THINGS THAT I AM HAPPY ABOUT

1. Fourth of July
2. Japanese and Korean soap dramas and foreign movies with English subtitles
3. Freshly cooked yellow corn
4. Water sprinklers on a hot summer day
5. Fridays

FUNNY CARTOON OF THE DAY

TODAY'S WORD

(www.joelosteen.com)

No Matter What

Today's Scripture

“I want you to know, brothers, that what has happened to me has really served to advance the gospel” Philippians 1:12 (ESV).

Today's Word from Joel and Victoria

We all could learn quite a bit from the apostle Paul. He was deliriously happy and joyous because of what Christ had done in his life. Even when he was chained and shackled in a dark prison because of his faith, Paul praised God and was excited to deliver his message of the gospel. He says in Philippians 1 that he knew he was suffering for a purpose and that he rejoiced because of the advancement of God's message even when he couldn't be out preaching the gospel. My friend, you can't defeat a person who gives God praise no matter what! And the best part is that God can work in your life the same way He worked in Paul's. God can turn some of the worst possible situations into some of the most worthwhile experiences if you have the right attitude. Praise God today . . . no matter what!

A Prayer for Today

God, I realize that You can take even my bad days and accomplish something great for Your glory. Thank You for the way You display Your power and love in my life. In Jesus' Name. Amen.

Long-Term Survival After Surgical Treatment of Patients With Takayasu’s Arteritis

CLINICAL INVESTIGATION REPORTS

http://circ.ahajournals.org/cgi/content/abstract/108/12/1474

Tetsuro Miyata, MD; Osamu Sato, MD; Hiroyuki Koyama, MD; Hiroshi Shigematsu, MD; Yusuke Tada, MD

From the Division of Vascular Surgery, Department of Surgery, Graduate School of Medicine, The University of Tokyo, Japan. Dr Sato is presently at the Department of Surgery, Saitama Medical Center, Japan. Dr Tada is presently at the Second Department of Surgery, Yamanashi Medical University, Japan.

Correspondence to Dr T. Miyata, Division of Vascular Surgery, Department of Surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail miyata-2su@h.u-tokyo.ac.jp
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Received February 6, 2003; de novo received April 10, 2003; revision received July 11, 2003; accepted July 11, 2003.

Background— Surgical interventions have been performed to ameliorate the complications of Takayasu’s arteritis. However, the efficacy of surgery to increase long-term survival has not been established.

Methods and Results— A retrospective review was performed on the survival of 106 consecutive patients with Takayasu’s arteritis who underwent surgical treatment during the past 40 years. Their ages ranged from 5 to 69 years (mean±SEM, 31.7±1.3 years). Survival was compared with the reported results of medically treated patients according to Ishikawa’s prognostic classification. There were 12 hospital deaths, and the remaining 94 patients were followed up from 8 months to 41.8 years (mean, 19.8 years). A serious long-term complication was anastomotic aneurysm, with a cumulative incidence at 20 years of 13.8%. Thirty-one late deaths were observed, and the major cause was congestive heart failure. The overall cumulative survival rate at 20 years was 73.5%. The prognostic classification by Ishikawa had little influence on the survival of surgically treated patients. For stage 3 patients, surgery seemed to increase survival; however, surgery-related complications conversely decreased the survival of stage 1 patients.

Conclusions— Surgery seems to increase the long-term survival of patients with stage 3 Takayasu’s arteritis, whereas conservative treatment is recommended for those with stage 1 or 2 disease. An anastomotic aneurysm may occur at any time after surgery, and regular follow-up using imaging modalities such as multi-detector CT, MRI, or ultrasonography at least once every several years for the rest of the patient’s life is mandatory for the early detection of anastomotic aneurysm.

TODAY'S WORD

Guard Against Bitterness

Today's Scripture
“When you go through deep waters and great trouble, I will be with you. When you go through rivers of difficulty, you will not drown” Isaiah 43:2 (TLB).

Today's Word from Joel and Victoria

Have you ever experienced something that truly tested your faith, your joy and your convictions? We're not talking about just having a bad day or having to deal with difficult people - but enduring an intense situation that rocks you to your very core. When many people face such soul-searching events, they let their happiness and joy turn into bitterness and anger. Make sure this doesn't happen to you. Don't give the evil one the victory by becoming an ineffective Christian due to lingering bitterness. Even if you're being tested, God has promised to remain faithful. He is all-powerful, and He can pull you out of your troubles at any moment. Choose to remain faithful and joyous despite your present circumstances.

A Prayer for Today

God, please help me to trust You and not give in to bitterness or anger, even in the middle of my trials. Thank You for the promise of Your never-failing love. In Jesus' Name. Amen.
Read another Word with Joel & Victoria

Comparative studies between Japanese and Korean patients: Comparison of the findings of TA

http://www.springerlink.com/content/w76u247v7263350h/

Comparative studies between Japanese and Korean patients: Comparison of the findings of angiography,HLA-Bw52, and clinical manifestations

(1) Michiyoshi Yajima1 , Ryutaro Moriwaki1, Fujio Numano1, Young B. Park2 and Young D. Cho3 Department of Internal Medicine, Tokyo Medical and Dental University, Bunkyo-ku, 113 Tokyo, Japan

(2) Department of Medicine, Seoul National University Hospital, Seoul, Korea

(3) Department of Radiology, Kosin Medical Center, 600 Pusan, Korea

Summary

A Japan-Korea cooperative survey on Takayasu arteritis has shown some differences in the features between Japanese and Korean patients with this disease. In angiographic findings, Japanese patients more frequently had lesions at the aortic arch and/or its branches (58% of 75 cases), while, in Korean patients, the abdominal aorta is the site of relatively frequent lesions (30% of 112 cases). Higher occurrence ofHLA-Bw52 was found in Japanese patients in comparison with Korean patients (46% vs 15%). The presence ofHLA-Bw52, however, might have a close association with Takayasu arteritis in Korea as well as in Japan. The complications in 126 Japanese and 88 Korean patients were also compared. The complications occurring with higher frequency in Japanese patients were aortic regurgitation, ischemic heart disease, and visual disturbances, while, in Korean patients, the more frequent complications were renovascular hypertension as well as hypertension of some other etiology.

Key words Takayasu arteritis - Aortography - HLA-Bw52 - Aortic regurgitation

Source:

Journal: Heart and Vessels
Publisher: Springer Japan
ISSN 0910-8327 (Print) 1615-2573 (Online)
Issue: Volume 7, Supplement 1 / March, 1992
DOI
10.1007/BF01744553
Pages: 102-105
Subject Collection
Medicine
SpringerLink Date
Monday, June 20, 2005

TODAY'S WORD

Relax and Let God Work

Today's Scripture

“Cease striving, and know that I am God” Psalm 46:10 (NAS).

Today's Word from Joel and Victoria

Psalm 46:10 is a great Scripture to pray daily. Turn to it and read it before you make any decision. You'll be amazed at the insight you get from waiting on God instead of striving to find the answers on your own. Don't always react on your first impulse - instead, think about what God would want from you and realize that He is in control. You'll be able to see His hand working in just about any situation when you take a step back and realize it's not your plan, but His. When you're absolutely confused, worried and don't have a clue what to do, relax for a minute and let God work. Don't let panic or worry guide your decisions when God is ready to help you.

A Prayer for Today

God, thank You for remaining in control even when I'm worried or stressed. Give me Your supernatural wisdom to make decisions that honor You and are for my good. In Jesus' Name. Amen.

LAUGHING BABIES VIDEO

Comprehensive Evaluation of Cardiovascular Complications in a Patient with Takayasu´s Arteritis

http://www.medical.siemens.com/webapp/wcs/stores/servlet/SMStandardContentView?storeId=10001&langId=-11&catalogId=-11&catTree=100001,18024,17997&pageId=53145&uCatTree=100004*3281799139*477251247
Authors:

Joon-Beom Seo, M.D.,

Tae-Hwan Lim, M.D.,

Department of Radiology, University of Ulsan College of Medicine,

Asan Medical Center, Seoul, Korea

History:

A 50-year-old female patient with a history of known Takayasu´s arteritis was presented with chest discomfort. The patient was diagnosed of Takayasu´s arteritis 20 years ago. She underwent coronary bypass graft surgery 10 years ago for diffuse narrowing of left main (LM), proximal left anterior descending (LAD), and proximal left circumflex (LCx). MSCT examination is requested by the cardiologist for evaluation of her cardiovadcular status.

Diagnosis and Comments:

ECG gated coronary CTA shows patent venous bypass graft which originates from ascending aorta and is anastomosed to distal LAD and diagonal branch [1]. Also shown is diffuse narrowing of left main coronary artery, proximal LAD, and LCx [2]. Non-gated CTA scan obtained immediately after coronary CTA without additional contrast agent shows total occlusion of left subclavian artery, and diffuse severe narrowing of left common carotid artery (LCC) [3]. The LCC originates anomalously from the right brachiocephalic trunk. Diffuse calcification of descending thoracic aorta with narrowing and dilation is also noted, which is the late manifestation of Takayasu´s arteritis. Thin slab MIP image [4] shows occlusion of left lower lobar pulmonary artery due to pulmonary arterial involvement of Takayasu´s arteritis. Also seen are tortuous bronchial arteries and many mediastinal small collaterals entering into left hilum to supply left lower lobe [5]. In the abdomen, mild narrowing of abdominal aorta with calcification at the level of renal artery origin is noted [6].

[1] VRT image shows patent venous bypass graft anastomosed to the distal LAD (arrow) and to diagonal branch (arrowhead) .

[2] VRT image shows diffuse narrowing of left main coronary artery (arrow), proximal LAD (thin arrow), and LCx (arrowhead) .

[3] Narrowing of left common carotid artery (arrow) and total occlusion of left subclavian artery (arrowhead) are seen.

[4] Sagittal slab MIP image shows total occlusion of left lower lobar pulmonary artery.

[5] VRT image shows dense calcification encircling the descending thoracic aorta (arrow) and multiple mediastinal collaterals (arrowheads) .

[6] VRT image of abdominal aorta shows mild narrowing of abdominal aorta with calcified patch at mid level. Diffuse narrowing of right external iliac artery is noted.

Siemens SOMATOM Sensation 16

Scan 1: CTA Coronary

Scan 2: Aorta

HANG ON LITTLE TOMATO

HANG ON LITTLE TOMATO

The sun has left and forgotten me
It’s dark, I cannot see
Why does this rain pour down
I’m gonna drown
In a sea
Of deep confusion

Somebody told me, I don’t know who
Whenever you are sad and blue
And you’re feelin’ all alone and left behind
Just take a look inside you and you will find

If you listen to your heart the whole night through
Your sunny someday will come one day soon to you

AFFIRMATION OF THE DAY

I meet my fear, pain or other emotions I tend to escape.
I thank the people or events that brought them up.

FUNNY CARTOON OF THE DAY

TODAY'S WORD

Go Ahead and Grow

From Joel & Victoria Osteen

joelosteen.com

Today's Scripture
“God is working in you, giving you the desire and the power to do what pleases him” Philippians 2:13 (NLT).

Today's Word from Joel and Victoria

Nothing can change God's love for you. He wants the best for you and desires for you to grow spiritually. God says in the Bible that His plans and purposes for your life are wonderful - and nothing can stop the almighty God from accomplishing great things through you! God orders certain circumstances in your life He knows will be a challenge and cause you to grow in your faith. God loves you far too much to leave you where you are. So why settle for a middle-of-the-road life when you can cross the finish line victoriously! God continually works in you to give you the power for abundant living -so believe it, receive it and use it mightily for Him!

A Prayer for Today

God, I'm so glad that You love me too much to leave me where I am. Help me to live in the obedience and victory that I know are Your desire for me. In Jesus' Name. Amen.

TODAY'S WORD

From Joel & Victoria Osteen
joelosteen.com

God is at Work for You

Today's Scripture

“I know what I am planning for you,” says the Lord. “I have good plans for you, not plans to hurt you. I will give you hope and a good future” Jeremiah 29:11 (NCV).

Today's Word from Joel and Victoria

Too often, we think God is just out there - watching and waiting for us to get things right. God is a big God, but He loves you and He wants to help bring the best things possible into your life. God is at work in your life each and every day, blessing you and preparing you for great and wonderful things that you can’t even imagine! Your entire perspective will radically change when you realize God is in your everyday experiences. Even when we are not completely faithful to Him, He is always faithful to us! Make God your hope and rely solely on Him, and He’ll faithfully work things out that will bless you, protect you and encourage you!

A Prayer for Today

God, thank You for always having my best in mind. I know that You love me and want the best for Your children. Help me to be faithful to You. In Jesus’ Name. Amen.

MUSIC VIDEO OF THE DAY: CORINNE BAILEY RAE

SCIENCE NEWS BREAKTHROUGHS IN GENETICS

http://www.hhmi.org/news/seidman20070608.html

June 08, 2007

Sensitive Genetic Analysis Reveals Vast Changes Associated with Hypertrophic Cardiomyopathy

The one-gene, one-disease concept is elegant, but incomplete. A single gene mutation can cause many other genes to start—or stop—working, and it may be these changes that ultimately cause clinical symptoms. Identifying the complete set of affected genes used to appear impossible. Not anymore.

Studying genetically modified mice, researchers led by Christine E. Seidman, a Howard Hughes Medical Institute investigator at Brigham and Women's Hospital, and her husband Jonathan G. Seidman, who is at Harvard Medical School, have identified hundreds of genes with altered expression in preclinical hypertrophic cardiomyopathy. The study, which is coauthored by colleagues at Harvard Medical School, is published in the June 9, 2007, issue of the journal Science. The discovery could help scientists define the pathways that lead to the disease and lead to the discovery of targets for early detection, prevention, and treatment.


“Some of these low-abundant molecules may be very important in altering cell biology in ways that may be part of the root cause, or a compensatory response to very early manifestations of disease.”
Christine E. Seidman

To obtain a complete picture of the genetic changes associated with the disease, the researchers developed a new gene sequencing technique called polony multiplex analysis of gene expression, or PMAGE. The technique can find messenger RNA transcripts—the directions for making a protein, spun out from the DNA of an active gene—that occur as rarely as one copy for every three cells.

To use PMAGE, researchers attach short sequences (called tags) cut from mRNAs to tiny beads. This tag is amplified, so that each bead contains millions of copies of the same mRNA tag sticking out from it like a minuscule Koosh ball. All of the beads — now called polonies (short for polymerase chain reaction of colonies) — are placed in one layer onto glass, and all of the tags are sequenced simultaneously. A computer program then matches the tags to known genes. The more tags associated with a gene, the higher the expression of that gene.

The industry standard for gene sequencing is serial active gene expression, or SAGE. "There are a couple of labs that have been dedicated to developing this technology," Seidman said, including HHMI investigator Bert Vogelstein at Johns Hopkins and George Church at Harvard. But PMAGE analysis costs between 1/20 and 1/9 of a comparable SAGE analysis, making it more appropriate for the kind of large-scale expression profiling undertaken in this study, she explained. "With SAGE, you can't afford to sequence 4 million transcripts."

Using PMAGE, the researchers compared a healthy group of mice to a group with a genetic mutation that causes hypertrophic cardiomyopathy (HCM) after about 25 weeks of age. In people with HCM, the heart muscle thickens and fails to relax normally after contraction. HCM is the most common cause of sudden death in athletes.

Seidman's group used cardiac tissue from 8-week-old mice to create two PMAGE libraries totaling 4.4 million mRNA tags. They found 706 genes that were overactive or underactive in HCM mice, compared with normal mice. Some genes already have been linked with HCM or heart development. Others are new to the scene.

Overactive genes included:

Nppa (natriuretic peptide precursor a), which encodes atrial natriuretic peptide, or ANP. This protein is an important marker for HCM.

Ctgf (connective tissue growth factor), Tgfß1 (transforming growth factor beta-1), and Postn (periostin), powerful regulators of fibrosis and collagen deposition. The early activation of these genes indicates that fibrosis is probably a primary contributor to heart dysfunction, not a reaction to other changes.

Vgll2 (vestigial-like 2 homolog) and Egr3 (early growth response-3), transcriptional regulators involved in the fetal development of the heart muscle

Nr1h3 (nuclear receptor subfamily 1, group h, member 3) and Nfkbie (nuclear factor kappa light polypeptide gene enhancer in B cells inhibitor epsilon), which have never before been linked with HCM

Underactive genes included:

Hod (homeobox-only protein) and Hand2 (hand and neural crest derivatives 2), transcriptional regulators involved in the fetal development of heart muscle

Abcc9 (adenosine triphosphate cassette subfamily C member 9), which encodes part of the cardiac potassium channel. This channel helps to regulate calcium balance. Mice who lack Abcc9 develop arrhythmias and myocardial calcium overload.

Sln (sarcolipin) and Pln (phospholamban), which regulate calcium uptake into muscle cells

"It's important that we could statistically quantify changes even in genes with very low expression levels," Seidman said. "Some of these low- abundant molecules may be very important in altering cell biology in ways that may be part of the root cause, or a compensatory response to very early manifestations of disease."

Seidman is now repeating the PMAGE sequencing using tissue from younger mice. "We want to get at the drivers of the pathology," Seidman said. "HCM largely affects structural proteins, and we don't really understand how a change in one protein affects the cascade that ultimately affects physiology. If we do this sequencing early enough, we'd like to think we'll see signals that point us to something that is fundamentally changing the whole downstream cascade."

Discovering those fundamental drivers of change could result in targeted therapies to halt HCM in its tracks, or even prevent it altogether.

"We're doing this in a mouse right now, but we have access to tissue from human patients," Seidman said. "With the deep, rich analysis we obtain from a biopsy or resection, we can jump into understanding the human biology of heart disease quite quickly."

-------------

February 27, 2005

Tailing the Cause of a Rare Heart Disease

Using genetic analyses and the translucent tail of a fish, researchers have pinpointed the underlying cause of a rare, mysterious heart disease that is preceded by hearing loss. Discovering the genetic cause of this disease provides researchers with a wealth of new ideas about the molecules involved in building the developing heart, as well as how diseases weaken heart muscle.

In an advance online publication on February 27, 2005, in the journal Nature Genetics , Howard Hughes Medical Institute investigators Christine E. Seidman and Jonathan G. Seidman and their colleagues identified the mutation that causes the disorder, dilated cardiomyopathy preceded by sensorineural hearing loss. The Seidmans and their colleagues at Harvard Medical School collaborated with researchers at University Hospital Würzberg in Germany, Massachusetts General Hospital, Children's Hospital Boston and The Wellcome Trust Sanger Institute in Britain.

“The finding that transcriptional regulation goes awry in this disorder gives us a top-down look at the molecules that must be appropriately expressed and regulated for normal function of the heart throughout life.”Christine E. Seidman

In dilated cardiomyopathy, muscle weakness causes the left ventricle to stretch. As a result, the heart becomes enlarged to the point where it can no longer pump blood efficiently. In earlier studies of patients with cardiomyopathy preceded by hearing loss, the Seidmans and their colleagues identified a region of chromosome 6 as the location of the culprit gene.

In the latest study, they sought to pinpoint the gene and identify the mutation that was responsible. A search of the human genome database identified candidate genes in the region, and subsequent tissue analysis revealed that one gene, called EYA4 , was expressed in both the heart and the cochlea of the ear. The researchers confirmed that affected people possess a characteristic mutation of the EYA4 gene, a finding which offered surprises, said Christine Seidman.

"The EYA4 gene had been implicated in hearing loss before, but in none of the patients where mutations had been characterized had there ever been an abnormality of the heart reported," she said. The Seidmans also found that the gene was expressed in adult heart tissues, which is unusual because other EYA gene family members are thought to function primarily during development.

Curiously, the gene does not code for a structural protein involved in known myocyte functions such as contraction, as is the case with other mutations that cause cardiomyopathies. Rather, EYA4 codes for a protein involved in activating other genes—controlling the copying, or transcription, of genetic information to messenger RNA that carries that genetic blueprint to the cell's protein-making machinery.

To confirm that the mutant EYA4 does indeed cause cardiomyopathy, the researchers turned to the zebrafish, whose genetic machinery for cardiovascular development closely resembles that of mammals. In their experiments with the fish, they used antisense genetic techniques to reduce the fish's production of eya4 protein and measured the resulting changes to the heart. The treated fish developed swelling of the heart ventricle that suggested cardiac dysfunction. High-speed video of the fish's beating heart—visible because the fish are translucent—indicated that the pumping function of the heart was dramatically reduced.

However, the researchers turned to the fish's translucent tail to confirm independently that blood flow was, indeed, reduced in the treated fish. "Since the cardiac imaging of zebrafish remains technically challenging," said Seidman, "we devised a means of tracking the movement of a single red blood corpuscle through the tail to assess flow. That analysis revealed a dramatically lower pumping velocity in the treated fish and provided a functional readout of heart performance," she said.

To understand the molecular mechanism by which the mutant eya4 protein might compromise cardiac function in humans, the researchers compared its function with that of other mutant forms that only caused hearing loss. They found that the mutant protein that caused both cardiomyopathy and hearing loss lacks a region necessary for the protein to attach to other proteins that help it enter the cell nucleus. Only if the eya4 protein enters the nucleus can it play the appropriate role in gene regulation, said Seidman.

"That finding suggests that this mutation causes a dramatic reduction in the amount of eya4 within the nucleus, and we presume that is what accounts for heart disease," said Seidman. "The implication of this finding is that the function of eya4 in the heart may be different than its functions in other tissues, such as the ear.”

Although the researchers' findings will not aid treatment of the cardiomyopathy immediately, said Seidman, they do offer the potential for important basic insights into the mechanisms of cardiomyopathies.

"Whenever a new disorder affecting the human population is identified, it adds new basic knowledge to the field of medicine," she said. "And sometimes rare disorders such as this one can provide very powerful insights into the biology of more common problems. In this case, the finding that transcriptional regulation goes awry in this disorder gives us a top-down look at the molecules that must be appropriately expressed and regulated for normal function of the heart throughout life."

DON'T GIVE UP

QUOTE OF THE DAY

When challenged to wait,

I learn how to wait and make good use of the time.

If no messages or directions about what to do next come up,

I am peaceful as I wait for the right timing of things.

MUSIC VIDEO OF THE DAY

Large Study Finds 12 New Disease-Related Genes

24 Genetic Risk Factors Tied to 7 Common Illnesses, British Scientists Say

LONDON - The largest ever study of genes in disease has found 24 genetic risk factors — half of them completely new — linked to seven common conditions, British scientists said on Wednesday.

It represents the biggest single haul of disease-associated genes so far, underlining an accelerating pace of discovery that will help researchers unpick the fundamental biology of major illnesses and may lead to more effective drugs.

Last week, researchers found a big batch of breast cancer genes and two months ago scientists identified a gene that contributes to obesity.

“We are just scratching the surface,” Peter Donnelly of the University of Oxford, who led the Wellcome Trust Case Control Consortium behind the project, told reporters.

“What will happen over the next couple of years, as these sorts of studies are extended, is that our understanding of the genetics of common diseases will change enormously.”

Scientists have known for years that genes, along with environmental factors, play a role in increasing the risk that people will develop problems like heart disease.

But they are still trying to work out which parts of the genome — the 3 billion sub-units of DNA in our cells — are actually responsible.

To find out more, Donnelly and colleagues from 50 research groups examined 500,000 genetic markers from each of 17,000 individuals, comparing the genomes of diseased and healthy volunteers.

Their findings, published in the journals Nature and Nature Genetics, included the discovery of four new chromosome regions containing genes that can predispose to type 1 diabetes and three new genes for Crohn’s disease, the most common form of inflammatory bowel disease.

They also found genetic links to coronary artery disease and hypertension, rheumatoid arthritis, bipolar disorder and type 2 diabetes.

New ideas for treatment

Significantly, many of the genes found were in areas of the genome not previously thought to have been related to the conditions, opening up completely new options for treatment.

In the case of Crohn’s disease, they uncovered the importance of a process known as autophagy, or “self eating,” which cells use to clear unwanted material, such as bacteria. John Todd of the University of Cambridge said this could be key to explaining the role gut bacteria play in the condition.

Scientists also, for the first time, found a gene linking Crohn’s and type 1 diabetes.
The overall increase in risk of disease conferred by the various genetic risk factors was between 1.2 and 1.5 times, suggesting routine testing is not worthwhile.

But Mark Walport, director of the Wellcome Trust medical charity, said there was a clear need for more research in even bigger projects, such as the UK Biobank scheme, which aims to test the DNA of half a million volunteers.

http://www.msnbc.msn.com/id/19074222/wid/11915773?GT1=10109

5 Things that I am Grateful and Happy

1. Good weather, the sun is out.
2. Pink Martini music.
3. Time to read.
4. Almost cleaned desk, filing stuff at work.
5. New laptop finally connected and in working order.

Cleveland Study on Takayasu’s Arteritis: Utility and Limitations of Magnetic Resonance Imaging in Diagnosis and Treatment

http://www.clevelandclinic.org/quality/outcomes/rheumaticAndImmunologic/takayasuTreatment.htm

Takayasu’s Arteritis: Utility and Limitations of Magnetic Resonance Imaging in Diagnosis and Treatment

Previous studies emphasized poor correlation of symptoms, signs and acute phase reactants with disease activity in about half of all patients with Takayasu’s arteritis (TAK). Invasive angiographic studies demonstrate vessel lumen anatomy. Sequential studies expose patients to high-dose ionizing radiation and catheter/procedure-related morbidity. Such studies do not provide qualitative information about the vessel wall. To determine the utility of vascular magnetic resonance (MR) technology in TAK patients, we previously reported (Tso E, et al. Arthritis Rheum. 2002;46:1634) our experience from 77 studies on 24 patients using ECG-gated MR images, “edema-weighted,” to evaluate the aorta and its primary branches in regard to the vascular lumen, vessel wall anatomy and vessel wall edema.

Ninety-four percent of studies, obtained when patients were thought to have unequivocally active disease, revealed evidence of vessel wall enhancement. In 81% of studies obtained during periods of uncertain disease activity, and in 56% of studies obtained during periods of apparent clinical remission, enhancement was also noted. The Westergren sedimentation rate and C-reactive protein did not correlate with either clinical assessment of disease activity or MR enhancement.

Following completion of our formal TAK-MR study, ten additional patients had MR images obtained just prior to vascular surgery procedures. In seven patients, the finding of edema on MR correlated with histopathologic proof of inflammation or vasculitis. In three patients, however, MR edema was present and inflammation absent within the biopsy, suggesting that vascular MR may not always be accurate.

This study was the first prospective analysis of the utility of recent technical advances in MR imaging in Takayasu’s arteritis. This technique can be an important supplement to the clinical and laboratory assessment of disease activity. The negative correlation we observed between ESR or CRP and MR signal intensity is similar to prior reports in which ESR was abnormal in 72% of patients during clinically active disease and was also abnormal in 44% of patients thought to be in remission.

Our observations should not be interpreted as suggesting that MR vascular imaging replace invasive angiography. Each technique has unique advantages and disadvantages. Sequential invasive angiography has been very informative in detecting new vascular lesions in TAK. It provides greater image resolution than MR in vessels other than the aorta, innominate and common iliac arteries, which makes it desirable for the preoperative planning of bypass surgery. Invasive angiography provides opportunities to record central blood pressure readings and gradient determinations in patients with vessel stenoses, allowing the clinician to assess the reliability of extremity blood pressure cuff measurements. Alternatively, the non-invasive, radiation-sparing qualities of MR and “edema-weighted” imaging techniques may lead to its preferred use for routine follow-up.

“Edema-weighted” MRI vs Invasive Angiography



A comparison of invasive angiography (A) and MR (B) demonstrates the superior resolution of the former study. The information gained from MR is considerable, and eliminates the risk of an invasive procedure and exposure to radiation.

A.

B.

Histopathologic specimen from a bypass procedure originating in the ascending aorta and inserting into the right subclavian and right carotid arteries.

Postscript

Since completion of this study, funding has been provided to the Vasculitis Clinical Research Consortium (Boston University, Johns Hopkins, Mayo Clinic and Cleveland Clinic) to further define the operating characteristics of MR, CT and PET scanning in large vessel vasculitis.

[KM McKinnon, TM Clark, GS Hoffman]

YOU GOTTA BE VIDEO CLIP

MUSIC VIDEO OF THE DAY: SEASONS OF LOVE

POSITIVE AFFIRMATION OF THE DAY

"If you believe, and if you persist, all things are possible."

Rieva Lesonsky

FUNNY CARTOON OF THE DAY

FUNNY CARTOON OF THE DAY: THE CHUBB CHUBBS

TODAY'S WORD

Fight the Good Fight

Today's Scripture

“That is why we never give up. Though our bodies are dying, our inner strength in the Lord is growing every day.” (2 Corinthians 4:16)


Today's Word from Joel and Victoria

Paul explained to the church at Corinth that giving up is not an option for a true Christian. As a follower of God, you are to fight the good fight in God’s strength and never surrender or give up. Being faithful means holding tight through tough and seemingly impossible times. Keep pushing whether you feel like it or not; keep going even when you run out of strength. Do the right thing, even when the wrong thing happens to you. In order to win the battle, you have to step out and take part in the struggle. Only after fighting the good fight can you experience the good victory that God has in store for you!


A Prayer for Today

God, thank You for giving me the strength to fight the good fight. Help me to keep my eyes on You for the endurance to keep moving forward. In Jesus’ Name. Amen.

TODAY'S WORD

From Joel & Victoria Osteen
www.joelosteen.com

Practicing Real Love

Today's Scripture

“My dear children, let’s not just talk about love; let’s practice real love.” (1 John 3:18)

Today's Word from Joel and Victoria

It’s important for you to let those special people in your life know how much you appreciate their love and faithfulness to you. It’s easy for human beings to let their love stop with words. Now loving words are certainly crucial to a love relationship, but words by themselves are not enough. The Bible says very clearly that we are to love not just by the words we say, but by the deeds of love that we do for others. There is absolutely no limit to the good things that can happen when you decide to let love be the driving force in your life. True love is so strong that the Bible says, “Many waters cannot quench love” (Song of Songs 8:7). That’s a wonderful promise that when you choose to love, your efforts will not be in vain. God will open the windows of heaven and rain down His joy, abundance and favor on you when you learn to love the way He loves.

A Prayer for Today

God, I want to live my best life for You, in love, in everything I do. Please show me the way today so that I may walk in love toward You and toward others. In Jesus’ Name. Amen.

AFFIRMATION OF THE DAY

I am still determined to be cheerful and happy, in whatever situation I may be; for I have also learned from experience that the greater part of our happiness or misery depends upon our dispositions, and not upon our circumstances. Martha Washington (1732-1802)

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FUNNY CARTOON OF THE DAY

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