Self-assembled bismuth nanocrystallites.
Using a high-temperature organic solution reduction method, highly crystalline and single domain bismuth nanoparticles have been synthesized and self-assembled.
Journal Article↗
Biomedical subjects
W L Zhou
Publications and source records attributed to W L Zhou.
Construction of copper halide networks within layered perovskites. Syntheses and characterization of new low-temperature copper oxyhalides.
The construction of two-dimensional (2D) copper halide networks within a variety of perovskite hosts by a low-temperature topochemical method is demonstrated. Ion exchange between some layered perovskite oxides of the type A'[An - 1(M,M')nO3n + 1] (A' = alkali metal, H, NH4; A = alkaline earth, rare earth, or Bi; M,M' = Nb, Ta, Ti; n = 2, 3) with CuX2 (X = Cl, Br) results in the oxyhalides (CuX)[An - 1(M,M')nO3n + 1]. Rietveld refinements from X-ray powder diffraction data show that the structures of these new copper oxyhalides contain edge-sharing CuO2X4 octahedra sandwiched between the M/M'O6 octahedra of the perovskite slabs. The compounds are low-temperature phases that decompose well below 700 degrees C. The copper oxyhalides exhibit antiferromagnetic ordering resulting from the magnetic exchange interactions within the planar Cu-X networks.
Journal Article↗
Prevalence and analysis of risk factors for infections caused by resistant Escherichia coli strains in Anhui, China.
BACKGROUND: This study analyzes the prevalence of hospital and community-acquired infections caused by Escherichia coli. PATIENTS AND METHODS: The antibiotic resistance pattern was used to characterize the isolates, and a retrospective observational study was performed to assess the relationship between antimicrobial use and bacterial resistance. The study was conducted during a 1-year and 7-month period in a 1,500-bed tertiary care hospital in Anhui, China. RESULTS: An E. coli infection was diagnosed in 1.4% of patients (519/36,179) admitted to the hospital between March 1, 1999 and August 31, 2000. Of the 519 isolates, 489 (94.2%) were resistant to at least one antimicrobial; 86% were resistant to ampicillin, 85% to cephalothin, 83% to piperacillin, 77% to ampicillin/sulbactam, 72% to trimethoprim/sulfamethoxazole (TMP-SMZ), 70% to ciprofloxacin, 61% to cefoperazone, 58% to tobramycin, 56% to gentamicin, 48% to ticarcillin-clavulanate, 44% to cefazolin, 43% to cefuroxime, 36% to cefoxitin, 32% to cefepime, 29% to aztreonam, cefetaxime and ceftriaxone, 28% to ceftazidime, 19% to piperacillin/tazobactam, 10% to amikacin, while all strains tested were susceptible to imipenem. CONCLUSION: Prior receipt of amtimicrobial therapy was significantly associated with infection caused by a resistant organism.
Adolescent↗
Regulation of capacitative Ca2+ entry by tyrosine phosphorylation in the neural retina of chick embryo.
Capacitative Ca2+ entry occurs in the neural retina of chick embryo during neurogenesis. We studied the effects of blockers of capacitative Ca2+ entry (SK&F 96365, Zn2+, Ni2+), genistein, a tyrosine kinase inhibitor and vanadate, a protein-phosphotyrosine phosphatase inhibitor in the embryonic chick retina with fura-2 fluorescence measurements. After incubation of the retina in a Ca2+-free solution with or without an inhibitor of Ca2+ pumps of intracellular Ca2+ stores, re-introduction of extracellular Ca2+ caused capacitative Ca2+ entry which was inhibited by SK&F 96365 (10 microM), Zn2+ (1 mM), Ni2+ (5 mM) and genistein (100 microM). On the contrary, vanadate (1 mM) enhanced the Ca2+ entry. These results suggested that tyrosine phosphorylation was involved in the activation of capacitative Ca2+ entry.
Animals↗
Lysophosphatidic acid-induced Ca(2+) mobilization in the neural retina of chick embryo.
Lysophosphatidic acid (LPA) plays various roles in the regulation of cell growth as a lipid mediator. We studied the effect of LPA on intracellular Ca(2+) concentration ([Ca2+]i) with Fura-2 in the neural retina of chick embryo during neurogenesis. Bath application of LPA (1-100 microM) to the embryonic day 3 (E3) chick retina caused an increase in [Ca2+](i) in a dose-dependent manner, with an EC(50) value of 9.2 microM. The Ca(2+) rise was also evoked in a Ca(2+)-free medium, suggesting that release of Ca(2+) from intracellular Ca(2+) stores (Ca(2+) mobilization) was induced by LPA. U-73122, a blocker of phospholipase C (PLC), inhibited the Ca(2+) rise to LPA. Pertussis toxin partially inhibited the Ca(2+) rise to LPA, indicating that G(i)/G(o) protein was at least partially involved in the LPA response. The developmental profile of the LPA response was studied from E3 to E13. The Ca(2+) rise to LPA declined drastically from E3 to E7, in parallel with decrease in mitotic activity of retinal progenitor cells. The signal transduction pathway and developmental profile of the Ca(2+) response to LPA were the same as those of the Ca(2+) response to adenosine triphosphate (ATP), which enhances the proliferation of retinal progenitor cells. The coapplication of LPA with ATP resulted in enhancement of Ca(2+) rise in the E3 chick retina. Our results show that LPA induces Ca(2+) mobilization in the embryonic chick retina during neurogenesis.
Animals↗
Involvement of P2 purinoceptors in the regulation of DNA synthesis in the neural retina of chick embryo.
The activation of P2 purinoceptors induces Ca2+ mobilization in the early embryonic chick neural retina. This purinergic Ca2+ response declines parallel with the decrease in mitotic activity during retinal development. To investigate the role of P2 purinoceptors in the regulation of retinal cell proliferation, we studied the effects of the P2 purinoceptor antagonists suramin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), and of the agonist ATP on DNA synthesis in retinal organ cultures from embryonic day 3 (E3) chick. Suramin inhibited [3H]-thymidine incorporation in a dose-dependent manner (IC50: approximately 70 microM). PPADS also reduced [3H]-thymidine incorporation with maximum inhibition of 46% at 100 microM. Exogenous ATP enhanced [3H]-thymidine incorporation in a dose-dependent manner to maximally 200% of control (EC50: approximately 70 microM). In dissociated retinal cultures from E7 chick, both antagonists showed similar inhibitory effects on [3H]-thymidine incorporation without affecting cell viability. In line with these observations, the presence of extracellular ATP was demonstrated both in vitro and in vivo. In the medium of E3 retinal organ cultures, the concentration of ATP increased 25-fold within 1 h of incubation and this concentration was kept for at least 24 h. In the chick amniotic fluid, the ATP concentration was nearly 3 microM at E3 and declined to 0.15 microM at E7. The results indicate that P2 purinoceptors activated by autocrine or paracrine release of ATP are involved in the regulation of DNA synthesis in the neural retina at early embryonic stages.
Adenosine Triphosphate↗
Ca2+ mobilization and capacitative Ca2+ entry regulate DNA synthesis in cultured chick retinal neuroepithelial cells.
Release of Ca2+ from intracellular Ca2+ stores (Ca2+ mobilization) and capacitative Ca2+ entry have been shown to be inducible in neuroepithelial cells of the early embryonic chick retina. Both types of Ca2+ responses decline parallel with retinal progenitor cell proliferation. To investigate their potential role in the regulation of neuroepithelial cell proliferation, we studied the effects of 2,5-di-tert-butylhydroquinone (DBHQ), an inhibitor of the Ca2+ pump of intracellular Ca2+ stores, and of SK&F 96365, an inhibitor of capacitative Ca2+ entry, on DNA synthesis in retinal organ cultures from embryonic day 3 (E3) chicks and in dissociated cultures from E7 and E9 chick retinae. We demonstrate that both antagonists inhibit [3H]-thymidine incorporation in a dose-dependent manner without affecting cell viability or morphology. The inhibition of [3H]-thymidine incorporation by SK&F 96365 occurred in the same concentration range (IC50: approximately 4 microM) as the blockade of capacitative Ca2+ entry in the E3 retinal organ culture. At a concentration of 5 microM SK&F 96365. DNA synthesis was reduced by 71, 40 and 32% in the E3, E7 and E9 cultures, respectively. Application of DBHQ at concentrations which led to depletion of intracellular Ca2+ stores also inhibited [3H]-thymidine incorporation with IC50 values of 20-30 microM in the different cultures. Our results suggest the involvement of Ca2+ mobilization and capacitative Ca2+ entry in the regulation of DNA synthesis in the developing neural retina.
Animals↗
Identification of Id2 as a globin regulatory protein by representational difference analysis of K562 cells induced to express gamma-globin with a fungal compound.
A fungus-derived compound (OSI-2040) which induces fetal globin expression in the absence of erythroid cell differentiation was identified in a high-throughput drug discovery program. We utilized this compound to isolate gamma-globin regulatory genes that are differentially expressed in OSI-2040-induced and uninduced cells in the human erythroleukemia cell line K562. Representational difference analysis (RDA) of cDNA revealed several genes that were significantly up- or down-regulated in OSI-2040-induced cells. One gene whose expression was markedly enhanced was the gene for the helix-loop-helix (HLH) transcription factor Id2. Southern analysis of RDA amplicons demonstrated progressive enrichment of Id2 with each successive subtraction of uninduced cDNA from induced cDNA. Northern analysis of OSI-2040-induced K562 cells confirmed that Id2 expression was directly up-regulated coordinately with gamma-globin. Analysis of other inducers of fetal globin demonstrated up-regulation of Id2 with sodium butyrate but not with hemin. Retrovirus-mediated overexpression of Id2 in K562 cells reproduced the enhancement of endogenous globin expression observed with OSI-2040 induction. Functional assays demonstrated that an E-box element in hypersensitivity site 2 is required for Id2-dependent enhancement of gamma-promoter activity. Protein binding studies suggest that alterations in E-box site occupancy by basic HLH proteins may influence this activity, thus expanding the potential role of these factors in globin gene regulation.
Blotting, Northern↗
Fluorophore toxicity in mouse eggs and zygotes.
Ion-sensitive fluorophores are commonly used for quantitative measurements of intracellular ion concentrations. However, both the method of intracellular loading--which for many fluorophores involves endogenous esterase-mediated removal of hydrophobic groups such as acetoxymethyl esters (AM)--and fluorescence excitation of fluorophores in the cell, can produce toxic metabolites and reactive species. Techniques used to measure intracellular ion concentrations in mammalian eggs and embryos are being increasingly employed, yet little information is available about any detrimental effects of the use of fluorophores. We have therefore used in vitro fertilisation (IVF) to assess potential fluorophore toxicity in mouse eggs, and whole cell patch-clamp recordings to detect fluorophore-associated membrane damage in zygotes. Four fluorophores were examined: SNARF-1 and BCECF (pH indicators), Fura-2 (Ca2+) and MQAE (Cl-). Cleavage of AM groups alone had no effect either on the success of IVF or on membrane electrical properties of mouse zygotes. Intracellularly loaded BCECF, SNARF-1 and Fura-2 followed by fluorescence excitation were not cell-toxic under the conditions examined. In contrast, MQAE demonstrated significant toxicity both alone and in combination with fluorescence excitation.
Animals↗
Angiotensin II receptors, AT1 and AT2 in the rat epididymis. Immunocytochemical and electrophysiological studies.
Previous work from our laboratory has provided evidence for the presence of a tissue renin-angiotensin system in the rat epididymis. In the current investigation, the regional localization of angiotensin II receptors, type I (AT1) and type II (AT2) was studied immunocytochemically using specific anti-peptide antibodies against the second extracellular loops of AT1 and AT2 receptors, and pharmacologically using specific receptor antagonists in conjunction with the short-circuit current technique. The immunocytochemical results showed that AT1 and AT2 immunoreactivities were predominantly localized in the basal region of the epididymal epithelium. Electrophysiological studies using the short-circuit current technique demonstrated a stimulatory effect of basolaterally applied angiotensin II on the epididymal electrogenic ion transport. This effect was inhibitable by the addition of AT1 antagonist, losartan but not by AT2 antagonist, PD123177, indicating a functional role of AT1 in epididymal electrolyte transport. The present finding suggests that angiotensin II receptors may play an important role in the regulation of epididymal function.
Angiotensin Receptor Antagonists↗
Local regulation of epididymal anion secretion by pituitary adenylate cyclase-activating polypeptide.
The present study investigated the role of pituitary adenylate cyclase-activating polypeptide (PACAP) in the regulation of electrogenic anion secretion by the rat cauda epididymal epithelium. PACAP38, which has been shown to affect secretory function in various exocrine and endocrine tissues, gave rise to a concentration-dependent increase in the short-circuit current (Isc). The PACAP38 effect was restricted to the apical aspect of the epididymal cells. The Isc response to PACAP38 was abolished in Cl-(-)free solution and completely inhibited by the Cl- channel blocker, diphenylamine-dicarboxylic acid. The Isc response to PACAP38 was also suppressed by pretreatment of the cells with the adenylate cyclase inhibitor, MDL12330A. The localization of PACAP38 was further investigated using an immunohistochemical technique. PACAP38 immunoreactivity was observed in the cauda epididymal tubules as well as in the cultured epithelium, indicating its epithelial origin. The present results suggest that Cl- secretion in the epididymis may be regulated by PACAP38, which could be locally synthesized and released by the epithelial cells, in a paracrine or autocrine fashion.
Adenylyl Cyclase Inhibitors↗
Different regulatory pathways involved in ATP-stimulated chloride secretion in rat epididymal epithelium.
The regulatory pathways involved in the ATP-stimulated Cl- secretion across rat epididymal epithelium were investigated by the short-circuit current (ISC) technique. Biphasic characteristic was observed in the ISC responded to ATP (0.01-10 microM). Inhibitor of P1 receptor, 8-phenyltheophylline (up to 100 microM), did not have any effect on both phases of the ATP-stimulated ISC. The order of potency for stimulation of the two phases in ISC was ATP > ADP >> AMP, adenosine, consistent with the presence of P2-purinoceptors. Cl- channel blocker, disulfonic acid stilbene (DIDS, 300 microM), only inhibited the first peak of the ATP-stimulated ISC while diphenylamine-dicarboxylic acid (DPC, 1 mM) reduced both, indicating the involvement of different conductance pathways. DIDS was found to have an inhibitory effect on Ca(2+)-activated ISC (induced by ionomycin, 10 microM) but not cAMP-activated ISC (induced by forskolin, 1 microM) which could only be blocked by DPC. Both peaks of the ATP-activated ISC could be significantly inhibited by pretreatment with a Ca(2+)-chelating agent, BAPTA-AM (50 microM). An increase in cellular cAMP content upon stimulation of ATP was measured by radioimmunoassay. No significant increase in cAMP production was observed in cells stimulated with adenosine. The ATP-induced cAMP increase was prevented by pretreatment with BAPTA-AM (100 microM) indicating that cAMP production upon ATP stimulation was secondary to an increase in intracellular Ca2+ concentration. These results indicate that the ATP-stimulated Cl- secretion could be mediated by Ca2+ and cAMP-dependent regulatory pathways giving rise to the biphasic nature of the ATP-induced ISC.
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
Extracellular ATP activates both Ca(2+)- and cAMP-dependent Cl- conductances in rat epididymal cells.
Activation of Ca2+ and cAMP-dependent Cl- conductances by extracellular ATP was studied using the whole-cell patch clamp technique. Immediately after addition of extracellular ATP (10 microM), activation of whole-cell Cl- current exhibiting delayed inactivation and activation kinetics at hyperpolarizing and depolarizing voltages, respectively, was observed. After prolonged activation, the kinetic characteristics of the ATP-induced Cl- current became time- and voltage-independent. When applied to the later phase of the ATP-activated whole-cell current, the disulfonic acid stilbene DIDS (200 microM) could only inhibit 64% of the current while diphenylamine-dicarboxylic acid (DPC, 1 mM) completely inhibited it. Inclusion of a peptide inhibitor for protein kinase A (PKI, 10 nM) in the pipette solution blocked ATP-induced time- and voltage-independent current activation but did not affect the delayed activating and inactivating current activation but did not affect the delayed activating and inactivating current which could be totally blocked by DIDS. Anion selectivity sequence was determined in the presence of either PKI or DIDS and found to be significantly different. Increased pipette EGTA (10 mM) or treatment of the cells with trifluoperazine (40 microM), an inhibitor of calmodulin, suppressed both types of ATP-induced Cl- currents. No current activation by ATP was observed when cells were dialyzed with the IP3 receptor blocker, heparin (10 ng/ml). These results suggest that extracellular ATP activates IP3-linked Ca(2+)-dependent regulatory pathway, which in turn activates cAMP-dependent pathway, leading to activation of both Ca2+ and cAMP-dependent Cl- conductances in epididymal cells.
Adenosine Triphosphate↗
[Determination of blood hormone levels in patients with "spleen deficiency" syndrome after major operations].
UNLABELLED: The character of "Spleen Deficiency" (SD) Syndrome was evaluated by determination of the blood levels of various gastroenteropancreatic hormones and thyroid hormone. Patients of SD group were diagnosed clinically by Syndrome Differentiation, and those of the normal group were volunteer blood donors. RIA was used to determine all the hormones except T3RUR. RESULTS: TT3, FT3 of the SD group were very significantly lower than that of normal group (P less than 0.001). The levels of rT3 in SD group were significantly higher than normal control (P less than 0.05). For TT4, T3RUR and FT4, there were no significant differences between the two groups. Among the gastroenteropancreatic hormones, gastrin in the SD group was significantly lower than that of the normal group (P less than 0.01), motilin was very significantly higher (P less than 0.002). The value of pp was similar in the two groups, under physiological conditions, however, in adults the hormone tended to increase with age. Since the average age of patients in the SD group was 54.9, and that of the normal group was 38.5, remarkably lower values were seen in the SD group. Other hormones such as VIP, SST, glucagon and insulin were of no significant difference between the two groups. The result showed that thyroid hormone and some of gastroenteric hormones in the blood of patients with SD after major operations were quite different from normal, and was common to patients with general SD Syndrome, with low T3 syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Immunologic diagnosis of schistosomiasis japonica by indirect immunoperoxidase on liver-egg section (LE-IIP).
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Animals↗
[Preliminary application of ELISA of liver sections of infected mice in the diagnosis of schistosomiasis japonica].
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Animals↗