Tony Pantalleresco Radio Show notes – November 29th 2014

Tony Pantallaresco

Welcome to Tony Pantalleresco Radio Show notes – November 29th 2014

Topics for this weeks show include:

Industrial pollution turning Canadian lakes into ‘jelly’
Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts
Derivative of vitamin B3 prevents liver cancer in mice
Energizing sick mitochondria with vitamin B3: Effective treatment for mitochondrial disease
Copper on the brain at rest
Copper can protect against Alzheimer’s disease

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Industrial pollution turning Canadian lakes into ‘jelly’
Published time: November 20, 2014 01:03

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Reuters / NASA / Handout

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Canada, Ecology, Science

The Canadian lakes are slowly but steadily turning into jelly since the industrial pollution has given jelly-clad organisms an edge over their calcium-protected competitors, researchers say, warning about potential impact on drinking water systems.—A battle between competing planktons in the delicate Ontario Lakes ecosystems is being won by “jelly-clad organism” called Holopedium that’s got an advantage over the planktonic Daphnia – all thanks to industrial pollution and acid rain – says new research by Cambridge University scientists published in Proceedings of the Royal Society B[F1] . The population of Holopedium – which has a “jelly” coat that gives them more protection from water predators – have doubled since the 1980s in many of the lakes, scientists behind the study say. [F2] — Eric Cai (@chemstateric) November 19, 2014 ———The dramatic decline in the water calcium levels has left Daphnia without crucial component to develop their exoskeleton defending them from predators. Thus Daphnia populations are declining, leaving more algae for other organisms to feed on, such as jelly-protected Holopedium. [F3] -“Lakes across eastern Canada have seen Holopedium populations explode in the last thirty years; particularly in lakes in the province of Ontario that have seen a recent Eurasian invasion of the spiny water flea – which also favours hunting Daphnia, affording Holopedium even more room in these ecosystems to expand,” Cambridge said in a press release. –Scientists warn that the “jellification” of Canada’s lakes will further prevent vital nutrients in the food chain flow and may eventually clog filtration and drinking water systems, as in Ontario, some 20 percent of drinking water comes from lakes with depleted calcium concentrations. [F4] –“As calcium declines, the increasing concentrations of jelly in the middle of these lakes will reduce energy and nutrient transport right across the food chain, and will likely impede the withdrawal of lake water for residential, municipal and industrial uses,” said study co-author Dr Andrew Tanentzap, from the University of Cambridge’s Department of Plant Sciences. [F5]

‘Daphnia Family’ by Karl Gaff, winner 2014 UCD Images of Research Competition @UCD_Research @ucdscience @UCDSciEx pic.twitter.com/4zhaGSSZnu —— UCD Innovation (@UCDinnovation) September 26, 2014 –Tanentzap says that industrialization in northern hemisphere deposited a lot of acid that displaced calcium from soil that feed these lakes. —-“Pollution control may have stopped acid deposits in the landscape, but it’s only now that we are discovering the damage wasn’t entirely reversed,” he says. –Besides Calcium loss, scientists also suggest that climate change is causing depletion of oxygen in the lakes that could lead to increasing populations of “larval midges – the main predator of Daphnia.” –“It may take thousands of years to return to historic lake water calcium concentrations solely from natural weathering of surrounding watersheds,” Tanentzap warned. “In the meanwhile, while we’ve stopped acid rain and improved the pH of many of these lakes, we cannot claim complete recovery from acidification. Instead, we many have pushed these lakes into an entirely new ecological state.” —

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Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts.

J Evid Based Complementary Altern Med. 2014 Apr;19(2):119-27

Authors: Ramachandran C, Quirin KW, Escalon E, Melnick SJ

Abstract
Ethnobotanical evidence suggests that herbs such as brahmi (Bacopa monnieri) and rosemary (Rosmarinus officinalis) may possess antioxidant and neuroprotective properties. We compared the antioxidant and neuroprotective effects of supercritical extract of Bacopa monnieri and rosemary antioxidant extract obtained from Rosmarinus officinalis as well as their combination to examine the effects on human glial (U-87 MG) and embryonic mouse hypothalamus cells. Bacopa monnieri extract, rosemary antioxidant extract, and their combination (1:1) are not cytotoxic in both glial and embryonic mouse hypothalamus cell lines up to 200 μg/mL concentration. The combination of extracts of Bacopa monnieri + rosemary antioxidant has better antioxidant potential and antilipid peroxidation activity than either agent alone[F6] . Although the extract of Bacopa monnieri + rosemary antioxidant showed almost similar inhibition of phospho tau expression as Bacopa monnieri or rosemary antioxidant extract alone, the combination has better inhibitory effect on amyloid precursor protein synthesis and higher brain-derived neurotrophic factor production in hypothalamus cells than single agents. These results suggest that the extract of Bacopa monnieri + rosemary antioxidant is more neuroprotective than Bacopa monnieri or rosemary antioxidant extract. –PMID: 24647092 [PubMed – indexed for MEDLINE]

Recipe—make either a tea or extract of these and make them separate as extracts—then when done—combine —as a tea take equal portions of each Boil together and drink as a tea—may see other benefits as well other then brain support —may see analgesic effects as well as heart –eye—and liver support

If you have powdered rosemary and bacopa then sprinkle on eggs and othee fats to increase protection of lipid issues and use as a brain tonic since all foods here mentioned are brain support

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Derivative of vitamin B3 prevents liver cancer in mice
Date-November 20, 2014–Source-Centro Nacional de Investigaciones Oncologicas (CNIO)

Liver cancer is one of the most frequent cancers in the world, and with the worst prognosis; according to the World Health Organisation (WHO), in 2012, 745,000 deaths were registered worldwide due to this cause, a figure only surpassed by lung cancer. The most aggressive and frequent form of liver cancer is hepato-cellular carcinoma (HCC); little is known about it and there are relatively few treatment options.–Researchers from the Spanish National Cancer Research Centre (CNIO), have produced the first mouse model that faithfully reproduces the steps of human HCC development, from the appearance of the first lesions in the liver to the development of metastasis. The results, published in the journal Cancer Cell, indicate that diets rich in nicotinamide riboside, a derivative of vitamin B3, protect these mice from developing HCC in its most initial stage, when genotoxic stress is damaging cellular DNA. [F7] They also show a curative effect of the diet in those mice that had previously developed the disease.

A MOUSE MODEL FOR HUMAN HEPATIC CANCER

One obstacle to the study of human HCC is the absence of mouse models that replicate the disease, which could be used to investigate molecular pathways or new therapies. Given that human HCC is associated to alterations in hepatocytes survival, and that the URI oncogene plays a role in this process, the researchers genetically engineered mice that contained high levels of URI only in the liver, in a controlled manner over time.-At 30 weeks, the mice with high levels of URI generated sporadic tumours in the liver and even metastasis when the induction lasted longer. The study details how deficiency in nicotinamide adenine dinucleotide (NAD+), a universal compound found in living organisms that is needed to burn calories via cell metabolism, orchestrates the development of the disease.[F8] –“An increase in URI reduces cellular NAD+ and as a consequence produces genotoxic stress and DNA damage,” says Nabil Djouder, leader of the study and Head of the Growth Factors, Nutrients and Cancer Group in the BBVA Foundation-CNIO Cancer Cell Biology Programme. “It is still not totally clear, however, why the deficit in NAD+ causes these lesions,” he adds.

ENERGY METABOLISM AND CANCER

The appearance of DNA damage is the first link in the chain of events that activate the carcinogenic process in the liver, even before apoptosis or cell death, as has been described in the literature. “We normally say that oncogenes induce DNA damage. Now we may be able to say, more appropriately, that oncogenes induce NAD+ depletion [or deficits in NAD+] which causes DNA damage,” says Djouder–The inverse relationship between NAD+ and cancer awakened the curiosity of the researchers: could an increase in NAD+ have beneficial effects on the disease? When the scientists supplemented the diet in genetically modified mice with nicotinamide riboside, a derivative of vitamin B3 that increases intracellular levels of NAD+, they did not observe tumour development. Surprisingly, when they gave this diet to mice that had already developed the disease, the size of the tumours was reduced and they eventually disappeared.–The results have been reproduced in other types of cancer such as pancreatic cancer. “We observed the same results in mice with pancreatic adenocarcinoma with regards to DNA damage[F9] , so we could conclude that this treatment is effective on tumours caused by oncogene[F10] -induced DNA damage and thus, deficit in NAD+,” says Krishna Tummala, first author of the study.–In addition to working with the mouse model, the authors have collated the results of nearly a hundred human samples. “Those from patients with HCC contain URI levels that double those of healthy samples,” according to the article. The data, which also associates URI with a worse prognosis or evolution of the illness, suggests that the gene could be a possible new HCC marker, and nicotinamide riboside boosting NAD+ levels may have a human relevance.

FUTURE RESEARCH——–Several epidemiological studies coincide in associating diets low in tryptophan [a NAD+ precursor] with an increased incidence of certain types of cancer[F11] . It has also been observed that daily supplements of vitamin B3 in populations with chronic nutritional deficiencies, reduces the incidence of some cancers including esophageal cancer.–Despite the results, the researchers underline that the efficiency of NAD+ enhancing nutritional supplements to protect healthy cells from chemotoxic stress as a combined therapy in oncology still needs to be demonstrated. Djouder’s team is collaborating with the CNIO Clinical Research Programme, lead by the oncologist Manuel Hidalgo to broaden these studies in mice and evaluate the possibility of carrying out clinical trials in humans in the future.

Story Source–The above story is based on materials provided by Centro Nacional de Investigaciones Oncologicas (CNIO). Note: Materials may be edited for content and length.–Journal Reference-Krishna S. Tummala, Ana L. Gomes, Mahmut Yilmaz, Osvaldo Graña, Latifa Bakiri, Isabel Ruppen, Pilar Ximénez-Embún, Vinayata Sheshappanavar, Manuel Rodriguez- Justo, David G. Pisano, Erwin F. Wagner & Nabil Djouder. Inhibition of De Novo NAD Synthesis by Oncogenic URI Causes Liver Tumorigenesis through DNA Damage. Cancer Cell, November 2014 DOI: 10.1016/j.ccell.2014.10.002

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Energizing sick mitochondria with vitamin B3- Effective treatment for mitochondrial disease
Date-April 7, 2014

Source-Helsingin yliopisto (University of Helsinki)

The researchers of the University of Helsinki, Finland, and École Polytechnique Fédérale de Lausanne, Switzerland, have shown that vitamin B3 form nicotinamide riboside can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.-Vitamins B have recently been turned out to be potent modifiers of energy metabolism, especially the function of mitochondria. Vitamin B3, (niacin) has been found to delay the signs of aging in animal models.–An international collaboration between the University of Helsinki and École Polytechnique Fédérale de Lausanne reported today in the journal Embo Molecular Medicine that vitamin B3 form, nicotinamide riboside, can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.–Mitochondria power up all cells in our bodies, by generating fuel, ATP, for all cellular functions. Dysfunction of these cellular engines can cause mitochondrial disorders, which are the most common cause of inherited metabolic diseases in adults and children. Mitochondrial myopathy is the most frequent form of adult mitochondrial disorder. The typical symptoms in the patients are muscle weakness, pain and cramps. Despite the progressive nature of these diseases, no curative treatment is available.–In their current publication, Dr Nahid Khan in Prof Anu Suomalainen Wartiovaara’s group showed that feeding mice with food supplemented with B3 form, nicotinamide riboside, delayed their mitochondrial myopathy[F12] . The treatment increased mitochondrial mass and function, and cured the structural abnormalities. These results clearly showed the potential of this vitamin B form, a natural constituent of milk, to activate dysfunctional mitochondrial metabolism.–“These results are a breakthrough for understanding the mechanisms of human mitochondrial muscle diseases and for exploring the efficient treatment options for these progressive disorders of adults. They also highlight the potent role of niacin in guiding mitochondrial energy metabolism,” Professor Anu Suomalainen Wartiovaara states.-Story Source-The above story is based on materials provided by Helsingin yliopisto (University of Helsinki). Note: Materials may be edited for content and length.-Journal Reference-Nahid A Khan, Mari Auranen, Ilse Paetau, Eija Pirinen, Liliya Euro, Saara Forsström, Lotta Pasila, Vidya Velagapudi, Christopher J Carroll, Johan Auwerx and Anu Suomalainen. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Molecular Medicine, April 2014 DOI: 10.1002/emmm.201403943

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Copper on the brain at rest
Date:November 26, 2014

Source:DOE/Lawrence Berkeley National Laboratory

Two-photon imaging of CF3 shows that the addition of acute BCS dosages also reduces labile copper pools in retinal neurons.

In recent years it has been established that copper plays an essential role in the health of the human brain. Improper copper oxidation has been linked to several neurological disorders including Alzheimer’s, Parkinson’s, Menkes’ and Wilson’s. Copper has also been identified as a critical ingredient in the enzymes that activate the brain’s neurotransmitters in response to stimuli. Now a new study by researchers with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) has shown that proper copper levels are also essential to the health of the brain at rest.-“Using new molecular imaging techniques, we’ve identified copper as a dynamic modulator of spontaneous activity of developing neural circuits, which is the baseline activity of neurons without active stimuli, kind of like when you sleep or daydream, that allows circuits to rest and adapt,” says Chris Chang, a faculty chemist with Berkeley Lab’s Chemical Sciences Division who led this study. “Traditionally, copper has been regarded as a static metabolic cofactor that must be buried within enzymes to protect against the generation of reactive oxygen species and subsequent free radical damage. We’ve shown that dynamic and loosely bound pools of copper can also modulate neural activity and are essential for the normal development of synapses and circuits.”–Chang , who also holds appointments with the University of California (UC) Berkeley’s Chemistry Department and the Howard Hughes Medical Institute (HHMI), is the corresponding author of a paper that describes this study in the Proceedings of the National Academy of Sciences (PNAS). The paper is titled “Copper is an endogenous modulator of neural circuit spontaneous activity.” Co-authors are Sheel Dodani, Alana Firl, Jefferson Chan, Christine Nam, Allegra Aron, Carl Onak, Karla Ramos-Torres, Jaeho Paek, Corey Webster and Marla Feller.–Although the human brain accounts for only two-percent of total body mass, it consumes 20-percent of the oxygen taken in through respiration. This high demand for oxygen and oxidative metabolism has resulted in the brain harboring the body’s highest levels of copper, as well as iron and zinc. Over the past few years, Chang and his research group at UC Berkeley have developed a series of fluorescent probes for molecular imaging of copper in the brain.–“A lack of methods for monitoring dynamic changes in copper in whole living organisms has made it difficult to determine the complex relationships between copper status and various stages of health and disease,” Chang said. “We’ve been designing fluorescent probes that can map the movement of copper in live cells, tissue or even model organisms, such as mice and zebra fish.”

For this latest study, Chang and his group developed a fluorescent probe called Copper Fluor-3 (CF3) that can be used for one- and two-photon imaging of copper ions. This new probe allowed them to explore the potential contributions to cell signaling of loosely bound forms of copper in hippocampal neurons and retinal tissue.–“CF3 is a more hydrophilic probe compared to others we have made, so it gives more even staining and is suitable for both cells and tissue,” Chang says. “It allows us to utilize both confocal and two-photon imaging methods when we use it along with a matching control dye (Ctrl-CF3) that lacks sensitivity to copper.”–With the combination of CF3 and Ctrl-CF3, Chang and his group showed that neurons and neural tissue maintain stores of loosely bound copper that can be attenuated by chelation to create what is called a “labile copper pool.” Targeted disruption of these labile copper pools by acute chelation or genetic knockdown of the copper ion channel known as CTR1 (for copper transporter 1) alters spontaneous neural activity in developing hippocampal and retinal circuits.[F13] – “We demonstrated that the addition of the copper chelator bathocuproine disulfonate (BCS) modulates copper signaling which translates into modulation of neural activity,” Chang says. “Acute copper chelation as a result of additional BCS in dissociated hippocampal cultures and intact developing retinal tissue removed the copper which resulted in too much spontaneous activity.”–The results of this study suggest that the mismanagement of copper in the brain that has been linked to Wilson’s, Alzheimer’s and other neurological disorders can also contribute to misregulation of signaling in cell−to-cell communications.–“Our results hold therapeutic implications in that whether a patient needs copper supplements or copper chelators depends on how much copper is present and where in the brain it is located,” Chang says. “These findings also highlight the continuing need to develop molecular imaging probes as pilot screening tools to help uncover unique and unexplored metal biology in living systems.”–Story Source-The above story is based on materials provided by DOE/Lawrence Berkeley National Laboratory. The original article was written by Lynn Yarris. Note: Materials may be edited for content and length.–Journal Reference-Sheel C. Dodani, Alana Firl, Jefferson Chan, Christine I. Nam, Allegra T. Aron, Carl S. Onak, Karla M. Ramos-Torres, Jaeho Paek, Corey M. Webster, Marla B. Feller, Christopher J. Chang. Copper is an endogenous modulator of neural circuit spontaneous activity. Proceedings of the National Academy of Sciences, 2014; 111 (46): 16280 DOI: 10.1073/pnas.1409796111

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Copper can protect against Alzheimer’s disease
Date:February 17, 2013

Source: Keele University

Researchers in The Birchall Centre at Keele University, Staffordshire, UK, have provided unequivocal evidence that under conditions which are approximately similar to those found in the brain, copper can only protect against beta amyloid forming beta sheets and as such it is highly unlikely that copper is directly involved in the formation of senile plaques in Alzheimer’s disease.–The research, published by Nature’s online journal Scientific Reports, may also imply that lower levels of copper in the brain may promote the mechanisms whereby beta amyloid is deposited as senile plaques in Alzheimer’s disease.–This research addressed the on-going question as to whether copper in the brain contributes to the formation of the senile plaques in Alzheimer’s disease. While previous research at Keele’s Birchall Centre pointed towards copper being potentially protective in preventing the protein beta amyloid from aggregating as beta sheets and forming senile plaques it had remained a controversial issue for some.–Story Source–The above story is based on materials provided by Keele University. Note: Materials may be edited for content and length.–Journal Reference–Matthew Mold, Larissa Ouro-Gnao, Beata M Wieckowski, Christopher Exley. Copper prevents amyloid-β1–42 from forming amyloid fibrils under near-physiological conditions in vitro. Scientific Reports, 2013; 3 DOI: 10.1038/srep01256

TOP D

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[F1]Chemtrail Fallout would be more the reality—them dumping tons of nanoparticles and nanometals have accumulated over time and now the water table is being poisoned—in a military exercise this would be considered as “poisoning the wells” where by the water would not be fir for consumption or irrigation and anything it would be exposed to —spread pathogens –in this case nanopoisoning

[F2]Polymers can ba a lipid or protein mix to create a “Jelly like effect”

[F3]Glyphosates in the region would case this as well –since glyphosates strip out minerals allowing pathogenic materials to become more predomnant

[F4]This sounds fishy—with the amount of GE chemicals such as glyphosates leeching into the water table this would be more credible as the cause and as a result this will now be in the drinking water which will further strip out of people vitals

[F5]Almost sounds like there is another reason to reduce the consumer usage—possible water rationing!!!

[F6]Protects Fat From Breaking down and going bad

[F7]B3 –used ot be used by medicicne to reduce cholesterol in the liver

[F8]And a lot have a B3 deficiency one way to tell is Sleep and rest depeleton—which without B3 you cannot regulate trytophan

[F9]Huge –info here –pancreatic and lung cancers are some of the hardest cancers to reverse—so this canbe effective as well

[F10]oncogene, genetic material that carries the ability to induce cancer. An oncogene is a sequence of deoxyribonucleic acid (DNA) that has been altered or mutated from its original form, the proto-oncogene

[F11]Foods with Tryptophan
(mg of Tryptophan per 100 grams)