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Anti-Psychotics Don't Kill Patients. Lack Of Health Care Does
In my last blog post, I talked about the shameful way that many with schizophrenia are treated (or not treated) for their other co-existing medical problems, like diabetes. There is ample evidence that this lack of proper medical treatment and the failure to exercise preventative measures for conditions like cardiovascular disease results in a shortened life span.
The latest research just released from California show that women with serious mental illnesses are not routinely screened for cervical cancer compared to women without mental illness.
(Photo: Istockphoto via Getty Images)
Despite the weight of all this evidence, the common belief among the anti-psychiatry, anti-medication group is that this reduced life expectancy for those with serious mental illness is the result of the medication they are given. That was one of the comments on my previous blog and it is the opinion of journalist Robert Whitaker of Mad in America fame.
The question we should be asking is what is mortality for those who do not take anti-psychotic medication, which is the standard starting treatment for people diagnosed with schizophrenia. If anti-psychotics are responsible for the shortened life span, then not taking them when diagnosed should result in less mortality. The answer to that can be found in one commentary published this month, in the Lancet, and a study published in Schizophrenia Bulletin. Mortality is quite a bit higher in those not properly treated with anti-psychotics than in those properly treated.
In the British Journal, the Lancet, author Cherrie Ann Galletly states that "Mortality in patients with schizophrenia seems to be highest among those who do not take antipsychotic drugs." The shocking extent of that mortality was demonstrated in a new U.S. study that just appeared in Schizophrenia Bulletin.
Those who died in the 12-month period received the least amount of outpatient care.
Michael Schoenbaum and colleagues examined the long-term patterns of treatment for those with health insurance in the U.S. aged 16-30 receiving a first observed diagnosis of psychosis in 2008-09. They limited their sample to only those with health insurance because, sadly, not having health insurance is itself a barrier in the U.S. to receiving proper medical care. Those identified for the study were followed for a year to find information on mortality, treatment and health resource utilization.
They found 154,322 people with psychotic illnesses. However, they limited their study to only those with a psychotic diagnosis while aged 16-30, continuous insurance coverage for the 12 months prior to diagnosis and 12 months after and a second psychosis diagnosis. This group comprised 1357 people. The second group was made up of 5488 people who had insurance at the time of diagnosis, but not for a year before and after and had only the one diagnosis.
Almost two-thirds of the people (61 per cent) did not fill their prescriptions for anti-psychotics in the year after diagnosis and 41 per cent did not receive any psychotherapy. Mortality for this group was anywhere between 24 times to 89 times greater than comparable for those aged 16-30 in the general U.S. population. The authors commented that "in the general population, only individuals over 70 years of age have all-cause mortality approaching the rate we observed among young psychosis patients here."
The study also found that there was very little medical oversight of these patients and only "modest" psychosocial treatment. Those who died in the 12-month period received the least amount of outpatient care.
Premature death for those with schizophrenia is complex and not as simple as the anti-psychiatry crowd suggests. It results from a combination of poor treatment and preventative care these people receive from the medical system, and the failure to treat their mental illness appropriately and aggressively. In the U.S., it appears to be confounded by the lack of universal health care.
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Former President Theodore Roosevelt champions national health insurance as he unsuccessfully tries to ride his progressive Bull Moose Party back to the White House. (Photo by Topical Press Agency/Getty Images)
President Franklin D. Roosevelt favors creating national health insurance amid the Great Depression but decides to push for Social Security first. (Photo by Keystone/Getty Images)
Roosevelt establishes wage and price controls during World War II. Businesses can't attract workers with higher pay so they compete through added benefits, including health insurance, which grows into a workplace perk. (Photo by Hulton Archive/Getty Images)
President Harry Truman calls on Congress to create a national insurance program for those who pay voluntary fees. The American Medical Association denounces the idea as "socialized medicine" and it goes nowhere. (Photo by Keystone/Getty Images)
John F. Kennedy makes health care a major campaign issue but as president can't get a plan for the elderly through Congress. (Photo by Keystone/Getty Images)
President Lyndon B. Johnson's legendary arm-twisting and a Congress dominated by his fellow Democrats lead to creation of two landmark government health programs: Medicare for the elderly and Medicaid for the poor. (AFP/AFP/Getty Images)
President Richard Nixon wants to require employers to cover their workers and create federal subsidies to help everyone else buy private insurance. The Watergate scandal intervenes. (Photo by Keystone/Getty Images)
President Jimmy Carter pushes a mandatory national health plan, but economic recession helps push it aside. (Photo by Central Press/Getty Images)
President Ronald Reagan signs COBRA, a requirement that employers let former workers stay on the company health plan for 18 months after leaving a job, with workers bearing the cost. (MIKE SARGENT/AFP/Getty Images)
Congress expands Medicare by adding a prescription drug benefit and catastrophic care coverage. It doesn't last long. Barraged by protests from older Americans upset about paying a tax to finance the additional coverage, Congress repeals the law the next year. (TIM SLOAN/AFP/Getty Images)
President Bill Clinton puts first lady Hillary Rodham Clinton in charge of developing what becomes a 1,300-page plan for universal coverage. It requires businesses to cover their workers and mandates that everyone have health insurance. The plan meets Republican opposition, divides Democrats and comes under a firestorm of lobbying from businesses and the health care industry. It dies in the Senate. (PAUL J. RICHARDS/AFP/Getty Images)
Clinton signs bipartisan legislation creating a state-federal program to provide coverage for millions of children in families of modest means whose incomes are too high to qualify for Medicaid. (JAMAL A. WILSON/AFP/Getty Images)
President George W. Bush persuades Congress to add prescription drug coverage to Medicare in a major expansion of the program for older people. (STEPHEN JAFFE/AFP/Getty Images)
Hillary Rodham Clinton promotes a sweeping health care plan in her bid for the Democratic presidential nomination. She loses to Obama, who has a less comprehensive plan. (PAUL RICHARDS/AFP/Getty Images)
President Barack Obama and the Democratic-controlled Congress spend an intense year ironing out legislation to require most companies to cover their workers; mandate that everyone have coverage or pay a fine; require insurance companies to accept all comers, regardless of any pre-existing conditions; and assist people who can't afford insurance. (Alex Wong/Getty Images)
With no Republican support, Congress passes the measure, designed to extend health care coverage to more than 30 million uninsured people. Republican opponents scorned the law as "Obamacare." (Mark Wilson/Getty Images)
On a campaign tour in the Midwest, Obama himself embraces the term "Obamacare" and says the law shows "I do care." (BRENDAN SMIALOWSKI/AFP/Getty Images)
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The Kingston Trio influenced popular song far beyond the boundaries of traditional folk music. Aesthetically they may have been a template for boy bands, handsome young men mugging cutely on their album covers. While there is a fair share of love songs in their repertoire, the Trio's more famous numbers are about Tom Dooley being bound to die, Tijuana jails and zombie jamborees. That's more Geto Boys than Backstreet Boys. In 1960, the Grammy Awards created a category for folk music (which the Trio won) in response to the genre's explosion in popularity. Mind you, this is when three-part harmony, a couple of acoustic guitars and a banjo could be described as something explosive. These days if you want to be explosive you simply put the sound of an explosion on the track. Click-click. Ka-boom! Here again, we see a correlation. The Kingston Trio is the great-grandfather of gangsta rap. The Kingston Trio lays down some old, old, incredibly old-school beats 7:30 p.m. Wednesday at the Bass Performance Hall, Fourth and Calhoun streets in Fort Worth. Tickets range from $35 to $45. Call 1-877-212-4280 or visit basshall.com.
Wed., Oct. 24, 7:30 p.m., 2007
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A basketball hoop made of durable steel tube with a diameter of 20 mm. It has 12 handles for grid. Ideal for mounting inside and outside.
Attached to the rim are:
- the mounting bolts - 3 pieces
- colored net rim - 1 piece
Material: Steel
Color: red
Handles for the net count: 12
The whole set is packaged in a cardboard box.
Mounting sketch


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Postgame Notes
Postgame Notes
Sept. 17, 2011
Recap | Final Stats | Quotes | Photo Gallery 1 | Photo Gallery 2
Postgame Notes
Purdue 59, Southeast Missouri 0
- Purdue is now 1-0 all-time against Southeast Missouri as Saturday's contest was the first-ever meeting between the two schools.
- Head Coach Danny Hope now owns a career record of 46-38, including a 11-16 mark at Purdue.
- Purdue is now 82-29-3 all-time when playing an opponent for the first time. Southeast Missouri is the 114th school to play the Boilermakers in program history.
- Purdue's 59-0 win is the largest margin of victory ever at Ross-Ade Stadium.
- The Boilermakers finished with 627 yards of total offense, its highest total under Hope and most since Nov. 20, 2004 against Indiana.
- The 393 yards rushing were Purdue's most since a 315-yard effort against Toledo on Sept. 5, 2009, and just shy of a 407-yard effort at Northwestern on Oct. 26, 2002.
- Purdue's defense limited the Redhawks to just 153 yards of total offense. It was the first time the Boilermakers held an opponent under 200 yards since Sept. 11, 2004 (vs. Ball State), and the first game under 100 yards passing since Oct. 10, 2009 (at Minnesota).
- The Boilermaker defense had 10 tackles for loss for 29 yards, including a pair of sacks.
- The Boilermakers topped the 50-point plateau for the first time since Sept. 5, 2009 (52-31 vs. Toledo).
- It was Purdue's first shutout since a 51-0 win vs. Syracuse on Sept. 5, 2004.
- Purdue improved to 8-1 under Hope when rushing for over 200 yards, including 2-0 this season.
- Purdue's 33 first downs were their most since Nov. 22, 2008 (35 vs. Indiana).
- Caleb TerBush completed 14-of-17 passes for 143 yards.
- Robert Marve made his first appearance of the season at quarterback. He completed 7-of-8 passes for 91 yards and a touchdown.
- Akeem Shavers led the Boilermakers with 70 yards rushing on 10 carries, scoring a pair of touchdowns.
- Ralph Bolden carried the ball 11 times for 57 yards and his first two touchdowns of the season. They were his 10th and 11th career rushing touchdowns and he now has 13 for his career.
- Antavian Edison had his first career rushing touchdown. He carried the ball three times for 32 yards and had one catch for 26 yards.
- Akeem Hunt saw his first career action at running back, rushing for 56 yards and two scores on six carries.
- Brandon Cottom also saw his first career carries in the backfield, rushing for 70 yards on seven attempts.
- Justin Siller and O.J. Ross paced the receiving core with five catches each. Siller had 61 yards and Ross had 46.
- Waynelle Gravesande smashed his career-highs with four receptions for 57 yards.
- Gary Bush scored his first touchdown of the season, his second-career scoring grab.
- Chris Carlino and Will Lucas led the Boilermaker defense with seven tackles apiece.
- Ricardo Allen grabbed his first interception of the season and fourth career pick.
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text: Springer Tiergartenstrasse 17 , Heidelberg , D-69121 Germany About Publications books magazines articles Latest news Companies Springer Books 11 Books found Books Breeding Plantation Tree Crops: Temperate Species 0 Comments Tree species are indispensable to human needs. Due to their long life cycle and environmental sensitivity, breeding trees for sustainable production is a formidable challenge in order to meet the demands of growing human population and industries. Fruit crops such as apple, cocoa, mango, citrus, litchi, pear, dates, and coconut or industrial crops including rubber and tea, improving yield under the optimal, sub-optimal and marginal areas call ... Breeding Plantation Tree Crops: Tropical Species 0 Comments Tree species are indispensable to human needs. Due to their long life cycle and environmental sensitivity, breeding trees for sustainable production is a formidable challenge on order to meet the demands of growing human population and industries. Fruit crops such as apple, cocoa, mango, citrus, litchi, pear, dates, and coconut or industrial crops including rubber and tea, improving yield under the optimal, sub-optimal and marginal areas call ... Continuous Cover Forestry 0 Comments The large-scale application of new silvicultural systems has become a political reality in many parts of the world. This involves a gradual tarnsformation of traditional silvicultural practice towards Continuous Cover Forestry (CCF), also know as near-natural forest management, favouring mixed uneven-aged stands, site-adapted tree species and selective harvesting. Today, CCF systems are encountered in many parts of the world, but forest managers ... Forest Trees 0 Comments Genome Mapping and Molecular Breeding in Plants presents the current status of the elucidation and improvement of plant genomes of economic interest. The focus is on genetic and physical mapping, positioning, cloning, monitoring of desirable genes by molecular breeding and the most recent advances in genomics. The series comprises seven volumes: Cereals and Millets; Oilseeds; Pulses, Sugar and Tuber Crops; Fruits and Nuts; Vegetables; Technical ... Mountain Timberlines 0 Comments This book is published as part of the broad area of research on the changing global climate and its impact on the environment. After an introduction into the complexities of the subject, the history and present state of timberline research are outlined. Chapters on the tree species at timberline and on the relationship of timberline elevation to marcroclimate, climate character and the mass-elevation effect follow. The main chapter deals with ... Sika Deer 0 Comments Sika deer, the graceful spotted deer of Japanese and Chinese art, originally were native to Asia from far-east Russia to Vietnam to the islands of Japan and Taiwan. They are widely raised in captivity to supply velvet antler for traditional medicine. They also were introduced to Europe, North America, and New Zealand, where they compete or interbreed with native deer. Sika deer typically occupy lowland hardwood forests with low winter snow ... Tropical Forest Seed 0 Comments The book aims at dealing with all practical issues in connection with practical tree seed procurement and supply in tropical countries, with necessary background information and documentation of applied methods. It starts with seed collection and follows the processes of the standard fates of seeds, from extraction, cleaning, drying, testing and storing to distribution and sowing in the field or in the nursery. The text covers simple hands-on ... Urban Forests and Trees 0 Comments This book covers all aspects of planning, designing, establishing and managing forests and trees and forests in and near urban areas. The disciplinary background of the authors is varied, ranging from forestry and horticulture to landscape ecology, landscape architecture and even plant pathology.The first chapters in the first part of the book deal with the concept, history, chapter deal with the form, function and benefits and functions of urba Beech Forests 0 Comments This volume compares the beech forests of eastern Asia, North America and Europe. Beech forests are important in each of these three regions. No other book covers beech on this scale. The author has personally studied beech forests in each region, and his large body of data is the starting point for comparison. For such a world-wide comparison to be justified, factors that have most strongly influenced the beech forests should be known. ... In vitro Culture of Trees 0 Comments Woody plants provide many challenges to the tissue culturist. Although there are many excellent tissue culture books and manuals available, these are generally strongly biased towards herbacious crops. Consequently, they often do not pay sufficient attention to the problems that specifically apply to in vitro culture of tree species. Culture of the latter often poses problems which are either absent or of lesser significance when culturing ... Tree Harvesting Techniques 0 Comments


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Great narration and very eye opening. Really liked the way the author didn't belittle Christianity in his closing but supported it, even though for him, it has lost its savor. This book is well worth reading. It brought the bible to life, made it very understandable and took out all the mystical elements and put them a perspective that is more real than trying to believe them as actually happening.
"Eh, it's alright"
Things I liked:
• provides a quick overview of some scholarly criticisms
• polite towards believers in God
• overall interesting perspective
Things I disliked:
• rambles toward the end (I feel like the book could've been shorter)
• writes in absolutes as if all biblical scholars accept certain things as facts, which is simply not true (I'm a biblical studies grad and view Ehrman's work as an interpretation/commentary)
• seems to contradict himself occasionally throughout the book
"Another great Ehrman book!"
I'll keep this short. For anyone trying to find a somewhat objective view of Christianity, Ehrman is the source. Professor Ehrman, please narrate your own books! Your passion comes through and makes your books better listens.
"A dull, one-sided critique of the New Testament"
The first half of this book would be of no interest to anyone except the bible-thumping, evangelical Christians. Progressive Protestant sects and Catholics have accepted for decades the "revelations" that Ehrman discloses. The actual authors of the New Testament is discussed at length in the two most important Catholic bibles. The fact that there are discrepencies in the telling of the same stories in the different Gospels as, for instance, the time in Jesus' ministry that an event occurred, are also obvious to most Christians and are of little significance.
In the second half Ehrman gets down to more meaty matters. Was Jesus God? Did he ever represent himself as God? Did Jesus mean to start a new religion?
I'm undecided on these questions but, not being a Biblical scholar, I have no way of judging the value of Ehrman's arguments. Ehrman, as someone who has left Christianity, cannot possibly be objective. What is needed is an objective presentation of both sides. Ehrman states that many of his friends who agreed with most of Ehrman's interpretation of the New Testament nevertheless remained Christians. A published debate with one of those friends would be of great interest.
"as a Christian..."
yes, because it makes you think on many levels about many things.
the story within the story
the last chapter was very revealing
no, it took me awhile. much to think about.
Though I'm a Christian i like this book very much. Such historical truths cause me to see God as bigger not smaller, and always make me ask, what is God doing? One of the discrepancies in the Bible that seems to disturb people most is the death of Judas. It is a story of betrayal. It is a story of what happens to one who betrays God, and like most of the Bible it is shrouded in layers of complexity and metaphor. And like most of the Bible the story of Judas is meant to speak to us as individuals, much like a dream; its language is full of archetypes at work in the subconscious of every man. Yet a psychotherapist, because he has studied Jung, would be foolish to think he knows exactly what a dream means to an individual without knowing anything about the individual's background or history. It's the same with the Bible. And the only psychotherapist who can tell us anything helpful is the Spirit of God, without whom the Bible is just an interesting artefact. Whatever else we wish He might do, this is done one human heart at a time.
Imagine you really were the God who created life on planet earth through evolution. What kind of book would you write? It has to last for thousands of years, it has to speak to everyone, and it has to be full of wisdom, warning and compassion. Would you lock yourself into one narrative, find a few heads, empty them out completely of their own ability to narrate and judge, fill them with this narrative and have them write it down verbatim? Not the God I know.
The Bible promises that many will have eyes and see without seeing, have ears and hear without hearing. I only ask for eyes and ears to see and hear. The God so many say isn't there certainly has His own way of answering.
"Knowledge is a wonderful thing…"
My praise for Bart D. Ehrman goes far beyond acknowledging his scholarship, he has done me an immense favor. Although baptized as a child, I am not a Christian and have always been made to feel that it was my fault. After listening to Jesus, Interrupted; I now understand why I am not a Christian and why I do not believe. The difference is that I can now articulate, with some degree of authority, just why I disbelieve. The coup de grace for me came when Bart asked the rhetorical question: Just how does one decide to believe one miracle and not another. Knowledge is a wonderful thing, especially if it inoculates a person from the mind-virus that is religion.
Hard Headed Stephen
"Mind blowing and right in front of your eyes"
Misquoting Jesus was one of my recomended downloads, but a reviewer suggested trying Jesus Interrupted first, so I did. I liked it so much and was so intrigued, I bought the book and downloaded his other works. Having grown up Protestant and Catholic, this really amazed me, more so when I opened the Bible to verify...WOW! I enjoyed his presentation of the material thoroughly and found it very hard to put down. I did not find it overly technical nor dry but quite fascinating. I agree whole heartedly that one should approach this open minded, considering what is said and what is written and referred to in the Bible. Man touched the Bible, therefore there will be mistakes. Professor shares his research yet suggests nothing but your deepest consideration of the facts. I have suggested it to my wife and children and many friends, I do to you as well!
"A must read to understand Christianity."
The author goes into the heart of Christianity and analyzes Jesus. Are the sayings from the Bible really from Jesus? Did he really teach the Sermon on the Mount? Which version of the Crucifiction is the most accurate? Dr. Ehrman shows us what the evidence supports. A good read for someone interested in Biblical history.
When I drive, I read... uhm listen. I like SciFi, Fantasy, some Detective and Espionage novels and Religion. Now and then I will also listen to something else.
"Bart's Systematic Theology (/Mythology)"
I have been reluctant to listen to this book from prof. Bart D. Ehrman for one reason, he claims that those who are pastors will not find anything new in this book. They would have been taught at seminary, most of the content of this book.
Ehrman's statement is only a half-truth. A lot of the issues I know, but what I didn't know is his own approach to the historical critical method of the Bible. You will get to know more about how Ehrman sees the world in this book, than just the things that pastors learned and haven't told their congregations.
As Ehrman concludes that the Bible cannot be the Word of God because of all its errors, in South Africa the view in theological faculties are that it is God's Word in Human Language. It is a midway from the Bible being the inerrant Word of God and the reality of the discrepancies in the Bible.
Ehrman is not scared to follow a train of argument through to the end of its consequences. This is probably on of the best popular books on the historical critical method of investigating the Bible. At the same time it is also a chapter by chapter "summary" of other books he has written.
I've recognised "Misquoting Jesus," "Forged," "Lost Christianities" as well as a little bit of "Did Jesus Exist?" his latest book. I you want to know what it is all about for Bart, then this is probably a good book to read.
I must say that I appreciated the tone of the book. He doesn't seem to want to convert Christians to atheism. Yet, I can see how having a few years of theology condensed into one book, can shake a person's faith. It challenges a lot of traditional beliefs.
Bart D. Ehrman does for the Biblical Sciences what Richard Dawkins did for the Natural Sciences. He takes a difficult topic and put it in a congestible format. Not only is the historical-criticism of the Bible a difficult subject, it also has tremendous consequences for Theology and in the end for Christians.
This book might challenge your belief-system to the core. Yet it is important information given in a digestible format. I personally think that it is sad that Ehrman doesn't believe. While he de-constructs the basics of the Christian faith, his reconstruction feels very empty.
The book is recommended, for anyone interested in the historical-critical approach of the Bible. It might not be everybody's cup of tea but it is an important perspective on the New Testament and needs to be heard.
"One of the best"
This is one of the best discussions of New Testament scholarship I've ever read (or listened to). Ehrman writes clearly and engagingly on a wide variety of topics: internal inconsistencies in the Bible, conclusions about the historical Jesus, early (non-orthodox) versions of Christianity, and much more. I've read several of his books, and I think this is a good one to start with; to some extent it works as a summary of some of his other work. Ehrman's scholarship is first rate, and his presentation is accessible and absorbing. Jason Culp does an outstanding job narrating the discussion


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Nunchaku Jutsu Kata - Martial Arts Weapons Kata
This page provides details about the martial arts weapons kata known as Nunchaku Jutsu. This kata incorporates angles and more footwork. It also includes the following stances; Nicho Ashi Dachi and Zenkustu Dachi. Please also visit Nunchaku and Nunchakujutsu for more details about this weapon.
Ensure when you have the nunchaku wrapped around your shoulder that the base of the top nunchaku is pointing down … Why? See the difference if you try to hit something with the base pointing to the ceiling as opposed to being angled down. Where the base points that will be where the nunchaku strikes. Do this kata imagining your opponent is your height.
Please note in some countries you will require a permit to use or even carry these, some requirements may include (not an exhaustive list):
Please visit Ryu Kon Kai - Fukyu Nunchaku for the first nunchaku kata.
Instructions for Kata
Demonstration Video of Kata - Nunchaku Jutsu
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Dr. Nolo is a board certified cardiologist at Princeton-Plainsboro Teaching Hospital. He is an unseen character.
In the season two premiere Acceptance, the case of a patient who's heart had started beating so fast it pumped out air was assigned to Dr. Nolo because he was a cardiologist. Dr. House stole Dr. Cuddy's password and found out about the case. He wanted it himself. Dr. Cuddy refused to give it to him and told him that Dr. Nolo had already been given the case. House said that Nolo was a useless drunk and that there were no usual reason that the patients symptoms would occur. This convinced Cuddy to give the case to House.
- Acceptance (mentioned)


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Having problems with your Fujitsu LifeBook B2131 Notebook ?
Stripe of discoloration
\015 I have a 2? year old Toshiba Satellite A135, and about a month ago i noticed a strange stripe that comes from about middle screen from the top to teh bottom. it discolors any light window a little bit darker, it does not affect any dark windows or the cursor.my OS is Vista Home Basic, i don't know whether it is Hardware or Software related, i have rebooted, hibernated, slept, and full shutdown. it has not affected it.\302\240\015\012Recently it has started to flash every now and then as well.\015
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Stripe of discoloration
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Discoloration I have a 2? year old Toshiba Satellite A135, and about a month ago i noticed a strange stripe that comes from about middle screen from the top to teh bottom. it discolors any light window a little bit darker, it does not affect any dark windows or the cursor. my OS is Vista Home Basic, i don't know whether it is Hardware or Software related, i have rebooted, hibernated, slept, and full shutdown. it has not affected it. Recently it has started to flash every now and then as well.
It sound like the screen is going bad try to hook it up to and external monitor and see if you have a clear picture if you do it could be a loose connection between the case and the Lcd or the inverter may be failing if yhttp://www.ask.com/bar?q=lapt ... Toshiba Satellite A135-S2386 Notebook (PSAD6U-01D00D) PC Notebook
Screen IBM Thinkpad 600E, Type 2645, Model 4AU, OS WIN/98 When I turn on the screen show me incorrect characters, discolored stripes vertical and horizonta. It don't allow me do nothing...please help
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Vertical stripes across my monitor.
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Stripes on my Samsung Monitor
The contrast may be to high.Adjust the brightness and contrast to make it go away but still readable.if that does not help the FL (backlight) is going and the unit will need to be replaced.Sorry. ... Samsung SyncMaster 913V 19" Flat Panel LCD Monitor
LG Flatron L1930B lcd monitor - 3 vert. stripes, center one dead
Sounds like the pixel controllers have gone bad or one or more of the color (RGB, RED, GREEN, BLUE) controllers have gone out. this is quite common in lcd monitors/tvs and is usually caused by pressure on the edges of the screen (you grabbed it too t ... LG L1930B 19" LCD Monitor
Acer 1711 17"Lcd monitor vertical stripe problem
That's pretty easy; not much is wrong. You have a backlight with several sections to it, and one section has gone dark on you; once you carefully take the monitor apart (on old towels, perhaps) and find the backlight circuits and LEDs or compact flu ... Acer AL1711 17" LCD Monitor
3 pixel wide stripe on lcd
Hi Casey,If the problem is getting worse, than either the pixels are dying (so to speak) or you might have a problem with the monitor's screen.Unfortunately, if either of the above are true, then the only way to fix it would b ... Acer AL1711 17" LCD Monitor
Striped color distortions on Nokia 300 Xa flat panel
This is power supply problem. \015\0121. First u replaced the power out put capacitors , 6V, 12V, etc.\015\0122. cheak the diodes. ... Computer Monitors
Intermittent 2" wide vertical stripe of color distortion
... Dell UltraSharp 2001FP 20.1" LCD Monitor
Installed a new Optical Drive and require assistance in the wiring
What kind of optical drive? Is this a CD, DVD?, Blue ray,or an opto-ferro-magnetic floppy?Generally:1) External drive: ============ a) just power it up and connect it to the PC using an USB or ... PC Desktops
Your screen is dieing your need to replace the screen the lamp are not working your screen has been damaged or they died they died ether way. I do refirsbeched LCD montiors and laptop screens.i've seen this before i have three line on my dell 17 i'm ... LG.Philips LCD LP150X05A2 Monitor
Netstar monitor has vertical stripes appx every 1.5 inches stripes are white and obscure the image. the parts of the image that does not have the stripes is fine. This happened after a 1.5 week period of monitor being turned off, when I came back and turned it on the stripes were there. Tried monitor on different pc and the problem stayed with the monitor. any suggestions
... Computer Monitors
Connect Digital and Analog cables at the same time.Any use?
Does not help. keep dvi connector (white one) on computer and in the back of monitor.\015\012and surely it will not take away those vertical stripes. \015\012those vert stripes... hmm... your monitor might have a problem which you can't f ... Dell UltraSharp 2001FP 20.1" LCD Monitor
Rewire a normal 24 pin Atx Psu to the 24 slim line connector
Okay, here is the pinout on the dc power supply:And here is the pinout of a "normal" power supply ... HP Compaq dc7100 PC Desktop
HD Pavillion Media CenterDv8225nr Notebood Pc. Verticle stripes
I would try a couple of things. First and cheapest way is to try and update your driver. If that does not work, then try to remove and reseat your memory card(s), and if all else fails you will need to buy a new graphics card approx 75 to 150 dependi ... IBM ThinkPad T21 Notebook
Magenta vertical stripe sets plus grid dots problem
Staples office supply store said it was the monitor and, after buying and installing a new $200 monitor, I discovered it wasn't the monitor. I brought my hard drive to a reputable computer repair place, who charged me $50 total to install a new video ... Acer P191WBD LCD Monitor
Right half of screen is Black with a White vertical stripe
Yeah, I have this exact same problem, except my mom slammed my laptop shut in frustration around half an hour ago, so that's why it's like this. The right half of my screen is black with two colorful stripes (mostly white), but the left half is visi ... HP Compaq FP 7317 17" Flat Panel LCD Monitor
Color distortion/blank screen on 50% of monitor
Full instructions from DELL at:\015\012\015\012http://support.dell.co ... Dell UltraSharp 2001FP 20.1" LCD Monitor
Need specs: CMOS battery for Toshiba Satellite M60 notebook, Euro
Sounds like you have several problems to solve.\015\012The LCD screen might only need the the video ribbon cable connector reseating otherwise it could be a video card problem. Connect an external monitor to the laptop, power up the monitor the ... Toshiba Satellite M60 Notebook
Cat 5 cabling
EIA/TIA\012568B\012WIRING STANDARD\012\012\012\012\012\012 PIN\012\012 WIRE COLOUR\012\012\012\0121\012\012White w/Orange\012Stripe\012\012\012\0122\012\012Orange\012w/White Str ... PC Desktops


text:
= I n d i g o =
My colourless afternoon
A shade of whatever in the damp sunless sky,
I wonder what world I wither with,
I wonder what rainbow died here,
The musk of nothingness drifts through
Scentless and sightless,
Nothing resembles a meaning,
No meaning resembles a word.
Wolves are bound to starless nights,
No moon to guide their howls,
No mate to call their beliefs,
So bullets without guns,
Dream sand without seas,
No sun in the sky,
No heart to the beat.
But I'm indigo,
Never thinking of a thing,
While you never think of me,
dreaming dreams of dreams so dreamily.


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Segorbe Spain Businesses For Sale
Searched the DealStream database for Segorbe Spain Businesses For Sale and found no matches. Expanded the search to nearby areas and found the following matches.
Electric Industrial Items Manu. Co. in Spain #465303 posted Mar 24, 2017
- Valencia, Valencia, Spain
- $6,000,000
Electric components company for sale a in city near Valencia, Spain. 3,000 square foot industrial warehouse space. This company manufactures and markets of the final product. It has a commercial network for more than 20 years, with a notable presence in the national and international markets.
Granier Franchise Bakery and Coffee Shop in Spain #465227 posted Mar 23, 2017
- Valencia, Valencia, Spain
- $161,000
This Bakery and Coffee Shop is a Franchise from a well known brand, Granier. There are 45 other franchise stores in the country and 10 prospects this year. It sells a wide variety of special breads and cakes. The coffee shop serves coffee, ice-cream, shakes, tea and snacks. Located in a busy tourist...
Medical Beauty Center in Valencia, Spain #465204 posted Mar 23, 2017
- Valencia, Valencia, Spain
- $193,000
Medical Beauty Center with the newest treatments with certified doctors for Medical Aesthetics, Laser and Beauty. There is a wide range of ethical, non-surgical beauty treatments designed to reduce wrinkles, remove blemishes and rejuvenates the face and body. Listing includes all the clientele and equipment....
Hotel "Four Stars", with Offices and Shops #462415 posted Feb 7, 2017
- Valencia, Valencia, Spain
Hotel "Four Stars", with offices and shops in the center of Valencia. The hotel has 192 rooms and a suite. Restaurant, bar. The complex includes a property for sale offices, shops, commercial and public parking. Valencia - a city in Spain, the autonomous community of the same name and the center of...
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text:
1,369pages onAdd New Page
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Malo was an Atlantean criminal who stole Neptune's Trident and used it against other Atlanteans. He was outwitted by Supergirl. However, this turned out to be a deception: Malo was actually Superman, who had disguised himself to give his cousin a birthday adventure. ("Supergirl's Busiest Day!")


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- Garden of Memories Funeral Home and Cemetery, Metairie, LA;
- Schoen Funeral Home, New Orleans, LA;
- Greenwood Funeral Home, New Orleans, LA;
- Tharp-Sontheimer-Tharp Funeral Home, Metairie, LA;
- Everly Community Funeral Care, Falls Church, VA; and
- Everly-Wheatley Funeral Home, Alexandria, VA.
HOUSTON, May 15, 2014 /PRNewswire/ -- Carriage Services, Inc. (NYSE: CSV) (the "Company") announced today it closed on its acquisitions from Service Corporation International. Mel Payne, Chief Executive Officer, stated, "We are excited and very proud to announce that today we closed the acquisition of six businesses in New Orleans and Alexandria, Virginia from Service Corporation International pursuant to a Consent Decree Application approved this past Monday by the Federal Trade Commission. We had a goal of being the first buyer in our industry to close on the large number of Service Corporation International divestitures resulting from their acquisition of Stewart Enterprises, and we achieved that goal through a team effort by a group of high performance 4E Leaders. This high quality group of operating businesses includes the following:


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Phooldol Gyaras is celebrated on Kamada Ekadasi (Shukla Paksha Ekadasi in Chaitra month) at Vrindavan Banke Bihariji Temple (Lord Krishna Temple). In 2016, Phooldol Gyaras date is April 17.
It marks the beginning of Phool Bangla Utsav which lasts for more than 3 and half months. In 2016, Phool Bangla Utsav starts on April 17 and ends on August 2.
On Phooldol Gyaras, the idol of Lord Krishna and the entire temple of Banke Bihariji is decorated with various types of flowers and garlands.
In 2015, Phooldol Gyaras date was March 31.
In 2014, Phooldol Gyaras date was April 11.
In 2013, Phooldol Gyaras date was April 22. In 2012, Phooldol Gyaras date was April 3.


text:
Heaven and Earth
He used to tell me that he'd found Heaven,
Right here, in this parking lot,
On this ordinary-ordinary Earth.
I didn't believe him, but I know that he
Could see through my fake smile, thin as it was.
The thing is, Heaven is extraordinary-extraordinary,
So it couldn't possibly reside here, could it?
But maybe, just maybe, extraordinary-ordinary
Things are alright, too, as long as they seem to fit.


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Organised, clean, love to cook, easy going, friendly, great sense of humor, never late with rent, love meeting new people, loves animals, not big partiers, enjoy friendly gatherings.
I am reliable, thoughtful and considerate of others. I enjoy good food and conversation and well as quiet times. I have recently moved here from Jindabyne to be closer to my girls and enjoy the coastal lifestyle.
My name is Tanika, I'm 19 years old and I work part time casual at a local coffee shop. I'm looking for a nice and tidy place to live and can definitely afford it. I'm sociable but respectful of people's private space, clean, tidy and definitely will not be throwing parties at my house. I have a 3 year old Labrador cross blue cattle named Marley who is the most beautiful natured dog I have ever met and I'm sure you will agree once meeting him. Feel free to contact me through here or email - Ps. If available my partner george, 26 who works full time as a call centre operator is looking for place to stay as well, so it would be even more convenient for a couple accomodation, we can both afford about $350 a week between us.. but price can be changed depending on the house and of Marley can stay etc..
Close to the water. I have a cat, need to get on with cats. No other pets are allowed. Some furniture provided, need own room furniture.
I'm working, reliable, a exceptionally good cook, I clean, happy to do lawns -gardens, am polite, easy going, down to earth, friendly and likable. :)
1 room available for rent in brand new house (currently nearing building completion, photos on request) available from late May 2017. Share with one male (owner/occupant) and one female, both in early 20's. Includes All Bills providing privilege is not abused (Reverse Ducted Air Conditioning, Electricity, Water, Gas and Unlimited Wifi on the NBN). Situated in new estate, approx. 5 min drive to CSU, Cafes and Coles. Rent period negotiable. Must be clean, tidy and sociable. Fully Furnished House, New Appliances, Two Seperate Living areas, shared Bathroom (will only be shared if another housemate there as have an ensuite also), separate Toilet, Internal Laundry with Dryer. 175 p/wk unfurnished, or can arrange as furnished - pretty flexible. Message me if you have any questions or want any further info! Welcome for inspections.
Very young, beautifully presented and well located, air conditioned, filled with natural light, quality design, premium inclusions, generous bedrooms, separate lounge and living areas, gourmet kitchen, landscaped gardens, near Charles Sturt University and hospital, 6 mins from CBD, built-in wardrobes and dishwasher.
Located very close to Charles Sturt University and Innes lake Coles. 2 story recently built house in a Quiet location with street parking
So I have just Updated my add to put it simply you can take the whole area at $350 pw OR I have 2 x Bedrooms 1 at $200 pw ( slightly smaller ) & 1 at $250 pw We are walking distance to the Charles Stuart University , St Columbia School , Shopping Centre & a short drive to the Public Hospital Only 10 min drive into town & beaches & if you don't drive there is a Bus stop just up road . My Husband & I are young retirees. You will live in part of our family home, We have our own part of the house separated from house mates but will still be accessing the house to use the laundry There are 2 x bedrooms & 1 bathroom for you both to share Full access to the kitchen & living room you Must clean up after yourself Looking for 2 easy going people to share, must have a great sense of humor & be animal lovers as we have dogs a cat & birds. Over all it's a very casual house You must be able to look after yourself by cooking , cleaning etc Non smoker , Occasionally having a drink is ok . But most of all be Respectful & Honest ...........NO PET'S ALLOWED SORRY............. This is not a Party House & Drugs will not be tolerated
Quiet area close to base hospital and uni. 2separate living areas. air conditioned, front and back courtyard
I have 1 bedroom available furnished with a queen size bed with bedside tables and walk in wardrobe, shared bathroom at $160 P/W inclusive of electricity, gas and water. . Two living areas, 1 large common sunroom close proximity to Lighthouse Beach area, outdoor area. Quiet relaxed house. Internet available at nominal cost. Prefer Employed person/student
Quiet, peaceful location. 3 min.drive to University of Newcastle, 5 min. to :- City centre, Charles Sturt University, Airport, Bunnings, Hospital and Town Beach. 10 min. to the Pacific Hwy. A pleasant garden with covered patio at rear of house. Small gym access, air-conditioning, large screen TV with Foxtel and second TV in dining area.New washing machine and full use of Laundry facilities. Private bathroom and toilet with separate walk in dressing room. Further information or inspection please phone .
Hello, I have a room to rent from the 22nd of May, off street parking available and a fifteen minute walk into town.
Great location, close to local shops, PO.Restaurants. Walk down the hill to the beach. 2 storey house with 2 living areas. Fully furnished shared areas,bedroom can be furnished or not if have own. BBQ area and pool. Small pet considered.
Lovely and modern, house is furnished besides for spare bedrooms. Decent sized rooms can fit queen bed.
Quiet neighbourhood in a great location. Close to the beach.
Room to rent in large clean furnished sharehouse with easy going working others. This house gets cleaned weekly & has large verandahs. It is in a quiet area in a great location which is central to all areas & has off street parking.. If you are a mature working, clean quiet easy going person that has respect for others, & would like to live in a quiet clean house thats peaceful, then this house could be for you. Must be of sober habits.Smoking accepted in designated areas only.. $170 PW Electricity Included . Phone Binny
Hello! I am a health professional who is looking to temporarily relocate to Port Macquarie from Sydney in approximately 2 weeks for 2 months. I am easy going, tidy, respectful of one's space and would love to have other female housemates to befriend during my stay.
Easy going clean tidy good to get along with keep to myself
I'm a vet working full time in Port Macquarie. Would like to eventually look at having my little dog up here too. Like living with people who are both happy to hang out and have dinner or watch a movie but also happy doing their own thing.
I am studying Diploma of Community Services at North Coast Tafe. I volunteer at a Non Government Organisation in Port Macquarie and also volunteer my time with a number of consumer groups. Outside of this I am cooking (I'm a qualified Chef), dog walking (not my own), surfing and jogging. I am very easy going and like to keep to myself but I am sociable when required.
quiet and non interfering while helpful and friendly


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Moxie goes 2-2 on weekend
By The Mercury
The Manhattan Optimist Moxie went 2-2 last weekend. The Moxie was 2-1 in pool play on Saturday, defeating the Salina Rockets and Topeka Legacy.
Winter Henry and Tyler Hoyt pitched for the wins. Moxie lost in pool play to Kansas Heatwave and in bracket play to the Olathe Vipers.
Against the Topeka Legacy, Abby Snow and Alexis Wilson went 2-for-3 and Cierra Lesperence hit a two-run home run.
Moxie will compete this weekend in Blue Valley (KC) in the NSC Recruiting Tournament.


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RANK, RANKL and osteoprotegerin in bone biology and disease
- First Online:
- Received:
- Accepted:
DOI: 10.1007/s12178-009-9046-7
- Cite this article as:
- Wright, H.L., McCarthy, H.S., Middleton, J. et al. Curr Rev Musculoskelet Med (2009) 2: 56. doi:10.1007/s12178-009-9046-7
- Citations
- 1.4k Downloads
Upon the discovery of RANK, RANKL and OPG in the late 1990s, their importance in the maintenance of the skeletal structure and their dramatic role in bone disease were largely unexpected. In recent years the understanding of these proteins, in particular their regulation, has greatly increased. This review aims to bring the interested reader up to date with the latest news and views on the mechanisms controlling bone resorption in normal and pathological conditions.
KeywordsReview Osteoprotegerin (OPG) Receptor-activator of nuclear factor kappa beta (RANK) Receptor-activator of nuclear factor kappa beta ligand (RANKL) Disease Structure
Bone is a specialised tissue with a complex composite structure that enables it to perform multiple mechanical and metabolic functions. In order to maintain these functions within the body, bone is in a constant state of remodelling. During this process, also known as bone turnover, osteoclasts demineralise and resorb old bone and osteoblasts deposit new bone to maintain a bone mass appropriate to the stresses placed on the skeleton. Any alteration in the process of bone turnover may alter bone mineral density (BMD), bone strength and bone micro architecture. This most commonly occurs when there is an increase in osteoclast activity, leading to increased bone resorption, resulting in diminished bone density (osteopenia). Osteopenia may also occur due to lack of vitamin D (rickets and osteomalacia) or an excess of parathyroid hormone (hyperparathyroidism). Disorders of the skeleton may also involve an increase in BMD (osteosclerosis), either due to defective osteoclast function (osteopetrosis), or as a result of too little parathyroid hormone (hypoparathyroidism).
Molecular biological investigations have led to an increased understanding of the mechanisms and proteins involved in bone resorption. This process is controlled by a system comprised of three key proteins, RANK (receptor-activator of nuclear factor kappa beta), its ligand RANKL (receptor-activator of nuclear factor kappa beta ligand) and a decoy receptor OPG (osteoprotegerin). This system is regulated by many osteotropic hormones and cytokines which either reduce (glucocorticoids, inflammatory cytokines e.g. interleukin-1 (IL-1), parathyroid hormone (PTH), prostaglandin E2 (PGE2), vitamin D3) or increase (transforming growth factor-β (TGF-β) and estrogens) the OPG/RANKL ratio [1].
Structural characteristics of RANK, RANKL and OPG
RANK was discovered by Anderson et al. [2] by directly sequencing cDNA from a human bone marrow-derived myeloid dendritic cell. Sequencing of the RANK gene showed it to be a type I transmembrane glycoprotein and further gene mapping showed this newly discovered protein to be located on chromosome 18q22.1 [2] and also a member of the tumour necrosis factor receptor (TNFR) family [3]. The expression of RANK has since been found on the surface of a wide variety of cells such as; osteoclast precursors (circulating monocytes) [4], mature osteoclasts [5], dendritic cells [2, 3], mammary gland epithelial cells [6], breast cancer cells [7] and prostate cancer cells [8].
The cognate ligand for RANK, RANKL, was reported almost simultaneously by four independent research groups [2, 12, 13, 14]. RANKL is a tumour necrosis factor (TNF)-related cytokine expressed by various bone cells including osteoblasts and their immature precursors [15], T lymphocytes [16], B lymphocytes [17] and megakaryocytes [18].
RANKL (Fig. 1b) is coded for by a single gene, however, alternative splicing results in the expression of three isoforms. In humans two of these isoforms are type II transmembrane bound glycoproteins of either 317 [11] or 270 aa, the latter differing only by a shorter intracellular domain [19]. The third isoforms of only 243 aa lacks both the transmembrane and cytoplasmic domains and acts as a soluble ligand (sRANKL) [19, 20]. Each of these isoforms is only capable of activating osteoclastogenesis when they associate forming homotrimeric molecules [16, 21].
The human and murine RANKL proteins share 83–87% homology, with the largest murine transmembrane isoform being 316 aa [11]. Sequence analysis of the murine RANKL gene (316 aa) compared to the human RANKL gene (317 aa) showed two potential N-glycosylation sites in the extracellular domain at amino acid fragment positions 197 and 263 [13].
Because of the existence of these splice variants in RANKL it is likely that they are regulated differently and have different functions. Although the exact explanations for various isoforms are unknown, one possibility is that membrane bound RANKL ensures cell–cell contact with osteoclasts and their precursors whereas sRANKL allows for diffusion to activate target cells. In the first case, bone resorption will be tightly localised to the cells expressing RANKL ensuring topographically accurate remodelling. In the second case, resorption will be more generalized perhaps allowing systemic resorption. sRANKL can also be formed by shedding, a process in which RANKL is cleaved from the cell surface membrane by sheddases such as matrix metalloproteinase 14 (MMP-14) [22].
OPG was first identified by sequence homology to the TNFR family during a rat intestine cDNA sequencing project [23]. They named the protein because of its protective effects in bone (Latin: os bone, protegere to protect). OPG is a soluble glycoprotein secreted by various mesenchymally derived cells such as osteoblasts [24] and bone marrow stromal cells [25].
Unlike RANK and RANKL, OPG does not have a transmembrane domain or cytoplasmic domain [2]. Composed of 401 aa, human and murine OPG consist of four cysteine rich pseudo repeats located in the N-terminal, two death domains, a heparin binding site located in the C-terminal and a 21 aa signal peptide [2] (Fig. 1c). The four cysteine rich pseudo repeats form an elongated structure and binds to one of the grooves of the active RANKL trimer [20] therefore preventing RANKL/RANK interaction and hence osteoclastogenesis.
This 401 aa structure gives OPG a monomeric molecular weight of 60 kDa which is then assembled at the cys-400 residue in the heparin binding domain to form a 120 kDa disulphide-linked dimer for secretion [26]. Prior to secretion of both the monomeric and dimeric forms of OPG, the signal peptide is cleaved from the N-terminal giving rise to a 380 aa mature OPG protein [2, 23].
The function of RANK, RANKL and OPG
The expression of RANKL in human and murine osteoblastic cells is stimulated by various cytokines (IL-1, TNFα and IL-11) [3, 29] and calciotrophic hormones including PTH, 1,25dihydroxyvitamin D3 (1,25D3) and prostaglandin E2 [29]. An increased production of RANKL by osteoblastic cells leads to osteoclast differentiation, activation and survival, which results in increased bone resorption. This, along with the involvement of the decoy receptor OPG is thought to be a key mechanism in the control of bone turnover.
The Wnt signalling pathway contains many proteins involved in embryogenesis, cancer and normal physiological processes and is a growing area of interest concerning the regulation of bone turnover. In brief, when canonical Wnt signalling is activated by one of the 19 secreted Wnts binding to one of 10 frizzled receptors (Fzd), a signalling cascade is initiated which results in the translocation of β-catenin into the nucleus. Once here, β-catenin binds with the transcription factor tcf/lef and initiates target gene transcription. Wnt signalling has been shown to be vital for normal osteoblast function [30, 31, 32]. sRANKL has been reported to bind secreted frizzled related protein (sFRP) [33], a soluble Wnt inhibitor produced by osteoblasts, another mechanism by which osteoblasts can inhibit osteoclast formation. This interaction may represent another way in which bone resorption may be controlled at the same time as Wnt signalling is inhibited.
OPG acts as a decoy receptor by binding with high affinity to RANKL therefore preventing the interaction with RANK [34]. As a consequence of binding to RANKL, OPG acts as an effective inhibitor of osteoclast differentiation, activation and survival and therefore inhibits bone resorption [34].
OPG expression and secretion by osteoblasts/stromal cells are modulated by various metabolic regulators: IL-1, TNF-α and TGF-β increase OPG secretion and it is decreased by various stimulators of bone resorption including PTH, PGE2 and 1,25D3 [15, 25, 29]. Using mouse calvaria treated with indomethacin to block endogenous prostaglandin production, the role of OPG in modulating the adhesion of osteoclasts between the bone surface and the endocranial membrane was investigated [29]. These authors found that OPG inhibited both the release of osteoclasts from the periosteum and adherence of the osteoclasts to the bone surface, therefore inhibiting bone resorption [29].
OPG has been shown to bind to TNF-related apoptosis inducing ligand (TRAIL) [35] although with less affinity than for RANKL [36]. TRAIL is a 33–34 kDa cell associated ligand which mediates apoptotic cell death particularly in cancer cells. TRAIL binds to specific cell surface receptors which contain cytoplasmic death domains. Following this binding, TRAIL transduces an apoptotic signal [37]. The binding of OPG to TRAIL was found to inhibit TRAIL-induced apoptosis of Jurkat cells in culture [35]. However, the biological significance of the binding of OPG to TRAIL remains unclear. OPG also has a basic heparin binding domain making interactions with heparin and heparin sulphates possible. Heparin sulphates are expressed on the cell surface as heparin sulphate proteoglycans (HSPGs). HSPGs are involved in cell-surface signalling, controlling cell behaviour, actin cytoskeleton regulation, cell adhesion and migration [4].
RANK, RANKL and OPG in disease
A summary of human diseases caused by mutations in the RANK, RANKL and OPG genes
18 bp duplication
Familial expansile osteolysis
27 bp duplication
Early onset Paget's disease
15 bp duplication
Expansile skeletal hyperphosphatasia
Deletion of amino acids 145-177
Autosomal recessive osteopetrosis
A single nucleotide change (596T-A) in exon 8 of both alleles
Autosomal recessive osteopetrosis
Deletion of two nucleotides (828_829delCG)
Autosomal recessive osteopetrosis
Deletion making OPG inactive
Juvenile Paget's disease
20 bp deletion resulting in premature termination of OPG translation
Juvenile Paget's disease
FEO is an inherited autosomal dominant disease with 100% penetrance resulting from the constitutive activation of RANK due to an 18-base pair tandem duplication. FEO is characterized by deafness which often occurs before the age of 10, early loss of teeth due to the resorption of the cervical region (where a tooth meets the gum), osteolytic lesions from late teenage years until late middle age [39] and increased bone remodelling [38]. Lesions in FEO mostly affect the tibia, ulna, humerus and femur, sparing the axial skeleton such as the skull and pelvis which are common sites for lesions found in Paget's disease of bone [39].
Another autosomal dominant disease caused by a mutation in RANK is early-onset Paget's disease [39, 40] which differs from classical Paget's disease by its early onset and instead of lesions being restricted to one or more bones they are scattered throughout the body. The patients studied with early-onset Paget's disease all presented with bone pain and/or deformity in their teens and early twenties and showed a 27-base pair duplication in the signal peptide region of the RANK gene causing constitutive activation [39].
RANK mutations in FEO and early-onset Paget's result in a failure to cleave the signal peptide. This leads to an increase in RANK-mediated activation of NF-кB, stimulation of osteoclast activity and a secondary stimulation of osteoblasts [39]. This stimulation in bone turnover leads to patients with early-onset Paget's disease to have enlarged and softened bones, particularly those that are long and weight bearing [38].
Expansile skeletal hyperphosphatasia (ESH) is an autosomal dominant disorder characterized by the premature loss of teeth, early-onset deafness, episodic hypocalcaemia, accelerated bone remodelling and widening of long bones causing pain in the finger bones [41]. Mutation screening of patients suffering from ESH revealed a 15-base pair tandem duplication in the signal peptide region of the RANK gene [42]. This mutation has the same affect on RANK as seen in FEO; however, there is not a great increase in osteoclast and osteoblast number and activity [38]. Anti-resorptive therapy with bisphosphonates can be effective in the treatment of FEO, early-onset Paget's disease and ESH [40], although very recently it has been reported that bisphosphonate toxicity during childhood can impair one remodelling and induce osteopetrosis during later life [41].
Autosomal recessive osteopetrosis is a rare genetic bone disease. Bone biopsies taken from four unrelated individuals with this disease showed an absence of osteoclasts and no improvement in bone remodelling following haematopoietic stem cell transplantation, which would be expected to replace the osteoclast population but not the osteoblast [43]. Genetic analysis of the RANKL gene in these four individuals revealed three different mutations. Patient one had an in-frame deletion of amino acids 145–177. The mutation deleted the entire βA strand and half of the AA loop, which are essential for the osteoclastogenic activity of RANKL. The second and third patients had a single nucleotide change (596T-A) in exon 8 of both alleles. The fourth patient had a genomic deletion of two nucleotides (828_829delCG), resulting in a frame shift starting at val277 and a premature stop codon. This mutation was thought to cause the loss of the βF, βG and βH strands of RANKL. These are all important for RANKL trimerisation and therefore the mutation would prevent the activation of osteoclastogenesis [43].
Mutations in the OPG gene cause a disease called juvenile Paget's disease, also known as idiopathic hyperphosphatasia [44]. This disease can be fatal if not treated with anti bone resorption drugs [45]. Juvenile Paget's disease is an autosomal recessive osteopathy which initially presents in infancy or early childhood and is characterized by rapidly remodelling woven bone, osteopenia, fractures, progressive skeletal deformity and increased bone remodelling throughout the skeleton [44, 45]. Individuals with this disease are also typically short in stature [46]. The location and type of gene mutation responsible for this disease was investigated by various groups.
The first group studied nine children from two generations of a family from New Zealand, three of whom displayed typical clinical and radiographical symptoms of juvenile Paget's disease. Biochemical analysis of the bone turnover markers ALP and N-telopeptide/creatinine ratio showed significantly raised levels in the three affected individuals. PCR analysis of each of the five exons of OPG identified a 3-base pair in-frame deletion of a critical aspartate residue in exon three. OPG was also detected in the plasma of the three affected children suggesting that the mutation does not affect secretion. The activity of the mutant OPG protein was then compared to the normal functional protein. This revealed that normal OPG inhibited bone resorption in mouse calvaria whereas the mutant protein did not. This suggests the mutant OPG with the three base pair deletion is inactive and results in uncontrolled bone remodelling and increased bone turnover [44].
The second group investigated two unrelated Navajo patients with juvenile Paget's disease. Patient one was a one-year-old male child with bone deformities as a result of the disease. Patient two was a 26-year-old Navajo female who was deaf, severely deformed and incapacitated by the disease. The bone turnover marker, serum alkaline phosphatase (ALP) activity was approximately 10 times above the normal range in both the male and female patient [45] indicating excessive osteoblastic activity. They then analyzed and sequenced the gene for OPG. PCR analysis of genomic DNA from patient one and his parents revealed no OPG gene product. Southern blotting of genomic DNA supported this finding confirming a 100 kilo base deletion that had completely deleted the gene for OPG [45].
A third mutation of OPG in juvenile Paget's disease was identified [47]. This group studied 10 affected individuals, each of these subjects had long-bone deformities, short stature, raised ALP activity, impaired mobility (7/10 subjects) and enlargement of the skull (6/10 subjects). PCR analysis revealed that three of the 10 individuals had a 3-base pair mutation of OPG. Other affected individuals had a much larger 20-base pair deletion also in exon three of the OPG protein. It is suggested that this mutation results in premature termination of OPG protein translation [47]. As with the 3-base pair deletion [44] and the 100 kb deletion [45] the 20-base pair deletion resulted in increased bone turnover, demonstrating that mutations in the OPG gene can cause autosomal recessive idiopathic hyperphosphatasia [47, 48].
Osseous malignancies
The RANK, RANKL and OPG system is also involved with many other metabolic bone diseases, where their expression is modulated either directly or indirectly by the tumour cell to promote its own survival. Bone metastases are unfortunately a common occurrence in patients with solid tumours such as breast cancer, prostate cancer and lung cancer often resulting in severe pain and pathological fractures amongst other complications [49]. Patients with solid tumours metastatic to bone have been shown to have a severe disruption in the RANK/RANKL/OPG system [50]. In these instances, quality of life and even life expectancy is dramatically reduced.
Breast cancer commonly metastasises to the skeleton causing painful osteolytic lesions [51]. Establishment of the metastatic tumour is gained by influencing the expression ratio of RANKL and OPG to favour bone resorption [51]. It is believed that some genes may predispose the likelihood for breast cancer to metastasise to bone [52].
Bone is the most common and sometimes the only site of metastasis in patients with advanced prostate cancer [53]. Prostatic bone metastases stimulate an increase in both rate of bone remodelling and bone volume [54]. Prostate cancer bone metastases produce RANKL thus enabling them to induce osteolysis through osteoclast activation [55]. Although mostly osteoblastic in nature, prostatic bone metastases can also appear osteolytic in order to promote tumour growth [54].
Lung cancer metastasises to bone in approximately 9–30% of all cases [56]. Lung cancer metastases are generally lytic in nature, although some have been found to also have osteoblastic characteristics [57]. Constitutive expression of the chemokine CCL22 by osteoclasts is thought in some cases to potentially promote the metastasis of lung cancer to bone [58].
Multiple myeloma (MM) is an osteolytic bone disease resulting from excessive bone resorption [59]. Although the exact mechanisms of invasion are unclear, it is believed the tumour invades surrounding bone by up regulating RANKL and down regulating OPG and therefore stimulating local bone resorption [59].
Murine knockout models
RANK deficient mice (RANK −/−) were generated in order to investigate the direct role of RANK in bone resorption [60]. RANK −/− mice were recognisable by their small-body size, shortened limbs and doming of the skull, which became apparent after weaning at 3 weeks of age. At 6 weeks radiography revealed an osteopetrotic phenotype including shortened long bones and increased radio-density in bone marrow cavities relative to the control mice (RANK +/+). Histological analysis showed disorganized chondrocytes at the growth plates and poorly remodelled osteocartilagenous structures blocking the marrow cavities. Staining for the osteoclast marker TRAP showed positively stained mature osteoclasts in the control mice, yet they were completely absent in the RANK −/− mice, suggesting an explanation for the osteopetrotic phenotype observed. The lack of RANK for RANKL to bind to inhibited osteoclast differentiation and maturation, causing a deficiency of mature osteoclasts at the bone surface [60].
The requirement of RANKL for osteoclastogenesis and bone remodelling, along with its function in modulating immune responses was investigated using RANKL −/− mice [5]. Similar to RANK −/− mice, RANKL −/− mice showed a normal rate of growth until weaning at 3 weeks old. After weaning their growth became severely stunted and teeth failed to erupt [34]. The RANKL −/− mice completely lacked TRAP positive stained osteoclasts, in contrast to the large number of TRAP positive cells in the RANKL +/+ control mice [5]. Radiographs showed osteopetrosis was visible from 2 days after birth, with shortened long bones with distinct broadening of the epiphyses. The axial skeleton (skull, vertebrae, sternum, breastbone and ribs) when visualized by X-ray showed a large increase in radio-density, 516 mg cm−3 in RANKL −/− mice compared with 242 mg cm−3 in RANKL +/+ mice [5].
OPG and its physiological role as a regulator of normal bone mass was investigated using targeted deletion of the gene in mice (OPG −/−) [50]. They found an increased mortality between birth and 4 weeks of age in OPG −/− mice when compared to the OPG +/+ control mice. The OPG −/− mice also had a higher prevalence of vertebral and bone fractures in the first 2 weeks of life indicating brittle bones and a possibility of low-bone density. OPG −/− mice that survived past weaning were fertile and females successfully carried litters to term. Offspring were also OPG −/− indicating that OPG is not required for normal embryonic development [61].
Radiography showed decreased BMD in OPG −/− mice compared to the OPG +/+ control mice, however, this was only evident from 1 month of age and became more prominent as the mice aged [61]. Histological examination of vertebrae and long bones from OPG −/− mice showed severe osteoporosis with almost a complete lack of trabeculae by 1–2 months of age [61]. OPG −/− mice have been shown to have a high bone turnover rate, disorganized matrix and an impaired attachment of new to old bone in the cement line due to excessive osteoclast activity [62]. Therefore, OPG plays a crucial role in blocking bone resorption. Radiographic investigation of a transgenic increase of OPG in mice revealed clear signs of osteopetrosis immediately following birth, with the severity increasing throughout adolescence and adult life [23].
With the discovery of RANKL came the ability to manufacture osteoclasts in vitro, which has accelerated up the discovery of other factors that affect bone loss and molecular details of differentiation and bone resorption. Further to this came the understanding of RANKL and OPG in diseases where bone is lost. This knowledge has provided new targets for modern therapies, for example re-engineered OPG and anti-RANKL antibodies.
Denusomab (AMG162) is a high affinity anti-RANKL antibody [63] able to prevent RANK/RANKL binding and inhibit bone resorption resulting in an increased bone mass. Denusomab is currently in phase III clinical trials for treatment of osteoporosis [63, 64] and also under investigation for the treatment of osteolytic bone metastases from diseases such as breast cancer (phase II clinical trials) [65], rheumatoid arthritis (phase II clinical trials) [66] and multiple myeloma [67]. Similar attempts have also been made with OPG [68, 69]. AMGN-0007 is a recombinant OPG construct and suppressed bone resorption when administered to MM and breast cancer patients during a phase I clinical trial [68]. A similar result has been observed using a recombinant adeno-associated viral (rAAV) vector in mouse model of osteolytic breast cancer [69].
Treatment of metastases to bone and their mechanisms of action remain elusive. Use of bisphosphonates, a common drug for the treatment of osteoporosis, has proved to be useful in preventing some metastases from breast, prostate and lung cancer by inhibiting the osteoclast [70]. Bisphosphonate treatment also has the added benefit of reducing bone pain caused by the metastases that general analgesics can sometimes fail to relieve [70]. Recent in vitro studies for the prevention/reduction in skeletal metastases include the intravenous administration of RANK-Fc, a chimeric protein that inhibits the RANK/RANKL interaction [57]. Treatment with RANK-Fc reduced osteoclastogenesis, reduced bone tumour volume and inhibited the lytic nature of the lesion [57].
Current publications also tend to discuss the function of these proteins in bone remodelling or they discuss the diseases that revolve around them. Here we have provided an in-depth synopsis of the structures of the RANK, RANKL and OPG proteins including structural diagrams and combined this with an in-depth review of diseases linked to these proteins. We have also reviewed how the osteoblast integrates systemic signals from calciotropic hormones like PTH and 1,25D3, and local signals from growth factors and cytokines to stimulate or inhibit bone resorption.
The discovery of the osteoclast differentiation factor RANKL, its receptor RANK and its decoy receptor OPG, has revolutionised our understanding of bone remodelling. There is currently a large wealth of knowledge already in publication surrounding RANK, RANKL and OPG although many questions remain unanswered.
Open Access
This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.


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When I was growing up, we had a beagle who liked to get into everything. He'd open the kitchen cabinet every day to rifle through the garbage. If food was left on the table, it was not safe from his hungry stomach. Anything left out had a chance of being eaten or slobbered upon. He even got into a whole bowl of chocolate. My mom was certain that would be the end of him, but he just left her a nasty present later that day. But through all of his craziness, we never dog-proofed the house.
When my son E was a baby, we bought childproofing devices with the intent of using them. However, he kept to himself and all we needed were some gates to protect him from falling down the stairs or getting into the kitchen. There was only one time when we forgot to block the stairs and that was the time he attempted to walk down them and fell instead. I almost had a heart attack, but a slice of cheese was all he needed to feel better.
And then came my next son, M. Since M became a toddler, we've had to cover our electrical outlets, install safety locks on our cabinets, and put all unsafe objects and electronics out of his reach. I've recently had to put a guard on his doorknob to keep him from potentially wandering around the house if he didn't want to go to sleep. It was also to keep him from locking himself into his room. This hasn't stopped him from getting into everything else though. We found him in his room one afternoon with all the contents of his "junk drawer" (which I thought he couldn't reach) strewn all over the room and his carpet as an artwork canvas. Luckily, the marker came out. However, I didn't know how to put the safety lock on his drawer (my dad is the one who installed everything in the kitchen), so I just taped the entire thing shut with a big strip of packing tape. It looks tacky, but it works. Then he managed to wrangle off the door guard and lock himself into his room. Again, packing tape to the rescue. I also cannot leave him to his own devices when it comes to bath time. He knows how to turn on the faucets (burn risk right there) and he is able to get in and out of the tub himself (even at the risk of slipping). He also manages to drink some bath water every time, even if he's just sneaking it off the washcloth.
I guess having a beagle prepared me for being a mother, except I haven't found garbage strewn all over the kitchen. However, M is very curious about what is in the garbage can…..


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Read Stuff, You Should: What Would Reagan Do?
Happy Birthday to Mercedes McNabb, 34.
Getting ready for the weekend with the good stuff:
1. Via Kevin Drum, a history lesson about Ronald Reagan from Dan Drezner. He points out that Reagan's pragmatism worked out pretty well when it came to the Soviets and other foreign policy threats, so emulating him is often a pretty decent idea.
2. All about deductibles and the Affordable Care Act, from Galen Benshoof.
3. More on money and access from David Broockman and Joshua Kalla.
4. Andrew Sullivan is losing patience with Barack Obama on torture.
5. Sean Trende wraps the Florida House special election.
6. And the importance of religion in the Ukraine confrontation, from Mara Kozelsky.
This column does not necessarily reflect the opinion of Bloomberg View's editorial board or Bloomberg LP, its owners and investors.
(Jonathan Bernstein covers U.S. politics for Bloomberg View. He is co-editor of "The Making of the Presidential Candidates 2012." Follow him onTwitter at @JBPlainblog.)
To contact the author on this story:
Jonathan Bernstein at firstname.lastname@example.com
To contact the editor on this story:
Max Berley at firstname.lastname@example.com


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Notice: On March 31, it was announced that Statalist is moving from an email list to a forum. The old list will shut down on April 23, and its replacement, statalist.org is already up and running.
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st: Joint Wald test after NLSUR
Regio Martins <firstname.lastname@example.com>
st: Joint Wald test after NLSUR
Wed, 28 Jul 2010 19:16:24 -0300
Dear Statalisters,
After the following NLSUR estimation:
nlsur (y1 = {a1}*x1 + {a2}*( {c} + x2 ) ) (y2 = {b1}*x1 + {b2}*( {c} + x2 ) )
how do I test the joint hypothesis that {a2} and {b2} are zero using the "test" command? I cannot find the right syntax to refer to these two parameters...
Thank you,
* For searches and help try:
* http://www.stata.com/help.cgi?search
* http://www.stata.com/support/statalist/faq
* http://www.ats.ucla.edu/stat/stata/


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April 17, 2017: The 3D printer is currently out of order. We will post a notice on this page when it is printing again.
Thanks to a gift from the Fremont Library Foundation, patrons can now design objects to print on our MakerBot Replicator 3D Printer!
3D printing allows you to create models, functioning prototypes, visual aids, real world products, educational materials, art, and more.
Our fifth generation MakerBot creates prints by building up layers of PLA filament that is pulled from a spool. Available colors are blue, clear, grey, and yellow. Want more colors? Consider donating to the Fremont Library Foundation!
Create a print
Search for and download a premade design from Thingiverse.com or using Yobi3D, a 3D print search engine. You can also use CAD (Computer Aided Design), software that allows you to create 2D and 3D designs on a computer, to make your own design. Keep in mind:
- Size is limited to 9.9 x 7.8 x 5.9 inches (25.2 L x 19.9 W x 15.0 H cm).
- Parts of a model that extend without support will not print successfully.
- The maximum allowable print time for each individual job may not exceed 8 hours. We will contact you if your print job is too large.
- You may submit one design at a time. Please wait for your print to be finished before submitting another design.
- Make sure your design is saved as an .stl file.
- Fill out the required fields on our submission page and upload your .stl file.
- The design will be reviewed to make sure it is not a weapon or copyrighted material, or a print job that will not print successfully. We will send a reply email if there are any problems.
- We will we will contact you when your design is ready to be picked up. Prints not picked up after six weeks will be used for library programs.
After the print is complete, you can remove any rafts or supports and sand your object with sandpaper (80 grit to 500 grit). Be sure to wear a mask and goggles! You can also prime and paint your model using hobby paints in a well-ventilated area.
Want to learn more about 3D printing?
Lynda.com offers several classes on 3D printing. Visit the library's Research page and use your library card to set up an account and start learning at your own pace.
Find premade files at Thingiverse.com or GrabCAD.com.
Create your own files using a CAD program:
- TinkerCAD is a free, web-based program. It works best in Google Chrome (v. 10 or newer) and Firefox (v. 4 or newer). Find it at tinkercad.com.
- SketchUp is a free downloadable design program, available at sketchup.com. You'll need to download this extension in order to save your work as an .stl file: http://extensions.sketchup.com/en/content/sketchup-stl.
Still want more? Visit the MakerBot website to see how it works, get ideas, and learn about the future of 3D printing.


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With every morning comes a new beginning. It is an opportunity for all of us to realize the potential of the day. And when we start the morning right, there's no end to what each day can bring.At Kellogg we believe that when you start with a great breakfast, great things can happen. That's why we make foods that you and your family know, trust and enjoy. A variety of great-tasting, good for you favorites that get you going so that you can make the most of every moment.That's the power of breakfast.
For more than 100 years, we've worked passionately to help families be their best. And it all starts with breakfast. That's why we're always looking to provide new ways to make a positive impact on the people we touch every morning.


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Wireless Door/Window Entry Alarm Kit Model RC3260
When you need an instant and immediate alert when a door or window is opened, the RC3260 by Carlon is a great product to choose.
Common Uses:
- Instant alert when door or gate to pool is opened
- Hear chime sound when closet door is opened
- Monitor when any door or window is opened
Here's What the Product Does:
When a monitored door is opened, the wireless door/window contact sends an immediate signal to the plug-in receiver featured in this kit and a selected chime sound is played. This kit may be expanded by adding more transmitters (sensors) as well as more receivers. The components in this kit are also compatible with the Carlon series or wireless door chime products that allow easy integration with other home alert and chime products. You can add push buttons, motion sensors, doorbell extenders and more to the components in this kit.
What's in the Kit?
The RC3260 is a wireless door/window alarm comes in two components. The sensor is indoor rated only and is powered by a 9 Volt battery (supplied). The sensor is comprised of two pieces one of which is magnetized. When these contacts are separated, the sensor is triggered and then wirelessly signals a plug-in chime receiver. The great thing about this product is that it uses the same receiver as the RC3253 so that you can easily expand the system by adding additional sensors and or additional receivers.
How the Products are Powered:
The door window sensors are battery operated – no wiring required. The range between the transmitter and receiver is roughly 150 feet. This range may be decreased by qualities such as metal doors, concrete, and stucco.
This product works best by a door or window that typically stays closed. It does not detect motion or other movement and is only triggered when the magnetic contacts are separated.
If you plan on placing your door sensor outside, we recommend ordering the RC2260. If not, go with the RC3260.
Common uses of this product
- There are two sound modes for this product:
- "Alarm" mode - plays alarm sound for 4 minutes, or until "chime" is selected on transmitter
- "Chime" mode - plays one of 13 tunes/melodies when transmitter is activated
- In chime mode, there is the option to have different transmitters play other sounds to differentiate other doors and or windows (13 different sounds).
- Under the transmitter cover is a push button to change the sound played by
- Wireless receiver with adjustable volume runs on 110 volts and plugs into a standard wall outlet within a 150-foot range
- Completely wireless, installs in minutes
- Alkaline battery powered - 6 volts (PX28A/RC2095)
- No false alarms - Alarm or chime is not activated until the door or window opens
- Maximum 150' range from transmitter to receiver is up to 150ft.
- 32 codes decrease interference
- Compatible with other Carlon wireless chimes and entry alert products. Expand listening area by adding receivers, add other sensors and transmitters to the system.
- Manufactured by Carlon
- One year manufacturer's warranty
Customer Reviews
Product Reviewed: Indoor Window/Door Alarm with Wireless Sensor
score average: 5 out of 5 , 11 review(s).
Absolutely perfect! I needed a chime for the door in my small retail store and this is just the right thing! Pleasant old-fashioned chime sound. Now, I hear my customers come in from the back room where I spend most of my time. Great product, easy to install.
Ontario Inn
(Ontario Oregon)
Replacing unit that was at our place when we bought it over 11 years ago. Reliable and dependable.
(Valley, AL)
I've been looking for a door entry chime for my small retail shop...most that I've found have poor reviews due to the inconsistent performance of the product. This one had decent reviews, so I gave it a try. rnrnI've had the door chime in place for 9 days. For the first 5 days or so, it worked just as it should. Then things started going awry. I have it set to give one loud "dong" when the door is opened, but after a few days, it started playing other tunes instead of the "dong". Then shortly after, it completely stopped alerting me that the door had opened.rnNow it seems to work as it should only some of the time. I can no longer rely on it.rnrnThe distance from the door transmitter to the receiver is only 30-35 feet and is completely unobstructed. So it's not the distance nor any interference. Just like all the others that have bad reviews, this one simply just can't be counted on.rnrnPass on this one...and I'll keep looking for a reliable model.
Great Bell. Very interesting to find the amount of chimes. I am using it for business and my crew is changing the chime sound based on the moods and the holidays. Great Bell, best price on the market.
I purchased my first one in 2009 and I have loved it ever since...I use it on the door to my shop and I can hear the chime every time the door is opened by a customer...I bought a new one this year 2015 to add to my other unit...I now have two receivers and I love the additional chimes...My customers love the different notes that it plays when I change it up for different seasons of the year...By the way, I originally bought a door chime from Lowe's and had to return it because it didn't work good...This Carillon Entrance Alert by Carlon RC3260 far exceeds my expectation of needing a door chime to alert me at all times...
Works well. Shipped quickly.
I bought the Door Alert Doorbell because my brother lives with me and he has Alzheimer's. Now when he gets up at night and opens his bedroom door, the receiver is in my bedroom and it alerts me so I can get up and take care of him. I have it set on chimes and set it on low and it always wakes me. This unit was so easy to install and only took about 3 minutes with the two sided sticky strip that came with it. There are a number of settings to choose from for the sound you want it to play and high, medium and low to choose how loud you want the sound. This is an excellent device and I highly recommend it. I have had it 3 weeks and it is exactly what I needed.
(Central New York)
After trying a door alarm from a local big box hardware store, what a refreshing product this is. I am using it to alert me in my office, which does not have sight to the entry door. The ability to have this chime notify me, without being a disturbance to others in the building and down the hallway (the other chime was a very loud high-pitched digital sound that even brought about complaints from coworkers), is a delight. I could have it set to the quietest setting (of low, med, hi), but my neighboring officemate likes the ability to hear it as well. Also, the fact that there are so many "chimes" -- really, some are recognizable songs, gives someone a chance to change it as often as they'd like. The one complaint I have is that I am needing to use tape to keep it in place, as I needed the spacer for the magnetic piece, and I was unable to screw it securely into the metal door frame. That being said, the weight of the magnet is too much for the sticky foam piece included. A piece of clear packing tape is holding nicely, is hardly visible and doesn't bring attention to it. I attached it close to the hinge side of the door, so most people don't notice it. I absolutely recommend this product to people who need a variable volume entrance notification system, and the customer service was knowledgeable and friendly.
New Customer
This door chime sounds just like a door bell. It is a refreshing change from the alarm sound that went off with our past door chime. A+
Fast, courteous service. Easy to install. Works great, I have one transmitter at both my garage entry doors and a receiver upstairs and in the basement. We know when someone enters the garage from either door, as these units work together. And being a name like Carlson, they are great quality. Highly recommended for single or multiple apps that work independent or simultaneously with distinguishable chimes for to let you know which door is being enteredrnrnThanks 1800 Doorbell!
Office User
Thank toy Lori for providing outstanding customer assistance in helping us determine the best chime for needs.The Door Chime works well in a medical office setting and has 3 loudness levels. Ours is set to a single tone at the lowest level and is perfect. We also have a remote receiver for the back section of the office and it works well too. Simple, effective chime for a good price.


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They are both beautiful specially the one with darker hair.... great legs!
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Both are absolutely wonderful - and each in his very own way - they really love each other -great gay sex !!! Love it !!
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Consultation sales end March 18th.
Consultation walk-ins accepted Friday night if space is available.
Consultation sales end March 18th.
Consultation walk-ins accepted Friday night if space is available.
Fairfax Genealogical Society Annual Spring Conference
Fairfax Genealogical Society
Friday, March 25, 2011 at 4:00 PM - Saturday, March 26, 2011 at 4:30 PM (EDT)
The first lecture begins at 9:00 a.m., the second at 10:45 a.m., third at 1:45 p.m., and last at 3:30 p.m. Each lecture is one hour. Click here for Satruday's lecture titles in a printable (pdf) matrix (table) format.
Track 1: "Putting the Pieces Together"
Track 2: "Western European Research"
Track 3: "Probate Records" (Mason)
Track 4: "Basics for Beginners and Beyond" (Dondero)
Further details on these items will be posted as it becomes available.
Warren Bittner, a genealogical researcher and lecturer, holds an M.S. degree in history from Utah State University. He is the owner of Ancestors Lost and Found, a small genealogical research firm. He is the former German Collection Manager for the Family History Library in Salt Lake City where he planned the German microfilming, indexing, book acquisitions, and internet publications.
Leslie Albrecht Huber is a freelance writer and speaker and has worked as a professional genealogist. She has published nearly 100 articles in over twenty different magazines and journals. Her website, www.understandingyourancestors.com, provides information for people tracing immigrant ancestors. Leslie is also involved in several genealogical societies.
Chuck is a Certified Genealogist SM, specializing in Southern New Jersey and 19th and 20th Century Death Records. He is a frequent contributor to the National Genealogical Society's magazine and authors "Genealogy News and Issues" a monthly article for their on-line newsletter "Up Front with NGS." In 2009 he received NGS's Distinguished Service Award.
Jennifer is a professional genealogist living in northern Virginia. In addition to lecturing she performs client research, specializing in lineage applications, southern research, and National Archives Records. She previously worked for the DAR before starting her own company. You can learn more about her at her website, www.jpgenealogy.com.
Learn about more genealogical events hosted by the Fairfax Genealogical Society at www.fxgs.org
The Fairfax Genealogical Society was established in 1974 as a non-profit organization to promote fellowship and cooperation among persons who are conducting genealogical research, to further the use of sound genealogical methods, standards of accuracy, and scholarly research, and to aid those doing research in our area. We currently have over 500 members, including not only many who live in or near Fairfax County, but also many who are searching for information in our area. We are pleased to also have the membership of several libraries and other societies nationwide.
In order to purchase these tickets in installments, you'll need an Eventbrite account. Log in or sign up for a free account to continue.


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Watch how to make this recipe.
Put the pepper and lemon slices in an old-fashioned glass and lightly muddle or crush. Fill the glass with ice and add the bourbon, agave nectar, and pineapple juice. Stir to combine the ingredients. Top the glass with ginger ale and enjoy.
Recipe courtesy of Darryl Robinson