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Read about Self in Python here!
PIP is a recursive acronym for “Preferred Installer Program” or PIP Installs Packages. It is a command-line utility that installs, reinstalls, or uninstalls PyPI packages with one simple command: pip. You may be familiar with the term package manager if you have used other languages like Ruby uses Gem, JavaScript uses npm for package management, and .NET uses NuGet. Pip has become the standard package manager for Python.
The Python installer installs pip automatically, so it is ready for you to use unless you have installed an older version of Python. You can also verify if pip is available on your Python version by running the command below:
On running the command mentioned above, a similar output should be displayed which will show the pip version, along with the location and version of Python. If you are using an older version of Python, the pip version will not be displayed. Then you can install it separately.
You can download pip from the following link: https://pypi.org/project/pip/
Follow the instructions to install pip in Python on Windows 7, Windows 8.1, and Windows 10:
In case you are a beginner and struggling to make inroads, we recommend taking a python programming course to shorten your learning curve.
Modern Mac systems have Python and pip pre-installed but the version of Python tends to be outdated and not the best choice for serious programming in Python. So, it’s highly recommended that you install a more updated version of Python and PIP.
If you want to use the pre-installed Python application but don’t have PIP available, you can install PIP with the following commands in Terminal:
If you want to install an updated version of Python, then you can use Homebrew. Installing Python with Homebrew requires a single command:
Installing Python with Homebrew will give you the latest version which should come packaged with PIP but if PIP is unavailable, you can re-link Python using the following commands in Terminal:
If your Linux distribution came with Python pre-installed, using your system’s package manager you will be able to install PIP. This is preferable since pre-installed versions of Python do not work well with the get-pip.py script used on Windows and Mac. Given below are the commands you should run in order to install pip in your system depending on the version of Python you are using:
Advanced Package Tool (Python 2.x):
pacman Package Manager (Python 2.x):
Yum Package Manager (Python 2.x):
Dandified Yum (Python 2.x):
Zypper Package Manager (Python 2.x):
Advanced Package Tool (Python 3.x):
pacman Package Manager (Python 3.x):
Yum Package Manager (Python 3.x):
Dandified Yum (Python 3.x):
Zypper Package Manager (Python 3.x):
You are most likely running Raspbian if you are a Raspberry Pi user as it is the official operating system designated and provided by the Raspberry Pi Foundation. PIP comes pre-installed on with Raspbian Jessie. It is one of the biggest reasons to upgrade to Raspbian Jessie instead of using Raspbian Wheezy or Raspbian Jessie Lite. If you are using an older version of Raspbian, you can still manually install PIP. Given below are the commands you should run in order to install pip on your system depending on the version of Python you are using:
On Python 2.x:
On Python 3.x:
Raspbian users, working with Python 2.x must use pip while Python 3.x users must use pip3 while running PIP commands.
After PIP is installed, we need to find a package to install. Packages are usually installed from the repository of software for the Python programming language which is the Python Package Index.
You won’t have to reference the pip install directory again and again if you set an environment variable.
Set: (default = C:\Python27\Scripts) in your Windows/Linux “PATH” environment variable.
Now that we know what PIP is and have successfully installed it on our computer, let's get started on how to use it:
Enter pip in the command terminal and it will show the following output on the screen.
Usage:pip
Commands:
Commonly used commands in pip are install, upgrade or uninstall.
General Options:
-h, --help: Shows help.
--isolated: To run pip in an isolated mode by ignoring environment variables and user configuration.
-v, --verbose: Give more output. Option is additive, and can be used up to 3 times.
-V, --version: Show version and exit.
-q, --quiet: Give less output. Option is additive, and can be used up to 3 times (corresponding to WARNING, ERROR, and CRITICAL logging levels).
--proxy: Specify a proxy in the form proxy.server:port.
--trusted-host: Mark this host as trusted, even though it does not have valid or any HTTPS.
--cert: Path to alternate CA bundle.
--client-cert: Path to SSL client certificate, a single file containing the private key and the certificate in PEM format.
--retries: Maximum number of retries each connection should attempt(5 times by default).
--timeout: Set the socket timeout(15 seconds by default).
--exists-action: Default action when a path already exists: (s)witch,(i)gnore, (w)ipe, (b)ackup, (a)bort).
--cache-dir: Store the cache data in
--no-cache-dir: Disable the cache.
--disable-pip-version-check: Don't periodically check PyPI to determine whether a new version of pip is available for download. Implied with --no-index.
Finding required packages:
To search any package, i.e. Flask command will be as shown below: pip search Flask
The following output will be displayed with all packages and description:
Flask-Cache - Adds cache support to your Flask applicationFlask-SeaSurf - An update CSRF extension for FlaskFlask-Admin - Simple and extensible admin interface framework for FlaskFlask-Security - Simple security for Flask appsFlask - A microframework based on Werkzeug, Jinja2 and good intentions
Installing a package:
To install the required package, in our case it is Flask, enter the following command :
pip install Flask
Pip – Show information
To check information about the newly installed packages enter:
Uninstalling a package:
To uninstall any package installed by PIP, enter the command given below.
That’s all. The PIP application has been uninstalled.
Although PIP application doesn’t receive updates very often, it’s still important to keep the application up to date with the newer versions because there may be important fixes to bugs, compatibility, and security holes. Fortunately, upgrading to the latest versions of PIP is very fast and simple yet quite a few learners often seek help from our experts leading a python programming advanced course on KnowledgeHut.
On Windows
python -m pip install -U pip
On Mac, Linux, or Raspberry Pi
pip install -U pip
Certain versions of Linux and Raspberry Pi, pip3 needs to be entered instead of pip.
The pip install command always installs the latest published version of a package, but you should install the particular version that suits your code.
You would want to create a specification of the dependencies and versions that you have used while developing and running your application, so that there are no surprises when you use the application in production.
Requirement files allow you to specify exactly the packages and versions that should be installed on your system. Executing pip help shows that there is a freeze command that displays the installed packages in requirements format. This command can be used to redirect the output to a file to generate a requirements file:
The freeze command is used to dump all the packages and their versions to standard output, so as to redirect the output to a file that can be used to install the exact requirements into another system. The general convention is to name this file requirements.txt, but it is completely up to you to name it whatever you want.
If you want to replicate the environment in another system, run pip install specifying the requirements file using the -r switch:
The versions listed in requirements.txt will match those of the packages:
$ pip list
You may submit the requirements.txt file to source control and can use it to create the exact environment in other machines.
The problem with hardcoding the versions of your packages and their dependencies is that the packages receive frequent updates with bug and security fixes, and you probably want to update to them as soon as they are published.
The requirements file format gives you a bit of flexibility to ensure that the packages are up to date by allowing you to enter dependency versions using logical operators, although specifying the base versions of a package.
Make the following changes by opening the requirements.txt file in your editor:
Change the logical operator to >= to install an exact or greater version that has been published. While you set a new environment using the requirments.txt file, pip searches for the latest version that supports the requirement and installs it. The packages in your requirements file can be updated by running the install command with the --upgrade switch:
In this case nothing was upgraded because latest versions have already been installed, but if a new version was published for a listed package, then the package would’ve been upgraded.
New versions can introduce changes that fix bugs and will make or break your application. In order to fine-tune your requirements, the requirements file syntax supports additional version specifiers.
Let us assume that a new version 3.0 of requests is published but it breaks your application as it introduces an incompatible change. In such a case, the requirements file can be modified to prevent 3.0 or higher versions from being installed:
Changing the version specifier for the requests package ensures that only the versions which are less than 3.0 get installed.
All packages which are installed during the development of your applications are not going to be application dependencies. During the development process, there are certain packages published to PyPI that are development tools or libraries that can be useful to you.
For example, you would require a unit test framework in order to unit test your application. Pytest is a popular framework for unit testing. You would want to install the unit testing framework in your development environment, but not in your production environment because it is not an application dependency.
To set up a development environment, you need to create a second requirements file (requirements_file.txt) to list additional tools:
To do this, you need to install both requirement files using pip: requirements.txt and requirements_file.txt. Pip allows for specifying additional parameters within a single requirements file. The requirements_file.txt can also be modified to install the requirements from the production requirements.txt file:
Notice that the exact same -r switch is being used in order to install the production requirements.txt file. The file format of the requirements file allows you to specify additional arguments right on a requirements file.
Pip is an essential tool for all Pythonistas which is used in developing many applications and projects for package management. This article gives you the basics of Pip for Python, but the Python community is very active in providing great tools and libraries for developers using other applications as well. These include alternatives to pip that try to improve and simplify package management.
Here are some package management tools other than pip that are available for Python:
Top Cities Where KnowledgeHut Conduct Python Certification Course Online
By now you know that pip is a package manager for Python that is used in many projects to manage dependencies. It is included with the Python installer; hence it is essential for all Python programmers to know how to use it.
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Protein kinase RNA-activated also known as protein kinase R (PKR), interferon-induced, double-stranded RNA-activated protein kinase, or eukaryotic translation initiation factor 2-alpha kinase 2 (EIF2AK2) is an enzyme that in humans is encoded by the EIF2AK2 gene on chromosome 2. PKR is a serine/tyrosine kinase that is 551 amino acids long.
PKR is inducible by various mechanisms of stress and protects against viral infections. It also has a role in several signaling pathways.
Protein kinase-R is activated by double-stranded RNA (dsRNA), introduced to the cells by a viral infection. In situations of viral infection, the dsRNA created by viral replication and gene expression binds to the N-terminal domain, activating the protein. PKR activation via dsRNA is length dependent, requiring the dsRNA to be 30 bp in length to bind to PKR molecules. However, excess dsRNA can diminish activation of PKR. Binding to dsRNA is believed to activate PKR by inducing dimerization of the kinase domains and subsequent auto-phosphorylation reactions. PKR can also be activated by the protein PACT via phosphorylation of S287 on its M3 domain. The promoter region of PKR has interferon-stimulated response elements to which Type I interferons (IFN) bind to induce the transcription of PKR genes. Some research suggests that PKR can be stimulated by heat shock proteins, heparin, growth factors, bacterial infection, pro-inflammatory cytokines, reactive oxygen species, DNA damage, mechanical stress, and excess nutrient intake.
Once active, PKR is able to phosphorylate the eukaryotic translation initiation factor eIF2α. This inhibits further cellular mRNA translation, thereby preventing viral protein synthesis. Overall, this leads to apoptosis of virally infected cells to prevent further viral spread. PKR can also induce apoptosis in bacterial infection by responding to LPS and proinflammatory cytokines. Apoptosis can also occur via PKR activation of the FADD and caspase signaling pathway.
PKR also has pro-inflammatory functions, as it can mediate the activation of the transcription factor NF-kB, by phosphorylating its inhibitory subunit, IkB. This leads to the expression of adhesion molecules and transcription factors that activate them, which induce inflammation responses such as the secretion of pro-inflammatory cytokines. PKR also activates several mitogen-activated protein kinases (MAPK) to lead to inflammation.
To balance the effects of apoptosis and inflammation, PKR has regulatory functions. Active PKR is also able to activate tumor suppressor PP2A which regulates the cell cycle and the metabolism. There is also evidence that PKR is autophagic as a regulatory mechanism.
PKR is in the center of cellular response to different stress signals such as pathogens, lack of nutrients, cytokines, irradiation, mechanical stress, or ER stress. The PKR pathway leads to a stress response through activation of other stress pathways such as JNK, p38, NFkB, PP2A and phosphorylation of eIF2α. ER stress caused by excess of unfolded proteins leads to inflammatory responses. PKR contributes to this response by interacting with several inflammatory kinases such as IKK, JNK, ElF2α, insulin receptors and others. This metabolically activated inflammatory complex is called metabolic inflammasome or metaflammasome. Via the JNK signaling pathway, PKR also plays a role in insulin resistance, diabetes, and obesity by phosphorylating IRS1. Inhibiting PKR in mice led to lower inflammation in adipose tissues, increased sensitivity to insulin, and amelioration of diabetic symptoms. PKR also participates in the mitochondrial unfolded protein response (UPRmt). Here, PKR is induced via the transcription factor AP-1 and activated independently of PACT. In this context, PKR has been shown to be relevant to intestinal inflammation.
Viruses have developed many mechanisms to counteract the PKR mechanism. It may be done by Decoy dsRNA, degradation, hiding of viral dsRNA, dimerization block, dephosphorylation of substrate or by a pseudosubstrate.
For instance, Epstein–Barr virus (EBV) uses the gene EBER1 to produce decoy dsRNA. This leads to cancers such as Burkitt's lymphoma, Hodgkin's disease, nasopharyngeal carcinoma and various leukemias.
PKR knockout mice or inhibition of PKR in mice enhances memory and learning.
First report in 2002 has been shown that immunohistochemical marker for phosphorylated PKR and eIF2α was displayed positively in degenerating neurons in the hippocampus and the frontal cortex of patients with Alzheimer's disease (AD), suggesting the link between PKR and AD. Additionally, many of these neurons were also immunostained with an antibody for phosphorylated Tau protein. Activated PKR was specifically found in the cytoplasm and nucleus, as well as co-localized with neuronal apoptotic markers. Further studies have assessed the levels of PKR in blood and cerebrospinal fluid (CSF) of AD patients and controls. The result of an analysis of the concentrations of total and phosphorylated PKR (pPKR) in peripheral blood mononuclear cells (PBMCs) in 23 AD patients and 19 control individuals showed statistically significant increased levels of the ratio of phosphorylated PKR/PKR in AD patients compared with controls. Assessments of CSF biomarkers, such as Aβ1-42, Aβ1-40, Tau, and phosphorylated Tau at threonine 181, have been a validated use in clinical research and in routine practice to determine whether patients have CSF abnormalities and AD brain lesions. A study found that "total PKR and pPKR concentrations were elevated in AD and amnestic mild cognitive impairment subjects with a pPKR value (optical density units) discriminating AD patients from control subjects with a sensitivity of 91.1% and a specificity of 94.3%. Among AD patients, total PKR and pPKR levels correlate with CSF p181tau levels. Some AD patients with normal CSF Aß, T-tau, or p181tau levels had abnormal total PKR and pPKR levels". It was concluded that the PKR-eIF2α pro-apoptotic pathway could be involved in neuronal degeneration that leads to various neuropathological lesions as a function of neuronal susceptibility.
PKR and beta amyloid
Activation of PKR can cause accumulation of amyloid β-peptide (Aβ) via de-repression of BACE1 (β-site APP Cleaving Enzyme) expression in Alzheimer Disease patients. Normally, the 5′ untranslated region (5′ UTR) in the BACE1 promoter would fundamentally inhibit the expression of BACE1 gene. However, BACE1 expression can be activated by phosphorylation of eIF2a, which reverses the inhibitory effect exerted by BACE1 5′ UTR. Phosphorylation of eIF2a is triggered by activation of PKR. Viral infection such as herpes simplex virus (HSV) or oxidative stress can both increase BACE1 expression through activation of PKR-eIF2a pathway.
In addition, the increased activity of BACE1 could also lead to β-cleaved carboxy-terminal fragment of β-Amyloid precursor protein (APP-βCTF) induced dysfunction of endosomes in AD. Endosomes are highly active β-Amyloid precursor protein (APP) processing sites, and endosome abnormalities are associated with upregulated expression of early endosomal regulator, Rab5. These are the earliest known disease-specific neuronal response in AD. Increased activity of BACE1 leads to synthesis of the APP-βCTF. An elevated level of βCTF then causes Rab5 overactivation. βCTF recruits APPL1 to rab5 endosomes, where it stabilizes active GTP-Rab5, leading to pathologically accelerated endocytosis, endosome swelling and selectively impaired axonal transport of Rab5 endosomes.
PKR and Tau phosphorylation
It is reported earlier that phosphorylated PKR could co-localize with phosphorylated Tau protein in affected neurons. A protein phosphatase-2A inhibitor (PP2A inhibitor) – okadaic acid (OA) – is known to increase tau phosphorylation, Aβ deposition and neuronal death. It is studied that OA also induces PKR phosphorylation and thus, eIF2a phosphorylation. eIF2a phosphorylation then induces activation of transcription factor 4 (ATF4), which induces apoptosis and nuclear translocation, contributing to neuronal death.
Glycogen synthase kinase 3β (GSK-3β) is responsible for tau phosphorylation and controls several cellular functions including apoptosis. Another study demonstrated that tunicamycin or Aβ treatment can induce PKR activation in human neuroblastoma cells and can trigger GSK3β activation, as well as tau phosphorylation. They found that in AD brains, both activated PKR and GSK3β co-localize with phosphorylated tau in neurons. In SH-SY5Y cell cultures, tunicamycin and Aβ(1-42) activate PKR, which then can modulate GSK-3β activation and induce tau phosphorylation, apoptosis. All these processes are attenuated by PKR inhibitors or PKR siRNA. PKR could represent a crucial signaling point relaying stress signals to neuronal pathways by interacting with transcription factor or indirectly controlling GSK3β activation, leading to cellular degeneration in AD.
PKR also mediates ethanol-induced protein synthesis inhibition and apoptosis which is linked to fetal alcohol syndrome.
Protein kinase R has been shown to interact with:
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