Objectives: . Head and neck squamous cell carcinoma (HNSCC) exhibits high recurrence rates, particularly in cases of radioresistant HNSCC (RR-HNSCC). Non-thermal plasma (NTP) therapy effectively suppresses the progression of HNSCC. However, the therapeutic mechanisms of NTP therapy in treating RR-HNSCC are not well understood. In this study, we explored the regulatory role of NTP in the RR-HNSCC signaling pathway and identified its signature genes. Methods: . After constructing two RR-HNSCC cell lines, we prepared cell lysates from cells treated or not treated with NTP-activated media (NTPAM) and performed RNA sequencing to determine their mRNA expression profiles. Based on the RNA sequencing results, we identified differentially expressed genes (DEGs), followed by a bioinformatics analysis to identify candidate molecules potentially associated with NTPAM therapy for RR-HNSCC. Results: . NTPAM reduced RR-HNSCC cell viability in vitro. RNA sequencing results indicated that NTPAM treatment activated the reactive oxygen species (ROS) pathway and induced ferroptosis in RR-HNSCC cell lines. Among the 1,924 genes correlated with radiation treatment, eight showed statistical significance in both the cell lines and The Cancer Genome Atlas (TCGA) cohort. Only five genes—ABCC3, DUSP16, PDGFB, RAF1, and THBS1—showed consistent results between the NTPAM data sequencing and TCGA data. LASSO regression analysis revealed that five genes were associated with cancer prognosis, with a hazard ratio of 2.26. In RR-HNSCC cells, NTPAM affected DUSP16, PDGFB, and THBS1 as activated markers within 6 hours, and this effect persisted for 12 hours. Furthermore, enrichment analysis indicated that these three DEGs were associated with the extracellular matrix, transforming growth factor-beta, phosphoinositide 3-kinase/protein kinase B, and mesenchymal-epithelial transition factor pathways. Conclusion . NTPAM therapy exerts cytotoxic effects in RR-HNSCC cell lines by inducing specific ROS-mediated ferroptosis. DUSP16, PDGFB, and THBS1 were identified as crucial targets for reversing the radiation resistance induced by NTPAM therapy, providing insights into the mechanisms and clinical applications of NTPAM treatment in RR-HNSCC.

Objectives: . Head and neck squamous cell carcinoma (HNSCC) exhibits high recurrence rates, particularly in cases of radioresistant HNSCC (RR-HNSCC). Non-thermal plasma (NTP) therapy effectively suppresses the progression of HNSCC. However, the therapeutic mechanisms of NTP therapy in treating RR-HNSCC are not well understood. In this study, we explored the regulatory role of NTP in the RR-HNSCC signaling pathway and identified its signature genes. Methods: . After constructing two RR-HNSCC cell lines, we prepared cell lysates from cells treated or not treated with NTP-activated media (NTPAM) and performed RNA sequencing to determine their mRNA expression profiles. Based on the RNA sequencing results, we identified differentially expressed genes (DEGs), followed by a bioinformatics analysis to identify candidate molecules potentially associated with NTPAM therapy for RR-HNSCC. Results: . NTPAM reduced RR-HNSCC cell viability in vitro. RNA sequencing results indicated that NTPAM treatment activated the reactive oxygen species (ROS) pathway and induced ferroptosis in RR-HNSCC cell lines. Among the 1,924 genes correlated with radiation treatment, eight showed statistical significance in both the cell lines and The Cancer Genome Atlas (TCGA) cohort. Only five genes—ABCC3, DUSP16, PDGFB, RAF1, and THBS1—showed consistent results between the NTPAM data sequencing and TCGA data. LASSO regression analysis revealed that five genes were associated with cancer prognosis, with a hazard ratio of 2.26. In RR-HNSCC cells, NTPAM affected DUSP16, PDGFB, and THBS1 as activated markers within 6 hours, and this effect persisted for 12 hours. Furthermore, enrichment analysis indicated that these three DEGs were associated with the extracellular matrix, transforming growth factor-beta, phosphoinositide 3-kinase/protein kinase B, and mesenchymal-epithelial transition factor pathways. Conclusion . NTPAM therapy exerts cytotoxic effects in RR-HNSCC cell lines by inducing specific ROS-mediated ferroptosis. DUSP16, PDGFB, and THBS1 were identified as crucial targets for reversing the radiation resistance induced by NTPAM therapy, providing insights into the mechanisms and clinical applications of NTPAM treatment in RR-HNSCC.

Objectives: . Head and neck squamous cell carcinoma (HNSCC) exhibits high recurrence rates, particularly in cases of radioresistant HNSCC (RR-HNSCC). Non-thermal plasma (NTP) therapy effectively suppresses the progression of HNSCC. However, the therapeutic mechanisms of NTP therapy in treating RR-HNSCC are not well understood. In this study, we explored the regulatory role of NTP in the RR-HNSCC signaling pathway and identified its signature genes. Methods: . After constructing two RR-HNSCC cell lines, we prepared cell lysates from cells treated or not treated with NTP-activated media (NTPAM) and performed RNA sequencing to determine their mRNA expression profiles. Based on the RNA sequencing results, we identified differentially expressed genes (DEGs), followed by a bioinformatics analysis to identify candidate molecules potentially associated with NTPAM therapy for RR-HNSCC. Results: . NTPAM reduced RR-HNSCC cell viability in vitro. RNA sequencing results indicated that NTPAM treatment activated the reactive oxygen species (ROS) pathway and induced ferroptosis in RR-HNSCC cell lines. Among the 1,924 genes correlated with radiation treatment, eight showed statistical significance in both the cell lines and The Cancer Genome Atlas (TCGA) cohort. Only five genes—ABCC3, DUSP16, PDGFB, RAF1, and THBS1—showed consistent results between the NTPAM data sequencing and TCGA data. LASSO regression analysis revealed that five genes were associated with cancer prognosis, with a hazard ratio of 2.26. In RR-HNSCC cells, NTPAM affected DUSP16, PDGFB, and THBS1 as activated markers within 6 hours, and this effect persisted for 12 hours. Furthermore, enrichment analysis indicated that these three DEGs were associated with the extracellular matrix, transforming growth factor-beta, phosphoinositide 3-kinase/protein kinase B, and mesenchymal-epithelial transition factor pathways. Conclusion . NTPAM therapy exerts cytotoxic effects in RR-HNSCC cell lines by inducing specific ROS-mediated ferroptosis. DUSP16, PDGFB, and THBS1 were identified as crucial targets for reversing the radiation resistance induced by NTPAM therapy, providing insights into the mechanisms and clinical applications of NTPAM treatment in RR-HNSCC.

Objective:To discuss the effect of Yes-associated protein(YAP)silencing on the proliferation,migration,and invasion capabilities of the human cervical cancer(CC)SiHa cells.Methods:The human CC SiHa cells were cultured in vitro,and the lentiviral YAP shRNA was transfected into the SiHa cells to establish stably transfected YAP-shRNA experimental group(sh-YAP group)and empty plasmid control group(control group).Western blotting method was used to detect the silencing effect of YAP;immunofluorescence method was used to detect the microfilament number and morphology of actin filaments(F-actin)in the cells in both groups;CCK-8 method was used to detect the survival rates of the cells in two groups;Transwell chamber assay and wound healing assay were used to detect the numbers of migration and invasion cells and scratch healing rates of the cells in two groups;Western blotting method was used to detect the expression levels of epithelial-mesenchymal transition(EMT)markers(E-cadherin and Snail),DNA damage repair-related proteins(γ-H2AX),and apoptosis-related proteins[c-MYC and B-cell lymphoma-2(Bcl-2)]in the cells in two groups.Results:The results of lentiviral YAP shRNA transfection into SiHa cells showed that the expression level of YAP protein in the SiHa cells was significantly decreased(P＜0.05).The immunofluorescence results showed that after YAP silencing,the F-actin in SiHa cells was sparse and regularly arranged,with a reduced number of cells and a shriveled appearance.The CCK-8 results showed that compared with control group,the survival rate of the SiHa cells in sh-YAP group was significantly decreased cultured for 24 and 48 h(P＜0.01).The results of Transwell chamber assay and the wound healing assay showed that compared with control group,the numbers of migration and invasion SiHa cells in sh-YAP group were significantly decreased(P＜0.01),and the cell scratch healing rates were signifiantly decreased(P＜0.05).The Western blotting results showed that compared with control group,the expression level of E-cadherin protein in the cells in sh-YAP group was increased(P＜0.05),and the expression levels of c-MYC,Bcl-2,and γ-H2AX proteins were decreased(P＜0.05 or P＜0.01).Conclusion:YAP gene silencing leads to the depolymerization of F-actin in the human CC SiHa cells and regulates the apoptosis and DNA damage repair,potentially reversing the EMT process,thereby inhibiting the proliferation and migration of the tumor cells.

Objective To study the protective effect and mechanism of maslinic acid (MA) on acute liver injury (ALI) in rats.Methods Fifty BALB/c mice were randomly divided into control group,model group,and low (12.5 mg/kg),medium (25.0 mg/kg) and high doses (50.0 mg/kg) of MA,with 10 rats in each group.The control group was intraperitoneally injected with normal saline.The other groups were intraperitoneally injected with lipopolysaccharide (LPS) (50 mg/kg) and D-Gal N (500 mg/kg) to prepare mouse AL[model.The MA groups were administered with 12.5,25.0,50.0 mg/kg MA 1 h before model establishment,respectively.All the mice were sacrificed 6 h after model establishment,and serum and liver tissues were collected.Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured.Hematoxylin-eosin staining was used to observe the pathological changes of liver tissue.Thiobarbituric acid method was used to determine malondialdehyde (MDA).H2O2 reaction product colorimetric was used to determine the content of myeloperoxidase (MPO).The tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in serum and liver tissue was detected by enzyme-linked immunosorbent assay,respectively.Western Blot was conducted to detect the expression of nuclear factor E2 related factor 2 (Nrf2),heme oxygenase-1 (HO-1) and the activation of nuclear factor-kappa B (NF-κB) pathway.Results Compared with the model group,the liver histopathology in the low,medium and high doses MA groups was significantly improved.The serum ALT and AST levels were decreased,and the differences were statistically significant (all P＜0.05).The contents of MDA and MPO in liver tissues were decreased,and the differences were statistically significant (all P＜0.05).The protein contents of Nrf2 and HO-1 were increased,the differences were statistically significant (all P＜0.05).The NF-κB pathway was inhibited,and the differences were statistically significant (all P＜0.05).The levels of TNF-α and IL-6 in serum and liver tissues were decreased,and the differences were statistically significant (all P＜0.05).Conclusions MA has a protective effect on LPS/D-Gal N-induced ALI,and its mechanism is related to inhibition of NF-κB pathway and activation of Nrf2/HO-1 pathway.

: Rehabilitation medicine is a medical branch which focused on functional recovery. Function Evaluation is very important in assessing the function of patients, the effect of treatment and the efficiency of rehabilitation. Comprehensive Function Evaluation includes evaluation of physical, psychological, speech and society. Vocal, mental and social evaluation have deep cultural and national background. Therefore every country must have its own Function Evaluation Method. Now we present our design for Comprehensive Evaluation. Based on the cooperation of Department of Rehabilitation, Department of Neurology, Department of Spinal Cord Injury, Department of Speech Therapy and Department of Psychology. The advantages of this method are as follows: 1. The style of ADL, speech and thinking are suitable for the condition of our country. 2. The evaluation result adopts hundred work system, it is easy for medical staff, patients and their family to understand and communicate the result. 3. We make it more accurate, comprehensive and reliable by some simple tests on speech pathology and psychology. 4. We overcome some disadvantages of evaluation indexes because it is not correct and is difficult to be understood before. Now every evaluation index has quantity standard. 5. It is simple and practical. Each subtest takes 20 minutes or more. 6. It has been tested by normal people. The norm and severity grade had been developed. 7. The reliability is tested and is proved to be dependable.

康复医学是以恢复患者功能为中心的医学分支。因此，功能评定无论是在客观地评定患者的功能方面，还是在最终评定治疗结果和康复效率方面都是极为重要的。全面的功能评定包括躯体、精神、言语和社会四个方面。其中，言语、社会功能和认知功能中的思维方式，都具有强烈的民族文化色彩。因此，每个国家都应该有切合自己国情的功能评定方法。但由于我国康复医学发展较晚，至今尚无一套既切合国情，又全面、实用和可靠的功能评定方法。有鉴于此，我们在“中心”顾问室、神经康复科、脊髓损伤康复科、言语治疗科、心理科和老年病科的通力合作下，经过近2年的研究，在吸收国际先进经验的基础上，密切结合国情，设计了本文所述的综合功能评定法。其优点有：1．在饮食、起居等生活方式方面以及在言语、社会、思维等方面，均切合我国国情。2．评定结果采用群众熟悉的100分制，使医务人员、患者和患者家属均易于理解，便于交流和沟通。3．在言语、认知等功能的评定方面，直接由言语和心理学家选择一些简易的言语和心理学测试项目，提高了量表的准确性、全面性和可靠性。4．各项评定指标的量化程度高，在言语、认知和社会方面尤其如此，克服了一些量表中对此类项目的评定指标不够具体和不易掌握的不足。5.简便实用，一次检查对正常人仅需20分钟左右，对患者则无负担。6.本法已在128名正常人中应用，并求出了正常值，据此拟定了功能障碍严重程度的等级，可供参考和应用。7.信度经过检验，证明可靠。 综合功能评定法的正常值、功能障碍严重程度分级及信度研究结果，将陆续报道。

Aim The mechanism of basic fibroblast growth factor(bFGF)in mediating increase of intracellular free magnesium ([Mg2+]i) in human umbilical vein endothelial cells (HUVECs), and the relationship between Mg2+and angiogenesis were investigated in this study.Methods The change of[Mg2+]i in HUVECs were quantitatively detected in intracellular cation measurement system via loaded with the fluorescent magnesium indicator mag-fura-2. Endothelial cells were primarily acquired by infusion of collagen enzyme solutioninto the lumens of human umbilical veins and cultured in M199 with 0.2 fetal bovine serum. The role of bFGF in angiogenesis was observed in presence of 0,1 mmol?L-1 or 2 mmol?L-1 of extracellular Mg2+.Results bFGF dose-dependently increased [Mg2+]i, and there was not any significant difference among the groups of 0,1 mmol?L-1and 2 mmol?L-1 of extracellular Mg2+;similar results were obtained in groups done with Na+ and Ca2+. Pretreatment with bFGF receptor-2 (KDR) inhibitor (SU1498) blocked the increase of [Mg2+]i induced by bFGF.Unlike in the group of 0 mmol?L-1extracellular Mg2+,the apparent angiogeneses were observed in the groups of 1 mmol?L-1 and 2 mmol?L-1 extracellular Mg2+ in the presence of bFGF.bFGF-induced angiogenesis was significantly blocked with SU1498 in the presence of 1 mmol?L-1 extracelluar Mg2+.Conclusions These results suggest that the increase of [Mg2+]i by bFGF come from intracellular Mg2+ pools mediated by KDR-dependent signaling pathways,thereby resulting in the bFGF-induced angiogenesis.