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Kuber Group 220 Patti – Carotenoid Raman signatures are better preserved in dehydrated cells of the desert cyanobacterium Chroococcidiopsis than their hydrated counterparts after high-intensity gamma irradiation.

Global codons optimized from GC to AU nucleotide composition indicate an early to late assignment of LUCA sequencing and formation.

Kuber Group 220 Patti

Kuber Group 220 Patti

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Federico Mucci Federico Mucci Scilit Preprints.org Google Scholar View Publications 1, 2, * , Donatella Marazziti Donatella Marazziti Scilit Preprints.org Google Scholar View Publications 1 , Alessandra Della Vecchia Alessandra Della Vecchia Google Scilit Scilit 1, 2 Bacilit Bacilit. .org Google Scholar View Publication 1 , Paolo Morana Paolo Morana Scilit Preprints.org Google Scholar View Publication 3 , Barbara Carpita Barbara Carpita Scilit Preprints.org Google Scholar View Publication 2 , Paola Mangiapane Paolaci Scilit Google Mangiapane. Scholar Publications 3 , Florinda Morana Florinda Morana Scilit Preprints.org Google Scholar View Publications 3 , Benedetto Morana Benedetto Morana Scilit Preprints.org Google Scholar View Publications 3 by Liliana Dell’Osso Liliana Dell’Osso Scilit Preprints.org Google View Publications.org

Manuscript accepted: March 28, 2020. / Revised: May 10, 2020 / Received: May 15, 2020 / Published: June 6, 2020

Evidence shows the involvement of inflammatory / immune systems and their interaction with neurotransmitters and various metabolic processes in mood disorders. Despite this, there is general agreement that the results obtained are still inconclusive. Therefore, more studies aimed at increasing the role of potential changes in biomarkers in the pathophysiology of mood disorders are needed, which may lead to more targeted and targeted treatments. This study is a comprehensive review of these topics, highlighting exciting avenues for the development of innovative treatment strategies for emotional disorders.

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Emotional disorders include various conditions characterized by changes in mood, psychomotor and biorhythms, causing great personal suffering and social and communication problems [1, 2, 3, 4]. Major depressive disorder (MDD) and bipolar disorder (BD) are the most severe and common types of mood disorders [5]. The first is characterized by depressive episodes, and the most common symptoms of BD are mood swings, mania or hypomania and depressive episodes [6, 7, 8]. The lifetime prevalence of major depressive disorder is about 7% (about 264 million people), while bipolar disorder is >1% (about 45 million people) [7, 8, 9]. As noted by the World Health Organization (WHO), it is the second cause of disability in 2020, which puts a heavy burden on the world economy [10, 11]. Several authors have hypothesized that unipolar and bipolar depression may represent different nosological entities that may be associated with different biological substrates and have tried to distinguish them phenomenologically [12]. Research on this topic is not complete, today the probabilistic and quantitative method (emotional spectrum model) prevails. Thus, various authors and clinicians tend to define MDD as part of a broader continuum called the “bipolar spectrum,” which includes depressive and manic symptoms of varying severity over time. In some patients, the onset of depression can lead to dementia, or often depressive symptoms appear mixed with mania in one episode [12].

Progress With Clinical Staging (section 2)

Although emotional disorders are one of the most common causes of disability among mental syndromes worldwide [7, 10, 13], their pathology is still unknown and their drug treatment is still a challenge due to the evidence that they are chronic diseases. 30% of patients experience complete remission of symptoms. For many years after the discovery of the first antidepressants (ADs), changes in monoamine neurotransmission, known as tricyclic AD, have been considered the most relevant mechanism of MDD syndrome [9]. However, the data supporting monoamine hypotheses are not inclusive, as they cannot explain the complex clinical picture [9, 13, 14, 15], and advertisements based on them have shown limited effectiveness. Only two-thirds of MDD patients can benefit from this pharmacological treatment; in addition, a number of responders relapse after initial improvement, even if they continue to take the medication [16].

Subsequent studies in AD and sensitized controls have shown that long-term exposure can trigger a cascade of activation of various genes involved in the expression and synthesis of various trophic factors [17, 18, 19]. In addition, neuronal plasticity has been shown to be associated with changes in cell morphology, synapse growth or reduction, and dendritic spine formation [20, 21, 22], and loss of neuronal trophism leads to impaired neuronal trophism. a decrease in the ability of brain regions that control emotions to respond to environmental stimuli. Together, these data contributed to the definition of the “neurotrophic theory”, based on the concept of loss of trophism in certain areas of the brain after a long period of stress. Experimental studies of rats with chronic stress have shown that neurons of the nucleus accumbens, hippocampus, and prefrontal cortex undergo a reduction in the density of dendritic spines and synapse formation, as well as loss of tone. “decreasing” [23, 24]. Depression, which is also observed in depressed patients and people with chronic stress, is significantly enhanced by AD [25]. The neurotrophins most involved in the pathophysiology of mood disorders are brain-derived neurotrophic factor (BDNF) and, to a lesser extent, glial-derived neurotrophic factor (GNDF). It has been hypothesized that compounds that can overcome the blood-brain barrier and act as modifiers on specific genes involved in trophic and/or immune system factors may provide opportunities for the development of new and more effective psychoactive compounds in the blood. almost later. However, preliminary data on the current experimental compounds are not encouraging due to their serious side effects [26, 27].

In addition to the monoaminergic and neurotrophic hypotheses, other neurological models of emotional disorders have been developed over the decades, ranging from hypothalamic-pituitary-adrenal (HPA) dysfunction of the inflammatory/immune axis to structural or functional changes in emotion. that is, the so-called “limbic cortex model” and “cortico-striatal model”) [28, 29, 30]. Increasing evidence indicates a central role of inflammation in mood disorders, consistent with all the proposed mechanisms including neurotrophins, neurotransmitters, and the HPA axis [31, 32, 33].

The purpose of this article is to review the available literature on the role of inflammation in the pathophysiology of mood disorders, considering its interactions with the immune system and other pathological factors.

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According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) [ 34 ], PubMed, Scopus, Embase, PsycINFO, and Google Scholar databases were accessed to search and collect articles published on the website only. English language. Free text words and MeSH headings were combined as follows: “(inflammation OR metabolic markers OR cytokines OR immune system) AND (mood disorder OR bipolar disorder OR depression)”. All authors agreed to submit abstracts, posters, and reports if published in journals listed at the review meeting. The following inclusion criteria were adopted: appropriate clinical studies using standard methods/evidence and clinical studies in children/adults with a reliable diagnosis of mood disorders based on structured interviews with established criteria and reliable evaluation of outcome measures. All authors contributed equally to identifying potential subject-specific information among the titles and abstracts of the publications. The first selection excludes 4223 names because: a) they were duplicates; b) are not related to the size of the paper; c) they did not have enough information. The second sample did not include 804 abstracts after reading and reviewing because the information reported did not match the scope of our work and/or the information presented was not relevant to the topic discussed. Another 144 publications were removed after thorough reading and evaluation because they did not provide sufficient information and/or did not provide sufficient results.

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