Objective To explore the high risk factors of brain injury in preterm infants,and to reduce its morbidity and improve the developmental outcome.Methods One hundred and thirty preterm infants,who were admitted to our neonatal intensive care unit(NICU)between Aug.2005 and Aug.2007,were scanned by echo in 1,3,4,7,15 days,and 1,3 and 6 months after birth,respectively.Those who had intraventricular hemorrhage(IVH)of grade Ⅰor Ⅱ were regarded as mild brain injury,whereas those who had IVH of grade Ⅲ or Ⅳ or periventricular leukomalacia(PVL)were regarded as severe brain injury.Logistic regression was adopted to analyze 17 factors:gestational age,birth weight,hypertension syndrome during pregnancy,premature rupture of membranes,modalities of delivery,fetal distress,asphy-xiate,resuscitation,surfactant,apnea,seizures,hypoxia,hypercarbia,hypocarbia,acidosis,use of oxygen,nasal constant positive airway pressure or mechanical ventilation.Results Among 130 preterm infants,88 cases(66.7%)were detected with brain injury,which included 29 cases(33%)with mild brain injury(5 cases with IVH of grade Ⅰ,24 cases with IVH of grade Ⅱ)and 59 cases(67%)with severe brain injury(53 cases with IVH of grade Ⅲ,1 case with IVH of grade Ⅳ and 5 cases with PVL).Gestational age and birth weight were the fundamental factors of brain injury in premature infants.The smaller the gestational age and the lower the birth weight,the highter the brain injury rate.Resuscitation,hypoxia,the use of auxiliary ventilation were also important high risk factors of brain injury in preterm infants.All these high risk factors could influence the autoregulation of cerebral blood and trigger or aggravate brain injury of preterm infants.Conclusions Smaller gestational age,lower birth weight,resuscitation,hypoxia,the use of auxiliary ventilation were all the high risk factors of brain injury in premature infants,which could influence the parameters of cerebral blood dynamics by influencing cerebral blood autoregulation of preterm infants and lead to the occurrence of brain injury in premature.

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.

Objective To observe the curative effects of monosialotetrahexosyl ganglioside(GM1)on neonates with moderate and severe hypoxic-ischemic encephalopathy(HIE).Methods Eighty-six neonates with HIE were randomly divided into GM1 treatment group and control group.The control group(42 cases)were received routine treatment(including cerebrolysin and citicoline);the treatment group(44 cases)were given GM1 on the basis of routine treatment as early as possible(within 6 hours after birth).Brain CT,neonatal behavioral neurological assessment(NBNA)and children's development center of China(CDCC)at 12 months after birth were proformed in both groups.Results Brain CT,NBNA and CDCC markers in treatment group were better than those in control group(Pa

Objective To explore the relationship between some single nucleotide polymorphisms (SNP)loci of interferon regulatory factor 6(IRF6)gene,transforming growth faetor-?(TGFA)gene and nonsyndromic cleft lip with or without cleft palate(NSCL/P)in nuclear families consisting of fathers, mothers and affected offspring with NSCL/P from southeast China.Methods Some SNloci of IRF6 and TGFA were detected by applying microarray technology in nuclear families,and then haplotype relative risk (HRR)and transmission disequilibrium test(TDT)were performed.Results There were no significant difference in genotypes and alleles distribution between patients and their parents.The SNP locus——V274I of IRF6 was associated with NSCL/P(HRR:?~2=4.5816,P

Objective To study the effect of rosiglitazone on plaque stability in ApoE-knockout mice. Methods Thirty-two 6-week-old ApoE knockout mice were used as atherosclerosis models in two groups: rosiglitazonegroup (n=18) and control group (n=14). Male and female mice were half separated into two groups. All mice were fed normal chow diet. Rosiglitazone group received rosiglitazone 17 mg/kg of body weight/day. The animals were sacrificed and aortae were prepared for analysis after fourteen weeks. Aortic root were cutted and prepared for paraffin section. The positive percentage of macrophage cells, smooth muscle cells, tumor necrosis factor-? and matrix metalloproteinase-9 in aortic lesions were measured by immunohistochemistry. The changes of grey gradient of collagen in lesion of both groups were measured by Masson stain. Results The positive percentage of smooth muscle cells [(38.5?7.2)%vs(18.6?6.7)%,P

BACKGROUNDAdipose-derived stromal cell (ADSC) differentiation into neural cells in vitro is becoming widely studied. However, there are few reports on astrocytes following differentiation, and particularly on maturation and electrophysiology. In this study, we used various methods to determine ADSC-derived astrocyte maturity.

METHODSChemical induction with isobutylmethylxanthine (IBMX) was used to differentiate adult ADSCs into astrocytes followed by hematoxylin-eosin (HE) staining to observe morphology and transmission electron microscopy for cellular ultrastructure assessment. Immunofluorescence was used to detect expression of neural stem cell marker nestin as well as glial markers glial fibrillary acidic protein (GFAP) and S-100. In addition, we measured membrane potentials in bis-(1,3-dibarbituric acid) trimethine oxanol-labeled ADSCs and astrocytes by stimulation with a high potassium solution under an inverted fluorescence microscope. Finally, cell cycle distribution was detected by flow cytometry.

RESULTSTypical astrocyte morphology was shown by HE staining after 48-hour differentiation. Glial fibril was observed with transmission electron microscopy. GFAP and S-100 were not expressed in the control group, but were expressed within 24-hour differentiation and reached a maximum at day 14 with no change up to day 28. Nestin was weakly expressed in control cells and also reached a maximum at day 14 with the percentage of positive cells constant until day 21 followed by a decrease. Differentiated cell membrane potentials after stimulation with potassium were slightly increased, and then gradually declined over time. There was no significant membrane potential change in the control group. Flow cytometry showed that the percentage of cells in G0/G1 phase was 93% and only 5% in S phase.

CONCLUSIONADSCs were differentiated into mature astrocytes with typical characteristics including morphology, ultrastructure, marker protein expression, mature potassium channels and mitotic capacity.

1-Methyl-3-isobutylxanthine ; pharmacology ; Adipose Tissue ; cytology ; Adult ; Astrocytes ; cytology ; Barbiturates ; pharmacology ; Cell Differentiation ; drug effects ; Cells, Cultured ; Electrophysiology ; methods ; Female ; Flow Cytometry ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Male ; Membrane Potentials ; drug effects ; Microscopy, Fluorescence ; S100 Proteins ; metabolism ; Stromal Cells ; cytology ; Young Adult

Objective To explore the molecular basis of familial hypercholesteraemia(FH)by analyzing the phenotype and genotype relationship through identify the low density liporotein receptor(LDL-r)gene mutation in a FH kindred.Methods A male patient of 15 years old was selected to examine the electrocardiogram,lipid.Color Doppler was used to examine heart and great vessels.The promoter region and the 18 exons of the LDL-r gene were screened by touch-down polymerase chain reaction(PCR)and DNA sequencing.Results The caro-tid intima-media thickness(IMT)was increased to 0.23 cm,while coronary flow velocity reserve(CFVR)was decreased to 1.57,and mode-rate mitral regurgitation was found in the proband.The genetic alteration G→A change at 1 448 of exon 10 causing premature stop codon(W462X).The same heterozygous nonsense mutation was also found in his father.The mutation had been reported in other Chinese patients.In vitro experiments showed that W462X mutation leads to low LDL binding and internalization ability.Conclusions The homozygous mutation(W462X)in exon 10 of the LDL-r gene were identified in the clinically heterozygous FH proband.The W462X mutation is the underl-ying cause of hypercholesterolaemia and clinical AS manifestations.W462X is recurrent mutation among Chinese FH patients.It might be a hot spot mutation in LDL-r in Chinese FH.J Appl Clin Pediatr,2009,24(1):18-20

OBJECTIVETo provide reference for the safe needling depth of Dazhui (GV 14), Jianzhongshu (SI 15), Xuanshu (GV 5) and Mingmen (GV 4) in clinical acupuncture and moxibustion treatment.

METHODSThirty-two adult volunteers were divided into 3 groups, thin person group, moderate person group and fat person group according to Luo's indexes, and computer-aided tomography was used to measure the needling depth of Dazhui (GV 14), Jianzhongshu (SI 15), Xuanshu (GV 5) and Mingmen (GV 4).

RESULTSThe safe depths of perpendicular needling were different for persons of different somatotypes, for example the needling depth for Dazhui (GV 14) was (32.86 +/- 3.96) mm for the thin person group, (37.76 +/- 4.91) mm for the moderate person group, and (47.93 +/- 5.30) mm for the fat person group.

Acupuncture Points ; Acupuncture Therapy ; Combined Modality Therapy ; Humans ; Moxibustion ; Tomography, X-Ray Computed

Acute Disease ; Animals ; Bone Marrow Cells ; cytology ; Cell Differentiation ; Female ; Liver Diseases ; pathology ; Male ; Mesenchymal Stromal Cells ; cytology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the correlation between the recurrence of cerebral infarction and aspirin resistance (AR)/Chinese medical (CM) constitutions.

METHODSTotally 413 cerebral infarction patients took Aspirin Enteric-coated Tablet (100 mg per day) while receiving routine therapy, 5 days at least in a week. They were followed-up for 12 months. Aspirin sensitivity (AS) was determined using turbidimetry. CM constitutions among patients with different AS were compared. Ratios of AR patients and AS patients of different CM constitutions in cerebral infarction recurrent patients were compared. Platelet membrane glycoproteins (GP) II b HPA-3 gene polymorphism was detected by polymerase chain reaction (PCR) method. Correlation between recurrence of cerebral infarction and AR, bb genotypes, CM constitutions times AS were analyzed by Logistic regression.

RESULTSTotally 11 patients dropped out, 101 (25.12%)with recurrent cerebral infarction and 301 (74.88%) without recurrent cerebral infarction. There were 152 (37.81%) AR patients and 250 (62.19%) AS patients. AR accounted for 26.6% (80/ 301) and AS accounted for 73.4% (221/301) in non-recurrent cerebral infarction patients. AR accounted for 71.3% (72/101) and AS accounted for 28.7% (29/101) in recurrent cerebral infarction patients. There was statistical difference in AR and AS ratios (χ2 = 64.287, P = 0.000). The proportion of yin deficiency constitution (YDC) was the largest [28.3% (43/152)] in AR patients. The proportion of blood stasis constitution (BSC) was the largest [23.6% (59/250)] in AS patients. There was statistical difference in CM constitutions between AR patients and AS patients (χ2 = 21.574, P < 0.01). The former 4 recurrent rates occurred in AR patients of YDC, BSC, damp-phlegm constitution (DPC), qi deficiency constitution (QDC). YDC occupied the first place [22.4% (34/152)]. The former 4 recurrent rates occurred in AS patients of BSC, QDC, DPC, damp-heat constitution (DHC). BSC occupied the first place [3.2% (2/250)]. Compared with non-recurrent cerebral infarction patients and AS patients, bb gene occurred most often, but aa gene and ab gene occurred obviously lesser in non-recurrent cerebral infarction patients and AR patients (χ2 = 20.171, χ2 = 55.139, P < 0.01). AR and bb gene were positively correlated with recurrent cerebral infarction (OR = 18.423, P = 0.000; OR = 1.304, P = 0.028). Body constitutions interacted with AS (OR = 0.707, P = 0.000).

CONCLUSIONSRecurrent cerebral infarction was closely related to AR and constitutional types. The recurrence rate was higher in AR patients of YDC. GP I b HPA-3 bb genotype might be a risk factor for AR and recurrent cerebral infarction.

Aspirin ; therapeutic use ; Body Constitution ; Cerebral Infarction ; Drug Resistance ; Humans ; Medicine, Chinese Traditional ; Neoplasms ; Recurrence ; Yin Deficiency