The therapeutic potential of heavy ion accelerators in malignant tumors is investigated through the analyses of precision dosimetry,biological optimization and side effects,evaluation of efficacy outcomes across diverse tumor types,and development prospects.By reviewing the recent literatures and clinical researches on heavy ion therapy,the study focuses on analyzing the physical characteristics and biological effects of heavy ion beams,summarizes their application achievements in complex lesions such as head and neck,chest and abdomen,and bone and soft tissue tumors,and explores their optimization strategies in light of current technological advancements.Research analysis has demonstrated that heavy ion therapy has distinct advantages in precise targeting and effective eradication of tumor cells,achieving high local control rate and success rate.In addition,heavy ion therapy significantly reduces the risk of radiation damage to normal tissues and improves the quality of life of patients.Heavy ion accelerator offers an efficient and safe option for malignant tumor radiotherapy.Its superior physical dose distribution and enhanced biological effects make it become a vital tool in modern precision cancer treatment.Through continued optimization of accelerator technology,heavy ion therapy is expected to become a mainstream treatment modality for more cancer patients.

The therapeutic potential of heavy ion accelerators in malignant tumors is investigated through the analyses of precision dosimetry,biological optimization and side effects,evaluation of efficacy outcomes across diverse tumor types,and development prospects.By reviewing the recent literatures and clinical researches on heavy ion therapy,the study focuses on analyzing the physical characteristics and biological effects of heavy ion beams,summarizes their application achievements in complex lesions such as head and neck,chest and abdomen,and bone and soft tissue tumors,and explores their optimization strategies in light of current technological advancements.Research analysis has demonstrated that heavy ion therapy has distinct advantages in precise targeting and effective eradication of tumor cells,achieving high local control rate and success rate.In addition,heavy ion therapy significantly reduces the risk of radiation damage to normal tissues and improves the quality of life of patients.Heavy ion accelerator offers an efficient and safe option for malignant tumor radiotherapy.Its superior physical dose distribution and enhanced biological effects make it become a vital tool in modern precision cancer treatment.Through continued optimization of accelerator technology,heavy ion therapy is expected to become a mainstream treatment modality for more cancer patients.

OBJECTIVETo explore the role of eukaryotic translation elongation factor 1A1 (eEF1A1) in regulating the invasion and metastasis of hepatocellular carcinoma (HCC) cells and the possible mechanism.

METHODSqRT-PCR and Western blotting were used to detect the mRNA and protein expression of eEF1A1 and NOB1 in different HCC cell lines and normal liver cells. The invasion and migration abilities of HCC cells with eEF1A1 knockdown or overexpression were examined using Transwell chamber assay and RTCA assay, and the changes in NOB1 mRNA and protein expressions in the cells were detected. The effects of increasing NOB1 expression in HCCLM3-sheEF1A1 cells and decreasing NOB1 expression in eEF1A1-overexpressing MHCC97h cells on eEF1A1 expression and cell invasion and migration abilities were analyzed using Western blotting, Transwell chamber assay and RTCA assay.

RESULTSThe expressions of eEF1A1 and NOB1 were significantly increased in positive correlation in HCC cells as compared with normal hepatocytes. Knockdown of eEF1A1 significantly decreased the invasion and migration of HCC cells and reduced the mRNA and protein expression of NOB1 ( < 0.01). Overexpression of eEF1A1 significantly enhanced invasion and migration of HCC cells and increased NOB1 mRNA and protein expressions ( < 0.01). Increasing NOB1 expression in HCCLM3-sheEF1A1 cells led to the restoration of NOB1 expression and cell invasion and migration abilities ( < 0.01), whereas decreasing NOB1 in MHCC97h-eEF1A1 cells resulted in inhibition of NOB1 expression and cell invasion and migration ( < 0.01).

CONCLUSIONSeEF1A1 positively regulates the expression of NOB1 to promote the invasion and migration of HCC cells .

Objective To study the correlation of wake-up stroke with progressive stroke.Methods Three hundred and twelve patients with acute ischemic stroke,admitted to our hospital from January 2014 to December 2015 were divided into progressive stroke group (n=70) and non-progressive stroke group (n=242).Demographic features,clinical characteristics,and incidence of wake-up stroke were compared between the two groups.The association between wake-up stroke and progressive stroke was analyzed.Results The incidence of wake-up stroke,homocysteine level,and fibrinogen level in progressive stroke group were significantly higher than those in the non-progressive stroke group (40.0％ vs.18.2％,P=0.000;[17.486±16.835] μmol/L vs.[14.321±7.251] μmol/L,P=0.023;[3.539±1.009] g/L vs.[3.134±0.775] g/L,P=0.000).Multivariate Logistic regression analysis showed that wake-up stoke,homocysteine and fibrinogen were the independent predictive factors of progressive stroke (OR=2.978,95％CI:1.623-5.464,P=0.000;OR=1.026,95％CI:1.002-1.052,P=0.035;OR=1.800,95％CI:1.310-2.472,P=0.000).Conclusion Wake-up stoke is a predictive factor of progressive stroke.

AIM: To investigate the role of nitric oxide in the development of brain edema after subarachnoid hemorrhage(SAH), and the influence of L-arginine on them. METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH plus L-arginine group. Dynamic changes of regional cerebral blood flow within 24 hours were measured. Serum nitric oxide level, brain water and sodium content at different time points within 24 hours were also detected. RESULTS: Regional cerebral blood flow and serum nitric oxide level at every time point after operation in SAH group were lower than those in sham-operated group, while brain water content and sodium content in the former group were higher than those in the latter group. Above pathological alterations in SAH plus L-arginine group were not so obvious as in SAH group. CONCLUSION: Decrease in serum nitric oxide plays a role in the development of brain edema after SAH, which may be partly reversed by administration of L-arginine.

AIM: To investigate the effect of Ginkgo biloba extrac (GBE) on cerebral ischemia during early stage of subarachnoid hemorrhage (SAH). METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH+GBE group. Dynamic change of regional cerebral blood flow (rCBF) was detected. Brain endothelin-1(ET-1) and calcium contents were also determined at different time point during 24 hours after the operation. Pathological change of neurons of hippocampus CA1 region was observed. RESULTS: In SAH group, rCBF decreased immediately and persistently after induction of SAH. Values of brain ET-1 content and calcium content at 1 hour, 6 hours and 24 hours were significantly higher than those in sham-operated group. Neurons of hippocampus CA1 region were damaged severely 3 days after onset of SAH. Above abnormal changes in SAH+GBE group were much slighter than those in SAH group. CONCLUSION: GBE may relieve cerebral ischemic damage after SAH.