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Find video protocols related to scientific articles indexed in Pubmed.
[Clinical and laboratory characteristics of chronic active Epstein-Barr virus infection in children.]
Zhongguo Dang Dai Er Ke Za Zhi
PUBLISHED: 11-20-2014
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To study the clinical and laboratory characteristics of chronic active Epstein-Barr virus (EBV) infection (CAEBV) in children and to provide a basis for the diagnosis and treatment of CAEBV.
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Isorhynchophylline treatment improves the amyloid-?-induced cognitive impairment in rats via inhibition of neuronal apoptosis and tau protein hyperphosphorylation.
J. Alzheimers Dis.
PUBLISHED: 10-22-2014
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The progressive accumulation of amyloid-? (A?) in the form of senile plaques has been recognized as a key causative factor leading to the cognitive deficits seen in Alzheimer's disease (AD). Recent evidence indicates that A? induces neurotoxicity in the primary neuronal cultures as well as in the brain. Previously, we have demonstrated that isorhynchophylline (IRN), the major chemical ingredient of Uncaria rhynchophylla, possessed potent neuroprotective effects. In the present study, we aimed to investigate the effect of IRN on cognitive function, neuronal apoptosis, and tau protein hyperphosphorylation in the hippocampus of the A?25-35-treated rats and to elucidate its action mechanisms. We showed that A?25-35 injection caused spatial memory impairment, neuronal apoptosis, and tau protein hyperphosphorylation. Treatment with IRN (20 or 40 mg/kg) for 21 days could significantly ameliorate the cognitive deficits induced by A?25-35 in the rats. In addition, IRN attenuated the A?25-35-induced neuronal apoptosis in hippocampus by down-regulating the protein and mRNA levels of the ratio of Bcl-2/Bax, cleaved caspase-3 and caspase-9, as well as suppressing the tau protein hyperphosphorylation at the Ser396, Ser404, and Thr205 sites. Mechanistic study showed that IRN could inhibit the glycogen synthase kinase 3? (GSK-3?) activity, and activate the phosphorylation of phosphatidylinositol 3-kinase (PI3K) substrate Akt. These results indicate that down-regulation of GSK-3? activity and activation of PI3K/Akt signaling pathway are intimately involved in the neuroprotection of IRN. The experimental findings provide further evidence to affirm the potential of IRN as a worthy candidate for further development into a therapeutic agent for AD and other tau pathology-related neurodegenerative diseases.
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[Dynamic accumulation regulation of curcumin, demethoxycurcumin and bisdemethoxyeurcumin in three strains of curcuma longae rhizome].
Zhongguo Zhong Yao Za Zhi
PUBLISHED: 10-03-2014
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The paper is aimed to study the dynamic accumulation regulation of curcumin (Cur), demethoxycurcumin (DMC) and bisdemethoxyeurcumin (BDMC) in three strains of Curcuma longa, and provide scientific references for formalized cultivation, timely harvesting, quality control and breeding cultivation of C. longa. The accumulation regulation of the three curcumin derivatives was basically the same in rhizome of three strains. The relative contents decreased along with plant development growing, while the accumulation per hectare increased with plant development growing. The accumulation of curcuminoids per hectare could be taken as the assessment standard for the best harvest time of C. longa. A3 was the best strain in terms of Cur and BDMC content.
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[Effect of L-ornithine L-aspartate granules in treating chronic liver disease in patients with high-level serum gamma-glutamyltransferase].
Zhonghua Gan Zang Bing Za Zhi
PUBLISHED: 09-10-2014
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To explore the clinical effect of L-ornithine L-aspartate (LOLA) granules in treating chronic liver disease in patients with high-level serum gamma-glutamyltransferase (G-GT) using a 24-week treatment course.
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Extensor digitorum brevis manus with "X" tendons.
Rom J Morphol Embryol
PUBLISHED: 09-03-2014
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During the educational dissection of a 72-year-old Chinese male cadaver, bilateral extensor digitorum brevis manus (EDBM) muscles were observed. The left EDBM muscle originated from the joint capsule ligament, running across the second dorsal interosseous muscle as double tendons (EDBM ulnar tendon and EDBM radial tendon) on the ulnar side of extensor digitorum communis (EDC)-index finger. The EDBM radial tendon positioned ventrally but inserted further to the ulnar tendon so that they made an "X" shape. The right EDBM muscle arose from dorsal radiocarpal ligament, coursing the second dorsal interosseous muscle and inserted into the ulnar side of EDC-index finger.
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Mesenchymal stem cells overexpressing integrin-linked kinase attenuate left ventricular remodeling and improve cardiac function after myocardial infarction.
Mol. Cell. Biochem.
PUBLISHED: 08-19-2014
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In the present study, we investigated whether mesenchymal stem cells (MSCs) overexpressing integrin-linked kinase (ILK) might regulate ventricular remodeling and cardiac function in a porcine myocardial infarction model. ILK-modified MSCs (ILK-MSCs) (n = 8), MSCs (n = 8) or placebo (n = 8) were injected into peri-infarct myocardium 7 days after ligation of the left anterior descending coronary artery. ILK expression was confirmed by immunofluorescence, real-time PCR, Western blot analysis, and flow cytometry. In vitro assays indicated increased proliferation and reduced apoptosis of MSCs due to overexpression of ILK. Echocardiographic, single-photon emission computed tomography and positron emission tomography analyses demonstrated preserved cardiac function and myocardial perfusion. Reduced fibrosis, increased cardiomyocyte proliferation, and enhanced angiogenesis were observed in the ILK-MSC group. Reduced apoptosis, as demonstrated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis, was also noted. In conclusion, ILK promotes MSC proliferation and suppresses apoptosis. ILK-MSC transplantation improves ventricular remodeling and cardiac function in pigs after MI. It is associated with increased angiogenesis, reduced apoptosis, and increased cardiomyocyte proliferation. This may represent a new approach to the treatment of post-infarct remodeling and subsequent heart failure.
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Role of glycosyltransferase PomGnT1 in glioblastoma progression.
Neuro-oncology
PUBLISHED: 08-03-2014
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Glioblastoma multiforme (GBM) is the most aggressive and invasive brain tumor, for which novel prognostic markers and predictors of therapeutic response are urgently needed. We reported previously that levels of peptide-O-linked mannose ?-1,2-N-acetylglucosaminyltransferase 1 (PomGnT1) in glioma specimens correlated with tumor grade. However, the prognostic significance of PomGnT1 in glioma patients and its function in GBM progression remain unknown.
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Could a traumatic epidural hematoma on early CT tell us about its future development? A multi-center retrospective study in China.
J. Neurotrauma
PUBLISHED: 07-23-2014
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Our aim of this study was to quantitatively develop an early EDH natural evolutionary curve, and to assess association of the most common radiological signs of initially nonsurgical supratentorial EDHs on early CT, added with their CT time for EDH enlargement. We retrospectively reviewed pertinent data of supratentorial EDH cases with CT ? 6h since injury (1997~2013) in three medical institutions in Shanghai. Cases involved were divided into 6 groups according to their initial CT time since injury (? 1h, 1~2h, 2~3h, 3~4h, 4~5h, and 5~6h for group 1 through 6, respectively). Time of initial CT, EDH-associated fractures, EDH volume, and EDH locations were the focus in present study. A total of 797 eligible cases were included. EDH growing curve showed EDH reached 98.1% of its final stabilized size by volume in 5~6h since injury. EDH volume and locations on initial CT could be highly associated with subsequent EDH increase ? 30ml and EDH increase requiring surgery when CT time was added. Multivariate analysis succeeded in determining two risk factors for EDH enlargement ? 30ml and EDH enlargement requiring surgery for EDH cases with an early CT: EDH volume > 10 ml on CT performed ? 2h and EDH located on temporal or temporoparietal region on CT ? 1h since head injury. Using recursive partitioning analysis, "high risk" identification criteria were derived to predict EDH enlargement ? 30ml with sensitivity of 90.5% (95% confidence interval, 77.9%~96.2%), specificity of 60.1% (95% confidence interval, 54.3%~65.7%); and EDH enlargement requiring surgery with sensitivity of 100.0% (95% confidence interval, 89.9%~100.0%), specificity of 59.9% (95% confidence interval, 54.1%~65.4%). A Redo-CT in 5~6 h post-impact for cases at "high risk" was recommended. Key Words: epidural hematoma; computed tomography; hematoma natural evolution; CT timing.
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Accessory slips of the extensor digiti minimi.
Rom J Morphol Embryol
PUBLISHED: 06-28-2014
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During the educational dissection of a 69-year-old Chinese male cadaver, an extensor digiti minimi (EDM) with five slips on the right hand was discovered. Except for the two slips of the little finger, the two radial slips were inserted into the dorsal aponeurosis of the middle finger and the ring finger, respectively. The middle slip was connected to the junctura tendinum in the fourth intermetacarpal spaces. Variations in this region are of paramount importance for the reconstructive surgeons, who may utilize the accessory slips to restore functional capacity of the fingers.
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Efficacy and Safety of Remifentanil and Sulfentanyl in Painless Gastroscopic Examination: A Prospective Study.
Surg Laparosc Endosc Percutan Tech
PUBLISHED: 06-10-2014
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We aim to assess efficacy and safety of remifentanil or sulfentanyl combined with propofol during painless gastroscopic examination in patients. In this study, 270 patients were randomly divided into 3 groups: propofol was given only in group P; propofol and remifentanil in group PR; propofol and sulfentanyl in group PS during the gastroscopic examination. Efficiency of group P was significantly lower than that of group PR and PS (P<0.01). Efficiency of group PR was lower than that of group PS (P<0.05). Incidence of chest wall rigidity and oxygen desaturation in group PR were higher than group P and PS (P<0.05), whereas there was no difference between groups P and PS (P>0.05). Propofol combined with remifentanil could provide satisfying anesthesia and more respiratory depression, whereas sulfentanyl at equivalent dose combined with propofol could also provide with satisfying anesthesia and less respiratory depression. Combined sufentanyl with propofol would be an effective anesthesia technique in the daytime procedure.
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Survival analysis for valproic acid use in adult glioblastoma multiforme: A meta-analysis of individual patient data and a systematic review.
Seizure
PUBLISHED: 05-19-2014
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Glioblastoma multiforme (GBM) is the most lethal type of primary brain tumor, and patients that undergo the maximum tumor resection that is safely possible and standard radiochemotherapy only achieve a median survival time of 14.6 months. Several clinical studies have reported that valproic acid could prolong survival of GBM patients. However, the results of these studies are inconsistent. We examined relevant studies and conducted a meta-analysis to assess the effects of VPA on survival times and recurrence.
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P450 enzyme-inducing and non-enzyme-inducing antiepileptic drugs for seizure prophylaxis after glioma resection surgery: a meta-analysis.
Seizure
PUBLISHED: 04-28-2014
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The prognoses of seizure treatment with P450 enzyme-inducing and non-enzyme-inducing antiepileptic drugs after glioma resection surgery were investigated across several clinical studies. However, the results of these studies are inconsistent. We examined the relevant studies and conducted a meta-analysis of these two types of anti-epileptic drugs.
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[Meta-analysis of magnesium isoglycyrrhizinate combined with nucleoside analogues in patients with chronic hepatitis B].
Zhonghua Gan Zang Bing Za Zhi
PUBLISHED: 04-17-2014
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To evaluate the efficacy and safety of the magnesium isoglycyrrhizinate plus nucleoside analogues (MGL + NA) combination therapy in patients with chronic hepatitis B using a meta-analysis approach.
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Relationship between intracranial pressure and aneurysmal subarachnoid hemorrhage grades.
J. Neurol. Sci.
PUBLISHED: 04-08-2014
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Intracranial pressure (ICP) is frequently elevated following aneurysmal subarachnoid hemorrhage (aSAH). In this prospective study, the factors associated with increased ICP and the relationship between ICP and the aSAH grade were evaluated.
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Isorhynchophylline improves learning and memory impairments induced by D-galactose in mice.
Neurochem. Int.
PUBLISHED: 04-08-2014
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Isorhynchophylline (IRN), an alkaloid isolated from Uncaria rhynchophylla, has been reported to improve cognitive impairment induced by beta-amyloid in rats. However, whether IRN could also ameliorate the D-galactose (D-gal)-induced mouse memory deficits is still not clear. In the present study, we aimed to investigate whether IRN had potential protective effect against the D-gal-induced cognitive deficits in mice. Mice were given a subcutaneous injection of D-gal (100mg/kg) and orally administered IRN (20 or 40mg/kg) daily for 8weeks, followed by assessing spatial learning and memory function by the Morris water maze test. The results showed that IRN significantly improved spatial learning and memory function in the D-gal-treated mice. In the mechanistic studies, IRN significantly increased the level of glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT), while decreased the level of malondialdehyde (MDA) in the brain tissues of the D-gal-treated mice. Moreover, IRN (20 or 40mg/kg) significantly inhibited the production of prostaglandin E 2 (PGE2) and nitric oxide (NO), and the mRNA expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), as well as the activation of nuclear factor kappa B (NF-?B) in the brain tissues of D-gal-treated mice. Our results amply demonstrated that IRN was able to ameliorate cognitive deficits induced by D-gal in mice, and the observed cognition-improving action may be mediated, at least in part, through enhancing the antioxidant status and anti-inflammatory effect of brain tissues via NF?B signaling.
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Use of lipolanthionine peptide, a toll-like receptor 2 inhibitor, enhances transdermal delivery efficiency.
Mol Med Rep
PUBLISHED: 04-01-2014
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The transdermal delivery system (TDS) is able to obtain a systemic therapeutic effect by administration through the skin, which has low side effects and is able to maintain a sustained blood concentration. However, due to the barrier presented by the stratum corneum, numerous drugs have poor percutaneous permeability. Therefore, the improvement of skin permeability is key to TDS. The main method of promoting transdermal absorption is through the usage of penetration enhancers. Dimethyl sulfoxide (DMSO) is a commonly used penetration enhancer, which has anti?inflammatory analgesic effects and is able to penetrate the skin. Retinoic acid (RA) and lipolanthionine peptide (LP) may also benefit the permeation efficiency of TDS. Therefore, the present study examined the function of DMSO, RA and LP as penetration enhancers in TDS. Firstly, the optimum concentration of DMSO was confirmed by detecting the expression of the LacZ gene in vitro. Secondly, different combinations of LP, RA and DMSO were applied to mouse skin to analyze the penetration enhancer combination with the greatest efficacy. All the animals were divided into five groups: The RA + LP + DMSO + pORF?LacZ group, the RA + DMSO + pORF?LacZ group, the LP + DMSO + pORF?LacZ group, the DMSO + pORF-LacZ group and the control group. Skin was soaked in combinations of LP, RA and DMSO for seven days and then the pORF?LacZ plasmids were daubed onto the skin once daily three days. On the 11th day, all the animals were sacrificed by cervical dislocation and the skin and blood samples were collected. The blood samples were used to detect the expression of the LacZ gene by quantitative polymerase chain reaction and the skin samples were used to detect the expression of claudin?4 and zonula occluden?1 (ZO?1) proteins by immunohistochemistry and western blot analysis. The results demonstrated that the combination of LP, RA and DMSO exhibited the greatest transdermal delivery efficiency, which verified that RA and LP were able to increase the penetration effects. Following treatment with LP, the symptoms of dermal edema were relieved and the capillaries contracted, which suggested that LP was a safe and effective penetration enhancer able to reduce the side?effects caused by DMSO. The present study provides a guideline for the synthesis of novel penetration enhancers.
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Clinical characteristics and current management of hepatitis B and C in China.
World J. Gastroenterol.
PUBLISHED: 03-24-2014
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To describe a population of outpatients in China infected by hepatitis B virus (HBV) and/or hepatitis C virus (HCV), and assess their current management status.
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Primary ectopic atypical meningioma in the renal hilum: a case report.
BMC Cancer
PUBLISHED: 03-16-2014
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Primary ectopic atypical meningioma involving the renal hilum is rare. This is, to our knowledge, only the second case report of a primary retroperitoneal meningioma and the first case of an atypical subtype in this location.
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Gamma knife surgery for pineal region tumors: an alternative strategy for negative pathology.
Arq Neuropsiquiatr
PUBLISHED: 03-08-2014
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Pineal region tumors (PRTs) are uncommon, and treatments vary among neoplasm types. The authors report their experience with gamma knife surgery (GKS) as an initial treatment in a series of PRT patients with unclear pathological diagnoses.
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Endogenous salicylic acid accumulation is required for chilling tolerance in cucumber (Cucumis sativus L.) seedlings.
Planta
PUBLISHED: 02-17-2014
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Salicylic acid (SA) is an important plant hormone, and its exogenous application can induce tolerance to multiple environmental stresses in plants. In this study, we examine the potential involvement of endogenous SA in response to chilling in cucumber (Cucumis sativus L.) seedlings. A low temperature of 8 °C induces a moderate increase in endogenous SA levels. Chilling stimulates the enzymatic activities and the expression of genes for phenylalanine ammonia-lyase (PAL) and benzoic acid-2-hydroxylase rather than isochorismate synthase. This indicates that the PAL enzymatic pathway contributes to chilling-induced SA production. Cucumber seedlings pretreated with SA biosynthesis inhibitors accumulate less endogenous SA and suffer more from chilling damage. The expression of cold-responsive genes is also repressed by SA inhibitors. The reduction in stress tolerance and in gene expression can be restored by the exogenous application of SA, confirming the critical roles of SA in chilling responses in cucumber seedlings. Furthermore, the inhibition of SA biosynthesis under chilling stress results in a prolonged and enhanced hydrogen peroxide (H2O2) accumulation. The application of exogenous SA and the chemical scavenger of H2O2 reduces the excess H2O2 and alleviates chilling injury. In contrast, the protective effects of SA are negated by foliar spraying with high concentrations of H2O2 and an inhibitor of the antioxidant enzyme. These results suggest that endogenous SA is required in response to chilling stress in cucumber seedlings, by modulating the expression of cold-responsive genes and the precise induction of cellular H2O2 levels.
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Tet and TDG mediate DNA demethylation essential for mesenchymal-to-epithelial transition in somatic cell reprogramming.
Cell Stem Cell
PUBLISHED: 02-13-2014
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Tet-mediated DNA oxidation is a recently identified mammalian epigenetic modification, and its functional role in cell-fate transitions remains poorly understood. Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three Tet genes and examine their capacity for reprogramming into induced pluripotent stem cells (iPSCs). We show that Tet-deficient MEFs cannot be reprogrammed because of a block in the mesenchymal-to-epithelial transition (MET) step. Reprogramming of MEFs deficient in TDG is similarly impaired. The block in reprogramming is caused at least in part by defective activation of key miRNAs, which depends on oxidative demethylation promoted by Tet and TDG. Reintroduction of either the affected miRNAs or catalytically active Tet and TDG restores reprogramming in the knockout MEFs. Thus, oxidative demethylation to promote gene activation appears to be functionally required for reprogramming of fibroblasts to pluripotency. These findings provide mechanistic insight into the role of epigenetic barriers in cell-lineage conversion.
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5mC Oxidation by Tet2 Modulates Enhancer Activity and Timing of Transcriptome Reprogramming during Differentiation.
Mol. Cell
PUBLISHED: 02-10-2014
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In mammals, cytosine methylation (5mC) is widely distributed throughout the genome but is notably depleted from active promoters and enhancers. While the role of DNA methylation in promoter silencing has been well documented, the function of this epigenetic mark at enhancers remains unclear. Recent experiments have demonstrated that enhancers are enriched for 5-hydroxymethylcytosine (5hmC), an oxidization product of the Tet family of 5mC dioxygenases and an intermediate of DNA demethylation. These results support the involvement of Tet proteins in the regulation of dynamic DNA methylation at enhancers. By mapping DNA methylation and hydroxymethylation at base resolution, we find that deletion of Tet2 causes extensive loss of 5hmC at enhancers, accompanied by enhancer hypermethylation, reduction of enhancer activity, and delayed gene induction in the early steps of differentiation. Our results reveal that DNA demethylation modulates enhancer activity, and its disruption influences the timing of transcriptome reprogramming during cellular differentiation.
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Developmental and activity-dependent expression of LanCL1 confers antioxidant activity required for neuronal survival.
Dev. Cell
PUBLISHED: 02-10-2014
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Production of reactive oxygen species (ROS) increases with neuronal activity that accompanies synaptic development and function. Transcription-related factors and metabolic enzymes that are expressed in all tissues have been described to counteract neuronal ROS to prevent oxidative damage. Here, we describe the antioxidant gene LanCL1 that is prominently enriched in brain neurons. Its expression is developmentally regulated and induced by neuronal activity, neurotrophic factors implicated in neuronal plasticity and survival, and oxidative stress. Genetic deletion of LanCL1 causes enhanced accumulation of ROS in brain, as well as development-related lipid, protein, and DNA damage; mitochondrial dysfunction; and apoptotic neurodegeneration. LanCL1 transgene protects neurons from ROS. LanCL1 protein purified from eukaryotic cells catalyzes the formation of thioether products similar to glutathione S-transferase. These studies reveal a neuron-specific glutathione defense mechanism that is essential for neuronal function and survival.
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Piperine reverses the effects of corticosterone on behavior and hippocampal BDNF expression in mice.
Neurochem. Int.
PUBLISHED: 01-23-2014
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A mouse model of depression has been recently developed by exogenous corticosterone administration. The present study aimed to examine the antidepressant-like effect and the possible mechanisms of piperine, a major alkaloid of black pepper (Piper nigrum Linn.) and long pepper (Piper longum Linn.), in corticosterone-induced depression in mice. The results showed that 3-weeks corticosterone injections caused depression-like behavior in mice, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test and tail suspension test. Moreover, it was found that brain-derived neurotrophic factor protein and mRNA levels in the hippocampus were significantly decreased in corticosterone-treated mice. Treating the animals with piperine significantly suppressed behavioral and biochemical changes induced by corticosterone. The results suggest that piperine produces an antidepressant-like effect in corticosterone-treated mice, which is possibly mediated by increasing brain-derived neurotrophic factor expression in the hippocampus.
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Genetic deletion of Rheb1 in the brain reduces food intake and causes hypoglycemia with altered peripheral metabolism.
Int J Mol Sci
PUBLISHED: 01-07-2014
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Excessive food/energy intake is linked to obesity and metabolic disorders, such as diabetes. The hypothalamus in the brain plays a critical role in the control of food intake and peripheral metabolism. The signaling pathways in hypothalamic neurons that regulate food intake and peripheral metabolism need to be better understood for developing pharmacological interventions to manage eating behavior and obesity. Mammalian target of rapamycin (mTOR), a serine/threonine kinase, is a master regulator of cellular metabolism in different cell types. Pharmacological manipulations of mTOR complex 1 (mTORC1) activity in hypothalamic neurons alter food intake and body weight. Our previous study identified Rheb1 (Ras homolog enriched in brain 1) as an essential activator of mTORC1 activity in the brain. Here we examine whether central Rheb1 regulates food intake and peripheral metabolism through mTORC1 signaling. We find that genetic deletion of Rheb1 in the brain causes a reduction in mTORC1 activity and impairs normal food intake. As a result, Rheb1 knockout mice exhibit hypoglycemia and increased lipid mobilization in adipose tissue and ketogenesis in the liver. Our work highlights the importance of central Rheb1 signaling in euglycemia and energy homeostasis in animals.
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Meta-analysis of peritumoural rCBV values derived from dynamic susceptibility contrast imaging in differentiating high-grade gliomas from intracranial metastases.
Int J Clin Exp Med
PUBLISHED: 01-01-2014
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In the preoperative period, it is very important to accurately differentiate high-grade gliomas from intracranial metastases, as treatment strategies vary. Hence we performed a meta-analysis to evaluate the sensitivity and specificity of peritumoural relative cerebral blood volume (rCBV) values derived from dynamic susceptibility contrast imaging (DSCI) in differentiating high-grade gliomas from intracranial metastases.
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Piperine reverses chronic unpredictable mild stress-induced behavioral and biochemical alterations in rats.
Cell. Mol. Neurobiol.
PUBLISHED: 01-01-2014
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Previous studies in our laboratory have demonstrated that piperine produced antidepressant-like action in various mouse models of behavioral despair, which was related to the serotonergic system. The present study aimed to examine the behavioral and biochemical effects of piperine in rats exposed to chronic unpredictable mild stress (CUMS). The results showed that CUMS caused depression-like behavior in rats, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test. In addition, it was found that serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) contents in the hippocampus and frontal cortex were significantly decreased in CUMS-treated rats. Treating the animals with piperine significantly suppressed behavioral and biochemical changes induced by CUMS. The results suggest that piperine produces an antidepressant-like effect in CUMS-treated rats, which is possibly mediated by increasing 5-HT and BDNF contents in selective brain tissues.
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[Study progress of spectral color science and its prospect of application in the field of Chinese medicine].
Guang Pu Xue Yu Guang Pu Fen Xi
PUBLISHED: 12-28-2013
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The paper reviewed the research progress in the spectral color science, including the common model, color measurement instrument in recent years, application of color measurement technology in agriculture, food, industry, medicine and other fields. The possibility to achieve the color quantization of Chinese medicine was explored by color measurement technology, and analyzed its application prospect in the field of Chinese medicine, provided a model for the study on quality control for Chinese medicine non-destructive online
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Involvement of substance P/neurokinin-1 receptor in the analgesic and anticancer activities of minimally toxic fraction from the traditional Chinese medicine Liu-Shen-Wan in vitro.
Biol. Pharm. Bull.
PUBLISHED: 12-21-2013
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Liu-Shen-Wan (LSW), an ancient preparation used to treat localized infection with pain, was recently reported to possess anticancer activity. The mechanism responsible for LSWs analgesic and anticancer activity is unclear. In the present study, we obtained a LSW supernatant (LSWS) fraction from ultrasound-assisted ethanol extraction (yield 15.9%) which proved to be safer than LSW in terms of hepatotoxicity. The LSWS (1 and 10 µg/mL) exhibited a potent inhibitory effect on the bradykinin-evoked rapid release of substance P from dorsal root ganglion (DRG) cells. At concentrations of 0.1 µg/mL and higher, the LSWS resulted in a concentration-related growth inhibitory effect on HepG2, a representative cancer cell lines. The LSWS significantly down-regulated the neurokinin-1 (NK-1) receptor expression in both HepG2 and bradykinin-treated DRG cells. In addition to the NK-1 receptor-dependent growth inhibition in HepG2 cells (0.1-100 µg/mL), the LSWS induced mitochondria-mediated apoptosis at a higher concentration (1-100 µg/mL). In conclusion, we recently isolated a safer LSW fraction which maintained its analgesic and anticancer activity, and found that the substance P/NK-1 receptor system was partly responsible for these effects. Our findings will be useful for developing more effective and less toxic LSW preparations.
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Blockage of the Upregulation of Voltage-Gated Sodium Channel Nav1.3 Improves Outcomes after Experimental Traumatic Brain Injury.
J. Neurotrauma
PUBLISHED: 12-06-2013
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Abstract Excessive active voltage-gated sodium channels are responsible for the cellular abnormalities associated with secondary brain injury following traumatic brain injury (TBI). We previously presented evidence that significant upregulation of Nav1.3 expression occurs in the rat cortex at 2?h and 12?h post-TBI and is correlated with TBI severity. In our current study, we tested the hypothesis that blocking upregulation of Nav1.3 expression in vivo in the acute stage post-TBI attenuates the secondary brain injury associated with TBI. We administered either antisense oligodeoxynucleotides (ODN) targeting Nav1.3 or artificial cerebrospinal fluid (aCSF) at 2?h, 4?h, 6?h, and 8?h following TBI. Control sham animals received aCSF administration at the same time points. At 12?h post-TBI, Nav1.3 messenger ribonucleic acid (mRNA) levels in bilateral hippocampi of the aCSF group were significantly elevated, compared with the sham and ODN groups (p<0.01). However, the Nav1.3 mRNA levels in the uninjured contralateral hippocampus of the ODN group were significantly lowered, compared with the sham group (p<0.01). Treatment with antisense ODN significantly decreased the number of degenerating neurons in the ipsilateral hippocampal CA3 and hilar region (p<0.01). A set of left-to-right ratio value analyzed by magnetic resonance imaging T2 image on one day, three days, and seven days post-TBI showed marked edema in the ipsilateral hemisphere of the aCSF group, compared with that of the ODN group (p<0.05). The Morris water maze memory retention test showed that both the aCSF and ODN groups took longer to find a hidden platform, compared with the sham group (p<0.01). However, latency in the aCSF group was significantly higher than in the ODN group (p<0.05). Our in vivo Nav1.3 inhibition studies suggest that therapeutic strategies to block upregulation of Nav1.3 expression in the brain may improve outcomes following TBI.
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Generation of stable 3-mRNA cleavage fragments induced by siRNA in cells with high-levels of duck hepatitis B virus replication.
Biochem. Biophys. Res. Commun.
PUBLISHED: 11-21-2013
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Therapeutic small interfering RNAs (siRNAs) have attracted a lot of interest both in basic biomedical sciences as well as in translational medicine. Apart from their therapeutic efficacy adverse effects of siRNAs must be addressed. The generation of stable mRNA cleavage fragments and the translation of N-truncated proteins induced by antisense oligodeoxynucleotides (ASOs) have been reported. Similar to ASOs, siRNAs are considered to function via an antisense mechanism that promotes the cleavage of the target mRNA. To further investigate whether the stable mRNA cleavage fragments also occur in siRNA we constructed a short hairpin RNA (shRNA) expression plasmid, pshRNA794, containing the same sequence reported in experiments using ASOs which directly targeted the overlapping region of the pre-genomic mRNA (pgmRNA) and sub-genomic mRNA (sgmRNA) of duck hepatitis B virus (DHBV). The shRNA resulted in a 70.9% and 69.9% reduction of the DHBV mRNAs in LMH and HuH-7 cells, respectively. In addition a 70% inhibition of the DHBV DNA level was observed. Interestingly, 3-mRNA cleavage fragments were detected in LMH but not in HuH-7 cells. Taken together, our findings demonstrate that the ASO sequence was also effective in siRNA. Importantly, our results provide direct evidence that stable 3-mRNA fragments were generated by siRNA in cells with high levels of DHBV replication. Whether these can cause adverse RNAi effects needs to be explored further.
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[Experimental observation of SIVmac239 Chinese rhesus monkey model at sub-acute phase of AIDS].
Zhongguo Zhong Yao Za Zhi
PUBLISHED: 11-16-2013
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To observe T lymphocyte subsets and indicators of changes in viral load in sub-acute period in Chinese rhesus monkey model of AIDS SIVmac239. To explore Virology related index variation in sub-acute period of the Chinese rhesus monkey model of AIDS.
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Brain-derived neurotrophic factor signalling mediates the antidepressant-like effect of piperine in chronically stressed mice.
Behav. Brain Res.
PUBLISHED: 10-09-2013
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Previous studies in our laboratory have demonstrated that piperine produced antidepressant-like action in various mouse models of behavioral despair. This study aimed to investigate the role of brain-derived neurotrophic factor (BDNF) signalling in the antidepressant-like effect of piperine in mice exposed to chronic unpredictable mild stress (CUMS). The results showed that CUMS caused depression-like behavior in mice, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test. It was also found that BDNF protein expression in the hippocampus and frontal cortex were significantly decreased in CUMS-treated mice. Chronic treatment of piperine at the dose of 10mg/kg significantly ameliorated behavioural deficits of CUMS-treated mice in the sucrose preference test and forced swim test. Piperine treatment also significantly decreased immobility time in the forced swim test in naive mice. In parallel, chronic piperine treatment significantly increased BDNF protein expression in the hippocampus and frontal cortex of both naive and CUMS-treated mice. In addition, inhibition of BDNF signalling by injection of K252a, an inhibitor of the BDNF receptor TrkB, significantly blocked the antidepressant-like effect of piperine in the sucrose preference test and forced swim test of CUMS-treated mice. Taken together, this study suggests that BDNF signalling is an essential mediator for the antidepressant-like effect of piperine.
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C-Myc negatively controls the tumor suppressor PTEN by upregulating miR-26a in glioblastoma multiforme cells.
Biochem. Biophys. Res. Commun.
PUBLISHED: 09-27-2013
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The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with oncogenesis in GBM through deregulation of miRNAs via the c-Myc-miR-26a-PTEN signaling pathway. This may be of clinical relevance.
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Telbivudine treatment corrects HBV-induced epigenetic alterations in liver cells of patients with chronic hepatitis B.
Carcinogenesis
PUBLISHED: 09-25-2013
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Hepatitis B virus (HBV) alters the expression of host cellular genes to support its replication and survival and to promote the liver cell injury. However, the underlying mechanism remained incompletely understood. In this study, we investigated HBV-induced epigenetic changes in HepG2 cells by profiling the landscapes of the active histone modification mark H3K4me3 and repressive mark H3K27me3 using chromatin immunoprecipitation-sequencing. HBV caused the altered histone modifications at thousands of genomic loci, which are critically involved in HBV entry, inflammation, fibrosis and carcinogenesis of host cells. Interestingly, treatment of the HBV-transformed HepG2 cells with the anti-HBV drug Telbivudine substantially restored the H3K4me3 level to that of untransformed HepG2 cells. More importantly, our analysis of liver samples from control and chronic hepatitis B patients revealed that treatment of the patients with Telbivudine not only corrected the target gene expression but also the epigenetic modification of critical genes. In addition, the expression of the histone methyltransferases SMYD3 and EZH2 that regulate histone H3-specific methylation showed no difference in HepG2 cell with or without HBV existence. Thus, our data suggest that abnormal histone modifications might critically involved in HBV-mediated liver pathogenesis and Telbivudine therapy might benefit patients with HBV-related chronic infection, liver cirrhosis and even hepatic carcinoma. Summary: Telbivudine substantially restores in vitro and in vivo HBV-caused abnormal expressions and histone H3K4me3 and H3K27me3 modifications at thousands of genomic loci that are involved in the pathogenesis of liver cells, revealing a novel mechanism for HBV-mediated liver damage.
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[Construction of a full-genome HCV replicon with self-cleaving double ribozyme sequences and characterization in vitro and in vivo].
Zhonghua Gan Zang Bing Za Zhi
PUBLISHED: 09-13-2013
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To construct a full-genome hepatitis C virus (HCV) replicon that will allow for direct initiation of replication and generation of infectious viral particles in an in vitro and in vivo cell system.
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[Progress in application of genetic control of mosquitoes].
Zhongguo Xue Xi Chong Bing Fang Zhi Za Zhi
PUBLISHED: 09-13-2013
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With the specific, environmental-friendly, fast and efficient characteristics, the genetic control of mosquitoes has been preliminary shown a good effect. However, the prejudices and misunderstandings to the genetic control limit its popularization and application. Therefore, in order to re-recognize and take full advantage of this method, the recent progresses towards applying the genetic control of mosquitoes are reviewed.
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The role of quantitative changes in the epxression of insulin receptor substrate-1 and nuclear ubiquitin in abnormal glycometabolism in the livers of KKay mice and the relative therapeutic mechanisms of Astragalus polysaccharide.
Int. J. Mol. Med.
PUBLISHED: 08-19-2013
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Ubiquitin and the ubiquitination pathway are important regulators of insulin signaling. The insulin receptor substrate?1 (IRS-1), an ubiquitin-interacting adaptor protein, serves as the key docking protein in insulin signaling. The effects of this dynamic interaction and the changes in ubiquitin expression on hepatic insulin signaling, as well as the relative therapeutic effects of Astragalus polysaccharide (APS) have not yet been elucidated. In this study, we aimed to investigate the abnormal changes which occur in the levels of IRS-1 and ubiquitin in the livers of mice (mice with insulin resistance and diabetes), and to elucidate the possible mechanisms responsible for these changes. A control group (CG), an insulin resistance group (IG) and a diabetes group (DG) were respectively composed of 12-week-old C57BL/6J mice fed a normal diet, C57BL/6J mice fed a high?fat diet and KKay mice fed a high?fat diet, and treatment groups were composed of corresponding groups treated with APS (CG + A, IG + A, DG + A). All the mice were age-matched and grouped at random. After eight weeks, the mouse models were successfully established and the related physiological or biochemical indexes were detected using corresponding methods. Ubiquitin expression in the liver was detected by immunohistochemisty, and western blot analysis was used to detect the expression of IRS-1 and ubiquitin. The results revealed that the expression of IRS-1 in the DG was significantly lower compared to that in the CG and IG; however, the nuclear expression of ubiquitin and the ubiquitination levels of IRS-1, including body weight and blood glucose and triglyceride levels in the DG were significantly higher compared to those in the CG or IG (P<0.05). There was a significant improvement in the ubiquitination levels in DG + A, including the blood glucose and triglyceride levels compared with the DG (P<0.05). From the stage of insulin resistance to the stage of diabetes, the reduced expression of IRS-1 and its enhanced ubiquitination levels combined with the overexpression of nuclear ubiquitin contributed to the abnormal glycometabolism and the disruption of insulin signaling. APS showed beneficial effects, such as lowering body weight, as well as blood glucose and triglyceride levels, and these effects correlated with the downregulation of the ubiquitination levels of IRS-1 and the nuclear expression of ubiquitin.
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Serum creatinine and creatinine clearance for predicting plasma methotrexate concentrations after high-dose methotrexate chemotherapy for the treatment for childhood lymphoblastic malignancies.
Cancer Chemother. Pharmacol.
PUBLISHED: 08-02-2013
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Monitoring of plasma methotrexate (MTX) concentrations allows for therapeutic adjustments in treating childhood acute lymphoblastic leukemia (ALL) or non-Hodgkin lymphoma (NHL) with high-dose MTX (HDMTX). We tested the hypothesis that assessment of creatinine clearance (CrCl) and/or serum Cr may be a suitable means of monitoring plasma MTX concentrations.
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Gain of Function of Mutant TP53 in Glioblastoma: Prognosis and Response to Temozolomide.
Ann. Surg. Oncol.
PUBLISHED: 07-28-2013
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Our aim was to investigate the relationship between mutant p53 and the prognosis of malignant glioma treated with temozolomide, and the regulation of mutant TP53 induced drug resistance, by molecular experimentation and a clinical trial.
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O-linked mannose ?-1,2-N-acetylglucosaminyltransferase 1 correlated with the malignancy in glioma.
J Craniofac Surg
PUBLISHED: 07-16-2013
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O-linked mannose ?-1,2-N-acetylglucosaminyltransferase 1 (PomGnT1) constitutes one third of the O-linked glycoproteins in brain tissue. However, its functions have been seldom investigated in brain cancers. In this study, immunohistochemistry was used for the detection of the PomGnT1 protein in 133 cases of glioma tissues. Spearman correlation analysis was used for the relationship between PomGnT1 staining and the glioma grade. Receiver operating characteristic curve was used to measure the diagnostic value of PomGnT1 protein in the degree of glioma malignance. We found that PomGnT1 expression was correlated with glioma grade, and it could be used as a marker to distinguish low- and high-grade gliomas. Stably transfected U87 cells were constructed to overexpress short hairpin RNA of PomGnT1. Immunofluorescence test detected that this protein also could restrain the generation of U87 cells pseudopodia. Western blotting further showed that the PomGnT1 protein had an impact on the c-myc protein level. In conclusion, our data suggest that PomGnT1 protein was correlated with the malignance of glioma progression, the mechanism involved in glioma cells pseudopodium formation, and the expression of c-myc protein.
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Magnetic resonance diffusion tensor imaging with fluorescein sodium dyeing for surgery of gliomas in brain motor functional areas.
Chin. Med. J.
PUBLISHED: 07-05-2013
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Tumor surgery in brain motor functional areas remains challenging. Novel techniques are being developed to gain maximal and safe resection for brain tumor surgery. Herein, we assessed the magnetic resonance diffusion tensor imaging (MR-DTI) and fluorescein sodium dyeing (FLS) guiding technique for surgery of glioma located in brain motor functional areas.
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Ascorbic acid enhances Tet-mediated 5-methylcytosine oxidation and promotes DNA demethylation in mammals.
J. Am. Chem. Soc.
PUBLISHED: 07-01-2013
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DNA hydroxymethylation and its mediated DNA demethylation are critical for multiple cellular processes, for example, nuclear reprogramming, embryonic development, and many diseases. Here, we demonstrate that a vital nutrient ascorbic acid (AA), or vitamin C (Vc), can directly enhance the catalytic activity of Tet dioxygenases for the oxidation of 5-methylcytosine (5mC). As evidenced by changes in intrinsic fluorescence and catalytic activity of Tet2 protein caused by AA and its oxidation-resistant derivatives, we further show that AA can uniquely interact with the C-terminal catalytic domain of Tet enzymes, which probably promotes their folding and/or recycling of the cofactor Fe(2+). Other strong reducing chemicals do not have a similar effect. These results suggest that AA also acts as a cofactor of Tet enzymes. In mouse embryonic stem cells, AA significantly increases the levels of all 5mC oxidation products, particularly 5-formylcytosine and 5-carboxylcytosine (by more than an order of magnitude), leading to a global loss of 5mC (?40%). In cells deleted of the Tet1 and Tet2 genes, AA alters neither 5mC oxidation nor the overall level of 5mC. The AA effects are however restored when Tet2 is re-expressed in the Tet-deficient cells. The enhancing effects of AA on 5mC oxidation and DNA demethylation are also observed in a mouse model deficient in AA synthesis. Our data establish a direct link among AA, Tet, and DNA methylation, thus revealing a role of AA in the regulation of DNA modifications.
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Protein expression profiling by antibody array analysis with use of dried blood spot samples on filter paper.
J. Immunol. Methods
PUBLISHED: 06-17-2013
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Dried blood spot samples (DBSS) on filter paper offer several advantages compared to conventional serum/plasma samples: they do not require any phlebotomy or separation of blood by centrifugation; they are less invasive; they allow sample stability and shipment at room temperature; and they pose a negligible risk of infection with blood-borne viruses, such as HIV, HBV and HCV, to those who handle them. Therefore dried blood spot samples (DBSS) on filter paper can be a quick, convenient and inexpensive means of obtaining blood samples for biomarker discovery, disease screening, diagnosis and treatment monitoring in non-hospitalized, public health settings. In this study, we investigated for the first time the potential application of dried blood spot samples (DBSS) in protein expression profiling using antibody array technology. First, optimal conditions for array assay performance using dried blood spot samples (DBSS) was established, including sample elution buffer, elution time, elution temperature and assay blocking buffer. Second, we analyzed dried blood spot samples (DBSS) using three distinct antibody array platforms, including sandwich-based antibody arrays, quantitative antibody arrays and biotin-label-based antibody arrays. In comparison with paired serum samples, detection of circulating proteins in dried blood spot samples (DBSS) correlated well for both low- and high-abundance proteins on all three antibody array platforms. In conclusion, our study strongly indicates the novel application of multiplex antibody array platforms to analyze dried blood spot samples (DBSS) on filter paper represents a viable, cost-effective method for protein profiling, biomarker discovery and disease screening in a large, population-based survey.
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The calcium-sensing receptor R990G polymorphism is associated with increased risk of hypertriglyceridemia in obese Chinese.
Gene
PUBLISHED: 06-14-2013
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We have demonstrated that the calcium-sensing receptor (CaSR) is involved in lipid metabolism; however, whether CaSR polymorphisms affect lipid metabolism in obesity is still unclear. The present study aimed to determine the effects of CaSR polymorphisms on HTG risk in obese Chinese.
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[Correlation between IDH1 mutation and prognosis in supratentorial high-grade astrocytomas].
Sichuan Da Xue Xue Bao Yi Xue Ban
PUBLISHED: 06-11-2013
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To study the correlation between isoeitratedehydrogenasel 1 (IDH1) mutation and prognosis in supratentorial high-grade astrocytomas.
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Effect of intravenous infusion of dexmedetomidine combined with inhalation of isoflurane on arterial oxygenation and intrapulmonary shunt during single-lung ventilation.
Cell Biochem. Biophys.
PUBLISHED: 06-05-2013
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To investigate the changes in arterial oxygenation and intrapulmonary shunt during one-lung ventilation (OLV) with intravenous infusion of dexmedetomidine combined with isoflurane inhalation. ASA I-II 60 patients aged 18-70 year, undergoing OLV during elective thoracic surgery were randomly allocated to two groups: (1) isoflurane + saline (group NISO, n = 30) and (2) isoflurane + dexmedetomidine (group DISO, n = 30). After induction, anesthesia was maintained with intravenous infusion of remifentanil 0.1-0.2 ?g kg(-1) min(-1) and inhalation isoflurane (1.0-2.0 %). In addition, anesthesia was maintained with intravenous infusion of dexmedetomidine 0.7 ?g kg(-1) h(-1) in DISO group and saline 0.25 ml kg(-1) h(-1) in NISO group. Bispectral Index values were maintained within 40-60 by changing the concentration of isoflurane in all groups. Arterial blood gas samples and central venous blood gas samples were taken as follows: during two-lung ventilation before OLV and during the first 40 min of OLV. 45 Patients completed the study, with 23 patients in DISO group and 22 patients in NISO group. The two groups were comparable in terms of demographic variables, hemodynamic, PaO2, Qs/QT, end expiration isoflurane and BIS levels during the operation. Compared with patients in the group NISO, there were significant increases with PaO2, significant decrease with Qs/QT, significant decrease with end expiration isoflurane, and significant decrease with HR in the group DISO during the first 40 min of OLV (P < 0.05). Dexmedetomidine infusions decrease the requirement for isoflurane, decrease intrapulmonary shunt, and moderate the change in PaO2 and may be useful in managing OLV.
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Hypoxia/ischemia up-regulates Id2 expression in neuronal cells in vivo and in vitro.
Neurosci. Lett.
PUBLISHED: 06-04-2013
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Inhibitor of DNA binding/differentiation 2 (Id2) belongs to a family of transcriptional modulators characterized by a helix-loop-helix (HLH) motif that lacks the basic amino acid domain necessary to bind DNA. The aim of this study was to obtain a better understanding of the role of Id2 in hypoxia/ischemia (H/I)-induced neuronal apoptosis. Following H/I induction in a rat model of middle cerebral artery occlusion (MCAO)/reperfusion, the number of TUNEL-positive cells in cerebral cortices of the penumbra area increased gradually, while the Id2 mRNA and protein expression were also significantly up-regulated. The hypoxia-mimetic, cobalt chloride (CoCl2)-treated rat neuroblastoma B35 cell line also demonstrated enhanced Id2 mRNA and protein expression as well as increased number of cells in the sub-G1 populations after H/I exposure. Consistently, the expression of Bax, a proapoptotic protein, was also up-regulated in vivo and in vitro. Moreover, triple immunofluorescence demonstrated the obvious co-localization of Id2, TUNEL and NeuN in neurons of the penumbra area. These data suggest that H/I up-regulates Id2 expression in neuronal cells, and Id2 might play an important role in H/I-induced neuronal apoptosis.
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Isorhynchophylline Protects PC12 Cells Against Beta-Amyloid-Induced Apoptosis via PI3K/Akt Signaling Pathway.
Evid Based Complement Alternat Med
PUBLISHED: 06-03-2013
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The neurotoxicity of amyloid- ? (A ? ) has been implicated as a critical cause of Alzheimers disease. Isorhynchophylline (IRN), an oxindole alkaloid isolated from Uncaria rhynchophylla, exerts neuroprotective effect against A? 25-35-induced neurotoxicity in vitro. However, the exact mechanism for its neuroprotective effect is not well understood. The present study aimed to investigate the molecular mechanisms underlying the protective action of IRN against A? 25-35-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Pretreatment with IRN significantly increased the cell viability, inhibited the release of lactate dehydrogenase and the extent of DNA fragmentation in A? 25-35-treated cells. IRN treatment was able to enhance the protein levels of phosphorylated Akt (p-Akt) and glycogen synthase kinase-3 ? (p-GSK-3 ? ). Lithium chloride blocked A? 25-35-induced cellular apoptosis in a similar manner as IRN, suggesting that GSK-3 ? inhibition was involved in neuroprotective action of IRN. Pretreatment with LY294002 completely abolished the protective effects of IRN. Furthermore, IRN reversed A? 25-35-induced attenuation in the level of phosphorylated cyclic AMP response element binding protein (p-CREB) and the effect of IRN could be blocked by the PI3K inhibitor. These experimental findings unambiguously suggested that the protective effect of IRN against A? 25-35-induced apoptosis in PC12 cells was associated with the enhancement of p-CREB expression via PI3K/Akt/GSK-3 ? signaling pathway.
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Hepatitis B virus induces IL-23 production in antigen presenting cells and causes liver damage via the IL-23/IL-17 axis.
PLoS Pathog.
PUBLISHED: 06-01-2013
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IL-23 regulates myriad processes in the innate and adaptive immune systems, and is a critical mediator of the proinflammatory effects exerted by Th17 cells in many diseases. In this study, we investigated whether and how hepatitis B virus (HBV) causes liver damage directly through the IL-23 signaling pathway. In biopsied liver tissues from HBV-infected patients, expression of both IL-23 and IL-23R was remarkably elevated. In vivo observations also indicated that the main sources of IL-23 were myeloid dendritic cells (mDCs) and macrophages. Analysis of in vitro differentiated immature DCs and macrophages isolated from healthy donors revealed that the HBV surface antigen (HBsAg) efficiently induces IL-23 secretion in a mannose receptor (MR)-dependent manner. Culture with an endosomal acidification inhibitor and the dynamin inhibitor showed that, upon binding to the MR, the HBsAg is taken up by mDCs and macrophages through an endocytosis mechanism. In contrast, although the HBV core antigen (HBcAg) can also stimulate IL-23 secretion from mDCs, the process was MR- and endocytosis-independent. In addition, IL-23 was shown to be indispensible for HBsAg-stimulated differentiation of naïve CD4(+) T cells into Th17 cells, which were determined to be the primary source of IL-17 in HBV-infected livers. The cognate receptor, IL-17R, was found to exist on the hepatic stellate cells and mDCs, both of which might represent the potential target cells of IL-17 in hepatitis B disease. These data provide novel insights into a yet unrecognized mechanism of HBV-induced hepatitis, by which increases in IL-23 expression, through an MR/endocytosis-dependent or -independent manner, produce liver damage through the IL-23/IL-17 axis.
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[A clinical and molecular study of long-term survival glioblastomas].
Zhonghua Wai Ke Za Zhi
PUBLISHED: 05-29-2013
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To analyze the long-term survivors of glioblastoma and to identify any prognostic factors that potentially contribute to survival.
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Hybrid DNA virus in Chinese patients with seronegative hepatitis discovered by deep sequencing.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 05-28-2013
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Seronegative hepatitis--non-A, non-B, non-C, non-D, non-E hepatitis--is poorly characterized but strongly associated with serious complications. We collected 92 sera specimens from patients with non-A-E hepatitis in Chongqing, China between 1999 and 2007. Ten sera pools were screened by Solexa deep sequencing. We discovered a 3,780-bp contig present in all 10 pools that yielded BLASTx E scores of 7e-05-0.008 against parvoviruses. The complete sequence of the in silico-assembled 3,780-bp contig was confirmed by gene amplification of overlapping regions over almost the entire genome, and the virus was provisionally designated NIH-CQV. Further analysis revealed that the contig was composed of two major ORFs. By protein BLAST, ORF1 and ORF2 were most homologous to the replication-associated protein of bat circovirus and the capsid protein of porcine parvovirus, respectively. Phylogenetic analysis indicated that NIH-CQV is located at the interface of Parvoviridae and Circoviridae. Prevalence of NIH-CQV in patients was determined by quantitative PCR. Sixty-three of 90 patient samples (70%) were positive, but all those from 45 healthy controls were negative. Average virus titer in the patient specimens was 1.05 e4 copies/µL. Specific antibodies against NIH-CQV were sought by immunoblotting. Eighty-four percent of patients were positive for IgG, and 31% were positive for IgM; in contrast, 78% of healthy controls were positive for IgG, but all were negative for IgM. Although more work is needed to determine the etiologic role of NIH-CQV in human disease, our data indicate that a parvovirus-like virus is highly prevalent in a cohort of patients with non-A-E hepatitis.
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No association between tea consumption and risk of renal cell carcinoma: a meta-analysis of epidemiological studies.
Asian Pac. J. Cancer Prev.
PUBLISHED: 05-18-2013
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To evaluate the association between tea consumption and the risk of renal cell carcinoma.
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MiR-26a enhances the radiosensitivity of glioblastoma multiforme cells through targeting of ataxia-telangiectasia mutated.
Exp. Cell Res.
PUBLISHED: 05-14-2013
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Glioblastoma multiforme (GBM) is notoriously resistant to radiation, and consequently, new radiosensitizers are urgently needed. MicroRNAs are a class of endogenous gene modulators with emerging roles in DNA repair. We found that overexpression of miR-26a can enhance radiosensitivity and reduce the DNA repair ability of U87 cells. However, knockdown miR-26a in U87 cells could act the converse manner. Mechanistically, this effect is mediated by direct targeting of miR-26a to the 3UTR of ATM, which leads to reduced ATM levels and consequent inhibition of the homologous recombination repair pathway. These results suggest that miR-26a may act as a new radiosensitizer of GBM.
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[Relationship between IDH1 mutation and clinic pathologic features in human supratentorial WHO grade II gliomas].
Sichuan Da Xue Xue Bao Yi Xue Ban
PUBLISHED: 04-23-2013
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To investigate the relationship between isocitrate dehydrogenase 1 (IDH1) mutation and clinicopathological features in human supratentorial WHO grade II gliomas.
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Calcineurin/NFAT pathway mediates wear particle-induced TNF-? release and osteoclastogenesis from mice bone marrow macrophages in vitro.
Acta Pharmacol. Sin.
PUBLISHED: 04-21-2013
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To investigate the roles of the calcineurin/nuclear factor of activated T cells (NFAT) pathway in regulation of wear particles-induced cytokine release and osteoclastogenesis from mouse bone marrow macrophages in vitro.
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Vitamin C modulates TET1 function during somatic cell reprogramming.
Nat. Genet.
PUBLISHED: 04-13-2013
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Vitamin C, a micronutrient known for its anti-scurvy activity in humans, promotes the generation of induced pluripotent stem cells (iPSCs) through the activity of histone demethylating dioxygenases. TET hydroxylases are also dioxygenases implicated in active DNA demethylation. Here we report that TET1 either positively or negatively regulates somatic cell reprogramming depending on the absence or presence of vitamin C. TET1 deficiency enhances reprogramming, and its overexpression impairs reprogramming in the context of vitamin C by modulating the obligatory mesenchymal-to-epithelial transition (MET). In the absence of vitamin C, TET1 promotes somatic cell reprogramming independent of MET. Consistently, TET1 regulates 5-hydroxymethylcytosine (5hmC) formation at loci critical for MET in a vitamin C-dependent fashion. Our findings suggest that vitamin C has a vital role in determining the biological outcome of TET1 function at the cellular level. Given its benefit to human health, vitamin C should be investigated further for its role in epigenetic regulation.
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Ki-67 overexpression in WHO grade II gliomas is associated with poor postoperative seizure control.
Seizure
PUBLISHED: 04-07-2013
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Seizures are the most common initial symptom in patients with low-grade gliomas, and approximately 30% of these patients still suffer from epilepsy after gross-total resection of the tumour. We examined the relationship between the overexpression of ki-67 in WHO grade II gliomas and seizure control.
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Genetic polymorphisms of glutathione S-transferase M1 and prostate cancer risk in Asians: a meta-analysis of 18 studies.
Asian Pac. J. Cancer Prev.
PUBLISHED: 03-29-2013
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Many studies have investigated associations between the glutathione S-transferase M1 (GSTM1) null polymorphism and risk of prostate cancer, but the impact of GSTM1 in people who live in Asian countries is still unclear owing to inconsistencies across results.
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Genome-wide characterization of phenylalanine ammonia-lyase gene family in watermelon (Citrullus lanatus).
Planta
PUBLISHED: 03-05-2013
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Phenylalanine ammonia-lyase (PAL), the first enzyme in the phenylpropanoid pathway, plays a critical role in plant growth, development, and adaptation. PAL enzymes are encoded by a gene family in plants. Here, we report a genome-wide search for PAL genes in watermelon. A total of 12 PAL genes, designated ClPAL1-12, are identified . Nine are arranged in tandem in two duplication blocks located on chromosomes 4 and 7, and the other three ClPAL genes are distributed as single copies on chromosomes 2, 3, and 8. Both the cDNA and protein sequences of ClPALs share an overall high identity with each other. A phylogenetic analysis places 11 of the ClPALs into a separate cucurbit subclade, whereas ClPAL2, which belongs to neither monocots nor dicots, may serve as an ancestral PAL in plants. In the cucurbit subclade, seven ClPALs form homologous pairs with their counterparts from cucumber. Expression profiling reveals that 11 of the ClPAL genes are expressed and show preferential expression in the stems and male and female flowers. Six of the 12 ClPALs are moderately or strongly expressed in the fruits, particularly in the pulp, suggesting the potential roles of PAL in the development of fruit color and flavor. A promoter motif analysis of the ClPAL genes implies redundant but distinctive cis-regulatory structures for stress responsiveness. Finally, duplication events during the evolution and expansion of the ClPAL gene family are discussed, and the relationships between the ClPAL genes and their cucumber orthologs are estimated.
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Genome-wide profiling of 5-formylcytosine reveals its roles in epigenetic priming.
Cell
PUBLISHED: 02-19-2013
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TET proteins oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC). 5fC and 5caC are excised by mammalian DNA glycosylase TDG, implicating 5mC oxidation in DNA demethylation. Here, we show that the genomic locations of 5fC can be determined by coupling chemical reduction with biotin tagging. Genome-wide mapping of 5fC in mouse embryonic stem cells (mESCs) reveals that 5fC preferentially occurs at poised enhancers among other gene regulatory elements. Application to Tdg null mESCs further suggests that 5fC production coordinates with p300 in remodeling epigenetic states of enhancers. This process, which is not influenced by 5hmC, appears to be associated with further oxidation of 5hmC and commitment to demethylation through 5fC. Finally, we resolved 5fC at base resolution by hydroxylamine-based protection from bisulfite-mediated deamination, thereby confirming sites of 5fC accumulation. Our results reveal roles of active 5mC/5hmC oxidation and TDG-mediated demethylation in epigenetic tuning at regulatory elements.
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ID1 affects the efficacy of radiotherapy in glioblastoma through inhibition of DNA repair pathways.
Med. Oncol.
PUBLISHED: 02-03-2013
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Glioblastoma multiforme (GBM) is characterized by poor therapeutic response and poor overall survival. It is crucial that more effective therapies be developed for the treatment of GBM. Inhibitor of DNA binding protein-1 (ID1) has been shown to maintain the self-renewal capacity of neural stem cells and might be involved in the therapeutic resistance of GBM. In the present study, we explored survival data from the The Cancer Genome Atalas database that were based on ID1 expression for patients diagnosed with primary GBMs. Interestingly, patients with high ID1 expression had better survival than patients with low ID1 expression, and a strong correlation was found between radiotherapy efficacy, ID1 expression, and overall survival. We further investigated the relationship between ID1 expression and the radiosensitivity of glioblastoma using glioblastoma cell lines. The clonogenic formation assay showed that U87 ID1-shRNA cells were much less sensitive to radiation. Moreover, both the results of the ?H2AX foci staining assay and the comet assay further revealed that ID1 negatively regulates DNA repair processes by downregulating the expression of genes such as DNA ligase IV (LIG4) and ataxia-telangiectasia-mutated. Additionally, ID1 induces G2/M arrest in U87 cells. Taken together, these results suggest that ID1 may be a new prognostic marker for GBM and have important implications for the therapeutic strategies used to treat GBM patients.
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Gamna-Gandy bodies of the spleen detected with susceptibility weighted imaging: maybe a new potential non-invasive marker of esophageal varices.
PLoS ONE
PUBLISHED: 01-31-2013
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Portal hypertension (PH) is a clinical sequelae of liver cirrhosis, and bleeding from esophageal varices (EV) is a serious complication of PH with significant morbidity and mortality. The aims of this study were to assess the ability of 2D multislice breath-hold susceptibility weighted imaging (SWI) to detect Gamna-Gandy bodies (GGBs) in the spleens of patients with PH and to evaluate the potential role of GGB number as a non-invasive marker of PH and EV.
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ID1 regulates U87 human cell proliferation and invasion.
Oncol Lett
PUBLISHED: 01-25-2013
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Despite therapeutic advances, the prognosis of patients diagnosed with malignant glioma has not improved in recent years. In particular, the molecular mechanisms that mediate glioma invasion remain poorly understood. The importance of ID1 in promoting tumor invasion and metastasis has recently emerged and a role for ID1 as a possible molecular marker of tumor aggressiveness has been proposed. To investigate the biological function of ID1 in glioblastomas, ID1-silenced U87 glioblastoma multiforme (GBM) cells were constructed using a small hairpin RNA (shRNA) sequence. The effect of the knockdown of ID1 on proliferation and invasion in these cells was analyzed using the 5-bromo-2-deoxy-uridine cell proliferation, Transwell invasion, scratch and cell adhesion assays. Compared with the controls, the U87 cells expressing ID1-shRNA exhibited a significantly decreased proliferation and invasion capacity (P<0.05), as well as increased cell adhesion. Furthermore, silencing ID1 reduced the expression of c-Myc, cyclin D1 and ?-catenin, while increasing E-cadherin expression in U87 cells. This study showed that ID1 regulates the metastatic potential of GBM cells by controlling the epithelial-mesenchymal transition. Therefore, ID1 is a potential prognostic indicator and therapeutic target in glioblastomas.
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miR-708 acts as a tumor suppressor in human glioblastoma cells.
Oncol. Rep.
PUBLISHED: 01-25-2013
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Glioblastoma (GBM) is one of the most lethal forms of human cancer, and new clinical biomarkers and therapeutic targets are urgently required. microRNAs (miRNAs) are small, non-coding RNAs that negatively regulate gene expression at the post-transcriptional and/or translational level by binding the 3 untranslated regions (3 UTRs) of target mRNAs. The dysregulated expression of several miRNAs has been reported to modulate glioma progression. In the present study, we defined the expression and function of miR-708, which, based on real-time PCR analysis, were downregulated in GBM cells. The overexpression of miR-708 inhibited cell proliferation and invasion and induced apoptosis in the human GBM cell lines A172 and T98G. Furthermore, the overexpression of miR-708 reduced the expression of Akt1, CCND1, MMP2, EZH2, Parp-1 and Bcl2 in A172 and T98G cells. Taken together, our study suggests that miR-708 affects GBM cell proliferation and invasion, and induces apoptosis. It is suggested that miR-708 may play an important role as a tumor suppressor in GBM and it may be an attractive target for therapeutic intervention in GBM.
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Strontium ranelate reduces cartilage degeneration and subchondral bone remodeling in rat osteoarthritis model.
Acta Pharmacol. Sin.
PUBLISHED: 01-21-2013
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Aim:To investigate whether strontium ranelate (SR), a new antiosteoporotic agent, could attenuate cartilage degeneration and subchondral bone remodeling in osteoarthritis (OA).Methods:Medial meniscal tear (MMT) operation was performed in adult SD rats to induce OA. SR (625 or 1800 mg·kg(-1)·d(-1)) was administered via gavage for 3 or 6 weeks. After the animals were sacrificed, articular cartilage degeneration was evaluated using toluidine blue O staining, SOX9 immunohistochemistry and TUNEL assay. The changes in microarchitecture indices and tissue mineral density (TMD), chemical composition (mineral-to-collagen ratio), and intrinsic mechanical properties of the subchondral bones were measured using micro-CT scanning, confocal Raman microspectroscopy and nanoindentation testing, respectively.Results:The high-dose SR significantly attenuated cartilage matrix and chondrocyte loss at 6 weeks, and decreased chondrocyte apoptosis, improved the expression of SOX9, a critical transcription factor responsible for the expression of anabolic genes type II collagen and aggrecan, at both 3 and 6 weeks. Meanwhile, the high-dose SR also significantly attenuated the subchondral bone remodeling at both 3 and 6 weeks, as shown by the improved microarchitecture indices, TMD, mineral-to-collagen ratio and intrinsic mechanical properties. In contrast, the low-dose SR did not significantly change all the detection indices of cartilage and bone at both 3 and 6 weeks.Conclusion:The high-dose SR treatment can reduce articular cartilage degeneration and subchondral bone remodeling in the rat MMT model of OA.
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Mesenchymal stem cells overexpressing integrin-linked kinase attenuate cardiac fibroblast proliferation and collagen synthesis through paracrine actions.
Mol Med Rep
PUBLISHED: 01-18-2013
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Mesenchymal stem cells (MSCs) transfected by integrin-linked kinase (ILK) transplantation may improve the function and compliance of the post-infarct cardiac ventricle. We investigated the effect of ILK-modified MSC contiditioned medium (ILK-MSC-CM) on the proliferation of cardiac fibroblasts (CFBs) and collagen synthesis in vitro and in vivo. Myocardial infarction (MI)-induced animals received mesenchymal stem cell conditioned medium (MSC-CM), ILK-MSC-CM, or complete medium alone, subepicardially. A group of animals with MI and no other former intervention served as controls. ILK-MSC-CM inhibited CFB proliferation, reduced the gene expression of type I (Col1a1) and type III collagen (Col3a1), tissue inhibitors of metalloproteinase?1 (TIMP-1) and ?2 (TIMP-2), ? smooth muscle actin (?-SMA), and connective tissue growth factor (CTGF). It also increased the gene expression of matrix metalloproteinase?2 (MMP?2) and -9 (MMP?9), as measured by qRT-PCR. Four weeks after the left anterior descending (LAD) coronary artery ligation, echocardiographic analysis demonstrated preserved cardiac geometry and contractility in the ILK-MSC-CM treated animals. Decreased infarct size and reduced fibrosis were observed in the ILK-MSC-CM group. Overexpression of ILK regulates paracrine actions of MSCs, and ILK-MSC-CM attenuates CFB proliferation and collagen synthesis through paracrine actions in vitro and in vivo.
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Antidepressant-like effects of paeoniflorin on the behavioural, biochemical, and neurochemical patterns of rats exposed to chronic unpredictable stress.
Neurosci. Lett.
PUBLISHED: 01-15-2013
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We have previously demonstrated that the total glycosides of peony exert antidepressant-like effects in animal models. Paeoniflorin is the main active glycoside of peony. The purpose of this study was to evaluate the antidepressant-like effects of paeoniflorin in a rat model of chronic unpredictable stress (CUS) and its active mechanisms. The results showed that CUS-exposed rats exhibited depressive-like behaviour with reduced weight, low motor activity as well as reduced consumption of sucrose, biochemical changes with increased concentrations of corticosterone and adrenocorticotropic hormone and neurochemical changes with reduced monoamine neurotransmitter levels. Paeoniflorin treatment markedly increased sucrose consumption and decreased serum corticosterone and adrenocorticotropic hormone levels in the CUS-treated rats. Furthermore, paeoniflorin treatment significantly attenuated CUS-induced reductions in noradrenaline, serotonin and its metabolite 5-hydroxyindoleacetic acid as well as CUS-induced increases in the ratio between the latter two factors. These results suggest that the modulation of the hypothalamic-pituitary-adrenal axis and up-regulation of serotonergic and noradrenergic systems are important mechanisms underlying the antidepressant-like effects of paeoniflorin in CUS-treated rats.
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Efficacy of pegylated interferon alpha2a in patients without HBeAg loss after the withdrawal of long-term lamivudine therapy.
Virol. J.
PUBLISHED: 01-11-2013
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ABSTRACT: BACKGROUND: Improving the HBe seroconversion rate of patients without HBeAg loss after long-term lamivudine therapy has become an urgent clinical problem that we have to face. Unfortunately, there is no consensus on the mananement of these patients. The aim of this study was to evaluate the efficacy of pegylated interferon (PEG-IFN) alpha2a in patients without HBeAg loss after the withdrawal of long-term lamivudine therapy. METHODS: Fifty patients with chronic hepatitis B without the loss of HBeAg after >=96 weeks of lamivudine treatment were enrolled to withdraw from treatment to induce a biochemical breakthrough. Patients who achieved a biochemical breakthrough within 24 weeks received 48-weeks of PEG-IFN alpha2a therapy, and were then assessed during a subsequent 24-week follow-up period. RESULTS: Forty-three (86.0%) patients achieved a biochemical breakthrough within 24 weeks of lamivudine withdrawal. The rates of combined response (both undetectable HBV DNA and HBeAg loss) and HBsAg loss were alone 51.2% and 20.9%, respectively after 48 weeks of PEG-IFN alpha2a therapy, and 44.2% and 18.6%, respectively, at 24 weeks after treatment cessation. The end-of-treatment combined response rate was 65.4% among patients with a baseline HBsAg <20,000 IU/mL, which was significantly higher than 29.4% of patients with HBsAg >=20,000 IU/mL (P=0.031). For patients with HBsAg levels<1,500 IU/mL at 12 and 24 weeks therapy, the end-of-treatment combined response rate was 68.2% and 69.0%, which were both significantly higher than patients with HBsAg>=1,500 IU/mL (33.3% and 14.3%; P=0.048 and 0.001). The end-of-treatment combined response rate was significantly higher among patients with HBV DNA<105 copies/mL (76.2%) compared to patients with HBV DNA>=105 copies/mL (27.3%) after 24 weeks of therapy (P=0.004). CONCLUSION: Retreatment with PEG-IFN alpha2a was effective and safe for patients without HBeAg loss after the withdrawal of long-term lamivudine therapy. HBsAg levels at the baseline, 12 and 24 weeks of therapy, and HBV DNA levels at 24 weeks of therapy, can predict the effect of PEG-IFN alpha2a after 48 weeks of therapy.
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