OBJECTIVETo study the combination of Mandibular distraction and orthognathic techniques for the reconstruction of adult hemifacial microsomia.

METHODSThe three-dimensional CT reconstruction data was used with Mimics for preoperation design. The osteotomy location, distraction vector, distraction distance were decided before operation with a surgical guider. At the first stage, internal distractor was implanted after ostetomy through an extra-oral approach. The distraction begun 5-7 days after operation with a frequency of 1 mm/day. After distraction, the distractor was maintained for 3-6 months. At the second stage, the distractor was removed. Le Fort I osteotomy was performed in order to correct the cross-bite and improve the facial contour. Usually, bone graft was inserted into the gap after Le Fort I osteotomy. The genioplasty was also performed if necessary.

RESULTS9 cases of adult hemifacial microsomia with severe mandibular deviation were treated. The facial asymmetry were improved greatly. 1 patient suffered an wound infection in the maxillary region after Le Fort I osteotomy and healed uneventfully with wound irrigation.

CONCLUSIONSMandibular distraction combined with orthognathic surgery is an effective procedure for adult hemifacial microsomia with complicated mandibular hypoplasia.

Adult ; Aged ; Bone Transplantation ; Facial Asymmetry ; surgery ; Goldenhar Syndrome ; surgery ; Humans ; Mandible ; surgery ; Osteogenesis, Distraction ; methods ; Osteotomy, Le Fort ; methods

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

Depression is a serious mental illness with a high incidence. At present, we do not fully understand the specific pathological mechanisms of depression, and the efficacy of drug treatments is very limited. Recent studies have shown that epigenetic changes that occur in specific brain regions may be a key mechanism by which environmental factors to interact with individuals to influence the risk of depression. Therefore, drugs that target epigenetic regulation may become a new direction for the development of antidepressants. Histone deacetylase inhibitors (HDACi) are a class of compounds that inhibit histone deacetylase activity, which has been reported to be associated with depression; this article addresses the use of HDACi in preclinical studies, and their potential therapeutic role and limitations of use in depression.

AIMTo explore the molecular biological mechanism of hemoglobin with high oxygen affinity in Tibetans by determining the sequence of globin cDNA in Tibetans living at high altitude.

METHODSTotal RNA was isolated from human bone marrow samples of three Tibetans who live in Qinghai-Tibet plateau. cDNA fragments coding for alpha and beta genes of human hemoglobin were obtained through RT-PCR and were ligated to plasmid pGEM-T easy vectors, and then the ligation liquid were transformed to Escherichia coli and cloned and sequenced. Nucleotide sequences were compared with GenBank data by BLAST method.

RESULTSsequence of a globin cDNA in Tibetans were the same with the registering globin genes in the GenBank, and Hb Abruzzo (beta143 (H21), His- > Arg) gene mutation, a high oxygen affinity beta globin mutation, was found in one Tibetan' beta goblin coding gene (CAC- > CGC).

CONCLUSIONThis hemoglobin gene mutation may be associated with high altitude adaptation of Tibetans living at high altitude.

Adult ; Altitude ; Asian Continental Ancestry Group ; genetics ; Cloning, Molecular ; DNA, Complementary ; genetics ; Hemoglobins, Abnormal ; genetics ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; RNA ; Sequence Analysis, DNA ; Tibet ; alpha-Globins ; genetics ; beta-Globins ; genetics

In order to enhance the antitumor efficacy of recombinant Newcastle disease virus, rNDV-IL15 was rescued in this study. Recombinant plasmid prNDV-IL15 was constructed, and BHK21 cells were transfected with the recombinant plasmid. Finally, the recombinant Newcastle disease virus rNDV-IL15 was successfully rescued. The growth curves of these two recombinant viruses were determined. Murine melanoma B16F10 cells were infected with rNDV-IL15 at MOI of 0.1, and the expression level of IL15 in the supernatant was detected by ELISA. The antitumor efficacy of rNDV-IL15 and rNDV was compared in vitro and in vivo. Results showed that prNDV-IL15 was constructed and recombinant virus rNDV-IL15 was successfully rescued. The growth curve of rNDV-IL15 showed that the growth of rNDV-IL15 had not been changed after insertion of IL15 gene. Results showed that there was high level of IL15 expression in the supernatant of rNDV-IL5-infected B16F10 cells (1 044.3 +/- 27.7 ng x mL(-1)). rNDV-IL15 and rNDV significantly inhibited the growth of B16F10 cells in vitro in a time-dependent manner. However, there was no significant difference between them. In animal experiments, rNDV-IL15 efficiently suppressed tumor growth in vivo when compared with rNDV, and the difference was statistically significant. The results suggested that rNDV-IL15 is a more effective antitumor agent.
Animals ; Body Weight ; Cell Line, Tumor ; Cell Proliferation ; Chick Embryo ; Cytotoxicity, Immunologic ; Female ; Genetic Therapy ; Interleukin-15 ; genetics ; metabolism ; Melanoma, Experimental ; pathology ; therapy ; Mice ; Neoplasm Transplantation ; Newcastle disease virus ; genetics ; Plasmids ; Recombinant Proteins ; genetics ; metabolism ; Transfection ; Tumor Burden

This study examined associations between MTHFR C677T polymorphism and serum folate concentrations with the risk of esophageal precancerous lesions (EPL) and esophageal squamous cell carcinoma (ESCC). The highest quartile of serum folate concentration significantly decreased the risk of ESCC compared with the lowest quartile (OR=0.11; 95% Cl, 0.04-0.33; P<0.05). MTHFR 677 C>T polymorphism was associated with the risk of ESCC by using chi-square tests (P<0.05). For the CT genotype, the risk of ESCC significantly increased in study participants with low serm folate concentrations (≤26.92 μg/L) compared with participants with high serum folate concentrations (>26.92 μg/L) by using multinomial logistic regression models. The MTHFR genotype may further modify associations between serum folate concentrations and the risk of ESCC, but it was not significantly associated with the risk of EPL.
Carcinoma, Squamous Cell ; blood ; genetics ; Chi-Square Distribution ; Esophageal Neoplasms ; blood ; genetics ; Folic Acid ; blood ; Genetic Predisposition to Disease ; Humans ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Polymorphism, Genetic

Reproductive toxicity research takes an important place in traditional Chinese medicine pre-clinical safety evaluation. Modern reproductive toxicity experiment includes drug-related miscarriage, fetal death, teratism, and adverse effects on fertility, genital system, embryonic development and fetus, which is different from contraindicated in pregnancy in traditional Chinese medicine theory. Now the three-phases reproductive toxicity study is the method mainly applied in traditional Chinese medicine reproductive toxicity evaluation. Besides that, alternative methods of whole embryos culture and embryonic stem cell test are also used in traditional Chinese medicine embryo toxicity evaluation. This article reviews research progress and pre-clinical evaluation on reproductive toxicity of traditional Chinese medicine.
Animals ; Drug-Related Side Effects and Adverse Reactions ; Drugs, Chinese Herbal ; toxicity ; Embryonic Development ; drug effects ; Embryonic Stem Cells ; drug effects ; Female ; Humans ; Medicine, Chinese Traditional ; Pregnancy ; Reproduction ; drug effects ; Toxicity Tests

OBJECTIVETo explore the association of the glycophorin A(GPA) gene mutation in peripheral erythrocytes and chronic benzene poisoning.

METHODSSixty-three patients with chronic benzene poisonings and 45 benzene-exposed workers who were engaged in the same job title were investigated. Fluorescence immunolabeling technique and flow cytometry were used to detect GPA mutation frequency in peripheral read blood cell.

RESULTSA significant decrease in WBC count and neutrophil count was found in patients with chronic benzene poisoning compared with control individuals (P<0.01). The WBC count and neutrophil count both decreased along with the GPA-NN frequency, and the trends were significant(P<0.05).Both WBC counts and neutrophil counts decreased as the frequency, and trends were significant(P<0.05). GPA-NN frequency increased along with the accumulative exposure score, and the trend was significant (P = 0.0026). There was no significant trend between the GPA-Nphi frequency and the accumulative exposure score (P = 0.2037).

CONCLUSIONA decrease in WBC count and neutrophil count is found in patients with chronic benzene poisoning, which can arise from genetic damage in bone marrow stem cells, namely gene-duplicating mutations (NN) at the GPA locus in bone marrow cells of MN-heterozygous subjects, GPA-NN mutagens contributed to the pathogenesis of chronic benzene poisoning.

Adult ; Benzene ; poisoning ; Bone Marrow Cells ; pathology ; Case-Control Studies ; Erythrocytes ; pathology ; Female ; Genetic Variation ; Glycophorin ; genetics ; Humans ; Leukocyte Count ; Male ; Middle Aged ; Mutation Rate ; Neutrophils ; pathology

AIMTo investigate the regulatory effects of various anti-inflammatory drugs on both endogenous and TNFalpha-induced NF-kappaB activation as well as the relative biological activity.

METHODSHEK293 cells were cultured in 96-well plate and 6-well plate, treated with meloxicam, indomethacin, dexamethasone and hydrocortisone, without or with 10 ng.mL(-1) TNFalpha for 24 hours. Then cell proliferation was measured by MTT and cell apoptosis was analyzed by pI stain-flow cytometry. HEK293/ kappaB-luc cells transfected stably with pElam-kappaB-luc vector, were cultured in 96-well plate and treated as above. Equal amounts of cell lysates were tested for luciferase activity which represents NF-kappaB activation.

RESULTSEndogenous NF-kappaB activation was present in HEK293 cells and its level can be increased about 2 times by 10 ng.mL(-1) TNFalpha-induction. Dexamethasone (1 x 10(-8) mol.L(-1)) and meloxicam (1 x 10(-7) - 1 x 10(-6) mol.L(-1)) can decrease both endogenous and TNFalpha-induced NF-kappaB activation. Hydrocortisone (1 x 10(-9) mol.L(-1)) increases endogenous NF-kappaB activation but decreases TNFalpha-induced one significantly. No influence of indomethacin on endogenous NF-kappaB activation was observed. However, its influence on TNFalpha-induced NF-kappaB activation is needed for further study. Cell apoptosis was observed after treatment with TNFalpha and 1 x 10(-8), 1 x 10(-6) mol.L(-1) dexamethasone and 1 x 10(-7) mol.L(-1) indomethacin, or only with dexamethasone. No significant effect of these anti-inflammatory drugs on cell proliferation was observed.

CONCLUSIONVarious anti-inflammatory drugs differ in their ability to regulate NF-kappaB activation in HEK293 cells, which indicates that NF-kappaB activation might be a potential useful target to study mechanism and for drug screening.

Anti-Inflammatory Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line ; Cell Proliferation ; drug effects ; Dexamethasone ; pharmacology ; Embryo, Mammalian ; Humans ; Hydrocortisone ; pharmacology ; Indomethacin ; pharmacology ; Kidney ; cytology ; metabolism ; NF-kappa B ; metabolism ; Thiazines ; pharmacology ; Thiazoles ; pharmacology

AIMTo investigate the effect of diazoxide preconditioning and the role of ERK and JNK in cellular signaling during diazoxide preconditioning protection in isolated spontaneous hypertension rat (SHR) hearts.

METHODSHearts were isolated from male SHR rats, and perfused on a Langendorff apparatus. Five groups were considered (n = 6). Con: after 40 min perfusion the hearts were submitted to 25 min ischemia followed by 30 min reperfusion. IP: the hearts were preconditioned with 2 periods of 5 min ischemia and 10 min reperfusion prior to 25 min ischemia. DP: the hearts were preconditioned with 2 periods of 10 min K-H solution with 50 micromol x L(-1) diazoxide and 5 min K-H solution reperfusion prior to 25 min ischemia. 5-HD: perfuse with 100 micromol x L(-1) 5-HD (a special mitochondrial ATP sensitive potassium channel blocker) for 10 min followed by 30 min K-H solution perfusion before 25 min ischemia. 5-HD + DP: 100 micromol x L(-1) 5-HD was given for 10 min before diazoxide preconditioning.

RESULTSDuring reperfusion, comparing with Con group, the recoveries of left ventricle developed pressure (LVDP), + dP/dt(max), - dP/dt(max) and left ventricle end diastolic pressure (LVEDP) were improved in IP and DP groups (P < 0.01 vs Con). At the end of reperfusion, compared with Con group, the expression of ERK in myocardium were higher in IP and DP groups (P < 0.01 vs Con), there was no significance between 5-HD and Con group, but 5-HD couldn't inhibit the expression of ERK induced by diazoxide preconditioning. The expression of JNK in IP and DP groups were decreased (P < 0.05 vs Con), this effect could been inhibited by 5-HD.

CONCLUSIONThese results indicated that diazoxide preconditioning could mimic ischemic preconditioning, the activation of ERK expression and the declining of JNK expression involved in diazoxide preconditioning in isolated SHR hearts.

Animals ; Diazoxide ; pharmacology ; In Vitro Techniques ; MAP Kinase Kinase 4 ; metabolism ; MAP Kinase Signaling System ; Male ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocardial Reperfusion Injury ; metabolism ; physiopathology ; Myocardium ; metabolism ; Rats ; Rats, Inbred SHR