Aged ; Female ; Humans ; Neurilemmoma ; Pharyngeal Neoplasms

OBJECTIVETo study technique of one-stage reconstruction of oral and maxillofacial soft tissue defect by using forearm free flap.

METHODSThe microsurgery procedure was used in the treatment of 4 oral cancer patients with oral and maxillofacial soft tissue defect after surgery.

RESULTSThe forearm free flap was survived, for 4-18 months the oral function was well, and the appearance was satisfactory.

CONCLUSIONThis is a good approach to the reconstruction of oral and maxillofacial soft tissue defect by using forearm free flap technique.

Aged ; Cystadenocarcinoma, Mucinous ; surgery ; Female ; Humans ; Male ; Middle Aged ; Mouth Neoplasms ; surgery ; Reconstructive Surgical Procedures ; methods ; Surgical Flaps ; Tongue Neoplasms ; surgery

AIMTo establish 3D QSAR model of propenamides with anti-malarial activities.

METHODSChemical synthesis combined with comparative molecular field analysis (CoMFA).

RESULTSGenerated QSAR models for activities of inhibiting chloroquine resistive malaria (W2) and chloroquine sensitive malaria (D6).

CONCLUSIONThe activity of anti-W2 depends mostly on steric interaction and the activity of anti-D6 depends on both steric and electrostatic interaction.

Acrylamides ; chemical synthesis ; chemistry ; pharmacology ; Animals ; Antimalarials ; chemical synthesis ; chemistry ; pharmacology ; Chloroquine ; pharmacology ; Drug Resistance ; Molecular Conformation ; Molecular Structure ; Plasmodium ; drug effects ; Quantitative Structure-Activity Relationship

Objective　To study the effect of IFN-γ inhalation via aerosol on cytokines of the immunocompromised rats. Methods　Immunocomprised rat model was established with cortisol acetate injection for 14 d and then Candida albicans fluid was injected by tracheal for establishing am immuno comprised with pulmonary infection model. IFN-γ was inhaled with aerosol 1 d before the bacterium injection and then for 1, 3 and 7 d respectively. The activity of TNF-α, and the levels of IL-1β and IL-6 in the supernatant of the cultured alveolar macrophage(AM), the activity of IFN-γ and TNF-α in bronchial alveolar lavage fluid (BALF), the expressions of IFN-γ,TNF-α, IL-1β, and IL-6 of the lung tissues, the level of IFN-γ,IL-1β, and IL-6 in the serum were investigated. Results　The activity of TNF-α, and the levels of IL-1β and IL-6 in the culture supernatant of the AM of the rats treated with IFN-γ were significantly higher than those of the control. The activity of IFN-γ and TNF-α in BALF was higher in the IFN-γ inhaled rats than in the control (except the activity of TNF-α on the 7th day). The expressions of IFN-γ and IL-1β in lung tissues was higher in the rats treated with IFN-γ than in the control. The expression of TNF-α in the rats treated with IFN-γ was less than that in the control rats. The expression of IL-6 had no difference between 2 groups. And no difference was found in the activity of IFN-γ, and the levels of IL-1β and IL-6 in the serum between 2 groups(except IL-1β on the 3rd day). Conclusion　Administration of IFN-γ via aerosol can obviously increase the activity or levels of some cytokines in the lung of the immunocompromised rats, but has no effect on them in serum of the immunocompromised rats.

Objective:To determine the location of the conus medullaris termination (CMT) in children under the magnetic resonance imaging (MRI).Methods:The children, aged 1 day to 15 yr, underwent MRI performed on the lumbosacral spine, were retrospectively analyzed.The CMT corresponding to the position of vertebral body was sequentially numbered.Each vertebral body was divided into upper (U), middle (M), and lower 1/3 unit (L), while the intervertebral disc was considered as an independent segment.From top to bottom of vertebral body, T 12-U1/3 was marked as 0, T 12-M1/3 was marked as 1, T 12-L1/3 was marked as 2, and T 12-L 1 was marked as 3, respectively.The children including male group and female group were divided into different age groups: <1 month, 1-5 months, 6-11 months, 1 yr, 2-4 yr, 5-9 yr and 10-15 yr.The children were divided into male group (M group) and female group (F group) according to gender, and the positions of CMT were compared. Results:A total of 231 children were enrolled in this study, including 122 males and 109 females, aged (4±4) yr.The corresponding number for the position of CMT in children aged <1 month, 1-5 months, 6-11 months, 1 yr, 2-4 yr, 5-9 yr and 10-15 yr was 7.3±2.0, 7.3±2.3, 6.4±1.8, 6.5±2.6, 5.4±2.2, 5.5±1.8, and 5.0±1.8, respectively.There was no statistically significant difference in the position of CMT between group M and group F ( P>0.05). Conclusion:The corresponding number for the position of CMT is 7.3, 7.3, 6.4, 6.5, 5.4, 5.5 and 5.0 in children aged <1 month, 1-5 months, 6-11 months, 1 yr, 2-4 yr, 5-9 yr and 10-15 yr, respectively.

This study was to determine the protective effect of ω-3 polyunsaturated fatty acids (ω-3PUFAs) on MK-801-induced cognitive impairment in schizophrenia (SZ) rats and the underlying mechanism.A rat model of schizophrenia was induced by MK-801.The cognitive function of rats was assessed using a Morris water maze.The number of hippocampal neurons was measured by Nissl staining.The expression of CREB,p-CREB,BDNF,TrkB,p-TrkB,AKT,p-AKT,ERK,and p-ERK in the hippocampus of rats was detected by Western blotting.The results showed that ω-3PUFAs attenuated MK-801-induced cognitive,impairment and hippocampal neurons loss,reversed the injury of the CREB/BDNF/TrtB pathway induced by MK-801,and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats.In conclusion,ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT,thereby increasing the synaptic plasticity and decreashng neuron loss,and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.

OBJECTIVETo study the gene mutation in a patient with multiple exostoses, identify the disease-causing gene mutation.

METHODSPolymerase chain reaction and DNA sequencing were used to screen the EXT1 or EXT2 gene mutation, while mismatch primer amplification and restriction endonuclease digestion were performed to confirm the mutation.

RESULTSBy DNA sequencing, a mutation in the seventh intron was detected and located at 26 bp of 3' splice site upstream in EXT1 gene, which was unreported before. Mismatch primer amplification and restriction fragment length polymorphism analysis suggested that this mutation was not detected in the normal control.

CONCLUSIONThe mutation 1633-26(C-->A) may be the disease-causing mutation in this patient with multiple exostoses.

DNA Mutational Analysis ; Exostoses, Multiple Hereditary ; genetics ; Female ; Humans ; Mutation ; N-Acetylglucosaminyltransferases ; genetics ; Young Adult

BACKGROUNDCD4(+)CD25(+) regulatory T cells (Tregs) mediate immune suppression through cell-cell contact with surface molecules, particularly cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR), and transforming growth factor beta (TGF-beta), but little is known about the exact role of Tregs in the pathogenesis of asthma. This study sought to characterize the expression of surface markers on peripheral blood mononuclear cells-derived Tregs in patients with atopic asthma and healthy subjects, and to investigate the effect of inhaled corticosteroid on them.

METHODSThe expression of surface molecules on CD4(+)CD25(high) Tregs was detected by flow cytometry. The effect of inhaled corticosteroid on expression of the surface molecules on Tregs was determined in vivo and in vitro. Total serum immunoglobulin E (IgE) and high-sensitivity C-reactive protein were measured by enzyme linked immunosorbent assay and latex enhanced immunoturbidimetric assay, respectively.

RESULTSEquivalent numbers of peripheral Tregs were found in patients with atopic asthma (stable and acute) and healthy subjects. Tregs preferentially expressed CTLA-4, GITR, toll-like receptor 4 (TLR4), latency-associated peptide (LAP/TGF-beta1), and forkhead box P3 (FOXP3). Patients with acute asthma had decreased numbers of CD4(+)CD25(high)LAP(+) T cells compared to healthy subjects and stable asthmatics. Inhaled corticosteroid enhanced the percentage of Tregs expressing LAP in vivo and in vitro dose-dependently. Furthermore, the percentages of Tregs expressing LAP were negatively correlated with total serum IgE levels and severity of asthma, but positively correlated with forced expiratory volume in one second percentage of the predicted value in patients with asthma.

CONCLUSIONSThe results suggest that membrane-bound TGF-beta1 is a potential candidate for predicting the severity of asthma, and may contribute to the sustained remission of asthma. Strategies targeting Tregs on their surface markers, especially TGF-beta1, are promising for future therapy of asthma.

Administration, Inhalation ; Adrenal Cortex Hormones ; administration & dosage ; Adult ; Antigens, CD ; blood ; Antigens, Differentiation ; blood ; Asthma ; drug therapy ; immunology ; Budesonide ; pharmacology ; CTLA-4 Antigen ; Female ; Forkhead Transcription Factors ; blood ; Glucocorticoid-Induced TNFR-Related Protein ; Humans ; Male ; Middle Aged ; Receptors, Nerve Growth Factor ; blood ; Receptors, Tumor Necrosis Factor ; blood ; T-Lymphocytes, Regulatory ; drug effects ; immunology ; Toll-Like Receptor 4 ; blood ; Transforming Growth Factor beta1 ; blood

BACKGROUNDBeta(2)-adrenoceptor (beta(2)AR) desensitization is a common problem in clinical practice. beta(2)AR desensitization proceeds by at least such three mechanisms as heterologous desensitization, homologous desensitization and a kind of agonist-induced rapid phosphorylation by a variety of serine/threonine kinases. It is not clear whether there are other mechanisms. This study aimed to investigate potential mechanisms of beta(2)AR desensitization.

METHODSTwenty-four BALB/c (6-8 weeks old) mice were divided into three groups, which is, group A, phosphate buffered saline (PBS)-treated; group B, ovalbumin (OVA)-induced; and group C, salbutamol-treated. Inflammatory cell counts, cytokine concentrations of bronchoalveolar lavage fluid (BALF), pathological sections, total serum IgE, airway responsiveness, membrane receptor numbers and total amount of beta(2)AR were observed. Asthmatic mouse model and beta(2)AR desensitization asthmatic mouse model were established. Groups B and C were selected for two-dimensional gel electrophoresis (2DE) analysis so as to find key protein spots related to beta(2)AR desensitization.

RESULTSAsthmatic mouse model and beta(2)AR desensitization asthmatic mouse model were verified by inflammatory cell count, cytokine concentration of BALF, serum IgE level, airway hyperreactivity measurement, radioligand receptor binding assay, Western blot analysis, and pathologic examination. Then the two groups (groups B and C) were subjected to 2DE. Two key protein spots associated with beta(2)AR desensitization, Rho GDP-dissociation inhibitor 2 (RhoGDI(2)) and peroxiredoxin 5, were found by comparative proteomics (2DE and mass spectrum analysis).

CONCLUSIONOxidative stress and small G protein regulators may play an important role in the process of beta(2)AR desensitization.

Albuterol ; therapeutic use ; Animals ; Asthma ; drug therapy ; metabolism ; Disease Models, Animal ; Electrophoresis, Gel, Two-Dimensional ; Female ; Guanine Nucleotide Dissociation Inhibitors ; analysis ; Lung ; chemistry ; pathology ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; Peroxiredoxins ; analysis ; Proteomics ; Receptors, Adrenergic, beta-2 ; physiology ; rho-Specific Guanine Nucleotide Dissociation Inhibitors

OBJECTIVE: To localize the gene of autosomal dominant familial dilated cardiomyopathy with conduction defect. METHODS: A Chinese family which was diagnosed as dilated cardiomyopathy with conduction defect was studied. Venous blood (3 - 5 mL) from some family members was collected, and genomic DNA was extracted from the blood. Then whole genome wide scan was performed after excluding the known markers on the candidate loci (CMD1A, CMD1 E, CMD1F, and CMD1H) by two-point linkage analysis. RESULTS: No significant evidence for linkage was found in the two point linkage analyses to the known markers in the analyzed family. And the whole genome wide scan showed the maximum LOD score reached 2.68 at marker D3S1614 ( at recombination fraction theta = 0). CONCLUSION The related gene in this kindred is located on 3q26 other than on CMD1A, CMD1H, CMD1E, and CMD1F.
Adult ; Arrhythmias, Cardiac ; etiology ; genetics ; Cardiomyopathy, Dilated ; genetics ; Chromosomes, Human, Pair 3 ; genetics ; Female ; Genetic Linkage ; Humans ; Male ; Microsatellite Repeats ; Middle Aged ; Pedigree