Child ; Humans ; Myelodysplastic Syndromes ; classification ; diagnosis ; Pediatrics ; World Health Organization

Humans ; Leukemia, Large Granular Lymphocytic

Blood Cells ; cytology ; Bone Marrow Cells ; cytology ; China ; Hematologic Tests ; standards ; Humans

Acute Disease ; Adolescent ; Adult ; Child ; Humans ; Leukemia ; diagnosis ; drug therapy ; Neoplasm, Residual ; Remission Induction

China ; Clinical Laboratory Techniques ; Humans ; Myelodysplastic Syndromes ; diagnosis

Adolescent ; Adult ; Angiography, Digital Subtraction ; Child ; Decompression, Surgical ; methods ; Female ; Humans ; Magnetic Resonance Angiography ; Male ; Middle Aged ; Optic Nerve Injuries ; diagnostic imaging ; pathology ; Young Adult

Adult ; Female ; Humans ; Magnetic Resonance Imaging ; Neuroma, Acoustic ; pathology ; surgery

Objective To investigate the relationship between amnestic mild cognitive impairment and functional genes associated with hyperphosphorylated tau protein.Methods One hundred and sixteen amnestic mild cognitive impairment (aMCI) patients and 93 normal controls were recruited for the study.Multi-dimension neuropsychologic tests were used to assess the cognitive function extensively.MassARRAY and iPlex systems were used to measure candidate SNP polymorphisms,analyze genotypic,allelic or haplotypic distributions and their interaction with ApoE ε4 and the correlation with the cognitive function in the subjects.Results ( 1 ) The scores of neuropsychologic tests in memory domain ( Auditory Verbal Learning Test (AVLT)-first immediate recall,AVLT-second immediate recall,AVLT-second immediate recall,AVLT-5 minute delayed recall,AVLT-20 minute delayed recall,AVLT-recognition,Rey-Osterrich Comolex Test-delay) in aMCI patients ( 3.0 ( 0-7.0 ),5.0 ( 1.0-10.0),6.0 ( 1.0-11.0 ),4.0 (0-11.0),3.0(0-10.0),20.0(8.0-24.0),11.2 ±8.3) were significantly lower than those in the normal controls(4.0(0-9.0),7.0(2.0-11.0),9.0(3.0-12.0),8.0(0-12.0),8.0(0-12.0),22.0 (10.0-24.0),16.1±8.0) (Z=-3.592,-6.802,-6.408,-8.173,-8.533,-5.647 andt=4.216 respectively,all P ＜0.01 ) ; (2) Genotypic distributions of rs242562 GG in aMCI (7.826％ ) were significantly lower than those in normal controls (20.65％,OR =0.3525,95％ CI 0.1411-0.8807,P =0.024 98),however there were no differences in the genotypic,allelic or haplotypic distributions between aMCI patients and controls of glycogen synthase kinase-3β,cyclin dependent protein kinase-5,calcium and calmodulin-dependent protein kinase-Ⅱ,cell division cycle 2,dual-specificity tyrosine-phosphorylation regulated kinase 1A and low density lipoprotein receptor-related protein 6; (3) MAPT/STH rs242562 genotype was correlated with AVLT-immediate recall,AVLT-delayed recall,Rey-Osterrieth Complex Test,Rey-Osterrieth Complex Test-delayed recall and Clock Drawing Test (H =9.763,12.258,10.508,9.624,10.767,F =3.700,3.123 and H =6.591 respectively,all P ＜ 0.05 ) ; (4) There were no differences in the distributions of MAPT/STH rs242562 GG genotype and ApoE ε4 haplotype between aMCI patients and normal controls.Conclusions MAPT/STH rs242562 GG genotype decreases the genetic risk of aMCI,which might have important role in memory function in aMCI.The interaction between rs242562 GG and ApoE ε4 doesn' t affect the susceptibility to aMCI.

The Japanese encephalitis virus (JEV), a leading cause of encephalitis, exists as quasispecies in clinical isolates. Using a limiting dilution method combined with immunohistochemistry to detect viral antigens, 10 biological clones were isolated and purified from a clinical JEV isolate (CNS138/9) derived from an autopsy brain. These biological clones were tested for neurovirulence in SK-N-MC and NIE-115 neuronal cells, and a 2-week-old, footpad-infected, JE mouse model. Nine clones were found to be neurovirulent; one clone neuroattenuated. Although further studies are needed to determine genotypic differences, if any, in these clones, the limiting dilution purification and neurovirulence testing methods described herein should be useful for phenotypic studies of quasispecies of neurotropic viruses in general, and JEV and other flaviviruses in particular.

ObjectiveTo examine whether the single nucleotide polymorphisms in inflammation-related genes are associated with the risk of amnestic mild cognitive impairment (aMCI).MethodsThe study recruited 116 aMCI patients and 93 matched healthy controls.All subjects underwent extensive assessment of cognitive function,genotyping was carried out on the platform of matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry.Results ( 1 ) There was prominent discrepancy between aMCI and controls in the memory,attention and executive functions,20 minutes delayed recall of auditory verbal memory test (AVMT) (3.0(0.0 ～ 10.0 ),8.0 (0.0 ～ 12.0),t =- 8.533,P ＜ 0.05 ),recall of Rey-Osterrieth complex figure test ( R-O CFT) (11.2 ±8.3,16.1 ±8.0,t=4.216,P＜0.05),digit span test (DST) (12.0(7.0 ～ 19.0),13.0(7.0 ～20.0),Z=-2.516,P＜0.05),trail making test A (TMTA) (80.0s(35.0 ～200.0)s,72.0s(29.0 ～512.0)s,Z=-3.113,P＜0.05),trail making test B (TMTB) ((180.1 ±72.7)s,(141,7 ±52.1)s,t=-4.385,P＜0.05 ).(2) No significant differences were found in frequencies of alleles,genotypes and hapolotypes of inflammation mediator genes ( interleukin 10,interleukin 1 A,interleukin 1 B,tumor necrosis factor,interleukin 6,α1- an-tichymotrypsin gene,transforming growth factor B1 ) between aMCI and controls (P ＞ 0.05 ).ConclusionThe results indicate that polymorphisms in the inflammation-related candidate genes do not appear to be involved in the risk of developing aMCI.