using tragedies to scam people.

But answering isn't the issue.

First, if you're a heavy hitter dropping a few thousand bucks on a single game, no sportsbook in the country is going to take that bet—unless it’s one of the ten biggest events globally, like the NBA, NFL, or Premier League. Only then will they touch those kinds of stakes.

Second, even if you play it smart and don't overdo it, once you start showing steady profits, every sportsbook in the world will eventually ban you. There's one exception, but they have their own ways of doing things.

When that happens, you could try organizing people across different states to place bets for you. You can't cover everything in just one place anyway; as soon as a bookie sees too much action on a specific game, they either pull the line or tank the odds.

That’s a massive headache and a total waste of time daily. Plus, most of those people are gamblers themselves, so there's always a risk someone loses their shirt and ends up causing problems for everyone involved.

It’s much more logical and easier to just sell your expertise. Why spend half your day stressing over how to place and fund your picks?

Sure, you can "live off subscribers," but you won't last long if you aren't actually delivering profit. Subscribers aren't idiots. They might pay you once, but they won't do it again if you fail, and there aren't enough suckers out there to make a living from one-time payments.

Besides, trust me, people do their homework before paying anyone.
There are millions of scammers online, which is why serious tipsters or sites use verified services. Those show a full history of every single bet, so everyone knows exactly what the profit or loss looks like.
No faking, no scams.

At the end of the day, is there really a massive difference between this and a financial advisor?
They invest your money, earn their fee, and take zero personal risk.
You could just as easily ask why they don't just take out a loan and invest for themselves instead of using other people's cash.

Gaston, I see you asked something similar, so there's your answer.

I don't have time to go buy CDs or DVDs either; it's faster to just grab them via torrent. But even that is slow, so we could just agree that one person downloads the movie, another grabs the porn, and then we find someone to sell it.😁

No faking or scamming involved there either...

Psychiatric evaluation costs $300? in Criminal and Misdemeanor Law · Mar 10, 2022

Usually, the Department of Justice or a judge—specifically an investigating magistrate—orders a psychiatric evaluation. It typically happens when someone has a documented history of mental health issues, or if family members or witnesses report bizarre behavior during the trial. Sometimes, a crime is just so brutal or strange that we have to suspect the perpetrator is dealing with some kind of mental disorder.

There’s a standard procedure for this, and here in the States, it takes a few days. We review the case files to find usable information, though some data is irrelevant. The real headache starts when the individual exercises their right to remain silent. For us psychiatrists, that makes it incredibly difficult to provide an accurate assessment of competency. Our job is to determine their mental state—whether they were fully competent, had diminished capacity, or were incompetent—and what kind of psychiatric treatment they actually need.

At our facility, we treat individuals who committed crimes while in an incompetent state. They don't go to prison because, legally speaking, they aren't held criminally responsible, even if they've been deemed dangerous. To manage that risk, they are placed in forensic institutions.

--------------------------------------------

Incompetent offenders (and those with diminished capacity who are found guilty) are handled based on the principle of public safety. They aren't "guilty" in the traditional sense, but they pose a threat to society given the severity of their actions. If no such danger is established for a defendant acting while incompetent, they'll be cleared of charges, and no legal mechanisms can be applied against them regarding that specific act.

-------------------------------------------

So what, the court still doesn't get it but keeps billing for its services? 🤔

Omicron variant in Coronavirus · Nov 30, 2021

Linda Harris59 said:That sounds exactly like the logic being used by scientists over in Japan.

They didn't claim that high vaccination coverage or herd immunity was the driver; they argued the virus essentially neutralized itself through mutation.

Here's a thought: how should we interpret that doctor's statement?

We’ve been conditioned to believe that every single physician is just a mercenary for Pfizer, tasked with pushing vaccines down our throats. Yet, when doctors in Japan suggest the virus simply mutated itself out of existence, it completely shatters the anti-vax narrative. It doesn't fit their worldview at all.

What does any of that have to do with doctors?

It's just basic Chemistry.🙏

Structural analyses of available receptor-binding domains show that the infectivity of certain coronavirus strains can be linked to mutations within these domains.
A review of mutation changes in the amino acid sequences and secondary structures of the receptor-binding domains of SARS-CoV-2 and SARS-CoV shows they are critical in interacting with the host cell membrane receptor.

In SARS-CoV, the receptor-binding domain consists of two α-helices and five β-sheets whereas in SARS-CoV-2 it consists of
four α-helices and ten β-sheets..

--------------------------

Wow, what kind of conspiracy theory is that?😵

The increased number of α-helices and β-sheets allows for more hydrogen bonds between the receptor-binding domain and the ACE2 receptor, which is linked to the increased infectivity of SARS-CoV-2.

Oh, I bet the college-educated moderators will call this a conspiracy theory now.😁

Crystal structures of the ACE2 and receptor-binding domain complexes for SARS-CoV-2 and SARS-CoV were analyzed. The analysis established that in SARS-CoV, the binding domain and the ACE2 receptor are connected by seven hydrogen bonds, one covalent bond, and one electrostatic interaction..

Meanwhile, in SARS-CoV-2, the binding domain and ACE2 are connected by eleven hydrogen bonds and one electrostatic interaction..

Lucky me, I actually paid attention in religion class.😁

Additionally, on the contact surface between ACE2 and the SARS-CoV-2 receptor-binding domain, key amino acids were identified as being responsible for maintaining their connection.

---------------------------------------------

This includes the amino acid residues Glu35, Tyr83, Asp38, Lys31, Glu37, and His34
of the ACE2 receptor, along with the amino acid residues Gln493, Gln498, Asn487, Tyr505, and Lys417 of the SARS-CoV-2 receptor-binding domain. Precisely because of the higher number of formed hydrogen bonds, the ACE2:receptor-binding domain complex of SARS-CoV-2 is more tightly and stably bound. This is further supported by the strength of the hydrogen bonds formed. Based on the distance between donor and acceptor, hydrogen bonds are categorized by strength as strong (2.2–2.5 Å), medium (2.5-3.2 Å), and
weak (3.2-4.0Å), with the hydrogen bonds formed between ACE2 and the SARS-CoV-2 receptor-binding domain falling into the medium-strength category, while those between ACE2 and the SARS-CoV receptor-binding domain fall into the weak category.

Once you read this, you'll have to go put on some leggings.😁

The SARS-CoV-2 receptor-binding domain (RBD) actually shows a much stronger affinity for ACE2 compared to the SARS-CoV RBD. We also learned something interesting about this interaction through cryo-electron microscopy. It turns out that while the SARS-CoV RBD stays mostly upright, the SARS-CoV-2 RBD tends to sit in a more reclined position, which makes it less available to bind with the ACE2 receptor. The downside
to this reduced availability is that it helps hide the domain from the immune response. While SARS-CoV relies on TMPRSS2 for proteolytic processing to enter cells, SARS-CoV-2 can also be proteolytically activated by furin alongside TMPRSS2. This furin activation allows SARS-CoV-2 to break into certain cells that don't have much TMPRSS2 on their membranes.

-------------------------------

Now they're going to try and explain how a satellite antenna works on a lunar rover to us. 🙏

Omicron variant in Coronavirus · Nov 29, 2021

Regarding these mutations

Researching that spike protein shows two different conformations.

Conformations are just different shapes a molecule takes when parts of it rotate around a single bond.

First, there's the closed conformation, where the virus struggles to fuse with a cell because conditions aren't ideal.
It has a low affinity for binding to the ACE2 receptor since there's less contact surface between the RBD and ACE2.

Once it hits the intercellular space in the human body, the spike is hit by
the cellular endoprotease furin, which shifts it into an open conformation. In this state, there's a high affinity for ACE2 due to the increased contact surface. Once it switches to open, the spike can't go back to being closed.

-----------------------------------
Only a few months after the first SARS-CoV-2 cases popped up in Wuhan in December 2019, new strains started appearing. Within a short window, numerous mutations were spotted globally; by June 1, 2020, about 35,000 strains
-----------------------------------

The D614G mutation

It's thought that replacing aspartate with glycine at position 614 speeds up how the S spike glycoprotein binds to the ACE2 receptor, making it easier to enter the cell.

In the study "The Effect of The D614G substitution on The structure of The spike glycoprotein of SARS-CoV-2", researchers found that 87% of the mutated spikes were in the open conformation, sometimes with one or two RBDs pushed out. By comparison, only 17% of the wild-type spikes were in the open conformation, while the rest stayed closed.

When the spike is stuck in the closed conformation, the RBD is physically blocked from interacting with the ACE2 receptor.
The G614 type mostly exists in a shape ready to bind to the receptor, so it doesn't even need furin to act on it—something the wild type needs to trigger the switch to the open conformation. Basically, the mutation removes a step in the entry mechanism, which significantly makes infecting cells easier.

---------------------------------------------

Proteins aren't static; they go through various conformational
changes that either stabilize or destabilize interactions at the amino acid level. These include non-covalent interactions, like the hydrophobic effect, which stabilize different conformations, and covalent ones that can stabilize or destabilize the structure.

D614

It was noted that aspartate (D) on monomer chain A (green) sits close enough (6.46 Å) to lysine (K) at position 854 B on monomer chain B (orange). This allows the negatively charged carboxyl group to create an attractive ionic interaction with the positively charged, protonated amino group of the lysine in the wild-type virus's closed conformation. To move to the open conformation, chains A and B have to pull apart so the RBD of chain B
can be pushed outward. That requires breaking several attractive interactions between the chains. Comparing the two, you have to overcome that attraction between the aspartate and lysine, requiring energy to push them far enough apart—specifically 8.25 Å—so the ionic bridge breaks.

Because of this interaction, the glycoprotein favors the closed conformation, staying in that shape about 83% of the time.

G614

With the mutation, the negatively charged aspartate is swapped for a neutral glycine. Since glycine is a tiny amino acid with no side chain, it can't maintain that interaction with the negatively charged lysine 854 B in the closed conformation.

It looks like glycine and lysine stay about the same distance apart—roughly 8.40 Å—whether they're in a closed or open conformation.

The idea is that the mutation kills off any stabilizing effect at position 614. Since there's less energy needed to flip into that open state under the right conditions, you barely
even need an enzyme to get it done. That’s why this mutated strain dominates at 87%, because it's much better at breaking into cells.

------------------------------
------------------------------

The reason this mutant is more infectious? It's got more conformational freedom because that ionic pull between aspartate and lysine is gone—replaced by glycine.

😁

Omicron variant in Coronavirus · Nov 29, 2021

rowdyranger44 said:Meanwhile, in China, they’ve wrapped up all their business and reported somewhere between Rwanda and the Maldives just 98,762 cases to this day...

There has to be something in their immunity; it's simply impossible to have such low infection rates in the Far East while we're all essentially using the same measures. That is, except for China, where you can't trust a single official figure anymore.

And you don't even get the quote right—it's the ACE2 receptor in humans

That's how the virus enters the cell. You can see in the image that these Jewish folks are highlighted in red

Omicron variant in Coronavirus · Nov 29, 2021

...we paired up an analysis of ACE2 coding variants across various groups with computational chemistry models to see how they impact the SARS-CoV-2/ACE2 interaction. The ACE2-K26R variant—which shows up most often in the Ashkenazi Jewish population —actually weakened the SARS-CoV-2/ACE2 electrostatic attraction. On the flip side, ACE2-I468V, R219C, K341R, D206G, and G211R all boosted the electrostatic attraction; listed here from weakest to strongest binding.

Any Ashkenaz representatives in here? 😁

Omicron variant in Coronavirus · Nov 29, 2021

Gerald Chavez7 said:Can you actually read an article and process it without spiraling straight into some conspiracy theory? It must be absolutely exhausting just trying to follow the news these days...

https://www.sciencedirect.com/scienc...05580820301072

https://www.preprints.org/manuscript/202002.0258/v2

So apparently science is just a conspiracy theory to you.

If you took religion class instead of biology, I guess how a virus enters a cell is just "mystery" to you.

It uses ACE2 receptors, but hey, that's a conspiracy too, right?

The receptors vary, oh no, aliens are attacking us.🍿

Omicron variant in Coronavirus · Nov 29, 2021

Gerald Chavez7 said:Whether Omicron hits harder than Alpha, Delta, or that first strain from Wuhan—honestly, it’s almost beside the point. What we’re actually waiting on is the data regarding how effectively it bypasses existing immunity, whether you got your shots or already fought it off.

If it turns out to be successful at dodging those defenses, it means the potential pool of susceptible people just got a whole lot larger...

Nobody's attacking anyone here. Why act like this? You clearly don't know the quote.

rowdyranger44 said:Everyone seems to be ignoring the very likely possibility that the Far East might possess some level of partial immunity to this virus, simply because their population has clearly encountered a similar strain in the recent past. Think back to the last WHO outbreak.

If Europe and the USA had implemented the exact same strategies as China, God knows what the fallout would have been. Shutting down such a massive territory would undoubtedly be far more devastating than the current disorganized mess we're dealing with, primarily because you wouldn't be able to maintain the distribution chains for essential goods and services—which, ironically, would just create more opportunities for the virus to spread further.

There’s an explanation, but this moderator can't even handle a quote.

https://pubmed.ncbi.nlm.nih.gov/32936832/

The virus enters the cell via the ACE2 receptor.

It was shown that the human Angiotensin-converting enzyme 2 (ACE2) is the receptor of recent coronavirus SARS-CoV-2, and variation in this gene may affect the susceptibility of a population. Therefore, we have analysed the sequence data of ACE2 among 393 samples worldwide, focusing on South Asia.

Z_K Clear enough now? Just use your head. It’s infuriating when people pretend to be stupid.

Omicron variant in Coronavirus · Nov 28, 2021

Linda Harris59 said:What on earth does that have to do with my explanation regarding mutations?

If you honestly think there is a connection, then please, enlighten me.

It’s about intelligence. You clearly lack it if you can't connect two pieces of data.

I explained that the virus enters the cell via the ACE2 receptor.

That receptor varies between Asian, African, and European populations... I gave you a chart, so Wand can analyze the numbers for you. 😁

It's obviously too complicated for you. Why isn't anyone debating this in public? 🤦

Studies have found that SARS-CoV-specific monoclonal antibodies and recombinant ACE2-Ig can potently neutralize SARS-CoV-2, and a hexapeptide of the receptor-binding domain of the spike protein binds to ACE2, thus blocking SARS-CoV entry

Clearly there are other ways to stop the virus, but they chose vaccines.

Question: Aren't you embarrassed by not grasping the basics? What part didn't you get—that the ACE2 receptor itself also mutates like the virus? Or will vaccines cause mutations in that ACE2 receptor and give us COVID-25?

----------------------------------------------

What if it turns out, say, Asians have a different ACE2 receptor that prevents the virus from entering cells? Could someone then violate the Constitution or the UN Charter by forcing movement restrictions without vaccination?

Omicron variant in Coronavirus · Nov 28, 2021

Linda Harris59 said:That is completely wrong. If you look at the data, the most dangerous mutations actually emerge from countries with very low vaccination rates. For instance, the Delta variant surfaced in India long before we even had a vaccine available.

It is true that a vaccine-resistant super-mutation could eventually become dominant in highly vaccinated nations like the USA. But the actual probability of a super-mutation developing within a vaccinated person is incredibly slim. Because there is a much smaller viral load and a shorter window of opportunity, antibodies strike the virus immediately, shutting down mass reproduction before it can mutate significantly.

Let me let you in on a little secret, just to see if you're a bot or a human, and to see if you'll keep blowing your horn after this.

The virus itself recognizes a very specific target to latch onto, which in this case is the ACE2 receptors.

That's an explanation for people like you, 😁

But check this out: those ACE2 receptors also have various mutations. Look at the link.

Investigation of the genetic variation in ACE2 on the structural recognition by the novel coronavirus (SARS-CoV-2)

https://translational-medicine.biome...86-7/figures/2

So what now? Just keep being stubborn... or actually realize what's happening.😉

Can't access BIOS in IT Support · Oct 29, 2020

Jack Cook7 said:Things have gotten messy over the last 40 years, thanks to Bill Gates, IBM, and Intel. To really break this down, I’d need a solid three pages of dense text. I touched on part of this in the thread about booting via network cards (PXE).

My advice? First, check the USB port versions on both the source and destination machines, then check what version of USB the stick itself is. Most PCs and laptops have a mix of 2.0 and 3.0.
Then we can go from there.

Also, EFI isn't the same thing as UEFI. UEFI supports MBR, FAT16, FAT32, and MFT, but like I said, things get complicated.

It’s true you need pages of text😁, but here’s a starting point:

UEFI and BIOS are low-level software that run when you power on a computer, but UEFI is the modern version. It supports larger drives and stuff—that has nothing to do with FAT16 or FAT32.
New computers come with UEFI, but they just call it BIOS so they don't confuse people who actually know what BIOS is.

Basically, BIOS looks for the MBR sector, reads it, and kicks off the bootloader.
Old BIOS can't recognize HDDs larger than 2TB, so a new 3TB drive won't work.
There's also BIOS emulation on newer computers, but I don't think that needs explaining.
And obviously, UEFI uses GPT instead of MBR to dodge those old BIOS limitations.

There. Hopefully, we've helped the user stop obsessing over USB 2.0 vs 3.0 ports and start looking for the actual reasons for the incompatibility.

E: drive has disappeared in IT Support · Sep 14, 2020

Sounds like I ran into the same thing. That cable probably just slipped a bit loose from the motherboard—hardly noticeable, but enough to mess things up. Try unplugging it and plugging it back in properly.

Need help with Microsoft Word in IT Support · Jul 9, 2020

Tyler Bennett73 said:So, I was working on some stuff in Microsoft Word and I’m trying to move my text over to another Microsoft Word doc, right? But here’s the kicker—it’s driving me absolutely insane. None of my bolded text or headers are actually sticking! It just dumps everything in as plain, boring, unformatted text. Like, seriously? How am I supposed to fix this mess?

https://support.microsoft.com/en-us/...0-fb9ce15bf3d6

Check the Paste options. I forgot the 😁
exact name.

How do I download this manual? in IT Support · Jun 28, 2020

rapidfox21 said:I’ve been going in circles trying to find a way to download this manual.
It says right here it's a PDF, but every single link just loops me back to the homepage
. Does anyone actually know how to make this work?

https://www.manualslib.com/manual/12...gd-3-8-A1.html

Click download at the top.

Schizophrenia - General Discussion in Psychology & Therapy · Jun 26, 2020

Nicholas Barnes74 said:Those spots you're seeing—those tiny little circles and dots drifting through your field of vision, and even the flashes—I deal with that too. It started when I was 15 with just one little speck, but now there are tons of them. And yeah, it's definitely not just "in your head."

It’s just fluid in the eye. When the eye muscles adjust the lens for near or far vision, that fluid shifts around. If it doesn't circulate enough, junk builds up. That’s why there are accommodation exercises—to keep that fluid moving so nothing sticks to the photoreceptors and messes with your sight.

Common "optimization" copy-paste tweaks that actually do nothing in IT Support · Jun 26, 2020

Jacob Cooper5 said:I'm sick of all these YouTube "experts" peddling useless performance hacks to people who don't understand how Windows works or even basic IT. I've been messing around with this stuff since the Windows XP days. My goal is to help people see through these myths and understand how these "tips" can actually screw up your system.

Setting up a larger pagefile.Pagefile.= better gaming performance.
The term "virtual memory" is outdated and poorly explained by Microsoft. They haven't done much to make sure users actually understand what's happening under the hood. Sure, there are reasons why they labeled disk paging as virtual memory, but the concept itself isn't just about the paging mechanism—it's about the principle of how applications perceive their available memory space.
Apps don't get direct access to memory or its addresses. The OS decides exactly where all that data gets written.
I won't go too deep into the mechanics here, but you need to get this: Windows views virtual memory as the total sum of your RAM + Pagefile available for use.

Claiming that tweaking your pagefile size will boost gaming performance is pure, unadulterated nonsense. It’s brainless. Disk paging is literally just moving data you aren't using right this second onto a drive for later. At best, it's a safety net for when you run out of physical memory. But once an app actually has to hit the swap because your RAM is maxed out? You're dead in the water. Performance tanks because an SSD or HDD is lightyears slower than the actual RAM modules on your motherboard. Period.
Don't bother disabling virtual memory, no matter how much RAM you're packing. It's not even about performance—it's just that some apps are hardcoded to look for it for various reasons.
Forget about "optimizing" virtual memory to get better performance. It’s a myth. There isn't a single benchmark out there that can actually prove it works.

SSD fragmentation and the fear over Windows 7+ optimization.
It’s true—defragging an HDD makes sense, but doing it to an SSD just wears it out. That said, ever since Windows 7, the OS actually recognizes when it's dealing with an SSD. Instead of defragging, it runs TRIM, which is what you actually need for performance and longevity.
Whatever. I still see YouTubers today warning people not to click "optimize" on their SSDs like it's some kind of disaster. It's obvious they have zero clue what they're talking about—they’re just recycling old legends from the Windows XP era.

3. Disabling Windows services
Windows is getting better and faster. Since Windows 7, disabling services doesn't even move the needle on app performance. As someone who’s always hunting for tweaks, I've never seen a single benchmark prove that turning off default services actually helps gaming performance. Not even back in the Windows XP days. It's a waste of time.

4. The whole HPET latency debate.
Windows 8 and up doesn't even touch HPET unless an app specifically demands it. If that happens, don't blame the OS—it's the app's fault. By default, Windows uses much faster timer generators built directly into the processor.
There were some issues with those Ryzen processors, but they're sorted now. Honestly, just leave Windows on the default settings. If you really need to prove it to yourself, grab TimerBench and compare the numbers.

Laptop owners using Nvidia high performance settings—what's the word?
I don't know about AMD, but setting things to high performance in the Nvidia control panel just means your GPU stays pinned at max clock speeds regardless of what you're actually doing. You really need that?
As a desktop user, this bugs me, so I can only imagine what it does to laptop users. Wasted battery life and pointless heating.
In the Nvidia control panel, you have the option to configure everything on a per-app basis. If you want your game to run at Nvidia high performance, just set it there.
It’s honestly baffling that those YouTube idiots don't get that.

6. Memory optimizers
Total garbage. These so-called memory optimizers or cleaners uselessly wipe the cache memory, which is actually designed to speed up the system by storing necessary data in RAM instead of on the disk. You end up with a slower system because once that cleaning is done, Windows has to re-cache everything it deems important based on your usage patterns.
The cache system works like this: the processor requests data from the disk, that data is written to memory, and then processed in memory as fast as possible. But then some asshole comes along and wipes that memory, and the Windows cache rises from the ashes, trying to become efficient again relative to your system and habits. Superfetch helps with this by tracking how often you launch certain apps so it can reserve space in the RAM to make them launch faster.

There are plenty of other senseless tweaks being peddled by YouTubers. These ones caught my eye recently.

Allocating more virtual memory (pagefile) = better gaming performance.

I didn't quite catch what you're claiming—is it better with a little or a lot?

SSD fragmentation and the fear of optimizing Windows 7+

I'm not sure what you meant there. Every single write to an SSD reduces the lifespan of that sector. Defragmentation is pointless because there isn't really a start or an end; it's just viewed as read/write cycles.

Disabling Windows services

Not everyone is just gaming. Why should processes you don't need and know you'll never use be sitting in your memory? They can even be buggy...

HPET latency dilemmas

Enabling HPET in BIOS is just halfway to Enabling HPET; it needs to be enabled in the OS too.
That might actually be a hardware issue, like usbport.sys...

Laptop owners and Nvidia high performance

This is something new, never seen before in this community. Those YouTube idiots 😁
You think there isn't a distinction between 2D and 3D, textures, and stuff on the GPU? 🤔

Memory optimizers

This is true, but you're confusing "advertised programs" with the actual problem. The goal is disabling things in memory that you don't need and will never need. Now, someone writes a program that wipes things from memory that you haven't used in an hour... Think about it. The problem is that after a few hours, that stuff has to be pulled from the disk again, whereas during that time, you could have been enjoying faster performance. 😁

Word Comparison in IT Support · Jun 11, 2020

Can someone start a new thread? Not sure if one exists. I want to actually solve code issues instead of dealing with all this nonsense. Or should we just pivot to arguing about Civil War history? What do you guys prefer?

Word Comparison in IT Support · Jun 11, 2020

Michael Jackson10 says:
Haven't had the time until now, but here it is. At least, this is my shorter version:

c=0
istaslova=""
word=input("Enter first word: ")
word2=input("Enter second word: ")
for i in range(len(word)):
--if istaslova.count(word)<min(word.count(word), word2.count(word)):
----istaslova=istaslova+word
----c=c+1

print("Common letters for the words are:",istaslova)
print("Total count:",c)

My previous attempt using find() was a complete bust. You'd have to manage some kind of pointer to track where you are in the words...

Anyway, isn't this decent for someone who's only had about 4 hours of Python classes with a nephew in middle school?
Wait until you see me struggle with Turtle 🤣
The Syntax trips me up. I've got one tab open with a W3Schools reference and another on Replit, but Python is actually pretty good for learning logic. You can interpret it instantly or drop in code to check variable states. The indentation-only structure is a pain, and I'm constantly checking casting since nothing is declared—I'm never sure what a function accepts or if I just messed up the Syntax... damn, my last "masterpiece" was in Cleveland... 🤦

Besides, you didn't even define the task right in your first post. It wasn't "how many identical letters they have" (since that ignores repeats: "aaaa" and "aaa" only share one unique letter), it's a "common subset" (where you treat every single letter as its own entity regardless of shape)

Man, we should start a new thread for coding challenges. We could post problems and try to hunt down solutions online, though people would probably accuse us of being "intellectually dishonest" or whatever. Is there anyone here doing actual "coding" who isn't intellectually dishonest, or are we just going to play around with Syntax errors?

Is there a thread for problem-solving? Not just Syntax, but actual discussion on how things should be done?

Word Comparison in IT Support · Jun 9, 2020

Michelle Bennett5 said:It's fine, I guess, but if you actually want to solve the problem correctly, you have to match those specific examples from the very first post. That's where the real trick is hidden.

c = 0
a = "potato"
b = "bread"
common_letters = ""
for x in a:
for y in b:
if x == y:
if x not in common_letters:
common_letters = common_letters + x
c = c + 1
print(c)
print (common_letters)

Who writes a program relying on food when we've got boolean usage matrices right here?

We aren't in a biology lab. Imagine your breaker trips and you start listing which appliances lost power...

I see you struggling to plug apples, eggs, butter, potatoes, and bread into the code. It's just what's inside the quotes; delete them and put whatever you want.

Word Comparison in IT Support · Jun 9, 2020

c = 0
a = "Benjamin Brooks2"
b = "Michelle Bennett5 Kok"
istaslova = ""
for x in a:
for y in b:
if x == y:
if x not in istaslova:
istaslova = istaslova + x
c = c + 1
print(c)
print(istaslova)