OBJECTIVETo discuss the influence of setup errors on the accuracy of pelvic cancer in IGRT, analysis setup errors and determine the CTV-to-PTV margins.

METHODS60 pelvic cancer patients treated with Varian 23IX, all of them were performed by CBCT before and after-correction three times in the first week and after that once a week. Then, to measure the setup errors at X(left-right), Y(superior-inferior), Z(anterior-posterior) axis and E(coronal), F(sagittal), G(axial) rotation directions.

RESULTS530 scans obtained in all, the setup errors in X, Y, Z, E, F, G were (-0.52 ± 4.18) mm, (0.73 ± 4.86) mm, (-0.36 ± 3.62) mm, (0.14 ± 1.20)degrees, (0.13 ± 1.34)degrees, (0.21 ± 1.73)degrees respectively and were much lower after correction at X, Y, Z axis, besides, CTV-to-PTV margins decrease a lot.

CONCLUSIONThe accuracy of radiotherapy can be highly increased with the use of IGRT in pelvic cancer.

Humans ; Pelvic Neoplasms ; radiotherapy ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted ; Radiotherapy, Image-Guided

Objective To study the inhibitory effect of curcumin on the proliferation,migration and invasion of non-small cell lung cancer cell A549,and to discuss further if it is closely related to the expression of c-Jun N-terminal kinase (JNK) and relative protein p38.Methods A549 cells were cultured by conventional method,and then treated with different concentration of curcumin (10,20,40,80 μmol · L-1).The proliferation,migration and invasion of A549 cells were measured by real-time cellular analysis (RTCA).The expression levels of JNK,p-JNK,p38 and P-p38 were detected by real-time PCR and Western blotting.Results Curcumin showed an antiproliferation effect against A549 cells with IC50 =40 μmol · L-1,and curcumin exhibited obviously inhibitory effect on the migration and invasion of A549 cells.Additionally,compared with control group,curcumin suppressed the expression of JNK and p38 at the gene level,and significantly inhibited the expression of JNK,P-JNK,p38 and p38 (P＜0.05) at the protein level.Conclusion These results demonstrated that curcumin can inhibit the proliferation,migration and invasion of A549 cells via reducing the level of JNK,p38 phosphorylation,and blocking JNK signal transduction pathway.

Objective:To analyze the performance of clinical theoretical examination of the five year clinical medical students in a medical school, and to explore the existing problems and direction involving in the medical education.Methods:The difficulty coefficient and degree of discrimination were used to analyze the quality of this test, and F test and LSD- t test were conducted with SPSS 24.0 to analyze the mastery rate of various modules and secondary disciplines including basic medicine, medical humanities, clinical medicine and preventive medicine. Results:The overall difficulty coefficient of the test was 0.74, and the degree of discrimination was 0.37. The coefficient of difficulty of each module is more than 0.70, and the degree of discrimination is about 0.40. The mastery rates of each module were all greater than 70%, with clinical medicine being the highest and medical humanities and basic medicine being the lowest, and the mastery rate of each secondary discipline was more than 60%, with a significant difference.Conclusion:This exam is sample, the degree of discrimination is good, and the overall knowledge is well mastered. However, it is still necessary to innovate education reform and improve the teaching quality based on weak points.

Objective:To explore the influence of virtual simulation experiment project on the experimental teaching effect of infectious diseases.Methods:Ten experimental contents were selected, including 3 703 students majoring in clinical five-year program, eight-year program, anesthesia, psychiatry and other majors of Medicine School of Central South University. The teaching effect and students' satisfaction were evaluated through examination and personal questionnaire survey. The measurement data was expressed by (mean ± standard deviation), the counting data was illustrated by percentage. The rate is compared by Chi-square test, and the difference is statistically significant when P<0.05. Results:All the students took part in the examination of 10 items. Except for item 8, the scores of students in all items had a large variance, with almost same number of high score students and low score students. Learning attitude is closely related to learning effect. Among the students who think it's necessary to learn, 20.5% and 53% have excellent learning effect and good learning effect, respectively. Compared with offline experiment teaching, virtual simulation teaching has both advantages and disadvantages, and needs to further improve the satisfaction of students.Conclusion:Virtual simulation teaching of infectious diseases is unable to completely replace offline teaching, and the combination of virtual and reality is more conducive to improving the quality of medical students.

OBJECTIVES: Acute kidney injury (AKI) can be caused by ischemia/reperfusion (I/R), nephrotoxin, and sepsis, with poor prognosis and high mortality. Leptin is a protein molecule that regulates the body's energy metabolism and reproductive activities via binding to its specific receptor. Leptin can inhibit cardiomyocyte apoptosis caused by I/R, but its effect on I/R kidney injury and the underlying mechanisms are still unclear. This study aims to investigate the effect and mechanisms of leptin on renal function, renal histopathology, apoptosis, and autophagy during acute I/R kidney injury. METHODS: Healthy adult male mice were randomly divided into 4 groups: a sham+wild-type mice (ob/+) group, a sham+leptin gene-deficient mice (ob/ob) group, an I/R+ob/+ group, and an I/R+ob/ob group (n=8 per group). For sham operation, a longitudinal incision was made on the back of the mice to expose and separate the bilateral kidneys and renal arteries, and no subsequent treatment was performed. I/R treatment was ischemia for 30 min and reperfusion for 48 h. The levels of BUN and SCr were detected to evaluate renal function; HE staining was used to observe the pathological changes of renal tissue; TUNEL staining was used to observe cell apoptosis, and apoptosis-positive cells were counted; Western blotting was used to detect levels of apoptosis-related proteins (caspase 3, caspase 9), autophagy-related proteins [mammalian target of rapamycin (mTOR), phosphorylated mTOR (p-mTOR), LC3 I, LC3 II], mTOR-dependent signaling pathway proteins [phosphate and tension homology (PTEN), adenosine monophosphate-activated protein kinase (AMPK), protein kinase B (AKT), extracellular regulated protein kinase (ERK), phosphorylated PTEN (p-PTEN), phosphorylated AMPK (p-AMPK), phosphorylated AKT (p-AKT), phosphorylated ERK (p-ERK)]. RESULTS: There was no significant difference in the levels of BUN and SCr between the sham+ob/+ group and the sham+ob/ob group (both P>0.05). The levels of BUN and SCr in the I/R+ob/+ group were significantly higher than those in the sham+ob/+ group (both P<0.05). Compared with the mice in the sham+ob/ob group or the I/R+ob/+ group, the levels of BUN and SCr in the I/R+ob/ob group were significantly increased (all P<0.05). There was no obvious damage to the renal tubules in the sham+ob/+ group and the sham+ob/ob group. Compared with sham+ob/+ group and sham+ob/ob group, both the I/R+ob/+ group and the I/R+ob/ob group had cell damage such as brush border shedding, vacuolar degeneration, and cast formation. Compared with the I/R+ob/+ group, the renal tubules of the mice in the I/R+ob/ob group were more severely damaged. The pathological score of renal tubular injury showed that the renal tubular injury was the most serious in the I/R+ob/ob group (P<0.05). Compared with the sham+ob/+ group, the protein levels of caspase 3, caspase 9, PTEN, and LC3 II were significantly up-regulated, the ratio of LC3 II to LC3 I was significantly increased, and the protein levels of p-mTOR, p-PTEN, p-AMPK, p-AKT, and p-ERK were significantly down-regulated in the I/R+ob/+ group (all P<0.05). Compared with the sham+ob/ob group, the protein levels of caspase 3, caspase 9, PTEN, and LC3 II were significantly up-regulated, and the ratio of LC3 II to LC3 I was significantly increased, while the protein levels of p-mTOR, p-PTEN, p-AMPK, p-AKT, and p-ERK were significantly down-regulated in the I/R+ob/ob group (all P<0.05). Compared with the I/R+ob/+ group, the levels of p-mTOR, p-PTEN, p-AMPK, p-AKT were more significantly down-regulated, while the levels of caspase 3, caspase 9, PTEN, and LC3 II were more significantly up-regulated, and the ratio of LC3 II to LC3 I was more significantly increase in the I/R+ob/ob group (all P<0.05). CONCLUSIONS Renal function and tubular damage, and elevated levels of apoptosis and autophagy are observed in mice kidneys after acute I/R. Leptin might relieve I/R induced AKI by inhibiting apoptosis and autophagy that through a complex network of interactions between mTOR-dependent signaling pathways.
AMP-Activated Protein Kinases/metabolism* ; Acute Kidney Injury/pathology* ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins/pharmacology* ; Autophagy ; Caspase 3/metabolism* ; Caspase 9/metabolism* ; Female ; Humans ; Ischemia ; Kidney/pathology* ; Leptin/pharmacology* ; Male ; Mammals/metabolism* ; Mice ; Proto-Oncogene Proteins c-akt/metabolism* ; Reperfusion/adverse effects* ; Reperfusion Injury/metabolism* ; TOR Serine-Threonine Kinases/metabolism*

Inflammatory caspase-11 senses and is activated by intracellular lipopolysaccharide (LPS) leading to pyroptosis that has critical role in defensing against bacterial infection, whereas its excess activation under pathogenic circumstances may cause various inflammatory diseases. However, there are few known drugs that can control caspase-11 activation. We report here that scutellarin, a flavonoid from Erigeron breviscapus, acted as an inhibitor for caspase-11 activation in macrophages. Scutellarin dose-dependently inhibited intracellular LPS-induced release of caspase-11p26 (indicative of caspase-11 activation) and generation of N-terminal fragment of gasdermin D (GSDMD-NT), leading to reduced pyroptosis. It also suppressed the activation of non-canonical nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome as evidenced by reduced apoptosis-associated speck-like protein containing a CARD (ASC) speck formation and decreased interleukin-1 beta (IL-1β) and caspase-1p10 secretion, whereas the NLRP3-specific inhibitor MCC950 only inhibited IL-1β and caspase-1p10 release and ASC speck formation but not pyroptosis. Scutellarin also suppressed LPS-induced caspase-11 activation and pyroptosis in RAW 264.7 cells lacking ASC expression. Moreover, scutellarin treatment increased Ser/Thr phosphorylation of caspase-11 at protein kinase A (PKA)-specific sites, and its inhibitory action on caspase-11 activation was largely abrogated by PKA inhibitor H89 or by adenylyl cyclase inhibitor MDL12330A. Collectively, our data indicate that scutellarin inhibited caspase-11 activation and pyroptosis in macrophages at least partly via regulating the PKA signaling pathway.