OBJECTIVE:To prepare oceanic lysozyme film and establish a method for its quality control.METHODS:Film agent was prepared with oceanic lysozyme as the principle agent and hydroxy propyl methylcellulose as the film-former.Folin-phenol method and agar plate diffusion method were used respectively to determine the concentration of albumen and enzyme activity of oceanic lysozyme;and the content of lysozyme in the oceanic lysozyme film was determined by ultraviolet spectrophotometry.RESULTS:Both albumen concentration and enzyme activity of oceanic lysozyme were up to the bacte?riostatic requirement.The average recovery rate of sample was101.0%(RSD=0.67%).Storing within6months,each index of the sample experienced no marked change.CONCLUSION:The preparation is simple in production,controllable in quality and it served as a new preparation for the clinical treatment of vaginitis.

Objective To comparatively study the difference status of lymphocyte subsets and activated T lymphocyte between preoperation and intraoperation,and to investigate the influence of operation on lymphocyte subsets and their activation in the pa-tients with malignant tumors.Methods The lymphocyte subsets and their activated cells were determined in 42 cases of common malignant tumors by the flow cytometry.Results The levels of CD3 + ,CD4 + ,CD8 + cells during intraoperation were obviously de-creased compared with preoperation,the difference in CD3 + and CD4 + had statistical significance(P <0.05),while the difference of CD8 + had no statistical significance(P >0.05).NK,CD19 + ,CD3 + HLA-DR+ were significantly increased,the difference of NK and CD19+ had no statistical significance(P >0.05),while the difference with CD3 + HLA-DR+ had statistical significance(P <0.05). Conclusion The cellular immune function in the patients with malignant tumor is in inhibitory status.Operation makes the cellular immune function to be further injured.The stress responses of operation and trauma increase the expression of NK,CD19 and acti-vated T lymphocytes.It is suggested that the patients with malignant tumor should use the immune response modifier before opera-tion to enhance the cellular immune function for ensuring the effect of postoperative radiochemotherapy sequential treatment.

Objective]To explore the aberrant expression of SOD1 gene in nasopharyngeal carcinoma tissues and adjacent tissues,as well as in NPC cell lines,then to observe the effect of SOD1 on NPC cells metastatic ability and investigate the intrinsic?mechanism.[Methods]Immunohistochemical technique was used to examine SOD1 expression in carcinoma tissues and adjacent tissues(n=10). Small interfering RNAs and inhibitor LCS-1 were used to knockdown of SOD1 expression and inhibit SOD1 activity, respectively. Then,wound healing test and migration assay were applied to detect cell metastatic ability in vitro. Real-time PCR and Western Blot were used to analyze the expression of EMT-related genes(E-cadherin,Vimentin,Twist).[Results]SOD1 was found to be significantly up-regulated in nasopharyngeal carcinoma tissues(n = 7 ,70%),compared to control. SOD1 was also highly expressed in highly metastatic potential NPC cell lines(CNE2,5-8F,S18)compared with low metastatic ability cell lines(6-10B). Knockdown SOD1 expression or inhibit SOD1 activity suppress cell motility in CNE2 and 5-8F cells. Finally,we demonstrate that SOD1 inhibition plays a role in induction of epithelial marker E-cadherin and has an opposite effect on mesenchymal marker vimen tin and transcriptional factor twist.[Conclusion]These results suggest that SOD1 contributes to EMT and might be important for tumor metastasis in NPC.

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.
Animals ; Apoptosis/*drug effects ; Cadmium/*toxicity ; Calcium/metabolism ; Cell Communication/drug effects ; Connexin 43/genetics ; Enzyme Activation/drug effects ; Gap Junctions/*drug effects ; Gene Expression Regulation/drug effects ; Hepatocytes/cytology/*drug effects ; Rats ; Signal Transduction/drug effects

The heterogeneity of exhausted T cells (Tex) is a critical determinant of immune checkpoint blockade therapy efficacy. However, few studies have explored exhausted T cell subpopulations in human cancers. In the present study, we examined samples from two cohorts of 175 patients with head and neck squamous cell cancer (HNSCC) by multiplex immunohistochemistry (mIHC) to investigate two subsets of Tex, CD8⁺PD1⁺TCF1⁺ progenitor exhausted T cells (TCF1⁺Tex^prog) and CD8⁺PD1⁺TCF1^- terminally exhausted T cells (TCF1^-Tex^term). Moreover, fresh tumor samples from 34 patients with HNSCC were examined by flow cytometry and immunohistochemistry to further investigate their properties and cytotoxic capabilities and their correlation with regulatory T cells (Tregs) in the tumor immune microenvironment (TIME). mIHC and flow cytometry analysis showed that TCF1^-Tex^term represented a greater proportion of CD8⁺PD1⁺Tex than TCF1⁺Tex^prog in most patients. TCF1⁺Tex^prog produced abundant TNFα, while TCF1^-Tex^term expressed higher levels of CD103, TIM-3, CTLA-4, and TIGIT. TCF1^-Tex^term exhibited a polyfunctional TNFα⁺GZMB⁺IFNγ⁺ phenotype; and were associated with better overall survival and recurrence-free survival. The results also indicated that larger proportions of TCF1^-Tex^term were accompanied by an increase in the proportion of Tregs. Therefore, it was concluded that TCF1^-Tex^term was the major CD8⁺PD1⁺Tex subset in the HNSCC TIME and that these cells favor patient survival. A high proportion of TCF1^-Tex^term was associated with greater Treg abundance.
CD8-Positive T-Lymphocytes ; Head and Neck Neoplasms/therapy* ; Humans ; Immunotherapy/methods* ; Prognosis ; Programmed Cell Death 1 Receptor ; Squamous Cell Carcinoma of Head and Neck/therapy* ; Tumor Microenvironment ; Tumor Necrosis Factor-alpha