E. Türkyılmaz, M. Özsoy, Merve Didem Eşkin Tanriverdi, B. Dinç, S. Aydoğan, Özlem Moraloğlu Tekin
Abstract Objectives The present study investigates the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the vaginal swabs of female patients diagnosed with coronavirus disease 2019 (COVID-19) based on a positive real-time reverse transcription polymerase chain reaction (RT-PCR) test on a combined throat and nasopharyngeal swab. Methods This study included 48 female patients hospitalized in two tertiary hospitals diagnosed with COVID-19 based on a positive RT-PCR test of the combined throat and nasopharyngeal swab samples, along with clinical and radiological findings. The IBM SPSS software package was used for the statistical analysis of the study data. Results SARS-CoV-2 positivity was detected in only one patient (2.08 %) in the present study from RT-PCR tests of vaginal swab samples. This patient was a 64-year-old, postmenopausal woman who tested positive for SARS-CoV-2 in a RT-PCR test of a vaginal swab sample six days after having tested positive in an RT-PCR test of a combined throat and nasopharyngeal swab. The patient’s partner also tested positive for SARS-CoV-2 in an RT-PCR of a combined throat and nasopharyngeal swab. Conclusions The present study is the first to report the presence of SARS-CoV-2 in vaginal secretions in Türkiye. The authors believe there is a need for studies investigating the presence of SARS-CoV-2 in the semen samples of the male partners of female patients to establish whether the presence of SARS-CoV-2 in vaginal secretions can play a role in the transmission of the virus.
{"title":"Investigation of SARS-CoV-2 in vaginal secretions of women with coronavirus disease 2019","authors":"E. Türkyılmaz, M. Özsoy, Merve Didem Eşkin Tanriverdi, B. Dinç, S. Aydoğan, Özlem Moraloğlu Tekin","doi":"10.1515/tjb-2023-0026","DOIUrl":"https://doi.org/10.1515/tjb-2023-0026","url":null,"abstract":"Abstract Objectives The present study investigates the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the vaginal swabs of female patients diagnosed with coronavirus disease 2019 (COVID-19) based on a positive real-time reverse transcription polymerase chain reaction (RT-PCR) test on a combined throat and nasopharyngeal swab. Methods This study included 48 female patients hospitalized in two tertiary hospitals diagnosed with COVID-19 based on a positive RT-PCR test of the combined throat and nasopharyngeal swab samples, along with clinical and radiological findings. The IBM SPSS software package was used for the statistical analysis of the study data. Results SARS-CoV-2 positivity was detected in only one patient (2.08 %) in the present study from RT-PCR tests of vaginal swab samples. This patient was a 64-year-old, postmenopausal woman who tested positive for SARS-CoV-2 in a RT-PCR test of a vaginal swab sample six days after having tested positive in an RT-PCR test of a combined throat and nasopharyngeal swab. The patient’s partner also tested positive for SARS-CoV-2 in an RT-PCR of a combined throat and nasopharyngeal swab. Conclusions The present study is the first to report the presence of SARS-CoV-2 in vaginal secretions in Türkiye. The authors believe there is a need for studies investigating the presence of SARS-CoV-2 in the semen samples of the male partners of female patients to establish whether the presence of SARS-CoV-2 in vaginal secretions can play a role in the transmission of the virus.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84117565","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}
Shirin Tarbiat, Demet Unver, Salih Tuncay, Sevim Isik, Kiyak Bercem Yeman, A. Mohseni
Abstract Objectives The current research examines the protective effects of the Piper cubeba ethanolic extract and its isolated lignans; Cubebin and Hinokinin fractions against Alzheimer’s Disease (AD) in vitro model. Methods Dried and powdered fruit of P. cubeba were extracted in ethanol and fractionated using silica gel column chromatography. Of the 15 eluted fractions, two fractions indicated presence of targeted Lignans; Hinokinin and Cubebin. They were monitored by thin layered chromatography and their structures were confirmed by LC-HRMS spectrometry and NMR analysis. Antioxidant activity of the crude extract and isolated lignan fractions were analyzed using FRAP, DPPH and ABTS assays. Anti-acetylcholinesterase activity was investigated in vitro and β-amyloid (Aβ) cytotoxicity on SHSY-5Y human neuroblastoma cell lines was studied using MTT assay. Results The crude extract showed similar if not significantly stronger antioxidant capacity compared to ascorbic acid in FRAP and DPPH assays. Both lignans exerted weaker yet potent activity. The crude extract yielded the strongest acetylcholinesterase inhibitory potential compared to the lignan fractions however, there was no significant difference (p<0.05) between IC50 values of lignan fractions. Significant neuroprotective effects against 50 μM Aβ at p<0.05 was observed for selected fractions compared to Aβ treated control. The crude extract was highly protective against Aβ at both 5 and 10 μg/mL. Cubebin and Hinokinin-containing fractions significantly improved the viability of the SH-SY5Y cells against Aβ cytotoxicity both only at the concentration of 100 μg/mL. Conclusions Results from our studies suggest that these phytoconstituents might be good candidates in prevention and treatment of AD.
{"title":"Neuroprotective effects of Cubebin and Hinokinin lignan fractions of Piper cubeba fruit in Alzheimer’s disease in vitro model","authors":"Shirin Tarbiat, Demet Unver, Salih Tuncay, Sevim Isik, Kiyak Bercem Yeman, A. Mohseni","doi":"10.1515/tjb-2023-0032","DOIUrl":"https://doi.org/10.1515/tjb-2023-0032","url":null,"abstract":"Abstract Objectives The current research examines the protective effects of the Piper cubeba ethanolic extract and its isolated lignans; Cubebin and Hinokinin fractions against Alzheimer’s Disease (AD) in vitro model. Methods Dried and powdered fruit of P. cubeba were extracted in ethanol and fractionated using silica gel column chromatography. Of the 15 eluted fractions, two fractions indicated presence of targeted Lignans; Hinokinin and Cubebin. They were monitored by thin layered chromatography and their structures were confirmed by LC-HRMS spectrometry and NMR analysis. Antioxidant activity of the crude extract and isolated lignan fractions were analyzed using FRAP, DPPH and ABTS assays. Anti-acetylcholinesterase activity was investigated in vitro and β-amyloid (Aβ) cytotoxicity on SHSY-5Y human neuroblastoma cell lines was studied using MTT assay. Results The crude extract showed similar if not significantly stronger antioxidant capacity compared to ascorbic acid in FRAP and DPPH assays. Both lignans exerted weaker yet potent activity. The crude extract yielded the strongest acetylcholinesterase inhibitory potential compared to the lignan fractions however, there was no significant difference (p<0.05) between IC50 values of lignan fractions. Significant neuroprotective effects against 50 μM Aβ at p<0.05 was observed for selected fractions compared to Aβ treated control. The crude extract was highly protective against Aβ at both 5 and 10 μg/mL. Cubebin and Hinokinin-containing fractions significantly improved the viability of the SH-SY5Y cells against Aβ cytotoxicity both only at the concentration of 100 μg/mL. Conclusions Results from our studies suggest that these phytoconstituents might be good candidates in prevention and treatment of AD.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"39 1","pages":"303 - 310"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86991945","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}
E. Baris, O. Simsek, Ozge Uysal Yoca, Ayse Banu Demir, M. Tosun
Abstract Objectives Inflammation can be endogenously modulated by the cholinergic anti-inflammatory pathway via calcium (Ca2+)-permeable alpha-7 nicotinic acetylcholine receptor (α7nAChR) ion channel expressed in immune cells. α7nAChR agonist choline and tryptophan metabolite kynurenic acid (KYNA) produces immunomodulatory effects. This study aimed to determine the effects of the choline and KYNA on the lipopolysaccharide (LPS)-induced cyclooxygenase (COX)-2 pathway. Methods In vitro inflammation model was produced via LPS administration in macrophage cells. To determine the effective concentrations, choline and KYNA were applied with increasing concentrations and LPS-induced inflammatory parameters investigated. The involvement of nAChR mediated effects was investigated with the use of non-selective nAChR and selective α7nAChR antagonists. The effects of choline and KYNA on COX-2 enzyme, PGE2, TNFα, NF-κB and intracellular Ca2+ levels were analyzed. Results LPS-induced COX-2 expression, PGE2 TNFα and NF-κB levels were decreased with choline treatment while intracellular calcium levels via α7nAChRs increased. KYNA also showed an anti-inflammatory effect on the same parameters. Additionally, KYNA administration increased the effectiveness of choline on these inflammatory mediators. Conclusions Our data suggest a possible interaction between the kynurenine pathway and the cholinergic system on the modulation of LPS-induced inflammatory response in macrophages.
{"title":"Effects of kynurenic acid and choline on lipopolysaccharide-induced cyclooxygenase pathway","authors":"E. Baris, O. Simsek, Ozge Uysal Yoca, Ayse Banu Demir, M. Tosun","doi":"10.1515/tjb-2023-0017","DOIUrl":"https://doi.org/10.1515/tjb-2023-0017","url":null,"abstract":"Abstract Objectives Inflammation can be endogenously modulated by the cholinergic anti-inflammatory pathway via calcium (Ca2+)-permeable alpha-7 nicotinic acetylcholine receptor (α7nAChR) ion channel expressed in immune cells. α7nAChR agonist choline and tryptophan metabolite kynurenic acid (KYNA) produces immunomodulatory effects. This study aimed to determine the effects of the choline and KYNA on the lipopolysaccharide (LPS)-induced cyclooxygenase (COX)-2 pathway. Methods In vitro inflammation model was produced via LPS administration in macrophage cells. To determine the effective concentrations, choline and KYNA were applied with increasing concentrations and LPS-induced inflammatory parameters investigated. The involvement of nAChR mediated effects was investigated with the use of non-selective nAChR and selective α7nAChR antagonists. The effects of choline and KYNA on COX-2 enzyme, PGE2, TNFα, NF-κB and intracellular Ca2+ levels were analyzed. Results LPS-induced COX-2 expression, PGE2 TNFα and NF-κB levels were decreased with choline treatment while intracellular calcium levels via α7nAChRs increased. KYNA also showed an anti-inflammatory effect on the same parameters. Additionally, KYNA administration increased the effectiveness of choline on these inflammatory mediators. Conclusions Our data suggest a possible interaction between the kynurenine pathway and the cholinergic system on the modulation of LPS-induced inflammatory response in macrophages.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"20 1","pages":"311 - 318"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81891129","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}
Muhammet Yusuf Tepebaşı, Okan Sancer, Pınar Aslan Koşar, A. Koşar, I. Ilhan
Abstract Objectives Transforming growth factor-beta (TGFβ1) is involved in tumorigenesis and metastasis. It provides this effect both by disrupting the thiol-disulfide balance and through the cancer-upregulated gene (CUG2) and transforming growth factor beta-induced (TGFBI) genes in the signaling pathway. In this study, the roles of TGFβ1 and related genes, as well as thiol-disulfide balance, in the formation of prostate cancer and metastasis were investigated. Methods Tissue samples were taken from 33 benign prostatic hyperplasia (BPH) and 35 prostate cancer (PC) patients to determine the Gleason score and metastasis. TGFβ1, CUG2, and TGFBI gene expression levels were measured by RT-PCR. Serum prostate specific antigen (PSA) levels were measured in patients, and PSA density (PSAD) was calculated. Total thiol and native thiol measurements in serum were performed spectrophotometrically, and disulfide was calculated. Results In patients with prostate cancer and metastases, PSA and PSAD levels were high, while total thiol and native thiol were significantly lower (p<0.05). TGFβ1, CUG2 and TGFBI gene expression levels were higher in patients with prostate cancer and metastases and were negatively correlated with total thiol and native thiol (p<0.001). Conclusions As a result of our study, we determined that the increase in TGFβ1, CUG 2 and TGFBI in prostate cancer plays an important role in cancer formation and metastasis by disrupting the thiol-disulfide balance.
{"title":"Investigation of the roles of TGFβ1, CUG2, TGFBI genes, and thiol-disulfide balance on prostate cancer and metastasis","authors":"Muhammet Yusuf Tepebaşı, Okan Sancer, Pınar Aslan Koşar, A. Koşar, I. Ilhan","doi":"10.1515/tjb-2022-0259","DOIUrl":"https://doi.org/10.1515/tjb-2022-0259","url":null,"abstract":"Abstract Objectives Transforming growth factor-beta (TGFβ1) is involved in tumorigenesis and metastasis. It provides this effect both by disrupting the thiol-disulfide balance and through the cancer-upregulated gene (CUG2) and transforming growth factor beta-induced (TGFBI) genes in the signaling pathway. In this study, the roles of TGFβ1 and related genes, as well as thiol-disulfide balance, in the formation of prostate cancer and metastasis were investigated. Methods Tissue samples were taken from 33 benign prostatic hyperplasia (BPH) and 35 prostate cancer (PC) patients to determine the Gleason score and metastasis. TGFβ1, CUG2, and TGFBI gene expression levels were measured by RT-PCR. Serum prostate specific antigen (PSA) levels were measured in patients, and PSA density (PSAD) was calculated. Total thiol and native thiol measurements in serum were performed spectrophotometrically, and disulfide was calculated. Results In patients with prostate cancer and metastases, PSA and PSAD levels were high, while total thiol and native thiol were significantly lower (p<0.05). TGFβ1, CUG2 and TGFBI gene expression levels were higher in patients with prostate cancer and metastases and were negatively correlated with total thiol and native thiol (p<0.001). Conclusions As a result of our study, we determined that the increase in TGFβ1, CUG 2 and TGFBI in prostate cancer plays an important role in cancer formation and metastasis by disrupting the thiol-disulfide balance.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"56 1","pages":"257 - 263"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74452362","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}
Y. Şahin, A. K. Devrim, M. E. Alçığır, A. Şenol, H. Ekici, T. Devrim, M. Sudağıdan, E. Yıldırım, M. Çınar, Merve Bişkin Türkmen, S. A. Peker
Abstract Objectives This study investigated the effect of krill oil (KO) on liver damage caused by acetaminophen (APAP). Methods In the present study, the control and APAP groups were given distilled water by gavage for 14 days. In addition, the KO and APAP+KO groups were given 500 mg/kg krill oil by gavage for 14 days. At the end of 14 days, 0.9 % sodium chloride solution (saline solution) administration was applied intraperitoneally to the control and KO groups. Meanwhile, 220 mg/kg acetaminophen was administered to the APAP and APAP+KO groups. While some biochemical parameters in plasma were examined, some oxidative stress parameters in plasma and liver tissue were evaluated. Apoptotic and inflammatory responses of some primer sequences determined by quantitative Real-Time PCR (qPCR) in liver tissue. After histopathological examination of liver tissue, immunohistochemical analysis was performed with Wnt inhibitory factor-1 (Wif-1), beta-catenin (β-Catenin), and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Results The Wif-1 positivity in hepatocytes increased significantly in the APAP group (5.29 ± 0.71) compared to the control (1.14 ± 0.51), and KO (2.14 ± 0.55) groups (p<0.001). The 8-OHdG positivity in hepatocytes increased significantly in the APAP group (19.57 ± 0.58) compared to the control (0.43 ± 0.20), KO (3.57 ± 0.48), and APAP+KO (4.00 ± 2.53) groups (p<0.001). Conclusions As a result, krill oil could be used as a nutritional supplement to protect the liver against acetaminophen-induced liver injury.
{"title":"The effect of krill oil on Wnt/β-catenin signaling pathway in acetaminophen-induced acute liver injury in mice","authors":"Y. Şahin, A. K. Devrim, M. E. Alçığır, A. Şenol, H. Ekici, T. Devrim, M. Sudağıdan, E. Yıldırım, M. Çınar, Merve Bişkin Türkmen, S. A. Peker","doi":"10.1515/tjb-2022-0289","DOIUrl":"https://doi.org/10.1515/tjb-2022-0289","url":null,"abstract":"Abstract Objectives This study investigated the effect of krill oil (KO) on liver damage caused by acetaminophen (APAP). Methods In the present study, the control and APAP groups were given distilled water by gavage for 14 days. In addition, the KO and APAP+KO groups were given 500 mg/kg krill oil by gavage for 14 days. At the end of 14 days, 0.9 % sodium chloride solution (saline solution) administration was applied intraperitoneally to the control and KO groups. Meanwhile, 220 mg/kg acetaminophen was administered to the APAP and APAP+KO groups. While some biochemical parameters in plasma were examined, some oxidative stress parameters in plasma and liver tissue were evaluated. Apoptotic and inflammatory responses of some primer sequences determined by quantitative Real-Time PCR (qPCR) in liver tissue. After histopathological examination of liver tissue, immunohistochemical analysis was performed with Wnt inhibitory factor-1 (Wif-1), beta-catenin (β-Catenin), and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Results The Wif-1 positivity in hepatocytes increased significantly in the APAP group (5.29 ± 0.71) compared to the control (1.14 ± 0.51), and KO (2.14 ± 0.55) groups (p<0.001). The 8-OHdG positivity in hepatocytes increased significantly in the APAP group (19.57 ± 0.58) compared to the control (0.43 ± 0.20), KO (3.57 ± 0.48), and APAP+KO (4.00 ± 2.53) groups (p<0.001). Conclusions As a result, krill oil could be used as a nutritional supplement to protect the liver against acetaminophen-induced liver injury.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"15 1","pages":"264 - 271"},"PeriodicalIF":0.0,"publicationDate":"2023-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82604128","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}
Abstract Objectives Schizophrenia (SZ) is a severe multifactorial disease. NRG1 is a gene acting in the development of SZ. A number of NRG1 single nucleotide polymorphisms (SNPs) and their haplotypes are associated with SZ. In the present study, we investigated the association of a NRG1 haplotype (G-C in rs6988339-rs3757930 frame) which was reported to be associated with SZ, and two other SNPs in the same gene (rs74942016, rs80127039) whose rare missense alleles were found in SZ patients. Also, we analyzed disease associations of potential new haplotypes constructed by the variants of these SNPs. Methods We genotyped 4 SNPs in a sample consisting of 302 SZ patients and 333 controls from a local Turkish population. We tested the disease associations of these variants at single SNP, haplotype and diplotype levels in case-control design. Results At single SNP level, the CC genotype of rs3757930 was associated with SZ (p=0.038). The previously reported association of G-C haplotype in rs6988339-rs3757930 frame was absent (p=0.416), but we found another haplotype (C-G in rs3757930-rs74942016, p=0.018) and three diplotypes (A-C/G-C diplotype of rs6988339-rs3757930 frame, C-G/C-G diplotype of rs3757930-rs74942016 frame, and A-C-G/G-C-G diplotype of rs6988339-rs3757930-rs74942016 frame) associated with schizophrenia in our sample. Conclusions Our study indicated the associations of a SNP, a haplotype, and a diplotype of NRG1 with schizophrenia and supported the involvement of NRG1 gene in the development of the disease. Since our sample was collected from a limited geographic area, the associations we have reported need to be supported by further studies in different populations.
目的精神分裂症是一种严重的多因素疾病。NRG1是参与SZ发生的一个基因。许多NRG1单核苷酸多态性(snp)及其单倍型与SZ相关。在本研究中，我们研究了与SZ相关的NRG1单倍型(rs6988339-rs3757930框架中的G-C)与在SZ患者中发现罕见错义等位基因的同一基因中的另外两个snp (rs74942016, rs80127039)的关联。此外，我们还分析了由这些snp变体构建的潜在新单倍型的疾病相关性。方法对来自土耳其当地人群的302例SZ患者和333例对照样本进行4个snp基因分型。我们在病例对照设计中测试了这些变异在单SNP、单倍型和双倍型水平上的疾病相关性。结果在单SNP水平上，rs3757930的CC基因型与SZ相关(p=0.038)。先前报道的rs6988339-rs3757930框架中G-C单倍型的关联缺失(p=0.416)，但我们发现了另一单倍型(rs3757930-rs74942016框架中的C-G, p=0.018)和三种双倍型(rs6988339-rs3757930-rs74942016框架中的C-G/ g - g双倍型，以及rs6988339-rs3757930-rs74942016框架中的A-C- g /G-C- g双倍型)与我们的样本中精神分裂症相关。结论本研究表明NRG1的一个SNP、一个单倍型和一个二倍型与精神分裂症相关，支持NRG1基因参与疾病的发展。由于我们的样本是从一个有限的地理区域收集的，我们报告的关联需要在不同人群中进一步研究来支持。
{"title":"Association of a haplotype in the NRG1 gene with schizophrenia: a case-control study","authors":"M. Sözen, S. Kartalci","doi":"10.1515/tjb-2022-0233","DOIUrl":"https://doi.org/10.1515/tjb-2022-0233","url":null,"abstract":"Abstract Objectives Schizophrenia (SZ) is a severe multifactorial disease. NRG1 is a gene acting in the development of SZ. A number of NRG1 single nucleotide polymorphisms (SNPs) and their haplotypes are associated with SZ. In the present study, we investigated the association of a NRG1 haplotype (G-C in rs6988339-rs3757930 frame) which was reported to be associated with SZ, and two other SNPs in the same gene (rs74942016, rs80127039) whose rare missense alleles were found in SZ patients. Also, we analyzed disease associations of potential new haplotypes constructed by the variants of these SNPs. Methods We genotyped 4 SNPs in a sample consisting of 302 SZ patients and 333 controls from a local Turkish population. We tested the disease associations of these variants at single SNP, haplotype and diplotype levels in case-control design. Results At single SNP level, the CC genotype of rs3757930 was associated with SZ (p=0.038). The previously reported association of G-C haplotype in rs6988339-rs3757930 frame was absent (p=0.416), but we found another haplotype (C-G in rs3757930-rs74942016, p=0.018) and three diplotypes (A-C/G-C diplotype of rs6988339-rs3757930 frame, C-G/C-G diplotype of rs3757930-rs74942016 frame, and A-C-G/G-C-G diplotype of rs6988339-rs3757930-rs74942016 frame) associated with schizophrenia in our sample. Conclusions Our study indicated the associations of a SNP, a haplotype, and a diplotype of NRG1 with schizophrenia and supported the involvement of NRG1 gene in the development of the disease. Since our sample was collected from a limited geographic area, the associations we have reported need to be supported by further studies in different populations.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"63 1","pages":"246 - 256"},"PeriodicalIF":0.0,"publicationDate":"2023-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91091490","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}
Hasim Akbalik, M. F. Polat, Ahmet Muderrisoglu, Z. Er, Ayşen Caniklioğlu, M. Ekim, H. Ekim
Abstract Objectives We aimed to evaluate PON1 QR192 polymorphism’s (rs662) effects on levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein, and paraoxonase-arylesterase activities among deep vein thrombosis patients and healthy subjects. Methods Forty-five deep vein thrombosis patients and 45 healthy subjects participated in the study. Genetic analysis was performed by using polymerase chain reaction and sequencing. Paraoxonase and arylesterase enzyme activities were determined by a spectrophotometer. Serum levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein were measured by a similar method. Results There were no statistically significant differences between patients and controls regarding the frequency of variant allele for the PON1 QR192 polymorphism, activities of paraoxonase-arylesterase, and level of high-density lipoprotein-cholesterol. Triglyceride, total cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein levels were significantly higher in patients compared to controls (p values were 0.005, 0.0002, 0.009, 0.0009, <0.0001, respectively.) Paraoxonase activity was found to be associated with PON1 QR192 genetic polymorphism (p<0.0001). However, we observed no association of PON1 QR192 polymorphism with arylesterase activity and, levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein. Conclusions There was no statistically significant difference between deep vein thrombosis patients and healthy subjects regarding variant allele frequency for the PON1 QR192 genetic polymorphism. In addition, paraoxonase and arylesterase activities were similar among the groups. These results indicate that PON1 QR192 genetic polymorphism and activity levels of paraoxonase-arylesterase have no effect on the development of deep vein thrombosis.
{"title":"Effects of PON1 QR192 genetic polymorphism and paraoxonase, arylesterase activities on deep vein thrombosis","authors":"Hasim Akbalik, M. F. Polat, Ahmet Muderrisoglu, Z. Er, Ayşen Caniklioğlu, M. Ekim, H. Ekim","doi":"10.1515/tjb-2022-0278","DOIUrl":"https://doi.org/10.1515/tjb-2022-0278","url":null,"abstract":"Abstract Objectives We aimed to evaluate PON1 QR192 polymorphism’s (rs662) effects on levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein, and paraoxonase-arylesterase activities among deep vein thrombosis patients and healthy subjects. Methods Forty-five deep vein thrombosis patients and 45 healthy subjects participated in the study. Genetic analysis was performed by using polymerase chain reaction and sequencing. Paraoxonase and arylesterase enzyme activities were determined by a spectrophotometer. Serum levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein were measured by a similar method. Results There were no statistically significant differences between patients and controls regarding the frequency of variant allele for the PON1 QR192 polymorphism, activities of paraoxonase-arylesterase, and level of high-density lipoprotein-cholesterol. Triglyceride, total cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein levels were significantly higher in patients compared to controls (p values were 0.005, 0.0002, 0.009, 0.0009, <0.0001, respectively.) Paraoxonase activity was found to be associated with PON1 QR192 genetic polymorphism (p<0.0001). However, we observed no association of PON1 QR192 polymorphism with arylesterase activity and, levels of triglyceride, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, glucose, and c-reactive protein. Conclusions There was no statistically significant difference between deep vein thrombosis patients and healthy subjects regarding variant allele frequency for the PON1 QR192 genetic polymorphism. In addition, paraoxonase and arylesterase activities were similar among the groups. These results indicate that PON1 QR192 genetic polymorphism and activity levels of paraoxonase-arylesterase have no effect on the development of deep vein thrombosis.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"73 1","pages":"319 - 326"},"PeriodicalIF":0.0,"publicationDate":"2023-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86409509","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}
Abstract Dementia is mostly caused by neurodegenerative diseases like Alzheimer’s disease (AD). AD is the most common form of dementia. It is caused by both genetic and environmental factors. Due to neuronal death in a number of brain regions, including the hippocampus, entorhinal areas, temporal lobe, and cingulate cortex, AD causes memory loss and gradual cognitive impairment. The condition’s two main pathogenic components are intracellular neurofibrillary tangles created by clusters of hyperphosphorylated tau protein and amyloid plaques made up of extracellular amyloid (Aβ) peptide aggregates. In contrast to the APOE- ε4 allele, which was found to have a significant impact on late-onset AD, presenilin 1, presenilin 2, amyloid precursor protein were genetic risk factors that were causal for early-onset AD. Misfolded proteins accumulate within the neuron, causing prolonged cellular stress in AD, a progressive neurodegenerative disease. Neurofibrillary tangles and senile plaques are two of the neuropathological hallmarks of Alzheimer’s disease that lead to the destruction of synapses and the death of neurons. AD is mostly caused by the death of nerves, particularly cholinergic nerves. In the absence of these cholinergic neurons, acetylcholine levels fall. This review discusses key genes involved in the pathogenesis and pathophysiology of AD, as well as the disease’s molecular mechanisms.
{"title":"Molecular mechanisms and genetics of Alzheimer’s disease","authors":"G. Öztan, H. Issever","doi":"10.1515/tjb-2023-0049","DOIUrl":"https://doi.org/10.1515/tjb-2023-0049","url":null,"abstract":"Abstract Dementia is mostly caused by neurodegenerative diseases like Alzheimer’s disease (AD). AD is the most common form of dementia. It is caused by both genetic and environmental factors. Due to neuronal death in a number of brain regions, including the hippocampus, entorhinal areas, temporal lobe, and cingulate cortex, AD causes memory loss and gradual cognitive impairment. The condition’s two main pathogenic components are intracellular neurofibrillary tangles created by clusters of hyperphosphorylated tau protein and amyloid plaques made up of extracellular amyloid (Aβ) peptide aggregates. In contrast to the APOE- ε4 allele, which was found to have a significant impact on late-onset AD, presenilin 1, presenilin 2, amyloid precursor protein were genetic risk factors that were causal for early-onset AD. Misfolded proteins accumulate within the neuron, causing prolonged cellular stress in AD, a progressive neurodegenerative disease. Neurofibrillary tangles and senile plaques are two of the neuropathological hallmarks of Alzheimer’s disease that lead to the destruction of synapses and the death of neurons. AD is mostly caused by the death of nerves, particularly cholinergic nerves. In the absence of these cholinergic neurons, acetylcholine levels fall. This review discusses key genes involved in the pathogenesis and pathophysiology of AD, as well as the disease’s molecular mechanisms.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"49 1","pages":"218 - 229"},"PeriodicalIF":0.0,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86356177","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}
Beril Altun, I. Cok, C. O. Noyan, E. Kadioglu, Alptekin Cetin, T. Şengezer, M. Altintas, Samet Kurnaz, N. Dilbaz
Abstract Objectives Given that drug addiction occurs as a result of complex gene-environment interaction, a number of studies claimed that cannabinoid receptor 1 (CNR1), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MGLL) single nucleotide polymorphisms (SNPs) are associated with the risk of substance use disorders such as cannabis, opioids, and, methamphetamine. However, scientific research on genetic susceptibility to synthetic cannabinoid addiction is limited. In this population-based case-control study, we aimed to evaluate the genetic susceptibility to synthetic cannabinoid use disorder in terms of these three endocannabinoid system genes in the Turkish population. Methods 100 individuals diagnosed with synthetic cannabinoid use disorder according to Diagnostics and Statistical Manual of Mental Disorders-5 criteria and 100 healthy volunteers have recruited for the study. Genotyping of the CNR1 rs1049353, FAAH rs324420, and MGLL rs604300 SNPs was performed using Real-Time Polymerase Chain Reaction hybridization probes. Results The patient and control groups consist of 98 % male, 2 % female, 80 % male, and 20 % female individuals, respectively. The genotype distributions were consistent with Hardy–Weinberg equilibrium for all SNPs (p>0.05). FAAH rs324420 and MGLL 604300 SNPs were genotyped for the first time in the Turkish population, and the variant allele frequencies were found as 0.205 and 0.085, respectively. Allele frequencies and genotype distributions CNR1 rs1049353, FAAH rs324420, and MGLL rs604300 SNPs were similar between the patient and control group (p>0.05). Conclusions These results indicate that CNR1, FAAH, and MGLL gene polymorphisms do not influence the risk of synthetic cannabinoid use disorder in the Turkish population.
{"title":"Assessment of the effects of CNR1, FAAH and MGLL gene variations on the synthetic cannabinoid use disorder","authors":"Beril Altun, I. Cok, C. O. Noyan, E. Kadioglu, Alptekin Cetin, T. Şengezer, M. Altintas, Samet Kurnaz, N. Dilbaz","doi":"10.1515/tjb-2022-0256","DOIUrl":"https://doi.org/10.1515/tjb-2022-0256","url":null,"abstract":"Abstract Objectives Given that drug addiction occurs as a result of complex gene-environment interaction, a number of studies claimed that cannabinoid receptor 1 (CNR1), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MGLL) single nucleotide polymorphisms (SNPs) are associated with the risk of substance use disorders such as cannabis, opioids, and, methamphetamine. However, scientific research on genetic susceptibility to synthetic cannabinoid addiction is limited. In this population-based case-control study, we aimed to evaluate the genetic susceptibility to synthetic cannabinoid use disorder in terms of these three endocannabinoid system genes in the Turkish population. Methods 100 individuals diagnosed with synthetic cannabinoid use disorder according to Diagnostics and Statistical Manual of Mental Disorders-5 criteria and 100 healthy volunteers have recruited for the study. Genotyping of the CNR1 rs1049353, FAAH rs324420, and MGLL rs604300 SNPs was performed using Real-Time Polymerase Chain Reaction hybridization probes. Results The patient and control groups consist of 98 % male, 2 % female, 80 % male, and 20 % female individuals, respectively. The genotype distributions were consistent with Hardy–Weinberg equilibrium for all SNPs (p>0.05). FAAH rs324420 and MGLL 604300 SNPs were genotyped for the first time in the Turkish population, and the variant allele frequencies were found as 0.205 and 0.085, respectively. Allele frequencies and genotype distributions CNR1 rs1049353, FAAH rs324420, and MGLL rs604300 SNPs were similar between the patient and control group (p>0.05). Conclusions These results indicate that CNR1, FAAH, and MGLL gene polymorphisms do not influence the risk of synthetic cannabinoid use disorder in the Turkish population.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"29 1","pages":"282 - 289"},"PeriodicalIF":0.0,"publicationDate":"2023-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78804703","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}
Abstract Objectives This study aimed to evaluate the calcium/magnesium (Ca/Mg) ratio in patients diagnosed with type 2 diabetes mellitus (T2DM). Methods This study is a retrospective cross-sectional study. Mg levels were determined by measuring the total serum Mg levels. Magnesium was measured by colorimetric method and HbA1c was measured by turbidimetric inhibition immunoassay method. Subject were divided into two groups (<7 % and ≥7 %) based on HbA1c levels. Also, subjects were divided into four groups (quartiles) based on serum Mg concentrations. Results A total of 891 (636F, 255M) patients diagnosed with T2DM were included in the study. The Mg increase in the group with good glycemic control was also remarkable. One of our most important findings is that as the Mg concentration increases, the fasting glucose, HbA1c, and Ca/Mg rate decreased with increasing Mg concentration. In the ROC analysis performed between the poor and good glycemic control groups, we found the AUC was 0.672, 0.650, 0.611, and 0.578 for Ca/Mg ratio, Mg, K, and Ca, respectively. Conclusions While the Ca/Mg ratio and Ca levels were significantly higher, Mg levels were significantly lower among poor glycemic control than good glycemic control T2DM. The Ca/mg ratio and Mg are important parameters for T2DM patients, but more comprehensive studies are needed before they can monitor glycemic control.
{"title":"Evaluation of calcium/magnesium ratio in patients with type 2 diabetes mellitus","authors":"Kamile Yücel, A. Gürbüz","doi":"10.1515/tjb-2023-0022","DOIUrl":"https://doi.org/10.1515/tjb-2023-0022","url":null,"abstract":"Abstract Objectives This study aimed to evaluate the calcium/magnesium (Ca/Mg) ratio in patients diagnosed with type 2 diabetes mellitus (T2DM). Methods This study is a retrospective cross-sectional study. Mg levels were determined by measuring the total serum Mg levels. Magnesium was measured by colorimetric method and HbA1c was measured by turbidimetric inhibition immunoassay method. Subject were divided into two groups (<7 % and ≥7 %) based on HbA1c levels. Also, subjects were divided into four groups (quartiles) based on serum Mg concentrations. Results A total of 891 (636F, 255M) patients diagnosed with T2DM were included in the study. The Mg increase in the group with good glycemic control was also remarkable. One of our most important findings is that as the Mg concentration increases, the fasting glucose, HbA1c, and Ca/Mg rate decreased with increasing Mg concentration. In the ROC analysis performed between the poor and good glycemic control groups, we found the AUC was 0.672, 0.650, 0.611, and 0.578 for Ca/Mg ratio, Mg, K, and Ca, respectively. Conclusions While the Ca/Mg ratio and Ca levels were significantly higher, Mg levels were significantly lower among poor glycemic control than good glycemic control T2DM. The Ca/mg ratio and Mg are important parameters for T2DM patients, but more comprehensive studies are needed before they can monitor glycemic control.","PeriodicalId":23344,"journal":{"name":"Turkish Journal of Biochemistry","volume":"48 1","pages":"327 - 334"},"PeriodicalIF":0.0,"publicationDate":"2023-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80741861","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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