scholarly journals Avian central clocking system

2018 ◽  
Vol 74 (1) ◽  
pp. 6043-2018
Author(s):  
Magdalena Prusik
Keyword(s):  
Pineal Gland ◽  
Molecular Mechanisms ◽  
Clock Genes ◽  
Biological Effects ◽  
Biological Rhythms ◽  
Species Differentiation ◽  
Direct Role ◽  
Environmental Light ◽  
Great Species ◽  
The Impact

In birds many life processes runs in diurnal (e.g. locomotor activity, feeding, melatonin secretion) and seasonal rhythms (e.g. reproduction, song, feathering, migration) depending on the environmental light and the activity of the central clock system (CCS). The structure and mechanisms of the activity of the avian CCS are the most complex among vertebrates. CCS consists of three oscillators (in the retina, SCN and pineal gland) possessing own sensory input system (photopigments) and effective output system (products for direct biological effects). So far in the CCS in birds 14 forms of photopigments (Opn1, Opn2, Opn3, TMT, Opn4x, Opn4m, Opn5, RGR, RRH, VA-opsins, pinopsin, Cry1, Cry2 i Cry4) and 12 clock genes making up oscillators (Bmal1, Bmal2, Clock, NPas2 called also Mop4 and Rorα – positive genes and Cry1, Cry2, Cry4, Per2, Per3, E4bp4 and Rev-erbα – negative genes) have been described. Photopigments are placed in all layers of the retina; in brain - mainly in regions of nuclei: septalis lateralis, premammillaris, habenularis and paraventricularis; in the pineal gland - in all kinds of pinealocytes. Most photopigments belonging to the opsin family are linked with nucleotide phototransduction path, typical for vertebrates, but in avian CCS also phosphoinositol phototransduction path, characteristic for invertebrates, is existing and concerns Opn4x and Opn5. Oscilators are placed in nuclei of cells of all layers of the retina, in mSCN and vSCN (with great species variability) and in pinealocytes. It is supposing, that all nonvisual photopigments have a direct role in the synchronization of the oscillator activity with the environmental light, but molecular mechanisms of the interaction between photopigments and the oscillator remain unknown. The impact of each of the three oscillators of CCS in generating of biological rhythms in birds show great species differentiation. The differences concern both the domination of one of oscillators over the others and the assignation of biological processes which individual oscillator synchronizes rhythmically with the environmental light..

scholarly journals Multi-Level Processes and Retina–Brain Pathways of Photic Regulation of Mood

2022 ◽  
Vol 11 (2) ◽  
pp. 448
Author(s):  
Julia Maruani ◽  
Pierre A. Geoffroy
Keyword(s):  
Emotional Processing ◽  
Ganglion Cells ◽  
Biological Effects ◽  
Biological Rhythms ◽  
Neural Basis ◽  
Brain Areas ◽  
Lateral Habenula ◽  
Light Effects ◽  
Brain Pathways ◽  
The Impact

Light exerts powerful biological effects on mood regulation. Whereas the source of photic information affecting mood is well established at least via intrinsically photosensitive retinal ganglion cells (ipRGCs) secreting the melanopsin photopigment, the precise circuits that mediate the impact of light on depressive behaviors are not well understood. This review proposes two distinct retina–brain pathways of light effects on mood: (i) a suprachiasmatic nucleus (SCN)-dependent pathway with light effect on mood via the synchronization of biological rhythms, and (ii) a SCN-independent pathway with light effects on mood through modulation of the homeostatic process of sleep, alertness and emotion regulation: (1) light directly inhibits brain areas promoting sleep such as the ventrolateral preoptic nucleus (VLPO), and activates numerous brain areas involved in alertness such as, monoaminergic areas, thalamic regions and hypothalamic regions including orexin areas; (2) moreover, light seems to modulate mood through orexin-, serotonin- and dopamine-dependent pathways; (3) in addition, light activates brain emotional processing areas including the amygdala, the nucleus accumbens, the perihabenular nucleus, the left hippocampus and pathways such as the retina–ventral lateral geniculate nucleus and intergeniculate leaflet–lateral habenula pathway. This work synthetizes new insights into the neural basis required for light influence mood

scholarly journals Marine Natural Products: A Source of Novel Anticancer Drugs

Marine Drugs ◽  
2019 ◽  
Vol 17 (9) ◽  
pp. 491 ◽  
Author(s):  
Shaden A. M. Khalifa ◽  
Nizar Elias ◽  
Mohamed A. Farag ◽  
Lei Chen ◽  
Aamer Saeed ◽  
...  
Keyword(s):  
Natural Products ◽  
Anticancer Drugs ◽  
Marine Natural Products ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Marine Organisms ◽  
New Drugs ◽  
Bioactive Metabolites ◽  
Chemical Structures ◽  
The Impact

Cancer remains one of the most lethal diseases worldwide. There is an urgent need for new drugs with novel modes of action and thus considerable research has been conducted for new anticancer drugs from natural sources, especially plants, microbes and marine organisms. Marine populations represent reservoirs of novel bioactive metabolites with diverse groups of chemical structures. This review highlights the impact of marine organisms, with particular emphasis on marine plants, algae, bacteria, actinomycetes, fungi, sponges and soft corals. Anti-cancer effects of marine natural products in in vitro and in vivo studies were first introduced; their activity in the prevention of tumor formation and the related compound-induced apoptosis and cytotoxicities were tackled. The possible molecular mechanisms behind the biological effects are also presented. The review highlights the diversity of marine organisms, novel chemical structures, and chemical property space. Finally, therapeutic strategies and the present use of marine-derived components, its future direction and limitations are discussed.

scholarly journals Challenging the Integrity of Rhythmic Maternal Signals Revealed Gene-Specific Responses in the Fetal Suprachiasmatic Nuclei

2021 ◽  
Vol 14 ◽  
Author(s):  
Vendula Lužná ◽  
Pavel Houdek ◽  
Karolína Liška ◽  
Alena Sumová
Keyword(s):  
Phase Shift ◽  
Clock Genes ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transient State ◽  
Suprachiasmatic Nuclei ◽  
Pregnant Rats ◽  
Behavioral Rhythm ◽  
Environmental Light ◽  
The Impact

During fetal stage, maternal circadian system sets the phase of the developing clock in the suprachiasmatic nuclei (SCN) via complex pathways. We addressed the issue of how impaired maternal signaling due to a disturbed environmental light/dark (LD) cycle affects the fetal SCN. We exposed pregnant Wistar rats to two different challenges – a 6-h phase shift in the LD cycle on gestational day 14, or exposure to constant light (LL) throughout pregnancy – and detected the impact on gene expression profiles in 19-day-old fetuses. The LD phase shift, which changed the maternal SCN into a transient state, caused robust downregulation of expression profiles of clock genes (Per1, Per2, and Nr1d1), clock-controlled (Dbp) genes, as well as genes involved in sensing various signals, such as c-fos and Nr3c1. Removal of the rhythmic maternal signals via exposure of pregnant rats to LL abolished the rhythms in expression of c-fos and Nr3c1 in the fetal SCN. We identified c-fos as the gene primarily responsible for sensing rhythmic maternal signals because its expression profile tracked the shifted or arrhythmic maternal SCN clock. Pathways related to the maternal rhythmic behavioral state were likely not involved in driving the c-fos expression rhythm. Instead, introduction of a behavioral rhythm to LL-exposed mothers via restricted feeding regime strengthened rhythm in Vip expression in the fetal SCN. Our results revealed for the first time that the fetal SCN is highly sensitive in a gene-specific manner to various changes in maternal signaling due to disturbances of environmental cycles related to the modern lifestyle in humans.

scholarly journals Transcriptional Profiling of the Chick Pineal Gland, a Photoreceptive Circadian Oscillator and Pacemaker

2003 ◽  
Vol 17 (10) ◽  
pp. 2084-2095 ◽  
Author(s):  
Michael J. Bailey ◽  
Phillip D. Beremand ◽  
Rick Hammer ◽  
Deborah Bell-Pedersen ◽  
Terry L. Thomas ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Molecular Mechanisms ◽  
Clock Genes ◽  
Transcriptional Profiling ◽  
Complex Form ◽  
Time Of Day ◽  
Constant Darkness ◽  
Immune Stress

Abstract The avian pineal gland contains both circadian oscillators and photoreceptors to produce rhythms in biosynthesis of the hormone melatonin in vivo and in vitro. The molecular mechanisms for melatonin biosynthesis are largely understood, but the mechanisms driving the rhythm itself or the photoreceptive processes that entrain the rhythm are unknown. We have produced cDNA microarrays of pineal gland transcripts under light-dark and constant darkness conditions. Rhythmic transcripts were classified according to function, representing diverse functional groups, including phototransduction pathways, transcription/translation factors, ion channel proteins, cell signaling molecules, and immune function genes. These were also organized relative to time of day mRNA abundance in light-dark and constant darkness. The transcriptional profile of the chick pineal gland reveals a more complex form of gene regulation than one might expect from a gland whose sole apparent function is the rhythmic biosynthesis of melatonin. The mRNAs encoding melatonin biosynthesis are rhythmic as are many orthologs of mammalian “clock genes.” However, the oscillation of phototransductive, immune, stress response, hormone binding, and other important processes in the transcriptome of the pineal gland, raises new questions regarding the role of the pineal gland in circadian rhythm generation, organization, and avian physiology.

scholarly journals The OFD1 protein is a novel player in selective autophagy: another tile to the cilia/autophagy puzzle

Cell Stress ◽  
2021 ◽  
Vol 5 (3) ◽  
pp. 33-36
Author(s):  
Manuela Morleo ◽  
Brunella Franco
Keyword(s):  
Basal Body ◽  
Primary Cilia ◽  
Molecular Mechanisms ◽  
Clinical Manifestations ◽  
Direct Role ◽  
Body Protein ◽  
Selective Autophagy ◽  
Mother Centriole ◽  
The Impact

The autophagy-lysosomal pathway is one of the main degradative routes which cells use to balance sources of energy. A number of proteins orchestrate the formation of autophagosomes, membranous organelles instrumental in autophagy. Selective autophagy, involving the recognition and removal of specific targets, is mediated by autophagy receptors, which recognize cargos and the autophagosomal membrane protein LC3 for lysosomal degradation. Recently, bidirectional crosstalk has emerged between autophagy and primary cilia, microtubule-based sensory organelles extending from cells and anchored by the basal body, derived from the mother centriole of the centrosome. The molecular mechanisms underlying the direct role of autophagic proteins in cilia biology and, conversely, the impact of this organelle in autophagy remains elusive. Recently, we uncovered the molecular mechanism by which the centrosomal/basal body protein OFD1 controls the LC3-mediated autophagic cascade. In particular, we demonstrated that OFD1 acts as a selective autophagy receptor by regulating the turnover of unc-51-like kinase (ULK1) complex, which plays a crucial role in the initiation steps of autophagosome biogenesis. Moreover, we showed that patients with a genetic condition caused by mutations in OFD1 and associated with cilia dysfunction, display excessive autophagy and we demonstrated that autophagy inhibition significantly ameliorates the renal cystic phenotype in a conditional mouse model recapitulating the features of the disease (Morleo et al. 2020, EMBO J, doi: 10.15252/embj.2020105120). We speculate that abnormal autophagy may underlie some of the clinical manifestations observed in the disorders ascribed to cilia dysfunction.

scholarly journals EFFECT OF FLUORIDE INTOXICATION ON HISTOHORMONE CONTENT IN EXPERIMENTS

2021 ◽  
pp. 13-16
Author(s):  
I. Yu. Bagmut ◽  
I. L. Kolisnyk
Keyword(s):  
Defense Mechanisms ◽  
Molecular Mechanisms ◽  
Biological Effects ◽  
Practical Importance ◽  
Research Work ◽  
Postgraduate Education ◽  
Normal Growth ◽  
The Body ◽  
Endocrine Organs ◽  
The Impact

Connection of work with scientific plans, topics. The work was performed in accordance with the research plan of the Kharkiv Medical Academy of Postgraduate Education of the Ministry of Health of Ukraine and is a fragment of research work of the Department of Clinical Pathophysiology, Topographic Anatomy and Operative Surgery "Pathophysiological mechanisms of radiotoxins on the body and principles of early diagnosis 2017–2021). SUMMARY. One of the important medical and biological problems is to elucidate the physiological and molecular mechanisms of the impact of harmful environmental factors on the body, including fluorine and its compounds, in particular sodium fluoride [1]. Solving this problem is of great theoretical and practical importance for understanding the intracellular defense mechanisms of the organism. Close attention to various aspects of the biological effects of fluoride on the body is due to the significant distribution of this halogen in nature. At physiological concentrations, it is necessary for normal growth and development of the organism, where it performs its specific metabolic function. Any changes in the external and internal environment are accompanied by changes in the function of the endocrine glands, which leads to certain changes in metabolism and energy. It is known that hormonal insufficiency is accompanied by a decrease in the body's resistance to various adverse factors, including physical, biological, chemical. Disturbance of hormone balance and functioning of endocrine organs and systems entails profound changes in metabolic processes and immunobiological reactivity of the organism, weakening of adaptive-protective mechanisms in support of homeostatic function [2,3]. It is important to study the effects of subchronic fluoride intake, which can in a relatively short time cause various intracellular and systemic disorders in the body.

The Impact of Ultraviolet Radiation on Barrier Function in Human Skin: Molecular Mechanisms and Topical Therapeutics

2019 ◽  
Vol 25 (40) ◽  
pp. 5503-5511 ◽  
Author(s):  
Abdulaziz Alhasaniah ◽  
Michael J. Sherratt ◽  
Catherine A. O'Neill
Keyword(s):  
Ultraviolet Radiation ◽  
Barrier Function ◽  
Molecular Mechanisms ◽  
Transepidermal Water Loss ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Epidermal Barrier ◽  
Positive Effects ◽  
Terrestrial Mammals ◽  
The Impact

A competent epidermal barrier is crucial for terrestrial mammals. This barrier must keep in water and prevent entry of noxious stimuli. Most importantly, the epidermis must also be a barrier to ultraviolet radiation (UVR) from the sunlight. Currently, the effects of ultraviolet radiation on epidermal barrier function are poorly understood. However, studies in mice and more limited work in humans suggest that the epidermal barrier becomes more permeable, as measured by increased transepidermal water loss, in response UVR, at doses sufficiently high to induce erythema. The mechanisms may include disturbance in the organisation of lipids in the stratum corneum (the outermost layer of the epidermis) and reduction in tight junction function in the granular layer (the first living layer of the skin). By contrast, suberythemal doses of UVR appear to have positive effects on epidermal barrier function. Topical sunscreens have direct and indirect protective effects on the barrier through their ability to block UV and also due to their moisturising or occlusive effects, which trap water in the skin, respectively. Some topical agents such as specific botanical extracts have been shown to prevent the loss of water associated with high doses of UVR. In this review, we discuss the current literature and suggest that the biology of UVR-induced barrier dysfunction, and the use of topical products to protect the barrier, are areas worthy of further investigation.

The Role of Vascular Aging in Atherosclerotic Plaque Development and Vulnerability

2019 ◽  
Vol 25 (29) ◽  
pp. 3098-3111 ◽  
Author(s):  
Luca Liberale ◽  
Giovanni G. Camici
Keyword(s):  
Atherosclerotic Plaque ◽  
Molecular Mechanisms ◽  
Driving Forces ◽  
Plaque Burden ◽  
Vascular Aging ◽  
Age Related ◽  
Plaque Development ◽  
Increased Risk ◽  
The Impact ◽  
Over Time

Background: The ongoing demographical shift is leading to an unprecedented aging of the population. As a consequence, the prevalence of age-related diseases, such as atherosclerosis and its thrombotic complications is set to increase in the near future. Endothelial dysfunction and vascular stiffening characterize arterial aging and set the stage for the development of cardiovascular diseases. Atherosclerotic plaques evolve over time, the extent to which these changes might affect their stability and predispose to sudden complications remains to be determined. Recent advances in imaging technology will allow for longitudinal prospective studies following the progression of plaque burden aimed at better characterizing changes over time associated with plaque stability or rupture. Oxidative stress and inflammation, firmly established driving forces of age-related CV dysfunction, also play an important role in atherosclerotic plaque destabilization and rupture. Several genes involved in lifespan determination are known regulator of redox cellular balance and pre-clinical evidence underlines their pathophysiological roles in age-related cardiovascular dysfunction and atherosclerosis. Objective: The aim of this narrative review is to examine the impact of aging on arterial function and atherosclerotic plaque development. Furthermore, we report how molecular mechanisms of vascular aging might regulate age-related plaque modifications and how this may help to identify novel therapeutic targets to attenuate the increased risk of CV disease in elderly people.

VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Aikebaier Maimaiti ◽  
Amier Aili ◽  
Hureshitanmu Kuerban ◽  
Xuejun Li
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Gallic Acid ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Dependent Manner ◽  
Lung Carcinoma Cells ◽  
Induced Apoptosis ◽  
The Impact

Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability.

scholarly journals SARS-CoV-2 and the Nervous System: From Clinical Features to Molecular Mechanisms

2020 ◽  
Vol 21 (15) ◽  
pp. 5475 ◽  
Author(s):  
Manuela Pennisi ◽  
Giuseppe Lanza ◽  
Luca Falzone ◽  
Francesco Fisicaro ◽  
Raffaele Ferri ◽  
...  
Keyword(s):  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Neurological Complications ◽  
Neurological Manifestations ◽  
Wide Range ◽  
Inflammatory State ◽  
Acute Polyneuropathy ◽  
The Central Nervous System ◽  
The Impact

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called “cytokine storm”), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.

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