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to get out of it, and, therefore, unreasonably magnify their grievances, and seek pretexts for neglecting their duty and disobeying orders. That they have set the authority of the Government at defiance, and have been assured that money and influence will not be spared in their behalf in their course of conduct, and that if they hold out a little longer their discharge will be granted. They say they have the legal opinion of eminent lawyers in Philadelphia that they cannot be held in the service. That the 208 who refused to come out of confinement and go to duty were induced to this course by the action of one or more of a committee who visited them from Philadelphia, and from letters received from friends. That they have allowed their personal feelings and conceived private grievances to outweigh the dictates of patriotism and a just sense of duty to their country in her most trying hour of peril and need. That, in a military sense, all reasonable means have been exhausted to induce them to return to duty, and awaken in them a feeling of pride and a proper sense of their sacred obligations to their Government and country without avail. That after making concessions to them, forgiving their past conduct, and giving them what they have claimed, a large number positively refuse all terms offered by their commanding general, and a large portion of those who did partially accept the terms offered, which were those they had claimed as their rights, did so, apparently, not in the right and proper spirit. That there is no good excuse for their mutinous and disobedient conduct, and that hundreds if not thousands of other troops in the Department of the Cumberland are closely watching the action of Government in this case, upon which their future action will be shaped. That the discipline, interests, and well being of the Army of the Cumberland depend materially upon the result of governmental action with regard to this regiment. It is an important case to the army, as affecting its efficiency and success. That there are leading spirits among the mutinous portion of the Anderson Cavalry, I have no doubt, who influence and control the others to a great extent. That there is a want of harmony of feeling between different portions of the regiment is manifest. There are many of those who have been confined who appear to be well meaning, and whom I believe would never have been guilty of such conduct but for the action of others who have influenced and urged them to it. That the good of the service requires an example to be made of a portion of this regiment, I have no doubt.
Most respectfully submitted.
Assistant Inspector-General, U. S. Army.
[Inclosure A.]
HEADQUARTERS ARMY OF THE OHIO, Huntsville, Ala., July 23, 1862.
His Excellency ANDREW G. CURTIN,
Governor of Pennsylvania, Harrisburg:
SIR: I am directed by Major-General Buell to address you as follows. On the 18th instant the following dispatch was forwarded, viz:
HUNTSVILLE, ALA., July 18, 1862.
Honorable E. M. STANTON,
Secretary of War, Washington:
I ask authority to arrange with the Governor of Pennsylvania for raising three companies of cavalry, to be united with the independent company raised last fall, and known as the Anderson Troop, Captain Palmer. This company is composed of supe-


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Clean Loop is a light weight, medium duty entrance mat which is particularly ideal for coastal and other sandy areas. The PVC loops on the surface of the mat assist in scraping sand, dirt and debris from footwear and retaining it in the mat, preventing it from being walked onto surrounding floor surfaces. The standard size mats have a pressed border, making it low profile and safe from trips on the mat edges and the edges are bonded to a non-skid backing preventing the mat from 'walking'. Custom sized mats can also be edged with a ramped black PVC Border. Clean Loop is UV resistant and can be used both indoors and outdoors situations. Regular cleaning by shaking, hosing or vacuuming is recommended to maintain the performance of the mat. Clean Loop is available in four standard sizes in either grey or black and can be custom sized.
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Forgot your password? Jamie Lynn Spears was cast as part of the show since the year up till the year Would you like to view this in our Asia edition?
Free Jamie Lynn Spears Nudes
This content is available customized for our international audience. Jamie Lynn posted a photo to Instagram in support of Britney and was quick to defend her in the comments. Potter, Elliott and Headley play three women from South Carolina who were best friends since high school and are still supporting each other to this day. In the show based on Sherryl Woods ' book series, Spears will play Noreen Fitzgibbons, a young woman who sets out to build a new life for herself following a series of not so great choices.


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The struggles continue for the Football Hogs as the SEC losing streak is now at 14 and things won't get any easier with Auburn this weekend and a trip to Tuscaloosa next weekend. Mike Irwin answers your questions about the state of the Razorbacks in his weekly "Ask Mike" segment.
1. Before we get started I want to say something to all of you.
2. Each week I get several fans asking… Mike do you think Chad Morris will be gone at the end of this year if this or this or this doesn't happen.
3. I'm not physic. I'm not tapped into Hunter Yurachek's brain.
4. It would be highly unusual for Morris not to get a least three years to get his program going.
5. So is that it? You guys have to go through another year of this no matter what?
6. Maybe but I'm not 100% sure about that.
7. Coming up with his big buyout is an issue with all the capital improvement projects they're paying for.
8. That's the best answer I can give.
*Okay, the first question this week comes from Kevin who asks: How do you continue to sell this hot mess to the fans?
1. I'm glad I'm not the one who has to do it.
2. The short answer is there's not much you can do if this team continues to lose.
3. You have a core of loyal fans who will continue to support the program because that's what they do….. win or lose.
4. Beyond that I guess if you're the AD you express concern. Say you're monitoring the situation. Working with the head coach to bring about some improvement.
*St. Hogustine wants to know: How involved was Jerry Jones in the Morris hire?
1. He didn't force it like, Hey I'm Jerry Jones. You better hire this guy.
2. But you had an interim AD who was being advised by a lot of boosters and Jerry Jones was one of them.
3. He said some very good things about Chad Morris and yes, his opinion carried weight.
*Lanny on Hogville is curious: Why does ARKANSAS hire unproven coaches and award them ridiculous buyouts
1. An inexperienced interim AD did that and it was approved by the Board of Trustees.
2. The Current AD…who did not hire Chad Morris… said right after HE was hired that he did not believe in big buyouts.
3. So we've probably seen the last of that.
4. If Hunter Yuracheck pulls the trigger on Chad Morris…based on how he handled the search for Eric Musselman…I'm confident that the search for a replacement would be handled much differently.
5. As in no boosters heavily involved.
*Kevin is back with this question: I am not a fan of firing assistant coaches, just seems like shuffling deck chairs on the Titanic, what are your thoughts?
1. Well it's done all the time and sometimes it works.
2. The big problem in this situation is….you're probably going to end up with out of work coaches who need a job as replacements.
3. Or coaches at lower level schools looking to move up.
4. A successful proven assistant at a Power 5 school probably wouldn't walk into this situation. They'd want more security.
Okay….I need a break. Let's step away from this heavy duty stuff for a couple of less weighty questions.
*Sivad asks:Which SEC schools treat you (visiting sports media) the best, and which treat you the worst?
1. The best I've been to is Georgia.
2. Those people will serve you brunch, lunch and dinner ..if you hang around long enough.
3. Plus great ice cream.
4. really nice folks.
5. I also like Ole Miss because they don't have a lot of rules.
6. I went off without my parking pass one year and they waved me right through to the media lot.
7. LSU is the worst.
8. To me it's called Death Valley because you'd almost rather die than go there.
9. A&M is a close second for the same reason.
10. Only I call that place Whackoville.
*Dr. Starcs says: I'd love for you to answer these hypothetical questions:
Mike, if you alone were responsible for the football hires, who are the two you would have realistically hired after Petrino and Bielema?
1. There would be only one.
2. I would have hired Mike Leach after Petrino and he'd still be here and he'd be winning.
3. But there's a catch. Leach is all offense.
4. He wants nothing to do with defense.
5. I would have put on a search for the right defensive coordinator just like the search for a head coach. Pay the guy top dollar.
6. Also Leach needs the support of the Board….AD and Chancellor wherever he is because he's not politically correct and most universities are eaten up with political correctness.
7. Like Texas Tech which fired him.
8. Tech's been going downhill in football ever since.
7. So I'd hire him.
8 Hire the right defensive coordinator.
9. Keep the liberal faculty off his back
10. And all of you Hog fans would have a winner.
Okay back to the depressing stuff – Redleg says: Do you see Hunter Yurachek stipulating certain "goals" for Chad Morris to reach in 2020, and if those "goals" aren't met, could we see a coaching change after next season?
Example: Morris' 2020 team must win enough games to go to a bowl.
1. Well that's logical.
2. The thinking would be…
3. In year three he has his players.
4. They've had time to learn his system.
5. Now lets see some real progress or your're gone.
6. But as I said earlier…I'm not 100 % sure he'll get year three.
*porksoda wants to know: Are there any winnable SEC games left of the schedule?
1. There could always be a crazy upset but realistically there's one left. Mississippi State. They are struggling this season. Probably not as good as Kentucky.
*Midway642 asks: I would like your comments on the Defense. Is it the talent level of round pegs in square holes? The score does not surprise me but the rushing yards did. It will interesting to see how many of the recruits will take a cue from the young man from Carthage, Tx and open their recruiting. Any thoughts Mike?
1. I've addressed this before. This is the second youngest starting lineup in BCS football.
2. The starting lineup is young and most of the backups are true freshmen.
3. The starters are on the field too much
4. Makes it worse when the Offense doesn't move the ball.
5. They can win this year with this defense.
6. The problem is the offense.
7. Specifically the QBs
8. It's been that way since Chad Morris arrived.
9.. Until they get a QB that can make the right decisions…
10. Especially in the red zone.
11. They will continue to get beat.
*gmarv asks:Mike what is your thoughts on this years teams personality, will they be able to keep trying all year long or do they quit somewhere along the way ?
1. I've certainly heard that there's some frustration with the players.
2. You always have to be aware of something like that considering the transfer portal.
3. But today Morris and John Chavis both said they've seen no sign of these players letting go of the rope.
Okay here's the part of this thing where I ask me a question. A question I wish some of you would have asked.
*Mike…How do you think the quarterback situation should be handled in the second half of the season?
Well Mike…
1. You've got two guys who have started and each have been up and down .
2. I'd go with Hicks against Auburn because he's played better than Starkel the last two games.
3. But he needs to be on a short leash.
4. If Arkansas is not scoring with him at quarterback give Starkel a shot.
5. And don't wait until the game is lost to do it.
6. The bench appears to be a motivator for these two.
7. This stuff about if you have two QBs you don't have one…that's great if you have one QB that is clearly superior.
8. And if one of them settles in as the starter clearly you go with that
8. But so far that not we have.
9. So deal with it.
10. Go with the hot hand.
11. Should the other two play?
12. Yes. K.J. Jefferson was the number 1 rated high school QB in Mississippi last year.
13. The number 2 guy is playing this year at Ole Miss.
14. Chad Morris is taking a conservative approach to almost everything right now.
15. Really where is that getting him?
16. He's losing games by being cautious.
17. I'm told he was more of a "go for it guy" at SMU because if "going for it" backfired nobody cared.
18. To me he's past the point of worring about something backfiring here.
19. Most fans I talk to would rather see him take some chances.
That's it for another week. I'll see you next Monday right here where YOU ask Mike.


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Tuesday 5 Mar 2019
Residents and passengers thanked as railway upgrade work between Swansea and Port Talbot is completed
- Region & Route:
- Wales
- Wales and Western
Network Rail has thanked residents and passengers for their patience following the successful completion of railway upgrade work between Swansea and Port Talbot, which will make the railway more reliable for passengers.
Over the weekend, Network Rail teams worked around the clock to remove old signal structures on the railway between Swansea and Port Talbot and to bring into use the new state of the art signalling system.
The £60m investment, which is the latest phase of the South Wales re-signalling programme, has seen the installation of 160 miles of new cable, 55 new LED digital signals, 160 metres of new track and new buffers at Swansea station.
Mark Neate, project manager for Network Rail Wales and Borders, said: "We would like to thank the local community and rail passengers for bearing with us whilst we delivered this work.
"The new signalling system between Swansea and Port Talbot will make the railway more reliable and resilient for passengers as it will allow railway traffic to be operated in either direction on the line. Although I understand disruption is never ideal, the work we have delivered will benefit rail users for many decades to come."
There will be changes to some weekend services between Cardiff and Camarthen on Saturday 9, Sunday 10, Saturday 23, Sunday 24, Sunday 31 March and Sunday 7 April, as Network Rail engineers undertake follow up works. Passengers are advised to check their journey before travelling at www.nationalrail.co.uk.
Notes to Editors
Notes to editor:
For engineers to safely and efficiently carry out follow up work, rail replacement buses will be in operation -
Saturday 9 and Sunday 10 March
Swansea – Llanelli (Long distance trains diverting via district line)
Swansea – Port Talbot Parkway (Long distance trains diverting via district line)
Swansea - Carmarthen
Sunday 17 March
Cardiff Central – Swansea (AM only)
Cardiff Central – Bridgend (All day)
Saturday 23 March
Swansea – Port Talbot Parkway
Sunday 24 March
Cardiff Central – Swansea
Contact information
Passengers / community members
Network Rail national helpline
03457 11 41 41
Latest travel advice
Please visit National Rail Enquiries
Network Rail press office - Bryony Parry
Media Relations Manager
07734 649220
About Network Rail
We own, operate and develop Britain's railway infrastructure; that's 20,000 miles of track, 30,000 bridges, tunnels and viaducts and the thousands of signals, level crossings and stations. We run 20 of the UK's largest stations while all the others, over 2,500, are run by the country's train operating companies.
Every day, there are more than 4.8 million journeys made in the UK and over 600 freight trains run on the network. People depend on Britain's railway for their daily commute, to visit friends and loved ones and to get them home safe every day. Our role is to deliver a safe and reliable railway, so we carefully manage and deliver thousands of projects every year that form part of the multi-billion pound Railway Upgrade Plan, to grow and expand the nation's railway network to respond to the tremendous growth and demand the railway has experienced - a doubling of passenger journeys over the past 20 years.
Follow us on Twitter: @networkrail
Visit our online newsroom: www.networkrailmediacentre.co.uk


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I'm studying analog to digital converters (ADC). I have a question about the least significant bit (LSB). If we have 10 bits and an analog range of 5 V, then the error would be $$ \frac{5}{2^{10}} = 4.9 \text{mV} \, ,$$ But there are other errors that are all included in LSB. For example, suppose that I have a 2 LSB error, now the error will be simply 10 mV approximately for all the measure that are between 512 and 1024 (2.5 V and 5 V).
Is this correct?


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My client is a well regarded European owned Manufacturing business, with a UK turnover of £25m and ambitious plans for additional growth over the next 3-5 Years.
Due to the above, they have now engaged FRS to assist with the recruitment of an ambitious commercially biased Qualified Accountant to join the business.
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Delivery & Returns
UK Delivery
All UK orders over £20 receive FREE Standard Delivery!
Delivery for UK orders valued at £20 or less is charged at £4.50.
UK deliveries are dispatched by Royal Mail - typically delivery can be expected within 2 to 5 working days of placing an order.
Please note: For your peace of mind, all parcels are sent on a fully tracked service. To enable our designated couriers to successfully deliver your parcel a signature on delivery may be required. If you are not available to sign for your goods please specify an alternative delivery address (e.g. work) or specify delivery instructions (e.g. leave with neighbour) during the checkout process.
Our clinic address is: Beautology 107 Coldharbour Road, Bristol BS6 7SD
European Delivery (countries within the EU)
European Delivery is available on selected brands. Delivery for European orders is £15.00. ANY ORDER OVER £100 TO EUROPE (WITHIN EU) WILL RECEIVE FREE DELIVERY.
European orders generally take between 3 - 20 working days to be delivered, depending on the country and location that the order is being dispatched to.
Important notices for certain international countries:
- Due to delivery time scales to the United Arab Emirates, all orders to the UAE must be sent on express delivery charged at £29.99, however if the order is over £600 the express delivery will be free of charge.
- Unfortunately, we can no longer offer express worldwide delivery to Brazil, Cambodia & Macau, however we can still offer standard worldwide delivery.
- Unfortunately, we can no longer offer delivery to Albania, Iran, North Korea, Syria, Cuba, Sudan, Russia & Turkey due to problems with parcels clearing customs in these countries.
Please note: We always aim to ensure European / Worldwide and express orders are delivered within the above time scales, however we cannot accept responsibility for delays caused by unforeseen circumstances, such as remote locations (e.g. offshore islands), customs clearance or busy holiday periods. In these instances, the original shipping costs cannot be refunded.
Further Delivery Information
Orders placed on Saturdays / Sundays or Bank holidays will be dispatched on the following working day (subject to stock availability).
During the Christmas and New Year period it might take longer to dispatch your order (up to 7 working days).
In the event of delivery not being possible within 14 days (UK) of receiving the order, we will undertake to keep you informed of any changes and give you the option to cancel the order and receive full refund of monies paid.
If an item is out of stock we will aim to contact you within 5 working days of your order being placed. We may offer alternative items or inform you of the date that we expect the missing item(s) to be back in stock.
The majority of orders will arrive within the delivery times stated above, however, please allow at least 10 working days for UK delivery & 25 working days for international delivery before contacting us, as we are unable to investigate with couriers until this time has passed.
Some international orders may have to pay customs duty; this is at the discretion of the country posted to. Beautology is in no way liable for any customs charges incurred by its customers.
If the customer does not agree to pay the customs duty, the parcel may be returned to Beautology and the value refunded will be less the customs duty or cost of return from the courier (if charged) and less the cost that Beautology paid to dispatch the parcel.
Beautology cannot accept responsibility on all orders include express international orders for delays caused by unforeseen circumstances, such as customs clearance or busy holiday periods. In these instances, the original shipping costs cannot be refunded.
If a parcel is deemed lost we will not be able to offer a replacement until 10 - 25 working days after the shipping date depending on the country posted to, subject to customers completing a non-receipt form. If a parcel is lost, we are not able to offer a straight refund, we will however send out a replacement.
Any goods not received within the above timescales must be reported to Beautology in writing 25 working days from the date of dispatch. Please note we cannot accept responsibility after this date due to courier regulations regarding the compensation for lost parcels.
Please ensure the delivery address provided at checkout is correct. We cannot be held responsible for failed deliveries whereby the address provided by the customer is not accurate. If a delivery fails due to a customer supplying an address incorrectly, we will not re-send or refund the order until the original parcel has been returned to our premises.
The products you order will be delivered to the delivery address you give when you placed your order, however, if you are a new customer placing an order for the first time we reserve the right to post only to the billing address provided should this differ from the delivery address.
Upon receipt of your order you may be asked to sign for the parcel received in good condition. If a parcel appears to be damaged in any way DO NOT accept the delivery and notify us immediately.
* Beautology FREE delivery applies to UK customers on orders over £20 and EU & Worldwide customers on orders over £100.
Please see our comprehensive returns information below, should you need to return an item(s) for any reason.
FAQ - Can I return an item?
We understand that on occasion you may need to return an item. Due to the nature of the products we sell, items cannot always be returned. Please see the below information on whether you can return an item (this does not effect your statutory rights).
You cannot return an item if…
- The product has been opened
- The product has been used
You can return an item if…
- It has not been opened or used
- It is in perfect resalable condition
- It is returned to us within 14 days of receipt of the order
To return an item(s), please download and print the returns form at the link below, complete it and return it with your invoice and goods to the following address. Any returns sent without the returns form cannot be accepted.
Please note: If you believe you have a product with a faulty pump, please contact us on 0117 2900 230 or firstname.lastname@example.com before returning an item. In many cases it will just be an airlock in the bottle, and we can explain how to release this and get the pump working as normal.
Beautology Returns Department
107 Coldharbour Road
Westbury Park
Standard Returns Terms and Information
The below information is extracted from our standard terms and conditions, which customers agree to when placing an order:
If a purchased product has been used or opened (hologram no longer intact, manufacturer / factory seal no longer in place or packaging damaged), then it will not be eligible for a return, refund or exchange.
If an item(s) is returned to us and it has been used / opened / is not in a resalable condition or does not pass the UV light checking process, the item(s) will be returned to the customer without prior notice.
Returns postage is at your own cost and risk. We would recommend that you return your items via a tracked delivery service. Please clearly state on the returns form the reason for return and whether you require a refund or exchange. Please put a contact number on your returns form should you require an exchange.
Any delivery charges paid for on an initial order are not eligible for a refund.
Some goods are non-returnable for hygiene reasons. Please note that this does not affect your statutory rights.
Once a refund has been issued you will receive a confirmation email detailing the amount that has been refunded, and the item(s) that we have received back.
Refunds can only be made to the billing details provided when ordering.
We aim to process all returns as quickly as possible and you should receive confirmation of this within a week of having returned the item.
If you exercise your right of cancellation after 14 days of receipt of the order, any returned goods must be in perfect resalable condition (inner and outer packaging fully intact) and are subject to a 25% re-stocking charge.
Items ordered from our Outlet section are not eligible to be returned for a refund or exchange.
Further Returns Information
It may be that you need to return an item for another reason other than listed above. This section provides more information on returns for the following:
- Damages / Shortages / Incorrect Products
- Faulty Products
- Reactions to Products
- Refused / Undeliverable Packages
Damages / Shortages / Incorrect Products
Please inspect goods fully on receipt. Any damages / shortages / incorrect products must be reported to Beautology in writing at email@example.com within 24 hours from receipt of goods, with full details of the issue, along with photographs of all packaging and contents.
If a return / refund / replacement / exchange is required, Beautology will provide full details on this process during email correspondence. This process may involve you completing a Non Receipt of Goods Declaration Form.
Beautology cannot accept responsibility for damages / shortages / incorrect products reported after the stated 24 hour period.
Faulty Products
If you feel that an item you have receive is faulty, please report this immediately in writing with detailed information on the issue to Beautology at email@example.com
Depending on the issue with the item, you may be required to complete a Product Query Form, and any item(s) deemed faulty might be sent back to the manufacturer for thorough testing.
If a return / refund / replacement / exchange is required due to a fault, Beautology will provide full details on this process during email correspondence.
Reactions to Products
Please note: It is the customer's responsibility to patch test any product prior to use. Always check compatibility of any purchased products with other material facts that can affect results described.
If you have followed the above process but feel that you have had a reaction to a product, please immediately report this in writing to Beautology at firstname.lastname@example.com
Depending on the issue with the item, you may be required to complete a comprehensive Product Reaction Authorisation Form, and any item(s) in question might be sent back to the manufacturer for thorough testing. This form must be fully completed within 48 hours, including photographs of the reaction.
If a return / refund / replacement / exchange is required due to a reaction, Beautology will provide full details on what to do during email correspondence.
Refused / Undeliverable Packages
In the case of a parcel being returned to Beautology due to an incorrect delivery address being provided or the customer not collecting from their postal office / depot, a re-delivery cost will be charged. The costs for this are as follows; £3 for UK delivery, £8 for European delivery (within the EU), £10 for Worldwide delivery or £30 for Express Delivery. Customers will be contacted via email should a parcel be returned to us.
If the customer chooses to cancel the order in this instance instead of re-posting, the original postage and packaging cost covered by Beautology will not be refunded (minimum £3).


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Received: 07 November 2019; Published on-line: 31 December 2019
PPARγ-mediated differences in energy substrate among T2DM patients differing in the stage of diabetic retinopathy
S.O. Rykov,1 Dr Sc (Med), Prof; L.V. Natrus,2 Dr Sc (Med), Prof; M.Iu. Bykhovets,1 Post-graduate Student
1 Shupik National Medical Academy of Postgraduate Education; Kyiv (Ukraine)
2 Bohomolets National Medical University; Kyiv (Ukraine)
E-mail: email@example.com
Background: Because fatty acid binding proteins (FABPs) and peroxisome proliferator-activated receptor (PPAR) γ physically interact, the ability of FABPs to modulate lipid signaling could be exploited for developing medications, improving therapeutic or prophylactic measures for the control of metabolic disorders, and for controlling the activity of their therapeutic targets such as PPARs.
Purpose: To examine PPARγ-mediated differences in energy substrate among type 2 diabetes mellitus (T2DM) patients differing in the stage of diabetic retinopathy.
Material and Methods: This study involved 101 T2DM patients (101 eyes) with different stages of diabetic retinopathy (DR) and 40 non-diabetics (controls) who were comparable in age, gender and body mass index. DR was graded using the ETDRS scale. The polymorphism was detected by real-time PCR on a Real-Time Gene Amp® PCR System 7500 (Applied Biosystems). ELISA was used to determine serum L-FABP levels with Human L-FABP ELISA kit (Hycult Biotech).
Conclusion: We found a significant variation in fatty acid (FA) concentrations in red blood cell membranes in T2DM patients differing in PPARγ-gene mediated phenotypes. Among wild-type carriers, arachidonic acid concentration increased 1.4-fold in those with the early stage of DR (р < 0.05) compared to controls and decreased 7.5-fold in those with DR progression (р < 0.05). Among carriers of the 12Ala allele, arachidonic acid concentration decreased twofold in those with the early stage of DR (р < 0.05) compared to controls, and further gradually decreased with DR progression. There was a gradual and not significant increase in L-FABP concentration with DR progression in T2DM patients carrying the wild genotype. Among carriers of the 12Ala allele, concentration of the chaperone increased fourfold in those with the early stage of DR compared to controls (р < 0.05), and gradually decreased with DR progression.
Keywords: diabetic retinopathy, type 2 diabetes mellitus, L-FABP, fatty acids, RBC membrane, lipid metabolism
Diabetic retinopathy (DR) is the leading cause of blindness among working-age adults around the world [1, 2]. This, coupled with the predicted increase in the prevalence of type 2 diabetes mellitus (T2DM), makes DR a serious and prevalent vision-threatening disease. Data from recent clinical trials demonstrate that dyslipidemia is an important, but often overlooked factor in the development of DR [3]. Patients with diabetic dyslipidemia have been found to have a high incidence of retinal damage [4]. However, unlike macrovascular complications, where direct correlation between pathology and circulating lipid levels is well established [5], the role of circulating lipids in microvascular complications is still controversial and intensively studied. Compared with controls at four years, type 2 diabetes mellitus (T2DM) patients that were administered fenofibrate for elevated triglycerides, or simvastatin for elevated cholesterol demonstrated reduced progression of DR [6]. Synthetic peroxisome proliferator-activated receptor γ (PPARγ) ligands like thiazolidinediones (TZDs) are used to treat T2DM; they, however, not only contribute to insulin sensitization, but also promote fat accretion, with yet unknown long-term effects [7]. In addition, the mechanism of the TZDs, and causes of their ambiguous efficacy and sometimes effects differing in different cases, are still to be elucidated [8,9].
PPARs are ligand-activated transcription factors and belong to a nuclear hormone receptor family. They have been shown to control genes of key enzymes involved in lipid and carbohydrate metabolism and to provide a link between external environmental factors and internal mechanisms of energy homeostasis. PPARγ has gained interest as a therapeutic target in the diseases in which dyslipidemia is pathogenetically involved, such as metabolic syndrome (MS), T2DM, obesity, and etc [9-11].
The impact of PPAR gene polymorphisms on phenotypic traits of energy metabolism has been intensively studied recently. The partial loss-of-function Pro12Ala mutation in the PPARγ2-specific B exon has been found to be associated with a lower body mass index (BMI), greater insulin sensitivity, and an improved lipid profile [12, 13]. In contrast to the hypomorphic Pro12Ala allele, the rare Pro115Gln substitution renders PPARγ constitutively active, and carriers of this mutation are extremely obese and insulin resistant [14].
Similar to PPARs, fatty acid binding proteins (FABPs) access the nucleus under certain conditions and also target fatty acids (FA) to transcription factors [9]. As lipid chaperones, FABPs protect cells from excessive fatty acid levels [15], and may actively facilitate the transport of lipids to specific compartments in the cell, such as to the lipid droplet for storage; to the endoplasmic reticulum for signaling, trafficking and membrane synthesis; to the mitochondria or peroxisome for oxidation; to the nucleus for lipid-mediated transcriptional regulation; or even outside the cell to signal in an autocrine or paracrine manner [16]. Under the unnaturally excessive and continuous caloric intake, decreased energy expenditure, and the distinctly stressful lifestyle of contemporary humans, FABPs may not be sufficient to maintain metabolic homeostasis, and hence no longer be beneficial. In this scenario, their presence now facilitates the formation of obesity, diabetes, dyslipidaemia, atherosclerosis and inappropriate immune responses [17,18,19].
Liver FABP (L-FABP) and PPAR physically interact, and therefore it has been suggested that L-FABP could be considered a co-activator in PPAR-mediated gene regulation. Therefore, the ability of FABPs to modulate lipid signalling and trafficking could be exploited for developing medications, improving therapeutic or prophylactic measures for the control of metabolic disorders, and for controlling the activity of nuclear hormone receptors as therapeutic targets [9, 20]. The association between L-FABP expression and the PPARγ gene polymorphism, remains, however, unclear. Clarifying this matter will be of importance to determine the features of impairments in lipid metabolism and pave the way for correction of these impairments.
The purpose of this study was to examine PPARγ-mediated differences in energy substrate among T2DM patients differing in the stage of diabetic retinopathy.
Material and Methods
This study involved 101 T2DM patients (101 eyes) in whom their eye examinations found different stages of DR. They underwent an eye examination including visual acuity assessment, refractometry, static Humphrey perimetry, tonometry, and biomicroscopy. In addition, gonioscopy, ophthalmoscopy with a Goldmann contact lens, and macular optical coherence tomography (Topcon DRI OCT Triton, Tokyo, Japan) were performed, when required. Fundus photography (the ETDRS seven standard fields) was performed with the fundus camera TRC-NW7SF (Topcon, Tokyo, Japan). Fluorescein angiography was performed when indicated.
Diabetic retinopathy was graded using ETDRS scale. The patients were divided into three groups based on the stage of DR: group DR1 included 30 patients (30 eyes) with mild, moderate or severe non-proliferative DR (NPDR), group DR2 comprised 34 patients (34 eyes) with mild, moderate or severe proliferative DR (PDR), and group DR3 comprised 37 patients (37 eyes) with progressive PDR. All patients had their thyroid hormone levels measured to exclude the presence of hormonal abnormalities. The control group comprised 40 non-diabetics without diagnosed metabolic abnormalities who had their medical check-up at the Clinical Diagnostic Laboratory of the Bohomolets National Medical University (NMU).
All biochemical, molecular genetic and gas-liquid chromatography studies were performed at the certified laboratories of the Bohomolets NMU Research Institute for Experimental and Clinical Medicine. The biochemical measurements were performed using biochemical assay kits from Diagnosicum Zrt (Hungary) and a semiautomatic biochemistry analyzer from Sinnowa Medical Science and Technology Co. Ltd (Nanjing, Jiangsu, China; Model: BS3000M ). ELISA was used to determine serum L-FABP levels with Human L-FABP ELISA kit (Hycult Biotech, Uben, the Netherlands). Gas-liquid chromatography was used to determine fatty acid composition of red blood cell (RBC) membranes following extraction of red blood cell mass from venous blood. We have identified the nine most informative fatty acids (denoted as 100%), and calculated relative abundance for (a) each of these, (b) the combination of saturated fatty acids (SFA; myristic C14:0, pentadecanoic (C15:0), palmitic (C16:0), and stearic (C15:0)), (с) the combination of unsaturated fatty acids (USFA; oleic (C18:1), linoleic (C18:2), linolenic (C18:3) and arachidonic (C20:4)), and the combination of essential polyunsaturated fatty acids (PUFA; C18:2, C18:3 and C20:4).
Venipuncture whole blood samples were collected using 2.5-mL collection tubes containing ethylenediaminetetraacetic acid and were used for molecular genetic studies. After collection, tubes were frozen at -20 °C.
Genomic DNA was extracted according to the manufacturer's instructions (PureLink® Genomic DNA Kits Invitrogen, USA). Briefly, blood cells were incubated in digestion buffer with proteinase K to lyse the membrane and pellet the DNA, and an additional incubation was performed with RNAse to prevent contamination.
Mutation detection was performed using TaqMan Mutation Detection Assays (Thermo Fisher Scientific) in a Real-Time PCR System 7500 (Applied Biosystems, USA). The rs1801282 polymorphism of the PPARG gene is located on chromosome 3 (Chr. 3:12393125 as per NCBI Build 37). The context sequence information was as follows: AACTCTGGGAGATTCTCCTATTGAC[C/G]CAGAAAGCGATTCCTTCACTGATAC.
The rs1801282 in the PPAR-gamma is characterized by a C-to-G substitution encoding a proline to alanine substitution at codon 12. The C allele is a considered a wild allele, whereas the G allele is considered a minor allele with its frequency index of 0.0703/352 according to MAF Source: 1000 Genomes (http://www.1000genomes.org/node/506). The material under study was incubated in the presence of DNA polymerase with primers flanking the DNA regions of interest in the Gene Amp® PCR System 7500 (Applied Biosystems, USA).
Data were analysed using IBM SPSS version 23 and MedStat software. Normality of quantitative data was established using the Shapiro–Wilk test. Most parameters were not normally distributed. Consequently, non-parametric statistical tests were used for statistical analyses at a significance level of 0.05. The descriptive statistical indices of median, and 25th and 75th percentile [Q1-Q3] for the groups are listed in tables. 95% confidence intervals for median and interquartile ranges were calculated. Bar charts are provided with 95% confidence intervals (CI). Kruskal-Wallis test was used for comparisons between groups. The Dunn's test or the Mann-Whitney test with Bonferroni correction was used for pairwise comparisons.
Results and Discussion
There have been numerous epidemiological studies on the frequencies of the heterozygous and homozygous polymorphisms of the PPARG gene within various populations and on their associations with metabolic disorders [19]. There were 18 carriers (45%) of the 12Ala allele in the control group; of these, 3 were (7.5%) homozygous carriers of the allele. In addition, there were 33 carriers (33%) of the 12Ala allele among diabetics; of these, only one (1%) was a minor homozygote. Previous studies by others [21, 22] reported that populations of Ukrainian patients with metabolic disorders carried predominantly the wild Pro12Pro genotype, and even suggested a protective role of the 12Ala allele in the development of DM and MS. In the current study, compared to the controls (Table 1), the percentage of carriers of the PPARG gene polymorphism was also decreased in all DR groups, but significantly only in group DR3.
We compared our patients with T2DM and non-diabetic controls regarding age, gender, mass, and BMI to investigate the factors that may influence the development of T2DM and the progression of DR (Table 2). Because 3 individuals in the control group were under the age of 30, there was a significant difference in age between patients of DR3 group and controls. Severity levels of DR (ETDRS severity scale) were correlated with the duration of diabetes (r = 0.401, р < 0.01). The percentage of women was lower in all DR groups compared to the controls, but not significantly. No expected significant difference in BMI was observed between controls and T2DM patients with different stages of DR. In addition, there was not an increase, but a gradual decrease in BMI from 29.3 kg/m2 [37.2-32.3] in the DR1 group with an increase in the stage of DR. Although the controls also had high BMI values, we did not use BMI ≥25 kg/m2 as an exclusion criterion for a more reliable comparison of effects on metabolism.
In patients of the DR1 and DR2 groups and controls, 12Ala allele carriers had higher BMI values, although differences were not significant. However, in the DR3 group, 12Ala allele carriers had lower BMI values. There are contradictions in the literature regarding this issue. Kaydashev and colleagues [21] found evidence of increased BMI in carriers of this polymorphism, whereas others [13] suggested a protective effect of the 12Ala allele against obesity.
PPARG-mediated analysis showed no significant difference in lipid profile characteristics between groups with different stages of DR. Previously, we have already noted no significant difference in lipid profile characteristics between groups with different stages of DR; however, taking genetic heterogeneity into account, we did find some differences in these characteristics between carriers of the polymorphism and wide-type subjects. In the current study, we exemplified only three lipid profile characteristics. Compared to wild-type subjects, serum total cholesterol levels in polymorphism carriers were lower for the DR1 and DR2 groups, and higher for the DR3 group and controls. Interestingly, 12Ala allele carriers had higher levels of triglycerides and high-density lipoproteins compared to wild-type carriers, but only for the DR1 group, and the difference was not significant.
It is believed that it is reasonable to analyze the fatty acid (FA) composition in the body through the analysis of FA concentrations in red blood cell (RBC) membranes since an RBC membrane is an established biological model of membranes of most cells in the body [20, 23]. Previously, we have analyzed concentrations of the nine particularly informative fatty acids in RBC membranes in groups of patients with different stages of DR against healthy controls. That analysis demonstrated a substantial and significant relative increase in saturated fatty acids (SFAs) with an increase in the stage of DR, indicating a pathological process, since accumulation of SFAs in the cell, especially, in the cell membrane, results in substantial changes in cell properties, plasticity, capacity for endocytosis, reactivity to ligand acceptance, and lateral movement of receptor rafts and integral proteins, leading to a reduced response to cytokines and reduced cell-to-cell interaction. In the DR1 and DR3 groups, SFAs were 1.5-fold to two-fold more abundant (p < 0.05) than unsaturated fatty acids (USFAs) at the expense of polyunsaturated fatty acids. In the DR2 group, the SFAs were practically as abundant as the USFAs. There was a tendency toward a decrease in myristic and arachidonic acid concentrations and increase in stearic and oleic acid concentrations with DR progression.
Our analysis of FA concentrations in RBC membranes in individuals with different PPARG-gene mediated phenotypes demonstrated a number of differences between patients with DR and healthy controls (Fig. 2). In the control group, there was practically no difference in FA concentrations among individuals differing in genotype. However, regarding USFAs, there was a tendency (р > 0.05) toward increased linoleic acid concentrations and decreased oleic and arachidonic acid concentrations for 12Ala allele carriers. As opposed to controls, the abundance of minor SFAs (myristic (C14:0), pentadecanoic (C15:0), and margaric (C17:0) acids) was significantly increased in patients (maximally, in the DR1 group, and minimally, in the DR3 group); however, a persistent increase was characteristic only of the polymorphism carriers. In the DR1 group, minor SFAs in 12Ala allele carriers were 2.6-fold and threefold more abundant than in carriers of the wild-type Pro12Pro genotype (р < 0.05) and controls (р < 0.05), respectively. In the DR2 group, palmitic acid in 12Ala allele carriers was 2.7-fold more abundant than in carriers of the wild-type Pro12Pro genotype (р < 0.05), but there was no substantial difference in stearic acid abundance between the former and latter carriers. Variation in oleic acid (C18:1) abundance was characteristic of only of DR patient carriers of the Pro12Pro genotype, with the least abundance found for the DR1 group, and the most, for the DR3 group. In addition, oleic acid concentration in carriers of the polymorphism was consistently elevated irrespective of the development of diabetic complication. A substantial variation in linoleic acid (C18:2) concentration was noted, especially among wild-type carriers. Concentration of C18:2 FA in the DR1 and DR3 groups was lower, whereas in the DR2 group, higher than in controls. In the DR2 group, there was a twofold difference (р < 0.05) in linoleic FA concentration between wild-type and polymorphism carriers. Among 12Ala carriers, linoleic FA concentration gradually increased from the DR1 to the DR3 group. A significant variation in arachidonic acid concentration was noted. Previously, we have observed a relative decrease in C20:4 FA with DR progression. However, in the current study, among wild-type carriers, total arachidonic acid concentration increased 1.4-fold in the DR1 group (р < 0.05), decreased twofold in the DR2 group (р < 0.05), and decreased 5.6-fold in the DR3 group (р < 0.05), compared to the controls. In addition, for polymorphism carriers, there was a consistent trend toward a relative decrease in C20:4 FA with DR progression, although this difference was less significant than that for wild-type carriers.
Previously, we have found a significantly elevated serum L-FABP level in patients with long duration of diabetes with DR. In the current study, L-FABP concentration increased 1.5-fold (р < 0.05), 1.3-fold, and 1.7-fold in the DR1, DR2 and DR3 groups, respectively, compared to controls. We believe that a reduced L-FABP expression in the DR2 group compared to the DR1 group reflects the body's adaptation to high levels of plasma fatty acids, and has a hampering effect on DR development and progression. Our examination of the relationship between L-FABP concentration and PPARG genotype (Fig. 3) showed a gradual and not significant increase in L-FABP concentration with DR progression in T2DM patients carrying the wild genotype. And, on the contrary, after a four-fold increased L-FABP level (р < 0.05) at the onset of DR, a gradual decrease in L-FABP level with DR progression, but without reaching the values of the control group, was found in T2DM patients carrying the 12Ala allele. In the control group, polymorphism carriers had lower L-FABP concentration (р < 0.05) compared to wild genotype carriers.
Therefore, we found substantial differences in concentrations of fatty acids (a major energy substrate in the body) in cell membranes, and L-FABP (an important intercellular lipid chaperone) between patients with different PPARG gene-mediated phenotypes and different DR stages. This reflects the factors influencing the development of metabolic disorders, particularly, T2DM, and genetically determined susceptibility to the development of microvascular diabetic complications.
Cock et al [7] reviewed a wide range of studies on PPARγ expression, including molecular and cellular studies, mouse genetic studies and human genetic studies, and concluded that (1) PPARγ is not only the master regulator of adipogenesis in vivo, but also a driving force of glucose and lipid homeostasis, and (2) moderate levels of PPARγ activation coordinate an important adaptive response [24], leading to efficient energy conservation and lipid storage in the adipocyte [7]. However, this evolutionarily maintained mechanism has been proved to be beneficial only under conditions of infrequent high caloric intakes and long periods of food shortages, which forced our progenitors to search for food throughout their life. Our present affluent style—characterized by a high caloric intake and a lack of physical exercise—now turns this once favorable energy conservation response into a detrimental one, which promotes dyslipidemia and related disorders like obesity, metabolic syndrome, and T2DM [17, 18].
Studies on characteristics of PPAR will offer the opportunity to utilize this mechanism for developing advanced therapeutic effects for the treatment of metabolic disorders, since full PPARγ agonists such as the TZDs, improve insulin sensitivity, glucose tolerance and the lipid profile in T2DM patients. Whereas enhanced PPARγ activity is invariably associated with increased fat mass, suboptimal PPARγ activation or PPARγ antagonism is neutral or even reverses weight gain. However, unlike the relationship between PPARγ and fat mass, PPARγ activity is not linearly related to insulin sensitivity, as both inactivation and activation of PPARγ can enhance insulin sensitivity [7]. This nonlinear relationship indicates that insulin sensitivity is an integrated effect, which is achieved predominantly by modulating PPARγ actions in the adipose tissue with effects on adipokine secretion and lipid storage, in addition to other tissue-specific PPARγ responses.
First, we found a significant variation in FA concentrations in RBC membranes in T2DM patients differing in PPARG-gene mediated phenotypes. Among wild-type carriers, arachidonic acid concentration increased 1.4-fold in those with the early stage of DR compared to controls (р < 0.05), and decreased 7.5-fold in those with DR progression (р < 0.05). Among carriers of the 12Ala allele, arachidonic acid concentration decreased twofold in those with the early stage of DR compared to controls (р < 0.05), and further gradually decreased with DR progression.
Second, there was a gradual and not significant increase in L-FABP concentration with DR progression in T2DM patients carrying the wild genotype. Among carriers of the 12Ala allele, concentration of the chaperone increased fourfold at the onset of DR compared to controls (р < 0.05), and gradually decreased with DR progression.
Finally, when developing therapeutic treatments with PPARγ agonists and antagonists and lipotropic medications targeted at the transport of lipids across plasma, one should take into account specific PPARγ-mediated metabolic characteristics that identify genetically determined mechanisms of abnormal lipid metabolism and metabolic complications.
1.Balashevich LI, Izmailov AS. [Diabetic ophthalmopathy]. St. Petersburg: Chelovek; 2012. Russian.
2.Pasyechnikova NV. [Diabetic maculopathy: current aspects of the pathogenesis, clinical manifestations, diagnosis and treatment]. Kyiv: Karbon LTD; 2010. Russian.
3.Hammer SS, Busik JV. The role of dyslipidemia in diabetic retinopathy. Vision Res. 2017 Oct; 139: 228–36.
4.Sacks FM, Hermans MP, Fioretto P, et al. Association between plasma triglycerides and high-density lipoprotein cholesterol and microvascular kidney disease and retinopathy in type 2 diabetes mellitus: a global case-control study in 13 countries. Circulation. 2014 Mar 4;129(9):999-1008.
5.Persistent Effects of Intensive Glycemic Control on Retinopathy in Type 2 Diabetes in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Follow-On Study. Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Eye Study Group and the Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Study Group. Diabetes Care. 2016 Jul;39(7):1089-100.
6.Shiomi Y, Yamauchi T, Iwabu M, et al. A Novel Peroxisome Proliferator-activated Receptor (PPAR)α Agonist and PPARγ Antagonist, Z-551, Ameliorates High-fat Diet-induced Obesity and Metabolic Disorders in Mice. J Biol Chem. 2015 Jun 5;290(23):14567-81.
7.Cock T-A, Houten SM, Auwerx J. Peroxisome proliferator-activated receptor-γ: too much of a good thing causes harm. EMBO Rep. 2004 Feb; 5(2): 142–7.
8.Saremi L, Lotfipanah S, Mohammadi M, et al. The Pro12Ala polymorphism in the PPARγ2 gene is not associated with an increased risk of NAFLD in Iranian patients with type 2 diabetes mellitus. Cell Mol Biol Lett. 2019; 24:12.
9.Grimaldi PA. Peroxisome proliferator-activated receptors as sensors of fatty acids and derivatives. Cell Mol Life Sci. 2007 Oct;64(19-20):2459-64.
10.Lee YK, Park JE, Lee M, Hardwicka J.P. Hepatic lipid homeostasis by peroxisome proliferator-activated receptor gamma 2. Liver Res. 2018 Dec; 2(4): 209–15.
11.Ma X, Wang D, Zhao W, and Xu L. Deciphering the Roles of PPARγ in Adipocytes via Dynamic Change of Transcription Complex. Front Endocrinol (Lausanne). 2018; 9: 473.
12.Deeb SS, Fajas L, Nemoto M, et al. A Pro12Ala substitution in the human PPARγ2 is associated with decreased receptor activity, improved insulin sensitivity, and lowered body mass index. Nat Genet. 1998 Nov;20(3):284-7.
13.Altshuler D, Hirschhorn JN, Klannemark M, et al. The common PPARγ Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes. Nat Genet. 2000 Sep;26(1):76-80.
14.Hu E, Kim JB, Sarraf P, Spiegelman BM. Inhibition of adipogenesis through MAP-kinase mediated phosphorylation of PPARγ. Science. 1996 Dec 20;274(5295):2100-3.
15.Esteves A, Ehrlich R. Invertebrate intracellular fatty acid binding proteins. Comp Biochem Physiol C Toxicol Pharmacol. 2006 Mar-Apr;142(3-4):262-74.
16.Choromańska B, Myśliwiec P, Dadan J, Hady HR, Chabowski A. The clinical significance of fatty acid binding proteins. Postepy Hig Med Dosw (Online).2011 Nov 24;65:759-63.
17.Boden G, Laakso M. Lipids and Glucose in Type 2 Diabetes. What is the cause and effect? Diabetes Care. 2004 Sep;27(9): 2253-9.
18.Rykov SO, Bykhovets MY, Natrus LV. [Features of the lifestyle as a risk factor for the development and progression of diabetic retinopathy in patients with type 2 diabetes mellitus]. Arkhiv Oftal'mologii Ukrainy. 2019. 7(1), 54-61. Ukrainian.
19.Rykov SO, Bykhovets MY, Natrus LV. [The role of metabolic disorders and genotype in the diabetic retinopathy development (review)]. Arkhiv Oftal'mologii Ukrainy. 2018. 6(3), 54-60. doi: http://dx.doi.org/10.22141/2309-8220.127.116.118.165211. Ukrainian.
20.Furuhashi M, Hotamisligil GS. Fatty acid-binding proteins: role in metabolic diseases and potential as drug targets. Nat Rev Drug Discov. 2008 Jun;7(6):489-503.
21.Kaydashev IP, Rasin AM, Shlykova OA, et al. Frequency of the Pro12Ala-polymorphism of the gene PPARγ2 in the Ukrainian population and its possible relation to the development of the metabolic syndrome. Cytol Genet. 2007; 41(5):43-7.
22.Ziablytsev SV, Mokrii VI. [Association of the 12Pro allele of PPARγ2 (rs1801282) and type 2 diabetes mellitus]. Klinichna endocrynologiia i endocrinna khirurgiia. 2016;55(3):34-8. Ukrainian.
23.Petrenko OV, Natrus LV, Tavartkiladze К. [Concentrations of fatty acids in blood cells of patients with diabetic retinopathy]. Arkhiv Oftal'mologii Ukrainy. 2017;3(19): 54-60. Ukrainian.
24.Auwerx J. PPARgamma, the ultimate thrifty gene. Diabetologia. 1999 Sep;42(9):1033-49.
The authors certify that they have no conflicts of interest in the subject matter or materials discussed in this manuscript.


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The GeoNames geographical database contains over 25 million geographical names and consists of over 11 million unique features whereof 4.8 million populated places and 13 million alternate names. All features are categorized into one out of nine feature classes and further subcategorized into one out of 645 feature codes.
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Version: 2.0.0


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If you have a parcel of shares under your name and you wish to transfer ownership to another entity, instead of a buy-and-sell process, you can perform what's known as an 'in-specie transfer' or 'in-specie contribution'.
An in-specie transfer is like a 'gifting' of asset where the ownership of the shares is transferred to another entity in whole, without selling the underlying investment. It is generally used to move ownership from one entity into a super fund, more commonly, Self-Managed Super Funds. The word 'in-specie' is a Latin phrase meaning 'in its actual form'.
Benefits of an in-specie transfer
There are a number of benefits to using an in-specie transfer. They include:
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There are restrictions on the type of in-specie contributions you can make to an SMSF. Currently, the law only allows the following assets to be transferred to an SMSF from a member:
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An in-specie transfer or contribution into an SMSF counts towards super contributions caps.
An example of an actual in-specie transfer scenario might be the following:
John earns $40,000 per annum. He also owns BHP shares which give him an additional $4,000 from dividend earnings. His total taxable income is therefore $44,000, which is taxed at the income tax rate of 32.5%.
John also has an SMSF where he would like to transfer the ownership of these BHP shares. He works out this is going to give him a tax saving, as putting the shares into the SMSF will mean it is taxed at 15% instead of 32.5%.
John prepares a 'deemed disposal' for the transfer of ownership which means completing an off-market share transfer form to the broker who will transfer the shares. John will need to pay Capital Gains Tax (CGT) as the disposal of the shares is considered a CGT event.
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Pleasant Hill United Brethren Church is having a Benefit Car Wash on Saturday, May 18th from 10am to 1pm in the parking lot at 169 S Antrim Way, Greencastle, PA . The cost is by donation and proceeds will go to benefit Over The Rainbow Children's Advocacy Center in Chambersburg, PA. For more information call 717-414-4029.


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Ezekiel 3:13-15
New Revised Standard Version, Anglicised
Ezekiel 3:13-15
New Revised Standard Version, Anglicised
13 it was the sound of the wings of the living creatures brushing against one another, and the sound of the wheels beside them, that sounded like a loud rumbling. 14 The spirit lifted me up and bore me away; I went in bitterness in the heat of my spirit, the hand of the Lord being strong upon me. 15 I came to the exiles at Tel-abib, who lived by the river Chebar.[a] And I sat there among them, stunned, for seven days.Read full chapter
- Ezekiel 3:15 Two Mss Syr: Heb Chebar, and to where they lived. Another reading is Chebar, and I sat where they sat
New Revised Standard Version, Anglicised (NRSVA)
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|This article is about the episode. You may be looking for 2019 Version of Episode.
|Is the Rumored Ri That Mother's Daughter
|Episode Information
|Dai Ni Juu San Wa
|43, 44, 45
|Staff Information
|Justin Cook (US)
|Jeremy Carlile, John Burgmeier (US)
|Music Information
|For Fruits Basket
|Chiisana Inori
|← Prince Yuki Fan Club
|The Curse of the Cat →
Is the Rumored Ri That Mother's Daughter (第ニ十三話, Dai Ni Juu San Wa) is the twenty-third episode of Fruits Basket.
Ritsu Sohma, the monkey from the zodiac, drops by Shigure's house. Tohru comes to the conclusion that Ritsu is a very sweet girl - but she really couldn't be more wrong!
On her way to the household residence, Tohru bumps into Ritsu Sohma, the Monkey of the Chinese zodiac. Ritsu is known for being a cross-dresser, very apologetic, and deeply depressed. As the two appear at the household residence, Ritsu gives some presents to Shigure. Ritsu decides to leave before he causes any trouble for Tohru and the others. However, Tohru wanted to serve him some tea before his departure. Unfortunately, after Tohru accidentally breaks one of the tea glasses, this sends Ritsu into a panic attack, thinking it was his fault. Tohru tries to stop him from stepping in the broken glass, but she turns him into a Monkey, getting cut in the process. Ritsu goes to the roof of the house to commit suicide, but after Tohru convinces him not to, he nearly falls off the roof, twisting his ankle in the furtherance. Ritsu asks to stay at the household residence for three days, with Hatori looking over him. While walking back from school, Tohru runs into Ritsu again, who plans to bring a bag of jelly buns for Shigure. Tohru and Ritsu sit on a park bench to talk about his cross-dressing, his apologizing, and his depression. Tohru comforts him by saying that everyone has a reason to live, a reason that everyone must search for.
- Tohru Honda
- Ritsu Sohma
- Shigure Sohma
- Okami Sohma (flashback)
- Yuki Sohma
- Ayame Sohma (mentioned/flashback)
- Kyo Sohma
- Hatori Sohma
- Kyoko Honda (flashback)
- Ritsu's Father (flashback)


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