Design of Ni(OH)2/M-MMT Nanocomposite With Higher Charge Transport as a High Capacity Supercapacitor.

Nano-petal nickel hydroxide was prepared on multilayered modified montmorillonite (M-MMT) using one-step hydrothermal method for the first time. This nano-petal multilayered nanostructure dominated the ion diffusion path to be shorted and the higher charge transport ability, which caused the higher specific capacitance. The results showed that in the three-electrode system, the specific capacitance of the nanocomposite with 4% M-MMT reached 1068 F/g at 1 A/g and the capacity retention rate was 70.2% after 1,000 cycles at 10 A/g, which was much higher than that of pure Ni(OH)2 (824 F/g at 1 A/g), indicating that the Ni(OH)2/M-MMT nanocomposite would be a new type of environmentally friendly energy storage supercapacitor.

miR-132 weakens proliferation and invasion of glioma cells via the inhibition of Gli1.

OBJECTIVE: Transcriptional factor Gli1 in Hedgehog signal pathway facilitates epithelial mesenchymal transition (EMT) and is associated with invasion or proliferation of multiple tumor cells. The previous study showed the correlation between miR-132 down-regulation and glioma pathogenesis. We investigated the role of miR-132 in mediating Gli1 expression and in affecting proliferation or invasion of glioma cells. PATIENTS AND METHODS: Dual luciferase reporter gene assay was used to confirm the targeted regulation between miR-132 and Gli1. Tumor tissues at different pathological grades (grade II, III and IV) were collected from glioma patients, in parallel with brain tissues from contusion surgery. The expression of miR-132 and Gli1 was measured by RT-PCR. Glioma cell line U251 was treated with miR-132 or si-Gli1 followed by measuring the expression of Gli1, E-cadherin, Vimentin and Cyclin D1. In addition, flow cytometry and transwell assay were performed to evaluate cell invasion potency. RESULTS: Bioinformatics analysis showed the complementary binding sites between miR-132 and 3'-UTR of Gli1 mRNA. Transfection of miR-132 mimic significantly reduced luciferase activity, indicating the targeted regulatory relationship between miR-132 and Gli1 mRNA. Compared with control group, miR-132 expression was decreased and Gli1 level was elevated in glioma tissues, both of which were correlated with the pathological grade. Transfection of miR-132 mimic or si-Gli1 remarkably suppressed the expression of Gli1, Vimentin or Cyclin D1 in U251 cells, up-regulated E-cadherin expression, suppressed cell proliferation and invasion. CONCLUSIONS: Our data indicated that over-expression of miR-132 could inhibit proliferation or invasion of glioma cells via targeted inhibition of Gli1 expression.

Characterization of cortical potentials evoked by oesophageal balloon distention and acid perfusion in patients with functional heartburn.

Oesophageal visceral hypersensitivity is thought to be important in generating symptoms in functional heartburn (FH). However, the neurophysiological mechanisms involved are poorly understood. The aim of this study was to compare the characteristics of oesophageal cortical evoked potentials (CEPs) induced by balloon distension and acid perfusion in FH and controls. We studied 21 FH patients and 12 healthy volunteers. Oesophageal mechanical stimulation was performed using the specially constructed mechanical pump. CEPs were recorded using the 10-20 international system of electroencephalogram recording. Oesophageal distention elicited recognizable, reproducible and muti-peak CEPs. CEP latencies for N1, P1 and N2 components were significantly shorter (P = 0.016, P = 0.003 and P = 0.031, respectively) in FH than in controls before perfusion. Acid perfusion significantly decreased the latencies of N1, P1 and N2 (P = 0.022, P = 0.007 and P = 0.041, respectively) and significantly increased the amplitude of P1-N2 components (P = 0.020) in FH patients, but not in controls. In conclusion, cortical evoked potential responses evoked by oesophageal distention and acid perfusion were greater in FH than in controls, suggesting that dysfunction of visceral neural pathways and/or alterations in cortical processing may produce and mediate oesophageal hypersensitivity in FH. These findings provide the evidence that central sensitization contributes to the development and maintenance of oesophageal hypersensitivity.

Clinical significance of PCR in Helicobacter pylori DNA detection in human gastric disorders.

AIM: To investigate the clinical significance of the PCR assay in the diagnosis of gastric Helicobacter pylori (Hp) infection. METHODS: Hp infection in gastric antral biopsied specimens was identified by using the polymerase chain reaction (PCR) to amplify the specific Hp urease gene fragments (PCR-Hp-DNA) in 154 patients with gastrointestinal disorders. Hp urease gene oligonucleotide primers specific for Hp (16s rRNA) were used. Urease test and enzyme-linked immunosorbent assay (ELISA) for anti Hp-IgG serum were also used as controls. RESULTS: PCR-Hp-DNA was detected in 140 (91%) of the 154 patients, where patients 114 and 125 were found infected with Hp by urease test and ELISA Hp IgG, respectively. There was a marked difference in the Hp-positive rate between the PCR-Hp-DNA and the urease test or ELISA-Hp-IgG (P < 0.05). The Hp infection rate increased with age, although a minority of infected people developed signs and symptoms of gastric disorders. Hp infection is closely related to adenocarcinoma in both the gastric antrum as well as the down body of the stomach. CONCLUSION: PCR is a sensitive and specific method for the detection of Hp in human gastric tissues. Detection of Hp DNA in vivo using this approach might improve the clinical diagnosis and epidemiological research related to H. pylori infection.

Expression of PDGF and its receptor as well as their relationship to proliferating activity and apoptosis of meningiomas in human meningiomas.

In this study, we detected the expression of platelet-derived growth factor (PDGF) and its receptor in 61 human meningiomas by immunohistochemistry and in situ hybridisation. The results showed that almost all the 61 meningiomas expressed PDGFBB and PDGF beta receptor and the positive rate of PDGFAA was 49%. Only two meningiomas expressed PDGF alpha receptor. The positive rate and the immunostaining intensity of PDGFBB and PDGF beta receptor were higher in atypical meningiomas than in benign types. There was no significant difference between the different types of benign meningiomas. The expression of PDGFB chain mRNA was coincident with that of PDGFB chain protein. There was no correlation between the expression of PDGFAA and the types or grades of meningiomas. The correlation between overexpression of PDGFBB/R beta and tumour grade provides a useful parameter in evaluating the prognosis of patients with meningiomas. The proliferative activity of meningiomas was evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI). In the 61 meningiomas, the average PCNA LI (%) was 1.8+/-1.3, 1.9+/-1.3, 1.7+/-0.8 and 11.6+/-5.3 (in fibrous, meningothelial, transitional and atypical meningiomas, respectively). Statistic analysis shows that the PCNA LI is higher in atypical meningiomas than that in benign types, and there was no significant difference between the different types of benign meningiomas. The expression of PDGFBB and PDGF beta receptor was significant enhanced in ascending order from low PCNA LI meningiomas to high ones. This result suggested that PDGFBB/R beta autocrine loop may stimulate the growth of meningiomas. In this study, we also detected the cell apoptosis of meningiomas by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) method. The average apoptosis labelling index (%) was 0.11+/-0.05, 0.08+/-0.04, 0.09+/-0.03 and 0.35+/-0.15 in fibrous, meningothelial, transitional and atypical meningiomas respectively. The apoptosis labelling index was higher in atypical meningiomas than that in benign types. There was a positive correlation between the apoptosis labelling index and PC NA LI of meningioma. When the positive rate of PDGFBB and/or PDGF beta receptor was higher in meningioma, the apoptotic cells was also increased. In conclusion, the overexpression of PDGFBB and its relevant receptor PDGFR beta in meningiomas was correlated with grade of meningiomas and the proliferative activity of meningiomas; PDGFBB/R beta autocrine loop may play an critical role in the pathogenesis of meningiomas.

[Detection of north-Asia tick-borne spotted fever in ticks and rodents along the Heilongjiang river-side by restriction fragment length polymorphism of PCR products].

In order to elucidate the natural foci of North-Asia tick-borne spotted fever along the bank of Heilongjiang river, we used PCR/RFLP to detect spotted fever group rickettsiae in ticks and rodents. The results showed that the wild samples of Dermacentor silvarum, Haemaphysalis concinna and Apodemus agrarius, Microtus fortis, Clethrionomys rufocanus and Ondatra zibethica were all positive with amplification, but typhus rickettsiae, tsutsugamushi fever rickettsiae and Q fever rickettsiae were all negative. Futher RFLP analysis of amplified products with PstI and Rsal demonstrated that their restriction endonuclease profiles were identical to Rickettsia sibirica, but were different from the other prototype strains of SFG rickettsiae, suggesting the possible existance of natural foci of North-Asia tick borne spotted fever in these areas.

Expression of matrix metalloproteinases and the tissue inhibitors of metalloproteinases and their local invasiveness and metastasis in Chinese human pancreatic cancer.

BACKGROUND AND OBJECTIVES: The objective was to evaluate the potent role of matrix metalloproteinases(MMPs) and the tissue inhibitors of metalloproteinases(TIMPs) in processes leading to metastasis and local invasiveness of Chinese human ductal adenocarcinomas of the pancreas. We also evaluated a possible biological association between the gene expression and clinical manifestations. METHODS: Northern blot and in situ hybridization have shown MMP and TIMP gene expression in the pancreas and alterations associated with neoplastic transformation. Fifteen cases of surgical pancreatic specimens were examined, using cDNA probes to MMP2, MMP9, and TIMP1. Findings were correlated with the size of tumor section, CA19-9, pathological classification, thrombosis, and infiltration of capsule and lymphonoids. RESULTS: Increased levels of the mRNA of MMP2, MMP9, and TIMP1 genes, MMP2 approximately MMP9

The diagnostic value of transendoscopic miniature ultrasonic probe for esophageal diseases.

BACKGROUND AND STUDY AIMS: To investigate the value of a transendoscopic miniature ultrasonic probe (USP) in the diagnosis of esophageal diseases. PATIENTS AND METHODS: Endoscopic ultrasonography was performed by means of USP in 53 patients with esophageal diseases, including 16 with esophageal leiomyoma, 14 with esophageal carcinoma, seven with achalasia, seven with reflux esophagitis, six with esophageal polyps and three with esophageal varices. RESULTS: USP clearly showed all 16 esophageal leiomyomas, whereas, conventional EUS could not show five small leiomyomas less than 1.0 x 1.0 cm in size. The appearance of esophageal leiomyoma was that of a hypoechoic mass with a homogeneous inner echogram arising from the fourth hypoechoic layer. All 14 patients with esophageal carcinoma underwent full endosonographic T and N staging with USP. In two cases passage of the malignant stenosis proved to be impossible using conventional EUS. The accuracy of USP on T staging and N staging was 80% and 30%, respectively. In the seven achalasia patients USP demonstrated a seven-layer structure of the esophageal wall, with thickening of the third and fifth layers. In the seven patients with reflux esophagitis no difference was found for the ultrasonic image between that with and that without Barrett's epithelium. All of the esophageal polyps were showed by USP as hypoechoic homogeneous lesion with indistinct margins. After endoscopic sclerotherapy the ultrasonographic feature of esophageal varices changed from submucosal multiple anechoic areas to high echoic areas. CONCLUSION: With refinement, the transendoscopic miniature ultrasonic probe will play an increasing role in the diagnosis of esophageal disease.

Polycystin-1 interacts with intermediate filaments.

Polycystin-1, the protein defective in a majority of patients with autosomal dominant polycystic kidney disease, is a ubiquitously expressed multi-span transmembrane protein of unknown function. Subcellular localization studies found this protein to be a component of various cell junctional complexes and to be associated with the cytoskeleton, but the specificity and nature of such associations are not known. To identify proteins that interact with the polycystin-1 C-tail (P1CT), this segment was used as bait in a yeast two-hybrid screening of a kidney epithelial cell library. The intermediate filament (IF) protein vimentin was identified as a strong polycystin-1-interacting partner. Cytokeratins K8 and K18 and desmin were also found to interact with P1CT. These interactions were mediated by coiled-coil motifs in polycystin-1 and IF proteins. Vimentin, cytokeratins K8 and K18, and desmin also bound directly to P1CT in GST pull-down and in in vitro filament assembly assays. Two observations confirmed these interactions in vivo: (i) a cell membrane-anchored form of recombinant P1CT decorated the IF network and was found to associate with the cytoskeleton in detergent-solubilized cells and (ii) endogenous polycystin-1 distributed with IF at desmosomal junctions. Polycystin-1 may utilize this association for structural, storage, or signaling functions.

A bacterially expressed peptide prevents experimental infection of primates by the hepatitis E virus.

A 23 kDa peptide of the major structural protein of the hepatitis E virus (HEV) expressed in E. coli was found to naturally interact with one another to form homodimers and the peptide was recognized strongly in its dimeric form by HEV reactive human sera. To determine if the peptide may confer protection against HEV infection, three monkeys were immunized with the purified peptide and three were given placebo. Both groups of animals were challenged with 10(5) genome equivalent dose of the homologous strain of HEV. All control animals excreted the virus for 10-12 days beginning 5 days after the infection. The viral genome was also present in the peripheral blood monocyte (PBMC) samples from two animals, but it was not detected in the plasma samples from any of the animals. The infection in two control animals was accompanied by HEV seroconversion. Immunization was found to abrogate HEV stool excretion in two animals and reduced the viral excretion to one day in the third. None of the immunized animals showed detectable HEV in plasma or PBMC samples nor did the animals showed evidence of HEV seroconversion. These results suggested that immunization with the bacterially expressed peptide may prevent experimental infection of primates with the homologous strain of HEV.