Radio-luminescence spectral features and fast emission in hafnium dioxide nanocrystals.

In this work, we investigate the optical properties of hafnium dioxide nanocrystals, upon X-ray irradiation, looking for spectral evolution following thermal treatments in air up to 1000 °C that modify the crystal size as well as their point defect concentrations. Radio-luminescence measurements from 10 K up to room temperature reveal a rich and evolving picture of the optical features. A complete spectral analysis of the broad luminescence spectra reveals the presence of several emission components in the visible and UV regions. The lower energy components peaking at 2.1, 2.5, and 2.9 eV are characterized by a thermal quenching energy of 0.08 eV, while the corresponding value for the UV bands at 4.1 and 4.7 eV is close to 0.23 eV. We tentatively assign the components ranging from 2 to 3 eV to the presence of optically active defects of an intrinsic nature, together with the occurrence of titanium impurities; conversely, the bands at higher energies are likely to be of an excitonic nature. The comparison with previous photo-luminescence studies allows evidencing characteristic differences between the features of luminescence emissions caused by intra-centre excitation and those occurring under ionizing irradiation. Finally, scintillation measurements in the visible range reveal the existence of a fast decay in the nanosecond time scale for the smallest hafnia nanocrystals. This study offers a clear description of HfO2 luminescence characteristics upon excitation by X-rays and can lead to a better comprehension of the structure-property relationship at the nanoscale in metal oxides.

Rationale for the crystallization of titania polymorphs in solution.

We use in situ X-ray absorption and diffraction studies to directly monitor the crystallization of different titania polymorphs in one and the same solution. We find that, despite the commonly accepted polymorphic-crossover from anatase to rutile triggered by the critical size of nanoparticles, in the solution their respective nucleation and growth are independent processes. Moreover, we find that 5.9 nm rutile nanoparticles are formed prior to the formation of 8.4 nm anatase nanoparticles. Our results suggest that the origins of this crystallization mechanism lie in the formation of an intermediate non-crystalline phase and in time-dependent changes in the chemical environment.

[Tremorgenic syndrome in a cattle herd after feeding silage contaminated with A. clavatus]. / Tremorgenes Syndrom in einem Rinderbestand nach Verfütterung einer mit A. clavatus befallenen Silage.

The clinical signs, pathological and laboratory findings of cattle suffering from a tremorgenic syndrome are described. Animals on a farm with a total of 22 cows, 18 heifers and 9 calves were fed mouldy grass and spent malt-grain silage. Five heifers were affected with muscular tremor, hyperexcitability and hypersensitivity. They were ataxic or in sternal recumbency, while their appetite remained normal. Haematology and blood chemistry in two heifers as well as cerebrospinal fluid from one sick animal were unremarkable. The pathological examination of one animal brought no macroscopic changes to light. Histological examination, however, revealed the degeneration of motor neurones in the midbrain, brain stem and spinal cord. Analysis of a silage sample provided evidence of the presence of Aspergillus clavatus, a mould capable of producing neurotoxic tremorgenic mycotoxins. Epidemiology, clinical findings, pathology and microbiological examination suggest that the five cattle were suffering from neuromycotoxicosis.

Cross-sectional study of Streptococcus species in quarter milk samples of dairy cows in the canton of Bern, Switzerland.

A total of 2538 quarter milk samples from 638 lactating dairy cows from 47 farms in the canton of Bern, Switzerland, were investigated for streptococci. A novel, simple and inexpensive laboratory method was used for the differentiation of Streptococcus species, and a risk factor analysis was carried out. The prevalence in the quarter milk samples was 0.2 per cent for Streptococcus agalactiae, 1.3 per cent for Streptococcus uberis, 1.3 per cent for Streptococcus dysgalactiae, 0.1 per cent for Enterococcus species and 2.9 per cent for minor Streptococcus species (designated Streptococcus-Lactococcus-Enterococcus [SLE] group). Based on the somatic cell count (SCC), S uberis and S dysgalactiae were classified as 'major' pathogens and the bacteria in the SLE group as 'minor' pathogens. For S uberis, S dysgalactiae and bacteria in the SLE group, the most significant risk factor was an intramammary infection (IMI) of a neighbouring quarter by the same pathogen. Other significant risk factors for S uberis infection were a positive California Mastitis Test (CMT) result and a SCC of more than 100,000 cells/ml. Significant risk factors for IMI with S dysgalactiae were a positive CMT result, teat injury and palpable abnormalities in the udder. Infection with bacteria in the SLE group was significantly associated with a SCC of more than 100,000 cells/ml, a lactation number of more than 2, the right rear quarter (as the location of infection) and a positive CMT result.

Binding sites of muscarinic and adrenergic receptors in gastrointestinal tissues of dairy cows suffering from left displacement of the abomasum.

Muscarinic acetylcholine (M) and adrenergic (AR) receptors mediate gastrointestinal motility. Using radioligand binding assays and real-time polymerase chain reaction, the densities of binding sites and mRNA levels of M2, M3, α2(AD)- and ß2-AR were compared in muscle tissues from the abomasal fundus, pylorus, duodenum, caecum, and external loop of the spiral colon of eight cows with left displacement of abomasum (LDA), and of eight healthy cows. Specific binding of the [³H]-ligands to each of the four receptors was competitive and saturable. Binding sites of M2 (all intestinal sites), M3 (duodenum and caecum), and of α2(AD)-AR (abomasal fundus) were lower (P < 0.05) in cows with LDA than in healthy cows. The coefficients of correlation between binding sites and mRNA transcripts of receptors were dissimilar in cows with LDA and healthy cows. The decrease in densities of M (intestine) and of α2(AD)-AR (abomasum) receptors suggests their implication in the impairment of motility associated with or leading to LDA.

Preparation of ligand-free TiO2 (anatase) nanoparticles through a nonaqueous process and their surface functionalization.

We here present a new method for preparing ligand-free titania nanoparticles, which are easily amenable to surface functionalization in an aqueous environment. The specific advantage of this method is that it combines the advantages of nonaqueous synthetic processes (high crystallinity) to those of a surface functionalization in a water medium, which allows for a wider variety of biofunctional (and nonorganic-soluble) groups to be added on the nanoparticles. In particular, we report on the characterization of the three phases of synthesis, dispersion in water environment and surface functionalization of the nanoparticles, focusing on a qualitative evaluation of the surface adsorption mechanism.

Adding a dialysis dose to continuous hemofiltration increases survival in patients with acute renal failure.

Acute renal failure (ARF) in critically ill patients is associated with high mortality. Optimal method and dose of continuous renal replacement therapy could improve survival in these patients. We studied the hypothesis that an increase in dialysis dose obtained by continuous veno-venous hemodiafiltration (CVVHDF) is associated with a better survival than continuous veno-venous hemofiltration (CVVH) among critically ill patients with ARF. In a prospective randomized trial, these two methods were compared in patients undergoing renal replacement therapy in two intensive care units (ICUs). The patients had either CVVH (1-2.5 l/h replacement fluid) or continuous CVVHDF (1-2.5 l/h replacement fluid+1-1.5 l/h dialysate) according to their body weight. 28- and 90-day mortalities, renal recovery, and duration of ICU stay were the main outcome measures. Two hundred and six patients were randomized from October 2000 to December 2003. Twenty-eight-day survivals (%) were, respectively, 39 and 59 (P=0.03) in the CVVH and CVVHDF groups. Three months survivals (%) were, respectively, 34 and 59 (P=0.0005) in the CVVH and CVVHDF groups. Apache II score, age, baseline blood urea nitrogen, and hemodiafiltration (hazard ratio 0.59, 95% confidence interval 0.40-0.87; P=0.008) were independent predictors of survival at 90 days. Renal recovery rate among survivors (71 versus 78% in the CVVH and CVVHDF groups respectively, P=0.62) was not affected by the type of renal replacement therapy. These results suggest that increasing the dialysis dose especially for low molecular weight solutes confers a better survival in severely ill patients with ARF.

Nitric oxide synthase (NOS) inhibition for one week improves renal sodium and water excretion in cirrhotic rats with ascites.

Normalization of the increased vascular nitric oxide (NO) generation with low doses of NG-nitro-L-arginine methyl ester (L-NAME) corrects the hemodynamic abnormalities of cirrhotic rats with ascites. We have undertaken this study to investigate the effect of the normalization of vascular NO production, as estimated by aortic cyclic guanosine monophosphate (cGMP) concentration and endothelial nitric oxide synthase (eNOS) protein expression in the aorta and mesenteric artery, on sodium and water excretion. Rats with carbon tetrachloride-induced cirrhosis and ascites were investigated using balance studies. The cirrhotic rats were separated into two groups, one receiving 0.5 mg/kg per day of L-NAME (CIR-NAME) during 7 d, whereas the other group (CIR) was administrated the same volume of vehicle. Two other groups of rats were used as controls, one group treated with L-NAME and another group receiving the same volume of vehicle. Sodium and water excretion was measured on days 0 and 7. On day 8, blood samples were collected for electrolyte and hormone measurements, and aorta and mesenteric arteries were harvested for cGMP determination and nitric oxide synthase (NOS) immunoblotting. Aortic cGMP and eNOS protein expression in the aorta and mesenteric artery were increased in CIR as compared with CIR-NAME. Both cirrhotic groups had a similar decrease in sodium excretion on day 0 (0.7 versus 0.6 mmol per day, NS) and a positive sodium balance (+0.9 versus +1.2 mmol per day, NS). On day 7, CIR-NAME rats had an increase in sodium excretion as compared with the CIR rats (sodium excretion: 2.4 versus 0.7 mmol per day, P < 0.001) and a negative sodium balance (-0.5 versus +0.8 mmol per day, P < 0.001). The excretion of a water load was also increased after L-NAME administration (from 28+/-5% to 65+/-7, P < 0.05). Plasma renin activity, aldosterone and arginine vasopressin were also significantly decreased in the CIR-NAME, as compared with the CIR rats. The results thus indicate that normalization of aortic cGMP and eNOS protein expression in vascular tissue is associated with increased sodium and water excretion in cirrhotic rats with ascites.

Increased renal and vascular cytosolic phospholipase A2 activity in rats with cirrhosis and ascites.

Indirect evidence suggests that the renal and vascular production of prostaglandins is increased in cirrhosis with ascites. However, the activity of the enzymes regulating the prostaglandin pathway has not been investigated in cirrhosis. The aim of the current study was to determine the activity of phospholipase A2 (PLA2), the key enzyme in the regulation of prostaglandin synthesis, in kidney and vascular tissue obtained from rats with carbon tetrachloride-induced cirrhosis and ascites (n = 9) and control rats (n = 6). PLA2 activity was assayed in vitro using [14C]arachidonyl-phosphatidylcholine (PC) and [14C]arachidonyl-phosphatidylethanolamine (PE) as substrates in the presence of Ca2+. Kidneys from cirrhotic rats had significantly higher PLA2 activity compared with control rats, with both PC and PE (35 +/- 5 and 40 +/- 6 vs. 21 +/- 2 and 26 +/- 3 pmol/mg/min, respectively; P < .05 for both). PLA2 activity was increased in the renal cortex as well as in the renal medulla. Fractionation of the kidney extracts by Mono-Q anion-exchange chromatography showed that the elution position of PLA2 activity corresponded to the cytosolic PLA2 isoform (cPLA2). Increased amounts of cPLA2 protein were found in kidney extracts immunoblotted with an anti-cPLA2 antibody However, reverse-transcriptase polymerase chain reaction (RT-PCR) analysis did not detect any difference in cPLA2 mRNA. PLA2 activity was also higher in aortic tissue from cirrhotic rats than in controls (PC 38 +/- 5 vs. 26 +/- 1 and PE 66 +/- 8 vs. 41 +/- 3 pmol/mg/min; P < .05 for both). Incubation of renal and aortic extracts from cirrhotic rats with anti-cPLA2 antibody reduced PLA2 activity by 64% and 88%, respectively. In conclusion, PLA2 activity is increased in kidneys and vascular tissue from cirrhotic rats with ascites. This can be accounted for by an induction of cPLA2, which would mediate, at least in part, the increased renal and vascular production of prostaglandins in cirrhosis.

Comparison of vascular nitric oxide production and systemic hemodynamics in cirrhosis versus prehepatic portal hypertension in rats.

Nitric oxide (NO) is postulated to play a role in the pathogenesis of arterial vasodilation in chronic portal hypertension. This present study investigates the relationship between systemic hemodynamics and the vascular production of NO, as estimated by measuring cyclic guanosine monophosphate (cGMP) in aortic tissue in two models of chronic portal hypertension in the rat: the partial portal vein ligation (PVL) model and CCl4-induced cirrhosis. NOS was also examined by Western blotting in aortic and mesenteric vessels. Sham-operated rats and rats given phenobarbital were used as controls. PVL rats and rats with cirrhosis and ascites showed a typical pattern of a hyperdynamic circulatory state, when compared with their respective controls: mean arterial pressure; PVL: 113 +/- 2 versus 124 +/- 2, P < .01 and cirrhotics: 103 +/- 5 versus 130 +/- 4 mm Hg, P < .01. Cardiac index; PVL: 32 +/- 2 versus 26 +/- 1, P < .01 and cirrhotics: 51 +/- 3 versus 30 +/- 1 mL . min-1 . 100 gm-1, P < .0001. Systemic vascular resistance; PVL: 3.7 +/- 0.1 versus 4.9 +/- 0.2, P < .01 and cirrhotics: 2.1 +/- 0.2 versus 4.4 +/- 0.2 mm Hg . min-1 100 g-1, P < .0001. Aortic cGMP was markedly increased in cirrhotic rats with ascites (728 +/- 83 fmol/ mg protein) as compared with phenobarbital-treated controls (244 +/- 31 fmol/mg, P < .001). This increase was abolished by chronic administration of N(omega)-nitro-L-arginine methyl ester. By contrast, PVL rats had an aortic cGMP concentration similar to sham-operated controls (282 +/- 16 fmol/mg vs. 274 +/- 33 fmol/mg, P = not significant) and significantly lower than that found in cirrhotic rats with ascites. Expression of cirrhotic aortic endothelial nitric oxide synthase (eNOS) was increased but PVL aortic eNOS did not differ from that of controls, whereas the mesenteric eNOS was increased in both PVL and cirrhotic rats as compared with the controls. These results suggest that vascular NO production is higher in cirrhotic rats than in PVL rats. This increased production may contribute to the more marked abnormalities in systemic hemodynamics seen in experimental cirrhosis as compared with PVL.

Upregulation of endothelial constitutive NOS: a major role in the increased NO production in cirrhotic rats.

Nitric oxide (NO) is postulated to mediate the peripheral arterial vasodilation in cirrhosis. However, it is not known which isoform of the nitric oxide synthase (NOS) is involved in the increased production of NO. This study was therefore undertaken to examine the expression of the NOS isoforms in arteries of cirrhotic rats compared with controls. Cirrhosis was induced by CCl4, and vessels were harvested for immunoblots using antibodies against inducible NOS (iNOS) and endothelial constitutive NOS (ecNOS). Endothelial cells were used as controls for ecNOS, and vascular smooth muscle cells treated with lipopolysaccharide or septic rats were used for iNOS controls. The results demonstrated an upregulation of ecNOS in both the aortas and mesenteric arteries of cirrhotic compared with control rats. Chronic inhibition of NOS decreased ecNOS in cirrhotic vessels. Although iNOS mRNA was found by reverse transcription-polymerase chain reaction in arteries of cirrhotic rats, iNOS protein was not detectable by immunoblotting compared with septic rats, suggesting a low vascular level of this isoform. In conclusion, the ecNOS seems to play a major role in the increased NO production in cirrhotic rats, whereas the role of iNOS remains elusive.

Endothelium-dependent vascular hyporesponsiveness without detection of nitric oxide synthase induction in aortas of cirrhotic rats.

The present experiments were designed to test if induction of nitric oxide synthase (NOS) plays a role in the systemic vasodilation observed in hepatic cirrhosis. Because endotoxin levels are elevated in cirrhosis, and endotoxin stimulates inducible nitric oxide synthase (iNOS) expression in several cell lines, aortas of carbon tetrachloride-induced cirrhotic rats with ascites were evaluated for iNOS expression. Endotoxin-treated rats were studied as positive controls. Phenylephrine contraction was decreased in aortic rings with endothelium from both endotoxin-treated and cirrhotic rats as compared with controls. However, after endothelium denudation, the reduced contractility persisted in endotoxin-treated rats but disappeared in cirrhotic rats. L-Nitro-arginine-methylester (L-NAME), a nonselective inhibitor of NOS, potentiated the phenylephrine contraction of aortic rings with and without endothelium from endotoxin-treated rats but only rings with endothelium from cirrhotic rats. Moreover, aminoguanidine (AG), a preferential inhibitor of iNOS, did not affect phenylephrine contraction of rings with or without endothelium from cirrhotic rats but reversed the blunted response in endotoxin-treated rats. Northern analysis detected iNOS RNA (mRNA) expression in aortas of endotoxin-treated rats but did not detect it from cirrhotic rats. In summary, although several previous studies provide evidence for in vivo overproduction of nitric oxide in cirrhosis, the present results do not support iNOS induction as the source of nitric oxide in aortas of cirrhotic rats. Rather, because the aortic vascular hyporesponsiveness in cirrhosis is endothelium-dependent, overexpression or overstimulation of the endothelial constitutive isoform of NOS appears to be involved.

Normalization of nitric oxide production corrects arterial vasodilation and hyperdynamic circulation in cirrhotic rats.

BACKGROUND & AIMS: Recent studies suggest that production of nitric oxide is increased in cirrhosis. This study determines to what extent this increased production contributes to arterial vasodilation and hyperdynamic circulation in cirrhosis. METHODS: Mean arterial pressure (MAP), cardiac index, and systemic vascular resistance (SVR) were determined in cirrhotic rats with ascites undergoing long-term treatment with different doses of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (3 mg or 0.5 mg.kg-1.day-1). Untreated cirrhotic rats with ascites and controls were also studied. The vascular production of NO was estimated by the aortic concentration of guanosine 3',5'-cyclic monophosphate (cGMP). RESULTS: Untreated cirrhotic rats had significantly lower MAP and SVR and higher cardiac index and aortic cGMP concentration than controls. When administrated to cirrhotic rats, an L-NAME dose of 3 mg.kg-1.day-1 induced a reduction of cGMP concentration less than normal levels. In these rats, MAP and SVR increased to greater than and cardiac index decreased to less than values in controls. By contrast, cirrhotic rats treated with 0.5 mg.kg-1.day-1 L-NAME had similar aortic cGMP concentrations as controls, suggesting a normalization of NO production. This was associated with a normalization of MAP, cardiac index, and SVR and a reduction in the elevated plasma renin activity and vasopressin concentration. CONCLUSIONS: Normalization of vascular NO production corrects systemic hemodynamic abnormalities in cirrhotic rats with ascites.

Beta-adrenoceptor stimulation increases neuropeptide Y release from sympathetic nerves in intact rats.

This study was undertaken to assess in conscious normotensive rats the effects of beta-adrenoceptor stimulation on plasma neuropeptide Y (NPY) levels. Wistar rats were subjected to adrenal demedullation on the right side and were either adrenalectomized or sham-operated on the left side. Eleven days later, the conscious rats were infused i.v. for 30 min with either isoproterenol (10 ng/min) or its vehicle. Plasma NPY levels were significantly lower (23.8 +/- 2.6 pM, means +/- S.E.M., n = 12, P < 0.01) in vehicle-treated medullectomized rats than in corresponding sham-operated controls (36.7 +/- 4.1 pM, n = 12). The medullectomized rats infused with isoproterenol showed plasma NPY levels (36.7 +/- 3.3 pM, n = 11) comparable to those of sham-operated rats having received the vehicle. These data therefore demonstrate that plasma NPY levels are lower in rats without adrenal medulla and that in these animals isoproterenol increases NPY release, most likely by activating pre-synaptic beta-adrenoceptors.

Increased aortic cyclic guanosine monophosphate concentration in experimental cirrhosis in rats: evidence for a role of nitric oxide in the pathogenesis of arterial vasodilation in cirrhosis.

Arterial vasodilation is considered to be the key factor in the development of sodium and water retention leading to ascites formation in cirrhosis. To determine if nitric oxide (NO) is involved in the pathogenesis of arterial vasodilation in cirrhosis, we measured the concentration of cyclic guanosine monophosphate (cGMP), the second messenger of NO, in arterial tissue from rats with carbon tetrachloride-induced cirrhosis. Aortic cGMP concentration was markedly increased in cirrhotic rats, particularly in those with ascites (ascites, 826 +/- 70; no ascites, 597 +/- 48; controls, 331 +/- 25 fmol/mg, ANOVA F = 23.1, P < .0001), and correlated inversely with arterial pressure (r = -.56, P < .0001) and systemic vascular resistance (r = -.69, P = .014) and directly with cardiac index (r = .74, P < .01). The chronic administration of the NO synthesis inhibitor NG-nitro-L-arginine-methyl-ester (L-NAME) (10 mg/kg/day for 7 days) induced a marked reduction in aortic cGMP concentration in cirrhotic rats with ascites to similar values obtained in L-NAME-treated control rats (86 +/- 14 vs. 89 +/- 8 fmol/mg, respectively, NS), indicating that the high-aortic cGMP content in cirrhotic rats was caused by an increased NO synthesis. Mean arterial pressure after L-NAME treatment increased to similar values in both groups of animals. These results suggest that in cirrhosis there is an increased vascular production of NO that may play a role in the pathogenesis of arterial vasodilation.

Expression and preferential inhibition of inducible nitric oxide synthase in aortas of endotoxemic rats.

Septic shock is associated with high mortality. There is in vitro evidence that the induction of nitric oxide synthase (iNOS) in vascular smooth muscle cells may be an important mediator of the systemic vasodilation and hypotension associated with sepsis. In this study, an in vivo murine model of sepsis was used to further examine this important question. Lipopolysaccharide (LPS), the major wall component of gram-negative bacteria, was administered to rats. By the use of a selective cDNA probe for iNOS, mRNA for iNOS was demonstrated in the aortas of these rats. The functional significance of this iNOS was then examined with aminoguanidine, a preferential inhibitor of iNOS. Aminoguanidine reversed the blunted phenylephrine-evoked contraction of endothelium-denuded aortic rings from LPS-treated rats or rings exposed to LPS in vitro. Aminoguanidine did not impair the relaxation of aortic rings with endothelium to acetylcholine, a known stimulator of endothelial NOS. The reversal of LPS-induced vascular hyporesponsiveness by aminoguanidine therefore strongly supports the functional importance of iNOS mRNA expression in the aorta of endotoxemic rats. Future clinical trials in treating septic shock should therefore consider the preferential inhibition of iNOS while maintaining the integrity of endothelial NOS.

Sympathetic nerve activity in conscious renal hypertensive rats treated with an angiotensin converting enzyme inhibitor or an angiotensin II antagonist.

OBJECTIVE: To assess in conscious two-kidney, one clip renal hypertensive rats whether angiotensin converting enzyme (ACE) inhibition with lisinopril, angiotensin II receptor blockade with losartan or vasodilation with sodium nitroprusside have similar effects on intra-arterial mean blood pressure, heart rate and splanchnic nerve activity. RESULTS: A bolus dose of lisinopril or losartan (both 10 mg/kg, intravenously) induced within 2 h an equal reduction in mean blood pressure, whereas sodium nitroprusside infused during the same period (at 10 micrograms/min) lowered mean blood pressure, but less strongly. The heart rate was accelerated significantly more during sodium nitroprusside infusion than during lisinopril or losartan treatment. Splanchnic nerve activity increased significantly only in those rats given sodium nitroprusside. No change in the parameters studied was observed in vehicle-treated rats. The doses of lisinopril and losartan were repeated after 12 and 24 h. Before administration of the last dose, the mean blood pressure was still low. Administration of lisinopril or losartan again 24 h after the initial dose had no further effect on the mean blood pressure, heart rate or splanchnic nerve activity. CONCLUSION: These results obtained in rats with a renin-dependent form of hypertension show that blockade of the renin-angiotensin system for 24 h produces an equivalent blood pressure reduction irrespective of whether it is due to ACE inhibition or angiotensin II antagonism. The results also indicate that there is less reflex activation of sympathetic nerve activity when blood pressure is lowered with a blocker of the renin-angiotensin system rather than with a direct vasodilator such as sodium nitroprusside.