text:
Paramount Airways yet to take off
By Shutapa Paul and Vishakha Talreja - NEW DELHI
Published: 23rd May 2013 09:42 AM
Last Updated: 24th May 2013 01:50 PM
A Rs 550 crore debt to a clutch of banks has come in the way of grounded Chennai-based airlines Paramount Airways from taking to the skies. Paramount Airways, promoted by M Thiagarajan, lost it licence in 2010 when aviation regulator, Director-General of Civil Aviation (DGCA) stopped its services for failing maintain the mandatory five aircraft in its fleet. The airline has now missed its earlier target of April to restart its services.
Thiagarajan met Union Aviation Minister Ajit Singh and DGCA officials in the capital in January. But soon after the meeting, six banks that had extended loans to Paramount Airways wrote to the DGCA asking the regulator to not to allow the airlines to commence operations till it settled its dues. Lenders including Bank of India, State Bank of India, Central Bank of India, Indian Bank and IDBI Bank wrote to the DGCA in February. The total exposure of Paramount Airways by all the lenders is around `550 crore.
"Our stand is that Paramount Airways should first make a settlement with the banks before applying again for a licence. There has been no movement in this regard since then. The airline should first settle its dues," Arun Mishra, DGCA said. In April, the Madras High Court appointed its official liquidator as the "provisional liquidator" to take charge of the assets of Paramount Airways for not clearing its dues.
The company management however has told Express that all debts have been cleared. "It (restarting operations) is progressing and in a month or so we will get started. We have cleared all our debts with the banks and received NOC."
Paramount renewed its efforts to take off after winning a lawsuit at a British court worth Rs 1,650 crore. It was over a lease agreement payment with GE Capital Aviation Services and Celestial Aviation Trading.
Paramount was also in talks with a number of foreign carriers for foreign direct investment coming at the back of easing of FDI norms in aviation.
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subset: commoncrawl


text:
DETROIT, MI – Walsh College in Troy is moving forward with a $15 million improvement project that will likely begin this summer, after the school's board of trustees gave the plan its formal approval.
The project calls for a two-story, 27,000-square-foot renovation and addition at the non-profit business school's original campus building on Livernois Road. That structure was built in the 1970s. There will also be a renovation to 28,000 square feet of interior space on the campus.
The modern addition, with a stone, brick and metal panel façade, will include a "student success center," which the college says will have technology that allows students to practice and record presentation in a variety of electronic formats, and that will offer digital conferencing.
The plans also include a new student lounge and additional study areas, as well as a student services center.
Chicago-based Valerio Dewalt Train Associates has been named architect.
Construction is expected to last about 18 months. The project is being funded with private capital as well as philanthropic donations.
"This initiative underscores Walsh College's long-term commitment to the growth and vibrancy that we see in southeast Michigan and Troy," Walsh College president and CEO Stephanie Bergeron said in a statement. "The improvements represent our high-quality educational programs, meet the needs of today's students, and put a contemporary face on the Walsh College business brand."
Walsh, founded in 1922, has about 4,200 students enrolled at the school. About 91 percent of its students are part-time.
David Muller is the business reporter for MLive Media Group in Detroit. Email him at firstname.lastname@example.com or follow him on Twitter or Facebook.


text:
The Bridge Children's Advocacy Center will postpone a groundbreaking ceremony for the agency's new center until 2 p.m. Friday at the proposed site, the corner of Plum Creek and Quail Creek drives, just east of the Amarillo Diagnostic Clinic.
Officials from The Bridge delayed the ceremony, originally scheduled for Wednesday, because of predictions of cold weather conditions this week.
The new center will accommodate space for Sexual Assault Nurse Examiner's Team exams, the multidisciplinary team case reviews and Child Fatality Review team investigations. It also will include child and family interview rooms, waiting and play areas and administrative office space.
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Your Travel Starts at Hisar . It Ends at Ch dadri.
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text: This is in reply to Mr. Gilbert's letter to the editor of April 26. In true liberal fashion, the writer has centered on a subject (and referred to a couple others) that have no relevant impact on this nation or the way it's being run. Rancher Bundy and his racist comments and the band of so-called vigilantes will fade out in the setting sun soon enough. He's just not that important.


text:
Sep 25, 2013
Banks are earning about as much in fees as they were a year ago, with a burst of ECM activity compensating for a sharply slower M&A market. Much now depends on market stability in the months ahead
But such pressure has so far this year failed to make a dent
in the earnings of the investment banks that service them: fees
are roughly flat on last year, thanks largely to the overall
resilience of the main business lines — even though
the sources of that revenue have changed.
Equity capital market activity picked up pace this year,
helping compensate for a slump in mergers and acquisitions. And
despite uncertainty over the direction of interest rates, debt
capital market revenue is down only slightly on last year,
tracking overall volume.
The fee pool for LatAm investment banking —
combining revenue from DCM, ECM, M&A and loans —
had reached $1.28 billion this year through September 6,
according to Dealogic data. This was up a hair...
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text:
Things could not have gone any worse for the French side in South Africa, as embarrassment supplanted success in 2010.
Players were dismissed, tantrums were thrown and the inability to advance from the group marked their 2010 campaign.
2014 offers a chance at redemption with a crop of young players and talented veterans headlining the French squad.
Are they ready for a deep run in 2014? Bleacher Report's Will Tidey and Ryan Bailey break it down. Watch this video and leave a comment below.


text:
Among developed nations, America stands out as an exceptionally religious country. While other wealthy nations grow ever more secular, the U.S. remains devoted to religion. New research on religion, however, finds that the U.S. may not be so exceptional after all. There is growing evidence linking religiosity to income inequality—countries where there are more haves than have-nots tend to be more religious than more egalitarian societies. The U.S., for all its wealth, is also a land of vast economic inequality. America's wealth exceeds that of European countries, but this wealth is spread out as unequally as it is in Uganda or Jamaica. And it is this high level of inequality that may help explain the so-called exceptional level of religiosity.
At least since Voltaire, scholars have predicted that religion would eventually be extinguished. It was seen as being ill-fitted for an enlightened, modern, rational world. Early sociologists saw society moving through an inevitable process of secularization. Eventually, went the theories, society would rid itself of the remnant of primitive superstition. Such theorists are still waiting for their Godot. Despite incredible rises in education, science, medicine, and overall quality of life during the 20th century, religion remains a common part of life around the globe.
In light of this continued vitality, a new take on secularization has emerged. Pippa Norris (Harvard) and Ronald Inglehart (Michigan) wrote in their book Sacred and Secular that people are more likely to be religious when their lives are at risk. Nations with harsher poverty are more likely to be religious; wealthier nations tend to be more secular.
Of course, material insecurity is not the only reason for religion. There are some societies that clearly buck this pattern. On one side are impoverished countries that have low levels of religiosity. China and Vietnam are the primary examples. Through force, these countries have been able to clamp down on religion (though not completely extinguish it). In the other direction, the major exception to the rule is the United States. Based on wealth, education, and other measures of development, the U.S. should be far less religious than it is. Indeed, America should be one of the least religious nations on earth.
But it isn't. Far from it. Religion continues as a prominent part of American life.
The reason may be due to inequality. The U.S. economy is distributed much more unequally than other Western economies. By the most common measures of inequality, the U.S. is ranked as the 39th most unequal economy (out of 136 countries). The U.S. is ranked near Uganda, Jamaica, Cameroon, and Cote d'Ivoire. Turkmenistan, Mali, and Cambodia have greater income inequality than the United States. Canada is ranked 101st; the entire European Union is ranked 111th. Sweden is considered the most equal nation.
Within the U.S., we can see the same pattern. States with high inequality, (e.g., states in the Mississippi Delta region) are also some of the most religious. States with more economic equality (e.g., states in New England and the Mountain West) are some of the least religious.
My own research with colleagues Fred Solt and Phil Habel (also from Southern Illinois University) shows that the U.S. is typical of countries with such high inequality. The U.S. is not unusually religious—it is typical for a country with such high inequality. We examine a dozen measures of religiosity, including prayer, church attendance, belief in God, and the self-identification of "religious people." In each case, inequality leads to greater religiosity.


text:
Singer Stylist 7258 | Kenmore 1503 | Brother 1034D
My Big 4 Sizing: Medium | Tops 14/16 | Pants 18 | Skirts 16/18.
My Measurements: 36 HB | 39.5 FB | 34 W | 44 Hip
------sewing brings joy and meaning to my life...
------Christine Central Coast NSW
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-- Edited on 3/17/13 4:51 PM --
------How is that still a thing?
This topic has been moved from NEW to PatternReview? to Pattern Reviews
This topic has been moved from Pattern Reviews to Computers AARGH!!!
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SALINEVILLE - Larry G. Adkins Sr., 73, of Salineville, Ohio, passed away Monday, September 10, 2012.
Born April 30, 1939 in Huntington, W.Va., a son of the late Hubert and Jenny (Elkins) Adkins, Larry was a Veteran of the United States Army and was a retired truck driver for Richmond Mills.
He was also preceded in death by his wife, Shirley (Halstead) Adkins; three sons, Chris Kessler, Jim Harris and Lee Harris; two grandchildren; four brothers, Robert, John, Bill and Collis Adkins and by two sisters, Mary Heath and JoAnn Byard.
Larry is survived by two sons, Carl Harris Jr. and Larry (Rhonda) Adkins Jr., all of Salineville; three daughters, Sharon (Lester) Harris of Salineville, Luella (Jim) Miller of Missouri and Brenda (Bryan) Rose of Salineville; 26 grandchildren and 31 great-grandchildren and also by a sister, Margaret Bellville of Newell.
Visitation will be held Wednesday, September 12 from 2-4 and 6-8 p.m. at Nixon Funeral Home in Newell, W.Va., where funeral services will be held at 11 a.m. Thursday, September 13, 2012.
Burial will follow at Shadow Lawn Memory Gardens, Newell, W.Va.


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Cynthia Boatright Raleigh
RE: August Schlageter
Thank you so much, I appreciate it!
Added by
Cynthia Boatright Raleigh
on Apr 08, 2013 1:49 PM
Beth Crowe
RE: Locust Hill Cemetery
I have done 15, 16, 17, 20, 21, 33, 34, 22 and 24. I did all the ones along the fence that goes around the P-5 area. I did some in P-5 and some in 26 last year until I realized you were working in that area. I'm trying to stick to the South side of the main gate so I don't duplicate what you are doing. I'm not sure where P-4 is but I may have done some there if it's close to P-5. I know I haven't gone into P-3 very much but I may have done some close to the road by P-5 hunting for shade last summer. I'm sorry if you wasted a trip. Hope this helps!
Added by
Beth Crowe
on Mar 31, 2013 2:20 PM
Glenda Barry
RE: Anna Hufnagel
Hi J.G.,
You're welcome, hope you have a beautiful day!
Added by
Glenda Barry
on Feb 27, 2013 10:17 AM
Tamara McDaniel Kincaide
RE: Johanna Moore Williamson
Thanks so much for the transfer and grave photo's of Sarah and daughter Johanna
Added by
Tamara McDaniel Kincaide
on Jan 21, 2013 9:29 AM
Tamara McDaniel Kincaide
Johanna Moore Williamson
Thanks so much for adding the photo of her marker I have searched several times without locating it and had planned another attempt soon. Thanks Tamara
Added by
Tamara McDaniel Kincaide
on Jan 20, 2013 3:48 PM
Bill Schraeder
RE: Mry Gyr
No thank you. I am not related. I was checking for a grave marker next to Joseph and Mary Gyr. There was no marker for the grave I was looking for. Bill
Added by
Bill Schraeder
on Oct 11, 2012 4:39 PM
Beth Crowe
RE: Friedericka Riebel
I should tell you, I did all the babies on the edge of the road across from P-3 and the first few rows back from that area into P-4 on the east end. I can't remember, but it was 3 or 4 rows. If it was in the shade, I took it. I think you or someone else already had some of them on but most were not so I added them.
Added by
Beth Crowe
on Jul 19, 2012 10:17 AM
Beth Crowe
RE: Friedericka Riebel
Someone has also entered information from a database too. I add pictures and make suggestions when I find different information. Some of the databases out there are not correct compared to census, birth, and death records.
Added by
Beth Crowe
on Jul 18, 2012 5:56 PM
RE: Jones
You are so welcome! I might go up there later on proble next month and take more. and probley retake Gilberth's grave stone too.
Added by
on Jul 17, 2012 10:20 PM
Beth Crowe
RE: Friedericka Riebel
I was in Section 26 according to the sign. I did the first four rows before my batteries died. (Forgot to replace my spares). I have since moved to Section 20 to avoid duplicating your efforts. I am not quite done going through the pics I took that day to check for any new ones. I took 124 pictures and have only found 2 new ones out of the first 52. It has just been so darn hot, I was looking for shade. Please let me know if there are any areas you have concentrated on so I can avoid them. Would it be safer for me to stick to the south side? Thank you for being so friendly.
Added by
Beth Crowe
on Jul 17, 2012 5:55 PM
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text:
Meg Loncharic: Mertens gives to campaign
Fairview resident Jean Belle Mertens recently made a large contribution to the Erie County Historical Society's Giving History a Home Capital Campaign.
Caleb Pifer, the group's executive director, said another $400,000 will be needed to meet the campaign's goal of $3 million. The campaign will run through the end of 2014.
Mertens' gift will fund the new archives and collections building, which will house the society's collection of 35,000 objects. The building will be known as the King Mertens Archive Building.
Mertens' late father, Eugene King, served as an officer and treasurer of Koehler Beer. The Kings and Mertens are related to the Curtze family that once lived in the historical society's Watson-Curtze Mansion at 356 W. Sixth St.
The Koehlers and Curtzes were united in marriage when Rose Koehler married Adolf Curtze, then president of the Erie Brewing Co. Their stately home, still known today as the Rose Koehler Curtze Mansion, is located at East 26th and Holland Streets.
Mertens' son, John Mertens, resides in Chevy Chase, Md., and her daughter, Mary Lou Lowry, in Chicago. They recently joined their 98-year-old mother in Erie.
The Watson-Curtze Mansion and adjacent carriage house are closed for renovations. When reopened in the spring of 2015, the project will include a visitors center, reading room, new galleries and increased storage space.
Choristers tour
The Young People's Chorus of Erie advanced choir recently returned from their annual tour. Highlights included a meeting in Washington, D.C., with U.S. Sen. Pat Toomey, who invited the group to give an impromptu performance in the rotunda of the Russell Senate Building. The choir also performed at the Pennsylvania Capitol Rotunda in Harrisburg, and for the patients at the Penn State Hershey Children's Hospital in Hershey.
On June 13, the Chorus hosted 130 guests at the Bayfront Convention Center at the annual White Party benefit.
A highlight of the event was the auction of four hand-painted conductor stands.
Musical celebration
"Let Me Be Your Star," the Erie Playhouse Youtheatre Concert, is set for July 21 and 22 at the Playhouse. The concert, which starts at 7 p.m., will feature popular Broadway, movie and TV show tunes.
Songs from "Wicked," "Pitch Perfect," "Les Mis�rables," "Beauty and the Beast," "The Book of Mormon," "Phantom of the Opera," "Kinky Boots" and many other shows will be featured.
Current and former Youtheatre participants will sing that night. They include former Youththeatre performers Allex Coles, Brandon Vogt, Devon Yates, Kyle Filbeck, Zach Hoffman, Riley Droney, Alanna Grafius, Eva Espy, Maeve Kirby, McKenna Priester, Leah Mathie, Alex Storer and Nathan Nitczynski.
The concert marks Emily Cassano's last official duty as Youtheatre education director. She will join the faculty at Penn State Behrend as the director of the theater program. In addition to teaching theater-related courses, Cassano will direct all productions at Behrend.
Chautauqua women
The Chautauqua Women's Club will celebrate 125 years during the 2014 season. Today's activities, from 1 to 5 p.m., include a silent auction, raffles, family and children's events and tours of the house, along with cupcakes and lemonade.
Garden camp
Fran Rosiak, recipient of a $1,700 American Association of University Women Community Education Grant, is coordinating a summer Garden Camp for inner-city girls ages 11 to 14, through July 18. Assisting Rosiak are Sister Pat Lupo, a member of the Order of St. Benedict and an educator at the Inner City Neighborhood Art House, and Ellen DiPlacido, of the Emmaus Grove Urban Farm. All three are certified master gardeners.
The two-week day camp, "Girls Growing with Gardening," is taking place at the Art House and nearby Emmaus Grove Urban Farm.
Academy grads convene
Peg Boniger Mitchell is organizing the committee for her 65th-year Academy High School reunion dinner in September at the Bel-Aire Clarion Hotel, 2800 W. Eighth St.
Assisting are Doreen Will Robertson, Wanda Szymanowicz, Russ Amendola, Marilyn George Moore, Joan Winarski Kuhl, Jerry Krafius and Don Hubert.
The next meeting takes place on Tuesday at the Amendola home, 306 Meade Ave., at 1 p.m.
"Our class numbered about 340 and we are sending out 163 invitations," Mitchell said. The reunion is set for Sept. 6. The following day there will be a picnic at the Our Lady of Mount Carmel picnic grounds, behind the school, beginning at 2 p.m.
Academy High closed in 1992 and reopened in the fall of 1998 as the Northwest Pennsylvania Collegiate Academy.
Incidentally, one of Peg Mitchell's six children, David Mitchell, is co-owner of All An Act productions, located in the old Columbus School auditorium, which is now called Columbus Square.
"David is satisfying his dream, while also working in the box office of the Station Dinner Theatre," Mitchell said.
POSTSCRIPT: If we could sell our experiences for what they cost us we'd be millionaires. -- Abigail Van Buren (1918-2013), columnist
MEG LONCHARIC's column appears in the Sunday Living section. Send e-mail to firstname.lastname@example.com or write to her in care of the Erie Times-News, 205 W. 12th St., Erie, PA 16534.


text:
Browsing Theses by Author "Barna, Laurentiu"
Now showing items 1-1 of 1
Barna, Laurentiu (2003-06-04)There is a continuous search for better and more natural human-computer interfaces. In the work the signal processing applications for three EMFi testing systems of human-computer interaction were implemented. EMFi was a ...
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text:
Why: The goal of the Tour de Blue bicycle ride is to raise funds to help provide free prostate cancer screenings to the poorest communities in the State of Alabama, and to increase awareness of the importance of early testing and treatment of prostate cancer. Since 2007, the Urology Health Foundation has screened thousands of men for prostate cancer for free in many Alabama counties. If an abnormality is found and the patient is unable to afford treatment, the Urology Health Foundation will assist in helping to find treatment at no cost to the patient.
How you can help: Please come out and ride the Tour de Blue. The courses are scenic, and the rest stops are staffed with happy folks eager to help you enjoy your day of cycling. Your contribution helps those who are at the greatest risk of developing prostate cancer. If you can't ride but want to donate to the Urology Health Foundation, please go to our Donate Page and give any amount you choose. Also, please consider volunteering your time; you can sign up for one of the volunteer positions at VolunteerSpot or by contacting Sherry Wilson at email@example.com. Thank you!


text:
I am terrified of heights this had me holding on tight......
Printable View
I am terrified of heights this had me holding on tight......
I have a friend who does that. Yes, he is very lean and very strong.
I'm getting dizzy
this scares the **** out of me
A few observations:
1. I wonder if he ever gets up there and says, "Man, that second cup of coffee/breakfast burrito/12 pack of beer last night was a bad idea".
2. Does he ever daydream at work?
3. Does this man make enough money to do this?
i would meet my neolithic death...
No safety harness? Did I hear him correctly!?
[QUOTE=TLoRu;981310]No safety harness? Did I hear him correctly!?[/QUOTE]
He had a safety harness, but if you watch closely, you will notice that he only uses it at certain times, usually when he stops climbing.
I was scared halfway to crying just watching that. No effing way am I going anywhere near that high.
he is very lean and very strong.


text: After launching its own e-commerce site in the U.S. just last year, fashion giant H&M has followed suit by launching an American web store for its upscale COS label. First reported last year by The Wall Street Journal, COS's U.S. debut positions H&M to compete with American labels like J.Crew – a brand whose prices are in the same ballpark and one who, like COS, tends to eschew more trendy affair in favor of tried-and-true classics and wardrobe staples. COS's Spring/Summer 2014 collection is now available online. The label is also celebrating the e-commerce launch by offering free shipping on all orders through June 30.


text:
Created in this Craftsy class
Master Palettes: Exploring Color Mixing taught by Scott Gellatly
Explore foundational color theory in oil painting as artist Scott Gellatly defines three art movement color palettes and their characteristics.
Other projects made as part of this class:
PaintingClassic Palette Still Life
PaintingThe Great Barrier Reef
PaintingMaster Palette class 1
Offer some kudos...
Join the conversation...
Ask a question...
Add your comment...
Very expressive and fun!
09/02/2014 Flag
Thank you!
10/31/2014 Flag
Good job! Your colors came out nice!
10/23/2014 Flag
Thanks! I did post the impressionist painting but didn't do the classical one
10/31/2014 Flag
Did you post your classical painting? I just did another one today, hoping it looked better than the first!
10/30/2014 Flag


text:
CHAMPION - As the superintendent of the Trumbull Career and Technical Center Board of Education prepares to retire, he will also be training his successor.
The TCTC Board of Education on Thursday unanimously accepted the resignation of Wayne McClain, who has served as superintendent since February 2002, and approved his recommendation to name Jason Gray, the center's director, as interim superintendent.
McClain recently announced plans to retire on July 31, 2013, and the board officially accepted his resignation on Thursday. He said his plan calls for him to work "alongside" Gray over the next year.
"I think it's a smart move," said Robert Faulkner, TCTC board member. "It will make the transition easier, smoother for everyone."
The board also named Mary Flint, who has served as supervisor of guidance and business, as TCTC's new director.
The only position that needs to be advertised and filled is the one Flint is vacating.
McClain, 69, came to TCTC after retiring as superintendent at the Trumbull County Educational Service Center. He has 48 years in education, 29 years as superintendent.
Gray, a former social studies teacher, also has been at TCTC since February 2002.
McClain said that the director's position at TCTC is comparable to a high school principal's post.


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A German shepherd thrown off an overpass in downtown Kansas City, Mo., earlier this year will be released from an animal clinic Wednesday.
The dog, named Lindey, suffered serious injuries to her front legs and has had multiple surgeries since she was found on Feb. 28.
Lindey is now well enough to go to a foster home. Officials said it will be more than eight weeks before she will be ready for adoption.


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Pacenti, Moniaa,1; Barzon, Luisaa,1; Favaretto, Francescaa,b; Fincati, Karinaa,c; Romano, Sarab; Milan, Gabriellab; Vettor, Robertob; Palù, Giorgioa
From the aDepartment of Histology, Microbiology and Medical Biotechnologies, University of Padova, Padova, Italy
bDepartment of Medical and Surgical Sciences, University of Padova, Padova, Italy
cCIVEN (Coordinamento Interuniversitario Veneto per le Nanotecnologie), Mestre, Venezia, Italy.
1Note: Monia Pacenti and Luisa Barzon equally contributed to this work.
Received 22 November, 2005
Revised 6 January, 2006
Accepted 12 January, 2006
Correspondence to L. Barzon and G. Palù, Department of Histology, Microbiology and Medical Biotechnologies, University of Padova, Via A. Gabelli 63, I-35121 Padova, Italy. Tel: +39 049 8218946; fax: +39 049 8272355; e-mail: email@example.com; firstname.lastname@example.com
Objective: To elucidate the pathogenesis of HAART-associated lipodystrophy, by investigating the effects of antiretroviral drugs on adipocyte differentiation and gene expression profile.
Design and methods: Analysis of gene expression profile by DNA microarrays and quantitative RT–PCR of 3T3-L1 preadipocytes treated with the nucleoside reverse transcriptase inhibitors (NRTI) lamivudine, zidovudine, stavudine, and zalcitabine, and with the protease inhibitors (PI) indinavir, saquinavir, and lopinavir during maturation into adipocytes.
Results: Under standard adipogenic differentiation protocols, PI significantly inhibited adipocyte differentiation, as demonstrated by cell viability assay and Oil Red O staining and quantification, whereas NRTI had mild effects on adipogenesis. Gene expression profile analysis showed that treatment with NRTI modulated the expression of transcription factors, such as Aebp1, Pou5f1 and Phf6, which could play a key role in the determination of the adipocyte phenotype. PI also modulated gene expression toward inhibition of adipocyte differentiation, with up-regulation of the Wnt signaling gene Wnt10a and down-regulation of the expression of genes encoding master adipogenic transcription factors (e.g., C/EBPα and PPARγ), oestrogen receptor β, and adipocyte-specific markers (e.g., Adiponectin, Leptin, Mrap, Cd36, S100A8).
Conclusions: This study identifies new genes modulated by PI and NRTI in differentiating adipocytes. Abnormal expression of these genes, which include master adipogenic transcription factors and genes involved in lipid metabolism and cell cycle control, could contribute to the understanding of the pathogenesis of HAART-associated lipodystrophy.
HAART, a treatment consisting of a combination of protease inhibitors (PI), nucleoside analogue reverse transcriptase inhibitors (NRTI), and non-NRTI, is associated with severe metabolic side-effects, including lipodystrophy [1]. The mechanism at the basis of HAART-associated lipodystrophy seems to involve dysregulation of fat cell growth and differentiation by both PI and NRTI [1–4]. In this study, we used microarray analysis to identify genes that are modulated by PI and NRTI in differentiating 3T3-L1 preadipocytes, a widely used in vitro model of adipogenesis [5].
3T3-L1 cells (clone 173, American Type Culture Collection, Rockville, Maryland, USA) were grown and differentiated into mature adipocytes according standard protocols and treated with NRTI and PI during differentiation (see Figs 1 and 2). Adipogenic differentiation and lipid content were measured by lipid-specific Oil-Red O staining. Gene expression profile of treated versus untreated 3T3-L1 cells was evaluated by DNA microarray analysis and quantitative real-time RT–PCR (See Fig. 2). For microarray analysis, polyA+ RNA was isolated from 3T3-L1 cells using Micro-Fast Track™ 2.0 Kit (Invitrogen, Milan, Italy) according to the manufacturer's instructions. For each sample, 3 μg polyA+ RNA was reverse transcribed and labelled using SuperScript II reverse transcriptase (Invitrogen), oligodT primers, and Cy3-dCTP or Cy5-dCTP dyes (Amersham Biosciences, Milan, Italy). Labelled cDNA probes were hybridized to microarray glass slides produced by CRIBI core facility (University of Padova, Italy), which contained 1 344 370 mer oligonucleotides (Operon version 1.1, designed on Mouse Unigene clusters). After hybridization, slides were washed and scanned on a Affymetrix 428™ Array Scanner (MWG-Biotech AG, Ebersberg, Germany) and the images analyzed by ImaGene 5.6 and GeneSight 4.1.6 softwares (BioDiscovery, El Segundo, California, USA). Data analysis included hierarchical clustering to group experimental conditions according to expression profile, differential regulation analysis to determine the significance of average change in expression (ratio of drug-treatment/control), and t test to determine the significance of differences between different experimental conditions. P < 0.005 was taken as significant. Microarray experiments were performed in duplicate and repeated two times. Each sample was analyzed in duplicate, including reciprocal labeling of fluorochromes.
Treatment of 3T3-L1 cells during differentiation with the NRTI zidovudine (ZDV) 10 μM and lamivudine (3TC) 20 μM, either alone or in combination, did not significantly alter cell viability and adipogenesis, as evaluated by counting the number of cells and the number adipocytes upon lipid staining (Fig. 1). At variance, treatment with the PI indinavir (IDV) 20 μM and saquinavir (SQV) 20 μM, either alone or in combination with NRTI, significantly reduced the number of differentiated cells, without any evident toxic effect, assayed by total cell counting. This effect was more evident with SQV than with IDV and in late phases of differentiation. In fact, on day 6 and 10, treatment with SQV and IDV reduced by 40% and 30%, respectively, the number of differentiated cells, which were characterized by the presence of smaller lipid droplets than control cells (Fig. 1a). A significant reduction in lipid accumulation of PI-treated 3T3-L1 cells was confirmed by spectrophotometric measurement upon Oil Red O staining (Fig. 1b). The stronger effect of PI than NRTI on adipocyte differentiation could in part be explained by the strong protein binding of PI in vivo, at variance with NRTI, which are not highly protein bound [6], and therefore the higher concentration of active PI drug in vitro.
To identify genes that were modulated in the process of adipocyte differentiation, the gene expression profile of 3T3-L1 cells grown in the presence of the differentiation medium was compared with 3T3-L1 preadipocytes grown in medium without supplementation of adipogenic factors. On day 3 of differentiation (early adipogenesis), a total of 1091 genes (8.1% of the expressed genes) were significantly altered as compared to 3T3-L1 preadipocytes. Up-regulated genes encoded adipocyte-specific transcription factors, enzymes involved in lipid and carbohydrate metabolism and adipocytokines, whereas down-regulated genes encoded mainly proteins of the extracellular matrix and cytoskeleton. On day 10 of differentiation (late adipogenesis), a total of 1084 genes were up- or down-regulated with respect to preadipocytes. Over-expressed genes included those encoding adipose tissue-specific marker and adipocytokines, such as aP2, angiotensinogen, haptoglobin, adipsin, adiponectin, CD36 antigen, and fat-specific gene 27. Under-expressed genes included those encoding Wnt signaling molecules, extracellular matrix proteins, and proteins expressed in fibroblasts (e.g., Wnt1 inducible signaling pathway proteins 1 and 2, high mobility group proteins, alpha actin, tissue inhibitor of metalloproteinase, stromal cell derived factor 1). A list of genes modulated during adipogenesis is given in Table 1.
Microarray analysis was subsequently performed to investigate the effect of antiretroviral drug combinations on gene expression profile of differentiating 3T3-L1 cells. Since the in vitro effect of antiretroviral drugs on gene expression of 3T3-L1 cells has been shown to occur mainly in the early phases of differentiation [2,7], the time point corresponding to day 3 of differentiation was chosen for microarray experiments. To analyse the effect of NRTI, 3T3-L1 cells were induced to differentiate in the presence or absence of ZDV 10 μM and 3TC 20 μM, whereas to analyse the effect of the combination of two NRTI with a PI, 3T3-L1 cells were grown in the presence of ZDV 10 μM and 3TC 20 μM, associated with either IDV 20 μM or SQV 20 μM. For each treatment protocol, the gene expression profile of drug-treated 3T3-L1 cells was compared with that of untreated (i.e., cultured in the same differentiation medium without antiretroviral drugs) 3T3-L1 cells at day 3 of differentiation. To analyse the global cellular genetic responses after the various treatments, microarray data were subjected to hierarchical clustering analysis, which showed that gene expression profiles of cells treated with the two combinations of PI–NRTI were quite similar, but markedly distinct from that of treatment with only NRTI. Moreover, drug combinations including a PI had a greater impact on cellular gene expression profile than treatment with NRTI, as suggested by the higher number of up- and down-regulated genes. In fact, when 3T3-L1 cells were treated with the combination of NRTI, a total of 58 genes were differentially regulated at 99% confidence level, whereas when cells were treated with the NRTI and IDV or SQV, the number of differentially regulated genes increased to 98 and 132, respectively. Of these genes, 44 were differently regulated and had the same expression pattern in all three treatment conditions and 26 were differently regulated in the two PI-including treatment conditions, but not in the treatment condition including only NRTI.
Of the 44 genes significantly modulated by NRTI, both alone and in combination with a PI, 32 were up-regulated by treatment, whereas 12 were inhibited (Table 2). Induced genes included transcription regulators and genes involved in signal transduction. Some of these genes showed increased expression during adipogenesis and were further enhanced by antiretroviral drugs, but others, such as Aebp-1 (adipocyte enhancer-binding protein 1) and Timp-2 (tissue inhibitor of metalloproteinase 2), were found to be repressed upon adipocyte differentiation, but markedly induced by treatment with NRTI. Aebp1 was originally characterized as a repressor of transcription of the adipocyte fatty acid binding protein gene aP2 [8], an important marker of adipocyte late differentiation. Aebp1 seems to correspond to aortic carboxypeptidase-like protein, i.e, a secreted protein associated with the extracellular matrix whose expression is induced during smooth muscle differentiation [9]. Over-expression of this protein in preadipocytes has been reported to inhibit adipogenesis [10,11] and to promote preadipocyte transdifferentiation into smooth muscle-like cells [10], even though this finding has not been confirmed by other authors [12]. Tissue inhibitors of metalloproteinase are a family of four secreted proteins (TIMP-1 to TIMP-4) that selectively inhibit matrix metalloproteinases. The proteolytic activity of matrix metalloproteinases has been hypothesized to play a critical role in the early step of adipocyte differentiation, as suggested by their differential regulation in adipose tissue and by the demonstration that inhibitors of matrix metalloproteinases decrease C/EBPβ expression and adipocyte differentiation [13].
Down-regulated genes included Faim (fas apoptotic inhibitory molecule), a negative regulator of apoptosis [14]; genes encoding transcription factors, such as Pou5f1 and Phf6; and genes encoding lipid metabolizing enzymes up-regulated in mature adipocytes, such as Hadh and Elovl3. Pou5f1 encodes a POU transcription factor expressed by early embryo cells and germ cells, whose activity is essential for maintaining pluripotency in embryonic stem cells [15]. Phf6 encodes a novel zinc finger gene of unknown function. Mutations of the corresponding human gene are responsible of the Borjeson–Forssman–Lehmann syndrome (BFLS; OMIM 301900), a X-linked disorder of intellectual disability, characteristic craniofacial features, hypogonadism, hypometabolism, obesity with marked gynecomastia, swelling of subcutaneous tissue of the face, short stature and epilepsy [16]. Hadh, which encodes hydroxylacyl–coenzyme A dehydrogenase, is a mitochondrial enzyme that catalyses a step of fatty acid β-oxidation. Over-expression of this enzyme allows the mitochondria to maintain a high rate of oxidative phosphorylation and production of ATP, whereas its down-regulation may determine cell death [17]. The Elovl3 gene belongs to the Elovl gene family coding for microsomal enzymes involved in elongation of very long chain fatty acids. Its expression is dramatically increased in mouse brown adipose tissue upon cold stimulation and this induction is under the control of PPARα, whereas it is inhibited by LXR agonists and SREBP-1 activation [18].
Some genes were modulated only by NRTI treatment, but not by treatment conditions including PI. Up-regulated genes included Bid3, an important inductor of apoptosis through the regulation of mitochondrial function and caspase-3 activation [19], whereas inhibited genes included the transcription factor Tcfcp2l3. An inactivating mutation of the corresponding human gene TFCP2L3 was identified in a large family with an autosomal dominant form of progressive non-syndromic sensorineural hearing loss [20].
Of the 26 genes significantly modulated by both treatment conditions including NRTI and a PI, but not by NRTI alone, 14 were up-regulated by treatment, whereas 12 were inhibited (Table 2). In particular, treatment with PI markedly induced the transcription factor Prdm1/Blimp1. Prdm1/Blimp1 is a transcriptional repressor with Krüppel-type zinc fingers which has been demonstrated to be essential for B-cell development [21] and, recently, also to play a critical role in the specification of mouse primordial germ cells and in the regulation of cell fate specification and morphogenetic processes [22,23]. Other genes induced by PI included those encoding extracellular matrix proteins (i.e., laminin gamma 2 and decorin), proteases (i.e., complement component 1r), and proliferins 1–3, which were found to be repressed in differentiated adipocytes. PI also induced expression of Δ-6 fatty acid desaturase (Fad2), a key enzyme in the biosynthesis of polyunsaturated fatty acids, such as arachidonic acid and decosahexaenoic acid, which is expressed in nearly all human tissues [24]. Transcription of Fad2 is induced by SREBP-1c and PPARα ligand activators [25,26], but suppressed by polyunsaturated fatty acids via inhibition of SREBP-1c [25,26] and by PPARγ agonists [27]. Increased Δ-6 desaturase activity has been associated with insulin resistance [27]. Of note is that PI dramatically induced expression of Wnt10a (wingless related MMTV integration site 10a) and repressed Lef1 (lymphoid enhancer factor 1), which are both involved in Wnt signaling pathway. Activation of the Wnt signaling pathway has been shown to inhibit the differentiation of 3T3-L1 preadipocytes by preventing the induction of C/EBPα and PPARγ [28], to block the development of white and brown adipose tissue and, in differentiated brown adipocytes, to promote their conversion to white adipocytes [29]. Wnt10a encodes a secreted signaling protein and has been demonstrated to be over-expressed in preadipocytes with decreased ability to differentiate into mature brown adipocytes [30]. The effect of Wnt signaling on adipogenesis has been shown to be mediated by both β-catenin-dependent and β-catenin-independent mechanisms [31]. LEF1 and the other members of this family of nuclear transcription factors, in response to Wnt signals, associate with β-catenin and activate Wnt-responsive target genes [32]. Analysis of Lef1-deficient mice indicated that LEF1 may have a function in epithelium-to-mesenchyme signaling networks. In fact, targeted inactivation of Lef1 resulted in a complete block of development of multiple ectodermal appendages, such as teeth, vibrissae, hair, and mammary glands [33,34]. Our results show that Lef1 expression is induced during adipogenesis and inhibited by PI, thus suggesting a role in adipocyte differentiation. In the Lef1-deficient mouse model, Wnt10a is expressed independently of Lef1 in the dental epithelium [34], in agreement with the discordant expression pattern observed in our study in adipocytes. In addition to Lef1, PI down-regulated expression of several other genes typically expressed in differentiated adipocytes and mainly involved in lipid metabolism, such as Fsp27 (fat specific gene 27), Lep (leptin), Adn (adipsin), Adipoq (adiponectin), and Pfkfb3 (inducible 6-phosphofructo-2-kinase), and already known to be inhibited by PI [2,7], as well as other genes induced during adipogenesis, but less well characterized, such as Mrap, Cd36/FAT, Hist1h4i, G0s2, and S100a8. Mrap encodes melanocortin 2 receptor accessory protein, which has been recently identified as an interacting partner of the ACTH receptor MC2R and has been supposed to have a role in the trafficking MC2R from the endoplasmic reticulum to the cell surface [35]. MRAP was first identified as a protein that is up-regulated upon differentiation of 3T3-L1 cells into adipocytes [36]. Interestingly, Mc2r is also up-regulated in 3T3-L1 cells during differentiation via PPARγ and mediates the lipolytic effects of ACTH [37]. The G0/G1 switch gene (G0s2) is involved in cell cycle regulation and has a temporal pattern of expression similar to that of Mrap, being induced during adipogenesis and further increased by PPARγ agonists [38]. CD36/FAT expression is also induced by PPARγ during adipocyte differentiation [39]. CD36/FAT mediates the uptake and accumulation of lipids in macrophages, adipose tissue and skeletal muscle [40] and its deficiency has been associated with dyslipidaemia and insulin resistance [41,42]. The role of CD36 in the pathogenesis of HAART-associated dyslipidaemia has already been investigated but with opposing findings. In fact, CD36 expression in circulating monocytes of HIV-infected patients treated with antiretroviral therapy including a PI has been reported to be reduced in a study [43], but increased in a more recent investigation in a larger population of patients [44]. Similarly, PI have been demonstrated to both inhibit [43] and induce [45] CD36 expression in different human cell lines in vitro. S100A8 belongs to the S100 family of calcium-binding proteins and, together with S100A9, is expressed in cells of the myeloid lineage where its is predominantly localized to the cytoplasm [46]. The secreted S100A8/S100A9 complex specifically binds polyunsaturated fatty acids (such as arachidonic acid) in a calcium-dependent manner [47] and interacts with CD36/FAT to facilitate cellular uptake of fatty acids [48]. Thus, PI could inhibit fatty acid accumulation and adipogenesis by down-regulation of both CD36/FAT and S100A8 expression. Indeed, polyunsaturated fatty acids, and in particular arachidonic acid, have been shown to stimulate adipogenesis probably by acting as PPARγ agonists [49]. In this context, up-regulation of Fads2 (Δ6-fatty acid desaturase) by PI could be the consequence of reduced intracellular polyunsaturated fatty acids. Finally, treatment with PI significantly inhibited expression of Esr2, which encodes oestrogen receptor β (ERβ). This result is in agreement with our findings in HIV-positive patients receiving antiretroviral therapy [50]. Our study demonstrated reduced ERβ mRNA levels in the subcutaneous adipose tissue of lipodystrophy patients, the down-regulation of ERβ expression in the adipose tissue of HIV-positive patients receiving antiretroviral therapy containing PI, and the restoration of ERβ mRNA levels after switching from PI [50]. Thus, ERβ could represent another nuclear transcription factor involved in the cascade of events triggered by PI that lead to impairment of adipocyte differentiation and metabolism. Overall, our observations with microarray experiments are consistent with previous reports which demonstrated that PI down-regulate the expression of lipogenesis genes, such as Fsp27, Lep, Adn, Pfkfb3, and Adipoq, which were reported to be repressed both in in vitro studies [2,7,51–53] and in vivo in the subcutaneous adipose tissue from lipodystrophic HIV-infected patients [7,50,54–56]. Moreover, our microarray study identifies new genes, such as Mrap, Cd36/FAT, and S100a8, that are inhibited in vitro by PI and that are also involved in adipogenesis and adipocyte function. Our results are thus in agreement with the presence of peripheral lipoatrophy in HIV-infected patients treated with PI [57]. Peripheral lipoatrophy, central fat accumulation, and lipomatosis are common problems in adult patients with HIV-1 infection on antiretroviral drugs. Many of the adverse metabolic effects associated with PI therapy, including hypertriglyceridaemia and insulin resistance, resemble those seen in patients with the rare congenital and acquired lipodystrophy syndromes [57]. Thus it has been proposed that peripheral lipoatrophy may be the primary effect caused by PI therapy, which subsequently leads to other adverse effects such as insulin resistance and many other endocrine disturbances ultimately leading to fat redistribution with an increase of the visceral fat and of lipids stored also inside the muscle fibres [58]. Therefore, the generation of the 'hypertrophic phase' in fat distribution must be seen as a secondary event linked to the alteration of the endocrine-metabolic milieu and the loss of the capacity by subcutaneous fat cells to store adequately the flux of free fatty acids within the cell and thus preferentially channelling these substrates towards other targets, which are the fat cells of the visceral area and other cells which get 'fatty', as is the case of muscle cells and hepatocytes [59]. Although what happens in vivo should be distinguished from what may be seen in in vitro models, our findings, together with the observations by others [7], support the general hypothesis of a primary damage of the subcutaneous adipose cell.
To confirm microarray results, the expression of a subset of genes modulated during differentiation and in response to treatment with NRTI and PI was further investigated using quantitative RT–PCR in a time-course experiment (Fig. 2). Overall, quantitative RT–PCR evaluation confirmed results obtained with microarray analysis. Expression of Srebp-1c, C/EBPα, C/EBPβ, and Pparγ mRNA was evaluated as early marker of adipogenesis, whereas expression of Leptin represented a marker of fully differentiated adipocytes. Among these genes, only Leptin expression was shown to be significantly modulated by antiretroviral drugs at microarray analysis and Srebp-1c probes were not represented in our microarray slides. As expected, in 3T3-L1 cells, Srebp-1c, C/EBPα, C/EBPβ, and Pparγ were rapidly and transiently induced during the early phase of adipocyte differentiation, whereas Leptin mRNA levels increased in the late phase of adipogenesis. Treatment with the NRTI ZDV and 3TC did not significantly modify expression of these genes at all time points of adipocyte differentiation, even though a slight decrease of Srebp-1c and Leptin mRNA as compared with untreated control cells could be observed during early and late adipocyte differentiation, respectively. These results are in agreement with Oil Red O staining which did not show a significant inhibition of adipocyte differentiation. At variance with NRTI, the PI SQV and IDV determined a significant inhibition of Srebp-1c, C/EBPα, Pparγ, and Leptin expression, and this inhibition was more evident with SQV than with IDV (Fig. 2). PI also determined a decrease, although not significant, of C/EBPβ transcript levels. The combination of a PI with two NRTI had the same effect on gene expression as treatment with only a PI.
Among the novel genes that microarray analysis demonstrated to be modulated by antiretroviral drugs, Mrap, Fads2, Aebp1, G0s2, Cd36 and Wnt10a were selected for further investigation using quantitative RT–PCR. These genes had different expression profiles during adipogenesis, since G0s2 was transiently induced during the early phase of adipogenesis, Mrap and Cd36 were induced during the late phase of adipogenesis, Aebp1 and Wnt10a were rapidly and markedly reduced during adipogenesis, whereas Fads2 expression remained unchanged during adipocyte differentiation. RT–PCR analysis showed that treatment with NRTI significantly increased Aebp1 mRNA levels as compared to untreated control cells, but had no effect on transcript levels of the other marker genes, thus confirming microarray results. Treatment with PI determined a marked reduction of Mrap, G0s2, and Cd36 mRNA levels and an increase of Wnt10a and Fads2 expression, both at early and late phases of differentiation. Even in this case, the association of a PI with two NRTI did not seem to modify the effect observed with the single drug treatment. The milder effect of NRTI than PI on adipocyte differentiation could in part be accounted to the relatively lower concentration of NRTI than PI used in our study. Although NRTI altered the gene expression profile in differentiating adipocytes, these effects were probably not so marked to be detectable at morphological examination and Oil Red O quantification.
The time-course experiments were replicated with different combinations of anti-retroviral drugs, including the NRTI zalcitabine (ddC) 0.2 μM and stavudine (d4T) 10 μM, which have been more strongly linked to lipoatrophy [60], and the PI lopinavir (LPV) 10 μM. Moreover, since the effects of NRTI on mitochondria and thus their presumed toxicity is time dependent, the time-course experiment was prolonged to 16 days (Fig. 3). Also with these combinations of NRTI, no significant alterations of cell proliferation or adipogenesis were observed, even after prolonged (16 days') treatment, whereas the number of differentiated adipocytes was reduced by LPV treatment. This effect of LPV on adipocyte differentiation was paralleled by abnormal expression of genes involved in adipogenesis (Fig. 3).
In this study, by microarray gene expression analysis, we identified genes modulated by NRTI and PI during early adipogenesis. We hypothesize that up-regulation of master transcription factors and modulation of the Wnt signaling pathway by PI could represent a key event leading to inhibition of adipocyte differentiation and down-regulation of expression of adipocyte-specific markers, such as adiponectin, leptin, MRAP, Cd36/FAT, and S100A8. With respect to PI, the effect of NRTI on adipocyte differentiation and gene expression profile was milder, even though NRTI modulated the expression of tissue inhibitors of metalloproteinases and transcription factors, such as Aebp1, which could play an important role in the determination of the adipocyte phenotype. As already demonstrated for ERβ [50], abnormal expression of these genes could be at the basis of HAART-associated lipodystrophy and could represent a potential target for the treatment of this syndrome.
Monia Pacenti is a recipient of a fellowship from IOV (Istituto Oncologico Veneto).
This work was supported by grants no. 40F.57 from ISS (Istituto Superiore di Sanità) and no. RSF 168/04 from Regione Veneto to Giorgio Palù, and by grant no. 2003061834_006 MIUR-PRIN to Roberto Vettor.
HAART; lipodystrophy; adipocytes; Wnt pathway; microarray analysis; nucleoside reverse transcriptase inhibitors; protease inhibitors
© 2006 Lippincott Williams & Wilkins, Inc.
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SDI's "Military Radar Market in Algeria to 2022: Market Brief" provides historic and forecast market sizing and market segmentation analysis.
SDI's "Military Radar Market in Algeria to 2022: Market Brief" provides a quantitative view of forecast market sizing and top performing categories in the market. The information in this Market Brief draws upon SDI's in-depth, primary research and proprietary databases to provide you with robust, segment specific data. It is an essential resource for professionals active across the industry value chain and for new players considering entry into the market.
- Provides key forecast statistics on Military Radar market to 2022.
- Features top performing categories in the Military Radar market in Algeria.
Reasons To Buy
- Understand the Military Radar market using SDI's market and segmentation analysis
- Identify trends in Algeria by analyzing the forecast market data
- Use the market size data to discover the future direction of the Military Radar market in Algeria
- Formulate crucial business strategies and make the right investment decisions using SDI's forecast figures.
1 Introduction
1.1 What is this Report About?
1.2 Definitions
1.3 Summary Methodology
1.4 About Strategic Defence Intelligence
2 Algeria Market Size and Forecast 2012-2022
2.1 Airborne military radar market to increase during the forecast period
2.2 Algeria expected to procure ground-based radar systems
3 Appendix
3.1 Methodology
3.2 Contact us
3.3 About SDI
3.4 Disclaimer Table 1: Algeria Military Radar Market Overview
Table 2: Major Algeria Military Radar Programs Figure 1: Military Radar Market in Algeria (US$ Million), 2012-2022
Figure 2: Military Radar Market Split by Sector in Algeria (%), 2012-2022
Figure 3: Airborne Military Radar Market Size in Algeria (US$ Million), 2012-2022
Figure 4: Ground-based Military Radar Market Size in Algeria (US$ Million), 2012-2022


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TAIPEI, Taiwan - Some liken it to a giant bamboo shoot of glass and steel. The less charitable see an outsize stack of Chinese food containers.
At 101 floors, Taipei's newest skyscraper is the world's tallest, and an ego boost for a people who feel snubbed by the world.
Reaching 1,679 feet into the sky, the Taipei 101 building is 188 feet taller than the previous record-holder, the Petronas Towers in Kuala Lumpur, Malaysia. The highest freestanding tower is still Toronto's 1,800-foot CN Tower, but Taipei 101 claims a hat trick for having the highest structural top, tallest roof and the highest occupied floor.
It also boasts the fastest elevators in the world, reaching a speed of 38 mph.
And it spells respect - or so the Taiwanese hope.
Although it is the world's first all-Chinese democracy and one of its biggest suppliers of laptops and computer chips, Taiwan can't call itself a country. China, its giant neighbor, regards it as a breakaway province, the product of an unfinished civil war, and most of the world, including the United States, refuses to recognize it or admit it to the United Nations.
"Taiwanese people are proud of their economic achievements and hope that having the highest skyscraper in the world will make the world sit up and notice this island," said Richard Lee, an independent architect not involved with the project.
Taiwanese President Chen Shui-bian recently echoed the sentiment.
"Taipei 101 is not only the tallest building in the world, it also symbolizes that Taiwan is in step with the world," he said.
Still, the building has an image problem: It stands on an island in a typhoon and earthquake belt. A quake in central Taiwan in 1999 killed more than 2,300 people. So a huge 733-ton ball near the top of the building moves about to counter strong winds and seismic vibrations.
In its base, a seven-story mall is packed with designer boutiques, gourmet restaurants and a giant screen showing fashion parades. It also has the capital's largest English-language bookstore and hopes to claim another record - for the world's highest hotel.
Cathy Yang, an executive with the Taipei Financial Center Corp., which manages the building, says negotiations are still under way with an international hotel group.
How long these records will stand is another question. East Asia has been in a virtual race to translate its economic power into ever higher skyscrapers, and Taipei 101 is likely to be eclipsed in this decade by a competitor in Manhattan - the 1,776-foot Freedom Tower replacing the World Trade Center that was demolished by the terrorism of Sept. 11, 2001.
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on October 12, 2011 - 12:01 AM
Family Sunday
Make family day a delicious one with lime chili-rubbed chicken breasts. In a small bowl, mix 2 teaspoons each chili powder and lime zest, 1/2 teaspoon coarse salt, 1/4 teaspoon garlic powder and 1/8 teaspoon cayenne pepper. Rub both sides of 4 boneless skinless chicken breasts with canola oil, then with spice mixture. Grill 10 to 12 minutes or until thickest part of breast is 165 degrees. Serve with pinto beans, coleslaw and whole-grain rolls. Buy a coconut pie for dessert.
Plan ahead: Grill enough chicken and save beans and pie for Monday.
Shopping list: Chili powder, lime, coarse salt, garlic powder, cayenne pepper, boneless skinless chicken breasts, canola oil, pinto beans, coleslaw, whole-grain rolls, coconut pie.
Heat and eat Monday
Make tacos with heated, chopped leftover chicken and pinto beans mixed with salsa. Spoon mixture into taco shells. Top with shredded 50 percent reduced-fat cheddar cheese. Alongside, add a shredded lettuce and diced avocado salad with a dollop of reduced-fat sour cream. Enjoy the leftover pie for dessert.
Plan ahead: If time permits, make Tuesday's chili tonight.
Shopping list: Salsa, taco shells, 50 percent reduced-fat cheddar cheese, lettuce, avocado, reduced-fat sour cream.
Budget Tuesday
We're always in the mood to try another chili recipe, and green chili chile's (see recipe) flavor measures up just fine. Serve it with mixed greens and cornbread (from a mix). Add chunky applesauce for dessert.
Plan ahead: Save enough chili for Thursday.
Shopping list: Canola oil, 95 percent lean ground beef, onion, chili powder, hot paprika, garlic, dark beer, salsa verde, canned diced green chiles, canned no-salt-added tomatoes, low-sodium pinto beans, 50 percent reduced-fat cheddar cheese, salad greens, cornbread mix, chunky applesauce.
Meatless Wednesday
Skip meat for vegetable paella (see recipe). Add a mixed green salad and whole-grain bread. Try peaches for dessert.
Shopping list: Olive oil, garlic, onion, fresh green beans, carrots, canned white beans, frozen green peas, fresh spinach, tomatoes, long-grain rice, vegetable broth, paprika, saffron threads, salad greens, whole-grain bread, peaches.
Kids Thursday
Make the kids happy with leftover chili over spaghetti. Top with shredded cheese. Serve with baby carrots and soft rolls.
For dessert, stir sliced bananas into instant chocolate pudding made with skim milk.
Shopping list: spaghetti, cheese, baby carrots, soft rolls, bananas, instant chocolate pudding mix, skim milk.
Express Friday
Dinner will be quick tonight with deli egg salad spread on toasted whole-grain English muffins. Top sandwiches with sliced tomatoes, lettuce and Canadian bacon. Serve with baked chips. For dessert, try plums.
Shopping list: Deli egg salad, whole-grain English muffins, tomatoes, lettuce, Canadian bacon, baked chips, plums.
Easy entertaining Saturday
Treat guests to an extra-easy and extra-tasty dinner of salmon with curried mustard sauce (see recipe). Serve the delicious entree with brown rice, sugar snap peas, a red-tip lettuce salad and baguettes.
Surprise your guests with blueberry pudding pie for dessert. Fill a graham cracker crust nearly to the top with blueberries and gently spread with a layer of vanilla pudding. Chill until pudding is set; slice and serve.
Shopping list: Salmon fillets, extra-virgin olive oil, coarse salt, pepper, low-fat plain yogurt, Dijon mustard, curry powder, lemon, brown rice, sugar snap peas, red-tip lettuce, baguettes, graham cracker crust, blueberries, vanilla pudding.
>GREEN CHILI CHILE (Tuesday)
Makes 8 servings
Preparation time: 15 minutes
Cooking time: About 1 hour
2 tablespoons canola oil
1 pound 95 percent lean ground beef
3 cups chopped onion
2 tablespoons chili powder
2 teaspoons hot paprika
10 cloves minced garlic
2 (12-ounce) containers dark beer
1 cup salsa verde
2 (4-ounce) cans diced green chiles
2 (15-ounce) cans undrained no-salt-added tomatoes
2 (15-ounce) cans rinsed low-sodium pinto beans
1/2 cup shredded 50 percent reduced-fat cheddar cheese
Heat a large Dutch oven on medium-high. Add oil and heat; add beef; cook 6 minutes or until no longer pink. Add chopped onion, chili powder and paprika; cook 6 minutes, stirring occasionally. Add garlic; cook 1 minute, stirring constantly. Stir in beer; bring to boil. Cook 15 minutes or until liquid almost evaporates. Add salsa, green chiles, tomatoes and beans; bring to boil. Reduce heat; simmer 30 minutes, stirring occasionally. (Adapted from Cooking Light magazine.)
Per serving: 309 calories, 22g protein, 8g fat (22 percent calories from fat), 2.2g saturated fat, 36g carbohydrate, 35mg cholesterol, 334mg sodium, 7g fiber.
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>VEGETABLE PAELLA (Wednesday)
Makes 4 servings
Preparation time: 15 minutes
Cooking time: 25 to 30 minutes
1 tablespoon olive oil
1 clove minced garlic
1/2 medium chopped onion
20 fresh green beans
1 diced carrot
1/2 cup drained canned white beans
1/2 cup frozen green peas
15 spinach leaves
2 medium diced tomatoes
1 cup long-grain rice
2 cups vegetable broth
1/2 teaspoon paprika
Pinch saffron threads, if desired
In a large nonstick skillet, heat oil over medium heat. Add garlic and onion; cook 5 minutes or until onion is softened. Add green beans, carrots, white beans, peas, spinach and tomatoes; cook 5 minutes or until carrots start to soften. Stir in rice, broth, paprika and saffron; bring to boil. Reduce heat; simmer gently without stirring for 15 to 20 minutes or until rice is tender and most of the liquid has been absorbed. At the end of cooking, you can remove the pan from heat; cover the paella with a damp cloth for a few minutes to allow flavors to blend. (Adapted from "The Best 30-Minute Vegetarian Recipes," Marie-Claude Morin; Robert Rose Inc., $24.95.)
Per serving: 309 calories, 9g protein, 4g fat (12 percent calories from fat), 0.7g saturated fat, 59g carbohydrate, no cholesterol, 623mg sodium, 6g fiber.
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>SALMON WITH CURRIED MUSTARD SAUCE (Saturday)
Makes 4 servings
Preparation time: 10 minutes
Cooking time: 15 to 20 minutes
1 pound salmon fillets cut into 4 portions
1 tablespoon extra-virgin olive oil
Pinch of coarse salt and pepper
1/2 cup low-fat plain yogurt
1 tablespoon Dijon mustard
1 teaspoon curry powder
2 teaspoons fresh lemon juice
Heat oven to 425 degrees. Place salmon, skin side down, in a 9-by-13-inch baking dish lined with foil. Rub each fillet with oil; sprinkle with a little salt and pepper. In a small bowl, combine yogurt, mustard, curry powder and juice; mix well; reserve half and refrigerate. Spread remaining mixture evenly over salmon. Bake 15 to 20 minutes or until cooked through and golden on top. Serve with reserved sauce. (Adapted from "The Essential Guide to Healthy Healing Foods," Victoria Retelny, RD, LDN, and Jovanka JoAnn Milivojevic; Alpha Publishing, $19.95.)
Per serving: 204 calories, 26g protein, 9g fat (42 percent calories from fat), 1.7g saturated fat, 3g carbohydrate, 55mg cholesterol, 185mg sodium, no fiber.


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@theMarket: Right Back Into the Range
The first week of earnings season is behind us. The results were not nearly as bad as investors feared. Some averages, such as the Russell small and mid-cap indexes, actually made new highs. However, all the indexes fell back into a trading range by the close on Friday.
As I suggested in my last column, on average 75 percent of companies actually beat earnings estimates. This quarter seems to be following the same pattern, at least so far. The money center banks reported pretty good numbers and even the worst of them got the benefit of the doubt from investors.
The really big moves came from the overseas markets. China, which has been a red-hot market all year, finally stumbled. After the Shanghai market closed on Thursday night (Friday, China time), the mainland regulatory authorities tightened margin rules. They also warned millions of individual investors (who have been the main players behind the stock boom) that they should not continue to borrow money or sell property to buy stocks. Some of these neophyte investors have no idea of what they are doing and yet they are buying and selling sometimes five or six times a day.
After the warning, the futures markets in Chinese stocks immediately plummeted over 6 percent, setting off a chain reaction throughout overseas markets. Aiding and abetting these China troubles, the economic woes of Greece continues to bedevil Europe.
As deadlines approach for various Greek debt payments to the IMF and the ECB, investors are worried that Greece will fail to make the deadlines. And if that happens, will European markets be facing a sudden and violent sell-off? Skittish investors decided not to wait for the outcome and instead sold European stocks on Friday by at least one percent or more. Germany was down almost 4 percent for the week.
In the meantime, this weekend the International Monetary Fund and World Bank meet in Washington, D.C. for their annual spring meeting. I expect a stream of new forecasts essentially reducing global growth to around 3 percent for the year. There may also be some commentary concerning the impact of a stronger dollar upon various economies.
At the same time, expect commentary from politicians this weekend on trade. On Thursday, the Senate agreed on the wording of a deal aimed at giving President Obama "fast track" authority to negotiate a wide-ranging trade deal with 12 countries in the Asia Pacific (excluding China). The new Trans-Pacific Partnership (TPP) would go beyond the traditional trade deals that focus on cutting tariffs and quotas. In addition, it would hammer out new rules on intellectual property, services and competition between state-owned enterprises and private competitors.
Given that Japan is the largest economy in the proposed TPP after the U.S. (which also includes NAFTA members Mexico and Canada), a lot is riding on the passage of the deal for the Japanese. Prime Minster Shinzo Abe is hoping Congress and the White House can present him with a done deal by the time he visits America on April 26. If so, expect that market to rally in response.
As for the down draft in world markets on Friday, I'm not worried. Foreign markets needed a pull back, especially in Shanghai and Hong Kong, after a quarter of remarkable out performance. Problems in Greece have been triggering sell offs in European markets since 2011. Every one of them has been a buying opportunity. I don't see this one as any different.
For those who missed putting some money to work overseas at the beginning of the year, this may be an opportunity to jump aboard. I strongly urge you to do so.
Bill Schmick is registered as an investment adviser representative with Berkshire Money Management. Bill's forecasts and opinions are purely his own. None of the information presented here should be construed as an endorsement of BMM or a solicitation to become a client of BMM. Direct inquires to Bill at 1-888-232-6072 (toll free) or email him at email@example.com.
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@theMarket: Earnings on Deck
This week launched the beginning of first-quarter earnings results for American companies. Wall Street doesn't expect much. It is bracing for a disappointing season, especially from U.S. exporters. Has the market discounted that news already?
Analysts expect that overall earnings will decline from 3 to 6 percent this quarter versus the same time last year. However, I have explained to readers how analysts play the earnings game. Well in advance of reporting, analysts revise down their earnings estimates to the point that only really out-of-touch corporate managers fail to "beat" estimates. On average, about 75 percent of companies meet or beat these lowered expectations. In which case, the markets may not experience the down draft that investors are so worried about.
Mergers and acquisitions continue to prop up the stock market and helping to keep investor's attention focused on what company will benefit from the next multibillion dollar buy out. It is a great time for corporations to acquire public assets. For most major corporations, borrowing huge sums of money is effectively free at these low to non-existent interest rates. Combined with the billions Corporate America has squirreled away on their balance sheets, it is a smart move to shop for strategic acquisitions.
Given the lead time and expense of building home grown assets, it is far easier to buy someone else's. If you throw the strengthening dollar into that equation, overseas companies seem exceptionally well-priced from the perspective of company managements on this side of the pond.
While investors fret about earnings, "Fed Heads" continue to play a guessing game on when the Fed will raise rates. Honestly, does it really matter if it is in June or September or the end of the year? In addition, economists are revising down their estimates for U.S. GDP growth for the year. In summary, the markets seem to me to be busily building a new wall of worry and you know what happens to markets when they do that. It goes up.
One reader asked if I still believe the U.S. market is the place to be, given my enthusiasm this year for buying foreign markets. The short answer is yes. Granted, year-to-date the S&P 500 Index is only up 1.6 percent, while India has gained over 5 percent, China, Japan and Hong Kong are up 14 percent, and Germany is pushing 24 percent, ex-currency.
I believe off-shore will continue to outperform, but America should see at least 5-7 percent gains by the end of the year. Most of those gains will be back-loaded toward the third and fourth quarter. But let's put this in perspective. Most U.S. indexes are only a percentage point or two from all-time highs. We need to take a break. That is all that is happening here.
All investors vacillate between fear and greed. Our natural reaction to a temporary slow-down in our market is to immediately dump it and buy what's moving, so that the feel-good euphoria of making more and more money keeps our high going. That's when you get into trouble.
It is better, in my opinion, to diversify some of your assets overseas--remembering that those are risky markets. If you have been following my advice since the beginning of the year, you already have a 10-25 percent exposure to foreign stocks, depending on your risk tolerance. Sure, in hindsight, you should have bought more so you could have scored big in just three months. But "could a, would a, should a," is a useless exercise and has no place in investing. You are doing just fine right where you are.
Bill Schmick is registered as an investment adviser representative with Berkshire Money Management. Bill's forecasts and opinions are purely his own. None of the information presented here should be construed as an endorsement of BMM or a solicitation to become a client of BMM. Direct inquires to Bill at 1-888-232-6072 (toll free) or email him at firstname.lastname@example.com.
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@theMarket: Will the Second Quarter Be Like the First?
By now you know that this year's first quarter was nothing to write home about. The benchmark S&P 500 Index managed to eke out a gain of just 0.4 percent for the quarter. The Dow posted a 0.3 percent loss, while the NASDAQ did gain 3.5 percent. Can we expect more of the same this quarter?
The short answer is yes. And that's not necessarily a bad thing. Investors have been conditioned to expect nothing but double digit gains in the stock market over the last few years. This "new normal," based on abnormally low interest rates, is coming to an end, at least in this country.
As I have written in the past, stock markets do not go straight up. Usually, we experience bouts of consolidation. Sometimes that means sharp sell-offs amounting to 10-20 percent and other times the consolidation is more benign. We may be in one of those times where markets digest previous gains by simply doing nothing for a few quarters. I would rather have that than a big sell-off any day.
But while most investors remain U.S.-centric, some foreign markets have done quite well. Back in January I made my investment case for China and Japan as well as Europe. At the time I believed (and still do) that these markets deserved your attention. That advice has paid off handsomely. China outperformed all other global markets. Japan, Asia's second best market, delivered an 8 percent return while Europe (ex-currency) gained double digits. Do I believe these foreign markets have more room to run?
China's market is climbing a great wall of worry. Their economy is slowing with the latest consensus forecast at a 7 percent growth rate for 2015. That's still far better than the rosiest forecast for our own economy at 2.5-3 percent. Chinese investors are convinced that the central government will use a combination of monetary and fiscal policy to offset this slower growth. So far that bet has paid off.
Over in Japan, where a full-fledged quantitative easing program is in full bloom, investors are buying stocks. They anticipate that their financial markets will react in a similar fashion to what occurred here in the aftermath of our QE programs. Once again that bet is paying off. Ditto for Europeans markets that saw their own QE launch in January.
Here at home the endless debate on whether, when or how much our central bank will begin to raise interest rates is a contributing factor to the underperformance of the American stock market. Today's nonfarm payroll number is a case in point. Although the stock market is closed today (in observance of Good Friday), the bond, currency and futures markets indicate that on Monday the markets will probably be down.
The economy added just 126,000 jobs, while economists were looking for at least 247,000 openings. That is the weakest growth in employment since 2013. Previous months' employments gains were also revised downward. Cold weather in the Northeast, the California dock strike and job losses in the oil patch explains the disappointing job number.
After the news the dollar fell, as did interest rates on the benchmark U.S. 10-year Treasury indicating that at least some investors believe that the Federal Reserve may now extend the timetable before raising interest rates here at home. I don't think so.
The good news is that hourly wages rose 2.1 percent, and that, I believe, is far more important to the Fed than one nonfarm payroll data point that will be revised up or down in the weeks ahead. Bottom line, however, the markets will most likely be down early next week and then earnings season will begin. Hold onto your hats.
Bill Schmick is registered as an investment adviser representative with Berkshire Money Management. Bill's forecasts and opinions are purely his own. None of the information presented here should be construed as an endorsement of BMM or a solicitation to become a client of BMM. Direct inquires to Bill at 1-888-232-6072 (toll free) or email him at email@example.com.
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@theMarket: The Fed Does It Again
Coming into this week's Federal Open Market Committee meeting, investors thought they had a handle on what the central bankers planned to do about interest rates. Once again, the Fed threw us a curve.
The bet was that the word "patient," in regard to when the Fed might raise interest rates for the first time in nine years, would be removed from the language of the FOMC policy statement. That would signal, according to Fed watchers, that the first hike in interest rates would occur as early as June.
It was a scenario that would almost guarantee that the dollar would continue to gain ground against the world's currencies, while oil continued to fall. Short-term interest rates would rise in anticipation of that move. But what happened was not quite what investors expected.
Yes, the word "patient" was removed, but Janet Yellen, the Federal Reserve chairman, made it clear that the change in wording did not mean that the Fed was suddenly "impatient" to raise rates. Quite the contrary, Yellen made it quite clear through her words and new central bank forecasts, that the Fed was in no hurry to raise rates. And, once they did, the rate rises would be far smaller than most economists expected.
Investors were once again taught the lesson that has held true since 2009 — don't fight the Fed. By the close of the market on Wednesday, the Dow was up 227 points (it had been down 100 points just prior to the 2 p.m. release of the rate decision) while the dollar and interest rates plummeted. The greenback had its greatest decline against the Euro in six years, while the 10-year Treasury note fell below 2 percent. Oil skyrocketed, as did other commodities. It was a good day for those who have been following my advice to stay invested.
Since then, however, the financial markets have continued to experience a heightened level of volatility, only now the currency world has joined the bond and stock markets in their daily gyrations. Thursday the dollar regained over one percent of its fall and then promptly gave it back on Friday. In sympathy, the stock market has run up and down alternating between acting like "Chicken Little'' and then the "Road Runner" on any given day.
I can commiserate with the day traders and HFT computers that are caught between a rock and a hard place. The Fed, by opening the door to an interest rate hike, has introduced a level of uncertainty in the markets that had not been there last week. Clearly, they plan to raise interest rates at some point. However, no one knows when. Will it be in June, September, the end of the year, or maybe even next year? That will depend on the data. Short term players can't cope with that.
All you need to know is that the Fed plans to raise interest rates in the months to come, and when they do; it will be so gradual that most of us won't even notice. The Fed also put dollar bulls on alert that the blistering pace of gains will likely be tempered in the months ahead. The dollar will continue to strengthen, but likely at a more sedate pace. That should also mean that oil (since it is priced in dollars), should see a more moderate rate of decline as well. My target for a low in the oil price is around $40/BBL and it almost reached that number last week.
As I warned readers in December, volatility will be on the upswing this year. So far that forecast has been spot on. How do you deal with volatility, by ignoring it? Stay focused on the year and not the weeks or months ahead. That's how your portfolio will profit in 2015.
Bill Schmick is registered as an investment adviser representative with Berkshire Money Management. Bill's forecasts and opinions are purely his own. None of the information presented here should be construed as an endorsement of BMM or a solicitation to become a client of BMM. Direct inquires to Bill at 1-888-232-6072 (toll free) or email him at firstname.lastname@example.com.
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@theMarket: Pay Attention to Diverging Markets
It was a turbulent week for U.S. stocks as the strong dollar and worries over possible rising interest rates spooked investors. But not all markets followed our lead. This divergence could be the beginning of a trend that could benefit your portfolio.
Normally, the American stock market is the big dog that wags the tail in international markets. When U.S. averages decline, foreign markets fall with them and vice versa. "De-coupling" occurs when the opposite happens like it did this week.
While U.S. stocks declined, both the Chinese and Japanese stock markets gained. Other Asian markets also did well, especially South Korea, which cut a key interest rate this week. So far in 2015, Japan is a clear winner, gaining 8.4 percent year-to-date, while China has trailed with only a 3.5 percent gain. However, those gains look good compared to the S&P 500 Index, which is flat for the year.
Europe, thanks to the launch of their own quantitative stimulus program, is up 15 percent so far this year but in all these cases appearances can be deceiving. If an American investor had purchased either European or Japanese shares without hedging the currency, those gains would have been much less. In the case of Europe, where the Euro has declined by 13 percent, the U.S. investors' gain is about 2 percent, still better than the U.S., but not by much.
Recently, many equity strategists are coming around to my point of view. As most readers know, I've been bullish on Japan since June, 2011, when the Nikkei was trading around 8,900, compared to over 19,000 today. Readers also know that I have reiterated my positive stand on China, Japan and Europe several times over the last year and with good reason.
The worldwide trend by central banks to lower interest rates and stimulate their slow-growing economies is having a predictable positive effect on many foreign stock markets (as it did in the U.S. over the last five years). In contrast, our own Federal Reserve Bank has wound down our stimulus program and is preparing to raise interest rates now that the country is growing again. That has triggered a rise in the dollar and demand for U.S. Treasury bonds.
All of this sounds good and it is over the long-term, but short-term it causes problems here at home. Most large U.S. companies depend on foreign markets for a healthy share of their profits. The 23 percent rise in the dollar against a basket of currencies since last June has hurt profits considerably. So much so that analysts are predicting that 2015 could be the worst year for corporate profits since 2009 (when earnings fell 5.5 percent).
I am not expecting that sort of shortfall, but first quarter 2015 profits could decline by over 2 percent and the second quarter should be down as well. And adding to the export woes, the decline in oil prices is also having a negative impact on corporations in the energy sector.
Given this wall of worry, is it any wonder that our stock market should be trapped in a trading range? So far this year we have vacillated in a range of -3 percent to 3 percent and I expect that to continue until we have more clarity on all of the above concerns. Does this mean I've turned cautious on the U.S. market?
Not at all; American corporations have coped and even prospered in a strengthening dollar environment in the past. The stock market has also done quite well when interest rates have risen throughout our history, as long as rates do not rise too much. Lower energy prices have also turned out to be a great boon for economies worldwide. All that is required is a little patience while we wait for our economy to adjust to these conditions. And as we wait, a little money in certain foreign markets is not such a bad idea.
Bill Schmick is registered as an investment adviser representative with Berkshire Money Management. Bill's forecasts and opinions are purely his own. None of the information presented here should be construed as an endorsement of BMM or a solicitation to become a client of BMM. Direct inquires to Bill at 1-888-232-6072 (toll free) or email him at firstname.lastname@example.com.
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Struma lymphomatosa (Hashimoto) is a rare type of abnormality of the thyroid gland, first described by Hashimoto in 1912.1 Because of the infrequency of its occurrence, this type of goiter has been discussed almost exclusively by pathologists who, following Hashimoto's work, occasionally have noted in certain cases the curious histology which he described. By clinicians this lymphoid infiltration of the thyroid is generally considered as a type of chronic thyroiditis, usually Riedel's struma, which it closely resembles in many respects.2 Since, however, pathologists3 occasionally report this rare condition, it is of importance that the clinical features of struma lymphomatosa be reviewed and the results of treatment noted.
The fundamental picture in struma lymphomatosa is that of a degenerative change in the thyroid gland, unaccompanied by evidence of acute inflammatory process. Microscopically one sees a diffuse lymphoid infiltration between the follicles, with the frequent formation of secondary nodules.
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