alexa A New RNA Synthesis of Cells: A Possible End of Birth Defects | Open Access Journals
ISSN: 2168-9547
Molecular Biology: Open Access
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

A New RNA Synthesis of Cells: A Possible End of Birth Defects

Aaron Wallman*

California State University, 401 Golden Shore, Long Beach, 90510, USA

*Corresponding Author:
Aaron Wallman
California State University, 401 Golden Shore
Long Beach, 90510, USA
Tel: 310-502-5889
E-mail: aaron.wallman@yahoo.com

Received date: February 07, 2017; Accepted date: February 21, 2017; Published date: February 28, 2017

Citation: Wallman A (2017) A New RNA Synthesis of Cells: A Possible End of Birth Defects. Mol Biol 6:187. doi:10.4172/2168-9547.1000187

Copyright: © 2017 Wallman A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Molecular Biology: Open Access

Abstract

According to Dr. Klaasmeir, each species has a specific ratio of nitrogen/phosphorous. In the case of plankton, for example, the nitrogen/phosphorous ratio would be N:P=16 and in deep oceanic water the ratio would be N:P=15. Dr. Karpinets believes nitrogen and phosphorous as this ratio dominate unicellular organisms. In addition, “the basic functions of initiation, elongation and termination in the ribosome of bacteria resemble those of eukaryotes”. Under adverse conditions, Dr. Karpinets thinks that the act of each gene’s encoding of cellular maintenance decreases as well.

Commentary

According to Dr. Klaasmeir, each species has a specific ratio of nitrogen/phosphorous. In the case of plankton, for example, the nitrogen/phosphorous ratio would be N:P=16 and in deep oceanic water the ratio would be N:P=15 [1]. Dr. Karpinets believes nitrogen and phosphorous as this ratio dominate unicellular organisms. In addition, “the basic functions of initiation, elongation and termination in the ribosome of bacteria resemble those of eukaryotes” [2]. Under adverse conditions, Dr. Karpinets thinks that the act of each gene’s encoding of cellular maintenance decreases as well.

With a birth defect like Downs Syndrome, Dr. Menkes contends that there are abnormalities in the chemical composition and the structure of such a person’s brain which I as well as some professors believe are from a faulty synthesis of RNA [3].

Dr. Konrad claims that, “the lack of a comparable reduction in protein synthesis during mitosis should be interpreted as evidence for the presence in these cells of a relatively stable messenger RNA [4].” Later in this article, I will mention those professors whom I believe link an unstable RNA messenger to birth defects.

Like Dr. Schultz’s discovery of the chemical compound reversine’s positive effect on the metaphase during mitosis, I believe that the influence of a chemical compound with a ratio as nitrogen/ phosphorous renews a cell’s abnormal instructions with normal ones as the two daughter cells separate on the metaphase plate during their mitosis [5]. To Dr. Maayan, the mitosis of cells reflect such a replication of this genetic material as they replicate as either an abnormal or normal trait of a person [6].

In more precise terms, Dr. Watts concludes that a person’s abnormal trait like congenital blindness can be traced to a faulty synthesis which to me leads to an unstable RNA messenger [7]. In even more specific terms, Dr. Haldeman-Englert observes that the origin of such a birth defect is from an extra chromosome or another type of error during their past meiosis which I believe is misdirected by its protein synthesis. Furthermore, I believe that its misdirection can be traced to an unstable RNA messenger [8].

In his article, “Cells Keep a Memory of their Tissue Origin During Axolotl Limb Regeneration,” Dr. Kragl thinks that cells keep a memory of their tissue origin during limb regeneration of an axolotl such as a Mexican lizard for example [9]. With such correct and matching input, which is traced to a faulty past meiosis of a person, I propose that in their laboratories, researchers should measure the ratio of nitrogen and phosphorous for a person’s new RNA synthesis which leads to a stable RNA messenger during the mitosis of his or her birth defect. Moreover, such an occurrence results in this birth defect’s end with the correct amino acid sequences.

Based on the data of this article, such elements of nitrogen and phosphorous along with protein underline the growth rate of either the birth defect or normal trait of an organism. In my opinion, an estimation of these two above elements as a chemical compound leads a human’s birth defect to have the correct amino acid sequence as previously mentioned and then become a normal trait. With the correct calculation of the compound of nitrogen and phosphorous for an unstable RNA messenger, which is traced to a birth defect, a researcher can discover the ideal growth rate for its stability as an RNA messenger and then its end as a birth defect. On this basis, I invite students and researchers to consider this point of mine with the data of this article.

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Relevant Topics

Recommended Conferences

Article Usage

  • Total views: 323
  • [From(publication date):
    April-2017 - Jul 23, 2017]
  • Breakdown by view type
  • HTML page views : 292
  • PDF downloads :31
 
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

agrifoodaquavet@omicsonline.com

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

clinical_biochem@omicsonline.com

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

business@omicsonline.com

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

chemicaleng_chemistry@omicsonline.com

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

environmentalsci@omicsonline.com

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

engineering@omicsonline.com

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

generalsci_healthcare@omicsonline.com

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

genetics_molbio@omicsonline.com

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

immuno_microbio@omicsonline.com

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

omics@omicsonline.com

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

materialsci@omicsonline.com

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

mathematics_physics@omicsonline.com

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

medical@omicsonline.com

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

neuro_psychology@omicsonline.com

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

pharma@omicsonline.com

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

social_politicalsci@omicsonline.com

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version