Revista de genética e investigación del ADN.

The Knowledge of Epigenetic mechanism significantly enlightens the dilemma ‘nature or nurture’ and constitutes a very important component for the outcome of psychotherapeutic relationship with patients or clients who report traumatic memories and had experienced negligence or maltreatment. The story starts from the beginning in the early 19th Century, when Lamarck argued that organisms can acquire characteristics and properties through their interaction and adaptation to the environmen. These new ‘personality traits’ can become lifelong stable and can be inherited by the next generation . The term ‘epigenetics’ which derived from Greek, was given to this organismic property. It means “above genetics”. There are two main mechanisms involved in epigenetics: DNA methylation and histone modification. A third mechanism concerning non coding RNA (ncRNA) needs to be more elucidated . DNA methylation occurs when one methyl group (CH3) is added on the amino acid cytosine. This is completed through the action of a methyltransferase only when cytosine is followed by guanine, and results in long term silencing of the expression of the specific gene. It is important to note that gene methylation is a multi-step procedure, while demethylation is performed through one single step.

These facts are highly important for the personality changes during psychotherapeutic interventions and psychiatry, since they show very high potential and flexibility on the multitude of lived experiences and they have a determining role in neuroplastic functions like learning, memorising and adaptive behaviour. The second mechanism concerns histone modification. Histones are proteins positively charged. Unused DNA which remains unneeded carries a negative charge and, through attraction, it is packaged around an octamer of histones [2]. Histone molecules are subjected to methylation, acetylation or phosphorylation and can repress the genes expression by increasing the electrostatic load and tightening the coils, thus silencing DNA expression. Histone modification is transient resulting in less permanent changes than DNA methylation

In accord with the new definition of addiction published by American Society of Addiction Medicine (ASAM) it is well-known that individuals who present to a treatment center involved in chemical dependency or other documented reward dependence behaviors have impaired brain reward circuitry. They have hypodopaminergic function due to genetic and/or environmental negative pressures upon the reward neuro-circuitry. This impairment leads to aberrant craving behavior and other behaviors such as Substance Use Disorder (SUD). Neurogenetic research in both animal and humans revealed that there is a well-defined cascade in the reward site of the brain that leads to normal dopamine release. This cascade has been termed the “Brain Reward Cascade” (BRC). Any impairment environmental influences on this cascade will result in a reduced amount of dopamine release in the brain reward site. Manipulation of the BRC has been successfully achieved with neuro-nutrient therapy utilizing nutrigenomic principles. After over four decades of development, neuro-nutrient therapy has provided important clinical benefits when appropriately utilized. This is a review, with some illustrative case histories from a number of addiction professionals, of certain molecular neurobiological mechanisms which if ignored may lead to clinical complications.

It is well established that DA and a number of other linked neurotransmitters are responsible for feelings of well being. However,attempts to attenuate irregularities in the brain reward circuits using pharmaceutical agents have been met with disastrous results [4,5] and in some cases suicidal ideation [6]. The result of using powerful neurotransmitter agonists is down regulation instead of the much needed up-regulation of the specific receptors being targeted [7]. Bromocriptine a powerful DA D2 agonist has been shown to down regulate DA D2 receptors following chronic administration [8]

Herbicide-resistant weeds pose a serious threat to weed Several factors govern the rate at which the resistant individuals (alleles) become dominant in the population [3]. Genetic factors, such as the initial frequency of resistant alleles present in the population, the dominance relationships among the alleles and fitness cost of the resistance gene(s) can significantly influence evolution of resistance to herbicides. Other factors, such as biology of weed species (e.g. life cycle, seed production capability, mating system), the herbicide and target site properties (chemical structure, herbicidetarget site interactions and residual activity), herbicide dose and application performance can impact dynamics of herbicide resistance evolution, as well. This review focuses on how genetic factors influence the evolution and spread of herbicide resistance in weeds and how herbicide use pattern can determine the genetics of herbicide resistance. Additionally, how this information can be useful in both proactive and reactive management of herbicide-resistant weeds is also discussed. management across the globe. Weeds evolve resistance to herbicides as a result of herbicide selection pressure. Under continuous herbicide selection, the resistant individuals dominate in a population Understanding the genetics of herbicide resistance will help assess frequency and spread of herbicide resistance allele(s) in a population, which will assist in formulating prudent weed management practices to delay the evolution of resistance

Dominant expression of the resistance allele also accelerates the process. Target-site resistance (TSR) is determined by a single gene, and is more likely a result of strong selection pressure. Although, non-target site resistance (NTSR) usually results under moderate selection pressure accumulating multiple alleles with minor effects imparting resistance, it may also involve a single gene when evolved under high selection pressure. Such monogenic resistances evolve and spread quickly, especially when the resistance is dominant and nuclearinherited. Herbicide mixtures with different modes of action when applied at recommended doses can effectively delay the evolution of both TSR and NTSR

Alzheimer’s disease (AD) is the most common form of dementia. It is a degenerative and incurable terminal disease. AD accounts for 75% of all forms of dementia all over the world. Its etiology is still unknown. Numerous risk factors of AD have already been discovered. In this paper, some preliminary results are presented. The results suggested that persons with AD often had cardiovascular disease in their history. Conversely, they did not have diabetes mellitus, hypertension and cerebrovascular disease. A relationship between the ApoE4 allele and a higher risk of AD was found (OR 2.52). Among ACE genotypes, the I allele increases the risk of AD, and in this pilot sample, the II genotype showed the OR on the borderline of significance (OR 1.43;95% CI 0.97- 2.12). It is generally accepted that Alzheimer’s disease (AD) is the most frequent form of dementia. The etiology of AD is still unknown and three risk factors are hypothesized to be involved indevelopment of the disease (a) vascular risk factors, (b) genetic risk factors and (c) behavioral risk factors [1]. For various reasons, no exact data on the incidence and prevalence of AD are available. There is no compulsory notification, it is difficult to distinguish between different forms of dementia and there is no exact diagnostic test.

Mostly, there are only estimates of the actual incidence or prevalence. Worldwide, there are about 38 million persons with dementia, with 75% of them having AD. In Europe, there are more than 7 million people with dementia, and in the Czech Republic, 120,000 cases of AD are notified [2-4]. Since 2010, an epidemiological study assessing the importance of selected vascular and genetic risk factors has been underway. The aim was to recruit 800 AD cases and 800 controls. In this paper, some preliminary results from analyses of 394 cases and 287 controls are presented. The diagnostic criteria for selection of subjects were (a) Mini Mental State Examination (MMSE) test score below 24 points (b) slow development of cognitive impairment and (c) other forms of dementia excluded by a CT scan in the group of cases, and (e) MMSE score above 28 and (f) matched gender and age (± 5 years) in the group of controls [5].

Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Do spite this, the general public remains largly unawar of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used. From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health. ASGM plants are gradually being introduced into European Union there is likely to be increasing public concern regarding potential health issues. Factories that are important in human health are fiber-rich plants. Because fiber in addition to its herapeutic properties, also help control weight, because excessive weight and weight gain can be threat to human health. If plant regeneration contributes increasing fiber content were. Modern maize has been obtained from a podcorn corn; this corn is completely different with other types of corn, and each of the grains is surrounded by a single pod.

Mostly, there are only estimates of the actual incidence or prevalence. Worldwide, there are about 38 million persons with dementia, with 75% of them having AD. In Europe, there are more than 7 million people with dementia, and in the Czech Republic, 120,000 cases of AD are notified [2-4]. Since 2010, an epidemiological study assessing the importance of selected vascular and genetic risk factors has been underway. The aim was to recruit 800 AD cases and 800 controls. In this paper, some preliminary results from analyses of 394 cases and 287 controls are presented. The diagnostic criteria for selection of subjects were (a) Mini Mental State Examination (MMSE) test score below 24 points (b) slow development of cognitive impairment and (c) other forms of dementia excluded by a CT scan in the group of cases, and (e) MMSE score above 28 and (f) matched gender and age (± 5 years) in the group of controls [5].