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Although anti-rheumatoid arthritis (RA) 33 antibodies have been reported to be present in various connective tissue diseases (CTDs), the clinical significance of anti-RA33 in CTDs is still obscure. This study was performed to explore the clinical significance of anti-RA33 in CTDs, especially systemic lupus erythematosus (SLE). A total of 565 patients with positive anti-nuclear antibodies who had been tested for anti-RA33 were included in this study and were further classified into RA33-positive and RA33-negative groups. The association between anti-RA33 and the clinical features of CTDs was examined. Receiver operating characteristic (ROC) analysis was performed to explore the diagnostic value of anti-RA33 in SLE and SLE-related organ involvement. The results showed that SLE was the most common disease in CTD patients positive for anti-RA33 (48.8%). Compared with the RA33-negative group, higher proportions of SLE-associated antibodies and SLE patients with a high disease activity as well as lower levels of serum complement components were observed in the RA33-positive group (all p

To observe the effect of electroacupuncture (EA) at "Zusanli"(ST36) on the phosphorylated tau levels in pancreas and hippocampus of type 2 diabetes mellitus (T2DM) rats，so as to explore the underlying mechanism of EA in diabetic demention rats.Forty-eight male Sprague-Dawley rats were randomly divided into control, model and EA groups, with 16 rats in each group. The T2DM model was established by 6 weeks of high-fat, high-sugar diet as well as intrape-ritoneal injection of streptozocin (STZ) solution (35 mg/kg). After that, EA (2 Hz, 0.1 mA) was applied to unilateral "Zusanli"(ST36) for 30 min, once a day, 6 times a week for 4 weeks. The survival rate was recorded every week, and the fasting blood glucose (FBG) was detected on the 1st, 6th and 11th week. The level of serum insulin (INS) was measured by using ELISA. The morphological structure of pancreas islet was observed by H.E. staining. The expressions of phosphorylated tau at the sites of Ser 396 (pS396) and Thr 231 (pT231), total tau (Tau5), phosphorylated glycogen synthase kinase-3β (pGSK-3β) and total glycogen synthase kinase-3β (GSK-3β) in pancreas and hippocampus were detected by Western blot. The expression and distribution of pS396 and pT231 in pancreas and hippocampus were assayed with immunohistochemistry.Compared with the control group, the survival rate presented a significant decline, the contents of FBG and INS were obviously higher(EA at ST36 can reduce the level of tau phosphorylation via regulating the activity of GSK-3β in the pancreas and hippocampus of T2DM rats, which may be related with the effect of EA on the brain function in T2DM rats.

Objective The study explored the effect of applying electroacupuncture (EA) preconditioning at ST 36 on mitochondria in rats with intestinal ischemia/reperfusion injury. Methods Forty SD rats were divided into four sets: sham operation group (sham group); intestinal ischemia/reperfusion group (I/R group); EA preconditioning at ST 36 followed by intestinal ischemia/reperfusion injury (ST 36 + I/R group); EA preconditioning at the lateral site away from ST36 0.5 cm followed by intestinal ischemia/reperfusion injury (N + I/R group). For the sham group, the rats were opened abdominal cavity for 3 h and 20 min and their abdominal cavities were covered with wet gauze avoiding drying and kept on the thermostat at 37 °C. For the ischemia/reperfusion (I/R) group, rats were anaesthetised and their abdominal cavities were opened to expose jejunum segments. The segment's collateral blood supply was restricted by bilateral ligation of the intestine. Next, one of the branches of a mesenteric artery was occluded with a thread for 20 min and then the thread was released after such ischemia conditions, keeping reperfusion for 3 h. For the ST36 + I/R group, the electroacupuncture at ST36 was first performed, then the intestinal ischemia/reperfusion model was constructed. For the N + I/R group, electroacupuncture at non ST36 acupoint, which is away from ST36 about 0.5 cm, and then the intestinal ischemia/reperfusion model was performed. Measurements of the levels of inflammatory markers tumour necrosis factor α (TNFα) and interleukin-1 beta (IL-1β), cytochrome c (CYCS), and the mitochondrial membrane pro-apoptotic protein (BAX), anti-apoptotic protein Bcl-2 were performed. Results Compared to I/R group, the intensity of cytoplasmic CYCS in intestinal tissues was significantly decreased in the ST 36 + I/R group (1.65 vs. 0.18, p Conclusion The results suggest the EA intervention has a protective effect upon mitochondria, preventing CYCS release and the subsequent activation of downstream apoptosis pathway. It is proposed that patients due to undergo gastrointestinal surgery get benefit from EA preconditioning at ST 36.

This work reported a new approach for the preparation of a promising lead nitroprusside (PbNP) and multi-walled carbon nanotubes (MWCNTs) composite electrode, which exploited the synergistic advantages of PbNP and MWCNTs. And the electrocatalytic performance of the new composite electrode toward glucose was also studied. Comparing with MWCNTs modified electrode and glassy carbon electrode, the new composite electrode exhibited advantages of low applied potential, high current response, good stability and reliability. The PbNP-MWCNTs composite electrode had superior performance, which was expected a good candidate for reliable glucose detection.

This work describes the preparation of multi-walled carbon nanotubes (MWCNT) and nickel oxide particles (NiO) composite modified electrode. The electrochemical catalytic performance of the new modified electrode toward sulfadiazine was studied by voltammetric method. The modified electrode exhibited good catalytic performance for the electrochemical oxidation of sulfadiazine at potential of 0.9 V, which was 0.2 V lower than that obtained by a normal glassy carbon electrode. The results of amperometric study suggested that the anodic current of the modified electrode linearly increased against the concentration of sulfadiazine in the range 1.0 - 7.9 μM.

A highly sensitive amperometric sulfadiazine sensor fabricated by electrochemical deposition of poly(cobalt tetraaminophthalocyanine) (poly(Co(II)TAPc)) on the surface of a multi-walled carbon nanotubes-Nafion (MWCNTs-Nafion) modified electrode is described. This electrode showed a very attractive performance by combining the advantages of Co(II)TAPc, MWCNTs, and Nafion. Compared with the bare glassy carbon electrode (GCE) and the MWCNTs-Nafion modified electrode, the electrocatalytic activity of poly(Co(II)TAPc)-coated MWCNTs-Nafion GCE generated greatly improved electrochemical detections toward sulfadiazine including low oxidation potential, high current responses, and good anti-fouling performance. The oxidation peak currents of sulfadiazine obtained on the new modified electrode increased linearly while increasing the concentration of sulfadiazine from 0.5 to 43.5 μmol/L with the detection limit of 0.17 μmol/L.

A new series of 4-aryl-3,4-dihydrocoumarins and 4-arylcoumarins were synthesized by the reaction of substituted cinnamic acids and 3-arylpropiolic acid with the corresponding phenols. These compounds were evaluated for antibacterial activity in vitro. The synthesized compounds displayed different degrees of antimicrobial activity against Staphylococcus aureus, Escherichia coli, and Bacillus dysenteriae, and Candida albicans (a fungus). Compounds with catechol moieties and 7,8-substituted dihydroxyls in the A ring were the most active antimicrobial agents.

A multicomponent modification on the surface of porous nickel with nanoparticles is conducted by an electrophoretic deposition (EPD) technique to prepare new composite-based cathodes for molten carbonate fuel cells (MCFCs). Two new ternary composite-based cathodes, (nano- LiCoO2-LiFeO2 )- Ni and (nano- LiCoO2-CeO2 )- Ni , are inclined to possess good morphology and homogeneous element distribution when prepared under moderate current density resulting from a medium deposition voltage and suspension pH value in this work. Both composite-based cathodes manifest excellent anti-deformation and anti-dissolution performances under conditions of a simulated MCFC startup stage and are thus expected to be useful for application in the MCFC industry.

To determine whether oxidative-stress damage play an important role in the mechanism of silicosis, the oxidative stress parameters were investigated in silicosis patients and controls group. 128 silicosis patients and 130 healthy controls were included. The serum superoxide dismutase (SOD) activity and the levels of malonyldialdehyde (MDA) and glutathione (GSH) were analyzed. The levels of GSH and MDA in silicosis patients were significantly higher than those of the controls group. SOD activity was higher in the silicosis group than that in the controls (p < 0.05) except for III stage. None of the 3 variables examined were associated with the age among both the controls and silicosis patients. The GSH level and SOD activity significantly declined over a prolonged disease period, while MDA levels remained largely unaffected by the disease duration. These results confirmed the role of oxidative stress in the mechanism of silicosis. Therefore, effective antioxidant therapy for inhibiting oxidative stress may be a therapeutic option in silicosis.Key words: Silica, silicosis, superoxide dismutase, glutathione, malondialdehyde.

This work describes the electrochemical deposition of poly(cobalt(II)-tetraaminophthalocyanine) (poly(CoIITAPc)) film onto a multi walled carbon nanotubes (MWNT) modified glassy carbon (GC) electrode (designated as poly(CoIITAPc)-MWNT-GC electrode) by cyclic voltammetric method and the effectiveness poly(CoIITAPc)-MWNT-GC electrode towards electrocatalytic oxidation of hydroxylamine. Cyclic voltammograms recorded during electropolymerization of cobalt(II) tetraaminophthalocyanine (CoIITAPc) indicated that good adherent layer of poly(CoIITAPc) was incorporated on to the surface of MWNT/GC electrode. The electrochemical detection of hydroxylamine was studied by amperometry at the new poly(CoIITAPc)-MWNT-GC electrode. The modified electrode exhibited good catalytic performance for the electrochemical oxidation of hydroxylamine with an anodic potential of 0.2 V, linear concentration range from 1.7 mmol/L to 0.20 mmol/Land a detection limit of 0.33 mmol/L.

An increased hippocampal neurogenesis has been observed in Alzheimer disease (AD), the most common neurodegenerative disorder characterized with accumulation of β-amyloid (Aβ) and hyperphosphorylated tau (p-tau). Studies in transgenic mouse models suggest that the amyloidosis suppresses adult neurogenesis. Although emerging evidence links tau to neurodevelopment, the direct data regarding tau phosphorylation in adult neurogenesis is missing. Here, we found that the immature neurons, identified by doublecortin (DCX) and neurogenic differentiation factor (neuroD), were only immunoreactive to p-tau but not to the non-p-tau in adult rat brain and human patients with AD, and the p-tau was coexpressed temporally and spatially with DCX and neuroD in the hippocampal dentate gyrus (DG) of the rat brains during postnatal development. A correlative increase of immature neuron markers and tau phosphorylation was induced in rat hippocampal DG by upregulating glycogen synthase kinase-3 (GSK-3), a crucial tau kinase, and the increased neurogenesis was due to an enhanced proliferation but not survival or differentiation of the newborn neurons. The hippocampal neurogenesis was severely impaired in tau knockout mice and activation of GSK-3 in these mice did not rescue the deficits. These results reveal an essential role of tau phosphorylation in adult hippocampal neurogenesis. It suggests that spatial/temporal manipulation of tau phosphorylation may be compensatory for the neuron loss in neurological disorders, including AD.

Enhanced neurogenesis has been reported in the hippocampus of patients with Alzheimer's disease (AD), the most common neurodegenerative disorder characterized with amyloid-β (Aβ) aggregation, tau hyperphosphorylation, and progressive neuronal loss. Previously we reported that tau phosphorylation played an essential role in adult hippocampal neurogenesis, and activation of glycogen synthase kinase (GSK-3), a crucial tau kinase, could induce increased hippocampal neurogenesis. In the present study, we found that treatment of D-galactose rats with Puerarin could significantly improve behavioral performance and ameliorate the enhanced neurogenesis and microtubule-associated protein tau hyperphosphorylation in the hippocampus of D-galactose rat brains. FGF-2/GSK-3 signaling pathway might be involved in the effects of Puerarin on hippocampal neurogenesis and tau hyperphosphorylation. Our finding provides primary in vivo evidence that Puerarin can attenuate AD-like enhanced hippocampal neurogenesis and tau hyperphosphorylation. Our finding also suggests Puerarin can be served as a treatment for age-related neurodegenerative disorders, such as AD.

This study was to investigate the effect of dehydroevodiamine (DHED) on Alzheimer's disease (AD)-like tau hyperphosphorylation induced by calyculin A (CA), an inhibitor of protein phosphatase (PP)-2A and PP-1, and the involvement of PP-2A in metabolically competent rat brain slices.Rat brain slices were pre-incubated at 33 degree centigrade in the presence (10, 100, and 200 micromol/L, respectively) or absence of DHED for 1 h. Then, CA 0.1 micromol/L was added and the slices were treated for another 2 h. Western blotting and/or immunohistochemistry were used to measure the phosphorylation level of tau and PP-2A.CA treatment could remarkably increase the immunoreactivity of pS262 and decrease the staining of Tau-1, representing tau hyperphosphorylation at Ser262 (pS262) and Ser198/ 199/202 (Tau-1, as the antibody reacts with unphosphorylated tau, therefore, decreased staining represents increased phosphorylation). Pre-incubation of the brain slices with DHED could efficiently attenuate the CA-induced tau hyperphosphorylation at the above AD-related sites. Additionally, DHED also decreased the basal phosphorylation level of tau at Ser396, although CA failed to induce tau hyperphosphorylation at this site. Furthermore, CA treatment induced an increased level of Tyr307-phosphorylated PP-2A, which represents inactivation of the phosphatase, whereas DHED arrested the elevation of the inhibitory modification of PP-2A.DHED can attenuate CA-induced tau hyperphosphorylation at multiple AD-related sites in metabolically active rat brain slices. The underlying mechanism may involve a decreased inhibitory phosphorylation of PP-2A at Tyr307.

Tau hyperphosphorylation and memory deficit are characteristic alterations of Alzheimer's disease (AD), and glycogen synthase kinase-3 (GSK-3) plays a crucial role in these AD-like changes. We have reported that activation of GSK-3 through ventricular injection of wortmannin and GF-109203X (WT/GFX, 100 microM each) induces tau hyperphosphorylation and memory impairment of rats [Liu, S.J. et al., 2003. Overactivation of glycogen synthase kinase-3 by inhibition of phosphoinositol-3 kinase and protein kinase C leads to hyperphosphorylation of tau and impairment of spatial memory. J. Neurochem. 87, 1333-1344]. By using this model, we explored in the present study the effects of dehydroevodiamine (DHED), a quinazoline alkaloid isolated from Evodia rutaecarpa Bentham, on the memory retention, tau phosphorylation and the activity of GSK-3. We found that pre-administration of DHED through vena caudalis for 1 week efficiently improved the WT/GFX-induced spatial memory retention impairment of the rats; it also antagonized tau hyperphosphorylation at multiple AD sites and arrested the overactivation of GSK-3 induced by WT/GFX. Our study gave the first in vivo evidence that DHED could suppress the overactivation of GSK-3 and improve tau hyperphosphorylation and spatial memory deficit of the rats, suggesting that this chemical may be served as a candidate for arresting AD-like pathological and behavioral alterations.

In this paper, cobalt tetraaminophthalocyanine (CoPc) was successfully deposited onto a carbon nanotubes modified electrode by consecutive cyclic scanning in supporting electrolyte containing CoPc to form phthalocyanine-containing chemically modified electrode. The electrochemistry of sulfadiazine was studied by voltammetric method and flow injection analysis at the new modified electrode. Compared with glassy carbon electrode, the new modified electrode exhibited exciting performance including low oxidation potential, high current response and promising flow injection response.

To investigate the serum myeloperoxidase (MPO) activity and serum paraoxonase-1 (PON-1) activity in patients with silicosis and observation subjects and their clinical significance.Seventy-two patients with silicosis (stage I: 30 cases, stage II: 22 cases, stage III: 20 cases) and 37 observation subjects were selected as a case group, and 110 healthy men were selected as a control group. Serum MPO activity was measured by double-antibody sandwich enzyme-linked immunosorbent assay, and serum PON-1 activity was measured by chemical spectrophotometry.Serum MPO activity was significantly higher in the case group than in the control group [(102.1 ± 15.7) U/L vs. (62.4 ± 11.4) U/L, P0.01], but serum PON-1 activity was significantly lower in the case group than in the control group [(85.4 ± 15.7) U/ml vs. (125.4 ± 13.7) U/ml, P0.01]. Serum MPO activity was significantly lower in patients with stages I, II, and III silicosis than in the observation subjects [(91.3 ± 13.5) U/L, (85.7 ± 14.4) U/L, and (88.6 ± 14.5) U/L vs. (128.4 ± 16.4) U/L, P0.01]. Serum PON-1 activity declined as the stage of silicosis increased; serum PON-1 activity was significantly lower in the patients with stages II and III silicosis than in the observation subjects and the patients with stage I silicosis [(70.4 ± 11.4) U/ml and (67.6 ± 13.7) U/ml vs. (101.5 ± 14.0) U/ml and (89.1 ± 10.1) U/ml, P0.01].Serum MPO activity and serum PON-1 activity are valuable for early diagnosis of silicosis and evaluation of patient's condition.

The current therapies for Alzheimer's disease (AD) are merely palliative that cannot arrest the pathologic progression of the disease. Therefore, it is critical to develop treatments that can target the disease-modifying molecule(s). In the present study, we found that treatment of tg2576 mice with melatonin from 4–8 months of age did not improve the pathology or behavioral performance of the mice. However, remarkable attenuation of tau and β-amyloid pathologies with memory improvement were observed when melatonin was supplied from the age of 8–12 months or 4–12 months of the mice; more importantly, the improvements were still significant when the mice survived to old age. We also found that the disease stage-specific alteration of glycogen synthase kinase-3β (GSK-3β) but not protein phosphatase-2A, was correlated with the alterations of the pathology and behavior, and the timely targeting of GSK-3β was critical for the efficacy of melatonin. Our finding suggests that melatonin treatment only at proper timing could arrest AD by targeting the activated GSK-3β, which provides primary evidence for the importance and strategy in developing disease-modifying interventions of AD.

Altered neurogenesis has been reported in Alzheimer disease (AD), the most common neurodegenerative disorder characterized with hyperphosphorylated tau and accumulation of β-amyloid (Aβ). Recent studies suggest that tau phosphorylation is essential for hippocampal neurogenesis, however, it is not known whether tau phosphorylation also play a role in neurogenesis of subventricular zone (SVZ), another main progenitor niche in the brain. Here, we examined the expression of phosphorylated tau (p-tau) in SVZ and analyzed the role of p-tau in adult SVZ neurogenesis. We found that the expression of p-tau increased during postnatal development and remains at a high level until adulthood, and the p-tau was colocalized with some SVZ neural precursors. However, up-regulating glycogen synthase kinase-3 (GSK-3), a crucial tau kinase, had no effect on SVZ neurogenesis in adult rat brain. The SVZ neurogenesis was also unaffected in tau knockout and human tau transgenic mice. These results suggest that tau phosphorylation and GSK-3 activation may not be essential for adult SVZ neurogenesis.

To study the effect of Astragalus mongholicus on renal gene expression profile in mice with diabetic nephropathy by cDNA microarray.The mice with diabetic nephropathy were fed A. mongholicus and normal saline respectively. cDNA microarray was used to measure gene expression profile in renal tissue after 12 weeks, and the data were analyzed by bioinformatics. RT-PCR was performed to detect the relative levels of some genes which were randomly selected.Eighty eight genes were found differently expressed in two chips. Among these genes, 81 genes were found differently expressed in reverse direction change, 7 genes were found differently expressed in same direction change. The genes altered were mainly related to material metabolism, immunity and inflammatory reaction, signal transduction, translation, transcription, et al. The expressions of genes tested by RT-PCR were in accordance with those detected by cDNA microarray.A. mongholicus may play protective roles in diabetic nephropathy through multiple pathways at gene level. The effect of A. mongholicus in genes related to material metabolism is more significant.