The occurrence and severity of radiotherapy-induced adverse events cannot be accounted for or predicted by therapeutic and clinical factors alone.Evidence suggests that genetic variants are associated with adverse effects following radiotherapy.Radiation genomics is the study of genetic variants associated with radiotherapy toxicity.Radiation genomics aims to develop a risk prediction model and uncover the biological mechanisms responsible for radiotherapy toxicity.With the advances in genomics and bioinformatics in the past two decades,radiation genomics has evolved from candidate gene studies to genome-wide association studies,with a series of progress.In this review,we will discuss the study background,design,approaches,challenges,and future directions for radiation genomics.

Objective To investigate the changes in TNF? content of sciatic nerve induced by chronic constriction injury (CCI) of sciatic nerve to determine the role of TNFa in the development of neuropathic pain. Methods Eight-four female health SD rats weighing 250-300g were anesthetized with sodium barbiturate. Unilateral sciatic nerve was exposed and ligated at the middle of thigh. Three ligatures (chromic catgut 4.0) were placed around the sciatic nerve and tied. The distance between the two ligatures was about 1 mm. Sham operation was performed on the contralateral thigh. The sciatic nerve was exposed and mobilized but not ligated. The thermal nociceptive threshold was determined by measuring the withdrawal latency of hindpaw placed on a 58℃ hot plate on days 0.5, 1, 3, 5, 7, 9, 11, 13 and 14 after surgery. Animals were sacrificed on days 0.5, 1, 3, 7, 10 and 14 after surgery. Sciatic nerves were removed from both thighs and frozen at - 80℃ for determination of TNF? content. Sciatic nerve from healthy animals was used as control. The percentage of maximal possible response (% MPR) , was determined for each group (CCI, sham operation, control) % MPR= (new withdrawal latency- average baseline latency)/( 15-average baseline latency) . The distribution of TNF? between supernatant and sediment was also determined. Results The average baseline nociceptive threshold (withdrawal latency) was (7.9?0.2)s. There was significant different in %MPR between the two hindpaws on days 1, 3, 5, 7, 9 and 11 after surgery. The TNF? content of sciatic nerve from healthy rats was (40.62? 0.24) pg/mg protein. The TNF? content of the ligated sciatic nerve was elevated abruptly in 12h after ligation, then abruptly declined to a plateau but was still significantly higher than that of sham-operated side on days 1 and 3. There was no significant difference in TNF? content of sciatic nerve between control group and sham-operation group. The relative content of TNF? content in the sediment of ligated sciatic nerve gradually increased and reached the peak on day 7 and then gradually decreased. Conclusion The TNF? content of peripheral nerves plays an important role in the development of neuropathic pain. Membrane-combined TNF? is involved in the process of nerve repairing.

Objective To investigate the effects of Polysaccharide Sulfate (PSS) on plasma von Willebrand factor (vWF) and thrombomodulin (TM) in patients with acute cerebral infarction.Methods 64 patients with acute cerebral infarction were randomly assigned to receive intravenous drip of PSS (150 mg/d for 14 days, 32 cases, PSS group) or Troxerutin (600 mg/d for 14 days, 32 cases, control group). All of the patients were tested for plasmatic levels of vWF and TM prior to and at 7 d, 14 d after treatment.Results The levels of vWF in PSS group at 7 d, 14 d after treatment were obviously decreased compared with control group (all P

Ischemic cerebral stroke is one of the diseases posing great threat to human health.It is of great value to have a correct evaluation and interpretation of cerebral angiography in interventional treatment of ischemic stroke together with efficacy.The authors reviewed the direct signs and collateral circulation of ischemic cerebral stroke and the evaluation of cerebral angiography in recent literature.

This study was aimed to analyze the composition principles of prescriptions for sequela of apoplexy collected in the CNKI by the Traditional Chinese Medicine Inheritance Platform (TCMIP), in order to provide a reference for clinical selection of medication. Prescriptions for the sequela of apoplexy treatment in CNKI were collected. Based on the TCMIP, the medication rules of prescription were analyzed by data mining method after data entry. A total of 190 prescriptions involving 204 herbs for sequela of apoplexy treatment were screened and studied. The herbs for blood-activating andqi-tonifying were used with higher frequency. There were 36 commonly used herbal pairs. The herb pair of Dang-Gui(Radix Angelicae Sinensis) andHuang-Qi (Radix Astragali) was with the highest frequency. The herbal combination with three types of herbs wasDi-Long (Pheretima),Dang-Gui andHuang-Qi. The herbal combination with four types of herbs wasChuan-Xiong (Rhizoma Chuanxiong),Di-Long,Dang-Gui andHuang-Qi. The analysis on association rule showed thatChuan-Xiong,Dang-Gui,Tao-Ren (Semen Persicae),Hong-Hua(Flos carthami) andHuang-Qiwere often combined with each other. A total of 48 core combinations and 11 new prescriptions were mined. It was concluded that the prescriptions for sequela of apoplexy were mainly composed with herbs for blood-activating,qi-tonifying and collateral-dredging. According to the flavor and meridian tropism theory of Chinese medicine, the herbal medication selection in the prescription was mostly warm and hot in nature, sweet and pungent flavor, and the meridian tropism of the liver and spleen meridian.

Objective To investigate the effects of rhG-CSF on the improvement of cognitive impairment and anti-apoptosis of Alzheimer disease (AD) induced by Aβ1-42 in rat. Methods Healthy male Wistarirats were randomly assigned to the Aβ group, treatment group and sham operation group. Aβ1-42 (10μg) was injected into bilateral hippocampus to create the rat model of AD. Rats in rhG-CSF group were subcutaneously subjected to 50μg/(kg · d) rhG-CSF for 5 days, while rats in Aβ group were subjected to normal saline. Morris water maze tests were done and expressions of caspase-3 protein were determined by immunohistochemical method on the 7th, 14th, 21st, and 28th day after administration. Results (1) The avoiding latent periods of rhG-CSF group ( ( 34. 33 ±6. 47 ) s, (42. 08 ± 6. 36 ) s, (46. 88 ± 7. 66 ) s, respectively ) were shorter than that of Ap group ((49.79 ±4.87)s, (50.25 ±6.81 )s, (51. 33 ±6.90)s, respectively). The percentages of swimming distances in the target quadrant in rhG-CSF group ( (41.00 ±7.62)% ,(43.33 ±8. 16)% ,(44. 67 ±8.07)% ,respectively) were increased comparing with Ap group((25.33 ±6.89)% , (23. 83 ±4.67)% ,(21.50 ±4.64)% ,respectively). The differences were all statistically significant (P<0.05). (2) Compared with sham operation group,the positive rate of caspase-3 protein in rat's hippocampus of Ap group significantly increased after injecting Aβ1-42 The positive rates of caspase-3 protein in rhG-CSF group on the 7th, 14th day ( (7. 93 ±6. 33) and (8. 83 ±5. 94) were lower than Aβ group ( ( 10.43 ±7. 16) and ( 11. 34 ± 5. 17 ) . The differences were statistically significant (P< 0.05). Conclusion RhG-CSF can improve the cognitive impairment of Alzheimer Disease (AD) induced by Aβ1-42 in rat, decrease the apoptosis of hippocampal neurons and delay the decline of its learning and memory ability to some extent.

Objective To investigate the effects of brain ischemic preconditioning (BIP) on peripheral blood EPCs and neovascularization in ischemic brain tissue in rats with cerebral ischemia reperfusion injury (IRI). Methods One hundred and eight male SD rats were randomly divided into three groups:SO group (n=36), MCAO group (n=36) and BIP group (n=36). Neurological function assessment was conducted at 0 h before MCAO-reperfusion, 3 h, 24 h and 3 d, 5 d as well as 7 d after MCAO-reperfusion (n=6 for each group in each time point). Flow cytometry was used to calculate the number of EPCs. Immunohistochemical staining was used to detect the capillary density. Results ①Although neurologi?cal deficit scores were significantly decreased in both BIP and MCAO groups after 3 h following MCAO-reperfusion, the scores were much lower in BIP group than in MCAO group(5 d:1.00±0.63;7 d:1.00±0.63, P<0.05).②The numbers of EPCs were decreased in MCAO group while was increased in BIP group at 3 h after MCAO-reperfusion. The numbers of EPCs were significantly higher in BIP group than in MCAO group(24 h:0.58±0.07;3 d:0.80±0.10;5 d:0.68±0.05;7 d:0.52 ± 0.03, P<0.01). ③ The new blood vessels could be detected at 3 d in BIP group and 5 d in MCAO group after MCAO-reperfusion. The numbers of new blood vessels were significantly higher in BIP group than MCAO group(5 d:14.53 ± 3.44; 7 d: 41.40 ± 5.62, P<0.01). ④ Pearson analysis showed a positive correlation between EPCs and capillary density (5 d: r=0.855, P<0.01; 7 d: r=0.946, P<0.01). Conclusion BIP can improve EPCs mobilization and function, which may contribute to neovascularization in the ischemic brain tissue.

rdial interstitial fibrosis.

BACKGROUND:Sensorineural hearing loss is mainly caused by missing or damaged hair cells in the inner ear. Application of adipose-derived mesenchymal stem cells to regenerate inner ear hair cells is an effective treatment for hearing loss. OBJECTIVE:To explore the feasibility of in vitro inducing adipose-derived mesenchymal stem cells to differentiate into inner ear hair cel-like cells in guinea pigs. METHODS:Adipose-derived mesenchymal stem cells from guinea pigs were isolated and cultured to the 3rd generation. cellphenotype was detected using flow cytometry. Cytokines were added for induction and differentiation by stages, including epidermal growth factor, basic fibroblast growth factor, insulin-like growth factor-1, al-trans retinoic acid, brain-derived neurotrophic factor, neurotrophin 3. RESULTS AND CONCLUSION:Adipose-derived mesenchymal stem cells of guinea pigs cultured in vitro were fusiform and showed a swirled adherent growth. Passage 3 cells were positive for CDCD29 and CD44, but negative for CD34 and CD45. After induction, the cells were positive for nestin and GFAP positive at early stage;after 10-day continuous induction, the cells expressed Myosin VIIa and Math1, specific markers of hair cells, indicating that cytokines can directly induce adipose-derived mesenchymal stem cells to differentiating into inner ear hair cells in guinea pigs.

Objective To investigate the relationships between the levels of plasma soluble CD40 ligand (sCD40L),fetuin-A and pregnancy-associated plasma protein A (PAPP-A) and carotid plaque in patients with acute ischemic stroke.Methods The patients with acute ischemic stroke were enrolled in the study.Carotid arteries were assessed by using carotid artery ultrasound.The patients were divided into either a carotid artery plaque group or a non-carotid artery plaque group according to the assessment results.The former were further divided into a stable plaque sub-group and an unstable plaque sub-group according the nature of plaque.Enzyme-linked immunosorbent assay was used to detect the levels of plasma sCD40L,fetuin-A and PAPP-A.The demography,previous history,complications,laboratory tests and plasma inflammatory biomarkers between the carotid artery plaque group and the non-carotid artery plaque group and between the stable plaque subgroup and the unstable plaque subgroup were compared.Multivariate logistic regression analysis was used to investigate the relationship between plasma inflammatory biomarkers and carotid plaques.Results A total of 200 patients with acute ischemic stroke were included.Among them,78 were females and 122 were males (aged 33 to 87 years,mean 60.1 ± 10.3 years); 139 patients were in the carotid artery plaque group and 61 were in the non-plaque group; 43 were in the stable plaque subgroup and 96 were in the unstable plaque subgoup.The mean age of the carotid artery plaque subgroup was significantly greater than that in the non-plaque subgroup (63.2 ± 8.7 years vs.50.3 ± 9.5 years; t ＝ 10.179,P =0.000),the constituent ratios of men (68.3％ vs.44.3％;x2＝ 10.336,P＝ 0.001),hypertension (71.2 vs.54.1％;x2=5.540,P=0.019),diabetes (46.8％ vs.29.5％ ;x2 =5.199,P =0.023),and hyperlipidemia (78.4％ vs.37.7％ ;x2 =31.31,P =0.000)in patients of carotid plaque group were significantly higher than those of the non-carotid plaque group.The levels of total cholesterol (5.7 ± 1.1 mmol/L vs.5.3 ± 1.0 mmol/L; t =2.433,P =0.016),low-density lipoprotein cholesterol (4.5 ± 1.0 mmol/L vs.4.1 ±0.9 mmol/L; t =2.683,P =0.008),fasting glucose (7.5 ±2.5 mmol/Lvs.6.4±2.1 mmol/L; t=3.002,P＝0.003),sCD40L (151.4 ± 55.8 pg/mlvs.102.8 ±65.9 pg/ml; t =5.360,P=0.000),fctuin-A (390.1 ± 80.6 μg/ml v.s.352.9 ± 98.6 μg/ml; t =2.591,P =0.011),and PAPP-A (11.49 ±4.67 mIU/L vs.8.46 ± 3.99 mIU/L; t =4.409,P =0.000) were significantly higher than those of the non-carotid plaque group.Multivariate logistic regression analysis showed that hyperlipidemia (odds ratio [OR] 6.582,95％ confidence interval [CI] 2.321-18.662; P =0.000),sCD40L (OR6.372,95％ CI 2.174-18.670;P=0.010),and fetuin-A (OR 4.101,95％ CI 1.012-16.619; P=0.048) were the independent predictors for carotid artery plaques in patients with acute ischemic stroke.The mean age of the stable plaque subgroup was significantly lower than that of the unstable plaque subgroup (59.6 ± 9.3 years vs.64.1 ± 7.2 years; t =3.231,P =0.002).The constituent ratio in patients with hypertension was significantly lower than that of the unstable plaque subgroup (55.8％ vs.78.1％ ; x2 =7.213,P =0.007).The levels of total cholesterol (5.4 ±0.9 mmol/L vs.6.0 ± 1.1 mmol/L; t =3.136,P =0.002),low-density lipoprotein cholesterol (4.0 ± 1.2 mmol/L vs.5.7 ± 1.0 mmol/L; t =8.696,P =0.000),fasting glucose (7.1 ± 2.3 mmol/L vs,7.9 ± 1.9 mmol/L; t =2.147,P =0.034),sCD40L (135.3 ±74.3 pg/ml vs.176.5 ±64.5 pg/ml; t =3.319,P ＝0.001),and PAPP-A (10.96 ± 5.02 mIU/L vs.13.98 ±4.63 mIU/L; t =3.463,P =0.001) were significantly lower than those of the unstable plaque subgroup,while the level of high-density lipoprotein cholesterol was significantly higher than that of the unstable plaque subgroup (1.2 ± 0.2 mmol/L vs.1.1 ± 0.3 mmol/L; t =2.314,P=0.022).Multivariate logistic regression analysis showed that HDL-C (OR 0.234,95％ CI0.060-0.906; P =0.022) was an independent protective factor for unstable plaques,while sCD40L (OR 5.290,95％ CI 1.613-17.351; P =0.029) and PAPP-A (OR4.125,95％ CI 1.281-13.283; P =0.021) were the independent predictors for unstable plaques.Conclusions The levels of sCD40L,PAPP-A,and fetuin-A were associated with the existence and stability of carotid artery plaque.The increased plasma sCD40L and fetuin-A were the independent predictors for carotid artery plaques in patients with acute ischemic stroke,and the increased levels of plasma sCD40L and PAPP-A were the independent predictors for carotid artery plaque instability in patients with acute ischemic stroke.