Recent studies have shown the potential of artificially synthesized conduits in the repair of peripheral nerve injury. Natural biopolymers have received much attention because of their biocompatibility. To investigate...Recent studies have shown the potential of artificially synthesized conduits in the repair of peripheral nerve injury. Natural biopolymers have received much attention because of their biocompatibility. To investigate the effects of novel electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits(biopolymer nanofiber conduits) on the repair of peripheral nerve injury, we bridged 10-mm-long sciatic nerve defects with electrospun absorbable biopolymer nanofiber conduits, poly(ε-caprolactone) or silicone conduits in Sprague-Dawley rats. Rat neurologica1 function was weekly evaluated using sciatic function index within8 weeks after repair. Eight weeks after repair, sciatic nerve myelin sheaths and axon morphology were observed by osmium tetroxide staining, hematoxylin-eosin staining, and transmission electron microscopy.S-100(Schwann cell marker) and CD4(inflammatory marker) immunoreactivities in sciatic nerve were detected by immunohistochemistry. In rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits, no serious inflammatory reactions were observed in rat hind limbs, the morphology of myelin sheaths in the injured sciatic nerve was close to normal. CD4 immunoreactivity was obviously weaker in rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits than in those subjected to repair with poly(ε-caprolactone) or silicone. Rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits tended to have greater sciatic nerve function recovery than those receiving poly(ε-caprolactone) or silicone repair. These results suggest that electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits have the potential of repairing sciatic nerve defects and exhibit good biocompatibility. All experimental procedures were approved by Institutional Animal Care and Use Committee of Taichung Veteran General Hospital, Taiwan, China(La-1031218) on October 2, 2014.展开更多
AIM To evaluate the incidence of lymph node metastasis （LNM） and its risk factors in patients with Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas.METHODS We enrolled 85 patients [69 men, 16 women; median age （ra...AIM To evaluate the incidence of lymph node metastasis （LNM） and its risk factors in patients with Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas.METHODS We enrolled 85 patients [69 men, 16 women; median age （range）, 67 （38-84） years] who had undergone esophagectomy or proximal gastrectomy for Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas. Predictive risk factors of LNM included age, sex, location of the tumor center, confirmed Barrett’s esophageal adenocarcinoma, tumor size, macroscopic tumor type, pathology, invasion depth, presence of ulceration, and lymphovascular invasion. Multivariate logistic regression analysis was used to identify factors predicting LNM. We also evaluated the frequencies of LNM for Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas in meta-data analysis.RESULTSLNMs were found in 11 out of 85 patients （12.9%, 95%CI： 5.8-20.0）. Only 1 of the 15 patients （6.6%, 95%CI： 0.0-19.2） who had a final diagnosis of pT1a adenocarcinoma had a positive LNM, whereas 10 of the 70 patients （14.2%, 95%CI： 6.0-22.4） with a final diagnosis of pT1b adenocarcinoma had positive LNM. Furthermore, only one of the 30 patients （3.3%, 95%CI： 0.0-9.7） with a tumor invasion depth within 500 μm from muscularis mucosae had positive LNM. Poor differentiation and lymphovascular invasion were independently associated with a risk of LNM. In meta-data analysis, 12 of the 355 patients （3.3%, 95%CI： 1.5-5.2） who had a final diagnosis of pT1a adenocarcinoma had a positive LNM, whereas 91 of the 438 patients （20.7%, 95%CI： 16.9-24.5） with a fnal diagnosis of pT1b adenocarcinoma had positive LNM.CONCLUSIONWe consider endoscopic submucosal dissection （ESD） is suitable for patients with Siewert type Ⅰ and type Ⅱ T1a adenocarcinomas. For patients with T1b adenocarcinoma, especially invasion depth is within 500 μm from muscularis mucosae with no other risk factor for LNM, diagnostic ESD could be a treatment option according to the overall status of patients and the presence of comorbidities.展开更多
To study the effects of Icariin on expression of osteopontin （OPN） mRNA and type Ⅰ collagen in rat osteoblasts in vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvar...To study the effects of Icariin on expression of osteopontin （OPN） mRNA and type Ⅰ collagen in rat osteoblasts in vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvaria of new-born new-born fetal Sprague-Dawley （SD） rats by means of modified sequential collagenase digestion and incubated in MEM medium and the cell morphology was observed under inverted phase contrast microscope, OB was identified by alkaline phosphatase （ALP） staining. Different concentration （0.1μg/mL, 1.0 μg/mL, 10 μ/mL） of Icariin was added to the OB and incubated. The effect of Icariin on the proliferation and osteogenesis of OB was monitored by MTT analysis. The expression of type l collagen was estimated with immunohistochemistry techniques. The expression levels of mRNA of OPN in the cells in every group were examined by reverse-transcriptase ploymerase chain reaction （RT-PCR）. The expression of OPN mRNA and type Ⅰ collagen was strengthened gradually with the increase of Icariin concentration and peaked with 10 μg/mL Icariin on the 5th day. Icariin could significantly promote the expression of OPN mRNA and type Ⅰ collagen in rat osteoblasts in vitro. The levels of expression of OPN mRNA and type Ⅰ collagen were changed with different concentration of Icariin. Icariin could effectively prevent and treat osteoporosis and promote the bone formation.展开更多
The Democratic Republic of the Congo holds important reserves of oil shale which is still under geological status.Herein,the characterization and pyrolysis kinetics of typeⅠkerogen-rich oil shale of the western Centr...The Democratic Republic of the Congo holds important reserves of oil shale which is still under geological status.Herein,the characterization and pyrolysis kinetics of typeⅠkerogen-rich oil shale of the western Central Kongo(CK)were investigated.X-ray diffraction,Fourier-transform infrared spectroscopy and thermal analysis(TG/DTA)showed that CK oil shale exhibits a siliceous mineral matrix with a consistent organic matter rich in aliphatic chains.The pyrolysis behavior of kerogen revealed the presence of a single mass loss between 300 and 550°C,estimated at 12.5%and attributed to the oil production stage.Non-isothermal kinetics was performed by determining the activation energy using the iterative isoconversional model-free methods and exhibits a constant value with E=211.5±4.7 kJ mol.1.The most probable kinetic model describing the kerogen pyrolysis mechanism was obtained using the Coats–Redfern and Arrhenius plot methods.The results showed a unique kinetic triplet confirming the nature of kerogen,predominantly typeⅠand reinforcing the previously reported geochemical characteristics of the CK oil shale.Besides,the calculation of thermodynamic parameters(ΔH~*,ΔS~*andΔG~*)corresponding to the pyrolysis of typeⅠkerogen revealed that the process is non-spontaneous,in agreement with DTA experiments.展开更多
Objective Neurofibromatosis typeⅠ(NF1)is an autosomal dominant disorder which is caused by loss-of-function mutations in neurofibromin 1 gene(NF1).Clinically,NF1 mainly manifests several typical features,such as mult...Objective Neurofibromatosis typeⅠ(NF1)is an autosomal dominant disorder which is caused by loss-of-function mutations in neurofibromin 1 gene(NF1).Clinically,NF1 mainly manifests several typical features,such as multiple neurofibromas and café-au-lait spots,as well as axillary freckling and Lisch nodules in iris.The aim of the current study is to identification a splicing mutation and genotype-phenotype correlation.展开更多
BACKGROUND Type Ⅰ diabetes(T1D)is characterized by insulin loss caused by inflammatory cells that excessively infiltrate and destroy the pancreas,resulting in dysregulation of tissue homeostasis,mechanobiological pro...BACKGROUND Type Ⅰ diabetes(T1D)is characterized by insulin loss caused by inflammatory cells that excessively infiltrate and destroy the pancreas,resulting in dysregulation of tissue homeostasis,mechanobiological properties,and the immune response.The streptozotocin(STZ)-induced mouse model exhibits multiple features of human T1D and enables mechanistic analysis of disease progression.However,the relationship between the mechanochemical signaling regulation of STZ-induced T1D and macrophage migration and phagocytosis is unclear.AIM To study the mechanochemical regulation of STZ-induced macrophage response on pancreatic beta islet cells to gain a clearer understanding of T1D.METHODS We performed experiments using different methods.We stimulated isolated pancreatic beta islet cells with STZ and then tested the macrophage migration and phagocytosis.RESULTS In this study,we discovered that the integrin-associated surface factor CD47 played a critical role in immune defense in the STZ-induced T1D model by preventing pancreatic beta islet inflammation.In comparison with healthy mice,STZ-treated mice showed decreased levels of CD47 on islet cells and reduced interaction of CD47 with signal regulatory proteinα(SIRPα),which negatively regulates macrophage-mediated phagocytosis.This resulted in weakened islet cell immune defense and promoted macrophage migration and phagocytosis of target inflammatory cells.Moreover,lipopolysaccharide-activated human acute monocytic leukemia THP-1 cells also exhibited enhanced phagocytosis in the STZ-treated islets,and the aggressive attack of the inflammatory islets correlated with impaired CD47-SIRPαinteractions.In addition,CD47 overexpression rescued the pre-labeled targeted cells.CONCLUSION This study indicates that CD47 deficiency promotes the migration and phagocytosis of macrophages and provides mechanistic insights into T1D by associating the interactions between membrane structures and inflammatory disease progression.展开更多
BACKGROUND Neurofibromatosis type Ⅰ(NF1) is the most frequent subtype of neurofibromatosis. Its related tumor-suppressor syndromes are characterized by a predisposition to multiple tumor types and other disorder pres...BACKGROUND Neurofibromatosis type Ⅰ(NF1) is the most frequent subtype of neurofibromatosis. Its related tumor-suppressor syndromes are characterized by a predisposition to multiple tumor types and other disorder presentations. In addition, the incidence of tumors is much higher in patients with neurofibromatosis type Ⅰ. However, there are very few reports at home and abroad on this topic. Here, we present a case of NF1 with spindle cell sarcoma.CASE SUMMARY A 50-year-old male was found to have a right axillary mass for 20 years.Specialist examination found cafe-au-lait spots on many parts of the skin,rounded nodules in the skin, a bulge in the right armpit, touching a lump(10 cm× 6 cm, hard, unclear boundary, poor mobility, local tenderness). The anterior side of the thigh felt weakened on the opposite side;in the right groin a swollen lymph node(hard, clear border, good mobility, local tenderness). According to the results of positron emission tomography/computed tomography, puncture pathology and immunohistochemistry, genetic testing, a diagnosis of NF1 with spindle cell sarcoma was confirmed. According to the genetic testing result, the patient was given a targeted treatment with crizotinib.CONCLUSION Surgery, chemotherapy and radiotherapy are the main treatment methods of NF1. However, with the continuous progress of molecular biology research,molecular targeted therapy may bring benefits for patients.展开更多
Objective:To investigate the effects of Sishen pill on the expression of type I interferon(IFN)and type III interferon and their receptors in colonic tissues of mice with acute ulcerative colitis(UC).Methods:Male C57B...Objective:To investigate the effects of Sishen pill on the expression of type I interferon(IFN)and type III interferon and their receptors in colonic tissues of mice with acute ulcerative colitis(UC).Methods:Male C57BL/6Cnc mice were randomly divided into control group,model group,sishenwan group and salazosulfapyridine group.The model was made with 0.2 mL 4%dextran sodium sulfate(DSS)for 5 days,and the control group was given 0.2mL normal saline by gavage.On the second day of modeling,sishen pill group was given 0.2mL 1.5 g·kg^(-1) sishen pill,and SASP group was given 0.2mL 0.25 g·kg^(-1) sulfasalazine,twice a day,for 7 days.During the administration period,the disease activity index(DAI)of mice was calculated every day.After administration,the histopathological changes of colon tissues of mice in each group were observed by hematoxylin eosin(HE)staining,and the histological scores were calculated.The expression of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 mRNAs in colon tissues of mice in each group were detected by qRT-PCR.The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 in colon tissues of mice in each group were detected by ELISA.Western blot was used to detect the expression of interferon receptors IFNAR1,IFNAR2 and IFNLR1 in colon tissues of mice in each group.Results:Compared with the control group,the DAI of mice increased significantly(P<0.001)in the model group.The inflammatory cells in colonic tissues infiltrated heavily,lymph nodes enlarged,colonic mucosal structure destroyed,crypt structure lost,inflammation involved a wide range,and the histological score increased significantly(P<0.001).The levels of IFN-α,IFN-βand IFNλ2 mRNA were significantly decreased(P<0.05,P<0.05,P<0.01).The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly decreased(P<0.01,P<0.01,P<0.001,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly decreased(P<0.01,P<0.05,P<0.01).Compared with the model group,the DAI decreased significantly(P<0.001)in Sishen pill group,the infiltration of inflammatory cells in colon tissue were significantly reduced,the structural regeneration of colon mucosa was significantly recovered,the crypt structure was significantly recovered,the lymph nodes were significantly reduced,the range of inflammation involvement was reduced,and the histological score was significantly reduced(P<0.001).The levels of IFN-α,IFN-βand IFN-λ2 mRNA were significantly increased(P<0.01,P<0.001,P<0.001).The levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly increased(P<0.01,P<0.001,P<0.01,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly increased(P<0.05,P<0.001,P<0.05).Conclusion:Sishen pill may alleviate the symptoms and signs of mice with acute ulcerative colitis by regulating the expression of type I and type III interferon and their receptors in colon tissues.展开更多
In this study, serum concentrations of carboxyterminal propeptide of type Ⅰ collagen(PICP) and carboxyterminal cross-linked telopeptide of type Ⅰ collagen (ICTP), which represent the rates of synthesis and degradati...In this study, serum concentrations of carboxyterminal propeptide of type Ⅰ collagen(PICP) and carboxyterminal cross-linked telopeptide of type Ⅰ collagen (ICTP), which represent the rates of synthesis and degradation of type Ⅰ collagen, were determined by radioimmunoassay in 56 patients with multiple myeloma (MM) and 22 healthy controls. It was discovered that serum concentrations of both PICP and ICTP were higher in MM than those in healthy controls (P<0. 01 ). With the disease progressing and the number of bone lesions increasing,serum concentration of ICTP elevated while serum concentration of PICP showed no significant change. Neither serum PICP nor ICTP concentration was related to M-component classes. Our results indicated that serum ICTP concentration was a good serological marker to reflect severity of bone lesions in MM and elevated serum PICP concentration might be due to compensatory increase in type Ⅰ collagen synthesis. Moreover, we also found that serum ICTP concentrations in MM correlated with serum interleukin-6 (IL-6) activities (r= 0. 610, P< 0. 01),which confirms the effectiveness of IL-6 as an osteoclast activating factor.展开更多
IKKε is an IκB kinase participating in the control of NF-κB and type Ⅰ IFN signal pathways in mammals.However,the function of IKKε in regulating immune response is largely unknown in teleost.Herein,an IKKε homol...IKKε is an IκB kinase participating in the control of NF-κB and type Ⅰ IFN signal pathways in mammals.However,the function of IKKε in regulating immune response is largely unknown in teleost.Herein,an IKKε homologue named AjIKKε was characterized in Japanese eel(Anguilla japonica).AjIKKε has an N-terminal kinase domain,a ubiquitin-like domain,and a coiled coil-containing domain(CC),which is conserved and similar to its counterpart in mammals.Expression analysis showed that AjIKKεcould be up-regulated in kidney,spleen,and particularly in liver under the stimulation of poly Ⅰ:C,LPS,and Aeromonas hydrophila infection.In vitro,the mRNA levels of AjIKKεwere significantly provoked in eel liver cells stimulated by LPS and poly I:C,or the different concentrations of A.hydrophila.The overexpression of AjIKKε could not only induce a significantly higher level of promoter activity of human NF-κB,AP-1,and IFN-β in a dose-dependent manner but also up-regulate the activation of promoters of Japanese eel cRel,AP1,IL6,IFN4,IRF3,and IRF7 in HEK293 cells.RNAi studies showed that after AjIKKε was knocked down,the expression levels of IL1,IL6,TNFα,c-Jun,IFN2,IFN3,MX1,MX2,and IRF3 genes were significantly down-regulated in liver,spleen,and kidney of Japanese eels.In addition,the mutants of AjIKKε-K39A,AjIKKε-S174A,and AjIKKε-ΔCC failed to activate Japanese eel IFN4,IRF3 and human IFN-β promoters in HEK293 cells.Collectively,these results suggest that AjIKKεmay function as a positive regulator of NF-κB,MAPK,and IRF3-mediated type Ⅰ IFN signaling pathways related to immune response evoked by bacterial and viral infection.展开更多
AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant...AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant hepatic failure （FHF）. METHODS： FHF was induced by lipopolysaccharide （LPS） in D-galactosamine （GAIN） sensitized BALB/c mice. There were 20 mice in normal saline （NS）-treated group, 20 mice in LPS-treated group, 20 mice in GaIN- treated group, and 60 mice in GalN/LPS-treated group （FHF group）. Liver and kidney tissues were obtained at 2, 6, and 9 h after administration. The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope. The expression of IP3R I in kidney tissue was tested by immunohistochemistry, Western blot and reverse transcription （RT）-PCR. RESULTS： Kidney tissues were morphologically normal at all time points in all groups. IP3R I proteins were found localized in the plasma region of glomerular mesangial cells （GMC） and vascular smooth muscle cells （VSMC） in kidney by immunohistochemical staining. In kidney of mice with FHF at 6 h and 9 h IP3R I staining was upregulated. Results from Western blot demonstrated consistent and significant increment of IP3R I expression in mice with FHF at 6 h and 9 h （t = 3.16, P 〈 0.05; t = 5.43, P 〈 0.01）. Furthermore, we evaluated IP3R I mRNA expression by RT-PCR and observed marked upregulation of IP3R I mRNA in FHF samples at 2 h, 6 h and 9 h compared to controls （t = 2.97, P 〈 0.05; t = 4.42, P 〈 0.01; t = 3.81, P 〈 0.01）. CONCLUSION： The expression of IP3R I protein increased in GMC and renal VSMC of mice with FHF, possibly caused by up-regulation of IP3R I mRNA.展开更多
基金supported by grants from the Taichung Veterans General Hospital and Central Taiwan University of Science and Technology,No.TCVGH-CTUST1047701(to CCS and BSL)Taichung Veterans General Hospital,No.TCVGH-1034907C(to CCS),Taiwan,China
文摘Recent studies have shown the potential of artificially synthesized conduits in the repair of peripheral nerve injury. Natural biopolymers have received much attention because of their biocompatibility. To investigate the effects of novel electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits(biopolymer nanofiber conduits) on the repair of peripheral nerve injury, we bridged 10-mm-long sciatic nerve defects with electrospun absorbable biopolymer nanofiber conduits, poly(ε-caprolactone) or silicone conduits in Sprague-Dawley rats. Rat neurologica1 function was weekly evaluated using sciatic function index within8 weeks after repair. Eight weeks after repair, sciatic nerve myelin sheaths and axon morphology were observed by osmium tetroxide staining, hematoxylin-eosin staining, and transmission electron microscopy.S-100(Schwann cell marker) and CD4(inflammatory marker) immunoreactivities in sciatic nerve were detected by immunohistochemistry. In rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits, no serious inflammatory reactions were observed in rat hind limbs, the morphology of myelin sheaths in the injured sciatic nerve was close to normal. CD4 immunoreactivity was obviously weaker in rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits than in those subjected to repair with poly(ε-caprolactone) or silicone. Rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits tended to have greater sciatic nerve function recovery than those receiving poly(ε-caprolactone) or silicone repair. These results suggest that electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits have the potential of repairing sciatic nerve defects and exhibit good biocompatibility. All experimental procedures were approved by Institutional Animal Care and Use Committee of Taichung Veteran General Hospital, Taiwan, China(La-1031218) on October 2, 2014.
文摘AIM To evaluate the incidence of lymph node metastasis （LNM） and its risk factors in patients with Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas.METHODS We enrolled 85 patients [69 men, 16 women; median age （range）, 67 （38-84） years] who had undergone esophagectomy or proximal gastrectomy for Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas. Predictive risk factors of LNM included age, sex, location of the tumor center, confirmed Barrett’s esophageal adenocarcinoma, tumor size, macroscopic tumor type, pathology, invasion depth, presence of ulceration, and lymphovascular invasion. Multivariate logistic regression analysis was used to identify factors predicting LNM. We also evaluated the frequencies of LNM for Siewert type Ⅰ and type Ⅱ pT1 adenocarcinomas in meta-data analysis.RESULTSLNMs were found in 11 out of 85 patients （12.9%, 95%CI： 5.8-20.0）. Only 1 of the 15 patients （6.6%, 95%CI： 0.0-19.2） who had a final diagnosis of pT1a adenocarcinoma had a positive LNM, whereas 10 of the 70 patients （14.2%, 95%CI： 6.0-22.4） with a final diagnosis of pT1b adenocarcinoma had positive LNM. Furthermore, only one of the 30 patients （3.3%, 95%CI： 0.0-9.7） with a tumor invasion depth within 500 μm from muscularis mucosae had positive LNM. Poor differentiation and lymphovascular invasion were independently associated with a risk of LNM. In meta-data analysis, 12 of the 355 patients （3.3%, 95%CI： 1.5-5.2） who had a final diagnosis of pT1a adenocarcinoma had a positive LNM, whereas 91 of the 438 patients （20.7%, 95%CI： 16.9-24.5） with a fnal diagnosis of pT1b adenocarcinoma had positive LNM.CONCLUSIONWe consider endoscopic submucosal dissection （ESD） is suitable for patients with Siewert type Ⅰ and type Ⅱ T1a adenocarcinomas. For patients with T1b adenocarcinoma, especially invasion depth is within 500 μm from muscularis mucosae with no other risk factor for LNM, diagnostic ESD could be a treatment option according to the overall status of patients and the presence of comorbidities.
文摘To study the effects of Icariin on expression of osteopontin （OPN） mRNA and type Ⅰ collagen in rat osteoblasts in vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvaria of new-born new-born fetal Sprague-Dawley （SD） rats by means of modified sequential collagenase digestion and incubated in MEM medium and the cell morphology was observed under inverted phase contrast microscope, OB was identified by alkaline phosphatase （ALP） staining. Different concentration （0.1μg/mL, 1.0 μg/mL, 10 μ/mL） of Icariin was added to the OB and incubated. The effect of Icariin on the proliferation and osteogenesis of OB was monitored by MTT analysis. The expression of type l collagen was estimated with immunohistochemistry techniques. The expression levels of mRNA of OPN in the cells in every group were examined by reverse-transcriptase ploymerase chain reaction （RT-PCR）. The expression of OPN mRNA and type Ⅰ collagen was strengthened gradually with the increase of Icariin concentration and peaked with 10 μg/mL Icariin on the 5th day. Icariin could significantly promote the expression of OPN mRNA and type Ⅰ collagen in rat osteoblasts in vitro. The levels of expression of OPN mRNA and type Ⅰ collagen were changed with different concentration of Icariin. Icariin could effectively prevent and treat osteoporosis and promote the bone formation.
基金financially supported by University of Mohammed V-Morocco under the Project No.SCH 04/09 and HassanⅡAcademy of Science and Technology,Morocco.
文摘The Democratic Republic of the Congo holds important reserves of oil shale which is still under geological status.Herein,the characterization and pyrolysis kinetics of typeⅠkerogen-rich oil shale of the western Central Kongo(CK)were investigated.X-ray diffraction,Fourier-transform infrared spectroscopy and thermal analysis(TG/DTA)showed that CK oil shale exhibits a siliceous mineral matrix with a consistent organic matter rich in aliphatic chains.The pyrolysis behavior of kerogen revealed the presence of a single mass loss between 300 and 550°C,estimated at 12.5%and attributed to the oil production stage.Non-isothermal kinetics was performed by determining the activation energy using the iterative isoconversional model-free methods and exhibits a constant value with E=211.5±4.7 kJ mol.1.The most probable kinetic model describing the kerogen pyrolysis mechanism was obtained using the Coats–Redfern and Arrhenius plot methods.The results showed a unique kinetic triplet confirming the nature of kerogen,predominantly typeⅠand reinforcing the previously reported geochemical characteristics of the CK oil shale.Besides,the calculation of thermodynamic parameters(ΔH~*,ΔS~*andΔG~*)corresponding to the pyrolysis of typeⅠkerogen revealed that the process is non-spontaneous,in agreement with DTA experiments.
文摘Objective Neurofibromatosis typeⅠ(NF1)is an autosomal dominant disorder which is caused by loss-of-function mutations in neurofibromin 1 gene(NF1).Clinically,NF1 mainly manifests several typical features,such as multiple neurofibromas and café-au-lait spots,as well as axillary freckling and Lisch nodules in iris.The aim of the current study is to identification a splicing mutation and genotype-phenotype correlation.
基金Supported by the National Natural Science Foundation of China,No.31701179the China Postdoctoral Science Foundation,No.2016M591877。
文摘BACKGROUND Type Ⅰ diabetes(T1D)is characterized by insulin loss caused by inflammatory cells that excessively infiltrate and destroy the pancreas,resulting in dysregulation of tissue homeostasis,mechanobiological properties,and the immune response.The streptozotocin(STZ)-induced mouse model exhibits multiple features of human T1D and enables mechanistic analysis of disease progression.However,the relationship between the mechanochemical signaling regulation of STZ-induced T1D and macrophage migration and phagocytosis is unclear.AIM To study the mechanochemical regulation of STZ-induced macrophage response on pancreatic beta islet cells to gain a clearer understanding of T1D.METHODS We performed experiments using different methods.We stimulated isolated pancreatic beta islet cells with STZ and then tested the macrophage migration and phagocytosis.RESULTS In this study,we discovered that the integrin-associated surface factor CD47 played a critical role in immune defense in the STZ-induced T1D model by preventing pancreatic beta islet inflammation.In comparison with healthy mice,STZ-treated mice showed decreased levels of CD47 on islet cells and reduced interaction of CD47 with signal regulatory proteinα(SIRPα),which negatively regulates macrophage-mediated phagocytosis.This resulted in weakened islet cell immune defense and promoted macrophage migration and phagocytosis of target inflammatory cells.Moreover,lipopolysaccharide-activated human acute monocytic leukemia THP-1 cells also exhibited enhanced phagocytosis in the STZ-treated islets,and the aggressive attack of the inflammatory islets correlated with impaired CD47-SIRPαinteractions.In addition,CD47 overexpression rescued the pre-labeled targeted cells.CONCLUSION This study indicates that CD47 deficiency promotes the migration and phagocytosis of macrophages and provides mechanistic insights into T1D by associating the interactions between membrane structures and inflammatory disease progression.
文摘BACKGROUND Neurofibromatosis type Ⅰ(NF1) is the most frequent subtype of neurofibromatosis. Its related tumor-suppressor syndromes are characterized by a predisposition to multiple tumor types and other disorder presentations. In addition, the incidence of tumors is much higher in patients with neurofibromatosis type Ⅰ. However, there are very few reports at home and abroad on this topic. Here, we present a case of NF1 with spindle cell sarcoma.CASE SUMMARY A 50-year-old male was found to have a right axillary mass for 20 years.Specialist examination found cafe-au-lait spots on many parts of the skin,rounded nodules in the skin, a bulge in the right armpit, touching a lump(10 cm× 6 cm, hard, unclear boundary, poor mobility, local tenderness). The anterior side of the thigh felt weakened on the opposite side;in the right groin a swollen lymph node(hard, clear border, good mobility, local tenderness). According to the results of positron emission tomography/computed tomography, puncture pathology and immunohistochemistry, genetic testing, a diagnosis of NF1 with spindle cell sarcoma was confirmed. According to the genetic testing result, the patient was given a targeted treatment with crizotinib.CONCLUSION Surgery, chemotherapy and radiotherapy are the main treatment methods of NF1. However, with the continuous progress of molecular biology research,molecular targeted therapy may bring benefits for patients.
基金National Natural Science Foundation of China(No.82160835)。
文摘Objective:To investigate the effects of Sishen pill on the expression of type I interferon(IFN)and type III interferon and their receptors in colonic tissues of mice with acute ulcerative colitis(UC).Methods:Male C57BL/6Cnc mice were randomly divided into control group,model group,sishenwan group and salazosulfapyridine group.The model was made with 0.2 mL 4%dextran sodium sulfate(DSS)for 5 days,and the control group was given 0.2mL normal saline by gavage.On the second day of modeling,sishen pill group was given 0.2mL 1.5 g·kg^(-1) sishen pill,and SASP group was given 0.2mL 0.25 g·kg^(-1) sulfasalazine,twice a day,for 7 days.During the administration period,the disease activity index(DAI)of mice was calculated every day.After administration,the histopathological changes of colon tissues of mice in each group were observed by hematoxylin eosin(HE)staining,and the histological scores were calculated.The expression of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 mRNAs in colon tissues of mice in each group were detected by qRT-PCR.The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 in colon tissues of mice in each group were detected by ELISA.Western blot was used to detect the expression of interferon receptors IFNAR1,IFNAR2 and IFNLR1 in colon tissues of mice in each group.Results:Compared with the control group,the DAI of mice increased significantly(P<0.001)in the model group.The inflammatory cells in colonic tissues infiltrated heavily,lymph nodes enlarged,colonic mucosal structure destroyed,crypt structure lost,inflammation involved a wide range,and the histological score increased significantly(P<0.001).The levels of IFN-α,IFN-βand IFNλ2 mRNA were significantly decreased(P<0.05,P<0.05,P<0.01).The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly decreased(P<0.01,P<0.01,P<0.001,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly decreased(P<0.01,P<0.05,P<0.01).Compared with the model group,the DAI decreased significantly(P<0.001)in Sishen pill group,the infiltration of inflammatory cells in colon tissue were significantly reduced,the structural regeneration of colon mucosa was significantly recovered,the crypt structure was significantly recovered,the lymph nodes were significantly reduced,the range of inflammation involvement was reduced,and the histological score was significantly reduced(P<0.001).The levels of IFN-α,IFN-βand IFN-λ2 mRNA were significantly increased(P<0.01,P<0.001,P<0.001).The levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly increased(P<0.01,P<0.001,P<0.01,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly increased(P<0.05,P<0.001,P<0.05).Conclusion:Sishen pill may alleviate the symptoms and signs of mice with acute ulcerative colitis by regulating the expression of type I and type III interferon and their receptors in colon tissues.
文摘In this study, serum concentrations of carboxyterminal propeptide of type Ⅰ collagen(PICP) and carboxyterminal cross-linked telopeptide of type Ⅰ collagen (ICTP), which represent the rates of synthesis and degradation of type Ⅰ collagen, were determined by radioimmunoassay in 56 patients with multiple myeloma (MM) and 22 healthy controls. It was discovered that serum concentrations of both PICP and ICTP were higher in MM than those in healthy controls (P<0. 01 ). With the disease progressing and the number of bone lesions increasing,serum concentration of ICTP elevated while serum concentration of PICP showed no significant change. Neither serum PICP nor ICTP concentration was related to M-component classes. Our results indicated that serum ICTP concentration was a good serological marker to reflect severity of bone lesions in MM and elevated serum PICP concentration might be due to compensatory increase in type Ⅰ collagen synthesis. Moreover, we also found that serum ICTP concentrations in MM correlated with serum interleukin-6 (IL-6) activities (r= 0. 610, P< 0. 01),which confirms the effectiveness of IL-6 as an osteoclast activating factor.
基金financially supported by“Nature Science Foundation of Fujian Province”(No.2020J01671,2021J01830).
文摘IKKε is an IκB kinase participating in the control of NF-κB and type Ⅰ IFN signal pathways in mammals.However,the function of IKKε in regulating immune response is largely unknown in teleost.Herein,an IKKε homologue named AjIKKε was characterized in Japanese eel(Anguilla japonica).AjIKKε has an N-terminal kinase domain,a ubiquitin-like domain,and a coiled coil-containing domain(CC),which is conserved and similar to its counterpart in mammals.Expression analysis showed that AjIKKεcould be up-regulated in kidney,spleen,and particularly in liver under the stimulation of poly Ⅰ:C,LPS,and Aeromonas hydrophila infection.In vitro,the mRNA levels of AjIKKεwere significantly provoked in eel liver cells stimulated by LPS and poly I:C,or the different concentrations of A.hydrophila.The overexpression of AjIKKε could not only induce a significantly higher level of promoter activity of human NF-κB,AP-1,and IFN-β in a dose-dependent manner but also up-regulate the activation of promoters of Japanese eel cRel,AP1,IL6,IFN4,IRF3,and IRF7 in HEK293 cells.RNAi studies showed that after AjIKKε was knocked down,the expression levels of IL1,IL6,TNFα,c-Jun,IFN2,IFN3,MX1,MX2,and IRF3 genes were significantly down-regulated in liver,spleen,and kidney of Japanese eels.In addition,the mutants of AjIKKε-K39A,AjIKKε-S174A,and AjIKKε-ΔCC failed to activate Japanese eel IFN4,IRF3 and human IFN-β promoters in HEK293 cells.Collectively,these results suggest that AjIKKεmay function as a positive regulator of NF-κB,MAPK,and IRF3-mediated type Ⅰ IFN signaling pathways related to immune response evoked by bacterial and viral infection.
基金Supported by National Natural Science Foundation of China, No. 30270607
文摘AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant hepatic failure （FHF）. METHODS： FHF was induced by lipopolysaccharide （LPS） in D-galactosamine （GAIN） sensitized BALB/c mice. There were 20 mice in normal saline （NS）-treated group, 20 mice in LPS-treated group, 20 mice in GaIN- treated group, and 60 mice in GalN/LPS-treated group （FHF group）. Liver and kidney tissues were obtained at 2, 6, and 9 h after administration. The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope. The expression of IP3R I in kidney tissue was tested by immunohistochemistry, Western blot and reverse transcription （RT）-PCR. RESULTS： Kidney tissues were morphologically normal at all time points in all groups. IP3R I proteins were found localized in the plasma region of glomerular mesangial cells （GMC） and vascular smooth muscle cells （VSMC） in kidney by immunohistochemical staining. In kidney of mice with FHF at 6 h and 9 h IP3R I staining was upregulated. Results from Western blot demonstrated consistent and significant increment of IP3R I expression in mice with FHF at 6 h and 9 h （t = 3.16, P 〈 0.05; t = 5.43, P 〈 0.01）. Furthermore, we evaluated IP3R I mRNA expression by RT-PCR and observed marked upregulation of IP3R I mRNA in FHF samples at 2 h, 6 h and 9 h compared to controls （t = 2.97, P 〈 0.05; t = 4.42, P 〈 0.01; t = 3.81, P 〈 0.01）. CONCLUSION： The expression of IP3R I protein increased in GMC and renal VSMC of mice with FHF, possibly caused by up-regulation of IP3R I mRNA.
