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Bear Walking Stick Top
A Bear Patrol Scout Walking Stick Top is the perfect way to remember your Wood Badge experience. On the top of your walking stick, this eye-catching piece will be a reminder and conversation starter of your accomplishments in Scouting's premier leadership program.
One of the key components of the Wood Badge course is the patrol method. As a Bear Patrol member, the camaraderie you form and the close ties you make with fellow Fox Patrol members will be kept for a lifetime.
This walking stick top resembles the imposing Bear. It is cast in plastic resin from original woodcarvings, and it fits on any walking stick or stave with a top of approximately 1-1/8" diameter. The hardware for attaching the top to the stave (a dowel screw) is included with each top.
Dimensions: 3" inches tall and approximately 1 1/8" inches at the base.


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Coffee Break: free coffee/hot chocolate at Bogomolny library
- When:
- Location:
- Bogomolny Library
- Room:
- 1st Floor
- Description:
Coffee Break
RLB Library is giving UB students some extra energy! Stop by the first floor of the library for FREE coffee, hot chocolate, and tea to stay alert while working on your final paper or studying for your finals.
Monday, Dec. 3 - Thursday, Dec. 6
8:30 am - 6 pm
First Floor Lobby - Contact Name:
- Mandy may
- Contact Email:
- email@example.com
Appropriate accommodations for individuals with disabilities will be provided upon request 10 days prior to a campus event and 30 days prior to an event requiring travel.

subset: commoncrawl


text:
Found occurrences of James Id in 1 document in the collection. Click on a column heading to sort by it, or to toggle ascending or descending sorting for the current column:
Click on a number to view all occurrences of the entity in the selected document
Document | Max. Freq. ⇩ | Min. Freq. ⇩ | ||
Emilio, Luis F., History of the Fifty-Fourth Regiment of Massachusetts Volunteer Infantry , 1863-1865 | 92 | 0 | Browse all entities in this document |


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Introduce your business and tell us your story: How did you decide on what to sell, and how did you source your products?
Boardies Apparel® is swimwear brand from the UK inspired by the hedonistic party scene around the world. We first saw a gap in the market for quality mens swim shorts with cool designs, available at accessible prices, whilst spending time at the all-day pool parties and clubs in Ibiza. Our creative team design exclusive Boardies® prints and we work with state of the art printers and factories, manufacturing mostly in the far east.
How did you earn your first sales? Which channels are now generating the most traffic and sales for you?
Back at the end of 2014 we launched our Shopify website and quite quickly our first sales started coming through. We has some early success by being selected by ASOS.com who took quite a wide selection of Boardies® styles, which helped to generate quite a lot of traffic to our web store. Some strong press followed in some key fashion and mens magazines which primed customers to check out our website.
Instagram is also an effective tool to showcase our brand and products to a targeted audience and this helps drive sales. We have found that a combination of online activity and physical wholesale stores drive the most traffic. Boardies® is available in the Selfridges store London and also on their website, so we get a double effect.
Tell us about the back-end of your business. What tools and apps do you use to run your store? How do you handle shipping and fulfillment?
We have managed to integrate many of Boardies®' systems with Shopify which drives many efficiencies. For example all our orders are processed via software like Stitchlabs and this feeds directly into Shopify, as well as with our accounts software. When we receive a sale, the notification goes straight to our warehouse and the shorts are picked, packed and shipped within 24 hours. The whole team at Boardies® uses Shopify and we have found it very intuitive and its constantly developing with new features.
What are your top recommendations for new store owners?
We advise new store owners to find a genuine gap in the market, doing something new or better than what's been done before. Research the market thoroughly and build a firm understanding of who your customer is. There are new swimwear brands launching every day, but we believe that Boardies® offers a unique point of difference which sets us apart. Finally, make sure you make the best use out of Shopify webinars and videos as there is so much helpful information readily available.


text: The Warehouse has an exceptional variety of T-shirt for men which are available in 3 colors (Black- White- Grey). These graphic tees are the trendiest and most comfortable you'll ever wear. We craft all of our T-shirts with extra care and love, so you can be sure you're getting the best of our product! T-shirts are easy to wash and quick to dry. They fit perfectly, as we have sizes available in a wide range of options. 100% Ultra-soft Jersey made of polyester You can add your own designs to this T-shirt through our customization feature.


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Pioneer DVR-S706-J
1. Retail Package - Installation
Review Pages
2. Data CD Reading Tests
3. CD Error Correction Tests
4. DVD reading tests
5. DVD Error Correction Tests
6. DAE Tests
7. Protected AudioCD Tests
8. Game Protection Tests
9. CD Recording Tests
10. Writing Quality Tests - 3T Jitter Tests
11. Writing Quality Tests - C1 / C2 / CU Error Measurements
12. DVD Recording Tests
13. PI/PO quality results for DVD+R/RW
14. PI/PO quality results for DVD-R/RW
15. BitSetting Tests
16. Conclusion
17. Noise Reduction
PIONEER DVR-S706 DVD±R/RW recorder - Page 1
The Pioneer DVR-S706 is an external 8x DVD dual format optical disc drive compatible with all current formats such as DVD-R/RW, DVD+R/RW and CDs. The external case has a fancy and stylish design and comes with connection interfaces for IEEE1394 firewire and USB2.0 ports. The drive can sit vertically or horizontally on your desk.
- Features
The DVR-S706 features 8x DVD±R writing, 4x DVD±RW rewriting, 24x CD-R writing, 24x CD-RW rewriting, 40x CD-ROM reading, 32x CD-RW reading and 12x DVD-ROM reading and 2x DVD-RAM reading. Buffer underrun protection is also supported.
Advanced technological features:
- Precision Recording Technology: Adapts drive to media characteristics for writing performance and quality.
- Smart Laser Driver: Controls laser pulse for accurate writing at high speeds.
- Quiet Drive Technology: Mechanism for quite operation, achieving 75% lower operation noise compared with previous drives.
- Specifications
Host/Interface |
Usable Discs
Supported Discs: 4.7GB DVD-RW Version 1.1 4.7GB DVD-RW Version 1.2 Read Supported
Discs: |
speed |
DVD-R: 8x-speed (Zone CLV), 6x-speed, 4x-speed, 2x-speed, 1x-speed DVD-RW: 4x-speed, 2x-speed, 1x-speed DVD+R: 8x-speed (Zone CLV), 6x-speed, 4x-speed , 2.4x-speed DVD+RW: 4x-speed, 2.4x-speed CD-R: 24x-speed (Zone CLV), 16x-speed , 8x-speed, 4x-speed US-RW: 24x-speed (Zone CLV), 16x-speed HS-RW: 10x-speed, 4x-speed |
Read speed |
DVD-R: Max.8x-speed DVD-RW: Max.8x-speed DVD+R: Max.8x-speed DVD+RW: Max.8x-speed DVD-RAM: 2x-speed (CLV) DVD-ROM
(Single Layer): DVD-ROM (Dual Layer): DVD-Video (Dual layer): CD-ROM: Max.40x-speed Video CD: Max.9.3x-speed Audio CD (Data extraction): CD-R: Max.40x-speed CD-RW: Max.32x-speed |
Buffer memory |
2 MB with Buffer Underrun Protection |
Weight |
2.1kg |
(WxDxH) |
167mm x 272.8mm x 56.2mm |
The drive uses a 2MB buffer memory store and supports RAW-DAO96 writing (CD). The drive does not support writing of DVD-RAM, DVD+R DL and Mount Rainier formats as well as DVD+R DL and CD+G reading features. The drive uses the RPC II region control, allowing a user to change the drive's region at most 5 times. There is "patched" firmware that can disable RPC1 protection, but is not recommended for amateur users. Use it at your own risk.
For our tests, we changed the region code to 2 (Europe) (hence the reason 4 changes left in the screenshot above). Using DVDInfoPro software we can also check the drive's features:
The screenshot above was taken after the tests were completed, and after Pioneer had released the new firmware, hence this is the reason why the Firmware Revision is shown as 1.16.
- Retail packageThe retail package includes an AC adaptor (AC100V), one USB cable (1m), two IEEE1394 cables, one 6pin - 6pin, 1.5m and one 6pin - 4pin, 1.5m. Also included are two stands for vertical mounting.
The drive's front panel's color is black and the case is silver. On the tray loader on the left side we can see the 8X8 DVD writing logo, in the middle the DVD-R/RW logo and on the right side the RW DVD+ReWritable logo, UltraSpeed Rewritable logo and the DVD Multi Player logo (the drive supports reading of DVD-RAM media).
Below from left to right we can also see the power/operation led (lights dark blue when on), the Pioneer logo and the eject button. The emergency eject hole is located below the 8x8 DVD writing logo.
On the rear panel you can see two firewire and one USB 2.0 connectors, the power button and the power connection.
- Installation
The device was connected to our test PC using a firewire connection and was identified as "Pioneer DVD-RW DVR-107D" under WinXP, which is the same id as the DVR-107D internal drive from Pioneer. All tests were done with firmware revision 1.15.
By the time we finished all tests, Pioneer had released a new firmware revision (v1.16) that supported more media types for 8X DVD-R writing:
- TDK8X New Dye Version (TTH01)
- Gigastorage 8X (GSC003)
The following pages include test results for the Pioneer DVR-S706 drive compared with the internal Pioneer DVR-107D drive to check performance differences between the external firewire and the internal atapi drive.
- Testing software
In order to perform our tests we used:
- Nero CD-DVD Speed v3.00
- CDVD Benchmark v1.21
- ExactAudioCopy v0.9 beta5
- Nero Info Tool v2.21
- KProbe v2.1.0 (Reader: LiteOn LDW-811S firmware vHS0Q, Reading speed 8X CAV)
- PlexTools v2.13 (Reader: Plextor PX-712A firmware v1.01, Reading speed 8X CLV for CD-R)
- DVDInfoPro v2.54
- Nero Burning Rom v18.104.22.168
Review Pages
2. Data CD Reading Tests
3. CD Error Correction Tests
4. DVD reading tests
5. DVD Error Correction Tests
6. DAE Tests
7. Protected AudioCD Tests
8. Game Protection Tests
9. CD Recording Tests
10. Writing Quality Tests - 3T Jitter Tests
11. Writing Quality Tests - C1 / C2 / CU Error Measurements
12. DVD Recording Tests
13. PI/PO quality results for DVD+R/RW
14. PI/PO quality results for DVD-R/RW
15. BitSetting Tests
16. Conclusion
17. Noise Reduction


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Posts Tagged: diarrhea
Giardia – It's a strain on everyone
What is it?
Giardiasis is an intestinal infection of animals. It is caused by a protozoan parasite called Giardia intestinalis. These single-celled parasites are not to be confused with more commonly known intestinal parasites; roundworms, hookworms, and tapeworms.
How do pets get it?
Giardia, in all life stages, is too small to be seen without a microscope. The infective stage of Giardia is the cyst, which is passed in the feces of infected wildlife and domestic animals. When an animal swallows the Giardia cysts, they enter the intestinal tract, causing infection.
There are many ways pets can ingest these cysts. Here are a few:
- Eating feces
- Stepping in feces and licking their paws
- Eating contaminated grass
- Drinking standing water
What are the symptoms?
Fortunately, even though the infection rate is high in cats and dogs, clinical disease is less common. Some animals infected with Giardia may show no clinical signs. When symptoms do arise they may include digestive upset, usually diarrhea and/or vomiting. Severe cases of untreated diarrhea and vomiting may lead to dehydration and more serious disease.
In the last 6 months, Becker Animal Hospital has diagnosed the infection in 50 pets!
How is it diagnosed?
Most often a microscopic examination of fecal material is used to diagnose Giardia. Occasionally the infection may be difficult to confirm because animals may not always shed the organism in their fecal material. In this case a blood test is used to confirm infection.
What's the Treatment:
The most common medication used to treat Giardia is metronidazole. It is usually given by mouth for 7-10 days. If the infection is persistent other medications may be added and treatment may continue for longer than one week.
Giardia in pets should be treated as a potentially communicable (zoonotic) disease. It is not known for certain if Giardia from pets directly infects humans, however, the same strains of Giardia have been known to infect dogs, cats and humans. Therefore, good hygiene should be observed when interacting with an infected animal and when cleaning up fecal material.
Thorough cleaning of the environment may help to decrease opportunities for reinfection. The cysts are sensitive to bleach dilutions (1 cup of bleach to 2 gallons of water). Cysts are also sensitive to heat and drying. Cold weather is no match for giardia cysts. It can live in 8°F! The protective shell of the cyst allows Giardia to survive for long periods of time.
All infected areas should be cleaned and dried well. Food bowls, bedding, toys and litter boxes should be washed with hot water. Bathing the pet may also be helpful during the course of treatment as well as picking up any fecal material present in the yard. It is important to reduce the chances of reinfection.
Important Points:
- Be sure to give any medications as prescribed; ending medications early may cause a chronic Giardia infection.
- Watch for signs of weakness, instability, appetite loss.
- Remember to use proper hygiene, wash bedding and bowls especially in multiple pet households
- Avoid allowing animals to drink untreated water.
- A fecal exam should be done at least once per year, even if your pet appears healthy.
When to call Becker Animal Hospital:
- If the condition is not improving:
- your pet continues to have diarrhea or if the diarrhea becomes more severe
- If your pet develops further digestive disorders:
- vomiting, not eating, weight loss, abnormal stool
- If your pet has had a reaction to medications or exhibits abnormal behavior.
For more information on Giardia:
CDC – The Center For Disease Control


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We currently do not have any treatment providers listed under Delaware. If you are looking for a treatment provider, please check back soon.
If you would like to be listed as a treatment provider, please visit www.edcatalogue.com/treatment-provider-directory-options/ for more information.
Gürze/Salucore is not a health care provider, and does not give medical advice or treatment. We offer this referral list as a resource only, and do not endorse any of the listed treatment providers or facilities. Each therapist listed in this directory works autonomously and has full, separate, legal and therapeutic responsibility for his/her clients. Treatment providers pay an annual fee to be listed, and supply their own information about their practices. Gürze/Salucore does not check for accuracy or verify credentials or licensing.
You are therefore responsible for interviewing and selecting an appropriate provider, and understand and agree that Gürze/Salucore is in no way responsible for the services provided. If you are under the age of 18, we recommend that you seek the advice of a trusted adult in choosing treatment options.


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Absolutely. Checking in with the doctor on a regular basis—usually every six months—is essential to keeping your smile looking its best. At Children's Dental Center of New Hampshire and Orthodontics TOO, we are proud to offer a number of preventive procedures to ensure the health of your mouth and the beauty of your smile. Your smile is just as important to us as it is to you!
Another good reason to visit our Amherst, New Hampshire office is to check for hidden issues in your mouth you may not even realize you had. Bacteria, tartar, and cavities are known to form in the hard-to-reach crevices of your mouth and may only be detected through a professional exam. If left untreated, these cavities and decay can get worse, requiring more extensive treatment, and costing you even more time and money down the road. During your routine exam, the doctor and our team will also check to make sure your fillings or other dental restorations you may have had are in good shape.
Preventing problems before they start is the key to optimal oral health. If it has been more than six months since your last visit, please contact our Amherst, New Hampshire dental office to schedule your routine checkup! See you soon!


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Shocking crash for cash footage shows the moment criminals deliberately cause a collision on busy road
and live on Freeview channel 276
This article contains affiliate links. We may earn a small commission on items purchased through this article, but that does not affect our editorial judgement.
Shocking dash cam footage shows the moment a gang of criminals deliberately caused a crash on a busy road in a bid to defraud insurers.
The frightening clip has been shared with NationalWorld by insurer LV= as new data reveals that Birmingham is the UK's worst city for "crash for cash" insurance scams.
Hide AdAdvertisement
Hide AdData from the Insurance Fraud Bureau (IFB) reveals that the city covers seven of the 30 worst postcodes for faked or deliberate collisions.
The three worst postcodes are all in the city, ahead of two more in Bradford, which is the second worst place in the country for the dangerous scam.
Behind them, Manchester, London and Luton are also hotspots for the crime, which involve criminal gangs staging or causing accidents in order to make inflated injury claims.
Almost 200,000 insurance claims a year could be linked to "crash for cash" scams, according to the latest figures, which show that of 2.7 million motor insurance claims submitted from October 2019 to December 2020, more than 170,000 could be linked to crash for cash networks.
Hide AdAdvertisement
Hide AdThese gangs of organised criminals cost the insurance industry millions of pounds a year in fraudulent claims, adding to the cost of everyone's premiums.
Crash for cash schemes range from fraudsters submitting claims for entirely fictitious crashes to staged incidents using pre-damaged vehicles. However, in the most dangerous cases such as that in our clip, they deliberately cause a collision in order to scam the innocent victim and their insurer.
Freddy Lovejoy, whose Land Rover Discovery was targeted in the above clip, has urged other drivers to be alert to the dangerous con. He said: "You never expect a crime like crash for cash to happen and I would strongly recommend drivers read up about it. There can be physical and mental impacts when involved in a car incident, and to think criminals do it on purpose is scary."
"At the time I was using a dashcam which provided crucial evidence for the case, so that would be my top tip to anyone. I was lucky to get support and justice, but others might not be so fortunate, so creating more awareness for the public is important."
Hide AdAdvertisement
Hide AdBen Fletcher, Director at the IFB, warned that as traffic returns to pre-lockdown levels, scammers could increase their activity. He said: "Crash for cash fraudsters bring devastation to countless victims and increase motor insurance costs for us all. The IFB's hotspots analysis is a stark reminder that although great strides have been taken in tackling the problem, these car crash scams are all too common.
"As traffic levels return to normal following the national lockdown, crash for cash fraudsters may look to make up for lost time. It is hoped that by shining a spotlight on the issue we will encourage road users to be alert and report any suspicious activity to the IFB's Cheatline on 0800 422 0421."
James Dalton, Director of General Insurance Policy at the Association of British Insurers, added: "These criminal gangs are often highly organised and put lives at risk. The amounts that they fraudulently claim can be huge, and can impact on the motor premiums paid by honest motorists. With more vehicles on the roads as we emerge from the pandemic restrictions, so the potential targets for these criminals increases. This is why it is so important for all motorists to be on their guard."
A message from the editor:
Thank you for reading. NationalWorld is a new national news brand, produced by a team of journalists, editors, video producers and designers who live and work across the UK. Find out more about who's who in the team, and our editorial values. We want to start a community among our readers, so please follow us on Facebook, Twitter and Instagram, and keep the conversation going.


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During my Star Trek Captain's Chair Restoration; I found myself wanting to paint match some powdercoat to the existing color of the plastic side panels on the chair.
Please note: Readers are responsible for their own sacrifices to the blood god. Safety first– if you injure yourself implementation of this guide; expect we'll take no responsibilities. Commentors at Hack-A-Day have indicated that MEK is flammable (as does the label) – so please take the appropriate precautions.
Required materials:
- Glass or metal mixing vessels (an airbursh jar works well)
- Methyl Ethyl Ketone (MEK)
- A set of Powder Coat colors to mix the colors
- A paint sprayer… HLVP, Gravity fed, or Airbrush
- A Panatone(r) Color Cue(TM) or similar device (optional).
Powdercoat using this method appears to be every bit as robust and scratch resistant as normal powdercoat. The author has seen no negative material properties from using MEK instead of a powder coating gun (electrostatic).
For the beginner; Harbor Freight may be a good stop for the primary colors – they usually carry White, Red, Black, and Yellow. Unsure about Green and blue. I also use HF touch up paint guns, HLVP, and airburshes to apply my MEK solutions. Caswell plating is also a good source for many a color. MEK can be purchase in the paint area of most home improvement stores – I buy mine at Lowes.
I wanted to paint match the powder coat because my chair controls have began to peel and rust. They'll need to be redone so I wanted them to match the newly retr0brighted side panels.
While the used of the color cue is a good starting place – it isn't required; you can manually mix colors by eye until you get it right… as you'll see; I used the color cue to get initial color suggestions (or base colors if you will); then added pure white to bring the color closer to that of the plastics.
I started by measuring the sRGB color of a retr0bright-ed side panel using my Pantone(r) Color Cue(tm) device which I got off of Ebay several months ago and it came up with r246 g230 b198. I pulled these values into the RGB to commercial Tints page at EasyRGB.com. This gave the closest RAL numbers which to match to. I then went to google and did a search for RAL-1013 powder coat which returned a result to powder365.com for their " Oyster White " powder coat. Then using the HTML code #F6E6C6
I also used the RGB browser to convert to "RAL Classic" listed six colors with % equivalent matches to my original scanned color.
% 1-?C | Color name |
96% | RAL 1015 Light ivory |
94% | RAL 1013 Oyster white |
93% | RAL 9001 Cream |
92% | RAL 1014 Ivory |
90% | RAL 9010 Pure white |
89% | RAL 9002 Grey white |
I also did searches for other color combinations and ended up selected the following three colors from powder365.
1lb x RAL 1013 OYSTER WHITE (340/10MIN)
1lb x RAL 7035 LIGHT GREY (340F/10MIN)
1lb x TEXTURED ALMOND (380F/20MIN)
The idea was to put each color on a test piece to see how close to match and pick one which looked the best.
For more information on color matching using the Color Cue; please see Pinball Pal's Color Cue page.
During my research; I also came across a post to caswellplating.com's forums which talked about mixing the powder with MEK to "melt" the powder into liquid form for the purpose of correct a blemish on an existing powder coated part. This sparked an idea – why not use the MEK to mix powders together to get an even better color match. I have a quart of MEK in the garage – so it was time to experiment.
I knew the grey wouldn't really match – it was too grey; so I used MEK to melt it and used a hobby paint brush to apply it to the scrap piece. I then used regular power coating equipment to lay down the almond and oyster for comparison. For the last color; I decided to mix some grey, 2 TSP of pure white (purchased at Harbor Freight), 2.5 TSP of oyster together with a generous helping of MEK to turn the powder to a grey-white "milky" formulation. I applied this with a paint gun:
From Left to Right: RAL-7035+MEK (under thumb), Almond, RAL 1013, and MEKMix
The Right most Grey is "uncured" IE that is how it goes on being applied with a paint gun. Looks fully cured already. and the lines were created with standard blue painters tape. Be-aware – that MEK powder liquid acts just like any paint… it will dry on everything. so protect from over-spray and wear gloves. Unlike the powder form of powdercoat; it can't just be wiped off of surfaces.
The cool thing about MEK powder-liquid is reportedly it can be used on Plastics and Wood… using low cure temperatures. Ideal for paint matching on cases or other non-metal projects.
With MEK; it looks like one could color match any color given enough patience and primary colors to choose from. Now with this knowledge; it was time to do some actual paint mixing for the purpose of matching the side panels.
I went to work on the control panels:
As you can see the control panels are in need of some TLC. As typical for this machine; the Fire control panel label has begun to deteriorate and is peeling away from the metal. So I removed the label manually – then used Xytol to soak the piece for about 5minutes to soften the label adhesive so it could be removed with a plastic paint scraper. I continued cleaning/soaking the bracket until all the label residue was removed:
Then I sandblasted the bracket w/ ALO2 to remove the rust and other residue. And then finally; I wiped the bracket clean with some clean MEK to remove and remaining dust and oil from the surface.
I then proceeded to powdercoat the underside to the bracket with the Oyster White Powder coat.
For the front; I did an MEK liquid mix as discussed previously. This time I started with a base of 2.5 TSP of Oyster White powder coat and added 1.5TSP of pure white Powder coat. I then mixed with approx 1/4cup of MEK to form a 2% milk-like consistency. I color checked the mixture by using a small paint brush to apply the color to the underside of on of my plastic pieces. This mixture was nearly a spot on match to the plastic so I decided to go with it. I loaded the MEK liquid powder coat to my touch up paint gun
And painted the front / sides with this MEK paint match. Here it is "air cured":
Once it is dry to the touch / safe to handle (usually about 20minutes); I place the bracket in my powder coat toaster oven for initial curing. during my test runs; I noticed that if you attempt a full cure (400F / 20minutes) with the MEK solution still wet – it will "Boil" the paint leaving rough spots. So I put the piece in the oven at 150F / Warming setting for 10minutes to allow the MEK to evaporate. Then I crank the piece up to 400F for 20minutes for the final cure.
Once the piece cooled to room tempeature; I did a test match against a retr0brighted piece. First; here's the stock Oyster White (back of bracket):
Notice the slight yellow hue vs the plastic piece.
Here's the MEK paint match 1.66:1 (oyster to pure white):
I call that a match!
Incidentally; The Color Cue captured an sRGB255 value of 237, 225, 192 for the color matched piece (color code EDE1C0).
Please check out the remainder of the worklog – where I used an airbrush and a laser cutter to create powdercoated labels on the pieces:


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A CDN resource is a specific server with content an end user wants to distribute via the CDN. The first step to configure the CDN is add the CDN resources.
1) Login to Exabytes Billing System via:
For MY client: https://billing.exabytes.com.my/mypanel/clientarea.php
For US client: https://billing.exabytes.com/mypanel/clientarea.php
For SG client: https://billing.exabytes.sg/mypanel/clientarea.php
2) Click on Service then My Service
3) Select the CDN service
4) Click on the New CDN Resources to create , select the HTTPD on Select CDN Resource Type section
5) Insert the CDN hostname and Origins .
*CDN Hostname which will be hostname to access CDN resources. Normally create as cdn.youdomainname
*Origins is the the location from where your data will be pulled which is the original domain
In short, if the domain is exatest.com, could create CDN hostname as cdn.exatest.com or *anything*.exatest.com
6) Select the edge group and click create CDN resources
*Edge Group is CDN server group location.
7) Once done, click on the Details of the CDN Resources
8) Under the DNS settings, it show the CNAME record that need to add. You need to add it as the subdomain CNAME record.
9) Once done, the CDN resources is ready.


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St. Charles Personal Injury and Car Accident Lawyer
In St. Charles, Dixon Law Office is the best personal injury law firm. Why? Dixon Law Office gets RESULTS for our clients. Dixon Law Office founder, G. Grant Dixon III, has been recognized as a Super Lawyer in multiple years.Less than 5% of all lawyers achieve this recognition.Grant is also member of the Million Dollar Advocate Forum.Only attorneys who personally get million dollar verdicts and settlements for their clients, are allowed to be members of this elite group.
Dixon Law Office clients love the law firm. More than 97% of Dixon Law Office clients rate their personal injury lawyer as OUTSTANDING. You can hear from them yourself and hear what great things they have to say about their experience here. Even the Better Business Bureau gives Dixon Law Office an A+ rating!
If you have a serious personal injury case in St. Charles, Dixon Law Office is the law firm for you. They have experience in all types of personal injury cases including:
- Automobile accidents
- Truck crashes
- Pedestrian accidents
- Medical malpractice
- Nursing home abuse
- Bicycle accidents
- Construction accidents and injuries
- Worker injury and worker's compensation
- Slip, trip and fall accidents
- Premises injury cases
If you have been injured in any kind of an accident in St. Charles, call Dixon Law Office right now at (888) 354-9880 or click here for a FREE review of your case. If we don't win, you pay no fee. Call today!
Information about St. Charles
St. Charles is in Kane County, Illinois. It has a population of 32974. In, St. Charles, there are these hospitals: None. The home nursing agencies are: Covenant Home Services. The home health care agencies are: Precious Life Home Health, LLC and Covenant Home Services.
Contact St. Charles personal injury and auto accident lawyer G. Grant Dixon III of Dixon Law Office. Call (888) 354-9880 or click here for a FREE review of your case. Call right now!


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Reclaim & Recovery services are designed to minimise the environmental impact of used refrigerants. Recovery services avoid the release of the used refrigerant into the atmosphere. Reclaim services allow the re-use of existing refrigerants avoiding the need to manufacture new refrigerant molecules.
Linde has always promoted the recovery and where possible, reclamation and reuse of refrigerants.
Most countries now have some form of environmental protection legislation to regulate emissions, and many have specific requirements to recover refrigerants.
Linde offers a range of recovery cylinders to allow the safe collection of used refrigerant, avoiding their release into the atmosphere. Many Linde Group companies also offer a range of additional recovery services including the collection of larger volumes of products in larger containers.
Once recovered, Linde can ensure that the refrigerant is destroyed in an environmentally friendly manner. In many locations, Linde group companies can also carry out reclaim of the recovered refrigerants. Reclaim involves bringing product back to "as-new" AHRI 700 specification.
In some geographies Linde also offers a wider range of refrigerant services in conjunction with Hudson Technologies (a US based leading refrigeration technology company).


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Label: FOSINOPRIL SODIUM tablet
Contains inactivated NDC Code(s)
NDC Code(s): 68258-6106-3 - Packager: Dispensing Solutions, Inc.
- This is a repackaged label.
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Drug Label Information
Updated July 22, 2013
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When used in pregnancy during the second and third trimesters, ACE inhibitors can cause injury and even death to the developing fetus. When pregnancy is detected, fosinopril sodium should be discontinued as soon as possible. See WARNINGS, Fetal/Neonatal Morbidity and Mortality .
Fosinopril sodium tablets are the sodium salt of fosinopril, the ester prodrug of an angiotensin- converting enzyme (ACE) inhibitor, fosinoprilat. It contains a phosphinate group capable of specific binding to the active site of angiotensin-converting enzyme. Fosinopril sodium is designated chemically as: L-proline, 4-cyclohexyl-1-[[[2-methyl-1-(1-oxopropoxy)propoxy](4-phenylbutyl)phosphinyl]acetyl]-, sodium salt, trans-.
Fosinopril sodium USP is a white to off-white crystalline powder. It is soluble in water (100 mg/mL), methanol, and ethanol and slightly soluble in hexane.
Its structural formula is:
Empirical formula: C30H45NNaO7P Molecular weight: 585.65
Fosinopril Sodium is available for oral administration as 10 mg, 20 mg, and 40 mg tablets. Inactive ingredients include: lactose, microcrystalline cellulose, carnauba wax, crospovidone, and zinc stearate.
Mechanism of Action
In animals and humans, fosinopril sodium is hydrolyzed by esterases to the pharmacologically active form, fosinoprilat, a specific competitive inhibitor of angiotensin-converting enzyme (ACE).
ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium.
In 647 hypertensive patients treated with fosinopril alone for an average of 29 weeks, mean increases in serum potassium of 0.1 mEq/L were observed. Similar increases were observed among all patients treated with fosinopril, including those receiving concomitant diuretic therapy. Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity.
ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of fosinopril sodium remains to be elucidated.
While the mechanism through which fosinopril sodium lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, fosinopril sodium has an antihypertensive effect even in patients with low-renin hypertension. Although fosinopril sodium was antihypertensive in all races studied, black hypertensive patients (usually a low-renin hypertensive population) had a smaller average response to ACE inhibitor monotherapy than non-black patients.
In patients with heart failure, the beneficial effects of fosinopril sodium are thought to result primarily from suppression of the renin-angiotensin-aldosterone system; inhibition of the angiotensin-converting enzyme produces decreases in both preload and afterload.
Pharmacokinetics and Metabolism
Following oral administration, fosinopril (the prodrug) is absorbed slowly. The absolute absorption of fosinopril averaged 36% of an oral dose. The primary site of absorption is the proximal small intestine (duodenum/jejunum). While the rate of absorption may be slowed by the presence of food in the gastrointestinal tract, the extent of absorption of fosinopril is essentially unaffected.
Fosinoprilat is highly protein-bound (approximately 99.4%), has a relatively small volume of distribution, and has negligible binding to cellular components in blood. After single and multiple oral doses, plasma levels, areas under plasma concentration-time curves (AUCs), and peak concentrations (Cmaxs) are directly proportional to the dose of fosinopril. Times to peak concentrations are independent of dose and are achieved in approximately 3 hours.
After an oral dose of radiolabeled fosinopril, 75% of radioactivity in plasma was present as active fosinoprilat, 20% to 30% as a glucuronide conjugate of fosinoprilat, and 1% to 5% as a p-hydroxy metabolite of fosinoprilat. Since fosinoprilat is not biotransformed after intravenous administration, fosinopril, not fosinoprilat, appears to be the precursor for the glucuronide and p-hydroxy metabolites. In rats, the p-hydroxy metabolite of fosinoprilat is as potent an inhibitor of ACE as fosinoprilat; the glucuronide conjugate is devoid of ACE inhibitory activity.
After intravenous administration, fosinoprilat was eliminated approximately equally by the liver and kidney. After oral administration of radiolabeled fosinopril, approximately half of the absorbed dose is excreted in the urine and the remainder is excreted in the feces. In two studies involving healthy subjects, the mean body clearance of intravenous fosinoprilat was between 26 mL/min and 39 mL/min.
In healthy subjects, the terminal elimination half-life (t1⁄2) of an intravenous dose of radiolabeled fosinoprilat is approximately 12 hours. In hypertensive patients with normal renal and hepatic function, who received repeated doses of fosinopril, the effective t1⁄2 for accumulation of fosinoprilat averaged 11.5 hours. In patients with heart failure, the effective t1⁄2 was 14 hours.
In patients with mild to severe renal insufficiency (creatinine clearance 10-80 mL/min/1.73m2), the clearance of fosinoprilat does not differ appreciably from normal, because of the large contribution of hepatobiliary elimination. In patients with end-stage renal disease (creatinine clearance <10 mL/min/1.73m2), the total body clearance of fosinoprilat is approximately one-half of that in patients with normal renal function (see DOSAGE AND ADMINISTRATION).
Fosinopril is not well dialyzed. Clearance of fosinoprilat by hemodialysis and peritoneal dialysis averages 2% and 7%, respectively, of urea clearances.
In patients with hepatic insufficiency (alcoholic or biliary cirrhosis), the extent of hydrolysis of fosinopril is not appreciably reduced, although the rate of hydrolysis may be slowed; the apparent total body clearance of fosinoprilat is approximately one-half of that in patients with normal hepatic function.
In elderly (male) subjects (65 to 74 years old) with clinically normal renal and hepatic function, there appear to be no significant differences in pharmacokinetic parameters for fosinoprilat compared to those of younger subjects (20 to 35 years old).
In pediatric patients, (N=20) age 6 to 16 years, with glomerular filtration rate ≥25 mL/min, given a single dose of fosinopril (0.3 mg/kg given as solution), the mean AUC and Cmax values of fosinoprilat (the active form of fosinopril) were similar to those seen in healthy adults receiving 20 mg (about 0.3 mg/kg for a 70 kg adult) of fosinopril as a solution. The terminal elimination half-life of fosinoprilat in pediatric patients was 11 to 13 hours, also similar to that observed in adults.
Fosinoprilat was found to cross the placenta of pregnant animals. Studies in animals indicate that fosinopril and fosinoprilat do not cross the blood-brain barrier.
Pharmacodynamics and Clinical Effects
Serum ACE activity was inhibited by ≥ 90% at 2 to 12 hours after single doses of 10 mg to 40 mg of fosinopril. At 24 hours, serum ACE activity remained suppressed by 85%, 93%, and 93% in the 10 mg, 20 mg, and 40 mg dose groups, respectively.
Administration of fosinopril sodium tablets to patients with mild to moderate hypertension results in a reduction of both supine and standing blood pressure to about the same extent with no compensatory tachycardia. Symptomatic postural hypotension is infrequent, although it can occur in patients who are salt- and/or volume-depleted (see WARNINGS). Use of fosinopril sodium in combination with thiazide diuretics gives a blood pressure-lowering effect greater than that seen with either agent alone.
Following oral administration of single doses of 10 mg to 40 mg, fosinopril sodium lowered blood pressure within one hour, with peak reductions achieved 2 to 6 hours after dosing. The antihypertensive effect of a single dose persisted for 24 hours. Following four weeks of monotherapy in placebo-controlled trials in patients with mild to moderate hypertension, once daily doses of 20 mg to 80 mg lowered supine or seated systolic and diastolic blood pressures 24 hours after dosing by an average of 8-9/6-7 mmHg more than placebo. The trough effect was about 50% to 60% of the peak diastolic response and about 80% of the peak systolic response.
In most trials, the antihypertensive effect of fosinopril sodium increased during the first several weeks of repeated measurements. The antihypertensive effect of fosinopril sodium has been shown to continue during long-term therapy for at least 2 years. Abrupt withdrawal of fosinopril sodium has not resulted in a rapid increase in blood pressure.
Limited experience in controlled and uncontrolled trials combining fosinopril sodium with a calcium channel blocker or a loop diuretic has indicated no unusual drug-drug interactions. Other ACE inhibitors have had less than additive effects with beta-adrenergic blockers, presumably because both drugs lower blood pressure by inhibiting parts of the renin-angiotensin system.
ACE inhibitors are generally less effective in blacks than in non-blacks. The effectiveness of fosinopril sodium was not influenced by age, sex, or weight.
In hemodynamic studies in hypertensive patients, after three months of therapy, responses (changes in BP, heart rate, cardiac index, and PVR) to various stimuli (e.g., isometric exercise, 45° head-up tilt, and mental challenge) were unchanged compared to baseline, suggesting that fosinopril sodium does not affect the activity of the sympathetic nervous system. Reduction in systemic blood pressure appears to have been mediated by a decrease in peripheral vascular resistance without reflex cardiac effects. Similarly, renal, splanchnic, cerebral, and skeletal muscle blood flow were unchanged compared to baseline, as was glomerular filtration rate.
Reduction of blood pressure with low (0.1 mg/kg), medium (0.3 mg/kg) and high (0.6 mg/kg) target doses of once-daily fosinopril was evaluated in a randomized, double-blind study of 252 pediatric patients 6 to 16 years of age with hypertension or high-normal blood pressure. Fosinopril doses in the medium and high dose groups were titrated to target doses after 1 week and the total duration of treatment was 4 weeks. The maximum dose studied was 40 mg once daily. At the end of 4 weeks of treatment, the mean reductions from baseline in trough systolic blood pressure were similar in all three dose groups. Withdrawal of fosinopril treatment resulted in an increase in blood pressure towards baseline over a 2-week period. Fosinopril was generally well tolerated.
Heart Failure
In a randomized, double-blind, placebo-controlled trial, 179 patients with heart failure, all receiving diuretics and some receiving digoxin, were administered single doses of 10 mg, 20 mg, or 40 mg of fosinopril sodium or placebo. Doses of 20 mg and 40 mg of fosinopril sodium resulted in acute decreases in pulmonary capillary wedge pressure (preload) and mean arterial blood pressure and systemic vascular resistance (afterload). One hundred fifty-five of these patients were re-randomized to once daily therapy with fosinopril sodium (10 mg, 20 mg, or 40 mg) for an additional 10 weeks. Hemodynamic measurements made 24 hours after dosing showed (relative to baseline) continued reduction in pulmonary capillary wedge pressure, mean arterial blood pressure, right atrial pressure and an increase in cardiac index and stroke volume for the 20 mg and 40 mg dose groups. No tachyphylaxis was seen.
Fosinopril sodium was studied in 3 double-blind, placebo-controlled, 12 to 24 week trials including a total of 734 patients with heart failure, with fosinopril sodium doses from 10 to 40 mg daily. Concomitant therapy in 2 of these 3 trials included diuretics and digitalis; in the third trial patients were receiving only diuretics. All 3 trials showed statistically significant benefits of fosinopril sodium therapy, compared to placebo, in one or more of the following: exercise tolerance (one study), symptoms of dyspnea, orthopnea and paroxysmal nocturnal dyspnea (2 studies), NYHA classification (2 studies), hospitalization for heart failure (2 studies), study withdrawals for worsening heart failure (2 studies), and/or need for supplemental diuretics (2 studies). Favorable effects were maintained for up to two years. Effects of fosinopril sodium on long-term mortality in heart failure have not been evaluated.
The once daily dosage for the treatment of congestive heart failure was the only dosage regimen used during clinical trial development and was determined by the measurement of hemodynamic responses.
Fosinopril sodium tablets are indicated for the treatment of hypertension. They may be used alone or in combination with thiazide diuretics.
Fosinopril sodium tablets are indicated in the management of heart failure as adjunctive therapy when added to conventional therapy including diuretics with or without digitalis (see DOSAGE AND ADMINISTRATION).
In using fosinopril sodium tablets, consideration should be given to the fact that another angiotensin-converting enzyme inhibitor, captopril, has caused agranulocytosis, particularly in patients with renal impairment or collagen-vascular disease. Available data are insufficient to show that fosinopril sodium tablets do not have a similar risk (see WARNINGS).
In considering use of fosinopril sodium tablets, it should be noted that in controlled trials ACE inhibitors have an effect on blood pressure that is less in black patients than in non-blacks. In addition, ACE inhibitors (for which adequate data are available) cause a higher rate of angioedema in black than in non-black patients (see WARNINGS, Anaphylactoid and Possible Related Reactions,Head and Neck AngioedemaHead and Neck andIntestinal Angioedema).
Anaphylactoid and Possible Related Reactions
Presumably because angiotensin-converting enzyme inhibitors affect the metabolism of eicosanoids and polypeptides, including endogenous bradykinin, patients receiving ACE inhibitors (including fosinopril sodium) may be subject to a variety of adverse reactions, some of them serious.
Head and Neck Angioedema
Angioedema involving the extremities, face, lips, mucous membranes, tongue, glottis, or larynx has been reported in patients treated with ACE inhibitors. If angioedema involves the tongue, glottis, or larynx, airway obstruction may occur and be fatal. If laryngeal stridor or angioedema of the face, lips, mucous membranes, tongue, glottis, or extremities occurs, treatment with fosinopril sodium should be discontinued and appropriate therapy instituted immediately. Where there is involvement of the tongue, glottis, or larynx, likely to cause airway obstruction, appropriate therapy, e.g., subcutaneous epinephrine solution 1:1000 (0.3 mL to 0.5 mL) should be promptly administered (see PRECAUTlONS, Information for Patientsand ADVERSE REACTIONS).
Intestinal Angioedema
Intestinal angioedema has been reported in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases there was no prior history of facial angioedema and C-1 esterase levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan or ultrasound, or at surgery, and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain.
Anaphylactoid Reactions During Desensitization
Two patients undergoing desensitizing treatment with hymenoptera venom while receiving ACE inhibitors sustained life-threatening anaphylactoid reactions. In the same patients, these reactions were avoided when ACE inhibitors were temporarily withheld, but they reappeared upon inadvertent rechallenge.
Anaphylactoid Reactions During Membrane Exposure
Anaphylactoid reactions have been reported in patients dialyzed with high-flux membranes and treated concomitantly with an ACE inhibitor. Anaphylactoid reactions have also been reported in patients undergoing low-density lipoprotein apheresis with dextran sulfate absorption.
Fosinopril sodium can cause symptomatic hypotension. Like other ACE inhibitors, fosinopril has been only rarely associated with hypotension in uncomplicated hypertensive patients. Symptomatic hypotension is most likely to occur in patients who have been volume- and/or salt-depleted as a result of prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting. Volume and/or salt depletion should be corrected before initiating therapy with fosinopril sodium.
In patients with heart failure, with or without associated renal insufficiency, ACE inhibitor therapy may cause excessive hypotension, which may be associated with oliguria or azotemia, and (rarely) with acute renal failure and death. In such patients, fosinopril sodium therapy should be started under close medical supervision; they should be followed closely for the first 2 weeks of treatment and whenever the dose of fosinopril or diuretic is increased. Consideration should be given to reducing the diuretic dose in patients with normal or low blood pressure who have been treated vigorously with diuretics or who are hyponatremic.
If hypotension occurs, the patient should be placed in a supine position, and, if necessary, treated with intravenous infusion of physiological saline. Fosinopril sodium treatment usually can be continued following restoration of blood pressure and volume.
Another angiotensin-converting enzyme inhibitor, captopril, has been shown to cause agranulocytosis and bone marrow depression, rarely in uncomplicated patients, but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Available data from clinical trials of fosinopril are insufficient to show that fosinopril does not cause agranulocytosis at similar rates. Monitoring of white blood cell counts should be considered in patients with collagen-vascular disease, especially if the disease is associated with impaired renal function.
Fetal/Neonatal Morbidity and Mortality
ACE inhibitors can cause fetal and neonatal morbidity and death when administered to pregnant women. Several dozen cases have been reported in the world literature. When pregnancy is detected, ACE inhibitors should be discontinued as soon as possible.
The use of ACE inhibitors during the second and third trimesters of pregnancy has been associated with fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death. Oligohydramnios has also been reported, presumably resulting from decreased fetal renal function; oligohydramnios in this setting has been associated with fetal limb contractures, craniofacial deformation, and hypoplastic lung development. Prematurity, intrauterine growth retardation, and patent ductus arteriosus have also been reported, although it is not clear whether these occurrences were due to the ACE-inhibitor exposure.
These adverse effects do not appear to have resulted from intrauterine ACE-inhibitor exposure that has been limited to the first trimester. Mothers whose embryos and fetuses are exposed to ACE inhibitors only during the first trimester should be so informed. Nonetheless, when patients become pregnant, physicians should make every effort to discontinue the use of fosinopril as soon as possible.
Rarely (probably less often than once in every thousand pregnancies), no alternative to ACE inhibitors will be found. In these rare cases, the mothers should be apprised of the potential hazards to their fetuses, and serial ultrasound examinations should be performed to assess the intraamniotic environment.
If oligohydramnios is observed, fosinopril should be discontinued unless it is considered life-saving for the mother. Contraction stress testing (CST), a non-stress test (NST), or biophysical profiling (BPP) may be appropriate, depending upon the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury.
Infants with histories of in utero exposure to ACE inhibitors should be closely observed for hypotension, oliguria, and hyperkalemia. If oliguria occurs, attention should be directed toward support of blood pressure and renal perfusion. Exchange transfusion or dialysis may be required as a means of reversing hypotension and/or substituting for disordered renal function. Fosinopril is poorly dialyzed from the circulation of adults by hemodialysis and peritoneal dialysis. There is no experience with any procedure for removing fosinopril from the neonatal circulation.
When fosinopril was given to pregnant rats at doses about 80 to 250 times (on a mg/kg basis) the maximum recommended human dose, three similar orofacial malformations and one fetus with situsinversuswere observed among the offspring. No teratogenic effects of fosinopril were seen in studies in pregnant rabbits at doses up to 25 times (on a mg/kg basis) the maximum recommended human dose.
Hepatic Failure
Rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
Impaired Renal Function
As a consequence of inhibiting the renin-angiotensin-aldosterone system, changes in renal function may be anticipated in susceptible individuals. In patients with severe congestive heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with angiotensin-converting enzyme inhibitors, including fosinopril sodium tablets, may be associated with oliguria and/or progressive azotemia and (rarely) with acute renal failure and/or death.
In hypertensive patients with renal artery stenosis in a solitary kidney or bilateral renal artery stenosis, increases in blood urea nitrogen and serum creatinine may occur. Experience with another angiotensin-converting enzyme inhibitor suggests that these increases are usually reversible upon discontinuation of ACE inhibitor and/or diuretic therapy. In such patients, renal function should be monitored during the first few weeks of therapy. Some hypertensive patients with no apparent pre-existing renal vascular disease have developed increases in blood urea nitrogen and serum creatinine, usually minor and transient, especially when fosinopril sodium has been given concomitantly with a diuretic. This is more likely to occur in patients with pre-existing renal impairment. Dosage reduction of fosinopril sodium and/or discontinuation of the diuretic may be required.
Evaluation of patients with hypertension or heart failure should always include assessment of renal function (see DOSAGE AND ADMINISTRATION).
Impaired renal function decreases total clearance of fosinoprilat and approximately doubles AUC. In general, no adjustment of dosing is needed. However, patients with heart failure and severely reduced renal function may be more sensitive to the hemodynamic effects (e.g., hypotension) of ACE inhibition (see CLINICAL PHARMACOLOGY).
In clinical trials, hyperkalemia (serum potassium greater than 10% above the upper limit of normal) has occurred in approximately 2.6% of hypertensive patients receiving fosinopril sodium. In most cases, these were isolated values which resolved despite continued therapy. In clinical trials, 0.1% of patients (two patients) were discontinued from therapy due to an elevated serum potassium. Risk factors for the development of hyperkalemia include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes, which should be used cautiously, if at all, with fosinopril sodium tablets (see PRECAUTIONS, Drug Interactions).
Presumably due to the inhibition of the degradation of endogenous bradykinin, persistent nonproductive cough has been reported with all ACE inhibitors, always resolving after discontinuation of therapy. ACE inhibitor-induced cough should be considered in the differential diagnosis of cough.
Impaired Liver Function
Since fosinopril is primarily metabolized by hepatic and gut wall esterases to its active moiety, fosinoprilat, patients with impaired liver function could develop elevated plasma levels of unchanged fosinopril. In a study in patients with alcoholic or biliary cirrhosis, the extent of hydrolysis was unaffected, although the rate was slowed. In these patients, the apparent total body clearance of fosinoprilat was decreased and the plasma AUC approximately doubled.
In patients undergoing surgery or during anesthesia with agents that produce hypotension, fosinopril will block the angiotensin II formation that could otherwise occur secondary to compensatory renin release. Hypotension that occurs as a result of this mechanism can be corrected by volume expansion.
Recent clinical observations have shown an association of hypersensitivity-like (anaphylactoid) reactions during hemodialysis with high-flux dialysis membranes (e.g., AN69) in patients receiving ACE inhibitors as medication. In these patients, consideration should be given to using a different type of dialysis membrane or a different class of medication (see WARNINGS, Anaphylactoid Reactions During Membrane Exposure).
Information for Patients
Angioedema: Angioedema, including laryngeal edema, can occur with treatment with ACE inhibitors, especially following the first dose. Patients should be advised to immediately report to their physician any signs or symptoms suggesting angioedema (e.g., swelling of face, eyes, lips, tongue, larynx, mucous membranes, and extremities; difficulty in swallowing or breathing; hoarseness) and to discontinue therapy (see WARNINGS, Anaphylactoid and Possible Related Reactions,Head and Neck AngioedemaandIntestinal Angioedema).
Symptomatic Hypotension: Patients should be cautioned that lightheadedness can occur, especially during the first days of therapy, and it should be reported to a physician. Patients should be told that if syncope occurs, fosinopril sodium should be discontinued until the physician has been consulted.
All patients should be cautioned that inadequate fluid intake or excessive perspiration, diarrhea, or vomiting can lead to an excessive fall in blood pressure, with the same consequences of lightheadedness and possible syncope.
Hyperkalemia: Patients should be told not to use potassium supplements or salt substitutes containing potassium without consulting the physician.
Neutropenia: Patients should be told to promptly report any indication of infection (e.g., sore throat, fever), which could be a sign of neutropenia.
Pregnancy: Female patients of childbearing age should be told about the consequences of second- and third-trimester exposure to ACE inhibitors, and they should also be told that these consequences do not appear to have resulted from intrauterine ACE-inhibitor exposure that has been limited to the first trimester. These patients should be asked to report pregnancies to their physicians as soon as possible.
Drug Interactions
Patients on diuretics, especially those with intravascular volume depletion, may occasionally experience an excessive reduction of blood pressure after initiation of therapy with fosinopril sodium tablets. The possibility of hypotensive effects with fosinopril sodium can be minimized by either discontinuing the diuretic or increasing salt intake prior to initiation of treatment with fosinopril sodium. If this is not possible, the starting dose should be reduced and the patient should be observed closely for several hours following an initial dose and until blood pressure has stabilized (see DOSAGE AND ADMINISTRATION).
Potassium Supplements and Potassium-Sparing Diuretics
Fosinopril sodium can attenuate potassium loss caused by thiazide diuretics. Potassium-sparing diuretics (spironolactone, amiloride, triamterene, and others) or potassium supplements can increase the risk of hyperkalemia. Therefore, if concomitant use of such agents is indicated, they should be given with caution, and the patient's serum potassium should be monitored frequently.
Increased serum lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors during therapy with lithium. These drugs should be co-administered with caution, and frequent monitoring of serum lithium levels is recommended. If a diuretic is also used, the risk of lithium toxicity may be increased.
In a clinical pharmacology study, co-administration of an antacid (aluminum hydroxide, magnesium hydroxide, and simethicone) with fosinopril reduced serum levels and urinary excretion of fosinoprilat as compared with fosinopril administered alone, suggesting that antacids may impair absorption of fosinopril. Therefore, if concomitant administration of these agents is indicated, dosing should be separated by 2 hours.
Nitritoid reactions (symptoms include facial flushing, nausea, vomiting, and hypotension) have been reported rarely in patients on therapy with injectable gold (sodium aurothiomalate) and concomitant ACE inhibitor therapy including fosinopril sodium.
Neither fosinopril sodium nor its metabolites have been found to interact with food. In separate single or multiple dose pharmacokinetic interaction studies with chlorthalidone, nifedipine, propranolol, hydrochlorothiazide, cimetidine, metoclopramide, propantheline, digoxin, and warfarin, the bioavailability of fosinoprilat was not altered by co-administration of fosinopril with any one of these drugs. In a study with concomitant administration of aspirin and fosinopril sodium, the bioavailability of unbound fosinoprilat was not altered.
In a pharmacokinetic interaction study with warfarin, bioavailability parameters, the degree of protein binding, and the anticoagulant effect (measured by prothrombin time) of warfarin were not significantly changed.
Carcinogenesis, Mutagenesis, Impairment of Fertility
No evidence of a carcinogenic effect was found when fosinopril was given in the diet to mice and rats for up to 24 months at doses up to 400 mg/kg/day. On a body weight basis, the highest dose in mice and rats is about 250 times the maximum human dose of 80 mg, assuming a 50 kg subject. On a body surface area basis, in mice, this dose is 20 times the maximum human dose; in rats, this dose is 40 times the maximum human dose. Male rats given the highest dose level had a slightly higher incidence of mesentery/omentum lipomas.
Neither fosinopril nor the active fosinoprilat was mutagenic in the Ames microbial mutagen test, the mouse lymphoma forward mutation assay, or a mitotic gene conversion assay. Fosinopril was also not genotoxic in a mouse micronucleus test in vivo and a mouse bone marrow cytogenetic assay in vivo.
In the Chinese hamster ovary cell cytogenetic assay, fosinopril increased the frequency of chromosomal aberrations when tested without metabolic activation at a concentration that was toxic to the cells. However, there was no increase in chromosomal aberrations at lower drug concentrations without metabolic activation or at any concentration with metabolic activation.
There were no adverse reproductive effects in male and female rats treated with 15 mg/kg or 60 mg/kg daily. On a body weight basis, the high dose of 60 mg/kg is about 38 times the maximum recommended human dose. On a body surface area basis, this dose is 6 times the maximum recommended human dose. There was no effect on pairing time prior to mating in rats until a daily dose of 240 mg/kg, a toxic dose, was given; at this dose, a slight increase in pairing time was observed. On a body weight basis, this dose is 150 times the maximum recommended human dose. On a body surface area basis, this dose is 24 times the maximum recommended human dose.
Pregnancy Category C (first trimester) and D (second and third trimesters): See WARNINGS, Fetal/Neonatal Morbidity and Mortality .
Nursing Mothers
Ingestion of 20 mg daily for three days resulted in detectable levels of fosinoprilat in breast milk. Fosinopril sodium should not be administered to nursing mothers.
Geriatric Use
Clinical studies of fosinopril sodium did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Pediatric Use
The antihypertensive effects of fosinopril have been evaluated in a double-blind study in pediatric patients 6 to 16 years of age (see CLINICAL PHARMACOLOGY, Hypertension ). The pharmacokinetics of fosinopril have been evaluated in pediatric patients 6 to 16 years of age (see CLINICAL PHARMACOLOGY, Pharmacokinetics and Metabolism ). Fosinopril was generally well tolerated and adverse effects were similar to those described in adults (see ADVERSE REACTIONS, Pediatric Patients ).
Fosinopril sodium has been evaluated for safety in more than 2,100 individuals in hypertension and heart failure trials, including approximately 530 patients treated for a year or more. Generally, adverse events were mild and transient, and their frequency was not prominently related to dose within the recommended daily dosage range.
In placebo-controlled clinical trials (688 fosinopril sodium-treated patients), the usual duration of therapy was two to three months. Discontinuations due to any clinical or laboratory adverse event were 4.1% and 1.1% in fosinopril sodium-treated and placebo-treated patients, respectively. The most frequent reasons (0.4% to 0.9%) were headache, elevated transaminases, fatigue, cough (see PRECAUTIONS, General, Cough), diarrhea, and nausea and vomiting.
During clinical trials with any fosinopril sodium regimen, the incidence of adverse events in the elderly (≥ 65 years old) was similar to that seen in younger patients. Clinical adverse events probably or possibly related or of uncertain relationship to therapy, occurring in at least 1% of patients treated with fosinopril sodium alone and at least as frequent on fosinopril sodium as on placebo in placebo-controlled clinical trials are shown in the table below.
Clinical Adverse Events In Placebo-Controlled Trials (Hypertension) Fosinopril Sodium
Incidence (Discontinuation)
Incidence (Discontinuation)
2.2 (0.4)
0.0 (0.0)
1.6 (0.0)
0.0 (0.0)
1.2 (0.4)
0.5 (0.0)
The following events were also seen at >1% on fosinopril sodium tablets but occurred in the placebo group at a greater rate: headache, diarrhea, fatigue, and sexual dysfunction. Other clinical events probably or possibly related, or of uncertain relationship to therapy occurring in 0.2% to 1.0% of patients (except as noted) treated with fosinopril sodium in controlled or uncontrolled clinical trials (N=1,479) and less frequent, clinically significant events include (listed by body system):
General: Chest pain, edema, weakness, excessive sweating.
Cardiovascular: Angina/myocardial infarction, cerebrovascular accident, hypertensive crisis, rhythm disturbances, palpitations, hypotension, syncope, flushing, claudication.
Orthostatic hypotension occurred in 1.4% of patients treated with fosinopril monotherapy.
Hypotension or orthostatic hypotension was a cause for discontinuation of therapy in 0.1% of patients.
Dermatologic: Urticaria, rash, photosensitivity, pruritus.
Endocrine/Metabolic: Gout, decreased libido.
Gastrointestinal: Pancreatitis, hepatitis, dysphagia, abdominal distention, abdominal pain, flatulence, constipation, heartburn, appetite/weight change, dry mouth.
Hematologic: Lymphadenopathy.
Immunologic: Angioedema. (See WARNINGS, Anaphylactoid and Possible Related Reactions,Head and Neck AngioedemaHead and Neck andIntestinal Angioedema).
Musculoskeletal: Arthralgia, musculoskeletal pain, myalgia/muscle cramp.
Nervous/Psychiatric: Memory disturbance, tremor, confusion, mood change, paresthesia, sleep disturbance, drowsiness, vertigo.
Respiratory: Bronchospasm, pharyngitis, sinusitis/rhinitis, laryngitis/hoarseness, epistaxis. A
symptom-complex of cough, bronchospasm, and eosinophilia has been observed in two patients treated with fosinopril.
Special Senses: Tinnitus, vision disturbance, taste disturbance, eye irritation.
Urogenital: Renal insufficiency, urinary frequency.
Heart Failure
In placebo-controlled clinical trials (361 fosinopril sodium-treated patients), the usual duration of therapy was 3 to 6 months. Discontinuations due to any clinical or laboratory adverse event, except for heart failure, were 8.0% and 7.5% in fosinopril sodium-treated and placebo-treated patients, respectively. The most frequent reason for discontinuation of fosinopril sodium was angina pectoris (1.1%). Significant hypotension after the first dose of fosinopril sodium occurred in 14/590 (2.4%) of patients; 5/590 (0.8%) patients discontinued due to first dose hypotension.
Clinical adverse events probably or possibly related or of uncertain relationship to therapy, occurring in at least 1% of patients treated with fosinopril sodium and at least as common as the placebo group, in placebo-controlled trials are shown in the table below.
Clinical Adverse Events in Placebo-Controlled Trials (Heart Failure) Fosinopril Sodium
Incidence (Discontinuation)
Incidence (Discontinuation)
11.9 (0.6)
5.4 (0.3)
9.7 (0.8)
5.1 (0.0)
4.4 (0.8)
0.8 (0.0)
Musculoskeletal Pain
3.3 (0.0)
2.7 (0.0)
2.2 (0.6)
1.6 (0.3)
2.2 (0.0)
1.3 (0.0)
Chest Pain (non-cardiac)
2.2 (0.0)
1.6 (0.0)
Upper Respiratory Infection
2.2 (0.0)
1.3 (0.0)
Orthostatic Hypotension
1.9 (0.0)
0.8 (0.0)
Subjective Cardiac
Rhythm Disturbance
1.4 (0.6)
0.8 (0.3)
1.4 (0.3)
0.5 (0.0)
The following events also occurred at a rate of 1% or more on fosinopril sodium but occurred on placebo more often: fatigue, dyspnea, headache, rash, abdominal pain, muscle cramp, angina pectoris, edema, and insomnia.
The incidence of adverse events in the elderly (≥ 65 years old) was similar to that seen in younger patients. Other clinical events probably or possibly related, or of uncertain relationship to therapy occurring in 0.4% to 1.0% of patients (except as noted) treated with fosinopril sodium in controlled clinical trials (N=516) and less frequent, clinically significant events include (listed by body system):
General: Fever, influenza, weight gain, hyperhidrosis, sensation of cold, fall, pain.
Cardiovascular: Sudden death, cardiorespiratory arrest, shock (0.2%), atrial rhythm disturbance, cardiac rhythm disturbances, non anginal chest pain, edema lower extremity, hypertension, syncope, conduction disorder, bradycardia, tachycardia.
Dermatologic: pruritus.
Endocrine/Metabolic: Gout, sexual dysfunction.
Gastrointestinal: Hepatomegaly, abdominal distention, decreased appetite, dry mouth, constipation,flatulence.
Immunologic: Angioedema (0.2%).
Musculoskeletal: Muscle ache, swelling of an extremity, weakness of an extremity.
Nervous/Psychiatric: Cerebral infarction, TIA, depression, numbness, paresthesia, vertigo, behavior change, tremor.
Respiratory: Abnormal vocalization, rhinitis, sinus abnormality, tracheobronchitis, abnormal breathing,pleuritic chest pain.
Special Senses: Vision disturbance, taste disturbance.
Urogenital: Abnormal urination, kidney pain.
Fetal/Neonatal Morbidity and Mortality
See WARNINGS, Fetal/Neonatal Morbidity and Mortality.
Potential Adverse Effects Reported with ACE Inhibitors
Body as a whole: Anaphylactoid reactions (see WARNINGS, Anaphylactoid and Possible Related Reactions and PRECAUTIONS,Hemodialysis Hemodialysis).
Other medically important adverse effects reported with ACE inhibitors include: Cardiac arrest; eosinophilic pneumonitis; neutropenia/agranulocytosis, pancytopenia, anemia (including hemolytic and aplastic), thrombocytopenia; acute renal failure; hepatic failure, jaundice (hepatocellular or cholestatic); symptomatic hyponatremia; bullous pemphigus, exfoliative dermatitis; a syndrome which may include: arthralgia/arthritis, vasculitis, serositis, myalgia, fever, rash or other dermatologic manifestations, a positive ANA, leukocytosis, eosinophilia, or an elevated ESR.
Laboratory Test Abnormalities
Serum Electrolytes: Hyperkalemia, (see PRECAUTIONS); hyponatremia, (see PRECAUTIONS, Drug Interactions, Diuretics).
BUN/Serum Creatinine: Elevations, usually transient and minor, of BUN or serum creatinine have been observed. In placebo-controlled clinical trials, there were no significant differences in the number of patients experiencing increases in serum creatinine (outside the normal range or 1.33 times the pre-treatment value) between the fosinopril and placebo treatment groups. Rapid reduction of longstanding or markedly elevated blood pressure by any antihypertensive therapy can result in decreases in the glomerular filtration rate, and in turn, lead to increases in BUN or serum creatinine (see PRECAUTIONS, General).
Hematology: In controlled trials, a mean hemoglobin decrease of 0.1 g/dL was observed in fosinopril-treated patients. In individual patients decreases in hemoglobin or hematocrit were usually transient, small, and not associated with symptoms. No patient was discontinued from therapy due to the development of anemia.
Other: Neutropenia (see WARNINGS), leukopenia and eosinophilia.
Liver Function Tests: Elevations of transaminases, LDH, alkaline phosphatase, and serum bilirubin have been reported. Fosinopril therapy was discontinued because of serum transaminase elevations in 0.7% of patients. In the majority of cases, the abnormalities were either present at baseline or were associated with other etiologic factors. In those cases which were possibly related to fosinopril therapy, the elevations were generally mild and transient and resolved after discontinuation of therapy.
Oral doses of fosinopril at 2600 mg/kg in rats were associated with significant lethality. Human overdoses of fosinopril have not been reported, but the most common manifestation of human fosinopril overdosage is likely to be hypotension.
Laboratory determinations of serum levels of fosinoprilat and its metabolites are not widely available, and such determinations have, in any event, no established role in the management of fosinopril overdose. No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine) that might accelerate elimination of fosinopril and its metabolites. Fosinoprilat is poorly removed from the body by both hemodialysis and peritoneal dialysis.
Angiotensin II could presumably serve as a specific antagonist-antidote in the setting of fosinopril overdose, but angiotensin II is essentially unavailable outside of scattered research facilities. Because the hypotensive effect of fosinopril is achieved through vasodilation and effective hypovolemia, it is reasonable to treat fosinopril overdose by infusion of normal saline solution.
No adverse clinical events were reported in 23 pediatric patients, age 6 months to 6 years, given a single 0.3 mg/kg oral dose of fosinopril sodium.
There is a published report of a 20-month-old female, weighing 12 kg, who ingested approximately 200 mg fosinopril sodium. After receiving gastric lavage and activated charcoal within one hour of the ingestion, she made an uneventful recovery.
Hypertension Adults
The recommended initial dose of fosinopril sodium tablets is 10 mg once a day, both as monotherapy and when the drug is added to a diuretic. Dosage should then be adjusted according to blood pressure response at peak (2 to 6 hours) and trough (about 24 hours after dosing) blood levels. The usual dosage range needed to maintain a response at trough is 20 mg to 40 mg but some patients appear to have a further response to 80 mg. In some patients treated with once daily dosing, the antihypertensive effect may diminish toward the end of the dosing interval. If trough response is inadequate, dividing the daily dose should be considered. If blood pressure is not adequately controlled with fosinopril sodium tablets alone, a diuretic may be added.
Concomitant administration of fosinopril sodium tablets with potassium supplements, potassium salt substitutes, or potassium-sparing diuretics can lead to increases of serum potassium (see PRECAUTIONS).
In patients who are currently being treated with a diuretic, symptomatic hypotension occasionally can occur following the initial dose of fosinopril sodium tablets. To reduce the likelihood of hypotension, the diuretic should, if possible, be discontinued two to three days prior to beginning therapy with fosinopril sodium tablets (see WARNINGS). Then, if blood pressure is not controlled with fosinopril sodium tablets alone, diuretic therapy should be resumed. If diuretic therapy cannot be discontinued, an initial dose of 10 mg of fosinopril sodium tablets should be used with careful medical supervision for several hours and until blood pressure has stabilized (see WARNINGS, PRECAUTIONS, Information for Patientsand Drug Interactions).
Since concomitant administration of fosinopril sodium tablets with potassium supplements, or potassium-containing salt substitutes or potassium-sparing diuretics may lead to increases in serum potassium, they should be used with caution (see PRECAUTIONS).
Pediatric Patients
In children, doses of MONOPRIL between 0.1 mg/kg and 0.6 mg/kg have been studied and shown to reduce blood pressure to a similar extent (see CLINICAL PHARMACOLOGY, Pharmacodynamics and Clinical Effects ). Based on this, the recommended dose of fosinopril sodium tablets in children weighing more than 50 kg is 5 mg to 10 mg once per day as monotherapy. An appropriate dosage strength is not available for children weighing less than 50 kg.
Heart Failure
Digitalis is not required for fosinopril sodium tablets to manifest improvements in exercise tolerance and symptoms. Most placebo-controlled clinical trial experience has been with both digitalis and diuretics present as background therapy.
The usual starting dose of fosinopril sodium tablets should be 10 mg once daily. Following the initial dose of fosinopril sodium tablets, the patient should be observed under medical supervision for at least two hours for the presence of hypotension or orthostasis, and if present, until blood pressure stabilizes. An initial dose of 5 mg is preferred in heart failure patients with moderate to severe renal failure or those who have been vigorously diuresed.
Dosage should be increased, over a several week period, to a dose that is maximal and tolerated but not exceeding 40 mg once daily. The usual effective dosage range is 20 mg to 40 mg once daily. The appearance of hypotension, orthostasis, or azotemia early in dose titration should not preclude further careful dose titration. Consideration should be given to reducing the dose of concomitant diuretic.
For Hypertensive or Heart Failure Patients With Renal Impairment
In patients with impaired renal function, the total body clearance of fosinoprilat is approximately 50% slower than in patients with normal renal function. Since hepatobiliary elimination partially compensates for diminished renal elimination, the total body clearance of fosinoprilat does not differ appreciably with any degree of renal insufficiency (creatinine clearances <80 mL/min/1.73m2), including end-stage renal failure (creatinine clearance <10 mL/min/1.73m2). This relative constancy of body clearance of active fosinoprilat, resulting from the dual route of elimination, permits use of the usual dose in patients with any degree of renal impairment. (See WARNINGS, Anaphylactoid Reactions During Membrane Exposureand PRECAUTIONS, Hemodialysis .)
Fosinopril Sodium Tablets for oral administration are available as:
20 mg: White to off-white, capsule-shaped tablets, debossed "E42" on one side and plain on the other side, packaged with a desiccant and supplied as:
Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature].
Dispense in a tight container as defined in the USP with a child-resistant closure, as required.
Protect from moisture.
To report SUSPECTED ADVERSE REACTIONS, contact Sandoz Inc. at 1-800-525-8747 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Sandoz Inc.
Princeton, NJ 08540
Rev. 05/13
fosinopril sodium tabletProduct Information Product Type HUMAN PRESCRIPTION DRUG Item Code (Source) NDC:68258-6106(NDC:0185-0042) Route of Administration ORAL Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength FOSINOPRIL SODIUM (UNII: NW2RTH6T2N) (FOSINOPRILAT - UNII:S312EY6ZT8) FOSINOPRIL SODIUM 20 mg Inactive Ingredients Ingredient Name Strength ANHYDROUS LACTOSE (UNII: 3SY5LH9PMK) CARNAUBA WAX (UNII: R12CBM0EIZ) CROSPOVIDONE (UNII: 68401960MK) CELLULOSE, MICROCRYSTALLINE (UNII: OP1R32D61U) ZINC STEARATE (UNII: H92E6QA4FV) Product Characteristics Color WHITE (Off-White) Score no score Shape CAPSULE Size 12mm Flavor Imprint Code E42 Contains Packaging # Item Code Package Description Marketing Start Date Marketing End Date 1 NDC:68258-6106-3 30 in 1 BOTTLE Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date ANDA ANDA076483 04/23/2004 Labeler - Dispensing Solutions, Inc. (066070785) Registrant - PSS World Medical, Inc. (101822682) Establishment Name Address ID/FEI Business Operations Dispensing Solutions, Inc. 066070785 relabel(68258-6106) , repack(68258-6106)


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DAMSEL FLIES FOR BLUEGILL (part I - Nymphs)
It is often necessary to ask the right question. "What is the best fly to use for bluegill?" is such a question. Of course, no two people will give you the same answer.
Adult bluegill feed primarily on insects. That means they will eat insects to the exclusion of everything else unless food is scarce enough to force them to seek out other items. They will eat insects in any stage of the insect's life cycle and are not particular; eating whatever insect is currently available. However, should availability include damsel flies, they will usually be near the top of the menu.


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ATLANTA (AP) — For more than a decade, Georgia Democrats struggled to lure highly qualified, big-name candidates to run for statewide office. With Republicans firmly in control of all constitutional positions and the state legislature, none wanted to take the risk.
This year is different.
Boosted by significant electoral victories in the 2020 election, a near-win of the governor's office in 2018 and rapidly changing state demographics, seven sitting Democratic lawmakers have declared candidacies for one of Georgia's eight statewide offices — a full nine months away from the 2022 qualifying deadline.
Among them are names that have drawn national notice, including Democratic state Rep. Bee Nguyen, a candidate for secretary of state who seeks to leverage her party's outrage over Georgia's restrictive new voting law to raise money nationwide, and state Sen. Jen Jordan, who is running for attorney general.
"I absolutely think it is going to be a strong field," Nguyen said. "I think we recognize we can win in Georgia. We saw it last year; we saw it in 2021."
Republicans, who still hold all of Georgia's constitutional statewide offices, hardly intend to concede. Most incumbents are gearing up for reelection and prominent GOP state lawmakers are also planning statewide runs.
Georgia is one of six Southern states where only Republicans hold statewide office. In others, Republicans are dominant. In Louisiana, Republican control is broken only by Democratic Gov. John Bel Edwards, while in Florida, Agriculture Commissioner Nikki Fried is the only Democrat in statewide office.
Still, as they look to the 2022 elections, few Republicans in Georgia expect the relatively easy victories that characterized the peak of GOP ascendance in the state in the 2010s.
That's because Georgia — as evidenced by the most recent elections — is evolving into the South's most electorally competitive state. In November, President Joe Biden became the first Democrat to win the state's 16 electoral votes since Bill Clinton in 1992. Democrats Raphael Warnock and Jon Ossoff then went on to win U.S. Senate seats in multimillion-dollar January runoffs that tipped control of the chamber to Democrats.
Candidates also hope to benefit from Stacey Abrams' expected retry for the governor's office in 2022. Abrams' narrow loss to then-Secretary of State Brian Kemp in 2018 bolstered the party that year, as did gains in the General Assembly.
Before Biden's victory, the last Democrats to win statewide were four incumbents who retained down-ballot offices in 2006, even as Republican Sonny Perdue swept to reelection as governor. Those victories came as voters split their tickets at a rate that has become unusual in Georgia today. Democrat Thurbert Baker won a third term as attorney general with 57% of the vote, at the same time Perdue won 58%.
But no statewide Democrats remained after the 2010 election, and the party's candidates became less competitive over the next two cycles.
The candidates who may have been the party's strongest challengers to GOP incumbents during that time said, 'No, not now, I'm not going to give up a sure thing for a longshot,'" noted University of Georgia political scientist Charles Bullock.
Some who did try didn't fare well. In 2014, the Democratic nominee for agriculture commissioner was Christopher James Irvin. Although he had huge name recognition as the grandson of a Democrat who held the post for 42 years, he raised only $52,000 compared to Republican victor Gary Black's $1.65 million.
Abrams has yet to announce plans for 2022, but other Democrats expect her to run again. Candidates are excited at the prospect of having her and Warnock atop the party's ticket.
"We are all sitting here waiting," said state Rep. William Boddie, a Democrat from the Atlanta suburb of East Point who is running for labor commissioner. "She brings a lot of energy, a lot of policy initiatives and a lot of drive to push Democratic values to any ticket."
Abrams is likely to raise a boatload of money, and some could find its way to other Democrats. Nguyen, for example, could cash in on opposition to Georgia's restrictive new election law in her race for secretary of state.
Democrats do face challenges. Like 2010, when Democrats were swept out of statewide office, 2022 falls in a midterm year, when the party that doesn't control the White House tends to pick up seats. With Biden in office, national gains by the GOP could drag down the state's Democratic ticket.
"It's not necessarily the easiest to recruit in this cycle for the constitutional offices," said Ross Rocketto, the cofounder of Run for Something, a political action committee that recruits and trains Democrats to run for office. "People are worried that it's not going to be that good of a year for Democrats."
But there are other factors that could push Democratic state lawmakers to run for higher office. When the legislature redraws district lines this fall for the 2022 elections, some Democrats could find themselves with unfriendly districts. In addition, the party overall is likely to remain in the minority in both chambers.
There's also the issue of pay. Statewide officers all make more than $120,000 a year, while state legislators make far less.
"You've essentially got two full-time jobs and one of them pays $17,000 a year," Bullock said of what lawmakers earn.
Being elected statewide also gives politicians a chance to set their own agenda, instead of being one voice among 236 in Georgia's expansive General Assembly. Jordan said that's part of the attraction of running for attorney general, a race in which she faces 2018 Democratic nominee Charlie Bailey. The winner will likely take on Republican incumbent Chris Carr.
To ensure victory, Democrats have to make sure their supporters don't just vote for top offices when they go to the polls, something that happened in January. Even as Warnock and Ossoff won, a fellow Democrat lost a runoff for a post on the Georgia Public Service Commission.
"Voters need to vote down the ticket, because Stacey can't do it by herself," Rocketto said.
For more from Fresh Take Georgia and the latest updates, follow us on Facebook and Twitter.


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PDA: Register for December's Professional Development Offerings
December 06, 2021
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