Hong-jie Huang, T. Deng, Jin Qian, Jie Hu, Yangyang Zhu, M. Tian, Xiaohong Guo, Lili Lu
Chidamide, a histone deacetylase (HDAC) inhibitor, displays antitumor activities in different tumor cells. Tongue squamous cell carcinoma (TSCC) is the most prevalent oral cavity malignancy with a high incidence and a high mortality rate. We describe the antitumor effects of chidamide on human TSCC SCC9 cells, which has not been reported before. Cell viability and wound healing assay and flow cytometry analysis were used to determine the proliferation, migration, cell cycle and apoptosis of chidamide-treated SCC9 cells in vitro. Western blotting was used to detect relative changes in protein levels. Our results reveal that chidamide inhibits SCC9 cell proliferation by decreasing ERK1/2 and mTOR phosphorylation and arresting the cell cycle in G0/G1 phase. Chidamide decreased cell migration in dose- and time-dependent manner by increasing E-cadherin expression. Chidamide induced SCC9 cells apoptosis by increasing the level of cleaved caspase-3 and decreasing the expression of Bcl-2. To sum up, chidamide displayed potent antitumor effects on SCC9 cells through multiple signaling pathways and has the potential to be developed as a new therapeutic agent to treat TSCC.
{"title":"Chidamide modulates proliferation, migration and apoptosis of human tongue squamous carcinoma SCC9 cells through multiple signaling pathways","authors":"Hong-jie Huang, T. Deng, Jin Qian, Jie Hu, Yangyang Zhu, M. Tian, Xiaohong Guo, Lili Lu","doi":"10.2298/abs210815035h","DOIUrl":"https://doi.org/10.2298/abs210815035h","url":null,"abstract":"Chidamide, a histone deacetylase (HDAC) inhibitor, displays antitumor activities in different tumor cells. Tongue squamous cell carcinoma (TSCC) is the most prevalent oral cavity malignancy with a high incidence and a high mortality rate. We describe the antitumor effects of chidamide on human TSCC SCC9 cells, which has not been reported before. Cell viability and wound healing assay and flow cytometry analysis were used to determine the proliferation, migration, cell cycle and apoptosis of chidamide-treated SCC9 cells in vitro. Western blotting was used to detect relative changes in protein levels. Our results reveal that chidamide inhibits SCC9 cell proliferation by decreasing ERK1/2 and mTOR phosphorylation and arresting the cell cycle in G0/G1 phase. Chidamide decreased cell migration in dose- and time-dependent manner by increasing E-cadherin expression. Chidamide induced SCC9 cells apoptosis by increasing the level of cleaved caspase-3 and decreasing the expression of Bcl-2. To sum up, chidamide displayed potent antitumor effects on SCC9 cells through multiple signaling pathways and has the potential to be developed as a new therapeutic agent to treat TSCC.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68389684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Lin, Shuo Cheng, Zhichao Yuan, Zhiqiang Yan, Jifa Zhang
Metformin is a drug used to treat type 2 diabetes based on its effectiveness as well as cardiovascular safety. Metformin has been shown to modulate proliferation and migration of vascular smooth muscle cells (VSMCs), but the underlying mechanisms of the effect of metformin on VSMC function remains unclear. We found that metformin inhibits VSMC proliferation and migration and upregulates the expression of nuclear receptor subfamily 4 group A member 1 (Nur77), ten-eleven translocation 2 (TET2), and calponin in vitro. In the carotid artery balloon injury model of rats, metformin effectively prevented neointimal hyperplasia in the carotid artery, including neointimal thickness, increased neointimal area, and the neointimal area/medial area ratio. It also reduced the number of proliferating cell nuclear antigen (PCNA)+ cells and increased the expression of Nur77, calponin and alpha-smooth muscle actin (?-SMA). These results show that metformin attenuates neointimal hyperplasia in balloon-injured carotid arteries via increased expression of TET2, Nur77 and calponin, and reduced expression of matrix metallopeptidase 9 (MMP-9).
{"title":"Metformin attenuates carotid neointimal hyperplasia by modulating the vascular smooth muscle cell phenotype transformation through upregulation of TET2, Nur77 and calponin","authors":"H. Lin, Shuo Cheng, Zhichao Yuan, Zhiqiang Yan, Jifa Zhang","doi":"10.2298/ABS201103009L","DOIUrl":"https://doi.org/10.2298/ABS201103009L","url":null,"abstract":"Metformin is a drug used to treat type 2 diabetes based on its effectiveness as well as cardiovascular safety. Metformin has been shown to modulate proliferation and migration of vascular smooth muscle cells (VSMCs), but the underlying mechanisms of the effect of metformin on VSMC function remains unclear. We found that metformin inhibits VSMC proliferation and migration and upregulates the expression of nuclear receptor subfamily 4 group A member 1 (Nur77), ten-eleven translocation 2 (TET2), and calponin in vitro. In the carotid artery balloon injury model of rats, metformin effectively prevented neointimal hyperplasia in the carotid artery, including neointimal thickness, increased neointimal area, and the neointimal area/medial area ratio. It also reduced the number of proliferating cell nuclear antigen (PCNA)+ cells and increased the expression of Nur77, calponin and alpha-smooth muscle actin (?-SMA). These results show that metformin attenuates neointimal hyperplasia in balloon-injured carotid arteries via increased expression of TET2, Nur77 and calponin, and reduced expression of matrix metallopeptidase 9 (MMP-9).","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68388654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nasim Ebrahimi, F. Amirmahani, Maryam Akbari, Azin Mosharf Ghahfarokhi, Bahareh Hajihashemi, R. Hamblin
Several long non-coding RNAs (lncRNAs) have recently emerged as potential biomarkers in cancer biology. In the present study, we examined the expression of four lncRNAs (CAT179, CAT1796, PRCAT47, and CAT1066) to evaluate their ability to discriminate prostate tumors from benign prostate hyperplasia (BPH). Expression of these four lncRNAs was examined in 20 prostate cancer and 20 benign prostate hyperplasia (BPH) samples, as well as in urine samples (11 BPH, and 11 cancer). Total RNA was extracted for cDNA syntheses. The expression of the candidate lncRNAs was evaluated by quantitative real-time PCR (qRT-PCR). The lncRNAs CAT1796 and CAT179 were both upregulated in prostate cancer compared to BPH clinical samples (P<0.05). ROC curve analysis showed that CAT1796 had high sensitivity and specificity for diagnosis of prostate cancer (AUC=0.8151[95%CI 0.65-0.97]), suggesting that CAT1796 lncRNA could be a prostate cancer biomarker.
{"title":"Two long non-coding RNAs, CAT179 and CAT 1796, differentiate between benign prostate hyperplasia and prostate cancer","authors":"Nasim Ebrahimi, F. Amirmahani, Maryam Akbari, Azin Mosharf Ghahfarokhi, Bahareh Hajihashemi, R. Hamblin","doi":"10.2298/abs210629033e","DOIUrl":"https://doi.org/10.2298/abs210629033e","url":null,"abstract":"Several long non-coding RNAs (lncRNAs) have recently emerged as potential biomarkers in cancer biology. In the present study, we examined the expression of four lncRNAs (CAT179, CAT1796, PRCAT47, and CAT1066) to evaluate their ability to discriminate prostate tumors from benign prostate hyperplasia (BPH). Expression of these four lncRNAs was examined in 20 prostate cancer and 20 benign prostate hyperplasia (BPH) samples, as well as in urine samples (11 BPH, and 11 cancer). Total RNA was extracted for cDNA syntheses. The expression of the candidate lncRNAs was evaluated by quantitative real-time PCR (qRT-PCR). The lncRNAs CAT1796 and CAT179 were both upregulated in prostate cancer compared to BPH clinical samples (P<0.05). ROC curve analysis showed that CAT1796 had high sensitivity and specificity for diagnosis of prostate cancer (AUC=0.8151[95%CI 0.65-0.97]), suggesting that CAT1796 lncRNA could be a prostate cancer biomarker.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68389617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inhibition of vascular endothelial growth factor (VEGF) has been widely applied in antineovascularization therapies. As a novel anti-VEGF agent, KH902 (conbercept) is designed to restrain pathological angiogenesis. However, the effects of KH902 on retinal hypoxia have not been well studied. In a mouse model of oxygen-induced retinopathy (OIR), we assessed retinal hypoxia at postnatal days 14 (P14) and P17, as well as retinal neovascularization (RNV) at P17. In addition, we evaluated the protein level of VEGF and galectin-1 (Gal-1). Changes of the neuroretinal structure were also examined. Our results indicated that KH902 could remit retinal hypoxia in OIR at P14 and P17, which was an exciting novel finding for KH902 function. Additionally, we confirmed that KH902 markedly reduces RNV. Our results indicated that administration of KH902 downregulated VEGF expression, as well as Gal-1. Damage of neuroretinal structure after KH902 injection was not observed, which was also an encouraging result. Our study suggests that KH902 plays a role in alleviating retinal hypoxia and that it could be used for the treatment of other neovascular ocular diseases.
{"title":"Intraocular injection of KH902 alleviates retinal hypoxia in a mouse model of oxygen-induced retinopathy","authors":"Ning Yang, Xuying He, Ningzhi Zhang, Y. Xing","doi":"10.2298/abs210814038y","DOIUrl":"https://doi.org/10.2298/abs210814038y","url":null,"abstract":"Inhibition of vascular endothelial growth factor (VEGF) has been widely applied in antineovascularization therapies. As a novel anti-VEGF agent, KH902 (conbercept) is designed to restrain pathological angiogenesis. However, the effects of KH902 on retinal hypoxia have not been well studied. In a mouse model of oxygen-induced retinopathy (OIR), we assessed retinal hypoxia at postnatal days 14 (P14) and P17, as well as retinal neovascularization (RNV) at P17. In addition, we evaluated the protein level of VEGF and galectin-1 (Gal-1). Changes of the neuroretinal structure were also examined. Our results indicated that KH902 could remit retinal hypoxia in OIR at P14 and P17, which was an exciting novel finding for KH902 function. Additionally, we confirmed that KH902 markedly reduces RNV. Our results indicated that administration of KH902 downregulated VEGF expression, as well as Gal-1. Damage of neuroretinal structure after KH902 injection was not observed, which was also an encouraging result. Our study suggests that KH902 plays a role in alleviating retinal hypoxia and that it could be used for the treatment of other neovascular ocular diseases.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68389633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Triclosan, produced as a broad-spectrum antibiotic in the early 1960s, is generally used as a preservative in personal care products, fabrics, plastic products such as kitchenware and toys. As a result of the high demand for triclosan, this chemical threatens the aquatic ecosystem by contaminating wastewater sources. Environmental pollutants affect the reproductive potential of fish, one of the most critical aquatic organisms. This study aimed to investigate the histopathological and apoptotic effects of triclosan in zebrafish gonads. Fish were exposed to sublethal concentrations of triclosan for 5 days, and general histological methods were applied. Histological sections were examined under a light microscope after staining with hematoxylin and eosin and toluidine blue. Triclosan exposure caused deterioration in ovarian tissue, such as shrinkage in the ooplasm, accumulation of proteinaceous fluid in the interstitial tissue, morphological changes of oocyte and the zona radiata. In testicular tissue, triclosan exposure caused fusion in seminiferous tubules, hypertrophy in spermatogenic and Leydig cells, edema in seminiferous tubules, and karyorrhexis in spermatogenic cells. The TUNEL assay was used for the determination of apoptotic cells. Brown-colored apoptotic cells were visualized under the light microscope. TUNEL positive cells were observed in all exposure groups. Triclosan administration was found to cause apoptosis in zebrafish gonads. These findings indicate that triclosan potentially affects fish reproduction, and that its judicious disposal is essential for protecting the environment and maintaining the reproductive potential of fish.
{"title":"Histopathological and apoptotic examination of zebrafish (Danio rerio) gonads exposed to triclosan","authors":"C. Akbulut","doi":"10.2298/abs210923040a","DOIUrl":"https://doi.org/10.2298/abs210923040a","url":null,"abstract":"Triclosan, produced as a broad-spectrum antibiotic in the early 1960s, is generally used as a preservative in personal care products, fabrics, plastic products such as kitchenware and toys. As a result of the high demand for triclosan, this chemical threatens the aquatic ecosystem by contaminating wastewater sources. Environmental pollutants affect the reproductive potential of fish, one of the most critical aquatic organisms. This study aimed to investigate the histopathological and apoptotic effects of triclosan in zebrafish gonads. Fish were exposed to sublethal concentrations of triclosan for 5 days, and general histological methods were applied. Histological sections were examined under a light microscope after staining with hematoxylin and eosin and toluidine blue. Triclosan exposure caused deterioration in ovarian tissue, such as shrinkage in the ooplasm, accumulation of proteinaceous fluid in the interstitial tissue, morphological changes of oocyte and the zona radiata. In testicular tissue, triclosan exposure caused fusion in seminiferous tubules, hypertrophy in spermatogenic and Leydig cells, edema in seminiferous tubules, and karyorrhexis in spermatogenic cells. The TUNEL assay was used for the determination of apoptotic cells. Brown-colored apoptotic cells were visualized under the light microscope. TUNEL positive cells were observed in all exposure groups. Triclosan administration was found to cause apoptosis in zebrafish gonads. These findings indicate that triclosan potentially affects fish reproduction, and that its judicious disposal is essential for protecting the environment and maintaining the reproductive potential of fish.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68389834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chunyan Huang, Shaofeng Li, Chao Xu, W-W Song, Lei Xu, Zhihui Lan, L. Liu
Efforts have been made to find a better therapeutic approach with fewer side effects in treating chronic obstructive pulmonary disease (COPD). This study investigated the effect of Buyuan decoction (BYD) on autophagy in COPD rats. An experimental model with Sprague-Dawley rats was established by lipopolysaccharide (LPS) injection and cigarette smoke exposure. Rats were randomly allocated into blank control (normal control), experimental model, low-dose BYD (8.0 g/kg/day), medium-dose BYD (16.0 g/kg/day), high-dose BYD (32.0 g/kg/day) and 3-MA (methyladenine) groups (6 rats/group). Cell and tissue morphology were observed using hematoxylin and eosin staining. Autophagic vesicles were examined with a transmission electron microscope. Protein expression of LC3-II/I, BNIP-1, ATG7, p62, PI3K and p-PI3K in lung tissue was detected by Western blotting. Compared with the experimental model group, the inflammatory infiltrate in lung tissue was reduced, the nuclei of the pulmonary epithelial cells were restored to normal, and the expression of LC3, BNIP1, ATG7 and p-PI3K was significantly downregulated, while p62 expression was significantly upregulated after treatment with the BYD. The effect was most significant in the lowdose BYD group (P<0.05, all groups). These findings suggest that the BYD inhibits the occurrence of autophagy in the pathogenesis of COPD and that it can be a potential treatment.
{"title":"Buyuan decoction inhibits autophagy in a rat model of chronic obstructive pulmonary disease","authors":"Chunyan Huang, Shaofeng Li, Chao Xu, W-W Song, Lei Xu, Zhihui Lan, L. Liu","doi":"10.2298/abs211104047h","DOIUrl":"https://doi.org/10.2298/abs211104047h","url":null,"abstract":"Efforts have been made to find a better therapeutic approach with fewer side effects in treating chronic obstructive pulmonary disease (COPD). This study investigated the effect of Buyuan decoction (BYD) on autophagy in COPD rats. An experimental model with Sprague-Dawley rats was established by lipopolysaccharide (LPS) injection and cigarette smoke exposure. Rats were randomly allocated into blank control (normal control), experimental model, low-dose BYD (8.0 g/kg/day), medium-dose BYD (16.0 g/kg/day), high-dose BYD (32.0 g/kg/day) and 3-MA (methyladenine) groups (6 rats/group). Cell and tissue morphology were observed using hematoxylin and eosin staining. Autophagic vesicles were examined with a transmission electron microscope. Protein expression of LC3-II/I, BNIP-1, ATG7, p62, PI3K and p-PI3K in lung tissue was detected by Western blotting. Compared with the experimental model group, the inflammatory infiltrate in lung tissue was reduced, the nuclei of the pulmonary epithelial cells were restored to normal, and the expression of LC3, BNIP1, ATG7 and p-PI3K was significantly downregulated, while p62 expression was significantly upregulated after treatment with the BYD. The effect was most significant in the lowdose BYD group (P<0.05, all groups). These findings suggest that the BYD inhibits the occurrence of autophagy in the pathogenesis of COPD and that it can be a potential treatment.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68389893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lidija Todorović, G. Stamenkovic, Biljana Vučetić-Tadić, K. Umezawa, A. Božović, S. Yamashita, B. Stanojević
The use of targeted inhibitors has shown promise as an effective approach in cancer therapy. However, targeted therapies based only on one drug, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), have limited success, partly because cancer cells engage alternate pathways for survival and proliferation. In the present study, we evaluated whether dehydroxymethylepoxyquinomicin (DHMEQ), a nuclear factor ?B (NF-?B) inhibitor, can enhance the antitumor activities of 17-AAG, a 90 kDa heat shock protein (Hsp90) inhibitor, in the anaplastic thyroid cancer cell line KTC2. We examined the effect of combined drug treatment vs single drug treatment on cell survival. Isobologram analysis was performed to distinguish the additive vs synergistic effects of the drug combination. Western blotting was performed to investigate apoptosis markers: caspase 3, poly(ADP-ribose) polymerase-one (PARP-1), B-cell lymphoma-extra large (Bcl-XL), X-linked inhibitor of apoptosis (XIAP) and cellular inhibitor of apoptosis 2 (cIAP-2). Compared to monotherapy, the combined treatment enhanced growth-inhibitory effects in a synergistic manner and strongly potentiated apoptosis. These results demonstrate the first in vitro evidence that a combination of Hsp90 and NF-?B inhibitors is a more effective modality for inhibiting cell proliferation and survival in anaplastic thyroid carcinoma cells than either agent alone, warranting further investigations.
{"title":"Synergistic effect of 17-allylamino-17-demethoxygeldanamycin with dehydroxymethylepoxyquinomicin on the human anaplastic thyroid carcinoma cell line KTC2","authors":"Lidija Todorović, G. Stamenkovic, Biljana Vučetić-Tadić, K. Umezawa, A. Božović, S. Yamashita, B. Stanojević","doi":"10.2298/abs201010055t","DOIUrl":"https://doi.org/10.2298/abs201010055t","url":null,"abstract":"The use of targeted inhibitors has shown promise as an effective approach in cancer therapy. However, targeted therapies based only on one drug, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), have limited success, partly because cancer cells engage alternate pathways for survival and proliferation. In the present study, we evaluated whether dehydroxymethylepoxyquinomicin (DHMEQ), a nuclear factor ?B (NF-?B) inhibitor, can enhance the antitumor activities of 17-AAG, a 90 kDa heat shock protein (Hsp90) inhibitor, in the anaplastic thyroid cancer cell line KTC2. We examined the effect of combined drug treatment vs single drug treatment on cell survival. Isobologram analysis was performed to distinguish the additive vs synergistic effects of the drug combination. Western blotting was performed to investigate apoptosis markers: caspase 3, poly(ADP-ribose) polymerase-one (PARP-1), B-cell lymphoma-extra large (Bcl-XL), X-linked inhibitor of apoptosis (XIAP) and cellular inhibitor of apoptosis 2 (cIAP-2). Compared to monotherapy, the combined treatment enhanced growth-inhibitory effects in a synergistic manner and strongly potentiated apoptosis. These results demonstrate the first in vitro evidence that a combination of Hsp90 and NF-?B inhibitors is a more effective modality for inhibiting cell proliferation and survival in anaplastic thyroid carcinoma cells than either agent alone, warranting further investigations.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68388410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Ladjevic, A. Vuksanović, O. Durutović, Jelena Jovičić, Nikola Ladjevic, I. Likic-Ladjevic, D. Nešić, Vesna Jovanovic
Urosepsis is defined as sepsis caused by urinary tract infection (UTI). Urosepsis represents a quarter of all cases of sepsis in adults. Complications of UTIs are the most common risk factor for urosepsis development. These infections, especially pyelonephritis, often occur in patients with structural or functional malformations that interfere with normal urine flow. The problem of a significant increase in UTIs with multiresistant bacteria should be emphasized, especially in patients with recurrent UTI and their frequent treatments. As the urogenital tract is one of the most common sources of infection in sepsis in general, a detailed assessment of the tract should be carried out in all septic patients. Even though urosepsis is associated with a relatively good prognosis and lower mortality than sepsis of another etiology, it occurs rapidly and progresses at a significant speed. Since urosepsis is mainly the result of obstruction of the urinary tract, the development of septic shock can most often be prevented by implementing early deobstruction. Knowledge of the most common causes of urosepsis and the category of high-risk patients will provide clinicians with the tools with which to prevent its occurrence.
{"title":"Urosepsis in adults","authors":"N. Ladjevic, A. Vuksanović, O. Durutović, Jelena Jovičić, Nikola Ladjevic, I. Likic-Ladjevic, D. Nešić, Vesna Jovanovic","doi":"10.2298/ABS210304015L","DOIUrl":"https://doi.org/10.2298/ABS210304015L","url":null,"abstract":"Urosepsis is defined as sepsis caused by urinary tract infection (UTI). Urosepsis represents a quarter of all cases of sepsis in adults. Complications of UTIs are the most common risk factor for urosepsis development. These infections, especially pyelonephritis, often occur in patients with structural or functional malformations that interfere with normal urine flow. The problem of a significant increase in UTIs with multiresistant bacteria should be emphasized, especially in patients with recurrent UTI and their frequent treatments. As the urogenital tract is one of the most common sources of infection in sepsis in general, a detailed assessment of the tract should be carried out in all septic patients. Even though urosepsis is associated with a relatively good prognosis and lower mortality than sepsis of another etiology, it occurs rapidly and progresses at a significant speed. Since urosepsis is mainly the result of obstruction of the urinary tract, the development of septic shock can most often be prevented by implementing early deobstruction. Knowledge of the most common causes of urosepsis and the category of high-risk patients will provide clinicians with the tools with which to prevent its occurrence.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68388681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
V. Vranic, K. Zeljic, D. Stefik, N. Ivkovic, D. Abazovic, N. Arsenijević, D. Vojvodić, G. Šupić
Vitamin D receptor (VDR) gene polymorphisms could play a significant role in the susceptibility and pathogenesis of osteoarthritis (OA), the most common degenerative joint disorder in humans. The current study involved 94 OA patients and 100 healthy, asymptomatic controls. VDR variants FokI (rs2228570), TaqI (rs731236), ApaI (rs7975232) and EcoRV (rs4516035) were genotyped using TaqMan-based real-time PCR. Adjusted odds ratio (OR) analysis showed that VDR TaqI and FokI polymorphisms are significantly associated with susceptibility to OA (OR=1.986, P=0.001 and OR=1.561, P=0.017, respectively). Joint-specific analysis showed that the VDR TaqI polymorphism was associated with risk of hip OA (OR=1.930, P=0.005) and knee OA (OR=1.916, P=0.028), while the VDR FokI polymorphism was associated with higher risk of knee OA (OR=2.117, P=0.012). VDR TaqI and FokI polymorphisms are associated with the occurrence of persistent pain (P=0.005 and P=0.027, respectively), while ApaI was associated with a family history of OA (p=0.004). The VDR FokI and TaqI genetic variants significantly contribute to osteoarthritis susceptibility, the occurrence of persistent pain, and potentially to joint-specific OA risk.
{"title":"Vitamin D receptor gene variants contribute to hip and knee osteoarthritis susceptibility","authors":"V. Vranic, K. Zeljic, D. Stefik, N. Ivkovic, D. Abazovic, N. Arsenijević, D. Vojvodić, G. Šupić","doi":"10.2298/ABS210329019V","DOIUrl":"https://doi.org/10.2298/ABS210329019V","url":null,"abstract":"Vitamin D receptor (VDR) gene polymorphisms could play a significant role in the susceptibility and pathogenesis of osteoarthritis (OA), the most common degenerative joint disorder in humans. The current study involved 94 OA patients and 100 healthy, asymptomatic controls. VDR variants FokI (rs2228570), TaqI (rs731236), ApaI (rs7975232) and EcoRV (rs4516035) were genotyped using TaqMan-based real-time PCR. Adjusted odds ratio (OR) analysis showed that VDR TaqI and FokI polymorphisms are significantly associated with susceptibility to OA (OR=1.986, P=0.001 and OR=1.561, P=0.017, respectively). Joint-specific analysis showed that the VDR TaqI polymorphism was associated with risk of hip OA (OR=1.930, P=0.005) and knee OA (OR=1.916, P=0.028), while the VDR FokI polymorphism was associated with higher risk of knee OA (OR=2.117, P=0.012). VDR TaqI and FokI polymorphisms are associated with the occurrence of persistent pain (P=0.005 and P=0.027, respectively), while ApaI was associated with a family history of OA (p=0.004). The VDR FokI and TaqI genetic variants significantly contribute to osteoarthritis susceptibility, the occurrence of persistent pain, and potentially to joint-specific OA risk.","PeriodicalId":8145,"journal":{"name":"Archives of Biological Sciences","volume":"1 1","pages":""},"PeriodicalIF":0.8,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68388837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G. Riezzo, A. Orlando, C. Clemente, B. D'Attoma, Anna Valentini Maria, R. Armentano, P. Giorgio, A. Pisani, F. Russo
Since tissue transglutaminase-2 (TG2) can represent a marker of inflammation for some gastrointestinal (GI) diseases, we aimed to evaluate TG2 and inflammatory markers? mucosal content in gastric antrum biopsies to shed light on the histological and biochemical background of chronic gastritis inflammation. Fifty-one of 78 patients who underwent upper GI endoscopy (UGIE) for dyspeptic symptoms, had a gastric biopsy. The symptom profile was assessed by a GI symptom rating scale (GSRS) score. Thirtyfive patients (69%) showed chronic gastritis. TG2, interleukin-6 (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-?, lipopolysaccharides (LPS) and toll-like receptor (TLR)-4 were evaluated in serum and the culture medium of gastric biopsies. TG2, IL-8, IL-10, TLR-4 and TNF-? were significantly higher in active chronic gastritis than in the inactive one and were linked to macrophage concentration. IL-6 was significantly lower in the active form of chronic gastritis than in the inactive one and negatively correlated with TG2. Lastly, IL- 10 significantly correlated with the macrophage score. TG2 can exert an active role in chronic gastritis pathogenesis by cooperating with different markers of inflammation. It seems that TG2 can represent a possible therapeutic target for modulating inflammation and disease progression.
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