A simple and efficient method for fabricating a novel surface-enhanced Raman scattering ( SERS) substrate with good reproducibility and high SERS activity was reported. Cu2 O was prepared by mixing CuCl2 ·2H2 O with ascorbic acid, which was then used as the templates for depositing of gold nanoparticles ( AuNPs) on their surfaces, forming Cu2 O@ Au with heterostructures. Transmission electron microscopy, scanning electron microscopy and X-ray diffraction observation revealed that Cu2 O had polyhedral structure and smooth surface, and AuNPs were closely deposited on the surface of Cu2 O. It was used as SERS substrate for detection of Rhodamine B with linear detection range of 1 × 10-2-5 × 10-6 mol/L, and detection limit of 3 ×10-7 mol/L. Cu2 O@Au showed good chemical stability, remained stable in acid, PBS and river samples, and could be used in the SERS detection of target in water sample.

Objective To explore the application of diffusion weighted imaging(DWI) in diagnosis of viral encephalitis in children.Methods Conventional MR imaging(T2WI and T1WI) and DWI were performed on 20 patients with viral encephalitis diagnosed clinically.Location and number of lesions demonstrated on these imagings and percents in their abnormality were compared.Results Percen-(tage of abnormality) demonstrated on DWI was significantly higher than that on T1WI(?~2=4.44 P

OBJECTIVETo compare the features of brain injury in neonatal rats with different severities of hypoxia-ischemia (HI), and explore the role of microglial activation and cytokines.

METHODSOne hundred and twenty 7-day-old rats were randomized to three groups: sham control, mild HI, and severe HI. The rats in the HI groups were subjected to right carotid artery occlusion and 8% oxygen hypoxia exposure (40 minutes, 34.5 Celsius degree in the mild HI group; 65 minutes, 35.5 Celsius degree in the severe HI group). MRI, microtubule associated protein (MAP2) and TUNEL staining were used to confirm the severity of brain injury. Changes in expression of activated microglia (ED1) and signs of cytokine involvement or oxidative stress (TNF-alpha, nitrotyrosine) were assessed immunohistochemically.

RESULTSIn the mild HI group, MRI scans demonstrated increased T2 values in the ipsilateral subcortical white matter and a slight loss of T2 values in the cortex, corresponding to a medium loss of MAP2 in the ipsilateral cortex. There was an increase in the number of TUNEL positive cells compared to the control group within the subcortical white matter. In the severe HI group, the T2 value increased in the majority of the hemisphere, corresponding to a severe loss of staining for MAP2 in the ispilateral hemisphere. The number of TUNEL positive cells significantly increased in the ipsilateral cortex and white matter. In the mild HI group, ED1, TNF-alpha and nitrotyrosine expression increased only in the acute stage and was only observed in subcortical white matter. In contrast, after severe HI, the increase in ED1, TNF-alpha and nitrotyrosine expression was observed in the whole ipsilateral hemisphere and prolonged for weeks.

CONCLUSIONSFollowing a mild HI a relatively selective white matter injury compares to the pannecrosis in the cortex and white matter following a severe HI. Microglial activation and over-expression of cytokines might contribute to the development of hypoxic-ischemic brain damage.

Animals ; Animals, Newborn ; Apoptosis ; Hypoxia-Ischemia, Brain ; etiology ; metabolism ; pathology ; Magnetic Resonance Imaging ; Microglia ; pathology ; Microtubule-Associated Proteins ; analysis ; Rats ; Tumor Necrosis Factor-alpha ; analysis ; Tyrosine ; analogs & derivatives ; analysis

Objective To compare the clinical effect of three kinds of gastric canal inserted method on patients with endotracheal intubation.Methods Two hundred and sixty-one cases of patients with endotracheal intubation were divided into group A(conventional group),B(inserting gastrotuhe by a guide-wire in it),C (pulling the tracheal under calm state),with each group of eighty-seven cases.The intubation successful rate,the time of gastric canal insertion,HR and SpO2 before and after inttthation,and the choking and blcoding occurrence during intubation were observed and compared.Results The intubation successful rate showed significantly higher in the group B(83.91%)than in the group A(70.11%,P＜0.05),and significantly higher in the group C(98.85%)than in the groups A and B(all P ＜ 0.01).In the time of gastrotuhe insertion,significantly quicker in the group B(43.25±5.56s)than in the group A(55.30±6.20)s(P ＜0.01),and significantly quicker in the group C(27.75±4.16)s than in the groups A and B(all P ＜ 0.01);In the total time of whole operation,significantly quicker in the group C(103.16±5.36)s than in the groups A and B(111.45±5.85 s、115.35± 5.25 s,all P ＜0.01),and significantly slower in the group B than in the group A(P ＜0.01).Before and after gastrotube insertion,there was no significant difference on HR in groups B and C(all P＞0.05),in the group A HR was obviously increased(P ＜0.05);while SpO2 there was no significant difference in group C,and the remarkably decreased in groups A and B(P ＜ 0.01,P ＜ 0.05).During the gastrotube insertion,The choking and blcoding occurrence in the group C(2.30%、O)was significantly lower than in the groups A(13.79%、9.20%)and B(8.05%,5.75%)(P＜0.01,P ＜ 0.05),and there was no significant difference in groups B and A(all P ＞0.05).Conclusions It shows higher accurate and less side effect for the endotracbeal intubation patients undergoing gastrotuhe insertion by pulling the tracheal under calm state.

Background The incidence of brain metastases in patients with breast cancer is approximately 10％-16％,and survival after diagnosis of brain metastases is usually short.This study was designed to evaluate the risk factors associated with brain metastases in advanced breast cancer patients,with a view to help predict patient groups with high risk of brain metastases.Methods In total,295 patients with advanced breast cancer were evaluated.All patients were pathologically confirmed and metastatic lesions were confirmed pathologically or by imaging.All patients were examined at least once every 6 months with head CT or MRI.Patients showing symptoms underwent immediate inspection,and brain metastatic lesions were confirmed by head CT and/or MRI.Results At a median follow-up of 12 months from the occurrence of metastases,brain metastases had occurred in 49 patients (16.6％).In our univariate analysis,variables significantly related to increased risk of brain metastases were hormone receptor-negative tumors,epidermal growth factor receptor 2 (HER2)-positive tumors,and multiple distant metastases.Patients with dominant tumor sites in soft tissue,or defined as Luminal A subtype,tended to have a lower risk of brain metastases than patients with visceral metastases,Luminal B subtype,triple-negative subtype or HER2-enriched subtype tumors.Conclusions Our results strongly suggest that factors such as Luminal B,triple-negative,and HER2-enriched subtypes are high risk factors for brain metastases.These data,therefore,provide pivotal clinical evidence towards a comprehensive understanding of the risk factors of brain metastases in advanced breast cancer patients.

This paper is to report the study of the metabolism of lidamycin in vitro including in plasma and microsomes to guide clinical therapy. Lidamycin was quantified by detecting its active ingredient using HPLC-MS/MS. The metabolic stability of lidamycin in rat, Beagle dog, monkey and human plasma and liver microsomes, and its inhibition to cytochrome P450 isoforms in human liver microsomes were studied. Results showed that lidamycin was metabolized in the four species of plasma, and the sequence of metabolic rates in plasma were in rat > in dog > in human > in monkey. But among the four species of liver microsomes, lidamycin was metabolized only in monkey liver microsomes. There was almost no inhibition to cytochrome P450 isoforms at the concentrations of between 0.0005 and 10 ng x mL(-1). Therefore, the property of lidamycin metabolism in human is similar with that in dog, and metabolism of other drugs would not be decreased by cytochrome P450 as used along with lidamycin in clinic.
Aminoglycosides ; blood ; metabolism ; Animals ; Antibiotics, Antineoplastic ; blood ; metabolism ; Chromatography, High Pressure Liquid ; Cytochrome P-450 CYP1A2 ; metabolism ; Cytochrome P-450 Enzyme System ; metabolism ; Dogs ; Enediynes ; blood ; metabolism ; Enzyme Activation ; Humans ; Macaca ; Microsomes, Liver ; metabolism ; Rats ; Tandem Mass Spectrometry

OBJECTIVETo investigate the effect of angiotensin II and angiotensin1-7 on alpha-smooth muscle actin (alpha-SMA)-induced Ca(2+)-independent pathways mediated by Rho kinase2 in hepatic stellate cells (HSCs).

METHODSHSC-T6 cells were treated with 10 micromol/L of AngII, Ang1-7, AngII +Ang1-7, and Ang1-7+A779. RT-PCR was used to detect the expression of Rho kinase2 (Rock2) in Ca(2+)-independent pathways, and alpha-SMA protein expression was detected by Western blotting.

RESULTSThe mRNA expression of Rock2 increased significantly in the cells after AngII treatment (P<0.01), but decreased following Ang1-7 treatment. Ang1-7 treatment significantly reduced alpha-SMA level in AngII-induced cells (P<0.01).

CONCLUSIONAng1-7 can inhibit AngII-induced activation of Rock2 and reduce alpha-SMA expression in HSCs.

Actins ; metabolism ; Angiotensin I ; pharmacology ; Angiotensin II ; pharmacology ; Animals ; Calcium ; metabolism ; Cell Line ; Gene Expression Regulation ; drug effects ; Hepatic Stellate Cells ; cytology ; drug effects ; metabolism ; Peptide Fragments ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Signal Transduction ; drug effects ; rho-Associated Kinases ; genetics

OBJECTIVETo investigate the effect of angiotensin II (AngII) type 1 (AT-1) receptor and angiotensin-converting enzyme (ACE) gene silencing on nuclear factor-kappaB (NF-kappaB) activity in hepatic stellate cells (HSCs).

METHODSpSilencer/AT-1 alpha receptor siRNA and pSilencer/ACE siRNA plasmids were transfected into cultured HSC-T6 cells, which were subsequently stimulated by 10(-6) mol/L AngII or ACE inhibitor (ACEI). The DNA binding activity of NF-kappaB in the transfected cells was analyzed using electrophoretic gel mobility shift assay (EMSA).

RESULTSs Gel shift studies showed that stimulation of the HSCs by AngII markedly increased the DNA-binding activity of NF-kappaB, which was inhibited by the transfection with pSilencer/ AT-1 alpha receptor siRNA plasmid or pSilencer/ACE siRNA plasmid.

CONCLUSIONAT-1 alpha receptor and ACE gene silencing result in inhibition of NF-kappaB activity in HSCs in vitro.

Cell Line ; Hepatic Stellate Cells ; cytology ; metabolism ; Humans ; NF-kappa B ; genetics ; metabolism ; Peptidyl-Dipeptidase A ; genetics ; RNA Interference ; RNA, Small Interfering ; genetics ; Receptor, Angiotensin, Type 1 ; genetics ; Transfection

BACKGROUNDLipid abnormalities are often complicated by renal dysfunction. 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are the first-line choice for lowering cholesterol levels. The present study was designed to investigate whether statins could prevent and invert the development of renal injury in cholesterol-fed rabbits and to find the possible mechanism of their effects by detecting gene and protein expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the renal artery.

METHODSTwenty-four male New Zealand white rabbits were divided into three groups: (1) control group, regular granules chow; (2) HC-diet group, granules chow with 1% cholesterol and 5% lard oil; and (3) fluvastatin group, 1% cholesterol and 5% lard oil diet plus fluvastatin [10 mg.kg(-1).d(-1)]. After 16 weeks, serum total cholesterol (TC), low-density lipoprotein (LDL) and creatinine (Cr) levels were measured. Renal hemodynamics and function, mainly including glomerular filtration rate (GFR) in vivo were quantified using (99m)Tc-DTPA single photon emission computed tomograph ((99m)Tc-DTPA SPECT). The thickness of the renal artery intima was quantitated in HE-stained segments by histomorphometry. Gene expression of LOX-1 in the renal artery was examined by semi-quantitative RT-PCR and its protein expression was evaluated by immunohistochemistry.

RESULTSHigh cholesterol diet induced hypercholesterolemia (HC) complicated by renal dysfunction with increased levels of serum lipid and Cr, decreased GFR and delayed excretion and extensively thickened renal arterial intima in the HC-diet group. Rabbits in the control group showed a minimal LOX-1 expression (mRNA and protein) in the endothelium and neointima of the renal artery. Intimal proliferation of the renal artery in the HC-diet group was associated with a marked increase of LOX-1 expression (protein and mRNA). Treatment with fluvastatin improved renal function, attenuated intimal proliferation of the renal artery and markedly decreased the enhanced LOX-1 expression in the endothelium and neointima of the renal artery in rabbits.

CONCLUSIONSFluvastatin treatment could prevent the development of renal injury in patients with HC and early atherosclerosis (AS). This beneficial effect might be mediated by its pleiotropic effects including a decrease in total cholesterol exposure level and prevention of LOX-1 expression in atherosclerotic arteries.

Animals ; Cholesterol ; blood ; Creatinine ; blood ; Fatty Acids, Monounsaturated ; pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Hypercholesterolemia ; drug therapy ; metabolism ; pathology ; Immunohistochemistry ; Indoles ; pharmacology ; Kidney ; drug effects ; pathology ; Male ; RNA, Messenger ; analysis ; Rabbits ; Receptors, LDL ; analysis ; genetics ; Receptors, Oxidized LDL ; Scavenger Receptors, Class E ; Tomography, Emission-Computed, Single-Photon

OBJECTIVETo investigate the signal transduction mechanism underlying the effects of angiotensin II (AngII) on extracellular signal-regulated kinase 1/2 (ERK1/2), early growth response-1 (EGR-1) and platelet-derived growth factor-B (PDGF-B) in hepatic stellate cells (HSCs).

METHODSHSC-T6 cells treated with AngII for 10 or 30 min were examined for phospho-P42/44 protein expression using Western blotting. In another experiment, the cells were preincubated for 1 h in the presence of U0126 (an inhibitor of the MAPK/ERK kinase), irbesartan (an AT-1 receptor blocker), or antioxidant-N-acetylcysteine (NAC) prior to AngII exposure, and the protein expression of phospho-P42/44 and PDGF-B were measured with Western blotting. The DNA binding activity of EGR-1 was analyzed using electrophoretic gel mobility shift assay (EMSA), and the expression of PDGF-B was detected immunohistochemically.

RESULTSAngII induced phospho-P42/44 expression in HSC-T6, which was abrogated by U0126 or irbesartan. NAC did not inhibit phospho-P42/44 expression. EMSA showed that AngII exposure of the HSC cells markedly increased EGR-1 DNA binding activity, reaching the maximum after 60 min of exposure followed by progressive declination; irbesartan and U0126 significantly suppressed AngII-induced EGR-1 activity enhancement. ACEI at 1 micromol/L and 10 nmol/L inhibited EGR-1 activity, but ACEI at the concentration of 0.1 nmol/L resulted in enhanced EGR-1 activity. NAC showed no obvious effect in suppressing EGR-1 activity. AngII increased PDGF-B protein level in the HSCs, the effect of which was inhibited by irbesartan. U0126, NAC and ACEI did not attenuate PDGF-BB protein level in the HSCs.

CONCLUSIONStimulation of the HSCs with AngII results in EGR-1 activation via the ERK1/2 pathway, leading to up-regulation of PDGF-B expression.

Angiotensin II ; pharmacology ; Blotting, Western ; Cells, Cultured ; Early Growth Response Protein 1 ; metabolism ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Hepatic Stellate Cells ; cytology ; drug effects ; metabolism ; Humans ; Immunohistochemistry ; Platelet-Derived Growth Factor ; biosynthesis ; Proto-Oncogene Proteins c-sis ; Signal Transduction ; drug effects