In recent years， as the incidence of ulcerative colitis （UC） is growing， intestinal mucosal injury has garnered increasing attention， and it is characterized by high recurrence， risk of inflammation-cancer transformation， and difficulty in repair. Intestinal mucosal injury in UC is centered on persistent inflammation and barrier dysfunction， with its pathological mechanisms involving endoplasmic reticulum stress （ERS）-mediated changes such as abnormal apoptosis， abnormal autophagy， and inflammatory responses. ERS induces apoptosis of intestinal epithelial cells， disrupts tight junction proteins， and exacerbates inflammatory responses through pathways such as protein kinase R-like endoplasmic reticulum kinase （PERK）， inositol-requiring enzyme 1 alpha （IRE1α）， and activating transcription factor 6 （ATF6）， ultimately causing intestinal mucosal injury. Traditional Chinese medicine （TCM） has a long history of research on UC. The theory of sores depending on spleen-earth holds that spleen deficiency is the fundamental cause of UC， while pathological products such as dampness-turbidity and blood stasis are the secondary manifestations. Dysfunction of the spleen-earth leads to insufficient production and transformation of Qi and blood， malnutrition of the intestinal mucosa， and invasion of external pathogens. In the active phase of UC， spleen deficiency is often accompanied by excessive pathogenic factors such as dampness-heat and heat-toxin， leading to acute intestinal mucosal damage. In the remission phase， however， it is mainly characterized by spleen deficiency and healthy Qi deficiency， accompanied by residual pathogens， resulting in weak intestinal mucosal repair. Studies have shown that the endoplasmic reticulum， as a key site for protein synthesis and folding， has functions highly similar to the TCM concept of the spleen governing transportation and transformation. From a TCM perspective， the endoplasmic reticulum can be regarded as the carrier of spleen transportation， and ERS is a microcosmic manifestation of spleen dysfunction， leading to intestinal mucosal injury. ERS impairs the structure and function of the endoplasmic reticulum， induces the generation of abnormal Qi， and triggers pathological changes， making inflammation difficult to be reduced and causing the aggravation of ERS， forming a vicious cycle of spleen deficiency-pathological products-intestinal injury. TCM has unique advantages in regulating ERS to prevent and treat intestinal mucosal injury. According to the theory of sores depending on spleen-earth and the modern medical understanding of ERS， this paper delves into the TCM and Western medicine pathogenesis of intestinal mucosal injury in UC. Furthermore， this paper discusses the roles of TCM active components and compound formulas in reducing intestinal mucosal injury in UC by regulating ERS under the guidance of the treatment principles of invigorating the spleen and replenishing Qi as the key and dispelling dampness and removing blood stasis as the supplementation， aiming to provide new ideas and methods for the prevention and treatment of UC.

Objective:To analyse the differences of related genes between serum alpha-fetoprotein (AFP) positive gastric cancer and AFP negative gastric cancer, and the relationship between related genes and prognosis of serum AFP positive gastric cancer.Methods:A total of 1 144 gastric cancer patients undergoing surgery at the 940th Hospital , Joint Logistic Support Force, People's Liberation Army from Jan 2013 to Dec 2018 were retrospectively analyzed. Of them, 47 cases were of AFP positive gastric cancer, and 47 serum AFP negative case were obtained by proper matching method.Results:Forty-seven patients with serum AFP positive gastric cancer, accounting for 4.1% of all gastric cancer patients during the same period. The prognosis of serum AFP negative gastric cancer is better than that of serum AFP positive gastric cancer. The 1-, 3- and 5-year cumulative survival rates were 95.6% vs. 63.8%, 48.9% vs. 23.4% and 26.7% vs. 14.9%, respectively. There were statistical differences in the immunohistochemistry of AFP, HER2, VEGF, GPC3, SALL4, P53 and Ki67 between the two groups ( χ2=67.758, P<0.001; χ2=4.004, P=0.044; χ2=19.299, P<0.001; χ2=5.232, P=0.022; χ2=6.359, P=0.012; χ2=6.224, P=0.013; χ2=5.232, P=0.022). The more co-positive expressions of AFP, GPC3, VEGF and SALL4, the more likely they were to affect pTNM stage, vascular invasion and liver metastasis ( χ2=5.328, P=0.021; P=0.013; χ2=5.887, P=0.015; χ2=3.923, P=0.048). Univariate and multivariate survival analysis of serum AFP positive gastric cancer showed:AFP, GPC3, VEGF and SALL4 were risk factors for AFP positive gastric cancer ( HR=3.700, P=0.036; HR=4.237, P=0.003; HR=3.916, P=0.004; HR=3.412, P=0.001). Conclusions:Serum AFP positive gastric cancer is a rare and highly invasive special type of gastric cancer. AFP, GPC3, VEGF and SALL4 are overexpressed in serum AFP positive gastric cancer, which is correlated with tumor stage, vascular invasion and liver metastasis. The final diagnosis of serum AFP positive gastric cancer still needs immunohistochemical examination. Preoperative serum AFP level is an important basis for AFP positive gastric cancer screening and AFP immunohistochemical examination.

Ganoderic triterpenoids (GTs) are the primary bioactive constituents of the Basidiomycotina fungus,

Objective:To investigate the effect of mechano-growth factor（MGF）on osteoclast activity and its mechanism.Methods:The RAW264.7 precursor osteoclast cell line was cultured with 25 ng/ml macrophage-colony stimulating factor（M-CSF）and 30 ng/ml receptor activator of NF-κB ligand（RANKL），and identified by tartrate resistant acid phosphatase（TRAP）staining after 7 days of culture. Western blot anslysis was used to determine the effect of 45 ng/ml MGF on the phosphoinositide-3-kinase/protein kinase B（PI3K/AKT）signaling pathway in separated osteoclasts，including levels of AKT，phosphorylation（p）-AKT，lactation mammalian target of rapamycin（mTOR），p-mTOR and TRAP at 0，4，8 and 12 hours. Real-time fluorescence quantitative PCR was used to expressions of TRAP in osteoclasts at 0，4，8 and 12 hours. The PI3K/Akt phosphorylation inhibitor LY294002（20 μmol/L）combined with MGF（45 ng/ml）was used to act on osteoclasts，and expression levels of Akt，p-Akt，mTOR，p-mTOR and TRAP were detected by Western blot at 0，4，8 and 12 hours.Results:After culturing RAW264.7 cells with M-CSF and RANKL for 7 days，a large number of osteoclasts with positive TRAP staining can be obtained. Western blot analysis showed expression levels of Akt and mTOR did not change significantly over time（ P>0.05），expression levels of p-Akt and p-mTOR increased continuously from（2.18±0.34）pg/ml and（0.83±0.10）pg/ml at 0 hour to（3.86±0.36）pg/ml and（1.56±0.19）pg/ml at 12 hours（ P<0.05），and expression level of TRAP decreased significantly over time，from（5.66±0.47）pg/ml at 0 hour to（3.76±0.38）pg/ml at 12 hours（ P<0.05）. Real-time fluorescence quantitative PCR analysis of expression of TRAP in osteoclasts showed that MGF inhibited the expression of TRAP in osteoclasts，which decreased from 1.02±0.06 at 0 hour to 0.53±0.11 at 12 hours（ P<0.05）. After acting LY294002 combined with MGF on osteoclasts，Western blot analysis showed expression levels of Akt and mTOR did not change significantly over time（ P>0.05），expression levels of p-AKT and p-mTOR decreased significantly from（3.28±0.18）pg/ml and（3.29±0.22）pg/ml at 0 hour to（2.06±0.34）pg/ml and（2.04±0.20）pg/ml at 12 hours（ P<0.05），and expression level of TRAP had no significant difference over time（ P>0.05）. Conclusions:MGF inhibits osteoclast activity by inhibiting the expression of TRAP in osteoclasts through PI3K/Akt signaling pathway. LY294002 inhibits the expression of PI3K/Akt signaling pathway in osteoclasts，further verifying the mechanism of MGF inhibiting osteoclast activity，and this finding puts forward new ideas for clinical prevention and treatment of osteoporosis.

Objective To explore the effect of focused nursing model on negative emotions and subjective well-being of lung cancer patients. Methods Eighty-six lung cancer patients hospitalized from November 2014 to November 2016 in our hospital were divided into two groups according to the order of admission in equal number. The control group was treated with routine care, and the observation group was with focused nursing model. The two groups were compared in terms of anxiety by SAS, depression by SDS, subjective well-being. Results The scores by SAS and SDS in the observation group were lower than those in the control group (P<0.05). The levels of objective support, subjective support, self-evaluation and subjective well-being index of the observation group were higher than the control group (P <0.05). Conclusion Focused nursing model can effectively relieve negative emotions, improve subjective well-being of lung cancer patients, worthy of clinical promotion.

PurposeTo explore and compare subtracted and unsubtracted volume rendering process on DSA apparatus in the diagnosis and treatment of intracranial aneurysms, and to provide a better reconstruction in clinic.Materials and Methods Twenty-seven patients with subarachnoid hemorrhage (SAH) underwent rotational cerebral angiography and 19 cases with embolization treatment underwent rotational cerebral angiography follow-up. 3D volume unsubtracted reconstruction and subtracted reconstructions were used respectively. Two sets of 3D volume reconstruction images were observed and analyzed by two neuroradiologists to compare the detection rate, image quality and post-embolization follow up.Results Thirty-three intracranial aneurysms were identiifed in 27 cases with SAH underwent three-dimensional digital angiography (3D-DA). False positives were found in 2 cases. 3D-DSA detected 33 intracranial aneurysms with no false positive case. There was no statistical signiifcance in intracranial aneurysms detection rate (χ2=1.943,P>0.05). There was no statistical significance in image quality of two reconstruction methods (Z=-1.445,P>0.05). In 19 cases with embolization treatment underwent the follow-up of rotational cerebral angiography, 3D-DA detected 3 cases with aneurysm remnants, while 3D-DSA detected 10. There was statistical signiifcance between 3D-DA and 3D-DSA when detecting aneurysm remnant (χ2=5.729,P<0.05).Conclusion Aneurysms can be well detected with better image quality by 3D-DSA and 3D-DA in the diagnosis and treatment of intracranial aneurysms. 3D-DSA can display more information on tiny vessels, and is better in detecting aneurysm remnants.

Objective To investigate the role of epigallocatechin gallate ( EGCG) in reversing the CpG island methylation of Rad23b and Ddit3 gene promoter and its mRNA expression induced by 0?5 Gy X-rays. Methods Thirty BALB/c male mice were randomly divided into 6 groups: control group, irradiation group, low/high dose of EGCG group, low/high dose of EGCG with irradiation group. For the irradiation group, mice were fractionally exposed with 6 MV X-rays for 10 d (0?05 Gy/d × 10 d). 2 hours after the final irradiation, all mice were killed and such tissues as blood, kidney, liver, spleen, brain, and lung were collected. Methylation and expression levels of Rad23b and Ddit3 were measured by bisulfate sequencing primers ( BSP) and Real-time PCR, respectively. Results Compare to the control group, Rad23b was hypermethylated in PBMC, liver, spleen, brain and lung (t= -20?19, -14?80, -12?05,-28?42, -12?58, P<0?05) in the irradiation group. Meanwhile, its mRNA expression level was down-regulated in PBMC, liver, brain and lung (t=25?25, 17?43, 11?53, 22?85, P<0?05). Similarly, a significant hypermethylation change of Ddit3 was observed in PBMC, liver and lung after irradiation ( t=-52?89, -20?31, -3?85, P<0?05) so that the mRNA expression of Ddit3 decreased in PBMC and liver ( t = 11?89, 16?52, P < 0?05 ). Compared to the irradiation group, EGCG with different concentrations of 10, 20 mg/kg significantly reduced the methylation level of Rad23b and Ddit3 ( t =-13?39-7?99, P<0?05), and induced re-expression of mRNA (t= -34?02 - -2?89, P<0?05). This change was more notable in the irradiation group with the high dose of EGCG. Conclusions As a natural drug, EGCG may play an important role in affecting DNA methylation and hence protects DNA from radiation damage.

OBJECTIVETo study the methylation changes in promoter CpG islands induced by low-dose X-ray radiation (LDR).

METHODSTwenty male BALB/c mice were randomly divided into control and fractionated radiation group exposed to 6 MV X-ray for 10 days (0.05 Gy/day). All the mice were sacrificed 2 h after the last radiation on day 10, and blood samples were collected for detecting DNA methylation changes using Roche-NimbleGen mouse DNA methylation 3×720K Promoter Plus CpG Island Array. MeDIP-qPCR was used to further validate the methylation status of specific genes.

RESULTSA total of 811 genes were found to show specific hypermethylation in fractional radiation group as compared with the control group, involving almost all the main biological processes by GO analysis. Eight candidate genes (Rad23b, Tdg, Ccnd1, Ddit3, Llgl1, Rasl11a, Tbx2, and Slc6a15) were confirmed to be hypermethylated in LDR samples by MeDIP-qPCR, consistent with the results of the methylation chip study.

CONCLUSIONLDR induces promoter hypermethylation on specific genes, which may contribute to radiation-induced pathogenesis.

Animals ; CpG Islands ; radiation effects ; DNA Methylation ; Dose-Response Relationship, Radiation ; Genome ; Male ; Mice ; Mice, Inbred BALB C ; X-Rays

Objective To study the methylation changes in promoter CpG islands induced by low-dose X-ray radiation (LDR). Methods Twenty male BALB/c mice were randomly divided into control and fractionated radiation group exposed to 6 MV X-ray for 10 days (0.05 Gy/day). All the mice were sacrificed 2 h after the last radiation on day 10, and blood samples were collected for detecting DNA methylation changes using Roche-NimbleGen mouse DNA methylation 3 × 720K Promoter Plus CpG Island Array. MeDIP-qPCR was used to further validate the methylation status of specific genes. Results A total of 811 genes were found to show specific hypermethylation in fractional radiation group as compared with the control group, involving almost all the main biological processes by GO analysis. Eight candidate genes (Rad23b, Tdg, Ccnd1, Ddit3, Llgl1, Rasl11a, Tbx2, and Slc6a15) were confirmed to be hypermethylated in LDR samples by MeDIP-qPCR, consistent with the results of the methylation chip study. Conclusion LDR induces promoter hypermethylation on specific genes, which may contribute to radiation-induced pathogenesis.

Objective To study the methylation changes in promoter CpG islands induced by low-dose X-ray radiation (LDR). Methods Twenty male BALB/c mice were randomly divided into control and fractionated radiation group exposed to 6 MV X-ray for 10 days (0.05 Gy/day). All the mice were sacrificed 2 h after the last radiation on day 10, and blood samples were collected for detecting DNA methylation changes using Roche-NimbleGen mouse DNA methylation 3 × 720K Promoter Plus CpG Island Array. MeDIP-qPCR was used to further validate the methylation status of specific genes. Results A total of 811 genes were found to show specific hypermethylation in fractional radiation group as compared with the control group, involving almost all the main biological processes by GO analysis. Eight candidate genes (Rad23b, Tdg, Ccnd1, Ddit3, Llgl1, Rasl11a, Tbx2, and Slc6a15) were confirmed to be hypermethylated in LDR samples by MeDIP-qPCR, consistent with the results of the methylation chip study. Conclusion LDR induces promoter hypermethylation on specific genes, which may contribute to radiation-induced pathogenesis.