Pancreatic cancer is a one of the most malignant digestive cancer.Because the lack of effective methods for early diagnosis,most patients have been ineligible for surgical resection when diagnosed.Kallikrein family is a group of serine proteases,because of its ability to decompose the extracellular matrix proteins,it may be closely related to the invasion and metastasis of various cancers.And some members of kallikrein family may become cancer diagnostic biomarkers.This paper reviews all the recent articles about kallikrein family study in pancreatic cancer.

Objective To evaluate the imaging features of acute necrotizing encephalopathy caused by children A H1N1 influenza.Methods CT and MRI brain imaging data of three children acute necrotizing encephalopathy caused by A H1N1 influenza virus and proved by clinical and laboratory investigation were analyzed.All the three children got CT and MRI scan because of coma while in hospital.Results All cases represented multifocal damage,and some were symmetrical.Bilateral thalamencephalons were involved in the all cases.Bilateral grey and white matters of frontal lobe,temporal lobe,parietal lobe and occipital lobe,and hippocampi,putamina,external capsule,brain stem,bilateral cerebellum,could be seen multifocal damage,and some were symmetrical.All the cases showed brain swelling in varying degrees.These region presented low density in CT,hypointensity on T1 weighted series and hyperintensity on T2 weighted series and FLAIR series in MRI.Conclusion The imaging features of acute necrotizing encephalopathy caused by children A H1N1 influenza represented multifocal and symmetrical damage and brain swelling.It may be characteristic that bilateral thalamencephaloas were involved.The patient was serious,and fatality rate was high.So we should pay much attention to acute necrotizing encephalopathy caused by children A H1 N1 influenza.

Objective: To test the expression of miR-1178 in pancreatic cancer and study its clinicopathological significance and mechanism. Methods: The expression of miR-1178 in 87 paired paraffin pancreatic ductal adenocarcinoma specimens and adjacent non- cancerous pancreatic tissue diagnosed by Pathology Department of Peking Union Medical College Hospital was detected by hybridization in situ. The relationship between the expression of miR-1178 and clinicopathological characters was analyzed.miR-1178 mimics and inhibitor were used to further detect the close relationship among miR-1178 and cancer invasion. Establish a nude mice subcutaneously transplanted tumor model, 4 weeks after vaccination for tumor volume and weight measurement.Student t-test, rank sum test, and χ² test was used respectively to compare the data between two groups. Cox regression was adopted to improve the single factor and multiple factors analysis. Results: The results of hybridization in situ showed the expression of miR-1178 was increased in 72 cases with pancreatic cancer compared to that in paired normal pancreatic tissues (50/72 vs. 11/72, χ²=43.26, P<0.05). miR-1178 expression was positively associated with tumor lymph node stage (χ²=4.189, P=0.041). Univariate and multivariate analysis revealed that miR-1178 was an independent adverse prognostic indicator for patients with pancreatic cancer (HR=2.364, 95%CI: 1.114-5.019, P=0.025). Transwell assay indicated the over-expression of miR-1178 increased the number of AsPC-1 cells that penetrated the ECM-coated membrane (177.0±19.8 vs. 119.7±15.9)(χ²=8.21, P<0.05). For the in vivo experiment, overexpression of miR-1178 significantly promoted tumor growth, compared with control group (tumor volume: (5 122.4±760.2)mm³ vs. (1 976.8±601.8)mm³, t=2.413, P<0.05; tumor weight: (1.55±0.21)g vs. (0.67±0.17)g, t=2.960, P<0.05). Over-expression of miR-1178 down-regulated the expression of Stub1 and elevated the expression of FAK/MMP-9 signal pathway(P<0.05). Conclusions MiR-1178 is overexpressed in pancreatic cancer, and is effective for predicting patients′ prognosis. MiR-1178 regulate Stub1/FAK/MMP-9 signal pathway and promote the invasion of AsPC-1 cells.

Objective: To investigate the expression of KLK7 in pancreatic cancer and its clinical significance. Methods: Immunohistochemistry was used to detect the expression of KLK7 protein in pancreatic cancer tissue microarray with 92 samples. Statistical analysis of the relationship between KLK7 and clinicopathological characteristics was finished. Pancreatic cancer cell lines were infected with lentiviuses in order to get cells with KLK7 stable overexpression.KLK7-siRNA was transfected into pancreatic cancer cells to knock down KLK7.Cell proliferation and chemosensitivity were detected by CCK-8 assay; Cell invasion and migration abilities were detected by Transwell assay. At the same time, subcutaneous xenograft tumor models were established in nude mice to observe the effect of KLK7 on tumor growth in nude mice. Data were statistically analyzed by rank sum test, χ² test and Logistic regression analysis. Results: The expression level of KLK7 in pancreatic cancer tissues was higher than that in paired adjacent tissues (P<0.05). KLK7 expression was correlated with vascular invasion(χ²=7.535, P<0.05). Further univariate and multivariate analysis showed that KLK7 expression was an independent risk factor for vascular invasion of pancreatic cancer(χ²=7.535, P<0.05). The overexpression of KLK7 in pancreatic cancer cell lines BxPC-3 and CFPAC can increase their proliferation abilities, reduce the chemosensitivity and promote their migration and invasion behaviour; The results of in vivo experiments showed that the volume of subcutaneously transplanted tumors in the overexpressing KLK7 group was significantly larger than that in the control group (t=4.479, P<0.05). The group of overexpressing KLK7 showed greater tumor weight than the control group(t=2.831, P<0.05). Conclusions The expression level of KLK7 in pancreatic ductal adenocarcinoma was higher than that in paired adjacent tissues and it is an independent risk factor for vascular invasion of pancreatic cancer.KLK7 can promote the proliferation of pancreatic cancer cells, reduce the chemosensitivity and increase the invasion and migration of pancreatic cancer cells.

Objective:To systematically evaluate the role of air pollutants in the development and exacerbation of autoimmune rheumatic diseases.Methods:We followed PRISMA guidelines and searched EMBASE, Scopus, PubMed, and Cochrane Library databases using keywords and MeSH terms from inception to July 2019. Observational studies reporting the relationship between autoimmune rheumatic diseases and exposure to certain air pollutants were included. Screening of literature according to established inclusion and exclusion criteria. No meta-analysis but the qualitative analysis was conducted due to the high methodological heterogeneity.Results:A total of 24 studies were included. Rheumatoid arthritis (RA) ( n=6), anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) ( n=1), ankylosing spondylitis (AS) ( n=1), systemic lupus erythematosus (SLE) ( n=3), childhood-onset systemic lupus erythematosus (cSLE) ( n=3), juvenile idiopathic arthritis (JIA) ( n=2), Kawasaki disease (KD) ( n=4), systemic autoimmune rheumatic diseases (SARD) ( n=4). The results of the study suggested that short-term elevation in particulate matter (PM)2.5 concentration was possibly associated with an increased risk of SLE and cSLE flare-ups, disease activity of AS, JIA and SARDs exacerbation. Studies demonstrated an increased risk of RA with cumulative exposure to carbon monoxide (CO), nitrogen dioxide (NO 2), ozone (O 3), and sulfur dioxide (SO 2). Only one study demonstrated an increased risk of KD admission with elevated O 3 levels. No association was found between AAV and ambient air pollution. Conclusion:Air pollution is likely to be involved in the development and exacerbation of certain autoimmune diseases. At the same time, the mechanism of autoimmune diseases of ambient air pollutants should be actively studied, so as to promote the early prevention of cardiovascular diseases.

Objective:To investigate the clinical manifestation, genetic characteristics, treatment and prognosis of Crouzon-like syndrome.Methods:Clinical data of one case of Crouzon-like syndrome diagnosed in Children′s Hospital Affiliated to Zhengzhou University in May 2019 were collected, including clinical test, treatment plan, follow-up outcomes. The clinical characteristics and the mutation characteristics of IL11RA-related Crouzon-like syndrome were analyzed combined with the literature.Results:The male proband, five years and four months old, was admitted with the main clinical manifestations including headache, vomiting, exophthalmos, ocular hypertelorism, nasal root flat and scaphocephaly. CT showed that the cerebellar tonsil moved down slightly, the occipital magnum was full, the bilateral cranial plates were locally thinner, the bilateral cranial diameters were increased, and the cranial seams were closed. Magnetic resonance imaging showed ChiariⅠmalformation. The mutation c.40_63del and splice site mutation c.811-2A>G of the patient′s IL11RA gene were screened by whole exome sequencing. Sanger sequencing showed that the mutations are compound heterozygous and both are first reported. The mutation c.811-2A>G was derived from the patient′s mother, and the other one is de novo.Conclusions:The main clinical manifestations of Crouzon-like syndrome are craniosynostosis and midface hypoplasia and ocular deformity. The study identified two novel mutations in the Crouzon-like syndrome related IL11RA gene. Genetic sequencing is helpful for accurate diagnosis and timely surgical treatment.

In recent years, the issue of end-of-life decision making has received broad attention. More and more people have been appealing for the respect for terminal patients’ wishes in decision making. Many scholars have proposed the application of advance medical decision to ensure the autonomy of terminally ill patients. Given that advance medical decision does not have legal effect in China, the Beijing Health Law Society proposed the "Expert Consensus on Legal Issues Related to End-of-life Decision Making" in July 2022. This consensus provides clear guidance on how to make medical decisions for terminally ill patients, based on the principle of respecting the patient’s wishes within the framework of current laws and regulations. The consensus aims to provide guidance for both doctors and patients about how to respect patients’ own wishes and protect their autonomy, as well as to provide reference for future law and policy formulation on related issues.