1.Advances in the study of precise radiotherapy for non-small-cell lung cancer
Journal of International Oncology 2006;0(10):-
With the development of computer techniques and medical imaging examining methods , precise radiotherapy is becoming the major direction of radiotherapy for tuomors. Both of tumor control probability and normal tissue complication probability are improved with precise radiotherapy. This paper critically review the value of PET-CT and breathing control in precise radiotherapy for non-small-cell lung cancer (NSCLC).
4.Regulatory effect of electroacupuncture on heart and stomach of rats.
Bin-bin REN ; Zh YU ; Ya-li WANG ; Bin XU
Chinese Journal of Integrated Traditional and Western Medicine 2014;34(10):1212-1215
OBJECTIVETo explore different regulatory effects of electroacupuncture (EA) at the same acupoint on the heart and the stomach.
METHODSEighty male SD rats were randomly divided into eight groups equally, i.e., the Neiguan (PC6) group, the Quchi (LI11) group, the Tianshu (ST25) group, the Danzhong (RN17) group, the Zusanli (ST36) group, the Sanyinjiao (SP6) group, the Xinshu (BL15) group, and the Weishu (BL21) group, 10 in each group. The regulatory effects of EA (2/15 Hz, 3 mA, 2 min) at different acupoints on the gastric motility (intragastric pressure) and the cardiac function (the left ventricular pressure) were observed. The mean values of effect of two-min pre-EA and after-EA were compared.
RESULTSCompared with the pre-EA in the same group, the left ventricular pressure decreased in the Neiguan (PC6) group, the Quchi (LI11) group, the Danzhong (RN17) group, the Sanyinjiao (SP6) group, and the Xinshu (BL15) group (P <0.05). The intragastric pressure increased in the Quchi (LI11) group, the Zusanli (ST36) group, the Sanyinjiao (SP6) group, and the Xinshu (BL15) group, while it decreased in the Tianshu (ST25) group, the Danzhong (RN17) group, and the Weishu (BL21) group (P <0.05). The difference of the left ventricular pressure was sequenced from high to low as Xinshu (BL15) >Danzhong (RN17) >Neiguan (PC6) >Sanyinjiao (SP6) >Quchi (LI11). The difference of the intragastric pressure was sequenced from high to low as Tianshu (ST25) >Weishu (BL21) > Xinshu (BL15) > Danzhong (RN17) > Zusanli (ST36) > Sanyinjiao (SP6) > Quchi (LI11).
CONCLUSIONSEA at the same acupoint (2/15 Hz, 3 mA) showed different regulatory effects on the heart and stomach. There existed some difference in the direction and size due to the acupoint location, meridians, dominant nerve segment or relating organs. A fixed effect direction to the specific target was also shown.
Acupuncture Points ; Animals ; Electroacupuncture ; Heart ; physiology ; Male ; Meridians ; Rats, Wistar ; Stomach ; physiology
5.Morphology and AFLP analysis of tetraploid plantlets of Atractylodes macrocephala.
Hong-juan WANG ; Ya-ting LI ; Zeng-xu XIANG
China Journal of Chinese Materia Medica 2015;40(3):404-409
In order to investigate the genetic basis of morphological variation of tetraploid plantlets of Atractylodes macrocephala, diploid plantlets were taken as experimental material, sterile filtration colchicine was used to soak 0.5-1.0 cm long buds. The difference between morphology and stomatal of diploid and tetraploid of A. macrocephala was compared, and genome polymorphism was explored by AFLP. The results showed that the buds dipped in 0.1% colchicine solution for 36 h was optimal conditions to induce tetraploid of A. macrocephala with induction rate of 32.0%. Morphological indexes such as leaf area index, leaf length and width, the density of stomas and the number of chloroplast of tetraploid were distinctly different from diploid. Four hundred and fifty-one bands ranging with 80-500 bp were amplified with 24 pairs of primers, the rate of polymorphism was 32.59%. These amplification sites of diploid were different from tetraploid of A. macrocephala, and the differences in morphology of them were reflected in the DNA polymorphism.
Amplified Fragment Length Polymorphism Analysis
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methods
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Atractylodes
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genetics
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Sequence Analysis, DNA
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Tetraploidy
6.Kawasaki disease complicated with cerebral infarction: a case report.
Yao-ming WANG ; Ya-chuan CAO ; Zhuang-jian XU
Chinese Journal of Pediatrics 2012;50(8):628-629
Aspirin
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administration & dosage
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therapeutic use
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Brain
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diagnostic imaging
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pathology
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Cerebral Infarction
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diagnosis
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drug therapy
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etiology
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Epilepsy
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diagnosis
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drug therapy
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etiology
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Humans
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Immunoglobulins, Intravenous
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administration & dosage
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therapeutic use
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Infant
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Male
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Mucocutaneous Lymph Node Syndrome
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complications
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diagnosis
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drug therapy
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Tomography, X-Ray Computed
8.Compound Heterozygosis Mutation of Low Density Lipoprotein Receptor Gene in Familial Hypercholestero-lemia Family
xiao-dong, PAN ; lu-ya, WANG ; jie, LIN ; peng-yu, SU ; ya, YANG ; shu, LIU ; lan-ping, DU ; xu, WANG
Journal of Applied Clinical Pediatrics 2006;0(13):-
Objective To identify mutations site and clinical characteristics of a familial hypercholesterolemia(FH) proband diagnosed clinically through DNA sequencing and family analysis in the proband and his family members of 3 generations.Methods Blood samples and clinical data of the kindred of total 29 from 3 generations members were collected.Proband had a physical examination electrocar-diogrom and vascular ultrasound.The proband and his family members took routine clinical exams,and genomic DNA was isolated.The promoter region and the 18 exons of low density liporotein receptor(LDLR) gene were screened by Touch down polymerase chain reaction -single strand conformation polymorphism(PCR-SSCP) and DNA sequencing.The result of sequencing were matched gene sequence published in the BLAST database.Results 1.Increased intima-media thickness and plaque were detected in the common carotid artery,right subclavian artery of the proband.Aortic valve regurgitation was found by echocardiography.2.No mutation R3500Q of ApoB100 was observed.3.Two heterozygous mutations in exon 10 and 13 of LDLR gene (W462X and A606T) were identified.The proband and 5 members of paternal relatives showed W462X heterozygosis mutation in exon 10 of LDLR gene which introduced the change from tryptophone to a new stop codon.The proband's mother and grandmother harboured A606T heterozygous mutation in exon 13 of LDLR gene due to a single base pair substitution of G for A in the codon for residue 1 879.Conclusions Disease causing mutations of proband are W462X and A606T compound heterozygosis mutation in exon 10 and 13 of LDLR gene inherited from mother and father.Proband shows homozyous phenotype though the genotype analysis indicates heterozygous mutations.
9.Synergetic effect of flue gases and arsenic on DNA injury in lymphocytes.
Yi WANG ; Chun-wei LU ; Lu WANG ; Ya-ping JIN ; Yuan-yuan XU ; Gui-fan SUN
Chinese Journal of Industrial Hygiene and Occupational Diseases 2006;24(3):175-177
Animals
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Arsenic
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toxicity
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Comet Assay
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DNA Damage
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drug effects
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Lymphocytes
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drug effects
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metabolism
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Male
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Malondialdehyde
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metabolism
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Rats
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Rats, Wistar
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Tobacco Smoke Pollution
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adverse effects
10.miR-498 inhibits A549 cell migration and invasion by down-regulating FOXM1
Xi TANG ; Ya HU ; Yanhua XU ; Chunlin WANG ; Ping QIU ; Xianghui WANG
Journal of Xi'an Jiaotong University(Medical Sciences) 2017;38(2):226-230
Objective To verify whether miR-498 can inhibit A549 cell migration and invasion by down-regulating FOXM1.Methods miR-498 mimic and miR-NC were transfected into A549 cells.Wound healing and Transwell method were employed to test the migratory ability and invasion ability of A549 cells;Western blot was used to detect the expressions of COL1A1,COL1A5 and FOXM1 in A549 cells.Luciferase assay was used to confirm whether FOXM1 is the target gene of miR-498.Results Compared with those in the control group,the expressions of COL1A1,COL1A5 and FOXM1 were decreased,and the migration and invasion abilities of A549 cells were decreased in the miR-498 group (both P<0 .01 ).The luciferase activity of the FOXM1-3′-UTR plasmid was significantly suppressed by miR-498 (P<0 .05 );over-expression of FOXM1 could reverse the effect of miR-498 on A549 cells.Conclusion miR-498 inhibits A549 cell migration and invasion by down-regulating FOXM1.