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But in a Rye Starbucks on an overcast Thursday morning, most folks were sticking to their usual orders. Many said it's something they'd get for their kids but looked too sweet for them.
"How many calories are in something like that?" asked Jon Watnick of Rye, who was busy sipping his back decaf. "It looks interesting but it's something my 11-year-old daughter would like, not me."
It was a sentiment echoed by Milan Yokuty, also of Rye, who has three children, ages three, six and seven.
Even Erin Colagiovanni, who had her young toddler in tow, said it's not something she'd get for him, despite the pretty pink and blue colors, sprinkles, and whipped cream.
"I could see coming back later, however, for my 5-year-old daughter," she said.
"Once she sees a picture of it, she'll totally want it."
According to Starbucks, the drink changes colors and flavors as you sip it, starting off "sweet and fruity transforming to pleasantly sour."
Emily Raho said it tasted like a sour milkshake. The Rye resident had been curious about the new concoction since seeing it on social media. The drink was introduced Wednesday, April 19.
A barista at the Rye Starbucks said, so far, the unicorn has been proven to be a hit, albeit among the shop's younger clientele. "Anytime something new comes out it's always very popular."
The unicorn frappuccino is available at participating Starbucks through Sunday, April 23. Tell us what you think or better yet, send a photo and post on our Facebook page.
Click here to follow Daily Voice Rye and receive free news updates.


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Well, my final 20 days of blogging post. It only took me two months to get through them! To be fair, I was actually posting about other things as well and not just stacking on my blogging.
It probably depends on how you define "last day of playing WoW". Is this my last day because I dont want to play any more? Or is this the last day because the game is being discontinued?
If it was the first one, I would probably give away my gold and shit to the people in game who I like and hold contests for some of them. Best transmog outfit etc.
If it was the second one, I would spend my time running the instances that I once loved or seeing content that I never got to see. I have never done AQ 40 for example. I have never completed Ulduar and ICC. These are things I would like to do, just to have the memory of it.
I would then take my character to a fitting place for the end of their lives. Maybe I would take my Paladin Zurlock to Uther's Tomb. I would take my Shaman to Aerie Peak (he is a Dwarf afterall). I would take my Warlock to the basement of the Slaughtered Lamb.
I would take my Gnome Rogue back to Gnomeregan and take it back before logging off as the new king of Gnomeregan.
I would take Darraxus to the floating island in Nagrand that has the corpse sitting against the tree. I would sit him down next to the skeleton and they could be company for eternity.
Either that, or I would have them go out in a blaze of glory, Trollslayer style. Go into and try to solo raid bosses, dying Heroically.

subset: commoncrawl


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SAMJ: South African Medical Journal
versão On-line ISSN 2078-5135
versão impressa ISSN 0256-9574
SAMJ, S. Afr. med. j. vol.100 no.6 Pretoria Jun. 2010
Arthur Charles Keast (30 may 1927 - 12 february 2010)
I first met Charles in Ward E1, Groote Schuur Hospital, in 1951, when he taught me to do a lumbar puncture.
Sadly he passed away on 12 February 2010.
Charles was born on 30 May 1927. He matriculated at Kingswood College in 1944 and graduated MB ChB at UCT in 1950. He did his internship training at Groote Schuur Hospital, and subsequently worked at Grey's Hospital, Pietermaritzburg, and King Edward VIII Hospital, Durban. He married Rosemary Slater in 1953. He then moved to London where he specialised in obstetrics and gynaecology, obtaining his MRCOG in 1959.
He started private practice in East London in 1960 and continued there until he retired in 1991. During this period he acted as a part-time consultant at Frere Hospital.
In 1992 he filled in locums in England and Canada.
The Border Branch Council of SAMA benefited from his membership. He was President in 1990 and Honorary Secretary in 1992/1993.
Charles and Rosemary had 4 children and 12 grandchildren, one of whom is a medical doctor.
He was a keen tennis player, played squash for Border, and travelled many hiking trails.
A staunch member of Rotary International, in 1973 he went to Canada as a group study exchange leader. He became a district governor in the 1990s and was presented with the Paul Harris Award.
Charles will be sadly missed by many sections of the community.
Dennis Smyth


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Accepted Scientific Name: Pritchardia hillebrandii Becc.
Malesia 3: 292 (1890)
Habit at Hanamu Rd Makawao, Maui, Hawaii (USA). June 03, 2009.
Origin and Habitat: Pritchardia hillebrandiiSN|24628]]SN|24628]] is endemic of Molokaʻi, Hawaii islands, USA.
Habitat: It grows in dry forest near sea level, only about 300 Pritchardia hillebrandiiSN|24628]]SN|24628]] are said to survive a top to Huelo an Islet rising from the ocean just off the windward coast of Molokaʻi, and a few other trees exist on nearby Mōkapu Islet this is let due to the absence of rats and goats. Up to 1970's a few palm were reported in the valleys at the base of the sea cliffs of north coast of Molokaʻi, but today they are extinct.
- Pritchardia hillebrandii Becc.
- Eupritchardia hillebrandtii (Becc.) Kuntze
- Styloma hillebrandii (Becc.) O.F.Cook
- Washingtonia hillebrandii (Becc.) Kuntze
Pritchardia hillebrandii Becc.
Malesia 3: 292 (1890)
Synonymy: 6
- Pritchardia hillebrandii Becc.
- Eupritchardia hillebrandtii (Becc.) Kuntze
- Styloma hillebrandii (Becc.) O.F.Cook
- Washingtonia hillebrandii (Becc.) Kuntze
- Pritchardia insignis Becc.
- Styloma insignis (Becc.) O.F.Cook
ENGLISH: Molokai Fan Palm, Loulu Lelo Palm, Blue Loulu, Hillebrand's pritchardia, Hawaiian Fan Palm
HAWAIIAN (ʻŌlelo Hawaiʻi): Wāhane, Noulu, Loulu, Hāwane, Loulu lelo
Description: Pritchardia hillebrandiiSN|24636]]SN|24628]] is a small to medium sized palm with large fan-shaped leaves.
Stem: Solitary, upright, about 5-7(-8) m tall and 25 cm in diameter, smooth or fibrous when young, with vertical fissures on a dark grey background, and obscurely ringed by leaf scars. .
Leaves: 120-200 cm across, costapalmate, induplicate, undulate, forming half to two-thirds of a circle, only slightly divided; Segments (leaflets), single-fold, rigid, leathery, bifid with stiff points, that don't droop much, if at all, light emerald green, silverish or bluish-green and smooth above; waxy greyish green cast (glaucous) below and devoid of scales; Petiole and lower ribs unarmed, densely covered in ash-grey felt. The leaf sheath breaks down into a mass of tawny fibres.
Flower: Inconspicuous, not showy, pale white to yellowish flowers. The inflorescence is shorter or equal to the petioles with panicles branched to three orders. The flowers are perfect, containing both male and female parts.
Fruit: Small globose, and characteristically ridged, measuring around 22 x 19 mm on fruit stalks as long as the leaf stalks (petioles) of about 90-100 cm in length.
Seeds: 11-13 mm in diameter.
Remarks: Pritchardia hillebrandiiSN|24647]]SN|24628]] is related to Pritchardia glabrataSN|24634]]SN|24625]], Pritchardia kaalaeSN|28613]]SN|28613]], Pritchardia maidenianaSN|24625]]SN|24634]], and Pritchardia remotaSN|24628]]SN|24647]]. It is also similar to Pritchardia affinisSN|24628]]SN|24636]] but the heavy waxy coating on leaves and the black, ridged fruit are distinctive. There is one a smaller form of this palm with blue colouration called Dwarf Blue in this variety, the waxy glaucous coating extends to the leaf upper surface.
Bibliography: Major references and further lectures
1) Forest & Kim Starr Pritchardia hillebrandii (Loulu lelo). Plants of Hawaii. <http://www.starrenvironmental.com>. Downloaded on 21 August 2014.
2) Wikipedia contributors. "Pritchardia hillebrandii." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 17 Mar. 2013. Web. 3 Sep. 2014.
3) Palmpedia contributors. "Pritchardia forbesiana." Palmpedia, PALM ENCYCLOPEDIA, <http://www.palmpedia.net> Downloaded on 26 Aug. 2014
4) Donald R. Hodel "Loulu-The Hawaiian Pritchardia" in the: The Palm Journal 193, page 12.
5) Native Plants Hawaii. "Pritchardia hillebrandii" web 21 August 2014. <http://nativeplants.hawaii.edu>
6) David Leaser "Growing Palm Trees in Hawaiʻi and Other Tropical Climates"
Don Ellison, Anthony Ellison "Cultivated Palms Of The World" UNSW Press, 01/May/2001
7) Gemmill, C. 1998. Pritchardia hillebrandii. The IUCN Red List of Threatened Species. Version 2014.2. <www.iucnredlist.org>. Downloaded on 03 September 2014.
8) Robert Lee Riffle & Paul Crafts "An Encyclopedia of Cultivated Palms", page 420.
9) Hawaiian Dictionaries http://www.wehewehe.org/
10) Donald R. Hodel "A Review of the Genus Pritchardia", pages S-3, S-8, S-19- 11) Audrey Sutherland "Paddling My Own Canoe", page 131.
12) PACSOA http://www.pacsoa.org.au/palms/Pritchardia/hillebrandii.html
Habitat aerial at Huelo Islet and Papaiki Flats North Shore, Molokai, Hawaii (USA). July 02, 2012. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
Habitat aerial at Huelo Islet North Shore, Molokai, Hawaii (USA). July 02, 2012. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
Habit in landscaping at Hanamu Rd Makawao, Maui, Hawaii (USA). June 03, 2009. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
Habit at Garden of Eden Keanae, Maui, Hawaii (USA). March 30, 2011. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
Habit at Kanaha Beach, Maui, Hawaii (USA). June 18, 2005. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
In pots at Makawao, Maui, Hawaii (USA). February 21, 2006. (Pritchardia hillebrandii) Photo by: Forest Starr & Kim Starr
Cultivation and Propagation: Many Pritchardias are fussy and difficult to grow outside the tropics, frequently suffering from a yellowing of the leaves, but Pritchardia hillebrandiiSN|24628]]SN|24628]] is a pretty robust grower, very modest in its requirement, that likes sand, cinder or coral soil, but is adaptable to clay and loam both slightly alkaline and acidic. Good drainage is also important. It vary in shape. Specimens raised in dry and/or infertile soils tend to be smaller in stature with smaller leaves. Light also affects the plant's form while those grown in full sun are more compact.
Fertilization: Need a perfect fertilizer diet including all micro nutrients and trace elements or slow release fertilizer. Micronutrient deficiencies are occasional problems. Fertilize often for faster growth. Potted or younger loulu planted in the ground appreciate a foliar feeding monthly or bi-monthly.
Water Requirements: It tolerates low levels of humidity, though it prefers evenly moist but not consistently wet medium. When supplied with adequate moisture and fertilizer it is also fairly fast growing. This palm is very drought tolerant once established. It dislikes soggy soils. The roots and lower trunk can rot if soil is kept too moist. Water young plants for healthy look and fastest growth.
Light: Prefers full sun but will tolerate half day sun.
Hardiness: It is adapted to tropical and subtropical climates but tolerate a wide range of climates and will even tolerate cool conditions and a little frost ; they should be grown in cold green houses or at least in a place where they are sheltered by the wind; However mature specimens can endure temperatures down to about -4°C (for short periods), while young plants are more cold sensitive. Best kept above 5° C.
Maintenance: The dead leaves, flowers and fruits can be removed in a landscape setting for a cleaner appearance. Do not prune the fronds that still have some green colour. Palms recycle nutrients from dead or dying fronds and use them for healthier fronds. Palms only have a set number of new leaves that can sprout and grow per year and removing fronds will not increase that number. If you cut off more than what will grow annually, you could be left with a pretty bare and bald palm.
Wind and salt tolerance: Due to the natural coastal habitat, it does very well in low elevation landscapes and tolerates some salt spray. With a particularly windy climate it is suggested to secure young palm to long solid stakes, to avoid that the wind could bare young and not very developed roots; specimens which are only a few years old might fear intense wind.
Pest & diseases: It is prone to leaf rollers, red spider mites and sugar cane borers. Rats will eat the fruit.
Early Hawaiian Use The hard wood of the trunk were fashioned into spears. The trunks loulu were notched for climbing to gather the immature fruits and fronds. Older specimens still bear notches that can be seen today. The fronds were used for thatching and as plaiting such as papale (hats) and fans.
Food use: The young fruits called hāwane or wāhane are edible and can be eaten after being peeled. The flavour of fruit with the soft interior is similar to coconut.
Ornamental: It is cultivated as an ornamental tree, and planted in gardens and parks in tropical and sub-tropical climates either as a single specimen in small groves of three or more palms. Culture in containers is possible although growth rates are slower. A bright patio will provide an excellent environment for young specimens which can eventually be planted in a sunny location.
Propagation: Mature seeds buried half way in pot of clean, well drained potting soil, water daily, germinates within 4 weeks and grows quickly, plants of 30 cm can be put in ground/larger pot; Because these palms easily hybridize with other Pritchardias, claiming a specific species requires seed collection from wild populations.
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Sao Luiz do Paraitinga (Plot 1)
Basic information
Sample name: Sao Luiz do Paraitinga (Plot 1)
Reference: D. B. Ribeiro, R. Batista, P. I. Prado, K. S. Brown, and A. V. L. Freitas. 2012. The importance of small scales to the fruit-feeding butterfly assemblages in a fragmented landscape. Biodiversity and Conservation 21:811-827 [ER 119]
Country: Brazil
State: Sao Paulo
Coordinate: -23.10° S, -45.20° W
Geography comments: Field work was carried out near the scarps of the Serra do Mar mountain range (p. 813)
Habitat: tropical/subtropical moist broadleaf forest
Altered habitat: fragment
Substrate: ground surface
Habitat comments: "The original vegetation of this area was dense humid forest. Over the past two centuries, forest fragmentation has drastically changed the landscape of the region. At the beginning of the eighteenth century, human activity in this landscape replaced native rain forest with ranching areas and small crop fields. Around 1760, massive coffee plantations were planted in this region, and deforestation rates increased. Defor- estation then accelerated with the decline of coffee plantations and the increase of dairy farming in the 1930s. Currently, most of the original vegetation is gone, and the remaining forest persists as small fragments surrounded by a matrix of crop fields, Eucalyptus plantations, ranching areas and abandoned pastures" (P. 813)
Life forms: butterflies
Site length: 30.000
Sampling methods: line transect, butterfly nets
Sample size: 562
Years: 2004-2005
Sample: 275
Contributor: John Alroy
Enterer: Albert Garcia Selles
Created: 2013-04-08 17:48:10
Modified: 2015-02-23 13:32:01
Abundance distribution
45 species
12 singletons
total count 562
extrapolated richness: 62.5
Fisher's α: 11.514
geometric series k: 0.9077
Hurlbert's PIE: 0.9375
Shannon's H: 3.0993
Good's u: 0.9787
Each square represents a species. Square sizes are proportional to counts.
• Find matching samples


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La Palma Island. Canary Islands. Spain
A Good Day is Coming
La Palma island, Canary Islands. Spain.
San Antonio Volcano
Teneguía Volcano
Waterfall of Clouds above The Witches Plains
Sea of Clouds and Canary Pine
Above the Clouds in Caldera del Taburiente
Waterfall of Clouds at The Witches Plains
Roque de Los Muchachos
The Canary laurel forest
Cubo de la Galga, La Palma island, Canary Islands. Spain.
Ancient Ferns
Believe it or not, these tiny kidney-shaped leaves belong to a species of fern, Adiantum reniform e. This is a very ancient species, dating from an "antediluvian" time, cooler than today, with a widely dispersed population that has given rise to different subspecies in different parts of the world.
Cubo de la Galga, La Palma island, Canary Islands. Spain.
In the Canary Islands are some of the last holdouts in the world of the ancient laurisilva or laurel forests. It is a botanical paradise. In the photo, you can see the leaves of an endemic canary species, rubus bollei.
Cubo de la Galga, La Palma island, Canary Islands. Spain.
Tilo Bark
Geranium canariense
Macaronesian Plants and the Sea
Male Western Canaries Lizard
This is a popular species endemic to these islands.
La Palma island, Canary Islands. Spain.
King of The Mountain
Mother and Cub
Wild rough-toothed dolphin and cub swimming in the sea surrounding Tazacorte.
La Palma island, Canary Islands. Spain.
Argiope trifasciata
Dawn at the Volcanic Coast
Sea at Night. Abstraction
Los Cancajos
Rainbow Waves
All photographs in this website are copyrighted by Jesús Ramón Campos Rodríguez. All rights reserved. These photographs cannot be reproduced, published, copied or transmitted in any way, including through Internet without permission of the author. Thank you for supporting creators.


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Wilson, Seahawks rally, but lose to Falcons 30-28
Pete Carroll called the game ''extraordinary'' and his Seahawks' comeback ''exquisite.'' Then, the coach called his rookie quarterback ''unbelievable.''
Russell Wilson did everything he could to deliver Seattle another comeback win in the playoffs.
Wilson led the Seahawks to three fourth-quarter touchdowns only to see Atlanta's Matt Bryant kick a 49-yard field goal with 8 seconds remaining to give the Falcons a 30-28 NFC divisional playoff win over Seattle on Sunday.
''(Wilson) put us in position to be in another game next week, but we couldn't finish it,'' Carroll said.
''That's just an amazing football team we have. ... It's a really good team and we're just getting started.''
The unflappable Wilson is the biggest reason for Carroll's optimism about the Seahawks' future.
The Falcons led 27-7 at the start of the final quarter before Wilson began Seattle's comeback. Wilson had a 1-yard touchdown run, passed to tight end Zach Miller for a 2-yard score and then led a go-ahead touchdown drive that was capped by Marshawn Lynch's 2-yard run with only 31 seconds remaining.
''I love it when games are on the line,'' Wilson said. ''I love it when games are a little bit tight. When others are nervous, that's when I love to play.''
There was ample reason for nerves on each sideline in the wild final quarter.
Wilson watched but didn't panic as Atlanta's Matt Ryan completed passes to Harry Douglas and Tony Gonzalez to set up Bryant's game-winning kick.
Wilson was left with 8 seconds.
''When we had the ball I knew we were going to win,'' Wilson said. ''I knew we were going to score. Obviously it didn't work out.''
Following a squib kickoff by Bryant, Wilson completed a short pass to Doug Baldwin to the Falcons 46.
''We called the route to see if we could get it down and get a shot at the field goal,'' Carroll said. ''That wasn't there so we threw it underneath.
That left Wilson only 2 seconds for one final desperation toss. The game ended with Falcons receiver Julio Jones, playing deep in the prevent defense, intercepting Wilson's pass in the end zone.
It was the only interception for Wilson, who completed 24 of 36 passes for 385 yards and two touchdowns. Wilson also had seven carries for 60 yards and a touchdown.
''I think he's an amazing football player,'' Carroll said. ''I think he proved it yet again. It's undeniable.''
Falcons coach Mike Smith, who last week compared Wilson to Fran Tarkenton, said the rookie ''did a great job extending plays.''
''We knew going into it, it was going to be tough for us. ... I believe there were 145 snaps in 17 games that he extended plays when I watched the entire season. We knew we had our hands full. He's an outstanding quarterback.''
The loss ended a six-game winning streak for the Seahawks (12-6).
Miller had eight catches for 142 yards and a touchdown. Golden Tate had six catches for 103 yards and a touchdown. Lynch was held to 46 yards rushing on 16 carries.
The Falcons claimed a surprising 167-123 edge in yards rushing as Michael Turner had 14 carries for 98 yards and Jacquizz Rodgers added 10 carries for 64 yards.
''We tackled so poorly against both guys,'' Carroll said. ''(Turner) kept blasting through us and then Jacquizz did the same thing.''
The Seahawks trailed 14-0 before rallying in last week's 24-14 victory over Robert Griffin III and the Washington Redskins in the opening round of the playoffs.
Wilson and the Seahawks narrowly missed joining the 1989 Los Angeles Rams as the only West Coast teams to win two postseason games at East Coast sites in the same year.
''Obviously it's very disappointing,'' Wilson said. ''We had high, high hopes for the rest of the season.
''When the game was over I was very disappointed but walking back into the tunnel I got so excited about next year. The resilience we showed was unbelievable.''
The loss also left the Seahawks to bemoan two lost scoring opportunities deep in Atlanta territory earlier in the game.
Wilson completed a 34-yard pass to Miller and added a 16-yard pass to Golden Tate to push the Seahawks deep into Atlanta territory in the second quarter. Robert Turbin was stopped on third-and-1 from the Falcons 11. On fourth down, Wilson handed to fullback Michael Robinson, who was dropped by Charles Mitchell for a 1-yard loss.
The Seahawks were stopped again as the first half ended after Wilson moved the Seahawks to a first down at the Atlanta 6. Wilson threw incomplete passes to Sidney Rice and Tate as Seattle used all its timeouts. On third down from the 11, Wilson was sacked by Jonathan Babineaux and time expired before the rookie quarterback could attempt a fourth-down pass.
Those failed chances left the Seahawks down 20-0.
''Nobody gave up. Nobody panicked,'' said rookie defensive end Bruce Irvin, who made his first start, replacing sacks leader Chris Clemons, who was injured his left knee last week.
''We knew we were going to make a run. We just kind of waited too late. We dug deep. (Atlanta) was executing a lot in the first three quarters. In the fourth, we stood up and played for each other and dug deep and got off the field.''
Online: http://pro32.ap.org/poll and http://twitter.com/AP-NFL
Follow Charles Odum on Twitter at www.twitter.com/CharlesOdum


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It has been pointed out more than once that I tend to skew towards the positive in my writing. That's not always the case, but generally it's a fair cop. Here's the main reason why: I don't like to eat bad food.
If I have a bad meal at a restaurant, I'm not likely to return. Why would I? There are already places in New Orleans that I don't have time to revisit because I'm on to the next new joint. Maybe it's because I'm more or less officially middle-aged now, but it has occurred to me that I have only so many meals left. I love you people, and I love this writing gig, but not enough to risk having two bad meals.
That said, I was talking to a friend recently about a restaurant I covered a few months ago. It wasn't the best meal I've ever had, but it wasn't bad either, and that's more or less what I said. He interpreted it as a full-on negative review. That's not what I intended, but I could see what he meant. I don't typically write negatively, so a less than enthusiastic review came off as a pan. If you regularly read what someone thinks about food, books, art, wine or decorative topiaries, you'll almost certainly end up with a barometer by which to compare their taste with your own.
It doesn't have to be someone with whom you agree, either. I know that if certain critics hate a film, there's a good chance I'll like it, for example. But more often I gravitate toward writers whose opinions and tastes I generally share, at least when I'm trying to decide what to read, where to eat, or how many Dalmations it takes to make a coat.
So if you follow this blog and notice that I sometimes am a bit faint with my praise, I hope that you understand I am not actually slamming a place. I've done it, and it's entirely possible I'll do it again, but for the most part if I'm writing about a meal, it's because I at least found it good enough to warrant comment.
There's another sort of writing I do here, of course, which is to share news. News such as the opening of a new Whole Foods Market in Mid-City, for instance.
I live in Mid-City, and from the moment I heard about the new Whole Foods, I was pretty excited. The old Schwegmann's at the corner of Broad and Bienville has been more or less derelict for years, so any development would have been preferable, but as I have noted in the past I shop at Whole Foods for certain things and the thing was ideal from my perspective.
All of which meant that my expectations were unreasonably high, so it's not all that surprising that the new Whole Foods disappointed me a bit. First things first: It's a Whole Foods, so you will find a good selection of excellent produce, the best meat and seafood offerings of any major retailer, cheese, wine and tons of organic items.
As Whole Foods goes, however, this is a pretty modest store. Yes, 25,000 square feet sounds like a lot, and it is if you're talking about a residence, but the place is small in comparison to the Metairie Whole Foods and it feels smaller than the one on Magazine Street. What that means as a practical matter is that you won't find quite the variety of products you will at those other stores, and that seemed to me to be true across the board.
It's also small in the parking lot department. Not as small as the Uptown store, and I imagine that once it's been open a few weeks the crowds will start to diminish, but as of now it's damn near impossible to get a parking space without driving around for 10 minutes or so.
None of these problems are deal-breakers in my opinion, because while Whole Foods tends to be a little more expensive than its competitors, if you shop with an eye for bargains, you can make out like a bandit. There's an organic baby food that my 20-month-old daughter loves (because of course she does), for example, that is .20 less at Whole Foods than either Rouses or Winn-Dixie; bulk beans, grains, rice and nuts are usually good deals, too, and the Whole Foods store-brand products are almost always high quality and reasonably priced.
Combine all of that with the aforementioned meat and seafood counters, and I'm still delighted the store moved into my neighborhood. I may not be as starry-eyed as I was, but I'm still smitten.
Hopefully that was at least critical enough to give me some credibility?


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Why is meat consumption a risk factor for diabetes? Why does there appear to be a stepwise reduction in diabetes rates as meat consumption drops? Instead of avoiding something in meat, it may be that people are getting something protective from plants. Free radicals may be an important trigger for insulin resistance, and antioxidants in plant foods may help. Put people on a plant-based diet, and their antioxidant enzymes shoot up. So, not only do plants provide antioxidants, but they may boost our own anti-endogenous antioxidant defenses, whereas, on the conventional diabetic diet, they get worse.
In my video, How May Plants Protect Against Diabetes, I discuss how there are phytonutrients in plant foods that may help lower chronic disease prevalence by acting as antioxidants and anti-cancer agents, and by lowering cholesterol and blood sugar. Some, we're now theorizing, may even be lipotropes, which have the capacity to hasten the removal of fat from our liver and other organs, counteracting the inflammatory cascade believed to be directly initiated by saturated-fat-containing foods. Fat in the bloodstream—from the fat in our bodies or the fat we eat—not only causes insulin resistance, but also produces a low-grade inflammation that can contribute to heart disease and non-alcoholic fatty liver disease.
Fiber may also decrease insulin resistance. One of the ways it may do so is by helping to rid the body of excess estrogen. There is strong evidence for a direct role of estrogens in the cause of diabetes, and it's been demonstrated that certain gut bacteria can produce estrogens in our colon. High-fat, low-fiber diets appear to stimulate the metabolic activity of these estrogen-producing intestinal bacteria. This is a problem for men, too. Obesity is associated with low testosterone levels and marked elevations of estrogens produced not only by fat cells but also by some of the bacteria in our gut. Our intestinal bacteria may produce these so-called diabetogens (diabetes-causing compounds) from the fats we eat. By eating lots of fiber, though, we can flush this excess estrogen out of our bodies.
Vegetarian women, for example, excrete two to three times more estrogens in their stools than omnivorous women, which may be why omnivorous women have 50% higher estrogen blood levels. These differences in estrogen metabolism may help explain the lower incidence of diabetes in those eating more plant-based diets, as well as the lower incidence of breast cancer in vegetarian women, who get rid of twice as much estrogen because they get rid of twice as much daily waste in general.
Either way, "[m]eat consumption is consistently associated with diabetes risk. Dietary habits are readily modifiable, but individuals and clinicians will consider dietary changes only if they are aware of the potential benefits of doing so." The identification of meat consumption as a risk factor for diabetes provides helpful guidance that sets the stage for beneficial behavioral changes. Meat consumption is something doctors can easily ask about, and, once identified, at-risk individuals can then be encouraged to familiarize themselves with meatless options.
Plant foods may also protect against diabetes by replacing animal foods. Learn more with my Why Is Meat a Risk Factor for Diabetes? video.
What if your entire diet was filled with plants? See Plant-Based Diets and Diabetes. Find out which plants may be particularly protective with these videos: Amla Versus Diabetes, Flaxseed vs. Diabetes, and Diabetics Should Take Their Pulses.
Unfortunately, cinnamon has fallen out of favor. See my Update on Cinnamon for Blood Sugar Control.
I also have an ever-growing series on the science behind type 2 diabetes:
- What Causes Insulin Resistance?
- The Spillover Effect Links Obesity to Diabetes
- Lipotoxicity: How Saturated Fat Raises Blood Sugar
- Diabetes as a Disease of Fat Toxicity
- What Causes Diabetes?
- Can Diabetic Retinopathy Be Reversed?
- How Not to Die from Diabetes
For more on the estrogen connection, see Relieving Yourself of Excess Estrogen and Breast Cancer and Constipation.
In health,
Michael Greger, M.D.
PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:
- 2012: Uprooting the Leading Causes of Death
- 2013: More Than an Apple a Day
- 2014: From Table to Able: Combating Disabling Diseases with Food
- 2015: Food as Medicine: Preventing and Treating the Most Dreaded Diseases with Diet
- 2016: How Not To Die: The Role of Diet in Preventing, Arresting, and Reversing Our Top 15 Killers


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DNA Testing Arkansas | DNA Medical Testing Service
DNA Testing Arkansas
DNA testing is often talked about as a way to prove who the father of a child is, but this is just a small
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Our results are used for child custody cases, child support disputes, inheritance issues, and changes of name within Arkansas, to give just a few examples.
You don't have to be a forensic scientist to learn how DNA and genetic testing can help — you only need to understand when and where DNA tests should be applied. We do all the science for you at ReliaLab. We can explain how the tests work and what the results mean so that you can learn about an individual's or a family's biological history, substance use, parental standing, relationships lineage and ethnicity.
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Paternity Testing in Arkansas
A paternity test is an accurate and scientifically sound test that can prove who is the father of a child, or at least show a probability of fatherhood.
Maternity Testing in Arkansas
Maternity tests establish who is the mother of a child (or who is not). This type of test is often used to prove a hospital has misidentified a baby.
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A sibling DNA test can establish whether twins are fraternal or identical. In addition, it can tell you whether two people are half siblings.
Avuncluar Testing (Aunt/Uncle)
Avuncular DNA testing (Aunt/Uncle) may be used if the alleged father is unavailable for testing.
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A grandparentage DNA test is used to establish a genetic family relationship between a possible grandparent and grandchild.
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An adoption DNA test may provide evidence of a biological relationship between an adoptee and their potential birth parent(s).
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Lubbock, TX – Lone Star State rivals square off in Lubbock on Saturday, as the 20th-ranked Texas Tech Red Raiders play host to the Texas Longhorns in Big 12 Conference action.
After a 4-0 start to the season, Texas rose to No. 11 in the country, but it promptly fell from grace following back-to-back losses to West Virginia (48-45) and Oklahoma (63-21). Since then, however, the Longhorns have righted the ship with two straight wins, including a come-from-behind road victory over Kansas last week, 21-17.
Texas Tech lost a home bout to Oklahoma on Oct. 6 (41-20), but it responded from that defeat incredibly well with two signature wins over West Virginia (49-14) and on the road against TCU (56-53). The Red Raiders had their most difficult test to date last week in facing No. 4 Kansas State, losing 55-24, causing them to fall from No. 14 to No. 20 in this week's AP Poll.
"Last week's game was a disappointment," head coach Tommy Tuberville said. "We can't turn the ball over against a team that doesn't turn the ball over and have a chance to win."
"Texas is a big game for us," he continued. "They've struggled up-and-down in some areas as we have -- pretty similar, same record -- so pretty much similar teams. We'll tee it up and see what happens."
Texas has dominated the all-time series with Texas Tech, winning 45 of the 60 previous meetings. The Red Raiders have not beaten the Longhorns since 2008.
The Longhorns rank in the bottom-half of the league in terms of total offense (442.9 ypg), but they still rack up 41.5 ppg. In the high-flying Big 12, they are one of seven teams that average at least 40 ppg (along with Texas Tech).
David Ash (215.8 ypg, .687 completion percentage, 12 TDs, five INTs) has been the starter all season, but after throwing two interceptions last week, he was replaced in the fourth quarter by Case McCoy, who sparked a comeback by going 6-of-8 for 109 yards and the game-winning touchdown to D.J. Grant in the final minute. Head coach Mack Brown is sticking with Ash as his starter for now, but knows that he can rely on McCoy if need be.
"Not much discussion, David has done a great job," Brown said. "We're lucky to have two (quarterbacks). That's what we fought for in the competition in the spring and summer. David struggled (last week), but the offense struggled. I was excited for Case that he was prepared to come in. We feel like Case is the guy we can use when needed."
Complementing the quarterbacks is a stable of talented running backs. Joe Bergeron (450 yards), Johnathan Gray (427 yards), and Malcolm Brown (245 yards) have all shown explosion, but when the Longhorns get near the goal line it's usually Bergeron doing the dirty work. He's plunged into the end zone 15 times on the ground, one behind K-State's Collin Klein for the league lead.
Mike Davis (34 receptions, 559 yards) and Jaxon Shipley (30 receptions, 334 yards) have been steady in the receiving game, hauling in four touchdown passes apiece.
The Texas defense (32.8 ppg) has been vulnerable this year, especially on the ground (218 rushing ypg).
Alex Okafor is one of the conference's best defensive linemen, racking up 10 tackles for loss, seven sacks, and 16 QB hurries. Quandre Diggs has 10 passes defended and three interceptions.
Despite tying a season-low with 24 points last week, Texas Tech is still more than capable of scoring points in bunches (40.5 ppg).
The Red Raiders have traditionally gotten strong play out of their quarterbacks, and Seth Doege has been no exception this season. He's one of the nation's best signal callers, ranking seventh in the FBS in yards (2,540), fifth in completion percentage (.707), and first in passing touchdowns (30). He has thrown for 300 yards or more in all but two games this season.
Doege does a good job disrupting his passes to many different receivers as 10 players have recorded double-digit catches. Darrin Moore (43 receptions, 440 yards, eight TDs) and Eric Ward (41 receptions, 517 yards, 10 TDs) are among the nation's leaders in receiving touchdowns.
Even with the high-powered passing attack, Texas Tech still finds time for an effective running game, as Kenny Williams (504 yards), Eric Stephens (358 yards), and SaDale Foster (330 yards) each average more than five yards per carry and have scored three touchdowns apiece.
After starting the season so well, the defense has been a major letdown over the past two games, surrendering a total of 111 points. Even with back-to-back duds, the unit's points allowed per game is respectable (25.8 ppg) and it still ranks 12th nationally in total defense (300.0 ypg).
Cody Davis not only has a team-high 64 tackles but he's also picked off three passes. The team doesn't get much pressure on the quarterback with just 12 sacks, led by four from Kerry Hyder.


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- Oak tree
- Ayla is the heroine of Jean Auel's Clan of the Cave Bear book series
The name Ayla
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CaribbeanFever / FeverEyes / CaribFever
Caribbean Fever - Your ONLY destination to all things Caribbean and more
India has unveiled a $35 computer prototype as part of its program to provide connectivity to its students and teachers at affordable prices.
Kapil Sibal, the country's human resources development minister, displayed what he called a low-cost computing and access device in New Delhi on Thursday.
The ministry said the price would gradually fall to $10 a piece.
India said connectivity to all its colleges and universities is key to achieving its education goals.
Home to a billion-plus population, the country's literacy rate stands at 65 percent, according to the 2001 census figures.
Nevertheless, the South Asian nation has made giant strides in various areas since it opened up its economy in the early 1990s.
The country ushered in a telecom revolution that delivered mobile telephony to nearly 600 million people in just a little more than a decade with highly competitive call tariffs.
Now, India is preparing for another leap into the digital world.
Recently, it auctioned off its airwaves for third-generation services to enable super-fast multimedia streaming of wireless.
The move is aimed at bringing India's online market on a par with its booming cell-phone business through Internet penetration with technology allowing quick access, data transfer and entertainment on mobile handsets.
The country has announced plans to link up all its 250,000 village councils by 2012 in a bid to plug massive broadband divides between rural and urban communities as it emerges as one of the world's few growth markets.
Authorities say technical institutions involved in designing the new device are now setting up research to address price and quality issues in developing budget gadgets for students.
"The aim is to reach such devices to the students of colleges and universities, and to provide these institutions a host of choices of low-cost access devices around Rs 1,500 ($35) or less in near future," the human resources ministry said at the launch of the computer.
Ministry spokeswoman Mamata Varma said the government aimed to introduce the new touch-screen computing tool at higher educational institutions in 2011.
The ministry, she said, is expected to tender out contracts to private companies for mass production of its prototype.
The Linux-based computer is equipped with an Internet browser, a PDF reader and several other facilities, she said.
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HANRAHAN, EDMUND, politician and public servant; b. in 1802 at Carbonear, Nfld.; d. at Ferryland, Nfld., on 6 Feb. or 13 Feb. 1875.
Edmund Hanrahan, a man of "humble origins," entered Newfoundland politics in December 1840 by contesting a by-election in Conception Bay. Both Hanrahan and his opponent, James Luke Prendergast, were Roman Catholics; Prendergast was backed by the Protestant merchants including John Munn, and Hanrahan was actively supported by the Roman Catholic clergy. The election was rendered abortive "by the ferocious conduct of a mob at Carbonear." Rowdyism at elections was, indeed, known for a time in Newfoundland as "Carbonearism," for it was at Carbonear that rioting occurred with regularity. Hanrahan was returned for Conception Bay in the general elections of 1842, 1848, and 1852; and, following the 1854 sub-division of districts, for Carbonear in 1855, 1859, and 1861. In the House of Assembly he was among the more radical of the Liberals and after 1850 supported Philip Francis Little* in the struggle for responsible government.
In 1855, on the introduction of responsible government, he was appointed to Little's cabinet as surveyor general. After Little's retirement, Hanrahan was continued in John Kent's cabinet until its dismissal by Governor Alexander Bannerman* in 1861. The weak and divided Liberal party lost the general election in May 1861. Although Hanrahan was re-elected as a Liberal for Carbonear, where there was again violence, he accepted the appointment of acting appraiser to the General Water Company from the Conservative government of Hugh Hoyles*. Hanrahan's resignation from his House of Assembly seat caused a by-election in Carbonear in November 1862 in which, for the first time in more than 20 years, a Conservative candidate, John Rorke, was elected. The following year Hoyles rewarded Hanrahan with the appointment of stipendiary magistrate at Ferryland, necessitating the retirement of the incumbent Peter Winser. The Liberal Record reported that "Hanrahan sold Carbonear . . . at the expense of an honest man . . . Peter Winser." In 1872 Hanrahan was elevated to the position of sheriff of the Southern District.
Hanrahan was married and the father of an apparently large family; four sons died young. After Hanrahan's death his widow Mary unsuccessfully petitioned the assembly for a pension in consideration of her husband's long service.
PANL, Newfoundland, Executive Council, Minutes, 1 March 1862. Newfoundland, Blue Books, 1842–74 (copies in PANL); House of Assembly, Journals, 1863, 8, 931. Courier (St John's), 20 March, 25, 29 Oct. 1862. Newfoundlander (St John's), 18 Oct. 1872, 17 Jan. 1873, 26 Feb. 1875. Newfoundland Patriot (St John's), 27 Feb 1875. Pilot (St John's), 8, 22 Jan. 1853. Public Ledger (St John's), 30 Oct., 14 Nov., 15 Dec. 1840; 28 Jan. 1862. Record (St John's), 8 March 1862, 15 Dec. 1863. Times and General Commercial Gazette (St John's), 4 Jan. 1843. E. A. Wells, "The struggle for responsible government in Newfoundland, 1846–1855," unpublished ma thesis, Memorial University of Newfoundland, 1966.
© 1972–2023 University of Toronto/Université Laval
Cite This Article
Elizabeth A. Wells, "HANRAHAN, EDMUND," in Dictionary of Canadian Biography, vol. 10, University of Toronto/Université Laval, 2003–, accessed September 28, 2023, http://www.biographi.ca/en/bio/hanrahan_edmund_10E.html.
The citation above shows the format for footnotes and endnotes according to the Chicago manual of style (16th edition). Information to be used in other citation formats:
|Author of Article:
|Elizabeth A. Wells
|Title of Article:
|Publication Name:
|Dictionary of Canadian Biography, vol. 10
|University of Toronto/Université Laval
|Year of publication:
|Year of revision:
|Access Date:
|September 28, 2023


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Punjab National Bank Mcc Two Raipur Branch IFSC Code - Raipur, PNB Mcc Two Raipur IFSC Code. Contact Phone Number, Address
Punjab National Bank (PNB) Mcc Two Raipur branch IFSC Code is PUNB0920800.
IFSC Code of Mcc Two Raipur Branch - Punjab National Bank (PNB)
Punjab National Bank
Mcc Two Raipur
IFSC Code:
Branch Code:
920800 (Last 6 Characters of the IFSC Code)
Postal Address of Punjab National Bank (PNB) Mcc Two Raipur branch
31236 Chhattisgarh Club Chowk Near Cm House Civil Lines Cg Raipu 492001
Contact Number of Punjab National Bank (PNB) Mcc Two Raipur branch
Contact Number: 11 23765326, 1800 1802222 / 1800 1032222
Email address of Punjab National Bank (PNB) Mcc Two Raipur branch
Email: email@example.com
Mcc Two Raipur Branch - Punjab National Bank IFSC, address, branch phone number, manager contact number, email address
Punjab National Bank - Mcc Two Raipur is located at Chhattisgarh state, Raipur district, Raipur city and the bank branch's address is [31236 Chhattisgarh Club Chowk Near Cm House Civil Lines Cg Raipu 492001]. Contact phone number / numbers - 11 23765326.
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First select your bank, select the state, now select your district and finally select the branch of your bank to find IFSC Code.Use the brown circle icons to change your bank or location.
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Looks to overhaul regulatory system and raise insurance levels
"We have real problems, and I'm very concerned about it,'' Menino said during an interview in his office. "We're not going to tolerate this nonsense.''
The mayor said he hopes to hire a nationally recognized taxi industry specialist within days and seek recommendations within two or three months that could dramatically reshape how Boston taxis are regulated and managed.
Menino said he wants to revamp the Hackney Division of the Boston Police Department, the chief enforcer of those who drive and those who own city-licensed taxis.
He said he will push the Legislature to mandate higher insurance for cabs, most of which now operate with the state minimum bodily injury coverage of $20,000, less than half the required coverage for bike messenger services and much lower than taxis must carry in many other large cities.
"If we can't get the Legislature to change it, we'll do it administratively,'' he said. "It's too low. There's no question about it.''
And the mayor said he wants to install a civilian advisory board to, among other things, help reduce and resolve disputes between drivers and fleet owners.
The top-to-bottom review comes after a nine-month Globe investigation found that drivers are routinely forced to pay petty bribes to get keys to their cabs while owners commonly violate Police Department regulations without fear of sanction. A federal criminal investigation is under way, the Globe reported Sunday.
The Spotlight report also highlighted a Byzantine insurance system used by the city's largest fleet owner, Edward J. Tutunjian. Instead of paying insurance premiums on each of his 372 taxis, the owner of Boston Cab self-insures his fleet by depositing $10,000 for each taxi with the state. He has earned hundreds of thousands of dollars in interest since 2003.
After the Globe's inquiry, state Treasurer Steven Grossman said he will ask the Legislature to end the program because it benefits only the few prosperous entities that can afford it. He added that the required $20,000 in coverage, whether paid through a traditional insurance policy or self-insurance, is inadequate to cover people's injuries.
Menino made it clear Monday that the Boston Police Department's oversight of the taxi industry will be a central focus of the upcoming review and that among its recommendations could be a call to get the police force out of the taxi regulation business entirely.
"I'm looking to revamp the division,'' Menino said after a meeting in his office with Police Commissioner Edward F. Davis and William F. Sinnott, the city's corporation counsel.
Neither Menino nor Davis would directly comment about the future of the leader of the hackney division, Mark Cohen, the civilian director of licensing for the Police Department. Cohen has been overseeing city taxis since the 1980s. Davis said the unit's top uniformed officer will now be given an enhanced role to supervise the division until the review is completed.
During interviews with the Spotlight Team, Cohen was unable to decipher the basic economics of his own division. And he quipped to two Globe reporters that he used to teach kindergarten, which he called a perfect training ground for working with cabbies.
Menino said Monday he was unaware of the abuse of taxi drivers, many of whom are poor immigrants who struggle to make a living wage while routinely working 60 hours a week or more. "Some of the stuff in there I have no control over,'' he said.
The mayor's call for a systematic review of the taxi industry was greeted with a combination of relief and skepticism from cabdriver advocates.
"Finally,'' said Donna Blythe-Shaw, an organizer for the United Steelworkers and the Boston Taxi Drivers Association.
Blythe-Shaw said she and taxi drivers have publicly called on the mayor and City Council to reform the industry every year since 2007, but their entreaties went nowhere. She wrote Menino in 2007 and delivered petitions to his office in 2008 and 2009 urging him to reform the industry, she said.
"It takes the Spotlight Team to open his eyes?'' she asked.
"The City Council has known about this as long as he's been around," she said of Menino. "They chose not to support hackney reform because they knew the mayor wouldn't go for it.''
If Cohen's future is clouded, Blythe-Shaw said, the mayor should clear the air immediately by firing him. Cohen, she said, was responsible for an "archaic, autocratic, oppressive, and dysfunctional regulatory system that wastes taxpayers' dollars and diverts police from neighborhood policing.''
Cohen declined to comment.
As for reforming the industry, Blythe-Shaw said it is imperative that taxi drivers be involved. "We need some drivers, we need the union involved," she said. "This is what we've been asking for since 2008.''
The union activist has called for a civilian commission, financed with funds from medallion renewals and resales, to supplant Cohen's Hackney Division.
During a 2011 hearing, drivers and advocates packed the City Hall chamber and Maureen Feeney, then a city councilor, said it was time to consider a different model to govern the industry.
"Much of the testimony that I've heard, as I've said, has been informative and educational, but it's also been upsetting and concerning,'' Councilor at Large Ayanna Pressley said then. "These cab drivers are risking their lives every day to provide a very important service for the residents of the city and for tourists, and for any of them to feel marginalized, exploited, or demoralized in any kind of way just doesn't sit well with anyone, and it shouldn't.''
Tutunjian and other fleet owners steadfastly opposed the idea of changing the way Boston has governed its taxi industry for generations. The plan went nowhere.
Cohen, who attended the University of Pennsylvania, has worked for the Boston police since 1985. He is credited with transforming Boston's taxi fleet from a scrubby collection of belching clunkers to an industry propelled by late-model vehicles, many of them gleaming new hybrids.
He sits on the board of an international association of taxi regulators and has helped usher in a requirement that all cabs accept credit cards.
He also drove the effort that introduced 100 wheelchair-accessible taxis into Boston's fleet.
The Globe reported this week that medallion owners who pleaded guilty to tax evasion, were suspected of misappropriating $200,000 from one cab association, and pleaded guilty to bribing a police sergeant were all allowed to keep their city-issued licenses.
Cohen said in earlier interviews that he could not recall a single instance where his division revoked a license, called a medallion, from an owner for misconduct.
The Menino-ordered examination of the cab business will also include whether the city should issue more medallions — they are capped at 1,825 — or other options to address increased demand from customers. The mayor said he also will institute a hot line to collect complaints from patrons and drivers. "For some reason we were not getting these allegations,'' Davis said of the Globe's report. "And we want to make sure we know of these things.''
The attorneys at Jason Stone Injury Lawyers have years of experience litigating accidents involving taxi cabs, and we are here to answer your questions. To contact us, please call us at (617) 543-4357.


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Tom Heehler
American author
Tom Heehler is an American author, known for his work The Well-Spoken Thesaurus.
Quotes Edit
The Well-Spoken Thesaurus (2011) Edit
- Common Sense and Education: The more you think you have of one, the less you think you need of the other.
- The foolish read to escape reality; the wise surrender to it.
- Good writers indulge their audience; great writers know better.
- The educated don't get that way by memorizing facts; they get that way by respecting them.
- Nuance: for best results apply with sledge hammer.
- Courage is the ability to ignore your options.
- If you are your own worst enemy, don't do yourself any favors.
- Fear not the tyrant; fear the tyrant's wake.
- Cultural pluralism is the only thing we all have in common.


text:
The Parliament – Parliamentary privileges -11
PARLIAMENTARY PRIVILEGES Meaning Parliamentary privileges are special rights, immunities and exemptions enjoyed by the two Houses of Parliament, their committees and their members. They are necessary in order to secure the independence and effectiveness of their actions. Without these privileges, the Houses can neither maintain their authority, dignity and honour nor can protect their members […]Read More »


text:
311 Philadelphia Green Moon Rock
- In stock, ready to ship
Official 311 print featuring art by Munk One.
From the August 10th Show in Philadelphia PA.
AP on Green Moon Rock paper
6 color screen print
Edition of 25
Numbered print signed by artist Munk One
Approx. 18" x 24"
Please note: That these ap's are from the same run as the show editions so the date shown on this print is August 18th. No returns.
Designed and Printed in California.
Please read Important Ordering Info at the link below before placing order. Only 1 of each print, set or variant allowed per household on the first day of sale. Multiple orders of the same exact print are refunded and returned to inventory without exception, even if placed by different accounts. All sales considered final and up to the discretion on Invisible Industries. Please make sure your shipping address is up to date on both your Paypal account and Shopify account BEFORE placing order. Changes of address after an order is placed will be refunded. CA residents pay sales tax. Colors vary from monitor to monitor and may vary slightly from actual product. Orders placed separately will not be combined.
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Only 1 copy of each print, variant, version or set allowed per household on the first day of sale. Meaning you if you buy 3, they should each be different versions. Orders containing multiples of the same exact print are refunded and returned to inventory at our discretion, even if placed through different accounts. We do not combine orders placed separately.
ALL shipping information provided must be 100% CORRECT. Delivery must be accepted by the customer or household. Changes of address after an order is placed are not allowed. We shall not be held liable for shipping to old, outdated or incorrect address, P.O. boxes that do not accept packages or loss of packages shipped to 3rd party shipping facilities.
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[181 U.S. 49, 50] On April 5, 1895, a certificate of membership, in the amount of $3, 000, was issued by the plaintiff in error to Frank E. Beck, payable on his death to his widow, Lillian H. Beck. The application for membership contained this stipulation:
On April 13, 1897, an action was commenced in the district court of the first judicial district of the state of Montana, in and for the county of Lewis and Clark, by his widow, to recover $3,000, the amount of the insurance. This action was removed by the defendant to the circuit court of the United States for the district of Montana. The answer set up specifically that the insured died from 'self-destruction and suicide,' and, further, 'that prior to said Beck taking his own life said Beck was attempting to and did violate the criminal laws of the state of Montana.' In the circuit court a trial was had, which resulted in a verdict and judgment for plaintiff. The judgment was taken by the defendant to the United States circuit court of appeals for the ninth circuit, and by that court affirmed May 16, 1899, 36 C. C. A. 467, 94 Fed. Rep. 751, to reverse which judgment of affirmance this writ of error was sued out.
Mr. Carlos S. Hardy for plaintiff in error.
Mr. C. B. Nolan for defendant in error.
Mr. Justice Brewer delivered the opinion of the court:
The principal question discussed by counsel for plaintiff in error, and the important question in the case is whether the trial court erred in refusing a peremptory instruction to find a [181 U.S. 49, 52] verdict for the defendant. It is said that the testimony established the fact of suicide, and that there was no sufficient doubt in respect thereto to justify a submission of the question to a jury. We have recently had before us a case coming, like this, from the trial court, through the court of appeals (Patton v. Texas & P. R. Co. 179 U.S. 658 , ante, p. 275, 21 Sup. Ct. Rep. 275), in which the action of the trial court in directing a verdict was vigorously attacked as an invasion of the province of the jury to determine every question of fact. That case stands over against this, for there the trial court directed a verdict. Here it refused to direct one. In each case its action was approved by the court of appeals. In that case, although the question was doubtful, we sustained the rulings of the lower courts; and the considerations which then controlled us compel a like action in the present case. We said that a trial court had the right, under certain conditions, to direct a verdict one way or the other (citing several cases to that effect), but added:
Neither can it be said that death came 'in violation of or attempt to violate any criminal law.' Before he left home with the gun he said he was going hunting. While from his conduct he apparently changed his mind, and doubtless went to the house where his wife was stopping with the view of persuading or compelling her to return home, and may have intended violence against her if she refused, yet the death resulted, not as a consequence of any violation or attempt to violate the criminal law. In this respect the court charged the jury as follows:
This instruction correctly states the law. The death must in some way come as a consequence of the violation or attempted violation of the criminal law, and the stipulation does not apply when it is simply contemporaneous and in no manner connected with the alleged violation or attempt to violate. For instance, if the deceased had started with the avowed intent to to kill his wife, and while walking down the street a tree had fallen and killed him, the fact that he was starting upon an intentional violation of the law would not make this stipulation applicable, because the cause of his death would be entirely disconnected from the criminal act. So here, whatever may have been the general thought and purpose running in his mind as he went to the house where his wife was, his act in going into and stepping out of the water-closet was in no manner connected with or part of an attempt to carry out any criminal purpose, and at that time came the shot, intentional or accidental, which killed him.
These are the substantial matters presented in the record. There are one or two minor questions. For instance, when the undertaker was on the witness stand, the defendant produced a gun, and asked him to show the jury how the mark which he said he found on the face of the deceased could be caused, and the gun was used for that purpose. On cross-examination it appeared that his arm was not long enough to reach the trigger, and, therefore, to fire if off in the position in which he had placed it, he needed a pencil or something of that kind. Subsequently, the plaintiff introduced testimony tending to show the length of the arm of the deceased and the improbability of his being able to reach the trigger, with his face on the muzzle, as described by the undertaker, which testimony was objected to on the ground that the gun had not been identified as the one which had caused the death, but the objection was overruled and the testimony admitted. There was testimony subsequently offered by her as to its identity, but that testimony was, to say the least, not clear and satisfactory, so that it cannot be said [181 U.S. 49, 56] that the gun was fully identified as the one which caused his death. Still, we cannot think that this furnishes a sufficient ground for reversing the judgment. The defendant produced the gun, and while it cannot be said that the mere production carried with it a declaration that this was the gun which caused the death, yet it certainly suggested the fact; and if not so it ought to have offered testimony to that effect. It presented the gun for use and illustration before the jury, and there was no material error in permitting the plaintiff to use the same gun for the purposes of other illustration, especially when she followed that with testimony tending, although, perhaps, only slightly, to identify it.
Another matter is that: The plaintiff in her proofs of loss stated that the deceased came to his death by suicide, and to that effect was the verdict of the coroner's jury. With respect to this matter the court charged that there was no estoppel; that the plaintiff could explain the circumstances under which she signed the statement, and that while standing alone it would justify a verdict for the defendant, yet if explained, and the jury were satisfied that the death did not arise from suicide, she was not concluded by this declaration. We see no error in this ruling. None of the elements of estoppel enter into the declaration. The condition of the defendant was not changed by it, and if under a misapprehension of facts she made a statement which was not in fact true, she could explain the circumstances under which she made the statement and introduce testimony to establish the truth.
Some other matters are mentioned in the brief of plaintiff in error, but nothing that we deem of sufficient importance to deserve notice. We see no error in the judgment, and it is affirmed.
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Are You Sure the Patient Has Diabetic Nephropathy?
Definition: Diabetic nephropathy (DN) is a clinical syndrome characterized by persistent albuminuria, a relentless decline in the glomerular filtration rate (GFR) and raised arterial blood pressure (BP). Persistent albuminuria (>300 mg/24 hr or >200 µg/min) in at least two of three consecutive nonketotic urine samples is the hallmark of diabetic nephropathy.
Epidemiology: About 20% to 30% of patients with type 1 or type 2 diabetes develop nephropathy, but in type 2 diabetes, a considerably smaller fraction progress to end-stage renal disease (ESRD). However, because of the much greater prevalence of type 2 diabetes, such patients constitute over half of the patients starting dialysis. Overall, DN occurs in almost 30% of all diabetics and is the leading cause of ESRD in the U.S. and Europe. Early diagnosis of diabetes and early intervention are critical in preventing the normal progression to renal failure seen in many type 1 and a significant percentage of type 2 diabetics.
In the United Kingdom Prospective Diabetes Study (UKPDS), the risk of a patient with type 2 diabetes progressing from normoalbuminuria to microalbuminuria was 2% per year, risk of progressing to macroalbuminuria was 2.8% per year, and the risk of macroalbuminuria to elevated creatinine level was 2.3% per year. However, in that study, the competing risk of death exceeded the risk of progression once macroalbuminuria had developed. Risk of death was 0.7% per year for normoalbuminuric patients, 3.5% per year for macroalbuminuric patients, and 12.1% per year for patients with elevated level of serum creatinine. There is considerable racial/ethnic variability in this regard, with native Americans; Hispanics, especially Mexican Americans; and African Americans having a much higher risk of developing ESRD than non-Hispanic whites with type 2 diabetes.
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Signs/symptoms of diabetic nephropathy
Albuminuria: Screening for microalbuminuria and an estimated glomerular filtration rate (eGFR) should be performed annually in type 1 diabetics with diabetes of duration >5 years, in all type 2 diabetics starting at diagnosis, and all patients with diabetes and hypertension.
Urinary albumin can be checked by three methods:
Albumin-to-creatinine ratio on a spot urine sample
24-hour urine collection
Timed urine collections
Normal albumin excretion on a spot collection should be <30 µg/mg of creatinine. Microalbuminuria is 30 to 299 µg/mg creatinine, while macro(clinical)-albuminuria is >300 µg/mg creatinine. Measuring timed or 24 hour urine collections is burdensome and adds little to the predictive value or accuracy of the spot sample.
Transient elevations in urinary albumin excretion can be seen in hyperglycemia, exercise, urinary tract infections (UTIs), marked hypertension, heart failure, and acute febrile illness.
Hypertension: In patients with type 1 diabetes, hypertension is usually caused by underlying diabetic nephropathy and typically becomes manifest around development of microalbuminuria. In patients with type 2 diabetes, hypertension is present at the time of diagnosis in about one-third of patients as part of the metabolic syndrome.
The mechanism of hypertension in DN is complex; it is not completely understood and involves excess sodium retention, activation of the sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS), endothelial cell dysfunction, and increased oxidative stress. It is usually associated with an expanded plasma volume, increased peripheral vascular resistance, and low renin activity. At any given level of GFR, BP tends to be higher in diabetic than nondiabetic patients with renal disease.
Other signs/symptoms of diabetic nephropathy
Peripheral edema may be the first symptom of diabetic nephropathy. Fluid retention may be present even with preserved renal function and a slight reduction in serum albumin.
There is usually a relentless, often linear but variable decline in GFR, ranging from 2 to 20 ml/min/yr.
What Else Could the Patient Have?
The differential diagnosis nephropathy in a patient with diabetes who had albuminuria and/or renal dysfunction should include:
Renal artery stenosis with/without renovascular hypertension
Primary or secondary glomerular disease
Interstitial nephritis
Chronic urinary obstruction
Key Laboratory and Imaging Tests
Diagnosis of diabetic nephropathy is based on detection of proteinuria. In addition, many patients will also have hypertension and retinopathy. The main diagnostic procedures to establish diagnosis are:
Determination of albuminuria or proteinuria
Measurement of BP which should be measured at every routine visit
Measurement of serum creatinine concentration and eGFR.
Renal ultrasound
Ophthalmologic examination
If proteinuria is found on urine analysis, it is important to rule out the various causes that can cause false-positive results, such as UTI.
This proteinuria, if confirmed, needs to be quantitated by one of the three methods mentioned in the albuminuria section. If the patient has typical diabetic nephropathy (i.e., type 1 diabetes for >10 years, retinopathy, prior microalbuminuria, no hematuria or red cell casts, and normal renal ultrasound), then no further workup is required. However, if the patient has no retinopathy, and has nephrotic range proteinuria without progression through microalbuminuria or has macroscopic hematuria or red cell casts, the patient needs to be evaluated further. It has to be noted that microscopic hematuria may be found in a third of patients with diabetic nephropathy, but red cell casts are very uncommon. Biopsies in such patients reveal nondiabetic renal disease in at least half of them.
Imaging studies
A renal ultrasound is usually obtained to evaluate for kidney size. In earlier stages on DN, the kidney may be enlarged because of hyperfiltration. With progression of diabetic renal disease, the kidney size often but not always decreases because of glomerulosclerosis. Also, chronic kidney/medical disease can be detected on renal ultrasound by assessing for hyperechogenicity. Ultrasound also helps in ruling out outlet obstruction as a cause of renal dysfunction.
Proteinuria in diabetes is occasionally due to a glomerular disease other than diabetic nephropathy. Patients with diabetes most often develop nephrotic-range proteinuria (>3.5 g/24 hr), but typically only after long-standing diabetes. A bland urine sediment supports the diagnosis of diabetes, although it is not uncommon to have some microscopic hematuria with advanced diabetic nephropathy.
Major clinical clues suggesting nondiabetic glomerular disease as etiology of proteinuria are:
Significant proteinuria without a long history of diabetes
No signs of other end-organ damage such as retinopathy or neuropathy (in type 1 diabetes). Although the presence of retinopathy supports diabetes as a cause of the proteinuria, lack of retinopathy does not rule out diabetes as the underlying etiology. This is especially true in patients with type 2 diabetes.
Acute onset of renal disease or of nephrotic syndrome
Presence of active urinary sediment containing red cells and cellular casts
Rapidly rising urinary protein level, or rapidly declining GFR
Indications for renal biopsy in diabetic patient
If retinopathy is not present in the type 1 diabetic patient (absence of retinopathy does not rule out DN in type 2 diabetes)
If onset of proteinuria is sudden or rapid, especially if in type 1 diabetic and duration of disease is <5 years or if evolution is atypical (without transitioning through usual stages of overt proteinuria)
If active urinary sediment (red cell casts or acanthocytes) or macroscopic hematuria is found
If decline of renal function is exceptionally rapid or if renal dysfunction is found without significant proteinuria
When a diabetic patient with impaired renal function is seen:
Assess the cause of renal failure
Assess the rate of progression and magnitude of proteinuria
Assess presence of microvascular and macrovascular complications of diabetes
Pathophysiology and natural history
As mentioned before, microalbuminuria is usually the first manifestation of DN. It is also called early or incipient nephropathy. It usually progresses to overt nephropathy in two-thirds of the patients. Natural history of DN is a process that progresses gradually over years.
Early DN is evidenced by glomerular hyperfiltration and an increase in GFR. This is believed to be related to changes in hemodynamics in renal microvasculature and increased cell growth and expansion of the kidneys, possibly secondary to hyperglycemia and its effects on insulin-like growth factor (IGF). Microalbuminuria typically occurs after 5 years in type 1 diabetes. Overt nephropathy, with urinary protein excretion >300 mg/day often develops after 10 to 15 years. However, type 2 diabetes has a more variable course. Patients often present at diagnosis with microalbuminuria; 40-60% of these patients will progress to overt nephropathy.
Long-standing hyperglycemia is a significant risk factor for development of DN. It may directly result in mesangial expansion and injury. The mesangium expands initially by cell proliferation and later by cell hypertrophy. Transforming growth factor (TGF-beta) is especially important in mediation of this expansion and later fibrosis via collagen and fibronectin deposition. Advanced glycosylation end products (AGEs) can be formed by the binding of glucose to proteins in kidneys and in the circulation. AGEs can form cross-links over years of hyperglycemia and can contribute to renal damage by stimulation of growth and fibrotic factors, as well as increasing oxidative stress. There can also be increased levels of mediators of proliferation and expansion, such as platelet derived growth factor, vascular endothelial growth factor (VEGF), and TGF-beta, and reduction in renal nitric oxide levels all of which can contribute to further renal and microvascular complications.
There is also activation of the renin-angiotensin system in the proximal tubular cells, podocytes, and mesangial cells. Angiotensin II (Ang II) is stimulated in diabetes. Even though the levels of plasma renin activity are suppressed in diabetics, as compared to controls, there is evidence that intrarenal levels of Ang II are increased.
Ang II preferentially constricts the efferent arteriole in the glomeruli, leading to higher intraglomerular pressure. Ang II also stimulates renal growth and fibrosis. It is because of this reason, pharmacologic interventions that inhibit production of Ang II or block ATI receptors that target RAAS are a cornerstone in the treatment of hypertension in DN patients. In addition stimulation of aldosterone by Ang II is also considered important in the pathogenesis.
Management and Treatment of Diabetic Nephropathy
Despite significant progress has been made in recent years in the understanding of the pathophysiology, prevention, and treatment of DN, we are far from optimal therapy. Both glycemic control and rigorous BP control have significant impact on prevention and progression of DN.
Studies in both type 1 and 2 diabetes patients have shown that use of angiotensin-converting enzyme (ACE) inhibitors leads to decreased albumin excretion and may postpone or even prevent overt nephropathy. Once overt nephropathy is present, progression cannot be halted, but only be slowed.
Lifestyle modifications: Should have a central role in managing these patients.
Smoking: Smoking increases risk and progression of DN. In the Appropriate BP in Diabetes Trial, 61% of enrollees were smokers. Analysis of a number of risk factors showed a 1.6 fold increased risk of DN among smokers.
Hyperlipidemia: common in diabetics. Aggressive lipid lowering is important, since diabetes is considered a coronary artery disease equivalent.
Weight reduction: marked decrease in proteinuria may be seen in diabetic patients who lose weight. Maintain body mass index (BMI) of 18.5 to 24.9 kg/m2.
Adopt DASH style diet eating plan: Diet rich in fruits, vegetables, and low fat dairy products.
Physical activity: regular aerobic physical activity at least 30 minutes per day, most days of the week
Dietary sodium reduction: to less than 2.4 g (100 mmol/day) sodium or 6 g sodium chloride.
Effect of glycemic control
The Diabetes Control and Complications Trial(DCCT) and United Kingdom Prospective Diabetes Study(UKPDS) have shown that intensive diabetes can significantly reduce the risk of development of microalbuminuria and overt macroalbuminuria. A Hb A1C of <7 is recommended by ADA guidelines, though AACE recommends Hb A1C <6.5%.
Close monitoring of glucose is required, as certain opposing influences may make glycemia control difficult to predict. On the one hand, renal failure can cause insulin resistance by accumulation of a (hypothetical) circulating factor interfering with the action of insulin leading to impaired glucose tolerance. On the other hand, the half-life of insulin is prolonged, causing the tendency to develop hypoglycemic episodes. Most sulfonylurea compounds accumulate in renal failure, except glimepiride and gliquidone. Glinides and glitazones do not accumulate. Hence any of these drugs that do not accumulate should be considered for use as oral hypoglycemics, once renal failure develops.
It had been the practice to discontinue Metformin when the creatinine is >1.5 mg/dl in males and >1.4 mg/dl in females. The FDA, based on its review of the literature, have recommended the eGFR be used to assess the suitability for use in patients with renal impairment. An eGFR should be obtained prior to initiating metformin. Metformin is contraindicated in patients with an eGFR < 30 ml/minute/1.73 M2 and is not recommended to be started in patients with an eGFR between 30-45 ml/minute/1.73 M2. In patients who are taking metformin and their eGFR falls between 30-45 ml/minute/1.73 M2 consideration of the risks and benefits of continuing or stopping metformin should be undertaken. However, there is an ongoing investigation to evaluate the benefits of continuing metformin in patients with advanced CKD.
Management of hypertension in DN
Target BP in DN
The American Diabetes Association guidelines recommend that most patients with diabetes and hypertension should be treated to achieve a blood pressure of < 140/90.
Current KDOQI guidelines recommend a BP of <130/80 mm Hg in patients with DN. Studies have shown that it takes an average of 2.9 appropriately dosed antihypertensive drugs to achieve BP control below target in diabetic patients with hypertension. If a patient has hypertension, diabetes, and renal disease, this average increases to about 3.5 medications.
However, the published guidelines from the Joint National Committee of Hypertension Management (JNC 8 published in 2014) recommends a target blood pressure of 140/90 mm/Hg in patients with diabetes based on the fact that none of the published major clinical trials including ACCORD-BP, UKPDS, or HOT have shown conclusive benefit in the outcomes by lowering BP to less than 140/90 mm/Hg. The ACCORD-BP study did not demonstrate a difference in outcomes in the primary prespecified endpoint between targeting a systolic blood pressure of <120 vs. <140. The SPRINT study, that used the same targets as in the ACCORD- BP study, demonstrated in high-risk hypertensive patients that targeting a systolic BP < 120. Both studies demonstrated increased adverse events and use of anti-hypertensive medications in the systolic BP <120 treatment arms. Additional studies may need to be performed to address the optimal lower systolic BP in patients with diabetes mellitus.
The essential goal of therapy is treatment of hypertension and reduction of proteinuria. Several studies have demonstrated the critical role of using drugs that block the RAAS in further slowing down the progression of DN. Use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blocker (ARB) has become the standard of care in patients with DN.
Antihypertensive Medications
In addition to lifestyle measures, all patients with diabetes and BP >140/90 mm Hg should be started on once daily RAAS blocker and the dose maximized within the first month of treatment if BP is not <130/80 mm/Hg. If the BP is >160/100, two pharmacologic agents should be initiated and titrated in addition to lifestyle measures. If BP is >20/10 mm Hg above goal, then combination therapy with RAAS blocker and either a diuretic (thiazide diuretic if GFR >30 ml/min or loop diuretic if GFR is lower) or a dihydropyridine calcium channel blocker (CCB) started.
When choosing an ACEI or ARB, the dose should be titrated to the maximally tolerated dose necessary to reach goal BP.
If an ACEI is started and the adverse effect of cough appears, treatment should be changed to an appropriate dose of an ARB.
If within a month of monotherapy titration the BP goal is not achieved, then either a low-dose thiazide diuretic such as 12.5 mg chlorthalidone or hydrochlorothiazide or CCB should be added. In patients with a GFR < 30ml/min, replace the thiazide diuretic with a loop diuretic.
If potassium levels are elevated (>5 mEq/L) before initiating RAAS blocking drugs, a review of all high potassium containing foods and substances, and drugs such as NSAIDS should be discussed with the patient. If potassium levels stay elevated, use of a loop diuretic twice or thrice daily maybe appropriate to allow use of the RAAS blocker. If hyperkalemia persists, replace ACEI with ARMs and if this does not lower potassium, discontinue ARBs.
Minimizing the number of antihypertensives improves patient adherence. Therefore, fixed drug combinations may be used.
If after 2 to 4 weeks of adding a diuretic or CCB, BP is still not at goal, titrate diuretic and/ or CCB to maximum tolerated dose. However, in at least 20% of the remaining cases, a fourth and possibly a fifth agent will be needed. If blood pressure is uncontrolled after administering 3 agents of which one is a diuretic, an evaluation for secondary causes of hypertension should be considered.
Inhibition of the RAAS: ACEI or ARB as monotherapy
Current recommendations are to use an ACEI or ARB as a first-line option in treating hypertension in patients with DN. The classic study with captopril published in the early 1990s showed that ACEI slow down the decline in GFR and prevent increases in albuminuria in patients with type 1 diabetes and DN. The Irbesartan in Diabetic Nephropathy Trial (IDNT) and Reduction in Endpoints in NIDDM with Angiotensin Antagonist Losartan (RENAAL) studies were sentinel studies establishing the efficacy of ARBs in patients with type 2 DM and nephropathy.
The IRbesartan in MicroalbuminuriA (IRMA) study demonstrated progression to macroalbuminuria was significantly reduced by Irbesartan in type 2 diabetics. The Diabetics Exposed to Telmisartan and Enalapril (DETAIL) study demonstrated that ARBs are noninferior to ACEIs in patients with type 2 diabetes and microalbuminuria on the basis of the outcome of GFR decline.
Thus these studies indicate that administration of an ACEI or ARB can be used as first-line therapy options for hypertension in patients with DN without evidence suggesting superior efficacy of active drugs to one another.
Inhibition of the RAAS: ACEI or ARB as dual therapy
Because ACEI or ARB are individually renoprotective, questions arose regarding the utility of combination therapy with ACEI and ARB. The concept behind this was more complete inhibition of Ang II, which can be produced through non-ACE pathways. Prior studies using combination therapy in patients with type 1 and 2 diabetes, showed significant reductions in albuminuria and/or BP and was generally well tolerated. Concerns about this strategy arose with the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET), which found no difference in primary endpoint of stroke, MI, and sudden cardiac death between groups. However, those in the combination group had higher rates of renal impairment and hyperkalemia. An ongoing multicenter study, VA NEPHRON-D Study (VA Nephropathy in Diabetes) is testing the efficacy and safety of an ACEI (lisinopril) + ARB (losartan) in reduction in GFR to >30 ml/min or >50%, ESRD, or death in DM2 and nephropathy. The results of the study were published in November 2013 and concluded that combination therapy resulted in increased risk of adverse events among patients with diabetic nephropathy.
Based on the ONTARGET results, it is better to avoid combination ACEI and ARB therapy.
Direct renin inhibitors (DRI) in DN
Renin levels are elevated with either ACEI or ARB and may produce Ang II through non-ACE pathways. Aliskiren is a direct renin inhibitor that lowers BP and albuminuria in patients with DN. Its utility as an add-on therapy is being investigated in the Aliskiren Trial in type 2 Diabetes Using Cardiovascular and Renal Disease Endpoints (ALTITUDE) where an ACEI or an ARB + DRI are being tested. The trial was stopped early by the data monitoring committee due to increased rate of adverse events, such as nonfatal stroke, hyperkalemia, and hypotension. The committee also stated that it was unlikely there would be a benefit to the use of aliskiren in the trial. At this time there is no recommendation to use aliskiren in patients with diabetes. Further studies will be needed to demonstrate the benefits.
Mineralocorticoid receptor antagonists in DN
With both ACEI and ARB, plasma aldosterone levels are expected to decrease. In some patients on maintenance therapy with these drugs, aldosterone levels increase to pretreatment levels through the phenomenon of "aldosterone escape." This may be seen in up to 40% of patients on either ACEIs or ARBs and may contribute to local renal damage, albuminuria, and possible systemic hypertension. A few studies have shown a small reduction in albuminuria but increased risk of hyperkalemia, especially in those with decreased renal function.
Renal Replacement Therapy Options
When GFR falls below 10 to 12 ml/min/1.73 m2, or signs and symptoms of volume overload or uremia develop, patients may need to be on some form of renal replacement therapy (RRT). The three forms of RRT are: hemodialysis, peritoneal dialysis, and renal transplant. Referral for evaluation for RRT should occur when the eGFR is <30 ml/min/1.73 m2.
Dialysis: Survival analysis shows that the two modalities (hemodialysis and peritoneal dialysis) are comparable with regard to patient outcomes. However, when compared to nondiabetics, diabetic patients on dialysis do much worse, with a 5-year survival rate as low as 5% in elderly type 2 diabetics. This survival can improve to 58% at 3 years, with meticulous management.
Issues that can decrease survival time in these patients can include: Cardiovascular disease, peripheral vascular disease, malnutrition, or access related infections.
Renal transplant: By far the best treatment for ESRD is a kidney transplant. This can be done alone or with a combined kidney-pancreas transplant. Patient survival time is much greater after transplant when compared to remaining on dialysis. Data from the Organ Procurement and Transplantation Network reported a 1-, 3-, and 5-year survival rate for transplanted diabetics of 90%, 79%, and 66%, respectively. This, compared to a 2-year survival rate of patients on hemodialysis of 58%, looks more promising. The renal transplant can come from a living donor or a deceased donor. Three-year allograft survival is better for the living donor than the deceased donor transplant. Preemptive transplant is an even better option as it offers a survival advantage over patients receiving a transplant while on dialysis.
Diabetic ketoacidosis (DKA) in ESRD patients
Development of DKA is not very common in ESRD patients. Some of the reasons for this are: Glycemic control may get better as renal function worsens, since insulin metabolism is decreased. Also, since many dialysis patients are anuric, fluid and electrolyte losses may be lesser due to lack of glycosuria and osmotic diuresis. On the other hand, hyperkalemia, metabolic acidosis and volume overload are more common.
Management of DKA in ESRD patients
Potassium supplementation should be avoided, since despite the hypokalemia seen on labs, the total body potassium stores may be high. However, if clinical suspicion or electrocardiographic findings of hyperkalemia are present, immediate potassium lowering therapies should be initiated, including emergent hemodialysis.
Dialysis dependent patients with DKA often present with profound metabolic acidosis, since the anuric kidneys cannot manage the increased acid loading secondary to ketogenesis. Aggressive fluid resuscitation to increase acid excretion is not a safe choice in anuric patients if they are not volume depleted. Bicarbonate therapy is usually not very effective in this patient population. If metabolic acidosis is very severe, emergent hemodialysis may be used to correct it.
If fluid resuscitation is required for a volume depleted patient, who is dialysis dependent, it should be done in small aliquots, with constant reevaluation for volume overload.
The most common indications for dialysis in a dialysis-dependent patient, presenting with DKA are: hyperkalemia, severe metabolic acidosis, and volume overload.
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- Are You Sure the Patient Has Diabetic Nephropathy?
- What Else Could the Patient Have?
- Key Laboratory and Imaging Tests
- Pathophysiology and natural history
- Management and Treatment of Diabetic Nephropathy
- Renal Replacement Therapy Options
- Diabetic ketoacidosis (DKA) in ESRD patients