Acute Disease ; Adult ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Male ; Neurotoxicity Syndromes ; therapy

Adult ; Female ; Gas Poisoning ; drug therapy ; Glycoproteins ; therapeutic use ; Humans ; Male ; Middle Aged ; Quinuclidines ; therapeutic use ; Treatment Outcome ; Young Adult

Adaptation, Physiological ; Animals ; Brain Stem ; Cloning, Molecular ; DNA, Complementary ; Gene Expression ; Gene Library ; Motion Sickness ; genetics ; Rats

Animals ; Disease Models, Animal ; Male ; Motion Sickness ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe cerebral protective effect of muscone (nasal administration) on traumatic brain injury model rats.

METHODSSD rats were divided into the sham-operation group, the model group, and the treatment groups according to random digit table, 50 in each group. Traumatic brain injury model was established by controlled cortical strike. Rats in the sham-operation group received surgery and anesthesia procedures only, with no strike. Muscone (1.8 mg/kg) was delivered to rats in the treatment group using in situ nasal perfusion, 30 min each time, twice daily for 7 successive days. Water content of brain tissue was detected in each group before intervention (T1), at day 3 of intervention (T2), day 5 of intervention (T3), and after intervention (T4), respectively. Expression levels of brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were detected using immunohistochemical analysis.

RESULTSCompared with the sham-operated group, water content of brain tissue increased (P < 0.05), and expression levels of NGF and BDNF decreased in the model group at T1, T2, T3, and T4 (P <0. 01). Compared with the model group, water content of brain tissue decreased (P < 0.05), and expression levels of NGF and BDNF increased (P < 0.01) in the treatment group at T1, T2, and T3.

CONCLUSIONNasal administration of muscone could reduce water content of brain tissue, alleviate cerebral edema, promote secretion of BDNF and NGF by olfactory ensheathing cells in traumatic brain injury rats.

Animals ; Brain ; drug effects ; Brain Injuries ; drug therapy ; Brain-Derived Neurotrophic Factor ; metabolism ; Cycloparaffins ; pharmacology ; Nerve Growth Factor ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Objective To investigate the clinical effects of dynamic mild hypothermia on patients with severe brain injury. Methods One hundred and seventy-four patients with severe brain injury, admitted to our hospital from 2003 to 2009, were chosen and randomly assigned to mild hypothermia treatment group, short-term mild hypothermia treatment group and control group; their clinical outcomes and complications were recorded. Results The difference on effective rate of the 3 groups was significant (84.48%, 67.24%, 48.27%, respectively, P<0.05); the mortality in the 3 groups was 8.62%, 15.51%, 36.20%, respectively. No significant difference of complications was showed in the 3 groups (46.55%, 46.55% and 48.27%, respectively, P>0.05). Conclusion Dynamic mild hypothermia therapy can improve the outcomes of severe brain injury according to the patients' condition.

Objective To evaluate the acute and delayed killing effect of high intensity focused ultrasound (HIFU) on Echinococcus granulosus(E. granulosus)protoscolices in vitro.Methods E. granulosus protoscolices were treated with different dosage of effective power(0,25,50,100,200,250 W)and time(5,10,20,30,40,50,60 s)of HIFU in vitro to obtain the dosage-effect curves.Then the survival pmtoscolices were incubated,and the mortality of each group was counted daily.The protoscolicidal effects were investigated by trypan blue exclusion assay.Results Compared with the untreated group,the Vitality of E.granulosus protoscolices significantly decreased immediately after treated by HIFU of different dosage(F=5201.59 vs 1865.65,P＜0.05),there were the interaction both different dosage and time(F=214.50,P＜0.05).The protoscolices were broken into pieces by HIFU of 250 W×40 s,whereas the growth of the surviving protoscolices after exposed to HIFU was obvious suppressed.Both the acute killing effect and the delayed inhibitory effect showed a dosage-dependant manner.The inhibitory effect increased along with the increased dosage of HIFU(P＜0.05).The inhibitory effect in 50 W×10 s group was stronger than 25 W×20 s group(P＜0.05).The mortality was increased in parallel with the increase of HIFU dosage.Conclusions HIFU show an effective immediately killing effect,as well as a growth-inhibiting effect on the E.granulosus protoscolices in vitro.

Objective To investigate the myocardial damage in rats fed with corn from Keshan disease area added with bean puree. Methods Male Wistar rats were randomly divided into 3 groups according to their body weights, and fed with corn, corn from Keshan disease area added with bean puree, corn from non-endemic area. The GSH-Px activity of vena cardalis blood was examined in 1 and 3 months, rats were sacrificed after being fed for 6 months to examine the heart changes with HE stain. Results The three groups of GSH-Px activity were different in 1 and 3 months respectively(F=23.60,72.46, all P<0.01); GSH-Px activity was (181.58±22.15), (44.76±28.59)U/L in rats fed with corn, was (195.03±17.66), (30.38±3.35)U/L in those fed with corn added with bean puree from Keshan disease area, lower than the group fed with corn of non-endemic area[(340.90±95.42), (125.17±13.64)U/L, all P < 0.01]. But the difference of GSH-Px activity between simple corn group and corn adding bean puree groups of Keshan disease area was not obvious(P>0.05). Myocardial damage incidence of the three groups was 3/9,1/9,2/7. Difference among three groups did not have statistical significance(χ2=1.33, P> 0.05). Conclusions Only corn from Keshan disease area may induce myocardial damage pathology change. Adding bean puree into corn does not increase damage.

OBJECTIVETo identify the region in PRL-3 gene promoter where the transcriptional factor Snail can bind.

METHODSPRL-3 promoter and the possible binding sites of the transcription factors were analyzed by bioinformatical methods. Chromatin immunoprecipitation and PCR were performed using the antibody specific for Snail to verify the binding of Snail to PRL-3 promoter.

RESULTSAccording to the prediction by TRED, a promoter prediction software, PRL-3 gene promoter was located between -700 bp to 299 bp of PRL-3 gene. Many possible transcription factor binding sites such as for Snail, n-MYC, ARNT, E74A, NF-kappaB, NRF-2 and AML-1 were predicted by Consite, a promoter analysis web system. Interestingly, a 5'-CACCTG-3' core sequence and other related sequences of Snail binding sites were found in the promoter region of PRL-3 genes by Consite software. Two regions in PRL-3 promoter were validated to allow binding of Snail by chromatin immunoprecipitation analysis of SW480 cells.

CONCLUSIONSSnail regulates the activity of PRL-3 gene by binding to the promoter of PRL-3 gene in SW480 cells.

Base Sequence ; Binding Sites ; Cell Line, Tumor ; Computational Biology ; Humans ; Molecular Sequence Data ; Neoplasm Proteins ; metabolism ; Promoter Regions, Genetic ; Protein Tyrosine Phosphatases ; metabolism ; Snail Family Transcription Factors ; Software ; Transcription Factors ; metabolism

OBJECTIVETo analyze the gene mutation in two pedigrees of inherited coagulation factor VII (FVII) deficiency, and investigate the relationship between the genotype and phenotype.

METHODThe coagulation function and coagulation factors activity of probands were detected for phenotype diagnosis, all exons and junctions of FVII gene from the family members' genomic DNA were amplified using polymerase chain reaction (PCR), and detected the gene mutation by direct sequencing. Mutations were confirmed by reverse sequencing.

RESULTThe prothrombin time (PT) of proband 1 was 265.2 s, FVII:C was 22% and the PT of proband 2 was > 120 s, FVII:C was 1%. Homozygous 17844G→A mutation in No. 8 exon of FVII gene was identified in the proband 1 resulting in Gly343Ser, and heterozygosity for the same mutations were confirmed in his parents and a sister. The proband 2 was compound heterozygous, one mutation was the same as the proband 1 but was a heterozygosity that can also found in his mother and brother; the other heterozygosity mutation was located on No. 8 exon 18055G→A that resulted in Gln413Arg which was inherited from his father.

CONCLUSIONNo. 8 exon of FVII gene encodes catalytic domain. Mutation found in those domain could change the FVII catalytic domain spatial structure, affected FVII function and stability, and the sufferer of homozygote and compound heterozygous may have clinical bleeding tendency. Almost no clinical findings in simple heterozygotes, however, a few of heterozygotes could have a tendency of bleeding because of genetic polymorphism which would reduce the FVII:C.

Blood Coagulation Disorders ; blood ; genetics ; Child, Preschool ; DNA Mutational Analysis ; Factor VII ; genetics ; Factor VII Deficiency ; blood ; genetics ; Heterozygote ; Homozygote ; Humans ; Infant ; Male ; Molecular Sequence Data ; Mutation ; Pedigree ; Polymerase Chain Reaction ; Prothrombin Time