目的:探讨腹腔镜结肠癌根治术对老年结肠癌患者胃肠激素、免疫功能及炎症因子的影响。方法:选取2016年1月~2019年3月我院肿瘤外科收治的的老年结肠癌患者142例,依据手术方式分为观察组(n=71)和对照组(n=71)。对照组采用开腹结肠癌根治...目的:探讨腹腔镜结肠癌根治术对老年结肠癌患者胃肠激素、免疫功能及炎症因子的影响。方法:选取2016年1月~2019年3月我院肿瘤外科收治的的老年结肠癌患者142例,依据手术方式分为观察组(n=71)和对照组(n=71)。对照组采用开腹结肠癌根治术治疗,观察组采用腹腔镜结肠癌根治术治疗。观察两组患者的疗效及术后并发症情况,比较其术前、术后胃泌素(GAS)、胃动素(MTL)、抑胃肽(GIP)、免疫功能指标及IL-6、IL-8、TNF-α及C反应蛋白(CRP)水平变化。结果:观察组术中出血量、手术时间、手术切口长度、术后的住院天数、镇痛时间、排气时间、引流量及下床活动时间均低于对照组(P<0.05)。两组患者术后并发症发生率差异无统计学意义(P>0.05)。两组患者术后GAS、MTL及GIP水平均低于术前(P<0.05),而观察组术后GAS[(83.20±8.42)vs(72.80±7.38)μmol/L]、MTL[(142.70±15.30)vs(117.53±12.36)ng/L]及GIP[(124.62±13.85)vs(101.40±11.18)pg/ml]水平均高于对照组(P<0.05)。术后观察组CD3+(63.74±9.52 vs 56.72±8.30)、CD4+(37.85±2.06 vs 33.40±1.93)及CD4+/CD8+(1.25±0.14 vs 1.03±0.11)均高于对照组(P<0.05)。两组患者术后IL-6、IL-8、TNF-α及CRP水平均高于术前(P<0.05)。观察组术后IL-6[(22.64±13.50)vs(33.62±16.70)μg/L]、IL-8[(18.62±5.52)vs(26.37±7.45)μg/L]、TNF-α[(67.84±12.60)vs(76.26±15.20)μg/L]及CRP[(21.38±8.17)vs(34.70±13.50)mg/L]水平均低于对照组(P<0.05)。结论:腹腔镜结肠癌根治术可促进老年结肠癌患者术后胃肠道恢复,炎症反应程度较轻且免疫功能影响较小,具有临床应用价值。展开更多
The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, K...The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, KRAS, TGFBR2, and TP53, whose mutations are frequently found in human colorectal cancers. Among them, the p53 mutation is found in ~60% of colorectal cancers, and a majority of mutations are missense-type at ‘hot spots’, suggesting an oncogenic role of mutant p53 by ‘gain-of-function’ mechanisms. Mouse model studies have shown that one of these missense-type mutations, p53 R270H (corresponding to human R273H), causes submucosal invasion of intestinal tumors, while the loss of wild-type p53 has a limited effect on the invasion process. Furthermore, the same mutant p53 promotes metastasis when combined with Kras activation and TGF-β suppression. Importantly, either missense-type p53 mutation or loss of wild-type p53 induces NF-κB activation by a variety of mechanisms, such as increasing promoter accessibility by chromatin remodeling, which may contribute to progression to epithelial–mesenchymal transition. These results indicate that missense-type p53 mutations together with loss of wild-type p53 accelerate the late stage of colorectal cancer progression through the activation of both oncogenic and inflammatory pathways. Accordingly, the suppression of the mutant p53 function via the inhibition of nuclear accumulation is expected to be an effective strategy against malignant progression of colorectal cancer.展开更多
Sleep disorders have become a global issue,and discovering their causes and consequences are the focus of many research endeavors.An estimated 70 million Americans suffer from some form of sleep disorder.Certain sleep...Sleep disorders have become a global issue,and discovering their causes and consequences are the focus of many research endeavors.An estimated 70 million Americans suffer from some form of sleep disorder.Certain sleep disorders have been shown to cause neurocognitive impairment such as decreased cognitive ability,slower response times and performance detriments.Recent research suggests that individuals with sleep abnormalities are also at greater risk of serious adverse health,economic consequences,and most importantly increased all-cause mortality.Several research studies support the associations among sleep,immune function and inflammation.Here,we review the current research linking sleep,immune function,and gastrointestinal diseases and discuss the interdependent relationship between sleep and these gastrointestinal disorders.Different physiologic processes including immune system and inflammatory cytokines help regulate the sleep.The inflammatory cytokines such as tumor necrosis factor,interleukin-1(IL-1),and IL-6 have been shown to be a significant contributor of sleep disturbances.On the other hand,sleep disturbances such as sleep deprivation have been shown to up regulate these inflammatory cytokines.Alterations in these cytokine levels have been demonstrated in certain gastrointestinal diseases such as inflammatory bowel disease,gastro-esophageal reflux,liver disorders and colorectal cancer.In turn,abnormal sleep brought on by these diseases is shown to contribute to the severity of these same gastrointestinal diseases.Knowledge of these relationships will allow gastroenterologists a great opportunity to enhance the care of their patients.展开更多
文摘目的:探讨腹腔镜结肠癌根治术对老年结肠癌患者胃肠激素、免疫功能及炎症因子的影响。方法:选取2016年1月~2019年3月我院肿瘤外科收治的的老年结肠癌患者142例,依据手术方式分为观察组(n=71)和对照组(n=71)。对照组采用开腹结肠癌根治术治疗,观察组采用腹腔镜结肠癌根治术治疗。观察两组患者的疗效及术后并发症情况,比较其术前、术后胃泌素(GAS)、胃动素(MTL)、抑胃肽(GIP)、免疫功能指标及IL-6、IL-8、TNF-α及C反应蛋白(CRP)水平变化。结果:观察组术中出血量、手术时间、手术切口长度、术后的住院天数、镇痛时间、排气时间、引流量及下床活动时间均低于对照组(P<0.05)。两组患者术后并发症发生率差异无统计学意义(P>0.05)。两组患者术后GAS、MTL及GIP水平均低于术前(P<0.05),而观察组术后GAS[(83.20±8.42)vs(72.80±7.38)μmol/L]、MTL[(142.70±15.30)vs(117.53±12.36)ng/L]及GIP[(124.62±13.85)vs(101.40±11.18)pg/ml]水平均高于对照组(P<0.05)。术后观察组CD3+(63.74±9.52 vs 56.72±8.30)、CD4+(37.85±2.06 vs 33.40±1.93)及CD4+/CD8+(1.25±0.14 vs 1.03±0.11)均高于对照组(P<0.05)。两组患者术后IL-6、IL-8、TNF-α及CRP水平均高于术前(P<0.05)。观察组术后IL-6[(22.64±13.50)vs(33.62±16.70)μg/L]、IL-8[(18.62±5.52)vs(26.37±7.45)μg/L]、TNF-α[(67.84±12.60)vs(76.26±15.20)μg/L]及CRP[(21.38±8.17)vs(34.70±13.50)mg/L]水平均低于对照组(P<0.05)。结论:腹腔镜结肠癌根治术可促进老年结肠癌患者术后胃肠道恢复,炎症反应程度较轻且免疫功能影响较小,具有临床应用价值。
文摘The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, KRAS, TGFBR2, and TP53, whose mutations are frequently found in human colorectal cancers. Among them, the p53 mutation is found in ~60% of colorectal cancers, and a majority of mutations are missense-type at ‘hot spots’, suggesting an oncogenic role of mutant p53 by ‘gain-of-function’ mechanisms. Mouse model studies have shown that one of these missense-type mutations, p53 R270H (corresponding to human R273H), causes submucosal invasion of intestinal tumors, while the loss of wild-type p53 has a limited effect on the invasion process. Furthermore, the same mutant p53 promotes metastasis when combined with Kras activation and TGF-β suppression. Importantly, either missense-type p53 mutation or loss of wild-type p53 induces NF-κB activation by a variety of mechanisms, such as increasing promoter accessibility by chromatin remodeling, which may contribute to progression to epithelial–mesenchymal transition. These results indicate that missense-type p53 mutations together with loss of wild-type p53 accelerate the late stage of colorectal cancer progression through the activation of both oncogenic and inflammatory pathways. Accordingly, the suppression of the mutant p53 function via the inhibition of nuclear accumulation is expected to be an effective strategy against malignant progression of colorectal cancer.
文摘Sleep disorders have become a global issue,and discovering their causes and consequences are the focus of many research endeavors.An estimated 70 million Americans suffer from some form of sleep disorder.Certain sleep disorders have been shown to cause neurocognitive impairment such as decreased cognitive ability,slower response times and performance detriments.Recent research suggests that individuals with sleep abnormalities are also at greater risk of serious adverse health,economic consequences,and most importantly increased all-cause mortality.Several research studies support the associations among sleep,immune function and inflammation.Here,we review the current research linking sleep,immune function,and gastrointestinal diseases and discuss the interdependent relationship between sleep and these gastrointestinal disorders.Different physiologic processes including immune system and inflammatory cytokines help regulate the sleep.The inflammatory cytokines such as tumor necrosis factor,interleukin-1(IL-1),and IL-6 have been shown to be a significant contributor of sleep disturbances.On the other hand,sleep disturbances such as sleep deprivation have been shown to up regulate these inflammatory cytokines.Alterations in these cytokine levels have been demonstrated in certain gastrointestinal diseases such as inflammatory bowel disease,gastro-esophageal reflux,liver disorders and colorectal cancer.In turn,abnormal sleep brought on by these diseases is shown to contribute to the severity of these same gastrointestinal diseases.Knowledge of these relationships will allow gastroenterologists a great opportunity to enhance the care of their patients.
