Aa
Inhibition on Hepatitis B virus in vitro of recombinant MAP30 from bitter melon
http://www.springerlink.com/content/j26q743782161u74/
not a cure at all because in vitro study only but bitter melon won t help hbv at least keeping us helthier as regards glucose kinetics
not a cure at all because in vitro study only but bitter melon won t help hbv at least keeping us helthier as regards glucose kinetics
I thought occult HBV was due to a mutated form of the virus that does not express HbSag?
no this is not ocrrect, they express a mutated hbsag in the "a" determinant, this mutation exsists naturally or induced by lamivudine/adefovir/telbivudine, many RT mutations induce hbsag mutations too.
architect and siemens have kits to detect hbsag mutant
in pisa they said the hbsag mutation is not too bad because the virus is very weak and can be eradicated by interferon and probably ntz too (nucs useless), hbsag is also very different to wild type and even HDV cannot use it
no this is not ocrrect, they express a mutated hbsag in the "a" determinant, this mutation exsists naturally or induced by lamivudine/adefovir/telbivudine, many RT mutations induce hbsag mutations too.
architect and siemens have kits to detect hbsag mutant
in pisa they said the hbsag mutation is not too bad because the virus is very weak and can be eradicated by interferon and probably ntz too (nucs useless), hbsag is also very different to wild type and even HDV cannot use it
"so i think there are many variables to put together since we probably dont know many things.one thing certain is that hbvdna zero is the mst important value correlated to liver dmage "
I agree, there are many variables and many unknowns. The immune system is complex, the virus is complex. Luckily, the scientists are working hard. If your above statement is correct, then antivirals must be highly recommended.
I thought occult HBV was due to a mutated form of the virus that does not express HbSag?
I agree, there are many variables and many unknowns. The immune system is complex, the virus is complex. Luckily, the scientists are working hard. If your above statement is correct, then antivirals must be highly recommended.
I thought occult HBV was due to a mutated form of the virus that does not express HbSag?
Taiwan study indicating normal ALT does not guarantee no progression of liver disease. I would like to know whether it is still the case if we use 30(for male) and 19(for female) as nul (normal upper limit). Also whether this uln should further be lowered in cirrhosis stage because there are lfewer liver cells to be damaged (as explained by Dr Misra on the Heplist.
well the best ranges for no liver related deaths are 10-15 but alt number is not always important if you see the cirrhosis regression study the regression is linked to platlets, PT, bmi, hbvdna and much less on alt value, there was regression even with alt 65 and no regression with lower alt.i also regressed with alt between 30-40
so i think there are many variables to put together since we probably dont know many things.one thing certain is that hbvdna zero is the mst important value correlated to liver dmage
in pisa they use hbsag quantity to understand immune response/control and much less on amount of cccdna (for that they prefer biopsy) if hbeag is negative
well the best ranges for no liver related deaths are 10-15 but alt number is not always important if you see the cirrhosis regression study the regression is linked to platlets, PT, bmi, hbvdna and much less on alt value, there was regression even with alt 65 and no regression with lower alt.i also regressed with alt between 30-40
so i think there are many variables to put together since we probably dont know many things.one thing certain is that hbvdna zero is the mst important value correlated to liver dmage
in pisa they use hbsag quantity to understand immune response/control and much less on amount of cccdna (for that they prefer biopsy) if hbeag is negative
To me any damage must be indicated by the the level of ALT.
no the damage is not always correlated with alt at all, the researchers don t even know what fibrosis is exactly and what leads to decompensated liver.
as an example occult hbv has no hbvdna or extremely low, normal alt but it makes the wrost damage to the liver than the other forms of the viruses: HCC and cirrhosis
i think everything happens inside the cell and at dna damage level too, infect even when there is no occult hbv but high hbvdna with normal alt there is a very high HCC risk especially in the geno B and C that often have this pattern in asia, normal alt high hbvdna but many HCC development
also my cirrhosis is an example, my alt and hbvdna were lower than my sister's but her liver is perfect mine had cirrhosis
no the damage is not always correlated with alt at all, the researchers don t even know what fibrosis is exactly and what leads to decompensated liver.
as an example occult hbv has no hbvdna or extremely low, normal alt but it makes the wrost damage to the liver than the other forms of the viruses: HCC and cirrhosis
i think everything happens inside the cell and at dna damage level too, infect even when there is no occult hbv but high hbvdna with normal alt there is a very high HCC risk especially in the geno B and C that often have this pattern in asia, normal alt high hbvdna but many HCC development
also my cirrhosis is an example, my alt and hbvdna were lower than my sister's but her liver is perfect mine had cirrhosis
I believe measuring HbSag quantity is a problem for genotype D HBV. I don't know whether this has been resolved.
Yes, it makes sense to say amount of HbSag is a marker of "active" cccDNA, rather than just any cccDNA in an infected liver cell. But I have trouble understanding the last sentence of the conclusion. Where is the damage coming from if you have zero HBVDNA, persistently normal ALT? To me any damage must be indicated by the the level of ALT. I know everyone uses the Taiwan study indicating normal ALT does not guarantee no progression of liver disease. I would like to know whether it is still the case if we use 30(for male) and 19(for female) as nul (normal upper limit). Also whether this uln should further be lowered in cirrhosis stage because there are lfewer liver cells to be damaged (as explained by Dr Misra on the Heplist.
it is now about 4 weeks i am taking bitter melon and i should have these dates hbsag quantifications, we might have a clue from it or nothing
in any case it helps for sure with insuline resistance/fatty liver:
20 jan 2011 don t know yet if pisa made the test on this date
7 march 2011 blood sample in a lab in my city trying to make quantification, they will let me know if they got correct hbsag reading in about 4 weeks
22 march 2011 will make test in a hospital were hbsag quant is routine, correct result in 7days
hbsag quant is also a little problematic because it has a steady pattern in non responders but it can have a wide range flactuating pattern on responders too, so it is very difficult to judge in single points unless the pattern is continuous decrease
i think the best point of comparison is interferon with a mean hbsag decrease of 0.5-1log decrease per year and use of alinia max dose 2-2.5g directly if no diarrea instead of using the small dose 1-1,5g like i did on 2010.
this is some of the research from my docotor, she is the one who discovered the importance of hbsag quantification and meaning then all other researchers followed.
to me hbsag (or biopsy cccdna) is the most important test if the goal is trying to eradicate virus
http://www.natap.org/2010/HBV/040710_03.htm
In conclusion, HBsAg serum levels are the resultant of the complex equilibrium between the virus and the host's immune system as well as the product of the transcription of specific mRNAs rather than viral replication. Thus, we may speculate that serum HBsAg is the indirect expression of transcriptionally active cccDNA rather than total intrahepatic cccDNA. Of course, we cannot exclude a role of integrated HBV-DNA in HBsAg synthesis; however, the evidence that HBsAg serum levels decline significantly with the duration of HBV infection, when the amount of integrated HBV-DNA is supposed to increase, weakens such a hypothesis. The substantial variations of total serum HBsAg in the different phases of HBV infection proposes quantitative HBsAg as a new diagnostic tool for the characterization of the HBV carrier in combination with HBV-DNA. The two HBV markers providing complementary information on the status of HBV infection (Fig. 1) may be very useful in clinical practice to define the specific condition of the single HBV carrier during the highly dynamic phases of chronic HBV infection, just as latitude and longitude allow to define the ship's position in the ocean. This will be of paramount importance to avoid the misclassification of an asymptomatic HBeAg negative CHB patient as an inactive carrier because of a single point serum test with normal transaminases and negative HBV-DNA caused by the typical intermittent disease profile of HBeAg negative CHB.
Well, I can't find any good information on preparation and dosage. Put this down as another "unproven" treatment.
BTW, I believe all HbSag are produced by gene expression of cccDNA in infected liver cells. Even in HbEag-ve patient. I can't see where else they can be produced. I don't think all experts agree that HbSag is a surrogate marker for cccDNA (well hardly anyone offers this as an explanation).
Just my opinion.
BTW, I believe all HbSag are produced by gene expression of cccDNA in infected liver cells. Even in HbEag-ve patient. I can't see where else they can be produced. I don't think all experts agree that HbSag is a surrogate marker for cccDNA (well hardly anyone offers this as an explanation).
Just my opinion.
Information in Italian (from a herbal company)
La famiglia: Cucurbitaceae
Il genere: Momordica
La specie: charantia
I sinonimi: Il chinensis di Momordica, M. l'elegans, M. l'indica, M. l'operculata, M. il sinensis, il fauriei di Sicyos
I Nomicomuni: il melone amaro, il papailla, il melao de il caetano di Sao, il bittergourd, la mela di balsamo, la pera di balsamo, il karela, il kurela di kua, il kor-kuey, il gua di ku, il pava-aki, il salsamino, il sorci, il sorossi, il sorossie, il sorossies, pareggia, il laut di peria, il peria
La parte Ha Usato: la pianta intera, le frutta, la semenza
http://fets3.freetranslation.com:5081/?Sequence=core&Language=English%2FItalian&Url=www.rain-tree.com/bitmelon.htm
La famiglia: Cucurbitaceae
Il genere: Momordica
La specie: charantia
I sinonimi: Il chinensis di Momordica, M. l'elegans, M. l'indica, M. l'operculata, M. il sinensis, il fauriei di Sicyos
I Nomicomuni: il melone amaro, il papailla, il melao de il caetano di Sao, il bittergourd, la mela di balsamo, la pera di balsamo, il karela, il kurela di kua, il kor-kuey, il gua di ku, il pava-aki, il salsamino, il sorci, il sorossi, il sorossie, il sorossies, pareggia, il laut di peria, il peria
La parte Ha Usato: la pianta intera, le frutta, la semenza
http://fets3.freetranslation.com:5081/?Sequence=core&Language=English%2FItalian&Url=www.rain-tree.com/bitmelon.htm
Lots of claims, no human studies, no preparation, no dosage.
http://www.houseofnutrition.com/bittermelon.html
Bitter melon also contains chemicals that show antiviral effects. One of the chemicals, Momordica anti-human immunodeficiency virus protein (MAP30), is found in bitter melon fruits and seeds. In laboratory studies, MAP30 activated natural killer (NK) cells, a type of white blood cells that specifically attack viruses and cancer cells. Additionally, MAP30 interfered with the actions of at least two enzymes needed by human immunodeficiency virus (HIV), the virus that causes AIDS, to divide and spread.
Dosage and Administration:
In countries where bitter melon grows, many individuals simply eat unripe bitter melon fruits or drink its juice several times a week. It is also available in a variety of commercial oral dosage forms, such as capsules, extract, tablets, and dried fruit powder. Injected bitter melon extract is used in some Asian countries, but it is not sold in North America. In most Western countries, individuals who take bitter melon supplements prefer capsules because they do not taste as bad as other oral dosage forms.
No set doses are recommended for bitter melon. Oral doses used in human studies varied widely from 200 mg per day to 1,000 mg (one gram) six times a day. Most of the studies lasted for 3 months or less.
It may also help to prevent HIV and other viruses from entering host cells, but it does not appear to damage normal cells. Another chemical in bitter melon increases the production of interferon gamma, a natural body substance that helps to fight all types of viruses. In laboratory studies, it has been effective against Epstein-Barr virus, hepatitis B virus, and herpes simplex virus. Bitter melon may also be active a
http://www.houseofnutrition.com/bittermelon.html
Bitter melon also contains chemicals that show antiviral effects. One of the chemicals, Momordica anti-human immunodeficiency virus protein (MAP30), is found in bitter melon fruits and seeds. In laboratory studies, MAP30 activated natural killer (NK) cells, a type of white blood cells that specifically attack viruses and cancer cells. Additionally, MAP30 interfered with the actions of at least two enzymes needed by human immunodeficiency virus (HIV), the virus that causes AIDS, to divide and spread.
Dosage and Administration:
In countries where bitter melon grows, many individuals simply eat unripe bitter melon fruits or drink its juice several times a week. It is also available in a variety of commercial oral dosage forms, such as capsules, extract, tablets, and dried fruit powder. Injected bitter melon extract is used in some Asian countries, but it is not sold in North America. In most Western countries, individuals who take bitter melon supplements prefer capsules because they do not taste as bad as other oral dosage forms.
No set doses are recommended for bitter melon. Oral doses used in human studies varied widely from 200 mg per day to 1,000 mg (one gram) six times a day. Most of the studies lasted for 3 months or less.
It may also help to prevent HIV and other viruses from entering host cells, but it does not appear to damage normal cells. Another chemical in bitter melon increases the production of interferon gamma, a natural body substance that helps to fight all types of viruses. In laboratory studies, it has been effective against Epstein-Barr virus, hepatitis B virus, and herpes simplex virus. Bitter melon may also be active a
The gene encoding MAP30 protein was cloned from bitter melon and recombinant MAP30 was expressed and purified. The human hepatoma G2.2.15 cells were exposed to different concentrations of MAP30. MTT assay was used to evaluate the cytotoxicity of the drugs and real-time PCR and Southern hybridization were applied to quantify extracellular HBV DNA and replicative intermediates intracellular and cccDNA in nucleus.
Test tube results only - inhibits production of hbv dna inside HBV infected animal liver cells and prevents release of HBSag manufactured from inside the cell. No dosage.
http://www.springerlink.com/content/j26q743782161u74/
HBsAg and HBeAg were assessed by enzyme-linked immunosorbent assay (ELISA). The results showed that exposure of HepG2.2.15 cells to MAP30 resulted in inhibition of HBV DNA replication and HBsAg secretion. After exposed to three different concentrations of MAP30 for 2, 4, 6, and 8 days respectively, the inhibition rates of extracellular HBV DNA, HBsAg, and HBeAg of each concentration decreased significantly (P < 0.05). After 9 days of treatment, the inhibition rates of extracellular HBV DNA of the different concentrations differed greatly (P < 0.001). The MAP30 could inhibit the production of HBV (P < 0.01) dose-dependently. The expression of HBsAg was significantly decreased by MAP30 dose-dependently (P < 0.001) and time-dependently (P < 0.001). Lower dose of MAP30 (8.0 μg/ml) could inhibit the expression of HBsAg and HBeAg.
Test tube results only - inhibits production of hbv dna inside HBV infected animal liver cells and prevents release of HBSag manufactured from inside the cell. No dosage.
http://www.springerlink.com/content/j26q743782161u74/
HBsAg and HBeAg were assessed by enzyme-linked immunosorbent assay (ELISA). The results showed that exposure of HepG2.2.15 cells to MAP30 resulted in inhibition of HBV DNA replication and HBsAg secretion. After exposed to three different concentrations of MAP30 for 2, 4, 6, and 8 days respectively, the inhibition rates of extracellular HBV DNA, HBsAg, and HBeAg of each concentration decreased significantly (P < 0.05). After 9 days of treatment, the inhibition rates of extracellular HBV DNA of the different concentrations differed greatly (P < 0.001). The MAP30 could inhibit the production of HBV (P < 0.01) dose-dependently. The expression of HBsAg was significantly decreased by MAP30 dose-dependently (P < 0.001) and time-dependently (P < 0.001). Lower dose of MAP30 (8.0 μg/ml) could inhibit the expression of HBsAg and HBeAg.
http://www.wellness.com/reference/herb/bitter-melon-momordica-charantia-l-curcurbitaceae-and-map30/dosing-and-safety
Due to the wide variations in preparation techniques of bitter melon, the proper dosing cannot be determined at the present time. Bitter melon has sometimes been administered as a fruit juice in doses of 50 milliliters or 100 milliliters in diabetic patients. Juice formulations have been reported to have more potent effects on blood sugar and lab values than the powder of the sun-dried fruit. However, safety and efficacy have not been established for any specific dose(s) of bitter melon.
Side Effects and Warnings
Headaches have been reported after the ingestion of bitter melon seeds. However, details regarding severity and duration of headaches are limited. Considerable rises in liver enzymes have been observed in animals after drinking bitter melon fruit juice and seed extract. These rises, however, have not been associated with significant damage or changes in the liver. The clinical relevance in humans has not been studied, so caution is advised, particularly in patients with underlying liver disease. The seeds and outer-rind of bitter melon contain a toxic chemical (lectin), which inhibits protein synthesis in the intestinal wall. Although this has not been correlated with signs or symptoms in humans, ingestion of bitter melon seeds or outer rind should be avoided due to potential adverse effects.
Bitter melon may lower blood sugar levels. Caution is advised in patients with diabetes or hypoglycemia (low blood sugar) and in those taking drugs, herbs, or supplements that affect blood sugar. Serum glucose levels may need to be monitored by a healthcare provider, and medication adjustments may be necessary. Two case reports have documented hypoglycemic coma and convulsions in children after the administration of a bitter melon tea.
Ingestion of bitter melon (or bitter melon seeds) should be avoided in patients with glucose-6-phosphate dehydrogenase (G6PDH) deficiency, due to the risk of hemolytic reaction and "favism." Favism is the onset of hemolytic anemia with symptoms including headache, fever, stomach pain, and coma. G6PDH deficiency and favism are most common in people from the Mediterranean and the Middle East.
The fertility rate of mice that were fed with daily bitter melon juice dropped from 90% to 20% in one study. Sperm production was inhibited in dogs that were fed a bitter melon fruit extract for 60 days. However, studies of a protein isolated from bitter melon seeds, called MAP30, have found that they do not affect sperm motility in laboratory studies.
Pregnancy & Breastfeeding
Bitter melon is not recommended during pregnancy; two proteins isolated from the raw fruit possess properties that may cause an abortion in animals. Lowered fertility rates are also possible.
Interactions
Interactions with Drugs
Bitter melon may lower blood sugar levels. Caution is advised when using medications that may also lower blood sugar. Patients taking drugs for diabetes by mouth or insulin should be monitored closely by a qualified healthcare professional, including a pharmacist.
Elevations in liver enzymes have been reported. Theoretically, bitter melon may interact with drugs metabolized by or affecting the liver.
The antiviral protein of bitter melon may enhance the therapies of the HIV antagonists, dexamethasone and indomethacin. Bitter melon may have antiviral and immunomodulating effects and therefore may have additive effects with other drugs with similar activity.
Bitter melon leaf extracts have been observed to reverse chemotherapy drug resistance.
Bitter melon may lower triglyceride levels and therefore may have additive effects with other drugs with similar activity.
Absorption, distribution, metabolism, and elimination (pharmacokinetics) of other drugs may be altered by bitter melon.
Bitter melon may induce abortion, reduce fertility rates, or inhibit production of sperm. Caution is advised in patients taking fertility agents or antifertility agents.
In theory, bitter melon may interact with medications used to treat parasites (anthelmintics).
Due to the wide variations in preparation techniques of bitter melon, the proper dosing cannot be determined at the present time. Bitter melon has sometimes been administered as a fruit juice in doses of 50 milliliters or 100 milliliters in diabetic patients. Juice formulations have been reported to have more potent effects on blood sugar and lab values than the powder of the sun-dried fruit. However, safety and efficacy have not been established for any specific dose(s) of bitter melon.
Side Effects and Warnings
Headaches have been reported after the ingestion of bitter melon seeds. However, details regarding severity and duration of headaches are limited. Considerable rises in liver enzymes have been observed in animals after drinking bitter melon fruit juice and seed extract. These rises, however, have not been associated with significant damage or changes in the liver. The clinical relevance in humans has not been studied, so caution is advised, particularly in patients with underlying liver disease. The seeds and outer-rind of bitter melon contain a toxic chemical (lectin), which inhibits protein synthesis in the intestinal wall. Although this has not been correlated with signs or symptoms in humans, ingestion of bitter melon seeds or outer rind should be avoided due to potential adverse effects.
Bitter melon may lower blood sugar levels. Caution is advised in patients with diabetes or hypoglycemia (low blood sugar) and in those taking drugs, herbs, or supplements that affect blood sugar. Serum glucose levels may need to be monitored by a healthcare provider, and medication adjustments may be necessary. Two case reports have documented hypoglycemic coma and convulsions in children after the administration of a bitter melon tea.
Ingestion of bitter melon (or bitter melon seeds) should be avoided in patients with glucose-6-phosphate dehydrogenase (G6PDH) deficiency, due to the risk of hemolytic reaction and "favism." Favism is the onset of hemolytic anemia with symptoms including headache, fever, stomach pain, and coma. G6PDH deficiency and favism are most common in people from the Mediterranean and the Middle East.
The fertility rate of mice that were fed with daily bitter melon juice dropped from 90% to 20% in one study. Sperm production was inhibited in dogs that were fed a bitter melon fruit extract for 60 days. However, studies of a protein isolated from bitter melon seeds, called MAP30, have found that they do not affect sperm motility in laboratory studies.
Pregnancy & Breastfeeding
Bitter melon is not recommended during pregnancy; two proteins isolated from the raw fruit possess properties that may cause an abortion in animals. Lowered fertility rates are also possible.
Interactions
Interactions with Drugs
Bitter melon may lower blood sugar levels. Caution is advised when using medications that may also lower blood sugar. Patients taking drugs for diabetes by mouth or insulin should be monitored closely by a qualified healthcare professional, including a pharmacist.
Elevations in liver enzymes have been reported. Theoretically, bitter melon may interact with drugs metabolized by or affecting the liver.
The antiviral protein of bitter melon may enhance the therapies of the HIV antagonists, dexamethasone and indomethacin. Bitter melon may have antiviral and immunomodulating effects and therefore may have additive effects with other drugs with similar activity.
Bitter melon leaf extracts have been observed to reverse chemotherapy drug resistance.
Bitter melon may lower triglyceride levels and therefore may have additive effects with other drugs with similar activity.
Absorption, distribution, metabolism, and elimination (pharmacokinetics) of other drugs may be altered by bitter melon.
Bitter melon may induce abortion, reduce fertility rates, or inhibit production of sperm. Caution is advised in patients taking fertility agents or antifertility agents.
In theory, bitter melon may interact with medications used to treat parasites (anthelmintics).
As for your damaged liver, do you know that long term suppression of viral load, using antiviral such as entecavir, can induce recovery of the liver?
yes it already did, the problem is noone knows the reason of decompensated liver.it is not due to cirrhosis or fibrosis since you can have decompensation even in acute hbv.researchers know only one thing a flare at 1000 alt can be dangerous but hbvdna und by entecavir should prevent flares both for interferon or gcmaf, what we expect from etv+ntz+interferon is just lowering of hbsag and hbsab appearance, the same thin should happen with gcmaf
yes i know hbsag is surrogate of cccdna especially on hbe pos and less on hbeag neg since hbsag in the second case is not all produced by cccdna.but in all the cases hbsag is a surrogate of immune system response
Still looking, but nothing on preparation.
As for your damaged liver, do you know that long term suppression of viral load, using antiviral such as entecavir, can induce recovery of the liver?
Also my theory that level of HbsAg is a surrogate marker of HBV cccDNA in liver cells is not mine, it was actually mentioned in s slide by A German research team. (that is what happens what we read too much, understand little, and forget most) :-(
As for your damaged liver, do you know that long term suppression of viral load, using antiviral such as entecavir, can induce recovery of the liver?
Also my theory that level of HbsAg is a surrogate marker of HBV cccDNA in liver cells is not mine, it was actually mentioned in s slide by A German research team. (that is what happens what we read too much, understand little, and forget most) :-(
same line of thinking here since macrophages are involved considerably in the type 1 immune response which may be the defense arm primarily affected by the hbs immunogen. need to modify the cell mediated immune response for those affected chronically. only then can the antigens be eliminated effectively by this reticuloendothelial system.
i do wish i ll be able to try gcmaf if researchers say it is not dangerous on my severely damaged liver
the researchers using gcmaf in europe are getting rid of cfs by making immune system work which makes all the viruses und so the link now is ultra clear
KDM researcher has got many good results, he s also very serious and charges gcmaf only 35euro per injection, he probably gets the drug for trials
I will try. I know Chinese eat bitter melon to help with their diabetes, like many other recommended food. All expressions of genes to produce proteins require RNA.
BTW, there is a longarticle in Nature about chronic fatigue syndrome:
"Judy Mikovits says that she will not abandon the hypothesis that XMRV and related viruses cause chronic fatigue syndrome, despite a growing chorus of critics."
BTW, there is a longarticle in Nature about chronic fatigue syndrome:
"Judy Mikovits says that she will not abandon the hypothesis that XMRV and related viruses cause chronic fatigue syndrome, despite a growing chorus of critics."
the precursors of hbv infection are rna, they come before development of cccdna and so on
so a comppond with minimum activity against rna like pgrna might be very useful comboed with interferon and antivirals, please help me understand and find where this map30 might be in the bitter melon (fruti, seeeds...)
and how much we can eat/drink of bitter melon to increase map30 quantity but safely
map30 has been extracted, produced synthetic and patented as broad antiviral, antitumor compound and research on this is very old since 1994...but this has never been produced.we should try to find which is the amount of map30 we can obtain by eating drinking bitter melon.
this is probably no cure because both we don t know if we can get enough map30 from plant directly, on experiment the used purified exteract and i don t understand the quantity they used
http://www.ncbi.nlm.nih.gov/pubmed/19747115
Curr Mol Med. 2009 Dec;9(9):1080-94.
Ribosome inactivating proteins (RIPs) from Momordica charantia for anti viral therapy.
Puri M, Kaur I, Kanwar RK, Gupta RC, Chauhan A, Kanwar JR.
Protein Biotechnology Laboratory, Department of Biotechnology, Punjabi University, Patiala, Punjab 147002, India. munish.***@****
Comment in:
Curr Pharm Biotechnol. 2010 Feb;11(2):229.
Abstract
This review describes the nature and applications of ribosome inactivating proteins (RIPs) from Momordica charantia (bitter melon). RIPs from the plant kingdom have received much attention in biomedical research because they target conserved host protein synthesis machinery and show specificity towards human and animal cell targets. Recent studies aimed at unravelling the enzymatic activities of the M charantia RIPs provide a structural basis for their activities. It has been reported that RIPs are member of the single chain ribosome inactivating protein (SCRIP) family which act irreversibly on ribosome by removing adenine residue from eukaryotic ribosomal RNA. Various activities of RIPs include anti-tumor, broad anti-viral, ribonuclease and deoxyribonuclease. MAP30 (Momordica Anti-HIV Protein), alpha- and beta-momorcharins inhibit HIV replication in acutely and chronically infected cells and thus are considered potential therapeutic agent in HIV infection and AIDS. Further, MAP30 improved the efficacy of anti-HIV therapy when used in combination with other anti-viral drugs. MAP30 holds therapeutic promise over other RIPs because not only it is active against infection and replication of both HSV and HIV but is non toxic to normal cells. Here we review the nature, action, structure function relationship and applications of RIPs from Momordica charantia and evaluate their potential for anti-cancer and anti-viral therapy.
so a comppond with minimum activity against rna like pgrna might be very useful comboed with interferon and antivirals, please help me understand and find where this map30 might be in the bitter melon (fruti, seeeds...)
and how much we can eat/drink of bitter melon to increase map30 quantity but safely
map30 has been extracted, produced synthetic and patented as broad antiviral, antitumor compound and research on this is very old since 1994...but this has never been produced.we should try to find which is the amount of map30 we can obtain by eating drinking bitter melon.
this is probably no cure because both we don t know if we can get enough map30 from plant directly, on experiment the used purified exteract and i don t understand the quantity they used
http://www.ncbi.nlm.nih.gov/pubmed/19747115
Curr Mol Med. 2009 Dec;9(9):1080-94.
Ribosome inactivating proteins (RIPs) from Momordica charantia for anti viral therapy.
Puri M, Kaur I, Kanwar RK, Gupta RC, Chauhan A, Kanwar JR.
Protein Biotechnology Laboratory, Department of Biotechnology, Punjabi University, Patiala, Punjab 147002, India. munish.***@****
Comment in:
Curr Pharm Biotechnol. 2010 Feb;11(2):229.
Abstract
This review describes the nature and applications of ribosome inactivating proteins (RIPs) from Momordica charantia (bitter melon). RIPs from the plant kingdom have received much attention in biomedical research because they target conserved host protein synthesis machinery and show specificity towards human and animal cell targets. Recent studies aimed at unravelling the enzymatic activities of the M charantia RIPs provide a structural basis for their activities. It has been reported that RIPs are member of the single chain ribosome inactivating protein (SCRIP) family which act irreversibly on ribosome by removing adenine residue from eukaryotic ribosomal RNA. Various activities of RIPs include anti-tumor, broad anti-viral, ribonuclease and deoxyribonuclease. MAP30 (Momordica Anti-HIV Protein), alpha- and beta-momorcharins inhibit HIV replication in acutely and chronically infected cells and thus are considered potential therapeutic agent in HIV infection and AIDS. Further, MAP30 improved the efficacy of anti-HIV therapy when used in combination with other anti-viral drugs. MAP30 holds therapeutic promise over other RIPs because not only it is active against infection and replication of both HSV and HIV but is non toxic to normal cells. Here we review the nature, action, structure function relationship and applications of RIPs from Momordica charantia and evaluate their potential for anti-cancer and anti-viral therapy.
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