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Archive for Caffeine
Browser-to-browser websocket tunnels with Caffeine and livecoded NodeJS
Posted in Appsterdam, consulting, Context, Smalltalk, SqueakJS with tags , , , , , , , , on 4 July 2017 by Craig Latta
network
In our previous look at livecoding NodeJS from Caffeine, we implemented tweetcoding. Now let’s try another exercise, creating WebSockets that tunnel between web browsers. This gives us a very simple version of peer-to-peer networking, similar to WebRTC.
Once again we’ll start with Caffeine running in a web browser, and a NodeJS server running the node-livecode package. Our approach will be to use the NodeJS server as a relay. Web browsers that want to establish a publicly-available server can register there, and browser that want to use such a server can connect there. We’ll implement the following node-livecode instructions:
• initialize, to initialize the structures we’ll need for the other instructions
• create server credential, which creates a credential that a server browser can use to register a WebSocket as a server
• install server, which registers a WebSocket as a server
• connect to server, which a client browser can use to connect to a registered server
• forward to client, which forwards data from a server to a client
• forward to server, which forwards data from a client to a server
In Smalltalk, we’ll make a subclass of NodeJSLivecodingClient called NodeJSTunnelingClient, and give it an overriding implementation of configureServerAt:withCredential:, for injecting new instructions into our NodeJS server:
configureServerAt: url withCredential: credential
"Add JavaScript functions as protocol instructions to the
node-livecoding server at url, using the given credential."
^(super configureServerAt: url withCredential: credential)
addInstruction: 'initialize'
from: '
function () {
global.servers = []
global.clients = []
global.serverCredentials = []
global.delimiter = ''', Delimiter, '''
return ''initialized tunnel relay''}';
invoke: 'initialize';
addInstruction: 'create server credential'
from: '
function () {
var credential = Math.floor(Math.random() * 10000)
serverCredentials.push(credential)
this.send((serverCredentials.length - 1) + '' '' + credential)
return ''created server credential''}';
addInstruction: 'install server'
from: '
function (serverID, credential) {
if (serverCredentials[serverID] == credential) {
servers[serverID] = this
this.send(''1'')
return ''installed server''}
else {
debugger;
this.send(''0'')
return ''bad credential''}}';
addInstruction: 'connect to server'
from: '
function (serverID, port, req) {
if (servers[serverID]) {
clients.push(this)
servers[serverID].send(''connected:atPort:for: '' + (clients.length - 1) + delimiter + port + delimiter + req.connection.remoteAddress.toString())
this.send(''1'')
return ''connected client''}
else {
this.send(''0'')
return ''server not connected''}}';
addInstruction: 'forward to client'
from: '
function (channel, data) {
if (clients[channel]) {
clients[channel].send(''from:data: '' + servers.indexOf(this) + delimiter + data)
this.send(''1'')
return ''sent data to client''}
else {
this.send(''0'')
return ''no such client channel''}}';
addInstruction: 'forward to server'
from: '
function (channel, data) {
if (servers[channel]) {
servers[channel].send(''from:data: '' + clients.indexOf(this) + delimiter + data)
this.send(''1'')
return (''sent data to server'')}
else {
this.send(''0'')
return ''no such server channel''}}'
We’ll send that message immediately, configuring our NodeJS server:
NodeJSTunnelingClient
configureServerAt: 'wss://yourserver:8087'
withCredential: 'shared secret';
closeConfigurator
On the NodeJS console, we see the following messages:
server: received command 'add instruction'
server: adding instruction 'initialize'
server: received command 'initialize'
server: evaluating added instruction 'initialize'
server: initialized tunnel relay
server: received command 'add instruction'
server: adding instruction 'create server credential'
server: received command 'add instruction'
server: adding instruction 'install server'
server: received command 'add instruction'
server: adding instruction 'connect to server'
server: received command 'add instruction'
server: adding instruction 'forward to client'
server: received command 'add instruction'
server: adding instruction 'forward to server'
Now our NodeJS server is a tunneling relay, and we can connect servers and clients through it. We’ll make a new ForwardingWebSocket class hierarchy:
Object
ForwardingWebSocket
ForwardingClientWebSocket
ForwardingServerWebSocket
Instances of ForwardingClientWebSocket and ForwardingServerWebSocket use a NodeJSTunnelingClient to invoke our tunneling instructions.
We create a new ForwardingServerWebSocket with newThrough:, which requests new server credentials from the tunneling relay, and uses them to install a new server. Another new class, PeerToPeerWebSocket, provides the public message interface for the framework. There are two instantiation messages:
• toPort:atServerWithID:throughURL: creates an outgoing client that uses a ForwardingClientWebSocket to connect to a server and exchange data
• throughChannel:of: creates an incoming client that uses a ForwardingServerWebSocket to exchange data with a remote outgoing client.
Incoming clients are used by ForwardingServerWebSockets to represent their incoming connections. Each ForwardingServerWebSocket can provide services over a range of ports, as a normal IP server would. To connect, a client needs the websocket URL of the tunneling relay, a port, and the server ID assigned by the relay.
As usual, you can examine and try out this code by clearing your browser’s caches for caffeine.js.org (including IndexedDB), and visiting https://caffeine.js.org/. With browsers able to communicate directly, there are many interesting things we can build, including games, chat applications, and team development tools. What would you like to build?
retrofitting Squeak Morphic for the web
Posted in Appsterdam, consulting, Context, Smalltalk, Spoon, SqueakJS with tags , , , , , , , , on 30 June 2017 by Craig Latta
Google ChromeScreenSnapz022
Last time, we explored a way to improve SqueakJS UI responsiveness by replacing Squeak Morphic entirely, with morphic.js. Now let’s look at a technique that reuses all the Squeak Morphic code we already have.
many worlds, many canvases
Traditionally, Squeak Morphic has a single “world” where morphs draw themselves. To be a coherent GUI, Morphic must provide all the top-level effects we’ve come to expect, like dragging windows and redrawing them in their new positions, and redrawing occluded windows when they are brought to the top. Today, this comes at an acceptable but noticeable cost. Until WebAssembly changes the equation again, we want to do all we can to shift UI work from Squeak Morphic to the HTML5 environment hosting it. This will also make the experience of using SqueakJS components more consistent with that of the other elements on the page.
Just as we created an HTML5 canvas for morphic.js to use in the last post, we can do so for individual morphs. This means we’ll need a new Canvas subclass, called HTML5FormCanvas:
Object
...
Canvas
FormCanvas
HTML5FormCanvas
An HTML5FormCanvas draws onto a Form, as instances of its parent class do, but instead of flushing damage rectangle from the Form onto the Display, it flushes them to an HTML5 canvas. This is enabled by a primitive I added to the SqueakJS virtual machine, which reuses the normal canvas drawing code path.
Accompanying HTML5FormCanvas are new subclasses of PasteUpMorph and WorldState:
Object
Morph
...
PasteUpMorph
HTML5PasteUpMorph
Object
WorldState
HTML5WorldState
HTML5PasteUpMorph provides a message interface for other Smalltalk objects to create HTML5 worlds, and access the HMTL5FormCanvas of each world and the underlying HTML5 canvas DOM element. An HTML5WorldState works on behalf of an HTML5PasteUpMorph, to establish event handlers for the HTML5 canvas (such as for keyboard and mouse events).
HTML5 Morphic in action
You don’t need to know all of that just to create an HTML5 Morphic world. You only need to know about HTML5PasteUpMorph. In particular, (HTML5PasteUpMorph class)>>newWorld. All of the traditional Squeak Morphic tools can use HTML5PasteUpMorph as a drop-in replacement for the usual PasteUpMorph class.
There are two examples of single-window Morphic worlds in the current Caffeine release, for a workspace and classes browser. I consider these two tools to be the “hello world” exercise for UI framework experimentation, since you can use them to implement all the other tools.
We get an immediate benefit from the web browser handling window movement and clipping for us, with opaque window moves rendering at 60+ frames per second. We can also interleave Squeak Morphic windows with other DOM elements on the page, which enables a more natural workflow when creating hybrid webpages. We can also style our Squeak Morphic windows with CSS, as we would any other DOM element, since as far as the web browser is concerned they are just HTML5 canvases. This makes effects like the rounded corners and window buttons trays that Caffeine uses very easy.
Now, we have flexible access to the traditional Morphic tools while we progress with adapting them to new worlds like morphic.js. What shall we build next?
Pharo comes to Caffeine and SqueakJS
Posted in Appsterdam, consulting, Context, GLASS, Naiad, Seaside, Smalltalk, Spoon, SqueakJS with tags , , , , , , , , , on 29 June 2017 by Craig Latta
Google ChromeScreenSnapz025
The Caffeine web livecoding project has added Pharo to the list of Smalltalk distributions it runs with SqueakJS. Bert Freudenberg and I spent some time getting SqueakJS to run Pharo at ESUG 2016 in Prague last summer, and it mostly worked. I think Bert got a lot further since then, because now there are just a few Pharo primitives that need implementing. All I’ve had to do so far this time is a minor fix to the input event loop and add the JavaScript bridge. The bridge now works from Pharo, and it’s the first time I’ve seen that.
Next steps include getting the Tether remote messaging protocol and Snowglobe app streaming working between Pharo and Squeak, all running in SqueakJS. Of course, I’d like to see fluid code-sharing of all kinds between Squeak, Pharo, and all the other Smalltalk implementations.
So, let the bugfixing begin! :) You can run it at https://caffeine.js.org/pharo/. Please do get in touch if you find and fix things. Thanks!
a faster Morphic with morphic.js
Posted in Appsterdam, consulting, Context, Naiad, Smalltalk, Spoon, SqueakJS with tags , , , , , , , , , , on 28 June 2017 by Craig Latta
Google ChromeScreenSnapz017
Caffeine is powered by SqueakJS. The performance of SqueakJS is amazingly good, thanks in large part to its dynamic translation of Smalltalk compiled methods to JavaScript functions (which are in turn translated to machine code by your web browser’s JS engine). In the HTML5 environment where SqueakJS finds itself, there are several other tactics we can use to further improve user interface performance.
Delegate!
In a useful twist of fate, SqueakJS emerges into a GUI ecosystem descended from Smalltalk, now brimming with JavaScript frameworks to which SqueakJS can delegate much of its work. To make Caffeine an attractive environment for live exploration, I’m addressing each distraction I see.
The most prominent one is user interface responsiveness. SqueakJS is quite usable, even with large object memories, but its Morphic UI hasn’t reached the level of snappiness that we expect from today’s web apps. Squeak is a virtual machine, cranking away to support what is essentially an entire operating system, with a process scheduler, window system, compiler, and many other facilities. Since, with SqueakJS, that OS has access to a multitude of similar behavior in the JavaScript world, we should take advantage.
Of course, the UI design goals of the web are different than those of other operating systems. Today’s web apps are still firmly rooted in the web’s original “page” metaphor. “Single Page Applications” that scroll down for meters are the norm. While there are many frameworks for building SPAs, support for open-ended GUIs is uncommon. There are a few, though; one very good one is morphic.js.
morphic.js
Morphic.js is the work of Jens Mönig, and part of the Snap! project at UC Berkeley, a Scratch-like environment which teaches advanced computer science concepts. It’s a standalone JavaScript implementation of the Morphic UI framework. By using morphic.js, Squeak can save its cycles for other things, interacting with it only when necessary.
To use morphic.js in Caffeine, we need to give morphic.js an HTML5 canvas for drawing. The Webpage class can create new DOM elements, and use jQuery UI to give them effects like dragging and rotation. With one line we create a draggable canvas with window decorations:
canvas := Webpage createWindowOfKind: 'MorphicJS'
Now, after loading morphic.js, we can create a morphic.js WorldMorph object that uses the canvas:
world := (JS top at: #WorldMorph) newWithParameters: {canvas. false}
Finally, we need to create a rendering loop that regularly gets the world to draw itself on the canvas:
(JS top)
at: #world
put: world;
at: #morphicJSRenderingLoop
put: (
(JS Function) new: '
requestAnimationFrame(morphicJSRenderingLoop)
world.doOneCycle()').
JS top morphicJSRenderingLoop
Now we have an empty morphic.js world to play with. The first thing to know about morphic.js is that you can get a world menu by control-clicking:
Google ChromeScreenSnapz018
Things are a lot more interesting if you choose development mode:
Google ChromeScreenSnapz019.png
Take some time to play around with the world menu, creating some morphs and modifying them. Note that you can also control-click on morphs to get morph-specific menus, and that you can inspect any morph.
Google ChromeScreenSnapz020.png
Also notice that this user interface is noticeably snappier than the current SqueakJS Morphic. MorphicJS isn’t trying to do all of the OS-level stuff that Squeak does, it’s just animating morphs, using a rendering loop that is runs as machine code in your web browser’s JavaScript engine.
Smalltalk tools in another world, with Hex
The inspector gives us an example of a useful morphic.js tool. Since we can pass Smalltalk blocks to JavaScript as callback functions, we have two-way communication between Smalltalk and JavaScript, and we can build morphic.js tools that mimic the traditional Squeak tools.
I’ve built two such tools so far, a workspace and a classes browser. You can try them out with these expressions:
HexMorphicJSWorkspace open.
HexMorphicJSClassesBrowser open
“Hex” refers to a user interface framework I wrote called Hex, which aggregates several JavaScript UI frameworks. HexMorphicJSWorkspace and HexMorphicJSClassesBrowser are subclasses of HexMorphicJSWindow. Each instance of every subclass of HexMorphicJSWindow can be used either as a standalone morphic.js window, or as a component in a more complex window. This is the case with these first two tools; a HexMorphicJSClassesBrowser uses a HexMorphicJSWorkspace as a pane for live code evaluation, and you can also use a HexMorphicJSWorkspace by itself as a workspace.
With a small amount of work, we get much snappier versions of the traditional Smalltalk tools. When using them, SqueakJS only has to do work when the tools request information from them. For example, when a workspace wants to print the result of evaluating some Smalltalk code, it asks SqueakJS to compile and evaluate it.
coming up…
It would be a shame not to reuse all the UI construction effort that went into the original Squeak Morphic tools, though. What if we were to put each Morphic window onto its own canvas, so that SqueakJS didn’t have to support moving windows, clipping and so on? Perhaps just doing that would yield a performance improvement. I’ll write about that next time.
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Вопросы с тегом 'utawarerumono'
я редактировал ответ, чтобы включить это Проверь свои источники программного обеспечения, убедитесь, что вы получаете обновления с главного сервера. У меня были проблемы в прошлом, со странными ошибкам ...
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Рекомендации для Программа веса для поддержки конкуренции боевых искусств
Я хотел установить VirtualBox 4.1 на удаленный сервер Ubuntu. Мне нужен только интерфейс командной строки для VirtualBox, мне не нужен этот пакет графического интерфейса. apt-получить установку в VirtualBox-4.1 приносит собой половину KDE, которые мне не нужны (а это занимает не менее 600 МБ). Можно ли установить VirtualBox без своего интерфейса? Я использую Убунту Люсид. ...
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Мой кот не хочет спать
Среды: ОС: Линукс Минт 19.2 Ноутбук: XPS13 9360 с последней версии BIOS Проблема: Я не могу понять почему, но если я закрываю либерал, мой ноутбук пойдет приостановить и возобновить, когда я либерал, он будет восстанавливаться. Вот это проблема, когда он оправится от приостановить, он автоматически отключается через несколько секунд. Это действительно странно :( Любой совет приветствуется! ...
13 дек. 2014 г., 19:50:23
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Patient education: Screening for hearing loss in newborns (The Basics)
Patient education: Screening for hearing loss in newborns (The Basics)
Why does my newborn need to be screened for hearing loss? — Screening is important because the sooner you know your baby has a hearing problem, the sooner they can get help. This will make it less likely that the hearing loss will cause problems with learning to talk
How will my newborn be screened for hearing loss? — There are 2 different tests for hearing loss in newborns:
Auditory brainstem response – For this test, the doctor will put 3 small devices called electrodes on your baby: on the forehead, back of the neck, and behind the ear. The electrodes connect to a machine that measures how your baby's brain responds to a clicking sound.
Otoacoustic emissions – For this test, the doctor puts a small microphone into your baby's ear. The microphone makes sounds (clicks or a tone) and measures sound waves from the cochlea, the area inside the ear that allows you to hear (figure 1).
Both of these tests are painless and take between 5 to 15 minutes. If a test suggests that your newborn has hearing loss, they will get another test. Your baby might also need to be checked by an expert in hearing problems, called an "audiologist."
Are some newborns more likely to have hearing loss? — Yes. Newborns with certain conditions are more likely to have hearing loss. These conditions include:
Being in the "neonatal intensive care unit" (also called the "NICU") for more than 2 days. Newborns spend time in the NICU if they are born too early or have other health problems.
A family history of hearing loss in childhood or other conditions that cause hearing problems
An abnormal shape to 1 or both ears
Infections
A serious form of a condition called "jaundice" that causes yellow skin and other problems
More on this topic
Patient education: When a baby is born premature (The Basics)
Patient education: What to expect in the NICU (The Basics)
Patient education: Jaundice in babies (The Basics)
Patient education: Jaundice in newborn infants (Beyond the Basics)
This topic retrieved from UpToDate on: Mar 03, 2022.
This generalized information is a limited summary of diagnosis, treatment, and/or medication information. It is not meant to be comprehensive and should be used as a tool to help the user understand and/or assess potential diagnostic and treatment options. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances. Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications. This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient. UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. The use of this information is governed by the Terms of Use, available at https://www.wolterskluwer.com/en/know/clinical-effectiveness-terms ©2022 UpToDate, Inc. and its affiliates and/or licensors. All rights reserved.
Topic 86382 Version 6.0
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Production of Oocytes from Human ES Cells
Funding Type:
SEED Grant
Grant Number:
RS1-00416
Award Value:
$385,466
Stem Cell Use:
Embryonic Stem Cell
Status:
Closed
Public Abstract:
The ability of human embryonic stem (hES) cells to form a wide variety of adult human cell types offers hope for development of novel therapies to treat human degenerative diseases such as Alzheimer’s, diabetes, and muscular dystrophy. However, to prevent rejection of the transplanted cells by a patient’s immune system it will be important to use hES cell derived tissues that are immunologically matched to the patient. One way to do this involves somatic cell nuclear transplantation (SCNT) where the nucleus containing the genetic information is transferred from a patient’s cell into a human oocyte (egg) from which the nucleus has been removed. The oocyte is then stimulated to divide into a small group of cells from which new hES cells are derived. As cells derived from these hES cells contain the patient’s DNA they will be immune-matched to the patient, thereby preventing tissue-rejection.While SCNT has been performed using cells and eggs from mice, it is not yet possible to do this on a routine basis using human cells and eggs. One reason for lack of progress concerns the scarce supply of human oocytes available for research. Oocytes are usually obtained from women undergoing hormonal treatment for infertility, when permission is given for unused and unwanted oocytes to be used for research. However, a severe shortage and great demand for such material has stimulated efforts to recruit suitable donors from the general public, often with financial incentive. There is significant health and ethical concern about such policies and the potential negative impacts of such procedures on long-term health of women are unclear.Remarkably, recent research with mice suggests that it may be possible to produce oocytes from hES cells. If so, the oocytes produced may be of use for SCNT to produce new lines of personalized-hES cells for treatment of patients. If successful, this would be expected to have at least two major benefits to the public. First, women would no longer be required as a source of eggs for research, which would reduce the risk of such treatments on women’s long-term health. Second, this would generate a theoretically infinite increase in the quantity of oocytes available for research, which would in increase the rate at which technical advances could be made in production of immune-matched hES via SCNT.Consequently, the proposed research will investigate methods for production of germ cells and oocytes from female hES cells. Specifically, we will test our prediction that it is possible to coax hES cells in culture to form germ cells and ultimately mature oocytes by exposing hES cells to different cell proteins and hormones that are normally used by the body to generate eggs. If successful, these protocols will help accelerate research on development of therapeutic cloning for a wide range of diseases. This would also obviate ethical concerns regarding egg-donation by women and would help protect women’s health.
Statement of Benefit to California:
The proposed research involves investigating how human embryonic stem (hES) cells form germ cells and oocytes, in a cell culture dish in the laboratory. The long-term goal of the research is to develop methods that enable production of such eggs in vitro. If successful, the research will benefit Californians in areas of healthcare and economy. Regarding healthcare, the ability to produce significant quantities of human oocytes in the laboratory will accelerate development of methods for reliable development of new hES cell lines from human oocytes following transfer of nuclei from a patient’s cell (i.e. therapeutic cloning). The ability to generate hES cells that are immunologically matched to a patient would also preclude the need for use of immunosuppressive drugs during treatment of patients with hES cell-derived material. Such drugs can have unwanted side effects on patients and could also have as yet unrecognized negative effects on ability of hES cell-derived tissues to engraft into a patient’s organs. Immunosuppressive therapy also increases the overall expense of treatment, due to the treatment itself as well as treating any side effects from its use.
Success of the proposed research would significantly reduce any requirement for donation of unused human oocytes. This would benefit California women by protecting them from undergoing unwanted and unnecessary hormonal stimulation for which the long-term health effects are currently unclear. If successful, the research could also have significant economic benefit to the State of California. First, successful development of this technology could be transferred to biomedical industry, and the potential worldwide market for such methods is considerable. This could stimulate employment in a variety of sectors as well as increasing state tax revenue. Equally important, a successful research outcome could also reduce the overall cost of healthcare to the State. It is anticipated that low-income individuals are more likely to be willing to donate eggs for research. While this may provide them with short term financial benefit, it is possible that such individuals could develop significant age-related health problems involving hormonal imbalance, such as infertility, polycystic ovarian syndrome, bone-loss, cognitive decline and obesity. In this event, the burden of providing healthcare to such individuals would likely fall to the State. Thus, reducing the incidence of egg-donation by in-state residents is likely to minimize any costs associated with treatment of such donors in the future.
Progress Report:
The original goal of this project was to generate oocytes (eggs) from human embryonic stem (hES) cells in cell culture dishes in the laboratory. Such oocytes could be of use as vehicles to reprogram the DNA from cells of patients with life-threatening or debilitating conditions, thereby allowing generation of new lines of hES cells that are immune matched to the patient. The paucity of donated human oocytes precludes research using such material, and production of human oocytes from hES cells in the laboratory would in theory provide a limitless source of material.
Since our last progress report another CIRM-funded group, Dr. Renee Reijo Pera’s lab at Stanford University, has published exciting results demonstrating successful production of primordial oocytes from mouse ES (mES) and human ES (hES) cells. Consequently, during the remaining period of the award we propose to use the Reijo Pera methods for production of female germ line cells in our lab using H9 and HUES-9 female hES cells. After accomplishing this, we will introduce human mtDNA containing mutations that cause either a severe or mild reduction in oxidative phosphorylation (energy) production into H9 and HUES-9 hES cells and investigate the impact of the different mtDNA mutations on the ability of hES cells to form cells with characteristics of PGCs, then primordial oocytes in vitro and in vivo. An important related goal of this research is to investigate whether development of oocytes from ES cells could be used as a method to remove deleterious mtDNA mutations from the hES cell population, thereby improving the utility and possibly safety of derived cell types for therapeutic purposes.
During this reporting period we have focused on our approved revised research plan. We continued our efforts to generate embryonic female germ cells from human embryonic stem (hES) cells in vitro using methods reported in the literature at the end of 2009. Our revised plan included the new goal of using in vitro developed female embryonic germ cells (oocytes) as a resource to investigate how mitochondrial genomic DNA containing deleterious mutations is segregated during female germ cell development. As well as providing novel information about the biology of germ cell development, this research may provide important information relevant to development of safe methods for therapeutic cloning. We began by using two different female hES cell lines (HUES-6 and H9) to investigate whether we could use the reported methods to develop female germ cells from hES in our lab. A third female hES cell line (HUES-9) we originally intended to use was found to have a high propensity to gain an extra chromosome (become aneuploid) and was therefore not used. Despite following the reported methods that demonstrated in vitro differentiation of hES cells into female germ cells, we were unable to reproduce the previously reported results in our own lab. The reasons for this are currently unclear but may involve subtle, but important, differences in the methodology or materials we used.
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Visualize Google Directory Data in Sisense
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Download for a free trial:
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Learn more:
Google Directory JDBC Driver
An easy-to-use database-like interface for Java based applications and reporting tools access to live Google Directory data (Domains, Groups, Users, Tokens, and more).
Create an ElastiCube in Sisense app with access to Google Directory data.
Sisense lets you join, analyze, and picture data to make more intelligent business decisions and craft effective strategies. The CData JDBC Driver for Google Directory makes it easy to integrate with Google Directory data in Sisense. This article shows how to create an ElastiCube that connects to Google Directory data and use the ElastiCube to visualize Google Directory data in Sisense.
Configure the Connection to Google Directory
Before creating the ElastiCube, note the installation location for the JAR file for the JDBC Driver (typically C:\Program Files\CDatat\CData JDBC Driver for Google Directory\lib) or copy the jar file (cdata.jdbc.googledirectory.GoogleDirectory.jar) to a new folder in the Sisense JDBC driver directory (typically C:\ProgramData\Sisense\DataConnectors\jdbcdrivers).
1. In the Data page of the Sisense application, create a new ElastiCube (or open an existing one).
2. In the Model Editor, click "+ Data" to open the Add Data dialog box.
3. Click Generic JDBC to open the JDBC settings.
4. Set the connection string property to the JDBC URL for Google Directory, adding required properties.
Google uses the OAuth authentication standard. You can authorize the data provider to access Google Spreadsheets as an individual user or with a Google Apps Domain service account. See the Getting Started section of the data provider help documentation for an authentication guide.
Built-in Connection String Designer
For assistance in constructing the JDBC URL, use the connection string designer built into the Google Directory JDBC Driver. Either double-click the JAR file or execute the jar file from the command-line.
java -jar cdata.jdbc.googledirectory.jar
Fill in the connection properties and copy the connection string to the clipboard.
When you configure the JDBC URL, you may also want to set the Max Rows connection property. This will limit the number of rows returned, which is especially helpful for improving performance when designing reports and visualizations.
A typical example follows:
jdbc:googledirectory:OAuthClientId=MyOAuthClientId;OAuthClientSecret=MyOAuthClientSecret;CallbackURL=http://localhost;InitiateOAuth=REFRESH
5. Set the JDBC JARs folder property to the location of the CData JDBC Driver JAR file (see above).
6. Set the driver's class name to the class name for the JDBC Driver: cdata.jdbc.googledirectory.GoogleDirectoryDriver
7. Leave the username and password properties blank.
8. Click Next.
Add Google Directory Data to an ElastiCube
Once you are connected to Google Directory, you can add tables and views to your ElastiCubes.
1. From the Tables list, select the tables and/or views you wish to work with.
2. (Optional) Click "+" to customize the data you want to import with SQL.
3. Click Done.
4. Click Build to build the ElastiCube for analytics.
Visualize Google Directory Data
With Google Directory tables added to your ElastiCube, you can perform analytics on your Google Directory data.
1. Navigate to the Analytics page of the Sisense application
2. Select a Dashboard (or create a new one)
3. Select your Data Source and click Create
4. Click "+ Select Data" and choose fields to add to your visualization.
With the CData JDBC Driver for Google Directory, you can access Google Directory data right in Sisense for powerful visualization and analytics. Download a free, 30-day trial and start working with Google Directory data in Sisense today!
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Skip to Content
ticarcillin
Generic Name: ticarcillin (tye KAR sil in)
Brand Name: Ticar
What is ticarcillin?
Ticarcillin is an antibiotic in a group of drugs called penicillins. Ticarcillin fights bacteria in the body.
The combination of ticarcillin is used to treat many different infections caused by bacteria, such as urinary tract infections, bone and joint infections, severe vaginal infections, stomach infections, and skin infections.
Ticarcillin may also be used for purposes other than those listed in this medication guide.
What is the most important information I should know about ticarcillin?
Do not use this medication if you are allergic to ticarcillin or to any other penicillin antibiotic, such as amoxicillin (Amoxil, Augmentin), ampicillin (Omnipen, Principen), carbenicillin (Geocillin), dicloxacillin (Dycill, Dynapen), oxacillin (Bactocill), penicillin (Beepen-VK, Ledercillin VK, Pen-V, Pen-Vee K, Pfizerpen, V-Cillin K, Veetids), and others.
Slideshow: The Shocking Truth About Antibiotic Resistance
Before using ticarcillin tell your doctor if you are allergic to cephalosporins such as Ceclor, Ceftin, Duricef, Keflex, and others, or if you have kidney disease, a bleeding or blood clotting disorder, low levels of potassium in your blood, a history of any type of allergy, or if you are on a salt-restricted diet.
Use this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Ticarcillin will not treat a viral infection such as the common cold or flu.
Ticarcillin can make birth control pills less effective. Use a second non-hormone method of birth control (such as a condom, diaphragm, spermicide) to prevent pregnancy while using ticarcillin.
What should I discuss with my healthcare provider before using ticarcillin?
Do not use this medication if you are allergic to ticarcillin or to any other penicillin antibiotic, such as:
• amoxicillin (Amoxil, Augmentin);
• ampicillin (Omnipen, Principen);
• carbenicillin (Geocillin);
• dicloxacillin (Dycill, Dynapen);
• oxacillin (Bactocill); or
• penicillin (Beepen-VK, Ledercillin VK, Pen-V, Pen-Vee K, Pfizerpen, V-Cillin K, Veetids, and others).
Before using ticarcillin, tell your doctor if you are allergic to any drugs (especially cephalosporins such as Ceclor, Ceftin, Duricef, Keflex, and others), or if you have:
• kidney disease;
• a bleeding or blood clotting disorder;
• an electrolyte imbalance such as low levels of potassium in your blood;
• a history of any type of allergy; or
• if you are on a salt-restricted diet.
If you have any of these conditions, you may not be able to use ticarcillin, or you may need a dosage adjustment or special tests during treatment.
FDA pregnancy category B. This medication is not expected to be harmful to an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant during treatment.
Ticarcillin can make birth control pills less effective. Use a second non-hormone method of birth control (such as a condom, diaphragm, spermicide) to prevent pregnancy while using ticarcillin.
It is not known whether ticarcillin passes into breast milk or if it could harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.
How should I use ticarcillin?
Use this medication exactly as it was prescribed for you. Do not use the medication in larger amounts, or use it for longer than recommended by your doctor. Follow the instructions on your prescription label.
Ticarcillin is given as an injection through a needle placed into a vein. Your doctor, nurse, or other healthcare provider will give you this injection. You may be given instructions on how to inject your medicine at home. Do not use this medicine at home if you do not fully understand how to give the injection and properly dispose of needles and other items used in giving the medicine.
Ticarcillin must be mixed with a liquid (diluent) before injecting it. Do not mix the medicine until you are ready to give yourself an injection.
Ticarcillin is usually given for 10 to 14 days, depending on the infection being treated. Follow your doctor's instructions.
Use each needle only one time. Throw away used needles and syringes in a puncture-proof container. If your medicine does not come with such a container, ask your pharmacist where you can get one. Keep this container out of the reach of children and pets. Your pharmacist can tell you how to properly dispose of the container.
Use this medication for the entire length of time prescribed by your doctor. Your symptoms may get better before the infection is completely treated. Ticarcillin will not treat a viral infection such as the common cold or flu.
Store unmixed ticarcillin, and the liquid diluent, at cool room temperature.
What happens if I miss a dose?
Use the missed dose as soon as you remember. If it is almost time for your next dose, skip the missed dose and use the medicine at the next regularly scheduled time. Do not use extra medicine to make up the missed dose.
What happens if I overdose?
Seek emergency medical attention if you think you have used too much of this medicine.
Symptoms of a ticarcillin overdose may include drowsiness, hyperactivity, or seizure (convulsions).
What should I avoid while using ticarcillin?
Antibiotic medicines can cause diarrhea, which may be a sign of a new infection. If you have diarrhea that is watery or has blood in it, call your doctor. Do not use any medicine to stop the diarrhea unless your doctor has told you to.
Ticarcillin side effects
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Call your doctor at once if you have any of these serious side effects:
• diarrhea that is watery or bloody;
• easy bruising or bleeding, unusual weakness;
• dry mouth, increased thirst, confusion, increased urination, muscle pain or weakness, fast heart rate, feeling light-headed, fainting;
• fever, chills, body aches, flu symptoms; or
• skin rash, bruising, severe tingling, numbness, pain, muscle weakness.
Less serious side effects may be more likely to occur, such as:
• mild diarrhea, gas, stomach pain;
• nausea or vomiting;
• headache;
• skin rash or itching;
• pain, swelling, or burning where the injection was given; or
• vaginal yeast infection (itching or discharge).
Side effects other than those listed here may also occur. Talk to your doctor about any side effect that seems unusual or that is especially bothersome. You may report side effects to FDA at 1-800-FDA-1088.
See also: Side effects (in more detail)
Ticarcillin dosing information
Usual Adult Dose for Febrile Neutropenia:
3 g IV every 4 hours. Therapy should be continued for approximately 14 days, or until more specific therapy may be substituted for a proven infection, or until the patient has been afebrile for 24 hours after the absolute neutrophil count has been greater than 500 cells/mm3.
Ticarcillin should be used in combination with another anti-infective agent, usually an aminoglycoside, for the empiric treatment of febrile patients.
Usual Adult Dose for Intraabdominal Infection:
3 g IV every 4 hours, for 7 to 14 days depending on the nature and severity of the infection.
Usual Adult Dose for Joint Infection:
3 g IV every 4 hours for up to 3 or 4 weeks, depending on the nature and severity of the infection. Longer therapy, sometimes up to 6 weeks, may be necessary for prosthetic joint infections.
Usual Adult Dose for Osteomyelitis:
3 g IV every 4 hours. Therapy should be continued for 4 to 6 weeks. Chronic osteomyelitis may require additional oral antimicrobial therapy, possibly up to 6 months.
Usual Adult Dose for Pelvic Inflammatory Disease:
3 g IV every 4 to 6 hours. Parenteral therapy should continue for 48 hours after clinical improvement is observed, at which time oral therapy may be initiated and continued for a total of 14 days of treatment.
If the patient is not pregnant, appropriate treatment for possible chlamydia infection should be initiated and any sexual partner(s) should be evaluated.
The Centers for Disease Control and Prevention currently recommend cefotetan or cefoxitin plus doxycycline, or clindamycin plus gentamicin for the treatment of pelvic inflammatory disease.
Usual Adult Dose for Peritonitis:
3 g IV every 4 hours. Ticarcillin is generally used as part of combination therapy when treating peritonitis. Therapy should be continued for approximately 10 to 14 days.
Intraperitoneal cefazolin plus ceftazidime are recommended for treatment of peritoneal dialysis-associated peritonitis.
Usual Adult Dose for Pneumonia:
3 g IV every 4 hours for 21 to 28 days, depending on the nature and severity of the infection.
Usual Adult Dose for Pyelonephritis:
3 g IV every 4 to 6 hours for 14 days, depending on the nature and severity of the infection.
Usual Adult Dose for Septicemia:
3 g IV every 4 hours for 14 days, depending on the nature and severity of the infection.
Usual Adult Dose for Skin or Soft Tissue Infection:
3 g IV every 4 hours for 7 to 10 days, or for 3 days after acute inflammation resolves, depending on the nature and severity of the infection.
Usual Adult Dose for Urinary Tract Infection:
Complicated: 3 g IV every 4 to 6 hours for 14 days, depending on the nature and severity of the infection.
Uncomplicated: 1 g IM or IV every 6 hours
Usual Pediatric Dose for Intraabdominal Infection:
Neonates:
< 7 days, birthweight < 2000 g: 75 mg/kg IV every 12 hours
< 7 days, birthweight > 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight < 1200 g: 75 mg/kg every 12 hours
> 7 days, birthweight < 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight > 2000 g: 75 mg/kg every 6 hours or 100 mg/kg IV every 8 hours
1 month to 12 years:
< 40 kg: 100 to 300 mg/kg/day IV in equally divided doses every 4 to 6 hours
> 40 kg: Adult dose
Usual Pediatric Dose for Pneumonia:
Neonates:
< 7 days, birthweight < 2000 g: 75 mg/kg IV every 12 hours
< 7 days, birthweight > 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight < 1200 g: 75 mg/kg every 12 hours
> 7 days, birthweight < 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight > 2000 g: 75 mg/kg every 6 hours or 100 mg/kg IV every 8 hours
1 month to 12 years:
< 40 kg: 100 to 300 mg/kg/day IV in equally divided doses every 4 to 6 hours
> 40 kg: Adult dose
Usual Pediatric Dose for Skin or Soft Tissue Infection:
Neonates:
< 7 days, birthweight < 2000 g: 75 mg/kg IV every 12 hours
< 7 days, birthweight > 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight < 1200 g: 75 mg/kg every 12 hours
> 7 days, birthweight < 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight > 2000 g: 75 mg/kg every 6 hours or 100 mg/kg IV every 8 hours
1 month to 12 years:
< 40 kg: 100 to 300 mg/kg/day IV in equally divided doses every 4 to 6 hours
> 40 kg: Adult dose
Usual Pediatric Dose for Septicemia:
Neonates:
< 7 days, birthweight < 2000 g: 75 mg/kg IV every 12 hours
< 7 days, birthweight > 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight < 1200 g: 75 mg/kg every 12 hours
> 7 days, birthweight < 2000 g: 75 mg/kg IV every 8 hours
> 7 days, birthweight > 2000 g: 75 mg/kg every 6 hours or 100 mg/kg IV every 8 hours
1 month to 12 years:
< 40 kg: 200 to 300 mg/kg/day IV in equally divided doses every 4 to 6 hours
> 40 kg: Adult dose
Usual Pediatric Dose for Urinary Tract Infection:
Uncomplicated infections:
1 month to 12 years:
< 40 kg: 50 to 100 mg/kg/day IV or IM in equally divided doses every 6 to 8 hours.
> 40 kg: Adult dose.
Complicated infections:
1 month to 12 years:
< 40 kg: 150 to 200 mg/kg/day IV in equally divided doses every 4 to 6 hours.
> 40 kg: Adult dose.
What other drugs will affect ticarcillin?
There may be other drugs that can affect ticarcillin. Tell your doctor about all the prescription and over-the-counter medications you use. This includes vitamins, minerals, herbal products, and drugs prescribed by other doctors. Do not start using a new medication without telling your doctor.
Where can I get more information?
• Your doctor or pharmacist has information about ticarcillin written for health professionals that you may read.
• Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
• Disclaimer: Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.
Copyright 1996-2012 Cerner Multum, Inc. Version: 1.05. Revision Date: 2010-12-15, 5:01:39 PM.
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What’s a Hemi?
What’s a Hemi?
My very first car as a kid in England was a 1946 Riley RME. I thought it was cool because it had a chrome grille like a ’34 Ford and it had a race-developed, twin-cam HEMI—whatever that was. Back then, there was no internet to look things up but a trip to the library revealed that the word HEMI was an abbreviation for hemispherical combustion chambers—whatever that was.
Combustion Chambers
Photo Credit: Tony Thacker
Believe it or not, HEMI-heads are nothing new and their history can be traced back to the early 1900s when they could be found in a number of European cars including the 1904 Welch Tourist, the Belgian Pipe of 1905, the 1907 Italian Fiat Grand Prix car, the French Grand Prix Peugeot of 1912 and the Italian Grand Prix Alfa Romeo of 1914—race-bred alright. However, it was the Welch design that became the blueprint for the many successors that included numerous motorcycle engines.
Chrysler HEMI
Photo Credit: Tony Thacker
Where the HEMI-head differs from other cylinder head designs such as the “flathead” Ford which is known as an “L” head design, is that their combustion chambers are hemispherical or half-bowl-shaped compared to most chambers that resemble a flattened, double egg. The chamber operates in a cross-flow configuration where the air-fuel mixture flows in one side; the more-or-less centrally located spark plug ignites the mixture and the exhaust gases exit on the opposite side from the inlet.
HEMI in a Dragster
Photo Credit: Tony Thacker
The use of a HEMI-head became prevalent in motorcycle engines because not only was it efficient, but it was not an overly complicated assembly in a single-cylinder application where the pushrods ran up the outside of the cylinder. Incidentally, a HEMI-head can be used with a pushrod, SOHC or DOHC valve train.
Believe it or not, HEMI-heads are nothing new and their history can be traced back to the early 1900s when they could be found in a number of European cars…
The concept even worked well in early air-cooled, radial airplane engines that are more-or-less a number of single cylinders arranged in a circle around a common crankshaft. In fact, by 1921 the U.S. Navy had announced it would only order aircraft fitted with air-cooled radials.
HEMI in a street rod
Photo Credit: Tony Thacker
Obviously, World War II propelled engineering development, as it did with much technology, as speed and power became all-important. Chrysler worked with Continental on the development of a giant, 1,792 cubic-inch (ci) V-12 that would be used in the Patton tank. It produced 810 horsepower and 1,560 pounds-feet (lb-ft) of torque and enabled Chrysler’s engineers to gather some valuable information that they put to good use in their post-War automobiles.
HEMI 392
Photo Credit: Tom West
In 1947, Zora Arkus-Duntov, the so-called “Father of the Corvette”, was commissioned by Ford Motor Company to improve the output of their aging flathead V8s. Zora, his brother Yuri and designer George Kudasch developed an overhead valve conversion (OHV) for the Ford V-8 that featured hemispherical combustion chambers. Tagged the “ARDUN”, which was a contraction of ARkus-DUNtov, their OHV heads looked great and increased the power, however, they were somewhat temperamental.
Only about 200 sets were made in the U.S. before Duntov moved to the U.K. to work with Sydney Allard where a few more sets were made for Allard’s J2 sports car. For many years, ARDUN heads were a much sought after hot rod accessory until the mid-90s when Don Orosco began to reproduce them. He made about 30 sets before the tooling was sold to Don Ferguson whose family continues to produce the heads albeit updated with some modern technology along with a compatible cast-aluminum block. Companies such as H&H Flatheads are known for building complete ARDUN engines.
Hardun HEMI
Photo Credit: Tony Thacker
While the Duntovs were working on the OHV Ford, Chrysler engineers John Platner, a graduate of the Chrysler Institute of Engineering, and William Drinkard, manager of the Engine Development department, got to work in 1948 downsizing that tank engine for use in an automobile.
The engine was tough and you could throw all kinds of power-enhancing devices from blowers to nitro and it thrived on it.
What they came up with was a 90-degree, 330 ci, cast-iron V8 engine with HEMI-heads. Code-named A-182, the “HEMI” was not quite ready for production and a lot of valve train development still needed to be done along with some ignition and crankshaft work.
Installing a HEMI
Photo Credit: Tony Thacker
Nevertheless, Chrysler debuted the HEMI V-8 for the 1951 model year as standard in the Imperial and New Yorker models and optional in the Saratoga. Initially, the “Fire Power” capacity was 331 ci due to an “oversquare” 3.81-inch bore and 3.63-inch stroke. With a 7:1 compression ratio (cr), it produced 180 hp and 312 lb-ft of torque but weighed a whopping 745 pounds—one head alone weighed almost 120 pounds and you’d better be wearing a belt when you lift one.
Chrysler HEMI
Photo Credit: Tony Thacker
Chrysler’s DeSoto division came out with their 276-ci “Fire Dome” version in 1952 and Dodge followed suit with their 241 ci “Red Ram” in 1953. Although all three engines differed in detail, they shared the same basic architecture.
In 1955, Chrysler claimed a dual 4-barrel (bbl) Carter version the first production car to produce 300 hp. The displacement was increased in 1956 to 354 ci and the engine now produced as much as 355 hp and became the first American engine to produce 1 hp per cubic inch.
Rat Trap 201 HEMI
Photo Credit: Kleet Norris
Two years later, the infamous 392 version was introduced and it was almost square having a 4-inch bore and a 3.906-inch stroke. It had a taller ‘raised deck’ compared to previous engines; however, the heads were cast with wider ports so that earlier manifolds could be used with the new heads on the new block. The following year, a single carb version with 9.25:1 cr was rated at 345 hp while a dual-carb version offered 375 hp.
Chrysler 392 HEMI
Photo Credit: Tony Thacker
The 392 is significant because it became the drag racer’s engine of choice, especially in the fuel ranks: Top Fuel, Funny Car, and Fuel Altered. The engine was tough and you could throw all kinds of power-enhancing devices from blowers to nitro and it thrived on it.
By 1958, the 392 was producing 380 hp but had reached the end of its production life. It wasn’t until 1964 that Chrysler re-introduced the engine and officially called it a HEMI. Nicknamed the “elephant engine,” because of its size and weight, the new Gen II HEMI displaced 426 ci. Not initially available to the public, it was used in NASCAR in ’64 but not in ’65 because it was not available in a production car and therefore could not be raced.
In the shop
Photo Credit: Tony Thacker
Not to be outdone, Ford also introduced a 427-ci HEMI in 1964. Nicknamed the “Cammer” because it had a single overhead cam (SOHC), engineers had worked hard to design a symmetrical combustion chamber with the plug located for maximum efficiency only to discover that the plug didn’t care where it was. The plugs were then located near the top of the cylinder for easy access. NASCAR wasn’t at all happy about these “special” racing engines, however, the “SOHC” motor (pronounced “sock”) remains a “halo” engine for Ford.
Ford 427 SOHC
Photo Credit: Tony Thacker
Ford SOHC 427 HEMI closeup
Photo Credit: Tony Thacker
Chrysler fixed their NASCAR problem in 1966 by introducing the “street” HEMI with lower compression, a milder cam, cast instead of tube headers and two 4 bbl Carter AFB carbs. The Gen II HEMI was produced until 1971 and was rated at 425 hp at 5,000 rpm and 490 lb-ft of torque at 4,000 rpm.
Of course, this is only the American version of HEMI history. Across the pond, in the homeland of the HEMI, the Europeans never left the concept alone.
Incidentally, the 426 HEMI is a HEMI in name only. Rather than build the new 426 from the old architecture of the 392, Chrysler engineers chose to use the existing 440 Wedge-head big-block. That said, the 426 evidences many improvements over the Wedge and indeed the 392 and became the modern drag racer’s engine of choice and was known colloquially as the “late model” compared to the 392 “early model.”
As the factory HEMIs came to the end of their respective lives Ed Donovan of Donovan Engines introduced a cast-aluminum 417 ci aftermarket version in 1971 that was based on the 392. That was followed in 1974 by Keith Black’s 426 HEMI based on the factory 426. Versions up to 573 ci are now available as are heads and numerous other parts milled from billet aluminum from numerous aftermarket manufacturers such as Hot Hemi Heads.
In fact, we use a billet 417 ci Donovan block with billet heads from Hot Hemi Heads in Ron Hope’s Rat Trap AA/Fuel Altered that we race. With a billet BDS supercharger and 90-percent nitro, it produces some 3,000 hp. However, in current Top Fuel/Funny car racing they use architecturally similar 500 ci blocks milled from forged billet aluminum.
Engine between drag strip rounds
Photo Credit: Tony Thacker
Hot Heads engine shot
Photo Credit: Tony Thacker
These proprietary blocks are produced in-house by Don Schumacher Racing and John Force Racing but similar blocks that can withstand in excess of 10,000 hp are available from companies such as Brad Anderson and Alan Johnson Performance—all based on that Chrysler HEMI.
Billet HEMI
Photo Credit: Tony Thacker
Of course, this is only the American version of HEMI history. Across the pond, in the homeland of the HEMI, the Europeans never left the concept alone. For example, Daimler, using Triumph motorcycle architecture, developed two aluminum-headed HEMI engines of 2.5 and 4.5-liters.
Other British brands such as Aston Martin and Jaguar both employed hemispherical combustion chambers in the DOHC V-8s and straight 6s respectively. However, no doubt the most well-known use of their HEMI-head was by Porsche in many of their engines—particularly the flat-six boxer engines of the 1963-’99 911s.
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Understand The Effect Of Sarms And Why Do You Wish to Take It.| provensarms.com | 2020
Published Date: November 10, 2021
girl, woman, fashion
This Is Everything You Need to Understand About SARMs
Key Takeaways
1. SARM means selective androgen receptor modulator, and it’s a type of drug that’s chemically comparable to anabolic steroids.
2. SARMs can increase muscle growth and weight loss like steroids, however to a lower degree.
3. SARMs likewise feature a number of the very same risks, disadvantages, and negative effects as steroids such as decreased natural testosterone production, increased loss of hair, and potentially an increased danger of cancer.
You’re watching your macros and calories.
You’re providing your exercises everything you’ve got.
You’re spending a small fortune on workout supplements.
And it’s all not enough. The needle simply isn’t moving as quickly as you desire.
Maybe you have actually thought about turning to steroids. You understand they work, however you also know about the negative effects and health risks, and you’re not all set to take that plunge (har har har).
And after that you stumble upon SARMs, and you can’t wonder however assist:
Are these the holy grail of bodybuilding supplements?
Can they truly help you gain muscle and lose fat almost as effectively as steroids, but without any of the downsides?
And they’re cheap and legal!?
It beggars belief.
That’s why many individuals are declaring that SARMs are the ultimate supplements for health-conscious bodybuilders, and why many athletes are singing their praises for efficiency enhancement and muscle-building purposes.
It certainly sounds too good to be real, but is it? What does the science state?
Well, in this post, we’re going to get to the bottom of all of it.
We’re going to look at what SARMs are, how they work, what research study says about how effective and safe they truly are.
What Are SARMs and How Do They Work?
SARM represents selective androgen receptor modulator, and it’s a type of drug that’s chemically comparable to anabolic steroids.
There are quite a few SARMs on the marketplace, and some are stronger and have a greater risk of negative effects than others.
Ivan Samkov
The more popular ones are …
1. MK-2866 or GTx-024 (Ostarine).
2. LGD-4033 (Ligandrol).
3. LGD-3303.
4. GSX-007 or S-4 (Andarine).
5. GW-501516 (Cardarine).
Why the strange alphanumeric names, you wonder?
Well, SARMs haven’t been authorized for medical usage, so pharmaceutical online marketers have not troubled naming them yet. Presently, they’re just sold as “research study chemicals” planned for scientific use, but more on that in a moment.
Now, to understand how these drugs work, we initially need to take a look at the physiology of hormones.
Hormonal agents are chemical messengers that your body utilizes to interact with cells.
You can think of them as outgoing mail which contains essential instructions, and when they reach the cells’ “mailboxes”– hormonal agent receptors– the commands are performed.
Androgens are hormones that produce masculinity (deeper voice, facial hair, more muscle and lower body fat levels, etc). The most well-known androgen is testosterone, but there are others.
Androgens exert their effects in the body in 3 main ways:
1. Binding to your cells’ androgen receptors.
2. Converting to the hormone dihydrotestosterone (DHT), which then binds to androgen receptors.
3. Transforming to the hormone estradiol (estrogen), which binds to a various type of receptor on cells (estrogen receptor).
Under regular situations, your body thoroughly regulates androgen production, counting on sensitive feedback systems to prevent imbalances.
When you present anabolic steroids into the body, however, your cells end up being flooded with androgens– many that all offered receptors become fully filled.
This sends an extremely effective message to all cells that are listening, consisting of muscle cells, which proliferate in action.
That sounds like great times to us weightlifters, but then there are the liabilities.
Research study reveals that some of the negative effects of steroid usage are reversible and some aren’t. Permanent damage is possible.
Reversible modifications consist of testicular atrophy (shrinking), acne, cysts, oily hair and skin, elevated blood pressure and “bad” cholesterol levels, increased aggression, and reduced sperm count.
Irreparable damage includes male-pattern baldness, heart dysfunction, liver illness, and gynecomastia (breast development).
Another significant downside to steroids is the risk of biological and psychological addiction.
One research study performed by scientists at Harvard Medical School discovered that 30% of steroid users developed a reliance syndrome, and if you talk to adequate truthful drug users, you’ll hear all about their addictive homes.
Now, for years, researchers have been attempting to develop steroids or steroid-like drugs that aren’t as damaging to people’s health and well-being, and supplement online marketers claim that SARMs are just that.
They’re non-steroidal drugs created to stimulate the androgen receptors in just muscle and bone cells, having little effect on the other cells in the body, and therefore the endocrine system as a whole.
In a sense, taking regular ol’ anabolic steroids is like carpet bombing your system with androgens. It gets the job done, but it’s careless and results in a lot of civilian casualties.
Taking SARMs, however, resembles drone striking just the asshole whistleblower journalists … er … I mean, bad guy terrorists.
Simply put, SARMs can tell your muscle cells to grow without all the noise and mess caused by anabolic steroids.
Technically speaking, SARMs achieve this in two ways:
1. They have a special affinity for certain tissues like muscle and bone, however not for others, like the liver, brain, and prostate.
2. They do not break down into unwanted particles that cause negative effects, like DHT and estrogen, as quickly.
This 2nd point is rather significant.
One key characteristic of SARMs is they’re not quickly transformed by an enzyme called 5-a reductase into DHT, a driver of numerous undesirable adverse effects of steroid use.
SARMs are likewise resistant to the enzyme aromatase, which converts testosterone into estrogen.
Because SARMs are less effective than routine steroids, they don’t suppress natural testosterone production as heavily, making them simpler to recuperate from.
SARMs are a synthetic drug that imitates a number of the impacts of testosterone in muscle and bone tissue, while (hopefully) having a very little effect on other organs. Hence, the theory is that you can have the benefits of steroids with none of the disadvantages.
Why Do Individuals Supplement With SARMs?
SARMs were initially established for individuals with diseases like muscle wasting, osteoporosis, anemia, and persistent fatigue.
They were meant to be a much healthier alternative to testosterone replacement therapy. Whether they’re going to meet that vision is yet to be identified.
Now, bodybuilders generally take SARMs for one of two factors:
1. To “get their feet wet” with anabolic substance abuse before going into conventional steroid cycles.
2. To increase the efficiency of steroid cycles without worsening adverse effects or health risks.
Since they help maintain lean mass however don’t seem to increase water retention, numerous bodybuilders likewise think that SARMs are specifically helpful for cutting.
How well do these drugs work?
Well, research study reveals that SARMs aren’t as powerful for muscle building as conventional steroids, however they’re definitely more efficient than anything natural you can take (like creatine).
They’re also popular amongst professional athletes because they’re more difficult to identify in drug screening.
Now, if whatever I have actually said so far has you wanting to go to Google, wallet in hand, not so quickly … we’re not done yet.
Are SARMs Safe?
Nonsteroidal SARMs have actually just been around for a couple of years and, unfortunately, are doing not have in human research.
We simply don’t understand sufficient about how they work and their prospective long-lasting side effects, which is a really genuine cause for issue.
In addition, because all SARMs offered online are technically black-market products, they’re exempt to any oversight whatsoever and quality assurance is often a concern. Mislabeling, contamination, and other shenanigans are common events.
Here’s what we do understand, though …
SARMs suppress your natural testosterone production.
Among the crucial selling points for a number of these drugs is the claim that they do not blunt your body’s production of testosterone.
This is a lie. They definitely do.
For instance, in one research study conducted by researchers at the behest of GTx, Inc., a pharmaceutical business that specializes in making SARMs, male subjects taking 3 mg of the SARM ostarine daily for 86 days experienced a 23% drop in totally free testosterone and 43% drop in total testosterone levels (throughout the trial).
As GTx, Inc. produces and sells SARMs, they had no reward to make the results look worse than they actually were. If anything, they were incentivized to do the opposite and underreport the unfavorable adverse effects (there’s no evidence this was done, however I’m simply making a point).
Comparable effects were seen in another study performed by scientists at Boston University with the SARM ligandrol. In this case, 76 guys aged 21 to 50 experienced a massive 55% drop in total testosterone levels after taking 1 mg of ligandrol per day for just 3 weeks. Disturbingly, it also took 5 weeks for their natural testosterone production to recuperate.
In fact, SARMs are being investigated as a male contraceptive due to the fact that they lower your levels of luteinizing hormone and follicle-stimulating hormonal agent, which decreases your sperm count and testosterone levels.
All this isn’t unexpected when you consider the basic physiology in play:
It acknowledges the spike and reacts by minimizing its own production of its own comparable hormonal agents when you introduce androgens into the body.
Regardless of what SARM hucksters declare, SARMs definitely due depress your natural testosterone production, and the more you take, the more your natural testosterone levels will drop.
The more SARMs you take, the more side effects you’ll experience.
SARMs aren’t entirely devoid of negative effects– they just tend to be very little at small dosages.
Bodybuilders do not typically take small dosages, however, and that’s why they often experience many of the negative effects related to steroid use, including acne and loss of hair.
This also applies to the suppression of testosterone you simply learnt more about. The more exogenous (stemming outside an organism) anabolic hormonal agents you present into your body, whether from SARMs or plain ol’ testosterone, the more your natural production will fall.
And according to a research study conducted by researchers at Copenhagen University, it’s possible that this decrease in natural testosterone production may continue for several years after you stop taking steroids (or SARMs).
On paper, SARMs appear to be simpler on the body than standard steroids, including testosterone. If you take enough to see considerable advantages, though, then opportunities are great you’ll also come across substantial side effects.
SARMs are probably easier to recover from than routine steroids.
We recall that they don’t convert into DHT or estrogen in the same way as steroids, which means they likewise do not affect your system as adversely.
SARMs also aren’t as anabolic as pure testosterone, which means they probably do not suppress natural testosterone as much, also (although there isn’t adequate research study offered to know for sure).
That stated, if you take enough to experience significant advantages, you’re most likely also taking enough to experience substantial negative results. That’s simply the nature of drugs– they cut both methods and you always need to weigh the excellent and the bad.
If you take sufficient SARMs to cause some of the more major side results such as hair loss, gynecomastia, and so on, they might be irreversible– just as with anabolic steroid use.
Anecdotally, many people do report recuperating from SARM use much faster than traditional steroid cycles. You have to take such stories with a grain of salt, though, as much of these individuals have also utilized significantly lower dosages of SARMs than they ever did of steroids, so it’s not a true apples-to-apples comparison.
Plus, as you’ll learn more about in a moment, it’s completely possible the stuff these people were taking wasn’t even SARMs.
The unfavorable effects of SARMs might be easier to recover from as soon as you stop taking them than conventional steroids, although this idea is largely based upon bodybuilder anecdotes rather than scientific research study.
SARMs might raise your risk of cancer.
Several big trials on the SARM cardarine needed to be canceled because it was causing cancerous developments in the intestinal tracts of mice.
You might have become aware of this, and that the doses utilized were much higher than us physical fitness folk would ever ingest, however that’s not true.
Rodents remove some drugs from their bodies much quicker than we do, so they have to get greater dosages to see the very same impacts.
In the event cited above, the mice were given 10 mg per kg of cardarine daily, which, when adjusted for a human metabolism, comes out to about 75 mg each day for a 200-pound male.
Poke around on bodybuilding online forums and you’ll quickly discover that many bodybuilders take substantially more than that.
Granted, you can’t extrapolate rodent research study to human beings (in spite of sharing ~ 98% of their DNA, we aren’t big mice), so it’s not clear if that drug or other SARMs in fact do increase our threat of developing cancer.
There’s also proof that SARMs might in fact prevent particular kinds of cancer, so we just do not know.
If you ask me, this is simply another reason why I think that SARMs are first and last a high-risk, low-reward proposition.
They’re billed as a less hazardous option to traditional steroids like testosterone, they’re likewise much less studied and comprehended, which is why many specialists believe SARMs are a riskier alternative. Better the devil you understand than the devil you do not.
There’s proof that SARMs might increase your danger of cancer and little understood about the security of these drugs in general. When you take them, you’re playing guinea pig and only time will inform what the results will be.
Numerous SARM products aren’t what they declare to be.
We recall that SARMs can only be lawfully sold as “research chemicals.”
In other words, the only individuals who are supposed to purchase SARMs are researchers seeking to learn more about how they really work and whether or not they have rewarding pharmaceutical uses.
Obviously, the vast bulk of SARMs you see for sale online never ever end up in a lab. Instead, they find their way into bodybuilders, professional athletes, and physical fitness buffs who want to get more jacked.
This opens the doors to all sort of skulduggery, including:
1. Infecting the drugs with harmful chemicals due to poor quality control or cutting corners during production.
2. Mixing them with weaker and in some cases harmful compounds to increase revenues.
3. Mislabeling them to increase earnings.
Damning evidence of this can be discovered in a study carried out by the United States Anti-Doping Firm (USADA) that involved buying 44 SARM products from 21 various online providers.
The researchers likewise took things a step further by asking all of the sellers to provide what’s called a “chain-of-custody” of the products, which determines whose hands the items passed through once they were produced (and hence who had the chance to damage them).
After evaluating the products, the researchers discovered that …
1. Only 52% of the products contained any traces of SARMs at all.
2. 25% of the products contained doses substantially lower than what was on the label.
3. 25% of the products consisted of no or just trace amounts of the SARM on the label, and instead contained unlabeled substances such as other SARMs and the estrogen blockers androstenetrione and tamoxifen.
The bottom line is the SARM market is a lawless free-for-all which most likely isn’t going to change anytime soon.
There’s presently no federal government company forcing SARMs producers to toe the line, and as the research study from USADA reveals, numerous producers are totally aware of this and are more interested in turning a profit than anything else.
A number of the products currently offered as SARMs either don’t include any SARMs or include other surprise chemicals and potentially hazardous substances.
The Bottom Line on SARMs
SARMs are drugs that provide some of the benefits of anabolic steroids with fewer of the short-term side-effects.
They aren’t as reliable as steroids, but they certainly do enhance muscle growth more than any natural supplement on the marketplace. They seem much safer, too, however don’t think that suggests they’re safe to take.
Research clearly reveals that they reduce natural testosterone production and negatively affect the endocrine system, and there’s evidence that they can increase the threat of cancer, too.
We have no concept if there are long-lasting health results of SARM usage, but provided the nature of the drugs, there likely are.
There’s likewise excellent proof that numerous of the items currently offered as SARMs do not actually include SARMs and may also contain other drugs, fillers, and damaging impurities.
So, if you want a cut-and-dried recommendation from me, it’s this:
Keep away from SARMs.
In my viewpoint, the risks far surpass the benefits, and they’re simply not required to construct a muscular, strong, and lean body that you can be pleased with.
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Scientific References
1. Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical Structure and Identifying of Substances Marketed as Selective Androgen Receptor Modulators and Sold by means of the Internet. JAMA.
2. Girroir EE, Hollingshead HE, Billin AN, et al. Peroxisome proliferator-activated receptor-β/ δ (PPARβ/ δ) ligands prevent growth of UACC903 and MCF7 human cancer cell lines.
3. Tachibana K, Yamasaki D, Ishimoto K, Doi T. The role of PPARs in cancer. PPAR Res. 2008. doi:10.1155/ 2008/102737.
4. Gupta RA, Wang D, Katkuri S, Wang H, Dey SK, DuBois Registered Nurse. Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates digestive tract adenoma growth. Nat Medication. 2004; 10( 3 ):245 -247. doi:10.1038/ nm993.
5. Rasmussen JJ, Selmer C, østergren PB, et al. Previous abusers of anabolic androgenic steroids display decreased testosterone levels and hypogonadal symptoms years after cessation: A case-control study.
6. Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014; 101( 5 ):1271 -1279. doi:10.1016/ j.fertnstert.2014.02.002.
7. Chen J, Hwang DJ, Bohl CE, Miller DD, Dalton JT. A selective androgen receptor modulator for hormone male birth control. J Pharmacol Exp Ther. 2005; 312( 2 ):546 -553. doi:10.1124/ jpet.104.075424.
8. Basaria S, Collins L, Dillon EL, et al. The security, pharmacokinetics, and results of LGD-4033, an unique nonsteroidal oral, selective androgen receptor modulator, in healthy boys. J Gerontol A Biol Sci Med Sci. 2013; 68( 1 ):87 -95. doi:10.1093/ gerona/gls078.
9. Dalton JT, Barnette KG, Bohl CE, et al. The selective androgen receptor modulator GTx-024 (enobosarm) improves lean body mass and physical function in healthy postmenopausal women and elderly males: results of a double-blind, placebo-controlled stage II trial.
10. Androgenic-anabolic steroids and the Olympic Games. 2008; 10( 3 ):384 -390. 2009; 12( 3 ):232 -240.
11. Gao W, Dalton JT. Broadening the therapeutic use of androgens through selective androgen receptor modulators (SARMs).
12. Yin D, Gao W, Kearbey JD, et al. Pharmacodynamics of selective androgen receptor modulators. J Pharmacol Exp Ther. 2003; 304( 3):1334 -1340. doi:10.1124/ jpet.102.040840. Gao W, Dalton JT. Ockham’s Razor and Selective Androgen Receptor Modulators( SARMs): Are we overlooking the function of 5α-reductase? Mol Interv. 2007; 7( 1 ):10 -13. doi:10.1124/ mi.7.1.3. Gao W, Dalton JT. Expanding the therapeutic use of androgens by means of selective androgen receptor modulators( SARMs ). Drug Discov Today. 2007; 12( 5-6):241 -248. doi:10.1016/ j.drudis.2007.01.003. Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG. Anabolic-androgenic steroid reliance: an emerging condition. Addiction. 2009; 104( 12 ):1966 -1978. doi:10.1111/ j.1360-0443.2009.02734. x. Research study links steroid abuse to key biological, mental attributes– Harvard Gazette. https://news.harvard.edu/gazette/story/2009/04/study-links-steroid-abuse-to-key-biological-psychological-characteristics/. Accessed October 6, 2019. Baggish AL, Weiner RB, Kanayama G, et al. Long-term anabolic-androgenic steroid usage is connected with left ventricular dysfunction. Circ Heart Fail. 2010; 3( 4 ):472 -476. doi:10.1161/ CIRCHEARTFAILURE.109.931063.
13. Hartgens F, Kuipers H. Results of androgenic-anabolic steroids in professional athletes. 2004; 34( 8 ):513 -554.
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15. Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical Structure and Labeling of Compounds Marketed as Selective Androgen Receptor Modulators and Offered through the Web. Tachibana K, Yamasaki D, Ishimoto K, Doi T. The selective androgen receptor modulator GTx-024 (enobosarm) enhances lean body mass and physical function in healthy postmenopausal females and senior men: outcomes of a double-blind, placebo-controlled phase II trial. Expanding the restorative use of androgens via selective androgen receptor modulators (SARMs). Broadening the therapeutic usage of androgens via selective androgen receptor modulators( SARMs ).
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