scholarly journals Micronuclei and Genome Chaos: Changing the System Inheritance

Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 366 ◽  
Author(s):  
Christine J. Ye ◽  
Zachary Sharpe ◽  
Sarah Alemara ◽  
Stephanie Mackenzie ◽  
Guo Liu ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Genome Instability ◽  
Common Mechanism ◽  
Cancer Evolution ◽  
Somatic Evolution ◽  
Causative Relationship ◽  
Key Issues ◽  
The Common ◽  
Genome Chaos ◽  
Genome Theory

Micronuclei research has regained its popularity due to the realization that genome chaos, a rapid and massive genome re-organization under stress, represents a major common mechanism for punctuated cancer evolution. The molecular link between micronuclei and chromothripsis (one subtype of genome chaos which has a selection advantage due to the limited local scales of chromosome re-organization), has recently become a hot topic, especially since the link between micronuclei and immune activation has been identified. Many diverse molecular mechanisms have been illustrated to explain the causative relationship between micronuclei and genome chaos. However, the newly revealed complexity also causes confusion regarding the common mechanisms of micronuclei and their impact on genomic systems. To make sense of these diverse and even conflicting observations, the genome theory is applied in order to explain a stress mediated common mechanism of the generation of micronuclei and their contribution to somatic evolution by altering the original set of information and system inheritance in which cellular selection functions. To achieve this goal, a history and a current new trend of micronuclei research is briefly reviewed, followed by a review of arising key issues essential in advancing the field, including the re-classification of micronuclei and how to unify diverse molecular characterizations. The mechanistic understanding of micronuclei and their biological function is re-examined based on the genome theory. Specifically, such analyses propose that micronuclei represent an effective way in changing the system inheritance by altering the coding of chromosomes, which belongs to the common evolutionary mechanism of cellular adaptation and its trade-off. Further studies of the role of micronuclei in disease need to be focused on the behavior of the adaptive system rather than specific molecular mechanisms that generate micronuclei. This new model can clarify issues important to stress induced micronuclei and genome instability, the formation and maintenance of genomic information, and cellular evolution essential in many common and complex diseases such as cancer.

scholarly journals Origins and Consequences of Chromosomal Instability: From Cellular Adaptation to Genome Chaos-Mediated System Survival

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1162 ◽  
Author(s):  
Christine J. Ye ◽  
Zachary Sharpe ◽  
Henry H. Heng
Keyword(s):  
Chromosomal Instability ◽  
Molecular Mechanisms ◽  
Evolutionary Model ◽  
Common Mechanism ◽  
Cancer Evolution ◽  
Two Phase ◽  
Cellular Adaptation ◽  
Somatic Evolution ◽  
New Research ◽  
Genome Chaos

When discussing chromosomal instability, most of the literature focuses on the characterization of individual molecular mechanisms. These studies search for genomic and environmental causes and consequences of chromosomal instability in cancer, aiming to identify key triggering factors useful to control chromosomal instability and apply this knowledge in the clinic. Since cancer is a phenomenon of new system emergence from normal tissue driven by somatic evolution, such studies should be done in the context of new genome system emergence during evolution. In this perspective, both the origin and key outcome of chromosomal instability are examined using the genome theory of cancer evolution. Specifically, chromosomal instability was linked to a spectrum of genomic and non-genomic variants, from epigenetic alterations to drastic genome chaos. These highly diverse factors were then unified by the evolutionary mechanism of cancer. Following identification of the hidden link between cellular adaptation (positive and essential) and its trade-off (unavoidable and negative) of chromosomal instability, why chromosomal instability is the main player in the macro-cellular evolution of cancer is briefly discussed. Finally, new research directions are suggested, including searching for a common mechanism of evolutionary phase transition, establishing chromosomal instability as an evolutionary biomarker, validating the new two-phase evolutionary model of cancer, and applying such a model to improve clinical outcomes and to understand the genome-defined mechanism of organismal evolution.

scholarly journals Genome Chaos, Information Creation, and Cancer Emergence: Searching for New Frameworks on the 50th Anniversary of the “War on Cancer”

Genes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 101
Author(s):  
Julie Heng ◽  
Henry H. Heng
Keyword(s):  
Cancer Research ◽  
Cancer Biology ◽  
Molecular Mechanisms ◽  
50Th Anniversary ◽  
Genome Project ◽  
Cancer Genes ◽  
Cancer Evolution ◽  
Volume Data ◽  
Architecture Theory ◽  
Genome Chaos

The year 2021 marks the 50th anniversary of the National Cancer Act, signed by President Nixon, which declared a national “war on cancer.” Powered by enormous financial support, this past half-century has witnessed remarkable progress in understanding the individual molecular mechanisms of cancer, primarily through the characterization of cancer genes and the phenotypes associated with their pathways. Despite millions of publications and the overwhelming volume data generated from the Cancer Genome Project, clinical benefits are still lacking. In fact, the massive, diverse data also unexpectedly challenge the current somatic gene mutation theory of cancer, as well as the initial rationales behind sequencing so many cancer samples. Therefore, what should we do next? Should we continue to sequence more samples and push for further molecular characterizations, or should we take a moment to pause and think about the biological meaning of the data we have, integrating new ideas in cancer biology? On this special anniversary, we implore that it is time for the latter. We review the Genome Architecture Theory, an alternative conceptual framework that departs from gene-based theories. Specifically, we discuss the relationship between genes, genomes, and information-based platforms for future cancer research. This discussion will reinforce some newly proposed concepts that are essential for advancing cancer research, including two-phased cancer evolution (which reconciles evolutionary contributions from karyotypes and genes), stress-induced genome chaos (which creates new system information essential for macroevolution), the evolutionary mechanism of cancer (which unifies diverse molecular mechanisms to create new karyotype coding during evolution), and cellular adaptation and cancer emergence (which explains why cancer exists in the first place). We hope that these ideas will usher in new genomic and evolutionary conceptual frameworks and strategies for the next 50 years of cancer research.

STUDY OF PEDIATRIC INJURIES: PATTERNS AND OUTCOME

2019 ◽  
Vol 3 (8) ◽  
Author(s):  
Yasir. B. Elshambaty
Keyword(s):  
School Level ◽  
Common Mechanism ◽  
Injury Patterns ◽  
Severe Injuries ◽  
Injured Child ◽  
Cross Sectional ◽  
Pediatric Injuries ◽  
Pediatric Injury ◽  
The Common ◽  
Structured Questionnaire

Purpose this study aims to show the patterns and outcome of pediatric injury among those living in Albaha region in Saudi Arabia Methods this is a cross-sectional descriptive household-based study, included children between 0-17 years old both male and female. The data were collected with structured questionnaire between 20 Nov – 20 Dec 2018 and  analyzed with SPSS version 25 Results the total of participants was 257 injured child. 199(77.4%) are male and 58(22.6%) are female. About 44%of them were injured at pre-school level and 56% were traumatized at school age. The least incidence of injury occurred in those less than 2 yrs and higher incidence in those between 3-10 yrs old. The most common mechanism of injury was falling from height. The most affected group age by RTA accidents was 11-17 yrs old. Approximately 83% of the injured children required hospital management. Only one third of the injuries were  associated complications. The most common injured anatomic part was the upper limb and the least affected part was the spine. Only 5% of the injuries were associated with a disability and the common was loss of organ or part of it. Paralysis occurred in less than 1% and head injury resulted in disabilities more than 1%. Conclusion the vast majority of the injuries in our participants are not serious. The severe injuries were associated with RTA-related trauma. Most of injuries due to falling from height are not serious. We recommend not to allow the children to drive cars. Keywords: pediatric injuries; injury patterns; household.

Multiple mechanisms are responsible for altered expression of gap junction genes during oncogenesis in rat liver

1994 ◽  
Vol 107 (1) ◽  
pp. 83-95
Author(s):  
M.J. Neveu ◽  
J.R. Hully ◽  
K.L. Babcock ◽  
E.L. Hertzberg ◽  
B.J. Nicholson ◽  
...  
Keyword(s):  
Gap Junction ◽  
Cellular Localization ◽  
Molecular Mechanisms ◽  
Northern Blotting ◽  
Mrna Abundance ◽  
Common Mechanism ◽  
Cx43 Expression ◽  
Bile Duct Proliferation ◽  
Altered Expression ◽  
Connexin Expression

Although several abnormalities in gap junction (GJ) structure and/or function have been described in neoplasms, the molecular mechanisms responsible for many of the alterations remain unknown. The identification of a family of GJ proteins, termed connexins, prompted this study of connexin32 (Cx32), connexin26 (Cx26) and connexin43 (Cx43) expression during rat hepatocarcinogenesis. Using antibody, cDNA and cRNA probes, we investigated connexin mRNA and protein expression in preneoplastic and neoplastic rat livers. In normal liver, Cx32 is expressed in hepatocytes throughout the hepatic acinus, Cx26 is restricted to periportal hepatocytes, and Cx43 is expressed by mesothelial cells forming Glisson's capsule. Most preneoplastic altered hepatic foci generated by diethylnitrosamine (DEN) initiation and either phenobarbital (PB) or 2,3,7,8-dichlorodibenzo-p-dioxin (TCDD) promotion exhibited decreased Cx32 or increased Cx26 staining. Foci from either protocol failed to display Cx43 immunoreactivity. In the majority of PB-promoted foci, Cx32 immunoreactivity decreased independently of changes in mRNA abundance. Continuous thymidine labeling, following cessation of PB promotion, showed that downregulation of Cx32 staining is reversible in foci that are promoter-dependent for growth, but irreversible in lesions that are promoter-independent for growth. Hepatic neoplasms from rats initiated with DEN and promoted with PB or TCDD also displayed modified connexin expression. While all 24 neoplasms studied were deficient in normal punctate Cx32 and Cx26 staining, altered cellular localization of these proteins was apparent in some tumors. Immunoblotting of crude tissue extracts revealed that neoplasms with disordered Cx32 staining showed immunoreactive bands with altered electrophoretic mobility. These observations show that hepatomas may downregulate Cx32 expression through changes in the primary structure of Cx32 or by post-translational modifications. Northern blotting of total tumor mRNAs failed to demonstrate consistent changes in the abundance of Cx32, Cx26 or Cx43 transcripts. Some tumors expressed steady-state transcripts without observable immunoreactivity, indicating that some hepatomas downregulate connexin immunoreactivity independently of mRNA abundance. Increased levels of Cx43 mRNA and protein were found in several neoplasms, but immunostaining was always localized to nonparenchymal cells. Areas of bile duct proliferation and cholangiomas displayed Cx43 staining, whereas, cholangiocarcinomas were deficient in immunoreactivity. These findings show that alterations in the expression of connexins, by either downregulation or differential induction, represent common modifications during hepatocarcinogenesis. Although our results imply that connexins represent useful markers for the boundary between tumor promotion and progression, preneoplastic and neoplastic rat hepatocytes fail to use a common mechanism to modify connexin expression.

Cross-species Transcriptomes Reveal Species-specific and Shared Molecular Adaptations for Plants Development on Iron-rich Rocky Outcrops Soils

2021 ◽  
Author(s):  
Mariana Costa Dias ◽  
Cecílio Caldeira ◽  
Markus Gastauer ◽  
Silvio Ramos ◽  
Guilherme Oliveira
Keyword(s):  
Circadian Rhythm ◽  
Differential Expression ◽  
Native Species ◽  
Molecular Mechanisms ◽  
Light Stimulus ◽  
Differential Expression Analysis ◽  
Common Mechanism ◽  
Dependent Manner ◽  
Rocky Outcrops ◽  
Species Specific

Abstract BackgroundCanga is the Brazilian term for the savanna-like vegetation harboring several endemic species on iron-rich rocky outcrops, usually considered for mining activities. Parkia platycephala Benth. and Stryphnodendron pulcherrimum (Willd.) Hochr. naturally occur in the cangas of Serra dos Carajás (eastern Amazonia, Brazil) and the surrounding forest, indicating high phenotypic plasticity. The morphological and physiological mechanisms of the plants’ establishment in the canga environment are well studied, but the molecular adaptative responses are still unknown. We aimed to identify molecular mechanisms that allow the establishment of these plants in the canga environment.ResultsPlants were grown in canga and forest substrates collected in the Carajás Mineral Province. RNA was extracted from pooled leaf tissue, and RNA-seq paired-end reads were assembled into representative transcriptomes for P. platycephala and S. pulcherrimum containing 31,728 and 31,311 primary transcripts, respectively. We identified both species-specific and core molecular responses in plants grown in the canga substrate using differential expression analyses. In the species-specific analysis, we identified 1,112 and 838 differentially expressed genes for P. platycephala and S. pulcherrimum, respectively. Enrichment analyses showed unique biological processes and metabolic pathways affected for each species. Comparative differential expression analysis was based on shared single-copy orthologs. The overall pattern of ortholog expression was species-specific. Even so, almost 300 altered genes were identified between plants in canga and forest substrates, responding the same way in both species. The genes were functionally associated with the response to light stimulus and the circadian rhythm pathway.ConclusionsPlants possess species-specific adaptative responses to cope with the substrates. Our results also suggest that plants adapted to both canga and forest environments can adjust the circadian rhythm in a substrate-dependent manner. The circadian clock gene modulation might be a central mechanism regulating the plants’ development in the canga substrate in the studied legume species. The mechanism may be shared as a common mechanism to abiotic stress compensation in other native species.

scholarly journals Evidence for biological shaping of hair ice

2015 ◽  
Vol 12 (14) ◽  
pp. 4261-4273 ◽  
Author(s):  
D. Hofmann ◽  
G. Preuss ◽  
C. Mätzler
Keyword(s):  
Organic Matter ◽  
Dead Wood ◽  
Complex Mixture ◽  
Fulvic Acids ◽  
Common Mechanism ◽  
Ice Growth ◽  
Physical Chemical ◽  
Broad Leaf ◽  
The Common

Abstract. An unusual ice type, called hair ice, grows on the surface of dead wood of broad-leaf trees at temperatures slightly below 0 °C. We describe this phenomenon and present physical, chemical, and biological investigations to gain insight in the properties and processes related to hair ice. Tests revealed that the biological activity of a winter-active fungus is required in the wood for enabling the growth of hair ice. We confirmed the fungus hypothesis originally suggested by Wegener (1918) by reproducing hair ice on wood samples. Treatment by heat and fungicide suppresses the formation of hair ice. Fruiting bodies of Asco- and Basidiomycota are identified on hair-ice-carrying wood. One species, Exidiopsis effusa (Ee), was present on all investigated samples. Both hair-ice-producing wood samples and those with killed fungus show essentially the same temperature variation, indicating that the heat produced by fungal metabolism is very small, that the freezing rate is not influenced by the fungus activity, and that ice segregation is the common mechanism of ice growth on the wood surface. The fungus plays the role of shaping the ice hairs and preventing them from recrystallisation. Melted hair ice indicates the presence of organic matter. Chemical analyses show a complex mixture of several thousand CHO(N,S) compounds similar to fulvic acids in dissolved organic matter (DOM). The evaluation reveals decomposed lignin as being the main constituent. Further work is needed to clarify its role in hair-ice growth and to identify the recrystallisation inhibitor.

scholarly journals Cytokine Imbalance as a Common Mechanism in Both Psoriasis and Rheumatoid Arthritis

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Yong Tan ◽  
Qiu Qi ◽  
Cheng Lu ◽  
Xuyan Niu ◽  
Yanping Bai ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Molecular Mechanism ◽  
Mononuclear Cells ◽  
Mitogen Activated Protein Kinase ◽  
Common Mechanism ◽  
New Paradigm ◽  
Peripheral Blood Mononuclear ◽  
The Common ◽  
Common Pathogenesis ◽  
Cytokine Imbalance

Psoriasis (PS) and rheumatoid arthritis (RA) are immune-mediated inflammatory diseases. Previous studies showed that these two diseases had a common pathogenesis, but the precise molecular mechanism remains unclear. In this study, RNA sequencing of peripheral blood mononuclear cells was employed to explore both the differentially expressed genes (DEGs) of 10 PS and 10 RA patients compared with those of 10 healthy volunteers and the shared DEGs between these two diseases. Bioinformatics network analysis was used to reveal the connections among the shared DEGs and the corresponding molecular mechanism. In total, 120 and 212 DEGs were identified in PS and RA, respectively, and 31 shared DEGs were identified. Bioinformatics analysis indicated that the cytokine imbalance relevant to key molecules (such as extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), colony-stimulating factor 3 (CSF3), interleukin- (IL-) 6, and interferon gene (IFNG)) and canonical signaling pathways (such as the complement system, antigen presentation, macropinocytosis signaling, nuclear factor-kappa B (NF-κB) signaling, and IL-17 signaling) was responsible for the common comprehensive mechanism of PS and RA. Our findings provide a better understanding of the pathogenesis of PS and RA, suggesting potential strategies for treating and preventing both diseases. This study may also provide a new paradigm for illuminating the common pathogenesis of different diseases.

Analysis of the molecular mechanisms by flavonoids with potential use for osteoporosis prevention or therapy

2021 ◽  
Vol 28 ◽  
Author(s):  
Valeria Rodríguez ◽  
María Rivoira ◽  
Gabriela Picotto ◽  
Gabriela Díaz de Barboza ◽  
Alejandro Collin ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Osteoporosis Treatment ◽  
Epidemiological Studies ◽  
Common Mechanism ◽  
Osteoporotic Bone ◽  
Osteoporosis Prevention ◽  
Mineral Density ◽  
Pubmed Database ◽  
Molecular Aspects ◽  
Potential Use

Background: Osteoporosis is the most common skeletal disorder worldwide. Flavonoids have the potential to alleviate bone alterations in osteoporotic patients with the advantage of being safer and less expensive than the conventional therapies. Objective: The main objective is to analyze the molecular mechanisms triggered in bone by different subclasses of flavonoids. In addition, this review provides an up-to-date overview on the cellular and molecular aspects of osteoporotic bones versus healthy bones, and a brief description of some epidemiological studies indicating that flavonoids could be useful for osteoporosis treatment. Methods: The PubMed database was searched in the range of years 2001- 2021 using the keywords osteoporosis, flavonoids, and their subclasses such as flavones, flavonols, flavanols, isoflavones, flavanones and anthocyanins, focusing the data on the molecular mechanisms triggered in bone. Results: Although flavonoids comprise many compounds that differ in structure, their effects on bone loss in postmenopausal women or in ovariectomized-induced osteoporotic animals are quite similar. Most of them increase bone mineral density and bone strength, which occur through enhancement of osteoblastogenesis and osteoclast apoptosis, decrease in osteoclastogenesis as well as increase in neovascularization on the site of the osteoporotic fracture. Conclusion: Several molecules of signaling pathways are involved in the effect of flavonoids on osteoporotic bone. Whether all flavonoids have a common mechanism or they act as ligands of estrogen receptors remain to be established. More clinical trials are necessary to know better their safety, efficacy, delivery and bioavailability in humans, as well as comparative studies with conventional therapies.

The Handbook of Language Assessment Across Modalities

2021 ◽  
Keyword(s):  
Second Language ◽  
Language Assessment ◽  
Spoken Language ◽  
Assessment Literacy ◽  
Signed Language ◽  
Key Issues ◽  
Relevant Field ◽  
The Common ◽  
New Perspective ◽  
First Time

In Language Assessment Across Modalities: Paired-Papers on Signed and Spoken Language Assessment, volume editors Tobias Haug, Wolfgang Mann, and Ute Knoch bring together—for the first time—researchers, clinicians, and practitioners from two different fields: signed language and spoken language. The volume examines theoretical and practical issues related to 12 topics ranging from test development and language assessment of bi-/multilingual learners to construct issues of second-language assessment (including the Common European Framework of Reference [CEFR]) and language assessment literacy in second-language assessment contexts. Each topic is addressed separately for spoken and signed language by experts from the relevant field. This is followed by a joint discussion in which the chapter authors highlight key issues in each field and their possible implications for the other field. What makes this volume unique is that it is the first of its kind to bring experts from signed and spoken language assessment to the same table. The dialogues that result from this collaboration not only help to establish a shared appreciation and understanding of challenges experienced in the new field of signed language assessment but also breathes new life into and provides a new perspective on some of the issues that have occupied the field of spoken language assessment for decades. It is hoped that this will open the door to new and exciting cross-disciplinary collaborations.

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