BACKGROUND Periodontitis is a chronic inflammation of periodontal supporting tissue caused by local factors. Periodontal surgery can change the gene expression of peripheral blood mononuclear cells. However, little is...BACKGROUND Periodontitis is a chronic inflammation of periodontal supporting tissue caused by local factors. Periodontal surgery can change the gene expression of peripheral blood mononuclear cells. However, little is known about the potential mechanism of surgical treatment for periodontitis. AIM To explore the potential molecular mechanism of surgical treatment for periodontitis. METHODS First, based on the expression profiles of genes related to surgical treatment for periodontitis, a set of expression disorder modules related to surgical treatment for periodontitis were obtained by enrichment analysis. Subsequently, based on crosstalk analysis, we proved that there was a significant crosstalk relationship between module 3 and module 5. Finally, based on predictive analysis of multidimensional regulators, we identified a series of regulatory factors, such as endogenous genes, non-coding RNAs (ncRNAs), and transcription factors, which have potential regulatory effects on periodontitis. RESULTS A total of 337 genes related to surgical treatment for periodontitis were obtained, and 3896 genes related to periodontitis were amplified. Eight expression modules of periodontitis were obtained, involving the aggregation of 2672 gene modules. These modules are mainly involved in G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger, and adenylate cyclasemodulating G-protein coupled receptor signaling pathway. In addition, eight endogenous genes (including EGF, RPS27A, and GNB3) were screened by network connectivity analysis. Finally, based on this set of potential dysfunction modules, 94 transcription factors (including NFKB1, SP1, and STAT3) and 1198 ncRNAs (including MALAT1, CRNDE, and ANCR) were revealed. These core regulators are thought to be involved in the potential molecular mechanism of periodontitis after surgical treatment. CONCLUSION Based on the results of this study, we can show biologists and pharmacists a new idea to reveal the potential molecular mechanism of surgical treatment for periodontitis, and provide valuable reference for follow-up treatment programs.展开更多
BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B...BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B protein and the severity of brain damage.METHODS:This article is a critical and descriptive review on S100 B protein in serum after ischemic brain injury.We searched Pubmed database with key words or terms such as "S100B protein", "cardiac arrest", "hemorrhagic shock" and "ischemia reperfusion injury" appeared in the last five years.RESULTS:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of ischemic brain injury will be dramatically increased.Ischemic brain injury elevated the level of serum S100 B protein,and the severity of brain damage.CONCLUSION:The level of S100 B protein in serum is elevated after ischemic brain injury,but its mechanism is unclear.展开更多
Objective:To observe the effect of captopril on the tumor necrosis factor-α(TNF- α) level and arterial blood gases in acute lung injury(All) induced by HCL in rats,and to analyze its protective mechanism.Methods:Fif...Objective:To observe the effect of captopril on the tumor necrosis factor-α(TNF- α) level and arterial blood gases in acute lung injury(All) induced by HCL in rats,and to analyze its protective mechanism.Methods:Fifty Wistar rats were selected and randomly divided into three groups,with 20 rats in Group Ⅰ and Ⅱ,respectively and 10 animals in Group Ⅲ.ALI model was constructed by intratracheal injection of diluted hydrochloric acid(pH=1.25.1.2 mL/kg).Group Ⅰrats received not any treatment after construction of AM model.Group Ⅱ rats were treated with captopril(5 mg/kg,i.p.) 5 min after induction of ALI.Group Ⅲ served as normal control without any treatment.Ninety minutes after construction of ALI model,all the rats were sacrificed.Blood was withdrawn for detection of TNF- α level and arterial blood gases index.And lung tissue slices of the three groups were prepared for observation of pathologic histology changes.Results:TNF- α level in serum of Group Ⅰ and Ⅱ rats was significantly higher than that in Group Ⅲ(P<0.05),while TNF- α level in serum of Group Ⅱ was significantly lower in Group Ⅰ(P<0.05).PaCO_2 level was significantly higher(P<0.05),while PaO_2 was significantly lower(P<0.05) in Group Ⅰ and Ⅱ rats than those in Group Ⅲ.PaCO_2 was significantly lower(P<0.05) and PaO_2 was significantly higher(P<0.05) in Group Ⅱ than those in Group Ⅰ.Histological observation showed diffuse congestion and severe edema of luug tissue,obvious thickening and structure damage of alveolar walls and a large amount of neutrophil infiltration in Group Ⅰ rats.Group Ⅱ rats showed mild edema of lung tissue;only a small portion of alveolar walls showed thickening and only a few of neutrophil infiltration could be observed.The degree of injury was remarkably slighter than that of Group Ⅰ rats.Group Ⅲ rats showed clear lung tissue structure and normal morphology:alveolar walls were uniform and the margin was smooth and few neutrophil could be observed.Conclusions:Captopril can significantly reduce serum TNF- α level,elevate PaO_2 and reduce PaCO_2 in rats with ALI.It has a protective effect on ALI rats.展开更多
Objective:To investigate the therapeutic effect of the intervention treatment with different doses of Captopril on TNF-α contents in serum of rheumatoid arthritis(RA) rats,and to provide the theoretical proofs for cl...Objective:To investigate the therapeutic effect of the intervention treatment with different doses of Captopril on TNF-α contents in serum of rheumatoid arthritis(RA) rats,and to provide the theoretical proofs for clinical application of Captopril in treatments ol rheumatoid diseases.Methods:Fifty Wistar rats were randomly divided into 5 groups,namely.Group A,Group 13.Group C.Group D,Group E with 10 rats in each group.Injection of Freund's complete adjuvant was employed to establish adjuvant-induced arthritis model in rats.Group A was model group;after model establishment,rats were treated with 20 mL normal saline as placebo(ip.).Rats in Group B were treated with 8 mg/kg cyclophosphamide(ip.).Rats in Group C.D and E were intraperitoneally injected with 30 mg/kg.100 mg/kg and 300 mg/kg Captopril respectively.Rats in each group were subjected to continuous treatment for 3 weeks,and then sacrificed.Eyeballs of rats were excised and blood was collected.TNF- α content in serum were detected using ELISA:each group rats were compared for the hind legs arthrocele.Right ankle tissues of rats were collected to prepare section,and microscopic observation of pathological changes was performed.Results:TNF- α content in serum of Group A rats was significantly higher than that of rats in other 4 groups(P<0.05).TNF- α content in serum of Group B rats was significantly lower compared with that of rats in Groups C.D and E.The highest TNF- α content in serum of rats treated with Captopril was found in Group C,followed by Groups D and E(P<0.05).Right ankle arthrocele of rats in Groups B.C.D and E in early stage showed no statistical difference compared with that of Group A rats(P>0.05).From Day 8,ankle arthrocele of rats in Groups B.C.D and E was obviously relieved compared with that of Group A rats:the anti-inflammatory effects were gradually enhanced with the extension of medication time.Treatments of Groups C.D and E showed significant activities against tardive aithrocele:the degree of ankle arthrocele in rats of these three groups was lower than that of Group A rats(P<0.01).Histological observation showed that large amount of inflammatory cells and plasmocyte infiltration was found in ankle synovial tissues of Group A rats.Relief of hyperaemia and edema of right ankle synovial tissues as well as significant decrease in synoviocyte layer hyperplasia,intra—articular inflammatory cells infiltration and cartilage articularis damage degree etc.were observed in Groups B.C.D and E.Conclusions:Intervention treatment with Captopril can effectively reduce the TNF- α content in serum of rheumatoid arthritis rats and inhibit the generation of inflammatory factors,so as to achieve the therapeutic effect.展开更多
In this paper,we focus on the vertex-fault-tolerant cycles embedding on enhanced hypercube,which is an attractive variant of hypercube and is obtained by adding some complementary edges from hypercube.Let Fv be the se...In this paper,we focus on the vertex-fault-tolerant cycles embedding on enhanced hypercube,which is an attractive variant of hypercube and is obtained by adding some complementary edges from hypercube.Let Fv be the set of faulty vertices in the n-dimensional enhanced hypercube Qn,k（1 ≤ k≤n- 1）.When ｜F_v｜ = 2,we showed that Qn,k-Fv contains a fault-free cycle of every even length from 4 to 2^n- 4 where n（n ≥ 3） and fc have the same parity;and contains a fault-free cycle of every even length from 4 to 2^n- 4,simultaneously,contains a cycle of every odd length from n — fc ＋ 2 to 2^n-3 where n（≥ 3） and fc have the different parity.Furthermore,when ｜Fv｜= fv ≤ n- 2,we proof that there exists the longest fault-free cycle,which is of even length 2^n- 2fv whether n（n 〉 3） and fe have the same parity or not;and there exists the longest fault-free cycle,which is of odd length 2^n-2fv- 1 in Qn,k — Fv where n（≥ 3） and fc have the different parity.展开更多
文摘BACKGROUND Periodontitis is a chronic inflammation of periodontal supporting tissue caused by local factors. Periodontal surgery can change the gene expression of peripheral blood mononuclear cells. However, little is known about the potential mechanism of surgical treatment for periodontitis. AIM To explore the potential molecular mechanism of surgical treatment for periodontitis. METHODS First, based on the expression profiles of genes related to surgical treatment for periodontitis, a set of expression disorder modules related to surgical treatment for periodontitis were obtained by enrichment analysis. Subsequently, based on crosstalk analysis, we proved that there was a significant crosstalk relationship between module 3 and module 5. Finally, based on predictive analysis of multidimensional regulators, we identified a series of regulatory factors, such as endogenous genes, non-coding RNAs (ncRNAs), and transcription factors, which have potential regulatory effects on periodontitis. RESULTS A total of 337 genes related to surgical treatment for periodontitis were obtained, and 3896 genes related to periodontitis were amplified. Eight expression modules of periodontitis were obtained, involving the aggregation of 2672 gene modules. These modules are mainly involved in G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger, and adenylate cyclasemodulating G-protein coupled receptor signaling pathway. In addition, eight endogenous genes (including EGF, RPS27A, and GNB3) were screened by network connectivity analysis. Finally, based on this set of potential dysfunction modules, 94 transcription factors (including NFKB1, SP1, and STAT3) and 1198 ncRNAs (including MALAT1, CRNDE, and ANCR) were revealed. These core regulators are thought to be involved in the potential molecular mechanism of periodontitis after surgical treatment. CONCLUSION Based on the results of this study, we can show biologists and pharmacists a new idea to reveal the potential molecular mechanism of surgical treatment for periodontitis, and provide valuable reference for follow-up treatment programs.
基金supported by a grant from 122 Project of Nanjing Military Command focusing on training(JQZD200905)
文摘BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B protein and the severity of brain damage.METHODS:This article is a critical and descriptive review on S100 B protein in serum after ischemic brain injury.We searched Pubmed database with key words or terms such as "S100B protein", "cardiac arrest", "hemorrhagic shock" and "ischemia reperfusion injury" appeared in the last five years.RESULTS:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of ischemic brain injury will be dramatically increased.Ischemic brain injury elevated the level of serum S100 B protein,and the severity of brain damage.CONCLUSION:The level of S100 B protein in serum is elevated after ischemic brain injury,but its mechanism is unclear.
基金supported by Science and Technology Research and Development Program of Tangshan City,Reference No.07130233d
文摘Objective:To observe the effect of captopril on the tumor necrosis factor-α(TNF- α) level and arterial blood gases in acute lung injury(All) induced by HCL in rats,and to analyze its protective mechanism.Methods:Fifty Wistar rats were selected and randomly divided into three groups,with 20 rats in Group Ⅰ and Ⅱ,respectively and 10 animals in Group Ⅲ.ALI model was constructed by intratracheal injection of diluted hydrochloric acid(pH=1.25.1.2 mL/kg).Group Ⅰrats received not any treatment after construction of AM model.Group Ⅱ rats were treated with captopril(5 mg/kg,i.p.) 5 min after induction of ALI.Group Ⅲ served as normal control without any treatment.Ninety minutes after construction of ALI model,all the rats were sacrificed.Blood was withdrawn for detection of TNF- α level and arterial blood gases index.And lung tissue slices of the three groups were prepared for observation of pathologic histology changes.Results:TNF- α level in serum of Group Ⅰ and Ⅱ rats was significantly higher than that in Group Ⅲ(P<0.05),while TNF- α level in serum of Group Ⅱ was significantly lower in Group Ⅰ(P<0.05).PaCO_2 level was significantly higher(P<0.05),while PaO_2 was significantly lower(P<0.05) in Group Ⅰ and Ⅱ rats than those in Group Ⅲ.PaCO_2 was significantly lower(P<0.05) and PaO_2 was significantly higher(P<0.05) in Group Ⅱ than those in Group Ⅰ.Histological observation showed diffuse congestion and severe edema of luug tissue,obvious thickening and structure damage of alveolar walls and a large amount of neutrophil infiltration in Group Ⅰ rats.Group Ⅱ rats showed mild edema of lung tissue;only a small portion of alveolar walls showed thickening and only a few of neutrophil infiltration could be observed.The degree of injury was remarkably slighter than that of Group Ⅰ rats.Group Ⅲ rats showed clear lung tissue structure and normal morphology:alveolar walls were uniform and the margin was smooth and few neutrophil could be observed.Conclusions:Captopril can significantly reduce serum TNF- α level,elevate PaO_2 and reduce PaCO_2 in rats with ALI.It has a protective effect on ALI rats.
基金supported by Science and Technology Research and Development Program of Tangshan City.Grant Number:07130233d
文摘Objective:To investigate the therapeutic effect of the intervention treatment with different doses of Captopril on TNF-α contents in serum of rheumatoid arthritis(RA) rats,and to provide the theoretical proofs for clinical application of Captopril in treatments ol rheumatoid diseases.Methods:Fifty Wistar rats were randomly divided into 5 groups,namely.Group A,Group 13.Group C.Group D,Group E with 10 rats in each group.Injection of Freund's complete adjuvant was employed to establish adjuvant-induced arthritis model in rats.Group A was model group;after model establishment,rats were treated with 20 mL normal saline as placebo(ip.).Rats in Group B were treated with 8 mg/kg cyclophosphamide(ip.).Rats in Group C.D and E were intraperitoneally injected with 30 mg/kg.100 mg/kg and 300 mg/kg Captopril respectively.Rats in each group were subjected to continuous treatment for 3 weeks,and then sacrificed.Eyeballs of rats were excised and blood was collected.TNF- α content in serum were detected using ELISA:each group rats were compared for the hind legs arthrocele.Right ankle tissues of rats were collected to prepare section,and microscopic observation of pathological changes was performed.Results:TNF- α content in serum of Group A rats was significantly higher than that of rats in other 4 groups(P<0.05).TNF- α content in serum of Group B rats was significantly lower compared with that of rats in Groups C.D and E.The highest TNF- α content in serum of rats treated with Captopril was found in Group C,followed by Groups D and E(P<0.05).Right ankle arthrocele of rats in Groups B.C.D and E in early stage showed no statistical difference compared with that of Group A rats(P>0.05).From Day 8,ankle arthrocele of rats in Groups B.C.D and E was obviously relieved compared with that of Group A rats:the anti-inflammatory effects were gradually enhanced with the extension of medication time.Treatments of Groups C.D and E showed significant activities against tardive aithrocele:the degree of ankle arthrocele in rats of these three groups was lower than that of Group A rats(P<0.01).Histological observation showed that large amount of inflammatory cells and plasmocyte infiltration was found in ankle synovial tissues of Group A rats.Relief of hyperaemia and edema of right ankle synovial tissues as well as significant decrease in synoviocyte layer hyperplasia,intra—articular inflammatory cells infiltration and cartilage articularis damage degree etc.were observed in Groups B.C.D and E.Conclusions:Intervention treatment with Captopril can effectively reduce the TNF- α content in serum of rheumatoid arthritis rats and inhibit the generation of inflammatory factors,so as to achieve the therapeutic effect.
基金Supported in part by the National Natural Science Foundation of China under Grant No.11371162 and 11171129National Natural Science Foundation of Hubei Province No.T201103
文摘In this paper,we focus on the vertex-fault-tolerant cycles embedding on enhanced hypercube,which is an attractive variant of hypercube and is obtained by adding some complementary edges from hypercube.Let Fv be the set of faulty vertices in the n-dimensional enhanced hypercube Qn,k（1 ≤ k≤n- 1）.When ｜F_v｜ = 2,we showed that Qn,k-Fv contains a fault-free cycle of every even length from 4 to 2^n- 4 where n（n ≥ 3） and fc have the same parity;and contains a fault-free cycle of every even length from 4 to 2^n- 4,simultaneously,contains a cycle of every odd length from n — fc ＋ 2 to 2^n-3 where n（≥ 3） and fc have the different parity.Furthermore,when ｜Fv｜= fv ≤ n- 2,we proof that there exists the longest fault-free cycle,which is of even length 2^n- 2fv whether n（n 〉 3） and fe have the same parity or not;and there exists the longest fault-free cycle,which is of odd length 2^n-2fv- 1 in Qn,k — Fv where n（≥ 3） and fc have the different parity.
