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				<title>Open Journal of Cell and Protein Science</title>
				<link>https://www.biolscigroup.us/journals/open-journal-of-cell-and-protein-science</link>
				<description>A Peertechz Open Access Journal</description>
				<language>en-us</language><item>
					  <title>Polyamine catabolism via spermine oxidase in the pathogenesis and treatment of hyperglycemia and diabetes mellitus-A short discussion</title>
					  <pubDate>01 Jun, 2023</pubDate>
					  
					  <link>https://www.biolscigroup.us/articles/OJCPS-6-105.php</link>
					  <description>Diabetes mellitus can be described as chronic, endocrine dysfunction of pathophysiological regulation related to glucose and insulin. Hyperglycemia is the most common and intensely related complication of this dysfunction and has countless methods of pathogenicity. Hyperglycemia has the ability to exacerbate a degenerative positive feedback loop within critical tissues. Considering the fact that pancreatic hormonal regulation has played an increasingly considerable role in serum glucose homeostasis, here we begin a discussion into the implication of polyamine catabolism as a pathway with a mechanism that would contribute considerably to the necrosis and dysfunction of islet cells in the pancreas. The pathogenicity of this mechanism focuses on how the sustained increase in free radical production by hyperglycemic induction extenuates several complications in diabetes mellitus. The oxidation of spermine to spermidine produces hydrogen peroxide, as well as 3-aminopropanol (which spontaneously converts to acrolein) and spermidine (the precursor for the substrate of this reaction). This increase in reactive oxygen species exhibits the ability to inhibit autophagy and apoptosis as well as stimulate fat necrosis within the cells of the pancreas. Considering the islet cells of the pancreas play an extremely important role in glucose homeostasis, small changes in concentrations of these ROS are able to eliminate large regulatory factors while going undetected in the analysis of disease processes and therapeutics. </description>
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					  <title>Expression of PAR2 and NF-κB in human primary dental pulp odontoblasts during the progression of caries</title>
					  <pubDate>06 May, 2022</pubDate>
					  
					  <link>https://www.biolscigroup.us/articles/OJCPS-5-104.php</link>
					  <description>Increased proteinase-activated receptor-2 (PAR2) expression is observed in various diseases related to inflammation. However, the expression of PAR2 in odontoblasts in response to dental caries has not been investigated. Therefore, to explore the functions of odontoblasts during the progression of carious infection, we measured PAR2 and NF-κB expression using immunofluorescence techniques in the odontoblast layer and pulpocytes in the sub-odontoblast region of 44 teeth extracted from children undergoing dental treatment (eight sound samples, 13 early carious samples, 16 advanced carious samples, and eight exposed pulp samples). PAR2 and NF-κB were expressed at moderate levels in sound teeth with non-carious pulp, and the expression levels changed as caries progressed. PAR2 was significantly upregulated in the odontoblast layer during early-stage and advanced-stage caries, and reduced below healthy levels in teeth with exposed pulp. NF-κB was significantly upregulated in early-stage caries and significantly downregulated in advanced-stage and late-stage caries. Moreover, in the sub-odontoblast region, NF-κB expression increased with the progression of caries. Overall, this study suggests PAR2 may represent a crucial cell signalling receptor in the dentine-pulp complex during dental inflammation, and that NF-κB may be one of the key pathways that regulate inflammatory immune responses in the dental pulp. </description>
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					  <title>Protein folding, misfolding, and coping mechanism of cells–A short discussion</title>
					  <pubDate>21 Jun, 2021</pubDate>
					  
					  <link>https://www.biolscigroup.us/articles/OJCPS-4-103.php</link>
					  <description>Proteins are not rigid structures, they are long polypeptide chains of ~50 or more “residues”. Proteins are generally thought to adopt unique structures determined by their amino acid sequences. However, proteins are not strictly static objects, but rather populate ensembles of (sometimes similar) conformations. Transitions between these states occur on a variety of length scales (tenths of Å to nm) and time scales (ns to s), and have been linked to functionally relevant phenomena such as enzyme catalysis [1] and allosteric signaling [2].
</description>
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					  <title>The DNA conformational energy landscape: Sequencedependent conformational equilibria of duplex DNA</title>
					  <pubDate>28 May, 2020</pubDate>
					  
					  <link>https://www.biolscigroup.us/articles/OJCPS-3-102.php</link>
					  <description>The free energy surfaces of duplex dinucleotide steps were mapped in a principal conformational subspace derived from crystal structure data on DNA duplex
oligomers. The three dimensional subspace, spanned by collective degrees of freedom representing linear combinations of the Cartesian coordinates of the backbone and
sugar atoms of both strands accounted for 77% of the total variance of the observed structural distribution. The features of the subspace free energy surface correspond
well to the distribution of observed structures exhibiting a clear separation of A- and B-family classes. The sequence dependence of the relative A / B-form conformational
equilibria was derived from the corresponding subspace free energy surfaces at physiological conditions. A B-philicity scale representing the mole fraction of the BI-form
vs the A-family for the 10 unique dinucleotide steps revealed three classes of sequences: highly B-philic (GC/GC &#x26; CG/CG), B-philic (AC/GT, AA/TT, AT/AT, CA/TG, AG/CT
&#x26; GG/CC) and A-philic (GA/TC &#x26; TA/TA). The high propensity of the TA/TA step to adopt the A-form conformation is in accord with single crystal X-ray diffraction data and
has biological signifi cance in view of the frequent presence of the TATA sequence motif in transcriptional promoter regions.</description>
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					  <title>Response to first-line erlotinib in a false EGFR mutation-negative patient with non-small-cell lung cancer: Make no assumptions</title>
					  <pubDate>01 Oct, 2018</pubDate>
					  
					  <link>https://www.biolscigroup.us/articles/OJCPS-1-101.php</link>
					  <description>So far, in the advanced non-small cell lung cancer (NSCLC) with clear epidermal growth factor receptor (EGFR) gene status, the treatment remmendations has reached an agreement: for patients with EGFR mutation-positive, epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) is the first choice, which can maximize the benefit from the treatment; while for the patients with wild-type EGFR gene, we should give priority to chemotherapy whether in the first-line or second-line therapy. However, about 70% of the patients were diagnosed at the late stage, so the pathological diagnosis and EGFR gene mutation detection depend on small specimens.</description>
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