BACKGROUND Lymphovascular invasion(LVI)and perineural invasion(PNI)are associated with decreased survival in colorectal cancer(CRC),but its significance in N1c stage remains to be clearly defined.AIM We retrospectivel...BACKGROUND Lymphovascular invasion(LVI)and perineural invasion(PNI)are associated with decreased survival in colorectal cancer(CRC),but its significance in N1c stage remains to be clearly defined.AIM We retrospectively identified 107 consecutive patients who had CRC with N1c disease radically resected at our hospital.Tumors were reviewed for LVI and PNI by one pathologist blinded to the patients’outcomes.Disease-free survival(DFS),overall survival(OS)and cancer-specific survival(CSS)were determined using the Kaplan-Meier method,with LVI and PNI prognosis differences determined by multivariate analysis using the Cox multiple hazards model.Results were compared using log-rank test.The receiver operating characteristic(ROC)curve was used to evaluate the prognostic predictive ability.RESULTS The median follow-up time was 63.17(45.33-81.37)months for DFS,with 33.64%(36/107)of patients experiencing recurrence;21.5%of tumors were found to be LVI positive and 44.9%PNI positive.The 5-year DFS rate was greater for patients with LVI-negative tumors compared with LVI-positive tumors(74.0%vs 35.6%),and PNI was similar(82.5%vs 45.1%).On multivariate analysis,LVI[hazard ratio(HR)=3.368,95%confidence interval(CI):1.628-6.966,P=0.001]and PNI(HR=3.055,95%CI:1.478-6.313,P=0.002)were independent prognostic factors for DFS.All patients could be divided into three groups of patients with different prognosis according to LVI and PNI.The 5-year ROC curve for LVI,PNI and their combination prediction of DFS was 0.646,0.709 and 0.759,respectively.Similar results were seen for OS and CSS.CONCLUSION LVI and PNI could serve as independent prognostic factors of outcomes in N1c CRC patients.Patients with LVI or PNI should be given more attention during treatment.展开更多
BACKGROUND The number of tumor deposits(TDs)does not play a part in the current tumor node metastasis staging.Negative lymph node(NLN)status is associated with the prognosis of colorectal cancer(CRC),but its clear rol...BACKGROUND The number of tumor deposits(TDs)does not play a part in the current tumor node metastasis staging.Negative lymph node(NLN)status is associated with the prognosis of colorectal cancer(CRC),but its clear role in N1c stage remains to be defined.AIM To evaluate the combination of TDs and NLNs as potential prognostic indicators in N1c CRC.METHODS We retrospectively identified 107 consecutive patients who had N1c CRC radically resected at China-Japan Friendship Hospital.The combination of TDs and NLNs was calculated by the formula NLNTD=NLN/(TD+1).Cutoff values of NLNs and NLNTD were determined using the R package“survminer”.Disease-free survival(DFS),overall survival(OS)and cancer-specific survival(CSS)were determined using the Kaplan-Meier method to assess the impact of NLNTD on prognosis.Results were compared using the log-rank test.RESULTS The median follow-up time was 63.17(45.33-81.37)months for DFS,with 33.64%(36/107)of patients experiencing recurrence during follow-up.Five-year DFS was 66.0%(57.3%-76.0%).There was no significant difference in prognosis between patients with>12 and≤12 NLNs(P=0.058)for DFS.Similar results were seen according to the number of TDs.The definition of NLNTD=NLN/(TD+1)with a cutoff value of 6 divided patients into two groups with different DFS(P=0.005).Five-year DFS for patients with NLNTD>6 was 73.5%(63.6%-85.0%),compared with 50.0%(35.7%-70.0%)for those with NLNTD≤6.These two groups had different prognosis without perineural invasion(P=0.012)or lymphovascular invasion(P=0.002)even neither(P=0.053).Similar results were seen for OS and CSS.CONCLUSION NLNTD could serve as important prognostic factor for outcomes in N1c CRC patients.These patients could be stratified for prognosis through NLNTD and the high-risk should be given more attention during treatment.展开更多
目的探讨“1+N”4C模式在糖尿病周围神经病变患者延续护理中的应用价值。方法选取2022年1月至10月在我科接受治疗的60例糖尿病周围神经病变患者,以随机数字表法将其分为对照组(30例,常规延续护理)和观察组(30例,“1+N”4C模式延续护理)...目的探讨“1+N”4C模式在糖尿病周围神经病变患者延续护理中的应用价值。方法选取2022年1月至10月在我科接受治疗的60例糖尿病周围神经病变患者,以随机数字表法将其分为对照组(30例,常规延续护理)和观察组(30例,“1+N”4C模式延续护理)。比较两组的干预效果。结果干预后,观察组的空腹血糖(FBG)、餐后2 h血糖(2 h PG)水平及糖化血红蛋白(HbA1c)均低于对照组(P<0.05)。观察组的健康教育知晓率高于对照组(P<0.05)。干预后,观察组的感觉神经传导速度(SNCV)、运动神经传导速度(MNCV)高于对照组(P<0.05)。干预后,观察组的生活质量综合评定问卷-74(GQOLI-74)各维度评分均高于对照组(P<0.05)。结论“1+N”4C模式用于糖尿病周围神经病变患者延续护理中能提高血糖控制效果和健康教育知晓率,改善神经传导速度,提升患者生活质量。展开更多
利用常规研究方法,对甜菜单体附加系M 14品系(B eta vu lg aris L.,VV+1C、2n=18+1)的生殖方式进行细胞学与胚胎学研究.结果表明:(1)甜菜单体附加系M 14的4代细胞学检查表明:染色体组分别为VV+1C、2n=18+1;VV+0、2n=18+0;VV+2C、2n=18+2...利用常规研究方法,对甜菜单体附加系M 14品系(B eta vu lg aris L.,VV+1C、2n=18+1)的生殖方式进行细胞学与胚胎学研究.结果表明:(1)甜菜单体附加系M 14的4代细胞学检查表明:染色体组分别为VV+1C、2n=18+1;VV+0、2n=18+0;VV+2C、2n=18+2;VVV+0、2n=27+0;VVV+1C、2n=27+1;VVV+2C、2n=27+2等,其中VV+1C、2n=18+1的植株传递率平均为96.7%,表现为稳定传递,具有二倍体孢子无融合生殖特性;其余各种分离植株的传递率总计为3.25%,有性生殖发生率较低.(2)胚胎学研究表明,二倍体孢子无融合生殖的胚珠中,珠孔处看不到花粉管,胚囊没有发生受精作用.2个助细胞提前退化,半数卵细胞的极性与正常卵细胞相反;卵与次生核不经受精而自发分裂,卵细胞自发分裂产生无性胚,次生核自发分裂产生核型胚乳,而且次生核自发分裂早于卵细胞分裂;有性生殖胚珠中,珠孔处可见多条花粉管,胚囊里见到精卵融合的图像.表明甜菜单体附加系M 14是以二倍体孢子无融合生殖为主要繁殖方式,有性生殖为次要敏殖方式的兼性无融合生殖体.展开更多
A systematic investigation of the microstructure of CrA1CxN1-x coatings as a function of carbon contents was conducted. Quaternary CrA1CxN1-x coatings were deposited on Si wafers by a hybrid coating system combining a...A systematic investigation of the microstructure of CrA1CxN1-x coatings as a function of carbon contents was conducted. Quaternary CrA1CxN1-x coatings were deposited on Si wafers by a hybrid coating system combining an arc-ion plating technique and a DC reactive magnetron sputtering technique using Cr and AI targets in the Ar/N2/CH4 gaseous mixture. The effect of carbon content on microstructure of CrA1C^N~ x coatings was investigated with instrumental analyses of X-ray diffraction, X-ray photoelectron, and high-resolution transmission electron microscopy. The results show that the carbon content of CrA1CxN1-x coatings linearly increases with increasing CH4/（CH4/N2） gas flow rate ratio. The surface roughness of the CrA1CxN1-x coating layer decreases with the increase of carbon content.展开更多
In a series of publications, the hypothesis of a special-type of endo-polyploidy, marked by 4-chromatid chromosomes (diplochromosomes), in the initiation of tumorigenesis has been presented from in vitro experiments. ...In a series of publications, the hypothesis of a special-type of endo-polyploidy, marked by 4-chromatid chromosomes (diplochromosomes), in the initiation of tumorigenesis has been presented from in vitro experiments. This review uses cellular happenings in benign pre-neoplasia to substantiate this idea, which appears to be linked to the wound-healing process of injured tissue. Rarer association between a wound healing process and a cancer occurrence has long been known. The wound healing multi-program-system involved a phase of tetraploidy that showed diplochromosomes. The hypothesis is that the inflammatory phase may not always be sufficient in getting rid of dead and damaged cells (by apoptosis and autophagy), such that cells with genomic damage (DNA breakage) may survive by genomic repair associated with change to diplochromosomal tetraploidy. In vitro data have shown division of these cells to be an orderly, mechanistic two-step, meiotic-like system, resulting in only two types of progeny cells: 4n/4C/G1 and 2n/2C/G1 pseudo-diploid cells with hyperplastic-like growth-morphology. In vivo damage to tissues can be from many sources for example, physical, toxic environment or from a disease as in Barrett’s esophagus (BE) with acid reflux into the esophagus. For this condition, it is acknowledged that damage of the esophagus lining is a pre-condition to hyperplastic lesions of pre-neoplasia. These initial lesions were from “diploid” propagating cells and, 4n cells with G2 genomic content (no mitosis) accumulated in these lesions before a change to dysplasia. Cell cycle kinetics put these 4n cells in G1, which with S-phase entry would lead to asymmetric tetraploid mitoses, characteristic for dysplastic lesions. This change in hyperplasia to dysplasia is the root-essential condition for a potential progression of pre-neoplasia to cancer. In BE the hyperplastic lesion showed increasing gains of cells with inactivated p53 and p16[ink4a] genes, which destroyed the retinoblastoma (Rb) protein-control over S-phase entry from G1. Rb-protein is a key controller of cycling advancement from G1 (also for normal cells), and is frequently inactivated in tumor cells. Thus in BE, 4n/4C/G1 cells with mutated p53 and p16[ink4a] genes gained cycling ability to tetraploid aneuploid cell cycles, which constituted the change from hyperplasia to dysplastic lesions. In general, such lesions have high predictive value for a cancerous change. Proliferation rates of pre-neoplasia and progression have been shown to be increased by a component of the wound healing program.展开更多
The geometries, bondings, and vibrational frequencies of C 2n H ( n =3-9) and C 2n -1 N( n =3-9) were investigated by means of density functional theory(DFT). The vertical excitation energies for th...The geometries, bondings, and vibrational frequencies of C 2n H ( n =3-9) and C 2n -1 N( n =3-9) were investigated by means of density functional theory(DFT). The vertical excitation energies for the X 2Π→ 2Π transitions of C 2n H( n =3-9) and for the X 2Σ→ 2Π and the X 2Π→ 2Π transitions of C 2n -1 N( n =3-9) have been calculated by the time-dependent density functional theory(TD-DFT) approach. On the basis of present calculations, the explicit expression for the wavelengths of the excitation energies in linear carbon chains is suggested, namely, λ 0=[1240 6A/(2+[KF(]3n+6-3n+3)](1-B e -Cn ), where A=3 24463, B=0 90742 , and C = 0 07862 for C 2n H, and A=2 94714, B=0 83929 , and C =0 08539 for C 2n -1 N. In consideration of a comparison of the theory with the experiment, both the expressions are modified as λ 1=0 92( λ 0+100) and λ 1= 0 95( λ 0+90) for C 2n H and C 2n -1 N, respectively. (1-B e -Cn ), where A=3 24463, B=0 90742 , and C = 0 07862 for C 2n H, and A=2 94714, B=0 83929 , and C =0 08539 for C 2n -1 N. In consideration of a comparison of the theory with the experiment, both the expressions are modified as λ 1=0 92( λ 0+100) and λ 1= 0 95( λ 0+90) for C 2n H and C 2n -1 N, respectively.展开更多
基金Supported by the National High Level Hospital Clinical Research Funding,No.2023-NHLHCRF-BQ-32 and No.2023-NHLHCRFYYPPLC-ZR-13the Elite Medical Professionals Project of China-Japan Friendship Hospital,No.ZRJY2024-GG01.
文摘BACKGROUND Lymphovascular invasion(LVI)and perineural invasion(PNI)are associated with decreased survival in colorectal cancer(CRC),but its significance in N1c stage remains to be clearly defined.AIM We retrospectively identified 107 consecutive patients who had CRC with N1c disease radically resected at our hospital.Tumors were reviewed for LVI and PNI by one pathologist blinded to the patients’outcomes.Disease-free survival(DFS),overall survival(OS)and cancer-specific survival(CSS)were determined using the Kaplan-Meier method,with LVI and PNI prognosis differences determined by multivariate analysis using the Cox multiple hazards model.Results were compared using log-rank test.The receiver operating characteristic(ROC)curve was used to evaluate the prognostic predictive ability.RESULTS The median follow-up time was 63.17(45.33-81.37)months for DFS,with 33.64%(36/107)of patients experiencing recurrence;21.5%of tumors were found to be LVI positive and 44.9%PNI positive.The 5-year DFS rate was greater for patients with LVI-negative tumors compared with LVI-positive tumors(74.0%vs 35.6%),and PNI was similar(82.5%vs 45.1%).On multivariate analysis,LVI[hazard ratio(HR)=3.368,95%confidence interval(CI):1.628-6.966,P=0.001]and PNI(HR=3.055,95%CI:1.478-6.313,P=0.002)were independent prognostic factors for DFS.All patients could be divided into three groups of patients with different prognosis according to LVI and PNI.The 5-year ROC curve for LVI,PNI and their combination prediction of DFS was 0.646,0.709 and 0.759,respectively.Similar results were seen for OS and CSS.CONCLUSION LVI and PNI could serve as independent prognostic factors of outcomes in N1c CRC patients.Patients with LVI or PNI should be given more attention during treatment.
基金Supported by the National High Level Hospital Clinical Research Funding,No.2023-NHLHCRF-BQ-32 and No.2023-NHLHCRFYYPPLC-ZR-13National Key Research and Development Program of China,No.2024YFE0198300Beijing Municipal Natural Science Foundation,No.7222316.
文摘BACKGROUND The number of tumor deposits(TDs)does not play a part in the current tumor node metastasis staging.Negative lymph node(NLN)status is associated with the prognosis of colorectal cancer(CRC),but its clear role in N1c stage remains to be defined.AIM To evaluate the combination of TDs and NLNs as potential prognostic indicators in N1c CRC.METHODS We retrospectively identified 107 consecutive patients who had N1c CRC radically resected at China-Japan Friendship Hospital.The combination of TDs and NLNs was calculated by the formula NLNTD=NLN/(TD+1).Cutoff values of NLNs and NLNTD were determined using the R package“survminer”.Disease-free survival(DFS),overall survival(OS)and cancer-specific survival(CSS)were determined using the Kaplan-Meier method to assess the impact of NLNTD on prognosis.Results were compared using the log-rank test.RESULTS The median follow-up time was 63.17(45.33-81.37)months for DFS,with 33.64%(36/107)of patients experiencing recurrence during follow-up.Five-year DFS was 66.0%(57.3%-76.0%).There was no significant difference in prognosis between patients with>12 and≤12 NLNs(P=0.058)for DFS.Similar results were seen according to the number of TDs.The definition of NLNTD=NLN/(TD+1)with a cutoff value of 6 divided patients into two groups with different DFS(P=0.005).Five-year DFS for patients with NLNTD>6 was 73.5%(63.6%-85.0%),compared with 50.0%(35.7%-70.0%)for those with NLNTD≤6.These two groups had different prognosis without perineural invasion(P=0.012)or lymphovascular invasion(P=0.002)even neither(P=0.053).Similar results were seen for OS and CSS.CONCLUSION NLNTD could serve as important prognostic factor for outcomes in N1c CRC patients.These patients could be stratified for prognosis through NLNTD and the high-risk should be given more attention during treatment.
文摘目的探讨“1+N”4C模式在糖尿病周围神经病变患者延续护理中的应用价值。方法选取2022年1月至10月在我科接受治疗的60例糖尿病周围神经病变患者,以随机数字表法将其分为对照组(30例,常规延续护理)和观察组(30例,“1+N”4C模式延续护理)。比较两组的干预效果。结果干预后,观察组的空腹血糖(FBG)、餐后2 h血糖(2 h PG)水平及糖化血红蛋白(HbA1c)均低于对照组(P<0.05)。观察组的健康教育知晓率高于对照组(P<0.05)。干预后,观察组的感觉神经传导速度(SNCV)、运动神经传导速度(MNCV)高于对照组(P<0.05)。干预后,观察组的生活质量综合评定问卷-74(GQOLI-74)各维度评分均高于对照组(P<0.05)。结论“1+N”4C模式用于糖尿病周围神经病变患者延续护理中能提高血糖控制效果和健康教育知晓率,改善神经传导速度,提升患者生活质量。
文摘利用常规研究方法,对甜菜单体附加系M 14品系(B eta vu lg aris L.,VV+1C、2n=18+1)的生殖方式进行细胞学与胚胎学研究.结果表明:(1)甜菜单体附加系M 14的4代细胞学检查表明:染色体组分别为VV+1C、2n=18+1;VV+0、2n=18+0;VV+2C、2n=18+2;VVV+0、2n=27+0;VVV+1C、2n=27+1;VVV+2C、2n=27+2等,其中VV+1C、2n=18+1的植株传递率平均为96.7%,表现为稳定传递,具有二倍体孢子无融合生殖特性;其余各种分离植株的传递率总计为3.25%,有性生殖发生率较低.(2)胚胎学研究表明,二倍体孢子无融合生殖的胚珠中,珠孔处看不到花粉管,胚囊没有发生受精作用.2个助细胞提前退化,半数卵细胞的极性与正常卵细胞相反;卵与次生核不经受精而自发分裂,卵细胞自发分裂产生无性胚,次生核自发分裂产生核型胚乳,而且次生核自发分裂早于卵细胞分裂;有性生殖胚珠中,珠孔处可见多条花粉管,胚囊里见到精卵融合的图像.表明甜菜单体附加系M 14是以二倍体孢子无融合生殖为主要繁殖方式,有性生殖为次要敏殖方式的兼性无融合生殖体.
基金Project supported by a grant from the Fundamental R&D Program for Core Technology of Materials funded by the Ministry of Knowledge Economy, KoreaProject (2010-0001-226) supported by NCRC(National Core Research Center) Program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology
文摘A systematic investigation of the microstructure of CrA1CxN1-x coatings as a function of carbon contents was conducted. Quaternary CrA1CxN1-x coatings were deposited on Si wafers by a hybrid coating system combining an arc-ion plating technique and a DC reactive magnetron sputtering technique using Cr and AI targets in the Ar/N2/CH4 gaseous mixture. The effect of carbon content on microstructure of CrA1C^N~ x coatings was investigated with instrumental analyses of X-ray diffraction, X-ray photoelectron, and high-resolution transmission electron microscopy. The results show that the carbon content of CrA1CxN1-x coatings linearly increases with increasing CH4/（CH4/N2） gas flow rate ratio. The surface roughness of the CrA1CxN1-x coating layer decreases with the increase of carbon content.
文摘In a series of publications, the hypothesis of a special-type of endo-polyploidy, marked by 4-chromatid chromosomes (diplochromosomes), in the initiation of tumorigenesis has been presented from in vitro experiments. This review uses cellular happenings in benign pre-neoplasia to substantiate this idea, which appears to be linked to the wound-healing process of injured tissue. Rarer association between a wound healing process and a cancer occurrence has long been known. The wound healing multi-program-system involved a phase of tetraploidy that showed diplochromosomes. The hypothesis is that the inflammatory phase may not always be sufficient in getting rid of dead and damaged cells (by apoptosis and autophagy), such that cells with genomic damage (DNA breakage) may survive by genomic repair associated with change to diplochromosomal tetraploidy. In vitro data have shown division of these cells to be an orderly, mechanistic two-step, meiotic-like system, resulting in only two types of progeny cells: 4n/4C/G1 and 2n/2C/G1 pseudo-diploid cells with hyperplastic-like growth-morphology. In vivo damage to tissues can be from many sources for example, physical, toxic environment or from a disease as in Barrett’s esophagus (BE) with acid reflux into the esophagus. For this condition, it is acknowledged that damage of the esophagus lining is a pre-condition to hyperplastic lesions of pre-neoplasia. These initial lesions were from “diploid” propagating cells and, 4n cells with G2 genomic content (no mitosis) accumulated in these lesions before a change to dysplasia. Cell cycle kinetics put these 4n cells in G1, which with S-phase entry would lead to asymmetric tetraploid mitoses, characteristic for dysplastic lesions. This change in hyperplasia to dysplasia is the root-essential condition for a potential progression of pre-neoplasia to cancer. In BE the hyperplastic lesion showed increasing gains of cells with inactivated p53 and p16[ink4a] genes, which destroyed the retinoblastoma (Rb) protein-control over S-phase entry from G1. Rb-protein is a key controller of cycling advancement from G1 (also for normal cells), and is frequently inactivated in tumor cells. Thus in BE, 4n/4C/G1 cells with mutated p53 and p16[ink4a] genes gained cycling ability to tetraploid aneuploid cell cycles, which constituted the change from hyperplasia to dysplastic lesions. In general, such lesions have high predictive value for a cancerous change. Proliferation rates of pre-neoplasia and progression have been shown to be increased by a component of the wound healing program.
基金Supported by the National Natural Science Foundation of China( Nos.2 0 1730 4 2 ,2 0 2 330 2 0 and2 0 0 2 10 0 2 ) and Trans-Century Training Programm e Foundation of the Educational Ministry of China
文摘The geometries, bondings, and vibrational frequencies of C 2n H ( n =3-9) and C 2n -1 N( n =3-9) were investigated by means of density functional theory(DFT). The vertical excitation energies for the X 2Π→ 2Π transitions of C 2n H( n =3-9) and for the X 2Σ→ 2Π and the X 2Π→ 2Π transitions of C 2n -1 N( n =3-9) have been calculated by the time-dependent density functional theory(TD-DFT) approach. On the basis of present calculations, the explicit expression for the wavelengths of the excitation energies in linear carbon chains is suggested, namely, λ 0=[1240 6A/(2+[KF(]3n+6-3n+3)](1-B e -Cn ), where A=3 24463, B=0 90742 , and C = 0 07862 for C 2n H, and A=2 94714, B=0 83929 , and C =0 08539 for C 2n -1 N. In consideration of a comparison of the theory with the experiment, both the expressions are modified as λ 1=0 92( λ 0+100) and λ 1= 0 95( λ 0+90) for C 2n H and C 2n -1 N, respectively. (1-B e -Cn ), where A=3 24463, B=0 90742 , and C = 0 07862 for C 2n H, and A=2 94714, B=0 83929 , and C =0 08539 for C 2n -1 N. In consideration of a comparison of the theory with the experiment, both the expressions are modified as λ 1=0 92( λ 0+100) and λ 1= 0 95( λ 0+90) for C 2n H and C 2n -1 N, respectively.
