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We find significant differences between degradation and healing at the surface or in the bulk for each of the different APbBr3single crystals (A = CH3NH3+, methylammonium (MA); HC(NH2)2+, formamidinium (FA); and cesium, Cs+). Using 1- and 2-photon microscopy and photobleaching we conclude that kinetics dominate the surface and thermodynamics the bulk stability. Fluorescence-lifetime imaging microscopy, as well as results from several other methods, relate the (damaged) state of the halide perovskite (HaP) after photobleaching to its modified optical and electronic properties. The A cation type strongly influences both the kinetics and the thermodynamics of recovery and degradation: FA heals best the bulk material with faster self-healing; Cs+protects the surface best, being the least volatile of the A cations and possibly through O-passivation; MA passivates defects viamethylamine from photo-dissociation, which binds to Pb2+. DFT simulations provide insight into the passivating role of MA, and also indicate the importance of the Br3−defect as well as predicts its stability. The occurrence and rate of self-healing are suggested to explain the low effective defect density in the HaPs and through this, their excellent performance. These results rationalize the use of mixed A-cation materials for optimizing both solar cell stability and overall performance of HaP-based devices, and provide a basis for designing new HaP variants.

We show a method to measure the topological charge of orbital angular momentum radiation in single-shot by exploiting the intrinsic local curvature of the helicoidal wavefront. The method is based on oriented Hartmann cells in a suitable detection scheme. We show experimental results and propose a Shack–Hartmann configuration with sectored photodiodes to improve resolution and detection time. The method can be applied for telecommunication applications in the far field of the radiation beam and more in general to measure the topological charge from a small portion of the radiation wavefront.

Micro- and macro-vascular complications are the leading causes of morbidity and mortality in type 1 and type 2 diabetic patients. Despite the vast clinical experience linking diabetic metabolic abnormalities to cardiovascular lesions, the molecular basis of individual susceptibility to diabetic cardiovascular injury is still largely unknown. Significant advances in this area may come from studies on suitable animal models. Although no animal model can accurately reproduce the human disease, experimental studies in animals have the great advantage to eliminate factors such as ethnicity, economic and geographic variables, drug interactions, diet, gender and age differences that importantly limit clinical studies. Indeed, appropriate animal models have provided important information on genetic and environmental risks of diabetes, and helped to dissect molecular mechanisms underlying the development, progression and therapeutic control of this disease. Unfortunately, none of the diabetic models presently available fully mimics the human syndrome. Therefore, the current knowledge on the pathogenesis of cardiovascular complications relies on the evaluation of distinct phenotypes from various diabetic models. In addition to strains prone to diabetes, this disease can be induced by surgical, pharmacological or genetic manipulation in several animal species. Rodents are the most used, although some studies are still performed in larger animals as rabbits, cats, pigs or monkeys. Far from being exhaustive, this work should serve as a general overview of the most relevant clues provided by major species and models for the overall comprehension of cardiovascular complications in type 1 and type 2 diabetes.

The Trypanosoma cruzi cyclophilin gene family comprises 15 paralogues whose nominal masses vary from 19 to 110 kDa, namely TcCyP19, TcCyP20, TcCyP21, TcCyP22, TcCyP24, TcCyP25, TcCyP26, TcCyP28, TcCyP29, TcCyP30, TcCyP34, TcCyP35, TcCyP40, TcCyP42 and TcCyP110. Under the conditions used, only some of the T. cruzi cyclophilin paralogue products could be isolated by affinity chromatography. The 15 paralogues were aligned with 495 cyclophilins from diverse organisms. Analyses of clusters formed by the T. cruzi cyclophilins with others encoded in various genomes revealed that 8 of them (TcCyP19, TcCyP21, TcCyP22, TcCyP24, TcCyP35, TcCyP40, TcCyP42 and TcCyP110) have orthologues in many different genomes whereas the other 7 display less-defined patterns of their sequence attributes and their classification to a specific group of cyclophilin's orthologues remains uncertain. Seven epimastigote cDNA clones encoding cyclophilin isoforms were further studied. These genes were found dispersed throughout the genome of the parasite. Amastigote and trypomastigote mRNAs encoding these 7 genes were also detected. We isolated 4 cyclosporin A-binding proteins in T. cruzi epimastigote extracts, which were identified by mass spectrometry as TcCyP19, TcCyP22, TcCyP28 and TcCyP40. Cyclosporin A-binding to these cyclophilins might be of importance to the mechanism of action of Cyclosporin A and its non-immunosuppressive analogues, whose trypanocidal effects were previously reported, and therefore, of potential interest in the chemotherapy of Chagas' disease.

Arginine, initially classified as a non-essential amino acid, participates to multiple biological processes including release of several hormones, collagen synthesis during wound healing, antitumor and antibacterial activities and non-specific immunity. Nitric oxide synthase and arginase competes for L-arginine as a substrate and this event appears to play a key role in the regulation of the inflammatory process. In this framework recent studies have identified complex patterns of interactions among these enzymes. This review will emphasizes some effects of L-arginine on immune cell functions, including triggering of L-arginine-nitric oxide and arginase pathways, its biological properties and therapeutical applications.

Second-harmonic cross-correlation operates a selection in time-phase among the randomly dephased contributions to an optical field that propagated through a scattering medium. It can thus be used to selectively detect the weak contribution remaining coherent with the incident field.

The aim of our study was to further investigatethe pathophysiological mechanism underlying idiopathicchronic constipation (ICC), a disorder of colonicmotility. A possible alteration of excitatory and inhibitory neurotransmission and also the roleof inhibitory neurotransmitters such as nitric oxide(NO), 5′-adenosine triphosphate (ATP), andvasoactive intestinal peptide (VIP) has been evaluatedon preparations of distal colon from patients with or withoutICC. The isometric tension was recorded from isolatedcircular muscle strips of both experimental groupsduring pharmacological and electrical field stimulation (EFS). The contractile response obtained byacetylcholine (ACh 20 μM), EFS (20 Hz, 20 V, 1 msec,pulse trains lasting 1 min) and substance P (SP 1 μM)was significantly lower in ICC than in controlpreparations. The effect of inhibitory nonadrenergic,noncholinergic innervation was evaluated using EFS atlow frequencies (0.5-8 Hz), after cholinergic andsympathetic blockade with atropine (3 μM) andguanethidine (3 μM). The maximum relaxation valueexpressed as percentage of inhibition of SP-inducedcontraction was significantly higher in ICC than incontrol preparations (87 ± 2.4 and 67 ±6.3, respectively; P < 0.05). Experiments with substances thatantagonize or reduce the effect of putative inhibitorymediators (VIP 6-28, apamin andNG-nitro-L-arginine) suggest that analteration in NO and ATP release is present in ICC preparations. In particularat a higher inhibitory frequency NO-mediated relaxationis enhanced in ICC vs control, supporting the hypothesisthat excessive NO production may be involved in pathophysiological mechanism ofconstipation.

The goal of the present study was to investigate a possible role for regulators of G protein-signaling (RGS) proteins in opioid receptor (OR) desensitization using cultured Xenopus laevis dermal melanophores. Morphine-induced pigment aggregation in a melanophore cell line stably expressing the murine mu OR (muOR) was quantified over time. Responses of the muOR (a G(i)-linked receptor) exhibited a time-dependent desensitization, which varied with the concentration of morphine used. In contrast, much less desensitization was observed in response to melatonin, effects mediated through the cells' endogenous melatonin receptor (which is also G(i)-linked). To further study OR desensitization, melanophores lacking a muOR were transiently transfected with plasmids encoding the muOR alone or in combination with plasmids encoding one of several RGS subtypes (RGS1, RGS2, RGS3, or RGS4). Overexpression of RGS2, but not the other RGS subtypes, produced a rightward shift in the morphine concentration-response curve. RGS protein overexpression also decreased the magnitude of morphine-induced responses. Finally, the effect of a mutant form of Galpha(i1), which is insensitive to RGS action, was investigated with respect to its ability to alter the response of the muOR to morphine. Expression of the mutant Galpha(i1) prolonged morphine-induced pigment aggregation and produced leftward shifts in concentration-response curves, compared with expression of wild-type Galpha(i1). These results demonstrate that specific RGS proteins can dampen signals initiated by agonist activation of the muOR, and support a possible role for RGS proteins in OR desensitization.

Praseodymium-doped fluoride fiber amplifiers at 1300 nm with different configurations and pumping sources have been developed. Performances obtained with various pumping wavelengths and active fibers are compared. The best results obtained with pumping at 1047 nm are 32.4 dB internal gain and 13.4 dBm saturation power. Copyright 1995, 1999 Academic Press

The present investigation was aimed to examine non-specific immunologic capabilities of spontaneously hypertensive rats (SHR) during the development of hypertension. In vitro phagocytosis and oxidative killing exerted by monocytes, polymorphonuclear cells (PMN) and splenic macrophages (SpMø) were evaluated in SHR at 5-, 8-, and 24-weeks of age. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls.Results showed that in pre-hypertensive stage (5-wk) there was no difference between SHR and WKY rats with regard to non-specific immunologic functions. Statistically significant differences in both phagocytosis and oxidative killing arose in early hypertensive stage (8-wk) and became more marked in adult SHR with established hypertension (24-wk).In conclusion, our data provide evidence of novel immunologic abnormalities in SHR in terms of ingestion and bactericidal phagocytic capabilities. The mechanisms responsible for these impaired immunologic functions may depend on various suppressive factors which will be object of discussion.

The aim of the liresent study was to investigate putative mechanisms implicated in the impaired phagocytic response of spontaneously hypertensive rats (SHR)1. The effect of in vitro treatment with isoproterenol (ISO), a β-adrenergic drug, on phagocytosis and respiratory burst by splenic macrophages (SpMØ) from normotensive Wistar-Kyoto rats (WKY) and SHR with established hypertension, respectively, was evaluated. Furthermore, the relaxant effect of ISO was determined in phenilephrine-precontracted thoracic aorta strips from SHR compared with age-matched WKY rats. Results indicate that exposure of rat SpMØ to ISO generate a significant and dose-dependent reduction of phagocytosis and oxidative burst which was antagonized, almost completely, by the β-adrenergic antagonist propranolol (PRO). Unlike normotensive, in hypertensive rats treatment with ISO fail to modulate phagocytosis and respiratory burst activity by SpMØ. At vascular level, aortic relaxation by ISO was reduced in SHR when compared to WKY rats. These findings suggest that SHR exhibit changes not only in vascular, but also in macrophage β-adrenoceptor-mediated responses. It is postulable that sympathetic overactivity could be responsible for impaired phagocytic functions and β-receptor alterations observed in SHR.

The development of optical fibre amplifiers has caused an impressive evolution in optical telecommunications systems since the end of the 1980s. The widespread application of active fibre amplifiers requires accurate tools to design and simulate these devices in very different operating conditions. The present work describes some physical aspects of active fibre amplifiers and a numerical model for the analysis of active optical fibres that can be applied to investigate spatial and spectral properties of amplifiers for the transmission windows of optical fibre telecommunications. Finally, various design issues relevant to the investigation of optimal fibre design of silica, fluoride erbium-doped and fluoride praseodymium-doped fibres are discussed and illustrated by means of examples.

Mode degeneration and mode conversion in multimode optical fibres are the main subjects of this work. In particular it is shown how fluctuations of the core shape can cause a rapid degeneration among the modes with the same azimuthal mode number. This allows a rigorous single variable approach to the second problem obtaining evident simplifications. The formalism proposed is applied to the study of mode distribution in the general case of microbending, of core-radius fluctuations in fibres with power law profiles and for simultaneous presence of microbending and ellipticity in parabolic fibres with differential mode attenuation.

The problem of scattering in multimode optical fibres is treated in a rigorous way by means of both a ray and a statistical approach. These two methods are interlaced and harmonized. Applications to microbending, ellipticity, core radius and maximum numerical aperture variations, and fluctuations of index profile shape are performed. Useful results about power distribution and fibre attenuation are derived in each case.

The refractive-index distribution of single-mode optical fibres can be obtained from transmitted near-field intensity measurements. The generalisation of the method from conventional fibres to noncircularly symmetric guides (e.g. polarisation-maintaining fibres) is discussed. Results obtained both on circular and on polarisation-maintaining fibres are presented.

A new dispersion measurement for monomode fibres is proposed. It is based on an elaboration of the near-field intensities at different wavelengths. The measurement is considerably simplified and the results are highly accurate.

A new discretisation procedure based on a finite difference approach is presented for the analysis of arbitrary two-dimensional optical dielectric waveguides. It is based on a longitudinally variant discretisation grid that allows an accurate treatment of waveguide changes of geometry to be obtained. Comparisons with the well known beam propagation method show a strong improvement in accuracy and computational time saving.

A new, easily implementable technique for mode-field radius measurement is described. It is based on a dynamical filtering and the detection of two harmonics of the fibre output radiation. The results are presented and discussed.

A finite difference method based on a Crank–Nicolson discretisation procedure has been implemented and applied to the analysis of propagation of optical beams in dielectric waveguides. It is based on a new formula which takes into account the correct boundary conditions. Comparisons with the well known BPM technique show a definite improvement in computer time saving, accuracy and ease of use.