Resenje za rak?
Started by
Uran
, Feb 06 2007 23:13
185 replies to this topic
#16
gaspod
-
- Members
- 238 posts
Posted 08 February 2007 - 13:09
Odličan ti je ovaj članak, još da znamo korisničko i lozinku pa da se načitamo ko veliki
#17
Indy
-
- Members
- 21,392 posts
Posted 08 February 2007 - 14:47
Kakvu lozinku? Kod mene ne trazi nista, mora da je neka greska. No, evo ga celog.
----
Gut Research Yields New Cancer Approach
Attacking Treatment-Resistant Tumors via Cell Skeletons
Researchers believe they have discovered by chance a new way to fight colorectal cancer, and potentially cancers of the esophagus, liver and skin. Early work shows that a group of compounds called peroxisome proliferator-activated receptor-gamma (PPARγ) inhibitors may have an unexpected cancer-fighting effect, according to research published today in the journal International Cancer Research. Furthermore, the new studies suggest that PPARγ inhibitors act through some of the same mechanisms as the blockbuster chemotherapy Taxol, but with key differences.
While studying whether compounds known to affect PPARγ could play a role in inflammatory bowel diseases, a team at the University of Rochester Medical Center found that medium-to-high doses of PPARγ inhibitor killed colorectal cancer cell lines. Despite the compound’s class name, the anti-cancer effect has nothing to do with the ability of the compounds to inhibit PPARγ function. Researchers believe that PPARγ inhibitors instead attack the “skeletons” of cancer cells that enable them to reproduce, grow and spread. Better solutions are needed because, according to the American Cancer Society, colorectal cancer remains the no. 2 cause of cancer death for men, and the no. 3 cause of cancer death for women.
“This is the first observation of a small molecule dramatically reducing levels of the proteins called tubulins, the building blocks of cancer cell skeletons,” said Katherine L. Schaefer, Ph.D., a research assistant professor within the Department of Medicine, Gastroenterology and Hepatology Division, at the University of Rochester Medical Center, and first author of the paper. “Because cells that line the colon are similar to those in the liver, esophagus and skin, we see potential for a new way to treat those cancers as well.”
In the study that led to the discovery of the anti-cancer effect, researchers were looking for new ways to reduce inflammation seen in Crohn’s disease and ulcerative colitis, bowel diseases that cause pain and diarrhea. Specifically, they were comparing the effect on inflammation of encouraging the action of the PPARγ protein (with activator compounds) against discouraging it (with inhibitors). The team conducted these experiments using colorectal cancer cells as study models because they arise from normal gut cells and share some of their qualities (e.g. normal inflammatory signals). Unlike normal gut cells, however, cancer cells do not die when removed from the gut wall. Living on in the absence of normal survival signals makes cancer cells dangerous in the body, but useful as cell lines for study.
While comparing PPARγ activators and inhibitors, Schaefer noted with frustration that her cancer cells were dying before she could complete her experiments. Retracing her steps, she found that she had used too much inhibitor. The team, led by Lawrence J. Saubermann, M.D., associate professor of Medicine at the Medical Center, realized they had come across a potentially new therapeutic effect, and launched experiments to confirm it.
Study Details
In the newly published study, researchers observed the effects of three compounds known from the literature to inhibit PPARγ, T0070907, GW9662 and BADGE, on the ability of colorectal tumor cells to survive. High doses (10-100 μM) of all three interfered with colorectal cancer cell growth, reduced the cells’ ability to spread through the bloodstream to cause new tumors elsewhere (metastasize) and caused cells to self-destruct, generally within 24 hours. Further experiments showed that high-dose PPARγ inhibition destroyed cancer cell microtubules, protein structures that form part of the skeleton of cells.
Beyond providing structural support and shape to cells, microtubules expand and shrink to generate the force needed for cells to divide, a basic process in tumor growth. Microtubules are made of two related proteins, alpha and beta tubulin, which pair up to form a chain and then wind into a helix. The current studies found that high-dose PPARγ inhibitors reduced levels of α and β tubulin by 60 to 70 percent.
Also described in the publication are studies where PPARγ inhibitors killed tumor cells in mice without causing significant toxicity. That provides at least the hope that the drug class may not be prohibitively toxic in humans, the researchers said. More formal toxicity studies are underway.
While PPARγ inhibitors reduce tubulin levels, older anti-microtubule drug classes; Vinca alkaloids, taxanes (including Taxol) and epithiolones; interfere with microtubule dynamics. To play their role in tumor growth, microtubules must remain flexible. Taxol, for example, “freezes” tubulin subunits, making the cell skeleton rigid and unable to make the shape changes necessary for cell division. Brought to the market by Bristol-Myers Squibb in 1993, Taxol had annual sales of $1.6 billion at its peak in 2000.
Unfortunately, Taxol and other standard, anti-tubulin drugs failed in colorectal cancer clinical trials. Gut tumor cells have evolved to include “efflux” proteins that recognize standard chemotherapies as foreign, and “pump them out” of tumor cells. Even for breast and lung cancer, the tumor types for which Taxol is most used, nearly 100 percent of these tumors eventually become resistant, said Alok A. Khorana, M.D., assistant professor of Medicine at the Medical Center. In cells with more drug efflux pumps, Taxol is not effective (e.g. pancreas, liver and colon), he said.
High-dose PPARγ inhibitors may overcome the limits of current treatment because the profile of molecules likely to be pumped out by drug efflux proteins is known, and at least one of the PPARγ inhibitors does not match it. In addition, PPARγ inhibitors do not bind to the standard tubulin-binding site that renders Taxol useless when binding sites change shapes thanks to ongoing genetic mutations.
With standard anti-microtubule not an option for colorectal cancer, current chemotherapy regimens feature 5-fluorouracil (5-FU) in combination with other chemotherapy drugs (oxaliplatin, irinotecan) and antibodies (bevacizumab, cetuximab). Once again, response rates of current drugs are low (less than 30 percent as single agents). Tumors generally begin growing again with a year.
Moving forward, the research team will seek to determine exactly which proteins are involved in the anti-cancer effect of PPARγ inhibitors. Combination therapy is the current leading strategy in treating cancer, and finding the mechanisms by which PPARγ inhibitors work could be a first step toward their safe combination with other treatments.
“The last work attempting to reduce tubulin levels was abandoned approximately 25 years ago under the assumption that such drugs would be toxic, destroying microtubules in healthy cells as well as cancer cells,” Schaefer said. “Our early studies, however, suggest that general toxicity does not rule out this approach as once feared. With new drug delivery technologies that help drugs target only cancer cells, we are very excited about the potential of this line of work.”
###
For more media inquiries, contact:
Greg Williams
(585) 273-1757
greg_williams@urmc.rochester.edu
----
Gut Research Yields New Cancer Approach
Attacking Treatment-Resistant Tumors via Cell Skeletons
Researchers believe they have discovered by chance a new way to fight colorectal cancer, and potentially cancers of the esophagus, liver and skin. Early work shows that a group of compounds called peroxisome proliferator-activated receptor-gamma (PPARγ) inhibitors may have an unexpected cancer-fighting effect, according to research published today in the journal International Cancer Research. Furthermore, the new studies suggest that PPARγ inhibitors act through some of the same mechanisms as the blockbuster chemotherapy Taxol, but with key differences.
While studying whether compounds known to affect PPARγ could play a role in inflammatory bowel diseases, a team at the University of Rochester Medical Center found that medium-to-high doses of PPARγ inhibitor killed colorectal cancer cell lines. Despite the compound’s class name, the anti-cancer effect has nothing to do with the ability of the compounds to inhibit PPARγ function. Researchers believe that PPARγ inhibitors instead attack the “skeletons” of cancer cells that enable them to reproduce, grow and spread. Better solutions are needed because, according to the American Cancer Society, colorectal cancer remains the no. 2 cause of cancer death for men, and the no. 3 cause of cancer death for women.
“This is the first observation of a small molecule dramatically reducing levels of the proteins called tubulins, the building blocks of cancer cell skeletons,” said Katherine L. Schaefer, Ph.D., a research assistant professor within the Department of Medicine, Gastroenterology and Hepatology Division, at the University of Rochester Medical Center, and first author of the paper. “Because cells that line the colon are similar to those in the liver, esophagus and skin, we see potential for a new way to treat those cancers as well.”
In the study that led to the discovery of the anti-cancer effect, researchers were looking for new ways to reduce inflammation seen in Crohn’s disease and ulcerative colitis, bowel diseases that cause pain and diarrhea. Specifically, they were comparing the effect on inflammation of encouraging the action of the PPARγ protein (with activator compounds) against discouraging it (with inhibitors). The team conducted these experiments using colorectal cancer cells as study models because they arise from normal gut cells and share some of their qualities (e.g. normal inflammatory signals). Unlike normal gut cells, however, cancer cells do not die when removed from the gut wall. Living on in the absence of normal survival signals makes cancer cells dangerous in the body, but useful as cell lines for study.
While comparing PPARγ activators and inhibitors, Schaefer noted with frustration that her cancer cells were dying before she could complete her experiments. Retracing her steps, she found that she had used too much inhibitor. The team, led by Lawrence J. Saubermann, M.D., associate professor of Medicine at the Medical Center, realized they had come across a potentially new therapeutic effect, and launched experiments to confirm it.
Study Details
In the newly published study, researchers observed the effects of three compounds known from the literature to inhibit PPARγ, T0070907, GW9662 and BADGE, on the ability of colorectal tumor cells to survive. High doses (10-100 μM) of all three interfered with colorectal cancer cell growth, reduced the cells’ ability to spread through the bloodstream to cause new tumors elsewhere (metastasize) and caused cells to self-destruct, generally within 24 hours. Further experiments showed that high-dose PPARγ inhibition destroyed cancer cell microtubules, protein structures that form part of the skeleton of cells.
Beyond providing structural support and shape to cells, microtubules expand and shrink to generate the force needed for cells to divide, a basic process in tumor growth. Microtubules are made of two related proteins, alpha and beta tubulin, which pair up to form a chain and then wind into a helix. The current studies found that high-dose PPARγ inhibitors reduced levels of α and β tubulin by 60 to 70 percent.
Also described in the publication are studies where PPARγ inhibitors killed tumor cells in mice without causing significant toxicity. That provides at least the hope that the drug class may not be prohibitively toxic in humans, the researchers said. More formal toxicity studies are underway.
While PPARγ inhibitors reduce tubulin levels, older anti-microtubule drug classes; Vinca alkaloids, taxanes (including Taxol) and epithiolones; interfere with microtubule dynamics. To play their role in tumor growth, microtubules must remain flexible. Taxol, for example, “freezes” tubulin subunits, making the cell skeleton rigid and unable to make the shape changes necessary for cell division. Brought to the market by Bristol-Myers Squibb in 1993, Taxol had annual sales of $1.6 billion at its peak in 2000.
Unfortunately, Taxol and other standard, anti-tubulin drugs failed in colorectal cancer clinical trials. Gut tumor cells have evolved to include “efflux” proteins that recognize standard chemotherapies as foreign, and “pump them out” of tumor cells. Even for breast and lung cancer, the tumor types for which Taxol is most used, nearly 100 percent of these tumors eventually become resistant, said Alok A. Khorana, M.D., assistant professor of Medicine at the Medical Center. In cells with more drug efflux pumps, Taxol is not effective (e.g. pancreas, liver and colon), he said.
High-dose PPARγ inhibitors may overcome the limits of current treatment because the profile of molecules likely to be pumped out by drug efflux proteins is known, and at least one of the PPARγ inhibitors does not match it. In addition, PPARγ inhibitors do not bind to the standard tubulin-binding site that renders Taxol useless when binding sites change shapes thanks to ongoing genetic mutations.
With standard anti-microtubule not an option for colorectal cancer, current chemotherapy regimens feature 5-fluorouracil (5-FU) in combination with other chemotherapy drugs (oxaliplatin, irinotecan) and antibodies (bevacizumab, cetuximab). Once again, response rates of current drugs are low (less than 30 percent as single agents). Tumors generally begin growing again with a year.
Moving forward, the research team will seek to determine exactly which proteins are involved in the anti-cancer effect of PPARγ inhibitors. Combination therapy is the current leading strategy in treating cancer, and finding the mechanisms by which PPARγ inhibitors work could be a first step toward their safe combination with other treatments.
“The last work attempting to reduce tubulin levels was abandoned approximately 25 years ago under the assumption that such drugs would be toxic, destroying microtubules in healthy cells as well as cancer cells,” Schaefer said. “Our early studies, however, suggest that general toxicity does not rule out this approach as once feared. With new drug delivery technologies that help drugs target only cancer cells, we are very excited about the potential of this line of work.”
###
For more media inquiries, contact:
Greg Williams
(585) 273-1757
greg_williams@urmc.rochester.edu
#18
gaspod
-
- Members
- 238 posts
Posted 08 February 2007 - 15:23
Ko sme tebi šta da traži, to samo malu raju smeju zajebavat
Dobar članak, skontao sam da je reč o antitubulinskoj substanci, a pošto su slične već registrovane (pomenuti Taxol) i proftabilne (1,6 bil $ za 7 god., malo li je) verujem da će se potruditi oko njega. Sad koliko znam propisi o uvođenju novih lekova su prilično konzervativni, a i nebili nakon DES-ova i drugih "katastrofa".
Možemo samo da navijamo za Kaću Šeferovu.
Dobar članak, skontao sam da je reč o antitubulinskoj substanci, a pošto su slične već registrovane (pomenuti Taxol) i proftabilne (1,6 bil $ za 7 god., malo li je) verujem da će se potruditi oko njega. Sad koliko znam propisi o uvođenju novih lekova su prilično konzervativni, a i nebili nakon DES-ova i drugih "katastrofa".
Možemo samo da navijamo za Kaću Šeferovu.
#19
Indy
-
- Members
- 21,392 posts
Posted 08 February 2007 - 23:20
QUOTE(gaspod @ 9 Feb 2007, 01:23)
... i proftabilne (1,6 bil $ za 7 god., malo li je) ...
Izostavio si ovaj put "nazalost". Dakle, kritika radi.
#20
gaspod
-
- Members
- 238 posts
Posted 08 February 2007 - 23:55
QUOTE(Indy @ 8 Feb 2007, 23:20)
Izgleda da je tamo "upeko mađar", ne žalostim se ja zbog toga. Samo neka oni zarađuju.
#21
Indy
-
- Members
- 21,392 posts
Posted 08 February 2007 - 23:57
QUOTE(gaspod @ 9 Feb 2007, 09:55)
Izgleda da je tamo "upeko mađar", ne žalostim se ja zbog toga. Samo neka oni zarađuju.
Dobro je, Herre. Mislio si da te necu prepoznati, sta? Tvoj jedinstveni fuckhead style je nemoguce imitirati (ili prikriti).
#22
gaspod
-
- Members
- 238 posts
Posted 09 February 2007 - 00:04
QUOTE(Indy @ 8 Feb 2007, 23:57)
Dobro je, Herre. Mislio si da te necu prepoznati, sta? Tvoj jedinstveni fuckhead style je nemoguce imitirati (ili prikriti).
Ili tebi stvarno nije dobro ili nešto debelo grešim?
#23
Indy
-
- Members
- 21,392 posts
Posted 09 February 2007 - 04:48
'Ajd da ne trollujemo vise... tvoje replike su bile taman nepotrebno provokativne koliko i neinformativne.
#24
gaspod
-
- Members
- 238 posts
Posted 10 February 2007 - 01:44
QUOTE(Indy @ 9 Feb 2007, 04:48)
.. a od kada sam postao nadžak čiča siguran sam da mi se neko šunja oko kuće.
Slobodno se opusti i misli pozitivno, ni ja ni Here ti više ne bismo smetali.
#25
Indy
-
- Members
- 21,392 posts
Posted 10 February 2007 - 01:52
QUOTE(gaspod @ 10 Feb 2007, 11:44)
Slobodno se opusti i misli pozitivno, ni ja ni Here ti više ne bismo smetali.
Ne, nisi Herr. Herr je ipak imao duha, na svoj naopak nacin.
#27
Isis
-
- Members
- 513 posts
Posted 10 February 2007 - 13:49
indy, odlican je onaj izvestaj us kongresa sto si ga linkovao.
sto se racunovodstvenog tretmana r&d troskova tice, nadam se da sledece moze pomoci.
troskovi se dele u tri kategorije:
1. operativni (oni koji su nastali u funkciji generisanja prihoda u tekucem periodu)
2. troskovi finansiranja (nebitni za ovu pricu)
3. kapitalni (oni koji nastaju da bi se pribavila imovina cijem koriscenjem se sticu koristi tokom vise perioda- recimo tangible assets-property, plant and equipment)
buduci da se finansijski izvestaji prave za odredjeni preiod (bilans uspeha, p&l account), odnosno na odredjeni dan (bilans stanja, balance sheet), a sa druge strane imas kapitalne troskove koji su nastali u vezi sa pribavljanjem aktive koju ces koristiti tokom vise perioda, neophodno je ukupne kapitalne troskove podeliti (shodno odredjenom metodu) na broj perioda tokom kojih ces koristiti tu imovinu. taj, za svaki period, pripadajuci deo troskova je ili depreciation (ukoliko je u pitanju tangible assets) ili amortisation (ukoliko je u pitanju intangible assets- patenti i licence recimo).
za pharma industriju je pitanje da li ce se r&d troskovi tretirati kao op expenses ( i u tom slucaju se od ukupnih prihoda oduzima celokupni deo r&d troskova koji su nastali u tom preiodu) ili kao capital expenditures ( i u tom slucaju je bilans uspeha tog perioda opterecen samo amortizacijom, koja je x- ti deo ukupnih r&d troskova).
prema us gaap (racunovodstvena pravila u usa), r&d troskovi se moraju tretirati kao op expenses, prema ias-u (rac. pravila za ostatak sveta), samo pod odredjenim uslovima se r&d troskovi mogu kapitalizovati (vrlo striktna pravila, tako da ta mogucnost kao i da ne postoji).
bitna razlika izmedju op expenses i cap expenditures je da op expenses ne kreiraju assets (imovinu, aktivu).
da se vratim na deo onog izvestaja koji se bavi efektom racunovodstvenog tretmana na profitabilnost pharma kompanija...
izvestaj se uglavnom bavi RoA merom prifitabilnosti (return on assets- odnos izmedju net income i assets koju si uposlio da bi realizovao taj profit).
tretiranje r&d troskova kao operativnih troskova na RoA ima efekat da:
1. u startu verovatno smanjuje operating income- od prihoda oduzimas sve troskove r&d nastale u tom periodu, a ne njihov amortizovani deo
2. prvi efekat je donekle ublazen poreskim efektom (tax deductibility of expenses; veci troskovi, veci i tax benefit)
3. ne uvecavaju assets (aktivu, imovinu)
ako je RoA= net income/ assets, a net income je u direktnoj vezi sa visinom op income-a, jasno je da je uticaj postojeceg racunovodstvenog tretmana r&d troskova na profitabilnost dvojak- kroz tacku 1 smanjujes profitabilnost (ali ne u odnosu 1:1 usled tacke 2), dok tackom 3 utices na povecanje profitabilnosti.
u opstem slucaju je tesko predvideti koji od ova tri (medjusobno donekle offsetting uticaja) ce prevladati. verujem da su, zarad pisanja tog izvestaja, analizirali celu industriju i zakljucili da je u proseku uticaj takav da sadasnji racunovodstveni tretman preuvelicava profitabilnost pharma industrije (preovladava tacka 3). mada, nisu dali opis konkretne metodoligije (ili jesu, al' ja nisam nasla, moguce). korektna formulacija bi bila da bi mogao da preuvelica (ali ne i da je to nuzno uvek slucaj).
generalno, kada bi reklasifikovali r&d troskove u kapitalne troskove i dozvolili njihovu amortizaciju tokom vremena, kakav bi uticaj na op income i profitabilnost bio, zavisice od: (i) starosti firme i visine r&d troskova (one koje postoje duze i koje imaju znacajnije r&d troskove imace i vecu promenu u visini assets-a), (ii) metoda amortizacije (iii) odnosa godisnje amortizacije i godisnjih r&d troskova (firme koje brzo rastu imaju trend da im r&d troskovi rastu tokom vremena, te bi reklasifikacija dovela do povecanja op income-a; u slucaju zrelijih kompanija koje imaju ujednacenije godisnje r&d troskove, reklasifikacija bi verovatno dovela do smanjenja op income-a).
ako ima neki racunovodja, mozda moze da doda nesto...
sto se racunovodstvenog tretmana r&d troskova tice, nadam se da sledece moze pomoci.
troskovi se dele u tri kategorije:
1. operativni (oni koji su nastali u funkciji generisanja prihoda u tekucem periodu)
2. troskovi finansiranja (nebitni za ovu pricu)
3. kapitalni (oni koji nastaju da bi se pribavila imovina cijem koriscenjem se sticu koristi tokom vise perioda- recimo tangible assets-property, plant and equipment)
buduci da se finansijski izvestaji prave za odredjeni preiod (bilans uspeha, p&l account), odnosno na odredjeni dan (bilans stanja, balance sheet), a sa druge strane imas kapitalne troskove koji su nastali u vezi sa pribavljanjem aktive koju ces koristiti tokom vise perioda, neophodno je ukupne kapitalne troskove podeliti (shodno odredjenom metodu) na broj perioda tokom kojih ces koristiti tu imovinu. taj, za svaki period, pripadajuci deo troskova je ili depreciation (ukoliko je u pitanju tangible assets) ili amortisation (ukoliko je u pitanju intangible assets- patenti i licence recimo).
za pharma industriju je pitanje da li ce se r&d troskovi tretirati kao op expenses ( i u tom slucaju se od ukupnih prihoda oduzima celokupni deo r&d troskova koji su nastali u tom preiodu) ili kao capital expenditures ( i u tom slucaju je bilans uspeha tog perioda opterecen samo amortizacijom, koja je x- ti deo ukupnih r&d troskova).
prema us gaap (racunovodstvena pravila u usa), r&d troskovi se moraju tretirati kao op expenses, prema ias-u (rac. pravila za ostatak sveta), samo pod odredjenim uslovima se r&d troskovi mogu kapitalizovati (vrlo striktna pravila, tako da ta mogucnost kao i da ne postoji).
bitna razlika izmedju op expenses i cap expenditures je da op expenses ne kreiraju assets (imovinu, aktivu).
da se vratim na deo onog izvestaja koji se bavi efektom racunovodstvenog tretmana na profitabilnost pharma kompanija...
izvestaj se uglavnom bavi RoA merom prifitabilnosti (return on assets- odnos izmedju net income i assets koju si uposlio da bi realizovao taj profit).
tretiranje r&d troskova kao operativnih troskova na RoA ima efekat da:
1. u startu verovatno smanjuje operating income- od prihoda oduzimas sve troskove r&d nastale u tom periodu, a ne njihov amortizovani deo
2. prvi efekat je donekle ublazen poreskim efektom (tax deductibility of expenses; veci troskovi, veci i tax benefit)
3. ne uvecavaju assets (aktivu, imovinu)
ako je RoA= net income/ assets, a net income je u direktnoj vezi sa visinom op income-a, jasno je da je uticaj postojeceg racunovodstvenog tretmana r&d troskova na profitabilnost dvojak- kroz tacku 1 smanjujes profitabilnost (ali ne u odnosu 1:1 usled tacke 2), dok tackom 3 utices na povecanje profitabilnosti.
u opstem slucaju je tesko predvideti koji od ova tri (medjusobno donekle offsetting uticaja) ce prevladati. verujem da su, zarad pisanja tog izvestaja, analizirali celu industriju i zakljucili da je u proseku uticaj takav da sadasnji racunovodstveni tretman preuvelicava profitabilnost pharma industrije (preovladava tacka 3). mada, nisu dali opis konkretne metodoligije (ili jesu, al' ja nisam nasla, moguce). korektna formulacija bi bila da bi mogao da preuvelica (ali ne i da je to nuzno uvek slucaj).
generalno, kada bi reklasifikovali r&d troskove u kapitalne troskove i dozvolili njihovu amortizaciju tokom vremena, kakav bi uticaj na op income i profitabilnost bio, zavisice od: (i) starosti firme i visine r&d troskova (one koje postoje duze i koje imaju znacajnije r&d troskove imace i vecu promenu u visini assets-a), (ii) metoda amortizacije (iii) odnosa godisnje amortizacije i godisnjih r&d troskova (firme koje brzo rastu imaju trend da im r&d troskovi rastu tokom vremena, te bi reklasifikacija dovela do povecanja op income-a; u slucaju zrelijih kompanija koje imaju ujednacenije godisnje r&d troskove, reklasifikacija bi verovatno dovela do smanjenja op income-a).
ako ima neki racunovodja, mozda moze da doda nesto...
#29
Indy
-
- Members
- 21,392 posts
Posted 12 February 2007 - 11:46
QUOTE(snaja @ 12 Feb 2007, 20:55)
Zasto nadrilekarski link na ovom podforumu? Je l' vas placaju?
http://www.quackwatc...r/laetrile.html
#30
snaja
-
- Members
- 8 posts
Posted 12 February 2007 - 12:45
zato sto kad ti ne preostaje nista drugo, hvatas se za bilo kakvu slamku. :-(
nije da verujem u taj lek, ali ta prica oko nacina ishrane mi pije vodu.
posto smo mi iz zemlje srbije, ne verujem da nam je taj lek (ili sta vec) dostupan.
ali ima ljudi koji ce mozda nesto ili neku informaciju izvuci iz ovoga, ko zna?!
jer mnoge detalje koje sam procitala na tom sajtu (bas vezane za ishranu) sam cula od doktora sa instituta u kamenici i to mnogo pre nego sto sam i saznala za taj sajt.
nije da verujem u taj lek, ali ta prica oko nacina ishrane mi pije vodu.
posto smo mi iz zemlje srbije, ne verujem da nam je taj lek (ili sta vec) dostupan.
ali ima ljudi koji ce mozda nesto ili neku informaciju izvuci iz ovoga, ko zna?!
jer mnoge detalje koje sam procitala na tom sajtu (bas vezane za ishranu) sam cula od doktora sa instituta u kamenici i to mnogo pre nego sto sam i saznala za taj sajt.
