This study aimed to investigate the expression and clinical significance of the long chain non-coding RNA SCHLAP1 in breast cancer tissues. The research included 60 breast cancer patients treated between June 2017 and September 2019. Cancer and adjacent tissues were collected for analysis. Furthermore, breast cancer cell lines MCF-7 and HCC1937, along with normal breast epithelial cell line MCF10A, were used to study the impact of LncRNA SCHLAP1 on breast cancer cell phenotypes. qRT-PCR was employed to measure LncRNA SCHLAP1 expression levels in cells and tissues. The results demonstrated that LncRNA SCHLAP1 was significantly up-regulated in breast cancer cells and patient tissues ( P <0.01). Moreover, differences in LncRNA SCHLAP1 expression were observed in patients with varying age, lymph node invasion, TNM staging, HER-2, and Ki-67 expression levels ( P <0.01). Patients with high LncRNA SCHLAP1 expression had a significantly lower two-year survival rate ( P <0.01). In vitro experiments revealed that down-regulated LncRNA SCHLAP1 inhibited the proliferation, migration, and invasion of MCF-7 cells, while promoting apoptosis ( P <0.01). This study suggests that LncRNA SCHLAP1 is associated with breast cancer progression and patient survival, serving as an independent predictor for breast cancer progression.
{"title":"Dysregulated Expression of LncRNA-SChLAP1 in Breast Cancer","authors":"Mengqi Yuan, Jie Pan, Tao Guo, Jian Ren","doi":"10.1166/jbn.2023.3702","DOIUrl":"https://doi.org/10.1166/jbn.2023.3702","url":null,"abstract":"This study aimed to investigate the expression and clinical significance of the long chain non-coding RNA SCHLAP1 in breast cancer tissues. The research included 60 breast cancer patients treated between June 2017 and September 2019. Cancer and adjacent tissues were collected for analysis. Furthermore, breast cancer cell lines MCF-7 and HCC1937, along with normal breast epithelial cell line MCF10A, were used to study the impact of LncRNA SCHLAP1 on breast cancer cell phenotypes. qRT-PCR was employed to measure LncRNA SCHLAP1 expression levels in cells and tissues. The results demonstrated that LncRNA SCHLAP1 was significantly up-regulated in breast cancer cells and patient tissues ( P <0.01). Moreover, differences in LncRNA SCHLAP1 expression were observed in patients with varying age, lymph node invasion, TNM staging, HER-2, and Ki-67 expression levels ( P <0.01). Patients with high LncRNA SCHLAP1 expression had a significantly lower two-year survival rate ( P <0.01). In vitro experiments revealed that down-regulated LncRNA SCHLAP1 inhibited the proliferation, migration, and invasion of MCF-7 cells, while promoting apoptosis ( P <0.01). This study suggests that LncRNA SCHLAP1 is associated with breast cancer progression and patient survival, serving as an independent predictor for breast cancer progression.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135707293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the current research, the effects of a regular sport program was investigated on peripheral nerve regeneration in a rat model. The critical sized peripheral nerve gap was created in a rat model and the nerve injury gap was bridged by an electrospun polycaprolacton/collagen-based neural conduit. After bridging the nerve gap, the animals received a regular exercise three times a week until week 8. Study showed that the regular exercise program significantly augmented the level of sciatic nerve repair as evidenced by histopathological examinations and functional recovery experiments. Gene expression studies showed that rats treated with regular exercise had higher expression levels of BDNF, NGF, and b-FGF genes.
{"title":"Curcumin-Loaded Nanocomposite Hydrogel for Healing in Spinal Cord Injury in a Rat Model","authors":"Qingdong Ling","doi":"10.1166/jbn.2023.3562","DOIUrl":"https://doi.org/10.1166/jbn.2023.3562","url":null,"abstract":"In the current research, the effects of a regular sport program was investigated on peripheral nerve regeneration in a rat model. The critical sized peripheral nerve gap was created in a rat model and the nerve injury gap was bridged by an electrospun polycaprolacton/collagen-based neural conduit. After bridging the nerve gap, the animals received a regular exercise three times a week until week 8. Study showed that the regular exercise program significantly augmented the level of sciatic nerve repair as evidenced by histopathological examinations and functional recovery experiments. Gene expression studies showed that rats treated with regular exercise had higher expression levels of BDNF, NGF, and b-FGF genes.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"111 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
For improving the wound healing probability of patients, this work discussed the application value and mechanism of nano-electrospinning (NES) composites combined with gelatin-Bletilla striata gum (BSG)/Salvia miltiorrhiza (SM) in the repair of orthopedic refractory wounds (ORWs). 40 patients with ORWs were included and randomly rolled into a control group (Ctrl group, treated with only NES composite) and an observation group (Obs group, NES+ gelatin-BSG/SM composite), with 20 cases in each. The expression levels of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor beta 1 (TGF- β 1) in the Obs group were higher than those in the Ctrl group ( P <0.05). NES composite combined with gelatin-BSG/SM could promote the formation of tissues and blood vessels in ORWs by upregulate VEGF, b-FGF, and TGF- β 1. Therefore, it was more conducive to the healing and repair of ORWs.
{"title":"Repair Effect and Mechanism of Electrospinning Nanocomposite Material with Gelatin-Bletilla Striata Gum/Salvia Miltiorrhiza on Orthopedic Refractory Wounds","authors":"Geliang Hu, Ming Deng, Yonggang Ma, Jianghua Ming","doi":"10.1166/jbn.2023.3672","DOIUrl":"https://doi.org/10.1166/jbn.2023.3672","url":null,"abstract":"For improving the wound healing probability of patients, this work discussed the application value and mechanism of nano-electrospinning (NES) composites combined with gelatin-Bletilla striata gum (BSG)/Salvia miltiorrhiza (SM) in the repair of orthopedic refractory wounds (ORWs). 40 patients with ORWs were included and randomly rolled into a control group (Ctrl group, treated with only NES composite) and an observation group (Obs group, NES+ gelatin-BSG/SM composite), with 20 cases in each. The expression levels of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor beta 1 (TGF- β 1) in the Obs group were higher than those in the Ctrl group ( P <0.05). NES composite combined with gelatin-BSG/SM could promote the formation of tissues and blood vessels in ORWs by upregulate VEGF, b-FGF, and TGF- β 1. Therefore, it was more conducive to the healing and repair of ORWs.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"92 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study investigated the impact of miR-29b on the proliferative ability and apoptosis of gallbladder cancer (GBC) cells by targeting TET3. The levels of miR-29b were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in GBC tissues and adjacent non-cancerous tissues. The clinical features of GBC patients were analyzed based on miR-29b expression. Overexpression of miR-29b in GBC-SD and NOZ cells was found to significantly reduce proliferation, as assessed by CCK-8 and colony formation assays, and increase apoptosis, as measured by flow cytometry. The regulatory mechanism between miR-29b and its target gene TET3 was confirmed through luciferase assays and rescue experiments. In a GBC mouse model, overexpression of miR-29b in GBC-SD cells suppressed tumor growth and reduced tumor weight. Low expression of miR-29b in GBC tissues was associated with advanced tumor stage, larger tumor size, and poor prognosis. TET3, which was upregulated in GBC tissues, showed an inverse correlation with miR-29b expression. Overexpression of TET3 counteracted the effects of miR-29b on proliferation and apoptosis in GBC cells. In summary, miR-29b inhibits the malignant progression of GBC by regulating TET3 and holds potential as a prognostic marker.
{"title":"miR-29b Inhibits the Malignant Progression of Gallbladder Carcinoma by Regulating Tet Methylcytosine Dioxygenase 3","authors":"Yunsheng Qin, Dianqian Wang, Dongxiao Ding","doi":"10.1166/jbn.2023.3684","DOIUrl":"https://doi.org/10.1166/jbn.2023.3684","url":null,"abstract":"This study investigated the impact of miR-29b on the proliferative ability and apoptosis of gallbladder cancer (GBC) cells by targeting TET3. The levels of miR-29b were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in GBC tissues and adjacent non-cancerous tissues. The clinical features of GBC patients were analyzed based on miR-29b expression. Overexpression of miR-29b in GBC-SD and NOZ cells was found to significantly reduce proliferation, as assessed by CCK-8 and colony formation assays, and increase apoptosis, as measured by flow cytometry. The regulatory mechanism between miR-29b and its target gene TET3 was confirmed through luciferase assays and rescue experiments. In a GBC mouse model, overexpression of miR-29b in GBC-SD cells suppressed tumor growth and reduced tumor weight. Low expression of miR-29b in GBC tissues was associated with advanced tumor stage, larger tumor size, and poor prognosis. TET3, which was upregulated in GBC tissues, showed an inverse correlation with miR-29b expression. Overexpression of TET3 counteracted the effects of miR-29b on proliferation and apoptosis in GBC cells. In summary, miR-29b inhibits the malignant progression of GBC by regulating TET3 and holds potential as a prognostic marker.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135707290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Huiping Wu, Jie Li, Tianhe Xia, Yue’e He, Tingting Wu, Zhenquan Wang, Shiyang Song, Maoping Chu, Xing Rong
Myocardial hypertrophy, a significant contributor to the development of heart failure, continues to be prevalent. Early growth response-1 (EGR-1) is closely linked to the development of diverse myocardial conditions. The target of EGR1 (TOE1) is a critical factor in myocardial hypertrophy, but its regulatory function remains unclear. Myocardial cell injury was induced by angiotensin II. TOE1 knockout mice and cells were generated to investigate its impact on myocardial hypertrophy. TUNEL staining was employed to assess cell apoptosis. Furthermore, western blotting and qRT-PCR were performed to measure the expression of target genes. The results revealed that knockout of TOE1 effectively inhibited myocardial hypertrophy and injury caused by transverse aortic constriction. In vivo experiments demonstrated that TOE1 knockout improved myocardial function and suppressed inflammatory factors, oxidative stress, apoptosis, and autophagy levels. In vitro , TOE1 knockout suppressed cell apoptosis, mitochondrial damage, and the intensity of reactive oxygen species. Additionally, it inhibited the expression of apoptosis- and autophagy-related genes. These findings introduce a promising avenue for preventing and treating myocardial hypertrophy.
{"title":"Inhibition of Transverse Aortic Constriction Induced Myocardial Hypertrophy by Knocking out the Target of the Early Growth Response-1 to Inhibit Apoptosis and Autophagy","authors":"Huiping Wu, Jie Li, Tianhe Xia, Yue’e He, Tingting Wu, Zhenquan Wang, Shiyang Song, Maoping Chu, Xing Rong","doi":"10.1166/jbn.2023.3674","DOIUrl":"https://doi.org/10.1166/jbn.2023.3674","url":null,"abstract":"Myocardial hypertrophy, a significant contributor to the development of heart failure, continues to be prevalent. Early growth response-1 (EGR-1) is closely linked to the development of diverse myocardial conditions. The target of EGR1 (TOE1) is a critical factor in myocardial hypertrophy, but its regulatory function remains unclear. Myocardial cell injury was induced by angiotensin II. TOE1 knockout mice and cells were generated to investigate its impact on myocardial hypertrophy. TUNEL staining was employed to assess cell apoptosis. Furthermore, western blotting and qRT-PCR were performed to measure the expression of target genes. The results revealed that knockout of TOE1 effectively inhibited myocardial hypertrophy and injury caused by transverse aortic constriction. In vivo experiments demonstrated that TOE1 knockout improved myocardial function and suppressed inflammatory factors, oxidative stress, apoptosis, and autophagy levels. In vitro , TOE1 knockout suppressed cell apoptosis, mitochondrial damage, and the intensity of reactive oxygen species. Additionally, it inhibited the expression of apoptosis- and autophagy-related genes. These findings introduce a promising avenue for preventing and treating myocardial hypertrophy.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"33 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135708225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yuzhi Cui, Zongqi Zhou, Yanhong Zhang, Jiafa Li, Jinmeng Ren, Lei Luo, Guanghui Wang
Deep vein thrombosis (DVT) is a common complication of malignancy, which greatly increases the mortality rate of tumor patients. Therefore, it is critical to understand the mechanism of malignancy and DVT. TWEAK expression in lung adenocarcinoma tissues from TCGA dataset was performed by using GEPIA and detected in 58 lung cancer patients with DVT by qRT-PCR. TWEAK shRNAs were transfected into endothelial progenitor cells (EPCs) to analyze the consequent alteration in EPCs behaviors through CCK-8, cloning formation, transwell, and flow cytometry assays. TWEAK was obviously declined in lung cancer patients with DVT and low expression of TWEAK was related to poor overall survival. The function experiments revealed that TWEAK over-expression facilitated EPCs proliferation, migration, invasion, and attenuated cell apoptosis. However, TWEAK inhibition showed the opposite effects on EPCs behavior. Mechanistically, TWEAK over-expression promoted the activation of p-p65 and p-IkBα. Moreover, NF-κB pathway inhibitor overturned the effects of TWEAK on EPCs proliferation, metastasis and apoptosis. TWEAK might inhibit venous thrombosis progression through the NF-κB signaling pathway in lung cancer.
{"title":"TWEAK Inhibits Venous Thrombosis Progression Through the NF-<i>κ</i>B Signaling Pathway in Lung Cancer","authors":"Yuzhi Cui, Zongqi Zhou, Yanhong Zhang, Jiafa Li, Jinmeng Ren, Lei Luo, Guanghui Wang","doi":"10.1166/jbn.2023.3667","DOIUrl":"https://doi.org/10.1166/jbn.2023.3667","url":null,"abstract":"Deep vein thrombosis (DVT) is a common complication of malignancy, which greatly increases the mortality rate of tumor patients. Therefore, it is critical to understand the mechanism of malignancy and DVT. TWEAK expression in lung adenocarcinoma tissues from TCGA dataset was performed by using GEPIA and detected in 58 lung cancer patients with DVT by qRT-PCR. TWEAK shRNAs were transfected into endothelial progenitor cells (EPCs) to analyze the consequent alteration in EPCs behaviors through CCK-8, cloning formation, transwell, and flow cytometry assays. TWEAK was obviously declined in lung cancer patients with DVT and low expression of TWEAK was related to poor overall survival. The function experiments revealed that TWEAK over-expression facilitated EPCs proliferation, migration, invasion, and attenuated cell apoptosis. However, TWEAK inhibition showed the opposite effects on EPCs behavior. Mechanistically, TWEAK over-expression promoted the activation of p-p65 and p-IkBα. Moreover, NF-κB pathway inhibitor overturned the effects of TWEAK on EPCs proliferation, metastasis and apoptosis. TWEAK might inhibit venous thrombosis progression through the NF-κB signaling pathway in lung cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Min Yin, Xi Ai, Yuanwei Pan, Lin Wang, Rui Liu, Weihong Zhu, Yalin Sun, Shuiying Wang, Zhouhui Jin
This study aimed to investigate the protective effects and underlying mechanisms of Panax notoginseng saponins (PNS) on glomerular endothelial cell (GEC) injury induced by high glucose, which is crucial in the development of diabetic nephropathy. GECs were treated with high glucose alone, PNS alone, or a combination of PNS and overexpression of endothelin-1 (ET-1), a key regulator in endothelial dysfunction. The results showed that high glucose inhibited cell viability, increased reactive oxygen species (ROS) levels, and upregulated the expression of fibronectin (FN), collagen type IV (Col-IV), protein kinase C (PKC), transforming growth factor-beta 1 (TGF- β 1), and ET-1. Additionally, high glucose downregulated the expression of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT). PNS treatment significantly protected against high glucose-induced GEC injury by promoting cell viability, reducing ROS generation, downregulating FN, Col-IV, PKC, TGF- β 1, and ET-1 expression, and upregulating SOD, GSH-Px, and CAT expression. However, ET-1 overexpression reversed the protective effects of PNS, indicating the involvement of the ET-1/protein kinase C (PKC)/TGF- β 1 pathway. In conclusion, PNS demonstrated a protective effect against high glucose-induced GEC injury by inhibiting the ET-1/PKC/TGF- β 1 pathway. These findings suggest that PNS may be a potential therapeutic target for diabetic nephropathy by antagonizing ET-1.
{"title":"Panax Notoginseng Saponins Alleviate High Glucose-Induced Glomerular Endothelial Cell Injury by Inhibiting the ET-1/PKC/TGF-<i>β</i>1 Signaling Pathway","authors":"Min Yin, Xi Ai, Yuanwei Pan, Lin Wang, Rui Liu, Weihong Zhu, Yalin Sun, Shuiying Wang, Zhouhui Jin","doi":"10.1166/jbn.2023.3668","DOIUrl":"https://doi.org/10.1166/jbn.2023.3668","url":null,"abstract":"This study aimed to investigate the protective effects and underlying mechanisms of Panax notoginseng saponins (PNS) on glomerular endothelial cell (GEC) injury induced by high glucose, which is crucial in the development of diabetic nephropathy. GECs were treated with high glucose alone, PNS alone, or a combination of PNS and overexpression of endothelin-1 (ET-1), a key regulator in endothelial dysfunction. The results showed that high glucose inhibited cell viability, increased reactive oxygen species (ROS) levels, and upregulated the expression of fibronectin (FN), collagen type IV (Col-IV), protein kinase C (PKC), transforming growth factor-beta 1 (TGF- β 1), and ET-1. Additionally, high glucose downregulated the expression of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT). PNS treatment significantly protected against high glucose-induced GEC injury by promoting cell viability, reducing ROS generation, downregulating FN, Col-IV, PKC, TGF- β 1, and ET-1 expression, and upregulating SOD, GSH-Px, and CAT expression. However, ET-1 overexpression reversed the protective effects of PNS, indicating the involvement of the ET-1/protein kinase C (PKC)/TGF- β 1 pathway. In conclusion, PNS demonstrated a protective effect against high glucose-induced GEC injury by inhibiting the ET-1/PKC/TGF- β 1 pathway. These findings suggest that PNS may be a potential therapeutic target for diabetic nephropathy by antagonizing ET-1.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this study, Galanthus nivalis extract was incorporated into chitosan nanoparticles and the resulting particles were loaded into alginate/chitosan scaffolds for the treatment of calvarial defects in a rat model. Cell viability assay, cytoprotection assay, scanning electron microcopy assay, cell migration assay, swelling assay, biodegradation assay, antiinflammatory assay, compressive strength measurement, and porosity assays were performed for characterizing the composite sponges. In Vitro studies showed that the scaffolds had a porous architecture and protected cells against oxidative stress. In Vivo study showed that bone healing activity of Galanthus nivalis extract-loaded scaffolds was significantly greater than polymer-only scaffolds and control group. Gene expression studies showed that the expression levels of osteopontin, collagen type 1, osteonectin, and TGF-B genes was improved in the Galanthus nivalis extract-containing scaffolds. This preliminary research shows that the combination of herbal medicine principles with bone tissue engineering is an effective strategy to treat bone injuries.
{"title":"Bone-Healing Activity of <i>Galanthus nivalis</i> Extract-Impregnated Alginate/Chitosan Nanocomposite Scaffolds for Bone Tissue Regeneration: An <i>In Vitro</i> and <i>In Vivo</i> Study","authors":"Yong Liu, Guogang Yang","doi":"10.1166/jbn.2023.3647","DOIUrl":"https://doi.org/10.1166/jbn.2023.3647","url":null,"abstract":"In this study, Galanthus nivalis extract was incorporated into chitosan nanoparticles and the resulting particles were loaded into alginate/chitosan scaffolds for the treatment of calvarial defects in a rat model. Cell viability assay, cytoprotection assay, scanning electron microcopy assay, cell migration assay, swelling assay, biodegradation assay, antiinflammatory assay, compressive strength measurement, and porosity assays were performed for characterizing the composite sponges. In Vitro studies showed that the scaffolds had a porous architecture and protected cells against oxidative stress. In Vivo study showed that bone healing activity of Galanthus nivalis extract-loaded scaffolds was significantly greater than polymer-only scaffolds and control group. Gene expression studies showed that the expression levels of osteopontin, collagen type 1, osteonectin, and TGF-B genes was improved in the Galanthus nivalis extract-containing scaffolds. This preliminary research shows that the combination of herbal medicine principles with bone tissue engineering is an effective strategy to treat bone injuries.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We tested physicochemical and biological properties of Smartee-Invisalign and found that it had superior light transmittance, good physical stability, and relatively unchanged tensile strength, elasticity modulus, and bending strength over time. It had good antibacterial properties and minimal toxic effects on oral cells and was thus safe to be wear. Physically, Smartee-Invisalign can correct malocclusion, and improve the patient’s chewing ability and quality of life without increasing the risk of periodontal bleeding. Mentally, it can improved patients’ psychological state, including engaging in more natural interpersonal interactions and significantly reducing depression and anxiety. Furthermore, it improved patients’ self-approval and self-aesthetics thus helping these patients to develop a healthier mental state. In conclusion, Smartee-Invisalign effectively improved the physical and mental health of patients with malocclusion.
{"title":"Physicochemical and Biological Properties of Smartee-Invisalign in Patients with Malocclusion","authors":"Qiaolong Yu, Guanbao Yuan, Qianqian Qiu, Gang Wu, Xingxing Wang, Yaochuan Shen, Juanjuan Chen, Zhumei Huang, Mingjing Gan, Xin Chen","doi":"10.1166/jbn.2023.3670","DOIUrl":"https://doi.org/10.1166/jbn.2023.3670","url":null,"abstract":"We tested physicochemical and biological properties of Smartee-Invisalign and found that it had superior light transmittance, good physical stability, and relatively unchanged tensile strength, elasticity modulus, and bending strength over time. It had good antibacterial properties and minimal toxic effects on oral cells and was thus safe to be wear. Physically, Smartee-Invisalign can correct malocclusion, and improve the patient’s chewing ability and quality of life without increasing the risk of periodontal bleeding. Mentally, it can improved patients’ psychological state, including engaging in more natural interpersonal interactions and significantly reducing depression and anxiety. Furthermore, it improved patients’ self-approval and self-aesthetics thus helping these patients to develop a healthier mental state. In conclusion, Smartee-Invisalign effectively improved the physical and mental health of patients with malocclusion.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bladder carcinoma is a complex and aggressive malignancy with limited treatment options. In this study, we aimed to investigate the expression pattern of TGIF2 in bladder carcinoma and its clinical significance, as well as its functional role and interaction with CD2BP2 in disease progression. Through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis, we found that TGIF2 was highly expressed in bladder carcinoma tissues compared to normal bladder mucosa. Furthermore, elevated TGIF2 levels were associated with advanced tumor stage and larger tumor size, indicating its potential as a prognostic marker in bladder carcinoma. Using knockdown models in bladder carcinoma cell lines (253j and J82), we observed that the inhibition of TGIF2 resulted in decreased proliferation and migration rates, suggesting a critical role of TGIF2 in promoting these malignant phenotypes. Additionally, our dual-luciferase reporter assay revealed a direct interaction between TGIF2 and CD2BP2, with CD2BP2 being upregulated in bladder carcinoma tissues and positively correlated with TGIF2 expression. Notably, the overexpression of CD2BP2 reversed the suppressed malignant phenotypes caused by TGIF2 knockdown. Collectively, our findings highlight the abundant expression of TGIF2 in bladder carcinoma tissues and its association with malignant characteristics. We demonstrate that TGIF2 promotes proliferative and metastatic capacities in bladder carcinoma by positively regulating CD2BP2. These insights provide a basis for further investigations into the potential of TGIF2 and CD2BP2 as therapeutic targets and prognostic markers in bladder carcinoma management.
{"title":"TGFB Induced Factor Homeobox 2 Induces Deterioration of Bladder Carcinoma via Activating CD2 Cytoplasmic Tail Binding Protein 2","authors":"Xiaobo Guo, Gang Li, Yufeng Zhao, Bo Zhao","doi":"10.1166/jbn.2023.3657","DOIUrl":"https://doi.org/10.1166/jbn.2023.3657","url":null,"abstract":"Bladder carcinoma is a complex and aggressive malignancy with limited treatment options. In this study, we aimed to investigate the expression pattern of TGIF2 in bladder carcinoma and its clinical significance, as well as its functional role and interaction with CD2BP2 in disease progression. Through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis, we found that TGIF2 was highly expressed in bladder carcinoma tissues compared to normal bladder mucosa. Furthermore, elevated TGIF2 levels were associated with advanced tumor stage and larger tumor size, indicating its potential as a prognostic marker in bladder carcinoma. Using knockdown models in bladder carcinoma cell lines (253j and J82), we observed that the inhibition of TGIF2 resulted in decreased proliferation and migration rates, suggesting a critical role of TGIF2 in promoting these malignant phenotypes. Additionally, our dual-luciferase reporter assay revealed a direct interaction between TGIF2 and CD2BP2, with CD2BP2 being upregulated in bladder carcinoma tissues and positively correlated with TGIF2 expression. Notably, the overexpression of CD2BP2 reversed the suppressed malignant phenotypes caused by TGIF2 knockdown. Collectively, our findings highlight the abundant expression of TGIF2 in bladder carcinoma tissues and its association with malignant characteristics. We demonstrate that TGIF2 promotes proliferative and metastatic capacities in bladder carcinoma by positively regulating CD2BP2. These insights provide a basis for further investigations into the potential of TGIF2 and CD2BP2 as therapeutic targets and prognostic markers in bladder carcinoma management.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"66 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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