Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

Objecfive To explore pathological mechanism and treatment of central hyponatrem-ia. Methods Synchronous assay was made to detect changes of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),endogenous digitalis-like substance(EDLS),antideuretic hormone (ADH),Na+ concentrations in blood and urine as well as osmotic pressure of plasma and urine in 68 pa-tients with traumatic brain injury(TBI). Results Of all,there were 27 patients with hyponatremia,mostly in patients with severe or critical TBI.There found syndrome of inappropriate secretion of antidi-uretic hormone(SIADH)in 7 patients and cerebral salt wasting syndrome(CSWS)in 20. Conclu-sions The central hyponatremia in patients with TBI may be related to the increased secretion of EDLS and ADH.The decrease of ANP and BNP in blood has no direct effect on Na+ concentration in blood.In-travenous injection of extrinsic thyrotropin releasing hormone(TRH)may inhibit dilutional hyponatremia resulted from increased secretion of ADH in TBI patients.

Objective:To evaluate the effects of resin infiltration in the treatment of post-orthodontic white spot lesions (WSLs)and compare it with microabrasion.Methods:1 0 subjects with 66 teeth with noncavitated and unrestored WSLs after multibracket treatment were recruited.A simple randomized,split-mouth and controlled design was used to allocate WSLs to the resin infiltration and micro-abrasion groups(n =33).The area of the WSLs were measured photographically by using image analysis software before treatment (T0),1 week(T2)and 3 months(T3)after treatment.Data were analyzed with multifactorial analysis of the variances with repeated measures at an a level of 5% and a power of 80%.Results:The area of the white spot lesions(R)decreased significantly in both groups(P <0.05).At T3 the success rate of resin infiltration group(88.68%)was significantly higher than that of microabrasion group (64.67%)(P <0.05).Conclusion:Resin infiltration is more effective than microabrasion in the treatment of post-orthodontic WSLs.

Objective:To evaluate the translucency,opalescence and fluorescence reflection of 6 light-cured resin composites. Methods:Disks of 6 resin composites including Filtek Supreme XT-YT(XT),Filtek Supreme XT-A3B(3M),Clearfil Majesty-A3 (MJ),Gradia Direct-A3(GC),Venus-A3(VE)and Charisma Diamond-A3(CA)were prepared in the diameter of 9 mm with the thickness 2.0 mm.PR-650 spectral scanning colorimeter was used to measure and caculate translucency parameters(TP),opal-escence parameter(OP)and fluorescence reflection(FL)and to draw the fluorescence reflection curves.Results:Except XT and MJ,TP value of other resin composites were in the range of natural tooth.Only OP value of XT was in the range of natural tooth en-amel.FL value of XT was close to that of natural tooth dentin.Fluorescent peak wavelength of GC,MJ,VE and CA were in the range of natural tooth,but fluorescent peak height was higher than that of natual tooth.TP was positively correlated with OP(r =0.85,P <0.05).There was no statistic correlation between TP and FL,between OP and FL.Conclusion:The 6 resin composites can simulate optical property of natual tooth,but the opalescence of resin composites is defective.

Objective To study the early expression of ca]pain Ⅱ and microtubule associated protein 2 (MAP2) mRNA in the hippocampus of the lateral fluid percussion injury rats. Methods 18 Male Sprague-Dawley rats were randomly divided into 3 groups. The changes of Calpaln Ⅱ and MAP2 mRNA in hippocampus 3 h after injury were detected by real-time PCR. Results Compared to the control group (n = 6), the expression for Ca]pain Ⅱ mRNA increased obviously(P <0.01)in the lateral fluid percussion injury group(n=6) ,the expression for MAP2 mRNA degraded obviously(P <0.01). Compared with the lateral fluid percussion injury group(n =6) ,the expression for calpuin Ⅱ mRNA in the mild hypothermia group degraded obviously (n = 6), the expression for MAP2 mRNA increased obviously(P <0.01). Conclusion Mild hypothermia may act as neuroprotection by inhibiting the expression of Ca]pain Ⅱ and easing the degradation of cytoskeleton.

Alcohols ; Animals ; Carbon Tetrachloride ; Collagen Type I ; metabolism ; Collagen Type III ; metabolism ; Disease Models, Animal ; Drug Therapy, Combination ; Glycyrrhetinic Acid ; therapeutic use ; Hepatocytes ; drug effects ; Interferon-alpha ; therapeutic use ; Liver Cirrhosis ; chemically induced ; drug therapy ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley

Objectives To study the molecular genetics of Niemann-Pick's disease (NPD), and its implication in the diagnosis of NPD. Methods The clinical data and blood samples of three unrelated families were collected. The genomic DNA was extracted from peripheral blood. The six coding exons and their lfanking intronic sequences of SMPD1 gene in all members of three pedigrees were ampliifed by polymerase chain reaction (PCR). The SMPD1 gene sequencing results were compared with the normal sequence from Genbank to identify possible causative mutations. The ampliifcation products of exons where mutations were located were cloned into TA vector for further conifrmation. Results Family 1 proband had homozygous T107C mutation and the parents had heterozygous T107C mutation. The homozygous delete mutation (c.108-113delGCTGGC) was detected and conifrmed by TA cloning in all members of family 2 and 3. The 20 normal control members did not have this delete mutation. Conclusions The genetic basis of NPD in the proband of family 1 is the homozygous T107C mutation in SMPD1 gene, while parents in family 1 are carriers of recessive T107C mutation. The homozygous mutation c.108-113delGCTGGC exists in SMPD1 gene in all members of the family 2 and 3. This delete mutation is considered to be genetic polymorphism.

Objective To screen the altered gene expression profile of hippocampus after traumatic brain injury(TBI)in rats. Methods Rats(n=3)in experimental group underwent moderate fluid-percussion(F-P)brain injury and the hippoeampus sample in the injured hemisphere was removed and conserved in liquid nitrogen three hours later.The rats(n=5)of the control group underwent the same procedure except for injury.Mfymetrix rat genome 230 2.0 array was used to detect the gene expression profile of hippocampus in two groups and find the altered gene expression profile. Results A total of 159 genes in the experimental group changed significantly(≥2 folds)compared with the control group,of which 136 genes were up-regulated and 23 genes down-regulated. Conclusions The significant gene expression changes of hippocampus,especially a large mount of up-regulated genes,are detected after moderate TBI in rats,suggesting that the secondary injury following TBI is a procedure involving multiple factors.

Objective To set up a rat model with acute traumatic coma and identify the variation of microRNA in mesencephalon. Methods After rats were injured moderately by central fluid percussion system, tissues of the mesencephalon were removed one hour after injury. RNA of brain tissue of the mesencephalon was isolated for microRNA array by using the exiqon microarray system. The data were analyzed statistically by Genepix Pro 6.0 after hybridization results were scanned and fluorescence intensity standardized. Resets Hybridization results showed 33 microRNAs with up-regulated expressions but 38 microRNAs with down-regulated activity. Conclusion Expression of microRNA array shows marked changes in the tissues of the mesencephalon in rats with traumatic coma, as may be injury mechanism of traumatic coma and also a way of neurobiological protection of coma.

Objective To investigate the mRNA and protein expressions of Nav 1.1 and Nav 1.2 in hippocampus following traumatic brain injury ( TBI) in rats.Methods After the lateral fluid percussion model was established in adult male Sprague Dawley rats,the rats were sacrificed at 2,12,24 and 72 hours after percussion and collected ipsilateral hippocampus for detecting mRNA and protein expressions of Nav 1.1 and Nav 1.2 by means of fluorescent quantitation RT-PCR,Western blot and immunofluo rescence staining.Results The mRNA expressions of Nav 1.1 and Nav 1.2 were significantly down-regulated (P<0.01) in hippocampus and reached the lowest level at 2 hours following TBI.The protein expression of Nav 1.1 was significantly down-regulated (P<0.01) but recovered near to level of control group at 72 hours after TBI.While there was no statistical difference on protein expression of Nav 1.2 in hippocampus after TBI compared with control group (P>0.05).Conclusion TBI induces significant down-regulated mRNA and protein expressions of Nav 1.1 in the hippocampus,which may be one of molecular mechanisms for functional alternation of sodium channels and excitotoxic action following TBI.