Creating a stream from an EventEmitter should remove listener on destruction

Consider:
const ee = new EventEmitter();
const s = highland('someEvent', ee);

typeof ee._events.someEvent; // function

s.destroy();

typeof ee._events.someEvent; // function

Given that highland adds a new listener to ee on creation it should also remove that listener on destruction.
We should be able to use _destructors to register the removal:
  function eeHandler () {
    var ctx = mapper.apply(this, arguments);
    self.write(ctx);
  }

  ee.on(xs, eeHandler);

  var removeMethod = ee['removeListener'] || ee['unbind'];

  if (removeMethod)
     this._destructors.push(function () {
       ee[removeMethod](xs, eeHandler);
    });

Closing since it's been fixed. Fix should be live in 2.10.5 or 3.0.0-beta.4.


[bug] Resources are not found if Linux bundle is installed anywhere else other than /usr

Describe the bug
Relative paths to resources in Linux should resolve to the ../lib/<name>/ directory relative to the executable location, instead of assuming the executable is always in /usr/lib/<name>/.
This was fixed for AppImage bundle (#1308) by looking for $APPDIR env var, and there's a "trick" to make it work when running from the deb bundle directory, by checking whether it's running from /data/usr/bin. Otherwise, it is simply assumed that the application was installed in /usr, which is not necessarily true.
That trick of making it work from the bundle directory causes confusion, because if we try to run it from there after we build it, it appears that the application works from anywhere, but when it is actually placed somewhere else (like /usr/local/ or /opt), resources are not found anymore.
It is work noting that, both for Windows and MacOS, the resource directory is resolved to a path relative to the executable. So, doing the same for Linux would be a simple change, and it could also work for the AppImage case without needing to special-case it, and of course, it would continue to work just as fine for standard bundle installations.
Reproduction

Create an application that accesses a resource file.
Build the deb bundle.
Copy the contents of the bundle data directory to somewhere else or unpack the deb file in a non-standard root.
Run the application from the new location.

Expected behavior
The application should find the resource file.
Full tauri info output
[✔] Environment
    - OS: Ubuntu 22.04 X64
    ✔ webkit2gtk-4.0: 2.42.5
    ✔ rsvg2: 2.52.5
    ✔ rustc: 1.76.0 (07dca489a 2024-02-04)
    ✔ cargo: 1.76.0 (c84b36747 2024-01-18)
    ✔ rustup: 1.26.0 (5af9b9484 2023-04-05)
    ✔ Rust toolchain: stable-x86_64-unknown-linux-gnu (default)
    - node: 20.11.1
    - yarn: 1.22.21
    - npm: 10.2.4

[-] Packages
    - tauri [RUST]: 1.6.0
    - tauri-build [RUST]: 1.5.1
    - wry [RUST]: 0.24.7
    - tao [RUST]: 0.16.7
    - @tauri-apps/api [NPM]: 1.5.3
    - @tauri-apps/cli [NPM]: 1.5.10

[-] App
    - build-type: bundle
    - CSP: unset
    - distDir: ../dist
    - devPath: http://localhost:1420/
    - framework: React
    - bundler: Vite

Stack trace
No response
Additional context
No response

Thanks for the report. This is a duplicate of #8679 though i really appreciate the extensive write up!


RHODS-4543 Updated GPU quick starts to work with getting-started-with-gpus repo

Description
RHODS-4543 required updates to the NVIDIA GPU quick starts and the notebook files in the https://github.com/rh-aiservices-bu/getting-started-with-gpus/ repository. These changes ensure the quick start remains accurate to the notebook resources.
The following MR contained the changes to the notebook files: https://github.com/rh-aiservices-bu/getting-started-with-gpus/pull/1
How Has This Been Tested?
Confirmed quick start format using the Patternfly Preview Quickstarts extension: https://marketplace.visualstudio.com/items?itemName=PatternFly.quickstarts-preview
Confirmed URLs work as expected.
Confirmed getting-started-with-gpus repo can be cloned by non-RH user.
Merge criteria:

[x] The commits are squashed in a cohesive manner and have meaningful messages.
[x] For commits that came from upstream, [UPSTREAM] has been prepended to the commit message.
[x] JIRA link(s): https://issues.redhat.com/browse/RHODS-4543
[ ] The Jira story is acked.
[x] Live build image: N/A
[x] Testing instructions have been added in the PR body (for PRs involving changes that are not immediately obvious).
[x] The developer has manually tested the changes and verified that the changes work.
[ ] QE contact acknowledges that this has been tested and is approved for merge.

@lugi0 This ping wouldn't work before :(

/assign @anishasthana

@LaVLaS @VaishnaviHire Can you review?

@lugi0 Are you able to LGTM?


Review local nav

Three issues in the local nav:

It seems the link to the main ILO website (the link that shows next to the language dropdown) does not show on the mobile designs.
We need designs for more breakpoints. As it can be seen on storybook, the layout seems to break on small widths. See screenshot below.
Perhaps we should clarify what we mean by 'Local nav', review perhaps the way we call it and document on Figma how it should be used. The local nav is meant to be used on ILO sub-sites, i.e. ILO websites that are not part of the main ILO corporate website. This is often the case for ILO databases, special campaigns/projects, etc.

Hey @inesdgomes
All the bullet points are done:

Included the "Go to main ILO website" on Mobile
Included Tablet breakpoints (See here)
So the thing with the Local Nav is that on Design we have it differently. It's not the same component nor developed the same.

Done @inesdgomes Made all the changes we talked about during our meeting and now we only have Main ILO and Subsite Nav https://www.figma.com/design/RRxsfLNxjoypKrfJg1EwJf/ILO-Components-Library?m=auto&node-id=6197-11062&t=QMNBGxgLNZZwntIx-1

Thanks @beatrizmartinmartins I still find this very confusing for someone without any background context. Can't we completely separate 'Main ILO website' nav and the 'ILO subsite nav'? A few other issues:

The order in which components are presented is not intuitive: why do we show sub-nav before main nav?
Do we really need the navigation strips to be separate components?
The mobile sub-nav shows the link to the main ILO site. This should only show in the mobile sub-nav for subsites, which should also include the space for the sub-brand logo.

Hey @inesdgomes
I just separate them into two different components:

Main Navigation Header
Subsite Navigation Header

Also removed the strips components, it didn't had any sense to have it there, and also fixed the sub-nav for subsites and main. Does it work now? Does it make sense?

Hi @beatrizmartinmartins Yes, great to have the headers as separate components. I left more comments in the file. Could you please address those before we complete this task? Thanks

@inesdgomes done

@beatrizmartinmartins Sorry, just one comment left to address on how the elements are organized and presented: https://www.figma.com/design/RRxsfLNxjoypKrfJg1EwJf?node-id=1433-3563#924857558

@inesdgomes moving this to in review after finalizing the comment

Sorry @GGKapanadze Ignore this one for now, I see there's still something we need to resolve in the design. @beatrizmartinmartins could you take a look at this comment: https://www.figma.com/design/RRxsfLNxjoypKrfJg1EwJf?node-id=3979-7043#926612144

@inesdgomes I made a test here Let's review it tomorrow

@inesdgomes Added what we talked about for the tablet version:

if we have 3 or less Menu items, we show them.
If we have more than 3 Menu Items, we hide them under the hamburger menu.

Check them here

This works! Just one comment to resolve here: https://www.figma.com/design/RRxsfLNxjoypKrfJg1EwJf?node-id=3979-7043#958928737

Comment solved @inesdgomes

Hi @beatrizmartinmartins Thanks, this works. In the meantime, there's an issue we'd need to solve related to this: https://www.figma.com/design/ulu2zb7ZOuT4VXu4M7Yp98?node-id=149-6177#961184293
I think showing the sub-site name under the logo on tablet and mobile doesn't really work, especially when the sub-site name is very short, such as ILO Live. Would it be possible to keep showing the sub-site name to the right of the logo on mobile? Will that limit us somehow?

@inesdgomes To review

Hi @beatrizmartinmartins I'll leave this in review until we address the sub-site component: https://github.com/orgs/international-labour-organization/projects/2/views/14?pane=issue&itemId=80747950&issue=international-labour-organization|designsystem|1223
Once that's resolved, I'll move this to development so Justin can tackle everything in one go.


Make public_key.pkcs7.pem a RSA public key instead of a X509 certificate

OpenSSL PKCS7 encrypt function needs a list of X509 certs to encrypt and sign data.
In hiera-eyaml, the certificate is only a vehicle to wrap the public key in order to use PKCS7 encrypt/decrypt functions. It has no signature checking function since the certificate serial number is harcoded to 1. All other attributes configured for the certificate are not involved in the decryption i.e: subject, start date, end date, digest, extensions.
In this PR, we propose to replace the format of the public key file from an X509 certificate with serial number 1, to an RSA public key file. Internally, we wrap the public key in a dummy certificate with an hardcoded serial number.
For the hiera-eyaml user, it is easier to understand that eyaml deals with a keypair. This is also what is documented. It is also make it easier for users to generate a keypair with openssl CLI.
We moved from serial number 1 to serial number 0 to make all tests pass. The test encrypted data were originally signed with a certificate serial number 0. The harcoded serial number was changed in commit f9fde79, but the encrypted data and the key files were not regenerated. Since it's been more than 10 years where the serial number has been 1, if this PR is accepted, we would updated the test data to make it sign with serial number 1 instead.
To upgrade, If the data has been encrypted with certificate serial number 1 (in the last 10 years), a user would only have to only have to extract the extracting the public key from the private key file:
openssl rsa -in private_key.pkcs7.pem -pubout -out public_key.pkcs7.pem

I'm :-1: on breaking changes unless they deliver a clear benefit or prevent a significant harm. After looking through this patch, it appears that hiera-eyaml will no longer be able to load existing .pem files that are in wide use today in production systems. It also looks like the code calls OpenSSL::X509::Certificate.new and ends up creating a certificate anyway --- so there is no actual change in how PCKS7 is being used.
So, I'm with Linus on this one: "don't break userland"

Hi!

This is also what is documented

@cmd-ntrf which documentation do you have in mind?

It is also make it easier for users to generate a keypair with openssl CLI.

Yes. But I think that's the reason why you can generate everything via eyaml createkeys?
I don't mind the additional support for plain private + public key, if the diff is easy to review and doesn't break existing setups.

A tool like cfssl can also be used to generate self-signed certificates with much less hassle than openssl, if you're looking for something that has fewer dependencies than a Ruby gem:
$ echo '{"CN": "hiera-eyaml", "key": {"algo": "rsa", "size": 4096}}' \
     | cfssl selfsign 'hiera-eyaml' - \
     | jq -r '.cert,.key'

2024/05/02 10:06:01 [INFO] generate received request
2024/05/02 10:06:01 [INFO] received CSR
2024/05/02 10:06:01 [INFO] generating key: rsa-4096
2024/05/02 10:06:03 [INFO] encoded CSR
*** WARNING ***

Self-signed certificates are dangerous. Use this self-signed
certificate at your own risk.

It is strongly recommended that these certificates NOT be used
in production.

*** WARNING ***

-----BEGIN CERTIFICATE-----
...
-----END CERTIFICATE-----

-----BEGIN RSA PRIVATE KEY-----
...
-----END RSA PRIVATE KEY-----

First, thank you for taking the time to review this properly. I appreciate it. I understand it is a breaking change. Let me try to answer your interrogations the best I can and I am open to discussion on how we could me make it break less things. My work on this started when asking myself why does hiera-eyaml requires the "public key" to decrypt. I found a partial solution to this and made PR #364. Then, I kept digging and realized the public key was not only a public key but a certificate.
I also found issue #137 where @gtmtech said this about public key being required:

Yes, when I implemented this, I noted that the public key and the private key are necessary to decrypt, and only the public key is necessary to encrypt. If you know otherwise, please let me know and will investigate.

So 9 years later, I decided to investigate and give a shot at a remedy.
@bastelfreak : > which documentation do you have in mind?
Starting with the README.md - Generate keys. It is mentioned that the command generate a private and a public key. No mention of certificate. In fact, the word certificate is never mentioned in the entire README. Users expecting a public key file will be surprised to find a certificate.
@Sharpie: > it appears that hiera-eyaml will no longer be able to load existing .pem files that are in wide use today in production systems
@bastelfreak: > I don't mind the additional support for plain private + public key, if the diff is easy to review and doesn't break existing setups.
Correct me I understand this improperly, but if we were to introduce backward compatibility with previous the previous public key format, it would make this PR acceptable? If so, I am confident that can be arranged.

Quick update: I think it ois possible to entirely remove that serial number constant by retrieving the certificate serial number value from the PKCS7 data object. This means decrypt would no longer require the public key, and therefore its format would no longer matter. There is a breaking in the test for Ruby 2.7, but I am confident I can fix it.
As for the encrypt function, it would be possible to support both the X509 certificate and the RSA public key format.
This would no longer make this a breaking change PR, but a feature PR to support RSA public key for encrypting.

Preserving backwards compatibility would be a requirement. However, I'm generally not a fan of complicating cryptographic workflows with branching logic --- especially when there are ways to generate the required input.

The PR is now backward compatible.

The encrypt function supports both public key file format X509 and RSA public key.
I have removed the commit changing the test public key file format.
I have removed the check on the ruby-openssl gem version. It is no longer required as we fetch the certificate serial number from the PKCS7 object.

It looks like 2 years ago I also got confused by the behavior of this backend, but I finally just did a copy of the code and adjusted it to use bare RSA keys: https://github.com/smortex/hiera-eyaml-rsa
At that time I was thinking that this module would make a lot of sense if it was able to handle a bunch of public keys (e.g. 1 for the puppet sever and 1 for each sysadmin) and when encrypting a secret allow to choose who will be able to decrypt it (e.g. the puppet server, and a selected group of admins).  In a bolt context where multiple small teams might need to have access to some secrets that should not be available to other teams, this could be handy.

@smortex : I started going down a similar route before stopping when I realized that there is a limit to the number of bytes that can be encrypted with an RSA key. It depends on the keysize, but for the default 2048 bits, a RSA only backend could only encrypt 214 bytes data. While the PKCS7 backend does support encrypting files of arbitrary size.


Refactor Gripp3r with main.py and README

Merged via https://github.com/pybricks/pybricks-projects/pull/19. Thanks!


Justeson and Katz patterns for .nouns()

"Take the longest sequence that fits one of the following parts-of-speech patterns:"
AN
NN
AAN
ANN
NAN
NNN
NPN
N = Noun
A = Adjective
P = Preposition
This is something discussed by Manning and Schutze as the “Justeson and Katz Filter" from their 1995 paper. It was focused on how to extract technical terminology.

@spencermountain I started playing with something like this:
         results = nlp(parsingText).match("#Noun #Preposition #Noun #Adjective? #Noun?").out('array')

But I would need to go through all permutations.  Something internal would be more performant. This is an example of a test I did on a small 200 document list.
noun-phrase-test-200-docs.txt
Here is the source:
nifa-data-all-200.txt
(Parsed only the 10th field)

heyyy, i did some of this yesterday, you may be pleased. I didn't copy their thing directly, but did lift a bunch of their examples/thinking.
https://github.com/nlp-compromise/compromise/blob/master/test/unit/subset/noun/nounPhrase.test.js
lemme know if you see anything weird/bad
cheers


dune: Update to Dune 3.15~alpha2

OK let's do this. Will upgrade to the final release once it's been tagged. Thanks!


Skip multiprocessing if no callback actions requested; Add sound param; Fix signal handling

Changes:

If there are no callbacks requested then there is no need for multiprocessing / listening / etc.
Fix the signal handling - the argument to sys.exit() is just the return code for the shell; it does not re-raise the SIGINT to call sys.exit(signal.SIGINT). Now it properly re-raises the trapped signal.
Add sound parameter as per the other PR https://github.com/Jorricks/macos-notifications/pull/25

In order to implement (1) I had to move the MacOSNotification class outside of the create_notification() method so it would not be redeclared every time create_notification() is called - see my comment.
Re: (2) I'm still not really convinced that trapping SIGINT in a package is the best idea and am kind of concerned about other unforeseen side effects but at least re-raising it seems to work as the user might expect.
Feel free to cherry pick and/or request changes.

It turns out that because the MacOSNotification class isn't getting redefined with every call to create_notification() any more forking the initial NotificationProcess was unnecessary - you only need multithreading to listen for responses, not trigger the initial notification - so i removed NotificationProcess altogether on this PR.

First of all, sorry for being so slow to respond.
Second, I went over the MR and it looks very nice and ready to merge. Please rebase it/fix the conflicts and we can get it in.


Do test Issue NFT while looping

abount 100 counts

this error is reason that did NFT.storage rate limit


Quick dockerfile fix

Updating the default entry user to conatiners built by pyk

There's a build failure I can't reproduce locally, or figure out what might cause.
When make test-pyk is run in the container as root, everything works fine. When however the user is set to user, it fails:
poetry run make -C pyk-tests
make[1]: Entering directory '/home/user/pyk-tests'
kompile ../k-files/d.k             \
    --output-definition definitions/d \
    --backend haskell                  \
    --emit-json
Error:  Critical: Could not write to ./definitions/d/scanner
(NoSuchFileException: ./definitions/d/scanner)
make[1]: Leaving directory '/home/user/pyk-tests'
make[1]: *** [Makefile:50: d.kompiled] Error 113
make: *** [Makefile:47: test-pyk] Error 2
Error: Process completed with exit code 2.

It looks like at that point, ./definitions/d/scanner should exist for rewriting, but it doesn't. The exception is probably raised here.
@ehildenb @radumereuta, any ideas what might cause this?

I haven't seen this before. Did you try running the tests again?

I haven't seen this before. Did you try running the tests again?

Yes, and the failure persists.

Running this locally I can see that kompile is trying to copy a generated scanner
from: /tmp/tmp-kompile-18140886876713790802
to: ./test-kompiled/scanner
Maybe running this in user mode doesn't allow you to copy from the /tmp directory?
I find it surprising that it's using the default /tmp dir instead of the .kompile-*** directory we usually use.
If this isn't something you can solve, we may be able to bypass this issue by changing how the scanners are generated in the front-end.

Thanks, @radumereuta, for looking into this, this might well be the root cause. @F-WRunTime, is it possible that the Docker container run on the worker restricts access to /tmp?

changing how the scanners are generated in the front-end

I think doing this might be a good idea in any case, especially if during kompilation other temporary files are created under .kompile-*.

I think doing this might be a good idea in any case, especially if during kompilation other temporary files are created under .kompile-*.
If you can't find a workaround with the container, please open an issue in the front end and we'll see how we can schedule such a fix.

That's a good question. The only thing I can find on this topic is the base container we use could have set the /tmp folder permissions such that we can't access it.
I tested this and didn't appear to have any issues with the container build process and creating a file within /tmp

The problem is not with the generation, but with the copy.
            Files.copy(scanner.toPath(), output.toPath(), StandardCopyOption.REPLACE_EXISTING);

If it was created as root, and the copy is done at the user level, then it might be an issue.
Or it's trying to override something already in the output directory and it fails.
But I'm just guessing.

The problem is not with the generation, but with the copy.
            Files.copy(scanner.toPath(), output.toPath(), StandardCopyOption.REPLACE_EXISTING);

If it was created as root, and the copy is done at the user level, then it might be an issue. Or it's trying to override something already in the output directory and it fails. But I'm just guessing.

Ah okay I think I found the root of the issue. We really should have done this where we mount the runner user into the container. And run out of shared folders, I forget why we didn't. But if we want to continue to work it the way we are with this 'user'. I'll post a quick and dirty solution in my next commit but ultimately I would strongly recommend we were running the 'docker run ` command something like this:
docker run                             \
          --name ${TAG_NAME}                 \
          --rm -it                           \
          --detach                           \
          --workdir ${{ github.workspace }} \
          --user $(id -u):$(id -g)                  \
          -v ${HOME}:${HOME}                 \
          -v "$(pwd):/opt/workspace"         \
          -v "/etc/passwd:/etc/passwd:ro"    \
          -v "/etc/group:/etc/group:ro"      \
          runtimeverification/${TAG_NAME}

This makes sense why none of us could reproduce. Likely case is we are all the FIRST user  on our accounts UID which I think almost always is given the 1001 uid which would match as we're building this such that 'user' (first user in the container) coincidentally has the same uid as we do.

This makes sense why none of us could reproduce. Likely case is we are all the FIRST user on our accounts UID which I think almost always is given the 1001 uid which would match as we're building this such that 'user' (first user in the container) coincidentally has the same uid as we do.

This was exactly the case. I changed the UID and GID of user, and was able to reproduce the issue locally.
The direct cause of the failure was that kompile couldn't create folder /home/user/pyk/pyk-tests/.kompile-* due to a permission issue. This was because the owner of the copied files were the host user (and this is only a problem with a host user other than 1000).
This is somewhat surprising, as the docker cp docs state the following:

Ownership is set to the user and primary group at the destination.

This seems to be true if the container is run as root, but not in general.
Anyways, I created a PR (https://github.com/runtimeverification/pyk/pull/63) that makes tests work with this generic non-root user. I also cherry-picked some commits from this PR.

We really should have done this where we mount the runner user into the container. And run out of shared folders, I forget why we didn't.

As our runners are not ephemeral, I wanted to copy rather than mount to avoid side-effects on the runner. Also, I find this approach more reproducible as it provides better isolation of guest from host.

This makes sense why none of us could reproduce. Likely case is we are all the FIRST user on our accounts UID which I think almost always is given the 1001 uid which would match as we're building this such that 'user' (first user in the container) coincidentally has the same uid as we do.

This was exactly the case. I changed the UID and GID of user, and was able to reproduce the issue locally.
The direct cause of the failure was that kompile couldn't create folder /home/user/pyk/pyk-tests/.kompile-* due to a permission issue. This was because the owner of the copied files were the host user (and this is only a problem with a host user other than 1000).
This is somewhat surprising, as the docker cp docs state the following:

Ownership is set to the user and primary group at the destination.

This seems to be true if the container is run as root, but not in general.
Anyways, I created a PR (#63) that makes tests work with this generic non-root user. I also cherry-picked some commits from this PR.

We really should have done this where we mount the runner user into the container. And run out of shared folders, I forget why we didn't.

As our runners are not ephemeral, I wanted to copy rather than mount to avoid side-effects on the runner. Also, I find this approach more reproducible as it provides better isolation of guest from host.

As long as we are running our jobs in containers they are ephemeral. The piece that won't be is if we try to install something to the host. But this method is fine. the _work folders where jobs run are ephemeral and won't liter or effect other jobs or jobs from the same repository. Regardless this approach is okay to do.
Should I delete this PR and the branch?


Tflite SSD Postprocessing

Adding custom operators to implement SSD postprocessing in mobilenet-ssd.

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After adding SSD Postprocessing ops,  how to convert mobilenet-ssd .pb model to tflite model ?

 You could use something like this script.
 You could use something like this script.
Then use toco, with something like this:
bazel-bin/tensorflow/contrib/lite/toco/toco \
    --input_file=/home/maly/tensorflow-lite/ssd_mobilenet_coco_2017-11-17_lite.pb \
    --input_format=TENSORFLOW_GRAPHDEF  --output_format=TFLITE \
    --output_file=/home/maly/tensorflow-lite/ssd_mobilenet_coco_2017-11-17_lite.lite \
    --inference_type=FLOAT   --input_data_type=FLOAT --input_array=image_tensor   \
    --output_arrays="Result/NumDetections,Result/Boxes,Result/Scores,Result/Classes" \
    --input_shape=1,300,300,3   --allow_custom_ops

@mohamedadaly , Thanks,
How to get "ssd-mobilenet-anchors.pb"  in  script?

You can find it here

Nagging Assignee @petewarden: It has been 14 days with no activity and this issue has an assignee. Please update the label and/or status accordingly.

You can find it here
https://www.dropbox.com/s/vanawje6zyocznt/ssd-mobilenet-anchors.pb?dl=0
On Mon, Jul 9, 2018 at 1:40 AM Wenguo.Li<EMAIL_ADDRESS>wrote:

@mohamedadaly https://github.com/mohamedadaly , Thanks,
How to get "ssd-mobilenet-anchors.pb" in script?
—
You are receiving this because you were mentioned.
Reply to this email directly, view it on GitHub
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.

@petewarden -- what is the state of this PR? Is it intended to be reviewed and merged?

Closing this PR as we've now pulled in code to do this elsewhere.


First draft of Unity SDK for Nether

Issue: #385

[ X] Tick here to confirm that you have run RunCodeFormatter.ps1

Description:
Added a few methods to use Nether SDK from a Unity game

@dgkanatsios,
Thanks for your contribution.
To ensure that the project team has proper rights to use your work, please complete the Contribution License Agreement at https://cla.microsoft.com.
It will cover your contributions to all Microsoft-managed open source projects.
Thanks,
Microsoft Pull Request Bot

@dgkanatsios, thanks for signing the contribution license agreement. We will now validate the agreement and then the pull request.
Thanks, Microsoft Pull Request Bot

@dgkanatsios can you have a look if there is a seeting in Unity to save assets, unity and meta files as text/ascii instead of binaries. I got some hints that that can be done, but don't have a direct link to a solution. Just need to be sure what we accept.

@krist00fer latest commit should address that, everything is serialized to text now (both assets and settings). Here is the relevant entry in the Unity documentation.

Just bumped into Unity's recommendation of what should be checked in into source control systems, leaving it here for reference
https://docs.unity3d.com/Manual/ExternalVersionControlSystemSupport.html

All assets are now as text, that looks much better. I'll go ahead and review the content again.


Latest package not on NPM

Hi,
I don't know if you own the right to be able to update the package on NPM, but your latest commits including 126bb11300cb207c8355372853cc1691d6857a07 are seriously needed on the NPM platform as their bugs are very noticeable.
I found this repository through here: https://www.npmjs.com/package/line-by-line
So I assume you have the right to update the package.
For now I have manually added the source to my project.

+1

+1

Done: https://www.npmjs.com/package/line-by-line


added graphing for Heart Rate Recorder

CHANGES

added graphing of latest 164 measurements of chosen record file
graphing code is based on batchart

Signed-off-by: Andrwe Lord Weber<EMAIL_ADDRESS>

Thanks! This looks great! I don't see anything that should really use the memory up too much though - so I'm a bit surprised about the large memory usage.
The big thing would be writing data into a standard JS array (rather than a types array) but it doesn't look like you do that?


update minikube and kubernetes version

Description
update to latest
Related links

xxx

Error from server (InternalError): error when creating "./rabbitmq-ingress.yaml": Internal error occurred: failed calling webhook "validate.nginx.ingress.kubernetes.io": Post https://ingress-nginx-controller-admission.kube-system.svc:443/extensions/v1beta1/ingresses?timeout=30s: dial tcp <IP_ADDRESS>:443: connect: connection refused
##[error]Process completed with exit code 1.


Remove excess icon

Duplicated with the SvgQualityUnknownIcon.tsx file?

 Thank you for your submission! We really appreciate it. Like many open source projects, we ask that you sign our Contributor License Agreement before we can accept your contribution.You have signed the CLA already but the status is still pending? Let us recheck it.

@hehehai Thanks for bringing this to our attention 👍.
I have made some additions. All icons are generated, so I made sure we remove all of them before generating new ones. I also added a warning that the icons are generated automatically.

@Ocupe thx! Cool, automatically generating resources is a good way to synchronize, and I found this problem when I copied resource files.
I'm trying to write vue components, But I see that the component library seems to be refactoring.
https://github.com/livekit/components-js/compare/main...hehehai:components-js:hehehai/support-vue


HTTP API

Hello!
Thank you for this. This is exactly what I have been planning to impement for myself for ages but couldn't due to the lack of spare time (and tbh I was just too lazy at times).
Is there HTTP API available for tagging?
Why am I asking? Well, there is the Spotify Destop extension solution called Spicetify. I made some experiments with it and found out that it's pretty simple to modify the Spotify context menu to add some custom functionality to it written in JS. The idea is to incorporate tagging directly into Spotify. One can just right click on a track/album/artist/playlist and apply a tag without the need to go somewhere else. I find this very convinient.
Here is the demonstration of rating and tagging respectively:
https://photos.app.goo.gl/rn5g3JXXq7jqAL2J8
https://photos.app.goo.gl/aT1izaivRybDWJk56
(I consider ratings to be just a special case of tags)
I just don't have a back-end for tagging for now. If your service had HTTP API I could use it as back-end. Of course, I would share the Spicetify extension I made too on Github so everyone could use it.
What do you think of my idea?

I just released the v1.0.2 version, it contains a BackendAPI.exe file that implements the HTTP API (the app automatically updates if you have not disabled that option).
A documentation for it can be found here
All the API endpoints you need are implemented.
In addition, the user needs to login before using the API (this login is seperate from the one the SpotifySongTagger.exe uses). When you open the BackendAPI.exe it will automatically prompt a login if the user is not logged in yet. The connection to spotify from the API can also be controlled with the connection endpoint.
In addition to GET tags/ I provided a GET taggroups/ for forward compatibility. Right now it just returns all tags in a default group, but once taggroups are implemented, this will be updated to properly return the taggroups.

@BenediktAlkin thank you very much. I have coronavirus now, will try out once I get well.

Unfortunately, I have a problem with the API.
The library Spicetify provides for HTTP requests can't handle content types other than JSON, so I got an error whenever the Tagger backend issues text/plain response, in particular connection/userid and all the endpoints for checking tags (get tags/{tag}/tracks|playlist|album?id=...). Would you please change the API endpoints to produce JSON?
Something like these would be good
get connection/userid returns {"userId": "{value}"}
get tags/{tag}/tracks?id={id} returns {"result": "NONE|SOME|ALL"}

I added json endpoints to the api. You can call endpoints that return something with prefixed json/ to get the result wrapped into json format.
GET connection/userid returns exampleuserid
GET json/connection/userid returns {"result":"exampleuserid"}

I've finished the extension. Been testing it. The API works fine. So I'm closing this.


Address coverity-reported NULL dereference in SSL_SESSION_print()

We need to check the provided SSL_SESSION* for NULL before
attempting to derference it to see if it's a TLS 1.3 session.

merged to master; closing


.Net: Bug: Can't create OpenAIAssistantAgent with CreateAsync()

Describe the bug
According to the source code and all of the examples and documentation, this method takes an OpenAIAssistantConfiguration object as the second parameter, but when I use it, IntelliSense tells me I must use an OpenAIClientProvider object. In fact, OpenAIAssistantConfiguration is not defined. Am I missing a NuGet package or did the implementation change?

    <PackageReference Include="Microsoft.SemanticKernel" Version="1.18.0-rc" />
    <PackageReference Include="Microsoft.SemanticKernel.Abstractions" Version="1.18.0-rc" />
    <PackageReference Include="Microsoft.SemanticKernel.Agents.OpenAI" Version="1.18.0-alpha" />

I am using OpenAIClientProvider.ForAzureOpenAI(_apiKey, new Uri(_endpoint)) for the parameter, but when it's executed, I get an exception: "HTTP 404 (invalid_request_error: ) Invalid URL (POST /v1/assistants)" with this stack trace:
   at Azure.AI.OpenAI.ClientPipelineExtensions.<ProcessMessageAsync>d__0.MoveNext()
   at System.Threading.Tasks.ValueTask`1.get_Result()
   at Azure.AI.OpenAI.Assistants.AzureAssistantClient.<CreateAssistantAsync>d__4.MoveNext()
   at OpenAI.Assistants.AssistantClient.<CreateAssistantAsync>d__46.MoveNext()
   at Microsoft.SemanticKernel.Agents.OpenAI.OpenAIAssistantAgent.<CreateAsync>d__23.MoveNext()
   at SKLasVegas.Program.<Agents>d__9.MoveNext() in C:\Users\MYeager\Dropbox\AI\SK DevIntersections Las Vegas 2024\SampleCode\SKVegas\Program.cs:line 208
   at SKLasVegas.Program.<Main>d__3.MoveNext() in C:\Users\MYeager\Dropbox\AI\SK DevIntersections Las Vegas 2024\SampleCode\SKVegas\Program.cs:line 34

Here is my code...
            OpenAIAssistantAgent agent =
                await OpenAIAssistantAgent.CreateAsync(
                    kernel: kernel,
                    clientProvider: OpenAIClientProvider.ForAzureOpenAI(_apiKey, new Uri(_endpoint)),
                    definition: new OpenAIAssistantDefinition(_defaultDeployment)
                    {
                        Description = "This is a test agent",
                        EnableCodeInterpreter = true,
                        EnableFileSearch = true,
                        EnableJsonResponse = true,
                        //ExecutionOptions = new OpenAIAssistantExecutionOptions {  }
                        Instructions = "This is a test agent", //system instructions
                        Name = "MyAgent",
                        Temperature = (float?)0.9,
                        //VectorStoreId = "??",
                    });

Platform

OS: windows 11 x64
IDE: Visual Studio 2022
Language: C#

Thanks in advance.

@MikeYeager The 1.18.0-rc code is not merged to main yet, the code is still in the feature-connectors-openai feature branch so please go here to see the samples https://github.com/microsoft/semantic-kernel/tree/feature-connectors-openai/dotnet/samples

Thank you for that. FYI, the samples appear to be broken at the moment.

Any news on this? 1.21.1 is out now and this branch no longer exists, but I'm still getting the same error. Should I open a new issue?


Add collapse feature to each school year

Explore the collapse feature of Bootstrap and add the feature to optionally collapse each school year (9th grade, 10th grade, 11th grade, 12th grade) so users can focus on a single year. Add labels for Fall/Winter/Spring to each card as well.  Most or all changes will be in the file terms.html.

Resolved in production version.


Dev

New Features / Significant Changes

Implement almost entire Etcd v2 API (user auth, roles, permissions)
Expand redis API implementation (strlen, multi, discard, exec, info)
Reduce memory usage for events significantly (>50%)
Reduce memory usage for services
Introduce non-atomic shared_ptr
Support requesting dependencies of the same type multiple times but with different properties (e.g. two IHttpConnection's to different addresses)
Support custom HTTP route matchers

Introduce an Ichor RegexRouteMatcher that supports capture groups for parsing e.g. /users/{id}?{queryParam1}={valueParam1}

Implement Small Buffer Optimization in Ichor::Any
Support converting Ichor::Any type and values to string for logging contents of Properties
Add Raspberry Pi model specific optimization flags
Add benchmark numbers on Raspberry Pi Model 4B
Add _FORTIFY_SOURCE=3 and other security related flags on non-windows builds when using hardening
Improve various compile/link modes, e.g. using libcpp instead of libstdc++ or creating a statically linked musl-aarch64-mimalloc build.
Support services having a priority lower than the default dependency priority, effectively enabling some control over which services get initialized first.
Have coroutines use the same priority for events as the services that create them

Third-party Libraries

Fork and update Mimalloc to 2.1.2

Forked because of this issue.
Allows using mimalloc with ASAN as well as on the combination of musl, aarch64
Use mimalloc's secure mode when hardening is turned on, even for release builds.

Update spdlog to v1.13.0
Update fmt to 10.2.1
Update Catch to 3.5.2
Update sole to 1.0.5
Update glaze to 2.0.6
Introduce CTRE 3.8.1
Introduce ankerl's unordered_dense 4.40, replacing std::unordered_map and abseil::btree_map entirely.
Remove abseil as a possible dependency (users are free to re-introduce it in their own projects, of course)

Bug Fixes

Fix bug  when sending multiple messages with HttpConnectionService
Fix data race with multiple threads creating services without dependencies
Fix data race in coroutine IO implementation
Fix bug in EventStatisticsService where collected events would be thrown away because a coroutine was not being run to completion
Fix bug where iterators to event interceptors might get invalidated by modifying the list of interceptors inside of an event intercept handler
Fix bug where realtime example would always try to re-enable SMT if option to disable it was missing

Codecov Report
Attention: 304 lines in your changes are missing coverage. Please review.

Comparison is base (dcbd0d7) 75.51% compared to head (e108f5b) 82.29%.
Report is 13 commits behind head on main.

:exclamation: Current head e108f5b differs from pull request most recent head 5972676. Consider uploading reports for the commit 5972676 to get more accurate results

Files
Patch %
Lines

include/ichor/glaze.h
0.00%
96 Missing :warning:

...nchmarks/utils_benchmark/ichor_utils_benchmark.cpp
62.35%
32 Missing :warning:

include/ichor/services/etcd/IEtcd.h
0.00%
30 Missing :warning:

include/ankerl/unordered_dense.h
93.58%
26 Missing :warning:

include/ichor/events/InternalEvents.h
79.26%
17 Missing :warning:

include/ichor/services/network/ClientFactory.h
65.30%
17 Missing :warning:

include/ichor/stl/ReferenceCountedPointer.h
86.53%
14 Missing :warning:

...ependency_management/ConstructorInjectionService.h
42.10%
11 Missing :warning:

...cy_management/IServiceInterestedLifecycleManager.h
12.50%
7 Missing :warning:

...dependency_management/DependencyLifecycleManager.h
86.84%
5 Missing :warning:

... and 17 more

:exclamation: Your organization needs to install the Codecov GitHub app to enable full functionality.
Additional details and impacted files
@@            Coverage Diff             @@
##             main      #32      +/-   ##
==========================================
+ Coverage   75.51%   82.29%   +6.78%
==========================================
  Files         143      183      +40
  Lines        6771     9834    +3063
==========================================
+ Hits         5113     8093    +2980
- Misses       1658     1741      +83

:umbrella: View full report in Codecov by Sentry.
:loudspeaker: Have feedback on the report? Share it here.


add Keybase

prioritise linking to Keybase, since it is supported for grin wallet transactions, and because we have enough eyes on that chat to quickly kick out spammers/scammers

As per Jan 17 decision Keybase should not be on website:

Decision: Managing chat channels

Only community promoted on website should be Gitter, because that is where development is taking place.
Add "Communities" page on wiki. This could be sorted by platform, members in community, etc. Have website link to this page.
Add "Events" page on wiki, functioning the same way, with links from the website.

So @sesam I would suggest you close this one.


Version 4.6.0: at least one new feature

property "debug" and new constructor keyword argument which enables verbose CLI output

Will reopen when ready to work on making release-worthy.


Twin normative modelling project

Hi all,
this PR contains my contributions to brainhack school 2022, the twin normative modelling project.
Please let me know if I need to add anything or should change any section.

hi @likeajumprope just seeing this now by random chance! Please open a PR to https://github.com/brainhackorg/school and add your project in a subfolder content/en/project/. This repo is the template for the md / yaml file, but it's meant to be used inside the school website.

ooohh will do! Thank you @pbellec!


feat/Qb946 video stream api

separate video stream caching and video stream http api
video caching downloads all slices once triggered
add signature to stream api

[INFO]2022/03/13 19:51:10 account.go:89: unlock wallet successfully
post this api
http://localhost:9608/unlock
response
{"errcode":500,"data":null,"message":"login failed, timeout"}


Couple things

Add in replicated-lint

Allow configuring of localPath and upstreamEndpoint via env vars

Fix bug where yaml without components fails linting

Few readme tweaks. Using $PRIVATE_ADDRESS in REPLICATED_OPTS
doesn't seem to resolve

update bind in readme to match default working dir (/) for docker image

Example of output with lint:
[getAppUpgrades:0fd01339] <- POST /v1/app/48e062db2e8aa2c18d689a33d6bbacf4/upgrades
[getAppUpgrades:0fd01339] <- {"CurrentVersion":32,"LastKnownVersion":32,"InstallationId":"93d2b4bf360349054d61133f4ab77973","FullUpdate":true}

1 errors in replicated/33.yaml:
{ rule: 'prop-schema-valid',
  type: 'error',
  positions:
   [ { path: 'lol',
       start: { position: 0, line: 0, column: 0 },
       end: { position: 8, line: 0, column: 8 } } ],
  message: 'Unknown property (not in schema) [lol]' }

0
1    replicated_api_version: 2.8.0
2    name: QA Application - Automation - PR
3    version: 1.0.0
4    release_notes: ' !"#$%&''()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_abcdefghijklmnopqrstuvwxyz{|}~'

Found 1 issues.

One or more releases were not included in the release list because they failed linting.
Please correct the errors in
  * replicated/33.yaml
[getAppUpgrades:0fd01339] => 200 {"Versions":[],"UpdatePolicy":"manual"}

I think this is almost ready, needs an info/warn/error/off toggle for linting I think before it goes in


fixed dialogue appearing only on top of the screen

When creating a new character using the Escoria Wizard, the floating dialogue appears only on the top of the screen, regardless of the position of the Dialogue Location set in the character scene.
The Wizard creates a instance of a ESCLocation class for the dialog_position:

Whereas the floating dialog requires an ESCDialogLocation class (addons/escoria-dialog-simple/types/floating.gd):

@balloonpopper I know you're really busy but whenever you have a minute if you could review this that'd be hugely appreciated. (We don't want to make any assumptions since this addon is your baby.)
Thanks!


This operating system is not supported.

this is error
[root@-VM ~]# uname
Linux
[root@-VM ~]# bash <(curl -fsSL git.io/warp.sh) install
System Information
Operating System: CentOS Linux 7 (Core)
Linux Kernel: 5.15.5-1.el7.elrepo.x86_64
Architecture: x86_64
Virtualization: kvm
[INFO] Installing Cloudflare WARP Client...
[ERROR] This operating system is not supported.
this is successful
[root@***-VM ~]# bash <(curl -fsSL git.io/warp.sh) d
I don't know why this happens.

The official WARP client is not available for CentOS 7


winget keeps redownloading/installing the same version

I've noticed that when I winget upgrade --all, a couple items always show up with the same version and winget downloads them and reinstalls them.
Ultimaker Cura [Ultimaker.Cura] Version 5.0.0
CrystalDiskInfo (I can't remember the version)
Originally posted by @myokeeh in https://github.com/microsoft/winget-cli/discussions/2248

Duplicate of #752
The second paragraph explains what is happening in this case.
Cura doesn't perform an upgrade. It installs the newer version. The reason the manifest hasn't been modified to "uninstallPrevious" is because Cura has settings that users might want to keep. So the Windows Package Manager sees the earlier version is still installed on the system and is attempting to upgrade it. We're going to add more logic such that if the latest version is already installed on the system it won't try to update the earlier version.
The version is included in the name, so you can winget list cura and winget uninstall "Ultimaker Cura <version>" to remove the version you want removed.
Trivia: Ultimaker.Cura was one of the first packages in the repository (even before public preview).


Added Test parser

Pull Request Test Coverage Report for Build 504

0 of 38 (0.0%)  changed or added relevant lines in 4 files are covered.
No unchanged relevant lines lost coverage.
Overall coverage decreased (-1.2%) to 84.397%

Changes Missing Coverage
Covered Lines
Changed/Added Lines
%

src/main/java/seedu/address/logic/parser/AddressBookParser.java
0
1
0.0%

src/main/java/seedu/address/logic/commands/OpenEndedTestCommand.java
0
8
0.0%

src/main/java/seedu/address/logic/parser/OpenEndedTestCommandParser.java
0
9
0.0%

src/main/java/seedu/address/model/test/openendedtest/OpenEndedTest.java
0
20
0.0%

Totals

Change from base Build 478:
-1.2%

Covered Lines:
2261

Relevant Lines:
2679

💛  - Coveralls

Pull Request Test Coverage Report for Build 554

0 of 38 (0.0%)  changed or added relevant lines in 4 files are covered.
No unchanged relevant lines lost coverage.
Overall coverage decreased (-1.2%) to 84.397%

Changes Missing Coverage
Covered Lines
Changed/Added Lines
%

src/main/java/seedu/address/logic/parser/AddressBookParser.java
0
1
0.0%

src/main/java/seedu/address/logic/commands/OpenEndedTestCommand.java
0
8
0.0%

src/main/java/seedu/address/logic/parser/OpenEndedTestCommandParser.java
0
9
0.0%

src/main/java/seedu/address/model/test/openendedtest/OpenEndedTest.java
0
20
0.0%

Totals

Change from base Build 478:
-1.2%

Covered Lines:
2261

Relevant Lines:
2679

💛  - Coveralls


[Bug]: The explore rounds won't detected by fall guys stats

What happened?
any other shows will work with fall guys stats but explore doesn't work and it doesn't change the round
Platform
Steam

I can confirm this issue and the reason: This issue happens when the FallGuysDB API (used to get info about played creative maps) is blocking the requests from your IP.

is it fixable??

The tracker should not stuck like this. The overlay should always display the creative map code if the FallGuysDB API doesn't return an expected result from the request.

oh wait FallguysDB can't determine the creative code so that's why it's stucked??

cloudseeker seems to work

wait you can use cloudseeker API it does work there

Yeah the tracker could use this API has a fallback API. 👍

the creator is the only one can change it right?

Everyone can propose a change in the code by sending a Pull Request (PR). The owner of this repository may do modifications himself or not (of course ^^).

is there anyways to change the API??

I'm working on it. ;)

oh I see

Sent PR #389 to add CloudSeeker API as a fallback API and even if both API are down, the tracker will not stuck anymore. ;)

thanks!

Here's the tracker with my patches, you can safety replace your current version with this one => https://github.com/ShootMe/FallGuysStats/actions/runs/11323362454/artifacts/2051959561

now it works


Update the mondo_release_diff.md

add a term label column for the following table/sections:

[X] Changed definition
[X] New obsoletion candidates
[X] previously candidate for obsoletion and are now not anymore:
[X] Obsoletions

Update the table for "Number of terms who were previously candidate for obsoletion and are now not anymore"

[X] This table should not include the terms which were obsoleted (it should include the terms which had the "obsoletion candidate" tag, but does not have the tag anymore AND was not obsoleted.

[ ] (please update the column titles to "Previous release definition" and "New release definition")

Apart from please update the column titles to "Previous release definition" and "New release definition" which would be a bit hacky (is this important to you?) i think its done.
I also tweaked some the tables to remove columns which may not be so useful to the user, like the "obsolete" status for new terms. This is how this all would look:
Overview:

Number of new terms: 168
Number of changed labels: 43
Number of changed definitions: 41
Number obsoleted terms: 24818
Number of new obsoletion candidates: 41
Number of terms who were previously candidate for obsoletion and are now not anymore: 21

New terms

Mondo ID
Label
Definition

MONDO:0023670
Bardet-Biedl syndrome 20

MONDO:0030258
pontocerebellar hypoplasia, type 14

MONDO:0030259
pontocerebellar hypoplasia, type 15

MONDO:0030260
pontocerebellar hypoplasia, type 1E

MONDO:0030261
pontocerebellar hypoplasia, type 1F

MONDO:0030263
leukodystrophy, hypomyelinating, 21

MONDO:0030266
immunodeficiency 80 with or without congenital cardiomyopathy

MONDO:0030268
developmental and epileptic encephalopathy 6B

MONDO:0030270
lymphatic malformation 9

MONDO:0030281
arthrogryposis multiplex congenita 6

MONDO:0030293
angioedema, hereditary, 5

MONDO:0030294
megacystis-microcolon-intestinal hypoperistalsis syndrome 3

MONDO:0030296
megacystis-microcolon-intestinal hypoperistalsis syndrome 4

MONDO:0030298
angioedema, hereditary, 8

MONDO:0030300
cardiomyopathy, dilated, 2D

MONDO:0030302
immunodeficiency 81

MONDO:0030307
spermatogenic failure 55

MONDO:0030308
immunodeficiency 82 with systemic inflammation

MONDO:0030309
Leber hereditary optic neuropathy, autosomal recessive

MONDO:0030311
combined oxidative phosphorylation deficiency 52

MONDO:0030312
spinocerebellar ataxia, autosomal recessive 29

MONDO:0030313
encephalopathy, acute, infection-induced (herpes-specific), susceptibility to, 10

MONDO:0030314
inflammatory bowel disease (infantile ulcerative colitis) 31, autosomal recessive

MONDO:0030316
lymphatic malformation 11

MONDO:0030317
cardiomyopathy, familial hypertrophic, 28

MONDO:0030318
spinocerebellar ataxia, autosomal recessive 30

MONDO:0030323
spinocerebellar ataxia, autosomal recessive 31

MONDO:0030326
mitochondrial dna depletion syndrome 16B (neuroophthalmic type)

MONDO:0030329
megacystis-microcolon-intestinal hypoperistalsis syndrome 5

MONDO:0030330
cardiomyopathy, familial restrictive, 6

MONDO:0030331
Ritscher-Schinzel syndrome 4

MONDO:0030332
ciliary dyskinesia, primary, 46

MONDO:0030333
immunodeficiency 84

MONDO:0030334
encephalitis, acute, infection (viral)-induced, susceptibility to, 11

MONDO:0030335
diarrhea 12, with microvillus atrophy

MONDO:0030337
cutis laxa, autosomal recessive, type 2E

MONDO:0030338
anencephaly 2

MONDO:0030339
microcephaly 28, primary, autosomal recessive

MONDO:0030341
myasthenic syndrome, congenital, 7B, presynaptic, autosomal recessive

MONDO:0030346
ciliary dyskinesia, primary, 47, and lissencephaly

MONDO:0030353
Joubert syndrome 38

MONDO:0030354
facioscapulohumeral muscular dystrophy 3, digenic

MONDO:0030355
facioscapulohumeral muscular dystrophy 4, digenic

MONDO:0030356
short-rib thoracic dysplasia 21 without polydactyly

MONDO:0030360
cholestasis, progressive familial intrahepatic, 6

MONDO:0030361
Aicardi-Goutieres syndrome 8

MONDO:0030362
Aicardi-Goutieres syndrome 9

MONDO:0030366
cardiomyopathy, dilated, 2E

MONDO:0100365
mucopolysaccharidosis or mucopolysaccharidosis-like disorder
Any disease that presents as a mucopolysaccharidosis or mucopolysaccharidosis-like disorder.

MONDO:0100366
occupational disorder
Any disorder that is realized in response to an exposure to occupation.

MONDO:0100367
port-wine nevi-mega cisterna magna-hydrocephalus syndrome
A rare developmental defect during embryogenesis syndrome characterized by a glabellar capillary malformation, congenital communicating hydrocephalus, and posterior fossa brain abnormalities, including Dandy-Walker malformation, cerebellar vermis agenesis, and mega cisterna magna. Seizures are occasionally associated. There have been no further descriptions in the literature since 1979.

MONDO:0100429
intrahepatic cholestasis of pregnancy
A cholestatic disorder characterized by (i) pruritus with onset in the second or third trimester of pregnancy, (ii) elevated serum aminotransferases and bile acid levels, and (iii) spontaneous relief of signs and symptoms within two to three weeks after delivery.

MONDO:0600030
B-cell acute lymphoblastic leukemia with t(1;19)(q23;p13.3); E2A-PBX1 (TCF3-PBX1)
A B-cell acute leukemia characterized by the presence of lymphoblasts that carry a translocation between the E2A gene on chromosome 19 and the PBX1 gene on chromosome 1. It occurs in children and less often in adults.

MONDO:8000000
infectious discitis
An infection of the intervertebral disc space.

MONDO:8000001
staphylococcus discitis
Discitis caused by infection with Staphylococcus.

MONDO:8000002
escherichia coli discitis
Discitis caused by infection with Escherichia coli.

MONDO:8000003
streptococcus pneumoniae discitis
Discitis caused by infection with Streptococcus pneumoniae.

MONDO:8000004
salmonella discitis
Discitis caused by infection with Salmonella.

MONDO:8000005
fungal discitis
Discitis caused by infection with fungi.

Changed terms
Changed label

Mondo ID
Label
Previous release
New release

MONDO:0007665
glaucoma 1, open angle, E
primary open angle glaucoma
glaucoma 1, open angle, E

MONDO:0019313
lymphatic malformation
hereditary lymphedema
lymphatic malformation

MONDO:0007883
periodic fever, immunodeficiency, and thrombocytopenia syndrome
lazy leukocyte syndrome
periodic fever, immunodeficiency, and thrombocytopenia syndrome

MONDO:0007919
lymphatic malformation 1
lymphedema, hereditary, 1A
lymphatic malformation 1

MONDO:0007920
lymphatic malformation 5
Meige disease
lymphatic malformation 5

MONDO:0007964
melanoma, cutaneous malignant, susceptibility to, 2
dysplastic nevus syndrome
melanoma, cutaneous malignant, susceptibility to, 2

MONDO:0008233
pheochromocytoma
phaeochromocytoma
pheochromocytoma

MONDO:0010118
inherited threoninemia
Threoninemia
inherited threoninemia

MONDO:0010301
obsolete thrombocythemia, X-linked
thrombocythemia, X-linked
obsolete thrombocythemia, X-linked

MONDO:0011293
obsolete Homocysteinemia
Homocysteinemia
obsolete Homocysteinemia

MONDO:0012317
visceral neuropathy, familial, 3, autosomal dominant
visceral neuropathy, familial, autosomal dominant
visceral neuropathy, familial, 3, autosomal dominant

MONDO:0012765
lymphatic malformation 2
lymphedema, hereditary, 1B
lymphatic malformation 2

MONDO:0012842
melanoma, cutaneous malignant, susceptibility to, 7
CMM7
melanoma, cutaneous malignant, susceptibility to, 7

MONDO:0012892
bone fragility with contractures, arterial rupture, and deafness
connective tissue disorder due to lysyl hydroxylase-3 deficiency
bone fragility with contractures, arterial rupture, and deafness

MONDO:0013278
lymphatic malformation 3
lymphedema, hereditary, 1C
lymphatic malformation 3

MONDO:0013759
melanoma, cutaneous malignant, susceptibility to, 8
MITF-related melanoma and renal cell carcinoma predisposition syndrome
melanoma, cutaneous malignant, susceptibility to, 8

MONDO:0013995
cholestasis, intrahepatic, of pregnancy, 3
cholestasis, intrahepatic, of pregnancy 3
cholestasis, intrahepatic, of pregnancy, 3

MONDO:0014393
lymphatic malformation 4
lymphedema, hereditary, 1D
lymphatic malformation 4

MONDO:0014797
lymphatic malformation 6
lymphedema, hereditary, type III
lymphatic malformation 6

MONDO:0014926
Bardet-Biedl syndrome 22
Bardet-Biedl syndrome 20
Bardet-Biedl syndrome 22

MONDO:0015009
lymphatic malformation 7
hydrops fetalis, nonimmune, and/or atrial septal defect, susceptibility to
lymphatic malformation 7

MONDO:0015318
obsolete Pierre Robin syndrome associated with collagen disease
Pierre Robin syndrome associated with collagen disease
obsolete Pierre Robin syndrome associated with collagen disease

MONDO:0015320
obsolete Pierre Robin syndrome associated with a chromosomal anomaly
Pierre Robin syndrome associated with a chromosomal anomaly
obsolete Pierre Robin syndrome associated with a chromosomal anomaly

MONDO:0015321
obsolete Pierre Robin syndrome associated with branchial archs anomalies
Pierre Robin syndrome associated with branchial archs anomalies
obsolete Pierre Robin syndrome associated with branchial archs anomalies

MONDO:0015322
obsolete Pierre Robin syndrome associated with bone disease
Pierre Robin syndrome associated with bone disease
obsolete Pierre Robin syndrome associated with bone disease

MONDO:0015543
obsolete hemophagocytic syndrome associated with an infection
hemophagocytic syndrome associated with an infection
obsolete hemophagocytic syndrome associated with an infection

MONDO:0015633
obsolete Bazex syndrome
Bazex syndrome
obsolete Bazex syndrome

MONDO:0015750
obsolete amelogenesis imperfecta-gingival hyperplasia syndrome
amelogenesis imperfecta-gingival hyperplasia syndrome
obsolete amelogenesis imperfecta-gingival hyperplasia syndrome

MONDO:0015938
obsolete systemic disease
systemic disease
obsolete systemic disease

MONDO:0016148
obsolete qualitative or quantitative defects of collagen 6
qualitative or quantitative defects of collagen 6
obsolete qualitative or quantitative defects of collagen 6

MONDO:0016329
obsolete familial syndrome associated with hypertrophic cardiomyopathy
familial syndrome associated with hypertrophic cardiomyopathy
obsolete familial syndrome associated with hypertrophic cardiomyopathy

MONDO:0017133
obsolete genetic systemic or rheumatologic disease
genetic systemic or rheumatologic disease
obsolete genetic systemic or rheumatologic disease

MONDO:0017274
obsolete autosomal ichthyosis syndrome with other associated signs
autosomal ichthyosis syndrome with other associated signs
obsolete autosomal ichthyosis syndrome with other associated signs

MONDO:0019687
obsolete type 11 collagen-related bone disorder
type 11 collagen-related bone disorder
obsolete type 11 collagen-related bone disorder

MONDO:0020012
obsolete systemic or rheumatic disease
systemic or rheumatic disease
obsolete systemic or rheumatic disease

MONDO:0020272
obsolete connective tissue disease with eye involvement
connective tissue disease with eye involvement
obsolete connective tissue disease with eye involvement

MONDO:0020277
obsolete ectodermal malformation syndrome associated with ocular features
ectodermal malformation syndrome associated with ocular features
obsolete ectodermal malformation syndrome associated with ocular features

MONDO:0020764
Brown-Pearce carcinoma
carcinoma, Brown-Pearce
Brown-Pearce carcinoma

MONDO:0035354
obsolete IgG4-related systemic disease
IgG4-related systemic disease
obsolete IgG4-related systemic disease

MONDO:0035363
obsolete IRF2BPL-related regressive neurodevelopmental disorder-dystonia-seizures syndrome
IRF2BPL-related regressive neurodevelopmental disorder-dystonia-seizures syndrome
obsolete IRF2BPL-related regressive neurodevelopmental disorder-dystonia-seizures syndrome

MONDO:0035369
obsolete MTHFS-related developmental delay-microcephaly-short stature-epilepsy syndrome
MTHFS-related developmental delay-microcephaly-short stature-epilepsy syndrome
obsolete MTHFS-related developmental delay-microcephaly-short stature-epilepsy syndrome

MONDO:0054844
pontocerebellar hypoplasia, type 1D
pontocerebellar hypoplasia, type 1d
pontocerebellar hypoplasia, type 1D

MONDO:0100027
obsolete febrile seizures plus, genetic epilepsy with febrile seizures plus
febrile seizures plus, genetic epilepsy with febrile seizures plus
obsolete febrile seizures plus, genetic epilepsy with febrile seizures plus

Changed definition

Mondo ID
Label
Previous release
New release

MONDO:0005550
infectious disease
A disorder resulting from the presence and activity of a microbial, viral, or parasitic agent. It can be transmitted by direct or indirect contact.
A disorder directly resulting from the presence and activity of a microbial, viral, or parasitic agent. It can be transmitted by direct or indirect contact.

MONDO:0005990
tracheitis
An inflammatory process affecting the wall of the trachea.
A tracheal disease which involves bacterial infection of the trachea often caused by Staphylococcus aureus and streptococci that follows a recent viral upper respiratory infection. The symptoms include barking croup cough, loud squeaking noise while breathing, scratchy feeling in the throat, high fever, and production of large amounts of pus-filled secretions.

MONDO:0017279
young-onset Parkinson disease
Young-onset Parkinson disease (YOPD) is a form of Parkinson disease (PD), characterized by an age of onset between 21-45 years, rigidity, painful cramps followed by tremor, bradykinesia, dystonia, gait complaints and falls, and other non-motor symptoms. A slow disease progression and a more pronounced response to dopaminergic therapy are also observed in most YOPD forms.
A form of Parkinson disease (PD) characterized by an age of onset between 21-45 years, rigidity, painful cramps followed by tremor, bradykinesia, dystonia, gait complaints and falls, and other non-motor symptoms. A slow disease progression and a more pronounced response to dopaminergic therapy are also observed in most YOPD forms.

MONDO:0019724
secondary glomerular disease
Secondary glomerular diseases are conditions with glomerular pathology in which an underlying cause can be established
Secondary glomerular diseases are conditions with glomerular pathology in which an underlying cause can be established.

MONDO:0009410
Addison disease
Addison disease (AD) is a chronic and rare endocrine disorder due to autoimmune destruction of the adrenal cortex and resulting in a glucocorticoid and mineralocorticoid deficiency. Properly speaking AD designates autoimmune adrenalitis, but it is a term commonly used to describe any form of chronic primary adrenal insufficiency (CPAI).
A chronic and rare endocrine disorder due to autoimmune destruction of the adrenal cortex and resulting in a glucocorticoid and mineralocorticoid deficiency. Properly speaking AD designates autoimmune adrenalitis, but it is a term commonly used to describe any form of chronic primary adrenal insufficiency (CPAI).

MONDO:0007489
dysplasia epiphysealis hemimelica
Dysplasia epiphysealis hemimelica (DEH), or Trevor's disease, is a rarecondition that most commonly affects the epiphysis (the end) of long bones in children.Early diagnosis and treatment are necessary to prevent jointdysfunction and deformity and may be surgical or non-surgical depending on the location and the symptoms. Due to the progressive nature of this disorder and the chance of worsening deformity, patients should be followed until skeletal maturity.Thecause ofdysplasia epiphysealis hemimelica is not known.
Dysplasia epiphysealis hemimelica (DEH), or Trevor's disease, is a rare condition that most commonly affects the epiphysis (the end) of long bones in children. Early diagnosis and treatment are necessary to prevent joint dysfunction and deformity and may be surgical or non-surgical depending on the location and the symptoms. Due to the progressive nature of this disorder and the chance of worsening deformity, patients should be followed until skeletal maturity. The cause of dysplasia epiphysealis hemimelica is not known.

MONDO:0019313
lymphatic malformation
Milroy disease is a frequent form of primary lymphedema characterized generally by painless, chronic lower-limb lymphedema found at birth or developing in the early neonatal period.
Primary lymphedema is caused by anatomic or functional defects in the lymphatic system, resulting in chronic swelling of body parts and lymphatic-system malformation.

MONDO:0007920
lymphatic malformation 5
Meige disease is a frequent form of late-onset, primary lymphedema characterized by lower limb lymphedema typically developing during puberty.
A frequent form of late-onset, primary lymphedema characterized by lower limb lymphedema typically developing during puberty.

MONDO:0008145
Ollier disease
Enchondromatosis is a rare primary bone dysplasia disorder characterized by the development of multiple mainly unilateral or asymmetrically distributed enchondromas throughout the metaphyses of the long bones.
A rare primary bone dysplasia disorder characterized by the development of multiple mainly unilateral or asymmetrically distributed enchondromas throughout the metaphyses of the long bones.

MONDO:0008156
autosomal dominant osteopetrosis 2
Albers-Schoenberg osteopetrosis is a sclerosing disorder of the skeleton characterized by increased bone density that classically displays the radiographic sign of ''sandwich vertebrae'' (dense bands of sclerosis parallel to the vertebral endplates).
A sclerosing disorder of the skeleton characterized by increased bone density that classically displays the radiographic sign of ''sandwich vertebrae'' (dense bands of sclerosis parallel to the vertebral endplates).

MONDO:0008199
late-onset Parkinson disease

A Parkinson disease that begins after around the age of 50.

MONDO:0018466
hereditary late onset Parkinson disease
Hereditary late-onset Parkinson disease (LOPD) is a form of Parkinson disease (PD), characterized by an age of onset of more than 50 years, tremor at rest, gait complaints and falls, bradykinesia, rigidity and painful cramps. Patients usually present a low risk of developing non motor symptoms, dystonia, dyskinesia and levodopa-induced dyskinesia (LID).
A form of Parkinson disease (PD) characterized by an age of onset of more than 50 years, tremor at rest, gait complaints and falls, bradykinesia, rigidity and painful cramps. Patients usually present a low risk of developing non motor symptoms, dystonia, dyskinesia and levodopa-induced dyskinesia (LID).

MONDO:0008771
amelogenesis imperfecta type 1G
Amelogenesis imperfecta-nephrocalcinosis, also called enamel-renal syndrome, is an extremely rare syndrome which is characterized by hypoplastic amelogenesis imperfecta (hypoplastic dental enamel) and nephrocalcinosis (precipitation of calcium salts in renal tissue). Oral manifestations include yellow and misshaped teeth, delayed tooth eruption, and intrapulpal calcifications. Nephrocalcinosis is often asymptomatic but can progress during late childhood or early adulthood to impaired renal function (e.g. recurrent urinary infections and renal tubular acidosis), and rarely to end-stage renal failure.
An extremely rare syndrome which is characterized by hypoplastic amelogenesis imperfecta (hypoplastic dental enamel) and nephrocalcinosis (precipitation of calcium salts in renal tissue). Oral manifestations include yellow and misshaped teeth, delayed tooth eruption, and intrapulpal calcifications. Nephrocalcinosis is often asymptomatic but can progress during late childhood or early adulthood to impaired renal function (e.g. recurrent urinary infections and renal tubular acidosis), and rarely to end-stage renal failure.

MONDO:0009303
anti-glomerular basement membrane disease
Goodpasture syndrome is an autoimmune disease that affects the lungs and kidneys and is characterized by pulmonary alveolar hemorrhage (bleeding in the lungs) and a kidney disease known as glomerulonephritis. Some use the term 'Goodpasture syndrome' for the findings of glomerulonephritis and pulmonary hemorrhage and the term 'Goodpasture disease' for those patients with glomerulonephritis, pulmonary hemorrhage, and anti-GBM antibodies. Currently, the preferred term for both conditions is “ anti-GBM antibody disease ”. Circulating antibodies are directed against the collagen of the part of the kidney known as the glomerular basement membrane (GBM), resulting in acute or rapidly progressive glomerulonephritis. Antibodies also attack the collagen of the air sacs of the lung (alveoli) resulting in bleeding of the lung (pulmonary hemorrhage). Symptoms may include general body discomfort or pain, bleeding from the nose and/or blood in the urine, respiratory problems, anemia, chest pain, and kidney failure. Anti-GBM disease is thought to result from an environmental insult (smoking, infections, exposure to certain drugs) in a person with genetic susceptibility, such as a specific human leukocyte antigen (HLA) type. Diagnosis is confirmed with the presence of anti-GBM antibody in the blood or in the kidney. The treatment of choice is plasmapheresis in conjunction with prednisone and cyclophosphamide.
An autoimmune disease that affects the lungs and kidneys and is characterized by pulmonary alveolar hemorrhage (bleeding in the lungs) and a kidney disease known as glomerulonephritis. Some use the term 'Goodpasture syndrome' for the findings of glomerulonephritis and pulmonary hemorrhage and the term 'Goodpasture disease' for those patients with glomerulonephritis, pulmonary hemorrhage, and anti-GBM antibodies. Currently, the preferred term for both conditions is “ anti-GBM antibody disease ”. Circulating antibodies are directed against the collagen of the part of the kidney known as the glomerular basement membrane (GBM), resulting in acute or rapidly progressive glomerulonephritis. Antibodies also attack the collagen of the air sacs of the lung (alveoli) resulting in bleeding of the lung (pulmonary hemorrhage). Symptoms may include general body discomfort or pain, bleeding from the nose and/or blood in the urine, respiratory problems, anemia, chest pain, and kidney failure. Anti-GBM disease is thought to result from an environmental insult (smoking, infections, exposure to certain drugs) in a person with genetic susceptibility, such as a specific human leukocyte antigen (HLA) type. Diagnosis is confirmed with the presence of anti-GBM antibody in the blood or in the kidney. The treatment of choice is plasmapheresis in conjunction with prednisone and cyclophosphamide.

MONDO:0009774
cloacal exstrophy
Cloacal exstrophy (EC) is a major birth defect representing the severe end of the spectrum of the exstrophy-epispadias complex (EEC) characterized by omphalocele, exstrophy, imperforate anus and spinal defects (also referred to as the OEIS complex), often associated with other malformations.
A major birth defect representing the severe end of the spectrum of the exstrophy-epispadias complex (EEC) characterized by omphalocele, exstrophy, imperforate anus and spinal defects (also referred to as the OEIS complex), often associated with other malformations.

MONDO:0017919
bladder exstrophy-epispadias-cloacal exstrophy complex
Exstrophy-Epispadias Complex (EEC) represents a spectrum of genitourinary malformations ranging in severity from epispadias (E) and classical bladder exstrophy (CEB) to exstrophy of the cloaca (EC) as the most severe form. Depending on severity, the EEC may involve the urinary system, the musculoskeletal system, the pelvis, the pelvic floor, the abdominal wall, the genitalia and sometimes the spine and the anus.
A spectrum of genitourinary malformations ranging in severity from epispadias (E) and classical bladder exstrophy (CEB) to exstrophy of the cloaca (EC) as the most severe form. Depending on severity, the EEC may involve the urinary system, the musculoskeletal system, the pelvis, the pelvic floor, the abdominal wall, the genitalia and sometimes the spine and the anus.

MONDO:0010079
Canavan disease
Canavan disease (CD) is a neurodegenerative disorder; its spectrum varies between severe forms with leukodystrophy, macrocephaly and severe developmental delay, and a very rare mild/juvenile form characterized by mild developmental delay.
A neurodegenerative disorder; its spectrum varies between severe forms with leukodystrophy, macrocephaly and severe developmental delay, and a very rare mild/juvenile form characterized by mild developmental delay.

MONDO:0010080
familial infantile bilateral striatal necrosis
Familial infantile bilateral striatal necrosis is the familial form of infantile bilateral striatal necrosis (IBSN), a syndrome of bilateral symmetric spongy degeneration of the caudate nucleus, putamen and globus pallidus characterized by developmental regression, choreoathetosis and dystonia progressing to spastic quadriparesis.
The familial form of infantile bilateral striatal necrosis (IBSN), a syndrome of bilateral symmetric spongy degeneration of the caudate nucleus, putamen and globus pallidus characterized by developmental regression, choreoathetosis and dystonia progressing to spastic quadriparesis.

MONDO:0015518
infantile bilateral striatal necrosis
Infantile bilateral striatal necrosis (IBSN) comprises several syndromes of bilateral symmetric spongy degeneration of the caudate nucleaus, putamen and globus pallidus characterized by developmental regression, choreoathetosis and dystonia progressing to spastic quadriparesis. IBSN can be familial or sporadic.
Several syndromes of bilateral symmetric spongy degeneration of the caudate nucleaus, putamen and globus pallidus characterized by developmental regression, choreoathetosis and dystonia progressing to spastic quadriparesis. IBSN can be familial or sporadic.

MONDO:0010371
Aland island eye disease
Aland Island Eye Disease (AIED) is an X-linked recessive retinal disease characterized by fundus hypopigmentation, decrased visual acuity, nystagmus, astigmatism, progressive axial myopia, defective dark adaptation and protanopia.
An X-linked recessive retinal disease characterized by fundus hypopigmentation, decrased visual acuity, nystagmus, astigmatism, progressive axial myopia, defective dark adaptation and protanopia.

MONDO:0011669
hypotonia-cystinuria syndrome
Hypotonia-Cystinuria syndrome (HCS) is a rare syndrome including neonatal and infantile hypotonia and failure to thrive, cystinuria type 1 and nephrolithiasis, growth retardation due to growth hormone deficiency, and minor facial dysmorphism.
A rare syndrome including neonatal and infantile hypotonia and failure to thrive, cystinuria type 1 and nephrolithiasis, growth retardation due to growth hormone deficiency, and minor facial dysmorphism.

MONDO:0015999
primary pigmented nodular adrenocortical disease
Primary pigmented nodular adrenocortical disease (PPNAD) is a form of bilateral adrenocortical hyperplasia that is often associated with adrenocorticotrophin hormone (ACTH) independent Cushing syndrome and is characterized by small to normal sized adrenal glands containing multiple small cortical pigmented nodules (less than 1 cm in diameter).
A form of bilateral adrenocortical hyperplasia that is often associated with adrenocorticotrophin hormone (ACTH) independent Cushing syndrome and is characterized by small to normal sized adrenal glands containing multiple small cortical pigmented nodules (less than 1 cm in diameter).

MONDO:0012608
autosomal recessive lower motor neuron disease with childhood onset
Autosomal recessive lower motor neuron disease with childhood onset is a rare, genetic, neuromuscular disease characterized by proximal muscle weakness with an early involvement of foot and hand muscles following normal motor development in early childhood, a rapidly progressive disease course leading to generalized areflexic tetraplegia with contractures, severe scoliosis, hyperlordosis, and progressive respiratory insufficiency leading to assisted ventilation. Cranial nerve functions are normal and tongue wasting and fasciculations are absent. Milder phenotype with a moderate generalized weakness and slower disease progress was reported.
A rare, genetic, neuromuscular disease characterized by proximal muscle weakness with an early involvement of foot and hand muscles following normal motor development in early childhood, a rapidly progressive disease course leading to generalized areflexic tetraplegia with contractures, severe scoliosis, hyperlordosis, and progressive respiratory insufficiency leading to assisted ventilation. Cranial nerve functions are normal and tongue wasting and fasciculations are absent. Milder phenotype with a moderate generalized weakness and slower disease progress was reported.

MONDO:0012892
bone fragility with contractures, arterial rupture, and deafness
Connective tissue disorder due to lysyl hydroxylase-3 deficiency is a rare, genetic disease, caused by lack of lysyl hydrohylase 3 (LH3) activity, characterized by multiple tissue and organ involvement, including skeletal abnormalities (club foot, progressive scoliosis, osteopenia, pathologic fractures), ocular involvement (flat retinae, myopia, cataracts) and hair, nail and skin anomalies (coarse, abnormally distributed hair, skin blistering, reduced palmar creases, hypoplastic nails). Patients also present intrauterine growth retardation, facial dysmorphism (flat facial profile, low-set ears, shallow orbits, short and upturned nose, downturned corners of mouth) and joint flexion contractures. Growth and developmental delay, bilateral sensorineural deafness, friable diaphragm and later-onset spontaneous vascular ruptures are additional reported features.
A rare, genetic disease, caused by lack of lysyl hydrohylase 3 (LH3) activity, characterized by multiple tissue and organ involvement, including skeletal abnormalities (club foot, progressive scoliosis, osteopenia, pathologic fractures), ocular involvement (flat retinae, myopia, cataracts) and hair, nail and skin anomalies (coarse, abnormally distributed hair, skin blistering, reduced palmar creases, hypoplastic nails). Patients also present intrauterine growth retardation, facial dysmorphism (flat facial profile, low-set ears, shallow orbits, short and upturned nose, downturned corners of mouth) and joint flexion contractures. Growth and developmental delay, bilateral sensorineural deafness, friable diaphragm and later-onset spontaneous vascular ruptures are additional reported features.

MONDO:0013060
autosomal recessive Parkinson disease 14
Adult-onset dystonia-parkinsonism is a rare neurodegenerative disease usually presenting before the age of 30 and which is characterized by dystonia, L-dopa-responsive parkinsonism, pyramidal signs and rapid cognitive decline.
A rare neurodegenerative disease usually presenting before the age of 30 and which is characterized by dystonia, L-dopa-responsive parkinsonism, pyramidal signs and rapid cognitive decline.

MONDO:0016536
autosomal recessive lymphoproliferative disease
Autosomal recessive lymphoproliferative disease is a rare combined T and B cell immunodeficiency with a predisposition to lymphoproliferative syndrome. It is characterized by persistent symptomatic EBV-viremia and hypogammaglobulinemia variably presenting with fever, lymphadenopathy and systemic inflammatory conditions including hepatitis, pneumonia and sepsis. It may be associated with lymphoma, hemophagocytic lymphohistiocytosis, and aplastic anemia.
A rare combined T and B cell immunodeficiency with a predisposition to lymphoproliferative syndrome. It is characterized by persistent symptomatic EBV-viremia and hypogammaglobulinemia variably presenting with fever, lymphadenopathy and systemic inflammatory conditions including hepatitis, pneumonia and sepsis. It may be associated with lymphoma, hemophagocytic lymphohistiocytosis, and aplastic anemia.

MONDO:0013172
polymicrogyria with optic nerve hypoplasia
Polymicrogyria with optic nerve hypoplasia is a rare genetic syndrome with central nervous system malformations characterized by severe developmental delay, neonatal hypotonia, seizures, optic nerve hypoplasia and distinct central nervous system malformations including extensive bilateral polymicrogyria, dysplastic or absent corpus callosum and malformed brainstem with loss of demarcation of the pontomedullary junction.
A rare genetic syndrome with central nervous system malformations characterized by severe developmental delay, neonatal hypotonia, seizures, optic nerve hypoplasia and distinct central nervous system malformations including extensive bilateral polymicrogyria, dysplastic or absent corpus callosum and malformed brainstem with loss of demarcation of the pontomedullary junction.

MONDO:0013759
melanoma, cutaneous malignant, susceptibility to, 8
MITF-related melanoma and renal cell carcinoma predisposition syndrome is an inherited cancer-predisposing syndrome due to a gain-of-function germline mutation in the MITF gene, associated with a higher incidence of amelanotic and nodular melanoma, multiple primary melanomas and increase in nevus number and size. It may also predispose to co-occurring melanoma and renal cell carcinoma and to pancreatic cancer.
An inherited cancer-predisposing syndrome due to a gain-of-function germline mutation in the MITF gene, associated with a higher incidence of amelanotic and nodular melanoma, multiple primary melanomas and increase in nevus number and size. It may also predispose to co-occurring melanoma and renal cell carcinoma and to pancreatic cancer.

MONDO:0014061
Steel syndrome

A rare genetic bone disease characterized by short stature, bilateral congenital hip dislocation, radial head dislocation, carpal coalition, scoliosis, pes cavus, and atlantoaxial subluxation. Dysmorphic facial features include broad forehead, broad nasal bridge, hypertelorism, and mild midface hypoplasia. Association with bilateral sensorineural hearing loss has also been described.

MONDO:0014500
atrial conduction disease
Atrial conduction disorder is a form of heart disease in which the conduction of the cardiac atrium is disrupted
Atrial conduction disorder is a form of heart disease in which the conduction of the cardiac atrium is disrupted.

MONDO:0014629
autoimmune interstitial lung disease-arthritis syndrome

A respiratory disease characterized by interstitial lung disease (often with pulmonary hemorrhage) and inflammatory arthritis, associated with high-titer autoantibodies (including anti-nuclear and anti-neutrophil cytoplasmic antibodies, and rheumatoid factor). Patients present from infancy to adolescence with tachypnea, cough, hemoptysis, and/or joint pain. Some patients may also develop glomerular disease.

MONDO:0015583
2p21 microdeletion syndrome
The 2p21 microdeletion syndrome consists of cystinuria, neonatal seizures, hypotonia, severe growthand developmental delay, facial dysmorphism, and lactic acidemia.
The 2p21 microdeletion syndrome consists of cystinuria, neonatal seizures, hypotonia, severe growth and developmental delay, facial dysmorphism, and lactic acidemia.

MONDO:0015633
obsolete Bazex syndrome
Bazex syndrome is a rare paraneoplastic syndrome characterized by acral psoriasiform lesions.

MONDO:0015750
obsolete amelogenesis imperfecta-gingival hyperplasia syndrome
This syndrome associates gingival fibromatosis with dental abnormalities including generalized thin hypoplastic amelogenesis imperfecta, intrapulpal calcifications, and delay of tooth eruption.

MONDO:0015938
obsolete systemic disease
A systemic disease is one that affects a number of organs and tissues, or affects the body as a whole.

MONDO:0016822
myalgia-eosinophilia syndrome associated with tryptophan
Myalgia-eosinophilia syndrome associated with tryptophan is a rare systemic disease characterized by severe myalgia and peripheral eosinophilia associated with tryptophan dietary supplementation. The symptoms do not subside after tryptophan discontinuation. Clinical presentation includes muscle tenderness and cramps, fatigue, weakness, paresthesia, peripheral edema, arthralgia, dyspnea, skin rash, dry mouth, and development of scleroderma-like skin abnormalities.
A rare systemic disease characterized by severe myalgia and peripheral eosinophilia associated with tryptophan dietary supplementation. The symptoms do not subside after tryptophan discontinuation. Clinical presentation includes muscle tenderness and cramps, fatigue, weakness, paresthesia, peripheral edema, arthralgia, dyspnea, skin rash, dry mouth, and development of scleroderma-like skin abnormalities.

MONDO:0017133
obsolete genetic systemic or rheumatologic disease
An instance of systemic or rheumatic disease that is caused by a modification of the individual's genome.

MONDO:0017213
postorgasmic illness syndrome
Postorgasmic illness syndrome (POIS) is a rare condition in which a man develops flu-like symptoms after ejaculation (when semen is released from the penis). Specific symptoms can include extreme fatigue, weakness, feverishness or sweating, mood changes or irritability, memory or concentration problems, and/or a stuffy nose or itching eyes. Symptoms may occur within seconds, minutes, or a few hours after ejaculation. Most symptoms last for 2 to 7 days and go away on their own. The underlying cause of POIS is poorly understood. Some scientists believe it may be due to a semen allergy that causes an immediate hypersensitivity reaction. There is no standard treatment for POIS, but some men have been treated with SSRIs, antihistamines, and/or benzodiazepines. Hyposensitization therapy (decreasing the immune response by exposure to semen) reportedly improved symptoms in two men with POIS.
A rare condition in which a man develops flu-like symptoms after ejaculation (when semen is released from the penis). Specific symptoms can include extreme fatigue, weakness, feverishness or sweating, mood changes or irritability, memory or concentration problems, and/or a stuffy nose or itching eyes. Symptoms may occur within seconds, minutes, or a few hours after ejaculation. Most symptoms last for 2 to 7 days and go away on their own. The underlying cause of POIS is poorly understood. Some scientists believe it may be due to a semen allergy that causes an immediate hypersensitivity reaction. There is no standard treatment for POIS, but some men have been treated with SSRIs, antihistamines, and/or benzodiazepines. Hyposensitization therapy (decreasing the immune response by exposure to semen) reportedly improved symptoms in two men with POIS.

MONDO:0019355
adult-onset Still disease
Adult-onset Still disease (AOSD) is a rare inflammatory multisystem disorder characterized clinically by fever of unknown origin, arthralgia or arthritis, hyperleucocytosis, and typical skin rash.
A rare inflammatory multisystem disorder characterized clinically by fever of unknown origin, arthralgia or arthritis, hyperleucocytosis, and typical skin rash.

MONDO:0100027
obsolete febrile seizures plus, genetic epilepsy with febrile seizures plus
These epilepsy syndromes are characterized by the presence of febrile seizures in an individual that may continue past the usual age where these are expected to resolve and/or be accompanied by afebrile seizures that may be generalized seizures (tonic-clonic, atonic, myoclonic, myoclonic-atonic or absence) or focal seizures. Febrile seizures plus and genetic epilepsy with febrile seizures plus are distinguished on the basis of family history. A number of dominantly inherited genes have been linked to these syndromes, with implications for specific genetic counseling, due to the variable severity of the resulting epilepsy in different family members.

MONDO:0100318
SARS-CoV-2-related disease
A related disease caused by infection with severe acute respiratory syndrome coronavirus 2 or the associated aftereffects of the disease.
A viral disease or post-viral disorder caused by infection with severe acute respiratory syndrome coronavirus 2 or the associated aftereffects of the disease.

Obsoletion candidates
New obsoletion candidates:

Mondo ID
Label

MONDO:0019708
primary bone dysplasia with disorganized development of skeletal components

MONDO:0000881
myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, and FGFR1

MONDO:0000882
myeloid and lymphoid neoplasms associated with PDGFRA rearrangement

MONDO:0000883
myeloid neoplasms associated with PDGFRB rearrangement

MONDO:0006475
unclassified renal cell carcinoma

MONDO:0006728
discitis

MONDO:0018232
primary bone dysplasia with micromelia

MONDO:0019700
primary bone dysplasia with multiple joint dislocations

MONDO:0017957
unclassified autoinflammatory syndrome

MONDO:0019703
primary bone dysplasia with increased bone density

MONDO:0019704
primary bone dysplasia with decreased bone density

MONDO:0017608
dystrophic epidermolysis bullosa

MONDO:0019299
unclassified genetic skin disorder

MONDO:0007600
primary Fanconi syndrome

MONDO:0018231
primary bone dysplasia with progressive ossification of skin, skeletal muscle, fascia, tendons and ligaments

MONDO:0020244
unclassified primitive or secondary maculopathy

MONDO:0007684
granulomatous disease, chronic, autosomal dominant type

MONDO:0007749
autosomal recessive infantile hypercalcemia

MONDO:0007815
immunodeficiency with defective leukocyte and lymphocyte function and with response to histamine-1 antagonist

MONDO:0008091
abnormal neutrophil chemotactic response

MONDO:0008122
olivopontocerebellar atrophy 5

MONDO:0009799
pachydermoperiostosis

MONDO:0018466
hereditary late onset Parkinson disease

MONDO:0008956
congenital neuronal ceroid lipofuscinosis

MONDO:0009004
combined inflammatory and immunologic defect

MONDO:0019705
primary bone dysplasia with defective bone mineralization

MONDO:0009494
Ketoadipicaciduria

MONDO:0009535
lymphedema, congenital recessive

MONDO:0009654
mucopolysaccharidoses, unclassified types

MONDO:0020241
unclassified familial retinal dystrophy

MONDO:0010527
microphthalmia-ankyloblepharon-intellectual disability syndrome

MONDO:0019302
mucopolysaccharidosis with skin involvement

MONDO:0011329
cerebral palsy, spastic quadriplegic, 1

MONDO:0016538
hypotonia-cystinuria syndrome type 1

MONDO:0015192
unclassified intestinal pseudoobstruction

MONDO:0016665
unclassified vasculitis

MONDO:0018139
scleredema

MONDO:0018348
polyglucosan body myopathy type 1

MONDO:0020313
unclassified myelodysplastic/myeloproliferative disease

MONDO:0020315
unclassified myelodysplastic syndrome

MONDO:0035398
hypomyelination of early myelinating structures

Number of terms who were previously candidate for obsoletion and are now not anymore:
No changes.
Obsoletions

Mondo ID
Label

MONDO:0010301
obsolete thrombocythemia, X-linked

MONDO:0011293
obsolete Homocysteinemia

MONDO:0015318
obsolete Pierre Robin syndrome associated with collagen disease

MONDO:0015320
obsolete Pierre Robin syndrome associated with a chromosomal anomaly

MONDO:0015321
obsolete Pierre Robin syndrome associated with branchial archs anomalies

MONDO:0015322
obsolete Pierre Robin syndrome associated with bone disease

MONDO:0015543
obsolete hemophagocytic syndrome associated with an infection

MONDO:0015633
obsolete Bazex syndrome

MONDO:0015750
obsolete amelogenesis imperfecta-gingival hyperplasia syndrome

MONDO:0015938
obsolete systemic disease

MONDO:0016148
obsolete qualitative or quantitative defects of collagen 6

MONDO:0016329
obsolete familial syndrome associated with hypertrophic cardiomyopathy

MONDO:0017133
obsolete genetic systemic or rheumatologic disease

MONDO:0017274
obsolete autosomal ichthyosis syndrome with other associated signs

MONDO:0019687
obsolete type 11 collagen-related bone disorder

MONDO:0020012
obsolete systemic or rheumatic disease

MONDO:0020272
obsolete connective tissue disease with eye involvement

MONDO:0020277
obsolete ectodermal malformation syndrome associated with ocular features

MONDO:0035354
obsolete IgG4-related systemic disease

MONDO:0035363
obsolete IRF2BPL-related regressive neurodevelopmental disorder-dystonia-seizures syndrome

MONDO:0035369
obsolete MTHFS-related developmental delay-microcephaly-short stature-epilepsy syndrome

MONDO:0100027
obsolete febrile seizures plus, genetic epilepsy with febrile seizures plus

I have committed this to master already, so if you are happy with the output above, you can just close this @sabrinatoro

It looks good to me.
And I don't think the "update the column titles to "Previous release definition" and "New release definition" " is a big deal (and I definitely don't think it is worth the extra effort.
Thank you @matentzn! Closing.


Support storing and reading ASCII format for BDDs

File Format
Tom van Dijk has suggested the following format for a BDD:

Options are (optional) key-value pairs; each written on a single line as follows
.<option> <value>

Possible options are:

option
name
count
order

type
string
uint
"pre", "post"

This is then followed by a set of nodes, starting with
.nodes

Terminals are given with the t key and are of the form.t "type" "value"

Nodes are of the formb <label> '-'?<then> '-'?<else>

where then is also known as high and else is also known as low. The optional '-' character marks an edge to be complemented, which depends on the attributed edge feature. Every node is identified by referencing its linenumber or the name of another bdd in the same file.

Finally, the list is ended with
.end

Parsing a file
This feature might be blocked until we support attributed edges.
The simplest way to implement this would be to do the following:

Read the entire bdd from a file and push it as edges { source_line, target_line } to a tpie::merge_sorter.
Run a bottom-up version of Reduce that merely puts it into the normal node based form.

By use of a b-tree we could also store the id of all prior nodes and then that way skip the merge sorter. Most likely this will not run as fast as using the sorter. Furthermore, it also takes up much more space
The "reference another bdd" also makes things much more complicated. At that point one probably has to first check whether some reference like this exists to then "inline" the other BDD inside of this one and then run the actual Reduce algorithm.
Comments
Notice, while this is quite close to #126 , it also is quite disjoint (both in terms of how to do these and the usecase they are solving. The purpose of this is to have a common file format that can be used between different BDD packages, while the other is supposed to be used for Adiar alone by using the least amount of space.

I wonder whether the "every node is identified by referencing its linenumber" is not extremely tedious, since adding a node in the middle will result in having to shift all other numbers?

The corresponding issue on Tom's Sylvan repo is here:
https://github.com/trolando/sylvan/issues/20

Alternatively, one can also investigate the lib-bdd format. A parser is implemented in https://github.com/SSoelvsten/bdd-benchmark/blob/main/src/apply.cpp