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WO3-Bi2WO6 heterostructures were synthesized by a facile hydrothermal method using WO3 nanorods and Bi(NO3)3 solution as raw materials. The Bi2WO6 nanosheets uniformly anchored onto the surface of the WO3 nanorods. The photocatalytic activity of the samples was assessed for degradation of rhodamine B (RhB) and phenol under solar light irradiation. The WO3-Bi2WO6 heterostructures showed higher photocatalytic activities than pure WO3 and Bi2WO6. As the content of Bi2WO6 increased, the photocatalytic activity of the WO3-Bi2WO6 heterojunction was enhanced and the optimal sample was WO3-Bi2WO6 with a nWO3 : nBi3+ mole ratio of 5 : 3. The efficient separation of electron-hole pairs because of the staggered band potentials between WO3 and Bi2WO6 may account for the higher photoactivity of WO3-Bi2WO6 hybrid structures. Radical scavenger experiments indicate that holes (h+) and superoxide radicals (.O2-) were the main active species for RhB degradation during the photocatalytic process. [ABSTRACT FROM AUTHOR]

Primary lymphoma of the bone (PLB) primarily arising from the medullary cavity is an extremely rare entity, with only retrospective studies and sporadic cases reported in the literature. The current study presents one case of PLB treated with chemotherapy and radiotherapy, and a review of the literature to elucidate the optimal treatment of PLB. A 73-year-old female presented with pain in the left hip that had persisted for two months. Plain X-ray and magnetic resonance imaging of the left hip showed lytic areas involving the left innominatum. Technetium-99m radionuclide imaging showed increased tracer uptake in the ilium, acetabulum and ischium. An 18F-fluorodeoxyglucose-positron emission tomography-computed tomography (FDG-PET-CT) scan showed high FDG uptake. A fine-needle aspiration biopsy of the lesion was performed, and histopathological and immunohistochemical examination confirmed a diagnosis of B-cell lymphoma. The patient received radiation therapy followed by six cycles of CHOP regimen (1,000 mg cyclophosphamide, 80 mg epirubicine and 2 mg vincristine on day one, and 100 mg prednisone on days one to five, every three weeks) and achieved a complete response, as confirmed by FDG-PET-CT. At present, the patient is in a good condition. This case is noteworthy, as it is a well-documented case in which the patient received successful treatment. This case demonstrates that PLB has an improved prognosis compared with primary lymphoma of other sites; however, combined therapy may further improve the patient outcome. [ABSTRACT FROM AUTHOR]

In this work, we engineered the α/β fold of mannanase Man23 based on its molecular structure analysis to obtain more stable variants. By introducing 31 single-site mutations in the α/β fold and shuffling them, the incorporation of four mutations (K178R, K207R, N340R, and S354R) displayed a good balance between high activity and stability at higher temperature and broader pH. This quartet variant was characterized by an almost threefold increased activity and a sevenfold increased stability compared to native mannanase Man23. Our results suggest that such work is safe to increase our target protein stability with no loss of activity. [ABSTRACT FROM AUTHOR]

Past studies of bone extracellular matrix phosphoproteins such as osteopontin and bone sialoprotein have yielded important biological information regarding their role in calcification and the regulation of cellular activity. Most of these studies have been limited to proteins extracted from mammalian and avian vertebrates and nonvertebrates. The present work describes the isolation and purification of two major highly glycosylated and phosphorylated extracellular matrix proteins of 70 and 22 kDa from herring fish bones. The 70-kDa phosphoprotein has some characteristics of osteopontin with respect to amino acid composition and susceptibility to thrombin cleavage. Unlike osteopontin, however, it was found to contain high levels of sialic acid similar to bone sialoprotein. The 22-kDa protein has very different properties such as very high content of phosphoserine (∼270 Ser(P) residues/1000 amino acid residues), Ala, and Asx residues. The N-terminal amino acid sequence analysis of both the 70-kDa (NPIMA(M)ETTS(M)DSKVNPLL) and the 22-kDa (NQDMAMEASSDPEAA) fish phosphoproteins indicate that these unique amino acid sequences are unlike any published in protein databases. An enzyme-linked immunosorbent assay revealed that the 70-kDa phosphoprotein was present principally in bone and in calcified scales, whereas the 22-kDa phosphoprotein was detected only in bone. Immunohistological analysis revealed diffusely positive immunostaining for both the 70- and 22-kDa phosphoproteins throughout the matrix of the bone. Overall, this work adds additional support to the concept that the mechanism of biological calcification has common evolutionary and fundamental bases throughout vertebrate species. [ABSTRACT FROM AUTHOR]

Background: Increasing evidence has suggested that differentiation of adventitial fibroblasts (AFs) to myofibroblasts plays an important role in arterial remodeling. The molecular mechanisms by which myofibroblast formation is regulated still remain largely unknown. This study aimed to evaluate the role of cyclic nucleotide phosphodiesterase 1A (PDE1A) in the formation of adventitial myofibroblasts induced by transforming growth factor (TGF)-β1. Methods and Results: AFs were cultured by the explant method. Western blot and immunocytochemistry were applied for α-smooth muscle actin (SMA) or protein kinase C (PKC) α protein analysis. Results showed that TGF-β1 upregulated PDE1A protein expression in rat aortic AFs and pharmacological inhibition of PDE1A blocked TGF-β1-induced α-SMA expression, a marker of myofibroblast formation, suggesting that the upregulation of PDE1A may mediate TGF-β1-induced AF transformation. Moreover, calphostin C (a PKC inhibitor) inhibited TGF-β1-induced α-SMA expression, whereas phorbol-12-myristate-13-acetate (a PKC activator) induced it. Finally, the upregulation of PKCα expression by TGF-β1 was also inhibited by PDE1A inhibition. Conclusions: Taken together, our data suggest that TGFβ1 induces α-SMA expression and myofibroblast formation via a PDE1A-PKCα-dependent mechanism. Our study thus unveils a novel signaling mechanism underlying TGF-β1-induced adventitial myofibroblast formation. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: There is much variation in the response of both individuals and different ethnic populations to opioids, with genetic differences being responsible for interindividual variation. The μ-opioid receptor single nucleotide polymorphism (rs number 1799971) at nucleotide position 118 (OPRM1 118A>G) affects the analgesic response to opioids. Objective: This study aimed to investigate the association between the OPRM1 118A>G polymorphism and the effects of fentanyl-induced analgesia, respiratory depression, and anesthetic recovery responses in a population of Han Chinese patients. Study Design: The study was a case series in a hospital setting, with 1 year of study and 1 year of follow-up.A total of 189 patients (92 males and 97 females; American Society of Anesthesiologists Physical Status I or II, Glasgow Coma Scale = 15) who were scheduled for laparoscopic abdominal surgery received intravenous midazolam (Versed®) 0.08-0.01mg/kg and fentanyl (Duragesic®) 5.0 mg/kg. The main outcome measure was the degree of postoperative pain, as assessed using the Visual Analog Scale (VAS). VAS scores were recorded 5, 15, 30, 45, and 60 minutes after a fentanyl bolus injection in the post-anesthesia care unit (PACU). The minute expiratory volume, end-tidal carbon dioxide concentration (EtCO2) and respiratory rate (RR) were measured continuously. The incidence of fentanyl-induced respiratory depression (RR <8/min and EtCO2 >45 mmHg) was recorded at its appearance and treated with respiratory assistance. Blood gas analysis was done 15, 30, 45, and 60 minutes after extubation. These parameters were correlated with genotyping results of genomic DNA extracted from whole blood. Results: Patients with theOPRM1118AGorGGgenotypes had significantly higher VAS pain scores 15 and 30 minutes after a fentanyl bolus injection in the PACU than AA genotype patients (p < 0.05). A small but statistically significant difference was observed between the 118 AA and 118 AG/GG genotypes with regard to the carbon dioxide arterial pressure (PaCO2) at 15 and 30 minutes from the fentanyl bolus injection after extubation (p < 0.05); however, no clinically significant difference in the frequency of respiratory depression was seen. Homozygous 118 GG genotype patients had a significantly shorter time to awakening (p = 0.018) and extubation (p = 0.024) than patients with the 118 AA genotype. When the 118 GG and 118 AG genotypes were combined for analysis, a significantly shorter time to awakening (p = 0.011) and extubation (p = 0.010), compared with the 118 AA genotype, was also seen. Conclusion: The OPRM1 118A>G polymorphism lessens the analgesic response to fentanyl and the time to awakening and extubation but has no clinically significant effect on the incidence of respiratory depression. [ABSTRACT FROM AUTHOR]

Abstract  At the neuropathological level, Parkinson’s disease (PD) is characterized by the accumulation of misfolded proteins, which can trigger the unfolded protein response (UPR). UCH-L1 is a component of ubiquitin proteasome system (UPS). It is reported that the loss of its function will impair ubiquitin proteasome system and cause toxicity to cells. But its mechanism has not been illustrated. In this study, we detected the protein expression of Bip/Grp78 and the spliced form of XBP-1 to examine the activation of unfolded protein response after SK-N-SH cells being treated with LDN-57444, a UCH-L1 inhibitor which could inhibit UCH-L1 hydrolase activity. Our data showed that UCH-L1 inhibitor was able to cause cell death through the apoptosis pathway by decreasing the activity of ubiquitin proteasome system and increasing the levels of highly ubiquitinated proteins, both of which can activate unfolded protein response. There is a lot of evidence that unfolded protein response is activated as a protective response at the early stage of the stress; this protective response can switch to a pro-apoptotic response when the stress persists. In this study, we demonstrated this switch by detecting the upregulation of CHOP/Gadd153. Taken together, our data indicated that the apoptosis induced by UCH-L1 inhibitor may be triggered by the activation of endoplasmic reticulum stress (ERS). Moreover, we provide a new cell model for studying the roles of UCH-L1 in Parkinson’s disease. [ABSTRACT FROM AUTHOR]

Aim: To examine the protective effect of propofol in renal ischemia/reperfusion (I/R) injury and the role of heme oxygenase-1 (HO-1) in this process. Methods: Sprague-Dawley rats were randomly divided into 3 groups: (i) sham-operated group; (ii) I/R group; and (iii) propofol group. Bilateral renal warm ischemia for 45 min was performed. After 2, 6, and 24 h reperfusion, blood samples and kidneys were collected for assessment of renal injury, and HO-1 expressions were analyzed by immunohistochemical analysis, RT-PCR and Western blotting. Results: Blood urea nitrogen and serum creatinine levels in the propofol group were significantly lower than that in the I/R group at 24 h after reperfusion. The mean histological score by Paller's standard showed that propofol significantly attenuated renal I/R injury after 6 h reperfusion. Propofol increased HO-1 mRNA and protein levels 2 h after reperfusion, whereas HO-1 expressions were present at exceedingly low levels in the I/R group and the sham-operated group at same time point. Propofol also markedly increased HO-1 mRNA and protein levels than I/R at 6 and 24 h after reperfusion. Conclusion: These results suggest that propofol mitigates renal I/R injury in rats. This protection may be partly through the induction of the HO-1 expression. [ABSTRACT FROM AUTHOR]

Bone sialoprotein (BSP) is one of the major non-collagenous glycosylated phosphoproteins of the extracellular matrix in bone. In vitro studies suggest that BSP may play important roles in the initiation and/or growth of calcium-phosphate crystals. To investigate the potential role of BSP in more complex in vivo environments, we implanted purified bovine BSP with type-I collagen as a carrier into surgically created rat calvarial defects and thoracic subcutaneous pouches. The responses to the implants were assessed by histochemistry, immunohistochemistry, in situ hybridization, quantitative real-time PCR, and biochemical analyses. BSP-collagen, but not collagen alone, elicited mineral deposition in the matrix of proliferating cells near the dura at days 4-5 followed by osteoblast differentiation and synthesis of new bone in the mid-portion of the calvarial defects. In contrast, implantation of BSP-collagen into subcutaneous pouches did not induce calcification or osteogenesis over the same experimental period. We explored the underlying mechanisms for the site-specific responses to BSP-collagen implants and found that higher levels of calcium content and alkaline phosphatase activity at the cranial site at days 2-5 were associated with the BSP-mediated calcification. We also found that BSP stimulated osteoblast differentiation through up-regulation of cbfa1 and osterix, key transcription factors of osteoblast differentiation, which occurred in the calvarial defects but not in the subcutaneous tissue. These results demonstrate that BSP stimulates calcification and osteogenesis in a site-specific manner, and that local environment and the specificities of responding cells may play critical roles in the function of BSP in vivo. [ABSTRACT FROM AUTHOR]