Imaging-anatomic Measurements of Carotid Artery Bifurcation

ABSTRACT Objective: To have anatomic measurements of carotid artery bifurcation (CAB) with 64-spiral computed tomography angiography (64-SCTA), and provide anatomic basis for related research. Methods: Imaging data of 92 subjects (45 males, 47 females, the age range 20-82 years and mean age 48.4 ± 6.1 years) without pathology of CAB, who underwent 64-SCTA in head and neck from June 1, 2008 to June 30, 2010, were selected from the Picture Archiving and Communication Systems in Zhongshan Hospital of Xiamen University, Fujian, China. On the 3D images, the angle and size of CAB were measured, and the statistical comparisons of measurements were made between the bilateral, sex and age groups. Results: The measurements of CAB were divided into young (≤ 40 years) and older (> 40 years) groups: bifurcation angle is 36.206° ± 10.210° and 49.343° ± 16.489°, respectively; the inner diameter of common carotid artery (CCA) is 6.820 ± 0.635 and 6.845 ± 0.838 mm, respectively; the proximal inner diameter of internal carotid artery (ICA) is 7.143 ± 0.992 and 7.476 ± 1.630 mm, of the enlargement is 7.568 ± 1.069 and 8.554 ± 1.733 mm, of the distal is 4.897 ± 0.508 and 5.123 ± 0.699 mm, respectively; the inner diameter of external carotid artery (ECA) is 4.324 ± 0.580 and 4.104 ± 0.638 mm, respectively. There were statistically significant differences in all the measurements between male and female groups, in the bifurcation angle, inner diameters of ICA and ECA between young and older groups, and in the bifurcation angle between the left and right (p < 0.05). Conclusion: A 64-SCTA with 3D image post-processing technique can clearly observe and show the CAB. All CAB measurements will provide the objective basis for applied anatomy, imaging diagnosis and surgery treatment.

VP1-binding protein glucose-regulated protein 78 as an important mediator for enterovirus 71 infecting human brain microvascular endothelial cells

Purpose: Enterovirus 71 (EV71) is one of the main pathogens causing hand, foot and mouth disease, which could even induce severe brain damage in some patients. As the underlying mechanism of the invasion and replication process still remains largely unknown, we investigated the role of candidate proteins expressed during EV71 invasion in human brain microvascular endothelial cells (HBMECs) to delineate the pathophysiological mechanism of EV-71 infection. Materials and Methods: Ninety-one candidate EV71-associated proteins which could bind the major capsid protein (viral protein 1 [VP1]) of EV71 on the HBMEC were identified by applying an analysis of glutathione-S-transferase pull-down coupling with liquid chromatography-electrospray ionisation-tandem mass spectrometry (LC-ESI-MS/MS). Seventy-eight kDa glucose-regulated protein 78 (GRP78) binding to the VP1 protein was further validated by co-immunoprecipitation, immunofluorescence and western blot analysis. To explore the role of GRP78 in EV71 infection, GRP78 was knocked down and overexpressed in HBMEC and was verified by TCID50 assay. Results: LC-ESI-MS/MS-identified 91 proteins were subjected to gene ontology analysis, and on molecular and biological function analysis revealed GRP78 act as an important binding protein in mediating EV71 infection. In addition, immunofluorescence demonstrated the co-localisation of GRP78 and VP1 in cytoplasm of the infected HBMEC. The TCID50 assay showed that knockdown of GRP78 could attenuate the replication capacity of EV71 in HBMEC, and the overexpression could increase the virus titre in HBEMC at 24 h post-infection suggesting that GRP78 was associated with the replication capacity of EV71 in HBMEC. Conclusion: These findings provided evidence that GRP78 plays an important role during the progression of EV71 infection as a mediator in HBMEC.

Expression of TRIM28 and p16 in esophageal squamous cell carcinoma and their clinicopathological signifi-cance / 实用医学杂志

Objective To investigate the expression of TRIM28 and p16 in esophageal squamous cell car-cinoma(ESCC)and explore the possible correlation with them and clinicopathological characteristics. Methods The expression level of TRIM28 and p16 were measured by immunohistochemistry S-P in 136 cases with ESCC and 37 cases with normal esophageal mucosa,selected from the First Affiliated Hospital of Hebei North University De-partment of Pathology.The relationship between them and the clinical-pathological features was also analyzed.The localization of TRIM28 and p16 protein in ESCC was detected by immunofluorescence. Results(1)The positive rates of TRIM28 and p16 in ESCC were 91.2%and 32.4%,respectively,whereas in normal esophageal mucosa the corresponding rates were 24% and 57%,respectively.(2)Immunofluorescence results showed that TRIM28 and p16 protein were all mainly distributed in the nucleus of ESCC.(3)The abnormal expression of TRIM28 and p16 protein were all related to the invasion depth,TNM staging and lymph node metastasis in ESCC(P < 0.05).(4) The expression of TRIM28 was negatively correlated to the expression of p16 in ESCC(r =-0.284,P = 0.001). Conclusions The abnormal expression of TRIM28 and p16 may have synergistic effect on the initiation and devel-opment of ESCC.Co-detection of the expression of them may be useful for diagnosis of ESCC and guiding the clini-cal therapy.

Analysis of serum microRNA expression in male workers with occupational noise-induced hearing loss

Occupational noise-induced hearing loss (ONIHL) is a prevalent occupational disorder that impairs auditory function in workers exposed to prolonged noise. However, serum microRNA expression in ONIHL subjects has not yet been studied. We aimed to compare the serum microRNA expression profiles in male workers of ONIHL subjects and controls. MicroRNA microarray analysis revealed that four serum microRNAs were differentially expressed between controls (n=3) and ONIHL subjects (n=3). Among these microRNAs, three were upregulated (hsa-miR-3162-5p, hsa-miR-4484, hsa-miR-1229-5p) and one was downregulated (hsa-miR-4652-3p) in the ONIHL group (fold change >1.5 and Pbon value <0.05). Real time quantitative PCR was conducted for validation of the microRNA expression. Significantly increased serum levels of miR-1229-5p were found in ONIHL subjects compared to controls (n=10 for each group; P<0.05). A total of 659 (27.0%) genes were predicted as the target genes of miR-1229-5p. These genes were involved in various pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway. Overexpression of miR-1229-5p dramatically inhibited the luciferase activity of 3′ UTR segment of MAPK1 (P<0.01). Compared to the negative control, HEK293T cells expressing miR-1229-5p mimics showed a significant decline in mRNA levels of MAPK1 (P<0.05). This preliminary study indicated that serum miR-1229-5p was significantly elevated in ONIHL subjects. Increased miR-1229-5p may participate in the pathogenesis of ONIHL through repressing MAPK1 signaling.

Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy

Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and β-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear β-catenin through restraining β-catenin from cytoplasm into nuclei or it could also promote β-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.

Effects of Neuromuscular Activation Training on Balance and Walking in Children with Hemiplegic Cerebral Palsy / 中国康复理论与实践

@#Objective To observe the effects of neuromuscular activation (Neurac) training on balance and walking in children with hemiplegic cerebral palsy. Methods 30 children with hemiplegic cerebral palsy from March to October, 2015 were divided into observation group (n=15) and control group (n=15). Both groups received routine rehabilitation, while the observation group received 30-minute Neurac training in addition, 5 times a week, for 3 months. They were assessed with D and E domains of Gross Motor Function Measure 88 (GM-FM-88), balance of Fugl-Meyer Assessment and footprints analysis before and after treatment. Results The scores of D and E domains of GMFM-88 and balance of Fugl-Meyer Assessment, and the step length, step width and velocity improved in both groups after training (t>7.31, P<0.001), especially in the observation group (t>2.08, P<0.05). Conclusion Neuroac training can further promote the recovery of gross motor function, balance and walking in children with hemiplegic cerebral palsy.

Effect of hyperbaric oxygenation on mitochondrial function of neuronal cells in the cortex of neonatal rats after hypoxic-ischemic brain damage

The timing and mechanisms of protection by hyperbaric oxygenation (HBO) in hypoxic-ischemic brain damage (HIBD) have only been partially elucidated. We monitored the effect of HBO on the mitochondrial function of neuronal cells in the cerebral cortex of neonatal rats after HIBD. Neonatal Sprague-Dawley rats (total of 360 of both genders) were randomly divided into normal control, HIBD, and HIBD+HBO groups. The HBO treatment began immediately after hypoxia-ischemia (HI) and continued once a day for 7 consecutive days. Animals were euthanized 0, 2, 4, 6, and 12 h post-HI to monitor the changes in mitochondrial membrane potential (ΔΨm) occurring soon after a single dose of HBO treatment, as well as 2, 3, 4, 5, 6, and 7 days post-HI to study ΔΨm changes after a series of HBO treatments. Fluctuations in ΔΨm were observed in the ipsilateral cortex in both HIBD and HIBD+HBO groups. Within 2 to 12 h after HI insult, the ΔΨm of the HIBD and HIBD+HBO groups recovered to some extent. A secondary drop in ΔΨm was observed in both groups during the 1-4 days post-HI period, but was more severe in the HIBD+HBO group. There was a secondary recovery of ΔΨm observed in the HIBD+HBO group, but not in the HIBD group, during the 5-7 days period after HI insult. HBO therapy may not lead to improvement of neural cell mitochondrial function in the cerebral cortex in the early stage post-HI, but may improve it in the sub-acute stage post-HI.

Treatment with 1,25(OH)2D3 induced HDAC2 expression and reduced NF-κB p65 expression in a rat model of OVA-induced asthma

Recent evidence indicates that a deficiency of 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) may influence asthma pathogenesis; however, its roles in regulating specific molecular transcription mechanisms remain unclear. We aimed to investigate the effect of 1,25(OH)2D3 on the expression and enzyme activity of histone deacetylase 2 (HDAC2) and its synergistic effects with dexamethasone (Dx) in the inhibition of inflammatory cytokine secretion in a rat asthma model. Healthy Wistar rats were randomly divided into 6 groups: control, asthma, 1,25(OH)2D3 pretreatment, 1,25(OH)2D3 treatment, Dx treatment, and Dx and 1,25(OH)2D3 treatment. Pulmonary inflammation was induced by ovalbumin (OVA) sensitization and challenge (OVA/OVA). Inflammatory cells and cytokines in the bronchoalveolar lavage (BAL) fluid and histological changes in lung tissue were examined. Nuclear factor kappa B (NF-κB) p65 and HDAC2 expression levels were assessed with Western blot analyses and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR). Enzyme activity measurements and immunohistochemical detection of HDAC2 were also performed. Our data demonstrated that 1,25(OH)2D3 reduced the airway inflammatory response and the level of inflammatory cytokines in BAL. Although NF-κB p65 expression was attenuated in the pretreatment and treatment groups, the expression and enzyme activity of HDAC2 were increased. In addition, 1,25(OH)2D3 and Dx had synergistic effects on the suppression of total cell infusion, cytokine release, and NF-κB p65 expression, and they also increased HDAC2 expression and activity in OVA/OVA rats. Collectively, our results indicated that 1,25(OH)2D3 might be useful as a novel HDAC2 activator in the treatment of asthma.

More than 10 years survival with sequential therapy in a patient with advanced renal cell carcinoma: a case report

Although radical nephrectomy alone is widely accepted as the standard of care in localized treatment for renal cell carcinoma (RCC), it is not sufficient for the treatment of metastatic RCC (mRCC), which invariably leads to an unfavorable outcome despite the use of multiple therapies. Currently, sequential targeted agents are recommended for the management of mRCC, but the optimal drug sequence is still debated. This case was a 57-year-old man with clear-cell mRCC who received multiple therapies following his first operation in 2003 and has survived for over 10 years with a satisfactory quality of life. The treatments given included several surgeries, immunotherapy, and sequentially administered sorafenib, sunitinib, and everolimus regimens. In the course of mRCC treatment, well-planned surgeries, effective sequential targeted therapies and close follow-up are all of great importance for optimal management and a satisfactory outcome.

Bone marrow mesenchymal stem cells overexpressing human basic fibroblast growth factor increase vasculogenesis in ischemic rats

Administration or expression of growth factors, as well as implantation of autologous bone marrow cells, promote in vivo angiogenesis. This study investigated the angiogenic potential of combining both approaches through the allogenic transplantation of bone marrow-derived mesenchymal stem cells (MSCs) expressing human basic fibroblast growth factor (hbFGF). After establishing a hind limb ischemia model in Sprague Dawley rats, the animals were randomly divided into four treatment groups: MSCs expressing green fluorescent protein (GFP-MSC), MSCs expressing hbFGF (hbFGF-MSC), MSC controls, and phosphate-buffered saline (PBS) controls. After 2 weeks, MSC survival and differentiation, hbFGF and vascular endothelial growth factor (VEGF) expression, and microvessel density of ischemic muscles were determined. Stable hbFGF expression was observed in the hbFGF-MSC group after 2 weeks. More hbFGF-MSCs than GFP-MSCs survived and differentiated into vascular endothelial cells (P<0.001); however, their differentiation rates were similar. Moreover, allogenic transplantation of hbFGF-MSCs increased VEGF expression (P=0.008) and microvessel density (P<0.001). Transplantation of hbFGF-expressing MSCs promoted angiogenesis in an in vivo hind limb ischemia model by increasing the survival of transplanted cells that subsequently differentiated into vascular endothelial cells. This study showed the therapeutic potential of combining cell-based therapy with gene therapy to treat ischemic disease.

Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock

The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.

The N-terminal 33 amino acid domain of Siva-1 is sufficient for nuclear localization

Siva-1 induces apoptosis in multiple pathological processes and plays an important role in the suppression of tumor metastasis, protein degradation, and other functions. Although many studies have demonstrated that Siva-1 functions in the cytoplasm, a few have found that Siva-1 can relocate to the nucleus. In this study, we found that the first 33 amino acid residues of Siva-1 are required for its nuclear localization. Further study demonstrated that the green fluorescent protein can be imported into the nucleus after fusion with these 33 amino acid residues. Other Siva-1 regions and domains showed less effect on Siva-1 nuclear localization. By site-mutagenesis of all of these 33 amino acid residues, we found that mutants of the first 1-18 amino acids affected Siva-1 nuclear compartmentalization but could not complete this localization independently. In summary, we demonstrated that the N-terminal 33 amino acid residues were sufficient for Siva-1 nuclear localization, but the mechanism of this translocation needs additional investigation.

Expression of the transforming growth factor beta-induced gene in human corneal tissue and cell in vitro / 中华实验眼科杂志

Background Clinical studies indicated that the pathogenesis of most corneal dystrophy is associated with the mutation of the transforming growth factor beta-induced (TGFBI) gene.However,the molecular mechanism of mutated TGFBI gene in corneal dystrophy is unclear. Objective The present study was to investigate the expression of the TGFBI gene in human corneal tissue and cells in vitro.MethodsHuman corneal epithelial cells and keratocytes were cultured and passaged,and donor corneal tissue was obtained for the section preparation.RT-PCR was used to detect the expression of TGFBI mRNA in human corneal tissue and cells.Immunofluorescence was used to test the expression of the TGFBI protein in the human corneal tissue,and immunohistochemistry was used to test the expression of the TGFBI protein in human corneal epithelial cells and corneal stromal cells.ResultsRT-PCR analysis showed that TGFBI mRNA could be detected as a 1274 bp band in human corneal tissue and corneal stromal cells,but no TGFBI mRNA was observed in corneal epithelial cells.Immunofluorescence assay revealed that corneal stromal cells were positive ly expressed for the TGFBI protein,but the corneal epithelial cells did not express the TGFBI protein.Immunohistochemistry indicated that the expression of TGFBI was detected the red fluoressence in the cytoplasm of corneal stromal cells;however,no positive response was found in corneal epithelial cells.ConclusionsThe expression of the TGFBI gene occurs in human corneal stromal cells but not in the corneal epithelial cells.This result might be of helpful for studying the function and role of TGFBI gene in pathogenesis of corneal dystrophy.

Experimental study on the atlanto-axial joint and related structures with regional anatomy and medical imaging / Estudio experimental de la articulación atlanto-axial y las estructuras relacionadas con la anatomía regional y la imagen médica

OBJECTIVE: To evaluate the anatomy and medical imaging characteristics in a study observing the atlanto-axial joint (AAJ) and related structures. METHODS: Eight cadaveric specimens of the AAJ segment were studied with both anatomical and imaging methods. The vertebral arteries of the AAJ segment (VA-A), the first and second cervical nerves (CN1, CN2) and synovial fold (SF) of the AAJ were observed and measured. RESULT: After extending from the vertebral canal, the CN1 goes between the posterior arch of the atlas and VA-A, and the CN2 passes between the posterior arch of the atlas and axis, and is posterior to VA-A. Among the eight cases, six were found in the SF in the central anterior AAJ and five in lateral. The vertebral arteries of the AAJ segment go along the AAJ with four curves, of which the second and fourth are away from the bone structure of the AAJ. The distance from CN1, CN2 to VA-A and that from the second, fourth curve of VA-A to AAJ is 0.0-2.2 mm, 0.0-3.6 mm and 0.0-4.8 mm, 2.0-7.9 mm respectively. There is no significant difference between the measurements made anatomically and those by the imaging method (p > 0.05). CONCLUSION: The anatomical method has advantages in observing the CN and SF, while the imaging method shows clearly and directly the VA-A and AAJ. Both are mutually complementary with consistent measurements. The combined use of the two provides a new way to study the complicated anatomy in this region.

OBJETIVO: Evaluar las características del método anatómico y el uso de la imagen médica en un estudio de observación de la articulación atlanto-axial (AAA) y estructuras relacionadas. MÉTODOS: Se estudiaron ocho especimenes cadavéricos del segmento de la AAA tanto con métodos anatómicos como con métodos de imaginología médica. Las arterias vertebrales del segmento de AAA (AV-A), el primer y el segundo nervios cervicales (NC1, NC2) y los pliegues sinoviales (PS) fueron observados y medidos. RESULTADO: Tras de extenderse desde el canal vertebral, el NC1 se extiende entre el arco posterior del atlas, y el NC2 pasa entre el arco posterior del atlas y el axis, y es posterior a las AV-A. Entre los ocho casos, se encontraron seis en los PS en la AAA anterior central, y cinco en la lateral. Las arterias vertebrales del segmento AAA van junto con la AAA con cuatro curvas, de las cuales la segunda y la cuarta están separadas de la estructura ósea de la AAA. La distancia del NC1 y NC2, a las AV-A, y la de la segunda y cuarta curvas de las AV-A a la AAA es 0.0-2.2 mm, 0.0-3.6 mm y 0.0-4.8 mm, 2.0-7.9 mm respectivamente. No hay ninguna diferencia significativa entre las mediciones realizadas anatómicamente y las hechas mediante métodos de imaginología (p > 0.05). CONCLUSIÓN: El método anatómico tiene ventajas al observar el NC y los PS, mientras que el método imaginológico muestra clara y directamente las AV-A y la AAA. Ambos son mutualmente complementarios con las mediciones. El uso combinado de los dos proporciona una nueva manera de estudiar la complicada anatomía de esta región.

High frequency of integrons related to drug-resistance in clinical isolates of Acinetobacter baumannii.

Purpose: As an opportunistic pathogen, Acinetobacter baumannii causes various nosocomial infections. In recent years, the increasing cumulative infection outbreaks involving A. baumannii have appeared worldwide. In addition, a perplexing trouble for clinical treatment is a severe drug-resistance problem with A. baumannii. In this study, we investigated the drug-resistance rates and integrons' distribution in A. baumannii clinical strains in East China. Furthermore, we explored the relationship between integrons and drug resistance. Materials and Methods: Strains were identified using non-fermenting bacteria identification cards by Vitek-32 system. Disk-diffusion method (Kirby-Bauer) was used to judge antimicrobial sensitivity. Integrons and the gene cassettes of integrons were identified by PCR, restriction enzyme digestion and DNA sequencing. Results: Except imipenem and cefoperazone/sulbactam, the drug-resistance rates of the A. baumannii clinical isolates to other 15 kinds of antibacterials, all surpassed 30%. Of 96 A. baumannii clinical isolates, 66 strains carried class 1 integrons (no class 2 or 3 integrons were found). Overall, the drug-resistance rates in integrons-positive A. baumannii to 14 kinds of antibacterials were higher than those in integrons-negative A. baumannii. Gene sequencing showed that 9 of 12 integrons contained seven different gene cassettes (aacA4, catB3, dfrA1, blam-1, orfX, aadA1, and sat2). The cassette arrays aacA4-catB3-dfrA1 was found in five detected integrons. Conclusions: High resistances in A. baumannii clinical strains to most common antimicrobial agents have appeared in East China, which was closely related with high frequencies class 1 integrons. A. baumannii integrons cassettes carried multi-drug-resistant gene codes. We believe that integrons cassettes gene could be taken as a marker of prognosticating A. baumannii antimicrobial resistance, but only reveal partial drug resistance profiles.

The role of autolysis loop in determining the specificity of coagulation proteases

We recently demonstrated that the substitution of the autolysis loop (residues 143 to 154 in the chymotrypsin numbering system) of activated protein C (APC) with the corresponding loop of factor Xa (fXa) renders the APC mutant (APC/fX143-154) susceptible to inhibition by antithrombin (AT) in the presence of pentasaccharide. Our recent results further indicated, that in addition to an improvement in the reactivity of APC/fX143-154 with AT, both the amidolytic and anti-factor Va activities of the mutant APC have also been significantly increased. Since the autolysis loop of APC is five residues longer than the autolysis loop of fXa, it could not be ascertained whether this loop in the mutant APC specifically interacts with the activated conformation of AT or if a shorter autolysis loop is responsible for a global improvement in the catalytic activity of the mutant protease. To answer this question, we prepared another APC mutant in which the autolysis loop of the protease was replaced with the corresponding loop of trypsin (APC/Tryp143-154). Unlike an ~500-fold improvement in the reactivity of APC/fX143-154 with AT in the presence of pentasaccharide, the reactivity of APC/Tryp143-154 with the serpin was improved ~10-fold. These results suggest that both the length and structure of residues of the autolysis loop are critical for the specificity of the coagulation protease interaction with AT. Further factor Va inactivation studies with the APC mutants revealed a similar role for the autolysis loop of APC in the interaction with its natural substrate.

NRSF Plays a Regulatory Role in Human Insulin Gene Transcription / 生物化学与生物物理进展

The transcriptional repressor RE1 silencer transcription factor(NRSF/REST) is an important factor that restricts some neuronal traits in neurons.Since these traits are also present in pancreatic islet cells,NRSF-regulated genes involved in islet function are searched.A NRSE-like motif was analysed in human insulin promoter.The role of NRSE was evaluated by generating a model of insulin-secreting cells that firmly express NRSF.The presence of NRSF led to a decrease in activity of human insulin promoter by stable or transient transfection with human insulin-promoter luciferase.The predicted NRSE-like motif also confers NRSF-dependent transcriptional repression in the context of a surrogate gene promoter.Specific binding activity of NRSF/REST to the NRSE-like motif was confirmed by EMSA.Moreover,the binding activity is competed by consensus NRSE sequence.These data showed that human insulin promoter is regulated by the transcriptional repressor NRSF/REST via the NRSE-like motif.

Detecting overexpression of P-glycoprotein-multidrug resistance gene in epileptic patient's peripheral blood lymphocytes / 中华神经科杂志

Objective To explore the relationship between the overexpression of P glycoprotein (P GP) multidrug resistance (MDR) gene in the epileptic patient's peripheral blood lymphocytes and the drug resistance of the intractable epilepsy Methods This is a prospective, observational study. First, the overexpression of P GP MDR in 85 epileptic patients' (M 39, F46,overage age 24 years) peripheral blood lymphocytes were investigated by using immunocytochemistry (ICT) or flow cytometer (FCE). Then, patients were given a single or a combining of two antiepilepstic drugs which they did not received before (including carbamazepine, valproic acid, phenobarbitone,phenytoin), when the single drug was not effective in observing the clinical efficacy Results In FCE study group, results showed that the 11 patients with overexpression of P GP MDR in the epileptic patient's peripheral blood lymphocytes became tolerant to antiepileptic drugs. Eighteen out of 32 patients without overexpression of P GP MDR are effective. In the ICT study group, it is effective that there are only 2 out of the 22 patients with overexpression of P GP MDR. Seven of 12 patients without overexpression of P GP MDR are effective Conclusion It is suggested that the overexpression of MDR in the intractable epileptic patient's peripheral blood lymphocytes might be a significant drug resistance marker. The sensibility of ICT method should be better than the FCE,though the latter may be more accurate.