R. S. Habeballa, Mutasim Mohamed Khalafalla Ali, R. S. Modawi
This research is conducted to study the genetic diversity of the genus Grewia tenax in Sudan. This plant has a common vernacular Sudanese Arabic name: “Gudeim”. It is mainly cultivated in North Darfur and Western Sudan. Common uses of Grewia species were overviewed in areas of nutrition, folk medicine and famine food. The genetic variation and genetic relationships among Grewia spp populations from different regions were efficiently determined using RAPD and ISSR markers.
The results of genetic analysis were statistically analyzed by STATISTCA and GenALEx 6.5 software. The results of molecular variance revealed that 74% of total genetic diversity was due to within populations variations as opposed to 26% due to variations between populations unweighted pair- group method with arithmetic average (UPGMA) were constructed for and RAPD + ISSR. The UPGMA results showed variability of Grewia genotypes.
It was concluded that both the marker systems RAPD and ISSR combination can be effectively used in determination of genetic relationships among Grewia tenax genotypes.
{"title":"Assessment of phylogenetic diversity and relationships among Grewia tenax population in Sudan using RAPD and ISSR molecular markers","authors":"R. S. Habeballa, Mutasim Mohamed Khalafalla Ali, R. S. Modawi","doi":"10.3934/molsci.2022001","DOIUrl":"https://doi.org/10.3934/molsci.2022001","url":null,"abstract":"<abstract> <p>This research is conducted to study the genetic diversity of the genus <italic>Grewia tenax</italic> in Sudan. This plant has a common vernacular Sudanese Arabic name: “Gudeim”. It is mainly cultivated in North Darfur and Western Sudan. Common uses of <italic>Grewia</italic> species were overviewed in areas of nutrition, folk medicine and famine food. The genetic variation and genetic relationships among <italic>Grewia spp</italic> populations from different regions were efficiently determined using RAPD and ISSR markers.</p> <p>The results of genetic analysis were statistically analyzed by STATISTCA and GenALEx 6.5 software. The results of molecular variance revealed that 74% of total genetic diversity was due to within populations variations as opposed to 26% due to variations between populations unweighted pair- group method with arithmetic average (UPGMA) were constructed for and RAPD + ISSR. The UPGMA results showed variability of <italic>Grewia</italic> genotypes.</p> <p>It was concluded that both the marker systems RAPD and ISSR combination can be effectively used in determination of genetic relationships among <italic>Grewia tenax</italic> genotypes.</p> </abstract>","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myosin is an actin-based motor protein that widely exists in muscle tissue and non-muscle tissue, and myosin of a diverse subfamily has obvious differences in structure and cell function. Many eukaryotes and even some unicellular organisms possess a variety of myosins. They have been well characterized in human, fungi and other organisms. However, the myosin gene family in Bemisia tabaci MEAM1 (Middle East-Asia Minor1 species) is poorly studied. In the study, we identified 15 myosin genes in B. tabaci MEAM1 based on a genome database. Myosin genes can be divided into ten classes, including subfamilies I, II, III, V, VI, VII, IX, XV, XVIII, XX in B. tabaci MEAM1. The amounts of myosin in Class I are the largest of the isoforms. Expression profiling of myosins by quantitative real-time PCR revealed that their expression differed among developmental stages and different tissues of B. tabaci MEAM1. The diversely may be related to the development characteristics of B. tabaci MEAM1. The BtaMyo-IIIb-like X1 was highly expressed in nymphs 4 instar which may be related to the development process before metamorphosis. Our outcome contributes to the basis for further research on myosin gene function in B. tabaci MEAM1 and homologous myosins in other biology.
{"title":"Characterization and analysis of myosin gene family in the whitefly (Bemisia tabaci)","authors":"Kui Wang, Zhifang Yang, Xiaohui Chen, Shunxiao Liu, Xiang Li, Liuhao Wang, Hao Yu, Hongwei Zhang","doi":"10.3934/molsci.2022006","DOIUrl":"https://doi.org/10.3934/molsci.2022006","url":null,"abstract":"<abstract> <p>Myosin is an actin-based motor protein that widely exists in muscle tissue and non-muscle tissue, and myosin of a diverse subfamily has obvious differences in structure and cell function. Many eukaryotes and even some unicellular organisms possess a variety of myosins. They have been well characterized in human, fungi and other organisms. However, the myosin gene family in <italic>Bemisia tabaci</italic> MEAM1 (Middle East-Asia Minor1 species) is poorly studied. In the study, we identified 15 myosin genes in <italic>B. tabaci</italic> MEAM1 based on a genome database. Myosin genes can be divided into ten classes, including subfamilies I, II, III, V, VI, VII, IX, XV, XVIII, XX in <italic>B. tabaci</italic> MEAM1. The amounts of myosin in Class I are the largest of the isoforms. Expression profiling of myosins by quantitative real-time PCR revealed that their expression differed among developmental stages and different tissues of <italic>B. tabaci</italic> MEAM1. The diversely may be related to the development characteristics of <italic>B. tabaci</italic> MEAM1. The <italic>BtaMyo-IIIb-like X1</italic> was highly expressed in nymphs 4 instar which may be related to the development process before metamorphosis. Our outcome contributes to the basis for further research on myosin gene function in <italic>B. tabaci</italic> MEAM1 and homologous myosins in other biology.</p> </abstract>","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-04-28DOI: 10.3934/molsci.2022004
Rahel Tekeste, Gregorio Garza, Song Han, Jianli Dong
Clopidogrel is a purinergic receptor P2Y12 (P2RY12)-blocking pro-drug used to inhibit platelet aggregation in patients at risk for major adverse cardiac events (MACE), such as coronary artery disease and stroke. Despite clopidogrel therapy, some patients may still present with recurrent cardiovascular events. One possible cause of recurrence are variants in the cytochrome P450 2C19 (CYP2C19) gene. CYP2C19 is responsible for the metabolism of many drugs including clopidogrel. Recent studies have associated pharmacogenetics testing of CYP2C19 variants to guide clopidogrel therapy with a decreased risk of certain recurrent MACEs. Through a different mechanism, diabetes mellitus (DM) and obesity are also associated with clopidogrel treatment failure. We describe the case of a 64-year-old Caucasian woman with a history of acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI), and DM/obesity, who presented to University of Texas Medical Branch (UTMB) in 2019 with a transient ischemic attack (TIA) while on clopidogrel/aspirin dual anti-platelet therapy. After CYP2C19 genetic testing revealed that she was an intermediate metabolizer with a heterozygous *2 genotype, ticagrelor replaced the clopidogrel treatment regimen. No future MACEs were documented in the two-year patient follow-up. Thus, ACS patients with DM/obesity who have undergone PCI and are intermediate CYP2C19 metabolizers may yield better treatment outcomes if prescribed ticagrelor instead of clopidogrel. Whether this improvement was due to genotype-guided therapy or the differing interactions of clopidogrel/ticagrelor in DM/obese patients is unknown based on available data. Regardless, CYP2C19 genotype-guided treatment of ACS/PCI patients, with consideration of DM/obesity status, may provide effective individualized therapy compared to standard treatment. The inclusion of DM/obesity in this study is clinically relevant because DM/obesity has become a major health issue in the United States and worldwide.
{"title":"Ticagrelor is more effective than clopidogrel in carrier of nonfunctional <i>CYP2C19</i> allele who has diabetes and acute coronary syndrome - case report and literature review.","authors":"Rahel Tekeste, Gregorio Garza, Song Han, Jianli Dong","doi":"10.3934/molsci.2022004","DOIUrl":"10.3934/molsci.2022004","url":null,"abstract":"<p><p>Clopidogrel is a purinergic receptor <i>P2Y12</i> (<i>P2RY12</i>)-blocking pro-drug used to inhibit platelet aggregation in patients at risk for major adverse cardiac events (MACE), such as coronary artery disease and stroke. Despite clopidogrel therapy, some patients may still present with recurrent cardiovascular events. One possible cause of recurrence are variants in the cytochrome P450 2C19 (<i>CYP2C19</i>) gene. <i>CYP2C19</i> is responsible for the metabolism of many drugs including clopidogrel. Recent studies have associated pharmacogenetics testing of <i>CYP2C19</i> variants to guide clopidogrel therapy with a decreased risk of certain recurrent MACEs. Through a different mechanism, diabetes mellitus (DM) and obesity are also associated with clopidogrel treatment failure. We describe the case of a 64-year-old Caucasian woman with a history of acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI), and DM/obesity, who presented to University of Texas Medical Branch (UTMB) in 2019 with a transient ischemic attack (TIA) while on clopidogrel/aspirin dual anti-platelet therapy. After <i>CYP2C19</i> genetic testing revealed that she was an intermediate metabolizer with a heterozygous *2 genotype, ticagrelor replaced the clopidogrel treatment regimen. No future MACEs were documented in the two-year patient follow-up. Thus, ACS patients with DM/obesity who have undergone PCI and are intermediate <i>CYP2C19</i> metabolizers may yield better treatment outcomes if prescribed ticagrelor instead of clopidogrel. Whether this improvement was due to genotype-guided therapy or the differing interactions of clopidogrel/ticagrelor in DM/obese patients is unknown based on available data. Regardless, <i>CYP2C19</i> genotype-guided treatment of ACS/PCI patients, with consideration of DM/obesity status, may provide effective individualized therapy compared to standard treatment. The inclusion of DM/obesity in this study is clinically relevant because DM/obesity has become a major health issue in the United States and worldwide.</p>","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":0.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9140224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48284388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction The clinical variability in the course of neuroblastoma (NB) is closely linked to diverse genetic changes acquired by tumor cells. Rapid NB progression is associated with oncogene MYCN amplification (MNA) and segmental chromosomal aberrations (SCA). Alternatively, numerical chromosomal alterations (NCA) have positive impact on treatment. So far, no studies have been undertaken to identify NCA that may group NB patients. Therefore, the aim of the study was to identify NCA typical for NB. Materials and methods Copy number alterations in NB tumor genome (fresh samples N = 94; formalin-fixed paraffin-embedded specimens N = 66) were analyzed with a pangenomic array CGH technique. Results The profile with NCA was observed in 72 (45%) cases, NCA+SCA in 37 (23%), normal in 35 (22%) and MNA in 16 (10%). Samples with NCA were characterized by whole chromosome gains: 17, 7, 6 (78%, 65%, 51%, respectively) and copy loss of chromosome 14 (57%). Similarly to NCA, patients with a combined NCA and SCA profile were also characterized by gain of whole chromosome 17 and 7 (35% both) and loss of chromosome 14 (38%), but with lower frequency. In the combined NCA and SCA profiles, typical NB changes such as deletion 1p36 (27%) and gain 17q (41%) were observed, as well as deletion 11q (24%). The same alterations were detected in MNA samples (44%, 44%, 19%, respectively). A difference was found in spanning 11q deletion between MNA and NCA+SCA subgroup, which may suggest new prognostic markers in NB. In MNA subgroup specific NCA was not indicated. Conclusions The hypothesis that NCA in NB tumors are more frequent in younger children with good prognosis was confirmed. To gain new insights into the pathogenesis of NB and to establish molecular targets for diagnosis and therapy, candidate genes in the altered chromosomal regions must be investigated.
{"title":"Typical numerical alterations in genome identified by array CGH analysis in neuroblastoma tumors","authors":"K. Szewczyk","doi":"10.3934/molsci.2021019","DOIUrl":"https://doi.org/10.3934/molsci.2021019","url":null,"abstract":"Introduction The clinical variability in the course of neuroblastoma (NB) is closely linked to diverse genetic changes acquired by tumor cells. Rapid NB progression is associated with oncogene MYCN amplification (MNA) and segmental chromosomal aberrations (SCA). Alternatively, numerical chromosomal alterations (NCA) have positive impact on treatment. So far, no studies have been undertaken to identify NCA that may group NB patients. Therefore, the aim of the study was to identify NCA typical for NB. Materials and methods Copy number alterations in NB tumor genome (fresh samples N = 94; formalin-fixed paraffin-embedded specimens N = 66) were analyzed with a pangenomic array CGH technique. Results The profile with NCA was observed in 72 (45%) cases, NCA+SCA in 37 (23%), normal in 35 (22%) and MNA in 16 (10%). Samples with NCA were characterized by whole chromosome gains: 17, 7, 6 (78%, 65%, 51%, respectively) and copy loss of chromosome 14 (57%). Similarly to NCA, patients with a combined NCA and SCA profile were also characterized by gain of whole chromosome 17 and 7 (35% both) and loss of chromosome 14 (38%), but with lower frequency. In the combined NCA and SCA profiles, typical NB changes such as deletion 1p36 (27%) and gain 17q (41%) were observed, as well as deletion 11q (24%). The same alterations were detected in MNA samples (44%, 44%, 19%, respectively). A difference was found in spanning 11q deletion between MNA and NCA+SCA subgroup, which may suggest new prognostic markers in NB. In MNA subgroup specific NCA was not indicated. Conclusions The hypothesis that NCA in NB tumors are more frequent in younger children with good prognosis was confirmed. To gain new insights into the pathogenesis of NB and to establish molecular targets for diagnosis and therapy, candidate genes in the altered chromosomal regions must be investigated.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70225772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Bwalya, R. M. Irekwa, Amos K Mbugua, Matthew Mutinda Munyao, Peter Kipkemboi Rotich, Tonny Teya Nyandwaro, C. W. Njoroge, A. Mwangi, J. Yego, Shahiid Kiyaga, S. Nzou
Visceral Leishmaniasis (VL) remains a major public health problem mainly affecting the poorest populations across Asia, Africa, Middle East, Europe, Southern and Central America. For seven-decade now, the first-line drug of choice for leishmaniasis has been pentavalent antimonials. However, the clinical value of these drugs is threatened by the emergence of drug-resistant parasites. Clinical resistance to sodium stibogluconate (pentostam) has been a challenge in the Indian subcontinent, raising concerns for the endemic countries in Africa. This study aimed to identify and describe Single Nucleotide Polymorphism (SNPs) in gene markers associated with drug resistance among the clinical samples. The study was an experimental laboratory investigation on Dry Blood Spots (DBS). DNA was extracted from 18 VL positive samples, and Internal Transcribed Spacer-1 Polymerase Chain Reaction confirmed the positivity. Two target resistance markers, aquaglyceroporin 1 ( AQP-1 ) and the Multi-Drug Resistant Protein A ( MRPA ), were PCR-amplified and resulting amplicons sequenced using the Sanger sequencing platform. Multiple sequence alignments were performed using ClustalW, and the phylogenetic tree was constructed in MegaX using the Maximum Likelihood method. A total of 84 SNPs in the AQP-1 gene were identified from six clinical samples. Fifty-nine of the SNPs (70.2%) were non-synonymous, while 25 (29.8%) were synonymous. Among the non-synonymous SNPs, three (5.1%) were nonsense, and 56 (94.9%) were missense point mutations. Two missense SNPs A188T and E185A in S17608 reported to be associated with drug resistance phenotype were observed. The study describes the resistance associated with the pentostam uptake by Leishmania donovani .
{"title":"Investigation of single nucleotide polymorphisms in MRPA and AQP-1 genes of Leishmania donovani as resistance markers in visceral leishmaniasis in Kenya","authors":"A. Bwalya, R. M. Irekwa, Amos K Mbugua, Matthew Mutinda Munyao, Peter Kipkemboi Rotich, Tonny Teya Nyandwaro, C. W. Njoroge, A. Mwangi, J. Yego, Shahiid Kiyaga, S. Nzou","doi":"10.3934/molsci.2021011","DOIUrl":"https://doi.org/10.3934/molsci.2021011","url":null,"abstract":"Visceral Leishmaniasis (VL) remains a major public health problem mainly affecting the poorest populations across Asia, Africa, Middle East, Europe, Southern and Central America. For seven-decade now, the first-line drug of choice for leishmaniasis has been pentavalent antimonials. However, the clinical value of these drugs is threatened by the emergence of drug-resistant parasites. Clinical resistance to sodium stibogluconate (pentostam) has been a challenge in the Indian subcontinent, raising concerns for the endemic countries in Africa. This study aimed to identify and describe Single Nucleotide Polymorphism (SNPs) in gene markers associated with drug resistance among the clinical samples. The study was an experimental laboratory investigation on Dry Blood Spots (DBS). DNA was extracted from 18 VL positive samples, and Internal Transcribed Spacer-1 Polymerase Chain Reaction confirmed the positivity. Two target resistance markers, aquaglyceroporin 1 ( AQP-1 ) and the Multi-Drug Resistant Protein A ( MRPA ), were PCR-amplified and resulting amplicons sequenced using the Sanger sequencing platform. Multiple sequence alignments were performed using ClustalW, and the phylogenetic tree was constructed in MegaX using the Maximum Likelihood method. A total of 84 SNPs in the AQP-1 gene were identified from six clinical samples. Fifty-nine of the SNPs (70.2%) were non-synonymous, while 25 (29.8%) were synonymous. Among the non-synonymous SNPs, three (5.1%) were nonsense, and 56 (94.9%) were missense point mutations. Two missense SNPs A188T and E185A in S17608 reported to be associated with drug resistance phenotype were observed. The study describes the resistance associated with the pentostam uptake by Leishmania donovani .","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hereditary Hemochromatosis (HH) is an autosomal recessive disorder of iron metabolism associated with HFE gene mutations, characterized by increased iron absorption and accumulation leading to multi-organ damage caused by iron overload toxicity. Beta thalassemia is caused by a mutation in the human beta globin gene. Imbalanced production of globin chain results in beta thalassemia, where the unpaired alpha chains precipitates in red cell precursors leading to ineffective erythropoiesis and reduced RBC survival. Both HH and beta thalassemia condition results in rapid accumulation of iron lead to iron overload in tissues and organs. The study aims to analyze the frequency of HFE variants among beta thalassemia cases and their effect on iron overload. The frequency of three HFE variants C282Y, H63D, S65C was analyzed by PCR RFLP method among Beta Thalassemia Trait (BTT) (n = 203), Beta Thalassemia Major (BTM) (n = 19) and age and sex-matched control samples (n = 200). The present study furnished allele frequency of H63D variant in BTT, BTM and controls 8.13, 15.8 and 6% respectively. Ten out of 33 heterozygous H63D variants exhibited iron overload with higher ferritin levels indicating HFE variant might aggravate the absorption of iron. The C282Y variant was present in heterozygous state in 1 case among beta thalassemia carriers. The C282Y variant was absent among BTM and control cases. S65C HFE variant was absent in the present study. Iron overload was completely absent in the control cases among all three HFE genotypes. Hence it is inferred from the present investigation, analysis of HFE genes and iron status will remarkably help to reason out the probable reason behind the iron status and support in proper management of beta thalassemia cases.
{"title":"Frequency of hereditary hemochromatosis gene mutations and their effects on iron overload among beta thalassemia patients of Chennai residents","authors":"Bhuvana Selvaraj, S. Soundararajan, Shettu Narayanasamy, Ganesan Subramanian, Senthil Kumar Ramanathan","doi":"10.3934/molsci.2021018","DOIUrl":"https://doi.org/10.3934/molsci.2021018","url":null,"abstract":"Hereditary Hemochromatosis (HH) is an autosomal recessive disorder of iron metabolism associated with HFE gene mutations, characterized by increased iron absorption and accumulation leading to multi-organ damage caused by iron overload toxicity. Beta thalassemia is caused by a mutation in the human beta globin gene. Imbalanced production of globin chain results in beta thalassemia, where the unpaired alpha chains precipitates in red cell precursors leading to ineffective erythropoiesis and reduced RBC survival. Both HH and beta thalassemia condition results in rapid accumulation of iron lead to iron overload in tissues and organs. The study aims to analyze the frequency of HFE variants among beta thalassemia cases and their effect on iron overload. The frequency of three HFE variants C282Y, H63D, S65C was analyzed by PCR RFLP method among Beta Thalassemia Trait (BTT) (n = 203), Beta Thalassemia Major (BTM) (n = 19) and age and sex-matched control samples (n = 200). The present study furnished allele frequency of H63D variant in BTT, BTM and controls 8.13, 15.8 and 6% respectively. Ten out of 33 heterozygous H63D variants exhibited iron overload with higher ferritin levels indicating HFE variant might aggravate the absorption of iron. The C282Y variant was present in heterozygous state in 1 case among beta thalassemia carriers. The C282Y variant was absent among BTM and control cases. S65C HFE variant was absent in the present study. Iron overload was completely absent in the control cases among all three HFE genotypes. Hence it is inferred from the present investigation, analysis of HFE genes and iron status will remarkably help to reason out the probable reason behind the iron status and support in proper management of beta thalassemia cases.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70225727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fazle Khuda, Nur Najmi Mohamad Anuar, B. Baharin, Nurrul Shaqinah Nasruddin
Matrix metalloproteinases (MMPs) are one of the most important endopeptidases in periodontal disease that generally degrade extracellular matrix (ECM) components of periodontal supporting tissues, leading to tooth loss. Among the MMP family, MMP-1, -8 and -13, which are also known as the collagenase group, play a vital role in the degradation of ECM collagen and non-collagen substances. Elevated levels of MMP -1, -8 and -13 are markedly significant within tissue, gingival crevicular fluid (GCF), and saliva of patients with periodontitis, which help to explain the progression pattern of the disease. This review provides an overview of MMP -1, -8, and -13 on their structures, functions and their critical role in periodontitis.
{"title":"A mini review on the associations of matrix metalloproteinases (MMPs) -1, -8, -13 with periodontal disease","authors":"Fazle Khuda, Nur Najmi Mohamad Anuar, B. Baharin, Nurrul Shaqinah Nasruddin","doi":"10.3934/MOLSCI.2021002","DOIUrl":"https://doi.org/10.3934/MOLSCI.2021002","url":null,"abstract":"Matrix metalloproteinases (MMPs) are one of the most important endopeptidases in periodontal disease that generally degrade extracellular matrix (ECM) components of periodontal supporting tissues, leading to tooth loss. Among the MMP family, MMP-1, -8 and -13, which are also known as the collagenase group, play a vital role in the degradation of ECM collagen and non-collagen substances. Elevated levels of MMP -1, -8 and -13 are markedly significant within tissue, gingival crevicular fluid (GCF), and saliva of patients with periodontitis, which help to explain the progression pattern of the disease. This review provides an overview of MMP -1, -8, and -13 on their structures, functions and their critical role in periodontitis.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70225814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Less than 2% of children are reported to test positive for SARS-CoV-2. However, increasing reports have described COVID-positive children demonstrating symptoms like Kawasaki disease (KD), an acute vasculitis in medium sized vessels. Characteristic clinical features of KD include fever, conjunctivitis, mucosal alterations, rashes, and cervical lymphadenopathy. We searched PubMed with six keywords including neutrophil and macrophage extracellular traps (NETs/METs), Kawasaki disease, vasculitis, COVID-19 and SARS-CoV-2. We discussed here how SARS-CoV-2 infection is accompanied by activation of proinflammatory cytokines, specifically IL-1 beta and production of neutrophil and macrophage extracellular traps (NETs/METs), structures formed through specialized types of cell death. In this review, we propose that the KD-like pathogenesis observed in COVID-19infected children could arise from infection of resident macrophages resulting in activation of NLRP3 inflammasomes and release of IL-1 beta in a genetically predisposed subset of infected children, mediated via NET/MET dysregulation and overproduction. We also propose potential avenues of diagnosis and treatment that could be utilized to aid such patients.
{"title":"Kawasaki like disease in SARS-CoV-2 infected children – a key role for neutrophil and macrophage extracellular traps","authors":"A. Yaqinuddin, Abdul Hakim Almakadma, J. Kashir","doi":"10.3934/molsci.2021013","DOIUrl":"https://doi.org/10.3934/molsci.2021013","url":null,"abstract":"Less than 2% of children are reported to test positive for SARS-CoV-2. However, increasing reports have described COVID-positive children demonstrating symptoms like Kawasaki disease (KD), an acute vasculitis in medium sized vessels. Characteristic clinical features of KD include fever, conjunctivitis, mucosal alterations, rashes, and cervical lymphadenopathy. We searched PubMed with six keywords including neutrophil and macrophage extracellular traps (NETs/METs), Kawasaki disease, vasculitis, COVID-19 and SARS-CoV-2. We discussed here how SARS-CoV-2 infection is accompanied by activation of proinflammatory cytokines, specifically IL-1 beta and production of neutrophil and macrophage extracellular traps (NETs/METs), structures formed through specialized types of cell death. In this review, we propose that the KD-like pathogenesis observed in COVID-19infected children could arise from infection of resident macrophages resulting in activation of NLRP3 inflammasomes and release of IL-1 beta in a genetically predisposed subset of infected children, mediated via NET/MET dysregulation and overproduction. We also propose potential avenues of diagnosis and treatment that could be utilized to aid such patients.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70225823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gracile axonal dystrophy (gad) mouse shows tremor, ataxia and muscular atrophy of hind limbs from about 80-days of age. These clinical features become progressively severe to death. Pathological examination reveals that main and early axonal degeneration exists in a long ascending nervous tract in dorsal column of the spinal cord: gracile nucleus and fascicules. Similar lesions are seen in axonal terminals of peripheral sensory (muscle spindles) and motor endplates. Most striking features of axonal dystrophy are “dying-back” axonal degeneration with partial swellings (“spheroids” in matured type) which come to be most frequently in gracile nucleus, followed by in order of gracile fasciculus of cervical, thoracic and lumber cord levels. Immunocytochemical increase of glial fibrillary acidic protein (GFAP) and substance P (SP) is seen in reactive astrocytes and degenerating axons. Likewise, amyloid precursor protein (APP) and amyloid β-protein (AβP) activity become positive in axons and astrocytes along ascending tract. Moreover, ubiquitin-positive dot-like structures accumulate in gracile nucleus, spinocerebellar tract, and cerebellum in gad mice after 9th-week old. Ubiquitinated structures are localized in spheroids with a larger diameter than normal. The gad mutation is caused by an in-frame deletion including exon 7 and 8 of UCH-L1 gene, encoding the ubiquitin c-terminal hydrolase (UCH) isozyme (UCH-L1) selectively expressed in nervous system and testis/ovary. The gad allele encodes a truncated UCH-L1 lacking a segment of 42 amino acids containing catalytic site. The evaluation as mouse models for Parkinson's and Alzheimer's diseases and the collapse of synapse-axon circulation around central nervous system from peripheral nervous system are discussed.
{"title":"Circular breakdown of neural networks due to loss of deubiquitinating enzyme (UCH-L1) in gracile axonal dystrophy (gad) mouse","authors":"T. Kikuchi","doi":"10.3934/molsci.2021024","DOIUrl":"https://doi.org/10.3934/molsci.2021024","url":null,"abstract":"Gracile axonal dystrophy (gad) mouse shows tremor, ataxia and muscular atrophy of hind limbs from about 80-days of age. These clinical features become progressively severe to death. Pathological examination reveals that main and early axonal degeneration exists in a long ascending nervous tract in dorsal column of the spinal cord: gracile nucleus and fascicules. Similar lesions are seen in axonal terminals of peripheral sensory (muscle spindles) and motor endplates. Most striking features of axonal dystrophy are “dying-back” axonal degeneration with partial swellings (“spheroids” in matured type) which come to be most frequently in gracile nucleus, followed by in order of gracile fasciculus of cervical, thoracic and lumber cord levels. Immunocytochemical increase of glial fibrillary acidic protein (GFAP) and substance P (SP) is seen in reactive astrocytes and degenerating axons. Likewise, amyloid precursor protein (APP) and amyloid β-protein (AβP) activity become positive in axons and astrocytes along ascending tract. Moreover, ubiquitin-positive dot-like structures accumulate in gracile nucleus, spinocerebellar tract, and cerebellum in gad mice after 9th-week old. Ubiquitinated structures are localized in spheroids with a larger diameter than normal. The gad mutation is caused by an in-frame deletion including exon 7 and 8 of UCH-L1 gene, encoding the ubiquitin c-terminal hydrolase (UCH) isozyme (UCH-L1) selectively expressed in nervous system and testis/ovary. The gad allele encodes a truncated UCH-L1 lacking a segment of 42 amino acids containing catalytic site. The evaluation as mouse models for Parkinson's and Alzheimer's diseases and the collapse of synapse-axon circulation around central nervous system from peripheral nervous system are discussed.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70226524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neurotransmitters play the role of electrochemical signalling molecules which are essential for suitable brain functioning. Their dysfunction causes several mental and health disorders. Neurotransmitters are present at a very low concentration in the nervous system and they are mixed with many other biochemical molecules. The precise detection and nursing of these molecules are pretty decisive in brain studies. This mini-review portrays the research on oxytocin and vasopressin as an exemplar for exploring the social neuroscience as the subject of social neuroscience has decisively explored the complex territory between perception and action. These neuropeptides, oxytocin and vasopressin are evolutionarily extremely conserved mediators in order to regulate the complex social cognition and behaviour. They play significant role in social interactions, in maternal care and closeness, development of general trust and cooperation, controlling of labor and breastfeeding, regulation of blood pressure, social recognition, sexual behaviours and response to stress. They find applications for several treatment approaches in mental disorders in the form of autism, borderline personality disorder, social anxiety disorder and schizophrenia.
{"title":"Oxytocin and vasopressin: the social networking buttons of the body","authors":"A. Mitra","doi":"10.3934/MOLSCI.2021003","DOIUrl":"https://doi.org/10.3934/MOLSCI.2021003","url":null,"abstract":"Neurotransmitters play the role of electrochemical signalling molecules which are essential for suitable brain functioning. Their dysfunction causes several mental and health disorders. Neurotransmitters are present at a very low concentration in the nervous system and they are mixed with many other biochemical molecules. The precise detection and nursing of these molecules are pretty decisive in brain studies. This mini-review portrays the research on oxytocin and vasopressin as an exemplar for exploring the social neuroscience as the subject of social neuroscience has decisively explored the complex territory between perception and action. These neuropeptides, oxytocin and vasopressin are evolutionarily extremely conserved mediators in order to regulate the complex social cognition and behaviour. They play significant role in social interactions, in maternal care and closeness, development of general trust and cooperation, controlling of labor and breastfeeding, regulation of blood pressure, social recognition, sexual behaviours and response to stress. They find applications for several treatment approaches in mental disorders in the form of autism, borderline personality disorder, social anxiety disorder and schizophrenia.","PeriodicalId":44217,"journal":{"name":"AIMS Molecular Science","volume":null,"pages":null},"PeriodicalIF":1.4,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70225869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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