From Science Daily website (see original article).
Read original article on Cancer Prevention Research journal
Jan. 9, 2013 — A high-fiber diet may have the clinical
potential to control the progression of prostate cancer in patients
diagnosed in early stages of the disease.
The rate of
prostate cancer occurrence in Asian cultures is similar to the rate in
Western cultures, but in the West, prostate cancer tends to progress,
whereas in Asian cultures it does not.
Why? A University of Colorado
Cancer Center study published in the January 2013 issue of the journal Cancer Prevention Research shows that the answer may be a high-fiber diet.
The
study compared mice fed with of inositol hexaphosphate (IP6), a major
component of high-fiber diets, to control mice that were not. Then the
study used MRI to monitor the progression of prostate cancer in these
models.
"The study's results were really rather profound. We saw
dramatically reduced tumor volumes, primarily due to the anti-angiogenic
effects of IP6," says Komal Raina, PhD, research instructor at the
Skaggs School of Pharmacy and Pharmaceutical Sciences, working in the
lab of CU Cancer Center investigator and School of Pharmacy faculty
member, Rajesh Agarwal, PhD.
Basically, feeding with the active
ingredient of a high-fiber diet kept prostate tumors from making the new
blood vessels they needed to supply themselves with energy.
Without
this energy, prostate cancer couldn't grow. Likewise, treatment with IP6
slowed the rate at which prostate cancers metabolized glucose.
Possible
mechanisms for the effect of IP6 against metabolism include a reduction
in a protein called GLUT-4, which is instrumental in transporting
glucose.
"Researchers have long been looking for genetic
variations between Asian and Western peoples that could explain the
difference in prostate cancer progression rates, but now it seems as if
the difference may not be genetic but dietary.
Asian cultures get IP6
whereas Western cultures generally do not," Raina says.
Foods high in fiber
* Whole grains and whole grain products
Bran cereals, oat bran, wheat bran, multigrain breads, granola, high-fiber bread.
* Beans and legumes
Whole beans, dried beans, fava beans, kidney beans, baked beans, black beans, peas.
* Nuts and seeds
Almond, flaxseed, sunflower seeds, pumpkin seeds.
* Fruits
Berries, dried fruits (figs, dates, apricot, prunes), guava, apples.
* Vegetables
Green leafy vegetables, green beans, broccoli, Brussels sprouts, squash.
venerdì 11 gennaio 2013
martedì 8 gennaio 2013
Pesticides and Parkinson's: Further Proof of a Link Uncovered
From Science Daily website (see original article).
Jan. 3, 2013 — For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson's disease. To date, paraquat, maneb and ziram -- common chemicals sprayed in California's Central Valley and elsewhere -- have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.
Now, UCLA researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.
Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.
Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.
The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.
The research is published in the current online edition of Proceedings of the National Academy of Sciences.
Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms -- including tremor, rigidity, and slowed movements and speech -- increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra. This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.
While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.
"As a result, environmental factors almost certainly play an important role in this disorder," Fitzmaurice said. "Understanding the relevant mechanisms -- particularly what causes the selective loss of dopaminergic neurons -- may provide important clues to explain how the disease develops."
Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.
The researchers wanted to explore whether there was a relationship between benomyl and Parkinson's, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure. But because a direct causal relationship between the pesticide and Parkinson's can't be established by testing humans, the investigators sought to determine if exposure in experimental models could duplicate some of the pathologic features of the disease.
They first tested the effects of benomyl in cell cultures and confirmed that the pesticide damaged or destroyed dopaminergic neurons.
Next, they tested the pesticide in a zebrafish model of the disease. This freshwater fish is commonly used in research because it is easy to manipulate genetically, it develops rapidly and it is transparent, making the observation and measurement of biological processes much easier. By using a fluorescent dye and counting the neurons, the researchers discovered there was significant neuron loss in the fish -- but only to the dopaminergic neurons. The other neurons were left unaffected.
Until now, evidence had pointed to one particular culprit -- a protein called α-synuclein -- in the development of Parkinson's. This protein, common to all Parkinson's patients, is thought to create a pathway to the disease when it binds together in "clumps" and becomes toxic, killing the brain's neurons.
The identification of ALDH activity now gives researchers another target to focus on in trying to stop this disease.
"We've known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson's," said Bronstein, who directs the UCLA Movement Disorders Program. "And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs."
Other authors of the study included Lisa Barnhill, Hoa A. Lam, Aaron Lulla, Nigel T. Maidment, Niall P. Murphy, Kelley C. O'Donnell, Shannon L. Rhodes, Beate Ritz, Alvaro Sagastig and Mark C. Stahl, all of UCLA; John E. Casida of UC Berkeley; and Myles Cockburn of the University of Southern California. The authors declare no conflict of interest.
Jan. 3, 2013 — For several years, neurologists at UCLA have been building a case that a link exists between pesticides and Parkinson's disease. To date, paraquat, maneb and ziram -- common chemicals sprayed in California's Central Valley and elsewhere -- have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.
Now, UCLA researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.
Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.
Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.
The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.
The research is published in the current online edition of Proceedings of the National Academy of Sciences.
Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms -- including tremor, rigidity, and slowed movements and speech -- increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra. This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.
While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.
"As a result, environmental factors almost certainly play an important role in this disorder," Fitzmaurice said. "Understanding the relevant mechanisms -- particularly what causes the selective loss of dopaminergic neurons -- may provide important clues to explain how the disease develops."
Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.
The researchers wanted to explore whether there was a relationship between benomyl and Parkinson's, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure. But because a direct causal relationship between the pesticide and Parkinson's can't be established by testing humans, the investigators sought to determine if exposure in experimental models could duplicate some of the pathologic features of the disease.
They first tested the effects of benomyl in cell cultures and confirmed that the pesticide damaged or destroyed dopaminergic neurons.
Next, they tested the pesticide in a zebrafish model of the disease. This freshwater fish is commonly used in research because it is easy to manipulate genetically, it develops rapidly and it is transparent, making the observation and measurement of biological processes much easier. By using a fluorescent dye and counting the neurons, the researchers discovered there was significant neuron loss in the fish -- but only to the dopaminergic neurons. The other neurons were left unaffected.
Until now, evidence had pointed to one particular culprit -- a protein called α-synuclein -- in the development of Parkinson's. This protein, common to all Parkinson's patients, is thought to create a pathway to the disease when it binds together in "clumps" and becomes toxic, killing the brain's neurons.
The identification of ALDH activity now gives researchers another target to focus on in trying to stop this disease.
"We've known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson's," said Bronstein, who directs the UCLA Movement Disorders Program. "And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs."
Other authors of the study included Lisa Barnhill, Hoa A. Lam, Aaron Lulla, Nigel T. Maidment, Niall P. Murphy, Kelley C. O'Donnell, Shannon L. Rhodes, Beate Ritz, Alvaro Sagastig and Mark C. Stahl, all of UCLA; John E. Casida of UC Berkeley; and Myles Cockburn of the University of Southern California. The authors declare no conflict of interest.
sabato 29 dicembre 2012
Esercizio fisico vigoroso: così il tessuto cardiaco ricresce dopo l'infarto
Tratto da "Salute 24" (vedi articolo originale)
Leggi articolo originale su European Heart Journal
Niente di meglio di un quotidiano e vigoroso esercizio fisico per favorire la riabilitazione dopo un attacco di cuore: secondo uno studio pubblicato sull'European Heart Journal dai ricercatori della Liverpool John Moores University (Regno Unito), il movimento fisico non blando aiuterebbe le cellule staminali cardiache «dormienti» ad attivarsi, stimolando la crescita di nuovo tessuto cardiaco e favorendo, quindi, il recupero post-insufficienza cardiaca.
Lo studio, per ora condotto su un gruppo di topi, ha dimostrato che lo sport - mezz'ora di tapis roulant 4 volte a settimana, per 4 settimane - rende attive più del 60% delle cellule staminali cardiache che solitamente, negli adulti, rimangono dormienti, oltre a migliorare la capacità aerobica e l'irrorazione sanguigna.
Dopo solo due settimane di esercizio aerobico i topi avevano infatti aumentato il numero di cardiomiociti - le cellule battenti del tessuto cardiaco - del 7%.
Questo studio è il primo del suo genere a suggerire che la riabilitazione basata sul movimento fisico potrebbe avere lo stesso effetto sulle cellule dormienti delle iniezioni di apposite sostanze chimiche che stimolino le staminali stesse a produrre nuovo tessuto, e aggiunge nuove evidenze scientifiche che confermano che il cuore può essere in grado di rigenerarsi autonomamente.
Altri studi dovranno però essere condotti per comprendere se gli stessi effetti possono essere sortiti sugli uomini.
Leggi articolo originale su European Heart Journal
Niente di meglio di un quotidiano e vigoroso esercizio fisico per favorire la riabilitazione dopo un attacco di cuore: secondo uno studio pubblicato sull'European Heart Journal dai ricercatori della Liverpool John Moores University (Regno Unito), il movimento fisico non blando aiuterebbe le cellule staminali cardiache «dormienti» ad attivarsi, stimolando la crescita di nuovo tessuto cardiaco e favorendo, quindi, il recupero post-insufficienza cardiaca.
Lo studio, per ora condotto su un gruppo di topi, ha dimostrato che lo sport - mezz'ora di tapis roulant 4 volte a settimana, per 4 settimane - rende attive più del 60% delle cellule staminali cardiache che solitamente, negli adulti, rimangono dormienti, oltre a migliorare la capacità aerobica e l'irrorazione sanguigna.
Dopo solo due settimane di esercizio aerobico i topi avevano infatti aumentato il numero di cardiomiociti - le cellule battenti del tessuto cardiaco - del 7%.
Questo studio è il primo del suo genere a suggerire che la riabilitazione basata sul movimento fisico potrebbe avere lo stesso effetto sulle cellule dormienti delle iniezioni di apposite sostanze chimiche che stimolino le staminali stesse a produrre nuovo tessuto, e aggiunge nuove evidenze scientifiche che confermano che il cuore può essere in grado di rigenerarsi autonomamente.
Altri studi dovranno però essere condotti per comprendere se gli stessi effetti possono essere sortiti sugli uomini.
Un ormone “stonato” alimenta il tumore
Tratto da "Salute 24" (vedi articolo originale)
Tumori e metastasi, colpa di una danza stonata.
Quella di un meccanismo utile allo sviluppo embrionale, che per un “cortocircuito” va in tilt e accende il gene della staminalità tumorale.
Grazie a gruppo di ricercatori dell’Università degli Studi di Padova, guidati da Stefano Piccolo – Piccolo ha appena ricevuto il premio scientifico FIRC “Guido Venosta” - è più chiaro il rapporto tra l'eccesso dell’ormone Wnt, normalmente coinvolto nella costruzione degli organi e nei processi rigenerativi, e il gene TAZ che “invia” staminali a supporto del tumore. Lo studio è pubblicato su Cell.
In condizioni normali lo sviluppo di un nuovo organo avviene solo durante lo sviluppo embrionale, e solo pochi organi, come il fegato, sono capaci di rigenerarsi dopo aver subito un danno.
Il cancro è un "organo" che ha scoperto il segreto di come riprodurre se stesso, ed è grazie alle sue cellule staminali che si possono sviluppare le metastasi, con ricadute dopo la chemioterapia.
Le cellule tumorali da sole però non riuscirebbero a fare molto e anche il più aggressivo dei tumori ha bisogno di ricevere parecchi segnali dall’ambiente che lo circonda.
Uno di questi segnali viene da un ormone che si chiama Wnt: un fattore attivo durante lo sviluppo embrionale e nei normali processi rigenerativi.
Lo studio di Stefano Piccolo, che porta la firma di Luca Azzolin e Michelangelo Cordenonsi, spiega come l'eccesso di Wnt attivi nella cellula un gene maestro della staminalità tumorale, chiamato TAZ.
TAZ era già noto ai ricercatori: è un gene che durante lo sviluppo di un organo controlla le sue dimensioni e animali che per difetti genetici nascono con troppo TAZ sviluppano organi giganteschi.
Lo stesso meccanismo viziato che può portare al processo di crescita di un tumore e la proliferazione delle metastasi, versione stonata di quella danza armoniosa che guida invece lo sviluppo embrionale.
La scoperta apre nuove prospettive terapeutiche: in futuro, grazie a farmaci mirati e anticorpi monoclonali sarà possibile colpire con un unico vettore sia Wnt che TAZ e arrestare, quindi, lo sviluppo della malattia.
Tumori e metastasi, colpa di una danza stonata.
Quella di un meccanismo utile allo sviluppo embrionale, che per un “cortocircuito” va in tilt e accende il gene della staminalità tumorale.
Grazie a gruppo di ricercatori dell’Università degli Studi di Padova, guidati da Stefano Piccolo – Piccolo ha appena ricevuto il premio scientifico FIRC “Guido Venosta” - è più chiaro il rapporto tra l'eccesso dell’ormone Wnt, normalmente coinvolto nella costruzione degli organi e nei processi rigenerativi, e il gene TAZ che “invia” staminali a supporto del tumore. Lo studio è pubblicato su Cell.
In condizioni normali lo sviluppo di un nuovo organo avviene solo durante lo sviluppo embrionale, e solo pochi organi, come il fegato, sono capaci di rigenerarsi dopo aver subito un danno.
Il cancro è un "organo" che ha scoperto il segreto di come riprodurre se stesso, ed è grazie alle sue cellule staminali che si possono sviluppare le metastasi, con ricadute dopo la chemioterapia.
Le cellule tumorali da sole però non riuscirebbero a fare molto e anche il più aggressivo dei tumori ha bisogno di ricevere parecchi segnali dall’ambiente che lo circonda.
Uno di questi segnali viene da un ormone che si chiama Wnt: un fattore attivo durante lo sviluppo embrionale e nei normali processi rigenerativi.
Lo studio di Stefano Piccolo, che porta la firma di Luca Azzolin e Michelangelo Cordenonsi, spiega come l'eccesso di Wnt attivi nella cellula un gene maestro della staminalità tumorale, chiamato TAZ.
TAZ era già noto ai ricercatori: è un gene che durante lo sviluppo di un organo controlla le sue dimensioni e animali che per difetti genetici nascono con troppo TAZ sviluppano organi giganteschi.
Lo stesso meccanismo viziato che può portare al processo di crescita di un tumore e la proliferazione delle metastasi, versione stonata di quella danza armoniosa che guida invece lo sviluppo embrionale.
La scoperta apre nuove prospettive terapeutiche: in futuro, grazie a farmaci mirati e anticorpi monoclonali sarà possibile colpire con un unico vettore sia Wnt che TAZ e arrestare, quindi, lo sviluppo della malattia.
venerdì 21 dicembre 2012
Cancer Study Overturns Current Thinking About Gene Activation
From Science Daily website (see original article).
Dec. 13, 2012 — A new Australian study led by Professor Susan Clark from Sydney's Garvan Institute of Medical Research shows that large regions of the genome -- amounting to roughly 2% -- are epigenetically activated in prostate cancer.
Regions activated contain many prostate cancer-specific genes, including PSA (prostate specific antigen) and PCA3, the most common prostate cancer markers.
Until now, these genes were not known to be regulated epigenetically.
A previous study from Professor Clark's lab showed that similarly large regions of the prostate cancer genome are also epigenetically silenced, demonstrating a structured rearrangement of the cancer epigenome.
Epigenetics looks at biochemical changes that affect how the genome is organised in the cell nucleus, which in turn controls how genes are expressed.
Attachment or detachment of certain molecules can literally open or close DNA's structure, allowing a gene to be expressed if the structure is opened, and silenced if the structure is closed.
Among other aspects of epigenetic activation, the new study shows that the epigenetic process known as 'methylation' can activate genes, often by changing the gene start site, overturning the prevailing dogma that DNA methylation can only silence genes.
The findings as a whole have extensive ramifications for cancer diagnosis and treatment, including epigenetic-based gene therapies, as they require the targeting of domains of genes, as opposed to single genes.
PhD student Saul Bert and Professor Clark used gene expression profiling data and genome-wide sequencing technology from prostate tumour cells to determine which parts of the genome were epigenetically activated in prostate cancer.
They then examined the mechanisms behind activation, publishing their findings in the international journal Cancer Cell.
DNA is made up of building blocks of nucleic acid known as 'base pairs', specifically guanine-cytosine (GC) and adenine-thymine (AT). Unlike other parts of the genome, there are dense clusters of CG pairs very close to gene start sites.
These CG clusters, known as 'CpG islands', are where methylation occurs.
"When I started my PhD, we were looking to see if there was loss of methylation at CpG islands, causing gene activation in cancer," said Saul Bert.
"We took a whole genome approach, looking at all the gene transcription start sites that included CpG islands.
What we saw surprised us, because we saw gene activation at hypermethylated sites -- that went against current thinking.
"We went on to show in the lab that if you methylate CpG islands that are very close to transcription start sites, but not exactly on top of them, then it's possible to turn genes on.
"While the realisation that methylation can trigger gene activation represents a paradigm shift in thinking, our other finding -- that the prostate cancer genome contains domains that harbour multiple gene families, tumour related genes, microRNAs and cancer biomarkers -- is equally important.
These domains are simultaneously switched on through significant epigenetic remodelling.
"In this study, we identified 35 domains including 251 genes. While the genes may seem to be functionally unrelated, their coordinated regulation in the cancer genome suggests the presence of epigenetic 'master controllers' that can switch on or off very large regions of DNA."
Project leader Professor Clark believes the study will have a significant impact on our understanding of diagnostic tests and on chemotherapy treatment.
"What we are seeing in prostate cancer would apply to other cancers.
The big new finding is about the ways in which neighbouring genes are being co-ordinately activated in cancer," said Professor Clark.
"The increased expression is not just due to genetic amplification -- but we now show is also due to unraveling of the cancer genome.
"We need to understand this process more deeply to determine the impact of current epigenetic therapies that are aimed at promoting gene activation rather than suppressing oncogene expression."
Dec. 13, 2012 — A new Australian study led by Professor Susan Clark from Sydney's Garvan Institute of Medical Research shows that large regions of the genome -- amounting to roughly 2% -- are epigenetically activated in prostate cancer.
Regions activated contain many prostate cancer-specific genes, including PSA (prostate specific antigen) and PCA3, the most common prostate cancer markers.
Until now, these genes were not known to be regulated epigenetically.
A previous study from Professor Clark's lab showed that similarly large regions of the prostate cancer genome are also epigenetically silenced, demonstrating a structured rearrangement of the cancer epigenome.
Epigenetics looks at biochemical changes that affect how the genome is organised in the cell nucleus, which in turn controls how genes are expressed.
Attachment or detachment of certain molecules can literally open or close DNA's structure, allowing a gene to be expressed if the structure is opened, and silenced if the structure is closed.
Among other aspects of epigenetic activation, the new study shows that the epigenetic process known as 'methylation' can activate genes, often by changing the gene start site, overturning the prevailing dogma that DNA methylation can only silence genes.
The findings as a whole have extensive ramifications for cancer diagnosis and treatment, including epigenetic-based gene therapies, as they require the targeting of domains of genes, as opposed to single genes.
PhD student Saul Bert and Professor Clark used gene expression profiling data and genome-wide sequencing technology from prostate tumour cells to determine which parts of the genome were epigenetically activated in prostate cancer.
They then examined the mechanisms behind activation, publishing their findings in the international journal Cancer Cell.
DNA is made up of building blocks of nucleic acid known as 'base pairs', specifically guanine-cytosine (GC) and adenine-thymine (AT). Unlike other parts of the genome, there are dense clusters of CG pairs very close to gene start sites.
These CG clusters, known as 'CpG islands', are where methylation occurs.
"When I started my PhD, we were looking to see if there was loss of methylation at CpG islands, causing gene activation in cancer," said Saul Bert.
"We took a whole genome approach, looking at all the gene transcription start sites that included CpG islands.
What we saw surprised us, because we saw gene activation at hypermethylated sites -- that went against current thinking.
"We went on to show in the lab that if you methylate CpG islands that are very close to transcription start sites, but not exactly on top of them, then it's possible to turn genes on.
"While the realisation that methylation can trigger gene activation represents a paradigm shift in thinking, our other finding -- that the prostate cancer genome contains domains that harbour multiple gene families, tumour related genes, microRNAs and cancer biomarkers -- is equally important.
These domains are simultaneously switched on through significant epigenetic remodelling.
"In this study, we identified 35 domains including 251 genes. While the genes may seem to be functionally unrelated, their coordinated regulation in the cancer genome suggests the presence of epigenetic 'master controllers' that can switch on or off very large regions of DNA."
Project leader Professor Clark believes the study will have a significant impact on our understanding of diagnostic tests and on chemotherapy treatment.
"What we are seeing in prostate cancer would apply to other cancers.
The big new finding is about the ways in which neighbouring genes are being co-ordinately activated in cancer," said Professor Clark.
"The increased expression is not just due to genetic amplification -- but we now show is also due to unraveling of the cancer genome.
"We need to understand this process more deeply to determine the impact of current epigenetic therapies that are aimed at promoting gene activation rather than suppressing oncogene expression."
giovedì 6 dicembre 2012
Il sistema nervoso parasimpatico
Il sistema nervoso parasimpatico si distingue in due sezioni: craniale e sacrale.
La sezione craniale è costituita da neuroni pregangliari situati nel tronco dell’encefalo, i cui cilindrassi raggiungono la periferia attraverso il III, VII, IX, X e XI paio di n. cranici.
Provvede, così, all’innervazione per la secrezione delle ghiandole lacrimali, sottolinguali e sottomascellari (n. intermediario di Wrisberg) e per la vasodilatazione; all’innervazione secretoria della ghiandola parotide (IX paio) e delle ghiandole faringee; all’innervazione delle fibre muscolari lisce dell’esofago (plesso faringeo), dei bronchi e dei polmoni (plesso bronchiale), del muscolo cardiaco (plesso cardiaco), dello stomaco (plesso gastrico), del fegato e della cistifellea (plesso epatico), di duodeno, pancreas, intestino fino al colon trasverso (plesso celiaco), con associata funzione vasoattiva.
La sezione sacrale è costituita da neuroni pregangliari posti alla base delle corna anteriori del midollo sacrale, i cui cilindrassi escono attraverso le radici anteriori II, III e IV sacrali. I neuroni postgangliari sono i gangli del plesso ipogastrico; le fibre postgangliari sono i nervi pelvici.
In particolare, le fibre postgangliari portano impulsi motori per il colon discendente, il retto, l’ano, la vescica e alcuni muscoli genitali esterni; impulsi inibitori per gli sfinteri interni dell’ano, della vescica e dell’uretra; impulsi secretori per la prostata, le ghiandole di Bartolini e Cowper; impulsi vasodilatatori per il retto, l’ano e i genitali esterni. Il sistema parasimpatico utilizza per la trasmissione sinaptica nei gangli, nelle fibre pregangliari e nelle fibre postgangliari, l’acetilcolina. I recettori per l’acetilcolina sono indicati come muscarinici e nicotinici, a seconda che mimino rispettivamente l’azione della muscarina o della nicotina.
I recettori postgangliari sono muscarinici; a livello gangliare e a livello muscolare i recettori sono di tipo nicotinico.
La sezione craniale è costituita da neuroni pregangliari situati nel tronco dell’encefalo, i cui cilindrassi raggiungono la periferia attraverso il III, VII, IX, X e XI paio di n. cranici.
Provvede, così, all’innervazione per la secrezione delle ghiandole lacrimali, sottolinguali e sottomascellari (n. intermediario di Wrisberg) e per la vasodilatazione; all’innervazione secretoria della ghiandola parotide (IX paio) e delle ghiandole faringee; all’innervazione delle fibre muscolari lisce dell’esofago (plesso faringeo), dei bronchi e dei polmoni (plesso bronchiale), del muscolo cardiaco (plesso cardiaco), dello stomaco (plesso gastrico), del fegato e della cistifellea (plesso epatico), di duodeno, pancreas, intestino fino al colon trasverso (plesso celiaco), con associata funzione vasoattiva.
La sezione sacrale è costituita da neuroni pregangliari posti alla base delle corna anteriori del midollo sacrale, i cui cilindrassi escono attraverso le radici anteriori II, III e IV sacrali. I neuroni postgangliari sono i gangli del plesso ipogastrico; le fibre postgangliari sono i nervi pelvici.
In particolare, le fibre postgangliari portano impulsi motori per il colon discendente, il retto, l’ano, la vescica e alcuni muscoli genitali esterni; impulsi inibitori per gli sfinteri interni dell’ano, della vescica e dell’uretra; impulsi secretori per la prostata, le ghiandole di Bartolini e Cowper; impulsi vasodilatatori per il retto, l’ano e i genitali esterni. Il sistema parasimpatico utilizza per la trasmissione sinaptica nei gangli, nelle fibre pregangliari e nelle fibre postgangliari, l’acetilcolina. I recettori per l’acetilcolina sono indicati come muscarinici e nicotinici, a seconda che mimino rispettivamente l’azione della muscarina o della nicotina.
I recettori postgangliari sono muscarinici; a livello gangliare e a livello muscolare i recettori sono di tipo nicotinico.
Il nervo vago e il cuore
In caso di mancata innervazione del ramo destro del nervo vago parasimpatico al nodo sino-atriale provoca delle tachicardie, mentre se viene a mancare quello sinistro, manca l’innervazione al nodo atrio-ventricolare e di conseguenza crea aritmie.
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