text:
Good move, A-Rod
The best thing Alex Rodriguez could've done in the wake of the SI.com report that indicated he used steroids during the 2003 season was simply come clean and admit it was true.
Andy Pettitte and Jason Giambi took that route before and have been able to continue with their careers without much controversy still tailing them. Barry Bonds and Roger Clemens kept denying and their historic careers will forever be tainted. Mark McGwire made a fool of himself in front of Congress and he's currently being kept out of the Hall of Fame.
On Monday, A-Rod came clean. He sat down with ESPN's Peter Gammons and said the SI report was correct, and Rodriguez took it a step further. He admitted to using performance enhancers in each of his three seasons with Texas from 2001-03. Will A-Rod's rep be tarnished? Sure. But, the game will be able to move on a bit easier now that he's fessed up to cheating.
When the report came out, I can't say that I was surprised. Why should any of us be surprised when we hear a player from this era tested positive for PHDs? As Rodriguez correctly points out in his comments, it was a loose era in the '90s and in the early part of this decade. Things have changed for the better in recent years with the new testing that's in place.
There's a good chart in the MLB.com article on A-Rod's admission. It breaks down his stats before, during and after the period in which he says he was using steroids. From 1996-2000, He averaged a .315 average, 36.8 homers and 114.8 RBIs in 145 games per season. From 2004-2008, the averages were .303/41.6/123.2 in 153.4 games. With Texas, A-Rod went .305/52/136.3 in 161.7 games on average.
You want to strip A-Rod of his tainted numbers? Go ahead. This guy is still a Hall of Famer. You want to strip Bonds of his totals from the point he is accused of using? Fine. He's still a Hall of Famer. Clemens? McGwire? Even someone like Sammy Sosa? I say put them in the Hall.
They are the product of an era when hitters AND pitchers were using. Put it right on their plaques in Cooperstown: "Achieved these feats during the so-called Steroids Era." Put it out there. Show what they did and why it was wrong and educate, but don't try to hide these players from the kids. They're in baseball's record books and they're not going anywhere.
That might not be the popular opinion, but that's mine. Then again, I'm also from the camp that believes Pete Rose should be enshrined as well. If cheating or character are really deciding factors, there are plenty of players in the Hall who you could make a case for removing. Asterisks could be applied for reasons well beyond steroids.
Bottom line: I was happy to see A-Rod fess up as quickly as he did. Waiting until he arrived for Spring Training would've been a mistake, as would denying the accusations. He's still going to hear plenty of "A-Roid!" chants when on the road and I'm sure Toronto will be one place that gives him a "warm" welcome.
Let's move on and get ready for this 2009 season. Spring Training is here and the World Baseball Classic is right around the corner. Maybe some of you Jays fans aren't as excited about this season, but you know what? Another baseball season is here and that's plenty to be pumped about. I'll be landing in Florida on Thursday and getting to work on Friday.
Here's the A-Rod interview for those who haven't seen it:
8 Comments
I am tired of the PEDS/ steroid era . As for A-Rod's interview yesterday , he had no choice but to come clean . His emotions were real though I think more due to the fact he got caught and his "clean" image was shattered than him being remorseful. I got the impression he is an insecure person and needs constant adulation from those around him and his fans . I do have a few problems with his interview . He said he was young , naive and stupid , he may have been naive about PEDS but in 2001-2003 he was 25-28 , not that young but I agree, he was stupid. He claims he didn't know what he was taking , I find that really difficult to believe coming from a man who is so meticulous about his appearance , workout and craves perfection from himself . He wants to be the best , to win all the accolades , then tries to say he didn't know what he was using , I don't buy that . He said the pressure of the contract and competition made him search for an edge to push him to the next level, if he felt that way going to Texas, then how do we believe he stopped taking them when he went to NY . We all know NY is the hot spot in baseball, the pressure is enormous ,the competition fierce and the fans can be brutal. If you watch the interview , he never really answers many of Gammon's questions buts skirts around them, offering such things as GNC sold over the counter things that you can test positive for . Does it matter what he took, probably not. Does he deserve to be in the HOF , not my decision but how do you leave out somebody that was potentially "clean" because his numbers aren't quite as good as those who used steroids. When a player decides to take PEDS it effects all of baseball not just him. I do agree with Jordan , if the steroid era players are in the HOF then Pete Rose deserves the same consideration. That debate will go on for years. Lastly I am a huge Delgado fan , if Delgado was clean , then he truly got ripped off in the 2003 MVP race. He and A-Rod's numbers were similar , A-rod having 5 more HR and Delgado 29 more RBIS. It has to be upsetting for Delgado to see this now, it was upsetting when he lost. I will look at baseball through different eyes . Have a great day all and take care
A-roid is scum,the only reason he came clean was because the Yankees told him to.
You can bet he was and still is on roids since day one.
I used to train race horses and when they found out how to detect one drug someone would come up with another one,the same with Roids.He will never be a HOF in my eyes.
It would be nice to see who the other 103 are,will there be any Jays on the list?????
I read all the blogs from the other teams,and they have 50 to 100 comments every day,but on this blog we have maybe 2 or 3 whats up with that,are their no true Jays fans out there anymore.
Whatever you do don't give up on the team,with out your support this blog will die so start posting and save it.
Although, A-Rod gained some respect for his admission yesterday, only one shoe has dropped. Coming out of THE steroid hotbed at Seattle and seeing how his HR numbers virtually doubled in 98 versus 97 suggests to me he's been on the juice since that timeframe. A quick look at picture of his body changes in that timeframe show a remarkable increase in size. In addition, I'm pretty convined he was still on it for at least the 2004 season, otherwise the COO of the players union wouldn't have tipped him on his upcoming drug test.
But the bigger issue is Major League Baseball and whether it truly wants to regain credibility from this era or continually sweep it under the rug and hope the stench goes away over time. Clearly, awarding A-Rod the MVP in 2003 knowing he tested positive for two banned drugs is laughable.
I expect we'll see players names released over time and the longer it takes for all names to come out, the lower the credibility of MLB will sink. There really is only one way to make this go away and that is to be upfront, release all the names and re-adjust the player awards for this timeframe.
Frankly, considering somewhere between 5 and 7% or 104 players tested positive, it really is the only fair thing to do for the guys who played the game the right way and didn't cheat. Delgado, Morris and countless others might suddenly rise in significance if they didn't test positive and whether they make it to the HOF or not isn't the issue. The issue is one of fairness to the guys who didnt cheat as well as the fans. The fans deserve to know the truth, the whole truth and nothing but the truth.
Nothing else will suffice.
I agree with Jordan about putting it right on the plaque. Let them still be in the hall though but do mention what they did to help them get in.
As for A-rod, he's always been and still is one of my favourite players to watch but as a person he comes off as a ***** (nothing new there). I refuse to give him credit for coming clean. If SI had never uncovered the truth he likely would've continued to deny that he's used it. I believe the main reason he did confess was because he's seen how Pettite and Giambi have moved on and how Clemens and Barry continue to be vilified, it's not because of remorse. Consider also, that he was on the same team as 2 guys who have moved on by admitting it. I don't think that's a coincidence. He even mentioned that in New York they like honesty obviously referring to the fact that Giambi and Pettite have moved on by admitting it. Makes me think that if those 2 had denied it he would've done the same.
Garry, personally I continue to read Jordan's blog and the site daily, I don't always post because I try and avoid the negativity (justified or not) but if there's ever a time when nobody posts i'll leave a comment or 2 just for the sake of it.
Anyone know if Matt Bush will be ready to compete for a spot right out of spring training or is this simply a move to add depth to triple A ?
The real question with Matt Bush is whether he's got himself under control, in order to get his baseball career under way. He's had a bit of history of run ins with the law apparently due to drinking.
I expect he'll start in Dunedin or lower to see if he's fully recovered from Tommy John surgury and whether he's serious about baseball or partying. That being said, the change of organizations might be good for him, he might have simply got off to a bad start with the Padres, since his first problem happened about one week after they signed him.
If he turns this behaviour around he could be a good addition, assuming of course we didnt pay too much for him and he's healthy.
JP has done it again…
Read the following on Bush… What a headache he is going to be…
SAN DIEGO (AP)—The San Diego Padres traded minor league pitcher Matt Bush to the Toronto Blue Jays on Tuesday for a player to be named or cash.
Bush, the No. 1 pick in the 2004 amateur draft, was designated for assignment Thursday, ostensibly to make room on the 40-man roster for slugger Cliff Floyd. However, hours after Floyd's signing was announced, the Padres acknowledged they were looking into another off-field incident involving Bush.
Police in suburban El Cajon later confirmed that the 23-year-old Bush was being investigated for allegedly assaulting members of a high school lacrosse team.
Originally drafted as a shortstop and given a $3.15 million signing bonus by his hometown team, Bush flopped as a position player with San Diego and was converted to pitcher. He developed elbow problems and had reconstructive surgery in August 2007, which caused him to miss all of last season.
Two weeks after he was drafted, Bush was suspended indefinitely by the Padres after he was arrested at a bar across the street from the team's complex in Peoria, Ariz. Among the charges were underage drinking and that he bit one of the bouncers who tried to escort him out of the bar. Assigned to the Padres' rookie-level Peoria team, Bush was reinstated a month later. He pleaded guilty to disorderly conduct, trespassing and underage possession or consumption of alcohol.
Bush was involved in a bar fight last summer, also in Peoria.
To make room on their roster for Bush, the Blue Jays released right-hander Dirk Hayhurst, claimed off waivers from San Diego last October.


text:
the twoTuesday, October 23, 2012
Cams and #168 Zenitude. Please email me your address and I will make sure a book lands in your hands. As always, I wish everyone could get a book.
I have a really fun giveaway coming up tomorrow.
See you then!
I have a really fun giveaway coming up tomorrow.
See you then!
5 comments
congratulations winners! so cute on the blackboards!ReplyDelete
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The leaves are really coming down around us, aren't they? Glad they rained down two great winners.ReplyDelete
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subset: commoncrawl


text:
Many women who have had a healthy pregnancy will have a vaginal birth. In a vaginal birth, the baby will come out through the birth canal. Most women give birth at around 38-41 weeks of pregnancy. However, there is no way to know exactly when you will go into labor.
Your doctor will review a list of possible complications, which may include:
Some factors that may increase the risk of complications include:
Be sure to discuss these risks with your doctor before giving birth.
During pregnancy you should:
Before "true" labor begins, you may have periods of "false" labor. These are irregular contractions of your uterus, called Braxton Hicks contractions. They are normal but can be painful. They are usually also felt in the stomach and not the back. Timing the contractions is a good way to tell the difference between true and false labor. Note how long it is from the start of one contraction to the start of the next. Keep a record for an hour. If the contractions are getting closer together, longer, stronger, and are being felt in your back, then it may be true labor. If you think you are in labor, call your doctor.
During this process, you will prepare to deliver your baby. At the beginning of labor, the uterus (where the baby grows during pregnancy) will begin to contract, moving the baby down the vagina (birth canal). The cervix, the opening of the uterus into the vagina, will slowly enlarge to a diameter of about 10 centimeters. This will allow the baby to pass through and be delivered through the opening of the vagina. This process usually takes a while. However, if you have delivered vaginally before, labor can be very quick.
Labor can cause severe pain, but keep in mind that every woman's labor is different. Everyone experiences pain differently. While planning the delivery, talk to your doctor about your options for pain relief.
In the early stages of labor, relaxation techniques (like meditation and rhythmic breathing) may be helpful. Some woman do not require any other pain control.
There are many medical options for pain control. All treatments to relieve pain during labor have risks and benefits. Make sure you discuss these with your doctor.
Once the cervix is fully dilated (opened) and the baby seems to be heading down the birth canal, the nurses will help prepare you for delivery. Your legs may be draped with cloths. Some doctors will clean the area around the vagina with an antiseptic solution.
You may put your legs into holders, especially if you have an epidural. The nurses and your support people may hold your legs in a comfortable position. This will help you to push. Your doctor may encourage you to find a position that is right for you. Each time you have a contraction, you will be instructed to push. This involves you bearing down, like you are trying to have a bowel movement.
"Crowning" is when the baby's head is seen at the opening to the vagina. When this happens, you may be asked to slow your pushing. Depending on your delivery plan, the doctor may massage your perineum to gently stretch it. An episiotomy is not routinely done, but in some cases, it is necessary.
Once your baby's head is out, you will be asked to stop pushing. The doctor will check to make sure that the umbilical cord is not around the baby's neck. Then, you will be able to push the rest of the baby out. If the baby appears healthy and is breathing well, he may be placed on your stomach. The umbilical cord will be clamped and cut. Within the next 20 minutes, the placenta will be delivered.
Sometimes the baby's head does not move as expected through the birth canal. If this happens, your doctor may use forceps or vacuum extraction to move the baby.
The average time for you to deliver your first baby and the placenta is 12 hours. This can vary greatly, though.
Labor causes severe pain during contractions. There may be brief periods of relief after each contraction. Talk to your doctor about your options for managing pain.
The usual length of stay for a vaginal delivery is 1-3 days. Your doctor may choose to keep you longer, however, if complications arise.
Having a baby will change you physically and emotionally.
Physically, you might have the following:
Emotionally, you may be feeling:
After you leave the hospital, contact your doctor if any of the following occurs:
In case of an emergency, call 911 .
The American Congress of Obstetricians and Gynecologists
American Pregnancy Association
Baby Center
Women's Health Matters
Depression during and after pregnancy. Women's Health.gov website. Available at: http://www.womenshealth.gov/faq/postpartum.htm . Updated April 2005. Accessed June 11, 2008.
Epidural anesthesia. American Pregnancy Association website. Available at: http://www.americanpregnancy.org/labornbirth/epidural.html . Updated August 2007. Accessed June 11, 2008.
Obstetrics: Normal & Problem Pregnancies . 3rd ed. New York, NY: Churchill Livingstone; 1996.
Spinal block. American Pregnancy Association website. Available at: http://www.americanpregnancy.org/labornbirth/spinalblock.htm . Updated December 2006. Accessed June 11, 2008.
2/5/2009 DynaMed's Systematic Literature Surveillance http://www.ebscohost.com/dynamed/what.php : Beckmann M, Garrett A. Antenatal perineal massage for reducing perineal trauma. Cochrane Database Syst Rev . 2009;CD005123
12/4/2009 DynaMed's Systematic Literature Surveillance http://www.ebscohost.com/dynamed/what.php : Marín Gabriel M, Llana Martín I, López Escobar A, et al. Randomized controlled trial of early skin-to-skin contact: effects on the mother and the newborn. Acta Paediatr. 2009 Nov 12. [Epub ahead of print]
Last reviewed October 2009 by ]]>Ganson Purcell Jr., MD, FACOG, FACPE]]>
Please be aware that this information is provided to supplement the care provided by your physician. It is neither intended nor implied to be a substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the advice of your physician or other qualified health provider prior to starting any new treatment or with any questions you may have regarding a medical condition.
Copyright © 2007 EBSCO Publishing All rights reserved.


text:
Each mojit you create can have some specific code called binders that is only deployed to the browser. The code can perform the following three functions:
A mojit may have zero, one, or many binders within the binders directory. Each binder will be deployed to the browser along with the rest of the mojit code, where the client-side Mojito runtime will call it appropriately. The view used to generate output determines which binder is used. Thus, if the simple view is used, the binder simple.js is used. This can be overridden by setting view.binder in the meta argument to ac.done. If no binder matches the view, then no binder is used.
To use binders, your application is required to have the following:
See Binding Events for a documented example that uses binders.
A binder essentially has the two essential functions init and bind. The init function initializes the binder and contains the mojitProxy object. The bind function allows the binder to be attached to the DOM.
The example binder below shows the basic structure of a binder. The binder is for the AwesomeMojit mojit and contains the init and bind functions that initialize and allow the binder code to be attached to the DOM.
YUI.add('AwesomeMojitBinder', function(Y, NAME) {
Y.namespace('mojito.binders')[NAME] = {
init: function(mojitProxy) {
this.mojitProxy = mojitProxy;
bind: function(node) {
}, '0.0.1', {requires: ['node']});
An instance of the binder above will be created whenever the index function of AwesomeMojit is executed, and its corresponding DOM node is attached to a client page. Mojito will select that DOM node and pass it into the bind function. This allows you to write code to capture UI events and interact with Mojito or other mojit binders.
The init method is called with an instance of a mojit proxy specific for this mojit binder instance. The mojit proxy can be used at this point to listen for events. It is typical to store the mojit proxy for later use as well. The mojit proxy is the only gateway back into the Mojito framework for your binder.
The bind method is passed a Y.Node instance that wraps the DOM node representing this mojit instance within the DOM. It will be called after all other binders on the page have been constructed and their init methods have been called. The mojit proxy can be used at this point to broadcast events. Users should attach DOM event handlers in bind to capture user interactions.
For Mojito to reference the DOM node representing the mojit instance and pass it to the bind function, the root element of the mojit's template must have the id attribute with the Handlebars expression {{mojit_view_id}}. Mojito will render {{mojit_view_id}} into a unique ID that can be used to select the DOM node.
For example, the root element
 in the template below has the id attribute with the value {{mojit_view_id}}. This id lets Mojito reference the Y.Node instance wrapping the DOM node representing the mojit instance within the DOM. If this
 element does not have this id value, no node will be passed to the bind function.

{{name}}

Each binder, when constructed by Mojito on the client, is given a proxy object for interactions with the mojit it represents as well as with other mojits on the page. This mojitProxy should be saved with this for use in the other parts of the binder.
From the mojitProxy, you can access properties that use the interface and provides the information below:
Mojit config - the instance specification for the mojit linked to the binder and uses the following syntax:
Mojit context - environment information such as language, device, region, site, etc.
Mojit children - the children of the mojit, which is defined in application.json.
Mojit type - the name of the mojit that attached the binder to the DOM.
Often all you want your binder to do is to refresh its associated view. From the mojitProxy object, you can call the refreshView method to render a new DOM node for the current mojit and its children, as well as reattach all of the existing binders to their new nodes within the new markup. Because all binder instances are retained, state can be stored within a binder's scope.
The code snippet below shows how to call the refreshView method with optional parameters. The refreshView method does not require a callback to manage the markup returned from the action invocation.
mojitProxy.listen('flickr-image-detail', function(payload) {
var urlParams = Y.mojito.util.copy(mojitProxy.context);
var routeParams = {
image: payload.data.id
params: {
url: urlParams,
route: routeParams
A mojit binder can attempt to destroy a child mojit on the page by calling the destroyChild method from the mojitProxy object. The destroyChild method accepts one parameter that identifies the child mojit to be destroyed. That parameter can either be the slot or _viewId that identify the child mojit.
After being destroyed, the child's DOM node is detached, destroyed, and its binder life-cycle events (unbind, destroy) are executed.
The code snippet below uses the destroyChild method to remove the child nodes based on the _viewId.
bind: function(node) {
this.destroy = node.one("#destroyButton").on('click', function() {
var childId = this.node.one('#' + this.mojitProxy._viewId).get('value');
}, this);
See the Class MojitProxy in the Mojito API Reference.
The following example shows a typical binder. To see how to use binders in a working example, see the Code Examples: Events.
YUI.add('ChickenMojitBinder', function(Y, NAME) {
Y.namespace('mojito.binders')[NAME] = {
init: function(mojitProxy) {
Y.log('Binder(' + mojitProxy.config.id + ')', 'debug', NAME);
// Store object and ID for later use
this.mojitProxy = mojitProxy;
this.id = mojitProxy.config.id;
// Listen for cluck events from other chickens
this.mojitProxy.listen('cluck', function(evt) {
Y.log(this.id + ' heard cluck from ' + evt.source.id);
if (this.node) {
this.node.append('
' + this.id + ' heard cluck from ' + evt.source.id + '
');
}, this);
bind: function(node) {
Y.log('bind(' + this.id + ')', 'debug', NAME);
this.node = node;
node.on('click', function() {
Y.log(this.id + ' clicked', 'debug', NAME);
}, this);
}, '0.0.1', {requires: ['node']});
This example binder shows how to use the methods refreshView and destroyChild.
YUI.add('ParentBinderIndex', function(Y, NAME) {
Y.namespace('mojito.binders')[NAME] = {
init: function(mojitProxy) {
this.mojitProxy = mojitProxy;
this.myid = Y.guid();
bind: function(node) {
var mp = this.mojitProxy;
var id = this.myid;
this.node = node;
this.buttonClickHandler = node.one('#' + mp._viewId + '_ParentRefresh').on('click', function() {
mp.refreshView(function(data, meta) {
Y.log('refresh complete', 'warn', NAME);
this.destroyHandler = node.one('#' + mp._viewId + '_destroyButton').on('click', function() {
var childId = this.node.one('#' + mp._viewId + '_destroyInput').get('value');
}, this);
this.moHandler = node.one('h3').on('mouseover', function() {
Y.log('parent: ' + id, 'info', NAME);
onRefreshView: function(node, element) {
Y.log(this.myid + ' refreshed', 'info', NAME);
this.bind(node, element);
destroy: function() {
console.error(this.myid + ' destroyed!');
}, '0.0.1', {requires: ['mojito-client']});


text:
You are here, Viewing: Sesame Shortcuts Full 2.2.1-beta1 (Unlocked) APK
App Name: Sesame Shortcuts
Version: 2.2.1-beta1 Full Unlocked
Package Name: ninja.sesame.app.edge
Requirements: Android 4.4 and up
File Size: 3.9 MB
www.underclassblog.com — Supercharge your Android with Sesame Shortcuts. Quick launch them from Nova Launcher!
• 100+ shortcuts added to your device
• Integrated into Nova Launcher App Search and app icon long press (requires Android 5.0 or >)
• Easy setup, just install Sesame and Nova Launcher
• Adds a Google Search option to Nova Launcher App Search
• Smart Search: matches first letters of words. Typing "S" "B" will bring "Spotify: The Beatles" to the top. Results are ranked by how often you've used them, next time just "S" will do.
• Full control via Settings. Turn ON/OFF at the app or individual shortcut level
• Make your own shortcuts
• Beta features: Lock Screen and Edge Launcher (these don't require Nova Launcher)
List of Shortcuts
Preloaded shortcuts
• Contacts with one touch to call, text, or email
• WhatsApp conversations (not group ones though)
• Settings (19 useful ones)
• Google Shortcuts (My flights, etc.)
• Yelp (42 common searches)
Android 7.1 App Shortcuts
Backported all the way to 4.4 devices
Create your own shortcuts for
Netflix, Maps, Chrome, Chrome Beta, Waze, YouTube, Spotify, Yelp, Google, Google Play Music, Google Play Store
API integrations
• Spotify: All albums, artists, and playlists in your Library
• Slack: your teams and channels
• Tasker: all your tasks. This let's you build complex actions in Tasker and quick launch them easily.
• Reddit: your subreddits. Works for Reddit Official App, BaconReader, and reddit is fun
Automatically creates these personal shortcuts
• Chrome: websites you visit (when you tap on a result in the URL bar). Does NOT make shortcuts when you're incognito :)
• Spotify: 1) new music you search for and click on 'Top Result' 2) when you click on a items from "Recently Played"
• Hangouts conversations: only for pre 7.0 devices and not too reliable
Version 2.2.1-beta1 (2017-09-27, build 5839):
- fixes (in many cases) dragged contact actions
- adds translations for Czech, German, Spanish, French, Italian, Portuguese, Russian, Swedish, Turkish, and Simplified & Traditional Chinese!
- adds About page
FULL version Unlocked | Analytics disabled
NOTE: If you experience difficulties with downloading Sesame Shortcuts Full 2.2.1-beta1 (Unlocked) APK from given links below, please try to login first to those file hosting before download (it's free to create an account), make sure to uncheck "Use our download manager and get recommended downloads" or similar, if any.
Sesame Shortcuts Full 2.2.1-beta1 (Unlocked) APK Posted on: http://www.underclassblog.com/2017/09/sesame-shortcuts-full-2-2-1-beta1-unlocked-apk.html


text:
Safe Kidney Care Cohort Study
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
|ClinicalTrials.gov Identifier: NCT01407367
Recruitment Status : Completed
First Posted : August 2, 2011
Results First Posted : November 6, 2018
Last Update Posted : October 18, 2019
- Study Details
- Tabular View
- Study Results
- Disclaimer
- How to Read a Study Record
Chronic kidney disease (CKD) is common, but it is often over-looked in patients with this disease when they are getting medical treatment. Patients with CKD have special needs for their medical treatment. When these special needs are not considered their medical care may lead to unintended harm (called safety events) which can cause hospitalization, more kidney problems, and even death.
This research study has two purposes. The first purpose is to determine how participants feel about wearing a medical alert bracelet or necklace that alerts health care workers that the user of the bracelet or necklace has decreased kidney function. Medical alert bracelets are often recommended for people who have other medical problems, such as diabetes. This medical alert bracelet or necklace has an address to an informational website about the safe care of patients with kidney problems. The investigators think that alerting health care workers that a person has decreased kidney function may decrease their chances of having a medical injury and improve the safety of their care.
The second purpose of this research study is to track how often people with kidney problems may be exposed to medicines, tests, or procedures that might increase their chance of having an accidental medical injury or safety event. Though some medical injuries can not be prevented, the investigators want to find out what medical events in patients with kidney problems might be preventable. The investigators also want to find out if other things might increase a patient's chances of getting a medical injury, such as physical weakness or medical instructions that might be confusing.
|Condition or disease
|Chronic Kidney Disease
Chronic kidney disease not requiring dialysis (CKD) is common, but under-recognized, among patients who frequent the health care system, where improving patient safety is a high priority. Poor recognition of the disease and several other features unique to CKD make it a high-risk condition for adverse, patient-safety incidents (PSIs). In this context, PSIs refer to events of unintended harm or injury related to medications or medical care. These adverse safety events may include those usually cited for the general population (PSI), but also, CKD-specific unsafe practices (CKD-PSI) all of which, in turn, can lead to frequent hospitalization, accelerated loss of kidney function, increased risk of end-stage renal disease (ESRD), and death - all common outcomes in CKD. CKD-PSIs have been established in prior work by the investigators of this study with the help of an expert panel but it is not known how commonly PSIs or CKD-PSIs occur or how to measure these reliably in the CKD population. Furthermore, it is not known what role poor disease recognition plays in the occurrence of such safety events. Finally, it remains to be determined whether CKD-PSIs contribute to the high frequency of adverse outcomes so common in this disease. If CKD-PSIs are common and account for a significant portion of the adverse events so common in this population, then it is possible that by reducing the incidence of CKD-PSIs, through increased disease recognition, outcomes can be improved in this patient population.
In this study, the investigators will enroll volunteers from the population with pre-dialysis CKD for the purpose of observing the frequency of CKD-PSI in the target population detected over time. The participants will be assessed annually for events that relate to CKD-PSI. The first 100 participants (Phase I) will be provided with a standard medical alert accessory (bracelet or necklace) which is commonly used to alert doctors and other providers of a patient's disease state. In this case the medical alert accessory will state "Decreased Kidney Function. For My Care, Please Visit (website) www.safekidneycare.org" Participants are asked to log onto the website using unique 4-digit identifier (ID) assigned by the PI to track the participant's use of the website and to further improve the website. Since all information on the website is available to the public, participants are not required to use the ID to access the content of the website. The website does not collect or store patient health information, except for the Internet Protocol (IP) address which provides limited information on the location of the computer used to access the website (city, state, zip, and area code).
The volunteers in Phase I will be tracked over time as to whether they use and tolerate this medical alert bracelet/necklace and for their incidence of CKD-PSI. Enrollment will continue after Phase I in Phase II (n = 250) with participants tracked on an identical study schedule for detection of CKD-PSI. All study procedures are the same for Phase II except for the medical alert accessory. The overall goal of this study will be to determine: the frequency of CKD-PSI in the target population, the acceptability of an alert device (Phase I only) intended to increase the recognition of CKD, and the contribution of CKD-PSI to the high incidence of adverse outcomes in CKD
|Study Type :
|Actual Enrollment :
|350 participants
|Observational Model:
|Time Perspective:
|Official Title:
|Does Under-recognition of Kidney Disease Affect Patient Safety?
|Actual Study Start Date :
|April 2011
|Actual Primary Completion Date :
|July 2017
|Actual Study Completion Date :
|July 2017
Phase I and Phase II
Phase I (First 100 participants):
Medical alert bracelet/necklace, Medical event diary, Medical event ascertainment, Repeated measurement of renal function and other electrolytes, Review for CKD-PSIs
Phase II (Next 250 participants):
Medical event diary, Medical event ascertainment, Repeated measurement of renal function and other electrolytes, Review for CKD-PSIs
- The Discrete Incidence of Any of the Chronic Kidney Disease Patient Safety Indicators (CKD-PSIs) Endorsed by the Consensus Expert Panel [ Time Frame: at the end of study (up to 4.25 years, depending on participant enrollment date) ]
The discrete incidence of any of the following CKD-PSIs endorsed by the consensus expert panel:
Class I events: Incidence of patient reported adverse events related to medical care or medicines incuding: Falling, Bleeding, Edema, Angioedema, Confusion or altered mental status, Rhabdomyolysis
Class II events: Incidence of adverse events detected at annual study visits such as: Hyperkalemia, Hypokalemia, Hypoglycemia, Hyperglycemia, Orthostatic Hypotension, Hypotension, Hypertension, Bradycardia
Class III events: Incidence of usage of medications or agents to be avoided in CKD and Incidence of improperly dosed medications in CKD
- Rate of All-cause Hospitalization [ Time Frame: at the end of study (up to 4.25 years, depending on participant enrollment date) ]Hospitalizations (following enrollment); including length of stay and safety events during hospitalization until time of end of study.
- Change in Renal Function From Baseline [ Time Frame: at the end of study (up to 4.25 years, depending on participant enrollment date) ]Renal function with estimated glomerular filtration rate (eGFR) based on serum creatinine measured annually until time of end of study.
- Number of Participants With End-stage Renal Disease (ESRD) Defined as Need for Renal Replacement Therapy (Dialysis or Transplant) [ Time Frame: at the end of study (up to 4.25 years, depending on participant enrollment date) ]ESRD defined as the need for renal replacement therapy with either dialysis (hemodialysis or peritoneal) for 3 months or more; or renal transplantation up until the time of end of study.
- Number of Deaths Among Participants (All-cause) [ Time Frame: at the end of study (up to 4.25 years, depending on participant enrollment date) ]determined until end of study.
Biospecimen Retention: Samples Without DNA
At each yearly research clinic visit (up to 4), 30 cc (6 teaspoons) of blood will be processed and stored for future assays related to kidney function.
At first research clinic visit, 9 cc urine will be processed and stored for future assays related to kidney function.
At each yearly research clinic visit, 1 swab of both nares, 1 pharyngeal swab and 1 skin swab will be obtained, processed and stored with future testing for multiple antibiotic resistant (MAR) organisms.
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.
|Ages Eligible for Study:
|21 Years and older (Adult, Older Adult)
|Sexes Eligible for Study:
|Accepts Healthy Volunteers:
|Sampling Method:
|Non-Probability Sample
Inclusion Criteria:
- estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2 (using Modified Diet in Renal Disease (MDRD) equation) based on the 2 out-patient serum creatinines obtained within the last 18 months and at least 90 days apart
Exclusion Criteria:
- <21 years of age,
- Expected to need dialysis within 12 months after time of enrollment,
- Expected to die within 12 months after time of enrollment,
- Unable to provide informed consent, or is a
- Prisoner
- Skin sensitivity or allergy to stainless steel and sterling silver (Phase 1 only)
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01407367
|United States, Maryland
|Baltimore VA Medical Center
|Baltimore, Maryland, United States, 21201
|University of Maryland Medical System
|Baltimore, Maryland, United States, 21201
|Principal Investigator:
|Jeffrey C Fink, MD, MS
|University of Maryland, Baltimore
Documents provided by Jeffrey Fink, University of Maryland, Baltimore:
|Responsible Party:
|Jeffrey Fink, Associate Professor, Nephrology, University of Maryland, Baltimore
|ClinicalTrials.gov Identifier:
|Other Study ID Numbers:
R01DK084017 ( U.S. NIH Grant/Contract )
|First Posted:
|August 2, 2011 Key Record Dates
|Results First Posted:
|November 6, 2018
|Last Update Posted:
|October 18, 2019
|Last Verified:
|October 2019
patient safety
chronic kidney disease
medical errors
Kidney Diseases
Renal Insufficiency, Chronic
Urologic Diseases
Renal Insufficiency


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What Atwal Eye Care Can Do For You
- Motto: "Change the way you see"
- Founded: 1980
- Led by: Dr. Amar Atwal
- Why They're Unique: Atwal Eye Care/Buffalo Eye Care Associates offers a wide variety of designer frames and the latest technology in lenses. Their licensed opticians will help you select the frame and lenses that best suit your lifestyle. They participate with many insurance companies, such as Community Blude, Spectera, Vision Service Plan (V.S.P) NVY, Eye Med, Univera, and Independent Health.
- They Can Answer Questions Relating to: Laser vision correction, allegretto wave eye q, cataract surgery, glasses and contacts.


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Generally when I think about a new topic a lot of ideas pop into mind. I've made the best attempt to semi-formalize this tendency of mine through an iterative process of writing and culling ideas. This blog post is the result of the only novel idea I've had regarding neuroscience and the singularity that I didn't end up trashing because it sounded stupid or strange a week later.
Now I'm gonna go out on a crazy limb here and say that I think one of the motivating goals of neuroscience (insofar as a "science" can be said to have a "goal") is to understand how the human brain—by which I mean the biological mass of fat, water, proteins, and amino acids—can give rise to what we perceive or interpret as consciousness, self-awareness, intelligence, and emotion (hereafter: "cognition"). And I think that in all likelihood we neuroscientists will eventually have to move beyond the currently-dominant paradigm of event-related behavioral experimentation combined with neuroimaging if we want a true and accurate scientific model of the human brain and cognition.
Okay, with that established: Where to from here? How can we proceed? Well there are researchers who are already well underway in building digital "brains" built using biologically-constrained rules. I've already talked a little bit about the Blue Brain Project which is one such endeavor (that I tritely summarized by saying that "thinking that modeling neurons makes a brain is like thinking that soldering together transistors makes a MacbookPro"... maybe a bit harsh). Another effort is being led by Eugene Izhikevich, who gave an excellent talk at Berkeley a few years ago where he showed a video of his large-scale neuronal model running for about one second of "real world" time.
So why try and build a digital brain? Well if we are going to understand how all of these intricate pieces work together we're going to need a better way to run neuroscientific experiments. Research on animals and humans involves many uncontrolled (and uncontrollable) variables which is why there are still so many big, open questions in the field (e.g., Nature/Nurture, the biological basis for psychological disorders, etc.). The best experiment is one where all variables are known and controlled for. Of course this is currently impossible in human neuroscience, but if we could build a biologically-plausible digital brain we might be able to conduct such an experiment.
On the flip side, we might not be able to build such a brain model without bootstrapping the brain from smaller, more tractable elements. This would be the neuroscientific equivalent of proof by exhaustion in mathematics where we would try all possible combinations of neuronal connectivity, synaptic plasticity, coding models, etc. to see which combination matches best the observed biological findings.
Regardless of how digital brains are used, I believe they pose a potential philosophical problem for researchers: what is our ethical responsibility with regards to activating a digital brain? What about deactivating it? I don't think this is just idle navel-gazing (omphaloskepsis!); I believe that a digital brain will be created (though I'm agnostic with regards to the time-scale of when). I believe that now is the best time to consider these kinds of ethical issues. Best to be proactive in this regard. After all, scientists are often criticized for allowing technology to exceed our humanity (as Einstein is oft-quoted as having said).
If we assume that our cognition and consciousness reduces to physical properties, and that those physical properties can be digitally represented and recreated, then in theory I could create a digital person. That person could be a copy of someone specific or it could be a random combination of neurons built in a person-like way. It doesn't matter for this argument.
Currently we can combine such neuronal elements in a crude manner that are based on—but are unlike—real animal brains. Currently there is no ethical problem in simulating millions of interconnected neurons. But what about when these models improve? What about when the models become 90% human? 99%? At what point do we say that the models are human-like enough that by stopping them we're effectively quenching a life?
This issue gets at the root of many philosophical problems: what are life and intelligence? What is consciousness? What are our ethical responsibilities as scientists? This is not unlike the current debate regarding animal research. To paraphrase Bill Crum's correspondence to Nature:
the stronger the evidence that [digital brains] provide excellent experimental models of human cognition, the stronger the moral case against using them for... experiments.


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Potato Gratin
2 cups whipping cream
1 cup creme fraiche
1 large garlic, minced
3 1/2 pounds russet potatoes, peeled, very thinly sliced
1 1/3 cups Gruyere cheese (about 5 ounces)
Slice the peeled potatoes, thinly. I have been using the Borner V-Slicer Mandoline
See here:
Do not wash the potato slices, you want the starch.
If cooking that day, preheat oven to 400.
Butter 13x9x2 inch glass baking dish.
Bring cream, creme fraiche and garlic to boil in heavy large sauce pan over medium heat.
Add sliced potatoes and cook until liquid returns to boil, about 4 minutes.
This takes time, but it makes for a much better dish. Take saucepan off heat and one at a time lay the potatoes, slightly overlapping, in rows in the buttered baking dish. After 2 layers, add a bit of the cream mixture and season generously with salt and pepper. Do another 2 layers, again do the potatoes one at a time and more of the cream mixture and season with salt and pepper. The rest of the potatoes should make the final two or three layers, add the rest of the cream mixture and again season with salt and pepper.
This can be done a day ahead and refrigerated covered with foil overnight.
Take the gratin out of the refrigerator and let come to room temperature, about 45 minutes to an hour.
Preheat oven to 400.
Bake the gratin covered for 45 minutes to 50 minutes or until potatoes are soft. Uncover casserole and sprinkle with the Gruyere cheese. Continue baking until potatoes are tender, cheese melts and sauce bubbles, about 15 minutes. Let stand 10 minutes and serve.


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Viewing the Tutorial
To view the tutorial, you will need the following:
- an Internet browser configured to allow pop-up windows;
- monitor resolution of 800x600 pixels or greater;
- Adobe Acrobat Reader; and
- Adobe Flash 8 player.
Speakers attached to the computer are not required to view the tutorial. However, they are necessary if you want to hear the audio narration that goes with each demonstration.
How do I know if my browser will allow pop-up windows?
This tutorial makes heavy use of pop-up windows. This makes it easier for you to get additional information if you want and to return to the main page of each module without having to use the browser's Back button.
How do I know my monitor's resolution?
Go to the Monitor Resolution section of Tech Tips for help determining your monitor's resolution.
The minimum monitor resolution of 800x600 pixels is recommended because the CDC website is 800 pixels wide. If you use a narrower width resolution, you will have to scroll side to side, as well as up and down.
How do I get the free Adobe Acrobat Reader?
You can download the free Adobe Acrobat Reader from Adobe's website at http://www.adobe.com/products/acrobat/readstep2.html.
All NHANES documentation is in Acrobat .PDF format. You will need the Reader to view and read the documentation that accompanies the data files.
How do I get the free Adobe Flash 8 or greater player?
You can download the free Adobe Flash player from Adobe's website at http://www.adobe.com/shockwave/download/download.cgi?P1_Prod_Version=ShockwaveFlash&promoid=BIOW. (See: Adobe Flash Player section of Tech Tips for more information.)
All of the tutorial animations are in Flash .SWF format. To view them you will need the Flash player. However, you do not have to view the animations to complete the tutorial, they are an additional method of delivery if you want to view them.
Running Sample Code
These requirements apply only to modules with sample code. You must have a software license to run these SAS and/or SUDAAN on your personal computer. If you do not wish to run the code in the tutorial you may view the demonstration of the code instead. Program code used in this tutorial follow procedures available in SAS 9.2, SAS 9.1, or SAS 8.0; and SUDAAN 9.0 or SUDAAN 8.0; and Stata 10.1 or Stata 9.0.
- SUDAAN (Version 9.0; Research Triangle Institute, Research Triangle Park, NC) and/or
- SAS Version 9.1 (Version 8.02; SAS Institute Inc, Cary, NC) statistical software and/or
- Stata Version 10.1; Version 9.0 (StataCorp, College Station, TX)
The sample code is all SAS, SAS-executable SUDAAN, or Stata code and the sample datasets provided in this tutorial are SAS or Stata datasets for Windows. If you are using a Macintosh or Unix computer, you should download the data files from the NHANES web pages, as these are in SAS transport format (.XPT), and can be extracted and used on Windows, Macintosh or Unix computers.
Contact Us:
- National Center for Health Statistics
3311 Toledo Rd
Hyattsville, MD 20782
- 1 (800) 232-4636
- firstname.lastname@example.com


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Nearly 400 LBD caregivers listened in on a recent scientific webinar on dementia with Lewy bodies (DLB) aimed at physicians and researchers, hosted by the Alzheimer Research Forum. Before and after the event LBD caregivers submitted over 100 questions on LBD clinical care to the panelists, which included Dr. Ian McKeith, Dr. James Galvin and Dr. James Leverenz who are members of LBDA's Scientific Advisory Council. (To view the webinar, click here.)
Due to the tremendous caregiver response, AlzForum turned to LBDA to provide answers to a broad assortment of caregiver questions. We are pleased to provide the first installment of answers to some of the most frequently asked caregiver questions.
Quick Links:
Symptoms and Diagnosis
Living with LBD
Physician Awareness
Caregiver Information
What is LBD?
Lewy body dementia (LBD) is a progressive neurological disorder. LBD is an umbrella term for two related diagnoses - Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB). The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms.
Do all people with DLB hallucinate? My dad has a recent DLB diagnosis but does not hallucinate, thank goodness. Does this mean his diagnosis is wrong?
This is great question. Not everyone with LBD hallucinates, though many will at some point. Likewise, not all patients will exhibit the other clinical signs associated with LBD. The diagnostic criteria requires a person to have dementia plus only TWO of any of the following: hallucinations, parkinsonism, fluctuating cognitive abilities, REM sleep behavior disorder, a severe sensitivity to antipsychotic medications, or an abnormal result on a brain scan that detects levels of dopamine.
Are the hallucinations/delusions the main difference between DLB and Alzheimer's? And can people presenting with delusions otherwise score quite well on standard cognitive testing, like the MMSE?
The MMSE is a commonly-used test to detect a general decline in cognitive function and memory. Because people with LBD typically fluctuate in their cognitive abilities and often perform well on the MMSE early in the disease, the MMSE is not sensitive enough to diagnose DLB, nor is it adequate by itself to diagnose Alzheimer's disease (AD).
There are a number of distinguishing features that help differentiate DLB from AD. For example, the cognitive profile in DLB features deficits in executive functioning, such as problem solving, abstract thinking, and reasoning, while Alzheimer's features a predominant decline in memory. Hallucinations occur earlier in Lewy body dementia, while they appear later in Alzheimer's disease. Severe sensitivity to antipsychotic medications used to treat hallucinations is common in LBD, but not so in Alzheimer's disease. REM sleep behavior disorder is common in DLB, but not in Alzheimer's. For a more detailed discussion, please visit LBDA's webpage on LBD symptoms.
Could you address sleepiness? My husband is very tired during the day. Are there ways to combat these symptoms of the disease?
Sleep disorders like sleep apnea, restless leg syndrome and REM sleep behavior disorder are common in LBDs. Sleep disorders often prevent the person with LBD and their caregiver from getting sleep. Excessive daytime sleepiness, despite adequate rest at night, is also common in LBD. Ask your physician to order a sleep study to identify and treat ALL underlying sleep disorders. It is also important to review sleep hygiene such as use of alcohol, caffeine, chocolate or other substances late in the day. Many foods and over the counter medications can have effects on sleep. If excessive daytime sleepiness is a severe problem, a sleep specialist may recommend the use of medication such as a stimulant to promote daytime arousal.
Does anyone with LBD ever recoup mental capabilities?
There are a number of things that can impact cognition in LBD in the short run. Cognitive abilities fluctuate in LBD, making a person appear to function better on one day, and worse on another. Illness, pain, infection, sleep disruption and other medical issues can impact cognition negatively as well. Some people with LBD respond to treatment with cholinesterase inhibitors (originally intended for Alzheimer's disease) very positively. But because LBD is a progressive disease, there is irreversible long term cognitive decline.
Are we getting any closer to confirming diagnosis prior to autopsy?
Right now, 2 out of 3 cases of dementia with Lewy bodies go undiagnosed, and there are no widely-available tests to definitively diagnose it. There are some very promising biological indicators in development to identify LBD through cerebral spinal fluid, blood, and brain imaging; however these are still several years from being ready for clinical use.
My father passed away from DLB, or so we thought. We donated his brain for research and the autopsy came back as having no Lewy bodies. Do LBD and Alzheimer's mimic each other?
Alzheimer's disease (AD) and Lewy body dementias are both neurodegenerative diseases and share many overlapping symptoms. The clinical criteria permit correct classification the majority of time however, the criteria are not perfect. Among the most common cause of disagreement between autopsy reports and clinical diagnosis is when an autopsied LBD cases was diagnosed with AD. Less commonly a clinically diagnosed LBD case will really be caused by AD. This highlights the need for more research to develop better clinical diagnostic tests.
How do I find a local neurologist who specializes in DLB?
Family physicians are a great, first-step resource if you are experiencing any cognitive, emotional, behavioral or physical changes. However, neurologists generally possess the specialized knowledge to diagnose specific types of dementia or movement disorders, as do geriatric psychiatrists and neuropsychologists. However, these specialists may require a referral from your primary care physician. Geriatricians, who specialize in treating older adults, are also frequently familiar with the different forms of dementia.
If you have access to a hospital affiliated with a medical school, the hospital may have a clinic specializing in dementia or movement disorders where you may find a high level of diagnostic and treatment capability.
The Lewy Body Dementia Association's Scientific Advisory Council is comprised of leading experts in Lewy body dementias. Click here to learn more.
What is the best treatment for DLB?
Right now, cholinesterase inhibitors are the gold standard in LBD treatment. People with LBD may obtain more benefit from these drugs than people with Alzheimer's disease. Treating sleep problems is also important, as any unresolved sleep disorders may increase confusion or behavioral problems. And very conservative treatment of parkinsonism or hallucinations is important in order to avoid medication side effects. Other symptoms, such as depression and changes in blood pressure regulation, should also be evaluated and treated.
Is DLB responding to any meds at this point? If so, which ones should be considered and what side effects are associated with them?
The symptoms of LBD are often quite responsive to treatment. Information on the most common LBD treatment options can be found at by clicking here.
Side effects vary for each person, but the most typical are as follows: Cholinesterase inhibitors, used to treat cognition, sometimes cause gastrointestinal upset. A recent report suggests that cholinesterase inhibitors may increase the risk of fainting spells (syncope). Levodopa, used to treat movement problems, can sometimes cause or worsen hallucinations. And many people with LBD are very sensitive to medications used to treat hallucinations.
NOTE: Up to 50% of patients with LBD who are treated with any antipsychotic medication may experience severe neuroleptic sensitivity, such as worsening cognition, heavy sedation, increased or possibly irreversible parkinsonism, or symptoms resembling neuroleptic malignant syndrome (NMS), which can be fatal. (NMS causes severe fever, muscle rigidity and breakdown that can lead to kidney failure.)
Is donepezil (Aricept) the best drug to counter memory loss in DLB? If not, what is?
There is no evidence that any one cholinesterase inhibitor is better than another for LBD cognitive symptoms.
Is Exelon likely to exacerbate hallucinations in DLB patients?
No, in fact, that class of drugs (cholinesterase inhibitors) has been shown to reduce hallucinations and other behavioral disturbances.
Does memantine (Namenda) have value for a DLB patient?
While there has been some conflicting data on memantine in LBD, new research from a small clinical trial shows memantine may be beneficial in LBD. Data from a larger trial is currently being analyzed and will provide a clearer picture in the near future.
It has been suggested to me that quetiapine (Seroquel) is the only medication that should be given to my husband who has DLB when he has "bad behavior." What is your opinion and suggestion for the best medication for these behavioral problems? They make caregiving much harder.
The first course of treatment for LBD, cholinesterase inhibitors, has been shown to be effective in treating hallucinations and other psychiatric symptoms of LBD. However, the effect is not immediate. If hallucinations they are disruptive or upsetting, physicians may recommend a cautious trial of a newer antipsychotic medication.
Your doctor is showing caution for a good reason. Severe sensitivity to neuroleptics is common in LBD. Neuroleptics, also known as antipsychotics, are medications used to treat hallucinations or other serious mental disorders. While traditional antipsychotic medications (e.g. haloperidol) are commonly prescribed for individuals with Alzheimer's with disruptive behavior, these medications can affect the brain of an individual with LBD differently, sometimes causing severe side effects. For this reason, traditional antipsychotic medications like haloperidol should be avoided. Some newer 'atypical' antipsychotic medications like risperidone may also be problematic for someone with LBD. Quetiapine is preferred by some LBD experts. If quetiapine is not tolerated or is not helpful, clozapine should be considered, but requires ongoing blood tests to assure a rare but serious blood condition does not develop. Hallucinations must be treated very conservatively, using the lowest doses possible under careful observation for side effects.
In what age range does DLB begin?
LBD is most often seen in the over-60 population, though like other neurodegenerative diseases, there is a small percentage of people who experience and earlier onset in their 40's and 50's.
What does the typical progression of DLB look like? Can you please describe the stages of the disease, so I know what to expect as it progresses?
Unlike Alzheimer's disease, which has clearly defined stages, LBD progression is much less predictable. Symptoms often appear in varying combinations and severity, making each person's experience unique. The prognosis is also different for each person and may be affected by your general health or the existence of unrelated illnesses. Because LBD progresses at varying rates for each individual, it is not possible to determine how long someone may live with the disease. The average duration of LBD is typically five to eight years after the onset of obvious LBD symptoms, but may range from two to twenty years. It is important to remember that this is a disorder that progresses gradually over years, not days or months.
My father was just diagnosed with DLB. It came on suddenly, though looking back we see other signs that we didn't realize at the time are a part of the disease. He doesn't know he has DLB. I don't want to tell him. Should I?
That decision may depend on the cognitive ability and temperament of the individual with LBD. While some people may find a dementia diagnosis distressing, a recent study indicates that most individuals actually find some relief in knowing the diagnosis and in understanding how this relates to their changing abilities.
My father has DLB. It wasn't until I went with him to a doctor's appointment that he got diagnosed (turns out he wasn't telling the whole story to his doctor). What I find most difficult in caring for my father is his thinking he is all right and everyone else has a problem. Patience is a great asset for repeating directions, plans, and whatever comes up. Is there anything else we can do to help him keep focused and slow the disease?
Not everyone with LBD retains an insight into why they cannot do some of the things they used to do. So maintaining a meaningful and structured life may benefit both the person with LBD and the family caregiver. Encourage him to be an active partner with you in a comprehensive treatment program, especially by remaining socially and physically active, as they are both good for overall cognition. And treatment with a cholinesterase inhibitor is highly recommended.
My husband's cognitive abilities go up and down like a yoyo. Is this "normal"? He was diagnosed three years ago with Alzheimer's, but has since been told he has LBD with Parkinson's symptoms. He is sometimes better now than he was three years ago.
As opposed to calling something "normal" or "abnormal", it is probably better to comment that the "yoyo-ing" or fluctuating course of your husband's disease is consistent with the cognitive fluctuation feature of LBD. His partial improvement may be attributed in part to his early treatment when he was diagnosed with AD.
How do I get family members to understand that some of the behaviors from our mom is the disease and not mom?
The best thing you can do is to educate them about the disease. Send them to the Lewy Body Dementia Association's website to learn more about LBD and to hear the stories of other families like yours, posted at LBDA's online community.
I have a family pattern of DLB. Can I prevent getting it?
Most dementias, including Alzheimer and Lewy body diseases are not genetic. Because research has not yet unlocked enough answers about LBD's root cause, we do not know yet how to prevent it. Living a heart-healthy lifestyle has been shown to reduce the risk of all forms of dementia, as has staying cognitively and socially active and physically fit.
My wife is now diagnosed with DLB after having had PD for 11 years. I need to know what I am in for. Please describe "rapid decline" regarding future months or years.
Technically this would be a case of PD dementia (PDD). Both PDD and DLB are Lewy body dementias – the difference being largely what the first symptom presentation was. Most individuals experience a gradual disease progression lasting well over 5 years, though a small percentage of people experience the full disease progression in as few as 2 years.
My husband has had two quadruple bypass surgeries, the last one in 1994 at age 60. Months after the last surgery he went back to work but the math he had to do for his job was too much for him. He just couldn't do it. He had to give up a job he loved and had been doing for over 30 years. He also made a mess of our checkbook many times. He was most difficult to live with, as opposed to normally being a kind, loving, and gentle man. He had vascular surgery again four times in 1997 and was off-the-wall difficult to handle. He was semi-conscious for days and used his hands to write in the air. He had a nurse with him 24/7 the first few days. He saw cats in the register overhead, etc. It was also after that that he could no longer do things around the house that he had always done. He just couldn't figure out how to do them. He finally asked me to help. I believe he began having DLB in 1994, most definitely since 1997. Is it possible that his dementia could have begun so long ago?
Sometimes DLB can have a very slow, progressive path. An illness or surgery may reveal LBD underlying symptoms that were not apparent at a clinical level, leading to a new diagnosis. People with LBD also often respond to certain anesthetics and surgery with acute states of confusion or delirium, and may have a sudden significant drop in functional abilities, which may or may not be permanent.
In addition, cerebral vascular disease is commonly co-existent with cardiovascular disease. Open-heart surgery is a tremendous stress for the body and the brain in particular. Many patients have periods of post-operative confusion, most recover but not all do.
It is always difficult to pinpoint exactly when neurodegenerative diseases begin because there is probably a period of several years where brain changes are occurring yet patients do not yet exhibit symptoms.
My father was diagnosed recently with DLB. He was in and out of different hospitals five times, then ended up in a care facility where he got better. So mom took him home and now he doesn't remember being sick. He seems fine. How can that be?
In all dementia, periods of time (particularly more recent events) may seem less clear or even forgotten. Some of these forgotten events can be quite climactic such as a recent hospitalization. In addition, certain medications can exacerbate LBD symptoms, as do pain, infection, and illness. In addition to addressing other underlying health problems, in-patient care sometimes provides the opportunity for physicians to discontinue certain medications, identify which ones may be problematic, and start them on more appropriate medication regimes.
My dad has DLB and Alzheimer's. The most distressing thing so far as a caregiver is some doctors' lack of knowledge about DLB and that DLB is different from other types of dementia when prescribing medication. Is this just my sense?
It can take many years from the time a new disease is defined and for awareness of that disease to make its way through the entire medical profession. The diagnostic criteria for DLB was first published in 1996, and while most neurologists, psychiatrists and geriatricians are becoming more familiar with it, awareness of the disease, its symptoms and treatment issues is still low among generalists and other specialties.
My wife sees a head of a clinical department at an Ivy League medical school for an eye condition. When I told him about her dementia with Lewy bodies, he asked: "What's that?" Where can I point the doctors so they can catch up on DLB?
The Lewy Body Dementia Association has just launched physician resources on their website. Physicians, nurses and other health care professionals will now find easy-to-read tables and figures on LBD diagnosis and treatment options along with family- and patient-centered publications that can be downloaded or ordered at no cost at www.lbda.org/go/physicians.
I am very much in agreement with the frustrations associated with diagnosis educating physicians! My husband was initially diagnosed with AD, which we treated for six years. Doing more reading, I discovered that he had all the symptoms of DLB. His REM sleep disorder goes back at least 30 years. He also has had no sense of smell for that many years. The Mayo clinic saw him in Scottsdale and agreed with the probable diagnosis of DLB. A well-regarded senior care physician made the statement that "while the universities may be trying to discern one type of dementia from another, they virtually all come down to Alzheimer's." Is that true?
The underlying brain pathology and symptoms are different among the many types of dementia, and there are important differences in treatment as well. People with Lewy body dementias need an early differential diagnosis to provide them with optimum care and to avoid unnecessary exposure to certain medications (like traditional antipsychotic medications, i.e. haloperidol) that may cause severe and sometimes irreversible side effects.
Many patients with LBD also have Alzheimer disease pathology at autopsy however, clinical, cognitive and behavioral features are distinct and research has shown differences in meaningful outcomes such as loss of functional abilities, nursing home placement and death.
How do I tactfully suggest that we have DLB, not Parkinson's and Alzheimer's?
If your physician is not familiar with Lewy body dementias, providing them with publications from the Lewy Body Dementia Association can provide them with the information they need to make an accurate diagnosis. You can request a physician packet be mailed to your doctor by emailing LBDA email@example.com.
What is the best way for caregivers to deal with DLB?
This is a complicated disorder with an often unpredictable course. So there are a number of things that will help. First and foremost, become educated about the disease and be prepared to educate those around you (including some medical professionals). Second, find the support you need for everyday caregiving and locate resources in your community BEFORE you need them. And last, but not least, connect with other LBD families for understanding and support. The Lewy Body Dementia Association's website, www.lbda.org, is a great place to start.
What is the best way to get DLB patients involved in activities to help stimulate them if they do not want to do them?
It is difficult to get people to do things they do not want to do, regardless of whether they have dementia. There can be many reasons for not wanting to participate; one of the more common ones is fear of the unknown. Slowly introducing a new activity in the comfort of a familiar surrounding may reduce anxiety.
Apathy (or lack of interest and motivation) is a common symptom of LBD, as is depression. Talk with your loved one's physician about whether or not there are symptoms of depression or apathy as the patient may benefit from an antidepressant medication.
Which websites are the most reputable for the latest DLB medical information?
The Lewy Body Dementia Association has a wealth of information on LBD for both families and physicians. Visit www.lbda.org. Related dementia and movement disorder organizations can also be found on LBDA's website by clicking here.
Is there a "beginner's book" for the caretaker and the family? We need to read up on what to expect, what we can do. Thanks!
The Lewy Body Dementia Association lists a number of books on LBD and related dementias on their website, which you can find by clicking here.
Is DLB hereditary?
Because DLB is biologically related to Parkinson's disease, from a genetics point of view, what holds true for Parkinson's will hold true for DLB. So, yes, a small proportion of families with DLB will have a genetic connection, but the vast majority of cases are considered 'sporadic,' meaning no genetic causes have been identified.
My husband is 66. He was diagnosed with Alzheimer's seven years ago. Four years ago after extensive testing, he was diagnosed with DLB with parkinsonian symptoms. He is on memantine (Namenda), carbidopa (Stelevo), selegiline (Zelapar) and the rivastigmine (Exelon) patch. He no longer drives and is having more trouble putting together sentences, dialing a phone, using the remote control, etc. He does mow the grass but misses a lot of it. He is now having much more trouble with grandchildren's names, etc. Do you think research is getting any closer to reversing his problems?
At this time, we don't know what causes LBD. We do know that naturally occurring proteins misfold in the brains of people with LBD but to date we do not know fully comprehend the steps that cause the proteins to misfold. Until we understand the underlying disease mechanism, we are unable to halt the progression of the disease or reverse it.
Is LBD being aggressively investigated the way that AD is starting to be? Is your research funded by the Alzheimer's funders? Should there be a movement to distinguish LBD on a fundraising level or is that counterproductive due to the disease overlap?
Research into LBD is gaining attention from both the Alzheimer's and Parkinson's disease research communities, as it represents a link between these neurodegenerative diseases. Thus, research into one of these diseases often contributes to the understanding of the others. However, LBD research funding still lags behind, despite having approximately the same patient population as Parkinson's disease.
For more information on how to contribute to LBD research, visit LBDA's website.
When my loved one passes away, should I consider allowing an autopsy to aid in research to LBD?
A brain autopsy is the only definitive way to diagnose Lewy body dementia, but an autopsy alone does not benefit LBD research. Participating in a research study that includes an autopsy is one of the best ways to contribute to the growing body of LBD knowledge.
What research agency do I contact if I am willing to participate in a study about early biomarkers of DLB?
www.ClinicalTrials.gov provides regularly updated information about federally and privately supported clinical research in human volunteers. ClinicalTrials.gov gives you information about a trial's purpose, who may participate, locations, and phone numbers for more details.
Edited by Dr. James Galvin, member of LBDA's Scientific Advisory Council


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EdMail: You are required to use it! It is the way we communicate with you.
The college assigns all students EdMail (email) accounts within a couple of days after you register for your first class. Note: if you are a former student returning after time away from school, check with the Enrollment Services Office to confirm what email address we have on file for you. Financial aid will use the address recorded in the Enrollment Services records. To activate your EdMail account, follow the steps at www.edcc.edu/edmail.
- We generally award students assuming they plan to attend school full-time (12 or more credits). You are not required to attend school full-time. See Enrollment Requirements (under "Awarding Aid" on the left) for additional information about how to notify us that you want to attend school part-time.


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Who knew? Don Draper can make a joke or two.
Suave AMC "Mad Men" star Jon Hamm made his second appearance on "Saturday Night Live" this weekend, hosting the show alongside musical guest Michael Buble in a program that poked fun at the State of the Union, "Jersey Shore" and Hamm himself.
Hamm, who stars as a slick advertising executive on the 1950s-era award-winning show, opened "SNL" with a monologue that inserted his dapper Don Draper persona into parodies of programs like "Saved by the Bell," Def Comedy Jam and the QVC Home Shopping Network.
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Stories that affect your life across the U.S. and around the world.
Hamm's monologue followed a sketch about Obama's State of the Union speech, which featured Fred Armisen as the commander in chief who enjoyed a brigade of standing ovations.
The "Mad Men" actor worked alongside "SNL" vet Kristen Wiig in several sketches, including a bit about a piano-playing twosome and a parody ad that also featured Will Forte as a unitard-clothed one-man closet organizer.
Wiig and Hamm continued the political parody with a sketch that featured Hamm as Massachusetts Senator-elect Scott Brown and Wiig as Speaker of the House Nancy Pelosi.
The actor also played alongside musical guest Michael Buble, starring in a short about "Hamm & Buble," a restaurant serving pork products and sparkling wine.
Saturday's episode also made use of tried-and-true standbys, most notably Bobby Moynihan's inspired impression of Nicole "Snooki" Polizzi from MTV's newly renewed series "Jersey Shore."
Hamm last hosted the program in 2008 alongside musical guest Coldplay.


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Trade Up: Ditch These Gadget Gifts Now
By Geoffrey A. Fowler and Joanna Stern
Let's just clear the air as we head into 2014: In the holiday buying frenzy, you might have ended up with a few tech regrets.
It's OK, Black Friday and awkward family members can do this to the best of us. That off-brand tablet in the bargain bin might have seemed like a good idea at the wholesale club. But if you have any tech gifts that sit unused after their unwrapping, you may have a problem.
We compiled our own list of gadget lumps of coal – and the diamonds you should swap them for.


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Orcas in Washington state waters will be counted and studied over the next nine months to determine whether they need to continue to be listed under the federal Endangered Species Act, the National Oceanic and Atmospheric Administration in Seattle announced Monday.
The federal listing is being challenged by an activist California-based law firm and two of its clients. The Pacific Legal Foundation, based in Sacramento, Calif., with an office in Bellevue, and two large farms in California's San Joaquin Valley are asking that the orcas be removed from the federal endangered species list.
The Center for Environmental Science, Accuracy and Reliability, based in Gold River, Calif., near Sacramento, worked with the groups on the 62-page petition.
The fact the petition will be reviewed does not mean orcas will be taken off the list, said Brian Gorman, a NOAA spokesman for the Seattle office, which is handling the request.
The agency has until next August to make a determination, Gorman said. If it decides delisting is warranted, the public would have a chance to comment before a decision is made.
"We go through a series of steps, each of which is a little bit tighter than the preceding one," he said.
The endangered status of the state's orcas has been given by government officials as a reason for restrictions on the amount of water available for irrigation from California rivers because they bear salmon that migrate north to Washington state waters where they form part of the orcas' diet, said Damien Schiff, an attorney for the Pacific Legal Foundation in Sacramento.
The California farms seeking the change in orca status are Empresas del Bosque in Fresno and Merced counties and Coburn Ranch near Dos Palos. Both rely on water from the Sacramento and San Joaquin river systems, Schiff said.
"New genetic analyses done since 2010 show that the orca whales (in Western Washington waters) are not genetically distinct from orca whales anywhere else in the world," he said.
The orcas were listed in 2005 as endangered under the federal Endangered Species Act. The listing covers three pods of orcas living in the Salish Sea between the southern end of Puget Sound and the Strait of Georgia in British Columbia. At the time of the listing, the pods numbered 89 orcas. Now there are 86, according to NOAA.
The orcas landed on the endangered list two years after region's chinook salmon were listed as threatened under the same federal law.
Just a few years earlier, NOAA had turned down requests to list the orcas, using the same arguments that the petitioners are using today — that the populations are not genetically distinct, Gorman said. After losing a court battle in 2003, NOAA researched the issue further and found that the Washington state orcas were biologically and socially distinct from neighboring populations, he said.
"This killer whale population doesn't seem to interbreed with any other," Gorman said.
Schiff of the Pacific Legal Foundation said that in addition to the orca listing's effect on the farms, "often times the law is used inappropriately to injure private property rights and other individual liberties and one way to keep this from happening is to make sure the decisions are based on the best possible science."
The firm also has filed separate suits over Obamacare and numerous other environmental regulations, according to its website.
"We're an action organization, battling in courtrooms across the country for limited government, property rights, free enterprise, and common sense in environmental regulations," the website says.
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Hello all, first time posting here.
I Recently picked up a platinum complete edition of neon genesis, and while I am pretty confident its is legit, I was hoping to get some second opinions. I linked to a google album of images I took of it (sorry for doing this in probably the most incorrect way possible)
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This page can be viewed at http://www.historycommons.org/context.jsp?item=a97maragingkang
This is a scalable context timeline. It contains events related to the event 1997: Shipment of Specialist Steel to North Korean Proliferator in Pakistan Intercepted in Britain. You can narrow or broaden the context of this timeline by adjusting the zoom level. The lower the scale, the more relevant the items on average will be, while the higher the scale, the less relevant the items, on average, will be.
After the BVD, a Dutch intelligence agency, informs the CIA that it intends to arrest A. Q. Khan over the passage of nuclear secrets to Pakistan (see Mid-October 1975), the CIA tells the Dutch to let Khan continue with his activities. Former Dutch Minister of Economc Affairs Ruud Lubbers will say, "The Americans wished to follow and watch Khan to get more information." Lubbers questions this and the CIA tells him to block Khan's access to the secrets, which the Dutch do by promoting him to a job where he no longer has access to sensitive data from the uranium enrichment company Urenco. Lubbers will later suggest that the real reason the US does not want Khan arrested is because of its interest in helping Pakistan, an enemy of Soviet-leaning India. Because Khan no longer has access to the sensitive data after his promotion, the CIA cannot find out anything by monitoring him. In addition, the promotion alerts Khan to the fact he may be under surveillance, and he flees to Pakistan in mid-December. Authors David Armstrong and Joe Trento will later comment: "What no one yet realized was that Khan had already absconded with the plans for almost every centrifuge on Urenco's drawing board, including the all-important G-2 [centrifuge]. It would prove to be one of the greatest nuclear heists of all time." (Armstrong and Trento 2007, pp. 54)
British Customs and Excise intercepts a shipment of maraging steel bound for Pakistan via Moscow at Gatwick Airport in London. The steel could be for use in Pakistan's nuclear weapons program and was to be delivered to Kang Thae Yun, a North Korean official who facilitates nuclear co-operation between Pakistan and his government. When it investigates Kang, Customs and Excise discovers that he has also brokered a deal to buy maraging steel from the All-Russian Institute of Light Alloys in Moscow, and the purchase was made on behalf of Pakistan. (Levy and Scott-Clark 2007, pp. 279)
The US begins to send Pakistan a series of demarches complaining about its nuclear proliferation activities. The sending of the demarches follows the receipt of intelligence about nuclear deals between Pakistan and North Korea. North Korea's plutonium program is in abeyance at this time, but it has begun a uranium enrichment project and the US is aware of this. However, according to State Department official Robert Einhorn, Pakistani nuclear scientist A. Q. Khan is never mentioned in the demarches, at the CIA's request. The CIA wants Khan's proliferation network to continue to run and is worried that mentioning him in them would tip him off to what the CIA knows. (Levy and Scott-Clark 2007, pp. 280)
Western intelligence agencies learn that Kang Thae Yun, a North Korean diplomat who facilitates nuclear co-operation between his government and Pakistan, is involved in negotiations between the Pakistan-based Tabani Corporation and a Russian company that makes mass spectrometers, lasers, and carbon fiber. They also learn he is discussing a purchase of maraging steel, which can be used in a nuclear program, but this steel is for his own government. The knowledge spurs MI6 and the CIA to increase their efforts to find out whether the North Koreans have established a cascade to weaponize uranium using technology obtained from Pakistani nuclear scientist A. Q. Khan. (Levy and Scott-Clark 2007, pp. 279-180)
The British intelligence service MI6 forms the opinion that Pakistani nuclear proliferator A. Q. Khan is using his North Korean connections in an attempt to purchase items for resale. The items include rare metals, magnets, and other difficult-to-source products. The purpose is to establish an export stock of goods that Khan can sell on to other countries. MI6 informs US intelligence agencies of its belief and the reasons for it (see 1997 and February 1998). (Levy and Scott-Clark 2007, pp. 279-280)
A Korean diplomat's wife named Kim Sa-nae is shot dead outside a guest house associated with Pakistani nuclear scientist A. Q. Khan in Islamabad, Pakistan. Government officials claim it was a tragic accident and that she was simply caught in a crossfire resulting from a domestic dispute. However, the US discovers that the woman had been shot execution-style and was the wife of Kang Thae Yun, a North Korean who was the economic counsellor at its embassy in Pakistan. Kang is already on the US nuclear watch-list and, based on interviews conducted by the CIA, the US comes to believes that Pakistan's ISI had her killed because she was preparing to pass on sensitive material about nuclear transfers between Pakistan and North Korea to Western contacts. This theory is supported by the fact that Kang represented the Changgwang Sinyong Corporation (CSC), also known as the North Korean Mining Development Trading Corporation, which had shipped No-dong missiles to Pakistan in 1994 (see January 1994). In addition, defectors have said that the most important job of North Korean embassies around the world is to help efforts to seek nuclear technology and this was Kang's primary role in Islamabad, where he frequently visited Khan. (Levy and Scott-Clark 2007, pp. 276-277) Kang disappears from Pakistan around the time his wife's body is flown home to North Korea (see Mid-June 1998).
Pakistani nuclear scientist A. Q. Khan takes five pieces of luggage, including two large crates that nobody is allowed to check, to North Korea. The crates contain P-1 and P-2 centrifuges for enriching uranium, drawings, technical data, and uranium hexafluoride, which is needed to start the uranium enrichment process. Khan takes the goods on a plane belonging to Shaheen Air International, which makes regular flights between North Korea and Pakistan to facilitate nuclear technology transfers (see (1998 and Possibly After)). The stated purpose of the flight is to carry the body of Kim Sa-nae, a North Korean diplomat's wife who was recently murdered in Pakistan (see Early June 1998). The diplomat, Kang Thae Yun, is said to be involved in North Korea's nuclear proliferation attempts and disappears around the time of this flight. (Levy and Scott-Clark 2007, pp. 278)
The White House convenes a small team of senior officials to look behind the nuclear program of North Korea, which appears to be attempting to start a uranium enrichment program, and focuses on Pakistani nuclear scientist A. Q. Khan. Khan travels to Pyongyang several times a month and, according to authors Adrian Levy and Catherine Scott-Clark, he is the "most visible common denominator" in Pakistan's proliferation network and "a flag to be followed." Levy and Scott-Clark point out that, although the US has been aware of Khan's activities for over two decades (see November 1975), this is the "first serious attempt at interdicting the Pakistani operation."
Experienced Officials Head Team - The officials include Robert Gallucci, President Clinton's special envoy on ballistic weapons and WMD, who has been monitoring Pakistan's nuclear program for 20 years and had helped negotiate an agreement with North Korea in 1994. Robert Einhorn, assistant secretary of state for non-proliferation, Karl Inderfurth, assistant secretary of state for South and Central Asian affairs, and Gary Samore, a senior director for non-proliferation at the National Security Council, are also on the team.
Problems - However, there are some initial problems. For example, the officials already have so much work that one will characterize it as a "five minute [info] dump on Khan." Levy and Scott-Clark will comment: "There was a surfeit of material, much of it higgledy-piggledy, since over the years no organized overview had been taken of Pakistan's illicit trade. Instead, a multiplicity of agencies in intelligence, defense, and foreign affairs had all assigned analysts to work on the Khan conundrum, stovepiping what they discovered, so no one agency knew everything."
More than Missiles - The group soon receives evidence showing that the dealings between North Korea and Pakistan do not involve just missiles, but also uranium enrichment technology (see 1997, 1998, (1998 and Possibly After), February 1998, February 1998 or Shortly After, Early June 1998, and Mid-June 1998). Einhorn will later say: "In 1998 we began to get some information of North Korean-Pakistani deals that went way beyond missiles. There was a nuclear dimension to this arrangement. There were Pakistani and North Korean weapons specialists getting together, including people from KRL [Khan Research Laboratories]. There was a pattern to the interactions." (Levy and Scott-Clark 2007, pp. 278-280)
Aircraft operated by Shaheen Air International, an airline run by Pakistan's Air Chief Marshal Kaleem Saadat, and Pakistani air force C-130 transporters make regular trips between North Korea and Pakistan. They carry technology the countries are exchanging for work on their missile and nuclear weapons programs. By January 1998, the US is observing at least nine flights per month between Islamabad and Pyongyang. (Levy and Scott-Clark 2007, pp. 278, 180) It is unclear how long these flights continue, although they presumably stop no later than when A. Q. Khan makes a public confession of his activities in 2004 (see February 4, 2004).
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text: I went down to Livestock for the Smile On Your Brother show last night and snapped some photos. It's up for two more nights – so you better catch it while you can. If you see a board you want, you can contact Annie or Mike here and place a bid. The auction closes near the end of October.


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Armour Bra Protegee B
Whether you're an A or a DD, an ill-fitting bra can rattle your focus, and even your self-confidence. We tested hundreds of prototypes, enlisted the experts, and asked the athletes. The result is the next-generation bra sized for both band and cup to deliver the perfect performance fit. No more digging, no more bunching, and—most importantly—no more bouncing. Just a comfortable, confident fit that changes the game for good.


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Tampa Bay Rays select Lumastream, local tech company, for lighting upgrade to Tropicana Field
ST. PETERSBURG, FL -- The Tampa Bay Rays announced today that they have selected LumaStream, Inc. (www.lumastream.com), the industry leader of Intelligent LED Lighting Systems, to upgrade the fan experience at Tropicana Field. This three-year agreement includes the replacement of lighting in concourse areas, helixes and multiple luxury suites. LumaStream was chosen for the quality and controllability of their lights and their strong return on investment.
"The Rays are proud to partner with LumaStream and showcase their game-changing technology in critical areas of the stadium," said Rays Senior Vice President Mark Fernandez, who views the agreement as a validation of the innovative technology that is thriving in the Tampa Bay business community. "It is remarkable that we have this world class company right here in St. Petersburg."
"We are thrilled to be aligned with the Rays organization and to install our technology," said Eric Higgs, CEO of LumaStream. "The Fan Experience will be enhanced by lighting scenes with interactive control for runs batted in and home runs. The future of stadium lighting is energy efficient, controllable and high quality LEDs. Kudos to the Rays for being on the leading edge."
LumaStream will celebrate the season opening game in the Left Field Terrace Suite "Powered by LumaStream", when the Rays play the Baltimore Orioles on April 2, 2013 at 3:10 p.m.


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