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Cake day: July 4th, 2023

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  • All remote based typing is awful, T9 included. I can’t speak for everyone, but I can type with swipe gestures on a virtual keyboard via remote faster than I can input T9 text. I’m unaware of any stock remote for a device with a full keyboard. I would argue Apple has text entry perfected at least as well as any other major manufacturer. You have virtual keyboard entry, solid voice-to-text, and it can be configured to push a notification to your iOS device when you enter a search bar which will auto-open to the remote app and pull up the keyboard. Because of this feature passwords can also be autofilled from Keychain to make logins easier.

    You may personally prefer T9, but I’ve never seen anyone in the last decade input anything into a TV via T9. And you’re asking why it doesn’t have voice input, when it does. You admit to having never used an Apple TV yourself. I hate the idea of app-only interfaces features, but this isn’t a case like that. Maybe you should understand the features of a product before you call it “fucking stupid”.


  • You’ll have to strike a balance between security and ease. Your two major options are reverse proxy and VPN (Tailscale is one option for VPN)

    For reverse proxy, you functionally open the app to the internet. Anyone with the correct web address can access the login page. This is inherently less secure than VPN, but not irresponsibly so. Beyond the reverse proxy itself, you’ll also have to learn how to configure an HTTPS certificate to increase security since it will be open to the internet.

    For VPN, every user you want to be able to access the service has to be tied into the VPN and have the VPN running throughout their access. Tailscale is arguably the easiest way to configure a VPN right now, as you won’t have to manually deal with VPN configuration files for every device. VPN use will functionally make it like you’re on your home network. VPN access to your network should not be given to tons of people if at all possible.




  • Section 2, first paragraph. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6956183/

    At their core phages are viruses, there is no reason to expect the host immune system to not recognize them as foreign and attempt to eradicate them outside the GI tract, where most serious infections occur. The GI tract, skin, and to some extent the lower UG tract will likely tolerate these through mechanisms we tolerate colonizing bacterial flora, but colonization, even with antibiotic resistant organisms, is not a primary indication for empiric treatment for eradication. In fact there are some studies that attempting to sterilize the UG tract in colonized asymptomatic women promote symptomatic UTI.

    These colonizations become problematic when growth becomes unchecked and infection develops, or they seed infection into another compartment. There is no reason to think something as foreign as a bacteriophage wouldn’t be recognized as foreign in a sterile space (kidneys for pyelonephritis, liver abscess from migrated gut flora, endocarditis, etc) where these serious infections occur.

    This ties in nicely with your suggestion of phage cocktail therapy. Yes, that can expedite the delivery of phages, however excessive use of phages could result in anti-phage antibodies, limiting future treatment in a method similar to the development of anti-drug antibodies in epoeitin analogues, insulin therapy, antivenin, and anti-inflammatory antibody therapies like adalimumab (Humira)




  • Hello all, I’m a pharmacist and 4th year medical student with a passion for antimicrobial stewardship and infectious disease. Just wanted to share my overall thoughts on the article.

    The author’s point of “finding out if you really need an antibiotic” is honestly one of the central issues in modern antimicrobial resistance coming from two fronts: patients who demand an antimicrobial for a non-indicated reason, and doctors who for various reasons excessively prescribe antibiotics. I could wax on this for hours, but at its core, the single most important thing we can do to decrease antimicrobial resistance is decreasing total antimicrobial exposure. That means fewer prescriptions for shorter courses of narrow-spectrum antibiotics. Unfortunately every bit of this requires more buy-in from patients and more work from clinicians.

    To go along with my point above, asking your doctor to make sure you’re getting the shortest possible duration is the single best thing you as a patient can do to help with these issues (other than just not demanding antibiotics if your doctor says no, but that’s a low bar). The key word here is ask though. There’s a huge amount of clinical experience and evidence that is used to determine when it is safe to stop antibiotics. And as much as I believe in patient autonomy and educating my patients, frankly antibiotic selection/course duration is not something the general public is capable of independently making decision on. Ask your doctor, and take what they prescribe for how long they’re prescribed for, and if you have issues then call them to discuss it.

    With regards to probiotics, it’s an interesting topic that we don’t have a ton of great data for and physicians are fervently behind or against them in my experience. The fact is we just don’t know enough about them, and most aren’t regulated well enough to give good information about them. Interestingly, there was a recent study which suggested higher rates of central line infections with the organisms in the probiotics in individuals given probiotics while they had a line in place.

    Lastly, I think I have to disagree with Dr. Blaser. Medicine doesn’t overvalue antibiotics. We certainly underestimate their risks, but antibiotics are some of the most effective and life-saving medications we as a species have ever developed. Countless lives have been saved solely from their development, and very very few therapies have a NNT as low as appropriate antimicrobial therapy. They truly are astonishingly good medications when they are indicated. The issue is simply prescribing them when they aren’t indicated, which is a big part of why we’re in the mess we’re in, and is in large part driven by underestimating the risks they pose.


  • The trouble is that, as a whole, antibiotics that work against resistant organisms are inherently more broad. Bacteria develop resistance by either mutating the target site of an antibiotic, decreasing/removing the expression of a target site, increasing removal of the drug from the bacterial cell, or preventing entrance to the cell.

    These changes are relatively antibiotic agnostic (in the sense that they do not target one specific antibiotic, they target a general chemical structure which is shared among a class of antibiotics), and in most cases, if you develop a drug which is able to circumvent one of these problems, it will continue to work on the wild-type bacteria of that species (by definition making it broader). I am unaware of any antimicrobial which is effective against drug-resistant organism which has no efficacy against the wild-type of that organism.

    I agree with the other poster that phage therapy likely represents a future avenue for antimicrobial resistance. Unfortunately antibiotics will (at least for the foreseeable future) be required as to effectively use phage therapy you must identify the organism and then select appropriate phages which will kill the bacteria, which takes time that a sick patient may not have without antibiotics. We also haven’t quite figured out how to keep our immune system from eradicating the bacteriophages, particularly for infections requiring longer treatment such as endocarditis.

    There is a currently existing technology which allows for genetic identification of bacteria and fungi in positive blood cultures approximately 1 day faster than classical methods of culture and biochemical testing. There is active research into changing these tests slightly to be able to function on other body fluids (pus, pulmonary secretions, urine, etc) as well as to be able to function on fresh blood samples instead of waiting 1-2 days for the culture to become positive from bacterial growth, but these technologies are not ready for clinical use, and until they are, broad spectrum antibiotics will be a necessity.



  • tl;dr - Asking your doctor for the shortest reasonable course is a good thing that will both protect you as a patient as well as minimize your risk of antimicrobial resistance. But the key phrase is ask your doctor, do not take it upon yourself to decide when to stop them. Take whatever course you’re prescribed.

    Pharmacist and 4th year medical student with a passion for antimicrobial stewardship and infectious disease.

    Historical treatment duration for most infections was truly quite arbitrary. Evidence for most infections, when it is actually tested, have pretty consistently demonstrated shorter treatment durations than were classically taught (10-14 days for pneumonia now generally 5-7, 14 days for Gram Negative Bacteremia now 7, etc). There is a subset of infectious disease doctors that are bucking the trend of historical “you have to complete your course advice” for some infections. In general, what I have seen is recommendations to discontinue antibiotics with significant clinical improvement AND a non-life-threatening infection in a non-sterile body cavity. So nobody is shortening course durations for empyemas or endocarditis.

    The issue becomes expecting patients to know what constitutes clinically meaningful recovery and whether or not their infection is one of the “safe” ones to stop antibiotics earlier.

    At the end of the day, I totally disagree with your premise, as we should always strive for the minimum safe antimicrobial exposure. However I do agree that telling patients “shorter is better” is bad advice because I don’t want laypeople making these decisions when usually no-ID physicians don’t make them.