Abstract Objective:  To define a complex of changes in hematologic parameters associated with subtypes (ST) of Blastocystis sp. infections and the status of immune function in Sprague Dawley (SD) rats, and lay the foundation for Blastocystis hominis pathogenesis research. Methods:  5 isolates of ST1, ST3 and ST7 were used, including 1 isolate of ST1 from symptomatic patient, 2 isolates of ST3 and ST7 from symptomatic patients and asymptomatic carrier separately. Immune compromise model was set up using dexamethasone (DEX) and infection models with 5 isolates of ST1, ST3 and ST7, and then examined the hematologic changes post infection 15 days using fully automatic hematology analyzer sysmex xe-2100. Results:  The results showed that infections of Blastocystis STs leaded to the increase of platelet indexes including MPV and PDW except ST3 isolated from asymptomatic carrier only with PDW increase and the higher values of PLT in ST7 isolated from asymptomatic carrier compared with the controls in the immune competence status (P < 0.05). However, the infections of Blastocystis ST7 isolated from symptomatic patient gave rise to higher values of WBC, LYMP, EO, MCV and RDW-SD while lower values of NEU% compared with the controls in immune compromise status (P < 0.05). Meanwhile, higher values of WBC and LYMP and lower NEUT% values were observed in ST1 infections compared with the controls (P < 0.05); lower NEUT values in ST1 infections and controls compared with ST3 and ST7 respectively were observed (P < 0.05); the infection of ST3 isolated from symptomatic patient resulted in higher values of MCV and RDW-SD while the asymptomatic isolate of ST3 only had higher RDW-SD (P < 0.05). Conclusion:  The virulence of Blastocystis sp. isolated from symptomatic patient is higher than that of the identical subtype one isolated from asymptomatic carrier. The infection of ST7 isolated from symptomatic patients may result in the most distinct hematologic changes among STs, and then followed by ST1 symptomatic isolate. And the severity of Blastocystis sp. infection may be mediated by the immune status of host.

Abstract Objective : To assess the correlation between Serum phospholipase A2 receptor antibody and clinicopathological features in patients with membranous nephropathy. Method:  The patients being hospitalized for renal biopsy were selected in this study from January 2016 to January 2018. And normal controls were randomly selected; all the patients were divided into idiopathic membranous nephropathy and non-idiopathic membranous nephropathy groups; patients with idiopathic membranous nephropathy were divided into three groups, namely stage I, stage II and stage III; using software for statistical analysis. Results:  A total of 357 patients were enrolled, including 155 patients with idiopathic membranous nephropathy, 183 patients with non-idiopathic membranous nephropathy, and 19 cases for normal controls. The average age of the idiopathic membranous nephropathy (IMN) group is higher than that of the membranous nephropathy group (P = 0.01). Different pathological stages of idiopathic membranous nephropathy general clinical characteristics analysis results showed that the age, cys c, serum creatinine (Scr) in stage III membranous nephropathy group were higher than those of the stage I and II membranous nephropathy (P values were 0.003, 0.000 and 0.000 respectively); titers of serum phospholipase A2 receptors antibody with stage II and III membranous nephropathy higher than the stage I membranous nephropathy group (P = 0.006); serum albumin (Alb) levels correlated inversely with serum anti-PLA2R antibody titers (rs = –0.234, P = 0.003), serum antiphospholipase A2 receptor (PLA2R) antibody titer level in patients with idiopathic membranous nephropathy was significantly higher than that in patients with non-membranous nephropathy (P < 0.001). Conclusion:  Baseline tite r of serum anti-PLA2R antibody is negatively correlated with Alb in the IMN patients ， and serum anti-PLA2R antibody level in patients with stage I IMN was significantly lower than stage II and III IMN patients.

Abstract Objective:   T o investigate inhibitory effect of TUA (2β, 3β, 23-trihydroxy-urs-12-en-28-oic acid) isolated from Actinidia chinensis Radix on the lung cancer xenografts in nude mice and explore its preliminary mechanism. Methods:  NCI-H460 cells were implanted into nude mice and the transplantation tumor block from nude mice of more than 2 generations was inoculated to the right armpits of BALB/c mice with dissecting needle to establish a lung cancer xenograft model. When the transplanted volume was about 50 mm 3 , the mice were randomly divided into 6 groups: (1) model group; (2) 10 mg·kg –1  cisplatin group; (3) 10 mg·kg –1  PDTC group; (4) TUA high dose group (30 mg·kg –1 ); (5) TUA middle dose group (12 mg·kg –1 ); (6) TUA low dose group (6 mg·kg –1 ). Administration approach was intratumoral injection. The effects of each group on the weight of transplanted tumor animals, the volume and weight of tumor were continuously observed for 14 days. Tumor volume growth curve was drawn and tumor inhibitory rate and index were calculated; HE staining was used to observe nude mice tumor tissue pathological changes. The effects of TUA on NF-κB signaling pathway related proteins were detected by immunohistochemistry and Western blot. Results: In vivo  experiments showed that the transplanted tumors in nude mice became smaller compared with the models. With the increase of TUA dose, the tumor tissue became smaller and smaller, especially in high TUA dose (30 mg·kg –1 ). It had the similar size with the NF-κB inhibitor PDTC (10 mg·kg –1 ) group. HE dyeing observation results confirmed the degree of tumor necrosis and fission in TUA treated tumor tissues obviously decreased. Immunohistochemical results showed that comparing the TUA treatment group with the model group, p65 expression in tumor tissues was reduced, and expression of IκBα increased. Western blot results also showed that the NF-κB related p65 protein expression levels decreased, at the same time IκBα protein expression level increased; the apoptosis related proteins S urvivin protein expression was depressed, Caspase-3 protein expression was promoted. Conclusion:  TUA significantly inhibits the growth of lung transplantation tumor and its mechanism. It may be related to the decreasing the expression of p65 , Survivin and increasing the expression of IκBα, Caspase-3 in tumor tissues.

Abstract Compared with other types of breast cancer, triple negative breast cancer has a poor survival prognosis due to its high aggressiveness and lack of effective therapeutic targets. Immune checkpoint (PD-1/PD-L1 and CTL-4) inhibitors have emerged as a breakthrough therapy in the treatment in various metastatic cancers. PARP inhibitors promote DNA damage in tumor cells, not only promoting immune initiation through a series of molecular mechanisms, but also leading to adaptive upregulation of programmed death ligand 1 (PD-L1) expression. Therefore, the  combination of the two inhibitors can improve the efficacy of tumor treatment. We reviewed the research progress of their combined use in triple negative breast cancer, and put forward relevant ideas for further development, hoping to find the best treatment mode of the combined use of the two .

Abstract Objective:  To detect the expression and distribution of I-FABP in intestinal tissue and the changes of serum concentrations at different time of acute intestinal ischemia , and explore the significance and mechanism of I-FABP in early diagnosis of acute ischemic bowel disease. Methods:  The selected 96 healthy adult SD rats were randomly divided into the experimental group and control group; 48 in each group. Each group was randomly subdivided into 6 groups with 8 rats in each group. The superior mesenteric artery was ligated in the experimental group and the peritoneal switch operation was performed in the control group. The venous blood samples were extracted from each group rats’ right ventricle at 0 . 5 h, 1 h, 2 h, 4 h, 8 h, 12 h after the operation and the concentration of I-FABP was tested respectively. Then the rats were killed, and the diseased intestinal tubes were cut out for paraffin sections. The I-FABP in intestinal tissue was stained by routine HE staining and direct immunofluorescence staining. Results:  The I-FABP was mainly expressed in the epithelial villi of intestinal mucosa, and there was a small amount of expression in the intestinal submucosa and even the muscularis. Within 1 hour of intestinal ischemia, the number of I-FABP positive granules in the intestine and intestinal cavity increased gradually, and then gradually decreased after 1 hour. The difference has statistically significant between the experimental group and the control group ( P  < 0.05). The serum I-FABP: In the experimental group, the serum I-FABP concentration began to increase at 0.5 h, and reached a peak at 1 h (290. 24 ± 156.69) μg·L –1 , then gradually decreased. Compared with the control group, the difference was statistically significant ( P < 0.05). Conclusion: I-FABP usually mainly exists in the epithelial cells of intestinal mucosa. When acute intestinal ischemia occurs, the epithelial cells of intestinal mucosa permeability changes; I-FABP expression rapidly releases to intestinal tissue and intestinal cavity, and is absorbed into the blood. Therefore, I-FABP has certain clinical significance in early diagnosis and treatment of acute intestinal ischemia .

Abstract Objective : To explore the expression and clinic significance of 8-OHdG in breast cancer .   Methods : Pre-operative serum 8-OHdG levels were detected with an enzyme-linked immunosorbent assay in a well-defined series of 173 breast cancer patients .  8-OHdG expression in cancer cells from 150 of these patients was examined by immunohistochemistry .  The HPLC-ECD method is used to determine 8-OHdG concentration in urine .   R esults : The serum 8-OHdG levels and immunohistochemical 8-OHdG expression were in concordance with each other ( P   < 0 . 05 , r = 0 . 163) .  Breast cancer p atients with n egative 8-OHdG immunostaining show lower survival  rate  according to the multivariate analysis ( P   < 0 . 01) .  This observation was even more remarkable in ductal carcinomas (n = 140) patients ( P   < 0 . 001) .  A low serum 8-OHdG level was associated statistically significantly with lymphatic vessel invasion and a positive lymph node status .  Comparison of 8-OHdG concentration in urine of breast cancer patients and healthy women was statistical significance ( P   < 0 . 01) .   Conclusion : Low serum 8-OHdG levels and a low immunohistochemical 8-OHdG expression were associated with an aggressive breast cancer phenotype .  In addition , negative 8-OHdG immunostaining was an independent prognostic factor for breast cancer-specific death in breast carcinoma patients .  Using 8-OHdG concentration in urine to predict DNA damage resulting from breast cancer can provide good biological indicators for detecting harm in early breast cancer .

Abstract Objective : T o study the potential therapeutic effects of active vitamin D 3   (1.25(OH) 2 D 3 ) in the experimental autoimmune neuritis (EAN). Methods : The EAN model was established by actively immunizing Lewis r at s  with synthetic P0 180 – 199   pepide and Freund ’ s complete adjuvant. 1.25(OH) 2 D 3   treatment was given, weight change of rats and clinical score were analyzed. HE staining was used to detect the inflammatory cell infiltration of sciatic nerve s  and demyelination of sciatic nerves was observed by transmission electron microscope (TEM) at the same time. The expressions of inflammatory cytokines IL - 17, IL - 10, TGF -β , IFN -γ  were detected by ELISA, and the expressions of Th17, Treg were examined by RT - PCR. Results : 1.25(OH) 2 D 3   ameliorated body weight loss and my e lin lesions. It  decreased expression s  of inflammatory cytokines IL - 17, IFN -γ  and RORrt while those of IL - 10, TGF -β  and FoxP3 were increased. Conclusions : 1.25(OH) 2 D 3   can improve the clinical pathological changes of EAN rats, and the mechanism may be related to the changes of inflammatory cytokines. 1.25(OH) 2 D 3   is expected to become a new strategy for the clinical treatment of GBS/EAN.

Abstract Sialic acid-binding immunoglobulin-like lectin 9 ( Siglec -9) is a receptor that expresses on the surface of immune cells. It plays an important role in the body ’ s immune response. Increased expression of Siglec -9 has been reported in infectious diseases, autoimmune diseases and cancer. Pathogenic microorganism and tumor cells can inhibit the recognition and killing of immune cells by upregulating their own specific sialic acid and binding with Siglec -9 on the surface of host immune cells, and suppress the release of pro-inflammatory cytokines and promote the release of anti-inflammatory cytokines, eventually leading to immunosuppression, tumor immune escape and the like. However, the immunosuppressive function of Siglec -9 may be advantageous for diseases such as neutrophil asthma and autoimmune diseases. Therefore, further research on the mechanism of action of Siglec -9 is of great significance.

Abstract Non-small cell lung cancer  ( NSCLC ) poses a serious threat to people’s health. Its morbidity and mortality are among the highest among all malignant tumors , and there is an urgent need for more effective new treatment methods. In recent years , NSCLC immunotherapy has made great progress , the first PD-1 inhibitor nivolumab  ( Nivolumab , O drug ) was approved by the US Food and Drug Administration  ( FDA ) in March 2015 , applying to the patients who progressed or has received platinum chemotherapy drugs in the past. Immunotherapy of advanced NSCLC has entered a new era. This article reviews the current research progress of NSCLC immunotherapy.

Abstract NK cell immunodeficiency has a variety of manifestations and complex mechanisms in the tumor .  NK cell immune deficiency is closely related to immune escape of acute leukemia . This paper demonstrates the immunological escape mechanism of acute leukemia from NK cell immune deficiency manifestation and cause .

Abstract Whether infection of Cryptococcus causes disease in host or not depends on the virulence of the pathogen and the immune defense ability of the host .  Cryptococcus neoformans (C .  neoformans) mainly causes opportunistic infections in the immunocompromised or immunodeficient patients. In contrast , Cryptococcus gattii (C .  gattii) mainly attacks the immunocompetent individuals .  On the one hand , the host immune cells can eliminate the invasive Cryptococcus through a complex immune mechanism; on the other hand , Cryptococcus can evade the clearance of host immune cells by adopting various strategies (immune escape) .  This review mainly focuses on the pathogenic mechanism of Cryptococcus, and the host’s immune defense mechanism against cryptococcal infection.

Abstract Tumor immune therapy, especially anti-programmed cell death ligand-1/programmed cell death-1  ( PD-L1/PD-1 ) treatment, is currently the focus of substantial attention. However, despite its enormous successes, the overall response rate of cancer immunotherapy remains suboptimal. There is an increased interest in combining PD-L1/PD-1 treatment with anti-angiogenic drug Apatinib to enhance antitumor effect. Presently available data seem to suggest that Apatinib may exert immune suppressive effects to make the PD-L1/PD-1 treatment works. Here, we review the extensive tumor microenvironment immune modulatory effects from antiangiogenic agents Apatinib in order to supporting VEGFR2 targettherapies in clinical trials are existing.