text: A while back on another list I was advised that auth.log (and syslog and a few others) are rotated by /etc/cron.weekly/sysklogd. I'm now interested in running a Perl program to generate a report from auth.log just before each rotation. Should I just insert my report-generating command into that file at one of the points marked below? Thanks, Adam #! /bin/sh #[comments snipped] test -x /usr/sbin/syslogd-listfiles || exit 0 test -x /sbin/syslogd || exit 0 test -f /usr/share/sysklogd/dummy || exit 0 set -e cd /var/log # insert the following? <------- /path/to/my_report auth.log |mail -s 'auth.log report' root for LOG in `syslogd-listfiles --weekly` do if [ -s $LOG ]; then # or is it safer to do it here? <------- if [ "$LOG" == "auth.log ]; then /path/to/my_report auth.log |mail -s 'auth.log report' root fi savelog -g adm -m 640 -u root -c 4 $LOG >/dev/null fi done # Restart syslogd # /etc/init.d/sysklogd reload-or-restart > /dev/null


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Study finds 15 common bee species suffer as temps rise
Staff Report
The urban heat island effect isn't just bad for people — it's also harming bees, according to a new study from North Carolina State University.
"We looked at 15 of the most common bee species in southeastern cities and – through fieldwork and labwork – found that increasing temperatures in urban heat islands will have a negative effect on almost all of them," said associate entomology professor Steve Frank.
"What's exciting is that we were able to use a relatively easy lab test on individual bees to predict how whole populations will fare at higher temperatures in urban areas," says Elsa Youngsteadt, a research associate at NC State and co-lead author of the paper. "This is a tool we can use for additional bee species in the future, giving us insights into how urban warming affects ecosystems."
The researchers established threshold maximum temperatures for 15 bee species in the lab, heating the insects in test tubes until they became incapacitated.
"After measuring the CTmax values, we still didn't know whether the way individual bees responded to temperature in the lab would correspond to how bee populations respond to higher temperatures in messy, real-world habitats," Youngsteadt says.
To address this question, the researchers sampled bee populations 11 times over two years at 18 urban sites in Wake County, North Carolina.
The researchers found that the response of the 15 bee species studied in the lab corresponded to each species' abundance in urban yards. In other words, the lower a species' CTmax, the more its numbers declined with urban warming.
"This is certainly relevant for urban heat islands, but it may also help us understand potential effects of global climate change on bee species," Youngsteadt says. "If species that have a lower CTmax are most sensitive to urban warming, they may also be most sensitive to warming in other environments."
The research was published in the Royal Society journal Biology Letters.


text:
This recipe for Sweet and Tangy Cocktail Meatballs is sponsored by Peapod. All opinions are 100% mine.
Hosting a Super Bowl party this weekend? If so – you really must add these Sweet and Tangy Cocktail Meatballs to the menu!
These easy turkey meatballs are packed with flavor, and that sauce?!? It's so good, you'll want to eat it with a spoon.
You can prepare these Sweet and Tangy Cocktail Meatballs ahead of time. Then, about an hour or so before your guests arrive, just place them in a slow cooker to heat through and keep warm through the entire game. (How easy is that?)
I think the best game day party menu should be filled with lots easy and delicious foods. After all, I want to watch the game – not slave over a stove!
And to make our party prep even easier, we order all of our groceries, snacks and beverages from Peapod grocery delivery. I just place our order online or via their mobile app, then schedule delivery when it's convenient for me.
Peapod carries thousands of items – including all of your game favorites. You can order the ingredients for today's Sweet and Tangy Cocktail Meatballs recipe, a deli platter of cold cuts and cheeses, party supplies and more! Check out this very cool Super Bowl Snack Stadium video (made with groceries from Peapod of course!). This is sure to be the talk of your party!
To learn more about Peapod's grocery delivery service, visit them here.
Click here to find the recipe for these Sweet and Tangy Cocktail Meatballs. You'll also find many more delicious recipes from me and my fellow bloggers over on From the Pod.
Enjoy the game!
You may also like these game day recipes made with groceries from Peapod:
Slow Cooker Tex-Mex Chicken Stew


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Time to Wine!
A Chef Emily Ellyn Fresh Take on Fresh Mozzarella.
Love a great wine? Crave Fresh Mozzarella? You've come to the right place. In this month's Fresh take on Fresh Mozzarella, Retro Rad Chef Emiy Ellyn brings you tips on how to pair your favorite cheese with your favorite wines.


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A frequent question I read is how to attach tin accessories, such as Marx light posts and light towers, to a layout in a semi-permanent but reversible manner. I have found a way to do this, and as a bonus, it also makes it easy to hide the wires that are feeding the lights and makes the wiring simpler.
Make display shelves out of rusty track
Some people try to fix rusty track, while others argue it isn't worth the bother. But if you're in the latter camp, you still have options besides trashing it: Make display shelves out of it.
My local train shop offers questionable track to his regular customers for free whenever he gets it, rather than trashing it or selling something that an unfamiliar customer might be unhappy with. I turned down a box of O31 track recently, then came to regret it a couple of weeks later when I remembered I could have used it. But that's OK–he'll probably have more next Saturday. Or the Saturday after that if not. I had plenty of disused track in a big tub under my layout anyway.
The common post on a Marx transformer
When you want to phase transformers, it's good to know the common (in Lionel terms) or base (in American Flyer terms) post. It's a shame that Marx didn't label which of its posts was common. So here's how to find the common post on a Marx transformer.
It's a good thing this is fairly easy to figure out, because Marx transformers are dirt cheap. I bought one for exactly one dollar at the last train show I attended, and the vendor wanted to sell me a box full of them for $5.
Sakai trains: The "Japanese Marx"
Sakai trains were made in HO and O gauge by a Tokyo-based manufacturer and sold abroad, particularly in the United States and Australia after World War II. Sakai's O gauge product bore a curious resemblance to Marx. I have read speculation that Marx once used Sakai as a subcontractor, and Sakai used the tooling to make its own trains rather than returning it to Marx, but there are enough differences that I don't think that's the case.
What I do know is that Sakai's O gauge product was a curious blend of cues from Lionel and Marx and the trains worked pretty well. They're hard to find today, but not especially valuable since few people know what they are. They turn up on Ebay occasionally.
How to install American Flyer track locks
To held tracks hold together without nailing them down permanently, AC Gilbert marketed its #694 track locks. Sometimes people also call these track clips. The locks are u-shaped pieces of tin that came in a brown envelope with instructions on the front. If you've lost the instructions, or bought the clips secondhand and never got them, here's how to install American Flyer track locks.
These track locks are indispensable for setting up a layout on the floor.
Visit your layout with a cheap camera
I've seen a number of videos lately made by people putting dashboard cameras on their trains, which gives a view of a layout that we don't usually get to see–the view from the trains themselves. I've found a cheaper option. Hit up Ebay for an SJ4000 camera, which, if you sort the buy-it-now listings, you should be able to get for less than $20.
If that's too rich for your blood, look for the Mini DVR 808, which is keychain sized and costs more like $5.
Don't expect the world for that kind of money, but you can get a surprisingly good view of your layout from a perspective you'll never see in person with one.
It's not quite like getting to ride in your trains, but it's not bad, either.
Marx 999 repair and service
I had a Marx 999 that didn't run well when I pulled it out of storage. When pushing it along the track a few times didn't yield any measurable improvement, I decided I'd better take it apart and give it a thorough cleaning.
In this case, I worked on a Marx 999, but everything I did applies to any other O gauge train Marx made except for the very late 490 locomotives, whose motors don't seem to have been designed to let you do any more than replace the brushes.
6 options for removing paint from model trains
It's not uncommon to find model trains with unwanted paint on them, or original paint that's damaged beyond the point of being able to rehabilitate it. Fortunately, the price is usually low on these trains, and there are numerous household chemicals that can strip the paint off these trains and give them a fresh start.
These tricks also work with other toys and plastic models, but while some of these methods seem to be unknown in the train community, some of them are very well known among collectors who restore vintage plastic model kits. This is an example where knowledge across disciplines can be very valuable, so I hope the car and airplane modelers won't mind me sharing their secrets.
All about the Lionel LW transformer
The Lionel LW Trainmaster is a 125 watt transformer that Lionel produced from 1955 to 1966. They are reasonably durable and Lionel made them for a long time. That means you can find them easily on the secondary market. They can be expensive if they have their original box and paperwork. But if you just want to run a train and don't care about the paper, you can get a serviced LW for $50-$60, and an as-is one for under $40. At 125 watts, it's the most powerful single-handle transformer of the postwar era.
The LW is a quirky transformer so there are some things about if you need to be aware of if you have other Lionel transformers, but as long as you keep those in mind, it's a fine transformer that will serve you well. The quirks have nothing at all to do with reliability. Lionel just designed its layout a bit differently than many of their other models. In some ways it's the ideal accessory transformer. We'll cover that later.
One thing to keep in mind: Unplug the LW when you're not using it. It doesn't have its own power switch. I plug my transformers into a power strip and turn all of them on and off with the strip's on/off switch.
Lionel CW-80 vs vintage transformers
Someone asked me recently about the Lionel CW-80 and how it compares vs older transformers. That's a fair question, and one that tends to stir up a lot of emotions on train forums. So I'll try to present the pros and cons in a fair manner.


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There is a class of jobs, which many users who lack UNIX skills think of as interactive jobs, but, which, in fact, aren't interactive at all. Applications which take input from a command line in some sort of an application dependent language fall in that category. Examples are Common Lisp, Smalltalk, Scheme, Octave, Matlab, Mathematica, Xplor, GeneHunter, etc.
Often a user has a command file prepared, which must be loaded into an application from an interactive session. Once the command file is loaded the application begins executing a program, which may take hours to complete. A user at that stage goes away leaving an active telnet connection or an X11 window on the display. The window was needed only to load the file and perhaps issue some start-up commands for the computation.
Jobs like that are not interactive at all and they can and should be run under LoadLeveler without asking for an xterm window and forking an unnecessary login shell.
The way to execute such jobs is to use the here-input feature of UNIX shells:
$ my_command << EOF one_line_of_input another_line_of_input EOF
Here is an example:
# @ shell = /afs/ovpit.indiana.edu/@sys/gnu/bin/bash # @ output = hello-lisp.out # @ error = hello-lisp.err # @ job_type = serial # @ class = test # @ notification = always # @ environment = COPY_ALL # @ queue clisp -q << EOF (load "hello.fas") (hello) EOF
Here I have a Common Lisp program stored on a file hello.fas. Normally, in order to execute that program I would have to enter a Common Lisp environment with the command clisp. Then I would have to load the file which contains the program, and finally I would have to evaluate the function, which has been defined on hello.fas, by typing (hello).
But all that can be accomplished also by typing
clisp -q << EOF (load "hello.fas") (hello) EOF
in a shell script without having to invoke xterm first. A UNIX shell (csh, tcsh, sh, ksh or bash) on encountering a construct like that will take the text enclosed by the
<< EOF ... EOFconstruct and will pass it to the program, in this case
clisp, as if it has been typed in by the user.
Long Matlab, GeneHunter, Xplor, etc., computations can and should be run like this too.


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Sports Mania » Motorsport » Big changes coming to 2018 NASCAR Cup schedule
Big changes coming to 2018 NASCAR Cup schedule
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Located in the Henry Hill Education Support Center in Independence. Enter through the 6th Street parking lot entrance, located by OCDC.


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TagsBig Day Out Bill Withers Bobby Womack Carl Craig Charles Bradley Chic Cosmo Cuban Brothers Danny Krivit David Mancuso Despacio Glastonbury Greg Wilson Harry Thumann Hot Chocolate Jarvis Cocker Karen Young LCD Soundsystem Loleatta Holloway Lucky Cloud Mardi Gras Miles Cleret Mr Scruff New Orleans Nicky Siano Nile Rodgers Optimo Paperclip People Paul Simon Primal Scream Richard Hawley Richie Hawtin Sonar Son of Dave The Loft Todd Terje
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The annual Glastonbury review (part 2)
Festivals are always a triumph of the human spirit. Where else can you party from midday til the sun comes up, then get up and do it all over again, five days in a row, always with a smile on … Continue reading
Posted in Festivals, Funk, Heroes, House, Rock / pop, Soul Tagged Antibalas, Bryan Ferry, Charles Bradley, Cuban Brothers, Daptone Super Soul Revue, DJ Sneak, Downlow Radio, Glastonbury, Illuminaughti Ball, John Grant, Justin RObertson, NYC Downlow, Saun & Starr, Sharon Jones, Son of Dave, Sugarman 3 2 Comments
Glastonbury countdown – 9 days to go: Dub Dot Dash selects
Since I've done such a slack job of keeping up with my daily recommendations as we count down the days (I managed to lose an entire weekend and only part of it was due to the alcohol), I thought it … Continue reading
Glastonbury (finally)
Ha! Obviously my plans to preview everything I was hoping to see at Glastonbury went horribly awry, and my plans to review it in a timely fashion have gone the same way. I was going to wax on about how the … Continue reading
Posted in Festivals Tagged Alice Russell, Alt-J, Ben Dorling, Bobby Womack, Charles Bradley, Charles Bradley & his Extraordinaires, Chic, Craig Charles, Dinosaur Jr, DJ Yoda, Don Letts, Dub Colossus, Fleetmac Wood, Glastonbury, Goat, I Am Kloot, Matthew E White, Nick Cave, Ondatropica, Pardon My French, PIL, Primal Scream, Rodriguez, Seasick Steve, Smashing Pumpkins, Steve Mason, The Bombay Royale, The Congos, The Stones, Tom Tom Club 4 Comments


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Northcentral Technical College AP tests
Think about what career is best suited for you, and where you want to study. Request more information now.
Think about what career is best suited for you, and where you want to study. Request more information now.
Think about what career is best suited for you, and where you want to study. Request more information now.
Find info concerning Northcentral Technical College AP tests, and registering for elective seminars and discussion sections. As a student, your first stop should be the registrar's office, where you can pick up a free copy of both the academic calendar and course catalog, in order to find available credit classes that you may be interested in taking. Then get a copy of the schedule of classes, so you can plan a workable weekly schedule for yourself. Finally, check with the admissions office for assistance with prerequisites, tuition payment deadlines, and Northcentral Technical College advanced placement exam information. Please use the form above to request admissions info for Northcentral Technical College.
For multiple-choice tests like the SAT Test or ACT Exam, look at the number of questions and the total number of minutes you're allowed. If there are more minutes than questions, you have over a minute for each. However, if there are more questions than minutes, you better scramble, as you have under a minute on each question. Round off all numbers you see, and look for tips in the test questions that point you to the correct answer. Look for word patterns in the vocabulary section, and in the math section, saving just a few seconds on each test question can lead to a much higher math score.
Exams are a huge portion of your final grade, and every professor will let you know in their own way which questions will be on the final exam. They may raise the pitch of their voice when stressing certain points, show slide presentations, or write course material on the blackboard. On the test day itself, arrive early after a good night's sleep, and pick a seat near the windows in order to get sunlight and oxygen. Trust your first instincts, and don't change your mind on a second pass. Beyond degree requirements such as Northcentral Technical College AP Exam, you may consider Samford University e-learning for complementary electives to your primary course of study.
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Previously participated in a team robotics event, such as FutureLeague's Team Robotics Level, 1 FLL, WRO, or Robofest
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New residential and commercial development throughout the Placentia-Yorba Linda Unified School District will be hit with increased school impact fees beginning next month, based on a recent unanimous vote by the district's five elected trustees.
The state-allowed charges, formally called "statutory school fees," will increase nearly 3.6 percent for residential development, while the hikes for various types of commercial projects will range from 3.7 percent to 25 percent.
Usually, developers recoup the fees they pay in the selling prices of the homes and buildings they construct, and they are expected to recover the upcoming increases in a similar manner.
Money generated from the fees are kept in an account "separately maintained, except for temporary investments, from other funds of the district," according to the six-page resolution.
Generally, the fees collected from both new residential and commercial development in the district can only be used to serve students that enroll in the district due to the development.
As specifically spelled out in the district's resolution, fee spending "will include construction or acquisition of school facilities, remodeling existing school facilities, the addition of technology and acquiring and installing additional portable classrooms and related school facilities…."
The "specific location of new schools, remodeling of existing schools and additional portables" are determined based on the residence of new students generated by the new residential and commercial development, "as well as any required central administrative and support facilities…."
Fees are based on the square footage of assessable space for residential construction that includes single-family homes, condominium and apartment units, manufactured and mobile homes, and the square footage of covered and enclosed space for commercial development.
The residential fee jumps to $3.48 per square foot, up close to 3.6 percent. Thus, the new charge for a 2,000-square-foot home increases to $6,960, up from $6,720.
The new per-square-foot fees for six types of commercial development include 45.5 cents, up 25 percent for retail; 56 cents, up 3.7 percent for office; 56 cents, up 13.6 percent for research and development; 53.9 cents, up 23.6 percent for industrial, warehouse and manufacturing; 55.1 cents, up 23 percent for hospital; and 22.7 cents, up 23.4 percent for hotel and motel.
The two justification studies conducted by a district-hired consultant are available for public review through June 12, when the new rates go into effect. A nine-step appeal process is in place to challenge the commercial fees.
The fee increases are authorized on a biannual basis by the 10-member State Allocation Board. Bob Huff, who represents Yorba Linda in the state Senate, is one of the members.
Jim Drummond is a longtime Yorba Linda resident. Email: email@example.com.


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November 23, 2014 Total Views: 6230 Today: 1
Hotel Apartamentos MLR Almirante Madrid, Set 500 metres from Cibeles Square, Apartamentos MLR Almirante offers a modern apartment with a very central location in Madrid. The property has air conditioning and free Wi-Fi. Featuring two balconies, the stylish apartment has a living room with a sofa and flat-screen TV. The kitchen has a dining table and is equipped with an oven and dishwasher. It also has a phone with free local calls. Apartamentos MLR Almirante is set in a lively area of Madrid, where guests can find many bars and restaurants. The famous Gran Vía Avenue is 700 metres away and the Retiro Park is 10 minutes' walk from the apartment. The metro stations of Colón, Chueca and Banco de España can be reached within 5 minutes' walk. Atocha Train Station is 1.6 km from the property and Madrid-Barajas Airport is 12 km away. (Hotel Apartamentos MLR Almirante Madrid hotels booking).


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(303) 667-7123
MLJ Financial Services, LLC
14 years in business2525 Arapahoe Ave Suite E4-836
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Fax Numbers
- (303) 955-8917
Additional Phone Numbers
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Business Started: 03/01/2003
Type of EntityLimited Liability Company
Business Management
- Mrs. Mary Heidbrier, Partner
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Licensing information is provided in the BBB Business Profiles to inform the public about industries that may require professional licensing, bonding, or registration. Better Business Bureau encourages you to check with the appropriate agency to be certain any requirements are currently being met.
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Integrative Cancer Therapies http://ict.sagepub.com/
The Present State of Antineoplaston Research (1) Stanislaw R. Burzynski Integr Cancer Ther 2004 3: 47 DOI: 10.1177/1534735403261964 The online version of this article can be found at: http://ict.sagepub.com/content/3/1/47
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Antineoplastons 10.1177/1534735403261964 Burzynski Antineoplastons
The Present State of Antineoplaston Research (1) Stanislaw R. Burzynski
Antineoplastons work as molecular switches, which regulate expression of genes p53 and p21 through demethylation of promoter sequences and acetylation of histones. They also inhibit the uptake of growth-critical amino acids, such as 1glutamine and 1-leucine in neoplastic cells. Phase II trials indicate efficacy of antineoplastons in low-grade glioma, brain stem glioma, high-grade glioma, adenocarcinoma of the colon, and hepatocellular carcinoma. The best results were observed in children with low-grade glioma, where 74% of patients obtained objective response, and in patients with adenocarcinoma of the colon with liver metastases whose survival rate of more than 5 years is 91% versus 39% in controls on chemotherapy. Gene array studies will explain antineoplaston-induced changes in gene expression. Keywords: antineoplastons; brain tumors; gliomas; colon cancer; liver cancer
The theory of antineoplastons originated in 1976 from the theory of autonomous cybernetic systems (ACS) and studies on peptides and amino acid derivatives in human blood.1 A cell can be compared to the ACS, which is connected with the environment through the information and energy pathways.1 Two types of gates connect the system with the environment: receptor is for information, and feeder is for energy. After crossing these gates, both pathways travel through systems that transform and store the energy (accumulator) and information (correlator). Accumulator and correlator are connected through homeostat, which influences both of them. Finally, the ACS possesses an effector, where both pathways converge and leave the system, which is responsible for a specific reaction. The ACS can be influenced through either the energy or information pathway. Most cancer treatments, known so far, were based on a "massive destruction" principle and employed a large amount of energy and a small amount of information, which resulted in poor specificity of the treatment and numerous side effects. The ideal cancer treatment should provide a large amount of information and a small amount of energy. Such targeted treatment will primarily influence the information pathway and consist of molecular switches, which control neoplastic DOI: 10.1177/1534735403261964
growth by "turning on" tumor suppressor genes and "turning off" oncogenes.2 Experience with imatinib mesylate (Gleevec; Novartis, East Hanover, NJ) proves the validity of such an approach. The practically infinite variety of peptides and amino acid derivatives that can be formed by combinations of the 20 common amino acids indicates the possibility of the existence of a peptide- and amino acid–based system that carries information from cell to cell and inside the cell and is able to correct errors in the program for normal development. I initiated the study of antineoplastic peptide fractions from the blood in 1967.3 The analysis of peptides and amino acids in the blood of healthy people and of patients suffering from various diseases, including cancer, revealed that there were significant deficiencies in peptide content in the serum of cancer patients. Subsequently, similar peptide fractions were found in urine, and it was postulated that they were synthesized in tissues and passed into the blood and urine. For economic reasons, urine was proposed as the main source for their isolation. The research on antineoplastic peptides from urine, by our team, resulted in the separation of urinary peptides in 119 fractions, which were further tested for their effect on the growth of neoplastic and normal cells. Fractions that inhibited the growth of neoplastic cells and did not inhibit the growth of normal cells were named antineoplastons.4-7 A hypothesis has been proposed that the human body possess a biochemical defense system, consisting of antineoplastons, which protects against the occurrence of abnormal cell growth. Normal cells differentiate according to the program encoded in the genes, eventually entering the stage of cellular senescence followed by apoptosis. Cancer cells, however, escape the fate of normal cells and, instead of dying, multiply endlessly.8,9 Growth and differentiation of the cells is regulated by influences from both outside the cells (growth factors, antineoplastons) and from inside (oncogenes, tumor SRB is at the Burzynski Research Institute, Houston, TX. Based on a presentation at the Comprehensive Cancer Conference, 2003. Correspondence: Stanislaw R. Burzynski, Burzynski Research Institute, 9432 Old Katy Road, Houston, TX 77055. E-mail: info@ burzynskiclinic.com.
INTEGRATIVE CANCER THERAPIES 3(1); 2004 pp. 47-58
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Burzynski suppressor genes). Errors in the early stages of differentiation result in highly malignant neoplasms. Middle and delayed disruption of the process leads to less aggressive cancers and benign tumors. Changes in the final steps cause abnormal production of proteins and may result in autoimmune and neurodegenerative disorders.2 Aging is a continuation of a process beginning in the embryo that depends on silencing some genes when they are no longer useful. When this silencing affects tumor suppressor genes, an aging person may develop cancer.10,11 Silencing of gene p53 leads to the development of many different types of cancer in the aging organism, and silencing of the WRN gene causes premature aging and formation of 5 different types of malignancies.12 Methylation of promoter sequences of the genes is the main mechanism silencing both of those genes (no longer necessary for development and other genes), which are gradually turned off during the aging process.10 Cancer patients have a marked deficiency of antineoplastons in plasma. Balancing this deficiency through introduction of antineoplastons in cancer treatment may control neoplastic growth.7,13 The initial studies concentrated on group A of antineoplastons with a broad spectrum of activity. Five formulations in this group, named antineoplastons A1, A2, A3, A4, and A5, consisting of peptide fractions isolated from urine, were the subjects of extensive tissue culture and animal toxicity studies and also phase I 14-26 The clinical studies in advanced cancer patients. studies revealed negligible toxicity and objective responses in difficult-to-treat cancers.14,24-26 Antineoplaston A2, which contributed to the highest number of complete responses in phase I clinical studies, was elected for final purification, isolation of the active components, and structure determination. The active ingredient was identified as 3-phenylacetylamino-2, 6-piperidinedione and was named 27 antineoplaston A10. A10 has been reproduced by synthesis involving condensation of l-glutamine with phenylacetyl chloride and subsequent cyclization of phenylacetylglutamine (PG).28 The metabolism of A10 in the human body yields PG, phenylacetylisoglutamine (isoPG), and phenylacetate (PN), which were reproduced synthetically and formulated into antineoplaston A10 injections (A10-I), AS2-1, AS5, and AS-25.29-33 Each of these formulations was submitted for basic research and phase I clinical studies.34-44 A10, A10-I, and AS2-1 were selected for phase II studies. Two initial phase II studies in astrocytoma and high-grade glioma began in 1988 and 1990 and were conducted outside the investigational new drug (IND) process.45,46 In 20 patients, in the astrocytoma study, complete and partial responses occurred in 48
30%, stable disease in 50%, and progressive disease in 45 20%. In the high-grade glioma study of 12 patients diagnosed with glioblastoma multiforme (GBM) and anaplastic astrocytoma (AA), 36% obtained complete and partial responses, 33% obtained stable disease, and 33% had progressive disease.46 The phase II study of AS2-1 capsules with low-dose diethylstibestrol in hormonally refractory cancer of the prostate revealed complete and partial responses in 36%, stable disease in 50%, and progressive disease in 14%.9 An independent review by the National Cancer Institute (NCI) of 7 patients with brain tumors concluded that an association existed between antineoplaston administration and objective tumor regressions.47 After this review, a phase II study was authorized by the US Food and Drug Administration (FDA) and sponsored by the NCI.48 The study was stopped after the treatment of 6 evaluable patients diagnosed with GBM and AA when it was found that the concentration of A10-I in patients' blood during the treatment was approximately 50 times lower than optimal concentration.49 48 There were no objective responses reported. Since 1994, the FDA has authorized 74 phase II studies with A10, A10-I, and AS2-1, under INDs 43,742 and 22,029, in advanced malignancies. In addition, 2 phase II studies were performed at Kurume University School of Medicine under the supervision of the Japanese government. Burzynski Research Institute sponsored all the studies. The preliminary results of the studies in primar y brain tumors have been previously published.50-52
Mechanism of Action of Antineoplastons The current theory of the mechanism of action of antineoplastons is their function as "molecular switches,� turning on tumor suppressor genes and turning off oncogenes. Such molecular switches should theoretically control cancer because they deal directly with its biochemical causes: increased activity of oncogenes and decreased expression of tumor suppressor genes. It is known that there are accelerators and brakes in the cancer process. Oncogenes are the accelerators, and normal tumor suppressor genes serve as brakes. PN and AS2-1 inhibit farnesylation of the p21ras protein and cause downregulation of Bcl2.53,54 While it causes inhibition of mevalonate 5pyrophosphate decarboxylase, it does not affect mevalonate kinase and mevalonate 5-phosphate kinase.55 PN and AS2-1 also activate the p53 gene. In most cases, protein p53 activates the p21 gene, which directs WAF1/Cip1 the synthesis of the p21 protein. This protein activates promoter sequences of the tumor suppressor INTEGRATIVE CANCER THERAPIES 3(1); 2004
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Antineoplastons gene p53, which are undergoing demethylation. DNA methylation of tumor suppressor genes is a common mechanism of silencing the genes.56 Removal of methyl groups activates the gene, which causes malignant cells to die through apoptosis. The reaction is facilitated by the enzyme methyltransferase. Methyltransferase can complete this reaction only if it is activated by binding to proliferating cell nuclear antigen (PCNA). In normal cells, PCNA binds to the p21WAF1/cip1 protein, leaving methyltransferase inactive. In cancer cells, in the absence of the p21WAF1/cip1 protein, the reaction of methylation proceeds uninhibited.57,58 Induction of p21WAF1/cip1 suppresses human glioma cell proliferation.59 At one of the previous comprehensive care conferences, we reported detailed data indicating that PN, which is the active ingredient of antineoplaston AS2-1, interrupts signal transmission in the ras pathway and activates tumor suppressor genes p53 and p21 through demethylation of their promoter sequences.53-55,57,58,60 Since the previous conference, our team has conducted research on the molecular mechanism of action of PG, the main ingredient of A10-I, and has concluded that • PG exhibits antineoplastic activity across a wide array of cancer cell lines; • PG inhibits the uptake of growth-critical amino acids, such as 1-glutamine and 1-leucine, in neoplastic cells; • the reduction in amino acid availability may contribute to the drug's antineoplastic activity; • human glioma (U-87) cells rapidly take up PG by a mechanism similar to facilitated diffusion; • upon the removal of PG from the media, PG rapidly and completely effluxes from the cell; and • PG enters cells via the stereospecific amino acid transporters for l-glutamine.61
Publications on these conclusions and supporting data are now in preparation.
Formulations of Antineoplastons Antineoplastons are a class of 12 antitumor agents. The following synthetic antineoplaston formulations are currently being used in phase II studies. • Antineoplaston® A10 capsules contain 500 mg of 3phenylacetylamino-2, 6-piperidinedione. • Antineoplaston® A10 injection is a mixture of the sodium salts of PG and isoPG in a 4:1 ratio. It is available in 500 mL and 1000 mL (300 mg/mL) plastic bags. • Antineoplaston® AS2-1 capsules containing 500 mg of a 4:1 PN and PG. • Antineoplaston® AS2-1 injection is a mixture of PN and PG in a 4:1 ratio. It is available in 250 mL (80 mg/ mL) plastic bags.
Clinical Trials With Antineoplastons in the United States All of the clinical trials in cancer in the United States are performed under FDA supervision (INDs 22,029 and 43,742). The government did not fund antineoplaston trials discussed here. Two additional trials are under way in Japan, supervised by the Japanese government. We have emphasized treatment of primary malignant brain tumors; colon, liver, esophageal, pancreatic, lung, and breast cancers; and nonHodgkin's lymphoma. The studies had the following common exclusion criteria: serious active infections, fever, or other serious concomitant disease that would interfere with the evaluation of the treatment drugs, (such as severe lung disease, hepatic failure, and history of cardiovascular or renal conditions that medically contraindicate administration of high dosages of sodium). Patients should have histological confirmation of the malignancy, except for cases of dangerous locations, where biopsy may entail unacceptable risk to the patient. There were no exclusions based on tumor size, multifocality, or leptomeningeal or systemic metastases except that the tumor size should be larger than 5 mm. Patients in the low-grade glioma group were excluded if less than 8 weeks had elapsed from the last dose of radiation therapy and 4 weeks from the last dose of chemotherapy (6 weeks from the last dose of nitroureas), immunotherapy, and surgery. In brain stem glioma, high-grade glioma, and GBM groups, there was a separate subgroup of patients who developed progression during standard therapy and within 4 weeks after chemotherapy (6 weeks after nitroureas) and also within 8 weeks after radiation therapy. Patients who had a Karnofsky performance status of less than 60 were excluded. Response criteria were as follows: Complete response (CR) is complete disappearance of all contrastenhancing tumors on imaging studies for at least 4 weeks without the use of corticosteroids. Partial response (PR) is more than 50% reduction in the sum of the products of the greatest perpendicular diameters of the contrast-enhanced tumors for at least 4 weeks with no appearance of new lesions on a decreasing or stable dose of corticosteroids. Objective response (OR) is either CR or PR. Minor response (MR) is at least 25% and less than 50% of tumor reduction. Stable disease (SD) is defined as less than 25% reduction and no progression. Progressive disease (PD) is a greater than 50% increase in the sum of the products of the greatest perpendicular diameters of the contrast-enhanced tumors, compared with nadir evaluation, or the appearance of new lesions. PD is often considered as a 25% increase in size of
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Burzynski measurable tumor. The reason for 50% PD in these studies is a long dose-escalation process, which extends to more than a month's time period, before the optimal dosage is reached. The patient may experience continuous tumor growth (more than 25%) on lower dosages and respond to the treatment at higher dosages. Some patients were not evaluable because they did not have follow-up scans, and others were not evaluable because it was too early for evaluation. Such patients were not included in the statistics. The results of our studies were compared with standard therapy. The comparison groups have a similar population of patients, as far as prognostic factors are concerned, including extent of prior resection, performance status, lag time to treatment, prior treatments, and so forth, unless stated otherwise. The patients were selected at the Burzynski Clinic (BC) from the general population of oncology patients. All consecutive patients who fulfilled entrance criteria were admitted to the trials, and remaining patients were treated with standard cancer treatment, including cytotoxic chemotherapy and immunotherapy. ORs have been confirmed by radiologists not associated with the BC. In addition, the FDA conducted an independent review of all medical records and films of patients who obtained OR. Because of the slow enrollment and similarity among protocols, the results were integrated into clinical and statistical reports for a faster and more meaningful review of the results of treatment of low-grade glioma in children, brain stem glioma, high-grade glioma, and GBM. Protocols are listed at www.clinicaltrials.gov. The accrual for studies BT-20 and CAN-01 is completed. To complete the remaining studies, we are still accruing the following number of patients: BT-06, 31; BT-07, 2; BT-08, 25; BT-09, 16; BT10, 27; BT-11, 10; BT-13, 30; BT-15, 15; BT-17, 29; BT18, 26; BT-21, 11; BT-22, 34; and BT-23, 30. Some detailed reports on individual clinical studies have been published or are in preparation for publication (Table 1).
Low-Grade Glioma in Children Protocols BT-10, BT-11, BT-13, BT-23, and CAN-01 • Nineteen evaluable children with a median age of 7 years were enrolled. • Only 16% of patients were not previously treated, except for tumor biopsy—the remaining 84% had developed tumor recurrence after surgery, radiation, or chemotherapy. • OR = 74%, MR = 5%, SD = 16%, PD = 5%. • Median overall survival from diagnosis (OSD) was 6.3 years.
Table 1.
Phase II Clinical Trials With Antineoplastons: Update on Efficacy, June 1, 2003 (in percentages)
Diagnosis Low-grade glioma in children Brain stem glioma High-grade glioma Glioblastoma multiforme
Objective Response
Minor Stable Progressive Response Disease Disease
Objective response = complete response and partial response.
• Median overall survival from start of treatment (OST) was 5.1 years with the majority of patients alive (26% deceased or status unknown). • Maximal survival (MS) is more than 17 years. • For progression-free survival (PFS), only 1 patient progressed after 24 months.
After completion of the study, the responses and survival will be evaluated for the following groups: (1) low-grade astrocytoma, (2) recurrent and progressive multicentric glioma, and (3) visual pathway glioma. Low-grade gliomas in children account for more than 50% of all primary central nervous system tumors in childhood. The main conventional treatment is surgery, but in many cases, the location of the tumor can be too risky. In addition, some patients develop multiple tumors throughout the brain and spine. Unfortunately, when only the conventional treatment is employed, most patients will experience disease progression and death, except in a small number of cases in which the tumor can be totally resected. With the use of aggressive chemotherapy, only 4% of patients obtained OR; SD was 74%, and PD was 22% (Figure 1).62
Case Study, Patient 1 This young man was 10 years old when diagnosed with low-grade astrocytoma in October 1997. Because his tumor grew in a difficult area of involvement, including the thalamus and brain stem, he was not a candidate for surgery and did not receive any standard treatment (Figure 2). He began treatment with antineoplastons in April 1998. His contrast-enhancing tumor decreased and finally could no longer be seen on magnetic resonance imaging (MRI) in March 1999. Repeated positron emission tomography (PET) scans did not show tumor recurrence. This patient has made a complete recovery. When he came to us for the first time, he was partially paralyzed and in a wheelchair (Figure 3). INTEGRATIVE CANCER THERAPIES 3(1); 2004
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Percentage of responses
CR – Complete Response PR – Partial Response MR – Minor Response SD - Stable Disease
A10 and AS2-1
(Mahoney et al.)
Figure 1 Phase II clinical trials with antineoplastons A10 and AS2-1 in children with low-grade glioma (as of June 1, 2003), comparison of responses. For the comparison study, see Mahoney et al.62 Figure 3 Patient 1 before and during the treatment with antineoplastons A10 and AS2-1.
• PFS 7 months = 43% of responding patients did not develop progression
Figure 2 Treatment of low-grade glioma with antineoplastons A10 and AS2-1 in a 10-year-old male (patient 1). The patient was diagnosed in October 1997 with inoperable astrocytoma, grade 2 of thalamus and brain stem. Magnetic resonance imaging (MRI) of the head with gadolinium. Images in the upper row show a large tumor before treatment. Images in the lower row confirm disappearance of the tumor after 11 months of treatment. Residual signal on posttreatment MRIs corresponds to old hemorrhage.
Brain Stem Glioma Protocols BT-11 and BT-22 • Eighteen evaluable patients with a median age of 11 years (15 children and 3 adults) • No prior treatment = 33%, and recurrence after radiation or chemotherapy = 67% • OR = 39%, MR = 11%, SD = 17%, and PD = 33% • OSD = 13.7 months • OST = 10.3 months • MS = more than 7.5 years
After completion of the study, the results will be evaluated separately for (1) brain stem glioma, (2) recurrent and progressive intrinsic brain stem glioma and for brain stem glioma that progressed during standard therapy and within 4 weeks after chemotherapy (6 weeks after nitroureas) and 8 weeks after radiation therapy. Brain stem gliomas are among the most difficult brain tumors to treat. Surgery usually is associated with great risk, while chemotherapy is ineffective. Therefore, radiation therapy remains the main treatment modality. Unfortunately, in most of the patients, the tumor will recur and cause death.
Case Study, Patient 2 This patient presented one of the most difficult brain stem glioma cases treated in our clinic (Figure 4). She arrived at the BC in October 1998, when she was less than 3 months old. The patient was diagnosed with a large brain stem glioma, measuring approximately 7 cm across its largest diameter. She was evaluated at City of Hope Medical Center in Duarte, California, and consulted with Beth Israel Hospital in New York. Unfortunately, there was no conventional treatment available for her. Her parents were told she would almost certainly die within 1 month. She came to us in terminal condition and began treatment immediately. After 4 months of treatment with antineoplastons, her contrast-enhancing tumor was no longer visible on MRI. She had been near death at the beginning of antineoplaston treatment and was being kept alive only by large dosages of corticosteroids. Pretreatment
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Figure 5 Patient 2 before and after the treatment with antineoplastons A10 and AS2-1.
Figure 6 Phase II clinical trials with antineoplastons A10 and AS2-1 in brain stem glioma (as of June 1, 2003), comparison of responses. For the comparison study, see Allen et al.63
Figure 4 Treatment of progressive intrinsic diffuse brain stem glioma with antineoplastons A10 and AS2-1 in 3-monthold female (patient 2). Patient was diagnosed shortly after birth with large inoperable brain stem glioma and presented for treatment with antineoplastons in terminal condition. Magnetic resonance imaging of the head with gadolinium shows decrease and disappearance of contrast-enhancing tumor.
photographs showed the child with facial nerve paralysis and extensive swelling of the face resulting from the corticosteroids. Six months later, her symptoms decreased and disappeared. Now, 5 years from her diagnosis, she is a completely normal and healthy child (Figure 5). A subgroup of 10 evaluable patients has been diagnosed with very difficult to treat recurrent diffuse intrinsic brain stem glioma. Among these patients, an OR was determined in 50%, MR in 30%, and PD in 20%. The longest survival (the patients are currently alive) is more than 7 years.52 We can compare these results to other studies. In a phase II PCNU trial, 18% 52
of patients obtained PR and 12% obtained SD, compared to the total of 80% of CR, PR, and MR in our study (Figure 6).63 In the study with thiotepa, in 14 cases there were no objective responses.64 A paper by Mandell et al analyzes the results of 66 patients treated with radiation therapy and chemotherapy with cisplatin. The study involved easier to treat cases of newly diagnosed patients than those in the 65 antineoplaston study. The percentage of patients surviving at 2 years in the antineoplaston study was 42% compared to 7.1% for radiation and chemotherapy (Figure 7).
High-Grade Glioma Protocols BT-06, BT-08, BT-09, BT-10, BT-11, BT-15, BT-17, BT-18, BT-21, BT-22, and CAN-01 • Sixty-two evaluable patients with a median age of 39 years (54 adults and 8 children) • No prior treatment = 24%; recurrence after surgery, recurrence during and/or after radiation or chemotherapy = 76% • OR = 36%, MR = 7%, SD = 29%, PD = 29% INTEGRATIVE CANCER THERAPIES 3(1); 2004
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Figure 7 Phase II clinical trials with antineoplastons A10 and AS2-1 in brain stem glioma (as of June 1, 2003). Comparison of patients' survival at 2 years. For the comparison study, see Mandell et al.65
Figure 8 Phase II clinical trials with antineoplastons A10 and AS2-1 in high-grade glioma (as of June 1, 2003), comparison of responses. For the comparison study, see Phuphanich et al.66
• • • •
OSD = 3 years OST = 1.15 years MS = more than 12.5 years PFS 12 months = 61% of OR patients had not progressed
Figure 9 Treatment of high-grade glioma with antineoplastons A10 and AS2-1 (patient 3). The patient is a 54-year-old male who underwent subtotal tumor resection for highgrade glioma on February 23, 1996. After the treatment with antineoplastons A10 and AS2-1 from March 27, 1996, to August 27, 1996, his tumor gradually decreased and disappeared. Magnetic resonance imaging of the head with gadolinium shows gradual decrease and disappearance of the tumor. 66
After completion of the studies, the results and survival will be evaluated separately for (1) high-grade glioma in children, (2) high-grade glioma in adults, (3) AA not treated with radiation and chemotherapy, (4) AA recurrent after radiation and chemotherapy, (5) recurrent anaplastic oligodendroglioma, (6) recurrent mixed glioma, and (7) high-grade glioma that progressed during radiation and chemotherapy and within 4 weeks after chemotherapy (6 weeks after nitroureas) and within 8 weeks after radiation therapy. High-grade gliomas are usually treated surgically, followed by radiation therapy and chemotherapy. Median survival without treatment is 17 months and with treatment may approach 3 years. For recurrent
tumors, median survival is reduced to 8 months. Ultimately, most patients will die from their tumors despite the treatment given. In one of the recent phase II studies in recurrent high-grade glioma with temozolomide and thalidomide, there were the following results: OR = 21%, SD = 14%, and PD = 65% (Figure 8).66
Case Study, Patient 3 The patient was a 54-year-old male diagnosed with high-grade malignant glioma (mixed astrocytoma, oligodendroglioma) on February 23, 1996. At the time of diagnosis, he underwent subtotal tumor resection and did not receive any standard treatment. He was treated with antineoplastons A10 and AS2-1 from
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Burzynski March 27, 1996, to August 27, 1997. He had a large tumor in the right temporal lobe, which gradually decreased and disappeared (Figure 9). He has been tumor free for more than 6 years. In the treatment of high-grade gliomas, including GBM, it is not unusual to see a rapid response to treatment and a complete response within 2 to 3 months.
Case Study, Patient 4 This case is a good example of a rapid response. The patient was 41 years old when on April 18, 2000, he underwent a partial resection of a brain tumor and was diagnosed with AA. After the surgery, he received radiation therapy, which was completed in June of 2000. On December 1, 2000, he underwent a second craniotomy for tumor recurrence, which confirmed the same diagnosis. After he developed a second recurrence, he began treatment with antineoplastons A10 and AS2-1 on February 22, 2001. His followup MRI on April 25, 2001, did not show a contrastenhancing tumor (Figure 10). The treatment with antineoplastons was discontinued on August 5, 2001. A follow-up PET scan on January 22, 2003, did not show any tumor recurrence (more than 3 years after his diagnosis). Glioblastoma Multiforme Protocols BT-06, BT-07, BT-09, BT-10, BT-18, BT-20, BT-21 and CAN-01 • Eighty evaluable patients with a median age of 46 years (72 adults and 8 children) • All patients underwent prior surgery (tumor resection = 87.5% and biopsy only = 12.5%), 74% developed recurrence after or during radiation and chemotherapy • OR = 19%, MR = 9%, SD = 21%, PD = 51% • OSD = 15 months • OST = 9 months • MS = more than 11 years • PFS 5 months = 53% of OR patients had not progressed
After completion of the study, the responses and survivals will be evaluated separately for GBM in children and in adults in the following groups: (1) GBM not treated with standard therapy, (2) recurrent GBM after completion of standard therapy, and (3) GBM that progressed during standard therapy and within 4 weeks after chemotherapy (6 weeks after nitroureas) and within 8 weeks after radiation therapy. As a glioma of the highest malignancy, GBM is difficult to control by standard therapy. The conventional treatment of recurrent GBM is disappointing. Curative therapies do not exist, and median survival is 54
Figure 10 Rapid response to treatment with antineoplastons A10 and AS2-1 in patient with high-grade glioma (patient 4). The patient is a 41-year-old male treated with antineoplastons after his anaplastic astrocytoma progressed after partial resection, radiation therapy, and a second resection. MRI of the head with gadolinium shows disappearance of contrast-enhancing tumor after the treatment with antineoplastons.
Figure 11 Phase II clinical trials with antineoplastons A10 and AS2-1 in recurrent glioblastoma multiforme (as of June 1, 2003), comparison of survival. For the comparison study, see Prados et al.67
approximately 4 months for patients not treated. For the recurrent GBM, the median survival is 6½ months with the newest forms of chemotherapy compared to INTEGRATIVE CANCER THERAPIES 3(1); 2004
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Figure 12 Phase II clinical trials with antineoplastons A10 and AS2-1 in glioblastoma multiforme (as of June 1, 2003), comparison of responses. For the comparison study, see Prados et al.67 67
15 months in our study (Figure 11). The percentage of objective responses (only partial responses) in patients treated with aggressive chemotherapy with 67 blood brain disruption was only 4.8% (Figure 12). Among our patients exhibiting objective responses, 1 is surviving more than 11 years, another patient for more than 9 years, and 3 additional patients for approximately 7 years.
Case Study, Patient 5 This 26-year-old female was diagnosed with GBM and underwent subtotal resection of the tumor on July 28, 1994. She received initial treatment with radiation therapy and chemotherapy with BCNU. In January of 1995, due to tumor recurrence, she received chemotherapy with procarbazine. After the second recurrence of her tumor, she received treatment with antineoplastons A10 and AS2-1 from April 2, 1996, to July 29, 1996. The tumor decreased and was no longer seen on repeated MRIs. She survived and is now in good health more than 9 years from tumor diagnosis (Figure 13).
Figure 13 Treatment of gl i obl astoma mul ti for me wi th antineoplastons A10 and AS2-1 in a 27-year-old female (patient 5). The patient was diagnosed with glioblastoma multiforme on July 28, 1994. She started antineoplastons A10 and AS2-1 on April 2, 1996, after tumor recurrence postsubtotal resection, radiation therapy, and 2 types of chemotherapy. Magnetic resonance imaging of the head with gadolinium shows gradual decrease and disappearance of the tumor. This patient's survival is more than 9 years.
Clinical Trials With Antineoplastons in Japan Colon Cancer According to preliminary results of the clinical trials conducted at the University of Kurume Medical School in Japan, A10 and AS2-1 given to patients with adenocarcinoma of the colon with metastases to the liver in conjunction with chemotherapy increased more than 5-year survival to 91%, compared with 39% in the control group treated with chemotherapy alone (Figure 14).68 The study was randomized and compared the results of treatment of 19 patients who received hepatic arterial infusion (HAI) of chemotherapeutics with antineoplastons and 56 patients who received HAI chemotherapy alone. HAI
Figure 14 Phase II clinical trials with antineoplastons A10 and AS2-1 in adenocarcinoma of the colon with liver metastases in University of Kurume Medical School of Japan. Comparison of survival, antineoplastons in conjunction with chemotherapy versus chemotherapy alone.
chemotherapy improved 5-year survival rate from 32% to 39% compared to standard chemotherapy.
Liver Cancer The same medical center described follow-up of 10 patients who had antineoplaston treatment during the
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Burzynski lower dosages of A10 in their study. On the other hand, A10 induces diuresis, which may result in rapid elimination of AS2-1 through the kidneys, which will lower the concentration of AS2-1 in plasma and reduce the chances for higher grade toxicity observed by Buckner et al.49
Figure 15 Phase II clinical trials with antineoplastons in heapatocellular carcinoma at the University of Kurume Medical School of Japan. Time to recurrence in patients given antineoplaston AS2-1 after standard chemotherapy compared to control group.
course of therapy for hepatocellular carcinoma (this was not a controlled study) (Figure 15). It was found that the time to recurrence was longer with AS2-1 po than that without AS2-1. Patients treated with AS2-1 had time to recurrence of 16 months compared with 5 months without AS2-1. In 7 patients, recurrence-free intervals were measured with and without AS2-1 treatment. The time to recurrence was longer after adding AS2-1 to the treatment (14 months vs 5 months).69,70 The Japanese group has reported encouraging results in case studies of 3 patients with advanced pancreatic, lung, and breast cancers.71,72
Adverse Reactions Treatment with antineoplastons is usually free from adverse reactions. Serious adverse reactions include anemia in 1.4% and hypernatremia and fever in 0.5% of patients. Additional moderate adverse reactions include skin rash (0.76%) and slurred speech (0.9%). Most patients experience increased diuresis, which may lead to dehydration and thirst. A complete list of rare adverse reactions occurring in less than 0.5% of patients is available on request. In general, however, adverse reactions observed during treatment with antineoplastons have usually been transient and mild. Buckner et al in their phase II study of antineoplastons described reversible grade 2 or 3 neurological toxicity, consisting of transient somnolence, confusion, and exacerbation of an underlying seizure disorder.48 Reversible grade 1 somnolence and confusion were also noted in our studies and were due to phenylacetate, which is the main ingredient of AS2-1. It is suspected that the other adverse reactions observed in our studies were due to A10. They were not observed by Buckner et al since they used approximately 50 times 56
We have accumulated substantial data on the safety and efficacy of antineoplaston treatment in supervised clinical trials. Some of our trials are nearing conclusion, but patients are still being accrued to most. A substantial number of patients are not yet evaluable, and for some indications, the time is too short for evaluation of survival; therefore, reported statistics may change in the future. Much of the data are positive, although we sometimes see a lack of efficacy in some types of cancer. The details of all cases are reported periodically to the FDA. A majority of the patients suffered from recurrent disease after standard treatment. Such patients usually have a smaller chance to respond to the next therapeutic regimen. Most patients had been told by previous physicians that they had only a few months to live and that there were no other treatments available for them. It is still possible, however, that some of these patients have already survived through many previous treatments and may simply represent a group that has less aggressive and more easily controlled disease.73 We are continuing to study the role of genes in cancer prevention and treatment. Gene array studies will explain antineoplaston-induced changes in gene expression. Other research may lead to formulations that are more powerful and faster acting or that have preventative capabilities. At this point, we remain convinced of the potentially important role of antineoplastons in the treatment of cancer.
Acknowledgments The studies were sponsored by the Burzynski Research Institute and supervised by its Institutional Review Board (IRB). The membership of the IRB was in agreement with the FDA. The authors express their appreciation to Lucy Rorke, MD, professor of pathology and neurology, University of Pennsylvania, Children's Hospital of Philadelphia, for review of pathology slides; Dieter Schellinger, MD, professor of radiology, chief, section of neuro-radiology, Georgetown Hospital, Washington, DC; and Joshua Pleasure, MD, M. D. Anderson Cancer Center, Houston, Texas, for evaluation of MRI and PET scans. The following physicians at the Burzynski Clinic (BC) participated in the study: Robert I. Lewy, Robert Weaver, Marc Bestak, Maxwell Axler, Alonzo Peters, Benjamin INTEGRATIVE CANCER THERAPIES 3(1); 2004
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Antineoplastons Saling, Barbara Burzynski, Tomasz Janicki, Jaroslaw Paszkowiak, Vishnu Alapati, Dmitri Davydov, Vsevolod Dolgopolov, Barbara Drynia, Andrzej Himmel, Wojciech Iwanowski, Gabor Jurida, Mohammad Khan, Eva Kubove, Grace Ormstein, Joseph Nguyen, Mohammed Radmard, Basel Salhoot, Barbara Szymkowski, and Marek Walczak. The following senior scientists (PhD), microbiologists, pharmacists, and engineers at the BRI and the BC participated in basic research: Robert Waldbillig, Majciej Klimczak, Elwira Ilkowska-Musial, Leszek Musial, Anna Baranowska, Piotr Kuligowski, Ryszard Madry, Donat Manek, Mike Mokrzycki, Andrzej Wieczorek, Anna Wisniewska, Kris Wisniewski, Irma Witkowska, Dennis Wright, and Iwona Zapedowski. References 1. Burzynski SR. Antineoplastons—history of the research (I). Drugs Exptl Clin Res. 1986;12(suppl 1):1-9. 2. Burzynski SR. Potential of antineoplastons in diseases of old age. Drugs Aging. 1995;7:157-167. 3. Burzynski SR. Investigations on unknown ninhydrin-reacting substances in human blood serum I. Attempts at identification of three such substances. Experientia. 1969;25:490-491. 4. Burzynski SR. Biologically active peptides in human urine: I. Isolation of a group of medium-sized peptides. Physiol Chemo Phys. 1973;5:437-447. 5. Burzynski SR, Ungar AL, Lubanski E. Biologically active peptides in human urine: II. Effect on intestinal smooth muscle and heart. Physiol Chem Phys. 1974;6:457-468. 6. Burzynski SR, Loo TL, Ho DH, et al. Biologically active peptides in human urine: III. Inhibitors of the growth of leukemia, osteosarcoma and HeLa cells. Physiol Chem Phys. 1976;8:13-22. 7. Burzynski SR. Antineoplastons: biochemical defense against cancer. Physiol Chem Phys. 1976;8:275-279. 8. Burzynski SR. Novel differentiation inducers. In: Adam D, ed. Recent Advances in Chemotherapy. Munich, Germany: Futramed; 1992. 9. Burzynski SR, Kubove E, Burzynski B. Treatment of hormonally refractor y cancer of the prostate with antineoplaston AS2-1. Drugs Exptl Clin Res. 1990;16:361-369. 10. Burzynski SR. Gene silencing—a new theory of aging. Med Hypotheses. 2003;60:578-583. 11. Burzynski SR. The methylation control of gene activation and silencing theory. In: Giampapa VC, ed. The Basic Principles and Practice of Anti-aging Medicine and Age Management for the Aesthetic Surgeon and Physician. Montclair, NJ: Giampapa Institute for Anti-aging Medical Therapy; 2003:33-34. 12. van Brabant AJ, Stan R, Ellis NA. DNA helicases, genomic instability, and human genetic instability, and human genetic disease. Ann Rev Genom Hum Genet. 2000;1:409-459. 13. Liau MC, Lee SS, Burzynski SR. Hypomethylation of nucleic acids: a key to the induction of terminal differentiation. Internat J Exptl Clin Chemother. 1989;2:187-199. 14. Burzynski SR, Stolzmann Z, Szopa B, et al. Antineoplaston A in cancer therapy (I). Physiol Chem Phys. 1977;9:485-500. 15. Gross S, Galicka N, Grabarczyk M, et al. Urinary peptides inhibit DNA synthesis in vitro in certain cultured neoplastic cells. Clin Chem. 1977;23:148-149. 16. Beall P, Szopa B, Burzynski SR, et al. Polypeptides that inhibit human breast cancer division. Cancer Biochem Biophys. 1979;3:93-96.
17. Lee SS, Mohabbat MO, Burzynski SR. Tissue culture and animal toxicity studies of antineoplaston A2. Drugs Exptl Clin Res. 1984;10:607-610. 18. Burzynski SR. Antineoplaston A2. Drugs of the Future. 1986;11:549-550. 19. Burzynski SR. Antineoplaston A3. Drugs of the Future. 1986;11:551-552. 20. Burzynski SR. Antineoplaston A5. Drugs of the Future. 1986;11:824-825. 21. Burzynski SR, Mohabbat MO. Chronic animal toxicity studies of antineoplaston A2. Drugs Exptl Clin Res. 1986;12(suppl 1):7375. 22. Lee SS, Mohabbat MO, Burzynski SR. In vitro cancer growth inhibition and animal toxicity studies of antineoplaston A3. Drugs Exptl Clin Res. 1987;13(suppl 1):57-60. 23. Lee SS, Burzynski SR. Tissue culture and animal toxicity studies of antineoplaston A5. Drugs Exptl Clin Res. 1987;13(suppl 1):31-35. 24. Burzynski SR, Kubove E. Initial clinical study with antineoplaston A2 injections in cancer patients with five years follow-up. Drugs Exptl Clin Res. 1987;13(suppl 1):1-12. 25. Burzynski SR, Kubove E. Phase I clinical studies of antineoplaston A3 injections. Drugs Exptl Clin Res. 1987;13(suppl 1):17-29. 26. Burzynski SR, Kubove E. Phase I clinical studies of antineoplaston A5 injections. Drugs Exptl Clin Res. 1987;13(suppl 1):37-43. 27. Burzynski SR, Hendry LB, Mohabbat MO, et al. Purification structure determination, synthesis and animal toxicity studies of antineoplaston A10. In: Proceedings of the 13th International Congress of Chemotherapy. Vienna, Austria; 1983:17, PS. 12.4 11-4. 28. Burzynski SR, Hai TT. Antineoplaston A10. Drugs of the Future. 1985;10:103-105. 29. Burzynski SR. Synthetic antineoplastons and analogs. Drugs of the Future. 1986;11:679-688. 30. Burzynski SR, Mohabbat MO, Lee SS. Preclinical studies of antineoplaston AS1-1 and antineoplaston AS2-5. Drugs Exptl Clin Res. 1986;12(suppl 1):11-16. 31. Burzynski SR, Khalid M. Antineoplaston A10 injections. Drugs of the Future. 1986;11:364-365. 32. Burzynski SR, Khalid M. Antineoplaston AS2-1. Drugs of the Future. 1986;11:361-363. 33. Burzynski SR. Antineoplaston AS2-5. Annual Drug Data Report. 1986;8:319. 34. Burzynski SR, Mohabbat MO, Burzynski B. Animal toxicology studies on oral formulation of antineoplaston A10. Drugs Exptl Clin Res. 1984;10:113-118. 35. Burzynski SR. Phase I clinical studies of antineoplaston AS2-5 injections. In: Ishigami J, ed. Recent Advances in Chemotherapy. Tokyo, Japan: University of Tokyo Press; 1985. 36. Burzynski SR, Burzynski B, Mohabbat MO. Toxicology studies of antineoplaston AS 2-1 injections in cancer patients. Drugs Exptl Clin Res. 1986;12(suppl 1):25-35. 37. Burzynski SR, Kubove E. Toxicology studies of antineoplaston A10 injections in cancer patients. Drugs Exptl Clin Res. 1986;12(suppl 1):47-55. 38. Lehner AF, Burzynski SR, Hendry LB. 3-phenylacetylamino2,6-piperidinedione, a naturally-occurring peptide analog with apparent antineoplastic activity may bind to DNA. Drugs Exptl Clin Res. 1986;12(suppl 1):57-72. 39. Ashraf AQ, Liau MC, Mohabbat MO, et al. Preclinical studies of antineoplaston A10 injections. Drugs Exptl Clin Res. 1986;12(suppl 1):37-45. 40. Ashraf AQ, Liau MC, Kampalath BN, et al. Pharmacokinetic study of radioactive antineoplaston A10 following oral administration in rats. Drugs Exptl Clin Res. 1987;13(suppl 1):45-50.
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Burzynski 41. Hendry LB, Muldoon TG, Burzynski, SR et al. Stereochemical modeling studies of the interaction of Antineoplaston A10 with DNA. Drugs Exptl Clin Res. 1987;13(suppl 1):77-81. 42. A s h r a f A Q , Bu r z y n s k i SR . C om p a r a t i v e s t u d y of antineoplaston A10 levels in plasma of healthy people and cancer patients. Adv Exptl Clin Chemother. 1988;2:19-28. 43. Ashraf AQ, Kampalath BN, Burzynski SR. Pharmacokinectic analysis of antineoplaston A10 injections following intravenous administration in rats. Adv Exptl Clin Chemother. 1988;6:3339. 44. Burzynski SR, Kubove E, Burzynski B. Phase I clinical studies of oral formulation of antineoplaston AS2-1. Adv Exptl Clin Chemother. 1988;2:29-36. 45. Burzynski SR, Kubove E, Burzynski B. Phase II clinical trials of antineoplastons A10 and AS2-1 infusions in astrocytoma. In: Adam D, ed. Recent Advances in Chemotherapy. Munich, Germany: Futuramed; 1992. 46. Burzynski SR, Kubove E, Szymkowski B. Phase II clinical trials of antineoplaston A10 and AS2-1 infusions in high-grade glioma. Paper presented at: 18th International Congress of Chemotherapy; June 1993; Stockholm, Sweden. 47. Hawkins MG, Friedman MA. National Cancer Institute's evaluation of unconventional cancer treatments. J Natl Cancer Inst. 1992;84:1699-1702. 48. Buckner JD, Malkin MG, Reed E, et al. Phase II study of antineoplaston A10 (NSC 648539) and AS2-1 (NSC 6200261) in patients with recurrent glioma. Mayo Clin Proc. 1999;74:137145. 49. Burzynski SR. Efficacy of antineoplastons A10 and AS2-1. Mayo Clin Proc. 1999;74:641-642. 50. Burzynski SR, Conde AB, Peters A, et al. A retrospective study of antineoplastons A10 and AS2-1 in primary brain tumours. Clin Drug Invest. 1999;18:1-10. 51. Burzynski SR. Antineoplastons. In: Novey DW, ed. Clinician's Complete Reference to Complementary/Alternative Medicine. St. Louis (MO): Mosby; 2000:496-507. 52. Burzynski SR, Lewy RI, Weaver RA, et al. Phase II study of antineoplastons A10 and AS2-1 in patients with recurrent diffuse intrinsic brain stem glioma (preliminary report). Drugs in R&D. 2003;4:91-101. 53. Shack S, Chen LC, Miller AC, et al. Increased susceptibility of ras transformed cells to phenylacetate is associated with inhibition of p21ras isoprenylation and phenotypic reversion. Int J Cancer. 1995;63:124-129. 54. Adam L, Crepin M, Savin C et al. Sodium phenylbutyrate induces growth inhibition and Bcl-2 down-regulation and apoptosis in MCF7 ras cells in vitro and in nude mice. Cancer Res. 1995;55:5156-5160. 55. Castillo M, Iglesias J, Zafra MF, et al. Inhibition of chick brain cholesterogenic enzymes by phenyl and phenolic derivatives of phenylalanine. Neurochem. 1991;18:171-174. 56. DiCroce L, Raker VA, Corsaro M, et al. Methyltransferase recruitment and DNA hypermethylation of target promoters by an oncogenic transcription factor. Science. 2002;295:10791082. 57. Gorospe M, Shack S, Guyton KZ, et al. Up-regulation and functional role of p21WAF1/Cip1 during growth arrest of human breast carcinoma MCF-7 cells by phenylacetate. Cell Growth Differ. 1996;7:1609-1615.
58. Liu L, Samid D. Mutant p53 as a target of phenylacetate in human glioblastoma [abstract 2580]. Proceedings of the 86th Annual Meeting of the American Association for Cancer Research. Toronto, Canada; 1995:433. 59. Kamitani H, Tanjura S, Watanbe K, et al. Histone acetylation may suppress human glioma cell proliferation with p21WAF1/Cip1 and gelsolin are induced. Neuro-Oncology. 2002;4:95-101. 60. Burzynski SR. Gene therapy with antineoplastons. Paper presented at: Comprehensive Cancer Care; 1998; Washington, DC. 61. Waldbillig RJ, Burzynski SR. Mechanism of action, uptake and g en e a r r a y s t u d i es on t h e a n t i n eopl a s t i c a g en t phenylacetylglutamine (PG) in human glioma cells U-87. Paper presented at: 8th Annual Meeting of the Society for Neuro-Oncology; November 13-16, 2003; Keystone, Colorado. 62. Mahoney DH, Cohen ME, Friedman HS, et al. Carboplatin is effective therapy for young children with progressive optic pathway tumors: a Pediatric Oncology Group phase II study. Neuro-Oncology. 2000;2:213-220. 63. Allen JC, Hancock, Walker R, et al. PCNU and recurrent childhood brain tumors. J Neurooncol. 1987;5:241-244. 64. Heideman RL, Packer RJ, Reaman GH, et al. A phase II evaluation of thiotepa in pediatric central nervous system malignancies. Cancer. 1993;72:271-275. 65. Mandell LR, Kadota R, Freeman C, et al. There is no role for hyperfractionated radiotherapy in the management of children with newly diagnosed diffuse intrinsic brain stem tumors: results of pediatric oncology group phase III trial comparing conventional vs. hyperfractionated radiotherapy. Int J Radiat Oncol Biol Phys. 1999;43:959-964. 66. Phuphanich S, Selph J, Snodgrass S, et al. Low dose thalidomide and temodar as salvage therapy for recurrent malignant glioma. Neuro-Oncology. 2002;4:374. 67. Prados M, Schold SC Jr, Fine HA, et al. A randomized, doubleblind, placebo-controlled, phase 2 study of RMP-7 in combination with carboplatin administered intravenously for the treatment of recurrent malignant glioma. Neuro-Oncology. 2003;5:96-103. 68. Ogata Y, Tsuda H, Matono K, et al. Long-term survival following treatment with antineoplastons for colon cancer with unresectable multiple liver metastases: report of a case. Surg Today. 2003;33:448-453. 69. Tsuda H, Sata M, Saitsu H, et al. Antineoplaston AS2-1 for maintenance therapy in liver cancer. Oncol Rep. 1997;4:12131216. 70. Kumabe T, Tsuda H, Uchida M, et al. Antineoplaston treatment for advanced hepatocellular carcinoma. Oncol Rep. 1998;5:1363-1367. 71. Tsuda H, Sata M, Ijuuin H. A novel strategy for remission induction and maintenance in cancer therapy. Oncol Rep. 2002;9:65-68. 72. Tsuda H, Sata M, Kumabe T, Uchida M, Hara H. The preventive effect of antineoplaston AS2-1 on HCC recurrence. Oncol Rep. 2003;10:391-397. 73. Richardson MA, Russell NC, Sanders T, et al. Assessment of outcomes at alternative medicine cancer clinics: a feasibility study. J Altern Complement Med. 2001;7:19-32.
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Published on Oct 18, 2011
Stanislaw R. Burzynski http://ict.sagepub.com/content/3/1/47 Published by: The online version of this article can be found at: http://www.sa...


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The Megaman 5W LED GX53 delivers huge energy and cash savings compared to halogen bulbs. It has a standard shape and size, directly replacing a 30W halogen equivalent, without needing to be changed as often. The LED GX53 is perfect for lighting small spaces and surface mounting inside cabinets where space is at a premium.

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I need to come up with a Hypothesis on crime. I also have to have a null hypothesis, independent and dependent variable as well as evidence to prove my hypothesis. Can anyone help me please?
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text: Hello everyone, I know Toshiba (and maybe Hitachi) allready have red/green lens filters with their sets, to improve the "purity" of the light the phosphor emits. However, I believe Sony and the majority of other manufacturers do not have such filters. Would it be possible to find such filters, and retrofit them to sets that do not allready have them? Are the filters on the Toshiba's separate, or are these filters "built-into" the actual mechanical lens assembly? I've looked online for filters, but the only hits I seemed to get were Toshiba's pages I know Guy Kuo mentioned doing this to a projector of his using certain gels, but I was wondering if there was some really good glass filters available? Thanks for any responses/comments! -Ryan Dinan


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One of the biggest problems that startup enterprises face is the fact that they register or prepare for tax. HMRC do make it reasonably easy to register your company on line after you have completed several checks via Firms Residence with regards to company name. And after you have registered, you can then start seeking at tax, what you might ought to pay but also any tax credits your company may possibly be eligible for, for instance for investigation and development. Get a lot more details about uk r&d tax credit
Tax and national insurance
The two simple types of business tax UK currently levy on each and every form of enterprise is tax and national insurance coverage. Tax is paid on profits while national insurance is paid on profits starting from a reduce quantity and is paid for staff of your business enterprise also as an employer.
When you are self-employed as a sole trader, then you definitely will spend tax on business enterprise earnings at the same time as Class two and Class 4 national insurance - employer and employee for want of a distinctive method to place it. After you run a restricted company with employees, you have to spend revenue tax via the Spend As You Earn or PAYE scheme as well as Corporation Tax at the same time as national insurance contributions. Based on the earnings from the enterprise, it may also pay to register for VAT exactly where you submit a quarterly return for payments and receipts of VAT.
The way that you know what tax and national insurance coverage is going to be due when starting a brand new company UK primarily based is by way of your bookkeeping. There are plenty of various ways to do this from the standard paper and pen ledger via to uncomplicated spreadsheets and onto additional complex account software program. But whatever system you use, it should commence from day one particular.
Legally, a company or sole trader have to retain correct financial records that detail all the income getting into and leaving the enterprise. Based on Get started Up Donut, these records should be kept for a minimum of six years, even if the enterprise stops trading.
The principle elements of a bookkeeping system contain a money book, a sales ledger, purchased ledger as well as a wages book. Most of this can now be computerised, even though a cash book is typically necessary when the enterprise uses petty cash to purchase supplies which include milk and sugar for the office kitchen or occasional office supplies. Some accountancy software program can connect to the business' bank account and automatically record all transactions, allowing you to dictate what they relate to and to exclude any individual transactions for a sole trader.
Finishing a tax return
Yet another region that quite a few startups fall afoul of in their first year is completing a tax return. Whilst the self-assessment system makes it theoretically straightforward to complete the relevant info, see what tax you owe and sort out the payment, the emphasis is totally on the individual completing the type to make positive it is correct. If anything goes incorrect, you'll be liable for the consequences.
Because of this, it can typically be a superb idea to get somebody to either comprehensive the kind on your behalf or to double check each of the details ahead of submitting it. If the small business has appointed an accountant to handle each of the bookkeeping troubles, then they may take care of this but otherwise, it may be worth in search of a professional for this area.
You may also speak to an professional in tax advice UK guidelines who can let you know if you can find any extras you could possibly be capable of claim for or schemes that your enterprise could qualify for that could lessen the tax you might want to spend and in some cases get you a tax credit. Examples contain machinery, fixtures and fittings for the premises which are claimed as a capital allowance. Cash spent to create the business enterprise can sometimes also qualify as this kind of expense.
Qualifying for R&D tax credit
A perfect example of this may be the analysis and development tax credit scheme the government presently operates. This is designed to give firms who are working to study and develop things in the region of science or technology a refund of monies paid in this research. The great thing is that the investigation doesn't even must be a success to qualify - but it does need to meet certain criteria to do so.
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Registering for VAT
Another big decision that sometimes can affect a startup business in its very first year is whether or not to register for VAT. Value Added Tax or VAT is charged on most goods and services inside the UK and also on some imported in the EU and outside it. Firms making more than £81,000 automatically have to register for it.
VAT is something of a cycle - a small business pays it on goods bought and charges it on goods sold, for example. The concept is the fact that the two equal out but if they don't then a small business can owe or be owed a payment from HMRC.
You'll find two primary reasons to voluntarily register for VAT if your enterprise doesn't make this figure. One reason is if customers are predominantly other VAT registered firms so it tends to make no real difference whether your business is VAT registered or not. The other is if you often find your business would be in a refund position and by registering, you may recoup this money from HMRC.
Getting the suitable tax advice is usually key for new firms. It can help understand any time you can expand, add new product ranges and try new markets too as ensuring you're always on top with the quantity of tax you'll need to pay each year.
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