text:
After going winless last season, Greene Central�s girls have already proven this year that they�re on the road back to contention.
On Friday, defending Eastern Plains 2A Conference champion Kinston proved that the road still runs through Viking Gym.
After going winless last season, Greene Central�s girls have already proven this year that they�re on the road back to contention.
On Friday, defending Eastern Plains 2A Conference champion Kinston proved that the road still runs through Viking Gym.
Kinston gave the upstart Rams a lesson in humility, building a 29-point lead before settling for a 72-53 victory to remain unbeaten in league play.
The loss dropped GC two games behind in the conference standings.
�We came to play,� Kinston coach Hubert Quinerly said. �We knew how important this game was. We had three excellent days of practice and then we came out and took care of business.�
Two big spurts propelled Kinston to victory.
Trailing 9-8 with 1:06 left in the first quarter, the Vikings (13-4, 6-0) reeled off 11 consecutive points bridging the end of the opening period and the first three minutes of the second frame.
The advantage grew steadily until intermission, reaching a high water mark of 32-15 when Alexis Williams found Xequoijah Washington for an easy layup at the 2:26 mark of the second period.
Williams finished with just five points but dished out a game-high eight assists.
The Rams (7-10, 3-2) ended the half on a 10-4 run and trailed by 11 at the break.
�We�re a young team and we have a tendency to get a little jittery when things don�t go our way,� first-year GC coach Meredith Franklin said. �We had several close calls go against us and I think it affected our mindset.�
That was even truer in the third quarter, which ultimately decided the outcome.
GC began the second half very tentative, committing seven of its 29 total turnovers and missing 12 of its 15 shot attempts in the third quarter.
Kinston, meanwhile, started hot and opened up a 51-27 margin on back-to-back 3-pointers by Hannah Vermillion, who came off the bench to score 12 points on 5-of-7 shooting.
�Hannah played lights out,� Quinerly said. �We got into some early foul trouble and she came in and really gave us a lift.�
The lead swelled to 58-29 in the final minute of the frame. With Quinerly substituting freely in the fourth quarter, the resolute Rams made a run of their own behind the dynamic freshman duo of Malaysia Lancaster and Dasheka Mason.
Lancaster tallied 14 of her game-high 26 points in the final eight minutes while Mason contributed seven of her 21 total markers.
Their energy forced Quinerly to reinsert his starters after the Rams closed to within 61-47 with 2:56 remaining.
�We were a little intimidated at times but I think we finally realized we could play with them,� Franklin said. �I�m proud of the way our girls battled back and didn�t quit.�
Brittany Drumgoole led three Vikings players in double figures with 15. Lydia Rivers collected another double-double with 12 points and 13 rebounds.
�We played with a bit of an edge tonight,� Quinerly said. �We�re going to have to continue to play that way if we hope to stay in first place.�
Kinston travels to SouthWest Edgecombe on Tuesday while the Rams host Wilson Beddingfield.
The boys game was as lopsided as the final score indicated.
Kinston scored the first nine points, led 26-3 after one quarter and 51-13 at halftime.
The Vikings (13-2, 6-0) outscored GC by at least 15 points in every quarter except the last when they emptied their bench.
�Obviously, we played very well,� Kinston coach Perry Tyndall said. �Offensively and defensively we were outstanding and every player contributed. As a coach, I couldn�t have been prouder of the effort.�
Denzel Keyes led four Vikings players in double figures with 15. Andrew Lopez added 14, Josh Dawson 12, and Brandon Ingram 10.
No GC player scored more than eight � Curtez Braswell.
�They (Kinston) come at you in waves,� said Rams coach Jim Cole, whose team fell to 3-14 overall, 0-5 in the league. �At least we kept working hard and didn�t quit. I told our kids that Kinston is the program we�re striving to be.�
Greene Central 3 10 7 13�33
Kinston 26 25 22 20�93
RAMS (3-14, 0-5) � Braswell 8, Bynum 6, Rozelle 6, Harper 3, Jones 3, Bates 2, Biggs 2, Ormond 2, Batchelor 1, Parker , Lee-Jones, Evans.
VIKINGS (13-2, 6-0) � Denzel Keyes 15, Andrew Lopez 14, Josh Dawson 12, Brandon Ingram 10, Williams 7, Dunn 6, Jackson 6, Ham 5, Jones 5, Canady 5, Joyner 3, Taylor 2, Rouse 2, White 1, Hart.
Greene Central 9 16 6 22�53
Kinston 12 24 22 14�72
RAMS (7-10, 3-2) � Malaysia Lancaster 26, Dasheka Mason 21, Payton 4, Moore 2, Robinson, Stevens, Barrett, Campbell.
VIKINGS (13-4, 6-0) � Brittany Drumgoole 15, Hannah Vermillion 12, Lydia Rivers 12, Lofton 8, Clark 6, Addison 5, Williams 5, Washington 4, Harper 4, Tice 1, Thi.


text:
For Sale: One L.A. Gossip Blog, Gently Used. Inquire Within.
We have exciting year-end news for anyone tired of Gawker Media's steady encroachment upon your Defamer-savoring experience: We're breaking free from the mothership!
According to this report from a very reputable news source, Gawker is looking to
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We suppose this is the part in the pitch where we flaunt our impressive statistics, like anatomical measurements in a Craigslist Casual Encounters ad. But let's face it—everyone makes that crap up, anyway. Just take our word that what you see is what you get—and since our recent lap band surgery, what you see has never looked better! So no chubby chasers, OK? That's not our flavor anymore.
Interested parties whose fortunes were not affected by the Madoff Ponzi scheme should contact Gaby Darbyshire.
Happy cutthroat outbidding!
Your Raise-Needy Friends at Defamer

subset: commoncrawl


text:
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TARPON SPRINGS, Fla. — The Greeks started filing into church about 8 a.m., but I'm neither Greek nor churchgoing, so I spent the morning walking.
I started where everyone would be in a few hours: the bayou just off the downtown, where more than 70 boys ages 16 to 18 would leap into the shallow, frigid water in pursuit of a cross tossed by a Greek Orthodox elder. Whoever retrieved the cross would win good luck for himself and his family for a year. He would be a town hero, a name on everyone's lips.
Locals already were setting up folding chairs and laying down blankets around the bayou's edge. Four TV trucks were in position for their live shots. The skies were gray and the air cool. Sheets of rain had fallen overnight.
It was Jan. 6, the Christian holiday of Epiphany (or Three Kings Day, if you prefer), and the annual religious and cultural highlight in this town of 23,000. Tarpon Springs, which has one of the highest percentages of Greeks in the country, has sent its boys into the water chasing crosses on this day for more than 100 years. The merging of cross and water commemorates Jesus' baptism.
I left the gathering crowd behind and wandered to St. Nicholas Greek Orthodox Cathedral, where cops waited outside to lead the four-block procession to the bayou. Across the street, in Fournos Bakery, the woman behind the counter told me everything in the glass case was baked that morning. I got a profoundly dense, chocolate-covered baklava and spinach pie with a deliciously creamy center. She asked where I was from. I said up North.
"Are you Greek?" she asked.
"No," I said. "Just checking out Epiphany."
Greeks started moving here as sponge divers in the late 1800s, and today they largely fuel the town, with Greek restaurant after Greek restaurant and the sponge docks, a collection of small tourist-ready shops. Tarpon Springs hasn't had much of a face-lift in recent decades, but the town is better off for it. Somehow Greek heritage seems more authentic when slightly weathered.
Though sponge diving brought Greeks here, its primary industry today is tourism — that is, being full of Greeks, and it is a tourist destination for that reason alone. But if there is one day to visit Tarpon Springs, it is Epiphany. On Jan. 6, the experience is more than being a tourist; you join them for a celebration of community, history and culture.
Back at the bayou, bodies were filling in — about 12,000, according to local estimates. The proselytizers were showing up with large signs about the afterlife, and the television reporters started going to work.
I squeezed into a spot beside two local women who never miss the cross chase. No one in town does, they said, never mind that it lasts no more than 30 seconds.
"You Greek?" one of the women asked.
"Nope," I said.
A helicopter started buzzing in place overhead. Epiphany was getting serious.
Just before 1 p.m., the procession showed up — the church hierarchy, including a Greek Orthodox honcho who had flown in from New York, and the stars of the day: the teenage boys, who were shivering in bathing suits and matching white T-shirts. Some looked ready for a fight. Bowed heads on others said they clearly did not want to be there.
The religious leaders, decked in long, flowing garb, took their places at the edge of the water and began to pray. The crowd was largely respectful but murmured lightly, ready for some splashing. The leader blessed the gathering, asked the Lord for mercy and then, in an ancient, accented voice, said, "Young divers, go." The boys hurled themselves into the water and sped to a series of boats arranged as a half-moon. They took their places in the boats and prepared to launch themselves when the cross was thrown. The family behind me started guessing who would win.
One said the kid in the blue swim trunks. One picked the kid in black. Another said the one in yellow. It seemed absurd. How could they pick correctly from so many boys?
After another few minutes of prayers, the cross went skyward. Cheers erupted, and the boys tore back into the water, all frenzied arms and legs, for the chance at victory and becoming a small-town celebrity. It didn't take more than 15 seconds for a kid whose family is well-known for — go figure — running a Greek restaurant to emerge from the pack. His competitors cheered him as loudly as anyone.
And behold — it was the kid in yellow. How did that woman get it right?
"Well, we come and bet on it every year," said Heather Iacovacci, 29, who sat with her brother and sister. "But really it's about the boat and what position he's in that determines it."
And with that, the cross chase was finished. Everyone walked back to the church for a brief ceremony to praise the winner before heading to the St. Nicholas community center for Greek food and dancing.
On the way, I heard a man lament that his kid didn't win. "I tell you, he almost got it," the man said. "I think the wind blew it."
Soon, for a mere $3, we were all packed into the community center, a combination of generic auditorium and generic gymnasium. Dozens of round tables topped with white paper tablecloths quickly filled with Greeks eating gyros, spinach pies and salads topped with feta cheese.
Children and adults decked in traditional Greek garb started dancing almost immediately as a band played the familiar sounds of Eastern Europe. At the booze line, while deciding what to drink, Angelo Gavrianis, 70, who lives in Brandon, Fla., counseled me to try the ouzo.
"This is my third," he said. "I haven't even been here an hour. Hey, you Greek?"
No, I said, and ordered ouzo. The licorice flavor warmed me.
Out back, a bunch of guys who went to high school together in the 1980s smoked Marlboro Lights, passed a bottle of Crown Royal and reminisced about chasing the cross 30 years ago.
Inside, the church hierarchy sat at a table at the head of the room, but when they rose to take part in the ceremonies, two women well into their 80s grabbed baklava from the priests' plate and giggled like schoolgirls. Stealing from a priest's dessert plate? On Epiphany?
"Yes!" one of the women said. "Here, take! Powder cookie!"
She put it in my hand and watched me eat it. It was quite delicious, made even more so by its illicitness.
"You Greek?" she asked, all smiles and baklava crumbs.
I was starting to wish I were.
If you go
Tarpon Springs is about 30 miles northwest of Tampa and an easy day trip while visiting the Tampa Bay area. It might not be necessary to stay in Tarpon Springs, but accommodations there tend to be on the cheaper side, so it can make for an affordable and quiet side trip.
Eating is a must. Many of the restaurants offer similar, if not identical, menus, and quality is relatively consistent. Hellas (307 Roosevelt Blvd., 727-934-8400, hellas-restaurant.com) and Plaka (769 Dodecanese Blvd., 727-934-4752, plakatarponsprings.com are both well-regarded.
Tarpon Springs, Fla.
TARPON SPRINGS, Fla. — The Greeks started filing into church about 8 a.m., but I'm neither Greek nor churchgoing, so I spent the morning walking.


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Remont Engineering & Design Group, LLC (RED Group) is a Professional Engineering firm specializing in Control Systems and Electrical Engineering. We are located in New Orleans, Louisiana serving a nationwide client base.
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We also have an in-house UL 508A & UL 698A Listed Panel Shop where we fabricate custom industrial control panels. We strictly follow industry standards and perform extensive quality control testing to ensure control panels meet exact specifications.


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BERLIN — The foreign ministers of Germany, France and Italy on Tuesday condemned the rise in anti-Semitic protests and violence over the conflict in Gaza, saying they will do everything possible to combat it in their countries.
"Anti-Semitic rhetoric and hostility against Jews, attacks on people of Jewish belief and synagogues have no place in our societies," German Foreign Minister Frank-Walter Steinmeier, France's Laurent Fabius and Italy's Federica Mogherini said in a joint statement issued in Brussels.
The three said that while they respect demonstrators' freedom of speech and right to assemble, they will also do everything possible to fight "acts and statements that cross the line to anti-Semitism, racism and xenophobia."
Since the outbreak of violence between Israel and Hamas, participants at anti-Israel demonstrations across Germany have frequently used anti-Semitic slogans and also called for Jews to be gassed.
In France, pro-Palestinian youths have clashed repeatedly with police, and on Sunday set fire to cars, pillaged stores and attacked two synagogues in the Paris suburbs, while Italy has also seen pro-Palestinian demonstrations.
Jewish groups have expressed shock and disgust about the growing anti-Semitism in Germany and other European countries with strong Muslim communities.
"We have reached a new level of hatred and violence in all of Europe that cannot even be compared to the anti-Semitism seen during previous conflicts in Israel," said Stephan Kramer, the director of the European office on anti-Semitism of the American Jewish Committee in Brussels. "It needs to be made very clear that violence is not an appropriate means of protesting."
French President Francois Hollande met Monday with Jewish and Muslim leaders in the Elysee Palace, where he told them that fighting anti-Semitism will be a "national cause."
In Berlin, police said Tuesday they had banned pro-Gaza protesters from chanting an anti-Semitic slogan at all protests in the city.
Police spokeswoman Cosima Pauluhn also said that they were investigating a sermon last week by imam Abu Bilal Ismail calling on worshippers at Berlin's Al-Nur mosque to murder Jews. The American Jewish Committee has filed a complaint with Berlin prosecutors seeking charges.
The mosque did not immediately return calls seeking comment.
At a pro-Palestinian protest in front of the Israeli embassy in Berlin on Monday, 13 protesters were detained and police were pelted with stones. A few hours after the protest, a man set fire to his pants in front of the embassy, but the flames were quickly doused by police officers and he was taken to the hospital without suffering serious injuries. The man, whose identity was not revealed other than saying that he was stateless, is currently in psychiatric evaluation.
Angela Charlton contributed to this report from Paris.


text:
The discussion in the links provides what is basically a manifesto on the topic, but I distilled what I'm pretty sure the actual workout is to
Code: Select all
Drop weight by 30-40% between sets
Set initial weight for 10-12 unassisted reps
Do 6-8 reps after failure
Monday: chest/calf
Tuesday: shoulder/tricep
Wednesday: rest
Thursday: back/bicep
Friday: legs
Saturday: rest
Sunday: rest
Exercise sets
Leg extension machine 3
Squat/press 1
Hamstring curls 2
Pec flies 3x2 (do three sets, rest, do three more)
Incline press 1
Calf press 4
Single arm lateral 3
Shoulder press 3
Tri machine 2
Pullover machine 3
Weighted rows 2
Lat pull-down 2
Machine curl 2
I can't seem to get the formatting quite right, but you get the idea.
Anyway, has anyone tried this? Does it sound workable?


text:
K-9 cop and his partner
'Is that a dog you got back there?'
Editor's note: Do you need something to smile about? Every day, WND selects the best joke offered up by readers and contributors to its Laughlines forum and brings it to you as the WND Joke of the Day. Here is today's offering:
A postman was assigned to a new mail route and came to a gate with a sign: "Beware of parrot!"
He glances around and sure enough, there's a parrot sitting on its perch on the porch.
He chuckles to himself, opens the gate and walks right up to the porch.
He gets as far as the perch when the parrot suddenly calls out, "REX, ATTACK!"
a great joke you want to share with the world? Write it up in the WND
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Janet Jackson is Prevention's July 2012 cover girl. The magazine got the chance to sit down for a chat with the 46-year-old singer and talked about her recent weight loss, body image, love, life itself, and how she sees herself these days. "I honestly don't even know what size I am. Now it's about looking in the mirror and saying, I feel good. I feel healthy," Janet confesses. Dishing on her public weight losses and gains, Jackson told the magazine that, "I think people really connect with the idea of someone who's gained and lost we... Read More


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2010 BlueCat Screenplay Competition CALL FOR ENTRIES?? ?
Since 1998, we have built a large community of writers passionately committed to writing original, unforgettable work.?
This starts with our exchange of feedback to each writer who enters BlueCat.
This year, we've created two new awards for international screenwriters, expanded our early analysis deadlines and resubmission programs and brought back our popular title contest to further our support and find the new writer.
Winner receives $10,000
Four Finalists receive $1500 each.
The best screenplay from the UK will be awarded the Cordelia Award and will receive $2500.
The best screenplay outside the USA, Canada and the UK will be awarded the Joplin Award and receive $2500.
The screenplay with the best title submitted in November and December, as voted by the public, will receive $1000.
Nov 1 - receive analysis by November 10
Dec 1, - receive analysis by January 5
January 20 - receive analysis by February 1
Feb 1 - receive analysis by March 1
March 1 – receive analysis by March 20
SAMPLE SCRIPT ANALYSIS: http://www.bluecatscreenplay.com/script_analysis
March 1, 2010 with an entry fee of $50.
LATE: April 1, 2010 with an entry fee of $60.
Any screenplay submitted early and having received our early analysis can be resubmitted by April 1, 2010 for the reduced fee of $35.
SUBMIT YOUR SCREENPLAY: http://www.bluecatscreenplay.com
BlueCat Screenplay Competition
PO Box 2635
Los Angeles, CA 90078
Email: info @ bluecatscreenplay.com
Website: http://www.bluecatscreenplay.com
Facebook: http://facebook.com/pages/BlueCat-Scree ... 0069287677
MySpace: http://www.myspace.com/bluecatscreenplay
Twitter: https://twitter.com/BlueCatPictures
2010 BlueCat Screenplay Competition
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Academics at Prescott College
Area of Study:
Global Studies
Enabling students to think critically across disciplines
Global Studies students learn to organize people, groups, and communities to effect social or environmental change. Our graduates are making to make the world a better place by working to advance social justice and human rights initiatives.
A bachelor's degree for people who want to change the world
This competence area takes an innovative approach to the College's liberal arts and environmental mission. Students have the opportunity to understand varied cultural responses to the human condition and its environmental surroundings.
The curriculum design enables students to think critically across a number of disciplines, including: anthropology, communication, economics, history, politics, and sociology. Students pursue a combination of local and field-based courses, and explore the interwoven forces of globalism and localism in a variety of cultural settings.
Students learn in the field, among the individuals and groups working to effect change now, in settings as varied as along the US-Mexico border, among the Maasai in Kenya, and at the Kino Bay Center for Cultural and Ecological studies on the Gulf of California, Mexico.
The rich variety of extracurricular activities at Prescott College complements and enhances this competence. Student clubs and organizations that promote social justice and human rights include: the Black Student Union, Mi Familia, the Queer Student Union, and the Prescott Asian Pacific Islander Student Union. These clubs and organizations often meet in The Frantz Fanon Community Strategy Center, the hub for student organizing and activism. The center is a space for Prescott College students as well as community members to meet and organize around social and political topics. There is also a lending library and a zine library located in the center.
Want to take your education further? Be sure to ask about our accelerated, tuition-free Master's degree in Social Justice and Human Rights, or our 100% online Masters in Social Justice and Community Organizing!
Ready to find out more? Connect with an admissions counselor. You can also connect with the amazing group of inspiring people who teach our courses. Just ask your admissions counselor to setup a time for you to connect with a faculty member. They are mentors and passionate leaders with first-hand experience organizing for social change.
Academic ElementsAcademic Elements
Each fall and spring, new Prescott College students find themselves in "the classroom," the breathtaking, sometimes raw, always diverse terrains and environments of the Southwest. New Prescott students are introduced to the natural environment of the Southwest, learn about themselves and each other, and experience the educational philosophies of Prescott College during Orientation, thus beginning the journey of developing relationships with their new home, community, and academic career.
For most students, Orientation will mean a three-week Desert, Mountain and Canyon Expedition (aka Wilderness Orientation). Students, as a small community of engaged learners, will be backpacking throughout ecologically diverse locations in Arizona. Studying - Connecting - Growing. Other students will participate in a Base Camp Orientation, or Community-Based Orientation.
Follow this link for detailed information on these Orientation options: Orientation Details
First Year Experience
In their first semester, freshmen will enroll in courses addressing the concerns and challenges of being a college student. First Year Students will choose from an array of immersive semester courses - like Water in the West, Art and Ecology, Foundations of Leadership, and Introduction to Psychology and Yoga - which continue to build community, forge relationships with faculty advisors, and develop academic inquiry.
In their first semester at Prescott College, transfer students participate in Crises of the 21st Century: Research Methods & Theories. Students from environmental and social disciplines, the arts, and humanities will be introduced to theoretical and research approaches that foster ways of integrating their questions through class discussions and personal research. Students enrolled in this course will be given individual support in creating a degree plan organizing courses they are transferring with into a pathway for graduation in their chosen fields.
Degree Plan
During the first semester of their junior year, students create a degree plan, with the assistance of their faculty adviser, which sketches the academic map of their journey. It includes an overview of courses and credits earned; brief descriptions of competence, breadth, and liberal arts areas; lists of courses completed and those to be completed; a tentative Senior Project plan and description; and additional honors or experience that contribute to competence or breadth. The Degree Plan is a living document that continues to evolve throughout the student's final three terms.
Senior Project
Prescott College requires every student, not just designated "honors" students, to design and carry out an ambitious Senior Project. This Project functions as both a demonstration of competence and a culmination of the undergraduate experience. It may take the form of an ambitious research project, a collection of original creative writing, a curriculum plan and implementation, a studio art exhibition, a performance, a case or field study, or a challenging internship. Another way of thinking about the Senior Project is as a bridge between a student's undergraduate career and work after graduation. The Senior Project stands as a calling card that proclaims to graduate schools, prospective employers, and the world, "Look, this is what I'm capable of doing."
Life & Career OutcomesLife & Career Outcomes
- High School Social Studies Teacher
- Historian
- Labor and Community Organizer
- Lawyer
- Non-Profit Manager
- Social Justice Activist
Academic ResourcesAcademic Resources
Maasai Community Partnership
The Maasai Community Partnership Project is a collaboration between the Maasai Environmental Resource Coalition (MERC), a grassroots umbrella organization of Maasai human rights and conservation efforts, and Prescott College in Arizona, a liberal arts college dedicated to social and environmental justice. The MCPP was created in 2004 by Meitamei Olol Dapash, MERC Executive Director and Mary Poole, Program Coordinator of Cultural and Regional Studies faculty at Prescott College, to support the Maasai community in its efforts to sustain its culture, achieve education, and become politically and economically empowered. It is based in Maasailand, at the MCPP center near Talek in Narok District, and in Prescott and includes many members in Maasailand and Prescott.
Media Center
The Media Center at Prescott College is a resource available to all students. Our media lab features twelve Mac computers equipped with software such as Adobe Creative Suite and Final Cut Pro, in addition to tools for sound editing, photo editing, flyer making and book design. The Media Center is used for classes such as Digital Storytelling, The Documentary, and Newspaper Journalism Practicum, while serving as the headquarters of the Raven Review Newspaper.
Prescott College Library
The Prescott College Library supports the curriculum with a variety of print and electronic resources. Our library catalog reflects not only our collection but that of more than 30 other libraries in Yavapai county. A system-wide library card allows borrowers to request books from any library in the county. Online resources include millions of full-text articles available through our article databases, and over 130,000 e-books available through ebrary.More Information


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After the wet spring, we had a very dry June. We only had 1.5 in. of rain the whole month. Fortunately, we had 2 in. of rain on July 11. We have a lot of corn in northwest Ohio that is only knee high. It is going to need plenty of rain to amount to anything. The wind that came with the rain pushed a lot of corn sideways. Fortunately, the majority of it straightened up.
Because of the wet spring, none of my cornfields received preemergence herbicide, and some of my fields were really getting weedy. I was surprised when my custom applicator started spraying one night after dark. It had been windy and he waited until the wind settled down. He was using a late model John Deere sprayer with HID lighting and field mapping with automatic boom shutoff. This was a first for our farm. We have never sprayed postemerge after dark. It is one example of how new technology is actually working.
To put nitrogen on my fields I used a Clark/Clymer applicator. It was built in a factory in Pandora, only two miles away from my home. When the plant owners sold the factory before retiring, the new owners discontinued making farm equipment. Now the factory makes storage racks, and the primary customers are Walmart warehouses. I guess it is a sign of the times.
For fun I cleaned up one of my three 4020 tractors and took it to a tractor show at my county fair. They put a microphone in front of all the participants, and each person had a chance to tell about his tractor. Among other things I said that I think this tractor could possibly be going to shows 100 years from now. All it needs is someone to keep it inside and give it some exercise once in a while.
The next day I ended up in a hospital emergency room with severe hip pains. The doctor said it was from jumping on and off tractors too much. I need to put ladders on my 4020s. Both Deere and aftermarket people make them. I figure in an average day I jump on and off 30 times. It is getting more difficult because I put taller tires on the tractors to raise the drawbars to make them more compatible to modern equipment. I use the tractors to do all of my hay and straw baling. I like them so well that I have no intention of ever trading them off.


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Thayer's Greek–English Lexicon of the New Testament
by Thayer, Joseph Henry•
Harper & Brothers 1889
Joseph Henry Thayer's Greek–English Lexicon of the New Testament is one of the greatest achievements in biblical scholarship at the turn of the twentieth century. As the culmination of nearly three decades of work, it contains more than 5,000 entries, references to hundreds of grammatical and exegetical works, detailed etymology, and complete summaries of both biblical and extra-biblical word usage. The publication of the revised edition of Thayer's Greek–English Lexicon in 1889 represents a watershed event in nineteenth-century Greek lexicography, and it remains an important tool for students and scholars of the Greek New Testament more than a century after its first appearance.
Thayer's Greek–English Lexicon is a revised and translated edition of C.G. Wilke's Clavis Novi Testamenti, which was first published in 1841. After numerous revisions by both Wilke and his successor, C.L. Wilibald Grimm, Joseph Henry Thayer took over the project. Thayer devoted nearly thirty years to the translation—making thousands of revisions based on the latest Greek scholarship. The first publication of Thayer's Greek–English Lexicon appeared in 1885, and an updated edition was published in 1889—the edition available from Logos Bible Software.
Key Features
- Complete, unabridged text of the 1889 edition
- Documentation of the historical change of a word's significance
- Notes on variation in meaning in the Greek text
- Detailed discussion of synonyms in the Greek text of the New Testament
- References to hundreds of grammatical works, commentaries, and exegetical works
- Hebrew equivalents
- Etymology
- Summaries of extra-biblical word usage
- Draws from Greek texts of the New Testament, plus 340 extra-biblical authors from the ancient world
- Appendices containing borrowed words, individual words exclusive to individual New Testament writers, helpful compilation of verbs, and more
- Links to cross-references
- Fully searchable text
- All Scripture references in Thayer's Lexicon are linked to the Greek texts and English translations in your library
Praise for the Print Edition
The publication of this lexicon unquestionably brings in a new epoch for English-speaking students of the Greek Testament. . . . It will affect commentaries, sermons, Sunday school expositions, and other religious literature.
—Methodist Review
Product Details
- Title: A Greek–English Lexicon of the New Testament
- Author: Joseph Henry Thayer
- Publisher: New York: Harper & Brothers
- Publication Date: 1889
- Pages: 728
About Joseph Henry Thayer
Joseph Henry Thayer was born in 1828 in Boston. He graduated from Harvard in 1850 and from Andover Theological Seminary in 1857. From 1858 to 1864 he served as a pastor—first in Quincy, Massachusetts, then in Salem—and served as a chaplain in the American Civil War. After the war, he returned to Massachusetts to become Professor of Sacred Literature at Andover Theological Seminary, where he taught until 1882. In 1884, he began teaching New Testament criticism at Harvard.
In addition to his Greek–English Lexicon of the New Testament, Thayer was also the editor or translator of numerous works, and the author of Biographical Sketch of Ezra Abbot, The Change in Attitude Toward the Bible, and Books and Their Use. His academic achievements were recognized with honorary degrees from Yale, Harvard, Princeton, and Dublin University. Thayer died in Cambridge, Massachusetts, in 1901—sixteen years after the first publication of his Lexicon, and the same year Adolf Deissmann's Bible Studies was published, which would revolutionize New Testament lexicography.


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The Wide-Ranging Effects of Nucleoside Analogs
A Look at Mitochondrial Toxicity
- Mitochondrial Biology
- Mitochondrial Toxicity of NRTIs
- New Long-term Mitochondrial Toxicities
- Risk Factors
- Problems Ranking the NRTIs
- Beyond DNA
- Contributing Toxicities
- Reversing or Preventing Mitochondrial Toxicities
- The Big Picture
- Selected Sources
September 25, 1999: A group of French doctors report on five cases of a rare syndrome of cerebral, neurologic, and/or retinal damage in 8 of 2,000 babies born to HIV positive mothers. This large mother-child cohort had received AZT (Retrovir) or AZT/3TC (Epivir) to prevent HIV transmission during pregnancy and delivery. The babies also displayed a variety of other abnormalities in muscle, heart, pancreas, and bone marrow activity. Underlying defects in energy production also were apparent. Two of the babies died after about a year. All were HIV negative.
**October 14, 1999:**U.S. Bioscience announces the termination of a trial of their experimental nucleoside analog or nucleoside reverse transcriptase inhibitor (NRTI) lodenosine because of "serious adverse events." On October 11, one of the trial participants died due to a striking liver failure syndrome that continued to worsen for a month after he had stopped taking lodenosine. Three similar deaths occurred in the seven weeks after the remaining trial participants were taken off lodenosine. Another nine persons had to be hospitalized for monitoring and treatment. In all, 75 trial participants exhibited some sign of liver damage in blood tests.
November 11, 1999: After U.S. Food and Drug Administration (FDA) prodding, Bristol-Myers Squibb sends physicians a letter warning about the dangers of combining three of their HIV treatments: d4T (Zerit), ddI (Videx), and hydroxyurea (Hydrea). The FDA also requires that Bristol-Myers emphasize the warnings about pancreatitis (inflammation of the pancreas) in the ddI package insert.
These notices followed two cases of fatal pancreatitis in the National Institutes of Health (NIH)-sponsored trial ACTG (AIDS Clinical Trials Group) 5025 as well as two other pancreatitis-related deaths in two separate industry-sponsored trials. All four of the deceased had been taking ddI plus d4T, but only the ACTG 5025 volunteers were also taking hydroxyurea. Inflammation of the pancreas, which secretes fat-digesting enzymes as well as the hormone insulin, is an occasional serious side effect of ddI. As with neuropathy (nerve disease characterized by numbness, tingling, and/or pain in the hands or feet), which is another but a less serious ddI side effect, combining ddI with certain other drugs raises the frequency of pancreatitis. D4T and ddI have similar, reinforcing side effects while hydroxyurea acts by enhancing ddI's potency within cells.
December 3, 1999: Gilead Sciences announces they are terminating development of adefovir, a nucleotide analog -- the first HIV treatment to be rejected by the FDA. Adefovir dosage causes progressive kidney failure in many people after six months on treatment. Kidney damage is first indicated by the appearance of protein in the urine. About one-half of the people taking the drug for a year exhibit serious loss of kidney function, which is marked by high serum creatinine (a metabolic waste product of muscle activity), and low serum phosphate and bicarbonate. Fanconi's syndrome, marked by low potassium, may be life-threatening. Despite these problems, adefovir is still being studied today, as a possible treatment for hepatitis B (HBV) infection, but at a much lower, 10 mg dose; the anti-HIV trials used 120 mg and 60 mg doses.
Mitochondrial Biology
These incidents are but the latest chapters in a long story. Almost since AZT was introduced in 1987, scientists have recognized that several drugs in the NRTI class are not very specific; they block the growth of HIV but they also can be toxic to human cells, sometimes with life-threatening consequences.
NRTIs including ddI, d4T, lodenosine, and adefovir work against HIV by disrupting the function of the virus's reverse transcriptase enzyme, which converts the HIV gene set into a DNA form that inserts itself into human cell genomes. Nucleoside analog drugs are essentially defective versions of natural nucleosides (precursor compounds). Natural nucleosides are first phosphorylated (chemically reconfigured) into nucleotides and then chained together to form DNA; this is done by both reverse transcriptase and the cells' own enzymes during gene replication. The chemical structures of NRTIs lack the necessary molecular hooks to continue this process; they terminate the chain being constructed by reverse transcriptase and block the infection of new cells.
NRTIs generally do not affect construction of new DNA in the nuclei (center) of somatic (body) cells because the enzymes that drive this process in the cells have a "proofreading" mechanism that snips out the nucleoside analogs if they are inserted into a new DNA chain. There is an exception to this rule, though: the cells' weak point lies in the mitochondria, the energy-producing components of the cell.
Eons ago, at the dawn of evolution, mitochondria apparently were independent bacteria-like cells. At some point, they took up abode in larger, more advanced cells with nuclei and entered into a symbiotic relationship. Today mitochondria retain some autonomy within nearly all nonbacterial cells. These organelles, which are small pouches of deeply folded membranes, break down sugar and fat to create energy that the cell can use for its myriad chemical processes.
Hundreds of mitochondria exist in each cell and replicate independently of the cell's own proliferation. The existing mitochondria are doled out to the daughter cells during mitosis (cell division); the mitochondria then replicate in each cell according to the cell's energy needs. Yet despite their integral role within cells, mitochondria retain certain unique genes that govern the production of a very small amount of proteins and enzymes. Two to ten redundant copies of the mitochondrial genome exist within each mitochondrion in the form of circular double-stranded DNA.
Mitochondrial genes are particularly prone to damage. DNA polymerase gamma, the enzyme that directs replication of the mitochondrial genes, is more primitive than the DNA polymerase enzymes found in the cell nucleus. Polymerase gamma has no "proofreading" function, so little repair of errors occurs when stringing nucleotides together. Nucleoside analogs therefore inhibit DNA polymerase gamma in the same way they do reverse transcriptase.
Mitochondria rely on their genetic redundancy to protect against errors in their genes. Defective DNA coexists and replicates alongside correct DNA, which covers for the defect. Similarly, functional mitochondria can compensate for defective mitochondria within the same cell.
The system breaks down only when damaged mitochondrial DNA reaches a threshold proportion somewhere above 70%. Cells then begin to suffer from energy deficiencies and turn increasingly to anaerobic processes (i.e., without using oxygen) outside the mitochondria. Anaerobic respiration is much less efficient than mitochondria's oxidative phosphorylation (use of oxygen to break down sugar and fat); furthermore, it causes the production of lactic acid, a substance that reduces the normal pH of blood.
The oxidative process in mitochondria also gives rise to toxic byproducts. These are reactive oxygen species (ROS), which are highly reactive forms of oxygen (O2-, H2O2, and OH-). ROS damage DNA and other molecules; they are produced when energy production is inhibited mid-stage. Antioxidant molecules (superoxide dismutase and glutathione) within mitochondria are supposed to eliminate ROS by reducing them to water while transferring their extra electrons to metals. However, this process is not always effective enough to prevent oxidative stress (increased levels of free radicals and other molecules, resulting in cell damage). A gradual buildup of dysfunctional mitochondria due to ROS reactions with mitochondrial DNA is thought to be one of the processes central to aging.
Mitochondrial Toxicity of NRTIs
Specific disease syndromes are also connected with rare inherited mitochondrial mutations. Mitochondria-related diseases vary in severity from person to person, and symptoms frequently appear only as a person ages. Tissues such as muscles and nerves, which require high levels of energy, are most often involved. Some of the specific conditions related to inadequately low mitochondrial activity are muscle wasting (myopathy); heart failure (cardiomyopathy); peripheral numbness and pain (neuropathy); generalized loss of the kidney's ability to filter the blood (proximal renal tubular dysfunction or Fanconi-like syndrome); low blood cell counts (anemia, leukopenia, thrombocytopenia, or pancytopenia); swelling and fatty degeneration of the liver (hepatomegaly with steatosis); and pancreatic inflammation (pancreatitis). Fatigue, psychological depression, and high lactic acid levels (lactic acidosis) are more generalized signs.
Researchers reported a connection between myopathy and AZT in 1990. A year later an article was published associating AZT with heart muscle damage in particular. Other signs of mitochondrial toxicity were associated with NRTIs in the years that followed. Why different NRTIs have different effects and why different individuals have varying sensitivity to those effects are currently unknown. The variations between individuals may relate to the mitochondrial mutations already present and to their distribution in various organs, which is not necessarily uniform.
The varying sensitivity of different tissues to specific NRTIs presumably arises from variations in the penetration of those drugs in different cells and the energy requirements of those cells. For example, adefovir selectively and severely affects kidney cells because it binds to a kidney cell transporter molecule (hOAT1). This binding causes adefovir to build up inside the cells lining the walls of renal tubules, where unwanted compounds are transferred from the blood to the urine.
D4T and ddC represent two critical cases in which mitochondrial-associated toxicity -- in these cases, neuropathy -- was noted to be so severe that dose levels had to be greatly restricted during research and development. Both compounds originally tested as highly potent antiretroviral agents. In the case of d4T, trials originally included daily doses as high as 900 mg. Trial participants reported immediate improvements in their health, but two-thirds were forced to quickly abandon the drug due to severe neuropathy.
In the end, the committee monitoring the large d4T parallel track program found that even 40 mg twice daily was too much; about a quarter of the persons taking that dose quit the parallel track program because of neuropathy. The development of neuropathy was noted to be mediated by CD4 cell count, i.e., the condition was more prevalent among people with lower CD4 cell counts. Peripheral neuropathy also developed after an average follow-up of 79 weeks in one-half of the participants in a d4T monotherapy trial who were using 40 mg twice daily. Nonetheless, 40 mg twice a day became the standard dose.
FDA-approved package inserts for all NRTIs carry a prominent warning that describes the potential side effect of liver degeneration. Specifically, the inserts warn: "Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs alone or in combination ... A majority of these cases have been in women. Obesity and prolonged nucleoside exposure may be risk factors." This hepatic degeneration resembles "acute fatty liver" of pregnancy, a maternal syndrome that threatens both mother and fetus and results from an inherited fetal inability to oxidize fatty acids in the mitochondria.
These warnings about liver degeneration are based on isolated incidents that were reported to occur after drug approval. It is difficult to say how frequent they are now. A 1989-1994 review of persons seen at Johns Hopkins' HIV Clinic recorded an incidence of 1.3 per 1,000 person-years of severe cases of hepatomegaly with steatosis and lactic acidosis. (The number of persons multiplied by the number of years equals person-years; e.g., one person followed for ten years equals ten person-years and ten persons followed for one year also equals ten person-years.) A more recent French study found a frequency of 8.4 per 1,000 person-years for symptomatic high lactic acid levels.
In the case of ddI, the incidence of severe pancreatitis has decreased in recent years as people's overall health has improved with the success of potent anti-HIV regimens. Frequent monitoring should be done to detect the presence of pancreatic enzymes in the blood -- an early sign of possibly developing pancreatitis. Sometimes, however, this condition develops rapidly and without forewarning; doctors therefore should not let their guard down. Somewhat alarmingly, the precise risk factors predisposing an individual on ddI to pancreatitis, as with other mitochondrial toxicities, remain unexplored. The effects of combining ddI with other drugs such as d4T and hydroxyurea also have come as a surprise. Even more surprising is that this situation emerged after a decade of testing and marketing ddI. Overall, more adverse effects are seen in the setting of alcohol abuse.
NRTIs rarely inflict severe mitochondrial damage -- with a few exceptions, notably adefovir's impairment of the kidneys; ddI, d4T and ddC's neuropathy; and high-dose AZT's anemia. Frequent monitoring of organ function through lab tests (specifically, tests of liver function, phosphorus, and carbon dioxide, as well as complete blood counts) usually can prevent serious outcomes. Monitoring serum lactate, while somewhat difficult because the test must be conducted immediately after blood is drawn, may also be useful, as indicated by one recent, preliminary report by Marianne Harris, MD, from the British Columbia Centre for Excellence in HIV/AIDS. Also, stopping the drugs commonly results in gradual recovery, probably because mitochondrial replication restores energy production. However, the FDA continues to receive reports of deaths from lactic acidosis, although mild increases in lactic acid levels that result in fatigue may be much more common than life-threatening cases.
New Long-term Mitochondrial Toxicities
After a decade's experience with one NRTI or another, there are now three or four potent, well-established drug combinations that include protease inhibitors (PIs) or non-nucleoside reverse transcriptase inhibitors (NNRTIs). Combining these drugs also combines their toxicities in new and unfamiliar ways. More importantly, antiviral drugs are now being taken for much longer periods of time than in the past. With durable suppression of HIV caused by highly active antiretroviral therapy (HAART), the health of the individual has stabilized but residual HIV survives (see HIV Persists despite HAART, Spring 2000 BETA). Not only is this a new era in HIV therapy; it is a new era with regard to long-term toxicities.
Chronic, unsuppressed HIV infection has long been known to trigger a wasting syndrome in which people with HIV lose lean tissue mass (mostly muscle), sometimes to a life-threatening extent. Some researchers have noted that subcutaneous (under the skin) fat loss accompanies the loss of lean tissue, especially in women and overweight men. The worst deficit, it appears, has been an inability to regain lean mass lost during severe opportunistic infections (OIs).
Today, some people taking HAART have trouble maintaining or restoring proper fat distribution. Fat tends to accumulate over time around the central organs and sometimes around the back or front of the neck. Meanwhile, lipoatrophy -- the depletion of subcutaneous fat stores, especially in the limbs and cheeks -- continues.
This widespread body fat rearrangement, affecting up to two-thirds of participants in various studies, has been a curious phenomenon (see Body Fat Changes: More than Lipodystrophy, January 1999 BETA, and HAART Attack: Metabolic Disorders during Long-Term Antiretroviral Therapy, April 1999 BETA). It was assumed at first that the new PIs were responsible for this "lipodystrophy" (now sometimes also referred to as HARS, HIV-Associated Adipose Redistribution Syndrome).
After the first flood of reports, physicians began to recall that they had seen some cases of fat accumulation at the base of the neck and between the shoulder blades (dorsocervical fat pads, commonly called "buffalo humps") in the pre-HAART days. This buildup sometimes was accompanied by lipoatrophy. In addition, there is a marked similarity between HAART-associated lipodystrophy and a form of multiple symmetrical lipomatosis (abnormal fat accumulations), also known as MSL or Madelungs disease. Both syndromes involve peripheral fat loss and buffalo humps. Persons with MSL do not have fat deposits in the torso, but they do exhibit neuropathy. Several reports indicate that mutations at a particular point in the mitochondrial DNA accompany MSL.
A recent survey of body fat abnormalities in Australia's HIV positive population recorded an overall prevalence of 54%, including 63% of those who had taken PIs and 32% of those with exposure to treatments that did not include PIs. The same research group, headed by Andrew Carr, MD, and David Cooper, MD, of St. Vincent's Hospital in Sydney, went on to compare 14 men receiving NRTIs only who were experiencing peripheral fat loss with or without fat accumulation with three different control groups without lipodystrophy. These three control groups were comprised of 32 treatment-naive men, 28 men on NRTIs only, and 44 men receiving NRTIs plus PIs. A fourth comparison group contained 102 men with lipodystrophy who were taking both NRTIs and PIs.
The NRTI-only cases of lipodystrophy were distinguished by higher lactic acid levels, which correlated with losses in body weight and signs of liver dysfunction. These signs included swollen livers and elevated liver enzymes in the blood, all of which are suggestive of mitochondrial toxicity.
Liver toxicity has particular implications for aggravating mitochondrial toxicity, since one of the roles of the liver is to remove lactic acid from the blood. Liver function is critical for fat metabolism, too, given that organ's central role in converting excess blood lipids (fats) into glucose (sugar) or vice versa as required by the body's activity level and dietary intake. PIs can lead to high lipid and insulin levels.
Recent weight loss, fatigue, and nausea were significantly more common in the Australians' NRTI lipodystrophy group than in the combined therapy lipodystrophy group. The lipodystrophic men on PIs had higher blood levels of lipids (cholesterol and triglycerides), glucose, and insulin than did their counterparts on NRTIs only.
Body shape alterations were similar in the two groups. However, in a study done in France by L. Maulin, MD, and colleagues, this was not the case. The French researchers found that those on PI-containing regimens had markedly more visceral (abdominal) fat than those either on NRTIs only or taking no anti-HIV drugs. Both the protease and nucleoside groups had about the same amount of subcutaneous fat, which was substantially less than in the treatment-naive group.
Risk Factors
Significant risk factors for lipodystrophy in the Australian study included current use of d4T and the number of years on any NRTI. Each year of NRTI use increased the risk of lipoatrophy 1.26-fold. In contrast, each year of PI use trebled the risk of any form of lipodystrophy. Discontinuing NRTIs led to reductions in blood lactic acid and liver enzymes, nausea, and fatigue, but lost weight was not recovered (over an average four months of follow-up).
The French study also showed a strong association between lipoatrophy and d4T. In 1999, the same researchers reported on what happened when 29 persons with peripheral fat wasting were taken off d4T and switched to another drug(s). Fourteen who were also receiving a PI changed from d4T to AZT or abacavir (Ziagen). The rest replaced their d4T-containing NRTI regimen with AZT/3TC/nevirapine (Viramune). After six months, blood triglyceride levels decreased by approximately 40% in both groups while subcutaneous fat rose 40%.
Problems Ranking the NRTIs
Glaxo Wellcome, the maker of AZT, 3TC, and abacavir, is quick to point to such studies. Whether d4T is especially culpable in lipoatrophy has yet to be decisively documented, however. Most persons on d4T have taken AZT previously and have lived longer with HIV infection.
Likewise, laboratory studies that attempt to rank the different NRTIs' respective mitochondrial toxicity are open to question since they may not reflect what happens in living cells in the body. There, toxicity is determined not just by the drugs' chemical inhibition of DNA polymerase gamma, but also by the concentration of each compound within mitochondria and the ease with which it is activated via phosphorylation (addition of a phosphate group) before DNA polymerase can process it.
The energy demands of cells in the body, for which they rely on their mitochondria, are yet another decisive factor in eliciting the NRTIs' inhibition of mitochondrial activity. Gender and HIV infection itself are major factors that influence the metabolic and, hence, the energy profile of cells throughout the body.
Beyond DNA
NRTIs also may have other effects on mitochondrial metabolism besides interference with DNA replication. For example, while lodenosine seemed to have little effect on mitochondrial DNA in lab tests, it causes serious heart toxicity in mice and fatal liver toxicity in humans in a way that resembles mitochondrial failure. This NRTI in fact does disrupt mitochondrial functioning, as evidenced by the heightened lactic acid levels and death in laboratory cell lines exposed to it. According to Yung-chi Cheng, a Yale University researcher who did the original mitochondrial assays on lodenosine, its toxic effect probably results from inhibition of lactic acid dehydrogenase, an enzyme that converts lactic acid into a compound that the mitochondria can oxidize.
A parallel situation exists for AZT, claims a recent study conducted in a laboratory liver cell line by Jean-Pierre Sommadossi, PharmD, and colleagues from the University of Alabama. Unlike ddC and ddI, AZT did not inhibit mitochondrial DNA synthesis in this case, but AZT increased lactic acid production in cell cultures whereas other NRTIs did not. The researchers found that exposure to AZT directly reduced the activity of several of the mitochondria's major energy-producing enzymes. This was thought to be the reason for the contradictory results.
Contributing Toxicities
At this past spring's Keystone Symposium on New Biological Approaches to HIV-1 Infection, Scott Raidel of the Department of Pathology at Emory University showed striking photos of mitochondria in the heart muscle of mice bioengineered to contain a gene for the Tat protein of HIV; the mitochondria were extremely elongated and their internal structures disrupted. That is, mice that were given genetic implants so that they developed higher levels of the Tat protein were then observed to have significant mitochondrial damage. Their DNA content was about 30% lower than in normal mice.
When NRTIs enter the body, they encounter an environment that may be already prone to the type of mitochondrial damage that these drugs promote. Tat is a protein that helps convert the HIV DNA genome within cells back into RNA for packaging in a new generation of virions (complete virus particles). Among other things, it suppresses the cells' antioxidant protective system, rendering them more sensitive to inflammatory activation by such cytokines as tumor necrosis factor (TNF). (Cytokines are hormones or messenger proteins that coordinate immune system responses.) Uninfected cells in lymph nodes are chronically exposed to Tat and suffer the effects of oxidative stress. Many die with swollen effects.
One widely advertised agent that has some effect in countering the anemia associated with certain NRTIs is erythropoietin (Procrit), a growth factor that stimulates red blood cell production. Erythropoietin helps reverse anemia caused by AZT but has no effect on other sources of fatigue, including muscle weakness or high lactic acid levels associated with mitochondrial dysfunction. People taking erythropoietin must continue to be monitored for such effects, and in some cases the offending drug still must be stopped or changed.
Reversing or Preventing Mitochondrial Toxicities
There are some potential but poorly researched ways to counteract mitochondrial toxicities. The agents involved are natural cofactors for mitochondrial energy production, and supplying them might increase the efficiency of that process. For example, there have been three individual cases of treating severe lactic acidosis with large amounts of riboflavin (vitamin B2), a micronutrient that is commonly deficient in people with HIV. Other suggested treatments along these lines have been coenzyme Q10 (an antioxidant) and the vitamins B1 (thiamine), B12, and K.
Another agent that might reduce mitochondrial toxicity is replacement L-acetyl carnitine, which is itself reduced by mitochondrial toxicity. L-carnitine is a product of protein breakdown that is used to transport fat components into the mitochondria for oxidation. L-acetyl carnitine, a variant of L-carnitine, shares this function and also helps damaged nerve cells regenerate. One four-person study has now indicated that L-acetyl carnitine promotes nerve growth and reduces symptoms in people with drug-related neuropathy. (Note that L-acetyl carnitine is not the L-carnitine sold in health food stores.)
A previous Italian study, led by Andrea Cossarizza of the University of Modena, of T-cells taken from people with primary (early) HIV infection found electric charge alterations in mitochondrial membranes and noted a strong tendency for these cells to undergo spontaneous cell death. In the test tube, L-acetyl carnitine, as well as N-acetyl cysteine and nicotinamide (niacin, a B vitamin), was able to rescue the cells, which correlated with the subjects' blood HIV and TNF levels. This association with TNF suggested that the cell rescue involved a process that reversed oxidative stress.
A Spanish study, led by José Garcia de la Asunción and colleagues at the University of Valencia, has tried a similar strategy using high doses of the antioxidant vitamins C (1 g per day) and E (0.6 g per day). Chemical markers of muscle damage and oxidative stress decreased in eight HIV positive persons on AZT plus the vitamins compared with a control group on AZT alone. The same was true in a group of study mice. Examination of the mitochondria in the mice's muscle cells further showed that the mice receiving AZT plus the vitamins retained normally organized mitochondria whereas the mice on AZT alone had swollen, disrupted mitochondria.
The Big Picture
Mitochondria play a vital role in the body's metabolism; protecting mitochondria is essential to sustaining life. Although an abundance of research suggests that certain NRTIs severely disrupt specific mitochondria, the exact significance and nature of that toxicity requires further elucidation. Development of nontoxic treatments to support energy production and of safer NRTIs is critically important. However, that research is still in rudimentary stages and lacks substantial industry or government support. Worse yet, the commercial implications of present NRTIs' mitochondrial toxicity threaten to disrupt the objective scientific process.
Still, it should be noted that mitochondrial toxicity results at least in part from the use of antiretroviral drugs -- and there are risks and benefits involved with the use of most if not all drugs, not only anti-HIV medications. Simply put, when the risks outweigh the benefits, the drug in question is not used; when the benefits outweigh the risks, the drug is used. While further research and data may change the risk-benefit ratio, the benefits for the vast majority of people with HIV whose lives have been improved and extended through the use of antiretroviral therapy still far outweigh the risks.
Dave Gilden is Director of Treatment Information Services at amfAR.
Selected Sources
Blanche, S. and others. Persistent mitochondrial dysfunction and perinatal exposure to antiretroviral nucleoside analogues. The Lancet 354(9184): 1084-1089. September 25, 1999.
Boxwell, D.E. and Styrt, B.A. Lactic acidosis (LA) in patients receiving nucleoside reverse transcriptase inhibitors (NRTIs). 39th Interscience Conference on Antimicrobial Agents and Chemotherapy. San Francisco. September 26-29, 1999. Abstract 1284.
Bridges, E.G. and others. Favorable interaction of _-L(-) nucleoside analogues with clinically approved anti-HIV nucleoside analogues for the treatment of human immunodeficiency virus. Biochemical Pharmacology 51(6): 731-736. March 22, 1996.
Brinkman, K. and others. Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy. The Lancet 354(9184): 1112-1115. September 25, 1999.
Carbonari, M. and others. Death of bystander cells by a novel pathway involving early mitochondrial damage in human immunodeficiency virus-related lymphadenopathy. Blood 90(1): 209-216. July 1, 1997. Carr, A. and others. A syndrome of lipoatrophy, lactic acidæmia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome. AIDS 14(3): F25-32. February 18, 2000.
Chen, C.H. and others. Effect of anti-human immunodeficiency virus nucleoside analogs on mitochondrial DNA and its implication for delayed toxicity.Molecular Pharmacology 39(5): 625-628. May 1991. Cossarizza, A. and others. Mitochondria alterations and dramatic tendency to undergo apoptosis in peripheral blood lymphocytes during acute HIV syndrome. AIDS 11(1): 19-26. January 11, 1997.
Dalaka, M.C. and others. Mitochondrial myopathy caused by long-term zidovudine toxicity. New England Journal of Medicine 322: 1098-1105. 1990.
Dutschman, G.E. and others. Metabolism of 2',3'-dideoxy-2',3'-didehydro-beta-L(-)-5-fluorocytidine and its activity in combination with clinically approved anti-human immunodeficiency virus beta-D(+) nucleoside analogs in vitro. Antimicrobial Agents and Chemotherapy 42(7): 1799-1804. July 1998.
Fortgang, I.S. and others. Hepatomegaly and steatosis in HIV-infected patients receiving nucleoside analog antiretroviral therapy. American Journal of Gastroenterology 90(9): 1433-1436. September 1995.
Fouty, B. and others. Riboflavin to treat nucleoside analogue-induced lactic acidosis. The Lancet 352(9124): 291-292. July 25, 1998.
Garcia de la Asunción, J. and others. AZT treatment induces molecular and ultrastructural oxidative damage to muscle mitochondria: prevention by antioxidant vitamins. Journal of Clinical Investigation 102(1): 4-9. July 1998.
Harris, M. and others. Lactic acidosis complicating antiretroviral therapy: frequency and correlates. 3rd International Workshop on Salvage Therapy for HIV Infection. Chicago. April 12-14, 2000. Abstract and oral presentation 34.
Harris, M. and others. Physiologic disturbance among HIV positive patients with elevated random venous lactic acid levels on antiretroviral therapy. 3rd Salvage Therapy Workshop. Abstract and oral presentation 35.
Hart, A.M. and others. Immunohistochemical quantification of cutaneous innervation in HIV-associated peripheral neuropathy: a study of L-acetyl carnitine therapy. 3rd Salvage Therapy Workshop. Abstract 36.
Ibdah, J.A. and others. A fetal fatty-acid oxidation disorder as a cause of liver disease in pregnant women. New England Journal of Medicine 340(22): 1723-1731. June 3, 1999.
Kotler, D.P. and others. Studies of body composition and fat distribution in HIV-infected and control subjects. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 20(3): 228-237. March 1, 1999.
Kulkarni, P.M. and others. Lactic acidosis and hepatic steatosis in HIV seropositive patients treated with nucleoside analogs. Digestive Disease Week 2000. San Diego, CA. May 21-24, 2000. Abstract and poster 95.
Lewis, W. and others. Mitochondrial ultra-structural and molecular changes induced by zidovudine in rat hearts. Laboratory Investigation 65: 228-236. 1991.
Lewis, W. and Dalaka, M.C. Mitochondrial toxicity of antiviral drugs. Nature Medicine 5(1): 417-422. January 1999.
Lo, J.C. and others. "Buffalo hump" in men with HIV-1 infection. The Lancet 351(9106): 867-870. March 21, 1998.
Luzzati, R. and others. Riboflavin and severe lactic acidosis. The Lancet 353(9156): 901-902. March 13, 1999. Maulin, L. and others. Emerging complication of antiretroviral therapy: symptomatic hyperlactatemia. 39th ICAAC. Abstract 1285.
Miller, J.E. and others. The Australian prevalence survey of lipodystrophy syndrome. 7th Conference on Retroviruses and Opportunistic Infections. San Francisco. January 30-February 2, 2000. Oral presentation 201.
Mulato, A. and others. Nonsteroidal anti-inflammatory drugs (NSAIDs) are protective against the in vitro cytotoxicity of adefovir (ADV) mediated by the human renal organic anion transporter 1 (hOAT1). 7th CROI. Abstract 64.
Mulligan, K. and others. Cross-sectional and longitudinal evaluation of body composition in men with HIV infection. Journal of Acquired Immune Deficiency Syndromes 15(1): 43-48. May 1, 1997.
Pan-Zhou, X.R. and others. Differential effects of antiretroviral nucleoside analogs on mitochondrial function in HepG2 cells. Antimicrobial Agents and Chemotherapy 44(3): 496-503. March 2000.
Parker, W.B. and Cheng, Y.C. Mitochondrial toxicity of antiviral nucleoside analogs. Journal of NIH Research 6: 57-61. March 1994.
Purnell, J.Q. and others. Effect of ritonavir on lipids and post-heparin lipase activities in normal subjects. AIDS 14(1): 51-57. January 7, 2000.
Raidel, S. and others. HIV-1 tat construct targeted to adult cardiac ventricular myocytes alters heart structure and function. Keystone Symposium on Novel Biological Approaches to HIV-1 Infection Based on New Insights into HIV Biology. Keystone, CO. April 4-10, 2000. Abstract 457.
Saint-Marc, T. and others. The effects of discontinuing stavudine therapy on clinical and metabolic abnormalities in patients suffering from lipodystrophy. AIDS 13(15): 2188-2189. October 22, 1999.
Saint-Marc, T. and others. Fat distribution evaluated by computed tomography and metabolic abnormalities in patients undergoing antiretroviral therapy: preliminary results of the LIPOCO study. AIDS 14(1): 37-49. January 7, 2000.
Savès, M. and others. Severe hepatic cytolysis: incidence and risk factors in patients treated by antiretroviral combinations: Aquitaine cohort, France, 1996-1998. AIDS 13(17): F115-121. December 3, 1999.
Savès, M. and others. Factors related to the presence of fat redistribution in HIV-infected patients treated with protease inhibitor (PI)-containing regimens: APROCO cohort, 1999. 7th CROI. Poster 14.
Tsai, C.H. and others. Effect of anti-HIV 2'-beta-fluoro-2',3'-dideoxynucleoside analogs on the cellular content of mitochondrial DNA and on lactate production. Biochemical Pharmacology 48(7): 1477-1481. October 7, 1994.
Wallace, D.C. Mitochondrial diseases in man and mouse. Science 283(5407): 1482-1488. March 5, 1999.
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Difference between revisions of "Fujitsu-Siemens Amilo Se 1520"
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This info may be helpful in addition to the Arch Linux Installation guide.
This info may be helpful in addition to the Arch Linux Installation guide.
Revision as of 12:53, 23 April 2012
This info may be helpful in addition to the Arch Linux Installation guide.
- CPU: Intel Core 2 Duo 1800Mhz, 1024MB ram, 60Gb SATA HD, CD-RW/DVD-RW (QSI).
- Video: Intel Mobile 945GM/PM/GMS/940GML
- Touchpad: Synaptics Mouse
- wifi: ipw3945
- Audio: HDA Intel
- Broadcom 440x 10/100 and Intel PRO/Wireless 2200GB.
- 4 USB ports
- Firewire
- Bluetooth
- 1 card slots.
Works, perfectly
You will need following packages:
- 915resolution
- xf86-video-i810
Add 915resolution to /etc/rc.conf to DAEMONS and change /etc/conf.d/915resolution to:
# Enter the VBIOS mode to patch MODE="5c" # Enter the desired resolution RESOLUTION="1280 800"
Part of my xorg.conf with explanations:
Section "Monitor" HorizSync 31.47-128.52 VertRefresh 59.9-128.52 Identifier "LCDi" VendorName "Fujitsu" #DisplaySize 260 165 #ModeLine "1280x800" 68.9 1280 1301 1333 1408 800 804 808 816 EndSection
I was not able to configure dual head. One way is to push FN + F3 button before X server starts, and then start it. HorizSync and VertRefresh is for my external monitor. But on resolution more that 1024x768 you can see a bug: two thin lines at left and right are swapped.
Section "Device" Identifier "Card0" Driver "i810" VideoRam 131072 Option "VBERestore" "true" Option "DevicePresence" "true" EndSection
VBERestore is needed when you close and open your laptop. Without this option you will need to switch terminal in order to have a picture on your screen.
Section "Screen" Identifier "Screen_local" Device "Card0" Monitor "LCDi" DefaultDepth 24 SubSection "Display" Viewport 0 0 Virtual 1280 800 Depth 24 Modes "1600x1200" "1280x800" "1024x768" "800x600" EndSubSection EndSection
Other resolution only for external monitor. You will be able to change them with xrandr.
Works poorly in Linux. Alsa is able to determine driver, but SPDIF doesn't work and external microphone too. Luckily internal microphone (above LCD) works good, though you can't change its' volume or disable it in alsamixer.
Install the synaptics driver with
pacman -S synaptics
In xorg.conf
Section "ServerLayout" Identifier "Layout0" Screen 0 "Screen_local" 0 0 InputDevice "Keyboard0" "CoreKeyboard" InputDevice "TouchPad" "CorePointer" InputDevice "ExtMouse" "SendCoreEvents" EndSection Section "InputDevice" Identifier "TouchPad" Driver "synaptics" Option "Protocol" "Auto" Option "Emulate3Buttons" Option "Device" "/dev/input/mouse0" Option "VertEdgeScroll" "true" Option "HorizEdgeScroll" "true" Option "SHMConfig" "true" EndSection Section "InputDevice" Identifier "ExtMouse" Driver "mouse" Option "Protocol" "Auto" Option "Device" "/dev/input/mice" EndSection
If you just change Driver to synaptics, external mouse will not work at all. This way you will have external mouse working and horizontal scrool on touch pad.
Also, I would recommend you to add following in ~/.xinitrc:
syndaemon -i 0.5 -d
It will disable touch pad, while you typing.
Fortunately, we have Linux native driver ipw3945, just install it and use wifi-radar
You will need to install powersave and add "powersaved" into /etc/rc.conf.
not tested
not tested
Alt+Function key commands work ok, but the special buttons on the left side of the keyboard do not work out of the box.
not tested
External Links
- This report is listed at the TuxMobil: Linux Laptop and Notebook Installation Guides Survey: Fujitsu-Siemens - FSC.
- See my personal page about, feel free a help