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Since 2003, Lori Ebbesen, this year's recipient of the James A. Murphy Award of Excellence, has been an active, engaged member of CACs, both regionally and nationally. An advocate in the Prairie region for enhancing the role of CACs in supporting CSC's mandate, Lori's dedication and commitment to public safety has served as a positive motivator for others and made her an effective leader.
Some highlights of her tireless work with CACs include developing the strategic plan for CSC's Regional Victim Advisory Committee (VAC) and her work on the Humanitarian Contribution to CSC's mission, values and goals. She has also held multiple positions, including Chairperson of the National Executive Committee and Chairperson, Regional Council, Prairies. We thank Lori for all her crucial work with CACs over the last 15 years, and congratulate her on her well-deserved recognition!
William Dickson, an eight-year CAC veteran from the Pacific region who was nominated for this year's Excellence Award, has been an advocate for the development and use of transferrable skills for inmates. For instance, William participated in the Buddy Benches Program, wherein CAC volunteers provided offenders at local institutions with lumber and wood to make benches for elementary schools. Children seeking companionship are encouraged to rest at the bench, signaling their desire for friendship. With such initiatives, it's clear that William's dedication to encouraging applicable skills for inmates highlights the social conscience of the restorative justice approach. We thank William for his inspiring, meaningful work, and look forward to highlighting it again in the future.
The Newfoundland Citizen Advisory Committee was also nominated for this year's award by the Atlantic region, thanks to a variety of effective, ongoing activities and projects. With eight dedicated members – who collectively total over 90 years of CAC volunteering – the committee is involved in creating gardening projects, offering counsel to CSC on mental health considerations, and consulting on homelessness and its interrelated issues. With a representative body that includes a retired provincial judge, banker, and both parole and correctional officers among its members, the Newfoundland Citizen Advisory Committee is an exemplary demonstration of the good-heartedness and generosity that fuels the CACs.


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How To Drag Race Your Diesel!
Tips and Tricks for Getting Down the Dragstrip
Related Video
Once a curious oddity on the dragstrip, diesel-powered pickups can now be seen tearing down tracks all across North America. In addition to pickups, compact cars like Volkswagen Jettas and Golfs are starting to get in on the action, as well as diesel-powered sports sedans and SUVs. With the popularity of diesel drag racing at an all-time high, we've created a list of tips and tricks for beginners and intermediate racers, including some sound advice from the pros of the sport—those who drag race diesels on practically a weekly basis.
Before You Hit the Track
Drag racing your hot-rodded diesel rig actually starts well before you hit the dragstrip. Almost all dragstrips have a mandatory process called a tech inspection, which is a basic once-over of your vehicle (performed by a track official) to ensure whatever you're racing is safe. Such hazards as nails or screws in tires, a cracked windshield, batteries that aren't properly secured, fluid leaks, or excess mud, dirt, or gravel in the bed are all reasons why you might be sent home rather than to the starting line. Even having improper clothing for racing like shorts, sandals, or tank tops can have you running to Walmart for acceptable gear. While a helmet isn't required until you run 13.99 seconds or faster in the quarter-mile, even a 15- or 16-second ride has to be safe before you make a pass. It's always a good idea to check with the dragstrip first to see if there are any special rules for diesels (like exhaust turn-ups) before heading to the strip.
The Staging Lanes and Starting Line
So you've gained entrance to the track and are ready to make your first run. After tech inspection, you'll most likely head to the pits. Please note that the pits are usually a pretty busy area, full of serious racers who might be unloading $100,000 cars. So, speeding, blowing smoke, or doing donuts is a definite no-no in the pit area. Just beyond the pit is an area called the staging lanes, where drag racers line up to race. Often, street vehicles will be designated a certain numbered lane, so make sure you know which lane you're supposed to be in before heading to the staging area. From there, it's just like rush-hour traffic: You sit in the staging lanes and move forward one lane at a time as more vehicles go down the dragstrip. Leaving your car or running your air conditioner (which creates condensation) is frowned upon, so make sure to stay close to your vehicle—and keep your A/C off—until it's your turn to go.
The Burnout Box and Staging
As you get close to the front of the line, you'll see a track official directing cars. Pay very close attention to this person, as he or she will be the one telling you which lane you need to be in and when to pull onto the track. At this point, your windows should be up, and you should be ready to race. Regardless of whether you're in a two-wheel-drive or four-wheel-drive rig, it's become common practice to pull around the water box that most tracks use for burnouts, then back into the puddle if you wish to do a burnout. After wetting the tires, you will be asked to pull forward slightly (maybe 6 inches or so), and then you can do a burnout of a few seconds to clean off the tires. Don't overdo it! While huge 300-foot burnouts may impress your friends, they'll earn you a warning from the starter. If you're done with your burnout or you just pulled around the water box and straight onto the track (common on four-wheel drives), then it's time to stage the truck at the starting line.
When pulling forward, note that the staging lights are actually in two small boxes on the ground, rather than up at the starting device that's better known as a "Christmas Tree." There are elements in the staging process. The first is "pre-stage" (the first yellow light at the top of the Christmas Tree is activated once the vehicle's tires break the first light beam that runs across the starting line), and then "staged," which occurs when a second light beam across the starting line is broken, which activates the second yellow bulb at the top of the Christmas Tree. The staged beacons are the starter's cue that a driver is ready for the green light.
Your First Pass: Launch and Hold On!
Once both the pre-stage and stage bulbs are lit, the lights on the Christmas Tree will flash "yellow, yellow, yellow, green," at half-second intervals. This is called a Sportsman or .500 tree; the driver should leave on the last yellow. If your tires spin, just try and modulate the throttle as best as you can, rather than do a giant burnout. If you're in a four-wheel drive, the vehicle should just grip and go. If something happens during the pass like smoke, a pop, or bang, pull over to the side of the track near the guardrail as quickly as you can. Driving all the way down the dragstrip with leaking oil or antifreeze is a good way of making other racers very irritated with you. Assuming everything goes right and your vehicle accelerates and shifts like it should, keep the hammer down until you cross the finish line, which should be indicated by a stripe or two orange timing lights in the middle of the track. At this point, let off, and start applying the brakes, but unless your truck is really fast, you probably don't need to stop abruptly. Once you've slowed, take the first turnout you can make to reach the return road, keeping in mind the vehicle in the lane nearest to the return road always has the right of way. From there, maintain a reasonable speed down the return road, and then collect your timeslip! Congratulations, you've just made your first pass.
Boosted Launches
If you're racing a four-wheel-drive (or two-wheel-drive with slicks or drag radials), then it's a good idea to start building boost as soon as both staging bulbs are lit, so you can launch under a good amount of power. While this is the best way to get quick elapsed times, it's also more difficult than one might think. After pulling up right before the pre-stage and staging lights, power-brake the truck (or car) so it builds about 5 psi of boost. Creep into the first staging beam by letting up slightly on the brake, until the pre-stage bulb is lit. At this point, the other competitor should be doing the same thing. Gradually give the vehicle a little more throttle and creep into the second beam.
At this point, you should be at about 10 to 15 psi of boost and ready to launch. If something goes wrong with the other competitor or the tree doesn't activate, don't just sit there against the torque converter, as this could result in serious transmission damage. If everything goes right and you're able to leave on the last yellow, floor the throttle rather quickly while stepping off the brake as fast as you can to achieve the best launch. Once you've mastered leaving the line with boost, you can start raising the boost levels to determine when the vehicle breaks traction. Diesels make so much torque that virtually no oil-burning truck or car (even all-out racing vehicles) can leave the line at maximum boost. Also, keep in mind that leaving the line hard can result in transmission, driveline, or suspension breakage, so play at your own risk when it comes to taking off with a good amount of boost.
Drivetrain and Chassis Tuning
The first pass you make will hardly be your best. There are many ways to whittle down your elapsed time while still running the same basic setup. For instance, we know of one driver who picked up a tenth of a second after creating his own ram-air system. Another picked up two tenths by removing unnecessary weight from his truck. A third competitor picked up three tenths by experimenting with suspension, tire pressure, and boost during the launch. A fourth was able to adjust the rate of torque converter lockup and gained two tenths. The point is, adding huge injectors and a big turbo might not be what you actually need to run the elapsed time you want, and all those tenths that come from refining a combination add up!
Final Thoughts
It makes no difference whether you drive an 8- or an 18-second truck, diesel drag racing can be fun for just about any competitor. Just like sled pulling, drag racing is meant to be a fun family activity, so don't be nervous about asking fellow competitors for advice. Having a combination where everything matches (such as the torque converter stall speed and turbocharger size) is perhaps the most important aspect of diesel drag racing, so make sure to do your homework before you make any big changes. Now get out there and have some fun! There's nothing like beating muscle cars in a 4-ton truck!
Tips from the Pros
"Before you start adding power, get used to your truck and how it goes down the dragstrip. Be as consistent as possible with your current combination; that way you'll already know how to drive it once you turn the power up." —"Idaho" Rob Coddens, NHRDA Super Street Record Holder (9.47 at 152 mph), 2013 Super Street Champion
"Diesels can be very consistent drag race vehicles at moderate power levels. My truck has made 457 hp at the rear wheels, runs low 13s, and I have about 800 dragstrip passes on it since 2004. I've gone from Washington to Indianapolis to race and then driven it back home." —Jim Calhoun, winningest driver in NHRDA history
"It's tempting to just put a diesel drag vehicle in the trailer after a race, but proper maintenance is very critical. It's better to catch a problem right after a race than a few days before the next one."—Jarid Vollmer, NHRDA Pro Street record holder (8.51 seconds at 160 mph) and three-time Pro Street Champion
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subset: commoncrawl


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We Protect The Rights Of Noncitizens Regarding Workers' Comp Benefits
The Pew Research Center reports that more undocumented immigrants live and work in California than in any other state. According to the Public Policy Institute of California, undocumented immigrants make up about 10 percent of the labor force in California.
If an illegal immigrant suffers a job-related injury, that worker is entitled to the same workers' compensation benefits that a U.S. citizen can receive. Employers must cover the full medical costs of an undocumented worker who is injured on the job. In addition, undocumented workers can receive permanent and temporary disability payments.
We Protect The Rights Of Non-U.S. Citizens
Understandably, given the increased focus on retaining and deporting foreign-born individuals who are in the U.S. illegally, many injured workers who are noncitizens are hesitant to report work-related injuries.
At the Law Offices of Anthony Choe, we help injured undocumented workers in Los Angeles and throughout Southern California obtain the workers' compensation benefits they are entitled to. We also protect these workers' rights.
If an employer fires or otherwise retaliates against an undocumented worker for filing a workers' compensation claim, we can file a discrimination lawsuit on their behalf.
We Are Ready To Assist You
If you or a relative is an undocumented worker who has suffered job-related injuries, we welcome the opportunity to review the facts of your case and discuss your options with you. Call 213-788-4448 or use our online contact form to schedule a meeting with our knowledgeable workers' compensation lawyer.
There are no upfront costs, and we only collect an attorney fee if we recover workers' comp benefits for you.


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We want to continue an abandoned mod if you interested you can join in the discord server we have hope we see you there! https://discord.gg/EUkZ2C
Hello, my name is Armado, im searching mods that can make a zombie mod for gta v, better than simple zombies, there was one we were making called Undead Streets but the dev dissapeared with the mod and the discord, it was top 5 so its kinda sad. The idea is to make a zombie survival mod with the features of simplezombies and make it even better with new features like zombie dogs or more atmosphere. But to make it first we need modders that would like to help us on the progress of the mod. There is already a plenty of people who wants it and who is concerned about the dissapearance of the mod. Thanks for reading, if you have a question or request you can send me an dm armado#0568


text: The CSCO team is pleased to announce that the Kennedy-Wright Opening lecture will be give this year by Professor Judith Lieu, Lady Margaret's Professor of Divinity, University of Cambridge on Monday 7th October at 4 pm in the Martin Hall, New College. Prof Lieu will speak on 'Marcion and the Corruption of the Gospel.' The event will be followed by a wine reception. As always, all are welcome!


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Links from Today's Show:
No Virus: https://www.lewrockwell.com/2022/07/no_author/wheres-the-virus/
Revelation 18 KJV: https://www.biblegateway.com/passage/?search=Revelation+18&version=KJV
Revelation 18 MSG: https://www.biblegateway.com/passage/?search=Revelation+18&version=MSG
The Great Reset is Coming for you Children: https://off-guardian.org/2022/07/16/protect-your-children-because-the-great-reset-is-coming-for-them/
Dave Daubenmire, a veteran 35 year high school football coach, was spurred to action when attacked and eventually sued by the ACLU in the late 1990's for mixing prayer with his coaching. As a result of the experience, Coach heard the call to move out of coaching a high school team, to the job of coaching God's team. PASS THE SALT was formed to encourage the Body of Christ to step into the cultural war. "For we wrestle not against flesh and blood…" PASS THE SALT is convinced that God has given the Body a window of opportunity to take our culture back.
Video Membership Site – https://coachdavelive.video
Register for Events – https://coachdavelive.com/event
Support Coach's Ministry – https://coachdavelive.com/donate
Buy a Cross Hat or Shirt – https://coachdavelive.com/shop


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Ubuntu Linux tablet will turn into a makeshift desktop
BQ's new slate just needs an external display and input to become a PC.
Want to use your mobile device as a desktop, but would rather not go the Windows route? BQ might have just what you're looking for. The Spanish device maker is teasing the launch of an Ubuntu-based tablet that touts Convergence, a feature that turns your mobile Ubuntu gear into makeshift PCs. If you can scrounge up an external display, mouse and keyboard, you'll have your own little Linux workstation.
BQ isn't saying much about the device itself, but OMG Ubuntu claims that it'll be an Ubuntu version of the Aquarius M10, a 10-inch budget model with a quad-core MediaTek processor, 2GB of RAM and a 1,280 x 800 screen. It won't be a powerhouse, then. However, you won't have to wait too long to get the full scoop. The company will unveil its Ubuntu slate at Mobile World Congress in late February, and its availability likely revolves around the release of Ubuntu 16.04 Xerus Xenial (which touts Convergence) in late April.


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Jim Shaughnessy Essential Witness
Sixty Years of Railroad Photography
By Jim Shaughnessy, Kevin P. Keefe.
Hardcover, 11.75x10.75", 192 pages, 150 dutone illustrations. 2017.
"Jim Shaughnessy Essential Witness is a comprehensive overview of this well-known image maker's sixty years of activity as a railroad photographer.
"Starting in the late 1940s, Shaughnessy began documenting in earnest the rapidly changing railroad scene in the northeastern United States. His interests and travels also took him to other areas of the country to document the Rio Grande narrow gauge in Colorado, the UP Big Boys in Wyoming, and various locations in Canada. His timing was perfect: he was there to record the dramatic transition between the steam and diesel eras as well as document and record for posterity the workers behind the machines operating in the depots, roundhouses, and back shops of the American railroad environment. Lucius Beebe once described Shaughnessy as a '…master in the massive effects of black and white.'
"Included in the book are some 150 duotone photographs taken between 1948 and 1970, with emphasis on the 1950s and 1960s. Images include landscapes, cities, and towns; action shots of formidable trains barreling down the tracks; snaps of weary railroad workers; nighttime photos of shadowy enclaves within the rail yard; and many more. Shaughnessy's photographs offer a stunning portrait of Americana through a transportation lens."
"Jim Shaughnessy is an American photographer. He lives in Troy, New York."
"Kevin P. Keefe is a journalist and former publisher and editor of Trains magazine. He lives in Milwaukee, Wisconsin."


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Written by: Jeff Lemire
Illustrated by: Travel Foreman
Presenting the Eisner Award-winning writer Jeff Lemire's New York Times bestselling two-and-a-half-year run on Animal Man.
Meet Buddy Baker: Everyman. Family man. Animal man.
Armed with the unique power to take on the abilities of any animal, Buddy is a hero-turned-activist struggling with the challenges of being a husband and father.
When his four-year-old daughter, Maxine, suddenly starts exhibiting her own disturbing animal-based powers, Buddy begins an odyssey that will change his and his family's lives forever! In the world of Buddy Baker, nothing is ever as it seems.
Animal Man by Jeff Lemire Omnibus features the stunning artwork of Travel Foreman (Immortal Iron Fist) and Steve Pugh (Vertigo's Animal Man), along with Rafael Albuquerque (American Vampire), Timothy Green II (Annihilation: Conquest--Starlord) and more. Collects Animal Man #0-29, Animal Man Annual #1-2, and Swamp Thing #12 and #17 along with a brand-new introduction by Lemire and more than 80 pages of behind-the-scenes artwork in the making of this modern classic.


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Jesus' Call to Mission
Listen to these words of Jesus reflecting this reality in His life ...
Jesus said to them, "My food is to do the will of Him who sent Me, and to accomplish His work." John 4:34
"I can do nothing on My own initiative. As I hear, I judge; and My judgment is just, because I do not seek My own will, but the will of Him who sent Me." John 5:30
"For I have come down from heaven, not to do My own will, but the will of Him who sent Me." John 6:38
"I know Him; because I am from Him, and He sent Me." John 7:29
"And He who sent Me is with Me; He has not left Me alone, for I always do the things that are pleasing to Him." John 8:29
"We must work the works of Him who sent Me, as long as it is day; night is coming, when no man can work." John 9:4
And Jesus cried out and said, "He who believes in Me does not believe in Me, but in Him who sent Me. And he who beholds Me beholds the One who sent Me." John 12:44-45
"For I did not speak on My own initiative, but the Father Himself who sent Me has given Me commandment, what to say, and what to speak." John 12:49
"Truly, truly, I say to you, he who receives whomever I send receives Me; and he who receives Me receives Him who sent Me." John 13:20
"And this is eternal life, that they may know Thee, the only true God, and Jesus Christ whom Thou hast sent." John 17:3
"For the words which Thou gave Me I have given to them; and they received them, and truly understood that I came forth from Thee, and they believed that Thou didst send Me." John 17:8
"As Thou didst send Me into the world, I also have sent them into the world." John 17:18
Jesus therefore said to them again, "Peace be with you; as the Father has sent Me, I also send you." John 20:21
What stands out to you from these verses?
How does this impact your understanding of being sent by Jesus?


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Since I am participating in Charcutepalooza, I have a lot of homemade bacon in the fridge and freezer. I have already cured another batch of bacon, and will be headed out to pick up more pork belly, probably sooner than later. No more store bought bacon for me!
Since I have so much of this delectable treat, I wanted to make something other than a BLT. I love scones and biscuits with cheese and other additions, so adding a bit of bacon seemed like a winner. And it was.
Savory Bacon-Cheese Scones
3 slices bacon, sliced into strips
2 cups AP flour 2 tsp baking powder
1/2 tsp baking soda
1/2 tsp salt
1/8 tsp pepper
4 TB chilled butter, cut into small pieces
1 cup grated Gouda cheese
1 cup heavy cream
Cook the bacon pieces until crisp. Remove them from the pan, and drain on a paper towel.
Place the flour, baking powder, baking soda, salt and pepper into a medium bowl. Lightly whisk the dry ingredients to mix them. Using your hand, quickly mix the chilled butter into the dry ingredients until the butter is pea sized, using a pinching and squeezing motion. Or you can use a pastry cutter, or make the dough in a food processor. I didn't feel like cleaning a whole lot of stuff, so I opted for the one bowl method.
Add the reserved bacon, cheese and cream to the bowl. Using a fork, mix until a sticky dough is formed. Turn the sticky dough out onto a floured surface and knead a few times until the dough comes together, and loses it's stickiness. This only takes a few turns, so DO NOT OVER-KNEAD THE DOUGH!
Pat the dough out into a rough circle about 1/2 inch thick. Cut the circle into 8 scones. Place the scones onto a baking sheet lined with parchment or a silicone mat.
Bake your scones for about 20 minutes, until lightly browned.
Eat these scones right out of the oven, with a little extra butter slathered on if you desire.


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Science in Medicine Free access | 10.1172/JCI33297
1Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St. Radboud, Nijmegen, The Netherlands. 2Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. 3Center for Neuroscience and Regeneration Research, West Haven VA Medical Center, West Haven, Connecticut, USA.
Address correspondence to: Joost P.H. Drenth, Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St. Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 31-24-3614760; Fax: 31-24-3540103; E-mail: firstname.lastname@example.com.
Find articles by Drenth, J. in: JCI | PubMed | Google Scholar
1Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St. Radboud, Nijmegen, The Netherlands. 2Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA. 3Center for Neuroscience and Regeneration Research, West Haven VA Medical Center, West Haven, Connecticut, USA.
Address correspondence to: Joost P.H. Drenth, Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St. Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 31-24-3614760; Fax: 31-24-3540103; E-mail: firstname.lastname@example.com.
Find articles by Waxman, S. in: JCI | PubMed | Google Scholar
Published December 3, 2007 - More info
The voltage-gated sodium-channel type IX α subunit, known as Nav1.7 and encoded by the gene SCN9A, is located in peripheral neurons and plays an important role in action potential production in these cells. Recent genetic studies have identified Nav1.7 dysfunction in three different human pain disorders. Gain-of-function missense mutations in Nav1.7 have been shown to cause primary erythermalgia and paroxysmal extreme pain disorder, while nonsense mutations in Nav1.7 result in loss of Nav1.7 function and a condition known as channelopathy-associated insensitivity to pain, a rare disorder in which affected individuals are unable to feel physical pain. This review highlights these recent developments and discusses the critical role of Nav1.7 in pain sensation in humans.
Pain is one of the most pervasive symptoms in clinical medicine; it occurs in a multitude of clinical conditions and is encountered by clinicians in every subspecialty. Yet treatment of chronic or recurrent pain remains challenging, in part because the therapeutic armamentarium is incomplete. Hopefully, this will change as a result of increased understanding of the molecular basis of pain. Over the past several years, elucidation of the genetic defects underlying three monogenic pain disorders has provided important insights about human pain and its molecular substrates. Here, we briefly review these recent advances.
The unraveling of the human genome may allow us to compare variations at the genetic level with interindividual differences in pain thresholds and pain perception. Most studies in the past have focused on genetic polymorphisms that might be responsible for interindividual differences in pain perception. For example, a common functional SNP (V58M) in the catechol-O-methyltransferase (COMT) gene modifies pain sensitivity (1). COMT has broad biological functions, including the metabolism of catecholamines, such as neurotransmitters, that modulate neuronal cell signaling. Individuals homozygous for the Val genotype are less sensitive to pain compared with those with Met homozygosity (1); however, the differences in pain sensitivity between groups are relatively subtle. A more dramatic set of observations has been reported in studies of rare Mendelian disorders. Over a decade ago, mutations in the voltage-dependent calcium channel, P/Q type 1A α subunit (CACNL1A4) were identified in families with familial hemiplegic migraine, a subtype of migraine with aura and paralysis (2). This finding indicated that channel dysfunction could lead to human disorders in which pain is a prominent symptom. More recent genetic studies have identified the voltage-gated sodium-channel type IX α subunit (SCN9A, referred to herein as Nav1.7) as a key player in three conditions in which recurrent pain or the inability to sense pain is a prominent symptom (3–8). These disorders — primary erythermalgia (PE), paroxysmal extreme pain disorder (PEPD), and channelopathy-associated insensitivity to pain (CIP) — are typified by very different pain phenotypes. Remarkably, recent work has shown that different types of channelopathies (diseases caused by disturbed function of ion channel subunits or the proteins that regulate them), all involving the same Nav1.7 sodium channel, underlie all three of these disorders (3–8). These discoveries allow better understanding not only of the molecular pathogenesis of these particular disorders but also of the molecular pathophysiology of pain (9).
Voltage-gated sodium channels play a critical role in the generation and conduction of action potentials and are thus important for electrical signaling by most excitable cells (10, 11). Sodium channels are integral membrane proteins and are comprised of a large α subunit, which forms the voltage-sensitive and ion-selective pore, and smaller auxiliary β subunit(s) that can modulate the kinetics and voltage dependence of channel gating (12). To date, we know of 9 isoforms of the sodium-channel α subunit (Nav1.1–Nav1.9), each with a unique central and peripheral nervous system distribution (10). Four closely related sodium channels (Nav1.1, -1.2, -1.3, and -1.7) are encoded by a set of 4 genes (SCN1A, SCN2A, SCN3A, and SCN9A, respectively) located within a cluster on chromosome 2q24.3. Mutations in the genes encoding Nav1.1, -1.2, and -1.3 are responsible for a group of epilepsy syndromes with overlapping clinical characteristics but divergent clinical severity (13, 14). Here, we focus on one of the α subunits, Nav1.7, because of its critical role in pain sensation.
Nav1.7 is encoded by SCN9A, a 113.5-kb gene comprising 26 exons (OMIM 603415) (Figure 1A). The encoded sodium channel is composed of 1977 amino acids organized into 4 domains, each with 6 transmembrane segments (15), and is predominantly expressed in the dorsal root ganglion (DRG) neurons and sympathetic ganglion neurons (16) (Figure 1B). Immunohistochemical studies show that Nav1.7 is present at the distal ends of the wire-like projections of neurons known as neurites, close to the impulse trigger zone where neuronal firing is initiated (16) (Figure 2). Interestingly, the large majority of DRG neurons that express Nav1.7 are pain sensing (nociceptive), suggesting a role for this sodium channel in the pathogenesis of pain (17). In addition to Nav1.7, Nav1.8 and Nav1.9 are also predominantly present in small nociceptive sensory neurons and the nerve fibers emanating from them (18, 19).
Mutations in the sodium-channel subunit Nav1.7 that are associated with the genetic pain disorders PE, PEPD, and CIP. (A) Nav1.7 is encoded by the 113.5-kb gene SCN9A, comprising 26 coding exons. The identity and location of known patient mutations in Nav1.7 that have been linked to PE (*), PEPD (^), and CIP (#) are shown. Note that the mutations are spread over the entire gene sequence; however, mutations linked to PEPD tend to be located closer to the 3′ end of the gene. (B) A schematic of the Nav1.7 sodium-channel subunit showing the 4 domains (D1–D4), each with 6 transmembrane segments. Locations of known mutations associated with genetic pain disorders PE, PEPD, and CIP are shown. COOH indicates the C-terminus of the peptide chain. HN indicates the N-terminus of the peptide chain.
Neuronal Nav1.7 channels. Nav1.7 (shown here in red after immunocytostaining with anti-Nav1.7 antibody; Alomone Reagents) within the tip of a growing neurite from rat DRG neuron in culture. Image kindly provided by Joel A. Black, Department of Neurology, Yale University, New Haven, Connecticut, USA.
In sensory neurons, multiple voltage-dependent sodium currents can be differentiated by their gating kinetics and voltage dependence and can also be defined by their sensitivity to the voltage-gated sodium-channel blocker tetrodotoxin (12). The Nav1.7 channel produces a rapidly activating and inactivating current that is sensitive to submicromolar levels of tetrodotoxin. This is in contrast with Nav1.8, which is also present within DRG neurons but is fairly resistant to tetrodotoxin. Nav1.7 appears to be important in early phases of neuronal electrogenesis. Nav1.7 is characterized by slow transition of the channel into an inactive state when it is depolarized, even to a minor degree, a property that allows these channels to remain available for activation with small or slowly developing depolarizations, usually mimicked by electrophysiologists as ramp-like stimuli (20). Thus, Nav1.7 acts as a "threshold channel" that amplifies small, subtle depolarizations such as generator potentials, thereby bringing neurons to voltages that stimulate Nav1.8, which has a more depolarized activation threshold and which produces most of the transmembrane current responsible for the depolarizing phase of action potentials (21). In this regard, Nav1.7 is poised as a molecular gatekeeper of pain detection at peripheral nociceptors.
A number of (inflammatory) mediators, such as prostaglandin (22), adenosine (23), and serotonin (24), affect the electrophysiological properties of voltage-gated sodium channels. These mediators increase the magnitude of the current, lead to activation of the channel at more hyperpolarized potentials, and enhance the rates of channel activation and inactivation. As a consequence, inflammation can sensitize nociceptive neurons. In an experimental model of inflammatory pain in which an irritant was injected into the hind paw in rats, Nav1.7 protein expression was upregulated within DRG neurons that project their axons to the inflamed area (25), a change that should increase excitability of these cells. Collectively, these data suggest that Nav1.7 contributes, at least in part, to pain associated with inflammation.
To obtain insight into the physiological role of Nav1.7, Nassar et al. generated targeted knockout mice that lack Nav1.7 within nociceptive DRG neurons (26). Selective deletion of Nav1.7 in nociceptors from mice produces a phenotype in which heat-induced pain thresholds are minimally altered, there is no change in punctate mechanical pain threshold, and cold-evoked channel activity is unchanged. In contrast, there is a general failure to develop pain or hypersensitivity in response to inflammatory stimuli, while neuropathic pain (chronic pain resulting from injury to the nervous system) remains intact. These results are consistent with an important role of Nav1.7 in setting the inflammatory pain threshold. To assess the role of Nav1.7 further, especially in relation to other sodium channels expressed in peripheral sensory neurons, the same researchers created mice deficient in both Nav1.7 and Nav1.8 (27). Mice deficient in Nav1.8 had deficits in sensing inflammatory pain (initiated by tissue damage/inflammation) and visceral pain (initiated by damage or injury to internal organs) but not neuropathic pain (28). The thermal pain threshold in mice deficient in both Nav1.7 and Nav1.8 mice was twice that of mice lacking only Nav1.7. There was no effect on induced neuropathic pain in the double knockouts, and the effect of the loss of Nav1.7 in raising the threshold for inflammatory pain was so overwhelming that no additional effect of Nav1.8 deletion was seen. Collectively, these results clearly implicate Nav1.7 as a major sodium channel in peripheral nociception and suggest a functional link to Nav1.8. Although insightful, these data should be interpreted with caution, as direct evaluation of pain in mice is not possible. Instead, researchers rely on behavioral changes of animals such as signs of paw guarding, lifting, and limping. As a consequence, the relevance of the observed changes to human pain remains to be determined.
Primary or idiopathic erythermalgia (OMIM 133020) is an autosomal dominant, inherited disorder. Clinically, PE is characterized by attacks or episodes of symmetrical burning pain of the feet, lower legs, and sometimes hands, elevated skin temperature of affected areas, and reddened extremities (Figure 3) (29–32). PE is sometimes termed erythromelalgia, although some authorities reserve the latter term for a condition that is caused by arteriolar inflammation as a result of platelet-rich thrombi in the end-arterial microvasculature, in which the platelet count is invariably elevated (> 400 × 109 cells/l) and a short course of aspirin brings swift relief (33). Platelet counts in PE are invariably normal, and aspirin is ineffective. Patients with PE usually develop symptoms within the first decade of life. As the disease progresses, the erythema can extend to the upper legs, nose tip, earlobes, and chin. In the early years of the disease, the erythema is intermittent, but at later ages, the feet and hands may be constantly red and edematous. Complaints are provoked by exercise, prolonged standing, or exposure to warmth, which usually compels patients not to wear socks or closed shoes, even during the winter. Patients typically sleep with uncovered feet, often cooled by a fan. Cold alleviates these complaints, and some patients search for relief by immersion of feet in ice-cold water. The greatest threat is that these actions can lead to trench foot with subsequent skin infections and even to limb amputations (34).
Red feet and lower legs in a patient with primary erythermalgia. Image courtesy of The Erythromelalgia Association.
A genome-wide linkage study in a large kindred of individuals with PE detected strong evidence for linkage with polymorphic markers on chromosome 2q (35). Haplotype analysis in four additional families confirmed the locus, and recombinant events defined the critical interval to 7.94 cM. Subsequent analysis of another family allowed narrowing of the region to 5.98 cM (3). This interval contains five genes encoding sodium-channel α subunits. After confirming the presence of this genetic interval in two affected families, two candidate genes, including SCN9A, were tested (3). A missense mutation (L858H) in SCN9A was identified that segregated with the disease in a three-generation Chinese family while an I848T mutation was present in a single sporadic case. Both mutations affected conserved residues in the pore-forming α subunit of the Nav1.7 channel, and multiple alignment indicated that the affected amino acids are conserved in sodium channels. Subsequent independent studies confirmed these findings and identified missense mutations (mutations in which one amino acid is replaced by another) in individuals from all of the families that had been examined in the original linkage study (4). To date, nearly a dozen SCN9A mutations in multiple families have been identified as causing PE (5, 6, 36–41). Most of these mutations have been found in families from The Netherlands, the United States, Belgium, France, Canada, and China, with a clear autosomal dominant inheritance pattern, although a few represent de novo founder mutations (a mutation that arose in the DNA of an individual several generations earlier and whom is considered to be a founder of a distinct population) (5, 6).
All of the PE mutations detected to date are missense mutations that change important and highly conserved amino acid residues of the Nav1.7 protein. The majority of mutations that cause PE are located in cytoplasmic linkers of the Nav1.7 channel, but some mutations (e.g., F216S and N395K) are located in transmembrane domains of the channel (Figure 1B). The PE mutations cause a hyperpolarizing shift in the voltage dependence of channel activation, which allows the channel to be activated by smaller than normal depolarizations, thereby likely enhancing the activity of Nav1.7. Most of the PE mutations also slow deactivation, thus keeping the channel open longer once it is activated (Figure 4). In addition, in response to a slow, depolarizing stimulus, most mutant channels will generate a larger than normal inward sodium current. Repriming, which is the recovery from inactivation, has been shown to be faster for channels possessing specific PE mutations (5, 6, 36, 38, 39, 42, 43). Each of these alterations in activation and deactivation can contribute to the hyperexcitability of pain-signaling DRG neurons expressing these mutant channels, thus causing extreme sensitivity to pain (hyperalgesia) (44). While the expression of PE Nav1.7 mutations produces hyperexcitability in DRG neurons, studies on cultured rat sympathetic ganglion neurons indicate that expression of these same PE mutations in sympathetic ganglion neurons, that is, another cell type in which Nav1.7 is normally expressed, leads to a reduction of excitability in these cells (43). This occurs because Nav1.8 channels, which are relatively resistant to inactivation by depolarization and are selectively expressed in addition to Nav1.7 in DRG neurons, are not present within sympathetic ganglion neurons (43). These PE mutations produce membrane depolarization due to an overlap between activation and steady-state inactivation, which inactivates sodium channels other than Nav1.8. The depolarization brings DRG neurons closer to the threshold of activation for the Nav1.8 channels that are present within DRG neurons, thus increasing the excitability of these cells. But in sympathetic ganglion neurons, which lack Nav1.8, the inactivation of the sodium channels results in reduced excitability. Introduction of Nav1.8 allows these cells to fire action potentials, despite depolarization of resting membrane potential (43). This illustrates an important principle, that the phenotype associated with a monogenic channelopathy is not predictable on the basis of the changes in physiology of the mutant sodium channel per se. The effect depends on the cell background in which the mutant channel is expressed, so that physiological interactions that are specific to particular types of neurons (in the case of PE, the physiological interaction of Nav1.7 and Nav1.8) may better explain the symptoms experienced by patients (45). These data provide an explanation of why PE presents with pain due to hyperexcitability of nociceptors together with sympathetic dysfunction (flushing/erythema) that is at least in large part due to hypoexcitability of sympathetic ganglion neurons (43).
Four clinical situations in which Nav1.7 channel activity is altered. PE and PEPD are autosomal dominant (AD) conditions, while CIP is inherited via an autosomal recessive (AR) trait. The mutations of the Nav1.7 channel grossly dictate that there is a gain of function (increased channel activity) in PE and PEPD, while Nav1.7 channel function is lost (absent) in CIP. The resultant phenotype is reflected in the lower row. In humans, the Nav1.7 mutations result in pain in the feet and hands (in PE) or ocular, mandibular, and/or rectal pain (in PEPD). In CIP, there is a loss of Nav1.7 channel function, resulting in an inability to register pain.
The condition first described in 1959 as rectal, ocular, and submaxillary pain (46) has recently been renamed PEPD (OMIM 167400) (47). PEPD is an autosomal dominant disorder characterized by paroxysmal episodes (of sudden onset and increased intensity upon recurrence) of pain at different body sites, accompanied by skin flushing. There are four well-defined types of painful episodes. The first occurs at birth with an archetypical red flush spread over the buttocks and down the backs of the legs to the soles of the feet (48). A second pattern involves rectal pain that is most evident in childhood and typically occurs at defecation, as a sudden (short-lived) onset of burning pain that moves down to the lower extremities (47). The pain is followed by red discoloration of the skin of the pubic area, scrotum, perineum, buttocks, and the backs of both legs and soles of the feet, lasting for about an hour. The ocular pattern of pain is described as an intense burning sensation, lasting 30–60 seconds, followed by conjunctival injection (nonuniform redness of the conjunctiva) and erythema of the eyelids and of the skin in the temporal region, lasting a few minutes (49, 50). Attacks may be precipitated by yawning and crying but also occur spontaneously. Last, there is paroxysmal pain in the mandibular region on both sides, with associated transient erythema of the overlying skin, together with autonomic manifestations such as salivation, lacrimation (tearing), and rhinorrhoea (running nose). Symptoms may be induced in these subjects by the ingestion of cold drinks or acidic or spicy foods. Moreover, these individuals are prone to a strange feeling of pressure or even a cramp-like sensation in the nose, following exposure of the face to bright sunlight or strong winds. In some patients, the painful crisis may be associated with nonepileptic tonic seizures and cardiac asystole (50). Carbamazepine, an antiepileptic drug, is effective in some patients, but high dosages may be needed to achieve efficacy (51). A principal target of anticonvulsant drugs in PEPD is most likely the sodium channels located in the peripheral sensory neuron (52).
A genome-wide linkage search in one large pedigree with PEPD led to linkage to a region of chromosome 2q24.3 (7). Haplotype analysis identified several recombinants, which narrowed the critical region down to 16 cM. As this region contained SCN9A, the investigators sequenced this gene and identified eight heterozygous missense mutations in eight families. All mutations were private, i.e., each family possessed a unique mutation. Interestingly, one individual was compound heterozygous for R996C and a de novo mutation (V1298D). This individual was more severely affected than his father. In another family in whom R996C was the only mutation identified, there was a less severe phenotype. In five families with typical PEPD, there were no SCN9A mutations found (7). These findings are consistent with the genetic heterogeneity of PE and suggest locus heterogeneity in PEPD.
Functional analysis of three mutations (I1461T, T1464I, and M1627K) that are attributed to PEPD was carried out in transfection experiments using a cell-based assay in which a mutant sodium channel was introduced into cells that normally do not express sodium channels (7). On the basis of these experiments, these mutations were reported to impair inactivation of the α subunit of the Nav1.7 channel (Figure 4). Steady-state inactivation was only partial in mutant channels and had shifted toward higher voltages in the context of near-normal activation. These changes are predicted to promote prolonged action potentials and repetitive neuron firing in response to provoking stimuli, such as stretching and exposure to cold temperatures (7). The different effects of PE mutations (which enhance channel activation) and PEPD mutations (which impair channel inactivation) might contribute in part to the different symptomatology in these two disorders. In either case, these results are in keeping with the notion that Nav1.7 plays a critical role in modulation of the pain threshold.
In contrast with PE and PEPD, CIP (OMIM 243000) is an autosomal recessive disorder (8, 53). Individuals with congenital indifference to pain have painless injuries beginning in infancy but otherwise normal sensory responses upon examination. Perception of passive movement, joint position, and vibration is normal, as are tactile thresholds and light touch perception. There is intact ability to distinguish between sharp and dull stimuli and to detect differences in temperature. The insensitivity to pain does not appear to be due to axonal degeneration, as the nerves appear to be normal upon gross examination (8). The complications of the disease follow the inability to feel pain, and most individuals will have injuries to lip or tongue caused by biting themselves in the first 4 years of life. Patients have frequent bruises and cuts, usually have a history of fractures that go unnoticed, and are often only diagnosed because of limping or lack of use of a limb. The literature contains very colorful descriptions of patients with congenital inability to perceive any form of pain. Individuals have been reported to walk over burning coals and to place knives through their arms and drive spikes through a hand as part of crucifixion reenactment (8).
Cox et al. described 6 patients stemming from three consanguineous families of northern Pakistani origin (8). The highly inbred population allowed for autozygosity mapping (homozygosity in which the two alleles are identical by descent), and a genome-wide search led to the identification of a 20-cM homozygous region on chromosome 2q24.3 with a maximum 2-point lod score of 3.2 (a lod score of 3 or more is generally taken to indicate that 2 gene loci are close to each other on the chromosome; a lod score of 3 means the odds are a thousand to one in favor of genetic linkage). Further refinement of the region to 11.7 Mb was facilitated by addition of a third family. A bioinformatics approach suggested SCN9A as the best candidate disease gene. Sequencing led to the identification of different homozygous mutations of SCN9A, and each family possessed a unique mutation. The mutations were identified in exon 10 (S459X), exon 13 (I767X), and exon 15 (W897X) (8). All mutations are nonsense mutations, that is, they change a codon that codes for one amino acid into a codon that does not specify any amino acid. These results were confirmed by two studies: one study in 9 western European and North and South American families (54) and another in a large Canadian family (55). Both studies used linkage analysis, searched for homozygous haplotypes, identified the same gene, and detected 10 truncating SCN9A mutations. The majority of affected patients were homozygous for SCN9A mutations, but 2 patients were compound heterozygous for different SCN9A mutations (54). Functional studies show that CIP-associated mutations cause loss of function of Nav1.7 (8, 55) (Figure 4). This is in contrast with the genetic basis of PE and PEPD, in which the disorders result from gain-of-function mutations. In DRG neurons expressing mutant Nav1.7, the firing of action potentials was greatly impaired and comparable to background (8).
Collectively, the data from recent studies indicate that Nav1.7 function is an essential and nonredundant requirement for nociception in humans. However, the genetic findings do not fully explain the clinical presentations described. Given the widespread expression of Nav1.7 throughout the sensory nervous system, it is remarkable that PE and PEPD have such different tissue distributions of pain. Moreover, the variability in age of clinical onset remains unexplained. Also, although physiological studies have revealed a temperature-dependent shift that brings the activation threshold of PE mutant channels close to that of wild-type Nav1.7 channels, possibly contributing to the alleviation of pain by cooling in PE (56), the paroxysmal nature of the painful attacks in PE and PEPD is not fully understood. These observations argue that there may be factors other than the mutated Nav1.7 channel, such as still–to be–identified binding partners (other protein molecules that the channel interacts with, such as fibroblast growth factor homologous factors, which are known to modulate the physiological properties of the sodium-channel isoforms) that are important in determining the topographic and temporal pattern of these symptoms (57, 58).
The important role of mutations that change the sequence of SCN9A in various pain disorders suggests that SCN9A polymorphisms might contribute to intersubject variability in the sensation of pain in humans. This should encourage researchers to look for SCN9A polymorphisms that are associated with chronic pain disorders other than PE and PEPD. It might also be expected that some SCN9A polymorphisms might confer protection against pain.
Neuropathic pain in PE is therapeutically challenging (59). Indeed, Nav1.7 represents a target that might be inhibited by small molecules in a subtype-specific or state-dependent manner during ectopic discharge, producing pain relief while sparing other neuronal functions. The development of subtype selectivity of potentially therapeutically useful molecules has proven to be a challenge. Several classes of drugs, including local anesthetics (e.g., lidocaine), systemic antiarrhythmics (e.g., mexiletine), and antiepileptic drugs such as phenytoin or carbamazepine, target sodium channels and act as channel blockers, although they do not show a high degree of channel subtype specificity and thus inhibit many types of sodium channels rather than selectively blocking Nav1.7 (52, 58). These agents, which act primarily through use-dependent blocks of sodium channels indeed are part of the armamentarium for the treatment of many types of chronic pain, including some forms of neuropathic pain. Several of these drugs have shown a degree of efficacy in patients with pain due to mutations in Nav1.7. Some PE patients have responded to oral mexiletine (600 mg daily) (60). Interestingly, some PE mutations attenuate the inhibitory effect on sodium channels of the sodium-channel blocker lidocaine, while other PE mutations do not, suggesting that the response to treatment with sodium-channel blockers in PE may depend on the specific genotype (61). Carbamazepine is effective in some patients with PEPD, as it stabilizes the inactivated state of sodium channels, meaning that fewer of these channels are available to open, making brain cells less excitable (7). In contrast, preliminary results in PE indicate low or absent effectivity of this drug (62). Moreover, in those cases in which lidocaine or mexiletine are helpful in PE, the efficacy of these agents is only partial or transient (63).
In conclusion, these observations, while drawn from a small number of patients, suggest that blockade of voltage-gated sodium channels is a promising therapeutic option for the treatment of pain but emphasize the need for the design of more highly focused, Nav1.7-specific blockers or genetically tailored pharmacological options for future testing. There will undoubtedly be progress along these lines in the future.
We thank the patients who participated in the studies that are described in this review. J.P.H. Drenth is a recipient of The Netherlands Organization for Health Research and Development VIDI award research grant. S.G. Waxman is the recipient of grants from the Department of Veterans Affairs and the Erythromelalgia Association.
Address correspondence to: Joost P.H. Drenth, Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St. Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 31-24-3614760; Fax: 31-24-3540103; E-mail: firstname.lastname@example.com.
Nonstandard abbreviations used: CIP, channelopathy-associated insensitivity to pain; DRG, dorsal root ganglion; Nav1.7, sodium channel encoded by SCN9A; PE, primary erythermalgia; PEPD, paroxysmal extreme pain disorder; SCN9A, voltage-gated sodium-channel type IX α subunit.
Conflict of interest: The authors have declared that no conflict of interest exists.
Reference information: J. Clin. Invest.117:3603–3609 (2007). doi:10.1172/JCI33297.


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King Solomon Mixed Different Religious Practices and God Was Not Pleased
In the Old Testament of the Bible, God tells his people to not marry those from other nations, folks who believe differently and worship other gods (Deuteronomy 7:3). This isn't so much to keep the bloodline of his chosen people pure but to keep them safe and their faith in God intact.
That's why he says to not worship other Gods (Exodus 34:14). Mixing religions never works.
King Solomon, the wisest man who ever lived, wasn't so wise when it came to women. Aside from having a ton of wives and lots of women on the side, many came from other nations who believed in different gods and not the God of the Bible.
It could be Solomon forgot what God commanded his people to do or that Solomon didn't care. It might be he thought the rule was silly or it didn't apply to him. Perhaps he assumed he was too smart to let his foreign-thinking wives influence him. Newsflash: he wasn't (1 Kings 11:2).
In his old age, his foreign wives distract him, turning his heart away from God and toward foreign gods. This divides his attention, and God isn't pleased.
Though Solomon doesn't fully turn his back on God, his devotion waivers. He splits his heart's focus. In addition to biblical God, Solomon also pursues Ashtoreth, the goddess of the Sidonians, and Molek, the god of the Ammonites. He honors these gods and worships them (1 Kings 11:4-13).
God Is a Jealous God
The Bible says that God is a jealous God (Deuteronomy 6:15 and Exodus 34:14). He's jealous of our attention and isn't content with part of it. He wants all of it. Because Solomon divides his attention, God removes some of the blessings he had previously given to the king and punishes him.
If we want a relationship with the God of the Bible, we need to do what the Bible says. We must give God our full attention. If we try to mix in other spiritual or religious practices into our pursuit of biblical God, it dishonors him and splits our attention.
If we're merely trying to make ourselves feel good or find some sort of enlightenment, we can pursue any course that works for us. We can mix religions, practices, and philosophies to produce something that makes us happy. But that's as far as it goes.
However, if we want a relationship with the God of the Bible, we need to do what the Bible says and pursue only him. Mixing different religious practices won't work. If we try that, we run the risk of making God into our own image instead of recognizing that he made us in his image.
Mixing different religious practices together is making up our own religion. It may make us feel good now, but it offers little hope of spending eternity with the God of the Bible. With time in perpetuity at stake, we better do what the Bible says and ignore all other ideas as mere distraction.
Peter DeHaan writes about biblical Christianity to confront status quo religion and live a life that matters. He seeks a fresh approach to following Jesus through the lens of Scripture, without the baggage of made-up traditions and meaningless practices.
Read more in his books, blog, and weekly email updates.


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The Power of Attorney and abuse of the elderly
By PATRICIA EDGAR and DON EDGAR | On 29 July 2020
Australia has a long way to go and COVID is lifting the scab revealing how neglect and absolute indifference have exposed these communities of older people to an end of life nightmare.
The interim report from the Australian Royal Commission into Aged Care, Quality and Safety titled 'A Shocking Tale of Neglect' pulls no punches in its description of the system of Age Care in Australia.
A 'Catch 22' is a dilemma from which there is no escape because of mutually conflicting conditions. The term, made famous in 1961, by Joseph Heller in his bitterly funny satire set in World War 11, was the story of a bombardier named Yossarian, who could never complete his flying missions because of a bureaucratic rule: a man is considered insane if he willingly continues to fly dangerous combat missions, but if he makes a formal request to be removed from duty, he is proven sane and therefore ineligible to be removed.
Deciding to grant an enduring Power of Attorney can be a Catch 22: we are prudent to sign one, given the hazards of old age, but increasing anecdotal evidence is showing we can be putting ourselves at risk from abusive and arbitrary decisions by the Attorney(s).
An enduring power of attorney is a legal document whereby you (the Principal), grant legal authority to someone else (such as a relative or friend) to make decisions for particular purposes on your behalf and in your best interests. It can be for financial matters, medical matters, personal matters or 'to do anything on your behalf.' There is no consistency in these documents across the states and territories, they are not well understood, their impact is unexamined and anecdotal evidence is piling up showing they can be used as a major enabler of elder abuse.
Elder abuse has been defined by the World Health Organisation as 'a single, or repeated act, or lack of appropriate action, occurring within any relationship where there is an expectation of trust which causes harm or distress to an older person'. Such abuse can take various forms, including financial, physical, psychological, emotional, and sexual abuse.
Financial abuse, possibly the most easily substantiated form of abuse is increasingly common as a Power of Attorney is well positioned to control and manipulate assets and property belonging to a principal, to delve into bank accounts to serve their own interests and if one sibling is holding the Attorney he or she has the clout and control over assets including bank accounts. Families have gone to war over the contents of the backyard shed.
Australia's Age Discrimination Commissioner, The Hon. Dr Kay Patterson AO has called on the state and territory Attorney-Generals to act urgently to implement the Australian Law Reform Commission's recommendations on powers of attorney at the COAG meeting July 27. She argues current rules for powers of attorney which differ from state to state cause confusion within families, within aged care facilities and among experts across jurisdictions.
COVID 19 has lifted a scab concealing the dysfunction in aged care facilities including elder abuse in its multiple forms. Financial hardship stemming from the pandemic has led to increasing cases revealed through lawyers, peak bodies and frontline workers of older people having their money misused or stolen by the people meant to be helping them manage their finances. There is growing evidence such abuse is often occurring within families.
If someone has their faculties there is Elder Rights Advocacy group (email@example.com) to appeal to if they are feeling pressured to make decisions you don't want to make, wanting information or support. But what of those who are unable to speak on their own behalf? Harmonising powers of attorney would enable a national education campaign to inform those making a power of attorney and those appointed about their responsibilities.
While evidence of financial abuse may be easier to ascertain, emotional or psychological abuse is well hidden and anyone attempting to expose such practices must follow a complex maze of legal apparatus with no clear exit.
We decided to test the system when a friend who was a regular visitor to Patricia's sister, who suffered from dementia and was in an aged care facility, was abruptly and arbitrarily ordered out, mid visit, when she believed loving interaction was occurring. Next day two more friends were denied access. Enquiries revealed these actions by the care provider occurred on the order of the Attorneys who wanted to block access of someone else so denied all access.
Global research indicates the critical importance to the well being of an individual in care to continued engagement with loving friends and family. There was no consideration of the fact that the interaction they interrupted was actively enjoyed by the resident or that the action reversed a long-standing norm of best practice by the residence.
We approached Office of the Public Advocate and The Victorian Equal Opportunity and Human Rights Commission ('the Commission') to see if the general principle of the duty of care of aged care facilities could be investigated and clarified. The Commission stated it was not their role to advocate nor provide legal advice.
Their role includes educating, reporting, reviewing and intervention functions under the Charter. If a person believes there has been a breach of their human rights under the Charter, and wishes to make a complaint committed by a "public authority" (such as a Local Council, a State Government Department or Statutory Authority), they can contact the Victorian Ombudsman who can investigate complaints about administrative actions and decisions made by government authorities.
The Public Advocate of Victoria also could not take up the issue and suggested an approach to the Victorian Administrative Appeals Tribunal (VCAT). That organisation's application for Order lists the categories they respond to relevant to any submission which include 'Declare whether an enduring power of attorney is valid' and 'Give advice about an enduring power of attorney' but when the application asked whether a care facility could arbitrarily deny access to visitors they ruled that an enduring power of attorney gave that authority and would make no comment on the role of the Aged Care facility in such a circumstance.
As we are living so much longer and medical science is keeping us alive with multiple co-morbidities, including dementia, there is no question we do need support and care in older age. We need the protection and advocacy of a trusted child or friend who will stand up for our rights, our dignity, our mental and physical well-being and protect us from neglect especially in aged care.
The interim report from the Australian Royal Commission into Aged Care, Quality and Safety titled A Shocking Tale of Neglect pulls no punches in its description of the system of Age Care in Australia, calling it 'unsafe and uncaring' 'cruel and harmful', 'poorly managed', lacking 'transparency and accountability' with older people 'left isolated and powerless'. The Report documents hideous examples of neglect: inadequate management of wounds, poor continence management, malnutrition, assaults by staff, widespread over medication, patchy palliative care with residents dying in distress.
No one looks forward to going into 'an old-folks- home', and when faced with no option, approach their future with dread and often subsequent trauma. An individual's contribution and hard work throughout life can lead to an end that is joyless, bereft of purpose and unsafe. It is the proverbial scrap heap so choosing an Attorney is a prudent choice.
Yet there is a problem? It is a hidden problem in our society as those who sign usually are not able to complain when things go wrong, even if they understand what is happening. And our system does not acknowledge there is any problem.
The Report includes 43 recommendations for law reform. The overall effect will be to safeguard older people from abuse and support their choices and wishes through:
? improved responses to elder abuse in residential aged care;
? enhanced employment screening of care workers;
? greater scrutiny regarding the use of restrictive practices in aged care;
? building trust and confidence in enduring documents as important advanced planning tools;
? protecting older people when 'assets for care' arrangements go wrong;
? banks and financial institutions protecting vulnerable customers from abuse;
? better succession planning across the self-managed superannuation sector;
? adult safeguarding regimes protecting and supporting at-risk adults.
Australia has a long way to go and COVID is lifting the scab revealing how neglect and absolute indifference have exposed these communities of older people to an end of life nightmare.
An important challenge is to ensure quality care in the best interests of the individual and as well as ensuring no institutional neglect and abuse that means overseeing the ways by which attorneys act towards the people in their care.


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Get Ideas For Your Freeform Swimming Pool
Need inspiration for the pool of your dreams? Freeform pools are the perfect tie-in to your nature-oriented landscaping. With the ability to fit perfectly into any space, these freeform swimming pools are not defined by straight lines or hard angles. Freeform pools are often lagoon-style or natural style and incorporate rock features, waterfalls, and stone decking. Freeform pools provide a natural design that is perfect for recreation, home enhancement, and entertaining. This swimming pool style is relaxed and allows for private, cozy corners and drifting aimlessly on a raft.
At Premier Pools and Spas, we design your freeform swimming pool to blend into the surrounding landscape. All measurements are customized to the specific site. We transform your backyard into a private retreat, where you can swim, splash, sun, relax and enjoy time together with friends and family.


text: Medium Dave: the question of race is a very contentious issue here (as is plainly obvious). SciFo does indeed have a preponderance of regular posters who regularly harp on this issue to advance their racist agendae. SciFo also has a preponderance of sockpuppets - banned posters returning under new names. It in no way means you are either of those things, it simply means that this is the reality here, and it needs to be taken in to consideration.


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Healthy Conversation, Communication and Agreements: More Resources
Communication by Connie Starzynski from the Art of Administration was written as a guide to administrators and Waldorf school leaders to shed light on the dynamics of communication of all kinds in a Waldorf school.
Speaking, Listening and Understanding by Heinz Zimmerman is a book that goes deeply into the art of conversation in groups and how, by bringing new consciousness into our speaking and listening we can transform our work together.
A Sample Communications Covenant is a document showing how one community created and articulated their agreements about communications.
Communication in a Young School from the Young Schools Guide is a short article by David Mitchell about the ways that groups involved in creating a school can focus their attention on the topic of healthy communications.
Non-Violent Communication: An Introduction by Marshall Rosenberg is a 35-page booklet that outlines the basics of NVC. Rosenbloom is the founder of the NVC movement and has helped thousands of people and organizations review, understand, refine and transform their skills in healthy communication.
Click on the article names to go to the document.


text:
Changes in Wind Turbine Setbacks
Author: | Europe, France, Germany, Health, Human rights, New Zealand, Noise, Nova Scotia, Ontario, Property values, Regulations, Safety, Scotland, Sweden, U.K.
Translate: FROM English | TO English
Translate: FROM English | TO English
Note that Setbacks can have both physical safety rationale – for reasons of potential injury – and noise rationale – for reasons of annoyance and health effects
United Kingdom
Derek Taylor, 1991, "How to Plan the Nuisance Out of Wind Energy", suggested setback from wind turbines with a 30 metre rotor to roadways and lot lines, of 50 metres adequate to a lightly traveled road, 100 metres to a heavily traveled road, and 120 to 170 metres to a home [4-5.7 times rotor diameter].
UK Noise Association, 2006, states, "It would be prudent that no wind turbine should be sited closer than 1 mile (1600 metres) from the nearest dwellings … Wind farms should only be located in areas where the "swish, swish, swish" of the turbines will not cause noise problems for people."
United Kingdom – Scotland
From the limits identified above …
Scottish Planning Policy SPP6 – Renewable Energy (2007)
From no limits for safety setbacks …
Original setbacks were that noise at night should not exceed 3 dBA above background sound at night (background may be 25 to 30 dBA at night in rural areas)
Administrative Court of Appeal, Lyon, April 2006, determined a "zone of protection of 500 metres" from wind turbines to areas where people can be.
Academy of Medicine, March 2006, recommended a setback of 1500 metres from wind turbines to homes until an epidemiological study could be carried out to determine health effects.
Nova Scotia
Pubnico Point Wind Farm – No standard resulted in setback from turbine to home of 370 metres, and sound up to 13 dbA above the Ontario limit of 40 dBA.
Glen Dhu Wind Farm, October 2008, established setbacks of 1200 metres from homes of participating residents, and 1440 metres from non-participating residences.
Safe setbacks: How far should wind turbines be from homes?
In 2000 used sound limits with a rising limit as ground level wind speed rose. Limit was 40 dBA at 1 m/s and increased to 50 dBA at 12m/s.
(Ontario used this as a model to develop its sound limits, although Ontario limits allowed 53 dBA at 12 m/s, and continue to allow 51 dBA at 11 m/s even after revision).
In 2007, the Netherlands changed to a fixed upper limit for wind turbine sound of 40 dBA – recognizing the change in wind profile at night. The Netherlands is currently investigating a new monitoring method based on Lden. This is a rating of community noise exposure that differentiates between daytime, evening and nighttime noise exposure, and penalizes nighttime noise.
Rural noise from wind turbines is limited to 35 dBA at night.
Compare Ontario's 51 dBA nighttime limit and Germany's 35 dBA limit -note that every 6 dBA (e.g. 35 vs 41 dBA) difference means the turbines in Germany will be twice as far away as in Ontario – a 12 dBA difference (e,g, 35 vs 47 dBA) means they are 4 times further away in Germany than Ontario.
Limits noise to 35 dBA in recreational areas in evening and at night, and to 40 dBA in residential areas at night. The measurement must be done with 10 metre wind speeds of 8 m/s. Ontario regulations permit 45 dBA at 8 m/sec.
European Union
Within the European Union the Commission has made a proposal for common noise immission level descriptions and evaluation methods. It is primarily intended for traffic noise but can be expanded to include other areas, such as wind power noise. It suggests an equivalent annual average sound level (Lden) where the night level has a penalty of 10 dBA and the evening level of 5 dBA. The day is in this case is 12 hours, the evening 4 hours and the night 8 hours.
New Zealand
NTS6808:1998, "The Assessment and Measurement of Sound From Wind Turbines", requires the calculation of a background noise level prior to construction of a wind farm. NTS68001:1991 limits sound from all activity except wind turbines to 35 dBA from 8:00 PM to 7:00 AM. NTS6808 limits sound from wind turbines to 40 dBA or 5dBA over background sound. Sounds with a "special audible characteristic" (clearly audible tones, impulses, or modulation of sound level) shall have a 5 dBA penalty.
The Environmental Court of New Zealand issued a decision July 20, 2007, that required that when the background sound conditions are at 25 dBA or less, the noise from a wind farm shall not exceed 35 dBA at any dwelling as an absolute limit.
Sound levels in rural Ontario are typically less than 35 dBA at night. Yet, Ontario continues to have guidelines that allow up to 51 dBA, and rejects applying a penalty for cyclic noise as New Zealand does.
Hydro One, System Networks
2005 to Dec 2007 – setback of overall height of turbine (tower plus blade radius) to edge of right of way. Dec 2007 to July 2008 – increased setback to greater of 150 metres or overall height of turbine.
As of July 2008 increased setbacks to edge of right of way for 500 kV assets (critical assets) of 500 metres, to 230 kV (redundant assets) of 250 metres, and to 115 kV assets (for which loss tends to be an inconvenience but not a significant one) of 150 metres.
CanWEA, Proposed By-Laws for Rural Municipalities in Ontario
Recommends setbacks to lot lines of non-participating property, road right of ways, or non residential buildings on a participating property need not exceed blade length plus 10 metres (typically 51 metres)
Recommends setbacks to residential buildings should not be less than 200 metres (or as required to meet MOE CofA requirements)
Interesting to compare the 51 metres that CanWEA reconnnds to protect the lives of people, compared to the 500 metre safety setback that Hydro One calls for to protect its critical assets.
From this should one conclude that the lives of people do not matter as much as a hydro line?
Download original document: "Changes in Wind Turbine Setbacks"
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Trenton Blackshear
Our great-grandfathers' legacies were built on the backs of the wars of their fathers. Born to soldiers, their fathers instilled in them the lessons of the age, yet the only lesson that they actually had to teach them was fear.
Thus, our great-grandfathers, who were practically born into the age of fear, grew up with a never-say-die attitude. They fought for themselves, and though they might not have been as accepting of other races as we are today, they were not afraid of fighting tooth and nail with businesses that were attempting to encroach upon the liberties their fathers laid out for them. In doing so, they left a path paved with effort and purpose all the way to the future.
Their legacy is Hard Work.
Due to our great-grandfather's nonacceptance of other people, they fought great wars and left the world emotionally broken and fearful of continued conflict. While they played a game of chicken on an extreme scale, the children were brought up to believe that anyone can be your enemy. Also, the government, despite whatever it tells you, is really only out for itself.
With things like the "Red Scare" and the ever-looming fear of a nuclear holocaust, is it any wonder our grandparents' generation wouldn't even trust their children with the future? Striving to change the way the government acted out its role, their generation fought in the streets. Racism, fascism and fear all eventually fell beneath their feet.
So our grandparents' legacy is Equality.
Equality is a dangerous thing, as our parents found out. Human beings are not equal, and not everyone can be on the same level.
While our grandparents were out marching in the streets, our parents were being subjected to talk of equality and hope. Those two things came eventually, but were either too late or didn't come as advertised.
Being confronted with the problem of the unreachable ideal of "total equality," yet being forced to attempt to make it work anyway, gave birth to a generation of hypocrites. The same businesses our great-grandfathers attempted to keep down reared their ugly heads, and our parents swallowed the entire tale they were fed.
Simultaneously preaching their goodness while neglecting the future and disrespecting the past is why our parents' legacy is Hypocrisy.
But what is our legacy? We're still in the middle of ours. Will our children say that we were the people who fought back against a generation which only cared about itself? Are we going to be the spark that lights our way back to the path our great-grandfathers walked? Or will we be the sheep, only living while being placated by the master's goodwill? We have in our hands better tools than our great-grandfathers could ever have dreamed. Yet what do we do with them?
We will light a fire to light our children's path. We refuse to be eaten by the wolves of our great-grandparents' generation. Our legacy will be the Spark of Change.


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This morning when I was feeding my dog, he did something a little strange.
I've taught Hamish to sit and wait while I put his food dish down . Then I point to my eye and say, 'look'.
He looks me right in the eye. It's a focus routine I've taught him because when you have a high energy and enthusiastic dog, you really do need a way to get their attention back in a snap. I've found that " sit and look" works well in a lot of situations where his ability to focus may go sideways on us and I need to get it back quickly.
After we do the sit and look routine I tell him 'dinner time ' and he dives into his dish and chows down like he hasn't eaten in about 100 years.
Everything went the same as usual as I got his meal ready- he tried to dive into his food bag, he tried to counter surf, he ran into the living room and found a couple of toys and dropped them at my feet- I think it's to reward me for feeding him FASTER.
When I went to put his food bowl down he sat on his own, which he does sometimes. But when I told him to 'look' he looked over my left shoulder instead. So I pointed to my eye and said 'look' a couple of times.
He kept looking over my shoulder.
I tried again and he looked at me and I said " dinner time " but he didn't move. He went back to looking over my shoulder and he did not move a muscle.
Hamish doesn't refuse to eat unless he's sick so I was concerned for a moment about that.
I kept trying to get his attention and he kept his eyes locked over my shoulder
Were his hackles up? Did he act like something out of the ordinary was happening?
No, he was fine.
The fact is, as he went through his routine I had the feeling he wasn't doing it for me.
We got back on track and he wolfed his meal down as usual.
In all, this wasn't an unnerving experience, but it was a curious one.
A curious incident, a day after Halloween.


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