Strain and size combined effects on the GaN band structure: VEELS and DFT study.

A nanoscale study of combined strain/size effects has been performed using monochromated valence electron energy-loss spectroscopy and density functional theory (DFT) calculations to locally explore the valence and conduction bands of a strained 2 nm GaN quantum well inserted between two fully relaxed AlN thick layers. Two main electronic transitions from the valence to the conduction band were experimentally detected and interpreted. The first transition was shown to be a collective oscillation (or plasmon), which was significantly blue-shifted in energy mainly due to the widening of the valence-band top-part. The second, however, had a single-particle character, that is: Ga-3d → Ga-4p, and was weakly affected by strain and size. In addition, our DFT calculations showed that strain and size can be adjusted separately to tune the GaN band-gap energy.

Tele-healthcare for diabetes management: A low cost automatic approach.

In this paper, a telemedicine system for managing diabetic patients with better care is presented. The system is an end to end solution which relies on the integration of front end (patient unit) and backend web server. A key feature of the system developed is the very low cost automated approach. The front-end of the system is capable of reading glucose measurements from any glucose meter and sending them automatically via existing networks to the back-end server. The back-end is designed and developed using n-tier web client architecture based on model-view-controller design pattern using open source technology, a cost effective solution. The back-end helps the health-care provider with data analysis; data visualization and decision support, and allows them to send feedback and therapeutic advice to patients from anywhere using a browser enabled device. This system will be evaluated during the trials which will be conducted in collaboration with a local hospital in phased manner.

[Anesthesia for minimally invasive cardiac procedure]. / Anesthésie pour interventions cardiaques minimalement invasives.

The objectives are to present the different minimally invasive cardiac surgery techniques to repair the mitral valve, TAVI and MitraClip, as well as the implications for the anaesthetist. Evaluate retrospectively the anaesthesist methods, change in monitoring and how the patients are selected. The mitral valve repair by minithoracotomy and video-surgery requires selective left intubation and monitoring by TEE. The TAVI methods seem to be working best under local anaesthesia and sedation for haemodynamic and neurologic monitoring. The MitraClip surgery requires an extensive monitoring during and after surgery. In conclusion, the care of patients that are candidates for a TAVI requires the same level of expertise as anaesthesiology in cardiac surgery. The number of procedures performed under sedation will increase. These patients require multidisciplinary care (surgeons, cardiologists, sonographers and anaesthesiologists) due to comorbidities, and the possible haemodynamic, neurologic and vascular complications. These patients have an Euroscore greater than 20% and a STS score greater than 10%. In our experience, 80% of the cases are done femorally, 17% of the cases are done through the subsclavian artery (Corevalve(®)). 80% of the patients have surgery with a local anaesthesia and sedation. 20% of the patients get surgery with general anaesthesia. For the Edwards-Sapien(®) valve, when the femoral approach is impossible, the patient can get surgery with general anaesthesia using the transapical access.

Is elevated plasma lactate a useful marker in the evaluation of pure carbon monoxide poisoning?

OBJECTIVE: To examine whether CO poisoning induces a significant increase in plasma lactate concentration. DESIGN AND SETTING: Prospective observational clinical study in the emergency department and intensive care unit in a university-affiliated teaching hospital. PATIENTS: 146 pure CO poisonings resulting from dysfunction of gas cookers or water heaters. MEASUREMENTS AND RESULTS: Patients were classified into four neurological impairment groups: 37% were severely, 8% moderately, and 45% mildly intoxicated, while 1% were asymptomatic. We found only very mild increases in plasma lactate concentration (median 2.30 mmol/l) which, however, was significantly correlated with the severity of neurological impairment and blood CO concentration (1.41 mmol/l, Spearman's test r=0.3). CONCLUSIONS: Plasma lactate is mildly elevated in pure CO-exposed patients. This mild increase and the extensive overlap between the groups of neurological impairment severity do not suggest the usefulness of systematic plasma lactate measurement in pure CO poisoning.

Lactoferrin is synthesized by activated microglia in the human substantia nigra and its synthesis by the human microglial CHME cell line is upregulated by tumor necrosis factor alpha or 1-methyl-4-phenylpyridinium treatment.

The presence of the iron-binding protein lactoferrin (Lf) in some specific areas of the central nervous system and particularly in the normal human substantia nigra, where it is found in dopaminergic (DA) neurons and some glial cells, led us to investigate Lf synthesis in this area. Lf mRNA were identified using in situ hybridization and found in small ameboid cells. These cells were identified using immunocytochemistry as activated microglia since they exhibited macrophage markers such as the CD68 and the CR1 antigens. Double immunofluorescent labeling confirmed that the two Lf immunostained cell populations were activated microglia and DA neurons. Since activated microglia contained both Lf and its messenger, these cells are the Lf producing cells. The presence of Lf in DA neurons in which no Lf messengers were visible, might be due to an endocytosis mechanism, DA neurons probably internalizing Lf produced in microglial cells located in their neighborhood. In neuropathological disorders, such as Alzheimer's and Parkinson's diseases, inflammatory process and oxidative stress are events that contribute to neuronal death. Since Lf concentration increases during these pathologies, we studied the level of Lf expression under these different stresses and showed, using RT-PCR, that the immortalized human embryonic microglial CHME cell line produced Lf transcripts under tumor necrosis factor alpha or 1-methyl-4-phenylpyridinium treatment whereas untreated cells did not. These data confirm that Lf is produced only when microglia are activated.

Tumor necrosis factor-alpha increases lactoferrin transcytosis through the blood-brain barrier.

Lactoferrin (Lf) is an iron-binding protein involved in host defense against infection and severe inflammation, which accumulates in the brain during neurodegenerative disorders. Prior to determining Lf function in pathological brain tissues, we investigated its transport through the blood-brain barrier (BBB) in inflammatory conditions. For this purpose, we used a reconstituted BBB model consisting of the coculture of bovine brain capillary endothelial cells (BBCECs) and astrocytes in the presence of tumor necrosis factor-alpha (TNF-alpha). As TNF-alpha can be either synthesized by brain glial cells or present in circulating blood, BBCECs were exposed to this cytokine at their luminal or abluminal side. We have been able to demonstrate that in the presence of TNF-alpha, whatever the type of exposure, BBCECs were activated and Lf transport through the activated BBCECs was markedly increased. Lf was recovered intact at the abluminal side of the cells, suggesting that increased Lf accumulation may occur in immune-mediated pathophysiology. This process was transient as 20 h later, cells were in a resting state and Lf transendothelial traffic was back to normal. The enhancement of Lf transcytosis seems not to involve the up-regulation of the Lf receptor but rather an increase in the rate of transendothelial transport.

Delayed transient loss of consciousness in acute carbon monoxide intoxication.

In acute carbon monoxide intoxication the presence of altered consciousness, ranging from transient loss of consciousness to coma, represents a poor prognostic factor and modifies the approach to therapy. Transient loss of consciousness is, as a rule, contemporaneous to the exposure, generally occurring at the scene of the intoxication. We report an unusual case of delayed transient loss of consciousness, occurring in the absence of any other evident aetiology, in one member of an orchestra composed of 110 members after a mass carbon monoxide poisoning.

Lactoferrin is synthesized by mouse brain tissue and its expression is enhanced after MPTP treatment.

The presence of iron in brain tissue in increased concentrations in Parkinson's disease cases, where it might be responsible for oxidative stress, and the parallel observation that the iron transporter lactoferrin (Lf) was present in increased amounts in surviving neurons, led us to study the synthesis of Lf in a mouse model of Parkinson's disease. In this context, the origin and expression of brain Lf in normal, aged and MPTP (1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine)-treated mice were investigated. Lf immunostaining was observed mainly on microvessels in the cerebral cortex of the adult mice and to a greater extent in older mice. Lf immunoreactivity was also present in the hippocampus only in the aged mouse brains, associated with structures which seemed to be pyramidal neurons and fibers. After RT-PCR (polymerase chain reaction), Lf transcripts were found in mouse brain tissue whatever the age of the animals studied but the level of their expression was very low. No up-regulation of Lf was detectable during aging. Lf distribution and expression in the MPTP-induced Parkinsonian mouse model were also investigated. A marked depletion of dopamine (DA) occurred in the high dose MPTP-treated mice. The level of Lf expression was found to be markedly increased in the same animals and this up-regulation occurred on the first day after MPTP administration. When the brain was stressed by the neurotoxin MPTP, Lf expression increased in line with antioxidant enzymes such as catalase and gamma-glutamylcysteine synthetase, which may permit the protection of brain tissue from oxidative damage induced by the drug.

Two distinct regions of cyclophilin B are involved in the recognition of a functional receptor and of glycosaminoglycans on T lymphocytes.

Cyclophilin B is a cyclosporin A-binding protein exhibiting peptidyl-prolyl cis/trans isomerase activity. We have previously shown that it interacts with two types of binding sites on T lymphocytes. The type I sites correspond to specific functional receptors and the type II sites to sulfated glycosaminoglycans. The interactions of cyclophilin B with type I and type II sites are reduced in the presence of cyclosporin A and of a synthetic peptide mimicking the N-terminal part of cyclophilin B, respectively, suggesting that the protein possesses two distinct binding regions. In this study, we intended to characterize the areas of cyclophilin B involved in the interactions with binding sites present on Jurkat cells. The use of cyclophilin B mutants modified in the N-terminal region demonstrated that the 3Lys-Lys-Lys5 and 14Tyr-Phe-Asp16 clusters are probably solely required for the interactions with the type II sites. We further engineered mutants of the conserved central core of cyclophilin B, which bears the catalytic and the cyclosporin A binding sites as an approach to localize the binding regions for the type I sites. The enzymatic activity of cyclophilin B was dramatically reduced after substitution of the Arg62 and Phe67 residues, whereas the cyclosporin A binding activity was destroyed by mutation of the Trp128 residue and strongly decreased after modification of the Phe67 residue. Only the substitution of the Trp128 residue reduced the binding of the resulting cyclophilin B mutant to type I binding sites. The catalytic site of cyclophilin B therefore did not seem to be essential for cellular binding and the cyclosporin A binding site appeared to be partially involved in the binding to type I sites.

Receptor-mediated transcytosis of lactoferrin through the blood-brain barrier.

Lactoferrin (Lf) is an iron-binding protein involved in host defense against infection and severe inflammation; it accumulates in the brain during neurodegenerative disorders. Before determining Lf function in brain tissue, we investigated its origin and demonstrate here that it crosses the blood-brain barrier. An in vitro model of the blood-brain barrier was used to examine the mechanism of Lf transport to the brain. We report that differentiated bovine brain capillary endothelial cells exhibited specific high (Kd = 37.5 nM; n = 90,000/cell) and low (Kd = 2 microM; n = 900,000 sites/cell) affinity binding sites. Only the latter were present on nondifferentiated cells. The surface-bound Lf was internalized only by the differentiated cell population leading to the conclusion that Lf receptors were acquired during cell differentiation. A specific unidirectional transport then occurred via a receptor-mediated process with no apparent intraendothelial degradation. We further report that iron may cross the bovine brain capillary endothelial cells as a complex with Lf. Finally, we show that the low density lipoprotein receptor-related protein might be involved in this process because its specific antagonist, the receptor-associated protein, inhibits 70% of Lf transport.

Lactoferrin is synthesized by mouse brain tissue and its expression is enhanced after MPTP treatment.

The biological role and origin of human lactoferrin (Lf) within the brain in normal and disease processes are as yet uncharted. In this context the origin and expression of brain Lf in normal and MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated mice were investigated using immunohisto chemistry, PCR amplification and in situ hybridization. Lf immunostaining was observed both on sections of mouse lactating mammary gland, which was used as a positive control, and brains from young, adult and aged mice. Lf immunoreactivity was present in the pituitary gland, the hippocampus and the cortex of mouse brains and to a greater extent in older mice. After reverse transcription, Lf transcripts were also found in these brain sections. Lf distribution and expression in the MPTP-induced parkinsonian mouse model were next investigated. A marked depletion of dopamine and its metabolites: dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxy indole acetic acid (5-HIAA) occurs in the high dose MPTP-treated mice. The level of Lf expression was found to be greatly increased in the same animals but Lf immunoreactivity detected in the same brain region was not found increased in the affected areas.

Contribution of HRTEM to the characterization of silica-incorporated copper-oxide catalysts prepared by the sol-gel technique.

The aim of the present work is a structural characterization study of silica-incorporated copper-oxide (CuO-SiO2) catalysts using HRTEM. The catalysts were prepared by the sol-gel synthetic route. Two calcined catalysts (at 400 degrees C and 800 degrees C, respectively) were analyzed before and after the "NOx + H2" catalytic reaction. It was found that in the 400 degrees C calcined catalyst, the copper is present as CuO crystallites in a structureless form, while in the 800 degrees C calcined catalyst, it was assumed that the copper is automatically dispersed into the silica matrix since no traces of crystalline copper were observed. Under a reducing atmosphere, i.e., after reaction, the former showed large crystallites of CuO, while in the latter a segregation of colloidal crystallites, a mixture of Cu2O and metallic Cu, was observed. It is worth noting that in the case of the 400 degrees C "after-reaction" catalyst, a change in color was observed after a few minutes of air exposure. This result suggested that the reduced copper-oxide phase obtained after reduction was unstable.

Changes in Helicobacter pylori ultrastructure and antigens during conversion from the bacillary to the coccoid form.

In vitro, Helicobacter pylori converts from a bacillary to a full coccoid form via an intermediate U-shaped form. Organisms with a full coccoid form keep a double membrane system, a polar membrane, and invagination structures. Western blots (immunoblots) of sera from colonized patients show that some high-molecular-mass antigenic fractions are expressed only in coccoids. Conversely, fractions of 30 and 94 kDa were more intensively detected in the bacillary forms. These results suggest that (i) coccoid conversion is not a degenerative transformation and (ii) antigens specific to the coccoid forms are expressed in vivo.

Hyperthermia complicating tricyclic antidepressant overdose.

We observed a 51-year-old woman who was admitted for severe amitriptyline overdose. Besides major cardiovascular complications, the patient developed severe hyperpyrexia with a central body temperature of more than 43 degrees C for 5 h. The patient died on day 3 from cardiocirculatory collapse and arrhythmias. Hyperthermia was unresponsive to cooling with ice water, gastric lavage, muscle relaxation, and dantrolene and bromocriptine administration. The possible mechanisms of refractory hyperthermia are discussed.

Mercury oxycyanide and mercuric cyanide poisoning: two cases.

BACKGROUND: Although cyanide poisoning can be serious or fatal, it is typically described as mild when the cyanide is ingested in the form of either mercuric cyanide or mercury oxycyanide. METHODS: We studied two patients with acute cyanide poisoning following ingestion of one of these two agents in each case. RESULTS: Both patients demonstrated features of life-threatening cyanide poisoning, including hemodynamic instability, severe lactic acidosis, and high blood cyanide concentration. One of the patients died, while the second demonstrated signs of mercury intoxication (acute renal failure and severe gastrointestinal symptoms), in addition to cyanide intoxication. CONCLUSION: Ingestion of either mercuric cyanide or mercury oxycyanide can result in life-threatening cyanide intoxication.

Structural determination of two N-linked glycans isolated from recombinant human lactoferrin expressed in BHK cells.

A full-length cDNA coding for human lactoferrin was isolated from a mammary gland library and the recombinant protein was expressed in BHK cells as described by Stowell K. M. et al. [1991, Biochem. J. 276, 349-355]. Two N-linked glycans from purified recombinant lactoferrin were released by hydrazinolysis and analyzed by 400-MHz 1H-NMR spectroscopy. The identified structures corresponded to N-acetyllactosaminic biantennary glycans and were alpha-2,3-disialylated forms (80%) or alpha-2,3-monosialylated (20%) forms. Moreover, 70% of total glycans were alpha-1,6-fucosylated at the GlcNAc residue linked to asparagine. In regard to its glycan moiety, the recombinant glycoprotein is close to native lactoferrins from milk or leucocytes but shows specific structural features which should be taken into account prior to in vivo and in vitro biological studies.

Rat mammary-gland transferrin: nucleotide sequence, phylogenetic analysis and glycan structure.

The complete cDNA for rat mammary-gland transferrin (Tf) has been sequenced and also the native protein isolated from milk in order to analyse the structure of the main glycan variants present. A lactating-rat mammary-gland cDNA library in lambda gt10 was screened with a partial cDNA copy of rat liver Tf and subsequently rescreened with 5' fragments of the longest clones. This produced a 2275 bp insert coding for an open reading frame of 695 amino acid residues. This includes a 19-amino acid signal sequence and the mature protein containing 676 amino acids and one N-glycosylation site in the C-terminal domain at residue 490. Phylogenetic analysis was carried out using 14 translated Tf nucleotide sequences, and the derived evolutionary tree shows that at least three gene duplication events have occurred during Tf evolution, one of which generated the N- and C-terminal domains and occurred before separation of arthropods and chordates. The two halves of human melanotransferrin are more similar to each other than to any other sequence, which contrasts with the pattern shown by the remaining sequences. Native rat milk Tf is separated into four bands on native PAGE that differ only in their sialic acid content: one biantennary glycan is present containing either no sialic acid residues or up to three. The complete structures of the two major variants were determined by methylation, m.s. and 400 MHz 1H-n.m.r. spectroscopy. They contain either one or two neuraminic acid residues (alpha 2-->6)-linked to galactose in conventional biantennary N-acetyl-lactosamine-type glycans. Most contain fucose (alpha 1-->6)-linked to the terminal non-reducing N-acetylglucosamine.

Stimulation of inositide degradation in clumping Stigmatella aurantiaca.

Numerous external signals which activate inositol phospholipid hydrolysis in eukaryotes are known; probably all of these signals are transduced by G proteins. So far, neither signal-transducing G protein nor receptor-regulated phospholipase C has been found in prokaryotes. However, a group of bacteria, the myxobacteria, displays cellular and tissue-like differentiation; therefore, it appeared that a search for the various activities involved in a signal-activated phosphatidylinositol cycle might be rewarding. Here, we report that in Stigmatella aurantiaca, under conditions which promote clumping, inositol phospholipid synthesis and degradation were stimulated with the resulting formation of inositol phosphate and inositol bisphosphate. The turnover was Ca2+ dependent and was increased by fluoride ions. Membrane preparations from these cells showed a phospholipase C activity which increased with the stage of incubation and which was stimulated by GTP gamma S, suggesting G protein dependency. To what extent this system in a prokaryotic cell shares properties of the phosphatidylinositol cycle in eukaryotes remains unexamined.