Angiogenesis plays a vital role in carcinogenesis and development of colorectal cancer. Treatment targeting VEGF signaling pathway acquires important survival prolong for advanced colorectal cancer patients. For advanced colorectal cancer patients,bevacizumab could furtherly prolongs survival time in the setting of first line,second line and continuing therapy after first-progression therapy combined with chemothe-rapy. Aflibercept used in combination with irinotecan-containing regimen improves the survival of advanced colorectal cancer patients in second-line setting. Regorafenib also improves the survival of advanced colorectal cancer patients who have progressed after all line treatment. Considering these suivival benefit and their favora-ble safety,anti-angiogenic agents should be taken into all lines of therapy in the management of advanced colo-rectal cancer.

Objective To improve differential diagnosis between acute disseminated encephalomyelitis ( ADEM) and classical multiple sclerosis ( CMS).Methods All 20 cases of ADEM and 24 cases of CMS were examined.Their epidemiological and clinical findings,laboratory features and magnetic resonance imaging ( MRI) data were analyzed using x2 test for categorical variables,Wilcoxon Rank-Sum tests for continuous variables.Results ADEM and CMS showed no sex predominance.Patients with ADEM ((27 ±15) years) were younger than CMS ((37 ±13) years,Z= -2.218,P =0.027).The following findings were more commonly seen in ADEM compared with CMS:predemyelinating infectious disease (75% vs 4%,x2 =23.652,P = 0.000),fever (65% vs 4%,x2 =18.609,P = 0.000),meningeal irritation sign (40% vs 0,x2 = 9.189,P =0.002),seizure (25% vs 0,x2 =4.514,P = 0.034),and encephalopathy.ADEM patients were more likely to present with blood leucocytosis ( (11.9 ± 5.8) ×109/L vs (8.0±3.2) ×109/L,Z= -2.030,P=0.042),high C-reactive protein (2.74 mg/L vs 0.49 mg/L,Z = - 3.028,P = 0.002),increased erythrocyte sedimentation rate (11.00 mm/h vs 7.00 mm/h,Z= -2.406,P =0.016),and cerebrospinal fluid leucocytosis (9 × 106/L vs 2×106/L,Z =- 2.781,P = 0.005).There were no differences in cerebrospinal fluid protein and oligoclonal band between the two groups.The following MRI lesions were more commonly seen in ADEM patients:cortical gray matter lesions (14/20,x2=15.213,P=0.000),basal ganglia gray matter lesions (14/20,x2 =8.910,P = 0.003),and brainstem lesions ( 14/20,x2 = 5.867,P = 0.015).In contrast,lesions in subcortical white matter (21/24,x2 = 17.628,P =0.000),periventricular area (21/24,x2 =15.213,P=0.000) and corpus callosum ( 14/24,x2 = 8.640,P = 0.003 ) were more common in the MRI image of CMS patients.The lesions in spinal cord were usually centrally distributed in ADEM (83% ),while peripherally in CMS (85%,x2 = 11.542,P = 0.001).The lesions had poorly defined margins in ADEM (95%),but well defined margins in CMS (75%,x2 =21.787,P = 0.000).Conclusion There are differences in epidemiological and clinical findings,laboratory features and MRI appearances between ADEM and CMS.

Objective To discuss the diagnosis and treatment of cerebral sparganosis. Methods To summary four cases of cerebral sparganosis, focusing on the clinical course and imaging findings, with the goal of better diagnostic skills. Results All 4 cases had some kind of misdiagnosis and improvement after surgery or parasiticidal pharmacotherapy. Cerebral MRI and CT scans revealed relatively extensive white matter degeneration and focal enhancements. Subsequent scans showed changes in shape and location of the enhanced foci, indicating the migration of sparganum. Pathologic findings of 3 patients who had undergone surgery showed granuloma and sparganum. Conclusions Cerebral sparganosis has relatively special manifestions on imaging, which are of diagnostic value. The spaganum should be as completely removed as possible during surgery.

Objective To investigate the expression of Notch1,Delta-like ligand 4 (DLL4),hairy and enhancer of split-1 (HES-1),microvessel density (MVD),lymphatic vessel density (MLD) in gastric carcinoma,so as to discuss their roles in the development of gastric carcinoma.Methods Gastric carcinoma,paracancer tissues which was apart from the edge of cancer tissue ＞ 60 mm obtained during operation and normal gastric mucosa obtained during gastroscopy were used as controls.All specimens were made tissue microarray.The expressions of Notchl,DLL4,HES-1 were detected by immunohistochemistry.Immunohistochenical double taining was used to detect MVD and MLD.The relationships between Notch1,DLL4,HES-1 expression and angiogenesis,lymphangiogenesis and their significances were analyzed.Results The positive rate of Notch1 in gastric carcinoma was 48.30％,significantly higher than that of paracancerous (25.00％,x2 =6.38,P ＜ 0.05) and control group (16.67％,x2 =10.18,P ＜0.05).The differences of the positive rate of DLL4 in gastric carcinoma (55.94％),paracancerous (45.70％) and control group (56.67％) were not significant (x2 =1.18,P ＞0.05 ; x2 =0.005,P ＞ 0.05).The differences of the positive rate of HES-1 in gastric carcinoma (36.64％),paracancerous (34.40％) and control group (33.33％) were not significant (x2 =0.05,P ＞ 0.05 ;,x2 =0.11,P ＞ 0.05).The mean of MVD in gastric carcinoma group was 28.84 ± 14.17,which was significantly higher than that in paracancerous group (17.02 ±8.54,t =4.03,P＜0.05) and control group (16.69 ±7.21,t =5.01,P＜0.05).The mean of MLD in gastric carcinoma group was 8.55 ±4.98,which was significantly higher than that in paracancerous group (4.05 ± 2.48,t =9.30,P ＜ 0.05) and control group (3.99 ± 1.56,t =10.32,P ＜ 0.05).The expression of DLL4 was correlated with MVD (t =2.77,P ＜ 0.05),but wasn't correlated with MLD (t =1.89,P ＞0.05).There were no correlations between the expression of Notch1,HES-1 and tissues MVD,MLD (P ＞0.05).Conclusion Notch1 plays important roles in the development of gastric carcinoma.There are many angiogenesis and lymphangiogenesis in gastric carcinoma.The expression of DLL4 in gastric carcinoma has certain effect in the formation of microvessel.

Objective To explore the role of the polymorphism of HLA-DRB1/DPB1 in patients with multiple scle-rosis (MS) and optica neuromyelitis (NMO). Methods Fifty-three patients with MS, 30 patients with NMO and 93 normal controls were enrolled in the present study. The HLA-DRB1/DPB1 gene polymorphism and allele frequencies were deter-mined by sequencing-based typing. All the subjects were Southern Han Chinese and were born in Southern China. Re-sults The frequencies of DPB1*0501 were higher in NMO patients than in controls, P=0.001, P (corrected)=0.022. The frequencies of DRB1*1602 DPB1*0501 haplotype were higher in NMO patients than in MS patients, P<0.001,P (cor-rected)=0.040. Conclusions There is significant difference in HLA-DRB1/DPB1 gene polymorphism between MS and NMO patients in a Southern Han Chinese population. The HLA-DPB1*0501 allele might be the susceptibility gene poly-morphism of NMO.

Objective To evaluate the detection of serum pepsinogen (PG) in screening of gastric cancer. Methods (1) To calculate the detection rate of gastric cancer in PG Positive patients from northeastern, noah-western and northern China. (2) To determine the PG positive rate in patients with chronic superficial and atrophic gastritis. (3) To calculate the detection rate of gastric cancer, H. pylori infection and esophageal cancer in PG positive patients from gastric cancer high risk areas. Results (1) The detection rate of gastric cancer in PC, positive patients from Changchun (northeastern China), Xihing (northwestern China) and Beijing ( northern China) was 22. 58%, 25. 2% and 0, respectively. The sensitivity of PG to seeen gastric cancer in Changchun and Xihing was 50. 9% and 35.6%, and the specificity was 82. 56% and 85.69%, respectively. (2) Only 25% of patients with chronic atrophic gastritis were PG positive. (3) The serum PG level was measured in 2346 cases from gastric cancer high risk areas, and PG positive rate was 27.02% (634/2346), in which 496 patients (76. 65%, 496/634) received endoscopy, and gastric cancer was detected in 10 (2. 02%, 10/496), including 9 cases of early gastric caner. The prevalence of gastric cancer was 0. 43% in common population and 1.58% in PG positive population. The infection rate of H. pylori was 70. 73% in 2346 subjects and 2 cases of esophageal cancer, including 1 case of early cancer was diagnosed. Conclusion Serum PG level cannot be used as a marker for gastric cancer or atrophic gastritis, while it may be of value for gastric cancer screening in high risk areas.

Objective To explore the effect of carrying out self and mutual medical aid training program after accidental injury for primary school students on the students ′relevant knowledge .Methods 98 primary school students in a certain primary school in Wuhan were selected by convenience sampling as objects . Training content and mode of self and mutual medical aid after common accidental injuries were designed basing on the students′age and interest .Their knowledge before and after the training was compared , and the training effect was thus determined .Results The students′post-training knowledge of self and mutual medical aid after common accidental injuries was higher than before the training , in the aspects of calling 120 correctly, 6-step hand washing method , treatment of small-area burn, bandaging of forearm skin damage , wound cleaning of animal bite (91.84%vs.57.14%, 83.67%vs.20.41%, 100.00% vs.67.35%, 77.55% vs.34.69%, 89.80%vs.25.51%) (P<0.01).Conclusions Reasonably-designed self and mutual medical aid training program after common accidental injuries can effectively strengthen primary school students ′relevant abilities , which makes it worth promoting in future training .

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.

Purpose: This study aimed to investigate the effect of the N6-methyladenosine (m6A) dependent ferroptosis on cisplatininduced Sertoli cell injury. Materials and Methods: A cisplatin exposure mouse model was established by intraperitoneal injection of cisplatin in our study. TM4 cell lines was used for in vitro study. Ferroptosis was detected according to metabolomic analysis and a series of assays, including malondialdehyde, glutathione, and glutathione disulfide concentration detection, 2′,7′-dichlorodihydrofluorescein diacetate and BODIPY 581/591 C11 probe detection, and transmission electron microscope imaging. Key ferroptosis-related genes were identified via transcriptomic analysis, western blot and immunohistochemistry. The m6A modification was demonstrated via m6A RNA immunoprecipitation and luciferase reporter assays. Immune cell infiltration was detected by mass cytometry, and verified by flow cytometry and immunofluorescence. Results: Ferroptosis, but not other types of programmed cell death, is a significant phenomenon in cisplatin-induced testis damage and Sertoli cell loss. Ferroptosis induced by cisplatin in Sertoli cell/TM4 cell is GPX4 independent but is regulated by SLC7A11 and ALOX12. Both SLC7A11 and ALOX12 are regulated via m6A dependent manner by METTL3. Furthermore, overexpressed ALOX12-12HETE pathway may result in macrophage polarization and inflammatory response in cisplatin exposure testis. Conclusions Cisplatin-induced Sertoli cell injury via ferroptosis and promoted ferroptosis in an m6A dependent manner. m6A modification of both SLC7A11 and ALOX12 mRNA could result in ferroptosis in our in vitro model. Further, overexpressed ALOX12 can cause more production of 12-HETE, which may be responsible for testis inflammation caused by cisplatin.