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 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.

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.

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 investigate the effect of electroacupuncture (EA) pretreatment on neurological function, and the expression of Toll-like receptor 4 (TLR4) and nuclear factorκB (NF-κB) protein in ischemic penumbra after cerebral ischemia-reperfusion (CIR) injury. Methods A total of 36 male Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12) and EA group (n=12). The later two groups were occluded their right middle cerebral arteries for two hours and reperfused. The EA group was pretreated with EA at Baihui (GV20) for two weeks before modeling. They were assessed with modified Neurological Severity Scores (mNSS), the injury in ischemic brain was detected with HE staining, and the expression of TLR4 and NF-κB protein in ischemic penumbra were detected with Western blotting, 24 hours after reperfusion. Results The score of mNSS decreased (P<0.05), the injury of brain tissue ameliorated, and the expression of TLR4 and NF-κB decreased in ischemic penumbra (P<0.05) in EA group compared with those in the model group. Conclu-sion EA pretreatment can reduce the injury and improve the neurological function in rats after CIR by down-regulating the expression of TLR4 and NF-κB protein in ischemic penumbra.

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.

Objective To evaluate the frequency of mutations that occur in PHEX,FGF - 23 and DMP - I genes associated with familial hypophosphatemic vitamin D resistant rickets among 6 patients from 4 families in China. Methods The peripheral blood samples from 4 families were collected and other 10 persons from different families were selected as normal controls,and then the total gene DNA was extracted from the whole blood. Using polymerase chain reaction(PCR)amplication,sequences of the exons and flanking zones in PHEX,FGF - 23 and DMP - I genes were sequenced by direct DNA sequencing and TA cloning,and then the mutations found were analyzed. Results In exon 6 of DMP - I gene,c1218 C ﹥ T and c1230 G ﹥ A mutations were detected in lineage 1,as same sense mutation (propositus and its sister:homozygous mutation;mother:heterozygous mutation);c1333 - 1334 GC ﹥ TT mutation,as missense mutation,was found in exon 12 of PHEX gene on the propositus of lineage 2,determined as heterozygous muta-tion,but the same mutation was not found from their parents. In exon 3 of FGF - 23 gene,c716 C ﹥ T,p. T239M hetero-zygous mutation was found on the propositus and its mother. In exon 6 of the DMP - I gene,c205 A ﹥ T homozygous mutation was detected in lineage 3. In lineage 3,c716 C ﹥ T mutation of the FGF - 23 gene was detected,and the pro-positus and their father had the same mutation. No disease causing mutations of the PHEX,FGF - 23 and DMP - I genes were detected in the family members of lineage 1,3 and 4. Conclusions The mutation c1333 - 1334 GC ﹥ TT detected in exon 12 of PHEX gene might be the cause of disease for the propositus of lineage 2,as missense mutation, which needs further verification;c716 C ﹥ T,p. T239M mutation of the FGF - 23 gene detected in lineage 2 and 3 might not be the causes of the hypophosphatemic rickets and abnormal phenotype.

BACKGROUND: Inert biomaterials such as metal usually hold poor biocompatibility and weak bonding force, which is against the effect of dental or bone implants. Therefore, how to improve their biocompatibility has become the research hotspot.OBJECTIVE: To prepare collagen-coated titanium alloy (Ti6Al4V), and to assess its biocompatibility.METHODS: Ti6Al4V served as the matrix, the 3-amino propyl triethoxy silane (KH550) as the crosslinking agent, and the three-dimensional printed titanium alloy coated by collagen type Ⅰ and Ⅱ was prepared,respectively. The coated materials were co-cultured with mouse preosteoblasts MC-3T3-E1 to evaluate its biocompatibility. The effect of different kinds of collagen on the cell differentiation was compared by differential recognition of surface proteins.RESULTS AND CONCLUSION: When the N content on the titanium alloy surface (Φ10 cm) was 8.41%, the cladding quantity of collagen type Ⅰ and Ⅱ was 0.81 and 0.77 mg, respectively. Compared with the bare titanium alloy, the cell adhered well and distributed extensively on the coated titanium alloy,which showed strong viability and fast proliferation.The cells cultured on collagen type Ⅰ coated materials expressed the proteins associated with matrix synthesis, and those on collagen type Ⅱ coated materials expressed the proteins associated with mineralization. These results clarify that the collagen coating can improve the biocompatibility of titanium alloy, and different types of collagens act on different functional proteins.

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