Treatment of polluted river water using pilot-scale constructed wetlands.
Explore the source record for details and available documents.
Biodegradation, Environmental↗
Biomedical subjects
X Ruan
Publications and source records attributed to X Ruan.
Solution structure and function of a conserved protein SP14.3 encoded by an essential Streptococcus pneumoniae gene.
Streptococcus pneumoniae is a major human pathogen that causes high mortality and morbidity rates and has developed resistance to many antibiotics. The genome of S. pneumoniae has recently been completely sequenced revealing many genes encoding hypothetical proteins of unknown function. We have found that the gene encoding one such conserved protein, SP14.3, is essential for growth of S. pneumonia. Since it is essential, SP14.3 represents a potential target for drug discovery. Here, we describe the three-dimensional solution structure of SP14.3 as determined by NMR spectroscopy. The structure consists of two domains each with an alpha/beta-fold. The N-terminal domain contains two alpha-helices and a three-stranded beta-sheet, while the C-terminal domain is composed of one alpha-helix and a five-stranded beta-sheet. The N-terminal domain of the protein contains a highly negatively charged surface and resembles the fold of the N-terminal domain of Thermus thermophilus ribosomal protein S3. The C-terminal domain has a protein fold similar to human small nuclear ribonucleoprotein Sm D3 and Haloarcula marismortui ribosomal protein L21E. The two domains of the protein tumble in solution overall as a whole with an overall molecular rotational correlation time (tau(m)) of 12.9 ns at 25 degrees C. The relative orientation of the two domains is not defined by the nuclear Overhauser effect data. Indeed, residual dipolar couplings and the structure calculations indicate that the relative orientation of the two domains is not rigidly oriented with respect to one another in solution.
Bacterial Proteins↗
Changes of absorption spectra during heat-induced denaturation of Photosystem II core antenna complexes CP43 and CP47: revealing the binding states of chlorophyll molecules in these two complexes.
The Photosystem II (PSII) core antenna complexes, CP43 and CP47, were prepared from spinach (Spinacia oleracea L.). The absorption spectra in the red region at room temperature were recorded for the PSII core antenna samples after increased temperature treatment (up to 80 degrees C). Derivative and difference spectra revealed the existence of two groups of chlorophyll a (Chl a) molecules in both CP43 and CP47. The one with the absorption peak in the shorter wavelength region was designated as CP43-669 and CP47-669, while the other with the absorption peak in the longer wavelength region was designated as CP43-682 and CP47-680. The results of the thermal treatment experiment demonstrated that CP43-669 and CP47-669 may exist as monomers of Chl a and that their binding sites on the polypeptides are insensitive to thermal treatment, whereas CP43-682 and CP47-680 may exist as dimers or multimers of Chl a and their binding regions in the polypeptide chains are more sensitive to heat treatment. The excitation energy transfer mechanism between these two different groups of Chl a molecules is also analyzed.
Apoproteins↗
Strong-light photoinhibition treatment accelerates the changes of protein secondary structures in triton-treated photosystem I and photosystem II complexes.
Changes in the protein secondary structure and electron transport activity of the Triton X-100-treated photosystem I (PSI) and photosystem II (PSII) complexes after strong illumination treatment were studied using Fourier transform-infrared (FT-IR) spectroscopy and an oxygen electrode. Short periods of photoinhibitory treatment led to obvious decreases in the rates of PSI-mediated electron transport activity and PSII-mediated oxygen evolution in the native or Triton-treated PSI and PSII complexes. In the native PSI and PSII complexes, the protein secondary structures had little changes after the photoinhibitory treatment. However, in both Triton-treated PSI and PSII complexes, short photoinhibition times caused significant loss of alpha-helical content and increase of beta-sheet structure, similar to the conformational changes in samples of Triton-treated PSI and PSII complexes after long periods of dark incubation. Our results demonstrate that strong-light treatment to the Triton-treated PSI and PSII complexes accelerates destruction of the transmembrane structure of proteins in the two photosynthetic membranes.
Electron Transport↗
Role of EP(2) and EP(3) PGE(2) receptors in control of murine renal hemodynamics.
The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE(2) E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE(2). Specifically, we determined the extent to which the EP(2) and EP(3) receptor subtypes mediate the actions of PGE(2) on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP(2) or EP(3) (-/-) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP(2) receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP(2)-/- mice [RBF EP(2)-/-: 5.3 +/- 0.8 ml. min(-1). 100 g kidney wt(-1); renal vascular resistance (RVR) 19.7 +/- 3.6 mmHg. ml(-1). min. g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 +/- 0.5 ml. min(-1). 100 g kidney wt(-1); RVR +/+: 25.4 +/- 4.9 mmHg. ml(-1). min. 100 g kidney wt(-1)). This was also the case for the peak RBF increase after local PGE(2) (500 ng) injection into the renal artery (EP(2)-/-: 116 +/- 4 vs. +/+: 112 +/- 2% baseline RBF). In contrast, we found that the absence of EP(3) receptors in EP(3)-/- mice caused a significant increase (43%) in basal RBF (7.9 +/- 0.8 ml. min(-1). g kidney wt(-1), P < 0.05 vs. +/+) and a significant decrease (41%) in resting RVR (11.6 +/- 1.4 mmHg. ml(-1). min. g kidney wt(-1), P < 0.05 vs. +/+). Local administration of 500 ng of PGE(2) into the renal artery caused more pronounced renal vasodilation in EP(3)-/- mice (128 +/- 2% of basal RBF, P < 0.05 vs. +/+). We conclude that EP(3 )receptors mediate vasoconstriction in the kidney of male mice and its actions are tonically active in the basal state. Furthermore, EP(3) receptors are capable of buffering PGE(2)-mediated renal vasodilation.
Animals↗
[Analysis on the trace element and amino acid content in xinjiang 6 series Rhodiola L. plant].
Trace elements Na, K, Mg, Ca, Mn, Fe, Cu, Zn, Se and 20 kinds of amino acid in Xinjiang 6 series of Rhodiola's root and rootstalk were measured. The result shows that contents of 9 kinds of trace elements in them are different. They contain from 8 to 18 kinds amino acid, and also contain from 3 to 7 kinds of indispensable amino acid respectively. Rhodiola rosea L. contains most kinds of amino acid among six kinds of Rhodiola L. in Xingjiang, and contents of trace elements in it are also moderate, so it is fittest to be a nutrious chinese traditional and herbal drug of six kinds of Rhodiola L. in Xingjiang.
Amino Acids↗
Spectroscopic study of trypsin, heat and triton X-100-induced denaturation of the chlorophyll-binding protein CP43.
Trypsin-, heat- and Triton X-100-induced denaturation of CP43, the core antenna complex of photosystem II purified from spinach, has been investigated using absorption, fluorescence and circular dichroism spectroscopy. Triton X-100 was found to bring about considerable dissolution of pigments from the protein to the monomeric state in solution and destruction of the interactions among the chlorophyll, carotene and protein. Heat induced significant unfolding of the protein secondary structure and loss of excitonic interactions of the pigments, but no apparent dissolution of the pigments from CP43. Trypsin caused structural changes in the extrinsic part of the protein but no change of the native state of the pigments. Trypsin, heat and Triton X-100 treatments increased the light sensitivity of chlorophyll in CP43 to different extents. The results suggest that the protein and beta-carotene can protect the chlorophyll from light-induced destruction in CP43.
Binding Sites↗
[The study of risk ratio on genetic factors in recurrent aphthous ulcer].
OBJECTIVE: To study the relation of SCE, MNR, CAR of lymphocytes in RAU patients and RAU. METHODS: SCE, MNR, CAR of 60 RAU patients were determined, and were analyzed by non-condition Logistic regression and the risk ratio of the 3 studying factors was calculated. RESULTS: SCE, MNR and CAR were important risk factors among many complicated causes of RAU. CONCLUSION: The results of the study showed essentially that RAU patients could have some pathological genetic predisposition and abnormal genetic materials congenitally.
Adolescent↗
[The alterations in vasoactive intestinal polypeptide-immune reaction positive neurons of cerebral tissues in epileptic rats induced by penicillin].
To further explore the action of vasoactive intestinal polypeptide(VIP) in epileptogenesis, we made an immunocytochemical analysis and observed the alterations in VIP-energic neurons of the cerebral cortex, hippocampus and amygdaloid in rats. The animals were divided into three groups: the control, the epileptic group in which seizure was induced by injected Penicillin(PNC) intraperitoneally, and the nimodipline(NIM) group in which seizure was impressed by giving PNC after NIM, a dihydropyridine calcium entry blocker, was injected. The results showed that the number of neurons of epileptic group increased, compared with that of control group (P < 0.01), the neuronic number of the epileptic group was higher than that of the NIM group(P < 0.01), whereas there was no significant difference in neuronic number between the control group and the NIM group(P > 0.05). These suggest that VIP and Ca2+ participate in the process of epileptogenesis.
Animals↗
[Analysis of trace elements contents in dry-fruit of xinjiang].
Ten kinds of trace element's contents in nine kinds of specialities of Xinjiang were measured by flame atomic absorption spectrometry and flame atomic emission spectrometry. The trace element's contents in these different specialities were compared with each other. The relationships between the over-accumulation of trace element in body and some illness of people were also studied. Statistics suggest that there are different contents of the ten kinds of trace elements in every kinds of dry-fruit. The statistics are valuable references.
China↗
Anti-inflammatory properties of cytochrome P450 epoxygenase-derived eicosanoids.
The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-kappaB and IkappaB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.
8,11,14-Eicosatrienoic Acid↗
Nitric oxide/cAMP interactions in the control of rat renal vascular resistance.
This study aimed to characterize the interaction between nitric oxide (NO)- and cAMP-related pathways in the control of renal blood flow. Using the isolated perfused rat kidney model, we determined the effects of inhibition of NO formation by Nomega-nitro-L-arginine methyl ester (L-NAME; 1 mmol/L) and of NO administration by sodium nitroprusside (SNP, 10 micromol/L) on renal vascular resistance under conditions of elevated vascular cAMP levels. cAMP levels were increased either by adenylate cyclase activation via isoproterenol or by inhibition of cAMP phosphodiesterases (PDEs) 1, 3, and 4. We found that L-NAME markedly increased vascular resistance and that this effect was completely reversed by SNP. Both isoproterenol and inhibitors of the cAMP PDEs lowered basal vascular resistance. In the presence of isoproterenol (3 nmol/L) and inhibitors of PDE-1 [8-methoxymethyl-l-methyl-3-(2-methylpropyl)-xanthine; 8-MM-IBMX, 20 micromol/L] and PDE-4 (rolipram, 20 micromol/L), L-NAME again substantially increased vascular resistance, and this effect of L-NAME was completely reversed by SNP. In the presence of the PDE-3 inhibitors milrinone (20 micromol/L) and trequinsin (200 nmol/L), however, both L-NAME and SNP failed to exert any additional effects. Because PDE-3 is a cGMP-inhibited cAMP PDE and because the vasodilatory effect of SNP was abrogated by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) (20 micromol/L), our findings are compatible with the idea that an action of NO on PDE-3 could account for the vasodilatory properties of NO on the renal vasculature. Moreover, our findings suggest that PDE-3 activity is an important determinant of renal vascular resistance.
Adenylyl Cyclases↗
Effect of interleukin-1 beta on the elevation of cytoplasmic free calcium of the cultured hippocampal neurons induced by L-glutamate.
To investigate the intracellular mechanism that interleukin-1 beta (IL-1 beta) facilitates epileptic seizure and neuronal damage, the effect of IL-1 beta alone or IL-1 beta plus glutamate (Glu) on the intracellular free calcium ([Ca2+]i) of single cultured hippocampal neuron was examined by using EPC-9 light-electricity measurement system. The results showed that IL-1 beta of different concentrations (5 x 10(3) U/L, 10 x 10(3) U/L, 20 x 10(3) U/L, 30 x 10(3) U/L, 50 x 10(3) U/L, 100 x 10(3) U/L) failed to affect the neuronal [Ca2+]i, but IL-1 beta could facilitate the augmentation of neuronal [Ca2+]i induced by Glu in a dose-dependent pattern. MK-801 inhibited the effect of Glu on [Ca2+]i, and also inhibited the effect of IL-1 beta on [Ca2+]i induced by Glu, while verapamil did not influence the effect of Glu or IL-1 beta. It is concluded that IL-1 beta, as a neuromodulator, can facilitate the activation of NMDA receptor by Glu, induce the increase of intracellular calcium, which enhances the excitement of neuron.
Animals↗
Carrier detection and presymptomatic identification of Wilson disease in Chinese by non-isotopic linkage analysis with four short tandem repeat polymorphisms.
Wilson disease (WD) is an autosomal recessive disorder of copper metabolism. To establish an efficient, accurate and fast diagnostic method for carrier detection and presymptomatic identification of WD in Chinese population, we studied haplotypes of short tandem repeat (STR) polymorphisms flanking the WD gene in 40 Chinese WD families. The results suggested that this genetic diagnosis system based on the four STR polymorphisms is of high value for the detection of potential carriers and WD homozygotes in families with at least one previously affected child. It is an efficient, accurate and fast diagnostic method that can be well suited for routine use in clinical laboratories.
Asian People↗
Impaired prostaglandin E(2)/prostaglandin I(2) receptor-G(s) protein interactions in isolated renal resistance arterioles of spontaneously hypertensive rats.
The protective effect of vasodilator agents linked to the cAMP pathway is less effective for buffering the vasoconstrictor effect of angiotensin II in young animals with genetic hypertension. To determine the underlying cellular mechanism, experiments were performed on freshly isolated preglomerular resistance arterioles obtained from kidneys of 7-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Specific high-affinity saturable binding of (3)H-prostaglandin (PG) E(2) revealed 1 receptor class in renal microvessels; PGE(2) receptor density was similar in SHR and WKY (106 versus 115 fmol/mg; P>0.8), as was receptor affinity (3.6 versus 3.5 nmol/L; P>0.7). Basal cAMP activity was similar in renal arterioles from SHR and WKY. A major finding was that PGE(2), PGI(2), and isoproterenol produced weaker stimulation of cAMP formation in arteriolar cells of SHR (P<0.02). In contrast, GTPgammas and forskolin stimulated cAMP generation to a similar degree in both rat strains, which suggests normal adenylate cyclase activity in hypertension-prone SHR. Immunoblots revealed the presence of 3 classes of G proteins (G(s), G(i), and G(q)) in preglomerular arterioles. The relative amounts of discernible G-protein alpha-subunits in renal resistance vessels did not differ between SHR and WKY. These results extend previous in vivo studies of abnormal renal vascular reactivity in SHR and more directly localize defective coupling of the prostaglandin and beta-adrenergic receptors to a stimulatory G protein and cAMP production in freshly isolated preglomerular arteriolar cells of young SHR. This dysfunction may be due to an abnormal interaction between prostaglandin receptors and G(s) protein that leads to inefficient coupling of initiating steps in the cAMP-protein kinase A cascade during the development of hypertension.
Animals↗
Renal vascular reactivity in mice: AngII-induced vasoconstriction in AT1A receptor null mice.
The present study describes methodology and its application to evaluate renal reactivity in acute studies on anesthetized mice. Renal blood flow (RBF) was measured using an ultrasonic transit-time flowmeter and a non-cannulating V-shaped probe. An intrarenal artery injection technique established feasibility and reproducibility of studies of renal vascular reactivity to angiotensin II (AngII) in adult wild-type mice. The study also examined whether AngII would affect RBF in mice lacking AT1A receptors due to gene targeting. Mean arterial pressure averaged 83 and 62 mmHg, respectively, in mice with and without AT1A receptors. The RBF was similar in both groups, averaging 7 ml/min per g kidney wt. AngII injection (10-microl bolus) into the renal artery produced transient, dose-dependent, selective reductions in RBF in AT1A knockout mice as well as wild-type mice. The response was considerably greater in mice with AT1A receptors: 10% for 0.1 ng, 30% for 1 ng, and 45% for 5 ng AngII in control animals versus respective decreases of 6, 15, and 17% in knockout mice. In other studies, angiotensin-converting enzyme (captopril) or renin (CP-71362-14) was inhibited. During inhibition of AngII formation, renal vascular reactivity to AngII increased twofold in both groups. Coadministration of the AT1 receptor antagonist losartan (1 to 1000 ng) elicited dose-dependent inhibition of AngII effects, with near maximum blockage of 80 to 90% in both groups of mice. The putative AT2 receptor antagonist PD 123319 inhibited 30 to 40% of AngII-induced vasoconstriction, whereas CGP 42112 had no effect in either group. In conclusion, AngII can elicit renal vasoconstriction, albeit attenuated, in AT1A knockout mice. The weaker RBF effects are most likely due to the absence of the AT1A receptor. Inhibition of the response by AT1 receptor antagonist suggests mediation by the AT1B receptor in these animals. The residual constrictor effect observed during AT1 receptor blockade and sensitive to PD 123319 appears to be mediated by a non-AT1 receptor.
Angiotensin II↗
[Influence of functional groups of huatanyuxin decoction on Ca2+ transmembrane influx in rat aorta].
OBJECTIVE: To study the Ca2+ antagonistic effect of functional groups of Huatanyuxin decoction. METHOD: The 45Ca transmembrane influx technique was used to measure the Ca2+ blocking effect of leak, receptor-operated Ca2+ channel (ROC) and potential-dependent Ca2+ channel (PDC) in rat aorta. RESULT: ROC and PDC could be blocked when the complex prescription was used at concentrations of 0.5-5 mg/ml. Among the functional groups, Huoxue group (activating blood) and Xinqi group (promoting and normalizing flow of vital energy) showed better Ca2+ antagonistic effect. CONCLUSION: The mechanism of therapeutic effect of Huatanyuxin decoction may be related to its Ca2+ blocking effect similar to verapamil.
Animals↗
Actions of angiotensin II on the renal microvasculature.
Angiotensin II (AngII) exerts powerful effects on the renal microcirculation to influence a variety of functions. This review summarizes some of the major findings over the past 10 years as they elucidate the multiple roles that AngII plays in the regulation of whole kidney blood flow, perfusion of cortical and medullary regions, and renal autoregulation. Topics of discussion include localization of AngII receptor types and subtypes in the renal vasculature, action of AngII on vascular smooth muscle cells of the afferent and efferent arterioles, and intracellular signaling pathways. Within the microvasculature, AngII causes potent constriction in both the afferent and efferent arterioles, with responses modulated by paracrine and autocrine factors of endothelial and macula densa origins. With regard to renal autoregulatory mechanisms consisting of the myogenic response and the tubuloglomerular feedback mechanism, the myogenic response appears to operate independent of the renin-angiotensin system. On the other hand, tubuloglomerular feedback activity is often directly proportional to concentrations of AngII, especially in high renin states. Of the two types defined to date, the AT1 is the predominant receptor in the adult rat kidney mediating the vascular effects of AngII. AT2 receptor is highly expressed in the fetal kidney and is important for renal development, but is very weakly expressed in adult animals. Nevertheless, AT2 receptors may mediate vasodilation under certain conditions. The signaling transduction pathways for AT1 receptors include Gq/11-protein and protein kinase C activation. AngII causes constriction of the afferent arteriole primarily by stimulation of calcium entry via voltage-sensitive, L-type channels, whereas AngII effects on the efferent arteriole are due to calcium release from intracellular stores and calcium entry through voltage-independent calcium entry channels. Future experiments should contribute to a more in-depth understanding of the modulation of AngII effects by other vasoactive agents and interactions between different second-messenger signaling pathways in health and disease.
Angiotensin II↗