Ahmad I Funjan*
Traditional identification methods for the soft rot Erwinias are both imprecise and time-consuming. We have used the 16S rDNA to aid in their identification.
Analysis of 16S rDNA-PCR and 16S rDNA-RFLP and gene sequencing was found to be simple, precise, and rapid method compared to other molecular techniques.
Analysis of the isolates genome by using their total DNA by amplifying their genome using the universal primer (fD1/rP2) indicated an amplified product of the
16S rDNA at 450 bp and the amplification using the specific 16S rDNA (EP16A/EP1GTC) was located of 700 bp. The restriction analysis of the universal amplified
product of 450 bp size using Hind III, proved the presence of different RFLP bands with some common bands. Variation in RFLP profile bands is an indication of
polymorphism in between the isolates. Whereas common bands indicates genetic stability among the isolates of the same spices or same genus. Sequencing of
the 16S rDNA universal primer amplified product showed a complete sequence of one isolate out of 10 isolate and the similarity between this isolate and the data
base indicated the presence of high similarity above 95% with other Enterobaceriaceae.
DOI: 10.37421/1747-0862.2023.17.632
Cancer is a complex and heterogeneous disease that results from genetic and epigenetic alterations in the genome. These alterations are known as drivers of cancer progression, which enable the acquisition of the hallmarks of cancer, including sustained proliferative signaling, evasion of apoptosis, and tissue invasion and metastasis. The identification of genetic and epigenetic drivers of cancer has led to the development of precision medicine approaches that aim to personalize cancer treatment based on the specific molecular alterations driving each individual patient's tumor. In this review, we discuss the genetic and epigenetic drivers of cancer progression and their implications for precision medicine.
Metabolic Syndrome (MetS) is a complex disorder that involves a cluster of metabolic abnormalities, including central obesity, insulin resistance, dyslipidemia, and hypertension. It is a significant public health problem and a leading cause of cardiovascular disease and type 2 diabetes mellitus. The molecular mechanisms underlying the development of MetS are multifactorial and involve a combination of genetic, environmental, and lifestyle factors. In this review, we discuss the molecular mechanisms of MetS and potential therapeutic targets.
DOI: 10.37421/1747-0862.2023.17.635
Cardos Garry*
Cardio-Vascular Disease (CVD) is a leading cause of death worldwide. The development of CVD is influenced by both environmental and genetic factors. Recent advancements in genomic technologies have allowed for the identification of genetic variants that are associated with increased risk of CVD. In this paper, we will review the current literature on the role of genetic variants in the development of CVD. We will discuss the various genetic variants that have been identified and their mechanisms of action. Furthermore, we will explore the potential clinical applications of genetic testing in predicting CVD risk and tailoring treatment strategies.
Danielly Viana Monteiro Santos*, Danilo Tokechi Amaral, Nathalia Teixeira Hatano, Leonardo Furtado Freitas, Catherine Marx and Lazaro Luis Faria do Amaral
Mowat-Wilson Syndrome (MWS) is a syndrome with multiple congenital abnormalities first clinically delineated by Mowat DR, et al. in 1998. All affected patients exhibit typical dysmorphic features in association with severe intellectual disability and most have microcephaly and seizures. Congenital anomalies such as Hirschsprung disease, congenital heart disease, hypospadias, genitourinary malformations, corpus callosum agenesis and short stature are also common. There is no consensus on clinical diagnostic criteria, but MWS should be suspected in individuals with the aforementioned clinical features and head imaging findings. We report a full-term male newborn with microcephaly, congenital megacolon, hypospadias, facial dysmorphism and heart defect. Thus, MWS was suspected and later confirmed by a mutation analysis of the ZEB2 gene.
Molecular and Genetic Medicine received 3652 citations as per Google Scholar report
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