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Article ; Online: Cognitive impairments in type 2 diabetes, risk factors and preventive strategies.

Sharma, Garima / Parihar, Arti / Talaiya, Tanay / Dubey, Kirti / Porwal, Bhagyesh / Parihar, Mordhwaj S

Journal of basic and clinical physiology and pharmacology

2020 Volume 31, Issue 2

Abstract: Mild cognitive impairment (MCI) is a modifiable risk factor in progression of several diseases including dementia and type 2 diabetes. If cognitive impairments are not reversed at an early stage of appearance of symptoms, then the prolonged pathogenesis ... ...

Abstract	Mild cognitive impairment (MCI) is a modifiable risk factor in progression of several diseases including dementia and type 2 diabetes. If cognitive impairments are not reversed at an early stage of appearance of symptoms, then the prolonged pathogenesis can lead to dementia and Alzheimer's disease (AD). Therefore, it is necessary to detect the risk factors and mechanism of prevention of cognitive dysfunction at an early stage of disease. Poor lifestyle, age, hyperglycemia, hypercholesterolemia, and inflammation are some of the major risk factors that contribute to cognitive and memory impairments in diabetic patients. Mild cognitive impairment was seen in those individuals of type 2 diabetes, who are on an unhealthy diet. Physical inactivity, frequent alcohol consumptions, and use of packed food products that provides an excess of cheap calories are found associated with cognitive impairment and depression in diabetic patients. Omega fatty acids (FAs) and polyphenol-rich foods, especially flavonoids, can reduce the bad effects of an unhealthy lifestyle; therefore, the consumption of omega FAs and flavonoids may be beneficial in maintaining normal cognitive function. These functional foods may improve cognitive functions by targeting many enzymes and molecules in cells chiefly through their anti-inflammatory, antioxidant, or signaling actions. Here, we provide the current concepts on the risk factors of cognitive impairments in type 2 diabetes and the mechanism of prevention, using omega FAs and bioactive compounds obtained from fruits and vegetables. The knowledge derived from such studies may assist physicians in managing the health care of patients with cognitive difficulties.
MeSH term(s)	Age Factors ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/prevention & control ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/psychology ; Diet ; Functional Food ; Humans ; Life Style ; Risk Factors
Language	English
Publishing date	2020-01-22
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1071737-7
ISSN	2191-0286 ; 0792-6855 ; 0334-1534
ISSN (online)	2191-0286
ISSN	0792-6855 ; 0334-1534
DOI	10.1515/jbcpp-2019-0105
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Zs.A 3207: Show issues

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Article ; Online: Flavonoid-based therapies in the early management of neurodegenerative diseases.

Solanki, Isha / Parihar, Priyanka / Mansuri, Mohammad Lukman / Parihar, Mordhwaj S

Advances in nutrition (Bethesda, Md.)

2015 Volume 6, Issue 1, Page(s) 64–72

Abstract: During the past several years, there has been enormous progress in the understanding of the causative factors that initiate neuronal damage in various neurodegenerative diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, ... ...

Abstract	During the past several years, there has been enormous progress in the understanding of the causative factors that initiate neuronal damage in various neurodegenerative diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington disease. Preventing neuronal damage and neuronal death will have a huge clinical benefit. However, despite major advances in causative factors that trigger these neurodegenerative diseases, to date there have been no therapies available that benefit patients who suffer from these diseases. Because most neurodegenerative diseases are late-onset and remain asymptomatic for most of the phases, the therapies initiated in advanced stages of the disease have limited value to patients. It may be possible to prevent or halt the disease progression to a great extent if therapies start at the initial stage of the disease. Such therapies may restore neuronal function by reducing or even eliminating the primary stressor. Flavonoids are key compounds for the development of a new generation of therapeutic agents that are clinically effective in treating neurodegenerative diseases. Regular consumption of flavonoids has been associated with a reduced risk of neurodegenerative diseases. In addition to their antioxidant properties, these polyphenolic compounds exhibit neuroprotective properties by their interaction with cellular signaling pathways followed by transcription and translation that mediate cell function under both normal and pathologic conditions. This review focuses on human intervention studies as well as animal studies on the role of various flavonoids in the prevention of neurodegenerative diseases.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyotrophic Lateral Sclerosis/drug therapy ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Brain/drug effects ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; Humans ; Huntington Disease/drug therapy ; Multiple Sclerosis/drug therapy ; Neurodegenerative Diseases/drug therapy ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Parkinson Disease/drug therapy ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use
Chemical Substances	Antioxidants ; Flavonoids ; Neuroprotective Agents ; Plant Extracts
Language	English
Publishing date	2015-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2583634-1
ISSN	2156-5376 ; 2156-5376
ISSN (online)	2156-5376
ISSN	2156-5376
DOI	10.3945/an.114.007500
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Article ; Online: Mitochondrial sirtuins: emerging roles in metabolic regulations, energy homeostasis and diseases.

Parihar, Priyanka / Solanki, Isha / Mansuri, Mohammad Lukman / Parihar, Mordhwaj S

Experimental gerontology

2015 Volume 61, Page(s) 130–141

Abstract: The energy production and metabolic homeostasis are well-orchestrated networks of carbohydrate, lipid and protein metabolism. These metabolic pathways are integrated by a key cytoplasmic organelle, the mitochondria, leading to production of many ... ...

Abstract	The energy production and metabolic homeostasis are well-orchestrated networks of carbohydrate, lipid and protein metabolism. These metabolic pathways are integrated by a key cytoplasmic organelle, the mitochondria, leading to production of many metabolic intermediates and harvest cellular energy in the form of ATP. Sirtuins are a highly conserved family of proteins that mediate cellular physiology and energy demands in response to metabolic inputs. Mitochondria inhabit three main types of sirtuins classified as Sirt3, Sirt4 and Sirt5. These sirtuins regulate mitochondrial metabolic functions mainly through controlling post-translational modifications of mitochondrial protein. However, the biological mechanism involved in controlling mitochondrial metabolic functions is not well understood at this stage. In this review the current knowledge on how mitochondrial sirtuins govern mitochondrial functions including energy production, metabolism, biogenesis and their involvement in different metabolic pathways are discussed. The identifications of potential pharmacological targets of sirtuins in the mitochondria and the bioactive compounds that target mitochondrial sirtuins will increase our understanding on regulation of mitochondrial metabolism in normal and disease state.
MeSH term(s)	Animals ; Apoptosis ; Citric Acid Cycle ; Energy Metabolism ; Fatty Acids/metabolism ; Glycolysis ; Homeostasis ; Humans ; Mitochondria/physiology ; Protein Processing, Post-Translational ; Reactive Oxygen Species/metabolism ; Sirtuins/physiology
Chemical Substances	Fatty Acids ; Reactive Oxygen Species ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	390992-x
ISSN	1873-6815 ; 0531-5565
ISSN (online)	1873-6815
ISSN	0531-5565
DOI	10.1016/j.exger.2014.12.004
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Zs.A 579: Show issues

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Article: Flavonoids in modulation of cell survival signalling pathways.

Mansuri, Mohammad Lukman / Parihar, Priyanka / Solanki, Isha / Parihar, Mordhwaj S

Genes & nutrition

2014 Volume 9, Issue 3, Page(s) 400

Abstract: Flavonoids, a family of polyphenols, generally found in various fruits and vegetables, as well as in many plant beverages such as tea, pomegranate juice, raspberry, blueberries, and red wine. Recently, studies on flavonoids have attracted scientific ... ...

Abstract	Flavonoids, a family of polyphenols, generally found in various fruits and vegetables, as well as in many plant beverages such as tea, pomegranate juice, raspberry, blueberries, and red wine. Recently, studies on flavonoids have attracted scientific attention as a potential nutritional strategy to prevent a broad range of chronic disorders. Many studies suggest that consumption of these flavonoids in sufficient amount plays neuroprotective, cardioprotective, anti-inflammatory, and chemopreventive roles. While there has been a major focus on the antioxidant properties, there is an emerging view that flavonoids and their in vivo metabolites do not act only as conventional antioxidants but may also exert modulatory actions on cellular system through direct action on various signalling pathways. These pathways include phosphoinositide 3-kinase, Akt/protein kinase B, mitogen-activated protein kinase, tyrosine kinases, and protein kinase C. Various inhibitory or stimulatory actions of flavonoids on these pathways greatly affect cellular functions by altering the phosphorylation state of targeted molecules. In addition, flavonoids also modulate various gene expressions through activation of various transcription factors. Thus, the present review will bestow a breathing overview regarding the prime role of flavonoids in modulation of survival signalling pathways at cellular system.
Language	English
Publishing date	2014-03-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2416599-2
ISSN	1865-3499 ; 1555-8932
ISSN (online)	1865-3499
ISSN	1555-8932
DOI	10.1007/s12263-014-0400-z
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Article ; Online: Amyloid-β as a modulator of synaptic plasticity.

Parihar, Mordhwaj S / Brewer, Gregory J

Journal of Alzheimer's disease : JAD

2010 Volume 22, Issue 3, Page(s) 741–763

Abstract: Alzheimer's disease is associated with synapse loss, memory dysfunction, and pathological accumulation of amyloid-β (Aβ) in plaques. However, an exclusively pathological role for Aβ is being challenged by new evidence for an essential function of Aβ at ... ...

Abstract	Alzheimer's disease is associated with synapse loss, memory dysfunction, and pathological accumulation of amyloid-β (Aβ) in plaques. However, an exclusively pathological role for Aβ is being challenged by new evidence for an essential function of Aβ at the synapse. Aβ protein exists in different assembly states in the central nervous system and plays distinct roles ranging from synapse and memory formation to memory loss and neuronal cell death. Aβ is present in the brain of symptom-free people where it likely performs important physiological roles. New evidence indicates that synaptic activity directly evokes the release of Aβ at the synapse. At physiological levels, Aβ is a normal, soluble product of neuronal metabolism that regulates synaptic function beginning early in life. Monomeric Aβ40 and Aβ42 are the predominant forms required for synaptic plasticity and neuronal survival. With age, some assemblies of Aβ are associated with synaptic failure and Alzheimer's disease pathology, possibly targeting the N-methyl-D-aspartic acid receptor through the nicotinic acetylcholine receptor, mitochondrial Aβ alcohol dehydrogenase, and cyclophilin D. But emerging data suggests a distinction between age effects on the target response in contrast to the assembly state or the accumulation of the peptide. Both aging and Aβ independently decrease neuronal plasticity. Our laboratory has reported that Aβ, glutamate, and lactic acid are each increasingly toxic with neuron age. The basis of the age-related toxicity partly resides in age-related mitochondrial dysfunction and an oxidative shift in mitochondrial and cytoplasmic redox potential. In turn, signaling through phosphorylated extracellular signal-regulated protein kinases is affected along with an age-independent increase in phosphorylated cAMP response element-binding protein. This review examines the long-awaited functional impact of Aβ on synaptic plasticity.
MeSH term(s)	Aging/metabolism ; Aging/pathology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/physiology ; Animals ; Humans ; Neuronal Plasticity/physiology ; Signal Transduction/physiology ; Synapses/physiology
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2010-09-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-2010-101020
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Zs.A 6084: Show issues

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Article ; Online: Study of apoptosis-related interactions in colorectal cancer.

Arora, Himanshu / Qureshi, Rehana / Rizvi, M A / Shrivastava, Sharad / Parihar, Mordhwaj S

Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

2016 Volume 37, Issue 11, Page(s) 14415–14425

Abstract: Abnormalities in apoptotic functions contribute to the pathogenesis of colorectal cancer. In this study, molecular interactions behind the apoptotic regulation have been explored. For this purpose, enrichment analysis was performed considering microRNAs ( ...

Abstract	Abnormalities in apoptotic functions contribute to the pathogenesis of colorectal cancer. In this study, molecular interactions behind the apoptotic regulation have been explored. For this purpose, enrichment analysis was performed considering microRNAs (miRNAs) that putatively target TP53 and altered during colon cancer. This revealed gene associated with both TP53 and miRNAs. Further analysis showed that a significant molecular interaction between the shortlisted candidates (TP53, miR-143, KRAS, BCL2, and PLK1) exists. Mutation study was conducted to confirm the clinical relevance of candidates. It showed that the mutation extent does not significantly alter survival in patients thus making these candidates suitable as drug targets. Overall, we showed the importance of interactions between TP53, miR-143, KRAS, BCL2, and PLK1 with respect to colorectal cancer using bioinformatics approach.
MeSH term(s)	Apoptosis/genetics ; Cell Cycle Proteins/genetics ; Cell Proliferation ; Colon/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; Mutation/genetics ; Protein Serine-Threonine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Polo-Like Kinase 1
Chemical Substances	BCL2 protein, human ; Cell Cycle Proteins ; MIRN143 microRNA, human ; MicroRNAs ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2016-09-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	605825-5
ISSN	1423-0380 ; 0289-5447 ; 1010-4283
ISSN (online)	1423-0380
ISSN	0289-5447 ; 1010-4283
DOI	10.1007/s13277-016-5363-9
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Zs.A 1598: Show issues

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Article: Flavonoid-Based Therapies in the Early Management of Neurodegenerative Diseases

Solanki, Isha / Parihar, Priyanka / Mansuri, Mohammad Lukman / Parihar, Mordhwaj S

Advances in food and nutrition research. 2015 Jan., v. 6, no. 1

2015

Abstract	During the past several years, there has been enormous progress in the understanding of the causative factors that initiate neuronal damage in various neurodegenerative diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington disease. Preventing neuronal damage and neuronal death will have a huge clinical benefit. However, despite major advances in causative factors that trigger these neurodegenerative diseases, to date there have been no therapies available that benefit patients who suffer from these diseases. Because most neurodegenerative diseases are late-onset and remain asymptomatic for most of the phases, the therapies initiated in advanced stages of the disease have limited value to patients. It may be possible to prevent or halt the disease progression to a great extent if therapies start at the initial stage of the disease. Such therapies may restore neuronal function by reducing or even eliminating the primary stressor. Flavonoids are key compounds for the development of a new generation of therapeutic agents that are clinically effective in treating neurodegenerative diseases. Regular consumption of flavonoids has been associated with a reduced risk of neurodegenerative diseases. In addition to their antioxidant properties, these polyphenolic compounds exhibit neuroprotective properties by their interaction with cellular signaling pathways followed by transcription and translation that mediate cell function under both normal and pathologic conditions. This review focuses on human intervention studies as well as animal studies on the role of various flavonoids in the prevention of neurodegenerative diseases.
Keywords	Alzheimer disease ; Parkinson disease ; amyotrophic lateral sclerosis ; animal models ; antioxidant activity ; cell death ; death ; disease course ; flavonoids ; humans ; neurons ; neuroprotective effect ; patients ; polyphenols ; risk reduction ; sclerosis ; signal transduction ; translation (genetics)
Language	English
Dates of publication	2015-01
Size	p. 64-72.
Publishing place	American Society for Clinical Nutrition
Document type	Article
ZDB-ID	1011108-6
ISSN	1043-4526
ISSN	1043-4526
DOI	10.3945/an.114.007500
Database	NAL-Catalogue (AGRICOLA)

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Article: Simultaneous age-related depolarization of mitochondrial membrane potential and increased mitochondrial reactive oxygen species production correlate with age-related glutamate excitotoxicity in rat hippocampal neurons.

Parihar, Mordhwaj S / Brewer, Gregory J

Journal of neuroscience research

2007 Volume 85, Issue 5, Page(s) 1018–1032

Abstract: Mitochondria are implicated in glutamate excitotoxicity by causing bioenergetic collapse, loss of Ca(2+) homeostasis, and generation of reactive oxygen species (ROS), all of which become increasingly important clinically with age. Little is known about ... ...

Abstract	Mitochondria are implicated in glutamate excitotoxicity by causing bioenergetic collapse, loss of Ca(2+) homeostasis, and generation of reactive oxygen species (ROS), all of which become increasingly important clinically with age. Little is known about how aging affects the relative importance of mitochondrial membrane potential (DeltaPsi(m)) and ROS production. To determine aging affects on DeltaPsi(m) and ROS production in individual somal and axonal/dendritic mitochondria, we compared ROS production while simultaneously monitoring DeltaPsi(m) before and after glutamate treatment of live neurons from embryonic (day 18), middle-aged (9-12 months), and old (24 months) rats. At rest, old neuronal mitochondria 1) showed a higher rate of ROS production that was particularly strong in axonal/dendritic mitochondria relative to that in middle-age neurons, 2) were more depolarized in comparison with neurons of other ages, and 3) showed no differences in ROS or DeltaPsi(m) as a function of distance from the nucleus. All DeltaPsi(m) grouped into three classes of high (less than -120 mV), medium (-85 to -120 mV), and low (greater than -85 mV) polarization that shifted toward the lower classes with age at rest. Glutamate exposure dramatically depolarized the DeltaPsi(m) in parallel with greatly increased ROS production, with a surprising absence of an effect of age or distance from the nucleus on these mitochondrial parameters. These data suggest that old neurons are more susceptible to glutamate excitotoxicity because of an insidious depolarization of DeltaPsi(m) and rate of ROS generation at rest that lead to catastrophic failure of phosphorylative and reductive energy supplies under stress.
MeSH term(s)	Aging/metabolism ; Animals ; Cells, Cultured ; Cellular Senescence/drug effects ; Cellular Senescence/physiology ; Glutamic Acid/metabolism ; Glutamic Acid/toxicity ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Membrane Potential, Mitochondrial/drug effects ; Nerve Degeneration/chemically induced ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/physiopathology ; Neurons/drug effects ; Neurons/metabolism ; Neurotoxins/metabolism ; Neurotoxins/toxicity ; Oxidative Phosphorylation/drug effects ; Oxidative Stress/drug effects ; Rats ; Rats, Inbred F344 ; Reactive Oxygen Species/metabolism
Chemical Substances	Neurotoxins ; Reactive Oxygen Species ; Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2007-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.21218
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Article: Mitoenergetic failure in Alzheimer disease.

Parihar, Mordhwaj S / Brewer, Gregory J

American journal of physiology. Cell physiology

2006 Volume 292, Issue 1, Page(s) C8–23

Abstract: Brain cells are highly energy dependent for maintaining ion homeostasis during high metabolic activity. During active periods, full mitochondrial function is essential to generate ATP from electrons that originate with the oxidation of NADH. Decreasing ... ...

Abstract	Brain cells are highly energy dependent for maintaining ion homeostasis during high metabolic activity. During active periods, full mitochondrial function is essential to generate ATP from electrons that originate with the oxidation of NADH. Decreasing brain metabolism is a significant cause of cognitive abnormalities of Alzheimer disease (AD), but it remains uncertain whether this is the cause of further pathology or whether synaptic loss results in a lower energy demand. Synapses are the first to show pathological symptoms in AD before the onset of clinical symptoms. Because synaptic function has high energy demands, interruption in mitochondrial energy supply could be the major factor in synaptic failure in AD. A newly discovered age-related decline in neuronal NADH and redox ratio may jeopardize this function. Mitochondrial dehydrogenases and several mutations affecting energy transfer are frequently altered in aging and AD. Thus, with the accumulation of genetic defects in mitochondria at the level of energy transfer, the issue of neuronal susceptibility to damage as a function of age and age-related disease becomes important. In an aging rat neuron model, mitochondria are both chronically depolarized and produce more reactive oxygen species with age. These concepts suggest that multiple treatment targets may be needed to reverse this multifactorial disease. This review summarizes new insights based on the interaction of mitoenergetic failure, glutamate excitotoxicity, and amyloid toxicity in the exacerbation of AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Brain/physiopathology ; Energy Metabolism ; Humans ; Mitochondria/metabolism
Language	English
Publishing date	2006-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00232.2006
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Article: Flavonoids in modulation of cell survival signalling pathways

Mansuri, Mohammad Lukman / Parihar, Priyanka / Solanki, Isha / Parihar, Mordhwaj S

Genes & nutrition. 2014 May, v. 9, no. 3

2014

Abstract	Flavonoids, a family of polyphenols, generally found in various fruits and vegetables, as well as in many plant beverages such as tea, pomegranate juice, raspberry, blueberries, and red wine. Recently, studies on flavonoids have attracted scientific attention as a potential nutritional strategy to prevent a broad range of chronic disorders. Many studies suggest that consumption of these flavonoids in sufficient amount plays neuroprotective, cardioprotective, anti-inflammatory, and chemopreventive roles. While there has been a major focus on the antioxidant properties, there is an emerging view that flavonoids and their in vivo metabolites do not act only as conventional antioxidants but may also exert modulatory actions on cellular system through direct action on various signalling pathways. These pathways include phosphoinositide 3-kinase, Akt/protein kinase B, mitogen-activated protein kinase, tyrosine kinases, and protein kinase C. Various inhibitory or stimulatory actions of flavonoids on these pathways greatly affect cellular functions by altering the phosphorylation state of targeted molecules. In addition, flavonoids also modulate various gene expressions through activation of various transcription factors. Thus, the present review will bestow a breathing overview regarding the prime role of flavonoids in modulation of survival signalling pathways at cellular system.
Keywords	antioxidant activity ; antioxidants ; blueberries ; cell viability ; flavonoids ; fruits ; gene expression ; juices ; metabolites ; mitogen-activated protein kinase ; phosphatidylinositol 3-kinase ; phosphorylation ; pomegranates ; protein kinase C ; red wines ; tea (beverage) ; transcription factors ; vegetables
Language	English
Dates of publication	2014-05
Size	p. 400.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	2416599-2
ISSN	1865-3499 ; 1555-8932
ISSN (online)	1865-3499
ISSN	1555-8932
DOI	10.1007/s12263-014-0400-z
Database	NAL-Catalogue (AGRICOLA)

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