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Setting up SaltStack is a fairly easy task. There is plenty of documentation here. This is not an install tutorial, this is an explanation and trouble shooting of what is going on with SaltStack Master and Minion communication. Mostly when using the CLI to send commands from the Master to the Minions.
After you have installed your Salt Master and your Salt Minions software the first thing to do after starting your Master is open your Minion's config file in /etc/salt/minion and fill out the line "master: " to tell the Minion where his Master is. Then start/restart your Salt Minion. Do this for all your Minions.
Go back to the Master and accept all of of the Minions keys. See here on how to do this. If you don't see a certain Minions key here are some things you should check.
Now lets say you have all of basic network and and key issues worked out and would like to send some jobs to your Minions. You can do this via the Salt CLI. Something like salt \* cmd.run 'echo HI'. This is considered a job by Salt. The Minions get this request and run the command and return the job information to the Master. The CLI talks to the Master who is listening for the return messages as they are coming in on the ZMQ bus. The CLI then reports back that status and output of the job.
That is a basic view of this process. But, sometimes Minions don't return job information. Then you ask yourself what the heck happened. You know the Minion is running fine. Eventually you find out you don't really understand Minion Master job communication at all.
By default when the job information gets returned to the Master and is stored on disk in the job cache. We will assume this is the case below.
The Salt CLI is just an small bit of code that interfaces with the API SaltStack has written that allows anyone to send commands to the Minions programmatically. The CLI is not connected directly to the Minions when the job request is made. When the CLI makes a job request, is handed to the Master to fulfill.
There are 2 key timeout periods you need be aware of before we go into a explanation of how a job request is handled. They are "timeout" and "gather_job_timeout".
When the CLI command is issued, the Master gathers a list of Minions with valid keys so it knows which Minions are on the system. It validates and filters the targeting information from the given target list and sets that as its list (targets) of Minions for the job. Now the Master has a list of who should return information when queried. The Master takes the requested command, target list, job id, and a few pieces of info, and broadcasts a message on the ZeroMQ bus to all of Minions. When all Minions get the message, they look at the target list and decide if they should execute the command or not. If the Minion sees he is in the target list he executes the command. If a Minion sees he is not part of the target list, he just ignores the message. The Minion that decided to run the command creates an local job id for the job and then performs the work.
When ever the Minion finishes job, it will return a message to the Master with the output of the job. The Master will mark that Minion off the target list as "Job Finished". While the Minions are working their jobs the Master is asking all of the Minions every 5 seconds (timeout) if they are still running the job they were assigned by providing them with the job id from the original job request. The Minion responds to "find job" request with a status of "still working" or "Job Finished". If a Minion does not respond to the request within the gather_job_timeout time period (5 secs), the Master marks the Minion as "non responsive" for the polling interval. All Minions will keep being queried on the polling interval until all of the responding Minions have been marked as responding with "Job Finished" as some point. Any Minion not responding during each of these intervals will keep being marked as "non responsive". After the last Minion that has been responding responds with "Job Finished", the Master polls the Minions one last time. Any Minion that has not responded in the final polling period is marked as "non responsive".
The CLI will show the output from the Minions as they finish their jobs. For the Minions that did not respond, but are connected to the Master, you will see the message "Minion did not return". If a Minion does not even look like it has a TCP connection with the Master, you will see "Minion did not return. [Not connected]".
By this time the Master should have marked the job as finished. The jobs info should now be available in the job cache. The above explanation is a high level explanation of how Master and Minions communicate. There are more details to this process than the above info, but this should give you a basic idea of how it works.
Sometimes you know there are Minions up and working, but you get "Minion did not return" or you did not see any info from the Minion at all before the CLI timed out. It is frustrating, as you can send the same Minion that just failed a job and it finishes it with no problem. There can be many reasons for this. Try/check the following things.
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I bought a Asus Z170-AR (the -A is almost identical except for DVI and VGA port). This motherboard (mobo) runs the latest Intel Skylake processors and has some of the newest chipsets on board. This means that you will likely need one of the newest Linux kernels out there to support these chipsets. But, if your running Ubuntu 14.04 LTS and want to run the latest hardware your going to have a problem.
Be advised this was an mobo/ram/proc upgrade and the OS was an original 14.04 install. 14.04.2 and newer point releases will ship with a much later and up to date kernel according to Canonical.
Very new hardware usually needs the latest drivers to work correctly. The closer you are to having the latest Linux kernel the better your chance is that your newer hardware will work. The newer the kernel the newer the driver. This is something that does not work well with Linux distributions that have long term releases in which the major kernel version does not get updated frequently. This is not to say you can go get more up to date kernel modules and build them but, when talking about built in support usually the kernels only get security updates and other fixes. Usually there are no features or support added. This does not bode well for using Ubuntu LTS releases on new hardware.
Ubuntu made LTS releases so people could stay on them for up to 5 years and not worry about upgrading every 6 months or not getting updates anymore. It is fantastic idea. The only problem is if you stay on an LTS release your were always stuck with the kernel that the release came with. Not any more.
Canonical (the makers of Ubuntu) decided that they wanted LTS releases to be able to be used on newer hardware. They wanted everyone who wanted the stability of an LTS release to be able to use a newer Linux kernel. This would enable to people to buy newer hardware and have better support for said hardware.
To make this a reality Canonical decided to make the LTS Enablement Stack.This set of packages are much more updated Linux kernel and X support for existing LTS releases.
As stated I upgraded a machine to an Asus Z170-AR motherboard with Ubuntu 14.04 already installed. Everything worked well except for the network adapter and the on board audio. These are some pretty important things so I just had to get them working. The following is what I did to do to get them working in Ubuntu 14.04.
With the stock 14.04 kernel (3.13.x) the Intel i219-V chip on the motherboard does not work. It also does not work with kernel version 3.15.x either. I had to go all the way to the latest 3.19.x kernel version to get the e1000e driver working with this adapter. To do this I installed the LTS enablement stack for 14.04. Follow that link and run the apt-get line. After reboot your ethernet adapter should be working.
Getting the Realtek ALC892 chip on the motherboard working was much harder than just updating the kernel. The 3.19.x kernel did not have a working sound kernel module for this chip. I could see the chip listed using lspci so I knew it was being seen by the kernel.
# sudo lspci -vv 00:1f.3 Audio device: Intel Corporation Device a170 (rev 31) Subsystem: ASUSTeK Computer Inc. Device 8698 Control: I/O- Mem+ BusMaster+ SpecCycle- MemWINV- VGASnoop- ParErr- Stepping- SERR- FastB2B- D ... Kernel driver in use: snd_hda_intel
It even said there was a kernel driver being used for it. Which was a good sign, but still there was no sound. Alsa did not show any cards listed either. If you run aplay and your audio chip is recognized by the kernel it will show up in Alsa.
# aplay -l
Not until I grepped the dmesg did I find out why the kernel module was loaded but it was still not working. I saw the following in dmesg output greping for the PCI address listed in the lspci output.
# dmesg | grep '00:1f.3' [ 10.538405] snd_hda_intel 0000:00:1f.3: failed to add i915_bpo component master (-19)
Now I have something to look for to see if anyone else was seeing the same error. Google turned up this post from someone with the exact same problem. Answer was to update to a very cutting edge Alsa kernel module. So I followed the instructions here to update 14.04's Alsa sound system with the latest kernel module. Be sure to choose the correct kernel module .deb package for your kernel on the "ALSA daily build snapshots" page. If your using 14.04.x choose "oem-audio-hda-daily-lts-vivid-dkms - ... ubuntu14.04.1" After installing the .deb package and rebooting, "aplay-l" saw the audio chip. Hooray!
Last thing to do to get the audio fully working is to choose the correct output in your desktops sound system. I use the XFCE desktop so what I had to do was Start "Pulse Audio Volume Control" then go to the "Configuration" tab and turn "HDA Nvidia" -> Off for my Nvida video card. Then in "Built in Audio" I had to select "Digital Stereo IEC958 Output" for my output. There are lots of outputs. My suggestion is to play an audio file on repeat, then go through each audio output to find the one that works.
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I have always been interested in Netflix streaming, but I could not get over not being able to adjust the playback speed. That and the movie selection stinks (out of 159 titles in my queue only 40 are available to be streamed). I still tried streaming for 30 days and really liked some of the original content Netflix had. During that time I did not find any native way to adjust the playback speed in their html5 player. This really stinks as I am used to watching video with Vlc, YouTube, and MythTV all of which allow for playback speed adjustment up to 2x. It is hard to watch anything at lower speeds anymore. After a bit more searching I finally found a way to change the playback speed in Netflix streaming video.
After much searching I found an Google Chrome extension called Video Speed Controller, which allows for the speedup of html5 video streams in the browser. Netflix has an html5 player so this works with Netflix streams. Hooray!! The speedup stream does not have any buffering issues and I've watched many things on with 2x playback without issue. Unfortunately you can't use this anywhere other than the browser. Come on Netflix please add playback speed adjust to all of your players on all platforms!!!
Beware that when speeding up video you will need to make sure your video card can handle the higher frame rates. When I stream a video file from local storage with a local program like Vlc at 2x, it is very smooth, without much jitter or video tearing. When streaming content from Netflix or YouTube or other sites using this browser plugin you are using the browser as the video player, and it might not be as clean of an experience. You might notice some more jitter in the video and some frame tearing on fast moving scenes. This usually happens if your hardware can't keep up rendering the video or if hardware acceleration is not enabled.
My testing for this is being done on Linux with Google Chrome using the accelerated Nvidia Drivers with a GeForce GT 520 a video card from 2011. What I had to do to get rid of the jitter and tearing is turn hardware acceleration on in Chrome. Google seems to be very careful about whether or not they turn on hardware acceleration. They usually don't turn it on unless they know for sure it will work. Mine was not turned on even though I had a video card that supported acceleration and the correct drivers. Chromes detection of this might not be the best or Google did not think the drivers for this were stable enough. What is great is you can turn this on anyways and it works great.
To see if your hardware acceleration is already turned on or not type "chrome://gpu" in your Chrome URL bar. If it's turned off you will likely see lots of red text indicating so. Look for "Video decode" and see if it says "Disabled". If so you will need to turn it on. If it says "Hardware accelerated" then your good and can skip the rest of this paragraph. To turn on the hardware acceleration in the Chrome URL bar type "chrome://flags". The first setting says "Override software rendering list". Click the "Enable" to turn on the override. Then restart Chrome. Go back to "chrome://gpu" and see if it says "Video decode: Hardware accelerated". If so go try to watch a movie again or a YouTube video and it should be much smoother and likely have less tearing. If you don't have less tearing, go into your video driver config and make sure you have Sync to VBlank enabled. Mine is in my Nvidia X server settings manager then under "OpenGL settings"-> Performance. Check the box "Sync to VBlank".
Netflix provides some hidden menus for stats and changing bit rates of your streams. Here are some different ones to try.I tried these using Chrome on Linux. They all worked for me.
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Response to Statement by Hillary Clinton
- 3 months ago
- Secretary Hillary Clinton was apparently offended by my presence at one of her campaign stops. She should understand that as a lifetime member of coal country and a proud West Virginian, I am interested in any suggestions she has to address the problems coal miners and coal communities face today. It is disappointing that she is choosing to promote her political campaign by demonizing me. It is[...]
Factual Discussions on America...
Most every country in the world, in one way or another, benefits from a strong, healthy America. All Americans, and in fact all the world, are stakeholders in our country. It is America, and Americans, that have led the world's progress in the improvement of people's quality of life...
Recent Essays
Mine Safety
- 3 months ago
- We Must Keep The Promise: Laws That Will Honor The Miners Mine safety regulations, or the lack thereof, are all too often written or not written to advance the popularity and electability of politicians rather than the safety of coal miners. The popular phrase politicians love to use after a mine tragedy is that "we must make sure this never happens again." Typically they then pass a bunch of la[...]
Lardieri Vents About Joe Main
- 2 years ago
- DISCLAIMER: This video is posted here to provide viewers an opportunity to see how MSHA, the government and Joe Main's actions are viewed by at least one working coal miner. Unfortunately, the coal industry itself has been unwilling to stand up for their miners and as with anything so egregious as is the idling of dust scrubbers in a coal mine the frustration of working miners is at a boilin[...]
Miner Says Enough Is Enough
- 2 years ago
- The opinions of this coal miner are his and his alone. However, I do agree and I know many coal miners that agree with many of his opinions as to MSHAs improper actions. At the same time I do not agree that MSHA is akin to Hitler. I also have no knowledge of the individual inspector nor of any specific inspections by that inspector. As most of you know, I have said that MSHA's idling of scrubbers [...]
Tuesday History
- 2 years ago
- Tuesday's election certainly was historical in West Virginia. Just 10 years ago most politicians would have laughed at the thought of having a Republican majority in the West Virginia legislature. Lots of things came together to accelerate West Virginia's conversion to Republican although the journey had already begun years ago, and it was only a matter of time. In fact some of the things that[...]
Regcession: How The EPA Is Destroying America
- 2 years ago
- The documentary makes clear that the Green Movement is a "big business" not a "big cause" It is not only a big business for those directly involved in the Green Movement like solar and wind companies but it is also big business for the media; the politicians, their friends and their families; foreign countries; multi-national corporations (many of which brand themselves as American companies); and[...]
Documentary Available Now
- 2 years ago
- The documentary titled "Regcession--Enough is Enough" has been released to YouTube and is available at savethecountry.com as well. We also plan to air it on WVAH channel 11 at 5PM Thursday October 23rd. The documentary explains the negative impacts that excessive EPA regulations (many of which are founded on the myth of Global Warming) are having on America. The hoax is costing millions of [...]
- 2 years ago
- Israel's Prime Minister Benjamin Netanyahu told the United Nations General Assembly today that ISIS and Hamas are part of the same 'poisonous' tree. The PM went on to claim Israel has photographic evidence that Hamas has used human shields to defend themselves from Israeli bombs.
Tidbits and an Apology to Senator Manchin
- 2 years ago
- The next documentary will not be finished in time for showing on Labor Day. The documentary will be one hour in length and it has proven to be a daunting task for the film production company. Their efforts have included thousands of miles of travel, dozens of interviews, weeks of research, and hundreds of hours of script writing and re-writing. The new target is to finish the documentary with[...]
O' Rahall
- 2 years ago
- If you believe Rahall is the man to represent West Virginia then u have to believe Obama is too.
McConnell Surrenders
- 2 years ago
- On October 31, 2013 I wrote how ridiculous it is that the politicians claim to be fighting so hard for coal when election time rolls around but that the rest of the time they sit on their hands as coal is destroyed. I specifically named as politicians who are disingenuous in this regard Nick Rahall, Joe Manchin, and Mitch McConnell. Afterward several coal and non-coal guys asked why I had inc[...]

subset: commoncrawl


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Give your jump course a natural look with this pair of Cedar Split Rail Fences. In maintenance-free polyethylene, they fit perfectly in a 10' or 12' jump.
The Burlingham Sports Starter Jump Set is a complete package of 4 jumps with 5' standards, 10' jump poles and standard jump cups. These are made of a durable polyethylene that won't shatter or splinter. Can be set up as singles, oxers or in combination lines that are great for both schooling and show use.
Add variety to your jump course with this Two-Piece Log Obstacle Set from Burlingham Sports. With the look of real logs without any of the maintenance, weight or hassle, these logs offer endless possibilities. Made of polyethylene. Each is 24" in diameter and 65" long. Pair.
The Burlingham Sports Wing Standard have the look of wood but are maintenance-free. 5' tall. Jumps from 1'3" to 4'9".
The Burlingham Sports gate is lightweight and easy-to-move . Gates are 11"H so you can set the jump can set the jump to 1'.
The Burlingham Log Wing Standards give your jump course the realistic look of logs--and they're weather-resistant and lighter than the real thing. These jump standards have keyhole tracks for use with pinless cups, and they can be placed on their sides to create an obstacle.
The Burlingham Sports Rock Set adds eye-catching appeal to your jump course. This set of jump decorations includes 5 single stones, the tallest of which is 22" high, and 5 single mountain and desert grass bushes.


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May captured Bulbasaur and Squirtle since FireRed and LeafGreen were released in her generation, and Dawn got an egg which later hatched into Cyndaquil as HeartGold and SoulSilver came out.
Do you think Serena will catch a Hoenn starter due to the fact that Omega Ruby and Alpha Sapphire were released almost two years ago?
I feel like it's too late for her to get one because I felt like she would've gotten one last year, although I would love it if she got one now - especially Mudkip! What are your thoughts?


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HPLJ 600 m602 49.06.65 error code
We have a HPLJ 600 M602 that has an error code of 49.06.65 in the display. The user states the printer keeps stalling and locking up when printing (from Mica and Citrix). I'd like to know what the error code indicates.
Thank you.
Additional: the user also indicates that prior to the error code they were sporadically getting "wingding" printouts with lots of symbols and many blank pages. Does this sound like hardware or software?
Re: HPLJ 600 m602 49.06.65 error code
Re: HPLJ 600 m602 49.06.65 error code
A 49.06.65 Error is a PCL5 Font Error. There was a generic font failure while printing a PCL5 job.
Do you have a Print Job that causes this error to happen each time it is printed? Or do you know if some fonts were installed on the printer and the printer gets the error when jobs are printed that use the installed fonts?
If you have a print job, or print jobs, that cause this error, if you would be willing to share those jobs with HP we can take a look at them.
If fonts have been installed in the printer and that appears to be causing the error, those fonts will need to be removed from the printer
In short, this sounds like it could be bad font data. But HP will need to get the job/font that is causing the problem to know for sure.
Please let me know if this helps.
Re: HPLJ 600 m602 49.06.65 error code
Printing files with unsupported programming commands.
A unique combination of user environment and user interactions with the product.
Interfacing with a third-party solution that was not designed to work with the product.
Specific timing, network traffic, or concurrent processing of jobs.
Each of these interactions could cause the product firmware to initiate an action that the product cannot accomplish. In situations like this, the product might present the error if it has no other option. When these errors occur, the only way to recover is to turn the products power off and back on.
Please follow the following steps to resolve the issue :
Step 2
>Turn off the printer and unplug the power cord. >Remove the HP Jetdirect card, third-party device, hard disk, parallel cable, or IFR cable from the formatter if one is installed. >If the error continues with accessories removed from the formatter, perform a cold reset on the printer. Ensure the HP Jetdirect card is not in the printer during a cold reset or the card settings will be changed back to default settings.
To perform a cold reset, do the following:
>Turn on the printer. >Watch the control panel. >When the memory starts counting, press and hold the green (Select ) button. >Continue holding the green check button until the Ready, Data, and Attention lights flash once, and then stay on steady. >Release the check button when the Ready, Data, and Attention light are on steady. >The control panel will display SELECT LANGUAGE . >Press (Down Arrow ) button once. The control panel will display COLD RESET . >Press (Select ). The printer will perform a cold reset and then continue its power-on sequence.
If the printer comes up to ready, print a Configuration page. If a 49 error occurs from printing internal pages, continue on to the next step.
>Turn the printer off and unplug the power cord. >Remove the eight screws around the formatter. >Remove the formatter. >Reseat the firmware and memory modules on the formatter. Check for any DIMMs that are non-HP and remove them. Non-HP DIMMs are not supported by HP and may cause this error. Replace with HP DIMMs, if necessary. >Install the formatter. >Turn the printer on again. >If it comes up to READY , print a configuration page. If a 49 error does not appear from printing internal pages, or at power up, continue to the next step.
Step 4
>Install the HP Jetdirect card and hard disk before installing the formatter. Verify that each device is properly seated. >Test any EIO devices, by turning off the printer, installing each device separately, and printing a Configuration page. Repeat for each EIO device. >If the 49 error occurs with any EIO device installed, replace that EIO device.
Kindly check the firmware date code & version from the configuration page and if required please upgrade it to the latest one.
You may check the latest firmware for your printer in below metioned link :
I work for HP in Printer's department.
Please send Kudos if you are satisfied with the suggestion.
Sohail Arshad


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Synonyms of repine in English:
literary even if I die, I doubt that he'll repine
fret, be/feel unhappy, mope, languish, eat one's heart out, be/feel miserable, be/feel upset, be/feel despondent, brood;
lament, grieve, mourn, sorrow, pine, agonize
Definition of repine in:
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The Sparkle Tattoo Parlor Cool Glam from Alex takes on the trend of glittery tattoos and puts them in an easy-to-use kit for kids. The kit includes 12 different tattoo stencils featuring stars, cherries, peace signs, and more. To use, start by selecting a stencil. Peel off the stencil's white backing and place it facedown on any area of skin. Peel off the clear cover and whip out the body glue to get started. Spread the glue over the exposed area of skin like you would apply a coat of nail polish. Peel off the stencil and wait until the glue turns clear, which takes about three minutes. Then choose from the four different colors of glitter (red, purple, silver, and blue), dip the small brush into the glitter, and brush it over the stenciled glue design. Use the big brush to dust away any excess glitter and your sparkly tattoo is ready to show off.
What we like about this kit is it's easy to use, and for kids who love a little sparkle this can be a fun way to accessorize their everyday look. The temporary aspect of these tattoos is also something that will appeal to parents.
The Sparkle Tattoo Parlor Cool Glam is for ages 8 and up.
The directions say to wait for the glue to dry before applying the glitter, which is a bit deceiving. You want the glue to be a bit sticky in order to hold the glitter, so just wait until it turns from white to clear.
The stencils are reusable, simply replace the white backing to save the stencil for later use.
The tattoos last between 3–7 days. If you want to remove the stencil, just rub on some lotion and let it set in for about 10 minutes. Then scrub away the tattoo.
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Upcoming Meetings, Workshops, and Classes
USCG License Class - 6 Pack to 100 GT Masters - CANCELLED
August 1–10, 2016
Unalaska, Alaska
Contact: Melissa Good
Aleutian Life Forum 2016: Building Resilience in the Face of Change
August 16–20, 2016
Unalaska, Alaska
Contact: Nikita Robinson
Smoked Seafood School
October 12–14, 2016
Kodiak, Alaska
Contact: Chris Sannito
Center for Salmon and Society Workshop: Long-term Challenges to Alaska's Salmon and Salmon-Dependent Communities
November 1–3, 2016
Anchorage, Alaska
Contact: Milo Adkison
HACCP – Kodiak
November 10–11, 2016, 8:00 am—5:00 pm
Kodiak, Alaska
Contact: Chris Sannito
Seafood Processing Quality Control Training
November 14–18, 2016
Kodiak, Alaska
Contact: Chris Sannito
Developing a Harmful Algal Bloom Action Plan for Alaska
December 8–9, 2016
Anchorage, Alaska
Contact: Ginny Eckert
Impacts of a Changing Environment on the Dynamics of High-latitude Fish and Fisheries
31st Wakefield Symposium
May 9–12, 2017
Anchorage, Alaska
Contact: Sue Keller
Recent events
Fishing Vessel - Drill Conductor Training (AMSEA)
May 27–28, 2016
Kodiak, Alaska
Contact: Julie Matweyou
HACCP – Kodiak
May 12–13, 2016, 8:00 am—5:00 pm
Kodiak, Alaska
Contact: Chris Sannito
Roe School
April 28–29, 2016
Kodiak, Alaska
Contact: Chris Sannito
Get Your Feet Wet!
April 1–May 31, 2016
Online event
Contact: Marilyn Sigman
View complete list of past meetings, workshops, and classes from 2011 to present.
View archives of selected meetings from 1996 to 2011.
About our meetings, workshops, and classes
Alaska Sea Grant and the Alaska Sea Grant Marine Advisory Program support public meetings, conferences, workshops, and classes on marine and coastal topics important to residents of Alaska, the Pacific Northwest, the United States, and the international community.
For more information on our events, contact us at firstname.lastname@example.com or phone (907) 474-7086.


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Awards for Rooms36
VisitEngland Guest House
All the national assessing bodies (VisitEngland*, VisitScotland, Visit Wales and the AA) now assess hotels and guest accommodation (including B&Bs) to the same criteria and award one to five stars. The star ratings reflect the overall quality of the experience. When choosing your accommodation look for the Quality Rose, the official marque of the Enjoy England national tourist board rating scheme.
Additional information on this classification scheme is available here.
AA GoldGuest House
AA Gold Stars are awarded to the very best of Guest Accommodation with the 3, 4 and 5 star ratings
Additional information on this classification scheme is available here.
Member of Cumbria Tourism
Cumbria Tourism is a membership organisation with over 2,600 members from the tourism industry, committed to developing, promoting and managing tourism in the county.
Additional information on this classification scheme is available here.
Self-assessed Accessibility Information
Self-assessed Accessibility Information provides a list of available facilities and services, highlighted as being of key importance by disabled people. Along with Access Statements, which provide a fuller written description of accessibility, it can help people with access needs make an informed choice as to whether accommodation, attractions, food & drink or shopping establishments meet their needs.
Self-Assessed Accessibility Details
- Designated parking for guests with disabilities
- Surface of the car park and pathway leading to entrance is
- Solid ie tarmac / concrete etc
- Gravel
- Drop-off point for guests outside entrance
- Route from the parking area to the entrance:
- Has steps and no ramp
- Meals for guests with special dietary requirements can be provided:
- Gluten free (coeliac)
- Organic
- Vegetarian
- Vegan
- Steps to the main entrance
- 12Number of steps to entrance
- Handrail by steps
- Entrance well lit
- Bell at main entrance
- Bedroom with non-allergenic bedding available
- Bathrooms available with:
- Separate shower unit
- Bath with shower
- Bath


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High School
Print without images
Saturday, February 12, 2011
Lincoln holds off Woodrow to clinch district title
By Travis L. Brown
DALLAS -- In the first matchup of the top two teams in District 12-4A, ĀDallas Woodrow Wilson gave Dallas Lincoln a run for its money before losing by two points.
Friday's rematch was another barnburner.
Lincoln almost gave the game away by missing key free throws late but held on to beat Woodrow, 67-64, at Forester Field House and clinch the outright district championship.
Lincoln star LeBryan Nash showed off his versatility by dunking and bombing his way to 28 points.
Lincoln, No. 2 in ESPNDallas.com's 4A rankings, missed nine free throws in the fourth quarter as Woodrow climbed within three points with under a minute remaining to play. The Wildcats, however, couldn't convert on two late 3-point shots.
"We missed free throws and we went down to the other end and didn't stop them," Lincoln coach Leonard Bishop said. "We either have got to make free throws or get a stop."
Lincoln began the game hot, riding newly minted McDonald's All-American
LeBryan Nash
to a 29-24 halftime lead. Nash finished the second quarter on fire, throwing down two authoritative slams.
"[Nash is] the straw that stirs us," Bishop said. "If he's playing well, and especially if he's shooting the ball well, then we've got a good ball club."
Nash was on target from outside Friday, complementing his dunking ability by hitting five 3-pointers and finishing with 28 points.
Curtis Davis
had an answer in the second half, penetrating to score baskets and draw fouls. His game-leading 32-point effort kept the Wildcats alive until the final buzzer.
"Woodrow is always fired up to play us," Bishop said. "[Davis] shoots the ball extremely well. They shot the ball well from outside."
Lincoln advanced to 10-0 in district play, building an insurmountable lead over 8-2 Woodrow with one game to play.
"What it does is it allows us to start looking at the people we have to play [in the playoffs] and get our game plan ready for those teams," Bishop said.


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How Can We Help You?
Upcoming Community Legal Aid Clinics:
Montgomery County | Covenant Life Church: June 11, 2016, July 9, 2016, August 13, 2016
Loudoun County | Reston Bible Church: June 18, 2016, July 16, 2016, August 20, 2016
Fairfax County | Columbia Crossroads: June 4, 2016, June 25, 2016, August 26, 2016
Announcing our newest clinic! Restoration Immigration Legal Aid (RILA) will focus on immigration
and welcomes clients from the entire DMV. The Clinic meets at Restoration Anglican Church,
1815 N. Quincy St., Arlington, VA. Call 571-429-5410 for information or an appointment. Upcoming clinic dates: June 23, 2016
Please remember GSA when you make your 2016 giving list! With your help we've already provided over 200,000 hours of free legal counsel to those in need in our community. With your continued help and support, we can reach even more people and provide more hours of service – your donation makes a difference!
Want to learn more about our service areas?
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Download our brochure, subscribe to our newsletter, or contact us to learn more.
Do you need legal help?
Request an appointment by calling one of our Community Legal Aid Clinic locations
or download our INTAKE form and submit it to our intake coordinators.
Upcoming Attorney Training
We are excited to partner with Bob Klima and the Private Court of Virginia to present a CLE on the family law courts and procedures. Think of it as a "Family Law 101" crash course so that we can better assist our neighbors. We'll also learn more about the use of Alternate Dispute Resolution in family law cases. Keep watching here for the date, time and place!


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Tae Kwon Do Students Compete in Tournament
On May 14th, some students from the Hillsboro Unified Tae Kwon Do School located at 125 W Elm Hillsboro, Texas competed in an invitational tournament in Austin, Texas. Among the students who competed were Juan Salas and two of his daughters from Frost, Texas. Juan returned home with two first place trophies, one in patterns and one in sparring. Analy and Joana returned home with trophies as well.


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Social media has become an integral part of life buy 1000 twitter followers and business. Long gone are the days when businesses used social media for mere presence. Today, social media has a wide array of uses for businesses some of which are interactions, advertisement, and brand visibility just to name a few. True to this, today, social media has become the new way by which businesses measure their social success and in extension their popularity and success. This makes social media a key part of any business growth and development, and like every key aspect of any business, a social media plan, or strategy is necessary to ensure the success of the endeavor regardless of why the business entity decides to use social media. Creating this document (the social media strategy document) is not a walk in the park; most businesses regardless of size are stuck at this point. To help you out, I have compiled a list of the top seven steps you need to create a simple but vibrant social media strategy.
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Posted May 12 2010 10:00PM
Forty-five minutes after sharing the big stage in the Lakers' Game 4 clincher over the Utah Jazz, Kobe Bryant and Pau Gasol shared a small folding table in the interview room.
As comfortable as they were on the floor, they combined for 65 points in the Lakers' 111-96 win, they were just as comfortable sharing the spotlight off of it.
In the past, neither of them would have been nearly as comfortable as they were Monday night. Gasol struggled to adjust to the glare when he was the bell cow for the Memphis Grizzlies. And Bryant always bristled at sharing the spotlight with Shaquille O'Neal when they were leading the Lakers' title three-peat at the start of the decade.
Somehow they've both managed to adjust and thrive as the Lakers' and perhaps the league's most dynamic duo.
"Kobe is arguably the best player in the league," Jazz point guard Deron Williams said. "And [Gasol] has to be what, one of the top five big men on the planet. That's a pretty tough combination to deal with, I don't care who you are."
The Phoenix Suns await in the Western Conference finals. And they have a dynamic duo of their own in two-time MVP Steve Nash and perennial All-Star Amar'e Stoudemire, who just like their Lakers' counterparts have fueled their team's run to the showdown that awaits.
If their performance in that Game 4 win over the Jazz is any indication, Bryant and Gasol are just getting started with what they can do. Gasol scored 33 points and grabbed 14 rebounds, while Bryant added 32, four assists and three rebounds.
"Pau had a really terrific game," Lakers coach Phil Jackson said. "Kobe was persistent, aggressive and stayed how he is in the course of the second half to carry the lead."
The fact is, Bryant and Gasol are playing some of the best basketball of their two-plus year union, a cosmic marriage of passionate and cultured men that has produced back-to-back trips to the NBA Finals.
They already have one title to show for it, having knocked off the Orlando Magic in the NBA Finals last year, and have the Lakers prepared to do whatever it takes to get another one.
"They got just about everything you want." Jazz coach Jerry Sloan said after his team was pushed aside by the Lakers. "They got experience. They got guys that are long and big and can play inside. Gasol can go inside and outside with his game and he's a terrific passer. They got all the size. They got a lot of guys that can pass the ball.
"That's a tremendous asset for any team and plus those guys have been in big games. They're tough to deal with and they put us out of sync because their defense is so good. Every shot you get is tough. They make you earn it. That's why they won the championship."
For Bryant, it's simply more of what he's always known.
He's just handling it better than ever.
It's hard to imagine him ceding as much of the spotlight as he has to Gasol, who in turn has infused the Lakers with a presence and versatility on the low block, alongside center Andrew Bynum, that was missing after O'Neal's departure and before the Spaniard's arrival on Feb. 1, 2008 in a trade-deadline deal with the Memphis.
Perhaps that has something to do with Gasol's easygoing nature. While his predecessor, O'Neal, had an ego and persona similar to Bryant's, Gasol has nothing of the sort.
After dominating the Jazz, he spent little time talking of himself and all the splendid damage he'd done in helping his team move on.
"I'm happy with the way I played," Gasol said. "But I'm more happy with the way we are playing. I think we are really doing a good job collectively, and we are improving as every game goes by and we are just getting better and better. It's really satisfying and I look forward to starting it up against a very good Phoenix team."
Sekou Smith is a veteran NBA reporter and the author of NBA.com's Hang Time blog. You can e-mail him here and follow him on twitter.
The views on this page do not necessarily reflect the views of the NBA, its clubs or Turner Broadcasting.
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Some members of the 2016 U.S. National Men's team are taught some Portuguese by Jerome Meyinsse.
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STAT4 is an important transcription factor that contributes to the incidence and severity of different autoimmune diseases and is implicated in the antiviral immune responses in mice. In this study, we evaluated the role of STAT4 in human and murine herpes simplex virus 2 (HSV-2) infections. We show that STAT4 regulates antiviral gamma interferon (IFN-γ) responses and disease severity during chronic HSV-2 infections in humans and vaccine-induced IFN-γ-mediated protection against HSV-2 infection in mice. In a cohort of 228 HSV-2-infected individuals, representing both patients with recurrent disease and asymptomatic HSV-2 carriers, we found that genetic variations in the STAT4 gene were associated with asymptomatic HSV-2 infection, as well as with increased in vitro secretion of IFN-γ in response to the virus. Mice that lacked STAT4 had impaired HSV-2-specific IFN-γ production and delayed-type hypersensitivity responses following vaccination, which led to impaired viral clearance in the genital tract of vaccinated animals after a genital HSV-2 challenge. We conclude that STAT4 plays an important role in IFN-γ-mediated HSV-2-specific immunity, affecting the severity of genital HSV-2 infection.
Genital herpes infection caused by herpes simplex virus 2 (HSV-2) is one of the most common sexually transmitted infections in the world. Up to 25% of the Swedish population is seropositive for HSV-2 (5, 11, 31), while the prevalence in some sub-Saharan African countries is as high as 80% (47). The clinical effects of HSV-2 infection range from no symptoms (asymptomatic infection) to severe and recurrent episodes of genital lesions and ulcers. Although the mechanisms underlying these different disease outcomes are not known, strong gamma interferon (IFN-γ) responses (10, 37), previous HSV-1 infection (22), high levels of mannan-binding lectin (13), specific HLA alleles (23), and variants of both the TLR2 gene (6) and the gene encoding mannose-binding lectin 2 (34) increase the likelihood of an asymptomatic infection.
Efficient HSV-2-specific acquired immunity requires CD4+ T cells and IFN-γ production. Mice that lack CD4+ T cells, IFN-γ, or the Th1-inducing transcription factor T-bet are unable to mount a protective immune response to HSV-2 following vaccination (14, 15, 40). However, the treatment of mice with IFN-γ circumvents the need for CD4+ T cells, which implies that the main function of CD4+ T cells in HSV-2-specific immunity is to produce IFN-γ (14). The situation is similar in humans, as HSV-2-infected individuals with recurrent disease have impaired virus-specific IFN-γ responses compared with asymptomatic HSV-2 carriers (10, 37).
IFN-γ secretion and Th1 differentiation are induced and maintained by two diverse and concurrent pathways that are characterized by the transcription factors T-bet and STAT4 (20, 42). Mice that lack either T-bet or STAT4 have impaired IFN-γ and Th1 responses but are still able to produce some IFN-γ, while mice that lack both T-bet and STAT4 have no Th1 responses, even under Th1-polarizing conditions (12, 20, 43). It is generally believed that Th1 differentiation is induced by T-cell receptor (TCR) activation, which leads to T-bet expression. In addition to IFN-γ secretion, T-bet induces the expression of the interleukin-12 (IL-12) receptor β2 on the T-cell surface (1), which allows the T cell to respond to IL-12 and to induce further IFN-γ production via STAT4 signaling (17, 18, 45). The secreted IFN-γ binds to the IFN-γ receptor and signals via Stat1 so as to amplify the expression of T-bet, thereby stabilizing the Th1 polarization (24).
Given that STAT4 is important for Th1 immunity, mice that are deficient for STAT4 are highly susceptible to infections (19). This is particularly true in the case of parasitic infections, whereby STAT4 deficiency is associated with increased parasitic burden and decreased IFN-γ responses to pathogens such as Leishmania major and Toxoplasma gondii (9, 38). Studies of viral infections, i.e., with lymphocytic choriomeningitis virus (LCMV), influenza virus, and HSV-1, have revealed diverse roles for STAT4 depending on the type of infection and the immune mediators that are involved in the antiviral response (2, 3, 7, 16, 29). As a consequence of the abrogated Th1 responses, STAT4-deficient mice have a decreased production of inflammatory cytokines (e.g., tumor necrosis factor alpha [TNF-α]) during autoimmune disease and are thereby resistant to the development of Th1-mediated autoimmune diseases, such as experimental autoimmune encephalomyelitis, arthritis, colitis, myocarditis, and diabetes (19).
Even though the role of STAT4 has been studied extensively in animal models of infectious diseases, little is known about its role in human infections. Most studies of human STAT4 have focused on correlations between variations in the STAT4 gene and the incidence of autoimmune diseases. These diseases include rheumatoid arthritis, systemic lupus erythematosus (SLE), and primary Sjögrens syndrome, for which single nucleotide polymorphisms (SNPs) in the STAT4 gene have been associated with the disease incidence in several different populations (21). Furthermore, genetic variations in STAT4 may also be involved in disease severity; a polymorphism in the STAT4 gene has been associated with a more severe disease outcome in SLE patients (44).
The present study was undertaken to evaluate the role of STAT4 in immune-mediated control of HSV-2 infection. For this purpose, DNA samples from 143 patients with recurrent HSV-2 infection and 85 asymptomatic carriers of HSV-2 were screened for variations in 7 SNPs of the STAT4 gene. The SNPs were subsequently correlated with HSV-2 disease severity and the levels of HSV-2-induced IFN-γ production by isolated peripheral blood mononuclear cells (PBMC). To study in greater detail the role of STAT4 during HSV-2 infection, mice that lack STAT4 were vaccinated and/or infected with HSV-2 and their abilities to mount a Th1 response and to resist the infection were monitored. We show that a variation in the human STAT4 gene is associated with increased HSV-2-specific IFN-γ production and asymptomatic disease. In addition, we show that STAT4 is required for adequate HSV-2-specific IFN-γ responses and for the induction of sterilizing immunity in mice.
DNA samples were collected from 228 HSV-2-infected individuals (male, 57%; female, 43%) who were recruited from the sexually transmitted disease (STD) clinics at Sahlgrenska University Hospital, Borås Hospital, and Uddevalla Hospital, Sweden. The average age of the subjects was 39 years for men (range, 20 to 70 years) and 37 years for women (range, 20 to 68 years). Permission for this study was granted by the Ethics Committee of the University of Gothenburg, and all patients gave informed consent. HSV-2 infection was confirmed serologically by enzyme-linked immunosorbent assay (ELISA) (see below). The patients were divided into two groups based on clinical status.
The symptomatic HSV-2 infection group comprised 143 patients: 77 males (54%; average age, 38 years; range, 23 to 70 years) and 66 females (46%; average age, 38 years; range, 23 to 68 years) who had a typical history of recurrent genital herpes. Symptomatic HSV-2 infection was confirmed by PCR, and serology and history clinical recurrence were recorded. The aim was to recruit individuals with more than six relapses per year to ensure the presence of clinical disease. Overall, 113 of the 143 symptomatically infected individuals fulfilled this criterion, whereas 30 of the symptomatic individuals had fewer than six relapses per year. In total, 56 of the symptomatic individuals were on antiviral treatment at the time of sampling.
The asymptomatic HSV-2 infection group comprised 85 patients: 54 males (64%; average age, 40 years; range, 21 to 66 years) and 31 females (36%; average age, 34 years; range, 20 to 52 years) who were seropositive for HSV-2 without any signs of clinical disease. Asymptomatic patients were recruited from an ongoing screening study of HSV-2 infection in visitors to the STD clinics and among the partners of the HSV-2-infected patients. All the subjects were provided with detailed information about the clinical spectrum of herpes and interviewed about genital symptoms. Putatively asymptomatic HSV-2-seropositive patients who after receiving the above information admitted to having genital symptoms were excluded from the study.
Three individuals (all symptomatic) were on immunosuppressive treatment (for rheumatoid arthritis, Bechterew's disease, and CNS vasculitis, respectively) at the time of sampling. Other diseases that were present in the study population were hepatitis B (one symptomatic individual), diabetes (two symptomatic individuals), allergic asthma (one symptomatic individual), multiple sclerosis (one symptomatic individual), and lichen sclerosis (one asymptomatic individual).
For the control group, 162 healthy HSV-2-negative adult blood donors were recruited from the Blood Bank at Sahlgrenska University Hospital. This group consisted of 54% males and 46% females with an average age of 40 and 41 years, respectively (ranges, 20 to 63 and 20 to 65 years, respectively). All individuals were screened for HSV-2 infection by ELISA. All the individuals were routinely screened (and found to be negative) for blood-derived contaminating diseases, including hepatitis A and B, HIV-1 and -2, and human T-lymphotropic virus I (HTLV-I) and -II.
DNA for genotyping was extracted from heparinized venous blood using the salting-out method. Genotyping was performed on 228 HSV-2-infected individuals and 162 control subjects for seven STAT4 SNPs [rs7574865 (T→G), rs4853543 (A→G), rs7572482 (A→G), rs13017460 (A→G), rs7601754 (G→A), rs3024896 (C→T), and rs6752770 (A→G)] using TaqMan allelic discrimination (premade or customized Applera assays) at the Core Facility of the Sahlgrenska Academy, Gothenburg University, Sweden. The seven SNPs were chosen based on the following criteria: (i) they are commonly detected in Caucasians (minor allelic frequency > 0.20, according to the Hap-Map-CEU northern and western European population data in the NCBI database), including the Swedish population (36); and (ii) they are spread across the entire STAT4 gene. The genotyping rate was ≥94.4% (range, 94.4% to 100.0%).
Plasma samples from HSV-2-uninfected individuals were screened for anti-HSV-2 glycoprotein G (gG) antibodies using an HSV-2 ELISA kit according to the manufacturer's manual (HerpesSelect2 ELISA IgG; Focus Technologies), and plasma samples from HSV-2-infected individuals were screened for mgG-2-specific antibodies using an ELISA, as previously described (46).
HSV-2 strain 333 and the attenuated strain Lyons (35) were obtained as described previously (40). For antigen preparation, the virus was inactivated by exposure to UV light for 30 min.
Freshly isolated PBMC (1 × 106 cells/ml) were cultured in 96-well plates in a total volume of 200 μl x-vivo medium (Lonza, Verviers, Belgium) supplemented with 1% l-glutamine, in the presence or absence of UV-inactivated HSV-2 (corresponding to 4 × 105 PFU/ml). Culture supernatants were collected after 48 h and stored at −20°C until assayed for IFN-γ using a human IFN-γ ELISA DuoSet kit (R&D Systems) according to the manufacturer's instructions.
For this study, 6-to-8-week-old female STAT4−/− and wild-type BALB/c mice were purchased from The Jackson Laboratory. All mice were maintained under standard conditions of temperature and light in the animal facilities at the Department of Rheumatology and Inflammation Research, University of Gothenburg. This study was approved by the Animals Ethics Committee in Gothenburg, Sweden.
Mice were pretreated with Depo-Provera (Pharmacia) and then vaccinated and infected as previously described (40). Mice were examined daily for vaginal inflammation, neurologic illness, and death. The severity of diseases was graded as follows: 0, healthy; 1, genital erythema (redness and swelling); 2, moderate genital inflammation (hair loss, small nonpurulent lesions); 3, severe and purulent genital lesions and/or generally bad condition; 4, hind-limb paralysis; and 5, death (26).
Vaginal washings were collected 2 days postinfection and stored at −70°C until further use. Spinal cords were collected and homogenized 7 days (unvaccinated mice) or 14 days (vaccinated mice) after infection and stored at −70°C until further use. DNA was extracted in a MagNA Pure LC robot (Roche Diagnostics, Mannheim, Germany) using a MagNA Pure DNA Isolation kit according to the manufacturer's instructions. The number of HSV-2 DNA copies was determined by quantitative PCR, as described previously (28), and is expressed in terms of genome equivalents (geq).
Delayed-type hypersensitivity (DTH) reactions were performed as previously described (40).
Assays of IFN-γ production from CD4+ spleen cells and IL-12 production from spleen cells were performed using a cell ELISA that utilizes murine IFN-γ and IL-12 DuoSet ELISA kits (R&D Systems), as previously described (40). CD4+ T-cell activation was performed with CD8-depleted splenocyte cultures in the presence of inactivated whole virus, as described previously (40). The 48-h culture supernatants from HSV-2-activated spleen cells were also analyzed using a Mouse Th1/Th2 10plex Ready-to-Use FlowCytomix Multiplex kit (eBioscience) and a FACSCanto flow cytometer (BD).
For human samples, genotype and allele frequencies were compared using the chi-square test. Differences were considered significant at P < 0.05. The calculations were conducted using online software. Hardy-Weinberg tests, haplotype association tests, and permutation tests were performed using Haploview software. Bonferroni's correction for multiple testing was used when appropriate. All the allele and genotype frequencies were found to be in Hardy-Weinberg equilibrium. Statistical analyses of human IFN-γ secretion and the mouse experiments were performed using the nonparametric Mann-Whitney U test and GraphPad Prism ver. 5 software. Differences were considered significant at P < 0.05.
To assess the role of STAT4 in HSV-2 infection, we compared seven different SNPs (rs7574865, rs4853543, rs7572482, rs13017460, rs7601754, rs3024896, and rs6752770) of the human STAT4 gene in asymptomatic and symptomatic HSV-2-infected individuals, as well as in healthy controls. We did not detect any correlations between the STAT4 SNPs and the incidence of HSV-2 infection when comparing HSV-2-infected individuals and healthy controls (data not shown). However, for one of the SNPs, rs7572482, which is located in an intron close to the 5′ untranscribed region (UTR), the minor A allele variant correlated with the incidence of symptomatic infection (Table 1) (P = 0.0184). However, this difference was not significant after Bonferroni's correction for multiple testing. We also investigated whether the minor A allele of rs7572482 correlated with the need for antiviral treatment. The A allele distribution was 45% in HSV-2-infected individuals who required acyclovir treatment, compared with 33% in HSV-2-infected individuals who did not require antiviral treatment (P < 0.02).
To assess further the role of STAT4 variations in HSV-2 infection, we analyzed the haplotype frequencies of the seven STAT4 SNPs. Of the seven STAT4 haplotypes with >4% frequency in at least one of the groups, the CAATAGG combination was significantly more common in asymptomatically infected individuals than in individuals with symptomatic HSV-2 infection and in healthy controls. The CAATAGG haplotype frequencies were 4% and 12% in symptomatically and asymptomatically infected individuals, respectively (P = 0.0029), and remained significant after 100,000 permutations (P = 0.012) (Table 2).
Given that previous HSV-1 infection correlates with asymptomatic infection, we compared the frequencies of HSV-1 seropositivity in the asymptomatic and symptomatic HSV-2-infected individuals but found no statistically significant differences.
Given the observed association of STAT4 variations with HSV-2 infection and the necessity for STAT4 in Th1-mediated immunity (20), we examined whether variations in the STAT4 gene affected IFN-γ production. For this purpose, we measured the levels of HSV-2-specific IFN-γ secretion in PBMC from HSV-2-infected individuals (both asymptomatic and symptomatic) who had different STAT4 rs7572482 genotypes, representative for the CAATAGG haplotype. The levels of HSV-2-specific IFN-γ production were higher in the PBMC from individuals who were homozygous for the major G allele than in those from individuals who were heterozygous or homozygous for the minor A allele (P = 0.04; Fig. 1). Following HSV-2 stimulation, the median level of IFN-γ secretion was more than 2-fold higher in the cells from HSV-2-infected individuals with the GG genotype than in individuals with the AA genotype (Fig. 1). We and others have previously reported that asymptomatic HSV-2 infection is associated with higher T-cell recall IFN-γ responses, compared with symptomatic HSV-2 infection (10, 37). However, we could not confirm this observation in the current patient cohort (data not shown).
To study the immune response to genital HSV-2 infection, naïve and vaccinated STAT4-deficient and wild-type mice were infected intravaginally with HSV-2 strain 333. The mice were examined daily for genital inflammation and neurologic illness, and the levels of viral DNA in vaginal washes and spinal cords were measured. Initially, we measured disease development during primary infection. No major differences between the STAT4−/− and wild-type mice were observed after genital inoculation of HSV-2. Neither disease development nor the survival rates were affected by STAT4 deficiency (data not shown). The STAT4−/− and wild-type mice had comparable levels of HSV-2 DNA in vaginal washes obtained 2 days postinfection (Fig. 2A) and in the central nervous system (CNS) on day 7 postinfection (Fig. 2B).
Subsequently, we challenged the vaccinated mice and assessed the viral loads and disease development. The viral load in the genital tract 2 days postinfection was significantly higher in the vaccinated STAT4−/− mice than in the wild-type mice (Fig. 2C). At this time point, we did not detect any viral DNA in the vaginal washes from wild-type mice whereas the median amount of viral DNA in the STAT4−/− mice was 4.4 × 106 (log10) copies of HSV-2 DNA/ml. Two weeks after the HSV-2 challenge, the vaccinated mice were sacrificed to measure the virus content in the CNS. None of the wild-type mice had any detectable levels of viral DNA, while 2 out of 10 STAT4−/− mice had measurable levels of HSV-2 DNA (data not shown). Nevertheless, the STAT4−/− mice were protected against terminal illness to the same extent as all the wild-type mice, and all the STAT4−/− mice survived the HSV-2 challenge.
To assess the role of STAT4 in virus-specific CD4+ T-cell responses, we measured the DTH and cytokine responses of the STAT4−/− and wild-type mice 4 weeks after HSV-2 vaccination. The mice that lacked STAT4 had impaired HSV-2-specific CD4+ T-cell responses both in vivo and in vitro. The in vivo CD4+ T-cell response was evaluated by measuring DTH footpad swelling 48 h after injection of inactivated HSV-2. The HSV-2-specific inflammatory responses were significantly lower in the STAT4−/− mice than in the wild-type mice (Fig. 3A). HSV-2-specific IFN-γ secretion in spleen cell cultures that were depleted of CD8+ T cells was measured using a cell ELISA. We found that the levels of HSV-2-specific IFN-γ secretion from the CD4+ T cells of the STAT4−/− mice were negligible compared to the high levels seen in the cells from the wild-type mice (Fig. 3B). In addition, we screened the 48-h culture supernatants of HSV-2-activated spleen cells for Th1, Th2, and Th17 cytokines. We confirmed that the IFN-γ levels were significantly reduced in the STAT4-deficient mice (Fig. 3C). However, there were no significant differences in the levels of the other Th1 cytokines (Fig. 3C) or Th2 cytokines (Fig. 3D) between the wild-type and STAT4−/− mice. We could not detect IL-17A in any of the culture supernatants (data not shown).
In the present report, we provide evidence to implicate STAT4 in HSV-2-specific immunity in both humans and mice. We show that a variation in the human STAT4 gene is associated with asymptomatic HSV-2 infection and increased HSV-2-specific IFN-γ secretion. In addition, we show that HSV-2 does replicate in the genital tracts of vaccinated STAT4-deficient mice, most likely due to their impaired HSV-2-specific IFN-γ responses.
Genetic variations in the human STAT4 gene have previously been associated with Th1-mediated inflammatory diseases, such as rheumatoid arthritis, SLE, and Sjögrens syndrome (21). The present study is, to the best of our knowledge, the first to show that STAT4 variations are associated with an infectious disease. In our study population, which consisted of 143 symptomatic and 85 asymptomatic HSV-2-infected individuals, we found that one of the haplotypes of the human STAT4 gene, consisting of seven SNPs from the same haplotype block, was associated with enhanced IFN-γ responses and asymptomatic HSV-2 infection. Therefore, STAT4 represents, together with certain HLA alleles (23), TLR-2 (6), and mannan-binding lectin gene 2 (34), a human gene variation that might predispose individuals to asymptomatic HSV-2 infection. However, the effect size of these associations is very modest and can serve only as an indication that the gene is important for the expression of a specific phenotype. This also implies that more-profound sequence changes in this immune-regulating gene may cause severe impairments of the antiviral immune response.
We were not able to correlate genetic variations in the STAT4 gene with susceptibility to HSV-2 infection. However, genetic variations in both innate and adaptive immune-regulating genes may affect susceptibility to HSV-2 infection; SNPs in the genes that encode the Th1-inducing transcription factor T-bet, TBX21 (39), and in the TLR3 gene (41) are risk factors for HSV-2 acquisition. Thus, the host repertoire of several immune-regulating genes may influence both susceptibility to and the severity of HSV-2-mediated disease.
The roles of STAT4 in human cells and during human infections have not been extensively studied. Similar to murine cells, human CD4+ T cells secrete IFN-γ upon IL-12 stimulation and STAT4 activation (4, 27). However, sufficient IFN-γ secretion is dependent upon IL-18 (27), as well as TCR stimulation and T-bet expression (32). In the present report, we show that a genetic variation in the human STAT4 gene affects the in vitro levels of IFN-γ produced in response to HSV-2 recall activation. The major allele of STAT4 rs7572482 is associated with increased HSV-2-specific IFN-γ secretion in vitro, as well as with asymptomatic HSV-2 infection. This supports the results of previous studies, in which increased IFN-γ responses were associated with symptom-free HSV-2 infection (8, 10, 37). Taken together, our data suggest that variations in the STAT4 gene are involved in the regulation of HSV-2 disease severity, possibly by modulating virus-specific IFN-γ responses.
The significance of IFN-γ and CD4+ T-cell responses in HSV-2 immunity has been well described in murine models of genital HSV-2 infection, in which IFN-γ (14, 25, 30), and T-bet expression (39) are critical for viral clearance and resistance to infection in the genital tract. Here, we show that vaccinated STAT4-deficient mice, in contrast to wild-type mice, do not develop sterilizing immunity to HSV-2 in the genital tract. The increased local viral load in STAT4−/− mice is associated with impaired CD4+ T-cell responses, as evidenced by the impaired DTH responses in vivo and reduced IFN-γ secretion in vitro. However, even though we detected considerable amounts of viral DNA in the genital tracts of the vaccinated STAT4−/− mice, it appears that the virus did not reach the CNS. This implies that STAT4 is important for the vaccine-induced prevention of vaginal viral replication, whereas it plays a marginal role in preventing the virus from spreading to the CNS. This notion differs from the conclusions drawn from studies using the closely related HSV-1. Allen and colleagues have shown in a model of ocular HSV-1 infection that vaccinated STAT4-deficient mice resolve the infection to the same extent as wild-type mice (2). This discrepancy could be due to the different routes of infection. Moreover, the validity of our findings for STAT4-deficient mice is strengthened by the results of our human experiments, which show that STAT4 variations affect HSV-2-specific IFN-γ production. Therefore, we propose that STAT4 is important for HSV-2-specific IFN-γ responses in both humans and mice.
None of the analyzed polymorphisms of the STAT4 gene were associated with the incidence of HSV-2 infection in humans. Likewise, STAT4 deficiency did not affect either the viral load or disease progression in primary HSV-2 infection in mice. This is somewhat different from previous findings obtained using a model of ocular HSV-1 infection. Allen et al. found that STAT4-deficient animals did not differ from wild-type animals with respect to survival or disease development, despite having higher levels of viral replication in the eye (2). Banerjee et al. have reported that STAT4−/− mice are more susceptible to HSV-1-induced encephalitis, although in their hands the animals also succumbed earlier to the infection (3). It is interesting that the two Th1 transcription factors STAT4 and T-bet play different roles in HSV-2 infection in both humans and mice. T-bet appears to be more important during primary infection (39, 40), while STAT4 controls viral reactivation. This is probably linked to the functional differences between these two transcription factors. While T-bet expression is required during the early phase of Th1 differentiation, STAT4 is required later on to stabilize and maintain the Th1 phenotype by amplification of both T-bet and IFN-γ expression (33). Thus, the importance of STAT4 appears to be in the long-time maintenance of the HSV-2-specific IFN-γ responses that are required to control viral reactivation.
In summary, we show that STAT4 regulates HSV-2-specific CD4+ IFN-γ responses in humans and mice. Genetic variations in the human STAT4 gene are associated with increased IFN-γ synthesis and asymptomatic HSV-2 infection, while vaccinated mice deficient in STAT4 have impaired HSV-2-specific IFN-γ responses and do not develop sterilizing immunity. We suggest that certain genetic variations in STAT4 affect HSV-2 replication and disease severity by altering the IFN-γ-mediated antiviral immune responses.
This work was supported by the Swedish Science Council, the Västra Götaland Region through LUA/ALF, Torsten and Ragnar Söderberg's Foundation, Inga-Lill and Arne Lundberg's Foundation, and Wilhelm and Martina Lundgren's Research Foundation.
We thank Christin Grimhag at the Sahlgrenska University Hospital for collecting the blood samples and Maria Bergquist for help with the MultiPlex analysis.
Published ahead of print 20 June 2012
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Oak Harbor village garage sale days scheduled
July 20, 2016 OAK HARBOR — Oak Harbor Area Chamber of Commerce is coordinating the seventh semi-annual Village Wide Garage Sale Days Aug. 26-27. more »»
Clyde student attends science conference
July 20, 2016 CLYDE — Through nomination, a Clyde High School soon-to-be sophomore got a chance to be a delegate at the 2016 Congress of Future Science and Technology Leaders June 29-July 1. more »»
Region briefs, July 20
July 20, 2016 T-SPL hosts reading program The junior department at Tiffin-Seneca Public Library is to host "Every Child Ready to Read @ Your Library Story Time" at 10: 30 a.m. Saturday in the Frost Kalnow Room. more »»
Driver cited, no injuries in crash
July 19, 2016 A driver was cited after a crash at CR 11 and CR 38 Monday afternoon. more »»
Council moves on land swap
July 19, 2016 Tiffin City Council heard the first reading of an ordinance expected to facilitate a property exchange with the Seneca County Agricultural Society during its meeting Monday. more »»
Carey readies for new mayor
July 19, 2016 CAREY — It took three meetings, but Carey Village Council finally approved five ordinances and resolutions that had been on the agenda since the death of former Carey Mayor Steven Smalley. more »»
Council member resigns
July 19, 2016 REPUBLIC — Republic council members accepted the resignation of Josh Watkins as councilman Monday evening. more »»
Mickey Mart opens in Green Springs
July 19, 2016 GREEN SPRINGS — Green Springs Village Council members heard about a new business opening in town during their meeting Monday night. more »»
County board sets agenda
July 19, 2016 Seneca County Board of Commissioners is to meet at 7 p.m. today at Eden Township Hall, 6571 SR 100, Melmore. In old business, the board is to discuss the Seneca County Museum Task Force. more »»
Man to undergo rehabilitation
July 19, 2016 A New Riegel man is to undergo rehabilitation. Seneca County Common Pleas Court Judge Michael Kelbley found Kade L. more »»
Grand jury hands down two indictments
July 19, 2016 Two people were indicted by a Seneca County grand jury. Timothy M. Harding, 44, of Fostoria, was charged with domestic violence, a fourth-degree felony. more »»
Lakota meeting rescheduled
July 19, 2016 KANSAS — The Lakota Board of Education has rescheduled its next regular meeting for 7 p.m. July 25 at 52000 CR 13. more »»
New Riegel sets special meeting
July 19, 2016 NEW RIEGEL — The New Riegle Board of Education is to have a special meeting at 4:30 p.m. Wednesday in the office conference room of the school, 44 N. Perry St. more »»
TCS committee plans meeting
July 19, 2016 The Tiffin City Board of Education's Finance Committee is to meet at 4:30 p.m. today at the Administration Building, 244 S. Monroe St. more »»
2, then 3, then 4
July 18, 2016 Tiffin Fire Rescue Division and Tiffin Police Department personnel work at the scene of a four-vehicle accident in the 6000 block of West Market Street Sunday evenin. more »»
Fine glass on display
July 17, 2016 David Hollingshead, of Kansas City, Kansas, looks over a piece of glass from his collection at Heminger Center, 350 Miami St. more »»
Dispatchers keep community running
July 17, 2016 Seneca County Sheriff's Office dispatchers Karen Aichholz and Stacey Saylors use teamwork and an ability to multitask to help county residents. more »»
Woman killed in crash
July 17, 2016 A Fostoria woman was killed after a two-vehicle accident at US 224 and CR 248 in Biglick Township Friday afternoon. According to a release from Hancock County Sheriff's Office, Jacob . more »»
Person transported after crash
July 17, 2016 A person was taken to ProMedica Fostoria Community Hospital after a one-vehicle accident Saturday night. more »»
Firefighters take down fire at hotel
July 17, 2016 Tiffin Fire Rescue Division personnel fought a fire at Holiday Inn Express, 78 Shaffer Park Drive, Saturday nigh. more »»


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THE PSYCHOLOGY OF DEMENTIA PRAECOXby Carl Jung
This work is the fruit of three years' experimental labor and clinical observation. In view of the difficulty and magnitude of the material, my work cannot and will not lay any claims either to perfection of treatment or to perfect certainty of conclusions and statements; on the contrary, it unites in itself all the disadvantages of
- LendMe LendMe™ Learn More
This work is the fruit of three years' experimental labor and clinical observation. In view of the difficulty and magnitude of the material, my work cannot and will not lay any claims either to perfection of treatment or to perfect certainty of conclusions and statements; on the contrary, it unites in itself all the disadvantages of eclecticism, which perhaps to many a reader will seem so peculiar that he will call my work rather a confession of faith than a scientific book. —Peu importe! What is of chief concern is that I may succeed in showing my readers how, by certain psychological investigations, I reached certain views, which I deem fit for the stimulation of the problems of the individual psychological basis of dementia praecox in a new and fruitful direction.
My views are no contrivances of a roving fancy, but thoughts which matured in almost daily intercourse with my venerable chief, Professor Bleuler. I owe special thanks to my friend, Dr. Riklin, of Rheinau, for considerably enriching my empirical material. Even a superficial glance at my work will show how indebted I am to the excellent conceptions of Freud. As Freud has not yet attained fair recognition and appreciation, but is opposed in the most authoritative circles, I hope to be allowed to define my position towards him. My attention was attracted to Freud by reading some of his articles, and indeed, at first accidentally by his "Traumdeutung," after which I studied also his other works. To be sure in the beginning I naturally entertained all the objections which are advanced in literature against Freud. However, I thought that Freud could only be refuted by one who himself had thoroughly tried the psychoanalytic method, and who should really investigate like Freud, that is, by studying out patiently and for a long time the daily life, hysteria and dreams from Freud's point of view. He who does not or cannot do this ought not to judge Freud, else he acts like those famous men of science who disdained to look through the telescope of Galileo. Fairness to Freud does not signify, as many fear, a conditionless submission to a dogma; indeed independent judgment can very well be retained beside it. If I, for instance, recognize the complex mechanisms of dreams and hysteria, it does not at all mean that I ascribe to sexual trauma in youth an exclusive significance, as Freud apparently does; still less does it mean that I place sexuality so preponderantly in the foreground, or that I even ascribe to it the psychological universality which Freud postulates under the impression of the very powerful role which sexuality plays in the psyche. As for Freud's therapy, it is at best a possible one, and perhaps does not always come up to expectations. Nevertheless, all these are only side issues which completely disappear beside the psychological principles, the discovery of which is Freud's greatest reward, and to which the critic does not pay enough attention. He who wishes to be fair to Freud should act in accordance with the words of Erasmus: Unumquemque move lapidem, omnia experire nihil intentatum relinque.
As my work is often based on experimental examinations, I hope that the reader will pardon me if he finds many references to the "Diagnostischen Associations-Studien."1
—C. G. Jung. Zürich, July, 1906.
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